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Casey: Neurology > Pance Pearls: Neuro > Flashcards

Pance Pearls: Neuro Flashcards

1
Q

4 lobes of the brain=

A

Frontal, parietal, temporal, occipital

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2
Q

Involuntary spasms or repetitive motions or abnormal voluntary movement

A

Dyskinesia

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3
Q

Sustained contraction (muscle spasm) esp of antagonistic muscles (ex simultaneous biceps and triceps contraction); twisting of body, abnormal posturing (ex torticollis, writer’s cramp)

A

Dystonia

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4
Q

Sudden brief sporadic single repetitive jerks/twitching of 1 muscle or muscle group (not suppressible)

A

Myoclonus

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5
Q

Sudden repetitive nonrhythmic movements or vocals using specific muscles groups (suppressible unlike myoclonus): Ex. tourette’s syndrome

A

Chorea

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6
Q

Muscle contractions; Tonic (prolonged sustained contraction/rigidity); Clonic (repetitive rapid movement)

A

Muscle spasms

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7
Q

Rhythmic movement of a body part

A

Tremors

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8
Q

Tremor at rest (ex. Parkinson’s)

A

Resting tremor

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9
Q

Tremors occurring while holding position against gravity

A

Postural tremor

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10
Q

Tremor occurring during moment or when nearing a target

A

Intentional tremor

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11
Q

Disorder associated with tremor, bradykinesia, rigidity, and postural instability

A

Parkinsonism

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12
Q

Loss of the dopamine producing cells of the substantia nigra (in basal ganglia)

A

Parkinsonism

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13
Q

Medications that block dopamine (dopamine antagonists)- ex. typical and atypical antipsychotics can cause this=

A

Parkinsonism

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14
Q

Disease with loss of anticholinergic neurons (similar to alzheimer’s) where the pt develops dementia and loss of dopaminergic neurons (sharing symptoms similar to Parkinson’s disease)

A

Lewy Body Dementia

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15
Q

Autosomal dominant inherited disorder or unknown etiology; onset of age usually in 60s; may begin at any age, worsened with emotional stress & intentional movement;; Tremor shortly relieved with alcohol ingestion; On finger to nose test, tremor increases as target approached; MC in upper extremities (usually spares legs)

A

Essential familial tremor

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16
Q

May be used to treat Essential familial tremor if severe:

A

Propranolol

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17
Q

Idiopathic dopamine depletion-> failure to inhibit acetylcholine in basal ganglia (Ach is excitatory CNS neurotransmitter, dopamine is INHIBITORY); Cytoplasmic inclusions (Lewy Bodies) & loss of pigment cells seen in substantial nigra (which produces dopamine)

A

Parkinson’s Disease

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18
Q

Classic: tremor, bradykinesia, rigidity with progressive postural instability (often occurs in ages 45-65)

A

Parkinson’s Disease

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19
Q

In Parkinson’s disease, worse at rest, emotional stress (lesseTened with voluntary activity/intentional movement & sleep); often first symptom; usually confined to one limb or one side for years before it becomes generalized

A

Tremor

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20
Q

MC sign in Parkinson’s disease

A

Resting tremor (“pill-rolling” tremor)

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21
Q

In Parkinson’s disease; slowness of voluntary movement & decrease in automatic movements: lack of swinging of arms while walking/shuffle gait

A

Bradykinesia

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22
Q

In Parkinson’s, increased resistance to passive movement (flexed posture); Festination (increased speed while walking); normal DTR; usually no muscle weakness

A

Rigidity

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23
Q

Signs include relative immobile face (fixed facial expressions), widened palpebral fissures, seborrhea of skin is common; Decreased blinking

A

Parkinson’s disease

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24
Q

In Parkinson’s, tapping the bridge of the nose repetitively causes a sustained blink

A

Myerson’s sign

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25
Q

Most effective tx in Parkinson’s disease

A

Levodopa/Carbidopa (Sinemet)

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26
Q

_____ is converted to dopamine

A

Levodopa

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27
Q

______ reduces the amount of levodopa needed reducing SE of the levodopa

A

Carbidopa

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28
Q

Bromocriptine, Pramiprexole, Ropinirole; directly stimulate dopamine receptors; Less SE than levodopa; sometimes used in young pts to delay use of levodopa

A

Dopamine agonists

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29
Q

Blocks excitatory cholinergic effects; indicated in pts

A

Anticholinergics

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30
Q

Increases presynaptic dopamine release & improves long term levodopa-induced dyskinesias

A

Amantadine

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31
Q

Autosomal dominant neurodegenerative disorder; the gene causes neurotoxicity, cerebral & caudate nucleus atrophy; Symptoms appear after 30yrs of age; usually fatal

A

Huntington Disease

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32
Q

Initial symptoms are behavioral changes (personality, cognitive intellectual, psych), chorea (atrophy of caudate nucleus in basal ganglia) & dementia; Chorea is rapid, involuntary or arrhythmic movement of the face, neck, trunk & limbs initially; may have facial grimacing, ataxia

A

Huntington disease

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33
Q

Diagnose by CT scan: shows cerebral and caudate nucleus atrophy

A

Huntington disease

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34
Q

Onset usually childhood (2-5y) & may be associated with obsession compulsions (50% have resolution of symptoms by 18yrs); Motor tics of face, head, and neck (blinking, shrugging, head thrusting, sniffling)

A

Tourettes syndrome

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35
Q

May include verbal/phonetic tics ex. grunts, throat clearing, obscene words (coprolalia), repetitive phrases, repeating phrases of others (echolalia), self-mutilating

A

Tourette syndrome

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36
Q

Can be managed with Dopamine blocking agents or Alpha-adrenergics

A

Tourette syndrome

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37
Q

Acute/subacute inflammatory demyelinating polyradiculopathy with symmetric LOWER–> UPPER extremity weakness (ASCENDING WEAKNESS)

A

Guillian Barre Syndrome

38
Q

Increased incidence with Campylobacter (MC) or other antecedent respiratory or GI infections, CMV, EBV, immunizations, surgery

A

Guillian Barre Syndrome

39
Q

Immune-mediated demyelination & axonal degeneration slows impulses –> symmetric weakness & paresthesias; thought to be secondary to post-infection immune responses which cross-reacts with peripheral nerve components (molecular mimicry)

A

Guillian Barre Syndrome

40
Q

Symptoms include weakness and paresthesias (usually symmetric); Decreased DTR; tachycardia, hypotension/hypertension, breathing difficulties

A

Guillian Barre Syndrome

41
Q

Dx by CSF with high protein & normal WBC count (albuminocytological dissociation)–> may be d/t altered nerve capillary-CSF barrier defect

A

Guillian Barre Syndrome

42
Q

Procedure done early in Guillian Barre Syndrome; removes harmful circulating Autoantibodies that causes the demyelination

A

Plasmapheresis

43
Q

Tx of Guillian Barre; suppresses harmful inflammation/autoantibody & induces remyelination

A

IV immune globulin (IVIG)

44
Q

Autoimmune disorder of the peripheral nerves; 75% have thymic abnormality (hyperplasia or thymoma) or other autoimmune disorders; MC in young women (HLA-DR3)

A

Myasthenia Gravis

45
Q

Inefficient skeletal muscle neuromuscular transmission d/t autoimmune Ab against Ach (nicotinic) post synaptic receptor @ NMJ (decrease Ach receptors)–> progressive weakness with repeated muscle use and recovery after periods of rest

A

Myasthenia Gravis

46
Q

Clinical manifestations include extra ocular muscle weakness–> diplopia; ptosis (eyelid weakness more prominent with upward gaze); pupils spared

A

Myasthenia gravis

47
Q

Generalized muscle weakness; least in the morning worsened with repeated muscle use throughout day (relieved w/ rest), fluctuation; bulbar (orapharyngeal) muscle weakness (weakness w/ prolonged chewing, dysphagia) ; Respiratory muscle weakness (leading to respiratory failure)

A

Myasthenia Gravis

48
Q

Test for Guillian Barre; rapid response to short acting IV edrophonium

A

Edrophonium (Tension test)

49
Q

Dx with + Ach-receptor Antibodies; + muscle specific tyrosine kinase Ab

A

Myasthenia Gravis

50
Q

Increases acetylcholine by decreasing acetylcholine breakdown

A

Acetylcholinesterase inhibitors

51
Q

Associated with small cell lung CA, develop Ab preventing Ach release; weakness is improved with continued use

A

Myasthenia

52
Q

Autoimmune inflammatory demyelinating disease of the CNS idiopathic origin with axon degeneration of white matter of the brain, optic nerve & spinal cord; MC in young adults (women) 20-40; associated with CNS IgG production abnormal T lymphocyte reaction

A

Multiple Sclerosis

53
Q

MC type of Multiple sclerosis=

A

Relapsing-remitting disease (RRMS)

54
Q

Clinical manifestation includes optic neuritis* (retrobulbar)-unilateral eye pain worse w/ eye movements, diplopia, scotoma/vision loss (esp color), blurry vision

A

Multiple sclerosis

55
Q

In Multiple Sclerosis; both pupils constrict when you shine light into the normal eye but pupil’s “DILATE” when you quickly shone the light into the affected eye (response d/t brain perceiving the delayed conduction of affected optic nerve as if light was reduced)

A

Marcus Gunn pupil

56
Q

Clinical manifestations include sensory deficits; weakness, parasthesisas, fatigue (75%); muscle cramping (spasticity); Uhthoffs’s phenomenon (worsening of sx w/ heat; pain, numbness, paresthesias in a limb, muscle cramping) & Lhermitte’s sign (neck flexion causes lighting-shock pain radiating from the spine down the leg)

A

Multiple sclerosis

57
Q

Includes spinal cord sxs: bladder, bowel, or sexual dysfunction; Charcot’s neurological triad(nystagmus, staccato speech & intentional tremor); Spasticity & positive (upwards) babinski*

A

Multiple Sclerosis

58
Q

Test of choice to confirm dx of Multiple Sclerosis

A

MRI* w/ gadolinium

59
Q

MRI will show white matter plaques* (hyperdensistites)

A

Multiple Sclerosis

60
Q

CSF will show increase IgG (oligoclonal bands)-sm, discrete bands in the gamma globulin seen on electrophoresis, which reflecting inflammatory cells penetrate the blood brain barrier)

A

Multiple Sclerosis

61
Q

CSF revealing ‘High IgG (oligoclonal) bands’

A

Multiple Sclerosis

62
Q

CSF revealing ‘High protein with NORMAL WBC cell count’

A

Guillian Barr Syndrome

63
Q

CSF revealing ‘High protein with INCREASED WBC (polymorphonuclear neutrophils), DECREASED glucose*’

A

Bacterial Meningitis

64
Q

CSF revealing ‘Normal glucose, Increased WBC lymphocytes’

A

Aseptic Viral Meningitis

65
Q

CSF revealing ‘Increased WBCs (lymphocytes) and decreased glucose’

A

Fungal Meningitis

66
Q

An acute, abrupt confused state (transient global disorder of attention) usually as a result of systemic problems with rapid onset and fluctuating mental status changes; Marked deficit in short term memory; usually 1 week with full recovery in most cases

A

Delirium

67
Q

Progressive, chronic deterioration of selective functions; MEMORY LOSS and loss of impulse control, motor & cognitive functions NOT d/t delirium, medications, or psychiatric illness

A

Dementia

68
Q

MC type of dementia; Loss of brain cells, amyloid deposition (senile plaques) in the brain, neurofibrillary tangles (tau protein); cholinergic deficiency–> memory, language, visuospatial changes; CEREBRAL CORTEX ATROPHY on CT scan*

A

Alzheimer’s disease

69
Q

Used to manage Alzheimer’s disease; reverses cholinergic deficiency, may not always slow down progression of dz but helps with sx

A

Acetylcholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine)

70
Q

Used to manage Alzheimer’s disease; blocks NMDA receptor, slowing calcium influx and nerve damage; Glutamate is excitatory receptor–this reduces Glutamate’s excitotoxicity

A

NMDA antagonists

71
Q

2nd MC type of Dementia; brain dz d/t chronic ischemia and multiple infarctions (ex. lacunar infarcts**); assoc w/ HTN

A

Vascular Dementia

72
Q

Type of dementia; Rare; Localized brain degeneration of the frontotemporal area may progress globally; marked personality changes*; aka Pick’s disease

A

Frontotemporal Dementia

73
Q

Abnormal protein deposits (Lewy bodies) in nerve cells; Visual hallucinations, delusions, Parkinsonism

A

Diffuse Lewy Body disease

74
Q

Rapid dementia d/t prions

A

Creutzfeldt-Jakob dz

75
Q

Predominantly middle-aged males with severe UNILATERAL periorbital/temporal pain (sharp, lacinating)* bouts lasting

A

Cluster headaches

76
Q

Physical exam reveals IPSILATERAL Horner’s syndrome (ptosis, miosis, anhydrosis)*, nasal congestion/rhinorrhea, conjunctivitis & lacrimation

A

Cluster Headaches

77
Q

First line tx in cluster headaches=

A

100% O2

78
Q

Prophylaxis tx for cluster headaces=

A

Verapamil

79
Q

MC in females; 2 types (w/ and w/o auras); Family hx 80%; Thought to be caused by vasodilation of the blood vessels innervated by the trigeminal nerve; Neuro findings d/t internal carotid constriction

A

Migraine headaches

80
Q

Lateralized, pulsatile/throbbing headaches associated with N/V, photophobia & photophobia for 4-72 Hr duration; worse w/ physical activity, stress, lack/excessive sleep, ETOH, certain foods, OCPs/menstruation

A

Migraine headaches

81
Q

Bilateral* tight band-like, constant daily HA worsened w/ stress, fatigue, noise, or glare (NOT ACTIVITY); usually not pulsatile; NO N/V or focal neurologic sx

A

Tension headaches

82
Q

Compression of trigeminal nerve root (by superior cerebellar artery or vein); Brief episodic, stabbing/lancinating pain in the 2nd/3rd division of the Trigeminal nerve (CN V) worse with touch, eating, drafts of wind, and movements (often unilateral): pain starts near mouth & shoots to eye, ear, nostril on ipsilateral side

A

Trigeminal Neuralgia

83
Q

First line tx for trigeminal neuralgia

A

Carbamazepine

84
Q

If this is present in younger pts, suspect Multiple sclerosis

A

Trigeminal Neuralgia

85
Q

MC type of stroke=

A

Ischemic

86
Q

Transient episode of neurological deficits caused by focal brain, spinal cord or retinal ischemia (WITHOUT acute infarction); MC due to embolus

A

Transient ischemic attack (TIA)

87
Q

Internal carotid artery: Amaurosis fugax (monocular vision loss-temporary “lamp shade down on one eye”), weakness in contralateral hand; sudden HA, speech changes, confusion

A

TIA

88
Q

Mild traumatic brain injury; alteration in mental status with or loss of consciousness; confusion, amnesia, HA, dizziness, visual disturbances, delayed responses and emotional changes; signs of increased intracranial pressure (persistent vomiting, worsening HA, increasing disorientation, changing levels of consciousness)

A

Concussion syndrome

89
Q

MC type of stroke; Most d/t thrombus (49%) others d/t embolus

A

Ischemic

90
Q

Type of ischemia stroke; small vessel disease (penetrating branches of cerebral arteries in pons, basal ganglia); MC is hemiparesis, hemiplegia; Ataxic hemiparesis weakness/clumsiness in LEG>arm; ;dysarthria (clumsy hand syndrome); hx of HTN (80%)

A

Lacunar infarcts

91
Q

On CT scan, small punched out hypotedense* area

A

Lacunar infarcts

Casey: Neurology (7 decks)

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