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neuro test 2 Flashcards

1
Q

how do you test CN I?

A

olfactory

sensory recognition of common odors (soap, coffee, tobacco, etc)

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2
Q

how do you test CN II?

A

optic

visual acuity (with corrective lenses)
far vision- SNELLEN CHART
near vision- ROSENBAUM POCKET SCREENER OR READING NEWSPRINT

visual fields (assessment of peripheral vision)

funduscopic exam
-optic disc color (creamy yellow)
-optic disc clarity (flat and sharp)
-increased intraocular pressure (glaucoma) cause optic
disk to depress-‘cupping’
-increased intracranial pressure causes optic disc to
elevate (“papilledema”)
-spontaneous venous pulsations are a normal finding

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3
Q

how do you test CN III?

A

oculomotor
Motor: EOMs (also CN IV and VI)
parasympathetic branch (PSNS constricts pupil, SNS dilates pupil)

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4
Q

how do you test CN IV?

A

trochlear

motor- EOMs (also CN III , VI)

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5
Q

how do you test CN V?

A

trigeminal

motor : muscles of mastication (temporalis, masseter) bulk
sensory:
-sensation in 3 divisions (ophthalmic, maxillary and manibular divisions) of Trigeminal nerve
-corneal touch reflex

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6
Q

how do you test CN VI?

A

abducens

motor: EOMs (also CN III, IV)
* *Eye can not move laterally

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7
Q

How do you test CN VII?

A

facial

Motor:

  • facial symmetry and movements (smile, puff cheeks, raise eyebrows)
  • close eyelids tightly against resistance
  • labial speech sounds (b,p,m)

sensory: sweet and salty taste on anterior 2/3 of tongue

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8
Q

how do you test CN VIII?

A

vestibulocochlear

SENSORY:
vestibular division (semicircular canal/vestibular nerve tests)
-stand on one leg and keep balance
-nylen-barany test (head movements to induce
nystagmus)
-cold calorics (cold water introduced into ear to induce
nystagmus)

cochlear division (hearing division)

  • assess auditory acuity (whisper or watch tick)
  • Rinne test (using 512 Hz tuning fork)
  • Weber test (using 512 Hz tuning fork)
  • Schwaback test (using 512 Hz tuning fork)
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9
Q

how do you test CN IX?

sensory and motor

A

glossopharyngeal

sensory:
- gag response (also CN X)
- sour/bitter taste on posterior 2/3 of tongue

motor:

  • movement of soft palate upon phonation (say “ahh”)
  • swallowing function (swallow cup of water - also CN X)
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10
Q

how do you test CN X?

A

vagus

sensory:
- gag response (also CN IX)

motor:

  • movement of soft palate upon phonation (say ‘‘ahh’’)
  • swallowing function (swallow cup of water - also CN IX)
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11
Q

how do you test CN XI?

A

accessory nerve

motor: trapezius and SCM muscle strength, against resistance

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12
Q

how do you test CN XII?

A

hypoglossal

motor:
- tongue midline position, movement and strength
- atrophy or fasciculations of tongue
- lingual speech sounds (l,t,d,n)

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13
Q

normal DTRs are?

A

bilaterally summetrical

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14
Q

DTRs

A
  • simple spinal reflex arcs
  • normally prevented from being hyperactive by inhibitory upper motor neurons - if they’re damaged (ie stroke), DTRs will be hyperactive on one side of the body)
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15
Q

Bicep DTR?

A

C5

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16
Q

brachioradialis DTR?

A

C6

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17
Q

triceps DTR?

A

C7

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18
Q

patellar DTR?

A

L2,L3,L4

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19
Q

Achilles DTR?

A

S1

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20
Q

what is a normal grade for a DTR?

A

2+

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21
Q

multiple contractions and relaxations of a muscle group occurring in rapid succession after forcefully moving the joint

A

clonus - just a couple beats of clonus is normal ( you must test for clonus in both upper and lower extremities)

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22
Q

normal DTRs are what?

A

bilaterally symmetrical. An absent of asymmetrically diminished DTR suggests a problem at that level of the spinal cord.

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23
Q

what does a hyperreflexive DTR suggest damage to?

A

the inhibitory upper motor neuron (often from a stroke)

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24
Q

superficial reflexes are decreased or absent if there is damage to what?

A

upper motor neurons

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25
Q

what refers to how loose or rigid (spastic) an extremity is when moved?

A

tone

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26
Q

what is normal strength?

A

5 (movement against gravity and full resistance)
4/5 - movement against gravity and some resistance
3/5 movement against gravity only
2/5 movement if gravity is eliminated
1/5 slight contractility (flicker) but no movements
0/5 no movement at all

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27
Q

what is the palmar (pronator) drift test and what do it test?

A

tests muscle power

patient is asked to extend his arms with the palms up and hold them there

this test is very sensitive for subtle motor motor strength weakness

abnormal test: the weak arm droops downward and pronates

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28
Q

what are “stress” gait evaluation?

A

walk on heels
walk on toes
“tandem” gait (heel-toe walking)

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29
Q

headaches due to another medical or neurological condition are what?

A

secondary headaches

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30
Q

this headache develops within the first few days after trauma and usually has a rapid resolution (days)

A

post-traumatic headache

10% of patients with persistent HA or other symptoms - average duration 3 months

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31
Q

when is ICP typically increased?

A

when laying down, not necessarily better when upright

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32
Q

what suggests chronicity of increased ICP?

A

papilledema on exam

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33
Q

when is intracranial hypotension worse?

A

when upright, better/resolves when laying down

may have worsening with cough/valsalva (paradoxical)

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34
Q

what is a classic example of intracranial hypotension?

A

post-lumbar puncture headage

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35
Q

treatment for intracranial hypotension

A

blood patching
caffeine
bed rest

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36
Q

is a headache a common symptom of ischemic stroke?

A

no, rare - must more strongly suggestive of hemorrhage (any type)

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37
Q

what headache should be considered for older patients (over 50 or 60) with new headache and repeated episodes of monocular vision loss? and what is the treatment?

A

temporal arteritis

treatment: steroids should be given before TA biopsy

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38
Q

red flags for secondary headache

A

new headache or change in headache quality (“worst headache of my life”)

age > 50 without prior history of headaches

trauma or known systemic disease associated with secondary headaches

focal neurologic deficits, impaired consciousness

systemic symptoms (fever, weight loss)

abrupt onset (“thunderclap”)

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39
Q

biggest cause of disability among headache disorders

A

migraine

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40
Q

phases of migraine

A

prodrome- several hours or more before “the migraine” starts. sleepiness, irritability, mood changes, food cravings

aura

attack (usually few hours)

postdromal phase -can last hours to days. tiredness, confusion, sluggishness, mild persistent headache

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41
Q

what is migraine aura?

A

present for about 20% of migraineurs, though not necessarily with every attack

precedes the attack by seconds to 60 minutes

usually has onset gradually and frequently stops with/before headache onset

most common are visual

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42
Q

what is necessary for a migraine diagnosis?

A

one of the following:

nausea and/or vomiting
both photophobia and phonophobia

also need at least 5 attacks over lifetime to make definitive diagnosis

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43
Q

acute treatment for migraines

A

rest/sleep
OTC analgesics
combination analgesics
triptans - serotonin receptor 1B agonists

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44
Q

migraine prevention drugs

A 
propranolol, other beta blockers
non-dihydropyridine calcium channel blockers
antidepressants
anticonvulsants 
riboflavin
CoQ10

lifestyle modifications (avoid trigger foods, alcohol, caffeine)
regular sleep and meals, staying hydrated, exercise
stress reduction

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45
Q

migraine with aura doubles the risk of what?

A

ischemic stroke (compared to migraine without aura) - more common with women

smoking and OCP use independently increase that risk further

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46
Q

true or false: migraine not considered a risk factor after age 50

A

true (much greater impact from HTN, DN, etc)

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47
Q

what is the most common headache disorder?

A

tension-type headache (70% in men, 85-95% in women)

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48
Q

what are the symptoms of a tension headache?

A

“band-like” tightness around the head
bilateral, occipital vs. frontal/temporal
should have no other associated neurological sx
can have photophobia or photophonia but not both

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49
Q

what is acute therapy for tension headaches?

A

NSAIDs, acetaminophen probably best

combination analgesics

narcotics can provide temporary relief but not a good long term option

heat and/or ice packs
muscle relaxers

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50
Q

what is chronic management of tension headaches?

A

tricyclic antidepressants
stretching, massage, heat/ice - PT
other migraine prophylaxis options all tried and can be effective (exception - propranol probably has no role)

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51
Q

family of primary headache disorders with a few common features:

unilateral severe headache, usually forehead/eye
associated ispilateral autonomic symptoms (lacrimation, congestions, conjunctival injection, rhinorrhea, sweating, miosis)

A

trigeminal autonomic cephalalgias

diagnosis hinges on timing, frequency, and duration of headaches

treatment is very different among the subtypes, so identifying the right syndrome is most important

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52
Q

characteristics of cluster headaches

A

attacks last 15m-3 hr
frequency btw every other day and 8x/day
clusters of headaches lasting weeks-months, with periods of remission lasting months-years
only primary headache syndrome more common in men

classic description- “restless”, pacing around —contrast migraines (want to rest, avoid physical activity)

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53
Q

cluster headache treatment

A

first line: oxygen
headaches usually too short to respond to pills
prevention: verapamil (board answer), lithium
corticosteroids during a cluster

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54
Q

headache attacks that last 3-20 minutes. frequency at least 5x/day, though can have periods of less frequent attacks. have to have at least 20 lifetime attacks. response to indomethacin is necessary for diagnosis

A

paroxysmal hemicrania

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55
Q

headaches that last 5 seconds-5 minutes. frequency anywhere from 3-200 per day. clinically can resemble trigeminal neuralgia (autonomic features not present in TN, and TN more likely V2/V3 rather than around the eye). always forehead and periorbital

A

SUNCT/SUNA

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56
Q

treatment for a spinal cord injury

A

ABCs
spinal immobilization
state imaging : MRI preferred
IV steroids

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57
Q

36 y/o male with no PMH presents with one week of tingling in legs, eventually spreading to arms. unable to walk; beginning to feel SOB

A

Neuromuscular respiratory failure

GUILLAIN-BARRE SYNDROME - preceded by infection (C jejuni, EVB, CMV)

diff dx:
myasthenia gravis
tetanus
botulism
organophosphate toxicity
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58
Q

what causes Guillian-barre syndrome?

A

preceded by infection - URI most common preceding, but C jejuni enterits is most commonly isolated organism

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59
Q

what is in the CSF for guillian-barre syndrome?

A

CSF with albuminocytologic dissociation (high protein, no WBCs- with the exception of HIV patients)

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60
Q

how do you know when someone is in respiratory distress?

A

increased RR and use of accessory muscles
inability to count to 20 on one breath

hypoxia is a late finding, usually hypercarbic and decreased mental status first- do not rely on pulse oximetry to monitor patients

61
Q

what is the acute management of neuromuscular respiratory failure?

A

intubation (VC

62
Q

what is the definition of status epilepticus?

A

continuous electrical or clinical seizure activity

or

repetitive seizures without regaining consciousness

> 5 min

can be generalized, focal (partial), nonconvulsive

63
Q

causes of status epilepticus

A

**AED noncompliance
**EtOH related (withdrawal)
drug toxicity
CNS infection
CNS tumor

64
Q

treatment for status epilepticus

A

ABCs
thiamine, glucose, IVF
AED levels (make sure complient), labs

BENZODIAZAPENES
lorazepam
(or diazepam or midazolam)

ANTICONVULSANTS
fosphenytoin, valproate, phenobartibal

65
Q

signs of increase ICP

A

altered consciousness (can’t count backwards)

cushing reflex (bradycardia, hypertension, irregular respirations)

dilated, fixed pupils (CN 3 palsy)

CN 6 palsy

papilledema (late finding)

projectile vomiting

66
Q

treatment of increased ICP?

A

immediately: designed to facilitate venous outflow

  1. head of bed up, head midline
  2. hyperventilation (bridge therapy) **manually
  3. mannitol or hypertonic (>.9%) saline

osmotherapy or steroids
remove mass, consider decompression craniectomy

67
Q

acute bacterial meningitis symptoms and physical findings

A

headache, photophobia
vomiting
lethargy
seizures

fever
impaired consciousness
kernig or brudzinski sign
nuchal rigidity

68
Q

bacterias responsible for community acquired bacterial meningitis

A 
S pneumoniae (47%)
N. meningitides (25%) - communal living, dorms, prisons
69
Q

bacterias responsible for acquired bacterial meningitis in patients older than 50

A

S. pneumoniae

70
Q

bacterias responsible for acquired bacterial meningitis in immunocompromised

A

listeria monocytogenes

71
Q

treatment for acute bacterial meningitis

A

ABCs

treat empirically: 
cefotaxime or ceftriaxone
vancomycin
consider ampicillin (for listeria)
steroids

image (CT) - cancer, seizures, alcoholics, comatose, elderly

LP

“no situation where you would pick one over the other” - do all at once

72
Q

how do you treat viral meningitis

A

supportive +/- acyclovir (herpes family only)

73
Q

who is at risk for wernicke’s encephalopathy?

A

chronic alcoholism or patients with other nutritional deficiency states (post gastric bypass, NPO)

74
Q

symptoms of wernicke’s encephalopathy

A

3 As
Ataxia
Ocular Abnormalities
Altered mental status/confusion

75
Q

42 year old man, history of alcohol abuse. found by his family at home, confused and unsteady.

exam shows: disoriented, inappropriate, abnormal eye movements, nearly falls when trying to walk

A

wernicke’s encephalopathy

76
Q

78 year old woman. 2 weeks of vertex headaches, painful to comb hair. brief left eye visual loss “like a shade being pulled down”. 2 month history of malaise, diffuse muscle aches. pain on chewing, soreness in hips. * nodular, ropey temporal artery. frail appearing, leg movement causes pain in hips/thighs, scalp tender to palpatiation. swollen optic disk and 20/200 in L eye.

A

giant cell arteritis

77
Q

what should you do for giant cell arteritis?

A

**stat ESR and CRP

steroids (oral)- IV if visual symptoms/loss

superficial temporal artery biopsy

chest CT and yearly CXR - aortic/thoracic aneurysms

78
Q

25 y/o man who took an unknown medication, presenting with confusion, temperature of 101.4, confusion, arms difficult to move, with myoclonus.

A

neuroleptic malignant syndrome

79
Q

symptoms of neuroleptic malignant syndroms

A

rigidity, myoclonus
dysautonomia
altered mental status
fever

80
Q

treatment for neuroleptic malignant syndroms

A

discontinue offending agent

81
Q

dysautonomia, altered mental status, myoclonus, hyperreflexia, seizures

A

serotonin syndroms

82
Q

what is the cause of malignant hyperthermia?

A

halogenated inhaled anesthetics

83
Q

symptoms of malignant hyperthermia?

A 
rigidity
fever
dysautonomia
acidosis
rhabdomyolysis
84
Q

treatment of malignant hyperthermia?

A

dantrolene

85
Q

state of being neither awake or aware

A

coma

86
Q

damage to ascending reticular activating system (brainstem, bilateral thalami, bilateral cortex)

A

coma

87
Q

treatment for coma

A 
ABCs
physical exam
correct hypothermia
thiamine, glucose, consider naloxone
labs (ABG, glu, CMP, everything)
CT/consider therapy for elevated ICP
consider LP
consider EEG
88
Q

most common type of brain tumor

A

metastatic tumors (1/2)

89
Q

where are most metastatic brain tumors from?

A

lung cancer

90
Q

brain tumor causing abulia, dementia, personality changes, apraxia, hemiparesis, dysphasia is likely where?

A

frontal lobe

91
Q

inability to perform particular purposive actions, as a result of brain damage.

A

apraxia

92
Q

brain tumor causing auditory or olfactory hallucinations, deja vu, memory impairment, visual field changes is likely where?

A

temporal lobe

93
Q

brain tumor causing contralateral motor or sensory impairment, homonymous hemianopsia, agnosia, apraxia is likely where?

A

parietal lobe

94
Q

brain tumor causing contralateral visual field deficits and alexia (impaired reading)

A

occipital lobe

95
Q

brain tumor causing cranial nerve deficits, ataxia

A

posterior fossa

96
Q

tumor is slow growing, extra axial, usually benign, arises from the arachnoid mater

A

meningioma

97
Q

tumor presenting with hormonal effects (cushing disease, acromegaly), bitemporal hemianopsia

A

pituitary adenoma

98
Q

most malignant brain tumor

A

astrocytoma WHO grade IV (median survival less than a year)

99
Q

standard steroid used in brain tumors and other meds

A

decadron

anti-epileptic medications , Keppra

DVT/PE - second leading cause of death in cancer patients- treat with LMWH (more efective than coumadin)

100
Q

any condition that affects the structure and/or function of the peripheral motor or sensory nerves

A

neuromuscular disorder

101
Q

neurological disorders related to the spinal cord.
may be structural (compressive) from spondylosis, neoplasms, MS, syringomyelia, abscesses etc. Or can be noncompressive from radiation, vascular disease, infections, metabolic.

A

myelopathy

102
Q

cervical myelopathy signs

A

neck pain without radiation
chronic DJD (degenerative joint disease)
posterior column symptoms (sensory changes, balance problems)
increase reflexes

103
Q

progressive motor loss of upper and lower motor neurons

A

Amyotrophic Lateral Sclerosis (ALS)

104
Q

average age of onset of ALS

A

60 (males 2-3x more likely than females)

105
Q

life expectancy from date of diagnosis of ALS

A

3 -5 years - shorter for bulbar predominant patients

106
Q

classic symptoms of ALS

A

painless weakness & atrophy, muscle fasciculations and cramping

laryngospasm

respiratory muscle weakness

head drop

107
Q

2/3 of patients with ALS present with what?

A

limb onset/LMN-D or PMA presentation

108
Q

one of the most common neurological problems. Pain along the course of one dermatone. elicited by specific maneuvers: straight leg raise, reverse straight leg. sensory or motor symptoms in one segment (cervical, thoracic, lumbosacral). diminished DTR

A

radiculopathies

109
Q

most common radiculopathies

A

L5 and S1

110
Q

impingement of lumbar nerve (L5-S1 space). commonly a lifting injury with acute onset. Unilateral. symptoms increase with sitting. decreased motor and sensation

A

lumbar radiculopathy

111
Q

clinical features: multiple levels of degenerative disease with compression of several nerve roots.
morning stiffness, increase pain with activity and prolonged standing
joint space narrowing and osteophyte (bone spurs) formation
BILATERAL pain, numbness and tingling

A

lumbar stenosis

112
Q

this neuromuscular disorder typically presents as pain restricted to a single limb - multiple nerve distributions can be affected if they share partial innervations. symptoms are usually pain, numbness, weakness, or absent reflexes

A

plexopathies

113
Q

brachial plexus plexopathies

A

upper trunk palsy

lower trunk palsy

114
Q

“erb palsy” typically during childbirth. “waiter’s tip” position .weak upper arm, strong hand

A

upper trunk palsy

115
Q

“klumpke” pulling arm up in child, cervical rib or lung tumor (pancoast tumor with Horner’s syndrome) Ulnar nerve. weak hand but strong upper arm

A

lower trunk pasy

116
Q

NM condition recognized by the combination of motor and sensory deficits localized to one nerve distribution. signs and symptoms should be distal to the site of injury

A

mononeuropathy

117
Q

which nerve fiber would present with decreased vibration and proprioception and + tingling

A

large fiber

118
Q

which nerve fiber would present with decreased pain and temperature and + burning

A

small fiber

119
Q

diagnostic tests recommended by the AAN to evaluate for distal symmetric polyneuropathy

A

fasting glucose, B12, SIFE

120
Q

this tests for motor and sensory problems through repetitive stimulations. a delayed response (F waves and H reflexes) - assess more proximal nerve segments

A

Nerve conduction studies (NCS)

121
Q

this is a needle examination that assesses spontaneous activity, motor unit action potentials (MUAPs), and recruitment rate. this is a single fiber analysis

A

electromyography (EMG)

122
Q

this NM condition has symmetric involvement and mainly affects distal nerves first. Sensory or motor nerves involved- often one predominate. patients experiences a burning/numbness in distal extremities ie “stocking glove distribution”

A

polyneuropathies

123
Q

neuropathy related to duration and severity of hyperglycemia. due to vascular insufficiency or nerve infarction. pure sensory and may lead to foot ulcers

A

diabetic neuropathy

124
Q

an acute inflammatory demyelinating polyneuropathy. clinical features are rapidly evolving areflexic motor paralysis with or without sensory involvement. “rubbery legs” 70% occur after infection.
CSF: elevated protein, normal cell counts

A

guillian barre syndrome

125
Q

treatment for GBS

A

IVIG or plasmapharesis

126
Q

what occurs in median mononeuropathy/carpal tunnel syndrom

A

thenar atrophy
sensory loss in digits 1,2,3
DTRs intact
worse at night

127
Q

autoimmune disorder caused by antibodies directed at acetylcholine receptors of skeletal muscle.
bimodal age of onset in second and seventh decades of life.
clinical presentation: fatigable, painless, asymmetric, muscle weakness

A

myasthenia gravis

128
Q

up to 85% of MG patients will have initial symptoms involving what?

A

ocular muscles (ptosis, diplopia or blurred vision)

129
Q

triad of muscle weakness, autonomic dysfunction, and hyporeflexia

A

lambert eaton syndrom

130
Q

muscles diseases are also known as what?

A

myopathies - typically involve shoulder, and hip girdle muscles ie large proximal muscles

131
Q

most frequent myopathy in adults; autosomal dominant. presents with myotonia (inability to relax after contraction -eyes)

A

myotonic dystrophy

132
Q

increased risk factors for MS

A 
geographical location
females (2-2.5X)
race
timing
genetics (not hereditary but there is a genetic link)
133
Q

neurological white matter

A 
optic nerve
brainstem
basal ganglia
spinal cord
lateral ventricles
134
Q

how does MS happen?

A

inflammation
scarring
degeneration

of myelin in white matter

135
Q

what is the classic first presentation of MS?

A

optic neuritis (unilateral pain, vision loss)

136
Q

other clinical signs of MS

A 
sensory symptoms (decreased pain, position, light touch)
Lhermitte's phenomenon
pain (back pain, visceral pain, spasms)
vertigo
nystagmus
weakness, coordination
137
Q

how does MS progress?

A

relapse/flare- weeks on then unknown remission, more frequent early in course, can happen with fever, activity

usually demyelinating events are in similar locations

138
Q

pregnancy’s effect on MS

A

decreases flares, especially in the third trimester, but flares increase in the post partum period

139
Q

term for MS involving a single attack consisting of 1 or more neurological symptoms secondary to a demyelinating inflammatory event.

A

clinically isolated syndrome

140
Q

term for MS - acute flares during which symptoms increase, plateau and resolve. +/- progression of disease during remission.

A

relapsing/remitting

141
Q

criteria used for MS

A

McDonald

142
Q

what diagnostic test is used for MS?

A

MRI, no single lab test

95 % of patients will have abnormal brain lesions

143
Q

test where peripheral stimulation evokes CNS electrical events that are measurable. VER/VEP used for MS if diagnosis is unclear

A

evoked potential testing

144
Q

how do you treat MS?

A

high dose steroids - methyprednisone

oral or IV both equally effective

145
Q

life expectancy of MS

A

30 years from onset

146
Q

most common type of seizure disorder?

A

partial seizure

147
Q

can’t see, can’t pee, can’t climb a tree

A

anykylosing spondylitis - an inflammatory disease that can cause some of the vertebrae in your spine to fuse together.

148
Q

Ptosis, miosis and anydrosis

A

horner’s syndrome

149
Q

Paralysis of one side, vertigo, difficulty speaking and contralateral leg weakness. Likely type of stroke?

A

basilar stroke

clin med (12 decks)

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