jdlevenson's version from 2015-06-21 02:11


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Paraneoplastic subacute cerebellar degeneration a/wSmall cell ung cancer; breast, ovarian and uterine malignancies. Progressively worsening dizziness, limb and truncal ataxia, dysarthria and visual disturbances.
Paraneoplastic subacute cerebellar degeneration causeImmune response against secreted tumor cells that cross-reacts with Purkinje neuron antigens. Antibodies Anti-Yo, anti-P/Q, anti-Hu
Neurological paraneoplastic syndromes as anAutoimmune phenomenon.


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Brain germimoma locationPineal gland
Precocious puberty (a/w b-HCG), Parinaud syndrome (paralysis of upward gaze and of convergence; compression of tectal area of the midbrain) and obstructive hydrocephalus (from aqueductal compression)Brain germinoma. Increaed ICP and parinaud.
Paralysis of upward gazeParinaud syndrome.


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Sensorineural hearling loss and tinnitusVestibular schwannoma/acoustic neuroma


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Most common type of schwannomaAcoustic, located at cerebellopontine angle at CN8.
Schwannoma on histologyBiphasic- highly cellularar areas (Antoni A; spindles cells that form palisading patterns with interspersing nuclear free zones called Verocay bodies) intermixed with myxoid regions of low cellularity (Antoni B).
Schwannoma can result from any cranial nerve exceptCN 2, which is covered by oligodendrocytes instead of Schwann cells.
Acoustic neuromas/ schwannomas present withIpsilateral tinnitus, vertigo and sensorineural hearing loss (CNV, with or without nystagmus, vertigo, which would be vestibule part) as well as loss of facial sensation and paralysis of muscles of mastication (CN V), and facial paresis and loss of taste and decreased lacrimation (CN VII).
Bilatearll acoustic neuromasNF2


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Craniopharyngiomas on neuroimaging? Macroscopic? Light?Neuroimaging – calcifications; macroscopically – cystic or partially cystic; on light – lined by stratified squamous epithelium. May or may not be keratin pearls. Cysts usually lined by yellow viscous fluid that is rich in cholesterol crystals.


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Attention and concentration testCounting down from 100 by intervals of 3 or 7 or reciting months of year in reverse order and spelling world backwards.
Short term memory testRecalling 3 unrelated words after 5 minutes.
Writing a complete sentence with noun-verb agreement is used forLanguage test.
Drawing intersecting pentagons is used forVisual-spatial.
Drwaing a clock oriented to the time requested is used forExecutive function.
DeliriumReversible, acute-onset confusional state with fluctuating levels of consciousness with deficits in attention, memory and executive function; vs. dementia- gradual, irreversible and does not involve flucutations in consciousness.


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Internal capsule stroke commonly leads toPure motor weakness of contralateral arm, leg and lower face.
UMN lesions affectAny part of pyramidal motor system- corticospinal tracts, medulla, pons, midbrain, internal capsule and precentral gyrus.
Stroke, irreversible damage is shown first inRed neurons during first 48 hours. Irreversible damage. Lysosomal enzymes released from ischemic neurons and neutrophils result in degradation (24-72 hours) and then microglia, 3-5 days after onset of ischemia.
Neutrophils vs Microglia after strokeMicroglia will have myelin and fragments of neurons and necrotic debris.
Where is liquefactive necrosis seen beyond brainAbscesses from bacterial or fungal infection.
Stroke on CTFocal parenchymal hypoattenuation and occipital horn effacement consistent with an evolving infarct
Astrocytes form glial scar bySurrounding cystic space left by microglial cells; enlarge and proliferate around area of necrosis. 1-2 weeks is when reactive gliosis and vascular proliferation around the necrotic area but it takes >2 weeks and sometime many months for a glial scar to form as a cystic area surrounded by gliosis.
SAH on CTHyperdensity in cisterns/ sulci. Recall, do CT without contrast. Should be done in first 24 hours of symptoms.
If suspicion of SAH remains high despite negative CT, thenLP/ CSF analysis looking for xanthochromia
Predisposing factors to SAHAVM (in children) and ADPKD and EH** -> aneurysms in circle of willis and ACOM.
Complications of SAHSecondary arterial vasospasm (very common) in vessels surrounding ruptured aneurysm which causes cerebral ischemia and new onset confusion and or focal neurological deficit (related to impaired brain autoregulation; may fail to see it on CT) and then also rebleeding, more dangerous and still fairly common (another svere headache with severe N/V and a change in level of consciousness and new neurological deficits) and also may have hydrocephalus from irritation leading to dysfunction of arachnoid villi.
SAH, prescribe what to prevent complicationsNimodipine to prevent vasospasm; it’s a selective CCB.
SAH, when does vasospasm potentially happenno earlier than 3 days after and usually 7-8 days after.
INTRACEREBRAL hemorrhage (ie charcot bouchard) presentationFocal neurological deficits (hemiplegia, hemianesthesia, cranial nerve deficits...)
Cerebral hypoperfusion/ global ischemia, what is most at risk of injuryHippocampus first (and its pyramidal cells) and purkinje cells of cerebellum next.
Non-pupil sparing third nerve palsy (down and out with ptosis) + unilateral headache + eye pain...Compression from aneurysm in PCA or more commonly PCOM; saccular aneurysm from HTN
Key risk factors for developing intracranial aneurysmsChronic smoking and poorly controlled hypertension
Third nerve is GVE and GSE and courses betweenPCA and superior cerebellar artery. GVE more susceptible to injury from compression whereas GSE more susceptible to injury from ischemia (DM).
PCA innervates what cranial nervesCN III and IV and other structures in the midbrain as well as thalamus, occipital lobe, splenium of corpus callosum and medial temporal lobe.
Fixed and dilated pupil may be from what kind of compression/ herniationIpsilateral transtentorial. Ptosis and down and out of eye too.
Stretching or rupture of the basilar artery leads toBrainstem hemorrhages/ duret hemorrhages in pons and midbrain. Usually fatal.
Artery of percheron is a normal variant that branches off right or left PCA and suppliesBilateral thalami or dorsal midbrain.
Bilateral wedge shaped strips of necrosis over the cerebral convexity parallel and adjacent to longitudinal cerebral fissureWatershed infarcts usually due to global cerebral ischemia/ ischemic hypoxic encephalopathy.
Unilateral wedge shaped strips of necrosis over cerebral convexity...Severe Carotid stenosis
MCA suppliesMotor and sensory (arm and face mostly), Broca’s and Wernicke’s, forntal eye field and internal capsule and basal ganglia
Broc’as area supplied byMCA**
PICA occlusion/ Wallenberg syndromeContralateral loss of pain and temperature sensation; ipsilateral deficits of CN V, VIII, IX< X, XI and Horner’s syndrome*
Which is dominant hemisphere in most peopleLEFT. Even left handed people.
Pure motor hemiparesis and small cavitary lesion** in the internal capsule thinkLacunar infarct. Ischemic stroke. Small penetrating vessels that supply the deep brain structures (basal ganglia, pons) and subcortical white matter (internal capsule and corona radiata). Small cavitary lesion as opposed to intraparenchymal hyperdensity of a hemorrhage in a charcot-bouchard stroke.
What causes a lacunar strokeChronic hypertension -> predisposes arterioles to lipohyalinosis, microatheroma formation and occlusion/ hypertensive arteriolar sclerosis. DM and smoking too. Leading to cavitary spaces filled with CSF called lacuna.
Lacunar stroke can present as pure motor hemiparesis (if it involves...) or pure sensory stroke (if it involves...) or ataxia-hemiplegia syndrome (if it involves...) or dysarthria-clumsy hand syndrome (if it involves...)Pure motor – posterior limb of internal capsule or basal pons; Pure sensory – VPL or VPM of thalamus; Ataxia... – if it involves posterior limb of internal capsule or basal pons (same as above) and dysarthria... – genu of the internal capsule or basal pons.
Ischemia vs Hemorrhage stroke on CTHypodensity (-> lacuna latter) v Hyperdensity
Cardiac embolism or carotid atherosclerosis -> stroke -> CT?Large territory ischemic infarctions of the cerebral cortex
Spontaneous lobar/ cortical occipital/ parietal hemorrhage in the elderlyCerebral amyloid angiopathy**
Progressive** headache and n/v following nonlocalizing neurologic symptomsHypertensive encephalopathy
Hypoxic encephalopathy presents withDecreaed consciousness as opposed to focal neurologic deficits with maybe some infarcts at watershed areas


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Scotoma defect is inRetia or optic nerve -> discrete area of altered vision surrounded by zones of normal.
Central scotoma is fromLesion in macula.
Arcuate scotomaVisual field defect in shape of nerve fiber pattern due to damage in a particular region of optic nerve head.
Macular degeneration, progressive loss of central vision, is fromDeposition of fatty tissue (drusen) behind retina (dry MD) and/or neovascularization of retina (wet MD). Most common cause of blindiness in people over 50.
Scotomas are usually in what disease processesMS, Diabetic retinopathy, Retinitis pigmentosa (i.e. ones that do not involve entire optic nerve)
Homonymous vs. Binasal vs. Bitemporal hemianopsiaHomonymous is same side (contralateral optic tract/ fibers linking optic chiasm to lateral geniculate body); Binasal is loss in nasal fields (calcified carotid arteries); or bitemporal hemianopsia (pituitary adenoma)
Most common cause of bitemporal hemianopsiaCompression of optic chiasm via pituitary adenoma
Pie in the skyMeyer’s loop injury in temporal lobe (lower retina -> temporal lobe -> lingual gyrus).
Optic fibers project to which nucleiLATERAL GENICULATE NUCLEUS*; also superior colliculus (reflex gaze), suprachiasmtic nucleus (ciracian rhythms), and pretectal area (light reflex).
Meyer’s loopLGN optic radation – Lower Optic fibers -> lower retina -> temporal lobe/ meyer’s loop -> lingual gyrus of striate cortex. Vs. Upper optic fibers -> upper retina directly from LGN, through parietal lobe -> cuneus gyrus of striate cortex.
Optic tract lesionContralateral homonymous hemianopia AND marcus gunn pupil/ relative afferent pupillary defect.
**Homonymous Hemianopia - Optic Tract Lesion vs Lateral Geniculate Nucleus/optic radiation defectBoth homonymous hemianopia but only optic tract lesion would lead to relative afferent pupillary defect/ marcus gunn pupil because the nasal portion of the retina contributes more input to the pretectal nucleus than the temporal portion of the retina.
Reflex pathway, efferent limbParasympathetic fibers of oculomotor.
Nucleus for reflex pathwayEdinger-westphal, which receives inputs from pretectal (which receives input from afferent).
Corneal reflexSensory – nasociliary branch, CNV1; Motor - temporal branch of facial, CNVII
CN IV / SO lesion leads toEye deviated upward and vertical and torsional diplopia
CN VI / LR lesion leads toEye deviated medially; horizontal diplopia
Diabetic neuropathies can be mono or poly or autonomic. Most common cranial nerve?CN III CN3.
Diabetic mononeuropaty of CN3 presentationAcute onset diplopia with down and out position of eye and ptosis but pupillary size and reactivity is normal because the autonomic reflexes are on the peripheral aspect of the nerve and that is relatively spared by the neuropathy.


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Which branchial arch regresses completely?5th arch.
Branchial arches, bony elements formed by? Muscular elements by?Muscular – mesoderm. Bony – neural crest cells.
First arch syndromePoorly formed first arch resulting in malformations of the mandible, maxilla, malleus, incus, zygoma, palate and temporal born. Recall, neural crest -> bony deform and mesodermal derivatives -> muscles. First arch is associated with Trigeminal nerve.
Second arch associated with what nerveFacial nerve/ 7. 2nd arch to muscles of facial expression, stylohyoid, stapedius, posterior belly of digastric.
Larynx made up by what archesCartilaginous structures of larynx.
Holoprosencephaly is example ofMalformation, i.e. primary defect in cells or tissues that form an organ/ intrinsic. Division of pro usually happens during 5th week of life.
Holoprosencephaly seen inTrisomy 13 and 18. And fetal alcohol syndrome.
CHD is example ofMalformation. Also polydactylyl, syndactylyl.
Malformation vs deformationMalformation is intrinsic whereas Deformation is due to extrinsic mechanical forces such as breech delivery can cause congenital dislocation of the hip.
Disruption isSecondary breakdown of a previously normal tissue or structure, such as rupture of amnion
SequenceSeries of abnormalities resulting from a single primary defect like Potter sequence.
Syringomyelia locationCentral cystic dilation in cervical spinal cord usually at C8-T1 causing damage first to ventral white commissure and then to anterior horns. May eventually expand to affect lateral corticospinal tract (UMN damage).
Loss of upper extremity extreme pain and temperature sensation, upper extremity weakness, hyporeflexia, lower extremity weakness and hyperreflexia and kyphoscoliosisSyringomyelia.
Syringomyelia, if pain and temperature is lost at T4, then where is spinal cord lesionT2 or T3 since first order axons briefly ascend in the zone of Lissaeur before synapsing