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Neuro Flashcards

1
Q

Valproic acid: potential adverse effects

A

BLACK BOX WARNINGS: pancreatitis, hepatotoxicity, fetal risk

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2
Q

phenytoin: potential adverse effects

A

gingival hyperplasia

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3
Q

Ototoxic meds

A

furosemide
erythromycin
ibuprofen

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4
Q

Sensorineural hearing loss is due to problems with which part of the ear?

A

The inner ear: Cochlea (organ of hearing), vestibular labyrinth (organ of balance)
Auditory nerve (CN VIII) or its central pathways

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5
Q

Conductive hearing loss is to due to problems with which part of the ear?

A

Outer ear: pinna, external ear canal
Middle ear: Tympanic membrane, ossicular chain (malleus, incus, stapes), and middle ear space

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6
Q

Weber test

A

Distinguishes between conductive and sensorineural hearing loss
-conductive: sound lateralizes to affected side
-sensorineural: sound lateralizes to contralateral side

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7
Q

Rinne test

A

Tests cranial nerve VIII
Evaluates conductive hearing loss
Strike a tuning fork and place it on the mastoid process

Normal: AC = 2x BC
Hearing loss: BC > AC

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8
Q

frontotemporal dementia: presentation

A

disruptions in personality and social conduct
may have primary language disorder

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9
Q

Lewy Body dementia: management

A

Medications can be used to treat agitation, hallucinations, and improve cognition or alertness, but do not decrease the rate of cognitive decline

Acetylcholinesterase inhibitors: 1st line
-donezpil, galantamine

If ineffective, atypical neuroleptics
-clozapine, quetiapine, aripiprazole

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10
Q

Lewy Body dementia

A

progressive degenerative dementia

most frequently characterized with bradykinesia and rigidity
-memory deficits
-reduced alertness
-visual hallucinations
-parkinsonian motor features: bradykinesia, resting tremor, rigidity, gait difficulty

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11
Q

vascular dementia: presentation

A

usually occurs after an infarct in a strategic location or with extensive white matter changes
does not cause visual hallucinations

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12
Q

CN I

A

Olfactory: smell

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13
Q

CN II

A

Optic: vision

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14
Q

CN III

A

Oculomotor: most EOMs, opening eyelids, pupillary constriction

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15
Q

CN IV

A

trochlear: down and inward eye movement

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16
Q

CN V

A

trigeminal: muscles of mastication; sensation of face, scalp, cornea, mucous membranes, nose

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17
Q

CN VI

A

abducens: lateral eye movement

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18
Q

CN VII

A

facial: move face, close mouth and eyes, taste (anterior 2/3), saliva and tear secretion

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19
Q

CN VIII

A

acoustic: hearing and equilibrium

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20
Q

CN IX

A

glossopharyngeal: phonation (1/3), gag reflex, carotid reflex swallowing, taste (posterior 1/3)

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21
Q

CN X

A

vagus: talking, swallowing, general sensation from the carotid body, carotid reflex

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22
Q

CN XI

A

spinal accessory: movement of the trapezius and sternomastoid muscles (shrug shoulders)

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23
Q

CN XII

A

hypoglossal: moves the tongue

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24
Q

CN III palsy

A

ptosis
dilated pupil
diplopia
eye deviated laterally and downward

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25
Q

Mini-mental status exam

A

ORArL 2, 3 RWD

Orientation to place AND time
Recognition (repeat three objects)
Attention (serial 7s counting backward from 100)
recall (ask to recall 3 objects 5 mins later)
Langauge
2 Identify names of 2 objects
3 Follow a 3-step command
Reading (e.g. Read this statement to yourself, do exactly what it says but do not say it aloud: “Close your eyes.”)
Writing
Drawing

Scoring:
- 0-17: severe dementia/delirium
- 18-23: mild dementia/delirium
- 24-30: no cognitive impairment

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26
Q

TIA classifications: vertebrobasilar

A

Occur as a result of inadequate blood flow from vertebral arteries

Presentations:
-vertigo
-ataxia
-dizziness
-visual field deficits
-weakness
-confusion

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27
Q

TIA classifications: carotid

A

due to carotid stenosis

Presentations:
-altered LOC
-aphasia, dysarthria
-weakness
-numbness

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28
Q

TIA: labs/Dx

A

CT: best for distinguishing between ischemia, hemorrhage, and tumor
MRI: best for detecting ischemic infarcts

EKG
Echocardiogram
Carotid doppler and ultrasound
Cerebral angiography

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29
Q

TIA: management

A

Aspirin
Plavix
Assess for HTN
CEA
- symptomatic low risk patients with 50-90% stenosis
- asymptomatic patients with >70% stenosis

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30
Q

CVA: labs/Dx

A

Large vessel stroke workup
-telemetry
-TEE with bubble study
-carotid imaging (US, CTA, MRA, angio)
-intracranial imaging (CTA, MRA, angio)

LP if grade I or II aneurysm to detect xanthochromia, but obtain head CT first
- contraindicated with large bleeds as brain stem herniation can be induced with rapid decompression of the subarachnoid space

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31
Q

CVA: Management by time of onset

A

<4.5 hours: tPA
- For thrombotic strokes, preferably <3 hours

<6 hours: mechanical embolectomy for all

6-24 hours: mechanical embolectomy for some

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32
Q

CVA: indications for ICP monitoring

A

Moderate: severe head injury who can’t be serially neurologically assessed

Severe head injury (GCS <8) + abnormal CT scan

Severe head injury (GCS <8) + normal CT if two of the following are present:
- Age >40
- BP <90
- Abnormal motor posturing

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33
Q

CVA: management for vasospasm

A

MAP goal 110-130 to treat cerebral vasospasm (if MCA spasms, it could interrupt blood flow to the brain and risk distal infarct)

Nimodipine (CCB) to counter vasospasm by preventing calcium from entering smooth muscle cells and causing contraction

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34
Q

Simple partial seizure

A

Common with cerebral lesions
No LOC
Rarely lasts >1 minute
Motor symptoms often start in single muscle group and spread to entire side of body
Parasthesias, flashing lights, vocalizations, hallucinations

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35
Q

Complex partial seizure

A

Common with cerebral lesions
Rarely lasts >1 minute
Motor symptoms often start in single muscle group and spread to entire side of body
Parasthesias, flashing lights, vocalizations, hallucinations
May have aura, staring, or automatisms such as lip smoking and picking at clothing
Followed by impaired level of consciousness

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36
Q

Absence (petit mal) seizure

A

Type of generalized seizure
Sudden arrest of motor activity with blank stare
Commonly discovered in children/adolescents
Begin and end suddenly

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37
Q

Tonic-clonic (grand mal) seizure

A

Type of generalized seizure
May have aura
Begins with tonic contraction (repetitive involuntary contraction of muscle), LOC, then clonic contractions (maintained involuntary contraction of muscle
Usually lasts 2-5 minutes
Incontinence may occur
Followed by postictal period

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38
Q

Status epilepticus

A

Seizure lasting >5 mins or more than 1 seizure within a 5-minute period without returning to normal level of consciousness
May occur when the patient is awake or asleep, but never regains consciousness between attacks

MEDICAL EMERGENCY

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39
Q

Seizures: assessment, labs/Dx

A

Assessment:
-presence of aura
-onset
-spread
-type of movement
-body parts involved
-pupil changes and reactivity
-duration
-loss/level of consciousness
-incontinence
-behavioral and neurological changes after cessation of seizure activity

EEG: most important test in determining classification
CT: indicated for all new onset seizures to r/o brain tumor

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40
Q

Seizures: management: Stabilization Phase

A

0-5 minutes

Stabilize: ABC’s, disability? neuro exam
Time seizure from onset
Ongoing vital signs assessment
O2 per n/c or mask; consider intubation
Continuous EKG monitoring
FSBG: if <60, IV thiamine and 50ml dextrose
Routine labs, tox screen, anticonvulsant levels

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41
Q

Seizures: management: Initial Therapy Phase

A

5-20 minutes

Choose one of the following:
- IM midazolam
- IV lorazepam
- IV diazepam

If none of these are available, choose one:
- IV pheonobarbital
- rectal diazepam
- intranasal midazolam, buccal midazolam

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42
Q

Seizures: management: Second Therapy Phase

A

20-40 minutes

Choose one of the following:
- IV fosphenytoin
- IV valproic acid
- IV keppra

If none of these are available:
- IV phenobarbital if not previously given

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43
Q

Seizures: management: Third Therapy Phase

A

40-60 minutes

Repeat second-line therapy OR

Anesthetic doses: choose one (with continuous EEG monitoring)
- thiopental
- midazolam
- pentobarbital
- propofol

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44
Q

Subsequent seizure prevention

A

Maintenance doses of long-acting anticonvulsants
-valproic acid (Depakene)
-phenobarbital (Luminal)
-phenytoin (Dilantin)
-carbamazepine (Tegretol)
-ethosuximide (Zarontin)
-primidone (Mysoline)

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45
Q

Myasthenia Gravis: cause

A

Autoimmune disorder resulting in the reduction of the number of acetylcholine receptor sites at the neuromuscular junction
Variable clinical course with remissions and exacerbations.

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46
Q

Myasthenia Gravis: incidence

A

Mostly 20-40 years old but may occur at any age
Incidence peaks in the 30s for females, 50-60s for males
More common in women

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47
Q

Myasthenia Gravis: S/Sx

A

Ptosis (common 1st complaint)
Diplopia
Dysarthria
Dysphagia
Respiratory difficulty
Extremity weakness, typically worse after exercise and better after rest
Fatigue

Sensory modalities and DTRs are normal

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48
Q

Myasthenia Gravis: labs/Dx

A

Antibodies to acetylcholine receptors

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49
Q

Myasthenia Gravis: management

A

Neurology referral
Anticholinesterase drugs block the hydrolysis of acetylcholine
- used for symptomatic improvement
- pyridostigmine bromide (Prostigmin)
Immunosuppressives
Plasmapheresis
Ventilator support during a crisis if needed

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50
Q

Multiple Sclerosis: Cause

A

Autoimmune disease marked by numbness, weakness, loss of muscle coordination, and problems with vision, speech, and bladder control
The body’s immune system attacks myelin
Variable clinical course with remissions and exacerbations

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51
Q

Multiple Sclerosis: Incidence

A

Greatest incidence is in young adults ages 20-50

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52
Q

Multiple Sclerosis: S/Sx

A

Weakness, numbness, tingling, or unsteadiness in one limb; may progress to all limbs (common 1st complaint)
Spastic paraparesis
Diplopia
Disequilibrium
Urinary urgency or hesitancy
Optic atrophy
Nystagmus

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53
Q

Multiple Sclerosis: labs/Dx

A

MRI: most specific, shows damaged myelin sheath
Evoked potentials test
LP
Blood tests to rule out other causes

54
Q

Multiple Sclerosis: management

A

No treatment to prevent progression
Neurology referral

Recovery from acute relapses hastened by steroids
Antispasmodics
Interferon therapy
Immunosuppressive therapy
Plasmapheresis

55
Q

Guillain-Barré syndrome

A

Acute, usually rapidly progressive form of inflammatory polyneuropathy characterized by demyelination of peripheral nerves resulting in progressive symmetrical ascending paralysis

56
Q

Guillain-Barré syndrome: cause

A

Usually preceded by a suspected viral infection accompanied by fever 1-2 weeks before onset of acute bilateral muscle weakness in lower extremities
Flaccid paralysis can result within 48-72 hours

57
Q

Guillain-Barré syndrome: S/Sx

A

Typically, a rapidly progressive ascending paralysis
Cranial nerve impairment, as evidenced by difficulties in speech, swallowing, and mastication
Hypoactive/absent reflexes
Impairment of the muscles of respiration as paralysis ascends

58
Q

Guillain-Barré syndrome: labs/Dx

A

CBC: early leukocytosis with left shift

LP
-CSF protein elevated, especially IgG

MRI
CT

59
Q

Guillain-Barré syndrome: management

A

Supportive treatment while myelin is regenerated
Symptoms begin to recede within 2 weeks with recovery in 2 years
Neuro consult

60
Q

Meningitis

A

infection of the membranes of the Pia mater and arachnoid mater of the brain or spinal cord

61
Q

What should be considered in any patient with fever and neurologic symptoms, especially if there is a history of other infection or head trauma?

A

meningitis

62
Q

Meningitis: pathogens

A

streptococcus pneumoniae
hemophilus influenzae
neisseria meningitidis

63
Q

Meningitis: S/Sx

A

fever 38.3-39.4C (101-103F)
severe headache
N/V
nuchal rigidity
+Kernig’s sign
+Brudinski’s sign
photophobia
seizures

64
Q

Kernig’s sign

A

pain and spasms of the hamstrings

65
Q

Brudinski’s sign

A

Legs flex at both the hips and knees in response to flexion of the head and neck to the chest

66
Q

Meningitis: labs/Dx

A

LP as soon as the diagnosis is suspected. CSF:
- cloudy or xanthochromic
- elevated pressure (bacterial)
- elevated protein
- decreased glucose
- +WBCs

Head CT

67
Q

Meningitis: organism and management if <50

A

organism:
- N. meningitidis
- S. pneumoniae

vancomycin + ceftriaxone

68
Q

Meningitis: organism and management if >50

A

Organism:
- S. pneumoniae
- N. meningitidis
- gram negative enterics (E. coli, Klebsiella, Enterobacter)
- L. monocytogenes

vancomycin + ampicillin + ceftriaxone

69
Q

Cushing’s Triad

A

physiological nervous system response to acute elevations of intracranial pressure

Widening pulse pressure (SBP increases in an attempt to maintain a constant CPP)
Decreased RR
Decreased HR

70
Q

Battle’s sign

A

bruising behind the ear at the mastoid process
sign of TBI

71
Q

raccoon eyes

A

sign of basilar skull fracture

72
Q

SCI to C4 or above: S/Sx

A

tetraplegia
may require mechanical ventilation

73
Q

SCI to C4-C5: S/Sx

A

tetraplegia
control of head, neck, shoulders, trapezius, and elbow flexion

74
Q

SCI to C5-C6: S/Sx

A

tetraplegia
some extension of wrist, index finger, thumb

75
Q

SCI to C6-C7: S/Sx

A

elbow extension
capable of feeding, dressing

76
Q

SCI to C7-T1: S/Sx

A

hand movement

77
Q

SCI to T1-T2: S/Sx

A

paraplegia
upper extremity control but no trunk control

78
Q

SCI to T3-T8: S/Sx

A

some trunk control

79
Q

SCI to T9-T10: S/Sx

A

bowel and bladder reflex
moves trunk and upper thigh

80
Q

SCI to T11-L1: S/Sx

A

Most leg and some foot movement
ambulation possible

81
Q

SCI to L1-L2: S/Sx

A

lower legs, feet, perineum
bowel, bladder, sexual dysfunction if S2-S4 spinal nerves are involved

82
Q

SCI: labs/Dx

A

spinal x-ray series
CT
MRI

83
Q

SCI: management

A

Consult neurology/neurosurgery
Methylprednisolone 30mg/kg IV bolus, followed by an infusion of 5.4 mg/kg/hr for 23 hours
-indicated for blunt trauma but not penetrating trauma

84
Q

SCI complications: C4 or above

A

respiratory compromise

85
Q

SCI complications: T4-T6

A

may lead to autonomic dysreflexia

86
Q

autonomic dysreflexia: S/Sx

A

diaphoresis and flushing above the level of injury
chills and severe vasoconstriction below the level of injury
hypertension
bradycardia
headache
nausea

87
Q

autonomic dysreflexia: treatment

A

stimulus removal
antihypertensives

88
Q

Brown Sequard Syndrome

A

Complication of SCI
Caused by damage to one half of the spinal cord

89
Q

Brown Sequard Syndrome: S/Sx

A

IPSILATERAL upper motor neuron paralysis and loss of proprioception
CONTRALATERAL loss of pain and temperature

90
Q

Brown Sequard Syndrome: treatment

A

MRI
steroids

91
Q

Cauda Equina Syndrome

A

complication of SCI
Caused by compression of nerve roots at the end of the spinal cord (cauda equina)

92
Q

Cauda Equina Syndrome: S/Sx

A

numbness in the lower legs, feet, or saddle region (groin, buttocks, genitals)

93
Q

Cauda Equina Syndrome: management

A

MRI
steroids
surgery for decompression

94
Q

Neurogenic shock

A

Complication of SCI to T6 or above
disruption of transmission of sympathetic impulses causing unopposed parasympathetic stimulation which leads to loss of vasomotor tone, including massive vasodilation

Results in hypovolemia, decreased venous return, and decreased cardiac output

95
Q

Neurogenic shock: treatment

A

sympathomimetic vasopressors (dopamine, norepinephrine) to maintain blood pressure

96
Q

Parkinson’s Disease

A

A degenerative disorder as a result of insufficient amounts of dopamine in the body

97
Q

Parkinson’s Disease: S/Sx

A

tremor: slow, most conspicuous at rest, may be enhanced by stress
rigidity
bradykinesia
wooden facies (mask-like face)
impaired swallowing
May see drooling
decreased blinking
Myerson’s sign (repetitive tapping over the bridge of the nose produces a sustained blink response; glabellar reflex)

98
Q

Parkinson’s Disease: labs/Dx

A

None
Dx of exclusion

99
Q

Parkinson’s Disease: management

A

Carvidopa-Levodopa (Sinemet)

Dopamine agonists (mimic dopamine)
- pramipexole (Mirapex)
- ropinirole (Requip)
- rotigotine (Neupro)

MAO-B inhibitors (help prevent the breakdown of dopamine)
- selegiline (Eldepryl, Zelapar)
- rasagiline (Azilect)
- safinamide (Xadago)

100
Q

Causes of delirium

A

Toxins
Alcohol/drug abuse
Trauma
Impactions in the elderly
Poor nutrition
Electrolyte imbalances
Anesthesia

101
Q

Causes of dementia

A

Alzheimer’s Disease - most common
Atherosclerosis
Neurotransmitter deficits
Cortical atrophy
Ventricular dilation
Loss of brain cells
Possible viral causes

102
Q

Dementia: labs/Dx

A

DEMENTIA to rule out other diseases
Drug reactions/interactions
Emotional disorders
Metabolic/endocrine disorders
Eye and ear disorders
Nutritional problems
Tumors
Infection
Arteriosclerosis

Labs:
- CBC
- BMP
- LFTs
- B12
- VDRL

CT to rule out tumors

103
Q

Alzheimer’s Disease

A

Development of multiple cognitive defects characterized by both memory impairment (impaired ability to learn new information and recall previously learned information) and one or more of the following:
- aphasia
- apraxia (inability to perform a previously learned task)
- agnosia (inability to recognize an object)
- Inability to plan, organize, sequence, and make abstract difference

Caused by overall acetylcholine deficiency throughout the body

104
Q

Alzheimer’s Disease: S/Sx

A

aphasia
apraxia
agnosia
inability to plan, organize, sequence, and make abstract difference
limb rigidity
flexion posture
disorientation
gait disturbances
impaired memory/judgment

105
Q

Alzheimer’s Disease: management

A

Neurology consult

Cholinesterase inhibitors – increase the availability of acetylcholine
- donepezil (Aricept): all stages of Alzheimer’s
- galantamine (Razadyne): mild to moderate Alzheimer’s
- rivastigmine (Exelon): mild to moderate Alzheimer’s

NMDA antagonist
- memantine (Namenda): moderate to servere Alzheimer’s

Combination preparation
- memantine and donepezil (Namzaric): moderate to severe Alzheimer’s

106
Q

Alcohol Use Disorder: screening test

A

CAGE
C: Have you ever felt the need to cut down on your drinking?
A Have people annoyed you by criticizing your drinking?
G Have you ever felt guilty about your drinking?
E Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover? (eye-opener)

107
Q

Myotonic muscular dystrophy

A

Most common adult form of muscular dystrophy
Often present with sustained involuntary contraction of a group of muscles
Stiffness and difficulty releasing their grip

108
Q

Muscular dystrophy

A

Autosomal dominant disease that often manifests in late childhood with gait abnormalities due to weakness of the foot dorsiflexors
Progression to weakness of the intrinsic muscles of the hands and wrist extensors, atrophy of facial muscles, ptosis
Other tissues may also be affected: cardiac arrhythmias, early frontal balding, endocrinopaties, testicular atrophy

109
Q

Causes / Risk factors associated with intracerebral hemorrhage

A

hypertension
septic emboli
brain tumor
vascular malformations
bleeding disorders
CNS infections
stimulants

110
Q

Causes/ risk factors associated with subarachnoid hemorrhage

A

aneurysms

111
Q

treatment for increased ICP

A

ICP is typically treated when it is over 20 mm Hg
If no obvious causes of increased ICP are present, analgesics (e.g. fentany) are used if the patient is having subclinical pain or agitation

112
Q

The progression of transtentorial herniation will require..

A

mechanical ventilation, as it leads to respiratory arrest

Also leads to hypertension and bradycardia

113
Q

transtentorial herniation: presentation

A

headache
altered LOC
dilation of one pupil
ptosis

Leads to respiratory arrest, bradycardia, hypertension

114
Q

idiopathic intracranial hypertension: presentation

A

headache
visual changes and disturbances

115
Q

idiopathic intracranial hypertension: risk factors

A

female of childbearing age
obesity
hypothyroidism
recent treatment with a tetracycline

116
Q

Horner syndrome

A

rare condition classically presenting with partial ptosis, miosis, and facial anhidrosis (absence of sweating) or hyperhidrosis due to a disruption in the sympathetic nerve supply

117
Q

Honer syndrome: labs/Dx

A

MRA head/neck to rule out carotid artery dissection

118
Q

Horner syndrome: management

A

Neurosurgery if aneurysm related
Vascular surgery if carotid artery dissection or aneurysm related

119
Q

Gold standard for identifying an intracranial lesion

A

MRI with contrast

120
Q

central cord syndrome

A

spinal cord injury where messages are unable to be transmitted to or from the brain below the level of injury
- upper extremity weakness out of proportion to lower extremity weakness

121
Q

anterior cerebral artery supplies which parts of the brain

A

medial portions of the frontal and parietal lobes and corpus callosum

122
Q

part of the brain that is partially responsible for voluntary movement

A

frontal lobe

123
Q

Visual loss is associated with an embolism in what part of the brain?

A

posterior cerebral artery

123
Q

Aphasia is associated with an embolism in what part of the brain?

A

middle cerebral artery

124
Q

Sensory loss is associated with an embolism in what part of the brain?

A

posterior cerebral artery

125
Q

First step in treating delirium

A

rule out or remove reversible causes

126
Q

When is intubation and ICP monitoring indicated?

A

Severe TBI w/GSC between 3-8 and abnormal head CT

127
Q

normal pressure hydrocephalus: S/Sx

A

increasing urinary incontinence
cognitive decline with disinhibition and apathy
gait disturbance resulting in falls

128
Q

Symptomatic cerebral salt wasting: treatment

A

3% NaCl
-rapidly increases serum sodium

129
Q

Biggest concern with severe head injury

A

High priority: cerebral edema d/t increased intracranial volume, causing increased ICP and ultimately leads to cerebral tissues being oxygen-deprived

Board Exam (18 decks)

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