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Final review for Step 2 Ck > Neuro > Flashcards

Neuro Flashcards

1
Q

Timeline for AD?

A

AD is a slow, progressive disease with cortical atrophy that progresses to personality changes, do not confuse with Pick frontotemporal dementia. Slow and gradual.

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2
Q

Does Lewy respond to dop agonism?

A

Lewy does not respond to dopa agonism

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3
Q

Most common place brain gets mets from?

A

The MCC of brain mets is lung CA, suspect in multiple brain densities on CT with h/o of smoking and no other abnormalties

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4
Q

S/s of GBS?

A

GBS causes ascending paralysis with absent DTR, sometimes sensory involed. CSF is normal other than high protein

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5
Q

How is GBS treated?

A

IVIg and plamaphoresis

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6
Q

First step in suspected Stroke?

A

CT before anything in suspected stroke

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7
Q

Where do emboli from Amaurosis Fugax come from?

A

Embolic from Amaurosis Fugax are usually from carotid bifurcation = get U/S of neck (Hollenhorst plaques)

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8
Q

What lesions are seen in spinal cord damage (UMN or LMN)

A

Spinal cord damage/acute injury is still an UMN as it happens before synapse at anterior horn (it can cause both injury, just remember spinal cord injury caues UMN too)

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9
Q

What do you get for a suspected ant/central/posterior cord syndrome?

A

For spinal cord, MRI is best imaging

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10
Q

best imaging for spinal cord?

A

MRI is best

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11
Q

Anterior cord syndrome associated with what breaks and s/s

A

Burst fracture and P/T sensation

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12
Q

S/s of intracranial bleed

A

Progressive syx with s/s of ICP which differentiates it, they progress and there is n/v and mental status deltas which DONT happen in ischemic strokes

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13
Q

What is the MOST IMPORTANT risk for ALL types of stroke?

A

The most important risk for ALL types of stroke is HTN

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14
Q

HTN is a risk for what strokes

A

The most important risk for ALL TYPES OF STROKE is HTN

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15
Q

what does a pronator drift mena

A

prontator drift is a UMN sign for upper extremities, may exist in absence of ther findings

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16
Q

Any suspected stroke first thing to do?

A

CT BEFORE ANYTHING, then Tpa if

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17
Q

When is ASA used and not tPA in stroke?

A

6 hours = ASA
3-4.5 = tPA
CT first
Add clop or dypyridamole if on ASA and having another ischemic stroke

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18
Q

What is MRI used for in stroke?

A

MRI is done AFTER CT and after therapy is started to localize a clot/vasculature that CT cannot pick up

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19
Q

What test shows an upper motor neuron lesion in upper extremities when high suspicion and other s/s may be absent?

A

Pronator drift

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20
Q

+ pronator drift?

A

Pronation when held out, if it drops without pronation it is only weakness, shows UMN deficit in upper extremities when other s/s absent

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21
Q

What do ALL stroke patients need within 24 hours?

A

Aspirin is only agent proven to prevent stroke, and is indicated in all stroke patients within 24hr

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22
Q

When do you suspect anterior cord syndrome

A

complete loss of function below lesion with P/T sensation loss

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23
Q

Central cord syndrome is associated in what demo?

A

cervical injury/upper extremities with incomplete paresis and some P/T loss in hyperextension of the elderly

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24
Q

Elderly with upper spondylolisis are predisposed to what spinal injury

A

Cental cord syndrome

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25
Q

what s/s might you see with a fluid filled cavity in the spinal column causing P/T loss?

A

You might see occipital headache and ataxia from arnold chiari cerebellar herniation

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26
Q

what is related to syringomyelia

A

arnold chiara- consider CT if synringomyelia diagnosed; P/T and some motor function loss in syringo.

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27
Q

where does anterior spinothalamic tract damage clinically manifest

A

P/T for spinothalamic tract disease manifests TWO LEVELS below the lesion. Damage at t12, syx at t10 (remember contralateral loss)

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28
Q

What is NOT lost in cerebellar hemorrhage?

A

There is NO sensory loss in cerebellar hemorrhage

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29
Q

What is the internal capsule

A

The internal capsule is where lateral corticospinal tract neurons cross over = motor defects

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30
Q

What two things make an internal capsule stroke clear as dx?

A

Internal capsule is descending lateral cortisopinal tract and is pure motor, and as has NO GAZE/ EYE defects (vs thalamic and cerebral hemisphere)

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31
Q

What causes paresis with characteristic NO EYE DEFECT

A

NO EYE DEFECT in internal capsule (vs cerebral deviation away and thalamic deviation toward the lesion)

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32
Q

What happens to eyes in internal cap, thalamic and cerebral lobe strokes?

A

internal = NO EYE SYX
Thal = T = TOWARD PARESIS OF BRAIN
Cerebral lobe = away from paresis of brain and TOWARD INFARCT

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33
Q

Where do eyes deviate for thalamic versus cerebral infarct

A 
Thalamic = TOWARD PARESIS OF BRAIN and 
Cerebral = AWAY FROM PARESIS OF BRAIN
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34
Q

What are classic s/s of thalamic stroke?

A

Thalamic stroke can cause severe pain syndrome, hypersensitivity to pain and athetosis with ballistic movements and eyes DEVIATE TOWARD PARESIS OF BRAIN

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35
Q

What are the s/s of lacunar stroke

A

lacunar strokes are deep penetrating arteries and usually just involve motor syx

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36
Q

What are some manifestations of lacunar stroke

A

lacunar usually involves internal capsule with pure motor syx and clumsy-hand syndrome affecting face/arms/legs

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37
Q

Associated lacunar stroke with what area of brain

A

internal capsule

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38
Q

MC site of HTN hemorrhage?

A

Putamen as it lies directly next to the internal capsule which is almost always involved

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39
Q

Total sensory stroke seen in what

A

Thalamus commonly may also have ballistic and athetosis

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40
Q

what part of thalamus is responsible for total sensory stroke?

A

VPL of the thalamus is why they get hypersensitivity to pain and pure sensory stroke

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41
Q

What are signs of vertebro basilar stroke?

A

There are many brain nuclei there that affect the cranial nerves and bulbar signs like dysphagia. Look for CN nerve signs and dysphagia along with paralysis

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42
Q

What is the gold number for endarectomy in men and wom ?

A

70%

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43
Q

what is the gold number for endarterectomy in men without syx?

A

60% in men asyx or 70% in either sex

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44
Q

what does vasospasm cause in SAH?

A

Vasospasm causes ischemic stroke in SAH

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45
Q

why give nimodipine in SAH and what timeline for cx does it prevent?

A

Namodipine is a CCB that presents vasospasm at 3d after SAH which would result in ischemic stroke

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46
Q

Ischemic stroke s/s 3d after SAH, why

A

Vasospasm causes ischemic stroke

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47
Q

Amyloid angiopathy in the brain results in what type of bleeds

A

Amyloid deposition causes lobar hemorrhages because all the blood vessels are extremely fragile, expect in elderly patients with dementia or RA or leukemias and CLL

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48
Q

What color is hemorrhage on CT

A

CT scan with hemorrhage is white (think epi and subdural hematoma)

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49
Q

what color is ischemia on CT

A

ischemia is dark (think of examples)

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50
Q

Subdural hematoma in ?

A

Alcs, warfarin elderly

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51
Q

what is damaged in subdural hematoma

A

crescent shaped, low pressure bleed of bridging veins

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52
Q

epidural hematoma in

A

trauma to middle meningeal

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53
Q

s/s of epidural hematoma

A

lucid period with convex mass and then sudden deterioration, high pressure arterial bleed, look for s/s of herniation

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54
Q

tx epidural

A

immediate neurosurg consult with relief of potential causes for herniation

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55
Q

can subdural hemorrhage be long-term

A

subdural is low-ressure bleed whcih can be chronic and cause dementia syx in elder versus epidural which kills from herniation suddenly after a lucid period

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56
Q

why does cavernous sinus syndrome happen

A

the cavernous sinus syndrome usually happens due to infection spread because the opthalmic vein system is valveless

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57
Q

what do you look for in cavernous sinus?

A

prior preseptal celluliitis which worsens to fever with pain with eye movements and s/s of neural ICP like n/v, papilledema

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58
Q

what is convern with cavernous sinus thrombosis

A

the concern with cavernous sinus thrombosis following infection form valvless optho system is that there will be brian herniation, you need to treat with IV antibiotics for several weeks and monitor for s/s of neural herniation and ICP like papilledema and n/v + down and out puil

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59
Q

How is sinus cavernous syndrome diagnosed?

A

Dx with MRI to find the internal carotid thrombosis (versus CT in sinusitis that is recurrent and don’t need to find specific artery)

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60
Q

s/s of cavernous sinus

A

papilledema, prior preseptal cellulitis, orbital pain and edema, n/v, FEVER
dx with MRI to find internal carotid
tx IV antibitoics for severeal weeks to avoid herniations

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61
Q

What are s/s of migriane

A

migraine is aura, pulsating headahce, worse with light and noise, triggers of food, stress and menses

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62
Q

how is migriane treated

A

try NSAID and then triptans

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63
Q

what is “abortive” therapy for refractory migraines

A

refractory migraines can be treated with triptans and TCAs early, other wise need antiemetcis like chrlopramzine, metochloprmaide in n/v

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64
Q

what headaches are promazines used for

A

promazines are used for migrines and hel with nausea and vomiting

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65
Q

when are SSRI and triptans used in migriane

A

SSRI and triptans are used in migraines early as abortive therapy, do not work late in course with n/v

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66
Q

what can be used for n/v in migraines

A

n/v in migraines can be treated with promazines and perazines

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67
Q

promazines and perazines treat what part of what headache?

A

they treat the s/s of n/v of migraine (promazines and perazines)

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68
Q

What is trigem neuralgia treated with

A

trigeminal neuralgia is treated with carbamazepine

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69
Q

why is trigeminal neuralgia treated with carbamazepine

A

trigem is really a simple, partial seizure of the CNV, and is treated with anticonvulsant carbamazepine

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70
Q

what do you have to worry about when treating with anti convulsant carbamazepine in trigem patient?

A

AE of carbamazepine is aplastic anemia

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71
Q

what is the main AE of carbamazepine?

A

carbamazepine is used for trigem neuralgia and causes aplastic anemia

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72
Q

what does chrlopromazine and prochlorperazine and IV metoclopramide do for n/v

A

treats n/v in migraine

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73
Q

what are classic s/s of cluster headaches

A

cluster headaches present with retroorbital pain, lacrimation, Horner’s syndrome and awakening from sleep

74
Q

can neuro deficits be present in cluster headaches?

A

yes they can have Horner’s syndrome along with night awakenings

75
Q

how is cluster treated acutely

A

cluster acute tx is O2 100%

76
Q

what is cluster prophylactic tx

A

cluster prophylactic tx is verapamil, Lithium or ergotamine

77
Q

Horner’s is associated with what headahce syndrome treated prophylactically with verapamil, Li or ergotamine?

A

horners, eye pain, lacrimation recurring = think cluster, acute tx is 100% O2 prophylax with verapamil, ergotamine, Li

78
Q

how is IIh diagnosed

A

You need to r/o tumor with CT or MRI and if WNL you can do an LP to relieve presure and document the elevated opening pressure and relieve some syx then give acetazolamide or furosemide

79
Q

who gets IIH

A

young, obese women with OCP, tetracycline and vit A (tretinoin) derivatives

80
Q

S/s of IIH

A

Like a tumor with vision changed, HA, diplopia, papilledema, CN VI defects, tinnitus and diplopia

81
Q

How is IIH diagnosed and why

A

First you need to rule out mass lesions in IIH, then after the MRI/CT is normal you can do LP even if there is s/s of ICP being raised because it is due to CSF and there won’t be herniation, unlike kids if they have papilledema you cannot do LP

82
Q

2 associations with lacunar infarcts?

A

think internal capsule and HTN

83
Q

HTN, internal capsule, pure motor think?

A

Lacunar infarct = HTN= motor= internal capsule

84
Q

How is cortisol - induced myopathy different from Polymyalgia Rheumatica myopathy

A

cortisol induced has lower extremity weakness with normal ESR and CK while PMR has increased ESR and when treated for and associated with Temporal arteririts, goes away with steroids. it also involves upper extremities

85
Q

Steroid muscle disease

A

Painless, lower extremity, normal ESR and CK

86
Q

NPH s/s and CT results and why

A

There is stretching of the ventricles permitting increase in CSF without increase in pressure. There is gait abnormalities, progressive dementia and urinary incontinence. Tx with LP or shunt if refractory. Opening pressure is NORMAL

87
Q

What is the opening pressure in NPH?

A

IT IS NORMAL PRESSURE CSF PRESSURE IS NORMAL ON LP, the ventricles expand to accomodate the volume

88
Q

HOw is NPH treated?

A

Treat NPH with large volume LP and IF IT WORKS, then do a shunt as these are curative

89
Q

When is shunt used in NPH

A

Use shunt IF SERIAL LP REDUCE SYX

90
Q

How is spinal abscess treated?

A

If suspected, you get MRI with gadolinium and treat with antibiotics and surgical debridement

91
Q

does spinal abscesss need surgery?

A

yes it, needs surgery for spinal abscess within 24 hours

92
Q

What CN is affected in IIH

A

IIH has CNVI palsy (lateral recture)

93
Q

what eye muscle is affected in IIH?

A

In IIH, the lateral rectus, CN VI is affected

94
Q

Common s/s of IIh

A

Headache, pulsatile tinnitus, diplopia, CNVI lateral rectal palsy, papilledema, double vision, h/o high BMI, isotretinoin / Vit A use and cyclnes

95
Q

VPL thalamic stroke causes

A

Athetosis/hemiballistic and extreme pain /sensory defect with touchgin post-stroke

96
Q

what is dysesthesia?

A

dysesthesia is characteristic of stroke in thalamus and is extreme pain afterward with touching

97
Q

AD signs that are not due to aging?

A

most important is loss of daily function; other key ones are lost in familiar places (visuospatial defects), and late behavior changes

98
Q

Essential tremor shows what with movement

A

Increased tremor with movement for ET

99
Q

PD shows what with movement?

A

Decreased tremor with purposeful movement

100
Q

How is essential tremor treated?

A

BB or primidone

101
Q

What type of hearing loss is prebycussis

A

prebycussis is high pitched sensorineural

102
Q

prebycussis is senosorinueral hearing loss of high pitched sounds common in elderly (bilateral), what is otosclerosis

A

otosclerosis is scarring of the middle ear bones causing conductive hearing loss common in middle aged people

103
Q

what are s/s of prebycussis

A

older person with issues with background noise hearing and high-pitch loss with inability to tolerate loud noises, it is bilateral and sensorineural

104
Q

what is the pathology of prebycussis

A

CNVIII cochlear damage leading to bilateral sensorineural hearing loss

105
Q

When is a brain tumor that is metastic resected?

A

Resect it when they have good functionability and have a single lesion, then follow it with whole brain radiation

106
Q

Difference between s. aureus brain abscess and s. viridans brain abscess?

A

Brain abscess due to direct extension (i.e ethmoid sinus) is commonly due to s. viridans, versus s. aureus which is puncture and surgery related

107
Q

What is classic sign of SiADH

A

suspect SiADH in lung disease or head trauma and presents with high urine osmo and low serum osmo, with high urine sodium; none of which corrects with fluid bolue

108
Q

how is SiADH treated?

A

Treat SiADH with fluid restriction and dememocycline and conivaptan

109
Q

What are demecocyline and conivaptan used for?

A

Demecocyline and conivaptan are anti-SiADH-R moleculres

110
Q

How is Nephro DI treated

A

Treat with fluid restriction and HCTZ

111
Q

What is the MCC of secondary AI

A

secondary AI is due to exogenous steroids meaning normal aldosterone axis with low ACTH and low cortisol

112
Q

Exogenous steroids use over time causing Cushing appearance is associated with what

A

Secondary adrenal insufficiency, aldosterone ok

113
Q

How is unilateraly hyperaldosternoism treated?

A

Eplerenone > spironolactone

114
Q

What is Conn’s syndrome

A

Hyperaldosteronism is Conn syndrome

115
Q

When and in what patients is total thyroidectomy indicated?

A

Medullary CA of thyroid happens in MEN2A/B and prophy thyroidectomy indicated with a positive RET oncogene test

116
Q

What is a partial seizure

A

partial seizure is a discrete region of the blrain

117
Q

what is complex seizure

A

complex seizure involves temporal lobe (different than generalized which is both hemispheres) and results in loss of consciousness

118
Q

what is a simple partial seizure example

A

conscious and aware of a muscle twitching

119
Q

What is general seizure

A

loss of consciouss and both hemispheres invovled (tonic clonic, absence, myoclonic, etc

120
Q

No postictal phase in absence, why unique?

A

because absence are actually generalized seizures involving both hemispheres and consciousness is lost

121
Q

First workup of seizure

A

ALl blood tests + CT, no need for EEG or MRI fi there is a reason

122
Q

Pediatric first line seizure prophylaxis?

A

Phenobarb

123
Q

Second line absence seizure tx?

A

It is generalized, can use valproic acid if not tolerating ethosuximide

124
Q

when to treat status epilepticus

A

seiuzre over 5m cause classic cortical necrosis, treat staticus at 5m mark with BDZ

125
Q

Lab values after seizure?

A

Lactic acidosis and elevated PRL that self resolve

126
Q

What type of hearing loss is otosclerosis

A

Conductive

127
Q

what type of hearing loss is prebycusis

A

bilateral high-pitch sensorineural

128
Q

how is benign positional vertigo treated

A

BPPV is due to otoliths and is positional and diangosed with dix hallpike and treated with epley maneuver, meclezine doesn’t work as it is a stone problem

129
Q

Dx of BPPV?

A

Nystagmus on Dix Hallpike maneuver. Tx is with Epley

130
Q

What is vestibulo-ocular reflex?

A

It diagnosis veticulopathy versus meniere/BPV, people cannot keep their eyes fixed on a target when rotating the head away; a + sign is veticulopathy, not Meniere and not BPV

131
Q

What is the way to tell if there is a MG crisis or a cholinergic crisis (too much pyridostigmine)

A

use edrophonium and see if it worsens it or improves it

132
Q

how is MG crises treated?

A

Intubate + IvIg + steroids

133
Q

How is MG treated first line?

A

Pyridostigmine for MG first line

134
Q

What is optic neuritis

A

Common in MS with pain on movmeent, scotoma, color cahnges and pupil defects and even swollen optic disks with diplopia

135
Q

What is LP used for in MS

A

MS presents with optic neuritis, bilateral trigemenal neuralgia, relapsing remiting loss of function and LP is used when clinical dx is not a enough and it shows NORMAL everything other than IgG increased index

136
Q

What is CSF like in MS

A

Normal, just some oligoclonal IgG bands

137
Q

Best imaging for MS

A

Best imaging for MS is T2 weight MRI, not CT

138
Q

is CT or MRI better for MS diagnosis

A

MRI is better for MS diagnosis, weighted T2 MRI is better for MS

139
Q

How is acute MS treated?

A

Acute MS is treated with IV steroids and plasma exchange if refractory and then glitarem,er IFN, MTx otherwise

140
Q

What is Glitarimer and IFN used for in MS?

A

Glitarimer and IFN prevent frequency/reduce frequence

141
Q

How is GBS treate

A

GBS is treated with IVIG and plasmaphoresis not steroids

142
Q

Why is GBS treated with IVIG and not steroids?

A

Treat GBS with IVIG and not steroids because antibody cross reaction, not cells is the issue

143
Q

What is the defect in Alz disesae?

A

There is decreased ACh in AD

144
Q

How is AD treated

A

Treat AD with reversible AChE-inhibitors as ACH is low in this disease

145
Q

What are the AChE-inhibitors names used in Alz Disease?

A

Rivastigmine, deonpezil

146
Q

What is galamantine?

A

NMDR inhibitor used in AD, otherwise use irvastigmine and donepezil AChE-i’s

147
Q

Pick disease affects what

A

frontotemporal dementia

148
Q

S/s of picks

A

frontotemporal dementia with family history and early behavior changes

149
Q

what is seen on NPH imaging

A

dilated ventricles

150
Q

how is pressure in NPH

A

NORMAL pressure that ventricles dilate to accommodate pressure at normal still – LP is NORMAL pressure

151
Q

How is NPH treated?

A

LP and CSF drainaged due to decreased CSF absorptoin and if suscessful then you can do a surgical shunt

152
Q

What part of brain is PD affecting?

A

Basal ganglia decreased dopamine

153
Q

How is RLS treated

A

treat RLS with DOPAMINE AGONISM (pramipexole) iron and gabapentin

154
Q

what dopamine agents are used in RLS

A

RLS = tx with dopamine agonism prampixole and iron and gabapentin

155
Q

What is trihexyphindyl used for?

A

trihexyphenidyl is used for resting tremor in PD

156
Q

what type of drug is trihyexyphenidyle and benztropine

A

trihexyphenidyle and benztropine are anticholinergics that are used to treat the syx of tremor only

157
Q

what treats tremor in PD

A

in PD, tremor is treated with anticholinergic trihexyphenidyl and benztropine which cause classic anticholinergic AE, but reduce the syx of tremor

158
Q

How is meningioma treaed?

A

Resect meningioma, epidural based masses with tails, resection is curatie

159
Q

Most common location of brain mets?

A

Most common location brain mets is from the lung

160
Q

why does medulloblastoma cause drop met?

A

It is cerebellar and in the fourth ventricle

161
Q

pilocytic astroma cytoma location, marker and staing?

A

GFAP, cerebellar, cystic and solid

162
Q

Whoe commonly gets craniopharyngioma?

A

Kids with Rathke pouch remnant and visual syx

163
Q

COmmon syx in craniopharyngioma

A

COmpression of the optic chiasm

164
Q

Brain lesions/tumors in non acute setting such as for veticular shwannoma are diagnosed how

A

diagnose brain lesions with MRI for tumors/not acute s/s (i.e shwanomma with tinnitus, hearing loss and vertigo)

165
Q

What is a complication of IIH

A

there is papilledema and CNVI defect and blindness is a complication of IIH

166
Q

s/s of cluster

A

retroorbital pain and horners, lacrimation isn’t alway spresent, commonly awakens patient from sleep

167
Q

Hy: male awoken from sleep with retrorbital pain and ptosis and miosis on the same side,cause?

A

Cluster headache

168
Q

What is biggest risk factor for any type of stroke?

A

Any stroke risk goes up with HTN, HTN, HTN, HTN biggest stroke risk

169
Q

MC place of ulnar nerve entrapment?

A

MC place of ulnar nerve entrapment is medil condylar groove at elbow

170
Q

What lies in medial epicondylar groove and commonly gets entrapped there? HY

A

The ulnar nerve lies in the medial epicondylar groove and commonly gets entrapped there HY

171
Q

How might dystonia due to metoclopramide bet treated?

A

dystonia due to metoclopramdie might be treated with benztropine or diphenhydramine

172
Q

Hemineglect invovles ignoring what side

A

Hemi neglect ignores the left side of their body and things (because right non-dom is infarcted)

173
Q

What is a common symptom of MG? (muscles not under voluntary control)

A

Bulbar syx with chewing/swallowing regurg are common in MG, don’t confuse with heart burn of sclerosis

174
Q

Lambert syndrome is due to?

A

Ab at presynaptic calcium channels

175
Q

S/s of lambert

A

weakness, smoker/lung CA, repetitive simulation increases response on EEG, normal CK

176
Q

Do Infective endocarditis patients need anticoagulation?

A

NO. In IE the antibiotics prevent the vegetations from forming and no anticoagulation is needed

177
Q

Brain death characterized by?

A

Loss of brain stem and cortical function

178
Q

What is Shy Drager syndrome?

A

Multiple system atrophy is Shy Drager syndrome and characterized by PD with autonomic dsyfunction and incontinence

179
Q

What are cx of heat stroke other than death?

A

heat stroke occurs in young individuals in military/sports/heat and complications are rhabo/renal failure and coagulation (epistaxis)

180
Q

what does heat stroke do to the blood

A

it causes rhabdo and renal failure and often results in coagulation deficiencies presenting as things such as nose bleeds

181
Q

S/s of MG that is overlooked?

A

Bulbar syx like dysphagia, dysarthyria and fatigable chewing can happen in MG

182
Q

What is seen in nuerons in PD?

A

PD shows alpha synuclein bodies in the substantia nigra pars compacta

Final review for Step 2 Ck (12 decks)

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