Neurology Flashcards

1
Q

What is Bell palsy?

A

hemifacial weakness/paralysis of muscles innervates by CN VII due to swelling of the cranial nerve

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2
Q

What are the characteristics of Bell palsy?

A
  • the prognosis is very good; 80% of patients recover fully within weeks to months
  • cause is uncertain
  • possible viral etiology (herpes simplex) - immunologic and ischemic factors implicated as well
  • upper respiratory infection is a common preceding event
  • there is an acute onset of unilateral facial weakness/paralysis
  • both the upper and lower parts of the face are affected (differentiate quickly from stroke - can wrinkle forehead)
  • diagnosis is clinical, but consider Lyme disease in endemic areas (do not use steroids if Lyme is suspected)
  • consider EMG testing if paresis fails to resolve within 10 days
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3
Q

What is the tx fo Bell Palsy?

A
  • usually, none is required, as most cases resolve in 1 month
  • a short course of steroid therapy (prenisone) and acyclovir, if necessary
  • patient should wear an eye patch at night to prevent corneal abrasion
  • surgical decompression of CN VII is indicated if the paralysis progresses or if tests indicate deterioration
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4
Q

What is a cerebral aneurysm?

A

weak bulging spot on the wall of brain artery like thin balloon/weak spot of inner tube; usually there’s a genetic predisposition
-usually asymptomatic unless ruptured; when ruptured = sudden, severe, headache

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5
Q

How is a cerebral aneurysm classified?

A

by size and shape

  • small: diameter <15 mm
  • large: 15 -25 mm
  • giant: 25-50 mm
  • supergiant: >50 mm
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6
Q

What is a saccular (“berry”) aneurysm?

A

MC type; account for 80-90% and MC cause of SAH; occur at arterial bifurcations and branches of large arteries at the base of the brain (circle of Willis)

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7
Q

What is a fusiform?

A

dilation of the entire circumference of the vessel

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8
Q

What is a traumatic?

A

caused by a closed head injury or penetrating trauma to the brain

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9
Q

What is a mycotic?

A

infected emboli

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10
Q

What is a ruptured (AVM)?

A

causes bleeding into CSF in subarachnoid space - ruptured berry account for 75% - mortality rate 50%

  • r/f: smoking, hypertension, hypercholesterolemia, heavy alcohol use; associated with polycystic kidney and coarctation of the aorta
  • s/sx: sudden onset unusually severe worst headache of life, n/v, seziure, altered state consciousness; increased bp, fever 102F
  • herald bleed: less severe headhace
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11
Q

How is a cerebral aneurysm dx?

A

found incidentally or when a patient presents with subarachnoid hemorrhage; non-contrast head CT for investigational

  • LP has elevated opening pressure, bloody fluid (xanthochromia, RBC)
  • cerebral angiography = gold standar
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12
Q

What is the tx for a cerebral aneurysm?

A

surgical clipping, endovascular coiling within first 24 hours; restore respiration

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13
Q

What is cerebral vascular accident?

A

there are two main types of cerebrovascular accident or stroke: An ischemic stroke is caused by a blockage; a hemorrhagic stroke is caused by a blockage; a hemorrhagic stroke is caused by a rupture of a blood vessel

  • acute onset of focal neurologic deficits resulting from - diminished blood flow (ischemic stroke) or hemorrhage (hemorrhagic stroke)
  • contralateral paralysis, motor function
  • right-sided symptoms = left side stroke
  • left-sided symptoms = right-side stroke
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14
Q

What is carotid/ophthalmic?

A

amaurosis fugal (monocular bling)

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15
Q

What is MCA?

A

aphasia, neglect, hemiparesis, gaze preference, homonymous hemianopsia

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16
Q

What is ACA?

A

leg paresis, hemiplegia, urinary incontinence

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17
Q

What is PCA?

A

homonymous hemianopsia

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18
Q

What is basilar artery?

A

coma, cranial nerve palsies, apnea, drop attach, vertigo

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19
Q

What is lacunar infarcts?

A

occur in areas supplied by small perforating vessels and result from atherosclerosis, hypertension, and diabetes: silent, pure motor or sensory stroke, “Dysarthria-Clumsy hand syndrome”, ataxic hemiparesis

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20
Q

How is cerebral vascular accident dx?

A

CT without contrast for acute presentation - important to diagnose as ischemic or hemorrhagic

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21
Q

What is the tx for cerebral vascular accident?

A

for occlusive disease treat with IV tPA if within 3-4.5 hours of symptom onset

  • can consider intra-arterial thrombolysis in select patients (major MCA occlusion) up to 6 hours after onset of symptoms
  • for embolic disease and hyper coagulable states give warfarin/aspirin once the hemorrhagic stroke has been ruled out
  • endarterectomy if carotid >70% occluded
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22
Q

What is a cluster headache?

A

unilateral, excruciating, sharp, searing, or piercing pain (often at nigh), lacrimation, and nasal congestion
-males > females

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23
Q

How do you tx cluster headache?

A

treat with oxygen 100% at 6-12 L/min for 15 minutes via nonrebreathing mask provides relief within 15 minutes and Imitrex

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24
Q

What is a coma?

A

a deep state of prolonged unconsciousness in which a person cannot be awakened
-fails to respond to normally to painful stimuli, light or sound; lacks a normal wake-sleep cycle; and does not initiate voluntary actions

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25
Q

What is the Glasgow Coma Scale/

A

score of < 9 = coma

  • score 13-15 may indicate mild dysfunction, although 15 is the score a person with no neurologic disabilities would receive
  • score 9 -12 may indicate moderate dysfunction
  • score 8 or less in severe dysfunction
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26
Q

What is complex regional pain syndrome?

A

idiopathic - a pain syndrome disproportionate to injury with continuing pain that is disproportionate to any inciting event

  • non-dermatomal limb pain
  • pain disproportionate to the injury
  • following trauma, injury
  • extremity pain and at least 1 other sensory, motor, vasomotor, edema, sudomotor symptom
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27
Q

How is complex regional pain syndrome dx?

A

Budapest consensus criteria for clinical diagnosis of continuing pain disproportionate to inciting event

  • At least 1 sx in 3 or 4 categories:
  • sensory: hyperalgesis and/or allodynia = evidence of hyperalgesia to pinprick/allodynia to light touch/temperature
  • vasomotor: skin, temperature, color aysmmetry = temperature asymmetric > 1C and/or skin color changes
  • sudomotor/edema: edema, sweating changes, sweating asymmetry = edema and/or sweating changes/asymmetry
  • motor/trophic: decreases ROM or motor dysfunction and/or trophic changes (hair, anil/skin) = weakness, tremor, dystonia
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28
Q

What is the tx of complex regional pain syndrome?

A
  • Stage 1: neuroontin, elavil, and bisphosphonates
  • Stage 2: add steroids
  • Stage 3: include pain management specialist = regional nerve block/spinal cord stimulators
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29
Q

What is a concussion?

A

a mild traumatic brain injury (TBI) due to contact or acceleration/deceleration injury

  • a concussion results in an altered mental state that may include becoming unconscious
  • concussions are characterized by a Glasgow Coma Score of 13-15 thirty minutes after injury
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30
Q

What is a Grade 1 concussion?

A

No LOC, post-traumatic amnesia and other symptoms resolve in < 30 minutes
-athlete may return to sports if asymptomatic for one week

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31
Q

What is a Grade 2 concussion?

A

+ LOC, 1 minute or post-traumatic amnesia and other symptoms last > 30 minutes but < 1 week
-athlete may return to sports in 2 weeks if asymptomatic at rest and exertion for at least 7 days

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32
Q

What is a Grade 3 concussion?

A

+ LOC > 1 minute or post-traumatic amnesia and other symptoms last > 1 week
-athlete may return to sports in 1 month if asymptomatic at rest and exertion for 7 days

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33
Q

How is a concussion dx?

A

Clinical evaluation and sometimes and sometimes neuroimaging to exclude more serious injuries

  • athletes with a possible concussion should be removed from play and evaluated; screening tools such as SCAT2 Standardized Assessment of Concussion may be helpful
  • neuroimaging is done if there is loss of consciousness, GCS < 15, focal neurologic deficit, persistently altered mental status, or clinical deterioration
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34
Q

What is the tx of a concussion?

A

there’s no specific cure for concussion = rest and restricting activities allow the brain to recover

  • patients should be instructed to temporarily reduce sports, video games, TV, or too much socializing
  • medications for headache pain, or ondansetron or other anti-nausea medications can be used for symptoms
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35
Q

How should athletic activies be resumed after a concussion?

A

gradually: after a concussion patients are more susceptible to repeat concussion for a period of time and must refrain from sports activities until they have been asymptomatic for 1 week or more (depending on the severity of injury)
- single concussion: if + LOC or symptoms of concussion lasting more than 15 minutes NOT to return to play sports until asymptomatic for at least one week
- Repeat concussions: if associated with either loss of consciousness or symptoms for more than 15 minutes NOT to return to play sports for that season

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36
Q

What is delirium?

A

an acute cognitive dysfunction secondary to some underlying medical condition and is usually reversible

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37
Q

What are the characteristics of delirium?

A
  • acute and rapid deterioration in mental status (hours-day), a fluctuating level of awareness, disorientation
  • visual hallucinations are the most common type experiences by patients with delirium
  • high-risk after surgery especially in those with heart disease or diabetes
  • delirium, unlike dementia,, is usually reversible
  • fall precautions - patients with delirium are six more times likely to fall
  • delirium is the mot common presentation of altered mental status in the inpatient setting
  • alcohol abuse is the most common cause of delirium, specifically, delirium tremens
  • delirium is a side effect of acute hyperthyroidism known as thyroid storm
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38
Q

What are the underlying organic causes of delirium?

A

UTI, pneumonia, metabolic changes, CVA, MI, TBI, medications (anticholinergics, benzodiazepines, opioids)

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39
Q

How is delirium dx?

A
  • mental status examination (MMSE)
  • labs (chemistry, B12/folate)
  • LP in a febrile, delirious patient (cerebral edema)
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40
Q

What is the tx for delirium?

A

treat the cause of delirium (almost always reversible) and provide supportive care, including sedation when necessary
-haloperidol for agitation/psychosis supportive

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41
Q

What is delirium vs neurocognitive disorders (dementia)?

A

delirium is an acute, usually reversible syndrome caused by a medical condition versus neurocognitive disorder which is a long-term impaired memory disease process that is usually irreversible such as Alzheimer’s disease

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42
Q

What are neuroconitive disorders?

A

(previously known as dementia) are described as those with a significant (major) or moderate (mild) impairment of cognition or memory that represents a marked deterioration from a pervious level of function

  • Increasing age
  • Insidious onset, progressive
  • preserved consciousness, rarely hallucinations present
  • no tremor unless due to Parkinson disease
  • typically irreversible
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43
Q

What are the characteristics of Alzheimer Disease (most common type)?

A
  • progressive cognitive decline; most common older than age 65 years
  • loss of brain cells, beta-amyloid plaques, and neurofibrillary tangles
  • physical exam: abnormal clock drawing test
  • Treatment: anti cholinesterase drugs (tacrine, donepezil)
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44
Q

What are the characteristics of Vascular Disease (second most common type)?

A
  • associated with arteriolosclerotic small vessel disease
  • multi-infarct, usually correlated with a cerebrovascular event and/or cerebrovascular disease
  • stepwise deterioration with periods of clinical plateaus
  • may cause a sudden decline
  • treatment: blood pressure control
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45
Q

What are the characteristics of frontotemproal lobar degeneration?

A
  • language difficulties, personality changes, and behavioral disturbances
  • personality changes precede memory changes
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46
Q

What are the characteristics of Lewy Body Disease?

A
  • parkinsonian symptoms
  • gradual, progressive decline in cognitive abilities
  • hallucinations and delusions, gait difficulties, and falls
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47
Q

What are the characteristics of Substance/medication use of dementia?

A

related to medication or non-prescription drug use

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48
Q

What is HIV infection dementia?

A
  • cognitive decline associated with HIV infection
  • substantial memory deficits, impaired executive functioning, poor attention and concentration, mental slowing, and apathy
  • cerebral atrophy is typically evident or brain imaging
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49
Q

What is encephalitis?

A

an acute inflammation of the brain; the infection may be bacterial or viral
-In some cases, encephalitis may be the result of an immune system disorder

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50
Q

What is the etiology encephaltiis?

A
  • usually viral
  • most common species: HSV
  • Immunocompromised: CMV
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51
Q

What are the symptoms of encephalitis?

A
  • fever, headaches, altered mental status, seizures, personality changes, exanthema
  • may present similar to meningitis but will see altered mental status, seizures, personality changes, exanthema
  • encephalitis is clinically differentiated from meningitis by altered brain functioning
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52
Q

How is encephalitis dx?

A
  • dx with lumbar puncture and MRI

- PCR for viruses

53
Q

What is the tx of encephalitis?

A

symptomatic

  • treat supportively + acyclovir until HSV and Zoster are ruled out, empiric antibiotics are often given until bacterial meningitis is excluded
  • HSV - acyclovir
54
Q

What is an essential tremor?

A

population: family history, autosomal dominant, elderly patients
- Intention/action tremor - hands and head
- shaking occurs with simple tasks such as tying shoelaces, handwriting, shaving or simply holding hands against gravity
- symptoms may be aggravated by stress, fatigue, caffeine, and temperature extremes
- better with alcohol

55
Q

What is the tx for essential tremor?

A

propranolol (first line) reduces limb tremor magnitude by ~50%

  • primidone, alprazolam, small amounts of alcohol, gabapentin, topiramate, or nimodipine
  • drug resistance cases - deep brain stimulation
56
Q

What is giant cell arteritis?

A

or temporal arteritis, is an inflammatory disease affecting the large blood vessels of the scalp, neck, and arms

  • Idiopathic +/- autoimmune viral infection = monocyte activation and inflammatory cytokines production, inflammation and tissue destruction
  • headache and jaw claudication with chewing
  • acute vision disturbances - amaurosis fugax (temporary monocular blindness) secondary to anterior ischemic optic neuritis
  • thickened temporal artery = scalp pain elicited by touching the scalp or combing the hair; aortic aneurysm
  • MC women > 50 y/o; associated with polymyalgia rheumatic
57
Q

How is giant cell arteritis dx?

A

diagnosed with temporal artery biopsy

-ESR > 100

58
Q

What is the tx for giant cell arteritis?

A

treat with high dose prednisone - do urgently to prevent blindness (do not wait for biopsy results)

  • 40-60 mg/day for 4 weeks then taper slowly and maintain 1-2 years
  • complications = blindness
59
Q

What is Guillain-Barre syndrome?

A

ascending paralysis beginning in distal limbs: leg weakness = total paralysis of all 4 limbs, facial muscles, eyes, loss of reflexes

  • often present after immunization
  • post-infectious cause: campylobacter jejuni = MC, CMV, Epstein-Barr, HIV
60
Q

How is Guillain-Barre syndrome dx?

A

based on lumbar puncture = elevated CSF protein with normal CSF WBC

61
Q

What is the tx for Guillain-Barre syndrome?

A

plasma exchange (remove circulating antibodies) and IVIG

  • monitor PFTs for paralysis of chest muscle/diaphragm
  • good prognosis
62
Q

What is Huntington Disease?

A

autosomal dominant, incurable neurodegenerative DZ = progressive motor/psychiatric dysfunction, dementia, chorea
-population: usually occurs between 30-50 yo, family history (autosomal dominant inheritance)

63
Q

What is the presentation of Huntington Disease?

A
  • dementia, mutism, dysphagia

- chorea = nonrepeating, complex, involuntary rhythmic movements that may appear purposeful

64
Q

How is Huntington Disease dx?

A

clinical symptoms, MRI, family history, genetic testing

  • genetic testing = 40+ CAG repeats
  • MRI = cerebral atrophy and atrophy of the caudate nucleus
65
Q

What is the tx for Huntington Disease?

A

currently incurable, may treat chorea with risperidone, haloperidol, all get speech therapy and eventually nursing care

  • tetrabenazine depletes dopamine = first drug to specifically treat chorea; neuroleptics also help
  • life expectancy 15-25 years symptom onset; high-risk suicide
66
Q

What is intracranial tumors?

A

a cancerous or noncancerous mass or growth of abnormal cells in the brain

  • 1/3 are glial cell origin, 1/3 meningioma, other: vestibular schwannoma, pituitary adenoma, neurofibroma, CNS lymphoma
  • most glial = malignant
  • astrocytoma: grade 4: glioblastoma = MC with poor prognosis
  • ependymoma: occurs in ependymal cells that line the ventricles/spinal canal
  • medulloblastoma: MC primary malignant in children (long term survival with tx = 70%)
  • MC source of intracranial metastasis = lung, breast, kidney, GI tract
67
Q

How are intracranial tumors dx?

A

Head CT or MRI with contrast medium may detect the lesion, define its location and size, evaluate the extent to which the normal anatomy is distorted, and the degree of any associated cerebral edema or mass effect

  • arteriography may demonstrate stretching or displacement of normal cerebral vessels as weel as the presence of tumor vascularity
  • EEG may demonstrate a focal disturbance resulting from the neoplasm or a more diffuse change reflecting altered mental status
68
Q

How are intracranial tumors tx?

A

complete superficial removal of tumor with radiation/chemotherapy
-steroids to help reduce cerebral edema, anticonvulsants

69
Q

What is meningitis?

A

an inflammation of the membranes (meninges) surrounding the brain and spinal cord

  • the swelling from meningitis typically triggers the classic triad of headache, fever, and a stiff neck (nuchal rigidity)
  • most cases of meningitis in the Untied States are caused by a viral infection, but bacterial, parasitic and fungal infections are other causes
  • unlike encephalitis no mental status changes
  • N. meningitides (most likely if pt. has a rash) = petechiae
70
Q

What is the physical exam of meningitis?

A
  • Kernig sign - knee extension causes pain in the neck

- Brudzinski sign - leg raise when bend neck

71
Q

What are the bacterial etiologies of meningitis?

A
  • Neonate: E.coli (gram-negative rods) and S.agalactiae (group B streptococcus)
  • most people: S. pneumonia (gram-positive diplococci), N. meningitides (gram-negative diplococci)
  • Immunocompromised: cryptococcus neoformans (diagnosis: india ink stain)
72
Q

What are the viral etiologies of meningitis?

A
  • most cases in the United Sates are caused by a group of viruses known as enteroviruses, which are most common in late summer and early fall
  • viruses such as herpes simplex virus, HIV, mumps, West Nile virus and other also cause viral meningitis
73
Q

What is the fungal etiology of meningitis?

A

cryptococcal meningitis is a common fungal form of the disease that affects people with immune deficiencies, such as AIDS

74
Q

How is meningitis dx?

A

spinal tap: increased opening pressure, decreased glucose, increased WBC (neutrophils), increased protein

75
Q

What are the CSF finding on lumbar puncture for meningitis?

A
  • bacterial: increased protein, decreased glucose (bacteria love to eat glucose)
  • viral: no specific characteristics but may have lymphocytes

make sure the patient does to have increased intracranial pressure prior to LP check fro papilledema, get a CT scan if you are unsure if there is swelling in the brain (risks include age > 60, immunocompromised, AMS, focal near finding or papilledema)

76
Q

What is the tx for meningitis?

A

Dexamethasone + Empiric IV antibiotics (Cephalosporin, Vancomycin, Penicillins)
-household contacts: treat with rifampin, cipro, Levaquin, azithromycin, ceftriaxone

77
Q

What is Aseptic meningitis?

A
  • etiology: enterovirus, HSV, TB, fungus
  • spinal tap - normal pressure, increased WBC (lymphocytes)
  • treatment: symptomatic or IV acyclovir for HSV
78
Q

What are migraine headaches?

A

a headahce of varying intesnity, often unilateral, and accompanied by nausea and sensitivity to light and sound

  • teens, female > male
  • pulsating, duration of 4-72 hours, unilateral, nausea, disabling, associated with photophobia and phnophobia
  • without aura = most common, N/V, photophobia, phonophobia
  • aura: scotoma, flashing lights, sound
  • HA follows aura w/in 30 min; visual = MC
79
Q

How are migraine headaches dx?

A

clinical

80
Q

What is the tx for migraine headaches?

A
  • abortive: triptans (do not use in ischemic heart disease), ergotamine (do not use in pregnant women)
  • prophylaxis: atenolol, propranolol, verapamil, or TCAs
81
Q

What is multiple sclerosis?

A

a disease in which the immune system eats away at the protective covering of nerves (myelin sheath)

82
Q

What are the characteristics of multiple sclerosis?

A
  • autoinflammatory disease = demyelination, neuronal loss, scarring of white matter in the brain and spinal cord
  • destruction of myelinated axons in the central nervous system
  • usually present with visual disturbances often over many years
  • MC problems: sensory loss, optic neuritis, weakness, paresthesias
  • Lhermitte’s sign: electrical shock sensation in limbs/torso brought on by flexion of the neck
  • Relapsing-remitting = MC type (85%) - episodic flare-ups over days/weeks between periods of neurologic stability; during attacks: new sx present and existing ones worsen; complete recovery/residual deficits may ensue following each out
83
Q

What is relapsing-remitting MS?

A

most common (85%) symptoms come and go - episodic flare-ups occurring over days to weeks between periods of neurologic stability

84
Q

What is secondary progressive MS?

A

(replapsing-remitting progresses to steady decline)

85
Q

What is primary progressive MS?

A

(no remission, steady decline from onset)

86
Q

What is progressive relapsing MS?

A

(combination, worse overtime with acute relapses. most rare

87
Q

How is multiple sclerosis dx?

A

MRI looking for plaques = Dawson fingers (white matter lesions)

  • diagnostic criteria:
  • two episodes/attacks of sx
  • two different areas of CNS involved
  • CSF: elevated IgG, oligocloncal bands
88
Q

How is multiple sclerosis tx?

A

steroids (for acute attacks), interferon betas (Avonex) - prevent relapses
-PT, symptomatic treatment for fatigue, urge incontinence, muscle spasm

89
Q

What is Myasthenia gravis?

A

autoimmune attack of acetylcholine receptors at the neuromuscular junction that results in motor problems

90
Q

What is the classical clinical presentation of myasthenia gravis?

A

a patient with (eye symptoms) ptosis, diplopia, and muscle weakness that worsens with use

  • the hallmark of myasthenia gravis is fatigability = weakness in everyday activities like brushing hair
  • It manifests as ptosis and diplopia; improves with rest
  • It is associated with thyme hyperplasia and thymoma
  • young women, older men
91
Q

How is myasthenia gravis dx?

A
  • acetylcholine receptor antibodies
  • Tennsilon test (edrophonium test) - short-actign anticholinesterase)
  • CT of the chest:
  • thymomas affect about 10-20% of patients with myasthenia gravis, patients diagnosed with myasthenia gravis should, therefore, have thymoma rules out via
92
Q

What is the Tensilon test?

A

uses the drug Tensilon (edrophonium) to diagnose myasthenia gravis

  • tensilon prevents the breaking down of the chemical acteylcholine, which then helps stimulate the muscles
  • a person tests positive for myasthenia gravis if their muscles get stronger after being injected with Tensilon
93
Q

What is the tx for myasthenia gravis?

A
  • acetylcholinesterase inhibitor (pyridostigmine/neostigmine) = first line = stops breakdown of acetylcholine
  • Immunosuppressive drugs (prednisone) = reduce the production of autoantibodies
  • thymectomy = reduces muscle weakness
  • myasthenic crisis: neuromuscular respiratory failure from dysphagia/aspiration (treat with plasma exchange, IVIG)
94
Q

What is Parkinson disease?

A

caused by degeneration of basal gangli in the substantial nigra leading to loss of dopamine-containing neurons located in the substantial nigra and locu coerules

  • age onset after 50 y/o
  • meds that cause parkinsonism: neuroleptics (chlorpromazine, metoclopramide, reserpine)
  • lewy bodies
  • acetylcholine/dopamine imbalance
95
Q

What are the cardinal features of Parkinson disease?

A

rest (pill-rolling) tremor, cogwheel rigidity and bradykinesia (slowness of movement)
-other clinical features: mask facies, loss of postural reflexes, decreased blink rate, shuffling gait, hypophonia, micrographia, gait arrest, and backward falling

96
Q

How is Parkinson disease dx?

A

based on the clinical impression

  • the gold standard for diagnosis is neuropathologic exam
  • MRI may be useful in evaluating the possibility of cerebrovascular disease, tumor, or multiple system atrophy as potential causes
97
Q

What is the tx of Parkinson disease?

A

Treatment is with dopamine agonists

  • < 65 dopamine agonists: bromocriptine, pramipexole, ropinirole
  • directly stimulates dopamine receptors, fewer side effects than Levodopa, used in younger patients to delay the use of Levodopa
  • > 65 Sinemet (levodopa/carbidopa)
  • common side effects of L-dopa: gastrointestinal upset with nauses and vomiting, vivid dreams of nightmares, psychosis, and dryskinesias
98
Q

What is the presentation of peripheral neuropathies?

A

symmetrical, stocking and glove distribution, postural hypotension

99
Q

What is the tx of peripheral neuropathies?

A

gabapentin, amitriptyline, topiramate, tramadol, and NSAIDs

-glycemic control

100
Q

What is a complication of peripheral neuropathies?

A

Charcot’s joints

101
Q

What are the characteristics of focal seziures with retained awareness (consciousness maintained)?

A
  • this type of focal seizure was previously known as a simple partial seizure
  • no alteration in consciousness, abnormal movements or sensations
102
Q

What are the characteristics of focal seziures with a loss of awareness (consciousness impaired)?

A
  • this type of focal seizure may also be called a focal dyscognitive seizure (previously known as a complex partial seizures)
  • altered consciousness, automatisms (ie. lip-smacking)
  • present with a poetical state (confusion and loss of memory) which differentiate them from absence seizures
103
Q

What is the tx for focal seziures?

A

phenytoin and carbamazepine are drugs of choice

104
Q

What are generalized seizures?

A

occur when there is widespread seizure activity in the left and right hemispheres of the brain
-start midbrain or brainstem and spreads to both cortices

105
Q

What are the characteristics of absence seizures (formerly known as petit mal)?

A

characterized by a brief impairment of consciousness with an abrupt beginning and ending
-at times involuntary movements may occur, but they are uncommon and the patient has no recollection and witnesses commonly miss them

106
Q

What are the characteristics of tonic-clonic or convulsive seizures (formerly known as grand mal)?

A
  • bilaterally symmetric and without focal onset
  • begins with a sudden loss of consciousness - a fall to the ground
  • tonic phase: very stiff and rigid 10-60 seconds
  • clonic phase: generalized convulsions and limb jerking
  • postictal phase: a confused state
107
Q

What are the characteristics of atonic seizures (also known as drop attacks)?

A

looks like syncope, sudden loss of muscle tone

108
Q

What are clonic seizures?

A

during a clonic seizure, a person may lose control of bodily functions and begin jerking in various parts of the body
-he/she may temporarily lose consciousness, followed by confusion

109
Q

What are tonic seizures?

A

extreme rigidity then immediate LOC, but not followed by a clonic phase

110
Q

What are myoclonic seizures?

A

muscle jerking, but not the tonic phase, occurs int he morning

111
Q

What are febrile seizure?

A

convulsion associated with an elevated temperature greater than 38 > 6 mos < 5 years, absence of central nervous system infection or inflammation

112
Q

What are infantile spasms?

A

infantile spasms are a type of epilepsy seizure but they do not fit into the category of focal or generalized seizures

113
Q

What is psychogenic non-epileptic seizures (PNES)?

A

are not due to epilepsy but may look very similar to an epilepsy seizure

114
Q

What is status epilepticus?

A

a single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without the person returning to normal between then

  • two forms: convulsive and nonconvulsive
  • convulsive status epilepticus presents with a regular pattern of contraction and extension of the arms and legs
  • nonconvulsive status epilepticus includes complex partial status epilepticus and absence status epilepticus
115
Q

What is the tx for status epilepticus?

A

benzodiazepines (lorazepam) are the preferred initial treatment after which typically phenytoin is given

116
Q

What is syncope?

A

refers to a transient loss of consciousness/postural tone secondary to an acute decrease in cerebral blood flow

117
Q

How is syncope characterized?

A

by a rapid recovery of consciousness without resuscitation

118
Q

What is cardiac syncope?

A

arrhythmias (eg AV block, sick sinus syndrome), obstruction of blood flow (eg aortic stenosis, hypertrophic cardiomyopathy), massive MI

119
Q

What is vasovagal syncope?

A

(neurocardiogenic) most common cause

120
Q

What is orthostatic hypotension?

A

defect in vasomotor reflexes, common in elderly, diabetics, patients taking certain medications (e.g diuretics, vasodilators)

121
Q

What is cerebral vascular disease?

A

a rare cause of syncope

122
Q

What are the other noncardiogenic causes of syncope?

A

metabolic causes (eg hypoglycemia, hyperventilation), hypovolemia (hemorrhage), hypersensitivity (syncope precipitated by wearing a tight collar or turning the head), mechanical reductio of venous return (e.g Valsalva maneuver, postmicturition) and various medications (beta-blockers, nitrates, anti arrhythmic agents)

123
Q

What is a tension headache?

A

a tension-type headache is typically described as bilateral, mild to moderate, dull pain

124
Q

What is the presentation of a tension headache?

A

bilateral, squeezing, sensation, mild to moderate, dull pain
-whereas a migraine is typically pulsating; unilateral; and associated with nausea, vomiting, and photophobia or phonophobia

125
Q

What is a transient ischemic attack?

A

a transient episode of neurologic dysfunction due to focal brain, retinal, or spinal cord ischemia without acute infarction

  • blockage in blood flow does not last long enough to cause permanent infarction
  • sudden onset of neurologic deficit, lasting minutes to <1 h (15 - 30 min on average), a reversal of symptoms within 24 h
126
Q

What are the clinical manifestations of a transient ischemic attack?

A
  • internal carotid artery: Amaurosis Fugax (monocular vision loss - temporary “lampshade down on one eye”) weakness in the contralateral hand
  • ICA/MCA/ACA: cerebral hemisphere dysfunction, sudden headache, speech changes, confusion
  • PCA: somatosensory deficit
  • Vertebrobasilar: brainsteam/cerebral symptoms (gait and proprioception)
127
Q

How is a transient ischemic attack dx?

A

by CT (without contrast), MRI more sensitive, carotid doppler ultrasound to look for stenosis, CT angiography, MR angiography of the neck

  • carotid endarterectomy if internal or common carotid artery stenosis is > 70%
  • aspirin within 24 hours, anti platelet therapy (e.g aspirin or clopidogrel or aspirin-dipyridamole) should be then initiated
128
Q

What is the tx of a transient ischemic attack?

A
  • hospital admission for new-onset and recurrent TIA, unless a confident diagnosis of the cause of the event can be made
  • antiplatelet therapy: aspirin +/- dipyridamole OR clopidogrel
  • note: if high risk - warfarin should be used
  • average 5% risk of recurrence per year