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USMLE Step 1 > Neurology > Flashcards

Neurology Flashcards

1
Q

what does the neural plate develop into?

A

neural tube and the neural crest cells

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2
Q

what does the notochord become?

A

nucelus polposus and eventually the intervertebral discs

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3
Q

what are the alar and basal plates?

A

alar- dorsal-sensory

basal-ventral-motor

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4
Q

what findings do you get with neural tube defects?

A

when neuropores fail to close during 4th week so you get opening between amniotic fluid and spinal canal. high AFP and high acetylcholinesterase (except spina bifida occulta- normal AFP)

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5
Q

what are the types of neural tube defects?

A
  1. spina bifida occulta- hole in neurpore, but no herniation so dura intact- tuft of hair or sacral dimple
  2. meningocele- meninges herniate, but no neural tissue
  3. myelomeningocele- meninges and neural tissue
  4. myeloschisis- exposed neural tissue with no meningeal or skin covering
  5. ancencephaly- failure of rostral neurpore to close so no forebrain
  6. holoencephaly- failure of right and left hemispheres to fuse (5-6 weeks)
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6
Q

what is the difference between type 1 and type 2 chiari malformations?

A
  1. ectopia of the cerebellar tonsils

2. vermis and tonsils through foramen magnum and stenosis of aqueduct

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7
Q

what is a dandy walker malformation?

A

agenesis of cerebellar vermis so get big 4th ventricle, non communicating hydrocephalus, spina bifida

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8
Q

what are the symptoms of a syringomyelia?

A

cape like loss of pain and temp sensation upper extremities, fine touch usually preserved

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9
Q

what are astrocytes?

A

glial cells- support, repair, extracellular K buffer, remove excess neurotransmitter
-derived neuroectoderm, GFAP is marker

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10
Q

where is myelin made?

A

oligodendrocytes in the CNS and schwann cells in the PNS

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11
Q

what types of cells are affected in guillian barre? what about multiple sclerosis

A
  1. Schwann cells in the PNS

2. Oligodendrocytes in the CNS

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12
Q

what are the three layers of the meninges?

A
  1. Dura mater (mesoderm)
  2. Arachnoid mater (neural crest)
  3. Pia mater (neural crest)
    Epidural space (between skull and dura-blood vessells and fat)
    CSF runs between arachnoid and pia
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13
Q

what makes up the blood brain barrier?

A

astrocyte foot process, tight junctions between non fenestrated capillary endothelial cells and basement membrane

  • non polar lipid soluble get through rapidly with diffusion and
  • glucose and AA’s get through with carrier mediated transport
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14
Q

what does the preoptic nucleus in the hypothalamus do?

A

thermoregulation and sexal urges-, GnRH (when the neurons don’t migrate, you get Kallman’s syndrome)

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15
Q

what are beta waves?

A

awake with eyes open, high frequency, low amplitude

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16
Q

what does the thalamus do? VPL and VPM?

A

major center for all ascending sensory information
VPL-spinothalamic and medial meniscus/dorsal column
VPM-gustatory and trigeminal
-all go to primary somatosensory cortex

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17
Q

what goes the lateral geniculate nucleus do?

A

all from CN2, optic tract, optic chiasm- goes to calcarine sulcus

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18
Q

medial geniculate nucleus?

A

hearing, everything from superior oliver and inferior colliculus of tectum

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19
Q

what does the ventral lateral nucleus do?

A

everything from basal ganglia and cerebellum- goes to motor cortex

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20
Q

what are the 4 dopaminergic pathways?

A
  1. Mesocortical- negative symptoms
  2. Mesolimbic- positive symptoms
  3. Nigrostriatal- decreased activity gives extrapyramidal symptoms-dystonia, akathisia, parkinsonism, tardive dyskinesia
  4. Tubuloinfindibular- dec activity= inc prolactin, dec libido, inc galactorrhea, gynecomastia
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21
Q

Is cerebral perfusion pressure more controlled by CO2 or O2?

A

CO2 until you get O2 less than 50mmHg, the CPP is proportional to pCO2 until it gets over 90mmHg

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22
Q

where is CSF made? where does it drain?

A

ependymal cells of choroid plexus

-drains into the arachnoid granules and then into the dural venous sinuses

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23
Q

what does the pineal gland do?

A

melantonin secretion and circadian rhythm

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24
Q

what are the vagal nuclei?

A
  1. nucleus solitarius- visceral sensory (taste, gut distension, baroreceptors) 7, 9, 10
  2. nucleus ambiguus-motor for the pharynx, larynx 9,10,11
  3. dorsal motor nucleus- autonomic (parasym) to heart, lungs, upper GI
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25
Q

at what vertebrae does the spinal cord terminate?

A

L1-L2

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26
Q

where do the eyes look when there is a lesion? where do the eyes look for seizures?

A

lesion- toward

seizures-away

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27
Q

what is a common lesion seen in MS?

A

medial longitudinal fasiculus, can’t adduct the eye with the side of the lesion and the contralateral eye gets nystagmus with abduction

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28
Q

what is the timeline for hypoxic damage in brain?

A

5 mins

  • CT can detect changes 6-24hr (noncontrast to look for hemorrhage)
  • diffusion weighted MRI (3-30mins)
29
Q

what is horners syndrome?

A

miosis (constriction of the pupil), anhidrosis (no sweating face) and ptosis (drooping of eyelid)

30
Q

what is trigeminal neuralgia?

A

CN V, shooting pain unilateral face, caused by chewing, talking, touching sides
-tx with carbamazepine

31
Q

what is athetosis?

A

snake-like writhing movements- basal ganglia

32
Q

what is syndenham chorea?

A

dance like purposeless movements associated with rheumatic fever

33
Q

what is hemiballismus?

A

flailing arm and ipsilateral leg-contralateral stroke, subthalamic nuceli-lacunar stroke

34
Q

what is the pathology of parkinsons?

A

lewy bodies with alpha synuclein- intracellular eosinophilic inclusion

35
Q

what is huntingtons?

A

AD CAG repeat in chr 4 HTT gene- get inc dopamine, dec GABA and Ach, degeneration of neurons in caudate and putamen

36
Q

what is Creutzfeldt Jakob disease?

A

Prion PrPc and PrPsc- periodic sharp waves on EEG, myoclonus, 14-3-3 protein on CSF

37
Q

what is communicating hydrocephalus?

A

decreased absorption of CSF by arachnoid granules

38
Q

what is normal pressure hydrocephalus?

A

wet, wobbly, wacky, increase ICP causes distortion of corona radiata so you get urinary incontinence, gait apraxia and cognitive dysfunction

39
Q

what is Charcot-Marie Tooth disease?

A

AD- hereditary sensory and motor neuropathy- lower extremity weakness, foot abnormalities (hammer toe), foot drop, sensory deficits

  • problem making proteins for peripheral nerves and myelin sheath
  • CMT1A PMP22 gene duplication
40
Q

what is STURGE weber?

A

sporadic, port wine stain, tram track calcifications in gyri, intellectual retardation, GNAQ gene, epilepsy
-affects small capillary sized blood vessels

41
Q

What is tuberous sclerosis?

A

TSC1 on Chr 9 or TSC2 on Chr16, AD

  • hamartomas on skin and CNS
  • angiofibromas
  • MR
  • ash leaf spots
  • cardiac rhabdomyomas, mental retardation, angiomyolipoma, seizures, shagreen patches
42
Q

What is NF1?

A

mutation in NF1 tumour suppressor gene, inhibitor of RAS, chr 17

  1. subcutaneous neurofibromas, cafe au lait spots, optic gliomas, pheochromocytomas, lisch nodules
    - AD
43
Q

What is NF2?

A

mutation chr 22, NF2

1. bilateral acoustic schwannomas, juvenile cataracts, meningomas and ependymomas,2 ears, 2 eyes, 2 parts brain

44
Q

What is Von hippel lindau?

A

deletion of VHL, chr 3p

  • hemangioblastomas of retina, brain stem, cerebellum and spine
  • renal cell carcinomas, pheochromocytomas, angiomastosis (hemangiomas of the skin
45
Q

how does a prolactinoma present in males and females?

A

males- infertility and low libido
females; galactorrhea, amenorrhea, low bone density
tx- dopamine agonist (bromocriptine, cabergoline

46
Q

what are the primary childhood brain tumours?

A
  1. pilocytic astrocytoma
  2. medulloblastoma
  3. ependymoma
  4. craniopharyngioma
  5. pinealoma
47
Q

what kind of cells do you see in medulloblastoma?

A

homer wright rosettes, primitive neuroectoderm tumour

48
Q

where is ependymoma usually found?

A

4th ventricle- get perivascular pseudorosettes

49
Q

where is craniopharygioma usually found?

A

supratentorial tumour, calcified

  • remnants of Rathke pouch (ectoderm)
  • cholesterol crystals found in motor oil like fluid into the tumour
50
Q

what can uncal herniation cause?

A

medial temporal lobe

-contralteral CN3 palsy and ipsalateral hemiparesis (false localizing sign

51
Q

what is spinal muscular atrophy?

A

AR

  • anterior horn degeneration
  • symmetrical weakness, LMN, marked hypotonia and fasiculations
52
Q

what is tabes dorsalis and what do you get?

A

tertiary syphilis- get knocked out dorsal column so dec proprioception, ataxia

53
Q

what does syringomelia cause?

A

bilateral cape like loss pain and temp

54
Q

B12 deficiency

A

knocks out dorsal columns and corticospinal tracts so you get ataxia, gait disturbance, impaired vibration, parathesias

55
Q

what is brown sequard?

A

hemisection of the spinal cord

  • ipsalateral UMN, LMN and vibration, proprioception and fine touch
  • contralateral pain and temp loss
56
Q

what is friedrich’s ataxia?

A

degeneration of lateral corticospinal, spinocerebellar and dorsal columns

  • AR, nucleotide repeat disorder (GAA) frataxin (iron binding protein)
  • diabetes, dilated cardiomyopathy, staggering gait, dysarthria, falling, nystagmus, hyphoscoliosis
57
Q

What is presbycusis?

A

age-related hearing loss

  • loss high frequency
  • bilateral, symmetrical
  • destruction of hair cells in cochlear base
58
Q

what is astigmatism?

A

abnormal curvature of the cornea- different refractive power on different axes, need cylindrical lens

59
Q

what is presbyopia?

A

age related change in lens so you can’t accommodate as well

-need reading glasses

60
Q

what is miosis?

A

constriction of the pupil (parasympathetic)

61
Q

mydriasis?

A

dilation (sympathetic)

62
Q

what is horner syndrome?

A

loss of sympathetic denervation of the face-miosis, ptosis and anhidrosis

63
Q

what is internuclear opthalmoplegia?

A

in MS-medial longitudinal fasiculus-so CN6 lateral rectus goes lateral, but can’t communicate for medial rectus on opposite eye to also coordinate inward to get the same direction of horizontal gaze

64
Q

what is first line for trigeminal neuralgia?

A

carbamazepine

65
Q

what is ethosuximide used for?

A

thalamic T type Ca channels blocked- absence seizures

66
Q

how does sumatriptan work?

A

5HT IB/ID agonist- for migraine, cluster headache, inhibits trigeminal nerve activation, prevents vasoactive peptide release and induces vasoconstriction

67
Q

how does levodopa work? what about carbidopa?

A

levodopa crosses BBB and converted by dopa decarboxylase to dopamine in CNS
carbidopa is a peripheral dopa decarboxylase inhibitor which is given with it to increase bioavailability of L dopa

68
Q

what is malignant hyperthermia and what do you give to treat it?

A

AD usually- mutation in genes for ryanodine receptors so you get increased Ca release in sarcoplasmic reticulum and give dantrolene

USMLE Step 1 (20 decks)

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