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Neurology Flashcards

1
Q

What is Bells palsy? Symptoms? tx?

A

Unilateral facial weakness with no evidence of other neurological dz. Involves CN VII (facial nerve)

Sxs: Paralysis of the forehead and lower face; cannot close eye, raise brow, or smile on the affected side

Pain on the ipsilateral ear; Loss of taste of the anterior 2/3 of the tongue

tx: oral prednisone

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2
Q

How does Guillian barre syndrome present? RF?

A

idiopathic polyneuropathy following minor infections, immunizations, and surgical procedures

Sxs: Symmetrical weakeness that begins distally; may have some sensory abnormalities; May begin with ataxia, pin and needles sensation in the feet

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3
Q

What reduces recovery time and neurological deficits in Guillian barre syndrome?

A

Plasmapheresis

Acute crisis: IV immunoglobulin

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4
Q

What is the pathophysiology of myasthenia Gravis?

A

Acquired autoimmune disorder that causes a decrease in Acetylcholine receptors

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5
Q

What are the s/s of Myasthenia gravis?

A
  • Sxs: muscle weakness and fatigability that improves with rest (trouble combing hair, climbing stairs, or lifting objects
  • Early stages: Affects eye muscles–>Ptosis and diplopia
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6
Q

How do you dx Myasthenia Gravis?

A
  • Tensilon Test: confirmed if marked clnical improvment with short-acting anticholinesterase
    • IV edrophonium or IM neostigmine results in improved strength within seconds to minutes
  • Check for elevated levels of circulating ach receptor antibodies (80-90%)
  • Do not forget CXR to r/o Thymoma!!
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7
Q

How do you treat Myasthenia gravis? what medication should be avoided?

A

Cholinesterase Inhibitor (Pyridostigmine)–improves strength

IgG plasmapharesis

Steroids, immunosuppressive drugs, IV immunoglobulins, –if refractory disease

Thymectomy if needed!

Aminoglycosides should be avoided!!

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8
Q

What is Lambert-Eaton Syndrome? Sxs? Tx?

A
  • Similar to Myasthenia Gravis, but associated with lung cancer (Small cell carcinoma) AND IMPROVES WITH ACTIVITY!
  • PROXIMAL muscle weakness
  • Defective release of ach in response to nerve impulse
  • may have dry mouth

Confirmed electrophysiologically

Tx: Plasmapheresis and immunosuppressive therapy

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9
Q

HOw do you treat Cluster headaches?

A

Prevention: Oral corticosteroids started immediately will often force a cluster cycle into remission and prevent future HA

Abortive Tx:

  • 100% oxygen
  • Ergotamine tartate (dihydroergotamine) and Sumatriptan
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10
Q

What is the most common viral cause of encephalitis?

A

Herpes simplex

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11
Q

HOw do you dx viral encephalitis/Meningitis?

A
  • Assess increased intracranial pressure first
  • LP and CSF analysis ASAP
    • Increased lymphocytes or monocytes
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12
Q

What are the S/S of bacterial meningits?

A

Rapidly progressive, can be fatal

Acute sxs of fever, HA, vomiting, stiff neck, Petechial rash (N. meningitidis)

PE: + kernig, + Bruzenski’s signs

CN abnormalities III, IV, VI, and VII

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13
Q

How do you diagnose Bacterial meningitis?

A
  • Dx: first CT
  • LP with CSF
  • May be turbid/purulent, elevated WBC (neutrophil predominant), decrased glucose, high protein
  • Gram stain/culture of CSF
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14
Q

Treatment of bacterial meningitis; What is the prophylaxis for close contacts?

A
  • Begin antibiotics immediately if CSF not clear and colorless
  • Vanocomycin plus ceftriaxone
  • neonates: Ampicillin pluse Cefotaxime
  • Immunocompromised/>50 y/o: Cefotaxime PLUS vancomycin PLUS Ampicillin
  • Hospital acquired: Ampicillin PLUS ceftazidime PLUS vancomycin

Prophlyaxis for close contacts: oral Rifampin

RPT LP and CSF after 24 hours of tx

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15
Q

What is Huntington Disease? what are the sxs?

A

Inherited autosomal dominant disorder (Chromosome 4)

  • Sxs: Presents with insidious onset of clumsiness and random, brief fidgety movements; behavioral changes (irritability, emotional liability) progressing to dementia
  • Choreic movements: worse with voluntary movement, dissapears with sleep
  • Choreiform movements: irregular gait and dance-like movements
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16
Q

When is the onset of Huntington disease? How is it treated?

A

Onset: 30-50 y/o

No cure or medical interventions (just symptomatic tx)

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17
Q

What is the pathophys of Parkinson disease? What is the clinical presentation?

A

Loss of dopaminergic neurons in the substantia nigra–>Imbalance of dopamine and acetylcholine

Clinical presentation:
Hallmark: resting tremor (“pill rolling”)
bradykinesia: slowing of movements; lack of facial expression (masked fascies), monotone speech
slow shuffling gait
Cogwheel rigidity

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18
Q

How do you treat Parkinson disease?

A
  • Anticholinergic drugs: more helpful with tremor and rigidity
    • Amantadine
  • Levodopa: converted to dopamine in the body
    • improves all s/s
    • Add carbidopa-Stops breakdown of Levodopa
  • If refractory to Levodopa therapy–>Dopamine agonist
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19
Q

What is the most common cause of nontraumatic subarachnoid hemorrhage?

A

Ruptured berry aneurysm

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20
Q

What is the initial diagnostic study for subarachonid hemorrhage? definitive dx?

A

Initial: CT scan

Definitive dx: Cerebral angiography: identifies source of the bleed

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21
Q

What is the definition of epidural hematoma? what artery is involved?

A

Defn: Accumulation of blood in the potential space btwn the dura and bone; usually results from a temporal bone fracture

Middle meningeal artery

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22
Q

What is the clnical presentation of Epidural hematoma? Dx? Tx?

A

Caused by head injury or skul fracture

Brief period of unconsciousness follwed by a lucid interval

PE: spinal fluid rhinorrhea; Dizziness; Enlarged pupil in one eye; HA, vomiting

DX: CT shows hyperdense lenticular-shaped

Tx: emergent craniotomy

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23
Q

What is the definition of subdural hematoma?

A

Accumulation of blood below the inner layer of the dura; Involves **bridging veins; **

Present more than 20 days after the trauma

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24
Q

What is the clinical presentation of Subdural hematoma? how is it dx? tx?

A

Sign and symptoms develop later; Confusion, hemiparesis, HA, seizures, visual disturbances

dx:CT scan: Crescent shaped clot

Tx: Burr holes

25
Q

What is Cerebral palsy

A

Disorder of movement and posture

Impairement of muscle tone, strength, coordination, and movement that results from insult to or anomaly of the immature central nervous system (during prenatal period)

NOT progressive

Commonly associated with seizures

26
Q

define Apraxia

A

Impaired ability to carry out motor activities despite intact motor function

27
Q

define Agnosia

A

Failure to recognize or identify objects despite sensory function

28
Q

What is the pathophys of Alzheimers? What is seen microscopically?

A

Unknown etiology but a protein called beta-amyloid deposits in neuritic plaques and aterial walls damages brain cells

MIcroscopically: Progressive loss of cortical neurons; Formation of amyloid plaques and intraneuronal neurofibrillary tangles

29
Q

HOw does the clinical presentation of vascular dementia differ from Alzheimers?

A

Vascular dementia involves Forgetfullness in the absence of depression and innattentiveness

30
Q

WHat is Frontotemporal dementa?

A

Formally called Picks diseaes

Presents as progressive change in personality or social behavior, progressive aphasia, limb apraxia

31
Q

Lewy body symptoms, How do you treat Lewy body dementia?

A

Sxs: fluctuating cognitive impairment, visual hallucinations, REM sleep disorder, Parkinsonism

Tx:

Acetylcholinesterase Inhibitors: Psychological function

Levodopa: motor function

32
Q

What is Creutzfield-Jakob disease? sxs? Dx?

A

caused by spontaneous transformation of normal prion proteins into abnormal proteins

Sxs: Initially flu like sxs, fatigue, cognitive impairment

Rapid cognitive dysfunction, pyramidal tract signs (weakness), cerebellar signs (clumsiness), myoclonic jerks

Labs: 14-3-3 protein in CSF

Histology: spongiosis and neuronal loss

Rapid onset and deterioration (weeks to months)

33
Q

What is Multiple sclerosis? Who does it affect? cliical presentation?

A
  • Chronic autoimmune demyelinating disease of the CNS
  • F>M, 18-45 y/o
  • Relapsing and remitting sxs of weakness, numbness, tingling, spastic paraparesis, neuritis, diplopia, urinary sphincter dysfunction, ataxia
    • sxs may last a few weeks and disapear
  • Upper Ext> lower ext
  • Positive Lhermittes sign: Sensation of electricity down back with passive neck flexion
  • Optic neuritis-blurry vision
34
Q

HOw do you diagnose MS?

A

MRI of brain and spinal cord show demylinating plaques in white matter

**2 or more regions of white matter lesions must be present for diagnosis**

35
Q

How do you treat MS?

A
  • Decrease frequency of relapses
    • Interferon B–TOC!
    • Glatiramer Acetate (mild)
  • High dose steroids for optic neuritis
  • Secondary progressive type:
    • Cyclophopamide or Azathioprine
36
Q

What is a tonic clonic seizure and how is it tx?

A

AKA Grand Mal

LOC, follwed by tonic (stiffening) then clonic (rhtymic jerking phases)
Urinary incontinence follwed by postictal period (altered state of consciousness post seizure)

Tx: First line: Carbamezapine

37
Q

What is an Absence seizure and how is it tx?

A

Petite mal

Brief abrupt and self limiting LOC (Pts appear awake)

Staring spells—>can have rapid eye blinking x 3-5 seconds

Tx: Only 2 drugs have FDA approval: Ethosuximide or Valproic Acid

38
Q

What is a myoclonic seziure? How is it treated?

A

short periods of muscle contraction that may reoccur x several minutes

NO LOC

Tx: Valproic acid

39
Q

What is a simple partial seizure and how is it tx?

A

Abnormal activity of a single limb; no loc

May be followed by a transient neurologic deficit (Todd’s paralysis)

TX: first line: Carbamezapine

40
Q

What is a Complex partial seizure and how is it tx?

A

Usually preceded by some type of sensory aura, followed by impaired consciousness (but not total LOC), along with an involuntary motor activity

Resolves in about 30 minutes and followed by postictal confusion

Ex. “Episod begins by upset stomach, appears confused, turns head to left, and raises Left arm in the ear–lasts 30 to 60 seconds-followed by fatigue x 1 hour”

Tx: first line: Carbamezapine

41
Q

What is the first line tx for Tourette syndrome?

A
  • Alpha 2 adrenergic receptor agonist
    • Clonidine
    • Guanfacine
42
Q

What are the most common organisms that cause bacterial meningitis in neonates? greater than 2 months?

A
  • Neonates: Group B strep, E. coli, listeria
  • Greater than 2 months: Strep pneumonia, N. Meningitides
43
Q

What is the gold standard diagnostic study for Guillian barre syndrome?

A

Nerve conduction studies or muscle biopsy

44
Q

WHat is the first line tx for Status Epilepticus?

A

Long acting benzodiazepines:

Lorazepam or diazepam

45
Q

What is central cord syndrome

A
  • Involves loss of motor function that is more severe in the upper extremities than in the lower extremities; and more severe in the hands
  • Usually hyperesthesia over the shoulders adn arms
46
Q

What is anterior cord syndrome?

A

Presents with paraplegia or quadriplegia, loss of lateral spinothalamic function with preservation of posterior column function.

47
Q

Absence of the knee jerk reflex suggests compression of what nerve roots?

A

L3-L4

48
Q

Absence of the Achilles (ankle jerk) reflex suggests compression of what nerve root?

A

S1,S2

49
Q

Absence of the Triceps reflex suggests compression of what nerve root?

A

C7, C8

50
Q

Abscence of the brachioradialis reflex suggests compression of what nerve roots?

A

C5, C6

51
Q

The presence of HA associated with papilledema raises concern for a brain tumor, but if MRI excludes this what is next on the differential?

A

Pseudotumor cerebri (AKA benign intracranial HTN)

May cause visual loss

Frequent in obese, adolescent girls and young women

May be associated with OCPs, vitamin A, or tetracycline

Tx: weight loss, diuretics, and steroids

52
Q

What is Horner’s syndrome?

A

unilateral, small pupil with mild ptosis in which pupillary response to light and accommodation is preserved.

may be ass. with ipsilateral anhydrosis

classic triad: Constricted pupil (Miosis), Partial ptosis, and loss of hemfacial sweating

53
Q

what is an Adie pupil?

A

Unilateral dilated pupil that is sluggish to direct light stimuli

After extended near focusing (or accomodation) the involved pupil may actually become tonic (remain constricted long after discontinuing accomodative effort).

Idiopathic

54
Q

What is an Argyll Robertson Pupil?

A

Usually affects both eyes; is irregular in shape, and poorly reactive to light, but can still constrict when pt focuses on a near object.

(Accomodate, but are not reactive)

Highly specific sign of neurosyphillis

55
Q

What are some causes of Horner’s syndrome?

A
  • Pancoast tumor (lung ca) or lung infxn
  • Dissecting carotid aneurysms
  • migraine
  • brachial plexus trauma
56
Q

What is the ACUTE treatment of choice for aborting a migraine HA?

A

5-HT receptor Agonists–Rizatriptan

57
Q

What is used as a preventative measure for Migraine HA?

A

Propanolol

If c/I due to Asthma, then Amitriptyline

58
Q

What diagnoses Narcolepsy?

A

Multiple sleep latency test

59
Q

What is a potential finding of a lower motor neuron process? Of an upper motor neuron process?

A

Lower motor neuron: Muscle weakness

Upper motor neuron: Hyperreflexia

“when the parents are away, the kids are at play”

PANCE-Flashcards (11 decks)

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