Neurology Flashcards
1
Q
- Nyeri retro-orbital dan paralise saraf keenam
A. Sindroma TOLOSA - HUNT
B. Sindroma GRANDENIGO
C. Sindroma RAEDER
A
(B)
Raeder’s para trigeminal neuralgia is often localized adjacent to the trigeminal nerve as it courses through the middle cranial fossa. The cause of this syndrome is often unclear, but it is usually characterized by a partial Horner’s syndrome and unilateral trigeminal nerve problems, including tic-like pain, numbness, and/or masseter weakness. Gradenigo’s syndrome, also known as apical petrositis, often consists of the classic triad of abducens nerve palsy, retroorbital pain, and a draining ear. Tolosa-Hunt syndrome is a diagnosis of exclusion; this condition is believed to result from inflammation adjacent to the superior orbital fissure. It is characterized by painful ophthalmoplegia, cranial nerves III, IV, and VI palsies, and recurrent attacks and remissions; it is typically treated with intravenous steroids (Greenberg, pp. 581-582 )
2
Q
- Optalmoplegia yang terasa sangat nyeri disertai paralise saraf ketiga, keempat dan kelima
A. Sindroma TOLOSA - HUNT
B. Sindroma GRANDENIGO
C. Sindroma RAEDER
A
A
Raeder’s para trigeminal neuralgia is often localized adjacent to the trigeminal nerve as it courses through the middle cranial fossa. The cause of this syndrome is often unclear, but it is usually characterized by a partial Horner’s syndrome and unilateral trigeminal nerve problems, including tic-like pain, numbness, and/or masseter weakness. Gradenigo’s syndrome, also known as apical petrositis, often consists of the classic triad of abducens nerve palsy, retroorbital pain, and a draining ear. Tolosa-Hunt syndrome is a diagnosis of exclusion; this condition is believed to result from inflammation adjacent to the superior orbital fissure. It is characterized by painful ophthalmoplegia, cranial nerves III, IV, and VI palsies, and recurrent attacks and remissions; it is typically treated with intravenous steroids (Greenberg, pp. 581-582 )
3
Q
6. Seorang anak berusia 7 tahun dibawa ke ruang gawat darurat dengan gejala terus tertawa tanpa dapat dikendalikan (kejang gelastik) dan pubertas prekok. Pemeriksaan MRI otak bisa menunjukkan lokasi kelainan dimana? A. Amigdala B. Hipokampus C. Girus singulate D. Hipotalamus E. Sella turcica
A
D.
An .MRI study of the brain in a patient with seizures accompanied by involuntary laughter (gelastic seizures) that alternates with crying or sobbing spells would likely show a lesion in the hypothalamus. A small series of cases hm•e been reported in the literature to date describing this phenomenon; in one report, 4 of 16 patients were found to harbor a hypothalamic hemartoma. Gelastic seizures or laughing fits have been reported to occur in up to 2 1 % of patients with hypothalamic hemartomas. Most patients with this lesion present with isosexual precocious puberty by the age of 3 years, although patients as old as 8 years have been reported. Hypothalamic hemartomas may be associated with midline deformities such as callosal agenesis, optic malformations, and hemispheric dysgenesis ( Kaye and Laws, pp. 593-596).
4
Q
Seorang pekerja bangunan, 52 tahun mencatat beberapa kelemahan pada tangannya saat dia
bekerja, yang diikuti oleh semakin parahnya masalah bicara dan menelan beberapa bulan kemudian. Meski pun kelemahannya adalah letih dan gatal extrenitas atas & bawah, pemeriksaan fisik tidak mencatat adanya mati rasa atau gangguan panca indera. Lengan, kaki,
dan lidahnya mengalami faskikulasia dan atropi yang jelas. serta gangguan refleks hiperaktif dan tanda-tanda Babinski
7. Diagnosis yang paling mungkin pada laki-laki usia pertengahan ini adalah sebagai berikut:
A. Mielopati servikal
B. Sklerosis majemuk
C. Miastenia Gravis
D. Sindroma GUILLAIN-BARRE
E. Sklerosis lateral amiotropik
A
E
In this patient , the multiple motor deficits and signs of anterior horn cell disease unaccompanied by any sensory abnormalities suggest a diagnosis of amyotrophic lateral sclerosis (ALS) . Most individuals with ALS die withir1 5 years of symptom onset, especially if there are both upper and lower motor neuron signs. There is a very high incidence of this disease among the Chamorro Indians of Guam, and there is also an association between ALS and a Parkinsonlike dementia complex (Merritt, pp. 7 10-7 12) .
5
Q
Seorang pekerja bangunan, 52 tahun mencatat beberapa kelemahan pada tangannya saat dia
bekerja, yang diikuti oleh semakin parahnya masalah bicara dan menelan beberapa bulan kemudian. Meski pun kelemahannya adalah letih dan gatal extrenitas atas & bawah, pemeriksaan fisik tidak mencatat adanya mati rasa atau gangguan panca indera. Lengan, kaki,
dan lidahnya mengalami faskikulasia dan atropi yang jelas. serta gangguan refleks hiperaktif dan tanda-tanda Babinski
8. Apa prognosisnya?
A. Relatif baik jika kadar gula di dalam darah dinaikkan
B. Seringkali pasien akan sembuh dalam jangka waktu yang lama dengan perawatan plasmaperesis dan steroid
C. Baik sekali jika diberikan medikasi antikolinergik
D. Pembedahan dapat membantu mencegah gejalanya menyebar menjadi neurologik
E. Seringkali akan menjadi fatal dalam jangka waktu 3 – 5 tahun
A
E
In this patient , the multiple motor deficits and signs of anterior horn cell disease unaccompanied by any sensory abnormalities suggest a diagnosis of amyotrophic lateral sclerosis (ALS) . Most individuals with ALS die withir1 5 years of symptom onset, especially if there are both upper and lower motor neuron signs. There is a very high incidence of this disease among the Chamorro Indians of Guam, and there is also an association between ALS and a Parkinsonlike dementia complex (Merritt, pp. 7 10-7 12) .
6
Q
Seorang pekerja bangunan, 52 tahun mencatat beberapa kelemahan pada tangannya saat dia
bekerja, yang diikuti oleh semakin parahnya masalah bicara dan menelan beberapa bulan kemudian. Meski pun kelemahannya adalah letih dan gatal extrenitas atas & bawah, pemeriksaan fisik tidak mencatat adanya mati rasa atau gangguan panca indera. Lengan, kaki,
dan lidahnya mengalami faskikulasia dan atropi yang jelas. serta gangguan refleks hiperaktif dan tanda-tanda Babinski
9. Penyakit ini bisa berasosiasi dengan penyakit atau kelainan apa?
A. Kejang-kejang bayi
B. Sindroma KLUVER-BUCY
C. Parkinson
D. Sindroma Down
E. Degenerasi sistem saraf otonom
A
C
In this patient , the multiple motor deficits and signs of anterior horn cell disease unaccompanied by any sensory abnormalities suggest a diagnosis of amyotrophic lateral sclerosis (ALS) . Most individuals with ALS die withir1 5 years of symptom onset, especially if there are both upper and lower motor neuron signs. There is a very high incidence of this disease among the Chamorro Indians of Guam, and there is also an association between ALS and a Parkinsonlike dementia complex (Merritt, pp. 7 10-7 12) .
7
Q
- Mutisme akinetik merujuk pada keadaan, dimana pasien meskipun tampak bangun, tetapi tetap tak bergerak dan diam. Keadaan umumnya dikaitkan dengan lesi yang melibatkan seluruh struktur di bawah ini, KECUALI
A. Hipotalamus
B. Sistem aktivasi dopaminergik menanjak
C. Girus singulate
D. Talamus
E. Nucleus raphe
A
E
Animal studies and case reports have disclosed two primary lesion sites that
8
Q
- Semua di bawah ini adalah karakteristik meningitis tuberculosa, KECUALI
A. Tingkat kematiannya seringkali lebih tinggi dibandingkan dengan meningitis bakterial
B. Perawatan awalnya meliputi isoniazid, rifampin, pirazinamid, dan etambutol
C. Jika perawatannya dimulai sejak dini, maka perawatan ini efektif dalam mencegah hasil yang buruk pada mayoritas pasien
D. Fokus utama infeksi tuberculosis kemungkinan berasal dari daerah di luar otak.
E. Meningitis bakterial ditandai oleh meningitis basal, sementara pada meningitis, basis pada otak relatif bebas infeksi.
A
E.
Tuberculous meningitis is always secondary to an infection elsewhere in the body, especially the lungs. It differs from infections caused by other common bacteria in that the time course is often more protracted, the mortality rate is higher, and the CSF changes may not be very helpful or diagnostic initially. Tuberculous meningitis is also often characterized by marked basal meningitis, as . opposed to bacterial meningitis, which tends to produce a n;eningeal reaction over the convexities of the brain. The diagnosis is often established by isolating the organism from the CSF. CSF findings include slightly increased pressure, moderate pleocytosis of 25 to 500 cells/mm3 with lymphocytic predominance, increased protein content, decreased glucose values in the range of 20 to 40 mg/dL, and the absence of growth on routine CSF culture media. The natural course of the disease is death within 6 to 8 weeks if left untreated. With early diagnosis and treatment, the recovery rate approaches 90%. Treatment is commonly started with four drugs , including isoniazid, rifampin, pyrazinamide, and ethambutol; streptomycin is an alternative in case one of the agents cannot be used. The drug regimen can be modified later, once sensiti\ •ities of the mycobacterium are known, but are typically administered for 18 to 24 months (Merritt, pp. 108-111).
9
Q
12. Sindrom GERSTMANN meliputi semua hal di bawah ini, KECUALI A. Agnosia jari B. Akalkulia C. Agrafia D. Kebingungan kanan dan kiri E. Anosognia
A
E.
Gerstmann’s syndrome can result from injury in the dominant inferior parietal lobule (angular and supramarginal gyri) and is characterized by confusion of the right and left limbs, difficulty in distinguishing the fingers on the hand (finger agnosia) , acalculia, and agraphia. Anosognosia, which is characterized by unawareness of the opposite side of the body, often results from lesions in the nondominant • parietal lobe and is not a feature of Gerstmann’s syndrome (Carpenter, p. 429).
10
Q
13. Cacad biokimiawi pada penyakit REFSUM telah dipastikan sebagai kekurangan enzim apa? A. Arilsulfatase A B. Pitanoil-koenzim A hidroksilase C. β-glukosilase D. α-galaktosidase E. Asam seramidase
A
B.
Refsum disease is an autosomal recessive disease caused by a deficiency of phytanoyl-coenzyme A hydroxylase and accumulation of phytanic acid in the body. This disease is unique among the lipidoses because phytanic acid is not synthesized in the body but is obtained exclusively from the diet. Limiting phytanic acid or its precursor, phytol (dairy products, ruminant fat, and chlorophyl-containing foods), from the diet reduces plasma phytanic acid levels. Plasmapheresis may further help eliminate phytanic acid from the body in seYere cases. Symptoms typically begin in childhood but in some patients may be delayed until the fifth decade. Night blindness typically appears first, followed by limb weakness and gait abnormalities. Some patients may develop psychiatric symptoms, peripheral neuropathy, pigmentary retinopathy, deafness, cataracts, bone deformities, or cardiac arrhythmias (Merritt, pp. 514-529 , 539-540 ) .
11
Q
Seorang perempuan berusia 65 tahun didiagnosis skizofrenia paranoid dan menjalani rawat inap. Perawatan dimulai dengan pemberian risperidon dosis rendah (Risperdal). Beberapa hari sebelum masuk perawatan rumah sakit ini, dia mengeluh karena sakit perut yang semakin lama semakin parah. Hasil pemeriksaan menunjukkan tidak terdapatnya kejang perut, tapi ditemukan adanya demam, leukositosis, diare, hipertensi dan tacikardia. Pemeriksaan melalui pencitraan otak dan rongga perut tidak begitu mencolok.
14. Diagnosis manakah yang paling mungkin?
A. Gangguan konversi
B. Skizofrenia dengan fitur-fitur depresif
C. Poripiria intermiten akut
D. Appendisitis
E. Sindroma infuse dengan picuan riperidon
A
C
The symptoms o f acute intermittent porphyria (AlP) are most commonly gastrointestinal, psychiatric, and neurologic. The precise etiology remains uncertain, but large and small nerve fibers, as well as autonomic nerves, have been shown to be affected. Abdominal pain is the most common finding, but often occurs concomitantly with a psychiatric or neurologic disorder. There is usually no abdominal rigidity, but fever, leukocytosis, diarrhea, tachycardia, and hypertension are often evident. Appendicitis or other serious abdominal problems may be difficult to rule out; in fact, some patients have been subjected to laparotomy for abdominal exploration. The most reliable test to confirm AlP is the assay for porphobilinogen deaminase activity in red blood cells, but often a good clinical histor
12
Q
Seorang perempuan berusia 65 tahun didiagnosis skizofrenia paranoid dan menjalani rawat inap. Perawatan dimulai dengan pemberian risperidon dosis rendah (Risperdal). Beberapa hari sebelum masuk perawatan rumah sakit ini, dia mengeluh karena sakit perut yang semakin lama semakin parah. Hasil pemeriksaan menunjukkan tidak terdapatnya kejang perut, tapi ditemukan adanya demam, leukositosis, diare, hipertensi dan tacikardia. Pemeriksaan melalui pencitraan otak dan rongga perut tidak begitu mencolok.
15. Uji atau intervensi yang paling dapat diandalkan untuk menguatkan diagnosis ini meliputi:
A. Sintase asam aminolevulinik
B. Uji sintetase homokistein
C. Uji aktivitas deaminase porpobilinogen
D. seliotomi eksploratoris
E. Diskriminasi medikasi antipsikotik dengan resolusi gejala
A
C
The symptoms o f acute intermittent porphyria (AlP) are most commonly gastrointestinal, psychiatric, and neurologic. The precise etiology remains uncertain, but large and small nerve fibers, as well as autonomic nerves, have been shown to be affected. Abdominal pain is the most common finding, but often occurs concomitantly with a psychiatric or neurologic disorder. There is usually no abdominal rigidity, but fever, leukocytosis, diarrhea, tachycardia, and hypertension are often evident. Appendicitis or other serious abdominal problems may be difficult to rule out; in fact, some patients have been subjected to laparotomy for abdominal exploration. The most reliable test to confirm AlP is the assay for porphobilinogen deaminase activity in red blood cells, but often a good clinical history
13
Q
Seorang perempuan berusia 65 tahun didiagnosis skizofrenia paranoid dan menjalani rawat inap. Perawatan dimulai dengan pemberian risperidon dosis rendah (Risperdal). Beberapa hari sebelum masuk perawatan rumah sakit ini, dia mengeluh karena sakit perut yang semakin lama semakin parah. Hasil pemeriksaan menunjukkan tidak terdapatnya kejang perut, tapi ditemukan adanya demam, leukositosis, diare, hipertensi dan tacikardia. Pemeriksaan melalui pencitraan otak dan rongga perut tidak begitu mencolok.
16. Sakit perutnya dapat segera sembuh secara dramatis dengan obat yang mana?
A. Propranolol
B. Barbiturat
C. Sulfonamid
D. Gabapentin
E. Merkuri
A
A
The symptoms o f acute intermittent porphyria (AlP) are most commonly gastrointestinal, psychiatric, and neurologic. The precise etiology remains uncertain, but large and small nerve fibers, as well as autonomic nerves, have been shown to be affected. Abdominal pain is the most common finding, but often occurs concomitantly with a psychiatric or neurologic disorder. There is usually no abdominal rigidity, but fever, leukocytosis, diarrhea, tachycardia, and hypertension are often evident. Appendicitis or other serious abdominal problems may be difficult to rule out; in fact, some patients have been subjected to laparotomy for abdominal exploration. The most reliable test to confirm AlP is the assay for porphobilinogen deaminase activity in red blood cells, but often a good clinical histor
14
Q
- Hal tersebut di bawah ini merupakan karakteristik neuropati dipteritis
(Diphtheritic Neuropathy), KECUALI
A. Organisme yang diisolasi dari laring dan paring seringkali adalah Corynebacterium diptheriae
B. Orgaisme-organisme seringkali melepaskan endotoksin yang dapat menyebabkan miokarditis atau neuropati asimetris
C. Neuropati seringkali dimulai dengan gangguan pada fungsi penglihatan
D. Dipteri dan neuropati yang berkaitan dengannya dapat dicegah dengan imunisasi
E. Seringkali menyebabkan neuropati demielinasi
A
B.
Diphtheria infection produces neuropathy in about 20% of infected patients. Corynebacterium diphtheriae is often isolated from the throat and releases an exotoxin (not endotoxin) that can cause myocarditis or symmetric neuropathy. The neuropathy is often characterized by poor visual accommodation, paresis of. throat muscles, quadriparesis, and slow ner;e conduction velocities secondary to demyelinating neuropathy. This disease can be prevented by immunization and often responds to antibiotics (Merritt, pp. 620-621).
15
Q
- Luka psikosis dari Korsakoff seringkali melibatkan struktur otak yang mana?
A. Nucleus dorsomedial (DM) dari thalamus
B. Nukleus globose
C. Amigdala
D. Vermis dari serebelum
E. Girus dentate
A
A.
Although \-ernicke’s and Korsakoff’s syndromes are often described together, these appear to be two distinct entities that result from thiamine deficiency. Wernicke’s syndrome consists of mental symptoms (global confusional state) , eye movement problems (nystagmus, lateral rectus palsy, and lateral gaze palsy), and gait ataxia, while Korsakoff’s syndrome is a purely amnestic syndrome usually associated with lesions in the DM nucleus of the thalamus and mammillary bodies. With treatment (thiamine) , ocular abnormalities, nystagmus, and global confusion often improve to varying degrees, leaYing Korsakoff’s amnesia in about 80% of patients. ( Merritt, pp. 924-925).
16
Q
- Di antara ciri klinis di bawah ini, ciri klinis manakah yang merupakan ciri klinis neuroborreliosis?
A. Radikulitis sensori yang terasa sangat sakit dan muncul sekitar 3 minggu setelah eritema migrans
B. Mononeuropati kranial
C. Paresis anggota badan
D. Arthalgia
E. Vertigo
A
A.
Lyme disease
17
Q
- Diantara gangguan di bawah ini, manakah yang BUKAN merupakan kelainan DNA mitokondrial?
A. Miopati mitokondrial, enselopalopati, asidosis laktik, dan episode-episode mirip stroke (MELAS)
B. Epilepsi mioklonik dengan serat-serat merah (MERRF)
C. Neuropati optik bawaan dari Leber (LHON)
D. Sindrom KEARNS-SAYRE (KSS)
E. Penyakit LEIGH
A
E.
MELAS, MERFF, LHON, and KSS are a group of disorders related to mitochondrial (mt) DNA abnormalities. Although specific syndromes are often identified by a variety of signs/symptoms, several clinical manifestations seem to be prevalent with mtDNA abnormalities and include short stature, hearing loss, and diabetes mellitus. Lactic acidosis is the most common laboratory finding, while pathologic sectioning reveals enlarged mi tochondria in muscle fibers, which forms the basis for ragged red fibers (RRF) . Leigh’s disease is a disorder of mitochondrial metabolism in which the primary defect involves proteins encoded by nuclear DNA instead of mitochondrial DNA (El l ison, pp. 457-465) .
18
Q
Tn. X, 74 tahun dengan penyakit vaskular peripheral dibawa ke ruang gawat darurat dengan lengan kiri terus terayun-ayun tanpa terkendali. Pencitraan resonansi magnetik (MRI) atas otak mengungkapkan adanya ventrikulomegali, atropi kortikal difusi, dan infark lakunar multiple
21. Diantara struktur-struktur di bawah ini, struktur manakah yang paling mungkin terkena sehingga menunjukkan ciri ini? A. Globus pallidus lateral B. Nukleus subtalamik C. Talamus D. Nukleus merah E. Nukleus caudate
A
B
Wild, involuntary flinging of an extremity may be secondary to a cerebrovascular accident affecting the subthalamic nucleus and is commonly referred to as hemiballismus. Normally, glutamatergic projections from the subthalamic nucleus to the Gpi and SNr suppress the motor nuclei of the thalamus. After damage to the subthalamic nucleus, the thalamic motor neurons are disinhibited and provide excessive activation of the motor cortex. The dopaminergic projections, howeYer, remain intact. pro,•iding a constant and unbalanced acti,•ation of motor neurons throughout the basal ganglia. This is the basis for using neuroleptic agents, including dopamine receptor blockers (haloperidol and perphenazine) and presynaptic dopamine depletors (reserpine and tetrabenazine ) to treat this disease process (Tarsy, p. 9; Pritchard, pp. 330-331).
19
Q
Tn. X, 74 tahun dengan penyakit vaskular peripheral dibawa ke ruang gawat darurat dengan lengan kiri terus terayun-ayun tanpa terkendali. Pencitraan resonansi magnetik (MRI) atas otak mengungkapkan adanya ventrikulomegali, atropi kortikal difusi, dan infark lakunar multiple
22. Di antara kelainan neurotransmitter di bawah ini, kelainan neurotransmitter manakah yang paling mungkin diderita pasien yang bersangkutan? A. Dopamin B. Glutamat C. GABA D. Norepineprin E. Asetilkolin
A
B
Wild, involuntary flinging of an extremity may be secondary to a cerebrovascular accident affecting the subthalamic nucleus and is commonly referred to as hemiballismus. Normally, glutamatergic projections from the subthalamic nucleus to the Gpi and SNr suppress the motor nuclei of the thalamus. After damage to the subthalamic nucleus, the thalamic motor neurons are disinhibited and provide excessive activation of the motor cortex. The dopaminergic projections, howeYer, remain intact. pro,•iding a constant and unbalanced acti,•ation of motor neurons throughout the basal ganglia. This is the basis for using neuroleptic agents, including dopamine receptor blockers (haloperidol and perphenazine) and presynaptic dopamine depletors (reserpine and tetrabenazine ) to treat this disease process (Tarsy, p. 9; Pritchard, pp. 330-331).
20
Q
Tn. X, 74 tahun dengan penyakit vaskular peripheral dibawa ke ruang gawat darurat dengan lengan kiri terus terayun-ayun tanpa terkendali. Pencitraan resonansi magnetik (MRI) atas otak mengungkapkan adanya ventrikulomegali, atropi kortikal difusi, dan infark lakunar multiple
23. Perawatannya bisa mencakup semua perawatan di bawah ini, KECUALI A. Haloperidol B. Perpenazin C. Reserpin D. Tetrabenazin E. L-DOPA
A
E
Wild, involuntary flinging of an extremity may be secondary to a cerebrovascular accident affecting the subthalamic nucleus and is commonly referred to as hemiballismus. Normally, glutamatergic projections from the subthalamic nucleus to the Gpi and SNr suppress the motor nuclei of the thalamus. After damage to the subthalamic nucleus, the thalamic motor neurons are disinhibited and provide excessive activation of the motor cortex. The dopaminergic projections, howeYer, remain intact. pro,•iding a constant and unbalanced acti,•ation of motor neurons throughout the basal ganglia. This is the basis for using neuroleptic agents, including dopamine receptor blockers (haloperidol and perphenazine) and presynaptic dopamine depletors (reserpine and tetrabenazine ) to treat this disease process (Tarsy, p. 9; Pritchard, pp. 330-331).
21
Q
- Diantara pernyataan-pernyataan mengenai penyakit Huntington di bawah ini, pernyataan manakah yang paling benar?
A. Merupakan gangguan berulang trinukeotida (CAG) yang menumpuk pada kromosom 4
B. Merupakan kondisi resesif autosomal dengan penetrasi tidak tuntas
C. Terutama merupakan penyakit yang menyerang proyeksi-proyeksi GABA/enkepalin dari amigdala ke stratum
D. Lebih lazim di kalangan perempuan dibandingkan dengan kalangan laki-laki
E. Memiliki onset lebih lambat pada generasi-generasi sesudahnya
A
A
HD is an autosomal dominant condition with complete penetrance that Yaries in symptom onset from ju,•eniles to late adulthood. \Yith a\•erage onset between 35 and 40 years of age. Sporadic cases of HD are rare. HD, a CHAPTER 3 Neurology Answers 67 trinucleotide repeat (CAG) disorder that localizes to chromosome 4, is more common in males than females and exhibits anticipation (earlier onset in successive generations). The abnormal gene product results in protein conformational changes that lead to aggregation in the cytosol and eventually cellular apoptosis. HD primarily affects the GABNenkephalin projections from the striatum to the external segment of the globus pallidus (indirect pathway) , resulting in thalamic facilitation of motor cortical areas and hyperkinesia. Haloperidol may be effective in suppressing abnormal movements early in the disease course, but the disease is inevitably progressive and usually results in death within 20 years from symptom onset (Merritt, pp. 659-664, 696-699).
22
Q
25. Tengkorak cloverleaf-shape A. Trigonosepalus B. Skaposepalus C. Plagiosepalus D. Brakisepalus E. Oksisepalus F. Kleebattschädel G. Bukan, A -F
A
G
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable “keel” along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492)
23
Q
26. Tengkorak tower A. Trigonosepalus B. Skaposepalus C. Plagiosepalus D. Brakisepalus E. Oksisepalus F. Kleebattschädel G. Bukan, A -F
A
E
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable “keel” along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
24
Q
27. Malformasi Chiarri A. Trigonosepalus B. Skaposepalus C. Plagiosepalus D. Brakisepalus E. Oksisepalus F. Kleebattschädel G. Bukan, A -F
A
F
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable “keel” along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
25
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28. Sinostosis metopik
A. Trigonosepalus
B. Skaposepalus
C. Plagiosepalus
D. Brakisepalus
E. Oksisepalus
F. Kleebattschädel
G. Bukan, A -F
```
A
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable "keel" along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
26
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29. Kepala datar pada satu sisi
A. Trigonosepalus
B. Skaposepalus
C. Plagiosepalus
D. Brakisepalus
E. Oksisepalus
F. Kleebattschädel
G. Bukan, A -F
```
C
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable "keel" along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
27
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30. Tengkorak boat-shape
A. Trigonosepalus
B. Skaposepalus
C. Plagiosepalus
D. Brakisepalus
E. Oksisepalus
F. Kleebattschädel
G. Bukan, A -F
```
B
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable "keel" along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
28
4. Seorang laki-laki berusia 56 tahun dengan riwayat merokok dan hipertensi dibawa kepada seorang neurolog dengan kelainan vaskular yang melibatkan bagian kranial dari nucleus ambiguus. Problem klinis manakah yang seringkali dapat dihindari pada kelainan ini ?
A. Paralisis palatal
B. Paralisis paringeal
C. Paralisis laryngeal
D. Bukan salah satu dari A sampai dengan C
E. A, B dan C semuanya benar
C .
Lesions within the nucleus ambiguus may occur as a result of vascular insults, tumors, syringobulbia, motor neuron disease, and inflammatory disease. Lesions in this location often result in palatal, pharyngeal, and laryngeal paralysis that is often associated with other adjacent cranial nerve and brainstem abnormalities. If the cephalad portion of the nucleus ambiguus is injured, however, laryngeal function is often spared due to the somatotopic organization of this motor nucleus. This is referred to as "palatopharyngeal paralysis of Avellis" (Brazis, pp. 321-322 ) .
29
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31. penutupan sutur sagital pradini
A. Trigonosepalus
B. Skaposepalus
C. Plagiosepalus
D. Brakisepalus
E. Oksisepalus
F. Kleebattschädel
G. Bukan, A -F
```
B
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable "keel" along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
30
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32. Kepala datar pada dua sisi
A. Trigonosepalus
B. Skaposepalus
C. Plagiosepalus
D. Brakisepalus
E. Oksisepalus
F. Kleebattschädel
G. Bukan, A -F
```
D
Craniosynostosis refers to the premature closure of cranial sutures. It is more common in males than females, and sagittal synostosis accounts for 50% of all cases of craniosynostosis. Sagittal synostosis is identified in a child with an oblong-shaped skull (scaphocephaly or dolichocephaly), which results in an increased AP skull diameter and a narrowed biparietal diameter. There is usually a palpable "keel" along the course of the sagittal suture. Trigonocephaly refers to premature closure of the metopic suture, and results in a wedge-shaped head. Unilateral suture closure (coronal or lambdoid) often results in a misshapen and unilaterally flattened head (plagiocephaly), while premature bilateral coronal or lambdoid suture closure often results in a broad biparietal skull diameter or brachycephaly. Other forms of craniosynostosis can result from premature closure of all the sutures, which can result in a tower-shaped skull (oxycephaly) or a grossly abnormal-appearing skull with a cloverleaf shape (Kleeblattschiidel). Lacunar skull can be seen in patients with Chiari II malformation, and does not result from premature closure of the cranial sutures. The indications for surgery with craniosynostosis are usually for intracranial hypertension (VP shunt) and cosmetic deformity (Wilkins, pp. 3673-3679; Merritt, pp. 491-492) .
31
33. Tn. X, 34 th dg HIV dibawa ke ruang gawat darurat dengan keluhan sakit kepala, pening, dan hemanopia homonimus kanan. MRI T1 dengan kontras menunjukkan lesi parietookipital kiri 3-4 cm yang tidak menyangat, yang menunjukkan naiknya sinyal pada citra-citra FLAR MRI. Diantara
luka-luka di bawah ini, luka manakah yang paling mungkin:
A. Infeksi measles yang menyebar ke otak
B. Serangan autoimun monophasik oleh sel-sel-T atas protein-protein dasar myelin
C. Peradangan perivenular dan demielinasi
D. Reaktivasi papovavirus menyerang oligodendrosit pada white matter subkortikal
E. Bukan salah satu dari A sampai dengan D
(D)
Progressive multifocal leukoencephalopathy (PML) i s a subacute demyelinating disease that results from reactivation of a papovavirus (JC virus) in immunocompromised patients. The reactivated JC virus infects oligodendrocytes, and results in multifocal areas of demyelination predominantly in the subcortical white mlltter. PML affects 4% of AIDS patients and has been associated with other illnesses characterized by defective cell-mediated immunity, such as lymphomas and leukemias. The lesions of PML are often parieto-occipital, nonenhancing, and exhibit increased signal on T2 and FLAIR MRI with no mass effect. Symptoms of PML depend on the location of lesions and include hemiparesis, visual field cuts, sensory changes, and eventually dementia. The diagnosis of PML is established by biopsy or PCR amplification of JC virus RNA in the CSF. The prognosis of PML is poor, and approximately 80% of patients die within 9 months of symptom onset. Choices A, B, and C are associated with subacute sclerosing panencephalitis (A) and acute disseminated encephalomyelitis ( B and C) (Merritt, pp. 151- 156).
32
34. Pasien-pasien yang mengalami koreksi cepat hiponatremia berisiko terkena masalah di bawah ini yang dapat menimbulkan kejang, disartria, palsi pseudobulbar, koma dan/atau kematian:
A. Penyakit MARCHIAFAVA-BIGNAMI
B. Mielinolisis pontin sentral
C. Leukoenselopalopati dengan penyebaran akut
D. Penyakit KRABBE
E. Penyakit ALEXANDER
B
Central pontine myelinolysis (CPM) is an acute demyelinating condition that primarily affects the pons, although 10% of cases have concomitant extrapontine myelinolysis. CPl\1 most common!
33
Laki-laki, 16 tahun sedang melakukan uji coba tim sepak bola sekolahnya dan memperhatikan
adanya kram kaki yang parah dan tidak kunjung mereda. Meski pun dia pernah mengalami masalah ini di masa lalu selama latihan, kram yang dialaminya belum pernah separah ini. Hasil pemeriksaan neurologi tidak begitu jelas tetapi tampaknya dia menderita kekurangan mioposporilase enzim yang sangat parah.
```
35. Diagnosis mana yang paling mungkin?
A. Penyakit VON GIERKE
B. Oenyakit Pompe
C. Penyakit McARDLE
D. Penyakit CORI
E. Distropi Duchene dengan onset lambat
```
C
Glycogen storage diseases a Fe primarily autosomal recessive disorders that result from deficiencies of the enzymes im•olved with the metabolism of glucose and glycogen. There are more than 12 different types of glycogenoses; they affect different tissues depending on the expression of the defective enzyme. Type I glycogenosis (Von Gierke's disease) is characterized by deficiencies of glucose-6-phosphatase and primarily affects the liver. Patients with Von Gierke's disease present with hepatomegaly and experience severe episodes of hypoglycemia. Type I I glycogenosis ( Pompe's disease) results from deficiencies of the enzyme acid maltase a.-glucosidase and has three different forms. The infantile type of Pompe's disease results in hYpotonia, macroglossia, hepatomegaly, cardiomegaly, and death by 2 years of age secondary to cardiac failure. The ju1•enile and adulthood variants of Pompe's disease are less se1•ere and present with myopathy. Type I I I glycogenosis ( debranching enzyme deficiency or Cori's disease) is rare and results in hepatomegaly, seizures, and growth retardation in children secondary to deficiencies of the debranching enzyme amylo-1 ,6-glucosidase. Type V glycogenosis
34
Laki-laki, 16 tahun sedang melakukan uji coba tim sepak bola sekolahnya dan memperhatikan
adanya kram kaki yang parah dan tidak kunjung mereda. Meski pun dia pernah mengalami masalah ini di masa lalu selama latihan, kram yang dialaminya belum pernah separah ini. Hasil pemeriksaan neurologi tidak begitu jelas tetapi tampaknya dia menderita kekurangan mioposporilase enzim yang sangat parah.
```
36. Apa yang mungkin tampak pada urinalisis pada pasien ini?
A. Mioglobinuria
B. Kelebihan garam
C. Hiperglikemia
D. Hiperkalsemia
E. Hiperposfatemia
```
A
Glycogen storage diseases a Fe primarily autosomal recessive disorders that result from deficiencies of the enzymes im•olved with the metabolism of glucose and glycogen. There are more than 12 different types of glycogenoses; they affect different tissues depending on the expression of the defective enzyme. Type I glycogenosis (Von Gierke's disease) is characterized by deficiencies of glucose-6-phosphatase and primarily affects the liver. Patients with Von Gierke's disease present with hepatomegaly and experience severe episodes of hypoglycemia. Type I I glycogenosis ( Pompe's disease) results from deficiencies of the enzyme acid maltase a.-glucosidase and has three different forms. The infantile type of Pompe's disease results in hYpotonia, macroglossia, hepatomegaly, cardiomegaly, and death by 2 years of age secondary to cardiac failure. The ju1•enile and adulthood variants of Pompe's disease are less se1•ere and present with myopathy. Type I I I glycogenosis ( debranching enzyme deficiency or Cori's disease) is rare and results in hepatomegaly, seizures, and growth retardation in children secondary to deficiencies of the debranching enzyme amylo-1 ,6-glucosidase. Type V glycogenosis
35
Laki-laki, 16 tahun sedang melakukan uji coba tim sepak bola sekolahnya dan memperhatikan
adanya kram kaki yang parah dan tidak kunjung mereda. Meski pun dia pernah mengalami masalah ini di masa lalu selama latihan, kram yang dialaminya belum pernah separah ini. Hasil pemeriksaan neurologi tidak begitu jelas tetapi tampaknya dia menderita kekurangan mioposporilase enzim yang sangat parah.
```
37. Cara penularan proses penyakit ini adalah:
A. Dominan autosomal
B. Resesif autosomal
C. Resesif rantai-X
D. dominan rantai-X
E. Penularan poligenetik
```
B
Glycogen storage diseases a Fe primarily autosomal recessive disorders that result from deficiencies of the enzymes im•olved with the metabolism of glucose and glycogen. There are more than 12 different types of glycogenoses; they affect different tissues depending on the expression of the defective enzyme. Type I glycogenosis (Von Gierke's disease) is characterized by deficiencies of glucose-6-phosphatase and primarily affects the liver. Patients with Von Gierke's disease present with hepatomegaly and experience severe episodes of hypoglycemia. Type I I glycogenosis ( Pompe's disease) results from deficiencies of the enzyme acid maltase a.-glucosidase and has three different forms. The infantile type of Pompe's disease results in hYpotonia, macroglossia, hepatomegaly, cardiomegaly, and death by 2 years of age secondary to cardiac failure. The ju1•enile and adulthood variants of Pompe's disease are less se1•ere and present with myopathy. Type I I I glycogenosis ( debranching enzyme deficiency or Cori's disease) is rare and results in hepatomegaly, seizures, and growth retardation in children secondary to deficiencies of the debranching enzyme amylo-1 ,6-glucosidase. Type V glycogenosis
36
38. Semua ciri ataksia dari Friedrich di bawah ini adalah benar, KECUALI
A. merupakan gangguan repeat trinukleotida (GAA) resesif autosomal yang melibatkan gen frataksin
B. Gejala-gejala awalnya biasanya tampak pada usia 10 sampai dengan 15 tahun
C. Seringkali menyebabkan degenerasi kolom belakang dan saluran sinoserebelar
D. Perubahan-perubahan iskemik kortikal serebelar dan serebral seringkali dapat diasosiasikan dengan kardiomiopati yang menyertainya.
E. Dengan perawatan yang efektif, perkembangan penyakit yang berasosiasi dengan degenerasi neuronal dapat dihentikan sekitar 60% dari waktunya, meski pun gagal jantung biasanya bersifat refraktoris atas terapi.
E.
Friedreich's ataxia (FA) is an autosomal recessive trinucleotide repeat ( GAA) disorder that involves repeat expansion in the frataxin gene, which encodes a mitochondrial protein and is located on chromosome 9q. The onset of symptoms with FA usually occurs by the age of 10 to 15 years; it is usually fatal by the fifth to sixth decades of life. FA results in degeneration of the posterior columns, spinocerebellar tracts, corticospinal tracts, and Clarke's nucleus in the spinal cord. The medulla (vestibular, cochlear, gracile, and accessory cuneate nuclei), subthalamic nucleus, and pallidum also exhibit evidence of gliosis. Symptoms of FA include ataxic gait, dysarthria, areflexia, lower limb weakness, and loss of vibratory sense and proprioception. Some patients with FA also develop cardiomyopathy, which can lead to cerebellar and cerebral cortical ischemic changes. F.A is associated with the development of peripheral neuropathy as well, with concomitant degeneration of the dorsal root ganglia. Orthopedic deformities, such as hammertoes, kyphoscoliosis, and pes cavus are also common. There is no effective treatment for FA (Merritt, pp. 645-646).
37
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39. Sindrom LESCH-NYHAN merupakan gangguan resesif rantai-X yang disebabkan kekurangan enzim yang mana?
A. Protein transporter-1 Glukose
B. Hidroksilase penilalanin
C. Fosforibosiltransferase hiposantin-
D. Sintase sistationin
E. Dekarboksilase purin
```
C.
Lesch-Nyhan syndrome ( LNS) is an X-linked recessive disorder of purine metabolism that results from deficiencies of the enzyme hypoxanthine-guanine phosphoribosyltransferase ( HPR'f). Levels of uric acid are increased in LNS secondary to increased purine metabolism, and urate deposition can result in severe nephropathy and gout. Patients with LNS exhibit mental retardation, choreoathetosis, spasticity, self-mutilating behavior, and usually die from renal failure in the second or third decade. Glucose transporter protein syndrome (GTPS) results from deficiencies of the glucose transporter-! protein (GLUT-I ) , which is responsible for the facilitative transport of glucose across the blood-brain barrier. Patients with GTPS exhibit decreased CSF glucose levels (hypoglycorrhachia), seizures, developmental delay, microcephaly, ataxia, and hypotonia. Phenylketonuria is an autosomal recessil•e disorder resulting from phenylalanine hydroxylase deficiency, and cystathionine
38
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40. Mungkin sifatnya sekunder, dengan kondisi utama kelemahan/lumpuh pada otot pratibial dan peroneal
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
D
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
39
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41. Penyakit Parkinson
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
B
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
40
```
42. Berasosiasi dengan sirkumduksi pada kaki
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
C
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
41
```
43. Sindrom WOHLFART-KUGELBERG-WELANDER kronis atau progresif
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
E
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
42
```
44. Mungkin menyertai lesi pada spine thorak
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
A
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
43
```
45. Seringkali tampak dengan foot drop
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
D
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
44
```
46. Infark pada kapsul interna
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
C
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
45
```
47. Batas anterior dan lateral sol sepatu seringkali rusak
A. Scissoring gait
B. Festinating gait
C. Hemiplegic gait
D. Steppage gait
E. Waddling gait
F. Reeling gait
G. Toppling gait
H. Bukan, A-G
```
C
Patients with infarcts or trauma involving the corticospinal tracts on one side often develop a hem iplegic gaic characterized by a stiff leg that does not freely flex at the hip, knee, or ankle. With movement, the involved leg tends to rotate outward in a semicircle (circumduction). and the toe and outer side of the sole often become worn (less commonly also seen with steppage gait). The arm on the affected side is also usually weak, and is often carried in a tlexed position iree of any natural movement. Festinating gait is a term used to describe the involuntary acceleration or hastening that often accompanies Parkinson's patients. Steppage or equine gait is caused by severe weakness or paralysis of the pretibial or peroneal muscles, with difficulty dorsiflexing and everting the foot. The steps are regular and even, but the advancing foot often hangs with the toes pointing down (footdrop) . Walking is accomplished by abnormally high elevation of the involved leg in order for the foot to clear the ground, often producing a characteristic slap as the foot strikes the floor. Waddling gait is characteristic of chronic or progressive muscular dystrophy (Wohlfart-Kugelberg-Welander disease) and congenital hip dislocation. Reeling gait is a term used to describe the gait of a severely intoxicated patient, which sways in many directions with no attempt to correct the staggering by watching the legs or trunk (as in cerebellar or sensory ataxia) . Toppling gait may be seen in patients with brainstem lesions, especially in the elderly with a recent stroke, where sudden lurches forward and frequent falls are a prominent feature. It has also been described as a feature of the lateral medullary syndrome (Wallenberg's) and in certain patients with progressive supranuclear palsy and advanced Parkinson's disease. Scissoring gait may result from lesions involving the thoracic spine, where abnormal gait may result from the combined effects of weakness and spasticity. The legs are usually maintained in an extended or slightly flexed position at the hips, and knees are often adducted at the hips. With severe spasticity, the legs may cross in front of each other during ambulation, causing a scissoring gait (Merritt, pp. 46-49; Adams, pp. 94-99) .
46
Perempuan, 34 tahun tiba-tiba mengalami hemiparesis kiri. Dia menderita trombosis venous yang dalam pada kaki kirinya sekitar 4 tahun sebelumnya.
```
48. Diantara penyebab-penyebab defisit dari pasien di bawah ini, penyebab manakah yang paling mungkin?
A. Fibrilasi atrial
B. Tumor otak metastatis
C. Sklerosis majemuk
D. Antikoagulan lupus
E. Cacad septal artrial
```
D
The lupus inhibitor can be found in up to one-third of systemic lupus erythematosus (SLE) patients . In SLE patients, the associated thrombosis risk can be as high as 10 to 1 5%, while the risk is less in patients without SLE but still in excess of normal. This disease process is associated with deep venous thrombosis of the legs, ischemic strokes in the brain, and miscarriages (placental dysfunction) . Abnormal bleeding does not typically occur, although laboratory findings include prolonged PT and PTT that does not reverse when the patient's plasma is mixed with normal plasma. Diagnosis can be confirmed by the thromboplastin inhibition test (TTI) and antiphospholipid antibody assays. Treatment to prevent thrombosis may include corticosteroids, antiplatelet drugs, and anticoagulation; plasmapheresis is not typically used. Anticoagulation appears to be the best therapy, with a goal of keeping the INR at least 3 . 0 . Atrial fibrillation and atrial-septal defects are common causes of stroke in certain patient populations, but there is no reason to suspect a rhythm or congenital heart problem in this patient. Multiple sclerosis and metastatic brain tumors are not typically associated with deep venous 'thrombosis unless the patient is immobilized for a prolonged time ( Merritt, p. 245).
47
Perempuan, 34 tahun tiba-tiba mengalami hemiparesis kiri. Dia menderita trombosis venous yang dalam pada kaki kirinya sekitar 4 tahun sebelumnya.
49. Ciri laboatoris non-spesifik dari gangguan ini mungkin meliputi :
A. PT dan PTT menahun yang tidak pulih
ketika plasma pasien tercampur dengan plasma normal
B. Pita oligoklional pada CSF
C. Kelainan gen distropia
D. Elevasi antibodi lgE pada serum
E. bukan salah satu dari A sampai dengan D
A
The lupus inhibitor can be found in up to one-third of systemic lupus erythematosus (SLE) patients . In SLE patients, the associated thrombosis risk can be as high as 10 to 1 5%, while the risk is less in patients without SLE but still in excess of normal. This disease process is associated with deep venous thrombosis of the legs, ischemic strokes in the brain, and miscarriages (placental dysfunction) . Abnormal bleeding does not typically occur, although laboratory findings include prolonged PT and PTT that does not reverse when the patient's plasma is mixed with normal plasma. Diagnosis can be confirmed by the thromboplastin inhibition test (TTI) and antiphospholipid antibody assays. Treatment to prevent thrombosis may include corticosteroids, antiplatelet drugs, and anticoagulation; plasmapheresis is not typically used. Anticoagulation appears to be the best therapy, with a goal of keeping the INR at least 3 . 0 . Atrial fibrillation and atrial-septal defects are common causes of stroke in certain patient populations, but there is no reason to suspect a rhythm or congenital heart problem in this patient. Multiple sclerosis and metastatic brain tumors are not typically associated with deep venous 'thrombosis unless the patient is immobilized for a prolonged time ( Merritt, p. 245).
48
Perempuan, 34 tahun tiba-tiba mengalami hemiparesis kiri. Dia menderita trombosis venous yang dalam pada kaki kirinya sekitar 4 tahun sebelumnya.
50. Yang dapat memperkuat Diagnosisnya adalah:
A. Membuktikan adanya reaksi-reaksi penghambatan di dalam sistem penggumpalan dengan uji hambatan trombioplastin (TTI) dan uji venom biper dari Russell
B. Penguatan adanya cacad pada faktor V
C. Luka majemuk pada materi putih dalam dengan MRI
D. Mencatat adanya cacad septal atrial dengan menggunakan ekokardiografi
E. Pendarahan yang berlebihan setelah mencukur
A
The lupus inhibitor can be found in up to one-third of systemic lupus erythematosus (SLE) patients . In SLE patients, the associated thrombosis risk can be as high as 10 to 1 5%, while the risk is less in patients without SLE but still in excess of normal. This disease process is associated with deep venous thrombosis of the legs, ischemic strokes in the brain, and miscarriages (placental dysfunction) . Abnormal bleeding does not typically occur, although laboratory findings include prolonged PT and PTT that does not reverse when the patient's plasma is mixed with normal plasma. Diagnosis can be confirmed by the thromboplastin inhibition test (TTI) and antiphospholipid antibody assays. Treatment to prevent thrombosis may include corticosteroids, antiplatelet drugs, and anticoagulation; plasmapheresis is not typically used. Anticoagulation appears to be the best therapy, with a goal of keeping the INR at least 3 . 0 . Atrial fibrillation and atrial-septal defects are common causes of stroke in certain patient populations, but there is no reason to suspect a rhythm or congenital heart problem in this patient. Multiple sclerosis and metastatic brain tumors are not typically associated with deep venous 'thrombosis unless the patient is immobilized for a prolonged time ( Merritt, p. 245).
49
Perempuan, 34 tahun tiba-tiba mengalami hemiparesis kiri. Dia menderita trombosis venous yang dalam pada kaki kirinya sekitar 4 tahun sebelumnya.
51. Terapi optimal untuk penyakit ini bisa mencakup:
1. Mempertahankan rasio normalisasi internasional (INR) pada ambang minimal 3.0 dari warfarin
2. Kortikosteroid
3. Agen-agen antiplatelet
4. Plasmaperesis
A
The lupus inhibitor can be found in up to one-third of systemic lupus erythematosus (SLE) patients . In SLE patients, the associated thrombosis risk can be as high as 10 to 1 5%, while the risk is less in patients without SLE but still in excess of normal. This disease process is associated with deep venous thrombosis of the legs, ischemic strokes in the brain, and miscarriages (placental dysfunction) . Abnormal bleeding does not typically occur, although laboratory findings include prolonged PT and PTT that does not reverse when the patient's plasma is mixed with normal plasma. Diagnosis can be confirmed by the thromboplastin inhibition test (TTI) and antiphospholipid antibody assays. Treatment to prevent thrombosis may include corticosteroids, antiplatelet drugs, and anticoagulation; plasmapheresis is not typically used. Anticoagulation appears to be the best therapy, with a goal of keeping the INR at least 3 . 0 . Atrial fibrillation and atrial-septal defects are common causes of stroke in certain patient populations, but there is no reason to suspect a rhythm or congenital heart problem in this patient. Multiple sclerosis and metastatic brain tumors are not typically associated with deep venous 'thrombosis unless the patient is immobilized for a prolonged time ( Merritt, p. 245).
50
Ny. X, 72 tahun yang sebelumnya sehat menderita halusinasi pendengaran dan depresi. Pasien mengalami kesulitan menjelaskan detilnya tapi dia yakin bahwa anak laki-lakinya memang sedang berbicara kepadanya. Selama wawancara, pasien tidak kooperatif, tetapi pemeriksaan fisik menunjukkan hasil yang tidak jelas. Setiap hari pasien mengkonsumsi multivitamin dan aspitrin
```
52. Diantara diagnosis-diagnosis di bawah ini, diagnosis manakah yang paling mungkin?
A. Hipertiroidisme
B. Kejang parsial kompleks
C. Penyakit Alzheimer
D. Demensia (pikun) multi-infract
E. Hiperparatiroidisme
```
C
Alzheimer's disease (AD) is a rare cause of new-onset auditory hallucinations in elderly patients. Typically, other forms of cognitive impairment are present, but hallucinations may occasionally precede other manifestations of this disease process. Low doses of haloperidol are often effective in treating the hallucinations, while medications such as tacrine and donepezil may slow the cognitive decline modestly early in the disease course. Several structures in the brain are affected in AD, including the hippocampus (especially CAl ) , mesial temporal lobe, frontotemporoparietal association areas, and the nucleus basalis of i\leynert (n.b.M) . The degeneration of cells in the n.b.M (and other basal forebrain nuclei) results in decreased•cortical cholinergic input and is associated with decreased levels of ACh and choline acetyltransferase in the hippocampus and neocortex. Patients with AD also exhibit decreased CNS levels of serotonin, norepinephrine, glutamate, and substance P. Ventriculomegaly accompanies the diffuse cerebral neocortical atrophy. Several genes are involved in the pathogenesis of AD including amyloid precursor protein (chromosome 2 1 ) , presenilin 1 (chromosome 14), and presenilin 2 (chromosome 1). The £4 allele of apolipoprotein E (chromosome 19) is associated with an increased risk of developing AD and is associated with 25 to 40% of all cases of AD. In any patient with suspected AD, treatable causes of dementia must be ruled out initially with a good history, physical examination, laboratory data, and imaging studies. Patients with AD are most often diagnosed with a detailed history and physical examination (Merritt, pp. 633 - 637 ) .
51
Ny. X, 72 tahun yang sebelumnya sehat menderita halusinasi pendengaran dan depresi. Pasien mengalami kesulitan menjelaskan detilnya tapi dia yakin bahwa anak laki-lakinya memang sedang berbicara kepadanya. Selama wawancara, pasien tidak kooperatif, tetapi pemeriksaan fisik menunjukkan hasil yang tidak jelas. Setiap hari pasien mengkonsumsi multivitamin dan aspitrin
53. Cara yang paling lazim untuk memperoleh diagnosis ini mencakup:
A. Ambil kadar hormon perangsang tiroid (TSH)
B. Elektroensepalografi
C. Riwayat detil dan pemeriksaan fisik
D. Biopsi otak
E. Ambil kadar enzim pengubah angiotensin
C
Alzheimer's disease (AD) is a rare cause of new-onset auditory hallucinations in elderly patients. Typically, other forms of cognitive impairment are present, but hallucinations may occasionally precede other manifestations of this disease process. Low doses of haloperidol are often effective in treating the hallucinations, while medications such as tacrine and donepezil may slow the cognitive decline modestly early in the disease course. Several structures in the brain are affected in AD, including the hippocampus (especially CAl ) , mesial temporal lobe, frontotemporoparietal association areas, and the nucleus basalis of i\leynert (n.b.M) . The degeneration of cells in the n.b.M (and other basal forebrain nuclei) results in decreased•cortical cholinergic input and is associated with decreased levels of ACh and choline acetyltransferase in the hippocampus and neocortex. Patients with AD also exhibit decreased CNS levels of serotonin, norepinephrine, glutamate, and substance P. Ventriculomegaly accompanies the diffuse cerebral neocortical atrophy. Several genes are involved in the pathogenesis of AD including amyloid precursor protein (chromosome 2 1 ) , presenilin 1 (chromosome 14), and presenilin 2 (chromosome 1). The £4 allele of apolipoprotein E (chromosome 19) is associated with an increased risk of developing AD and is associated with 25 to 40% of all cases of AD. In any patient with suspected AD, treatable causes of dementia must be ruled out initially with a good history, physical examination, laboratory data, and imaging studies. Patients with AD are most often diagnosed with a detailed history and physical examination (Merritt, pp. 633 - 637 ) .
52
Ny. X, 72 tahun yang sebelumnya sehat menderita halusinasi pendengaran dan depresi. Pasien mengalami kesulitan menjelaskan detilnya tapi dia yakin bahwa anak laki-lakinya memang sedang berbicara kepadanya. Selama wawancara, pasien tidak kooperatif, tetapi pemeriksaan fisik menunjukkan hasil yang tidak jelas. Setiap hari pasien mengkonsumsi multivitamin dan aspitrin
```
54. Rezim perawatan untuk halusinasi pendengaran ini dapat meliputi:
A. Takrin
B. Donepezil
C. Vitamin E
D. Haloperidol
E. A, B, C dan D
```
D
Alzheimer's disease (AD) is a rare cause of new-onset auditory hallucinations in elderly patients. Typically, other forms of cognitive impairment are present, but hallucinations may occasionally precede other manifestations of this disease process. Low doses of haloperidol are often effective in treating the hallucinations, while medications such as tacrine and donepezil may slow the cognitive decline modestly early in the disease course. Several structures in the brain are affected in AD, including the hippocampus (especially CAl ) , mesial temporal lobe, frontotemporoparietal association areas, and the nucleus basalis of i\leynert (n.b.M) . The degeneration of cells in the n.b.M (and other basal forebrain nuclei) results in decreased•cortical cholinergic input and is associated with decreased levels of ACh and choline acetyltransferase in the hippocampus and neocortex. Patients with AD also exhibit decreased CNS levels of serotonin, norepinephrine, glutamate, and substance P. Ventriculomegaly accompanies the diffuse cerebral neocortical atrophy. Several genes are involved in the pathogenesis of AD including amyloid precursor protein (chromosome 2 1 ) , presenilin 1 (chromosome 14), and presenilin 2 (chromosome 1). The £4 allele of apolipoprotein E (chromosome 19) is associated with an increased risk of developing AD and is associated with 25 to 40% of all cases of AD. In any patient with suspected AD, treatable causes of dementia must be ruled out initially with a good history, physical examination, laboratory data, and imaging studies. Patients with AD are most often diagnosed with a detailed history and physical examination (Merritt, pp. 633 - 637 ) .
53
55. Seorang pengacara berusia 45 tahun mengeluh kesulitan memegang dan menggunakan pena. Dia mencatat bahwa dia mengalami kejang-kejang pada lengan kanan dan tangannya selama tiga bulan sebelumnya hanya pada saat menulis. Pemeriksaan fisik kurang begitu
menggembirakan,. Diantara etiologi-etiologi di bawah ini, etiologi manakah yang paling mungkin berasosiasi dengan tanda-tanda /gejala pada pasien?
A. Penyakit Parkinson dini
B. Atetosis
C. Radikulopati C7
D. Distonia
E. Sindrom saluran Carpal
D .
Writer's cramp i s a focal dystonia o f unknown etiology. Patients develop sustained muscle contractions that yield abnormal postures or twisting movements when attempting to write. It differs from athetosis by the persistent nature of the abnormal posture or movement. It can be focal (writer's cramp), segmental (e.g. , face), or rarely multifocal (e.g., face and leg) . Dystonia can also be either primary (inherited) or secondary (stroke, toxin, medication, etc. ) . The medical treatment is variable, often empiric, and can include local botulinum toxin injections, anticholinergics, benzodiazepines, anticonvulsants, lithium , reserpine, baclofen, and levodopa. Micrographia can be seen with Parkinson's disease but is often accompanied by signs of rigidity, tremor, and bradykinesia. Carpal tunnel syndrome is clue to pressure on the median nerve and is asso.ciated with numbness. weakness, and pain. A cervical radiculopathy rarely if ever presents with the findings seen in this patient; instead. there is pain, weakness, numbness, and ret1ex changes in the distribution of the affected nerve ( Merritt, pp. 669- 6 7 7 )
54
```
56. Antibodi yang diisolasi dengan karsinoma paru-paru sel kecil, neuropati sensoris, ensepalomielitis
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
A
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
55
```
57. Sindrom miastenik LAMBERT-EATON
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
E
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
56
```
58. Sindroma Opsoklonus-mioklonus
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
B
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
57
```
59. Bereaksi terhadap del-sel Punkinje dari serebelum
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
F
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
58
```
60. Polimiositis
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
C
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
59
```
61. Penyakit HODGKIN
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
F
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
60
```
62. Antibodi yang terutama ditemukan pada pasien dengan kanker testikular
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
G
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
61
```
63. Degenerasi retinal
A. Antibodi anti-Hu
B. Antibodi anti-Ri
C. Antibodi anti-Jo
D. Antibodi anti-Yo
E. Antibodi anti-VGCC
F. Antibodi anti-Tr
G. Antibodi anti-Ta
H. Bukan, A-G
```
B
| Refer to Table 3 . 56-3.63A (Merritt, pp. 767, 894-895; Rolak. pp. 237-239 ) .
62
64. Seorang ibu membawa bayi laki-lakinya yang berumur 4 bulan ke kantor anda setelah menyaksikan satu episode yang ditandai oleh kejang-kejang ekstensor yang tiba-tiba, dan melibatkan kepala, tangkai dan anggota badan. Yang paling mungkin ditunjukkan oleh EEG adalah:
A. Pengosongan gelombang-percik 3-Hz
B. Pengosongan epileptiform dengan lateralisasi berkala (PLEDs)
C. Hipsaritmia
D. Pelambatan yang semakin lama semakin umum
E. gelombang kejut 4 – 6 Hz
C.
| Refer to Table 3 .64A ( Merritt, pp. 813-836)
63
65. Peningkatan latensi refleks-H bersama-sama dengan latensi gelombang F melokalisasi luka pada lokasi yang mana?
A. Pertemuan neuromuscular
B. sel-sel tanduk depan dari spinal cord
C. Akar-akar dorsal
D. Akar-akar ventral
E. Bukan salah satu dari A sampai dengan D
C.
The F wave and H reflex evaluate certain aspects of nerve conduction. Whereas sensory nerve action potentials (SNAP) and compound muscle action potentials (Ct--1AP) are best at evaluating distal nerves, the F wave and H reflex are the two most commonly used methods in evaluating the proximal portions of nerves. The F wa1•e (F response) measures the entire length of the nerve, including the ventral root. It results from supramaximal stimulus of distal motor nerves with impulse propagation in an antidromic direction. The stimulus tra1•els proximally up the motor nerve and stimulates the anterior horn motor neurons. The variable backfiring of nonreiractory anterior horn cells then results in impulse propagation back down the ventral root and motor nerve to the distal electrode. F-wave latencies are most sensitive for disorders causing generalized or multifocal demyelination (GBS or extensive plexopathies). This is because any focal conduction slowing is diluted by the normal conduction velocity over most of the F-11•ave pathway. The H retlex is the electrical equi1•alent of the stretch retlex and is obtained with submaximal stimulation of the median and tibial nerves. The H reflex therefore involves an afferent (sensory) limb and an efferent (motor) limb, similar to monosynaptic reflex arcs. The H reflex exhibits increased latency in proximal neuropathies and radiculopathies (i.e., C6, C7, or Sl root lesions). Increased H-reflex latencies in conjunction with normal F-wm•e latencies localize lesions to the dorsal roots (Adams, pp. 1022-1025; Merritt, pp. 73-7 6 ) .
64
1. Sindroma HORNER dan hipestesi wajah
A. Sindroma TOLOSA - HUNT
B. Sindroma GRANDENIGO
C. Sindroma RAEDER
(C)
Raeder's para trigeminal neuralgia is often localized adjacent to the trigeminal nerve as it courses through the middle cranial fossa. The cause of this syndrome is often unclear, but it is usually characterized by a partial Horner's syndrome and unilateral trigeminal nerve problems, including tic-like pain, numbness, and/or masseter weakness. Gradenigo's syndrome, also known as apical petrositis, often consists of the classic triad of abducens nerve palsy, retroorbital pain, and a draining ear. Tolosa-Hunt syndrome is a diagnosis of exclusion; this condition is believed to result from inflammation adjacent to the superior orbital fissure. It is characterized by painful ophthalmoplegia, cranial nerves III, IV, and VI palsies, and recurrent attacks and remissions; it is typically treated with intravenous steroids (Greenberg, pp. 581-582 )
65
```
5. Kelemahan muskulus trapezius dan sternokleidomastoideus ipsilateral, disponia dan dispagia, hilang rasa pengecap pada sepertiga belakang dari lidah, dan berkurangnya sensasi pada faring merupakan ciri-ciri khas sindroma:
A. Collet-Sicard
B. Vernet
C. Schmidt
D. Garcin
E. Weber
```
B.
The spinal accessory nerve enters the j ugular foramen accompanied by cranial nerves IX and X. Lesions of the jugular foramen including tumors, infections, and fractures can result in Verner's syndrome, which is characterized by ipsilateral trapezius and sternocleidomastoid muscle weakness, dysphonia and dysphagia, loss of taste over the posterior third of the tongue, and depressed sensation over the pharynx (Brazis, pp. 330-331).
66
66. Semua karakteristik di bawah ini adalah karakteristik neuropati demielinasi pada pemeriksaan-pemeriksaan konduksi saraf motorik, KECUALI
A. Latensi distal menahun
B. Menurunnya kecepatan segmental
C. Amplitudo respons yang jika dipicu tetap normal atau hanya menurun sedikit
D. Penurunan gelombang F
E. Dispersi temporal
D.
Nerve conduction studies (NCSs) vary in conditions that result in either demyelination or axonal degeneration. Conduction velocity. amplitude of evoked response, latency (latency from the stimulus to recording electrodes) , and duration of response all provide information about the integrity of motor and sensory nerves. NCSs of the sensory nerves generate a sensory nerve action potential (SNAP), while NCSs of motor nerves generate a compound muscle action potential
67
```
67. Semua karakteristik di bawah ini adalah karakteristik potensi unit-motorik-tunggal normal pada EMG, KECUALI
A. Durasi 5-15 milidetik
B. Dua sampai empat fase
C. 0,5 – 3 mV
D. Potensi fibrilasi
E. Aktivitas insersional
```
D.
| Normal muscle potentials appear as waveforms with a duration of 5 to 1 5 ms, 2 to 4 phases, and an amplitude of 0 .
68
```
pic
68. Spindel tidur dan kompleks K
A. Tahap 1
B. Tahap 2
C. Tahap 3
D. Tahap 4
E. Rapid Eye Movement (REM)
F. Bukan salah satu dari A sampai dengan F
```
B,C
| Refer t o Table 3 . 68- 3 . 73A ( Merritt, p. 64).
69
```
pic
69. Gelombang delta > 50%
A. Tahap 1
B. Tahap 2
C. Tahap 3
D. Tahap 4
E. Rapid Eye Movement (REM)
F. Bukan salah satu dari A sampai dengan F
```
D
| Refer t o Table 3 . 68- 3 . 73A ( Merritt, p. 64).
70
```
pic
70. Transisi dari gelombang α ke aktivitas voltase-rendah lambat
A. Tahap 1
B. Tahap 2
C. Tahap 3
D. Tahap 4
E. Rapid Eye Movement (REM)
F. Bukan salah satu dari A sampai dengan F
```
A
| Refer t o Table 3 . 68- 3 . 73A ( Merritt, p. 64)
71
```
pic
71. Apnea tidur merusak dapat diasosiasikan dengan tahap tidur ini
A. Tahap 1
B. Tahap 2
C. Tahap 3
D. Tahap 4
E. Rapid Eye Movement (REM)
F. Bukan salah satu dari A sampai dengan F
```
E
| Refer t o Table 3 . 68- 3 . 73A ( Merritt, p. 64).
72
```
pic
72. Teror malam
A. Tahap 1
B. Tahap 2
C. Tahap 3
D. Tahap 4
E. Rapid Eye Movement (REM)
F. Bukan salah satu dari A sampai dengan F
```
C,D
| Refer t o Table 3 . 68- 3 . 73A ( Merritt, p. 64)
73
```
pic
73. Adanya tahap tidur ini selama EEG di siang hari mengisyaratkan
A. Tahap 1
B. Tahap 2
C. Tahap 3
D. Tahap 4
E. Rapid Eye Movement (REM)
F. Bukan salah satu dari A sampai dengan F
```
E
| Refer t o Table 3 . 68- 3 . 73A ( Merritt, p. 64).
74
```
74. Temuan EEG ini paling sejalan dengan kelainan yang mana?
A. Penyakit CREUITZFELDT-JACOB
B. Enselopalopati Hepatik
C. Infarksi serebral massif
D. kejang-kejang motorik fokal
E. Mati otak
```
B.
Triphasic waves are a type of generalized, pseudoperiodic pattern consisting of sharp discharges occurring at typical frequencies of 1 to 2 per second. This is a nonspecific pattern and has to be distinguished from other generalized periodic patterns (CJD, status epilepticus; and hypoxicischemic injury) . Approximately 50% of patients with triphasic waves have hepatic encephalopathy; the other half have other toxic-metabolic encephalopathies, includingrenal failure. Creutzfeldt-Jakob disease is characterized by generalized periodic sharp waves, an acute destructive cerebral lesion (stroke) often results in periodic lateralizing epileptiform discharges (PLEDs) on EEG, and brain death is marked by no activity on EEG ( Merritt, p p . 64-65) .
75
75. Semua karakteristik di bawah ini adalah karakteristik narkolepsi, KECUALI
A. Berasosiasi dengan mengandung yang amat sangat pada siang hari, paralysis tidur, katapleksi dan halusinasi hipnagogis
B. Narkoleptik mungkin akan mengalami lumpuh otot selama periode awal dan akhir siklus tidur, yang seringkali melibatkan otot-otot ekstraokuler.
C. Halusinasi hipnagogis seringkali terjadi pada awal siklus tidur
D. Mungkin menunjukkan kadar oreksin yang menurun
E. Berasosiasi dengan allele DR2
B .
Narcolepsy i s a sleep disorder characterized by excessive daytime sleepiness, sleep paralysis, cataplexy, and hypnagogic hallucinations. Narcolepsy affects males and females equally, is associated with the DR2 allele, and usually presents between the ages of 1 S and 30 years. Patients with narcolepsy experience increased daytime sleepiness and irresistible sleep attacks during the day that last between S and 30 minutes. Patients \Yith narcolepsv sleep more frequently than normal people, but the amount of total sleep is the same in narcoleptics and healthy adults. Narcoleptics also display attacks of cataplexv, which is the abrupt loss of muscle tone and is often precipitated by emotion. Cataplexy reflects REM sleep paralysis during periods of normal "•akefulness. RElit periods occur earlY in the sleep cycles of patients \Vith narcolepsy (sleep-onset RE!II) , and this is diagnostic of the condition. Narcoleptics may experience paralysis of voluntarv muscles (sleep paralysis ) during the initial and terminal periods of the sleep cycle, often with sparing of the extraocular muscles. Hvpnagogic hallucinations occur at the beginning of the sleep cycle in narcoleptics; these hallucinations can be auditory or visual . Abnormalities in the hypothalamic projecting system are common in narcolepsy, and patients with this condition exhibit decreased levels of orexin. The treatment of narcolepsy involves adrenergic stimulants, such as methylphenidate (Ritalin), pemoline, and amphetamines. Cataplexy can often be effectively controlled with antidepressants (tricyclics and 88Rls), which suppress REM sleep (Merritt, p p . 843-844).
76
```
pic
76. Temuan klinis yang paling mungkinberasosiasi dengan EEG untuk seoranganak perempuan berumur 10 tahun dibawah ini akan meliputi:
A. Serangan drop
B. Kejang-kejang bayi
C. Starring spell
D. Autisme oral-alimentaris
E. Sentakan mioklonik
```
C
The absence seizure is characterized by a generalized,. symmetric, and synchronous 3-Hz spikeslow- wave discharge. This is diagnostic of an absence seizure and is best treated with medications such as ethosuximide ( Zarontin) or sodium valproate ( Depakote). The common acti,•ating procedures usually performed on patients with suspected seizures are hyperventilation, photic stimulation, and sleep. As soOI1" as 3-Hz spike-and-wave bursts stop and the seizure ceases, the EEG returns to its interictal state immediately with no postictal depression or slowing (Merritt, p. 66: Rolak. pp. 365-366) .
77
```
pic
77. Secara umum, prosedur-prosedur aktivasikejangmanakah yang dapat digunakanuntuk merangsang aktivitas kejang?
A. Hiperventilasi
B. Kurang tidur
C. Stimulasi photik
D. 1 dan 3 saja
E. A, B, C dan D, benar
```
E
The absence seizure is characterized by a generalized,. symmetric, and synchronous 3-Hz spikeslow- wave discharge. This is diagnostic of an absence seizure and is best treated with medications such as ethosuximide ( Zarontin) or sodium valproate ( Depakote). The common acti,•ating procedures usually performed on patients with suspected seizures are hyperventilation, photic stimulation, and sleep. As soOI1" as 3-Hz spike-and-wave bursts stop and the seizure ceases, the EEG returns to its interictal state immediately with no postictal depression or slowing (Merritt, p. 66: Rolak. pp. 365-366) .
78
pic
78. Begitu kejang-kejang pasien berhenti,aktivitas EEG diperkirakan akan:
A. Kembali ke keadaan interiktal begitudepresi postikal berhenti atau menurun
B. Kembali ke keadaan interiktal setelahbeberapa saat terjadi pengosongan aruslateralisasi
C. Kembali ke keadaan interiktal setelahbeberapa saat terjadi aktivitas bi-okipitalparoksimal
D. Kembali ke irama mu normal yang lazimtampak pada gangguan ini.
E. Kembali ke keadaan interiktal dengandepresi aktivitas yang jelas pada semua daerah
A
The absence seizure is characterized by a generalized,. symmetric, and synchronous 3-Hz spikeslow- wave discharge. This is diagnostic of an absence seizure and is best treated with medications such as ethosuximide ( Zarontin) or sodium valproate ( Depakote). The common acti,•ating procedures usually performed on patients with suspected seizures are hyperventilation, photic stimulation, and sleep. As soOI1" as 3-Hz spike-and-wave bursts stop and the seizure ceases, the EEG returns to its interictal state immediately with no postictal depression or slowing (Merritt, p. 66: Rolak. pp. 365-366) .
79
```
79. Kolikulus bawah
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
E
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
80
```
80. Saraf pendengaran
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
A
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
81
```
81. Tubuh genikulat medial
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
F
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
82
```
82. Olive atas
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
C
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
83
```
83. Nukleus koklear
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
B
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
84
```
84. Radiasi pendengaran
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
G
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
85
```
85. Lemniskus lateral
A. Gelombang I
B. Gelombang II
C. Gelombang III
D. Gelombang IV
E. Gelombang V
F. Gelombang VI
G. Gelombang VII
```
D
Brainstem auditory evoked potentials (BAEPs) are elicited with specific auditory stimuli and result from several important components of the auditory pathway. There are generally seven peaks in the K\EP. \Yhich result from the auditory nerve (wave I ) , cochlear nuclei (wave I I ) , superior olive or trapezoid body ( \\•m•e I I I ) , lateral lemniscus (wave IV) , inferior colliculus ( wave \•), medial geniculate body (wave VI), and auditory radiations (wave VII ) . BAEPs are usually preserved with metabolic abnormalities and exhibit prolonged latencies with structural lesions of the brainstem or auditory nerves. BAEPs are abnormal in 90% of patients with acoustic neuromas and usually consist of delayed conduction from CN VIII to the lower pons (prolongation of waves I to III). BAEPs are also abnormal in 33% of multiple sclerosis patients and usually involve increased interpeak latency of waves I I I to V (Merritt, p p . 68-69).
86
86. Bagaimana kita mencoba menormalkanirama yang digambarkan pada EEG dibawah ini?
A. Dengan memberikan dilantin
B. Prosedur bedah
C. Pemberian Penobarbital
D. Pemberian ACTH
E. Irama ini secara klasik tidak pekaterhadap setiap intervensi medismaupun bedah
B.
A breach rhythm is a rhythmic sharp wave pattern that appears in the region of a skull defect. The skull acts as a "low-pass filter" and screens out high frequencies generated by the cortex. The skull defect allows these higher frequencies to appear. This is the EEG of a man with a history of head trauma and a surgical scar noted within the right frontocentral region (F4, C4) ( Rolak, pp. 359-360 ) .
87
```
87. Pusat primer dari fungsi bladder yangmenyelaraskan kontraksi bladder denganrelaksasi spinkter uretral diyakini beradapada lokasi yang mana?
A. Tegmentum otak tengah
B. Hipotalamus
C. Amigdala
D. Pons
E. Talamus
```
D
There are three major muscle groups that need to be coordinated during micturition: the detrusor muscle, the internal sphincter, and external sphincter . .1\tlotor control of the bladder results primarily from parasympathetic function. The detrusor muscle and internal sphincter are heavily intluenced by parasympathetic (PN8) fibers with their cell bodies located within the 82, 83, and S4 segments of the spinal cord. Increased PN8 activity results in contraction of the detrusor muscle of the bladder and reflex inhibition of the internal sphincter, which aids bladder emptying. The external sphincter, although under voluntary control (pudendal nerve), relaxes in a retlex-type manner after internal sphincter opening and allows for micturition to occur in a synchronous fashion. The sympathetic supply to the bladder originates in cells of the intermediolateral gray column of the upper lumbar cord and passes through spinal nerves to reach the inferior mesenteric ganglia. From there, they travel as postganglionic fibers to the wall of the bladder and internal sphincter. They heavily innervate the bladder neck and trigone (a-adrenergic) and cause bladder neck closure, which aids bladder filling. The primary coordinating center for bladder function is the pontine micturition center, which synchronizes bladder contraction with sphincter relaxation. This center is inhibited by higher cortical leYels in adults but not i n children. This forms the basis for the uninhibited bladder in children, which contracts when it reaches a critical capacity. This is also seen in adults after severe head injury or the presence of tumors, hydrocephalus, stroke, or other cerebral insults. Injury to the spinal cord above the sacral Yoiding center (82-4) often produces detrusor hyperretlexia ( involuntary bladder contractions and smooth sphincter synergy) secondary to preservation of the ,•oiding center (82-4) and striated or external sphincter
88
```
88. Di antara kelainan-kelainan kandung kemihdi bawah ini, kelainan manakah yang paling mungkin disebabkan oleh adanya sindromkauda equina akut?
A. Hiperrefelsia derusor
B. Arefleksia destrutor
C. Kepatuhan bladder yang menurun
D. Tingkat arus urine naik
E. Bukan, A-D
```
B
There are three major muscle groups that need to be coordinated during micturition: the detrusor muscle, the internal sphincter, and external sphincter . .1\tlotor control of the bladder results primarily from parasympathetic function. The detrusor muscle and internal sphincter are heavily intluenced by parasympathetic (PN8) fibers with their cell bodies located within the 82, 83, and S4 segments of the spinal cord. Increased PN8 activity results in contraction of the detrusor muscle of the bladder and reflex inhibition of the internal sphincter, which aids bladder emptying. The external sphincter, although under voluntary control (pudendal nerve), relaxes in a retlex-type manner after internal sphincter opening and allows for micturition to occur in a synchronous fashion. The sympathetic supply to the bladder originates in cells of the intermediolateral gray column of the upper lumbar cord and passes through spinal nerves to reach the inferior mesenteric ganglia. From there, they travel as postganglionic fibers to the wall of the bladder and internal sphincter. They heavily innervate the bladder neck and trigone (a-adrenergic) and cause bladder neck closure, which aids bladder filling. The primary coordinating center for bladder function is the pontine micturition center, which synchronizes bladder contraction with sphincter relaxation. This center is inhibited by higher cortical leYels in adults but not i n children. This forms the basis for the uninhibited bladder in children, which contracts when it reaches a critical capacity. This is also seen in adults after severe head injury or the presence of tumors, hydrocephalus, stroke, or other cerebral insults. Injury to the spinal cord above the sacral Yoiding center (82-4) often produces detrusor hyperretlexia ( involuntary bladder contractions and smooth sphincter synergy) secondary to preservation of the ,•oiding center (82-4) and striated or external sphincter
89
```
89. Semua hal di bawah ini dapat digunakanuntuk merawat hiperrefleksia detrusor,
KECUALI
A. Propantelin (Pro-Banthine)
B. Oksibuntinin (Ditropan)
C. Tolterodin (Detrol)
D. Flavoksat (Urispas)
E. Betanekol (Urecholine)
```
E
There are three major muscle groups that need to be coordinated during micturition: the detrusor muscle, the internal sphincter, and external sphincter . .1\tlotor control of the bladder results primarily from parasympathetic function. The detrusor muscle and internal sphincter are heavily intluenced by parasympathetic (PN8) fibers with their cell bodies located within the 82, 83, and S4 segments of the spinal cord. Increased PN8 activity results in contraction of the detrusor muscle of the bladder and reflex inhibition of the internal sphincter, which aids bladder emptying. The external sphincter, although under voluntary control (pudendal nerve), relaxes in a retlex-type manner after internal sphincter opening and allows for micturition to occur in a synchronous fashion. The sympathetic supply to the bladder originates in cells of the intermediolateral gray column of the upper lumbar cord and passes through spinal nerves to reach the inferior mesenteric ganglia. From there, they travel as postganglionic fibers to the wall of the bladder and internal sphincter. They heavily innervate the bladder neck and trigone (a-adrenergic) and cause bladder neck closure, which aids bladder filling. The primary coordinating center for bladder function is the pontine micturition center, which synchronizes bladder contraction with sphincter relaxation. This center is inhibited by higher cortical leYels in adults but not i n children. This forms the basis for the uninhibited bladder in children, which contracts when it reaches a critical capacity. This is also seen in adults after severe head injury or the presence of tumors, hydrocephalus, stroke, or other cerebral insults. Injury to the spinal cord above the sacral Yoiding center (82-4) often produces detrusor hyperretlexia ( involuntary bladder contractions and smooth sphincter synergy) secondary to preservation of the ,•oiding center (82-4) and striated or external sphincter
90
90. Unsur-unsur penelusuran potensi denganpicuan aomatosensor (SSEP) atas saraf
median meliputi semua unsur di bawah ini,KECUALI
A. Pleksus brakial (Titik Erb)
B. Abu-abu sentral dari spinal cord (B13)
C. Caudal medial lemniscus (P14)
D. Otak tengah rostral (N18)
E. Daerah Broadman 5 dan 7 (N24)
E.
Somatosensory evoked potentials (SSEPs) result from stimulation of peripheral nerves (median and posterior tibial) and are generated by components of the dorsal column sensory pathways. The components of the SSEP tracing of the median nerve include Erb's point (brachial plexus) , N13 ( central gray of cervical spinal cord), P14 (caudal medial lemniscus), N18 (rostral brainstem), and N20 (primary sensory cortex) , but not Brodmann's areas 5 and 7, which are located posterior to the primary sensory cortex. SSEPs are affected by many different pathological conditions that intluence the somatosensory system, including strokes, syringomyelia, spondylosis, subacute combined deficiency, and multiple sclerosis. SSEPs are frequently utilized intraoperatively during neurosurgical procedures to monitor the integrity of the spinal cord. Some anesthetics that suppress SSEPs include benzodiazepines, halothane, and thiopental sodium (Pentothal) (Merritt, p. 7 0 ) .
91
```
91. Tn. X, 52 tahun dengan riwayat diabetesmellitus dan hipertensi dibawa ke bagiangawat darurat lokal dengan keluhanhemiparesis dan infarct yang meradang dan melibatkan bagian-bagian daridistribusi arteri serebral tengah (MSA)Angiogram pembuluh-empat yang dilakukan terhadap otak mengungkapkanadanya oklusi MSA kanan di dekat pencabangannya.Data yang diperoleh daripercobaan The National Institute ofNeurologis Disor-ders (NINDS)menunjukkan pemberian t-PA dalamjangka waktu berapa jam kejut yangdihasilkan pada level hasil yang menunjukkan perbaikan, jika administrasiini dilaksanakan selama 3 bulan dan satu tahun?
A. 3 jam
B. 6 jam
C. 8 jam
D. 12 jam
E. 24 jam
```
A.
The safety and efficacy of thrombolytic therapy has been extensively studied in acute stroke. Data obtained from the National Institute of Neurologic Disorders and Stroke (NINDS) trial showed that administering t-PA within 3 hours of symptom onset resulted in improved functional outcome at 3 months and 1 year. The benefit \\'as seen across all stroke types and was not affected by age, sex, or ethnicity. Although symptomatic i ntracerebral hemorrhage was higher in the t-PA group, there was no difference in mortality at 3 months. Other trials have assessed the safety of other thrombolytic agents with or without the addition of neuroprotective agents with mixed results. Data from the ATLANTIS trial have provided further information concerning the efficacy and safety of administering t-PA beyond the 3-hour window established by the NINDS trial. Although the drug was not shown to be effective beyond the 3-hour ,,•indo,,-_ the safety profile was similar to that of the NINDS trial. This information provides physicians with some flexibility in administering t-PA beyond the 3-hour \\'indo\\', although CHAPTER 3 Neurology Answers 73 most still advocate its administration in a time frame similar to that established by NINDS (Youmans, pp. 1595-1502) .
92
92. Karena berbagai faktor lainnya dapatmempengaruhi percepatan, termasuk tekanan darah dan aliran darah serebralsecara keseluruhan, membedakan kenaikan vasospastik dari kenaikan hiperemik dalampercepatan aliran darah MCA denganmenggunakan Doppler transkranial akan
paling baik hasilnya dengan
A. Menentukan karakter semua percepatanyang lebih tinggi dari 200 cm/detiksebagai hasil dari vasospasma
B. Mengulang penelitian Doppler dalamwaktu 1 jam untuk menguatkan hasilpembacaannya
C. Memberikan satu agen vasodilasibersama-sama dengan pemeriksaanDoppler untuk menilai perubahanpersentase alirannya
D. Mengukur “Rasio Lindegaad” untukmembantu membedakan keadaan vasospastik dari keadaan hiperemik
E. Dengan menggambar percepatandengan diperbandingkan dengandiameter pembuluh darah denganmenggunakan skala logaritmik
D.
Since other factors can influence velocities, including blood pressure and overall cerebral blood flow, distinguishing vasospastic from hyperemic increases in MCA blood tlow velocities by transcranial Doppler is best achieved by measuring the cervical carotid artery velocities in addition to the intracranial blood velocities. A "Lindegaard ratio" of V
93
```
93. Pernafasan Cheyne-Stokes
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
A
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
94
```
94. Hiperventilasi neurogenis sentral
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
B
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
95
```
95. Pernafasan kluster
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
C
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
96
```
96. Pernafasan Apneustik
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
B
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
97
```
97. Pernafasan ataksis
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
D
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
98
```
98. Pernafasan Stertorus
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
F
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
99
```
99. Ondine's curse
A. Hemisfir diensepalon/serebral bilateral
B. Pons
C. Medulla atas/Pons bawah
D. Medulla
E. Otak tengah bawah/pons atas
F. Bukan, A-E
```
D
Cheyne-Stokes respiration consists of briefs periods of hyperpnea alternating \\'ith even shorter periods of apnea and often results from large supratentorial lesions affecting either the cerebral hemispheres or diencephalon. The respiratory drive with this respiratory pattern is highly dependent on the pC02 and accumulation causes hyperpnea, which in rurn induces a drop in the pC02_ With this drop in pC02, the respiratory stimulus ceases, and a period of apnea ensues. Central neurogenic hyperventilation most often results from pontine lesions in which patients have prolonged and rapid breathing. This breathing pattern can also result from midbrain/ high pontine lesions. It may be responsive to morphine or methadone. Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds before it is released. It appears to result from lesions of the lateral tegmentum of the pons. Cluster breathing is characterized by a series of breaths following each other in an irregular sequence, which can result from low pontine or high medullary lesions. Ataxic breathing (Biot breathing) has a completely irregular pattern in which breaths with diverse amplitude and length are mixed with periods of apnea, which often follows damage to the dorsomedial medulla. Loss of automatic breathing with preserved voluntary breathing ( " Ondine's curse" ) can also occur with medullary lesions, although they tend to occur in a somewhat lower location than those c,ausing ataxic breathing. Ondine's curse has also been noted to occur after lesions involving the vemrolateral high cervical spinal cord, a location transmitting fibers from the primary medullary respiratory centers. Stertorous breathing is a sign of airway obstruction (Brazis, pp. 568-5 7 1 ; Greenberg, p. 121; Merritt, p. 18).
100
100. Seorang pasien hipertensi dengan kontrolyang buruk tiba-tiba menunjukkan gejala
menderita hemiplegia dan menurunnyaindera peraba dan posisi, kesemuanyamengenai sisi kanan, tapi sensasi atas rasasakit dan sensasi atas suhu pada kedua sisitubuh tidak berubah. Juga tampakkelemahan lain pada sisi kanan lidah sertanistagmus pukulan ke atas, tapi tidak tampak adanya keriput pada wajah. Infarctyang menyebabkan simptomatologi ini
paling mungkin terdapat pada lokasi yangmana?
A. Pontine tegmentum
B. Medulla dorsolateral
C. Tegmentum otak tengah
D. Medulla paramedian
E. Anggota badan bagian belakang darikapsul internal
D.
The tracts that were most likely affected in this patiem run along a paramedian plane in the medulla. In ventrodorsal order they consist of the pyramidal tract, medial lemniscus. medial longitudinal fasciculus, and hypoglossal nucleus. This region receives blood from the paramedian branches of the vertebrobasilar system and anterior spinal artery. The face was spared because corticobulbar fibers to the facial nucleus typically depart before reaching the medulla. Pain and temperature were spared because the lateral spinothalamic tracts run in the lateral parts of the medulla, which is supplied by the circumferential arteries. This patient is suffering from medial medullary syndrome (Dejerine's anterior bulbar syndrome) (Carpenter pp. 115-150; Brazis, pp. 345-346)
101
tabel
| 101. Transkortikal campuran
F
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
102
tabel
| 102. Konduksi
C
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
103
tabel
| 103. Motorik transkortikal
D
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
104
tabel
| 104. Global
G
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
105
tabel
| 105. Broca
A
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
106
tabel
| 106. Sensoris Transkortikal
E
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
107
tabel
| 107. Wernicke
B
| Refer to Table 3 . 10 1-3. 107 A. ( Merritt, pp. 7-11) .
108
108. Optalmoplegia internuklir bilateral dapatdibedakan dari luka nuklir rektus medialmelalui
A. Adanya pergerakan medial normaldengan sakkade pada INO bilateral
B. Adanya pergerakan medial normaldengan stimulasi vestibular pada INObilateral
C. Adanya konvergensi normal pada INObilateral
D. Adanya pergerakan lateral normal padaluka nuklir rektimedial garis tengah
E. Adanya pergerakan lateral normal padaINO bilateral
C.
It is extremely difficult to differentiate between bilateral INO and bilateral medial rectus subnucleus damage unless there is an absence of convergence (as seen with medial rectus subnucleus damage). ( Kl i ne, pp. 63-66; Merritt, pp. 2 15-2 1 7 ) .
109
```
109. Mioritmia okulomastikaloris paling seringtampak dengan kelainan yang mana?
A. Penyakit HALLERVORDEN-SPATZ
B. Palsi supranuklir-progresif
C. Penyakit WHIPPLE
D. Malformasi Arnold-Chiari
E. Penyakit CREUITZFELDT-JACOB
```
C
Oculomasticatory myorhythmia refers t o acquired pendular vergence oscillations of the eyes associated with concurrent contraction of the masticatory muscles, which may persist during sleep. This distinct disorder has been recognized only in Whipple's disease (Brazis, p. 231).
110
dari nistagmus vestibular peripheral adalah:
A. Supresi nistagmus peripheral denganfiksasi
B. Aksentuasi nistagmus sentral denganfiksasi
C. Adanya unsur torsional dengannistagmus sentral
D. Adanya kenaikan nistagmus denganarah-pandangan kepada fase nistagmuslambat
E. Adanya arah-pandangan miokloniksejalan dengan nistagmus peripheral.
A.
Two main differences that differentiate peripheral from central nystagmus include the effects of fixation on nystagmus as well as the direction of nystagmus. Fixation of the eyes suppresses peripheral but not central nystagmus. Also, peripheral nystagmus, particularly when vertical, usually has a torsional component. Pure vertical and torsional nystagmus are central (Brazis, pp. 223-224) .
111
```
111. Amantadin dapat diklasifikasi-kan sebagaijenis medikasi yang mana?
A. Agonis reseptor dopamin
B. Antagonis reseptor dopamin
C. Blocker muskarinik
D. Aktivator muskarinik
E. Bukan A sampai dengan D
```
E .
Amantadine i s an indirect dopaminergic agent that augments dopamine release from storage sites and possibly blocks dopamine reuptake into presynaptic terminals (Merritt, p. 688 )
112
```
112. Gerakan ke atas vertikal murni dari pupil ketika posisi pupil adalah 510 ke arah hidung (teraduksi).
A. Muskulus rektur atas
B. Muskulus rektur bawah
C. Muskulus rektur lateral
D. Muskulus rektus medial
E. Muskulus oblik atas
F. Muskulus oblik bawah
```
F
The globe of the eye is moved by the action of the superior and inferior oblique muscles as well as the lateral, medial, superior, and inferior recti. The superior rectus muscle ele\•ates the eye when it isabducted (23 degrees), while the inferior rectus muscle depresses the eye when the globe is abducted (23 degrees). By contrast, when the eye is adducted, the superior rectus muscle intorts the eye (moves it counterclockwise in the case of the left eye), while the inferior rectus muscle extorts the eye (moves the left eye clockwise) . The oblique muscles have a similar and complementary action in moving the eyes in a vertical plane. They move the eyeball in a vertical plane when the eye is adducted ( 5 1 degrees ) and act as rotators (intort, extort) when it is abducted (39 degrees) . Unlike the rectus muscles, however, they function as would be expected from their insertional points on the globe. The superior oblique muscle depresses the adducted eye or twists it inwardly when the eye is abducted (coun terclockwise i n the case of the left eye), and the inferior oblique muscle ele,•ates the adducted eye or extorts it when abducted (moves the left eye clockwise). The action of the lateral and medial rectus muscles causes the eyes to deviate laterally and medially, respectively (Brazis, pp. 156-157).
113
```
113. Pergerakan ke bawah murni dengan abduksi mata 230
A. Muskulus rektur atas
B. Muskulus rektur bawah
C. Muskulus rektur lateral
D. Muskulus rektus medial
E. Muskulus oblik atas
F. Muskulus oblik bawah
```
B
The globe of the eye is moved by the action of the superior and inferior oblique muscles as well as the lateral, medial, superior, and inferior recti. The superior rectus muscle ele\•ates the eye when it isabducted (23 degrees), while the inferior rectus muscle depresses the eye when the globe is abducted (23 degrees). By contrast, when the eye is adducted, the superior rectus muscle intorts the eye (moves it counterclockwise in the case of the left eye), while the inferior rectus muscle extorts the eye (moves the left eye clockwise) . The oblique muscles have a similar and complementary action in moving the eyes in a vertical plane. They move the eyeball in a vertical plane when the eye is adducted ( 5 1 degrees ) and act as rotators (intort, extort) when it is abducted (39 degrees) . Unlike the rectus muscles, however, they function as would be expected from their insertional points on the globe. The superior oblique muscle depresses the adducted eye or twists it inwardly when the eye is abducted (coun terclockwise i n the case of the left eye), and the inferior oblique muscle ele,•ates the adducted eye or extorts it when abducted (moves the left eye clockwise). The action of the lateral and medial rectus muscles causes the eyes to deviate laterally and medially, respectively (Brazis, pp. 156-157).
114
```
114. Pergerakan ke bawah murni dengan abduksi mata 510
A. Muskulus rektur atas
B. Muskulus rektur bawah
C. Muskulus rektur lateral
D. Muskulus rektus medial
E. Muskulus oblik atas
F. Muskulus oblik bawah
```
E
The globe of the eye is moved by the action of the superior and inferior oblique muscles as well as the lateral, medial, superior, and inferior recti. The superior rectus muscle ele\•ates the eye when it isabducted (23 degrees), while the inferior rectus muscle depresses the eye when the globe is abducted (23 degrees). By contrast, when the eye is adducted, the superior rectus muscle intorts the eye (moves it counterclockwise in the case of the left eye), while the inferior rectus muscle extorts the eye (moves the left eye clockwise) . The oblique muscles have a similar and complementary action in moving the eyes in a vertical plane. They move the eyeball in a vertical plane when the eye is adducted ( 5 1 degrees ) and act as rotators (intort, extort) when it is abducted (39 degrees) . Unlike the rectus muscles, however, they function as would be expected from their insertional points on the globe. The superior oblique muscle depresses the adducted eye or twists it inwardly when the eye is abducted (coun terclockwise i n the case of the left eye), and the inferior oblique muscle ele,•ates the adducted eye or extorts it when abducted (moves the left eye clockwise). The action of the lateral and medial rectus muscles causes the eyes to deviate laterally and medially, respectively (Brazis, pp. 156-157).
115
```
115. Pergerakan ke atas murni dengan abduksi mata 230
A. Muskulus rektur atas
B. Muskulus rektur bawah
C. Muskulus rektur lateral
D. Muskulus rektus medial
E. Muskulus oblik atas
F. Muskulus oblik bawah
```
A
The globe of the eye is moved by the action of the superior and inferior oblique muscles as well as the lateral, medial, superior, and inferior recti. The superior rectus muscle ele\•ates the eye when it isabducted (23 degrees), while the inferior rectus muscle depresses the eye when the globe is abducted (23 degrees). By contrast, when the eye is adducted, the superior rectus muscle intorts the eye (moves it counterclockwise in the case of the left eye), while the inferior rectus muscle extorts the eye (moves the left eye clockwise) . The oblique muscles have a similar and complementary action in moving the eyes in a vertical plane. They move the eyeball in a vertical plane when the eye is adducted ( 5 1 degrees ) and act as rotators (intort, extort) when it is abducted (39 degrees) . Unlike the rectus muscles, however, they function as would be expected from their insertional points on the globe. The superior oblique muscle depresses the adducted eye or twists it inwardly when the eye is abducted (coun terclockwise i n the case of the left eye), and the inferior oblique muscle ele,•ates the adducted eye or extorts it when abducted (moves the left eye clockwise). The action of the lateral and medial rectus muscles causes the eyes to deviate laterally and medially, respectively (Brazis, pp. 156-157).
116
```
116. Intorsi murni dengan abduksi mata 390
A. Muskulus rektur atas
B. Muskulus rektur bawah
C. Muskulus rektur lateral
D. Muskulus rektus medial
E. Muskulus oblik atas
F. Muskulus oblik bawah
```
E
The globe of the eye is moved by the action of the superior and inferior oblique muscles as well as the lateral, medial, superior, and inferior recti. The superior rectus muscle ele\•ates the eye when it isabducted (23 degrees), while the inferior rectus muscle depresses the eye when the globe is abducted (23 degrees). By contrast, when the eye is adducted, the superior rectus muscle intorts the eye (moves it counterclockwise in the case of the left eye), while the inferior rectus muscle extorts the eye (moves the left eye clockwise) . The oblique muscles have a similar and complementary action in moving the eyes in a vertical plane. They move the eyeball in a vertical plane when the eye is adducted ( 5 1 degrees ) and act as rotators (intort, extort) when it is abducted (39 degrees) . Unlike the rectus muscles, however, they function as would be expected from their insertional points on the globe. The superior oblique muscle depresses the adducted eye or twists it inwardly when the eye is abducted (coun terclockwise i n the case of the left eye), and the inferior oblique muscle ele,•ates the adducted eye or extorts it when abducted (moves the left eye clockwise). The action of the lateral and medial rectus muscles causes the eyes to deviate laterally and medially, respectively (Brazis, pp. 156-157).
117
```
117. Ekstorsi murni dengan abduksi mata 390
A. Muskulus rektur atas
B. Muskulus rektur bawah
C. Muskulus rektur lateral
D. Muskulus rektus medial
E. Muskulus oblik atas
F. Muskulus oblik bawah
```
F
The globe of the eye is moved by the action of the superior and inferior oblique muscles as well as the lateral, medial, superior, and inferior recti. The superior rectus muscle ele\•ates the eye when it isabducted (23 degrees), while the inferior rectus muscle depresses the eye when the globe is abducted (23 degrees). By contrast, when the eye is adducted, the superior rectus muscle intorts the eye (moves it counterclockwise in the case of the left eye), while the inferior rectus muscle extorts the eye (moves the left eye clockwise) . The oblique muscles have a similar and complementary action in moving the eyes in a vertical plane. They move the eyeball in a vertical plane when the eye is adducted ( 5 1 degrees ) and act as rotators (intort, extort) when it is abducted (39 degrees) . Unlike the rectus muscles, however, they function as would be expected from their insertional points on the globe. The superior oblique muscle depresses the adducted eye or twists it inwardly when the eye is abducted (coun terclockwise i n the case of the left eye), and the inferior oblique muscle ele,•ates the adducted eye or extorts it when abducted (moves the left eye clockwise). The action of the lateral and medial rectus muscles causes the eyes to deviate laterally and medially, respectively (Brazis, pp. 156-157).
118
```
118. Pada paraplegik T6 (bagian urat utuh)adanya hipertensi, sakit kepala, diaporesis,dan bradikardia harus dirawat dengan:
A. Propanolol
B. Kateterisasi bladder
C. Arfonad (blocker ganglionik)
D. 1000 cc bolus dari salinasi normal
E. Nitrogliserin
```
B.
Bladder retention and autonomic instability in a T6 paraplegic patient typically resolve with bladder catheterization ( Brazis, p. 89; Merritt, p. 422).
119
```
119. Pupil pinpoint kecil mungkin dapat dilihatpada semua hal sebagai berikut, KECUALI
A. Luka tegmental Pontine
B. Disfungsi diensepalik bilateral
C. Intoksikasi narkotik
D. Kompresi saraf okulomotor
E. Obat-obatan kolinergik
```
D.
Oculomotor nerve compression typically causes a dilated pupil, whereas a pontine hemorrhage, bilateral diencephalic injury, narcotic administration, and cholinergic drug therapy typically result in small pupils (Merritt, pp. 18-19).
120
120. Sakit bahu yang parah yang beberapa harikemudian diikuti oleh lumpuh pada tangan di sekitarnya merupakan ciri khas dari
A. Sindrom Erb-Duchene
B. Sindroma PARSONAGE-TURNER
C. Sindroma DEJERINE-KLUMPKE
D. Sindroma Benedict
E. Bukan salah satu dari A sampai dengan D
```
B.
Neurogenic amyotrophy (Parsonage-Turner syndrome) is characterized by se,•ere. acute pain located in the shoulder and radiating into the arm , neck, and back. To prevent pain, movement of the arm is a\•oided and the arm is held in a position of flexion at the elbow and adduction at the shoulder (flexion-adduction sign). The muscles innervated by the axillary, suprascapular, and long thoracic nerves are most often affected. The pain usually disappears but is then followed by paresis of the shoulder and proximal musculature (Brazis, p. 5 7 ) .
```
121
```
121. Semua hal berikut ini melibatkan motorikbawah CN VII KECUALI
A. Sindroma RAMSAY-HUNT
B. Sindroma Meige
C. Sindroma FOVILLE
D. Sindroma Benedict
E. Sindroma MILLARD-GUBLER
```
D.
Benedikt's syndrome consists o f ipsilateral oculomotor paresis, usually with a dilated pupil. as well as contralateral involuntary movements including intention tremor, hemichorea, or hemiathetosis due to red nucleus damage. Ramsay-Hunt syndrome, lvleige's syndrome, Foville's syndrome, and the Millard-Gubler syndrome involve the facial nerve (CN VII) ( B razis, pp. 359-360)
122
122. Galaktorea bisa disebabkan oleh hal-halsebagai berikut, KECUALI
A. Luka iritatif pada dinding dada bagiandepan
B. Levodopa/karbidopa
C. Hipotiroidisme
D. Adenoma Kromopobe pituitaris
E. Obat-obatan kontraseptik
B.
| Levodopa/carbidopa does not typically produce galactorrhea (Merritt, pp. 687-691).
123
```
123. “Sindroma diensepalik paramedian”mencakup semua hal di bawah ini, KECUALI
A. Hipersomnolens
B. Lupa ingatan
C. Palsi gaze horisontal
D. Apatis
E. Hemiataksia
```
C.
Infarcts involving the paramedian region of the midbrain and pons may result in decreased le,•el of conciousneness, behavioral changers ( agitation, confusion, lack of initiative, apathy), memory loss, vertical gaze and convergence disorders, contralateral hemiataxia, asterixis, motor weakness, and action tremor in the contralateral limbs . Lateral gaze palsies are not typically associated with this syndrome (Brazis, pp. 408-409).
124
124. Sindroma “Dejerine dan Rousy” palinglazim terjadi pada
A. Nuklei ventral-lateral (VL) dari thalamus
B. Nuklei ventral-posterior dari thalamus
C. Nuklei intralaminal dari thalamus
D. Nuklei genikulat
E. Nuklei subtalamik
B.
The syndrome of " Dejerine and Roussy" is characterized by contralateral sensory loss to all modalities, severedysesthesias of the involved side (thalamic pain) , vasomotor disturbances, transient contralateral hemiparesis, and choreoathetoid or ballistic movements. It is most often the result of infarction in the ventral posterior (VP) nuclei of the thalamus, which are supplied by the penetrating branches of the posterior communicating artery (Brazis, p. 548 ) .
125
```
125. Hemorase vitreus yang berasosiasidengan hemorase subaraknoid dikenalsebagai
A. Sindroma KARSON
B. Sindroma TERSON
C. Sindroma Collaret
D. Sindroma VICARD
E. Sindroma HEUBNER
```
```
B.
Subarachnoid hemorrhage (or any intracranial hemorrhage) may result in vitreous hemorrhage, also known as Terson's syndrome (Brazis, p. 559)
```
126
```
126. Protekolipid myelin
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
D
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
127
```
127. Galaktoserebrosidase
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
A
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
128
```
128. Aryl Sulfatase A
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
B
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
129
```
129. Arginase
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
G
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
130
```
130. Aspartoasilase
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
G
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
131
```
131. Transporter pengikat ATP
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
C
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
132
```
132. Metabolisme asam lemak rantai panjang
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
F
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
133
```
133. Defisiensi ATPase tembaga
A. Penyakit KRABBE
B. Leukodistropi metakromatik
C. Adrenoleukodistropi
D. Penyakit PELIZAEUS-MERZABACHER
E. Penyakit ALEXANDER
F. Sindroma Zwellweger
G. Bukan, A-G
```
G
| Refer to Table 3. 126-3 . 133A. Arginase deficiency is associated with urea
134
```
134. Sphingomielinase
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
E
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
135
```
135. α-galaktosidase A
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
C
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
136
```
136. β-glukoserebosidase
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
D
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
137
```
137. β-galaktosidase
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
I
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
138
```
138. Heksosaminidase A tidak ada; heksosaminidase B naik
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
A
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
139
```
139. Heksosaminidase A dan B kurang
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
B
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
140
```
140. Seramidase asam
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
J
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519)
141
```
141. Lipase asam
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
F
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
142
```
142. Tioesterase palmitoilprotein
A. Penyakit Tay-Sachs (GM3gangliosidosis)
B. Penyakit SANDHOFF
C. Penyakit FABRY
D. Penyakit GAUCHER
E. Penyakit NIEMANN PICK
F. Penyakit WOLMAN
G. Penyakit BATTEN (Lipofuskinosis keroidneuronal)
H. Xanthomatosis Serebrotendinus
I. GM1gangliosidosis
J. Penyakit FARBER
K. Bukan, A-J
```
G
| Refer to Table 3 . 13-!-3 . 142. ( Merritt, pp. 5 18-519) .
143
```
143. Apa yang menjadi pola bawaan telangiestasia hemorargis keturunan (HTT):
A. Resesif autosomal
B. Dominan autosomal
C. Rantai-X
D. Sporadis
E. Bukan, A-D
```
B
HHT or Rendu-Osler-Weber disease, is an autosomal dominant neurocutaneous syndrome that involves mutations i n the TGF-P receptor gene. Patients with HHT develop arteriovenous malformations of the liver, lungs, brain, and spine, in descending order of frequency. Patients with HHT also exhibit telangiectasias of the skin and mucosa, and often present with epistaxi . One key distinguishing feature of HHT is the presence of nail bed telangiectasias. The pulmonary shunts that are commonly associated with HHT put patients at significant risk for the deYelopment of brain abscesses. Patients \Yith HHT also experience paradoxical cerebral emboli, strokes. and subarachnoid hemorrhage (due to an increased risk of intracranial aneurysms) ( Merritt, p. 3 7 1; Osborn D N , pp. 106-107 ) .
144
```
144. HHT berasosiasi dengan mutasi-mutasiyang mana?
A. EGFR
B. TNF-α
C. TGF-β
D. Dismutase superoksida
E. Bukan, A-D
```
C
HHT or Rendu-Osler-Weber disease, is an autosomal dominant neurocutaneous syndrome that involves mutations i n the TGF-P receptor gene. Patients with HHT develop arteriovenous malformations of the liver, lungs, brain, and spine, in descending order of frequency. Patients with HHT also exhibit telangiectasias of the skin and mucosa, and often present with epistaxi . One key distinguishing feature of HHT is the presence of nail bed telangiectasias. The pulmonary shunts that are commonly associated with HHT put patients at significant risk for the deYelopment of brain abscesses. Patients \Yith HHT also experience paradoxical cerebral emboli, strokes. and subarachnoid hemorrhage (due to an increased risk of intracranial aneurysms) ( Merritt, p. 3 7 1; Osborn D N , pp. 106-107 ) .
145
```
145. Pasien dengan HHT berisiko tinggimenderita
A. abses otak
B. Sklerosis majemuk
C. Limpoma
D Hipoglisemia
E. Mioglobinuria
```
A
HHT or Rendu-Osler-Weber disease, is an autosomal dominant neurocutaneous syndrome that involves mutations i n the TGF-P receptor gene. Patients with HHT develop arteriovenous malformations of the liver, lungs, brain, and spine, in descending order of frequency. Patients with HHT also exhibit telangiectasias of the skin and mucosa, and often present with epistaxi . One key distinguishing feature of HHT is the presence of nail bed telangiectasias. The pulmonary shunts that are commonly associated with HHT put patients at significant risk for the deYelopment of brain abscesses. Patients \Yith HHT also experience paradoxical cerebral emboli, strokes. and subarachnoid hemorrhage (due to an increased risk of intracranial aneurysms) ( Merritt, p. 3 7 1; Osborn D N , pp. 106-107 ) .
146
```
146. Berapakah risiko stroke 1-tahun dari stenosis arteri carotid 80% asimtomatis?
A. 3%
B. 10%
C. 15%
D. 33%
E. 50%
```
A .
Symptomatic carotid artery stenosis a n d significant asymptomatic carotid artery stenosis are associated with an increased risk of stroke. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) provided strong evidence for the benefit of carotid endarterectomy over maximum medical management of patients with symptomatic ipsilateral carotid artery stenosis bet)veen 70 and 99%. In the NASCET study group, patients with mild strokes or ipsilateral hemispheric or retinal TIAs within the past 120 days exhibited a 1 7% decrease in the rate of all ipsilateral strokes (26% in medical group versus 9% in surgical group), and a 10.6% decrease in major or fatal ipsilateral stroke ( 13 . 1 % in medical group versus 2 . 5% in surgical group) at 2 years com-pared to medical management. Symptomatic patients with less than 50% carotid stenosis should not undergo carotid endarterectomy, and stenosis between 50 and 69% is controversial, with a 6 . 5% reduction in stroke rate with surgery. Asymptomatic carotid artery stenosis of greater than 75% is associated with a 3 .3% risk of stroke per year (2.5% risk of ipsilateral stroke), and stenosis of less than 75% is associated with a 1 .3% risk of stroke per year. The Asymptomatic Carotid Atherosclerosis Study (ACAS) concluded that patients with asymptomatic carotid artery stenosis greater than 60% have reduced stroke rates with carotid endarterectomy compared to medical management at 5 years ( 1 1 . 0% stroke rate in medical group versus 5 . 1 % stroke rate in surgical group). However, these results apply to patients in reasonable health and to medical centers that perform carotid endarterectomy with less than 3% perioperative morbidity and mortality ( Executive committee for ACAS, pp. 1421-1428; NASCET, pp. 445-453; Merritt, pp. 228, 2 5 7 ) .
147
```
147. Semua gangguan berikut ini berasosiasidengan pemulihan DNA cacad, KECUALI
A. Pigmentosa Xeroderma
B. Anemia Franconi
C. Sindroma BLOOM
D. Telangiestasia Ataksia
E. Sindroma KLINEFELTER
```
E . Cockayne's syndrome, ataxia telangiectasia, xeroderma pigmentosa, Fanconi's anemia, and Blooms syndrome are associated with defective DNA repair, whereas Klinefelter's syndrome is associated with an increase in the number of sex chromosomes (X.'CY) (Osborn D N , pp. 1 1- 1 2 ) .
148
```
148. Sindroma MILLER-DIEKER
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
H
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
149
```
149. Sindroma Down
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
A
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
150
```
150. Sindroma CRI DU CHAT
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
G
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
151
```
151. Sindroma PATAU
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
C
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
152
```
152. Sindroma PRADER-WILLI
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
E
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
153
```
153. Sindroma EDWARD
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
B
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
154
```
154. Sindroma Fragile X
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
I
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
155
```
155. Sindroma TURNER
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
I
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
156
```
156. Berasosiasi dengan Sindroma Dandy-Walker untuk beberapa kasus
A. Trisomi 21
B. Trisomi 18
C. Trisomi 13
D. Trisomi 9
E. Delesi lengan panjang, kromosom 15
F. Delesi lengan pendek, kromosom 4
G. Delesi lengan pendek, kromosom 5
H. Delesi lengan pendek, kromosom 17
I. Penurunan jumlah kromosom seks
J. Bukan, A-I
```
D
| Refer to Table 3 . 148-3 . 1 56A (Osborn DN, pp. 1 1-12) .
157
```
157. Semua gangguan di bawah ini berasosiasidengan titik “cherry red”, kecuali
A. Penyakit TAY-SACHS
B. Penyakit SANDHOFF
C. Stalidosis
D. Penyakit NIEMANN PICK
E. Galaktosemia
```
E.
| Galactosemia is associated with cataracts, not "cherry-red" spots (Geyer, p. 114)
158
```
158. Pigmentasi kulit yang meningkatberasosiasi dengan gangguan apa?
A. Penyakit TAY-SACHS
B. Penyakit Hurler
C. Penyakit HUNTER
D. Sindroma COCKAYNE
E. Homokistinuria
```
A.
Increased skin pigmentation is one of the features of adrenoleukodystrophy, while Hurler's syndrome, homocystinuria, and Cockayne's syndrome are associated with corneal clouding (Geyer, pp. 113-114) .
159
```
159. Lidah atropis
A. Bulbar palsy
B. Pseudobulbar palsy
C. A dan B
D. Bukan A, B dan C
```
A
Patients with bulbar palsy typically have an atrophic tongue with fasciculations, flaccid speech, a weak face, absent jaw-jerk and gag reflexes, and diminished extraocular movements. Patients with pseudobulbar palsy have a normal-sized tongue with spastic speech, a weak face, emotional lability, the presence of jaw-jerk and gag (hyperactive) ret1exes, diminished extraocular movements, and the absence of fasciculations ( Brazis, p. 3 2 1 ; Merritt, p. 239; Geyer, p. 133)
160
```
160. Muka lesu
A. Bulbar palsy
B. Pseudobulbar palsy
C. A dan B
D. Bukan A, B dan C
```
C
Patients with bulbar palsy typically have an atrophic tongue with fasciculations, flaccid speech, a weak face, absent jaw-jerk and gag reflexes, and diminished extraocular movements. Patients with pseudobulbar palsy have a normal-sized tongue with spastic speech, a weak face, emotional lability, the presence of jaw-jerk and gag (hyperactive) ret1exes, diminished extraocular movements, and the absence of fasciculations ( Brazis, p. 3 2 1 ; Merritt, p. 239; Geyer, p. 133)
161
```
161. Refleks jaw-jerk tidak ada
A. Bulbar palsy
B. Pseudobulbar palsy
C. A dan B
D. Bukan A, B dan C
```
A
Patients with bulbar palsy typically have an atrophic tongue with fasciculations, flaccid speech, a weak face, absent jaw-jerk and gag reflexes, and diminished extraocular movements. Patients with pseudobulbar palsy have a normal-sized tongue with spastic speech, a weak face, emotional lability, the presence of jaw-jerk and gag (hyperactive) ret1exes, diminished extraocular movements, and the absence of fasciculations ( Brazis, p. 3 2 1 ; Merritt, p. 239; Geyer, p. 133)
162
```
162. Gerakan ekstraokular menurun
A. Bulbar palsy
B. Pseudobulbar palsy
C. A dan B
D. Bukan A, B dan C
```
C
Patients with bulbar palsy typically have an atrophic tongue with fasciculations, flaccid speech, a weak face, absent jaw-jerk and gag reflexes, and diminished extraocular movements. Patients with pseudobulbar palsy have a normal-sized tongue with spastic speech, a weak face, emotional lability, the presence of jaw-jerk and gag (hyperactive) ret1exes, diminished extraocular movements, and the absence of fasciculations ( Brazis, p. 3 2 1 ; Merritt, p. 239; Geyer, p. 133)
163
```
163. Labilitas emosi
A. Bulbar palsy
B. Pseudobulbar palsy
C. A dan B
D. Bukan A, B dan C
```
B
Patients with bulbar palsy typically have an atrophic tongue with fasciculations, flaccid speech, a weak face, absent jaw-jerk and gag reflexes, and diminished extraocular movements. Patients with pseudobulbar palsy have a normal-sized tongue with spastic speech, a weak face, emotional lability, the presence of jaw-jerk and gag (hyperactive) ret1exes, diminished extraocular movements, and the absence of fasciculations ( Brazis, p. 3 2 1 ; Merritt, p. 239; Geyer, p. 133)
164
```
164. Cara berjalan hiperaktif
A. Bulbar palsy
B. Pseudobulbar palsy
C. A dan B
D. Bukan A, B dan C
```
B
Patients with bulbar palsy typically have an atrophic tongue with fasciculations, flaccid speech, a weak face, absent jaw-jerk and gag reflexes, and diminished extraocular movements. Patients with pseudobulbar palsy have a normal-sized tongue with spastic speech, a weak face, emotional lability, the presence of jaw-jerk and gag (hyperactive) ret1exes, diminished extraocular movements, and the absence of fasciculations ( Brazis, p. 3 2 1 ; Merritt, p. 239; Geyer, p. 133)
165
```
165. Poliovirus
A. Virus DNA
B. Virus RNA
C. A dan B
D. Bukan A, B dan C
```
```
B
Enteroviruses ( poliovirus, coxsackievirus, and echovirus), arboviruses ( t1m•i\•iruses, bunyaviruses, alphaviruses , rubiviruses), rhabdoYiruses (rabies virus), and arenaviruses (lymphocytic choriomeningitis) are RNA viruses, while the herpesviruses CHAPTER 3 Neurology Answers 77 (HSV- 1 , HSV-2, varicella zoster virus, cytomegalovirus, and HHV-6) are DNA viruses. Viral infections of the CNS can result in meningitis, ventriculitis, encephalitis, and myelitis. CSF in patients with viral syndromes of the CNS reveals increased pressure, lymphocytic pleocytosis, mild elevations in protein, and normal glucose levels. Viral (aseptic) meningitis usually peaks in the summer and fall seasons, whereas bacterial meningitis is more common during the winter. The most common causes of viral meningitis are the enteroviruses, but togaviruses are also frequent pathogens. Encephalitis often results from infections with herpes simplex virus, mumps, or arbodruses (Merritt, pp. 134- 174).
```
166
```
166. Echovirus
A. Virus DNA
B. Virus RNA
C. A dan B
D. Bukan A, B dan C
```
```
B
Enteroviruses ( poliovirus, coxsackievirus, and echovirus), arboviruses ( t1m•i\•iruses, bunyaviruses, alphaviruses , rubiviruses), rhabdoYiruses (rabies virus), and arenaviruses (lymphocytic choriomeningitis) are RNA viruses, while the herpesviruses CHAPTER 3 Neurology Answers 77 (HSV- 1 , HSV-2, varicella zoster virus, cytomegalovirus, and HHV-6) are DNA viruses. Viral infections of the CNS can result in meningitis, ventriculitis, encephalitis, and myelitis. CSF in patients with viral syndromes of the CNS reveals increased pressure, lymphocytic pleocytosis, mild elevations in protein, and normal glucose levels. Viral (aseptic) meningitis usually peaks in the summer and fall seasons, whereas bacterial meningitis is more common during the winter. The most common causes of viral meningitis are the enteroviruses, but togaviruses are also frequent pathogens. Encephalitis often results from infections with herpes simplex virus, mumps, or arbodruses (Merritt, pp. 134- 174).
```
167
```
167. Virus herpes simplex-1
A. Virus DNA
B. Virus RNA
C. A dan B
D. Bukan A, B dan C
```
```
A
Enteroviruses ( poliovirus, coxsackievirus, and echovirus), arboviruses ( t1m•i\•iruses, bunyaviruses, alphaviruses , rubiviruses), rhabdoYiruses (rabies virus), and arenaviruses (lymphocytic choriomeningitis) are RNA viruses, while the herpesviruses CHAPTER 3 Neurology Answers 77 (HSV- 1 , HSV-2, varicella zoster virus, cytomegalovirus, and HHV-6) are DNA viruses. Viral infections of the CNS can result in meningitis, ventriculitis, encephalitis, and myelitis. CSF in patients with viral syndromes of the CNS reveals increased pressure, lymphocytic pleocytosis, mild elevations in protein, and normal glucose levels. Viral (aseptic) meningitis usually peaks in the summer and fall seasons, whereas bacterial meningitis is more common during the winter. The most common causes of viral meningitis are the enteroviruses, but togaviruses are also frequent pathogens. Encephalitis often results from infections with herpes simplex virus, mumps, or arbodruses (Merritt, pp. 134- 174).
```
168
```
168. Arenavirus
A. Virus DNA
B. Virus RNA
C. A dan B
D. Bukan A, B dan C
```
```
B
Enteroviruses ( poliovirus, coxsackievirus, and echovirus), arboviruses ( t1m•i\•iruses, bunyaviruses, alphaviruses , rubiviruses), rhabdoYiruses (rabies virus), and arenaviruses (lymphocytic choriomeningitis) are RNA viruses, while the herpesviruses CHAPTER 3 Neurology Answers 77 (HSV- 1 , HSV-2, varicella zoster virus, cytomegalovirus, and HHV-6) are DNA viruses. Viral infections of the CNS can result in meningitis, ventriculitis, encephalitis, and myelitis. CSF in patients with viral syndromes of the CNS reveals increased pressure, lymphocytic pleocytosis, mild elevations in protein, and normal glucose levels. Viral (aseptic) meningitis usually peaks in the summer and fall seasons, whereas bacterial meningitis is more common during the winter. The most common causes of viral meningitis are the enteroviruses, but togaviruses are also frequent pathogens. Encephalitis often results from infections with herpes simplex virus, mumps, or arbodruses (Merritt, pp. 134- 174).
```
169
```
169. Flavivirus
A. Virus DNA
B. Virus RNA
C. A dan B
D. Bukan A, B dan C
```
```
B
Enteroviruses ( poliovirus, coxsackievirus, and echovirus), arboviruses ( t1m•i\•iruses, bunyaviruses, alphaviruses , rubiviruses), rhabdoYiruses (rabies virus), and arenaviruses (lymphocytic choriomeningitis) are RNA viruses, while the herpesviruses CHAPTER 3 Neurology Answers 77 (HSV- 1 , HSV-2, varicella zoster virus, cytomegalovirus, and HHV-6) are DNA viruses. Viral infections of the CNS can result in meningitis, ventriculitis, encephalitis, and myelitis. CSF in patients with viral syndromes of the CNS reveals increased pressure, lymphocytic pleocytosis, mild elevations in protein, and normal glucose levels. Viral (aseptic) meningitis usually peaks in the summer and fall seasons, whereas bacterial meningitis is more common during the winter. The most common causes of viral meningitis are the enteroviruses, but togaviruses are also frequent pathogens. Encephalitis often results from infections with herpes simplex virus, mumps, or arbodruses (Merritt, pp. 134- 174).
```
170
```
170. Coxsackievirus
A. Virus DNA
B. Virus RNA
C. A dan B
D. Bukan A, B dan C
```
```
B
Enteroviruses ( poliovirus, coxsackievirus, and echovirus), arboviruses ( t1m•i\•iruses, bunyaviruses, alphaviruses , rubiviruses), rhabdoYiruses (rabies virus), and arenaviruses (lymphocytic choriomeningitis) are RNA viruses, while the herpesviruses CHAPTER 3 Neurology Answers 77 (HSV- 1 , HSV-2, varicella zoster virus, cytomegalovirus, and HHV-6) are DNA viruses. Viral infections of the CNS can result in meningitis, ventriculitis, encephalitis, and myelitis. CSF in patients with viral syndromes of the CNS reveals increased pressure, lymphocytic pleocytosis, mild elevations in protein, and normal glucose levels. Viral (aseptic) meningitis usually peaks in the summer and fall seasons, whereas bacterial meningitis is more common during the winter. The most common causes of viral meningitis are the enteroviruses, but togaviruses are also frequent pathogens. Encephalitis often results from infections with herpes simplex virus, mumps, or arbodruses (Merritt, pp. 134- 174).
```
171
```
171. Berapa percepatan normal sarafperipheral manusia jika diuji denganmenggunakan elektromiografi?
A. 5 – 10 meter per detik
B. 10 – 20 meter per detik
C. 20 – 30 meter per detik
D. 30 – 40 meter per detik
E. 40 – 60 meter per detik
```
E .
The normal conduction velocity of a human peripheral nerve, as tested by electromyography, is approximately 40 to 60 m/s (Adams, p. 1023)
172
```
pic
172. Apakah neurotransmitter A?
A.Glutamat
B.GABA
C.Asetilkolin
D.Dopamin
E.Senyawa P
```
A
This i s a highly simplified depiction of the basal ganglia circuitrv. The neurotransmitters utilized by these neurons are as follows: A, D, and G utilize glutamate; B, C, and E utilize GABA, while F neurons utilize dopamine (Youmans, p. 2684) .
173
```
pic
173. Apakah neurotransmitter C?
A.Glutamat
B.GABA
C.Asetilkolin
D.Dopamin
E.Senyawa P
```
B
This i s a highly simplified depiction of the basal ganglia circuitrv. The neurotransmitters utilized by these neurons are as follows: A, D, and G utilize glutamate; B, C, and E utilize GABA, while F neurons utilize dopamine (Youmans, p. 2684) .
174
```
pic
174. Apakah neurotransmitter E?
A.Glutamat
B.GABA
C.Asetilkolin
D.Dopamin
E.Senyawa P
```
B
This i s a highly simplified depiction of the basal ganglia circuitrv. The neurotransmitters utilized by these neurons are as follows: A, D, and G utilize glutamate; B, C, and E utilize GABA, while F neurons utilize dopamine (Youmans, p. 2684) .
175
```
pic
175. Apakah neurotransmitter G?
A.Glutamat
B.GABA
C.Asetilkolin
D.Dopamin
E.Senyawa
```
A
This i s a highly simplified depiction of the basal ganglia circuitrv. The neurotransmitters utilized by these neurons are as follows: A, D, and G utilize glutamate; B, C, and E utilize GABA, while F neurons utilize dopamine (Youmans, p. 2684) .
