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Neurology 2 > Misc Neuro Disorders > Flashcards

Misc Neuro Disorders Flashcards

1
Q

Multiple Sclerosis

  • what is this?
  • most common in who?
  • dx at what age?
  • most commonly seen in what regions?
A

What: body makes abys and wbc against proteins in the myelin sheath, this results in inflammation and injury to the sheath and nerves. The result is scarring eventually damage can slow or block the nerve signals that control muscle coordination, strength, sensation, and vision.

  • brain, spinal cord, and optic nerve
  • Relapsing-remitting*

Most common in women

Dx between ages 30-50yo

Not found between +40 to - 40 degrees (around the equator), found in northern latitudes; western european lineage
*increased risk if HLA-DR2 gene

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2
Q

Causes of MS

A
  • environmental factors
  • genetics
  • viruses/bacteria; epstein barr
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3
Q

Signs & Sx of Multiple Sclerosis

A
  • weakness, numbness, tingling, or unsteadiness in a limb “Lhermittes Sxs”
  • unilateral visual impairment
  • fatigue
  • spastic paraparesis
  • diplopia
  • disequilibrium
  • sphincter disturbance
  • dysarthria
  • mental disturbance

Signs:

  • optic neuritis
  • ophthalmoplegia
  • nystagmus
  • spasticity or hyperreflexia
  • babinski sign
  • absent abd reflexes
  • labile or change in mood
  • *UMNL**
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4
Q

MS
-describe onset in younger and older pts

-what are the types?

A

young=subacute or acute sx
older=insidious

Types:
-Benign = no disability, return to normal between attacks

-relapsing-remitting*= interval months to years after initial episode before new sx develop or original ones reoccur. (get progressively worse, but only after attack)

Secondary progressive: steady deterioration occurs, unrelated to acute relapses

Primary progressive: steady increase in disability w/o attacks

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5
Q

How do you dx MS?

-what is definitive dx?

A
  • MRI w/ contrast= gold standard
  • LP if you dont see anything on MRI and you still have high suspicion, looking for protein, lymphocytosis, elevated IgG, myelin abys, oligoclonal bands

Clinical Dx:
-2 or more exacerbations greater than 1-2mo apart that sx take longer than 24hrs to resolve.

Definiative dx:
-intermittent or progressive CNS sx with TWO OR MORE CNS white matter lesions in an appropriately aged patient

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6
Q

What scale is used to measure disease progression of MS?

A

-Kurtzke Explanded Disability Status Scale

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7
Q

MS

  • Tx
  • -minimally ill
  • -exacerbations
  • -rest of people
  • -symptomatic
A
  • minimally affected pts:
  • -no tx
  • -encourage healthy lifestyle
  • -PT

Rest of people:
-Corticosteroids; mainstay for acute exacerbations = reduce inflamm, improve nerve conduction

  • immune modifiers; IFN 1a, IFN 1b, Glatiramer acetate
  • immunosuppressents; clyclophosphomide(Cytoxan), imuran (azathioprine)

IVIG can reduce clinical attack rates

Tysabri (Natalzumab); decreases movement of immune cells from the blood stream across the BBB into the brain and spinal cord.
*only used if cannot tolerate any other therapies…we dont ever use this.

symptomatic tx
-spasticity: dantrolene, baclofen

  • fatigue: provigil, amantadine
  • bladder problems: cholinergics (Bethanechol
  • depression- antidepressants
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8
Q

Cerebral Palsy

  • what is this?
  • when is this commonly dx?
  • cause
A

What: abnormalities in parts of the brain that control muscle movements

Commonly dx 18mo-3years

Causes:

  • damage to young developing brain, can occur:
  • -during pregnancy; infections, insufficient perinatal oxygen, prematurity, Rh incompatibility

–during birth: asphyxia during labor and delivery

–after birth: brain injuries occuring in the first 2 years of life; infections such as meningitis, head injuries (trauma, child abuse)

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9
Q

What are the 4 major classifications to describe the different movement impairments of cerebral palsy?

All of these are characterized by what?

A
  1. Spastic
  2. Athetoid
  3. Ataxic
  4. mixed

Characterized by abnormal muscle tone, posture, reflexes, motor development, and coordination.

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10
Q

Spastic Cerebral Palsy:

-presentation

A
  • *most common**
  • hypertonic
  • spastic hemiplegia (one side)
  • spastic diplegia (legs)
  • spastic quadriplegia
  • spasticity of the limbs
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11
Q

Athetoid or Dyskinetic Cerebral Palsy:

-presentation

A
  • have trouble holding themselves upright, steady position for sitting or walking
  • requires a lot of concentration to get their hand to a certain spot
  • may not be able to hold onto things
  • mixed muscle tone (hypertonic, hypotonic)
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12
Q

Ataxia Cerebral Palsy

-presentation

A
  • hypotonia and tremors
  • writing, typing, using scissors may be difficult
  • problems with balance while walking
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13
Q

Signs of Cerebral Palsy in Newborns and older children?

A

Newborns: floppy movements, unable to roll over, unable to sit crawl, or walk, birth defects such as irregular spine, small jawbone, or small head

older children:

  • walking with one foot or leg dragging
  • walking on the toes
  • muscle tone that is either too stiff or too floppy
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14
Q

Cerebral Palsy:

-sx

A

seizures, spasms, involuntary movements, speech or communication disorders, hear or vision impairments, cognitive disabilities, learning disabilities, behavioral disorders

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15
Q

Cerebral Palsy

-dx

A
  • may take months to years
  • clinical, parental observations, medical hx, PE, screening tests

Evaluate childs muscle tone; floppy or stiff

Check reflexes; persistence of primative reflexes:

  • moro reflex (startling)
  • walking reflex
  • rooting reflex
  • sucking reflex
  • tonic neck reflex
  • palmar grasp
  • babinkski

See if baby has developed handedness by 12mo (most dont develop this until after 12mo)

CT, MRI, US of brain may be done….though they may not be helpful

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16
Q

What are some secondary consequences of Cerebral Palsy?

A

-orthopedic deformities such as scoliosis and hip dislocation

  • shafts of bones are often thin (gracile)
  • metaphyses are enlarged (ballooning)
  • shorter in height
  • bones may grow at different lengths (one leg longer than the other)
17
Q

Cerebral Palsy

  • prognosis
  • tx
A

brain damage does not progress, but symptoms DO progress

Tx: 
cannot be cured 
-PT, OT, ST
-Drugs to control seizures, relax muscle spams, allieviate pain
-surgery to correct anatomical abnormalities or release tight muscles 
-braces/orthotics 
-Wheelchair, rolling walkers
-communication aids
18
Q

Amyotrophic Lateral Scerlosis

  • aka
  • what
  • pathophysiology
  • what do these patients usually die of?
A

aka: Lou Gehrigs Dz

What;
-fatal neuromuscular dz characterized by progressive muscle weakness resulting in paralysis

Patho:

  • attacks nerve cells in the brain and spinal cord. Motor neurons which control movement of voluntary muscles deteriorate and eventually die, once these are dead the brain can no longer initiate and control muscle movement, these muscles weaken and deteriorate.
  • degeneration of the upper and lower motor neurons.
  • bowel and bladder sphincters and eye movement are usually spared.

Usually die of PNA or respiratory failure, generally within 2-5 years of dx

19
Q

ALS

  • common at what age?
  • what gender is most affected?
  • cause
  • earliest sx
A

Can strike at any age, most between 40-70yrs

More common in men

Cause:

  • unknown, may have genetic component (5%)
  • may be associated with veterans & repeated concussions

Sx:

  • weakness, muscle atrophy
  • twitching, cramping, stiffness of muscles
  • slurred and nasal speech
20
Q

What are the two types of onset in ALS?

Dx of ALS

A

75% Limb onset

25% bulbar onset; difficulty speaking, slurred nasal speech, difficulty swallowing

Dx:

  • no test can provide definitive dx of ALS; clincal
  • must have signs and sx of both upper and lower motor neuron damage that cannot be attributed to other causes

EEG, EMG/Nerve Conduction Velocity, MRI

21
Q

ALS patients may develop frontotemporal dementia, have mild problems with word generation, attention, and decision making, T/F?

A

True

22
Q

ALS Tx

A

Riluzole (Rilutek)

  • may offer neuroprotective effects, though it does not reverse the damage already done to the motor neurons.
  • lengthens survival by several months

-BIPAP for ventilatory support if resp muscles weakened

23
Q

Wernicke-Korsakoff Syndrome

  • cause
  • who gets this?
  • characterized by?
A

Cause: deficiency of Thiamine (B1)

Who: chronic alcoholism

Characterized: confusion, amnesia, confabulation

Confabulation = memory disturbance, production of fabricated or distorted memories about oneself or the world w/o the intention to deceive.

other features:

  • weakness
  • Paralysis of EOM
  • Nystagmus
  • Ataxia
  • peripheral neuropathy
  • diplopia
24
Q

Dx of Wernicke-Korsakoff Syndrome

A

sx

CBC (r/o infection)

Coags (r/o bleeding disorder)

serum/urine drug test

liver enzymes

CT (r/o head trauma)

MRI** will show acute lesions of Wernickes
^^diagnostic^^

25
Q

Tx Wernicke-Korsakoff Syndrome

A

Supplemental Thiamine (IV, IM, PO) and then glucose

Wernickes = reversible; give thiamine

Korsakoff = chronic does not get better

Neurology 2 (8 decks)

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