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Final FA review > 3/23 Neuro > Flashcards

3/23 Neuro Flashcards

1
Q

subthalamic nucleus

  • whats it do?
  • lesion here causes what?
A
  • inhibits movement on the contralateral side of the body.

- Hemiballismus of the contralateral side, or wild, uncontrollable movement of the right arm and leg.

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2
Q

Parkinsons

-chemical imbalance?

A

dec. dopamine

inc. ACh

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3
Q

Lewy bodies

  • seen in what disease?
  • composed of what?
A
  • Parkinsons, Lewy body dementia

- α-synuclein

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4
Q

Huntingtons

  • chemical imbalance?
  • mnemonic?
A

Expansion of CAG

  • Caudate loses ACh & GABA.
  • dec. ACh
  • dec. GABA
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5
Q

Huntingtons

-what causes the neuronal death?

A

-NMDA-R binding and glutamate toxicity.

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6
Q

Hemiballismus

-usually caused by what?

A

-lacunar infarct

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7
Q

Athetosis

  • define:
  • seen in what?
A
  • Slow, writhing movements; especially seen in fingers.

- damage to basal ganglia (ie. huntingtons).

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8
Q

Dystonia

  • define:
  • examples:
A
  • Sustained, involuntary muscle contractions.

- Writer’s cramp; blepharospasm (sustained eyelid twitch).

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9
Q

Resting tremor

-what relieves it?

A

-tremor alleviated by intentional movement.

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10
Q

Klüver-Bucy syndrome

  • wheres the lesion?
  • Sxs?
  • associated w/which viral infection?
A
  • Amygdala (bilateral).
  • hyperorality, hypersexuality, disinhibited behavior.
  • HSV-1
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11
Q

Spatial neglect syndrome (agnosia of the contralateral side of the world).
-wheres the lesion?

A

Right parietal-temporal cortex.

*agnosia = inability to process sensory information.

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12
Q

agnosia

-define

A

Inability to process sensory information.

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13
Q

Agraphia, acalculia, finger agnosia, and left-right disorientation.

  • wheres the lesion?
  • whats this disease called?
A
  • Left parietal-temporal cortex

- Gerstmann syndrome

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14
Q

Reduced levels of arousal and wakefulness (e.g.,coma)

-wheres the lesion?

A

Reticular activating system (midbrain)

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15
Q

Wernicke-Korsakoff syndrome

  • wheres the lesion?
  • mnemonic for Sxs?
  • associated w/which vitamin def?
A

Mammillary bodies (bilateral)

  • CAN of beer:
  • Confusion, Ataxia, Nystagmus.
  • thiamine (B1)
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16
Q

Damage to cerebellar hemispheres

-contra or ipsilateral deficits?

A

ipsilateral

-fall toward side of lesion.

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17
Q

Cerebellar vermis lesion

-Sxs?

A
  • Truncal ataxia, dysarthria.
  • Vermis is centrally located—affects central body.
  • as opposed to cerebellar hemispheres which = laterally located and affect lateral limbs.
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18
Q

Paramedian pontine reticular formation lesion

-eyes look toward or away from side of lesion?

A

Eyes look away from side of lesion.

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19
Q

Frontal eye fields

-eyes look toward or away from side of lesion?

A

Eyes look toward lesion

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20
Q

Central pontine myelinolysis

  • aka?
  • cause?
  • mnemonic?
A
  • Ostmotic demyelination syndrome.
  • Caused by overly rapid correction of hyponatremia.
  • “From low to high, your pons will die” (CPM)
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21
Q

Fast dec. in serum sodium

  • can cause what?
  • mnemonic?
A

“From high to low, your brain will blow”.

-cerebral edema/herniation

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22
Q

Central pontine myelinolysis

  • Sxs:
  • which two tracts are most commonly affects?
A
  • Can cause “locked-in syndrome.”
  • Acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness.
  • corticobulbar & corticospinal tracts.
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23
Q

dysarthria

-define:

A

Motor speech disorder

-movement deficit. As opposed to aphasia which is a language deficit.

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24
Q

Where is the brain is the speech center?

-what artery supplies this area?

A

-Left cerebral hemisphere, in a vascular area supplied by the left middle cerebral artery.

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25
Q

Conduction aphasia

  • what is it?
  • wheres the lesion?
A
  • Poor repetition but fluent speech, intact comprehension.

- left superior temporal lobe and/or left supramarginal gyrus.

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26
Q

Nonfluent aphasia with good comprehension and repetition.

-whats the disease?

A

Transcortical motor aphasia

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27
Q

Poor comprehension with fluent speech and repetition.

-whats the disease?

A

Transcortical sensory aphasia

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28
Q

Nonfluent speech, poor comprehension, good repetition.

-whats the disease?

A

Mixed transcortical aphasia

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29
Q

lenticulostriate

-off what big artery?

A

MCA

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30
Q

PCA branches off basilar artery at the:

A

pontomesencephalic junction.

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31
Q

brain

  • watershed zones
  • what Sxs will you see in severe hypotension?
A
  • upper leg/upper arm weakness.

- defects in higher-order visual processing.

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32
Q 
Therapeutic hyperventilation (brain)
-what is it?
A

When you have acute inc. ICP/cerebral edema:

-your body hyperventilates, so you dec. pCO2 which leads to vasoconstriction & dec. cerebral perfusion => dec. ICP.

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33
Q

MCA stroke

-Sxs:

A
  • language defects (if in dominant hemo = left hemi).
  • contralat. hemineglect if in non-dom side.
  • motor/sensory for contralateral upper limb and face.
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34
Q

ACA stroke

-Sxs:

A

-motor/sensory for contralateral lower limbs.

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35
Q

Lenticulo-striate stroke

  • what region do they feed?
  • Sxs:
A
  • Striatum, internal capsule.

- Contralateral hemiparesis/hemiplegia.

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36
Q

(hemi) paresis =

(hemi) plegia =

A 
paresis = weakness
plegia = paralysis
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37
Q

fasciculations

-sign of LMN or UMN lesion?

A

LMN

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38
Q

brisk DTR

-UMN or LMN lesion?

A

UMN lesion

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39
Q

why does macula get spared in a PCA infarct (which feeds occipital lobe).

A

Gets collateral blood from MCA.

*the part of the lobe that processes macular information is what we’re talking about.

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40
Q

Cystic degeneration of putamen

-seen in what disease?

A

Wilson’s disease

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41
Q

apixaban, rivaroxaban

  • mech:
  • use:
A
  • directly inhibit factor 10a.

- Tx & prophylaxis of DVT/PE/stroke.

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42
Q

Why is PT so minimally inc. w/heparin admin?

A

The PT reagent has chemicals that neutralize heparin.

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43
Q

Intimate partner violence

-whats your first step?

A
  • supportive open ended inquiry & identification of emergency safety plans.
  • do not pressure the partner to disclose, report the abuse, or leave the partner.
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44
Q

Bupropion

-reuptake inhibitor for which chemicals?

A

-dopamine & NE.

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45
Q

Pain in shoulders & hips then sudden blindness in a 65 year old woman.

A

polymyalgia rheumatica & temporal arteritis.

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46
Q

qualitative study

A

Using discussion groups, interviews, & other anthropological methods to obtain narrative info that may explain quantitative findings.

47
Q

phenelzine

-what is it?

A

nonselective MAO inhibitor

48
Q

TCAs

-block reuptake of which chemicals?

A

NE & serotonin

49
Q

Which drugs can cause drug-induced parkinsons?

-tx:

A

D2 receptor blockers

  • antipsychotics (1st gen>2nd gen)
  • anti-emetics (metoclopramide, prochlorperazine).

-Tx: benztropine, diphenhydramine

50
Q

Why can’t you use levodopa or dopamine agonists to treat drug-induced parkinsons caused by anti-psychotics?

A

bc they can induce psychosis.

-problem was too much dopamine in the first place.

51
Q

fluoxetine

-what is it?

A

SSRI

52
Q

imipramine

-what is it?

A

TCA

53
Q

Take atropine & sudden eye pain.

-Dx?

A

mydriasis = exacerbated angle-closure glaucoma.

54
Q

pramipexole, ropinirole

A

dopamine agonists

55
Q

neuroblastoma vs wilms tumor

-which can cross the midline?

A

neuroblastoma can cross the midline.

56
Q

factitious disorder

  • what is its?
  • subtypes?
A
  • consciously creating Sxs so you can assume the “sick role” & to get medical attention.
  • munchaushen & munchausen by proxy.
57
Q

binge/purge anorexia vs bulimia nervosa

-difference?

A
  • The anorexic pt has very low BMI & amenorrhea.

- The bulimic has normal BMI.

58
Q

Conversion disorder

A

Sudden loss of sensory or motor function s/p acute stressor.

-chick w/severe weakness in left leg s/p fiance breaking up with her.

59
Q

schizophreniform

-time frame?

A

1-6 months

60
Q

Parinaud syndrome

  • whats is it?
  • cause?
A
  • paralysis of upward gaze.

- due to lesion in superior colliculi (ie. pinealoma).

61
Q

B12 deficiency

  • whats it called?
  • what part of spinal cord gets fucked up?
A

“Subacute combined degeneration”

  • dorsal columns
  • lateral corticospinal tracts
  • axonal degen of periph. nerves.
62
Q

Stroke - ASA (ant. spinal art).

-whats damaged?

A
  • Lateral corticospinal tract.
  • Medial lemniscus.
  • Caudal medulla—hypoglossal nerve.

*Dorsal columns spared.

63
Q

Stroke - ASA (ant. spinal art).

-Sxs:

A
  • Contralateral hemiparesis—upper and lower limbs.
  • Dec. contralateral proprioception.
  • Ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally).
64
Q

Stroke - PCA

-Sxs:

A

-Contralateral hemianopia with macular sparing.

65
Q

Stroke - Basilar artery

-Sxs:

A
  • “Locked-in syndrome.”

- just like Central pontine myelinosis bc basilar artery feeds the pons.

66
Q

Acom

  • most common lesion?
  • Sxs?
  • mnemonic:
A

Berry aneurysm

  • Visual field defects
  • “A Com (communications) major must be good w/visuals.”
67
Q

PCom

  • most common lesions?
  • Sxx?
A

Berry aneurysm

-CN3 palsy (eye is down and out) w/ptosis & mydriasis.

68
Q

A lesion in which art will => CN 3 palsy?

A

PCom

69
Q

Central post-stroke pain syndrome

-where are the lesions?

A

-Neuropathic pain due to thalamic lesions.
-Initial sensation of numbness and tingling followed in
weeks to months by allodynia and dysaesthesia.

70
Q

allodynia

A

-ordinarily painless stimuli cause pain.

71
Q

dysaesthesia

A

-Abnormal, unpleasant sense of touch. Typically w/pain.

72
Q

middle meningeal art = branch of what? which is a branch of what?

A

External carotid => maxillary art. => middle meningeal a.

73
Q

What type of brain hematoma causes CN3 palsy?

A

epidural hematoma

74
Q

Epidural hematoma

  • can blood cross suture lines?
  • can blood cross falx?
  • can blood cross tentorium?
A
  • cross suture = no
  • cross falx = yes
  • cross tentorium = yes
75
Q

Subdural hematoma

  • can blood cross suture lines?
  • can blood cross falx?
  • can blood cross tentorium?
A
  • cross suture = yes
  • cross falx = no
  • cross tentorium = no
76
Q

Bloody or yellow (xanthochromic) spinal tap

  • seen in what?
  • what does this predispose to?
A

-Subarachnoid hemorrhage
-2–3 days afterward, risk of vasospasm due to blood
breakdown and rebleed.

77
Q

Subarachnoid hemorrhage

-vasospasm, Tx?

A

nimodipine

78
Q

berry aneurysms

-lack what layer?

A

media

79
Q

Ischemic brain disease

-irreversible damage after how long?

A

Irreversible damage begins after 5 min of hypoxia.

80
Q

Brain: where is most vulnerable to ischemia?

A

-hippocampus, neocortex, cerebellum, watershed areas.

81
Q

What scan has highest sensitivity for early brain ischemia?

A

MRI

82
Q

How long to see ischemia on CT scan?

-what do you see?

A

12-24 hrs.

-dark abnormality.

83
Q

How long after ischemic event do you see red neurons?

A

12-48 hrs

84
Q

How long after ischemic event do neutrophils show up & necrosis start happening?

A

24-72 hrs

85
Q

How long after ischemic event do macros show up?

A

3-5 days

86
Q

How long after ischemic event does reactive gliosis & vascular prolif start?

A

1-2 weeks

87
Q

How long after ischemic event is there a glial scar?

A

> 2 weeks

88
Q

Most common site of intracerebral hemorrhage?

A

basal ganglia

89
Q

hemorrhagic vs ischemic stroke presentation:

A

-hemorrhagic stroke presents w/acute onset of
focal neuro deficits. Ischemic stroke evolves
over a few hours.

90
Q

Ischemic stroke

-which is only one that wont be hemorrhagic due to reperfusion?

A

thrombotic (hypertensive)

  • the thrombus is not going to break down.
  • keep in mind its a thrombus on top of an atheroma.
91
Q

ischemic stroke

-Tx:

A

tPa

92
Q

Dural venous sinuses

-drain into what vein?

A

internal jugular vein

93
Q

Lateral ventricle => 3rd ventricle

-goes thru what?

A

foramina of monroe

94
Q

3rd ventricle => 4th ventricle

-goes thru what?

A

aqueduct of sylvius

-aka cerebral aqueduct

95
Q

Normal pressure hydrocephalus

  • mnemonic?
  • clinical triad?
  • cause?
A

“wet, wobbly, & wacky like Mark”.

  • urinary incontinence, ataxia, and cognitive dysfunction.
  • corona radiata distorted by expansion of ventricles.
96
Q

Hydrocephalus ex vacuo

-cause?

A

-brain atophy = dec. neural tissue.

97
Q

How many Spinal nerves

-name the segments & how many there are:

A 
-31 total
cervical = 8
thoracic = 12
lumbar = 5
sacral = 5
coccyx = 1
98
Q

Do spinal nerves exit above or below the corresponding vertebrae?

A
  • Nerves C1–C7 exit above the corresponding
    vertebra. All other nerves exit below.
  • so C7 has one nerve exiting above and one below = C7 and C8. Thats where the extra C comes in.
99
Q

Vertebral disc herniation

  • whats herniating out of what?
  • which direction?
  • which levels?
A
  • nucleus pulposus (soft central disc) herniates thru annulus fibrosus.
  • usually posterolaterally.
  • L4-L5 or L5-S2 = most common
100
Q

Lower border of s. cord?

Lower border of subarachnoid space?

A
  • s.cord ends at L2

- subarachnoid space ends at S2

101
Q

Stimulus control therapy

-what is it?

A

Leave the room if you cant fall asleep for 20 min.

-goal = dissociate bedroom from any stimulating activities.

102
Q

normal action potential

-when is membrane most permeable to K?

A
  • Its not at the peak of the membrane potential, but once the repolarization has already started that the membrane is most permeable to K.
  • so not the top of the peak (in the overshoot), but once the cell has already repolarized a bit.
103
Q

primidone

  • use?
  • what are its metabolites?
A
  • first line med for benign essential tremor.

- metabolites = phenobarbital phenylethylmalonamide.

104
Q

Upper extremity LMN signs & lower extremity UMN signs in the setting of scoliosis.
+loss of upper extremity pain/temp sensation.

A

syringomyelia

105
Q

restless leg syndrome

-tx:

A

dopamine agonist

-ie. pamipexole, ropinirole.

106
Q

Middle cerebellar peduncle

  • connects what structures?
  • landmark for what?
A
  • cerebellum to pons

- trigeminal nerve (CN 5)

107
Q

Which is the only CN to decussate before innervating its target?

A

Trochlear nerve.

-so it innervates the contralateral superior oblique.

108
Q

narcolepsy

  • lack of what chemicals in the CSF?
  • where are these chemicals made?
A
  • hypocretin 1 (orexin A)
  • hypocretin 2 (orexin B)

-made in lateral hypothalamus.

109
Q

Homovanillic acid (HVA)

  • breakdown product of what?
  • CSF conc. in parkinsons?
A
  • dopamine

- dec. CSF conc. in parkinsons.

110
Q

CN3

-courses btwn which arteries as it leaves midbrain?

A

PCA & SCA (superior cerebellar)

111
Q

thiopental

-where does it rapidly redistribute to?

A

skeletal muscle & fat.

112
Q

diphenoxylate

-what is it?

A

opiate

113
Q

opsoclonus-myoclonus syndrome

  • what is it?
  • what disease is it associated with?
A
  • non-rhythmic conjugate eye movement associated w/myoclonus.
  • paraneoplastic syndrome associated w/neuroblastoma.

Final FA review (52 decks)

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