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Q Bank Quickies > Neurology > Flashcards

Neurology Flashcards

1
Q

Premature infant with blood in lateral ventricles? What if the baby was term?

A

Germinal matrix –> intraventricular hemorrhage. Germinal matrix is a very vascularized area where neurons and glial cells develop. They migrate out and it regresses at 24-32 weeks, then choroid plexus bleed is most common cause. Another risk for hemorrhage with prematurity is not being able to autoregulate blood flow.

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2
Q

Tuft of hair or skin dimple on lower back?

A

Spina bifida occulta. Bony spinal canal never closed but no herniation.

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3
Q

Meningocele vs meningomyelocele

A

Meningocele is just meninges herniating through spinal canal defect, meningomyelocele is both meninges and spinal cord herniating through

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4
Q

Thoraco-lumbar myelomeningocele and paralysis below the defect. Also decreased swallowing, dysphonia, stridor, apnea.

A

Arnold Chiari malfornation (Chiari II). Cerebella tonsillar and vermian herniation through forament magnum with aqueductal stenosis and hydrocephalus. The medulla going down too causes all those symptoms. II = more severe. With I–> just get cerebellar ataxia when older, and increased risk of syringomyelia

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5
Q

Agenesis of cerebellar vermis and cystic enlargement of 4th ventricle.

A

Dandy Walker. Also see hydrocephalus and spinal bifida

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6
Q

What embryo layer are microglia from?

A

Like macs, from mesoderm

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7
Q

Path of TAI and how do you image?

A

Shear injury –> axonal membrane injury –> influx of sodium and calcium –> axonal swelling –> accumulation of amyloid precursor protein. Need to use DTI to image.

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8
Q

Enlargement of cell body, eccentric nucleus, enlarged nucleolus, dispersion of Nissl substance. What’s going on?

A

Axonal reaction in response to loss of axon.

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9
Q

Where is NE made?

A

Locus ceruleus (pons)

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10
Q

Where is DA made?

A

Ventral tegmentum and SNc (midbrain)

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11
Q

Where is 5-HT made?

A

Raphe nucleus (pons and rostral medulla). Raphe means seam, neurons are in a line in the middle.

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12
Q

Where is ACh made?

A

Basal nucleus of Meynert

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13
Q

Where is GABA made?

A

Nucleus accumbens

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14
Q

Patient is an infant who is failing to thrive. Which hypothalamic area has been destroyed and what is this area usually responsive to?

A

Lateral. Does hunger, inhibited by leptin.

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15
Q

Patient has hyperphagia. Which hypothalamic area has been destroyed and what is this area usually responsive to?

A

Ventromedial hypothalamus. Satiety. Stimulated by leptin. Destroyed in cranipharyngioma.

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16
Q

Which part of the hypothalamus does cooling? What ANS does it do?

A

Fanterior! Also does parasympathetic.

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17
Q

Which part of the hypothalamus does heating? What ANS does it do?

A

Posterior (pHOTerior). Does sympathetic.

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18
Q

Where does ADH come from? Oxytocin?

A

Post pit. Receives projections from supraoptic (ADH) and paraventricular (oxytocin)

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19
Q

Where does DA come from in the hypothalamus?

A

Arcuate nucleus. Inhibits prolactin

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20
Q

Pain, temp, pressure, touch, vibration, and proprioception all travel together to the thalamus. What nucleus is their relay, and what is their destination?

A

VPL via spinothalamic, dorsal columns/medial lemniscus (dorsal decussate then travel in ML), then go to primary sensory. VPL think vibration pain,pressure,props, and light touch

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21
Q

Face sensation and taste travel to the thalamus via which inputs? Where do they relay and where do they go?

A

Trigems and gustatory pathway (solitarius) take them there, relay on VPM and then hit up primary sensory. VPM think M for muscles of mastication, then you’ll be thinking V. And face and taste almost rhyme.

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22
Q

What nucleus in thalamus does vision? Where does it go after?

A

LGN –> calcarine sulcus. LGN for light.

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23
Q

What nucleus in thalamus does hearing? Via what inputs?

A

CNVIII –> Superior olive in pons –> lateral lemniscus –> inferior colliculus of tectum –> MGN of thalamus. MGN for music.

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24
Q

Motor thalamus? Input?

A

VL via basal ganglia.

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25
Q

Striatum of BG =

A

Putamen (motor) and caudate (cognitive)

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26
Q

Lentiform of BG=

A

Putamen and GP

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27
Q

Hyperorality, hypersexuality, disinhibited behavior. Lesion? Associations?

A

Kluver Bucy syndrome. Bilateral amygdala lesion. Associated with HSV1

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28
Q

Cerebellar hemisphere lesion vs cerebellar vermis lesion

A

Hemispheres are lateral and affect lateral limbs. Fall toward side of lesion. Vermis lesions are central, affect trunk. Cause truncal ataxia and dysarthria

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29
Q

STN damage causes contralateral or ipsilateral ____?

A

Contralateral hemiballismus

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30
Q

Paramedian pontine reticular formation damage vs FEF damage

A

Pons –> eyes look away from side of lesion, FEF –> eyes look toward side of lesion. IDK if this is true but think of pons as doing the bidding for FEF, FEF is like okay make eyes look away, and pons is like okay and pons is ipsilateral by then so defect makes eyes look away (trying to bring it towards)

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31
Q

What causes locked in syndrome?

A

Central pontine myelinosis. Commonly caused by overly rapid correction of Na+ levels (hyponatremia). See massive demyelination in pontine white matter tracts.

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32
Q

Poor repetition but fluent speech and intact comprehension

A

Conduction aphasia

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33
Q

A patient has a stroke and is hyperventilating. The doctor says the hyperventilation is helping the patient. How?

A

Hyperventilation helps cases of ICP like stroke (causing acute cerebral edema) by decreasing cerebral perfusion. PCO2 will be low, and PCO2 is what determines perfusion. Hypoxemia only influences when PO2 < 50 mmHg

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34
Q

MCA and ACA, which does hand and which does leg?

A

LACA (lower) and UMCA (upper).

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35
Q

What causes medial medullary syndrome? Lateral medullary syndrome?

A

Medial: Anterior spinal artery stroke/ vertebral artery stroke. Lateral: PICA lesion. FYI: PICA = branch of vertebral

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36
Q

Contralateral hemiparesis, decreased contralateral proprioception, ipsilateral hypoglossal dysfunction

A

Medial medullary syndrome. Infarct of paramedian branches of ASA/ vertebral arteries. Hitting the CST before it decussates, the medial lemniscus (has the cuneatus and gracilis info after they decussate), and the hypoglossal nerve as it exits.

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37
Q

Vomiting, vertigo, nystagmus, ipsilateral loss of pain and temp on face, contralateral loss of pain and temp on body, dysphagia, hoarseness, loss of gag reflex, ipsilateral horner’s, ataxia, dysmetria

A

Lateral medullary syndrome. PICA. If you see nucleus ambiguous effects –> PICA.
Vomiting, vertigo, nystagmus is from vestibular nucleus (located laterally near ICP)
Ipsilateral loss of pain and temp on face is from descending spinal trigems tract
Contralateral loss of pain and temp on body is from hitting the spinothalamic tract
Dysphagia, hoarseness, loss of gag reflex is from hitting the nucleus ambiguous.
Dysmetria and ataxia from hitting ICP
Ipsilateral horner’s is from loss of descending sympathetic control fibers that run near spinothalamic

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38
Q

Nucleus ambiguous vs nucleus solitarius

A

Ambiguous is motor –> dysphagia and hoarseness with damage (X and IX). Ambiguous is at same level as hypoglossal (rostral medulla). Solitarius = sensory and taste (VII, IX, X in rostral medulla, below does visceral like heart)

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39
Q

Vomiting, vertigo, nystagmus, paralysis of face, decreased lacrimation, decreased taste from anterior 2/3 of tongue, decreased salivation, decreased corneal reflex, face has decreased pain and temp sensation, ipsilateral hearing loss, ipsilateral horner’s

A

Lateral pontine syndrome. Damage to anterior inferior cerebellar artery.
Vomiting, vertigo, nystagmus: Vestibular nucleus
Paralysis of face, decreased lacrimation, decreased salivation (does all salivary except parotid which is CNIX), decreased taste from anterior 2/3 of tongue, and decreased corneal: hitting CN VII
Decreased pain and temp sensation of face: hitting CN V
Ipsilateral hearing loss: Cochlear nucleus
Horner’s: loss of descending sympathetic control fibers that run near spinothalamic

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40
Q

Blood supply to medulla

A

Anterior/medial = anterior spinal artery. Anterior/Lateral = vertebral arteries. Posterior/lateral = PICA.

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41
Q

Lateral cuneate nucleus vs cuneate nucleus

A

Lateral is what Clarke’s nucleus is for the upper extremity. Clarke’s got all the proprioceptive info for the lower extremity (instead of post columns) and sends it up dorsospinocerebellar tract, then for upper extremity the cuneate tract just gets everything, including what needs to go to the cerebellum. So the cuneatus sends the thalamic info to the cuneate nucleus and the cerebellar to the lateral cuneate.

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42
Q

Blood supply to pons

A

Medial= basilar. Lateral = AICA. Upper pons is just basilar.

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43
Q

Damage to abducens nucleus on L will produce what symptoms?

A
  1. Can’t abduct left eye
  2. L MLF damage, so neither eye will move when try to look to left.
  3. L facial droop because CN VII loops around there, also loss of corneal reflex
44
Q

What forms the MLF?

A

CN VI and vestibular. Does conjugate gaze/ adjusting gaze to head rotation

45
Q

Superior colliculus vs inferior colliculus

A

Superior does visual attention/ saccades, inferior does auditory

46
Q

Consensual light pathway

A

Retina –> CN II –> pretectal (bilaterally) –> parasympathetic –> cilliary muscles

47
Q

Contralateral hemianopia with macular sparing. What is fucked and what other things can get fucked by this blood supply?

A

PCA. MCA and PCA share the macula. PCA also supplies thalamus and midbrain, so can eff up CN III and CN IV and all the relays!

48
Q

Anterior communicating damage vs posterior communicating damage. Causes and consequences?

A

Cause = saccular/berry aneurysm. Most frequent is AComm, but common in PComm too. AComm –> impingement of CN II –> visual field defects (classically bitemporal hemianopsia via optic chiasm compression). PComm –> impingement of CN III –> effects para first and motor second (motor is on inside). Remember, ischemia affects motor first and para second.

49
Q

What do you give for subarachnoid hemorrhage?

A

Calcium blocker to prevent vasospasms. (Such as nimodipine)

50
Q

What is the cause of recurrent hemorrhagic strokes in elderly patients?

A

Cerebral amyloid angiopathy. Small, parenchymal (lobar) strokes, less severe than HTN strokes. From beta amyloid deposition in arterial wall –> weakened wall more prone to rupture

51
Q

Subfalcian herniation hits what vessel?

A

ACA

52
Q

Transtentorial herniation hits what vessel? What else happens?

A

PCA. Also hits CN III and pushes brainstem down –> Duret hemorrhages. And pushes brainstem to side, squishes contralateral CP.

53
Q

What happens with cerebellar tonsilar hemorrhage?

A

Compression of medulla (tonsils through foramen magnum) –> death

54
Q

Hydrocephalus ex vacuo

A

Apparent increase in CSF but really just brain atrophy

55
Q

A young, obese woman presenting with headache and papilledema. Increased ICP with normal CSF and imaging

A

Pseudotumor cerebri. Small block that you can’t see causing increased ICP probably.

56
Q

Which sensory system reaches cortex without relay in thalamus?

A

Olfactory. Makes sense, already up there.

57
Q

How is the spinal cord affected with polio? How is polio transmitted?

A

Hits LMN. Fecal oral, replicates in small intestine first.

58
Q

Macroscopically, see thin anterior roots and atrophy of precentral gyrus. Microscopically, see loss of anterior horn and lateral CST, as well as loss of CN V, IX, X, XII motor. What is it and what is the most common cause of death and what is the path and what can you treat it with?

A

ALS. Combined UMN and LMN defects and can hit cranial nerves.
Can be caused by defect in superoxide dismutase 1
Pneumonia from aspiration or other resp complications is caused of death usually
Riluzole treatment can modestly increase survival by decreasing glutamate release

59
Q

Myelin vacuolization and axonal degeneration in dosral columns, lateral CST, and peripheral nerves.

A

B12 or E deficiency –> subacute combined degeneration

60
Q

Werdnig Hoffman disease

A

Looks like polio except congenital –> hits LMN. AR.

61
Q

Kid has high arched foot, hammer toes, kyphoscoliosis. Genetic analysis shows a GAA trinucleotide repeat. What is it and what are other symptoms and what is most common cause of death?

A

Friedrich’s ataxia. AR.
Mitochondrial dysfunction.
See staggering gait, frequent falling, nystagmus, dysarthria, and hypertrophic cardiomyopathy is most common cause of death.

62
Q

Low back pain radiating to legs, loss of anocutaneous reflex (pinprick in perianal area doesn’t cause contraction of anal sphincter), bowel/bladder dysfunction, loss of ankle jerk with plantar flexion of feet, loss of ability to have erection

A

Cauda equina syndrome. Bowel and bladder –> S3-S5. Loss of ankle reflex is S1-S2. S2-S4 = pudendal (does erection, S2,3,4 keep the penis off the floor).

63
Q

Biceps reflex tests what nerve?

A

C5. Fiveceps

64
Q

Triceps reflex tests what nerve?

A

C7. Triseven.

65
Q

Patellar reflex tests what nerve?

A

L4

66
Q

Achilles reflex tests what nerve?

A

S1. AchilleS1

67
Q

Moro reflex

A

Startled one where abduct/extend limbs then draw together

68
Q

Galant reflex

A

Stroking along one side of spine while newborn is in ventral suspension (head down) causes lateral flexion of lower body toward stimulated side

69
Q

Paralysis of upward gaze. What would you expect to see? Other symptoms you might see?

A

Pinealoma (pineal gland tumor). Mass effect is squozing superior colliculus, which is the conjugate vertical gaze center. Pinealoma is a germinoma –Malignant tumor from embryonic germ cells –> precocious puberty from beta HCG, Parinaud syndrome (the paralysis of conjugate gaze), and obstructive hydrocephalus.

70
Q

What nerve innervates the tensor tympani?

A

Trigems. Does external part of tympanic membrane and will regulate membrane tension via tensor tympani

71
Q

What innervates the inner surface of the tympanic membrane?

A

IX

72
Q

What innervates the posterior part of the auditory canal?

A

X. Can have fainting with ear exam

73
Q

Gag reflex afferent and efferent

A

Afferent = IX, efferent = X

74
Q

Dorsal motor nucleus

A

Sends parasympathetic fibers to heart, lungs, and upper GI. X

75
Q

What goes through the jugular foramen?

A

CN IX, X, XI, jugular vein

76
Q

Opthamoplegia and decreases corneal and maxillary sensation with normal vision

A

Cavernous sinus syndrome. Extraocular paralysis because they all pass through there, as do V1 and V2.

77
Q

Rinne test is abnormal in R ear and when put tuning fork on your head can hear it better in R ear…

A

Conductive hearing loss in R ear. Bone > air (Abnormal Rinne), and Weber is localized to affected ear because loss of conduction masks ambient noise in room, allowing vibrations to be better heard

78
Q

Normal rinne, abnormal weber localized to R

A

Sensorineural hearing loss localized to L ear.

79
Q

Patient has tinnitus, vertigo, and sensorineural hearing loss. They have been having exacerbations and remissions of these three symptoms. What is it? What if it was constant?

A

Meniere’s disease: disorder of inner ear, increased endolymph secondary to decreased resorption –> damage. If it was constant, would probably be acoustic neuroma–> mass lesion at cerebropontine angle.

80
Q

What muscles open the jaw?

A

Masseter, temporalis, medial pterygoid.

81
Q

What muscles close the jaw?

A

Lateral pterygoid.

82
Q

Path of presbyopia.

A

Ciliary muscles squeeze to cause miosis. In presbyopia, hardened lens that can’t thicken upon ciliary contraction –> can’t do accommodation (see up close). Age related. And if it happen in near-sighted people, can help with distance vision and can retain up close vision! 437 for drawing.

83
Q

Acute, painless monocular vision loss in a 65 year old. See retinal whitening and cherry-red spot on fundoscopic exam.

A

Central retinal artery occlusion. Embolic occlusion. preceded by amaurosis fugax (transient monocular vision loss) from embolus coming and passing through. Macula preserved from other blood supply.

84
Q

Painless loss of vision of top half of visual field in a 40 year old. On exam, see swollen, pale disc.

A

Anterior ischemic optic neuropathy. Ischemia of optic nerve head due to disease of posterior ciliary arteries.

85
Q

Painful eye with dirty looking retina on exam in a 65 year old.

A

Central retinal vein occlusion. Venous stroke –> central retinal vein clotted –> backpressure –> venous HTN –> dirty looking retina

86
Q

Where do muscarinics, beta, alpha and PGF2a act in terms of glaucoma?

A

Muscarinics –> ciliary muscle (contract to cause miosis)–> pilocarpine, carbachol.
Beta on ciliary epithelium that makes aqueous humor (can use timolol for glaucoma).
Alpha 1 dilates the iris.
And PGF2a increases outflow through Canal of Schlemm (latanoprost, ends in prost)
438 for drawing

87
Q

Open angle vs closed angle glaucoma

A

Open angle –> angle is open so buildup is in front of iris. Painless, more common in US.
Closed angle –> angle is closed so buildup behind iris. Acute –> opthalmic emergency –> very painful, rock hard eye, do not give epi because of mydriatic effect

88
Q

Enlarged blind spot and elevated optic disc with blurred margins on fundoscopic exam. Headache.

A

Papilledema. Optic disc swelling due to increased ICP (secondary to mass effect)

89
Q

You see decreased bilateral pupillary constriction when you shine the light in the L eye. If I told you the lesion was in the optic tract, where in the optic tract is it?

A

R side. This happens because nasal portion contributes more to consensual constriction signal to pretectal than temporal, and nasal crosses. So damage to L nasal and R temporal running in optic tract together would cause a L sided Marcus Gunn pupil

90
Q

Flashes and floaters followed by monocular vision loss like a curtain drawn down.

A

Retinal detachment. Surgical emergency. Separation of neurosensory layer of retina from outermost pigmented epithelium (support of retina) –> degeneration of photoreceptors

91
Q

You see deposition of yellowish material beneath retinal pigment epithelium… What if it was cotton wool spools?

A

Age related macular degeneration. That stuff is drusen. This is dry stage, can progress to wet stage with VEGF –> subretinal hemorrhage.
Cotton wool spools –> diabetic retinopathy. Very similar except whole retina involved not just macula. Cotton wool spools from little infarcts in retina, also can have wet phase.

92
Q

Causes of bitemporal vs binasal hemianopia

A

Bitemporal is compression of medial optic chiasm (nasal retinal sees temporal, remember, and this is the part that crosses)–> pituitary adenoma. Binasal is compression of lateral –> think calcified carotids

93
Q

ApoE4 vs ApoE2

A

2 is protective for Alzheimer’s, 4 increases risk.

94
Q

What are Pick bodies?

A

Spherical tau protein aggregates

95
Q

What are Lewy bodies?

A

Alpha-synuclein defect

96
Q

Which type of dementia involves beta pleated sheets resistant to proteases? What would you see in terms of symptoms and on histo

A

Creutzfeldt-Jakob disease
Myoclonus with dementia
See vacuolization and reactive gliosis
Noninflammatory

97
Q

Which neuropathology makes it look like the ventricles are enlarged but really the caudate is just small? What is the mechanism of cell death?

A

Huntington’s. Loss of neurons in caudate and putamen. Excitotoxicity is the mechanism of cell death.

98
Q

Painful, monocular, slow vision loss.

A

Optic neuritis. Inflammatory demyelination of the optic nerve. Associated with MS.

99
Q

Symmetric ascending muscle weakness/paralysis beginning in lower extremities. You see papilledema. What is the prognosis? Associations?

A

GBS. Prognosis is good. Associated with Crampylobacter and CMV. Hits peripheral myelin./
Papilledema is from increased protein, in CSF see increased protein with normal cell count.

100
Q

Subacute sclerosing encephalitis vs progressive multifocal leukencephalopathy

A

SSE: measles missing M protein so can’t be cleared from CNS –> inflammation, demyelination, gliosis. Progresses slowly to dementia and death. See viral nuclear inclusions
PML: JC virus (a polyomavirus) reactivated in AIDS patients. See ground glass intranuclear inclusions in oligos. NONINFLAMMATORY! RAPIDLY progressive –> fatal.

101
Q

Charcot-Marie-Tooth

A

Hereditary motor and sensory neuropathy. Defective production of proteins involved in structure and function of peripheral nerves or myelin sheath. Often presents as weakness of foot dorsiflexion (common peroneal nerve)

102
Q

Positional testing shows delayed horizontal nystagmus? Positional testing shows immediate nystagmus in any direction?

A

Delayed horizontal: Peripheral vertigo. More systematic.

Immediate nystagmus in any direction: Central vertigo. Think of this one as just crazy fucked because it’s central.

103
Q

Spindle cells, compact (antoni A) and loose (antoni B) areas, encapsulated, slow growing

A

Schwannoma

104
Q

Small, round, blue cell tumors with neuropil in a kid. Positive for NSE, chromogranin, synaptophysin, S100. N-myc. Increased urinary HVA and/or VMA. What is it and clinical symptoms?

A

Neuroblastoma NOT pheo! Tumor of adrenal medulla but no episodic HTN. May see nonrhythmic eye movements with myoclonus (paraneoplastic)

105
Q

GFAP + processes tapering toward blood vessels in a kid. Where in brain? Prognosis?

A

Ependymoma. Often in fourth ventricle. Poor prognosis, causes hydrocephalus.

106
Q

Foamy cells and high vascularity in the cerebellum in a kid. Also see polycythemia. What is it and associations?

A

Hemangioblastoma. Associated with von-Hippel-Lindau when found with retinal angiomas.

107
Q

Solid, cystic structures filled with machinery oil and calcified components in a kid. Cysts lined by squamous epithelium. What is it, what do you confuse it with, where does it come from?

A

Craniopharyngioma. Confused with pituitary adenoma because both can cause bitemporal hemianospia. Derived from ectoderm (anterior pituitary precursor)

Q Bank Quickies (11 decks)

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