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Neuro 2 Flashcards

1
Q

Characteristic feature of NMJ disorders?

A

Muscle weakness in the absence of UMN or LMN signs

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2
Q

Presentation of MG?

A

Fluctuating and fatiguable extraocular (eg, diplopia, ptosis) and bulbar (eg, dysarthria, dysphagia) muscle weakness as well as symmetrical proximal weakness of the neck and extremities (upper>lower)

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3
Q

Pathogenesis of MG?

A

Autoantibodies against acetylcholine receptors in the motor end plate

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4
Q

List the 3 major types of muscular dystrophy.

A
  1. Duchenne
  2. Becker
  3. Myotonic
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5
Q

Compare the genetics of the 3 major types of muscular dystrophy.

A

Duchenne and Becker: X-linked recessive deletion of dystrophin gene on chr Xp21

Myotonic: AD expansion of a CTG trinulceotide repeat in DMPK gene on chr 19q 13.3

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6
Q

Compare the presentations of the 3 major types of muscular dystrophy

A
  1. Duchenne: onset age 2-3 of progressive weakness, Gower maneuver, calf pseudohypertrophy
  2. Becker: onset age 5-15, milder weakness compared to Duchenne
  3. Myotonic: onset age 12-30, facial weakness, hand grip, myotonia, dysphagias
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7
Q

Compare the comorbidities of the 3 major types of muscular dystrophy.

A
  1. Duchenne: scoliosis and cardiomyopathy
  2. Becker: cardiomyopathy
  3. Arrhythmias, cataracts, balding, testicular atrophy/infertility
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8
Q

Compare the prognosis of the 3 major types of muscular dystrophy.

A
  1. Duchenne: wheelchair dependent by adolescence, death by 20-30 from respiratory or heart failure
  2. Becker: death by 40-50 from heart failure
  3. Death from respiratory or heart failure depending on age of onset
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9
Q

Risk factors for a febrile seizure?

A

Fever from mild viral illness

Family history

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10
Q

Dx criteria for febrile seizure?

A

Typically age 3 months to 5 years
No previous afebrile seizure
No meningitis or encephalitis
No acute metabolic cause

Simple febrile seizures are generalized, last <15 minutes, and do not recur within 24 hours

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11
Q

Manage febrile seizure?

A

Abortive therapy if 5+ minutes

Reassurance

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12
Q

Prognosis of febrile seizure?

A

Normal development/intelligence
~30% risk of recurrence
<5% risk of epilepsy

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13
Q

Next step in a simple febrile seizure after treating the fever?

A

No further evaluation or treatment required; discharge home with education and supportive care

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14
Q

Frequent, prolonged, focal febrile seizures may be concerning for ___.

A

Dravet syndrome

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15
Q

When is hospitalization and observation required in a patient with a febrile seizure?

A

If they have not returned to neurologic baseline

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16
Q

Features of essential tremor?

A

Bilateral action tremor of the hands, usually without leg involvement
Possible isolated head tremor without dystonia
Usually no other neurologic signs
Relieved with alcohol in many cases

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17
Q

Features of tremor in Parkinson’s disease?

A

Resting tremor that decreases with voluntary movement
Usually involves legs and hands
Facial involvement is less common

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18
Q

Features of cerebellar tremor?

A

Usually associated with ataxia, dysmetria, or gait disorder

Tremor increases steadily as the hand reaches its target

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19
Q

Features of a physiologic tremor?

A

Low amplitude, not visible under normal conditions
Acute onset with increased sympathetic activity (drugs, hyperthryoidism, anxiety, caffeine)
Usually worse with movement, can involve face and extremities

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20
Q

Rx essential tremor?

A

Propranolol, especially helpful if patient has coexistent hypertension

Other options - anticonvulsants (primidone and topiramate)

Benzos are effective but should be restricted de to potential for dependence

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21
Q

Rx Parkinson disease?

A

Carbidopa/levodopa

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22
Q

True or false - caffeine use is correlated with the severity of essential tremor

A

False

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23
Q

Presentation of basal ganglia (puaminal) hemorrhage?

A

Sudden focal neurologic deficits that gradually worsen over minutes to hours, progresses to headache, N/V, AMS due to increased ICP

Almost always involves the adjacent internal capsule -> contralateral hemiparesis and hemianesthesia (disruption of corticospinal and somatosensory fibers in the posterior limb)

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24
Q

Most common cause of spontaneous deep intracereberal hemorrhage?

A

Hypertensive vasculopathy involving the small penetrating branches of the major cerebral arteries

Chronic HTN leads to the formation of Charcot-Bouchard aneurysms, which may rupture and bleed within the deep brain structures

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25
Q

ACA deep branches supply blood to what structures?

A

Head of caudate nucleus and the anterior limb of the internal capsule

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26
Q

MCA deep branches supply blood to what structures?

A

Lentiform nucleus = putamen and globu pallidus

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27
Q

PCA deep branches supply blood to what structures?

A

Thalamus

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28
Q

Anterior choroidal artery supplies blood to what structure?

A

Internal capsule (posterior limb)

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29
Q

What is the most common cause of spontaneous lobar/cortical hemorrhage in the elderly?

A

Cerebral amyloid angiopathy

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30
Q

Most common cause of intraparenchymal hemorrhage in children?

A

AV malformation

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31
Q

Common cause of subarachnoid hemorrhage?

A

Ruptured saccular (berry) aneurysms

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32
Q

Bridging vein tears cause ___.

A

Subdural hematoms

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33
Q

Mengingeal artery tears cause ___.

A

Epidural hematomas

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34
Q

Risk factors for subdural hematoma?

A

Elderly and alcoholics (cerebral atrophy, increased fall risk)
Infants (thin-walled vessels)
Anticoagulant use

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35
Q

Clinical presentation of acute subdural hematoma?

A

Gradual onset 1-2 days after injury
Impaired consciousness, confusion
Headache, N/V (increased ICP)

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36
Q

Clinical presentation of chronic subdural hematoma?

A

Insidious onset weeks after injury

Headache, somnolence, confusion, lightheadedness, focal neuro deficits

37
Q

Dx chronic subdural hematoma?

A

Head CT with crescent shaped hyperdensity (acute) or hypodensity (chronic) crossing suture liones

38
Q

Rx subdural hematoma?

A

Reverse/discontinue anticoagulants

Surgical evacuation of symptomatic or large bleeds

39
Q

Neuroimaging findings of cardioembolic stroke?

A

Multiple lesions at the grey-white matter jnction

40
Q

Cause of lacunar stroke?

A

Chronic HTN causes hyalinosis of small penetrating branches of the major cerebral arteries, leading to lacunar stroke in deep brain structures

41
Q

Cause of normal-pressure hydrocephalus?

A

Decreased CSF resorption by the arachnoid granulations

42
Q

Imaging findings of NPH?

A

Ventricular enlargement that is out of proportion to sulci enlargement

43
Q

Cause of diffuse axonal injury?

A

Result of trauma acceleration/deceleration shearing forces that diffusely damage axons in the brain

44
Q

Causes of myoclonus?

A

Genetic disorders
Seizures
Medications
Prolonged hypoxia

45
Q

What is myoclonus status epilepticus?

A

Acute form of post-hypoxic myoclonus that typically develops within 24 hours after the initial hypoxic insult while the patient is still unconscious

46
Q

Characteristics of myoclonus status epilepticus?

A

Generalized, often symmetric, myoclonus that typically involves the axial, limb, and facial muscles; intermittent eye opening, upward gaze deviation, and swallowing problems

47
Q

What is Lance-Adams syndrome?

A

Chronic form of PHM, presents days to weeks after the initial insult once the patient has regained consciousness

48
Q

Characteristics of Lance-Adams syndrome?

A

Focal
Exacerbated by action
Negative myoclonus can also occur, leading patients to drop things or fall

49
Q

What should be obtained to distinguish between seizure and PHM?

A

EEG

50
Q

Management of acute and chronic PHM?

A

Antiepilpetics and supportive care

51
Q

DDx - myopathy

A
  1. Glucocorticoid-induced myopathy
  2. Polymyalgia rheumatic
  3. Inflammatory myopathies
  4. Statin-induced myopathy
  5. Hypothyroid myopathy
52
Q

Clinical features of glucocorticoid-induced myopathy?

A

Progressive proximal muscle weakness and atrophy WITHOUT PAIN or tenderness
Lower extremity muscles are more involved (lower before upper)

53
Q

Clinical features of polymyalgia rheumatica

A

Muscle PAIN AND STIFFNESS in the shoulder and pelvic girdle
NORMAL MUSCLE STRENGTH
Tenderness with decreased ROM at the shoulder, neck, and hip
Responds rapidly to glucocorticoids

54
Q

Clinical features of inflammatory myopathies?

A

Muscle pain, tenderness, and proximal muscle weakness

Skin rash and inflammatory arthritis may be present

55
Q

Clinical features of statin-induced myopathy?

A

Prominent muscle pain/tenderness with or without weakness

Rare rhabdomyolysis

56
Q

Clinical features of hypothyroid myopathy?

A

Muscle pain, cramps, and weakness involving the proximal muscles
Delayed tendon reflexes and myoedema
Ocasional rhabdomyolysis
Features of hypothyroidism

57
Q

Compare the ESR levels in the different types of myopathies.

A

Normal: glucocorticoid-induced, statin-induced, hypothyroid

Elevated: polymyalgia rheumatica, inflammatory

58
Q

Compare the CK levels in the different types of myopathies.

A

Normal: glucocorticoid, polymyalgia rheumatica

Elevated: inflammatory, statin-induced, hypothyroid

59
Q

What is the most frequent precipitant of GBS?

A

Campylobacter jejuni

Other precipitants include HSV, Mycoplasma, H. influenzae

60
Q

What is the most common cause of fatal sporadic encephalitis in the US?

A

Herpes encephalitis

61
Q

Presentation of herpes encephalitis?

A 
Acute onset (<1 week duration) of focal neurological findings (altered mentation, focal CN deficits, ataxia, hyperreflexia, focal seizures)
Fever (90% of patients)
Behavioral changes, including hypomania, Kluver-Bucy (hyperphagia, hypersexuality), amnesia
62
Q

CSF findings in HSV encephalitis?

A

Lymphocytic pleocytosis
Increased number of erythrocytes (hemorrhagic destruction of temporal lobes)
Elevated protein levels
Low glucose levels are generally not seen

63
Q

Brain imaging findings in HSV encephalitis?

A

Temporal lobe lesions (MRI preferred to CT)

64
Q

EEG findings in HSV encephalitis?

A

Focal findings (prominent intermittent high amplitude slow waves) occur in >70-80% of patients and can be used in some cases as corroborative evidence

65
Q

Dx HSV encephalitis?

A

PCR analysis of HSV DNA in CSF (highly sensitive and specific) -> gold standard

66
Q

Rx HSV encephalitis?

A

IV acyclovir

67
Q

Classic CSF findings in cryptococcal meningitis?

A

Elevated opening pressure
Low leukocytes with mononuclear predominance
Slightly elevated proteins
Low glucose levels

68
Q

Dx cryptococcal meningitis?

A

India ink preparation

69
Q

Classic CSF findings in bacterial meningitis?

A

Markedly increased PMNs and decreased glucose levels

70
Q

Clinical features of post-concussive syndrome?

A

Headache, confusion, amnesia, difficulty concentrating/multitasking, vertigo, mood alteration, sleep disturbance, anxiety

71
Q

What is the classic symptom triad of NPH?

A

Cognitive impairment
Urinary incontinence
Gait abnormalities

Other symptoms may include depressed affect (frontal lobe compression) and UMN signs in lower extremities

72
Q

Dx NPH?

A

Neuroimaging shows ventriculomegaly out of proportion to the sulci

Confirm with LP -> normal opening pressure and transient clinical improvement following high-volume CSF removal

73
Q

Rx NPH?

A

Ventriculoperitoneal shunt

74
Q

How might OTC cold medications provoke a warfarin-associated intracerebral hemorrhage?

A

Contain acetaminophen -> potentiates anticoagulant effect of warfarin

Decongestants contain phenylephrine -> may elevate BP

75
Q

Management of warfarin-associated intracerebral hemorrhage?

A

Reverse anticoagulation immediately to reduce the risk of death and permanent disability

Initial therapy -> IV vitamin K (sustained response, takes 12-24 hours to be effective by promoting clotting factor synthesis in the liver + Prothrombin complex concentrate (PCC) -> vitamin K-dependent clotting factors (eg, II, VII, IX, X) that rapidly reverse warfarin

76
Q

If PCC is not available for reversing warfarin, what can be given?

A

Fresh frozen plasma

77
Q

Why should LP be avoided in patients with acute intracerebral hemorrhage?

A

Risk of inducing herniation as a result of increased ICP

78
Q

When is protamine sulfate indicated?

A

When urgent reversal of heparin is needed

79
Q

Sources of foodborne botulism?

A 
Improperly canned foods
Aged seafood (eg, cured fish)
80
Q

Pathogenesis of foodborne botulism?

A

Toxin inhibits presynaptic ACh release at NMJ

81
Q

Presentation of foodborne botulism?

A

Prodrome: GI discomfort, dry mouth, sore throat

Acute onset within 36 hours of ingestion:

  • Bilateral cranial neuropathies -> blurred vision (due to fixed pupillary dilation), diplopia, facial weakness, dysarthria, dysphagia
  • Symmetric descending muscle weakness
  • Diaphragmatic weakness with respiratory failure
82
Q

Dx foodborne botulism?

A

Serum analysis for toxin

83
Q

Rx foodborne botulism?

A

Equine serum heptavalent botulinum antitoxin for adults and children >1 y/o

Supportive care

84
Q

Presentation of cholinergic toxicity caused by organophosphate poisoning?

A

Bradycardia, miosis, bronchospasm, vomiting, diarrhea

85
Q

Rx cholinergic toxicity? MOA?

A

Atropine and pralidoxime

Atropine blocks peripheral effects of ACh at muscarinic receptors

Pralidoxime aids in the reactivation fo AChE

86
Q

What is the edrophonium test used to diagnose?

A

MG (temporarily improves muscle weakness as a short-acting AChE inhibitor)

87
Q

Presentation of tick paralysis?

A

Paresthesias and fatigue followed by ascending muscle paralysis

88
Q

Rx GBS and MG crisis?

A

Plasmapheresis

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