Neurology Flashcards
Neonatal Abstinence Syndrome
Classic Signs - 5
TYT Does Heroin
- Tremors
- Yawning
- Tachypnea
- Diarrhea
- High Pitched Cry
Caused by maternal opioid (Heroin) use during pregnancy
Which Germ Layer does the ANT Pit come from?
Surface Ectoderm
A: Primary CNS Lymphoma is the ___ most common cause of _____ in HIV pts
B: What virus is this associated with?
C: What WBCs would you expect to see in the brain tissue
A: 2nd most common cause of ring enhancing lesions in HIV pts (1st = Toxoplasmosis Gondi)
B: EBV
C: B-lymphocytes
A: What function does the iliohypOgastric nerve have (3)
B: What happens when Surgery (Appendectomy) damages it? (2)
A:
- [Suprapubic Sensation]
- [Gluteal Region Sensation]
- [Anterolateral Abd Mucle Motor]
B: Loss of the above areas + [Suprapubic Burning]
Dandy Walker Malformation
Clinical Manifestation (2)
(Dan - D - Walk - Er = 4 syllables = 4th Vt Dilitation (2/2 → )
+
Can’t walk with NO CEREBELLUM FORMATION!
A: Wilson Disease MOD
B: Wilson Disease Mode of Inheritance and genetic cause
A: Damaged Hepatocytes leak free copper and the copper deposits in other tissues (basal ganglia / cornea)
B: [Auto Recessive ATP7B gene mutation]
Wilson Disease Clinical Manifestation (4)
- Hepatic (Acute Liver Failure - Cirrhosis & Chronic Hepatitis)
- Neuro - (Gait Ataxia / Parkinsonism)
- Psych - Personality Changes
- Cornea - Kayser Fleishcer rings
Wilson Disease
A: Dx (2)
B: Tx
A: DEC Ceruloplasmin and [INC Urinary Copper Excretion]
B: D-Penicillamine
Causes of Congenital Hydrocephalus (4)
- Congenital Obstruction (aqueductal stenosis vs. [Chiari malformation Type 2])
- Acquired Obstruction (infection vs. posthemorrhagic)
A: Congenital Hydrocephalus Clinical Manifestations (6)
B: Tx
PEDS w/ Mushy Brain
- Macrocephaly
- Bulging Fontanelle
- Enlarged Ventricles
- Poor feeding
- Developmental Delay
- [Spasticity & Hyperreflexia (from periventricular pyramidal tract stretching)]
B: Ventriculoperitoneal Shunt
Most common [1° CNS Tumors] in PEDs (3)
PEDs
Pilocytic Astrocytoma = MOST COMMON
Ependymoma
meDulloblastoma (PNET tumor) = 2nd most common
Which 2 Pediatric Brain Tumors occur in the [Cerebellar Vermis]
[Pilocytic Astrocytoma] and meDulloblastoma
Cerebellar Vermis = Midline POST fossa
Image shows [Pilocytic Astrocytoma]
A: Histology for [PNET - Primitive NeuroEctodermal Tumors] (MeDulloblastoma)
B: Pgn
A: Sheets of [small, primitive blue cells] + [abundant mitotic figures]
B: POOR! (PNET tumors are undifferentiated and aggressive)
A: Histology for [Pilocytic Astrocytoma] (3)
B: Pgn
A:
Pilocytic Astrocytes (spindle cells with hair-like glial processes)
+
Rosenthal Fibers
+
[Cerebellar Vermis Cyst]
B: (Better than MeDulloblastoma since it is well-differentiated)
A: Describe Opsoclonus-Myoclonus Syndrome
B: What Childhood tumor is it associated with?
A: [Non-Rhythmic Conjugate Eye mvmnts] with myoclonus= “Dancing Eyes and Feet”
B: Neuroblastoma (onset 2 y/o)
Neuroblastoma Histology
[Homer Wright Rosettes] made of [small round blue cells w/purple nuclei]
A: Neuroblastoma Genetic cause
B: Neuroblastoma Pgn
A: N-myc amplifcation
B: [Better pgn for pts < 1 yo]
Describe the Neuroblastoma metastasis process (6)
image
Histology for [Acute Neuronal Injury] (AKA ___ _____) (4)
[Acute Neuronal Injury (AKA RED NEURON)]
- Cell Body Shrinks
- Nuclei Pyknosis
- Loss of Nissl substance
- Eosinophilic Cytoplasm
THIS IS IRREVERSIBLE INJURY that eventually –> Neuronal Degeneration!
What causes [Acute Neuronal Injury] (AKA ___ _____) and When do the changes appear?
[Acute Neuronal Injury (RED NEURON)]
12-24 Hrs post [Transient Severe Insult]
Histology for [Chromatolysis Axonal Rxn (Loss of Axon)] (4)
[Chromatolysis Axonal Rxn (Loss of Axon)]
- Cell Body ENLARGES
- Nucleolus ENLARGES
- Eccentric nucleus
- Dispersion of Nissl substance
Histology for [Neuronal Atrophy 2° to Degenerative Dz] (2)
- Neuronal Loss eventually (compensated for by Gliosis)
- Reactive Gliosis = Astrocyte proliferation in area of neuron degeneration –> Glial Scar (compensates for volume loss)
Can come After [Acute Neuronal Injury (AKA RED NEURON)]
A: What are Craniopharyngiomas
B: What type of tissue do they arise from
A: Suprasellar Pediatric tumors
B: Remnants of Rathke’s Pouch (Embryonic Precursor of ANT Pituitary)
A: Craniopharyngiomas Composition
B: What type of tissue do they arise from
A: [Brownish Calcified Cyst containing cholesterol and [wet keratin]
B: Remnants of Rathke’s Pouch (Embryonic Precursor of ANT Pituitary)
A: Deep [Intraparenchymal HTN Hemorrhage] is most commonly caused by _____, which results in rupturing of _____
B: This begins as a ______ Aneurysm
A: Deep [Intraparenchymal HTN Hemorrhage] is most commonly caused by HTN, which results in rupturing of [lenticulate small penetrating arteries]
B: Charcot Bouchard Aneurysm
Acute [Intraparenchymal HTN Hemorrhage] in image
Where does Charcot Bouchard Aneurysms occur (4)
Charcot Bouchard Tears Pink
- Basal Ganglia
- Cerebellum
- Thalamus (shown in image below)
- Pons
Acute [Intraparenchymal HTN Hemorrhage] in image
- What’s the Difference in size between [Charcot Bouchard Aneurysms] and [Berry Saccular Aneurysms]?
- Which is associated with Subarachnoid Hemorrhage?
- [Charcot Bouchard Aneurysm] = < 1 mm
vs.
[Berry Saccular Aneurysm] = 2-25 mm variable
- [Berry Saccular Aneurysm] = Subarachnoid Hemorrhage
What conditions are associated with [Berry Saccular Aneurysm]? (5)
“Eating AppleBerries Can Sound Heavenly”
- ADPKD**
- [Ehlers Danlos Syndrome]
- HTN
- SAH
- Coarctation of Aorta (associated w/HTN)
Where do [Berry Saccular Aneurysms] occur?
Circle of Willis
Dx for Multiple Sclerosis (3)
- MRI: [Periventricular demyelinating plaques with lipid laden macrophages]
- CSF Oligoclonal IgG bands
- Visual Assessment (test conduction velocity)
A: Syringomyelia MOD
- How does this manifest (2)
Formation of [CSF filled syrinx cavity] in cervical region of spinal cord –> damages [Ventral white commissure (crossing fibers for STT)] –> [Bilateral Pain/Temp Loss in Arms & Hands]
***Eventually Ventral Horns are destroyed also –> LMN signs (FAW) - Fasciculations / Atrophy & Areflexia / Weakness
Destructive Site for Syringomyelia
A
What type of Hydrocephalus is shown
Normal Pressure Hydrocephalus
CT: Symmetrical Dilation of Ventricles
A; Normal Pressure Hydrocephalus Sx (3)
B: What causes Normal Pressure Hydrocephalus
Wacky, Wobbly & Wet!
Wacky (dementia)
Wobbly (ataxia)
Wet (Urinary Incontinence from compressing periventricular cortex white fibers traveling to sacral micturition center)
B: Idiopathic; Episodic; Occurs in Elderly. Does not INC SubArachnoid space volume.
Which vessels are affected by [TUMTL-Transtentorial Uncal Medial Temporal lobe] Herniation? (5) What manifestations result from this?
[TUMTL Hernation–> Compression of [COPPR- [Crus Cerebri CTL] / PCA / [Oculomotor CN3] / Paramedian Pontine vessels/ Reticular Formation] –>
- [Crus Cerebri CTL] compression –> CTL Hemiparesis
- [PCA compression] –> Occipital lobe infarct –> CTL homonymous hemianopsia w/Macular sparing
- Oculomotor CN3 compression –> [Ipsilateral “Down & Out” Eye + Dilated Pupil + Ptosis]
- Paramedian Pontine vessel compression –> Duret Hemorrhage
- Reticular formation compression–> Altered Mental Status
- Clinical Manifestation for [MIOS-MLF Internuclear Ophthalmoplegia Syndrome] (3)
2: MIOS seen in Younger pts indicates _____
3: MIOS seen in OLDER pts indicates ______
[MIOS-MLF Internuclear Ophthalmoplegia Syndrome]
1.
*[Impaired ADDuction of affected eye]
+
[Normal ADDuction of affected eye during [near reflex convergence]
+
*[Nystagmus of UNaffected eye when attempting to ABduct]
C:
1) Younger pts= Multiple Sclerosis
2) Older pts= Ischemic infarction
Clinical Manifestation of Multiple Sclerosis (9)
Charcot classic triad of MS is a [SLUM SiiiN] !
Sensory sx
Lheurmitte sign = pain when chin is touched to chest
Uhthoff phenomenon (heat sensitivity)
Motor sx
Scanning Speech
[Internuclear Ophthalmoplegia (MIOS) w/eye pain] / Intention Tremor / Incontinence
Neuritis Optic - Loss of vision with Marcus Gunn Pupils
Ocular Clinical Presentation for Diabetic Mononeuropathy (3)
DM –> Oculomotor CN3 Central Ischemia
- Ptosis (from Levator Palpebrae paralysis)
- Down & Out Eye
- NORMAL PERRL (since Parasympathetic fibers are spared)
Which part of the Cerebellum would cause Truncal and Gait Ataxia? What system is affected?
Upper Vermis - Medial Descending System
Which part of the Cerebellum would cause Vertigo/Nystagmus (2)? What system is affected?
Flocculonodular Lobe
+
Medial Descending System
Vestibular Nuclei
Which part of the Cerebellum would cause [Limb Dysmetria & Rebound Check Response loss]? What system is affected?
Intermediate Hemispheres - [Lateral Descending system]
Which part of the brain demonstrates the most atrophy in Alzheimer’s Dz? (2)
Hippocampus and Temporoparietal Lobe
Identify
image
Identify
image
What 2 brain cells come from Neuroectoderm?
Astrocytes and Oligodendrocytes
Embryologically, where does Microglia originate from?
[Mesoderm - Bone Marrow Monocytes]
Describe Oligodendrocyte Histology
Pale halO surrounding [small / round / dark nuclei] cells
[Creutzfeldt Jakob Dz] MOD
PrP (prion protein), normally in neurons as [a-helical structure] converts–> [INFECTIOUS Beta pleated sheets] –> Protease resistance –>
Vacuoles in [Gray Matter Neurons & Neutrophils] develop –> Cyst = [Spongiform Gray Matter]
Microscopic findings for [Creutzfeldt Jakob Dz]
Vacuoles in [Gray Matter Neurons & Neutrophils] develop –> Cyst = [Spongiform Gray Matter]
Remember: These PrP are INFECTIOUS!
Facial CN7 Functions (4)
FACE
- Facial Muscles
- Afferents(Somatic) from [Ear Pinna (Pain/Temp)] & [External Auditory Canal (stapedius m.)]
- Cry: Parasympathetics to [Lacrimal/Salivary/Sublingual/Submandibular/]
- Eat: Taste from ANT 2/3 Tongue
Clinical Manifestations for [Bells Palsy] (4)
Bells Palsy = Facial CN7 paralysis
Loss of F –> Unilateral Paralysis
Loss of A –> Hyperacusis
Loss of C–> DEC Eye lacrimation (tearing)
Loss of E –> Loss of ANT 2/3 Tongue Taste
FACE
- Facial Muscles
- Afferents(Somatic) from [Ear Pinna (Pain/Temp)] & [External Auditory Canal (stapedius m.)]
- Cry: Parasympathetics to [Lacrimal/Salivary/Sublingual/Submandibular/]
- Eat: Taste from ANT 2/3 Tongue
What Spinal Columns are affected in [Subacute Combined Degeneration]?-3 ; How does this manifest?-3
[SuBACute Combined Degeneration]
[Demyelinating lesions] in 3 Thoracic Spinal Columns:
- [Dorsal–> Loss of 2TVP]
- [Lateral CST –> UMN Weak MESH + Ataxia]
- Spinocerebellar
Causes of [Subacute Combined Degeneration] (3)
[SuBACute Combined Degeneration]
1) B12 Deficiency
2) Copper Deficiency
3) AIDS/HIV
* Affects Dorsal / Lateral CST / Spinocerebellar Tracts (Combined)*
Describe SChWannoma Histology (3)
SChWannoma
- Cellularity with Biphasic pattern (Antoni A & B areas)
- [Verocay Bodies within Antoni A areas]
- S100 positivity (indicates neural crest origin) - also seen in melanoma
Verocay Bodies = Interspersing nuclear free zones within Antoni A palisading pattern: shown in image
Where does SChWannomas arise from (3)
SChWannoma
Peripheral n. vs. Nerve Roots vs. [All CN except 2]
Most common type of Intracranial SChWannoma. Where is it located?
SChWannoma
Acoustic Neuroma: located at [CN8 Cerebellopontine Angle]
Verocay Bodies = Interspersing nuclear free zones within Antoni A palisading pattern: shown in image
Identify the arrow AND what Dz it’s associated with
SChWannoma
Verocay Bodies = Interspersing nuclear free zones within Antoni A palisading pattern: shown in image
Myotonia Dystrophy Clinical Manifestation (5)
My Tonia, My Toupee, My TV Viewers, My Ticker, My Testicles,
Tonia = MyoTonia = [sustained muscle contraction with Weakness & Atrophy]
Toupee = Frontal Balding
TV viewer = Cataracts
Ticker = Arrhythmia
Testicle = Testicular Atrophy
Myotonia Dystrophy MOD
My Tonia, My Toupee, My TV Viewer, My Ticker, My Testicles,
Auto Dom [CTG repeat] on [DMPK (Dystrophy Myotonia Protein Kinase) gene] –> Type 1 Dystrophy
Describe Histological finding for [Ischemic Hypoxic Encephalopathy]
Bilateral Wedge shaped strips of necrosis over the cerebral convexity, parallel & adjacent to the [longtitudinal cerebral fissure]
List the Location of Watershed infarcts in the Brain (2)
Between perfusion Zones of [ANT-Middle] and [Middle-POST] Cerebral a.
Bilateral Wedge shaped strips of necrosis over the cerebral convexity, parallel & adjacent to the [longtitudinal cerebral fissure]: shown in image
Chiari Malformation MOD
Congenital Underdevelopment of [POST Fossa] –> [Cerebellar and Medulla herniation] through foramen magnum
Describe Chiari Malformation Type 2
Type 2 is TOO BAD:
SEVERE NEONATAL ONSET –> [LUMBAR MYELOMENINGOCELE] & [CONGENITAL HYDROCEPHALUS]
Huntington’s Dz MOD
[AUTO DOM [Chromo 4 CAG repeats]] —> Degeneration of (Caudate nc. inside the ((I)ndirect Striatum) –> [DEC GABA]
“Hunting 4 food is way too aggressive & dancey”
Huntington’s Dz Clinical Presentation (2)
“Hunting 4 food is way too aggressive & dancey”
1st: Aggressive Dementia w/ strange behavior
2nd: Dance-like Chorea mvmnts
When does Huntington’s Dz onset
30 - 40 y/o
Parkinsonism Clinical signs (7)
PARK & ham
[Pill Rolling Resting Tremor]
[Rigidity Cogwheel]
BradyKinesia
[AReflexia posturally] –> Fall
+
- hypOphonic speech
- Autonomic Dysfunction (constipation / bladder problems / orthostatic hypOtension)
- micrographia
- PARK = primary signs*
Friedreich Ataxia involves Degeneration of the ______, [____ and ____ spinal columns]
FriEdreich Ataxia involves Degeneration of the [Dorsal and Spinocerebellar spinal columns]
FriEdrecih is Fratastic! He’s your fav. twisted frat brother, always studdering and falling, but has a sweet, big heart
A: Deficency of what Vitamin mimics Friedreich Ataxia
B: Friedreich Ataxia Mode of Inheritance
FriEdreich Ataxia
A: Vitamin E (will also have Hemolytic anemia)
B: [Chromo 9 Auto Recessive]
Describe Friedreich Ataxia (8)
FriEdreich is Fratastic! He’s your fav., twisted frat iHouse brother, always studdering and falling, but has a sweet, big heart
FriEdreich = [Vitamin E Deficiency] mimics it
Fratastic has 9 letters = [Chromo 9 Auto Recessive]
twisted = Kyphoscoliosis @ childhood
frat = [frataxin (iron binding protein) defect]
iHouse = [(iron binding protein) defect]
studdering = Dysarthria
falling = [Falls + Gait Ataxia + (Pes Cavus High Foot Arch)]
sweet = DM
big heart = Hypertrophic Cardiomyopathy
Involves Degeneration of [Dorsal, Lateral CST & Spinocerebellar]
Explain the MOD for this Dz process (2)
Liquefactive Necrosis
Hypoxic CNS Injury —> Lysosomal complete digestion of necrotic tissue –> cystic cavity formation
vs.
Bacteria or Fungal Abscess formation also –> Liquefactive Necrosis
What causes Coagulative Necrosis
Irreversible Ischemic Injury (every organ EXCEPT BRAIN)
What causes FAT Necrosis
Acute Pancreatitis
What causes Caseous Necrosis (5)
TB vs. Histoplasma vs. Cryptococcus vs. Coccidioides vs. Nocardia
Morphology for Coagulative Necrosis (2)
- Preserved Tissue Architecture (since lytic enzymes denature b4 they have a chance to break dwn)
- Anucleated Cells with eosinophilic cytoplasm
Morphology for FAT Necrosis
Release of Lipase allows fatty acids to combine with Ca+ –> [Chalky White Saponification]
Morphology for Caseous Necrosis (2)
- Cheesy Tan-White Appearance
- Granuloma
What structures does the lenticulostriate vessels perfuse (5)
lenticulostriate vessels perfuse everything in [Be TIPC] EXCEPT PONS!
Basal Ganglia
Thalamus = pure sensory stroke
[Internal Capsule / / Corona Radiata] = pure motor stroke
Lacunar Stroke MOD
lenticulostriate vessels perfuse [Be TIPC]
Lacunar Stroke= [HTN Arteriolosclerosis] of lenticulostriate vessels –> [cystic infarcts < 15 mm] –> Lacunar Syndrome
Describe the Lacunar Syndrome
lenticulostriate vessels perfuse [Be TIPC]
Lacunar Stroke= [HTN Arteriolosclerosis] of lenticulostriate vessels –> [cystic infarcts Lacunar Syndrome (listed below)
1A: [Internal Capsule/Pons/Corona Radiata] Stroke–> pure Motor stroke (ataxia vs. clumsy hand)
1B: ThalamuS Stroke –> pure Sensory stroke
Most common [1° CNS Tumors] in Adults (3)
GMS
Glioblastoma (GRADE 4 - MALIGNANT - MOST COMMON)
MeninGioma
SChWannoma
Glioblastoma Radiographic Findings (2)
- Midline shift from Lateral Vt. Compression (Red arrow)
- Butterfly lesion from crossing Corpus Collosum
Glioblastoma Histological Findings (5)
CREEPY
- Cystic Change
- Reddish brown hemorrhage
- Endothelial Cell Hyperplasia on Histo
- Pseudopalisading Necrosis on Histo - image
- Yellow necrosis
What’s the marker for Glioblastoma?
GFAP
A: [LEMS - Lambert Eaton Myasthenic Syndrome] MOD
B: Clinical Presentation (2)
A: [Autoimmune attack against (Presynpatic Ca+ channel)–> No ACh release]
B:
- Fatigable Weakness of [Proximal limbs and trunk] mimicking myopathy
- Autonomic sx (Dry mouth /Orthostasis / Impotence)
What other condition is [LEMS - Lambert Eaton Myasthenic Syndrome] associated with?
“LEMS has a good SOLC(soul)”
SOLC-Small Oat cell Lung Carcinoma
Name 3 Differentiating Factors for Myasthenia Gravis vs. [Lambert Eaton Myasthenic Syndrome]
- [LEMS] improves with exercise/exertion during the day!
- [LEMS] will show no imprvmnt with [Tensilon Edrophonium] injection
- [LEMS] nerve testing shows INC muscle responses
What other condition is [Myasthenia Gravis] associated with?
May cause Thymoma(thymic hyperplasia)
[Myasthenia Gravis] MOD
Autoantibodies block and degrade [postsynpatic nicotinic ACh Receptors]] –> [DEC motor end plate potential]
[Myasthenia Gravis] Clinical Presentation (6)
Generalized= P DDD WF
[Ptosis
[Diplopia from Disconjugate gaze]
Dysarthria
Dysphagia
[Weakness(Respiratory / limbs / Extraocular m.)
[Fatigue that worsens throughout day]
Violent Infant Shaking —> ________. This is characterized by what 3 things?
B: How is this differentiated from similar conditions?
Violent Infant Shaking –> [AHT- Abusive Head Trauma]! =
- Subdural Hemorrhage (from tearing bridging veins between Dura and Arachnoid)
- Retinal Hemorrhages Bilaterally (from congested retinal vein ruptures)
- POST rib fractures
B: Accidental Fall is not sufficient for Subdural Hemorrhage OR Retinal Hemorrhage
AHT is formely known as Shaken Baby Syndrome
[Von Hippel Lindau Dz] Clinical Presentation (3)
[Cerebellar Hemangioblastoma]
+
[Cyst of Kidney vs. Liver vs. Pancreas]
+
Pheochromocytoma
[Von Hippel Lindau Dz] MOD
[Tumor cells lose [Chromo 3 VHL Tumor suppressor gene] –> [INC VEGF from Hypoxia Inducible Factor]
Tuberous Sclerosis MOD
([Hamartin C1 9q] and [Tuberin C2 16p])–> HAMARTOMASSS
Tuberous Sclerosis Clinical Presentation (12)
HAMARTOMASSS
[Hamartomas benign]
[Angiofibroma on Face-triad] - image
Mitral Regurgitation
[Ash Leaf Macules]
[Rhabdomyoma Cardiac –> Valvular Obstruction]
Tuberous Sclerosis
AUTO DOM
Mental Retard-triad
[AngioMyoLipoma Kidney]
Seizures-triad
SEGA (SubEpendymal Giantcell Astrocytoma)
[Shagreen forehead patches]
Genetic Cause of Neurofibromatosis Type 1
[chromo 17 mutation]–> [NeurofibroMin loss]. NeurofibroMin tumor suppresses (RAS GTPase activating protein
Characteristics of Neurofibromatosis Type 1 (6)
CLAP ON type 1!”
- Neurofibroma PLEXIFORM
- Acoustic Schwannoma-Unilateral (HA/Tinnitus/Vertigo)
- [Optic n. Glioma]
- Lisch nodules
- [Cafe Au Lait Spots]
- Pheochromocytoma
Neurofibromatosis Type 2 Genetic Cause
[chromo 22 tumor suppresor gene mutation–> (Merlin cytoskeletal protein)]
Neurofibromatosis Type 2
Clinical Manifestation (2)
- [Bilateral Acoustic Schwannomas] (HA/Tinnitus/Vertigo)
- Multiple Meningiomas
Bilateral Acoustic Schwannomas @ Cerebellopontine angle
A: [HIV Encephalopathy] Histology
B: [HIV Encephalopathy] PGN
A: Microglial Nodules (microglial formed around necrotic areas) –> fuse & form [multinucleated Giant Cells]
B: [Subcortical Dementia from HIV attacking gray matter] –> Progressive cognitive decline
Describe Decerebrate Posturing
[dEcErEbrate ExtEnsor posturing]
Rigid ExtEnsion of UE and LE
Describe Decorticate Posturing
[Decorticate Flexion Posturing] “Flex toward ur Core”
Rigid Flexion of UE
but
LE Extension
Describe [Cavernous Hemangiomas] and list the 2 things they put pts at risk of developing
Vascular malformations in the brain parenchyma –> INC risk of [intracerebral hemorrhage & Seizures]
This Mass is a Vascular Malformation that INC pt risk for Intracerebral hemorrhage and Seizures
What is this lesion and where does it occur?
Cavernous Hemangioma occur in [Brain Parenchyma above Cerebellar Tentorium]
Which Fish bind to Na+ channels (Brain & Heart) and inhibit Na+ influx –> prevents action potential conduction? (2)
- [Tetrodotoxin Puffer Fish]
- [Saxitoxin Red Tide Dinoflagellates]
will have DEC Deep Tendon Reflexes
Which Fish bind to Na+ channels (Brain & Heart) and KEEP IT OPEN –> PERSISTENT depolarization? (2)
- [Ciguatoxin Exotic Fish vs. Moray eel]
- [Batrachotoxin South Amr. frog]
Name the Major UMN signs (5)
UMN signs = Weak MESH
Weakness
[Spastic Paralysis]
[Exaggerated Reflexes (Babinski)]
Mental Status change
HemipLegia
A: What 2 microbes is [1° CNS Lymphoma] associated with?
B: Which lymphocytes are involved and what’s pgn?
- EBV
- HIV/AIDS
B: B-cell lymphoma that’s a high-grade tumor = POOR PGN!
Alzheimer’s Dz MOD (3)
Alzheimers MOD = CHA
**Cleavage, Hemorrhage, ACh **
- Cleavage of [transmembrane amyloid precursor glycoprotein] –> Beta-amyloid which accumulates–> [Neuritic Senile plaques] in temporal lobe early on.
- Eventually Beta-amyloid starts to deposit in cerebral vessels –> [Spontaneous Occipital/Parietal hemorrhages]
- Beta-amyloid accumulation causes defective [Choline acetyltransferase] in the [Basal nc. of Meynert] & Hippocampus –> DEC ACh in those areas –> Alzheimer Sx
How do you diagnose Alzheimer’s Dz? (2)
- Apple Green Birefringence when stained with Congo red under polarized light
- [Hyperphosphorylated Tau Neurofibrillary Tangles]
[Amyotrophic Lateral Sclerosis] (Lu Garret’s) MOD
[Superoxide Dismutase gene mutation] –> copper-zinc dysfunction —>[Upper AND Lower Motor Neuron Disease!]
UMN Dz includes loss of neurons in motor nc. 5/9/10/12
A: Tx for ALS
B: What do pts with ALS end up dying from?
ALS (AKA Lu Garrets Dz)
A: RiLuzole (DEC Glutamate release since Glutamate over excites neurons)
B: Respiratory Complications (PNA vs. failure)
[Carpal Tunnel Syndrome] MOD
BILATERAL Median n. Compression from the [Flexor Retinacular Transverse carpal ligament] –> Peripheral mononeuropathy
[Flexor Retinacular Transverse Carpal ligament] can be surgically incised for relief
[Carpal Tunnel Syndrome] Clinical Manifestation (4)
- Paresthesia vs. Pain with Median n. Distribution (worst at night)
- Thenar Atrophy from motor weakness (flexion/ABduction/Opposition impairment)
- Tinel Sign (tapping over flexor surface DEC sx)
- Phalen Sign (flexing Wrist INC sx)
CARPEL TUNNEL IS BILATERAL
Which parts of the brain are the most susceptible to injury post [Global Cerebral Ischemia] (3)
- Hippocampus (pyramidal cells) <—AFFECTED FIRST!
- [Cortex pyramidal - layers 3/5/6]
- Cerebellar Purkinje Cells
What [mini mental state exam] do you use to test for: Concentration & Attention?
Reciting months of the year backwards
What [mini mental state exam] do you use to test for: Comprehension?
Following multistep commands
[Wernicke Korsakoff Syndrome] Clinical Presentation (3)
Wernicke problems come in a CAN of beer!
[Confusion & Confabulation]
Ataxia (Gait & Postural)
[Nystagmus + Oculomotor Dyf] (Opthalmoplegia)
beer = chronic alcoholism is most common cause
What serious finding is most likely to occur despite treatment in [Wernicke Korsakoff Syndrome]?
Memory Loss is permanent!
Antero and Retrograde
Causes of [Wernicke Korsakoff Syndrome] (2)
Wernicke Problems come in a CAN of beer!
[Thiamine B1 Deficiency] from:
- Chronic Alcoholism = MOST COMMON
- Giving [Glucose that doesn’t have B1] to a B1-deficient pt (i.e. homeless malnutrition pt)
Tx for [Wernicke Korsakoff Syndrome] (2)
- IV [Thiamine B1]
- Glucose administration
A: Parkinson’s Disease Histology
B: What other Dz shares this Histology and how do you tell the diff. clinically?
A: Lewy Bodies = [intracell eosinophilic inclusions] made of a-synuclein
B: [Lewy Body Dementia] (will aso have visual hallucinations and attention deficit clinically)
Describe the Prodromal phase of [Measles RubeOla Paramyxovirus] (4)
1st: Fever
2nd: 3 C’s of Measles= [Cough / Coryza / Conjunctivitis]
3rd: Koplik spots
4th: Maculopapular Rash starting from head then down
What are the dangerous potential sequelae of [Measles RubeOla Paramyxovirus] (3)
- Encephalitis (days later)
- [Acute Disseminated Encephalomyelitis] (weeks later)
- [SSPE- Subacute Sclerosing PanEncephalitis] (years later)
Identify the Finding & Dz associated
Koplik spots found in [Measles RubeOla Paramyxovirus]
Prodromal phase:
1st: Fever
2nd: 3 C’s of Measles= [Cough / Coryza / Conjunctivitis]
3rd: Koplik spots
4th: Maculopapular Rash starting from head then down
Why does [Chromatolysis Axonal Reaction (Loss of Axon)] changes occur?
Cell body attempts to repair/regain Axon by INC protein synthesis –> Enlargement of Cell Body
What syndrome occurs from rapidly correcting Na+ levels from low to High ?
“Rapid Na+ From low to HIGH, your pons will DIE” =
[Osmotic Central Pontine Demyelination]
Osmotic demyelination of pons white matter