Neurology Flashcards

Question

Neuroleptic Malignant Syndrome

Answer 1

Defn: Due to massive dopamine blockade; risk factors neuroleptics, antiemetics [high-dose or rapid dose increase], concurrent illness dehydration\exhaustion\poor nutrition Sx: FARM (24-72 hours) fever (\>39), autonomic hyperreactivity, rigidity, MSE Findings: elevated CK, LDH, AST, leukocytosis, myoglobinuria Mgmt: discontinued drug ( results in 1-2 weeks), aggressive hydration, cooling measures, dantrolene Note:

Answer 2

Defn: Sx: usually within 12-48 h after last drink, chronic ETOH Findings: TC, usually singular, status rare Mgmt: BZD, phenobarbital Note: Dilantin is ineffective

Answer 3

Transient global amnesia is syndrome of reversible anterograde amnesia. Prognosis is generally benign. Anatomically, temporal lobe and hippocampus are sites of neurologic involvement. No clear etiology. Patients are disoriented in time and often repetitively ask questions about date or their environment. Immediate recall is intact, but delayed recall is impaired. Retrograde amnesia is common. A loss of self-awareness excludes TGA. Patients have no problems with complex motor tasks. Treatment is not required. Attention is spared, visual-spatial skills are intact, and social skills are retained. Symptoms typically last less than 24 hours. As the syndrome resolves, the amnesia improves, but the patient may be left with a distinct lapse of recollection for events during the attack.

Answer 4

Defn: distention of the labyrinthine system compressing the perilymphatic spaces Sx: vertigo lasting hours, N&V, since selling euro hearing loss tinnitus and aural fullness Findings: audiometric confirmation is suggestive Mgmt: betahistine Note:

Answer 5

The sensitivity of head CT for detecting SAH is highest in the first 6 to 12 hours after SAH (nearly 100 percent) Xanthochromia for the detection of cerebral aneurysms had a sensitivity and specificity of 93 and 95 percent. The presence of xanthochromia indicates that blood has been in the CSF for at least two hours. Only limited data   

Answer 6

* Indications for LP include the following: * First or worst headache of a patient's life * Severe, rapid-onset, recurrent headache * Progressive headache * Unresponsive, chronic, intractable headache * Neuroimaging (CT or MRI scan) should precede LP to rule out a mass lesion and/or increased intracranial pressure.

Answer 7

Meningiomas can occur anywhere from dura. Seizures common with focal deficits (visual changes), progressive unilateral visual loss, hearing loss (cerebellopontine angle), extremity weakness (parasagittal meningioma), progressive sequence of ipsilateral arm, then leg, then contralateral weakness from foramen magnum meningioma, progressive leg weakness and numbness (spinal).

Answer 8

Defn: Sx: Findings: Mgmt: Note:

Answer 9

Defn: Sx: Findings: Mgmt: Note:

Answer 10

**Drug-induced hypersensitivity syndrome** — Anticonvulsant hypersensitivity syndrome (AHS) is a rare but serious event associated with aromatic antiepileptics. idiosyncratic drug reaction, 1 in 1000 to 1 in 10,000 patients treated with phenytoin; fatality of 10 %. Symptoms - fever, rash, lymphadenopathy, pharingitis and other organ involvement. When severe, the syndrome can include hepatitis, megaloblastic anemia, rhabdomyolysis, and arteritis. Occurs two months of starting phenytoin. The diagnosis is frequently missed, and must be considered in any patient on phenytoin with suggestive symptoms. Patients who develop the hypersensitivity syndrome are at risk for recurrence and may exhibit similar reactions to other anticonvulsants

Answer 11

• Damage to the third, fourth, or sixth cranial nerves, which control eye movements. • Cancer • Trauma • Multiple sclerosis • Fluoroquinolone antibiotics[6] • Botulism • Guillain-Barré syndrome • Brain tumor • Sinusitis • Abscess • Wernicke's syndrome • Graves disease • Drunkenness • Orbital myositis • Myasthenia gravis[7] • Salicylism • Strabismus Lyme Disease

Answer 12

Indication: SEs: Dosage: Notes:

Answer 13

Defn: Sx: Findings: Mgmt: Note: positive babinski r/o Despite frequent complaints of paresthesias, objective sensory changes are minimal. A well-demarcated sensory level should not be observed in patients with GBS; such a finding calls the diagnosis of GBS into question. Reflexes are absent or reduced early in the disease course. Hyporeflexia or areflexia of involved areas represents a major clinical finding on examination of the patient with GBS. Pathologic reflexes, such as the Babinski sign, are absent. Hypotonia can be observed with significant weakness.

Answer 14

Defn: Sx: Findings: Mgmt: Note: r/o malignant Otitis externa

Answer 15

Defn: Sx: Findings: Mgmt: Note: ## Footnote is bilateral motor paresis greater in the upper than in the lower extremities. The paresis is usually greater distally than proximally, and there is variable sensory involvement (figure 2). This pattern occurs because the most central portions of the spinal tracts contain fibers from the upper extremities. Impairment in the upper extremities is usually greater than in the lower extremities and is especially prevalent in the muscles of the hand. Sensory loss is variable, although sacral sensation is usually present. Anal wink, anal sphincter tone, and Babinski reflexes should be tested. Muscle stretch reflexes may initially be absent but will eventually return along with variable degrees of spasticity in affected muscles. Bladder dysfxn is common

Answer 16

Defn: Sx: Findings: Mgmt: Note:

Answer 17

Defn: Sx: Findings: Ddx: MS Other causes include Friedreich’s ataxia, spinocerebellar degeneration, and cerebellar infarction.

Answer 18

Defn: Sx: Findings: Mgmt: Note: Could have all 3 tremors

Answer 19

Perilymphatic or labyrinthine fistula is a condition in which an abnormal communication is present between the perilymphatic space of the inner ear and the middle ear or mastoid. The manifestations of this disease vary in severity and complexity, commonly ranging from very mild to incapacitating. Perilymphatic fistulas (PLFs) may induce hearing loss, tinnitus, aural fullness, vertigo, disequilibrium, or a combination of these symptoms. Weber et al, in a follow-up article, confirmed that surgical repair of perilymph fistula does not result in a significant risk of postoperative hearing loss and that fistula repair may prevent further hearing loss, even in patients in whom a perilymph fistula was not identified at the time of surgery

Answer 20

Red flag symptoms: - thunderclap head ache - progressive head ache over days to months - new onset after age 40 - precipitated by valsalva maneurver or exertion, nocturnal occurrence or morning awakening, systemic syptoms, neurologic symptoms, etc.

Answer 21

* Pathologic response *

Answer 22

CEA should be considered for any patient with carotid artery stenosis in whom surgery will improve the natural history of the disease to a greater degree than the corresponding medical treatment would.[[7]](javascript:showrefcontent('refrenceslayer');) In symptomatic good-risk patients with surgical morbidity and mortality (stroke and death) of less than 6%, proven indications for CEA include the following: * One or more transient ischemic attacks (TIAs) in the preceding 6 months and carotid artery stenosis exceeding 50%[[3] ](javascript:showrefcontent('refrenceslayer');) Acceptable but not proven indications include the following: * Ipsilateral TIA and carotid artery stenosis exceeding 70%, combined with required coronary artery bypass grafting (CABG) * Progressive stroke and carotid artery stenosis exceeding 70% In asymptomatic good-risk patients treated by surgeons with surgical mortality and morbidity of less than 3%, the proven indication for CEA is stenosis exceeding 60%.[[4]](javascript:showrefcontent('refrenceslayer');)

Answer 23

Beta-adrenergic agonists  Terbutaline  Metaproterernol  Isoetharine  Epinephrine Psychiatric drugs  Lithium  Neuroleptics  SSRI Stimulants  Amphetamine  methylphenidate  midodrine  cocaine Heavy metals  Mercury  Lead  Arsenic  Bismuth  Methyl bromide Anticonvulsants  Valproate sodium Methylxanthines  Caffeine  Theophylline

Answer 24

**Phenytoin Toxicity:** -rarely fatal -neurological symptoms: -variable: nystagmus → ataxia → coma -binds to voltage gated sodium channels → increases membrane threshold for depolarization -excessive inhibition → incoordination altered LOC arrythmia (SA and AV node blocks) -propylene glycol in which it is storeed → hypotension, cardiac arrhythmias -70% bioavailable after oral ingestion -significant protein binding → may be displaced from plasma proteins by other drugs causing toxicity -increased concentration: protiein binding becomes saturated therfore only a small incremental dose can cause dramatic rise in free phenytoin concentrations → toxicity. -renal and hepatic clearance so renal failure could impact, but not renally dosed!

Answer 25

Aspirin for Stroke prevention * Works if previous TIA, stroke, CAD but not without a prior hx of cerebrovascular or coronary disease, even in those with carotid bruits. * The AHA/ASA 2011 recommend ASA 75-325mg for patients with obstructive atherosclerosis involving the carotid artery for prevention of ischemic cardiovascular events, acknowlding that “the benefit has not been established for prevention of stroke in asytmpomatic patients”

Answer 26

Bipap but no prophylactic abx

Answer 27

The primary symptom is diplopia from misalignment of the visual axes, and the pattern of image separation is the key to diagnosing which particular cranial nerve (and extraocular muscle) is involved. With unilateral third cranial nerve palsy, the involved eye usually is deviated down and out (infraducted, abducted), and there is ptosis, which may be severe enough to cover the pupil. In addition, pupillary dilatation can cause symptomatic glare in bright light (if the ptotic lid does not cover the pupil), and paralysis of accommodation causes blurred vision for near objects.

Answer 28

* PCA aneurysm * Cavernous sinus lesion

Answer 29

More diffuse lesions within the cavernous sinus, often inflammatory in nature, typically give rise to simultaneous involvement of the third, fourth, sixth, and first 2 divisions of the fifth cranial nerves in various combinations, which serve to define a cavernous sinus syndrome. Nonspecific or granulomatous inflammation within the cavernous sinus is referred to as Tolosa-Hunt syndrome.

Answer 30

* Peroneal nerve damage - Examination typically reveals weakness in foot dorsiflexion and foot eversion (deep and superficial peroneal nerve-innervated, respectively), with normal inversion and plantar flexion (posterior tibial nerve). Sensory disturbance is confined to the dorsum of the foot. Reflexes are normal * S1 radiculopathy – Pain radiates down the posterior aspect of the leg into the foot from the back. Weakness of plantar flexion (gastrocnemius muscle) is specific. Sensation is generally reduced on the posterior aspect of the leg and the lateral edge of the foot. Ankle reflex loss is typical.

Answer 31

Ventral CN III fascicular syndrome (Weber's Syndrome, lesion affecting cerebral peduncle) * Contralateral hemiplegia including lower face d/t CST, CBT involvement * Ipsilateral oculomotor paresis incl parasympathetic CN III (i.e. mydriasis)

Answer 32

If midbrain involved, (i.e. nuclear or fascicular third nerve lesion) almost always occurs with other neurologic signs or symptoms, which identifies the midbrain location of the lesion: * Contralateral ataxia will be present if the red nucleus/superior cerebellar peduncle is involved * Cerebellar tremor may be present in Claude syndrome (ipsilateral third nerve palsy and contralateral cerebellar signs) * Contralateral hemiparesis may be present in a cerebral peduncle lesion (Weber syndrome) * Contralateral choreiform movements or tremor are present when red nucleus/substantia nigra involvement occurs (Benedikt syndrome)

Answer 33

Brainstem stroke syndromes refer to a group of syndromes that occur secondary to occlusion of small perforating arteries of the posterior circulation. The resulted infarction has characteristic clinical picture according to the involved area however, generally there is ipsilateral cranial nerve palsy and contralateral hemiplegia/hemiparesis and sensory loss. Medulla oblongata lateral medullary syndrome (Wallenberg syndrome) medial medullary syndrome (Dejerine syndrome) hemimedullary syndrome (Babinski-Nageotte syndrome) Pons lateral pontine syndrome (Marie-Foix syndrome) inferior medial pontine syndrome (Foville syndrome) locked-in syndrome ventral pontine syndromes ventral pontine syndrome (Raymond syndrome) ventral pontine syndrome (Millard-Gubler syndrome) facial colliculus syndrome Midbrain Weber syndrome Benedikt syndrome Claude syndrome

Answer 34

* 5 — Muscle contracts normally against full resistance. * 4 — Muscle strength is reduced, but muscle contraction can still move joint against resistance. * 3 — Muscle strength is further reduced such that the joint can be moved only against gravity with the examiner’s resistance completely removed. As an example, the elbow can be moved from full extension to full flexion starting with the arm hanging down at the side. * 2 — Muscle can move only if the resistance of gravity is removed. As an example, the elbow can be fully flexed only if the arm is maintained in a horizontal plane. * 1 — Only a trace or flicker of movement is seen or felt in the muscle, or fasciculations are observed in the muscle. * 0 — No movement is observed.

Answer 35

**- Diabetic amyotrophy**: L2-L4 and occasionally L5? * Not a pure lumbosacral plexopathy because it also affects the lumbosacral nerve roots and peripheral nerves * The most likely cause is ischemic injury from a nonsystemic microvasculitis * Typically occurs in patients with *_type 2 diabetes mellitus_* that has been _recently diagnosed_ (this can be the presenting feature) or _has been under fairly good control_. * Traditional features – acute, asymmetric, focal onset of pain followed by weakness involving the proximal leg, with associated autonomic failure and weight loss. * Progression occurs over months and is followed by partial to full recovery in most patients. * Diabetic amyotrophy was the presenting feature of diabetes in 21 percent. * Most patients in the series had proximal and distal sensory loss, Diabetic lumbosacral plexopathy often occurs in conjunction with significant recent weight loss (commonly 10-40 pounds) and is associated with poor glycemic control.

Answer 36

* Subacute Combined Degeneration Classic picture of subacute combined degeneration of the dorsal (posterior) and lateral spinal columns (specific for Cbl deficiency, is due to a defect in myelin formation of unknown mechanism. ) * The neuropathy is symmetrical and affects the legs more than the arms. * It begins with paresthesias and ataxia associated with loss of vibration and position sense, and * Can progress to severe weakness, spasticity, clonus, paraplegia, and even fecal and urinary incontinence * Early in the course, poor joint position and vibration sense predominate. Typically, the legs are affected before the arms. Rarely are all limbs affected simultaneously. A Romberg sign is commonly found. The gait may be wide based. * On presentation, 50% of patients have absent ankle reflexes with relative hyperreflexia at the knees. Plantars are initially flexor and later extensor. A Hoffman sign may be found. * As the disease progresses, ascending loss of pinprick, light touch, and temperature sensation occurs. Later, depending on the predominance of posterior column versus cortical spinal tract involvement, ataxia or spastic paraplegia predominates. Then, PNS involvement causes distal limb atrophy. * Cognitive testing may reveal mild impairment or frank dementia.

Answer 37

Vertigo and disequilibrium are uncommon presenting symptoms among patients with acoustic tumors. Rotational vertigo (the illusion of movement or falling) is uncommon and is occasionally seen in patients with small tumors. Disequilibrium (a sense of unsteadiness or imbalance), on the other hand, appears to be more common in larger tumors. Overall, if carefully questioned, approximately 40-50% of patients with an acoustic neuroma report some balance disturbance. However, balance disturbance is the presenting symptom in less than 10% of patients.

Answer 38

**Burning mouth syndrome** — Burning mouth syndrome is characterized by an intraoral burning sensation for which no medical or dental cause can be found [[2](http://www.uptodate.com/contents/central-craniofacial-pain/abstract/2)]. Prior to making the diagnosis, it is important to rule out oral mucosal diseases, such as herpes simplex and aphthous stomatitis. A treatment algorithm for neuropathic pain has been proposed based upon a systematic review of randomized clinical trials in various central and peripheral neuropathic pain conditions [[41](http://www.uptodate.com/contents/central-craniofacial-pain/abstract/41)]. The following recommendations were made for central neuropathic pain: * Tricyclic antidepressants are first-line agents. * [Gabapentin](http://www.uptodate.com/contents/gabapentin-drug-information?source=see_link)/[pregabalin](http://www.uptodate.com/contents/pregabalin-drug-information?source=see_link) are second choices. However, these agents are first choices in the elderly or when tricyclics are contraindicated. * Opioids are third-line agents. When medications of choice fail, a trial-and-error approach can be attempted with other drugs that have been used for neuropathic pain, including but not limited to, [phenytoin](http://www.uptodate.com/contents/phenytoin-drug-information?source=see_link), [carbamazepine](http://www.uptodate.com/contents/carbamazepine-drug-information?source=see_link), [clonazepam](http://www.uptodate.com/contents/clonazepam-drug-information?source=see_link),[valproate](http://www.uptodate.com/contents/valproate-drug-information?source=see_link), phenothiazines, serotonin-norepinephrine reuptake inhibitors,[mexiletine](http://www.uptodate.com/contents/mexiletine-drug-information?source=see_link), and [baclofen](http://www.uptodate.com/contents/baclofen-drug-information?source=see_link) [[6](http://www.uptodate.com/contents/central-craniofacial-pain/abstract/6)].

Answer 39

Corrected Phenytoin = Measured Phenytoin Level / ( (0.2 x albumin) + 0.1)

Answer 40

**Lewy body syndromes** — The Lewy body syndromes are characterized by cytoplasmic neuronal inclusions (Lewy bodies) found in the brain and peripheral autonomic nerves of affected patients. There are three different but overlapping phenotypes: * Pure autonomic failure (PAF) with idiopathic peripheral autonomic failure as the sole clinical finding. * Parkinson disease (PD) with motor abnormalities and varying degrees of autonomic failure. * Dementia with Lewy bodies (DLB), with severe cognitive impairment associated with parkinsonism and autonomic dysfunction. * Some small number of patients with PAF may progress to develop PD or DLB [[11](http://www.uptodate.com/contents/mechanisms-causes-and-evaluation-of-orthostatic-and-postprandial-hypotension/abstract/11)], but PAF usually progresses gradually, responds well to therapy, and has a substantially better prognosis than PD or DLB [[12](http://www.uptodate.com/contents/mechanisms-causes-and-evaluation-of-orthostatic-and-postprandial-hypotension/abstract/12)]. **Multiple system atrophy (MSA)** — Another neurodegeneration with autonomic failure is MSA, also referred to as Shy-Drager syndrome, which affects the central nervous system but spares peripheral autonomic neurons. MSA has two phenotypes: parkinsonian and cerebellar, both with prominent autonomic failure. **Neuropathies** — Autonomic failure can result from peripheral neuropathies as well as autoimmune and paraneoplastic neuropathy. * Peripheral neuropathies include those caused by diabetes or amyloidosis that affect postganglionic autonomic nerves. * Autoimmune autonomic neuropathy with ganglionic nicotinic acetylcholine receptor (nAChR) autoantibodies (autoimmune autonomic ganglionopathy) is usually associated with subacute (less than three months) clinical onset of dysautonomia. In addition to orthostatic hypotension, patients also have dry eyes and dry mouth, severe upper gastrointestinal dysautonomia, large pupils that react poorly to light and accommodation, and neurogenic bladder. There is usually no objective sensory loss or motor or reflex changes. Patients are young to middle aged adults and are more likely to be female than male (ratio 2:1). * Paraneoplastic autonomic neuropathy occurs commonly in association with anti-Hu antibodies (also known as type 1 anti-neuronal nuclear antibody ANNA-1), most often in patients with small cell lung cancer, but it can be seen in other malignancies. Also associated with paraneoplastic autonomic neuropathy are Purkinje cell cytoplasmic antibodies type 2 (PCA-2) and antibodies to the neuron cytoplasmic protein, collapsin response-mediator protein-5 (CRMP-5). Bowel hypomotility, intestinal obstruction, bladder dysfunction, orthostatic hypotension, pupillomotor and sudomotor dysfunction and xerophthalmia are prominent clinical findings.

Answer 41

Lateral Medullary Infarction (Wallenberg Syndrome) * Most common syndrome related to _IC vertebral artery_ occlusion. * **Vestibulo-cerebellar** (nearly always present) - vestibular nuclei and connections, Cerebellar peduncle affected. Vertiginous sensation (variable forms) Difficulty sitting upright - often lean towards ipsilateral side. Hypotonia in ipsilateral arm (a cerebellar sign) Blurred vision/diplopia, oscillopsia. Nystagmus (both horizontal and rotatory usually) Ocular torsion - ipsilateral eye tilted downward. Limb ataxia (ipsilateral) * **Sensory Symptoms** * Pain or unpleasant feeling in *_ipsilateral_ face (s*pinal nucleus of V) * Loss of P/T in *_contralateral_ trunk and limbs* (spinothalamic tract) * The most common pattern of sensory abnormality with lateral medullary infarcts is loss of pain and temperature sensation in the ipsilateral face and the contralateral trunk and limbs. The next most frequent combination is hypalgesia in the ipsilateral face and contralateral face, trunk, and limbs. * **Bulbar Muscle Weakness** * Very prominent feature when infarct extends medially (lower CNs) * Paralysis of ipsilateral palate, pharynx, larynx - hoarseness/dysphagia, apsiration * Ipsilateral Vocal cord paralysis, Uvula deviates to side contralateral to infarct. * Odine's Curse - Failure of autonomic respirations, esp during sleep.(Caudal lesions) * Autonomic Dysfunction - Horner's in ipsilateral eye, CV insatbility (tachycardia, orthostasis with inappropriate HR response, bradycardia)

Answer 42

**POSTERIOR INFERIOR CEREBELLAR ARTERY** – Cerebellar infarction in posterior inferior cerebellar artery (PICA) distribution can involve just the vermis, or the lateral surface, or the full PICA territory. Full PICA territory infarcts are often accompanied by edema formation and mass effect (so-called pseudotumoral cerebellar infarcts). The combination of lateral medullary and PICA cerebellar infarction occurs when the intracranial vertebral artery (ICVA) is occluded and blocks the orifice of both PICA and the lateral medullary penetrators. Sometimes medial PICA territory infarcts are accompanied by dorsal medullary infarcts since the medial PICA branch has some supply to the dorsal medulla [[4,16,17](http://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/abstract/4,16,17)]. Infarcts limited to the medial vermis in medial PICA territory usually cause a vertiginous labyrinthian syndrome that closely mimics a peripheral vestibulopathy. Severe vertigo with prominent nystagmus are the major findings. Some patients also have truncal lateropulsion characterized by feelings of magnetic pulling of the trunk to the ipsilateral side. Lateral cerebellar hemisphere PICA territory infarcts are usually characterized by minor degrees of dizziness and gait incoordination with veering to the side of the lesion. Minor limb hypotonia and incoordination are found. A common syndrome is acute unsteadiness with ataxia but without vertigo or dysarthria. Body sway towards the side of the lesion, ipsilateral limb ataxia, and abnormal rapid alternating movements are also common. When the full PICA cerebellar territory is involved, headache is usually present in the occiput or high neck on the ipsilateral side. The head may also be tilted with the occiput tending to tilt toward the ipsilateral side. Vomiting, gait ataxia, truncal lateropulsion, and limb incoordination are other common findings. The truncal dysfunction is similar to that found in the lateral medullary syndrome; the body is often tilted or pulled ipsilaterally upon sitting or standing. The limb incoordination consists mostly of hypotonia rather than a rhythmic intention tremor. **Pseudotumoral cerebellar infarction** — The syndrome of pseudotumoral cerebellar infarction, with edema formation and mass effect, is most often associated with large full posterior inferior cerebellar artery (PICA) territory infarcts. After the first day or so, patients with this form of cerebellar infarction typically develop increased headache, vomiting, and decreased consciousness, with drowsiness followed by stupor. Bilateral Babinski signs are an early sign of cerebellar mass effect. Characteristic oculomotor abnormalities of large cerebellar space-taking infarcts can develop and include the following features: * Most common are a conjugate gaze paresis to the side of the lesion or a paresis of abduction limited to the ipsilateral eye * Bilateral sixth nerve paresis may occur * Later bilateral horizontal gaze palsies may develop, often accompanied by ocular bobbing These signs are due to compression of the pontine tegmentum by the swollen cerebellar infarct. Stupor is followed by deep coma when the oculomotor abnormalities become bilateral.

Answer 43

**POSTERIOR CEREBRAL ARTERIES** — Most posterior cerebral artery (PCA) territory infarcts are due to embolism from the heart, aorta, or vertebral arteries. Atherosclerosis and dissection of the PCAs is not common. The combination of hemisensory loss and hemianopia without paralysis is virtually diagnostic of infarction in the PCA territory. The occlusive lesion is within the PCA before the thalamogeniculate branches to the lateral thalamus. Rarely, occlusion of the proximal portion of the PCA causes a hemiplegia, which is probably due to infarction in the lateral midbrain [[3,35-37](http://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/abstract/3,35-37)]. Involvement of the corticospinal and/or corticobulbar tracts in the cerebral peduncles is thought to cause hemiplegia in these cases. **Left PCA territory symptoms and signs** — When the left PCA territory is infarcted, alexia without agraphia, anomic aphasia or transcortical sensory aphasia, and Gerstmann syndrome (acalculia, agraphia, finger agnosia, and right-left disorientation) may be found. Defective acquisition of new memories is common when both medial temporal lobes are damaged but also occurs in lesions limited to the left temporal lobe. The memory deficit in patients with unilateral lesions is usually not permanent but may last up to six months. Patients cannot recall what has happened recently and, when given new information, they do not recall it moments later. They often repeat statements and questions spoken only minutes before. Some patients with left PCA territory infarction have difficulty in understanding the nature and use of objects presented visually (associative visual agnosia). They can trace with their fingers and copy objects, demonstrating that visual perception is preserved; they can name objects presented in their hand and explored by touch or when verbally described. **Right PCA territory symptoms and signs** — Infarcts of the right PCA territory are often accompanied by prosopagnosia, which is difficulty in recognizing familiar faces. Disorientation to place and an inability to recall routes or to read or visualize the location of places on maps are also common. Patients with right occipitotemporal infarcts also may have difficulty visualizing what a given object or person look like. Dreams may be devoid of visual imagery. Visual neglect is much more common after lesions of the right than of the left PCA territory.

Answer 44

Anatomic approach Central * Hypothalamus * brainstem (Wallenberg's) / spinal cord (syringomyelia/myelitis) pre-ganglionic * pulmonary: Pancoast tumor * cervical rib, aneurysm or dissection of the aorta, lymph nodes, neuroblastoma * Iatrogenic: CT placement, CVC post-ganglionic * Int. carotid dissection * para trigeminal syndrome * carotid cavernous fistula * herpes zoster NOTE: imp to rule out cervicothoracic dissection or acute cavernous sinus syndrome

Answer 45

Hereditary motor sensory neuropathy (HMSN), also known as Charcot-Marie-Tooth (CMT) disease, is really a spectrum of disorders caused by a specific mutation in one of several myelin genes that result in defects in myelin structure, maintenance, and formation. Hereditary motor sensory neuropathy (Charcot-Marie-Tooth disease) has been classified as CMT types 1 through 7 and is genetically heterogeneous with more than 40 genes/loci identified to date. The major division comprises type 1 and type 2, which together are the most common hereditary peripheral neuropathies [[4](http://www.uptodate.com/contents/hereditary-primary-motor-sensory-neuropathies-including-charcot-marie-tooth-disease/abstract/4)], with an estimated prevalence of 40 per 100,000. Common features include both motor and sensory nerve manifestations with distal leg weakness, foot deformities (pes cavus, hammer toes), and sensory deficits. * CMT-1: onset first and second decade. The most common. Early complaints may include frequent sprained ankles caused by distal muscle weakness or difficulty running and keeping up with peers. The only obvious physical findings may be loss of reflexes, pes cavus foot deformity, and hammer toes. * Distal calf muscle atrophy often occurs, causing the classic "stork leg deformity." Walking is clumsy because of both muscle weakness and sensory loss. Sensory loss is gradual and mainly involves proprioception and vibration. * Later changes include atrophy of the intrinsic hand and foot muscles. Palpable enlargement of the peripheral nerves may occur secondary to nerve hypertrophy. In addition, kyphosis or scoliosis often develops. * Ambulation is variable but usually is maintained through life. Life expectancy is not affected. * Disease exacerbation can occur in pregnancy, an effect that may be mediated by increased plasma progesterone. * In addition to the typical findings discussed above, patients with type 1A HMSN may have associated sleep apnea. Nerve conduction studies (NCS) - severe slowing of conduction velocity in both the motor and sensory nerves to less than 60 percent of normal, degree often does not correlated with physical findings. Sural nerve biopsy shows demyelination that affects primarily the large nerve fibers. Onion bulbs are a characteristic feature; they reflect repeated demyelination and remyelination and represent redundant Schwann cells, collagen, and fibroblasts. Secondary axonal changes are present. The classic features of CMT2 include distal weakness, atrophy, sensory loss, decreased deep tendon reflexes and variable foot deformity [[37](http://www.uptodate.com/contents/hereditary-primary-motor-sensory-neuropathies-including-charcot-marie-tooth-disease/abstract/37)]. The onset of symptoms usually is in the second or third decade of life. The clinical course is similar to that of CMT1, but sensory symptoms, with loss of vibration and proprioception, typically predominate over motor symptoms, and peripheral nerves are not palpably enlarged. Distal trophic ulcerations in the feet may occur. Management of CMT is supportive. Specific disease-modifying therapy is not available. Daily stretching exercises early in the course of the disease may help delay ankle contractures. Orthotics are often used to help stabilize the ankles. Orthopedic foot surgery often is required by the time the patient reaches adolescence to treat the pes cavus deformity and hammer toes.

Answer 46

**DOPAMINE AGONISTS** — The dopamine agonists (DAs) are a group of synthetic agents that directly stimulate dopamine receptors. The drugs currently approved by the United States Food and Drug Administration (FDA) include [bromocriptine](http://www.uptodate.com/contents/bromocriptine-drug-information?source=see_link), [pramipexole](http://www.uptodate.com/contents/pramipexole-drug-information?source=see_link), [ropinirole](http://www.uptodate.com/contents/ropinirole-drug-information?source=see_link), [rotigotine](http://www.uptodate.com/contents/rotigotine-drug-information?source=see_link), and injectable [apomorphine](http://www.uptodate.com/contents/apomorphine-drug-information?source=see_link) ([table 1](http://www.uptodate.com/contents/image?imageKey=NEURO%2F69053&topicKey=NEURO%2F4896&rank=2%7E150&source=see_link&search=parkinsons+disease)). Pergolide has been voluntarily withdrawn from the United States market and is best avoided because it is associated with a risk of cardiac valve problems. [Apomorphine](http://www.uptodate.com/contents/apomorphine-drug-information?source=see_link) and lisuride are additional DAs that can be administered parenterally for "rescue therapy" in patients experiencing sudden akinetic episodes. Lisuride is not currently approved in the United States, but is available in Europe. Injectable apomorphine has been approved by the United States FDA for treatment of motor fluctuations in PD [[50](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/50)]. Apomorphine infusion pumps may also be useful, but are not available in the United States. Unlike [carbidopa-levodopa](http://www.uptodate.com/contents/carbidopa-levodopa-drug-information?source=see_link) (Sinemet), these drugs are direct agonists that do not require metabolic conversion, do not compete with amino acids for transport across the gut or into the brain, and do not depend upon neuronal uptake and release. An additional advantage over immediate-release forms of levodopa is the longer duration of action of most of these agents. **Monotherapy** — Dopamine agonists (DAs) were initially introduced as adjunctive treatment for advanced PD complicated by reduced levodopa response, motor fluctuations, dyskinesia, and other adverse effects of levodopa. However, the hypothetical concern that free radicals generated by the oxidative metabolism of dopamine contribute further to the degeneration of dopaminergic neurons has prompted some investigators, despite lack of conclusive evidence, to advocate the early use of DAs as an levodopa-sparing strategy [[51,52](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/51,52)]. With this approach, treatment with levodopa can be postponed and saved for a later time in the course of the disease, when disability worsens and the less effective agonists no longer provide adequate benefit. This strategy is based upon the unproven concept that the long-term duration of a given patient's responsiveness to levodopa is finite and that the drug, like money in a savings or retirement account, should be rationed. However, whether reduced responsiveness to levodopa over time is due to a decline in drug response or progression of underlying PD is currently uncertain. Given the potential that DAs are associated with fewer motor fluctuations and the evidence that there is a higher incidence of levodopa-related dyskinesia in young-onset PD, some experts suggest using DAs as initial treatment for PD in patients younger than age 60, and using the more effective agent levodopa in patients 60 and older [[53](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/53)], although other factors should be weighed in making this treatment decision. **Effectiveness of DAs** — Controlled trials have shown that [bromocriptine](http://www.uptodate.com/contents/bromocriptine-drug-information?source=see_link), pergolide, [pramipexole](http://www.uptodate.com/contents/pramipexole-drug-information?source=see_link), and [ropinirole](http://www.uptodate.com/contents/ropinirole-drug-information?source=see_link) are all effective in patients with advanced PD complicated by motor fluctuations and dyskinesia. Other studies have found that [pramipexole](http://www.uptodate.com/contents/pramipexole-drug-information?source=see_link), [ropinirole](http://www.uptodate.com/contents/ropinirole-drug-information?source=see_link), transdermal [rotigotine](http://www.uptodate.com/contents/rotigotine-drug-information?source=see_link), and pergolide are effective as monotherapy in patients with early disease. However, DAs are ineffective in patients who have shown no therapeutic response to levodopa. The decision to initiate symptomatic medical therapy in patients with PD is determined by the degree to which the patient is functionally impaired. The timing of this decision varies greatly among patients but is influenced by a number of factors, including [[1](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/1)]: * The effect of disease on the dominant hand * The degree to which the disease interferes with work, activities of daily living, or social and leisure function * The presence of significant bradykinesia or gait disturbance * Personal philosophy regarding the use of drugs The major drugs available for symptomatic therapy include: * Levodopa * MAO B inhibitors * Dopamine agonists * COMT inhibitors * Anticholinergic agents * [Amantadine](http://www.uptodate.com/contents/amantadine-drug-information?source=see_link) Either levodopa or a dopamine agonist (DA) can be used initially for patients who require symptomatic therapy [[2-4](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/2-4)]. Practitioners should always try to find the lowest but still effective dose of dopaminergic medication, either singly or in combination, for patients with PD, each of whom must be evaluated and managed in a highly individual way. In addition to these agents, low-dose estrogen may be helpful as adjunctive therapy in postmenopausal women. Most patients with PD can go without antiparkinson medications when oral intake is temporarily restricted (eg, when perioperative, or when NPO for testing), or when seriously ill. In patients who are critically ill and bedbound, the parkinsonian symptoms are typically overshadowed by the burden of other medical problems, and antiparkinson medications may not provide any clear benefit. There have been reports of patients with PD who developed neuroleptic malignant syndrome in the context of sudden withdrawal of levodopa or dopamine agonists. However, the occurrence of neuroleptic malignant syndrome in this situation is highly unusual and is typically of more theoretical than real concern. Brief withdrawals (ie, for \<24 hours) of these medications under careful supervision during hospitalization should not be an issue. When treatment is still desired for patients who are NPO, options include transdermal [rotigotine](http://www.uptodate.com/contents/rotigotine-drug-information?source=see_link) and [apomorphine](http://www.uptodate.com/contents/apomorphine-drug-information?source=see_link) by injection or continuous infusion. The use of apomorphine requires a test dose prior to ongoing treatment. Transdermal rotigotine is available in Europe, but in the United States the drug has been recalled and future availability is uncertain. Levodopa (L-dopa) is well established as the most effective drug for the symptomatic treatment of idiopathic or Lewy body PD. It is particularly effective for the management of akinetic symptoms and should be introduced when these become disabling and are uncontrolled by other antiparkinsonian drugs. Tremor and rigidity can also respond to levodopa therapy, but postural instability is less likely to do so. Adverse Effects: Nausea, somnolence, dizziness, and headache are among the more common early side effects that may accompany treatment with levodopa, but they are not likely to be serious in most patients. More serious adverse reactions to levodopa (mainly in older patients) may include confusion, hallucinations, delusions, agitation, and psychosis. A substantial number of patients develop levodopa-induced complications within several years of starting levodopa. These include motor fluctuations (the wearing-off phenomenon), involuntary movements known as dyskinesia, abnormal cramps and postures of the extremities and trunk known as dystonia, and a variety of complex fluctuations in motor function. It is estimated that such motor complications occur in at least 50 percent of patients after 5 to 10 years of treatment

Answer 47

**MAO B INHIBITORS** — [Selegiline](http://www.uptodate.com/contents/selegiline-drug-information?source=see_link) (Eldepryl), a selective monoamine oxidase (MAO) type B inhibitor ([table 1](http://www.uptodate.com/contents/image?imageKey=NEURO%2F69053&topicKey=NEURO%2F4896&rank=2%7E150&source=see_link&search=parkinsons+disease)) [[38](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/38)], is modestly effective as symptomatic treatment for PD [[39](http://www.uptodate.com/contents/pharmacologic-treatment-of-parkinson-disease/abstract/39)] and may have neuroprotective properties. In many individuals, however, [selegiline](http://www.uptodate.com/contents/selegiline-drug-information?source=see_link) monotherapy does not produce a functionally significant benefit. However, the use of selegiline in early PD is a reasonable option as long as the patient understands its limitations. In terms of MAOB inhibitors, _Selegiline_ has mild symptomatic benefit, and it may be used in patients with early PD. Its use should be limited to patients with early disease since the symptomatic benefits are unlikely to be significant in those with more advanced PD.

Answer 48

Progressive Multifocal leukoencephalopathy: **_Progressive multifocal leukoencephalopathy_** * JC Virus * Lesions usually in white matter: cortical symptoms. * Asymmetric, focal neurologic symptoms * Motor deficits (hemiparesis or monoparesis), limb ataxia, gait ataxia, and visual symptoms such as hemianopia and diplopia. Progressive multifocal leukoencephalopathy (PML) is a severe demyelinating disease of the central nervous system that is caused by reactivation of the polyomavirus JC (JC virus). Asymptomatic primary infection with JC virus occurs in childhood and antibodies can be found in 86 percent of adults [[4](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/4)]. In most individuals, JC virus remains latent in kidneys and lymphoid organs, but, in the context of profound cellular immunosuppression, JC virus can reactivate, spread to the brain, and induce a lytic infection of oligodendrocytes, which are the CNS myelin-producing cells. Progressive multifocal leukoencephalopathy occurs almost exclusively in immunosuppressed individuals. There are only isolated case reports of PML in patients without apparent immunosuppression. There are, however, reports of PML affecting patients who have conditions associated with minimal or occult immunosuppression, such as hepatic cirrhosis and renal failure. PML was initially described in patients with lymphoproliferative and myeloproliferative diseases such as chronic lymphocytic leukemia, chronic myeloid leukemia, and Hodgkin lymphoma [[11-16](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/11-16)]. It was subsequently reported in rare patients with solid organ malignancies, granulomatous and inflammatory diseases, solid organ transplant recipients, and with the use of certain drugs. Prior to the widespread use of highly active antiretroviral therapy (HAART) in the United States and Europe, PML was recognized as a major opportunistic infection associated with AIDS in adults, with a prevalence of 1 to 5 percent. PML has also been reported in patients treated with [belatacept](http://www.uptodate.com/contents/belatacept-drug-information?source=see_link) [[32,33](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/32,33)], efalizumab [[34,35](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/34,35)], fludarabine [[12-16](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/12-16)], infliximab [[36](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/36)], rituximab [[37-39](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/37-39)], mycophenolate [[40-42](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/40-42)], and glucocorticoids. PML usually manifests with **subacute neurologic deficits** including altered **mental status, motor deficits (hemiparesis or monoparesis), limb ataxia, gait ataxia, and visual symptoms such as hemianopia and diplopia**. Most patients with HIV infection and PML are profoundly immunosuppressed with CD4-positive T-cell counts \<200 per mm³. Initial symptoms may vary greatly from patient to patient, depending on the location of their lesions in the central nervous system (CNS) white matter. PML typically spares the optic nerves and the spinal cord, although incidental finding of PML lesions in the spinal cord has been reported in the post-mortem examination of one patient with HIV infection who died from hemispheric PML [[46](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/46)]. Although PML lesions are located mainly in the white matter, PML symptoms are frequently indicative of a cortical disorder. These cortical symptoms have been attributed to white matter lesions that undercut relevant cortical areas. As examples, aphasia may result from lesions underlying the language areas in the left frontal and temporal lobes, and lesions in the occipital lobe white matter can mimic symptoms of cortical blindness. However, neuropathologic study has revealed that cortical demyelination is a frequent finding with PML, suggesting that cortical symptoms in PML may arise from cortical demyelinating lesions. Seizures are usually thought to be a manifestation of cortical injury rather than white matter disease. Nonetheless, seizures occur in up to 18 percent of patients with PML, mainly when PML lesions are located immediately adjacent to the cortex [[47](http://www.uptodate.com/contents/progressive-multifocal-leukoencephalopathy-epidemiology-clinical-manifestations-and-diagnosis/abstract/47)]. The disease course of PML is usually progressive and fatal. The median survival of patients without HIV infection is only a few months. Survival in the era of highly active antiretroviral therapy is longer, but survivors are often left with severe neurologic sequelae.

Answer 49

The diagnosis of PSP is clinical. Key features typically develop over time. Participants in a National Institute of Neurological Disorders and Stroke (NINDS)/Society for PSP conference have formulated and validated clinical research criteria for the diagnosis of PSP.[1] In this system, criteria for possible PSP are as follows: Gradually progressive disorder with onset at age 40 years or older Either vertical supranuclear palsy or both slowing of vertical saccades and prominent postural instability with falls in the first year of onset No evidence of other diseases that can explain the clinical features

Answer 50

Vision loss and eye pain Afferent pupillary defect Central scotoma Papillitis with hyperemia and swelling of disk, blurring of disk margin, loss of colour vision

Answer 51

While rarely the presenting symptom, visual symptoms are common in patients with papilledema. These are typically visual obscurations that clear completely, are often unilateral, and typically very brief (just seconds) They may occur spontaneously or with changes in position, and they are believed to represent transient fluctuations in nerve head perfusion. Their presence correlates with the degree of intracranial pressure elevation. Increasing intensity, frequency, and duration of these symptoms can be a prognostic sign for visual loss. In papilledema, it is unusual for patients to have deficits of visual acuity or field loss until quite late in the course. Untreated, chronic papilledema can lead to progressive visual field loss in the form of peripheral field contraction, nerve fiber bundle defects, and even blindness

Answer 52

**PTOSIS** Congenital Ptosis (levator muscle problem) Amblyopia, strabismus also common Aponeurotic ptosis Horner Syndrome Ipsilateral Miotic Pupil Myasthemia Variable, Fatigable. Diplopia/EOM abn often +. Muscle disease May also affect Orbicularis/Extraocular/Bulbar muscle CN 3 Palsy (many causes) Nucleus **Ipsi** complete 3^rd, **Ctrl** Ptosis + SR weakness Infarct, Hemorrhage, Tumor Fascicles **Ipsi** ataxia; **Ctrl** tremor or hemiparesis (i.e. midbrain syndromes) Infarct, Hemorrhage, Tumor, Demyelination Subarachnoid space Typically **Isolated Ptosis.** +/- headache, orbital pain **ICA/PCom**/Basilar/PCA Aneurysm, **Microvascular (Ischemic),** Tumor (Pit), Meningitis, Herniation, Trauma Cavernous Sinus Horner. Prominent Pain Tumor, Inflmmation, Carotid aneurysm, Ischemic, Thrombotic, AV fistula Orbital Apex Proptosis, Visual loss, CN IV, VI, V1, V@ also affected, Horner, Pain Tumor, Trauma, Inflammation, Infection (Fungal)

Answer 53

* Earlier symptoms of CTS are pain and numbness with repetitive wrist motion. * Numbness along the Palmer aspect of the first to fourth digits; weakness comes later * Phalen's and Tinels have Se50% Sp75% _Diagnostic Criteria for Carpel Tunnel:_ * One or more of the following symptoms affecting at least part of the median nerve distribution of the hand: paresthesias; hypesthesia; pain; or numbness * One or more of the following objective findings: physical findings of median nerve compression including a positive Hoffman-Tinel sign or a positive Phalen test; diminished or absent sensation to pin prick in the median nerve distribution; or electrodiagnostic findings indicative of median nerve dysfunction across the carpal tunnel.

Answer 54

Given the available trial data, we recommend early treatment with oral glucocorticoids for all patients with Bell's palsy. Treatment should preferably begin within three days of symptom onset. Our suggested regimen is prednisone (60 to 80 mg/day) for one week. For patients with severe facial palsy, we suggest early combined therapy with prednisone (60 to 80 mg per day) plus valacyclovir (1000 mg three times daily) for one week.

Answer 55

Nerve root entrapment in lumbar spinal stenosis is caused by narrowing of the spinal canal (congenital or acquired), nerve root canals, or intervertebral foramina. This narrowing is usually caused by bony hypertrophic changes in the facet joints and by thickening of the ligamentum flavum. Disc bulging and spondylolisthesis may contribute. Symptoms of significant lumbar spinal stenosis include back pain, transient tingling in the legs, and ambulation-induced pain localized to the calf and distal lower extremity, resolving with rest.

Answer 56

* There are four prerequisites before one can begin considering a patient "brain dead" ## Footnote 1. the cause of brain death / coma should be known. 2. Exclusion of complicating medical conditions or drug intoxication or poisoning, which may confound the clinical assessment 3. Core temperature 36ºC (90ºF). There is little evidence base for a choice of threshold temperature. Because of this, Canadian forum recommendations published in 2006 substituted 34ºC as a standard 4. Abnormal Neurologic exam (any findings) * Examination must demonstrate absent cerebral or brainstem function with all of the following findings: - Coma - Absent motor response - Absent pupillary light reflex; pupils are midposition or dilated (4 to 9 mm) - Absent corneal reflexes - Absent oculocephalic reflexes (Doll's eyes) - Absent oculovestibular reflexes (caloric responses) - Absent gag reflex - Absent cough with tracheal suctioning - Absent sucking or rooting reflexes - Apnea as demonstrated by apnea test, described below * Following above, can do apnea test (spontaneous breathing trial) - Pre-oxygenate with 100% O2 for 10min - Disconnect from vent - Observe for resp efforts x 8-10min - Do ABG and reconnect to vent - Need PaCO2 to be \> 60 and \> 20 from baseline Uniform Determination of Death Act, which has been adopted by most state laws in the United States.

Answer 57

1. Carbidopa levodopa; SEs (delusion, hallucinations, dyskinesia); 2. DA: are all effective in patients with advanced PD complicated by motor fluctuations and dyskinesia; can be used in monotherapy (only if not refractory to levodopa) 3. MAOI: Selegiline; modest effective and does not significantly improve fxn.

Answer 58

Bilateral adduction difficulties = INO Internuclear ophthalmoplegia (INO) is a specific gaze abnormality, characterized by impaired horizontal eye movement with weak adduction of the affected eye and abduction nystagmus of the contralateral eye. In typical cases, convergence is spared. Abnormalities of vertical gaze are common but are not required features of an INO

Answer 59

paraneoplastic syndrome

Answer 60

is a relatively weak antiparkinsonian drug with low toxicity that is most useful in treating patients with early or mild PD and perhaps later when dyskinesia becomes problematic.

Answer 61

REfeeding Syndrome (low phosphate)

Answer 62

* Vegetative state—complete unawareness of the self and environment despite preservation of some brain functions (often cardiovascular and autonomic control). * Persistent vegetative state \>1 month after initial injury. * Permanent vegetative state \>6 months of unresponsiveness. * Minimally Concious state - In contrast to PVS, they may intermittently demonstrate limited interaction with the environment by visually tracking, following simple commands, signaling yes or no (not necessarily accurately), or having intelligible verbalization or restricted purposeful behavior. * Brain Death

Answer 63

The NIHSS is a 15-item impairment scale, intended to evaluate neurologic outcome and degree of recovery for patients with stroke. The scale assesses level of consciousness, extraocular movements, visual fields, facial muscle function, extremity strength, sensory function, coordination (ataxia), language (aphasia), speech (dysarthria), and hemi-inattention (neglect)

Answer 64

PCA * Most due to embolism from the heart, aorta, or vertebral arteries * Most frequent complaint is hemianopia. Superior quadrant field defect - just the lower bank of the calcarine fissure (the lingual gyrus). Inferior quadrantanopia if lesion affects the cuneus on the upper bank of the calcarine fissure. * Lateral thalamic infarction is the major reason for somatosensory symptoms and signs * The combination of hemisensory loss and hemianopia without paralysis is virtually diagnostic of infarction in the PCA territory.

Answer 65

Retinal Ischemia more commonly associated with embolism from ipsilateral carotid rather than heart disease (in contrast to TIAs involving cerebral hemisphere). Only about 23.8% experience the typical altitudinal visual loss, but when present, highly suggestive of retinal embolism. Episodes generally last from seconds to minutes, rarely more than 15 minutes When contralateral hemispheric symptoms (motor, sensory, aphasia) accompany visual loss, carotid disease is very likely; however, TMVL is more often an isolated symptom

Answer 66

Domains of MMSE

Answer 67

a. The classic triad of Wernicke's encephalopathy (WE) includes: 1. gait ataxia 2. encephalopathy 3. occulomotor dysfunction (nystagmus and/or palsy). WE is diagnosed in patients with two of the following four Caine criteria: * Dietary deficiency * Oculomotor abnormalities * Cerebellar dysfunction * Either altered mental status or mild memory impairment **Rx: R**ecommended regimen 500 mg of thiamine IV over 30 minutes, TID x 2 days then 500 mg IV/IM daily x 5 additional days in combination with other B vitamins Expect ocular palsies to improve within hours-days; Gait ataxia – 2 weeks; confusion – days to weeks

Answer 68

The available evidence suggests that early anticoagulation with heparin or low molecular weight heparin is associated with a higher mortality and worse outcomes compared with [aspirin](http://www.uptodate.com/contents/aspirin-drug-information?source=see_link) treatment initiated within 48 hours of ischemic stroke onset. Although full anticoagulant therapy was associated with about nine fewer recurrent ischemic strokes per 1000 patients treated, it was also associated with a nine per 1000 increase in symptomatic intracranial hemorrhage. Similarly, anticoagulants avoided about four pulmonary emboli per 1000, but this benefit was offset by an extra nine major extracranial hemorrhages per 1000

Answer 69

features that are relatively specific for TLE, including a rising epigastric sensation (often likened to a "roller coaster" sensation), and psychic or experiential phenomena, such as deja vu, jamais vu, or fear. taste and smell are less common but are also relatively specific for TLE. Unilateral automatisms are usually ipsilateral to the seizure focus, while dystonic posturing almost invariably occurs on the contralateral side. Head deviation at seizure onset is usually ipsilateral to the seizure; when it occurs later, it is contralateral

Answer 70

* L4-L5 and L5-S1 - about 90 to 95 percent of compressive radiculopathies (evenly split) * Next in frequency is L4. *Other levels are uncommon.* (And also unlikely to cause bilateral findings?) * Far lateral herniations are seen more often at the L2-4 levels. *They may affect the rostral root.* (rare, as only 10 percent of far lateral herniations will result in nerve root compression)

Answer 71

* Symmetric Polyneuropahty, Autonomic Neuropathy, Polyradiculopathies (of which amyotrophy is one), mononeuropathies (CN, Peripheral nerve, MN)

Answer 72

* Neither (mimics) - can experience PAIN! * Locked-in: pons injury from basilar artery infarct; only blinks + vert eye movmt * Akinetic mutism: prefrontal/premotor injury; tracks only * Arousal: located in the ARAS (pons, midbrain); 4 subtypes * confusion/delirium: "grumpy" * drowsiness: "dopey" - can wake up * stupor: "sleepy" - wakes up only with noxious stimuli * coma: "comatosey" - can't wake up * Awareness: Cerebrum with multiple inputs * Abulia: no will - frontal/prefrontal/basal ganglia, ACA, psych * catatonia: no movm't - NMS * conversion disorder: no dz * dissociative state: no one (multiple personality)

Answer 73

Lesions in the bilateral midbrain or pontine areas result in a decerebrate posturing, characterized by opisthotonus and extension with internal rotation of all four extremities. A hemispheric disease or upper midbrain lesions (classically above the red nucleus) can result in a decorticate posturing, characterized by extension with internal rotation of the lower extremities and flexion with adduction of the upper extremities.

Answer 74

**Pseudobulbar palsy** results from an [upper motor neuron lesion](http://en.wikipedia.org/wiki/Upper_motor_neuron_lesion) to the [corticobulbar pathways](http://en.wikipedia.org/wiki/Corticobulbar_pathway) in the [pyramidal tract](http://en.wikipedia.org/wiki/Pyramidal_tract). Patients have difficulty chewing, swallowing and demonstrate slurred speech (often initial presentation). Individuals with pseudobulbar palsy also demonstrate inappropriate emotional outbursts. Causes * [Vascular](http://en.wikipedia.org/wiki/Vascular) causes: Bilateral hemisphere infarction, [CADASIL syndrome](http://en.wikipedia.org/wiki/CADASIL_syndrome) * [Progressive Supranuclear Palsy](http://en.wikipedia.org/wiki/Progressive_Supranuclear_Palsy) * [Amyotrophic lateral sclerosis](http://en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis) (ALS) * [Parkinson's disease](http://en.wikipedia.org/wiki/Parkinson%27s_disease) * Multiple System Atrophy (related to Parkinson's disease) * Degenerative disorders: [motor neuron disease](http://en.wikipedia.org/wiki/Motor_neuron_disease) * [Inflammatory](http://en.wikipedia.org/wiki/Inflammation) disorders: [Multiple sclerosis](http://en.wikipedia.org/wiki/Multiple_sclerosis) * [Malignancy](http://en.wikipedia.org/wiki/Malignancy): High [brain stem](http://en.wikipedia.org/wiki/Brain_stem) tumors * Metabolic causes: [osmotic demyelination syndrome](http://en.wikipedia.org/wiki/Osmotic_demyelination_syndrome)[^[1]](http://en.wikipedia.org/wiki/Pseudobulbar_palsy#cite_note-pmid7484639-0) * Brain trauma Symptoms These include: * [Dysphagia](http://en.wikipedia.org/wiki/Dysphagia) (difficulty in swallowing) * [Labile affect](http://en.wikipedia.org/wiki/Labile_affect)[^[2]](http://en.wikipedia.org/wiki/Pseudobulbar_palsy#cite_note-pmid17167648-1) * [Dysarthria](http://en.wikipedia.org/wiki/Dysarthria) Signs These include: * Speech is slow, thick and indistinct * [Gag reflex](http://en.wikipedia.org/wiki/Gag_reflex) is normal, exaggerated or absent * [Tongue](http://en.wikipedia.org/wiki/Tongue) is small, stiff and [spastic](http://en.wikipedia.org/wiki/Spastic) * [Jaw jerk](http://en.wikipedia.org/wiki/Jaw_jerk) is brisk * There may be [upper motor neuron lesion](http://en.wikipedia.org/wiki/Upper_motor_neuron_lesion) of the limbs. Bulbar palsy is a similar disorder but is caused by [lower motor neuron lesions](http://en.wikipedia.org/wiki/Lower_motor_neuron_lesion)

Answer 75

1. Epileptic Seizures: -Congenital - brain malformations, inborn errors of metabolism -Drugs - withdrawal, overdose, illicit -Infections - menigintis, febrile siezures. -Structural - tumour, infarct, stroke, cerebral degeneration, truama 2. Physiologic Non-epileptic: -Metabolic - electrolyte, hypo/hyperglycemia (non-ketotic), hypoxia, hyperthryoid -Other - arrhythmia, acute intermittent porphyria 3. Psychogenic Non-epileptic - major emotional trauma, stressful psychological conflicts. 4. Seizure Mimics - syncope/TIA/migraine/BPV/hypoglycemia/sleepdisorders/periodic paralysis/ breath holding spell. Types - 1) Simple (conscious), 2) Complex (reduced LOC), 3) partical (part cortex), 4, generalized - bilateral cortex, unconscious Epilepsy \>1 unprovoked seizure Status epilepticus - \>30 min generalized seizure and warrants admission. First seizure: History, Seizure preceiptiatnts (strong emotions, intesnse exercise, loud music, flasshing lights, fever, menstrual period, lack of sleep, stress) auras (simple partial complex) , history seizures, post-ictal sate. Then labs: Screning to rule out metabolic, toxic. Then LP: essential if history suggestive of infection or cancer that might met to mengines - rule out space occupying lesion with CT! EEG - essential to diagnosis. if abnromal, routin interictal EEG may aid in supporting diagnosis. suggest general vs partial. -abnormal in 23% presenting with first sieuzre ---\> increases likelihoood of secont seizure in 2 years. -can also use sleep depreivation and provokative meausres to increase yield. -IF NORMAL DOES NOT RULE OUT EPILEPSY. -many are non-specifically abnormal. Then neuro imaging. When to Treat? -risk of reucrrent seizures is high. -Risk with single unprovoked seizure - 14% at oneyear, 29% at 3 years, 34% t 5 years. 2 year recurrecen is 40-50%. 3 RF for recurrence: 1) Epileptiform activity on EEG, 2) remote symptomatic cause - history or neuroimaging, 3) abnormal neuro exam. -consider AED if any high RF after first seizures, otherwise, generally only start after second seizure ---\> 75% risk of recurrence. -OTHER RFS for reucrrence: status epilepticus, multi seizures in one day, prior history of febrile seizures, family history, occurs during sleep. -no difference between various AED. -beware of TENS/SJS with arbemazepine, valproate, phenytoin.

Answer 76

TMC's: tension migraine cluster and chronic * Tension-type; most common type; **Bilateral, dull and viselike/band;** non-pharm tx * Migraine headache, 2nd most common, **worse with exertion,** has four phases: The prodrome—premonitory phenomena occurring hours to days prior to headache onset The aura—focal neurologic symptoms (visual), usually \<60 minutes. The headache—**unilateral, throbbing**, mod-severe intensity, and aggravated by exertion. Other symptoms: nausea, vomiting, **sensory excitability**, systemic symptoms (i.e., anorexia, diarrhea, abdominal cramps, diaphoresis, lightheadedness, irritability). Hemicranial. The postdrome—feeling tired, washed out, or depressed. * Chronic daily headache—any type of headache that occurs ≥15 days per month. Medication overuse headaches, when related to overuse of medications (e.g., nonsteroidal anti-inflammatory drugs). Tx is to limit drugs to \<=2 days/wk * Cluster headache—≥5 attacks/d of severe, **stabbing**, unilateral, **periorbital**, and/or temporal pain lasting 15-180 minutes assoc ipsilateral lacrimation, conjunctival injection, rhinorrhea, nasal congestion, forehead and facial sweating, miosis, ptosis, or eyelid edema. **Tx is 100% O2; Li or verapamil to abort.** * Thunderclap headache—maximal at onset **"explosive"**. Global * Hemicrania continua—**continuous**, **daily** unilateral headache, associated with autonomic features (miosis, ptosis, lacrimation, rhinorrhea). **Responds to Indomethacin.** * Trigeminal Neuralgia, **brief paroxysms,** shock-like w/ facial triggers * GCA, temporal, tender scalp, jaw claudications and visual changes; PMR

Answer 77

Remember 1- 2-3-4-5!! one of the phobias, 2/4, up to 3 days, at least 5 attacks five attacks are needed, each lasting 4 to 72 hours and having two of the following four characteristics: unilateral location, pulsating quality, moderate to severe intensity, and aggravation by routine physical activity. In addition, the attacks must have at least one of the following: nausea (and/or vomiting), photophobia, or phonophobia.

Answer 78

For initial treatment of patients who present to the hospital emergency department with severe migraine, particularly if the migraine is accompanied by severe nausea or vomiting, we suggest treatment with intravenous (IV) metoclopramide or prochlorperazine * Triptans (Serotonin 1b/1d agonists, inhibit the release of vasoactive peptides, promote vasoconstriction, and block pain pathways in the brainstem); Triptan for outpatients with moderate to severe migraine. There are no efficacy data that definitively support use of one triptan versus another. Based on limited evidence, it is still recommended that ?? Based on limited evidence, it is still recommended that triptans be avoided in patients with familial hemiplegic migraine, basilar migraine, ischemic stroke, **ischemic heart disease**, Prinzmetal's angina, uncontrolled hypertension, and pregnancy. Also recommend giving first dose under observation if over age 40 and risk factor for CHD even if no known CHD. * Ergotamine: drug of choice in few patients with migraine because of issues of efficacy and side effects. Ergots should be avoided in patients with coronary artery disease because they cause sustained coronary artery constriction, peripheral vascular disease, hypertension, and hepatic or renal disease. * Analgesics, antiemetics, anxiolytics In a small randomized trial, prochlorperazine was shown to be as effective as subcutaneous sumatriptan Cleveland clinic Review

Answer 79

* How to select patients for prophylaxis? * Preventive medications for migraines include antidepressants, anticonvulsants, beta-blockers, and calcium channel blockers. * Level A evidence is available for antiepileptic drugs (AEDs; divalproex sodium, sodium valproate, topiramate), beta blockers (metoprolol, propranolol, timolol), and triptans (frovatriptan for short-term menstrual-associated migraines). * Among the beta-blockers, propranolol appears to be the most effective, probably because it penetrates the blood–brain barrier the best, but is no longer the most recommended migraine preventive medication (unless \>4 /month). * Among the AEDs, valproic acid is probably the most effective, but the side effects of hair loss and lack of safety in pregnancy make it difficult to use in the patient population that is more likely to have migraines—young women. Gabapentin is another useful anticonvulsant that is not metabolized by the liver and has a minimal side effect profile. Among the tricyclic antidepressants, amitriptyline is widely used, with a good level of supportive evidence, but it also has the most side effects: dry mouth, constipation, blurred vision, and some degree of confusion and drowsiness. * Onabotulinumtoxin A, the first agent to receive U.S. Food and Drug Administration approval for chronic migraine, is likely safe and well tolerated.

Answer 80

Colchicine: * Neurological examination shows predominantly proximal muscle weakness (more in LE than UE), which is accompanied by distal areflexia and minor distal sensory loss. * CK levels are almost always elevated, usually 10 to 20-fold above normal. * Electromyography shows myopathic changes, while electron microscopy of muscle biopsy samples shows **vacuolar changes** and an accumulation of lysosomes and autophagic vacuoles. * Myopathy generally disappears a few weeks after the cessation of medication, but neuropathy may persist for a long time.

Answer 81

_ANTERIOR CEREBRAL ARTERY (embolic \>thrombotic):_ * motor and sensory deficit (leg \>face, arm) * frontal release signs (grasp, snout, root, and suckling reflexes) * abulia, paratonic rigidity, gait apraxia, personality D _MIDDLE CEREBRAL ARTERY (left dominant hemi- spheric, embolic \>thrombotic):_ * aphasia, right hemiparesis, and sensory deficit (face, arm \>leg) * may be complete hemiplegia if internal capsule involved * right spatial neglect, right homonymous hemianopia, impaired right conjugate gaze _MIDDLE CEREBRAL ARTERY (right non-dominant hemi- spheric, embolic \>thrombotic):_ * anosognosia, left motor and sensory deficit (face, arm \>leg) * left spatial neglect, left homonymous hemianopia, impaired left conjugate gaze _DEEP (SUBCORTICAL/LACUNAR) HEMISPHERE OR BRAIN STEM (small artery infarct):_ * hemiparesis (pure motor stroke); sensory loss (pure sensory stroke) * dysarthria and clumsy hand; ataxic, hemiparesis * No abnormalities of cognition, lan- guage, or vision _POSTERIOR CEREBRAL ARTERY (embolic \>thrombotic):_ * homonymous hemianopia with macular sparing * alexia without agraphia (dominant hemisphere), visual hallucinations, visual perseverations (calcarine cortex), choreoathetosis, spontaneous pain (thala- mus), third nerve palsy, paresis of vertical eye movement, sensory loss, motor deficit (cerebral peduncle, midbrain) _VERTEBROBASILAR ARTERY (brain stem, embolic =thrombotic):_ * motor or sensory loss in ALL 4 limbs; crossed signs (ipsilateral cranial nerve palsy with contralateral motor/sensory deficit), dysconju- gate gaze, nystagmus, ataxia, dysarthria, dysphagia _CEREBELLUM:_ * ipsilateral limb ataxia, gait ataxia _INTERNAL CAROTID ARTERY (thrombotic \>embolic):_ * progressive or stuttering onset of MCA syndrome * occasionally ACA syndrome as well

Answer 82

refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to an upper and lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.

Answer 83

PSP: The initial symptoms in two-thirds of cases are loss of balance, lunging forward when mobilizing, fast walking, bumping into objects or people, and falls. Other common early symptoms are changes in personality, general slowing of movement, and visual symptoms. Later symptoms and signs are [dementia](http://en.wikipedia.org/wiki/Dementia) (typically including loss of inhibition and ability to organize information), [slurring of speech](http://en.wikipedia.org/wiki/Relaxed_pronunciation), [difficulty swallowing](http://en.wikipedia.org/wiki/Difficulty_swallowing), and difficulty [moving the eyes](http://en.wikipedia.org/wiki/Eye_movement_(sensory)), particularly in the vertical direction. The latter accounts for some of the falls experienced by these patients as they are unable to look up or down. Some of the other signs are poor [eyelid](http://en.wikipedia.org/wiki/Eyelid) function, [contracture](http://en.wikipedia.org/wiki/Contracture) of the [facial muscles](http://en.wikipedia.org/wiki/Facial_muscles), a backward tilt of the head with stiffening of the [neck muscles](http://en.wikipedia.org/wiki/Table_of_muscles_of_the_human_body:_Neck),[sleep disruption](http://en.wikipedia.org/wiki/Sleep_disorder), [urinary incontinence](http://en.wikipedia.org/wiki/Urinary_incontinence) and [constipation](http://en.wikipedia.org/wiki/Constipation). The visual symptoms are of particular importance in the diagnosis of this disorder. Notably, the [ophthalmoparesis](http://en.wikipedia.org/wiki/Ophthalmoparesis) experienced by these patients mainly concerns voluntary eye movement. Patients tend to have difficulty looking down (a downgaze [palsy](http://en.wikipedia.org/wiki/Palsy)) followed by the addition of an upgaze palsy. Involuntary eye movement, as elicited by [Bell's phenomenon](http://en.wikipedia.org/wiki/Bell%27s_phenomenon), for instance, may be closer to normal. On close inspection, eye movements called "square-wave jerks" may be visible when the patient fixes at distance. These are fine movements, that can be mistaken for [nystagmus](http://en.wikipedia.org/wiki/Nystagmus), except that they are saccadic in nature, with no smooth phase. Difficulties with [convergence](http://en.wikipedia.org/wiki/Convergence_(eye)) (convergence insufficiency), where the eyes come closer together while focusing on something near, like the pages of a book, is typical. Because the eyes have trouble coming together to focus at short distances, the patient may complain of [diplopia](http://en.wikipedia.org/wiki/Diplopia)(double vision) when reading. Cardinal manifestations: * Supranuclear ophthalmoplegia * Neck dystonia * [Parkinsonism](http://en.wikipedia.org/wiki/Parkinsonism) * [Pseudobulbar palsy](http://en.wikipedia.org/wiki/Pseudobulbar_palsy) * Behavioral and Cognitive impairment * Imbalance and Difficulties walking * Frequent falls Prognosis There is currently no effective treatment or [cure](http://en.wikipedia.org/wiki/Cure) for PSP, although some of the [symptoms](http://en.wikipedia.org/wiki/Symptom) can respond to nonspecific measures. The average age at symptoms onset is 63 and survival from onset averages 7 years with a wide variance. Differential diagnosis PSP is frequently misdiagnosed as [Parkinson's disease](http://en.wikipedia.org/wiki/Parkinson%27s_disease) because of the slowed movements and gait difficulty, or as [Alzheimer's disease](http://en.wikipedia.org/wiki/Alzheimer%27s_disease) because of the behavioral changes. It is one of a number of diseases collectively referred to as [Parkinson plus syndromes](http://en.wikipedia.org/wiki/Parkinson_plus_syndrome). A poor response to levodopa along with symmetrial onset can help differentiate this disease from PD.[^[4]](http://en.wikipedia.org/wiki/Progressive_Supranuclear_Palsy#cite_note-3)

Answer 84

The Confusion Assessment Method (CAM) is a simple tool that can be used by clinicians to integrate their observations and identify when delirium is the most probable diagnosis. CAM questionaire if positive ---\> strongly argues for delerium +LR 10.3 CAM questionnaire if negative → argues against -LR 0.2 Need BOTH major criteria and one minior for test to be positive.

Answer 85

Horner syndrome is the clinical combination of ptosis, anhydrosis (decreased sweating) and miosis (constriction of pupil). It is caused by a lesion or compression on one side of the cervical or thoracic sympathetic chain. In order to get that plus a L body weakness (UMN) the lesion would need to be high up and likely prior to decussation (at the medulla oblangata). So you are looking at where the sympathetic chain meets a motor tract above the medulla. The cerebral peduncle is a region of the midbrain. It carries the corticospinal (pyramidal [carries motor signals from the brain to the spinal cord) and corticobulbar tracts (motor information from the cranial nerve nuclei to the spinal cord).

Answer 86

Overview of gait disorders: * UMN gait: When walking, the toes do not adequately clear the ground because the hip flexors are weak, and the toes scuff with each step. The strategy of circumduction at the hip helps with toe clearance. Inspection of the patient's shoes may show wearing of the soles at the tips. * LMN gait: In a patient with LMN foot drop, the gait is high stepping because the hip flexors are strong and compensate for the weakness to allow foot clearance. There may be an audible slap as the foot hits the ground. * Myopathic gait: In myopathy, because of limb girdle weakness, the gait is waddling and there is abnormal pelvic tilt with each step. * Parkinson’s: shuffling gait. In B12 deficiency, the neuropathy is symmetrical and affects the legs more than the arms. It begins with paresthesias and ataxia associated with loss of vibration and position sense, and can progress to severe weakness, spasticity, clonus, paraplegia, and even fecal and urinary incontinence.

Answer 87

Picture of blurred optic disc, inc central scotoma. This is likely optic neuritis associated with MS. MS – Common symptoms include viual loss, diplopia, sensory symptoms in limbs or face, acute or subacute motor weakness, gait disturbance and balance problems, Lhermitte's sign (electric shock-like sensations that run down the back and/or limbs upon flexion of the neck), bladder problems, limb ataxia, acute transverse myelopathy, and pain. In MS, optic neuritis (ON) is the most common type of involvement of the visual pathways. It usually presents as acute or subacute unilateral eye pain that is accentuated by ocular movements. This is followed by a variable degree of visual loss (scotoma) affecting mainly central vision. In ON, disc edema (papilledema) may be observed on fundus examination when the acute ON lesion involves the head of the optic nerve Other eye findings in MS are internuclear ophthalmoplegia (INO) refers to abnormal horizontal ocular movements with lost or delayed adduction and horizontal nystagmus of the abducting eye. It is caused by a lesion of the medial longitudinal fasciculus on the side of diminished adduction.

Answer 88

CN VII innervates the platysma. However, it does not decrease hearing. If anything, since it innervates the stapedius, sounds will seem louder (hyperacusis). If the defect was from a central cause, then no facial asymmetry with spontaneous smile. Bell's palsy typically presents with the sudden onset (usually over hours) of unilateral facial paralysis. Common findings include the eyebrow sagging, inability to close the eye, disappearance of the nasolabial fold, and the mouth drawn to the non affected side. Associated manifestations may include decreased tearing, hyperacusis, and/or loss of taste sensation on the anterior two-thirds of the tongue. Central Peripheral Lesion Location UMNContralateral motor cortex Descending pyramidal tractsLMNPeripheral nerve / facial nucleus in the ipsilateral ponsWeakness Predominantly lower facial musclesBoth upper and lower facial muscles Movements affected: All facial movements on the side affected Causes Unilateral- Stroke, demyelination (MS)- Cerebral tumours Bilateral- Pseudobulbar palsy, poliomyelitis - motor neuron disease Pontine (ass. with CN 5 and 6 lesions)- Aneurysm, Tumour, Syringobulbia, MSPosterior fossa (ass. with CN 8)- Acoustic neuroma, meningioma, meningitisPetrous Temporal Bone (Facial Canal)- Bell’s Palsy, Ramsay-Hunt, Otitis mediaass with hyperacusis and/or loss of tasteParotid Gland- Tumour, SarcoidBilateral- Sarcoid, GBS, MG, Myopathies

Answer 89

status = seizures longer than 5 min tx: ativan 0.1 mg/kg / diazepam (can be given rectally)

Answer 90

1st Line: Levetiracetam

Answer 91

**LAW OF 3's (Three Stooges)** * Single, unprovoked **OR** sz w/ med change: Investigations and 3 months * Epilepsy on meds: No sz for 6 months (except for the following) * Epilepsy postop: No sz for 12 months * Epilepsy diagnosed: No sz for 2 yrs; otherwise wait 12 months * Epilepsy drug taper: No sz for 5 yrs (off meds) and clear EEG in prev 6 mos * ETOH: abstinent AND sz free for 6 mos after rehab program * Auras/Simple partial: Stable dz for 12 months [https://www.cma.ca/secure/assets/assets-library/document/en/CMA-Drivers-Guide-8th-edition-e.pdf](https://www.cma.ca/secure/assets/assets-library/document/en/CMA-Drivers-Guide-8th-edition-e.pdf)

Answer 92

* Neurologic Exam: Definitely * Drug screen: Considered but NO evidence of benefit * Neuroimaging: Definitely; MRI preferred but emergent CT may be considered * EEG: Definitely; may be done as outpt except in non-convulsive status (useful for prognosis as well as tx determination) * ECG: Definitely; sz-like attacks with a cardiovascular cause may be misdiagnosed as epilepsy [http://www.epilepsytoronto.org/.../download.php?...Recommendations%20in%...](http://www.epilepsytoronto.org/.../download.php?...Recommendations%20in%...)

Answer 93

**LAW of FIVE** 1. ONE drug whenever possible 2. TWO drugs together only when switching and tapering off 3. THREE important Drugs: * Valproate * Carbamazepine * Phenytoin 4. FOUR important reactions: 1. Pregnancy/teratogenicity 2. STS/TENS: carbamazepine in Hans Chinese 3. Hepatotoxicity 4. Renal Injury 5. FIVE Reasons to monitor levels: 1. Therapeutic Range 2. Compliance 3. Pregnancy 4. Hospitalization or comorbid dz 5. New meds http://www.epilepsytoronto.org/.../download.php?...Recommendations%20in%... [NICE clinical guidelines, 2012] http://www.ncbi.nlm.nih.gov/books/NBK2597/#ch14.s1

Answer 94

* Myoclonic Epilepsy * Pseudoseizures * Hypnagogic Hallucinations * Absence Seizures * Encephalopathy *

Answer 95

* Non-tumors **(ABCD/QRST)**: Abscess, Blood vessels (AVM), Cysts, Demyelinating DZ; "Quirky" toxo, radiation induced, Sarcoidosis, TB * Tumors: Primary vs. Mets * Mets: multifocal with **ring enhancement @ GW jxn**; Breast, Lung, melanoma, Lymphoma * Primary: Histological (or benign vs malignant) * Glioma (30%): may enhance and can be bihemispheric; astocytoma/gliobalstoma (bleeding), ependymoma, oligodendroglioma (honeycomb pattern) * Meningioma (35%): **Extradural, calcified, "light bulb" lesions** * Schwannoma: Cerebropontine angle * Medulloblastoma: Posterior fossa +/- **hydrocephalus** * Craniopharyngioma (1%) * Pituitary (12%)/Pineal * Notes: * Rule of 1/3's: two of the major types are ~30% each; 30% of all types are malignant and 5yr mortality are ~30% * Always get family hx: FAP, Li-Fraumeni, neurofibromatosis * MMSE must \>24 in order to be considered to drive MKSAP 16

Answer 96

* Common presentation of carotid artery embolism * Temporary monocular blindness "shade over vision" * medical emergency

Answer 97

1. vertigo: illusion of movement often related to a disorder of the vestibular system 2. near syncope: lightheadedness related to inadequate cerebral perfusion 3. disequilibrium: and unsteadiness related to a lack of sensory input or processing

Answer 98

is for neurocardiogenic or supected cardiac syncope

Answer 99

definition: traumatically induced transient disturbance of brain function, involving a complex pathophysiological process. * immediate cessation from activities and prompt assessment by a licensed health care provider. * Initial assessment should be guided by a symptom checklist, cognitive evaluation, balance test, and for the neurologic examination. * In suspected or diagnosed concussion the individual should be monitored for deterioration * hypnotics should be avoided in the first 10 hours * patient cannot return to activity on the same day, even without headaches * routine imaging is not indicated and is reserved for patients with neurologic symptoms

Answer 100

1. Iron deficiency anemia 2. diabetes 3. end-stage renal disease

Answer 101

ulnar neuropathies are characterized by normal grip, triceps reflex and lack of the Tinel sign at the elbow.

Answer 102

* M.D., most common form of muscular dystrophy and adults, affects one in 8000 persons worldwide. it has a variable presentation with an autosomal dominant inheritance pattern. It is a multiorgan disease that is incurable. * Type I (Steinert): DM, primary hypogonadism, and testicular atrophy are common problems. Cardiac arrhythmias may also be seen. * Type II: generally milder in symptoms

Answer 103

IV methyl prednisolone 1 g daily 3-5 days; no conclusive evidence that it reduces disability at six months but it may shorten symptoms.

Answer 104

Defn: calcium debris in semicircular canal Sx: Brief vertigo after changes in position; nystagmus +/-nausea vomiting Findings: Dix-Hallpike Mgmt: Epley maneuver Note: can be caused by head trauma

Answer 105

* Peripheral * BPV, * labyrinthitis - ativan, antinauseants, * vestibular neuritis, recurrent vestibulopathy, * toxic vestibulopathy: AG, loop diuretics, NSAIDs, cytotoxtic, AED *

Answer 106

* a.k.a. "rocker bottom" foot * etiology: diabetic neuropathy related inflammation * x-ray should be the initial imaging modality: subtle fractures or subluxations

Answer 107

* Apraxia (inability to perform multistep task) is an early indication of frontal parietal problems such as Alzheimer's disease

Neurology Flashcards

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