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*USMLE* > Neuro > Flashcards

Neuro Flashcards

1
Q

Middle Cerebral Artery Stroke: Signs / Sx etc.

A

contralateral hemiparesis + hemisensory loss of the FACE and UPPER LIMB

other features = anosognosia (insight lack), contralateral spatial neglect (if in non-dominant parietal lobe), conjugate gaze deviation TOWARD lesion side, contralateral homonymous hemianopsia (optic radiation damage in subcortical temporoparietal)

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2
Q

Anterior Cerebral Artery Stroke: Signs / Sx etc.

A

contralateral hemiparesis of LOWER limb

if bilateral ACA occlusion, may have ABULIA (lack of initiative/will), primitive reflexes (Moro, grasp), urinary incontinence (prefrontal cortex damage)

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3
Q

Posterior Cerebral Artery Stroke: Signs/ Sx etc.

A

contralateral hemianopia with macular sparing (due to collateral circ. from MCA) via visual cortex infarction

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4
Q

Basilar Artery Occlusion: Signs/ Sx etc.

A

damages corticospinal / -bulbar tracts

quadriplegia; bulbar dysfunction (facial weakness, dysarthria) and oculomotor issues (horizontal gaze palsy)

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5
Q

Anterior Inferior Cerebellar Artery occlusion: Signs / sx etc.

A

LATERAL PONTINE SYNDROME

ipsilateral pain/temp loss (trigeminal nucleus)
ipsi facial weakness (facial nucleus)
ipsi hearing loss (cochlear nucleus)
contra pain/temp trunk/limbs (lateral spinothalamic)
cerebellar dysfunction (ataxia, dysmetria)

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6
Q

Anterior Communicating Artery aneurysm: signs sx etc

A

compresses central optic chiasm

bitemporal hemianopia

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7
Q

Posterior Communicating Artery aneurysm: signs sx etc.

A

compresses CN III

ipsilateral mydriasis, ptosis + “down n out” deviation

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8
Q

Histopathology of brain biopsy shows:

amyloid deposits in cortical vessels

what’s the condition?

A

cerebral amyloid angiopathy

beta amyloid; usually asymptomatic, can be assoc. with hemorrhage or Alzheimer’s dementia

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9
Q

Histopatho of brain shows:

Congo red staining plaques in hippocampus

what’s the condition?

A

Alzheimer’s

neuritic (senile) plaques of EC beta amyloid surround dystrophic neurites (Congo+ and often hippocampal)

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10
Q

Histopatho of brain shows:

Eosinophilic, round cytoplasmic neuronal inclusions

what’s the condition?

A

Rabies

Negri bodies, especially in Purkinje and hippocampal pyramidal cells

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11
Q

Histopatho of brain shows:

profound neuronal loss in caudate nucleus

what’s the condition?

A

Huntington disease (AD)

choreiform movement, psych disturbance, dementia

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12
Q

Histopatho of brain shows:

Slit-like white matter cavities with surrounding gliosis

what’s the condition?

A

Lacunar infarction

recurrent in vascular dementia, with stepwise cognitive decline + focal deficits (older pt with CV risk factors such as DM and htn)

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13
Q

Histopatho of brain shows:

Microglial nodules and multinucleated giant cells

what’s the condition?

A

HIV-associated dementia

HIV enters CNS via infected macrophages and infects microglia > subcortical dementia with memory deficits, executive dysfunction + slow info processing

CD4 < 200/mm3

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14
Q

Meningioma: histo, signs / sx, etc.

A

slow-growing benign tumor of arachnoid meningothelium

“whorled” cell pattern of syncytial nests; psammoma bodies

well-circ round mass attached to dura at falcine, parasagittal, tentorial or lateral brain convexities

s/s are seizure via compression; HA/nausea/vom via ICP (worse lying or sleeping); focal neuro deficits by size/location

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15
Q

Ependymoma: epidemiology, histo, site

A

10% of posterior fossa tumors in kids

histo = characteristic perivascular rosettes (pink fibrous material around vessel); GFAP+ processes tapering towards vessels

paraventricular tumors in kids (eg, floor of fourth ventricle, other sites of ependymal cells); spinal ependymomas in adults

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16
Q

Glioblastoma: histo, morpho, site, epidemiology

A

1 primary malignant brain tumor of adults (40-70)

soft + poorly defined; can be very large –> mass effects and midline shift; areas of necrosis + hemorrhage with microvascular prolif.

seen in cerebral hemispheres (frontal, temporal, basal ganglia) + may cross corpus callosum with “butterfly glioma” appearance on img

histo = hypercellular areas of atypical astrocytes that border regions of necrosis (“pseudo-palisading”); poorly diff, pleomorphic astrocytes; nuclear atypia + many mitoses

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17
Q

Medulloblastoma: epidemiology + histo

A

malignant cerebellar tumors in children

small blue cells (primitive neuroectodermal tumor, PNET) with high mitotic index

Homer-Wright rosettes (cells surround neuropil) in 20%

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18
Q

Oligodendroglioma: site, morpho + histo

A

white matter of cerebral hemispheres; well-circumscribed gray mass with calcification

“fried egg” cells (round nucleus + halo of clear cytoplasm)

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19
Q

Pilocytic Astrocytoma: epidemiology; site; histo

A

usually benign in cerebellum (or brainstem, hypothalamus, optic path) of kids / young adults

histo = eosinophilic granular bodies and elongated hairlike processes (Rosenthal fibers: pink fibrous material); well-diff with spindle cells + hair-like glial processes + microcysts

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20
Q

Schwannoma: site, histo

A

mostly benign; vestibular branch of CN VIII at cerebellopontine angle

histo = spindle cells with palisading nuclei around “Verocay bodies” with an eosinophilic core (Antoni A pattern)

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21
Q

Craniopharyngioma: epidemiology, site, histo

A

benign suprasellar tumor in kids

cords/nests of palisading squamous epithelium with internal areas of lamellar “wet keratin”

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22
Q

Primary CNS Lymphoma: epidemiology, morpho

A

immunocompromised (HIV, transplant) pts; in HIV can be via EBV infection

multiple lesions in deep grey matter, white matter + cortex

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23
Q

Brain metastases: morphology / imaging, common primary tumor sites

A

lung, breast, kidney and skin (melanoma)

typically multiple, well-circ masses at grey-white matter junction

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24
Q

Neuroblastoma:

site, epidem, histo + markers

mutation

A

1 extracranial solid tumor in kids

small, round, blue cell tumors; “neuropil” (neuritic process pathognomonic of neuroblastoma cells)

NSE, chromogranin, synaptophysin and S-100 positive on IHC

urinary HVA and/or VMA high in 90%

N-MYC (chr. 2) is mutated

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25
Q

Pituitary Apoplexy: etiology, s/s, dx and tx

how to diff from aneurysm rupture near optic chiasm?

A

acute pituitary hemorrhage assoc. with pituitary adenoma

sudden severe HA
bitemporal hemianopsia
ophthalmoplegia (CN III)
hemodynamic instability (low cortisol)
altered sensorium
antecedent loss of libido (high PRL)
chronic mild HAs

dx by CT or MRI
tx by surgery and steroids

diff from saccular aneurysm rupture by history of pituitary dysfunction prior to acute event + CV collapse during event

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26
Q

Basal ganglia hemorrhage: etiology, s/s

A

usually via chronic hypertensive vasculopathy

neuro deficits that gradually worsen over minutes - hrs

contralateral hemiparesis, hemianesthesia (corticospinal + somatosensory tract disruption)

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27
Q

Carotid dissection: etiology, s/s

A

trauma, chronic htn, CT disease or smoking can cause

unilateral HA, transient vision loss, ptosis + miosis (partial Horner syn.)

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28
Q

Cerebral venous sinus thrombosis: etiology, s/s

A

thrombophilia, pregnancy, contraceptives, malignancy or infection can cause

presents with HA, vomiting, seizure and focal neuro deficits

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29
Q

anoxic brain injury MRI findings

A

loss of grey-white matter differentiation

sulcal effacement

(common in cardiac arrest)

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30
Q

pupillary reflex pathway

A

retina > optic nerve > superior colliculus-level midbrain > pretectal nucleus > BILATERAL Edinger-Westphal nuclei > oculomotor nerve (preganglionic PSNS) > ciliary ganglion > postganglionic fibers to sphincter pupillae

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31
Q

Epidural hematoma: vessel, location, clinical s/s, CT

A

middle meningeal artery; btwn skull + dura

lucid interval, followed by loss of consciousness

biconvex hematoma on CT

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32
Q

Subdural hematoma: vessel, location, clinical s/s, CT

A

bridging cortical veins; btwn dura + arachnoid

gradual onset HA/confusion

crescent shaped hematoma on CT

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33
Q

SAH hematoma: vessel, location, clinical s/s, CT

A

ruptured aneurysm/AV malformation of ant/post communicating arteries or MCA; btwn arachnoid + pia

sudden severe headache, fever, NUCHAL RIGIDITY (develops within 24 hrs as blood irritates meninges)

may see PAPILLEDEMA or PUPILLARY DILATION (but no focal neuro deficits)

blood in basal cisterns on CT

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34
Q

L2 radiculopathy: sensory + motor sx

A

upper anteromedial thigh

weak hip flexion (iliopsoas)

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35
Q

L3 radiculopathy: sensory + motor sx

A

lower anteromedial thigh

weak hip flexion (iliopsoas), hip adduction, knee extension (quad)

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36
Q

L4 radiculopathy: sensory + motor sx

A

lower anterolateral thigh, knee, medial calf + foot

weak hip adduction, knee extension (quad) and PATELLAR reflex

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37
Q

L5 radiculopathy: sensory + motor sx

A

buttocks, posterolateral thigh, anterolateral leg, dorsal foot

weak foot dorsiflexion + inversion (tibialis anterior), foot eversion (peroneus), and toe extension (extensor hallucis + digitorum)

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38
Q

S1 radiculopathy: sensory + motor sx

A

buttocks, posterior thigh + calf, lateral foot

weak hip extension (glut max), knee flexion (hamstrings), foot plantarflexion (gastroc) and ACHILLES reflex

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39
Q

Babinski sign

what does it indicate, how is it done, associated sx

A

stroke sole from lateral heel to ball of foot

dorsiflexion with toe spreading is positive in adults + indicates UPPER MOTOR NEURON LESION

assoc. findings are spasticity, hyperreflexia, muscle weakness/paralysis

(dorsiflexion normal in babies due to incomplete myelination of corticospinal tracts)

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40
Q

Acute cerebellitis

AKA? epidemiology + causes? Sx and course?

A

aka post-viral cerebellar ataxia

children 2-3 wks old via varicella, measles, or EBV

ataxia, nystagmus + dysarthria; usually resolves by 3 weeks

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41
Q

Cerebellar Infarction

presentation? biopsy/autopsy findings?

A

vertigo, nystagmus, IPSILATERAL limb ataxia, and TRUNCAL LATEROPULSION (fall toward lesion)

autopsy shows liquefactive necrosis (acute infarct) and glial scarring (chronic infarct)

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42
Q

Opsoclonus-Myoclonus syndrome

s/s, association

A

nonrhythmic conjugate eye movements, involuntary limb + trunk jerking

rare paraneoplastic condition from NEUROBLASTOMA (thought to be via an auto-ab)

(N-myc, SRB cells, Homer-Wright rosettes and urinary HVA/VMA)

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43
Q

Hypothalamic nuclei functions:

ventromedial, lateral, anterior, posterior

A

ventromedial - monitors blood glucose; mediates SATIETY; lesions cause HYPERPHAGIA

lateral - mediates HUNGER; lesions cause ANOREXIA

anterior - mediates heat dissipation; lesions cause HYPERthermia

posterior - mediates heat conservation; lesions cause HYPOthermia

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44
Q

Hypothalamic nuclei functions:

arcuate
paraventricular
supraoptic
suprachiasmatic

A

arcuate - secretes dopamine (inhibits PRL), GHRH and GnRH

paraventricular - ADH, CRH, oxytocin + TRH secretion

supraoptic - ADH + oxytocin secretion

suprachiasmatic - circadian rhythm + pineal gland function

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45
Q

Tumors of hypothalamus

most common in kids? most common in adults?

A

gliomas in kids

metastases in adults

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46
Q

Cavernous Hemangioma in CNS

where? s/s? complications?

A

in brain parenchyma ABOVE TENTORIUM CEREBELLI

seizures + progressive neuro deficits due to mass effects

tend to bleed > intracerebral hemorrhage

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47
Q

Transtentorial Herniation

what is it? cause?

ocular sx?

A

herniation of the medial-most portion of the temporal lobe (uncus) around/below the tentorium cerebelli

large cerebral hemorrhages, tumors etc. with mass effects can cause it

ipsilateral CN III disruption > ipsilateral fixed DILATED pupil with “DOWN AND OUT” deviation

herniation progression > midbrain + upper pons injury causes MID-POSITION and fixed pupil BILATERALLY w/ loss of vestibulo-ocular reflex

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48
Q

Decerebrate Posturing

what is it? what causes it?

A

EXTENSOR posturing via loss of RUBROSPINAL descending upper limb flexor excitation and unopposed VESTIBULOSPINAL extensor output

BRAINSTEM damage AT/BELOW RED NUCLEUS (midbrain tegmentum / pons)

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49
Q

Decorticate posturing

what is it? what causes it?

A

FLEXOR posturing due to loss of DESCENDING INHIBITION of the red nucleus (upper limb flexion)

damage to structures ABOVE RED NUCLEUS such as CEREBRAL HEMISPHERES or INTERNAL CAPSULE

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50
Q

Cerebellar vermis damage

signs?

A

vermis controls AXIAL/PROXIMAL LIMB muscle coordination

damage causes GAIT / TRUNCAL ATAXIA; may also cause nystagmus/vertigo via role in vestibular function

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51
Q

Thalamus damage

signs?

A

thalamus is relay station for almost all ascending sensory info

damage > sensory loss; bilateral damage may cause coma

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52
Q

Multiple Sclerosis

signs + symptoms

A

sx are EPISODIC + PROGRESSIVE

sensory disturbance; motor weakness; bowel/bladder issues

ocular issues: OPTIC NEURITIS (painful movement, intermittent vision decrease, optic disc swelling); INTERNUCLEAR OPHTHALMOPLEGIA (impaired adduction on lateral gaze)

cerebellar dysfunction: INTENTION TREMOR and BROAD GAIT

LHERMITTE SIGN: electrical sensation in limbs/back with neck flexion

UHTHOFF PHENOMENON: sx worse with increased body temp (slow conduction in damaged nerves)

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53
Q

Multiple Sclerosis

risk factors (race, gender, genetics, environment)

A

white females

HLA-DRB1

US / Europe; colder climates

low vitamin D and smoking

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54
Q

Multiple Sclerosis

diagnosis (clinical, imaging, other)

A

episodic/progressive sx disseminated over time/space

MRI shows HYPERINTENSE T2 lesions (demyelinating plaques)

CSF shows OLIGOCLONAL IgG bands

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55
Q

Wallenberg syndrome

cause? s/s?

A

LATERAL MEDULLA lesion - affects pain/temp tracts plus CN V 5, 9, 10 and 11

vertigo/nystagmus; ipsilateral ataxia + dysmetria (cerebellar)

loss of pain/temp in IPSILATERAL FACE + CONTRALATERAL BODY

bulbar weakness (dysphagia)

ipsilateral Horner

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56
Q

Colloid cyst

what? where? histo? complications?

A

BENIGN cyst in THIRD VENTRICLE

rare mitoses

lethal obstructive hydrocephalus

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57
Q

Pleomorphic Xanthoastrocytoma

what? in whom? histo? progression?

A

astrocytoma in KIDS / YOUNG ADULTS

RETICULIN deposits and CHRONIC WBC INFILTRATES

may progress to glioblastoma multiforme (rarely)

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58
Q

What is Wallerian degeneration?

How does it occur in CNS? Timeline?

A

axon damage > axon degeneration + myelin sheath breakdown DISTAL TO INJURY (begins few days after lesion)

in CNS, occurs more slowly due to BBB

macros/microglia enter more slowly > MYELIN DEBRIS PERSISTS FOR YEARS causing slower axonal growth

GLIAL SCAR in weeks/months after injury also slows process

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59
Q

Substructures + sheathing of nerves

A

Nerve is surrounded by EPINEURIUM and made up of FASCICLES (bundles of axons) surrounded by PERINEURIUM

Each axon is surrounded by an ENDONEURIUM

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60
Q

Guillain Barre histo

A

ENDONEURIAL inflammation

perivenular lymphos and macros btwn vessel and its assoc. axon

macros may appear LIPID LADEN after engulfing myelin

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61
Q

1 diagnosed movement disorder

cause? s/s? tx?

A

Essential tremor
(aka familial tremor, sometimes follows AD inheritance)

worsens while maintaining a certain posture (eg, holding an object)

improves with alcohol consumption

PROPRANOLOL is first-line

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62
Q

Thalamus VPL nucleus

inputs from where? what sensations?

A

contralateral…

spinothalamic tract - touch, pain, temp

dorsal columns - vibration + proprioception

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63
Q

Thalamus VPM nucleus

inputs from where?

A

trigeminal pathway

touch and pain in face

64
Q

Lacunar infarct

affects what structures? what vessels?

A

basal ganglia, posterior limb internal capsule, pons + cerebellum

small penetrating arteries (eg, lenticulostriate)

65
Q

Lacunar infarct

causes?

pathogenesis / histo (2 main features)?

A

uncontrolled HYPERTENSION and DIABETES

LIPOHYALINOSIS - leakage of plasma proteins > hyaline vessel thickening, sclerosis and foamy macros

MICROATHEROMAS - foamy macros accumulate near origin of penetrating vessel

Liquefactive necrosis > small cavitary infarct

66
Q

Amyotrophic Lateral Sclerosis

in whom? MC-COD?
what tracts / areas damaged?

A

middle-aged pt
COD = respiratory complications (aspiration pneumonia)

affects ANTERIOR HORNS (lmn lesion) and LATERAL CORTICOSPINAL TRACTS (umn lesion)

also MOTOR nuclei of CN V, IX, X, XII

67
Q

Amyotrophic Lateral Sclerosis

mutation? histo of muscle? tx?

A

SOD1 mutation - codes for copper-zinc superoxide dismutase

muscle shows DENERVATION ATROPHY with SMALL, ANGULAR FIBERS

Riluzole - decreases Glu release

68
Q

Neurofibromatosis Type I

inheritance + gene? two skin manifestations and their origin?

A

von Recklinghausen disease; AD inherited mutation of NF1 tumor suppressor

Cafe-Au-Lait Spots - hyperpigmented macules of the trunk (melanocytes); soon after birth

Cutaneous neurofibromas - early adolescence; multiple raised tumors; grow and multiply with age (< 2cm); from Schwann cells

all from neural crest cells

69
Q

NF type I

risk of what?

A

CNS neoplasms such as OPTIC GLIOMA and PILOCYTIC ASTROCYTOMA

70
Q

Oculomotor Palsy

causes? s/s?

A

tumors, aneurysms (specif. POST. COMMUNICATING A.)
nerve ischemia, trauma

ptosis (levator palpebrae)
DIAGONAL DIPLOPIA
impaired adduction (medial rectus)
impaired depression (inferior rectus)
impaired elevation (superior rectus)
impaired constriction + accommodation

causes a DOWN AND OUT deviation, via unopposed lateral rectus and superior oblique action

71
Q

Trochlear palsy

s/s?

A

SUPERIOR OBLIQUE function is disturbed (poor abduction, internal rotation + depression when adducted)

eye deviates UPWARD
vertical + torsional diplopia

72
Q

Abducens palsy

s/s?

A

LATERAL RECTUS function disturbed (poor abduction)

eye deviates MEDIALLY > HORIZONTAL diplopia

73
Q

Trigeminal Neuralgia

s/s? trigger? duration?

tx?

A

stabbing/electric pain in CN V (esp. V/2 and V/3) distribution, usually UNILATERAL

lasts only SECONDS but REPEATEDLY and episodes can occur for months

trigger is any CN V stimulus: chewing, toothbrushing, shaving, washing face, swallowing, hot/cold

CARBAMAZEPINE is tx
(aplastic anemia / CYP induction >monitor CBCs and other drug levels)

74
Q

Wernicke encephalopathy

s/s? iatrogenic cause?

A

ataxia, nystagmus, ophthalmoplegia, anterograde amnesia

IV dextrose without thiamine in chronic alcoholic with low thiamine at baseline

(dextrose precipitates use of all available thiamine and then a severe thiamine defic.)

75
Q

Korsakoff psychosis

cause? brain area damaged? s/s?

(other brain area that MAY be affected, but not always)

A

CHRONIC thiamine defic. > MAMMILLARY BODY necrosis

antero-/retrograde amnesia, apathy, lack of insight, confabulation

(anterior nucleus of thalamus… also part of Papez circuit like mammillary bodies, can be affected)

76
Q

Locus Ceruleus

Creates what? Involved in what? Injured by what?

A

Norepinephrine

involved in RETICULAR ACTIVATING SYSTEM (arousal), mood, sleep-wake states, cognition, BP control

dysfunction in ANXIETY DISORDERS (panic attacks, etc.)

BILATERAL PONTINE HEMORRHAGE - causes coma due to reticular activating system damage; also paralysis with EXTENSOR posturing (corticospinal/bulbar tract injury) and PINPOINT PUPILS

77
Q

Transtentorial Herniation (aka uncal)

what can be compressed / occur? (4)

A
  1. OCULOMOTOR NERVE - ispilateral; first pupil is fixed and dilated, then muscles are paralyzed and a ptosis and “down and out” position occurs (sup. oblique + lateral rectus still function)
  2. POSTERIOR CEREBRAL ARTERY - ipsilateral artery > contralateral homonymous hemianopsia w/ macular sparing
  3. CONTRALATERAL CEREBRAL PEDUNCLE - damage to contralateral corticospinal tract > ipsilateral hemiparesis
  4. BASILAR ARTERY - can be stretched/ruptured causing brainstem (Duret) hemorrhage in pons/midbrain; often fatal
78
Q

Subfalcine herniation

cause? result?

A

subdural hematoma causes cingulate gyrus to compress under falx cerebri

can compress ANTERIOR CEREBRAL ARTERY

79
Q

Hemiballism

cause? structure affected? s/s?

A

LACUNAR STROKE (long-standing DM or htn) damamges the SUBTHALAMIC NUCLEUS, which no longer excites the globus pallidus internus > no longer inhibits the thalamus

wild, involuntary, large amplitude flinging movements of proximal limbs on ONE SIDE OF BODY (hemi-)

80
Q

diff dx of hemiballism and Huntington’s motor issues

A

hemiballism - large amplitude movements of proximal limbs (subthalamic nucleus)

Huntington - low amplitude movements of distal limbs (caudate nucleus) plus dementia + behavioral issues

81
Q

internal capsule damage

via what? what deficits?

A

lacunar infarct, tumor, etc.

contralateral pure motor or sensorimotor deficit

82
Q

Wilson’s disease

affects what part of brain?

A

Lentiform nucleus (GP and putamen)

so-called “hepatolenticular degeneration” bc liver involved too

depression + personality changes
dysarthria and movement disorders

83
Q

glossopharyngeal nerve functions

somatic motor?
PSNS?
general sensory?
special sensory?

A

somatic motor - STYLOPHARYNGEUS, elevates larynx on swallowing

psns - PAROTID SECRETION

general sensory - inner tympanic membrane, eustachian tube, post 1/3 tongue, tonsils, upper pharynx (gag!), carotid body + sinus

special sensory - post 1/3 tongue taste

84
Q

what is the path for innervation of the parotid?

5 steps

A
  1. INFERIOR SALIVATORY NUCLEUS (inf. dorsal pons)
  2. travels along CN IX (glossophar.)
  3. OTIC GANGLION (infratemp fossa)
  4. AURICULOTEMPORAL n. (CN V/3)
  5. parotid gland
85
Q

What are the 5 seizure types?

2 major categories plus subtypes

A
  1. FOCAL - 1 hemisphere at onset
    - Simple - no loss of consciousness
    - Complex - loss of consc. + POST-ICTAL state
  2. GENERALIZED - both hemispheres at onset
    - Tonic-clonic - lost consc., contraction + jerking
    - Myoclonic - no lost consc. brief jerking
    - Absence - brief consc. loss + automatisms
86
Q

How is epilepsy treatment divided?

3 divisions

A

FOCAL seizures can be tx with NARROW SPECTRUM drugs (even if they evolve into tonic-clonic after onset!)

GENERALIZED seizures can be tx with BROAD SPECTRUM DRUGS

ABSENCE seizures are tx with ETHOSUXIMIDE

87
Q

Pineal gland mass

common s/s?

(2 main syndromes plus 3 s/s for one and 3 s/s for the other)

A

OBSTRUCTIVE HYDROCEPHALUS - via aqueductal stenosis; causes 1) papilledema, 2) HA worse when lying 3) vomiting, usually in morning

DORSAL MIDBRAIN (Parinaud) SYNDROME - compression of pretectal midbrain; causes 1) limited upward gaze, 2) bilateral eyelid retraction (Collier sign), 3) light-near dissociation (accommodation without pupillary constriction)

88
Q

What is the #1 pineal gland mass?

where else might it show up? in whom?

A

GERMINOMA - midline malignant tumor of embryonic germ cells

can also be suprasellar, gonad or mediastinum

more common in YOUNG BOYS

(causes obstructive hydrocephalus and Parinaud syndrome = downward gaze, eyelid retraction and light-near dissociation = pupils accommodate but don’t react to light)

89
Q

What is “locked in” syndrome + what can cause it?

A

spastic quadriplegia (extensor posturing) and paralysis of most cranial nerves but PRESERVED CONSCIOUSNESS + EYE MOVEMENTS

via pontine hemorrhage or tumors

90
Q

what do medial medulla lesions cause?

3 things

A

MEDIAL MEDULLARY SYNDROME

  1. contralateral SPASTIC PARALYSIS (umn lesion)
  2. contralateral VIBRATION/PROPRIO loss (dorsal columns)
  3. ipsilateral FLACCID TONGUE PARALYSIS (CN XII)
91
Q

Charcot-Bouchard vs. Berry aneurysm

assoc. conditions
location

A

Charcot-Bouchard - ONLY via HYPERTENSION; found in basal ganglia (mostly PUTAMEN), thalamus, cerebellum + pons

Berry - via PCKD, Ehlers-Danlos and hypertension; in the CIRCLE OF WILLIS

92
Q

Charcot-Bouchard vs. Berry aneurysm

size, result of rupture + s/s

A

Charcot-Bouchard - smaller (<1 mm); cause INTRACEREBRAL hemorrhage with PROGRESSIVE FOCAL DEFICITS +/- headache

Berry - variable (2-25 mm); cause SUBARACHNOID hemorrhage; sudden SEVERE HA without focal neuro sx

93
Q

anterior 2/3 of internal capsule carries what?

posterior 1/3?

internal capsule lesions cause what?

A

anterior 2/3 - motor fibers (corticospinal tract)

posterior 1/3 - sensory fibers (thalamocortical tracts)

most lesions are CONTRALATERAL PURE MOTOR or SENSORIMOTOR (it would take a very small lesion to the posterior only to produce a pure sensory lesion)

94
Q

What is INTERNUCLEAR OPHTHALMOPLEGIA?

what two nuclei + which tract are involved?

A

a disorder of CONJUGATE HORIZONTAL GAZE movements

communication between the ABDUCENS NUCLEUS (dorsal pons) and the contralateral OCULOMOTOR NUCLEUS (dorsal midbrain) via the MEDIAL LONGITUDINAL FASCICULUS is disrupted

95
Q

Explain how CONJUGATE HORIZONTAL EYE MOVEMENT works

tracts + nuclei

A
  1. FRONTAL EYE FIELD - in frontal cortex, goes to…
  2. contralateral PARAMEDIAN PONTINE RETICULAR FORMATION, sends efferents to…
  3. ipsilateral ABDUCENS NUCLEUS (dorsal pons) to abduct ipsilateral eye, which sends efferents to…
  4. contralateral OCULOMOTOR NUCLEUS (dorsal midbrain) via MLF to adduct the contralateral eye
96
Q

3 sx of internuclear ophthalmoplegia

what 2 things are preserved?

A
  1. IMPAIRED CONJUGATE HORIZONTAL GAZE - eye opposite the gaze can not adduct to look in the same direction as the abducting eye
  2. DIPLOPIA
  3. HORIZONTAL NYSTAGMUS of the abducting eye

(pupillary light reflex and convergence are preserved)

97
Q

Jugular Foramen Syndrome

cause? s/s?

think about what goes thru the jugular foramen

A

tumor, trauma or infection affection affecting structures that pass thru the jugular foramen (CN IX, X, XI, jugular vein)

  • posterior 1/3 taste loss (CN IX)
  • gag reflex loss (CN IX, X)
  • dysphagia (CN IX)
  • dysphonia/hoarseness (CN X)
  • soft palate drop; uvula toward unaffected side (CN X)
  • SCM and trapezius paralysis = “shoulder drop” (CN XI)
98
Q

Main SC tracts affected in subacute combined degeneration (3)

A
  1. DORSAL COLUMN - position/vibration (proprioception); sensory ataxia with POSITIVE ROMBERG
  2. SPINOCEREBELLAR TRACT - ataxia
  3. LATERAL CORTICOSPINAL - spastic paresis
99
Q

Romberg test

A

Premise = patient needs at least 2 of the 3 systems of proprioception, vestibular system and vision to maintain balance

Normal pt can close eyes and still have proprioception and vestibular system to maintain balance

POSITIVE ROMBERG pt closes eyes and cannot balance because both vision and PROPRIOCEPTION IMPAIRED (as in dorsal column damage, like subacute combined degeneration in B12 defic.)

100
Q

MAIN SC LESIONS in poliomyelitis / spinal muscular atrophy (aka Werdnig-Hoffman)

A

loss of anterior horn motor neurons

causes FLACCID PARALYSIS, atrophy and fasciculations (twitches)

101
Q

MAIN SC LESIONS in multiple sclerosis

A

pattern is RANDOM and ASYMMETRIC

102
Q

MAIN SC LESIONS in tabes dorsalis of tertiary syphilis

A

ONLY the DORSAL COLUMNS and DRGs

as opposed to SCD which affects lateral corticospinal and spinocerebellar tracts as well

103
Q

MAIN SC LESIONS in syringomyelia

A

central cavitation affects the ANTERIOR WHITE COMMISSURE of the SPINOTHALAMIC TRACT

(is usually cervical > BILATERAL PAIN/TEMP LOSS in UPPER LIMBS, may progress to legs

can expand to ventral horns > flaccid paralysis of hands)

104
Q

Syringomyelia

most common location of dilation

A

C8 to T1 levels of SC

extends rostral, caudal and centrifugal

105
Q

Syringomyelia

what skeletal sx is seen and why?

A

kyphoscoliosis

paresis of paravertebral muscles

106
Q

Neuroblastoma

cell origin + where is it? who gets it?

what are the main signs (4) clinically?

A

neural crest cells

in adrenal medulla + sympathetic chain of kids <2

  1. Abdominal Mass
  2. Periorbital bruise (metastases)
  3. Opsoclonus-Myoclonus - eye, trunk + limb jerking
  4. “DUMBBELL TUMOR” appearance on imaging due to sc compression/epidural invasion
107
Q

What is the general progression of muscle weaknesses associated with lumbosacral radiculopathy from L2 to S1?

A
  • Generally higher segments (L2 - L4) will affect HIP FLEXION and KNEE EXTENSION (picture a crane kick)
  • Lower segments (L5 - S1) will affect FOOT movements, HIP EXTENSION and KNEE FLEXION (picture a superman stretch)
108
Q

What two lumbosacral radiculopathy segments affect important reflexes and which reflexes?

A

L4 - affects the PATELLAR REFLEX

S1 - affects the ACHILLES REFLEX (“ankle jerk reflex”)

109
Q

Subacute Cerebellar Degeneration

cause? s/s? labs?

A

paraneoplastic issue from SCLC, breast, ovary and uterine tumors

progressive dizziness, limb/trunk ataxia, dysarthria, visual disturbance (diplopia, oscillopsia)

anti-tumor Abs cross react with Purkinje cell Ags > acute-onset rapid cerebellar degeneration

antibodies are anti-Yo, anti-P/Q and anti-Hu

110
Q

Bilateral anterior cerebral artery occlusion can cause what?

A

Sensorimotor - leg/foot numbness + weakness

BEHAVIORAL SX - abulia (lack of will/initiative - prefrontal)

INCONTINENCE - frontal micturition center; medial frontal lobe + cingulate gyrus

111
Q

Mnemonic for which CNs are sensory, motor and both

A

Some Say Marry Money But My Brother Says Big Brains Matter Most

112
Q

Vagal Nuclei

3 and what they do

A
  1. nucleus Solitarius - visceral Sensory info (VII, IX, X)
  2. nucleus aMbiguus - Motor innervation of pharynx, larynx and upper esophagus (IX, X, XI)
  3. dorsal motor nucleus - autonomic fibers to heart, lungs and GI (X only)
113
Q

ALS

lesions + s/s

A

UMN and LMN lesions (corticobulbar/-spinal and medullary/SC anterior horn)

LMN - dysarthria, dysphagia, asymmetric limb weakness, fasciculations, atrophy

UMN - pseudobulbar palsy (facial movement disorder also with dysarthria/-phagia), emotional lability, spastic gait, clonus

114
Q

ALS

enzyme deficit + treatment

A

SUPEROXIDE DISMUTASE 1

tx is with RILUZOLE, but is still fatal

115
Q

Cerebral Amyloid Angiopathy

is the MCC of what? and what areas of the brain does it affect?

A

CAA is the mcc of SPONTANEOUS LOBAR HEMORRHAGE, especially in pts > 60

tends to be RECURRENT and in OCCIPITAL / PARIETAL LOBES (frontal rarer, but possible)

116
Q

Considering what parts of the brain it mostly affects…

what are the clinical results of CEREBRAL-AMYLOID ANGIOPATHY-related lobar hemorrhage?

A

occipital - HOMONYMOUS HEMIANOPSIA

parietal - CONTRALATERAL HEMISENSORY LOSS

(frontal - more rare, but CONTRALATERAL HEMIPARESIS)

117
Q

Hypertensive encephalopathy

presentation?

A

PROGRESSIVE headache > nausea + vomiting

NONLOCALIZED neuro sx (confusion, etc.) in setting of hypertension

118
Q

differential between cerebral hemorrhage due to AVM and cerebral amyloid angiopathy

A

AVM - a SINGLE lesion in a CHILD

CAA - MULTIPLE lesions in an OLDER ADULT (esp. parietal / occipital)

119
Q

What is “pseudotumor cerebri”?

other name? in whom? presentation?

A

“Idiopathic Intracranial Hypertension”

YOUNG OBESE WOMEN

  • daily HEADACHE
  • bilateral symmetric PAPILLEDEMA (optic disc edema with blurred borders on funduscopy)
  • TRANSIENT visual disturbances - worsened by Valsalva (bend down, cough, etc.)
120
Q

Broca aphasia

spontaneous speech? comprehension? repetition?

A

sparse + nonfluent speech (slow and mostly nouns + verbs)

PRESERVED comprehension

impaired repetition

121
Q

Broca aphasia

area damaged? associated features?

A

INFERIOR FRONTAL gyrus of the dominant (usually LEFT) hemisphere (Br. 44 + 45)

associated FACE + ARM HEMIPARESIS (usually right-sided, due to proximity of lesion to primary motor cortex)

122
Q

Wernicke aphasia

spontaneous speech? comprehension? repitition?

A

Fluent + voluminous NONSENSICAL speech

DIMINISHED comprehension

impaired repetition

(also lack insight)

123
Q

Wernicke aphasia

area damaged? assoc. features?

A

POSTERIOR SUPERIOR TEMPORAL gyrus (Br. 22) usually of the dominant (left) hemisphere

assoc. with SUPERIOR VISUAL FIELD DEFECT (usually R sided)

124
Q

Frontal eye field

where is it? what does a lesion here cause?

A

POSTERIOR MIDDLE FRONTAL gyrus (just above Broca area)

lesion causes EYE DEVIATION to IPSILATERAL SIDE

125
Q

What is CONDUCTION APHASIA?

spontaneous speech? comprehension? repetition?

A

fluent with PHONEMIC errors (as in saying “thumb” instead of “dumb”… replacing one phoneme with another)

PRESERVED comprehension

VERY POOR repetition

126
Q

what is damaged in CONDUCTION APHASIA?

A

the ARCUATE FASCICLE

connection btwn Broca and Wernicke areas within frontal + parietal lobes

127
Q

Meningioma

common sites + resulting sx

A

dural reflections

eg, falx cerebri, tentorium cerebelli

falx > disruption of contralateral LEG sensation/motor (due to location on homunculus)

128
Q

What is the major difference in seizure type that determines whether broad spectrum or narrow spectrum anti-epileptics should be used?

A

Focal vs. generalized

focal = 1 hemisphere AT ONSET = narrow spectrum

generalized = both hemispheres AT ONSET = broad spectrum

129
Q

what is the difference between “simple” and “complex” seizures?

A

simple = no lost consciousness

complex = lost consciousness

130
Q

Huntington disease

inheritance? gene affected?

A

AD inheritance - history in 1st deg relative

increased CAG repeats in HTT gene on Chr. 4 for Huntingtin protein

(in Huntington the Caudate has less Acetylcholine and Gaba … CAG; “hunt” is 4 letters > chr. 4)

131
Q

Huntington disease

sx onset? s/s?

A

onset at 20-50 yrs old (dep on anticipation); 35-45 most common and will live 15-20 yrs after

CHOREA - from fidgeting to uncontrollable swinging of limbs

DEMENTIA - memory + cognitive decline

BEHAVIOR - aggressive, apathy, depression

132
Q

Huntington disease

macro + micro brain changes

A

Macro - CAUDATE ATROPHY with some putamen/frontal atrophy

Micro - NEURON LOSS in CAUDATE/PUTAMEN

133
Q

Huntington disease

decreased what where?

mechanism of neuron damage?

A

decreased ACh, GABA and Substance P in “striatum” (caudate + putamen)

excitotoxicity - NMDA-Rs bind Glu and overexcite > neuronal death

134
Q

injury to WHAT nerve WHERE can cause Trendelenburg gait?

A

injury to SUPERIOR GLUTEAL NERVE in the SUPEROMEDIAL quadrant of a buttock

will paralyze the ipsilateral gluteus medius/minimus and cause contralateral Trendelenburg

ie, left nerve issue will weaken left abductors > right hip will drop when right foot is lifted during walking

(common in IM injection in wrong place, give superolateral or anterolateral buttock)

135
Q

Hypothalamic Nuclei: what is the function of…

ventromedial?

A

satiety

damage > hyperphagia

(remember medial + lateral oppose each other’s actions in appetite regulation

“I SAT MEDitating then HUNG LANTerns”)

136
Q

Hypothalamic Nuclei: what is the function of…

lateral?

A

hunger

damage > anorexia

(remember medial + lateral oppose each other’s actions in appetite regulation

“I SAT MEDitating then HUNG LANTerns”)

137
Q

Hypothalamic Nuclei: what is the function of…

anterior?

A

heat dissipation

damage > hyperthermia

(remember ant + post oppose each other’s actions in temp regulation

“I DISliked my AUNT’s CONSERVative POST on Facebook”)

138
Q

Hypothalamic Nuclei: what is the function of…

posterior

A

heat conservation

damage > hypothermia

(remember ant + post oppose each other’s actions in temp regulation

“I DISliked my AUNT’s CONSERVative POST on Facebook”)

139
Q

Hypothalamic Nuclei: what is the function of…

arcuate?

A

secretion of DOPAMINE > prolactin inhibition

GHrH and GnRH release also

140
Q

Hypothalamic Nuclei: what is the function of…

Paraventricular?

A

ParaVenTriCular

Vasopressin (and oxytocin)
Thyrotropin-releasing hormone
Corticotropin releasing hormone

(look for the V T C in VenTriCular + oxytocin/vasopressin go together)

141
Q

Hypothalamic Nuclei: what is the function of…

Supraoptic?

A

SuprAOptic

ADH
Oxytocin

142
Q

Hypothalamic Nuclei: what is the function of…

Suprachiasmatic?

A

SupraChiasmatic

Circadian rhythm + pineal function

143
Q

Cognitive testing for…

COMPREHENSION

A

follow a MULTISTEP COMMAND

144
Q

Cognitive testing for…

CONCENTRATION / ATTENTION

A

Recite months BACKWARDS

Count DOWN from 100 by 7s

Spell “world” BACKWARDS

145
Q

Cognitive testing for…

SHORT TERM MEMORY

A

Repeat 3 unrelated words AFTER 5 MINUTES

146
Q

Cognitive testing for…

LONG TERM MEMORY

A

Recall PAST LIFE EVENTS

147
Q

Cognitive testing for…

VISUAL-SPATIAL

A

DRAW INTERSECTING PENTAGONS

148
Q

Cognitive testing for…

EXECUTIVE FUNCTION

A

DRAW a CLOCK oriented to a REQUESTED TIME

149
Q

Dementia dx criteria (2)

A
  1. Impairment in AT LEAST ONE cognitive domain

2. FUNCTIONAL IMPAIRMENT in daily life

150
Q

Spinal Stenosis

3 pathophysiological changes in spine

A
  1. LIGAMENTUM FLAVUM thickening - compresses SC
  2. Hypertrophic FACETS - on vertebrae, plus…
  3. DISC BULGING - both cause foraminal stenosis
151
Q

Spinal Stenosis

sx (3)?

what exacerbates / improves the pain?

A
  1. leg pain
  2. numbness / paresthesia
  3. weakness

WALKING worsens pain (“neurogenic claudication”) as well as anything that EXTENDS LUMBAR SPINE (due to further canal narrowing)

LUMBAR FLEXION decreases pain (leaning on shopping cart, walking uphill)

152
Q

Spinal Stenosis

MCC

A

Osteoarthritis of the spin

mostly pts > 60

153
Q

What is the cause of…

UNILATERAL vs. BILATERAL internuclear ophthalmoplegia?

A

unilateral - stroke, usually older pt

bilateral - MS, usually younger pt

154
Q

What are the 2 neuron types / areas in the CNS most vulnerable to hypoxic injury via ischemia?

A
  1. PURKINJE cells of cerebellum

2. PYRAMIDAL cells of hippocampus and neocortex (zones 3, 5, 6)

155
Q

What GENERAL areas of the brain are susceptible to ischemia?

A

watershed regions between areas supplied by ACA, MCA and PCA

156
Q

What/where is the FRONTAL EYE FIELD?

Activation of a UNILATERAL frontal eye field (as in seizure) causes what?

A

cerebral cortical region that controls HORIZONTAL EYE MOVEMENT; located just above Broca’s area

activation of one side causes EYE DEVIATION TO OPPOSITE SIDE

(but after a seizure “post-ictal neuroinhibition” of that area would cause deviation to the same side)

*USMLE* (28 decks)

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