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clin med IV > motor disorders > Flashcards

motor disorders Flashcards

1
Q

myasthenia gravis (MG)

A
  • painless weakness and fatiguability of skel muscles
  • disease of NMJ
  • bimodal age distribution: women 20-30, men 50-60
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2
Q

most common pathophys of MG

A
  • autoab directed against AcH receptors
  • decreased AcHR at post synaptic muscle membrane
  • causes weak contractions
  • AcH does not get repleated fast enough
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3
Q

pathophys of MG in 15% of pts

A
  • MuSK ab -> decreased AChR on membrane

- impacts trafficking of receptors

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4
Q

what is usu assoc with MG

A
  • thymus disorder
  • hyperplasia in young
  • thymoma in older: benign or malignant
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5
Q

si/sx of MG

A
  • weakness and fatiguability- worse with repetitive stim
  • exacerbations and remissions possible
  • infx or systemic disorders -> crisis
  • diplopia
  • ptosis
  • facial weakness
  • nasal timbre speech
  • difficulty swallowing -> aspiration risk
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6
Q

diagnosis of MG

A
  • Ab to AChR, MuSK, or Ipr4
  • electro diagnostic testing: repetitive nerve stimulation -> reduced amplitude
  • edrophonium -> improved muscle strength
  • CT or MRI to exclude intracranial lesions
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7
Q

treatment of MG

A
  • long acting anticholinesterase: pyridostigmine or neostigmine
  • immunosuppressants
  • surgical thymectomy
  • plasmapheresis in crisis
  • IV IG in crisis
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8
Q

immunosuppressants used in MG

A
  • steroids*
  • cyclosporine A
  • azathioprine
  • mycophenolate mofetil
  • MTX
  • cyclophosphamide
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9
Q

what is a tic

A
  • brief, rapid, recurrent, purposeless motor contraction

- motor vs sensory

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10
Q

types of motor tics

A
  • simple: individual muscle groups
    complex: multiple muscle groups
  • phonic ticks: simple vs complex
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11
Q

tourette’s syndrome

A
  • multiple motor tics often present with vocalizations/ phonic tics
  • mainly affects males
  • can suppress tic for short period of time but then experience irresistible urge to express them
  • varies in intensity
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12
Q

etiology and pathogenesis of tourette’s syndrome

A
  • thought to be genetic
  • no specific gene mutation
  • may have enviorn influence
  • possibly d/t decreased dompamine, opioids, second messenger systemics
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13
Q

treatment for tourette’s

A
  • education, counseling
  • no singular effective tx
  • alpha adrenergic agonists: clonidine, guanfacine
  • neuroleptics: typical vs atypical
  • botulism inj if focal tic
  • deep brain stimulation possible
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14
Q

guillain barre syndrome

A
  • acute, severe fulminant polyradiuclopathy
  • acute onset immune mediated demyelinating neuropathy
  • does not impact CNS
  • majority occur 1-3 weeks after acute respiratory or GI infx
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15
Q

causes of GBS

A
  • campylobacter jejuni most common in US
  • CMV, EBV
  • HIV
  • mycoplasma pneumonia
  • flu, rabies vaccine
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16
Q

si/sx of GBS

A
  • rapidly evolving ascending paralysis
  • weakness evolves over hours- days
  • asoc with tingling dysesthesias in extremities
  • legs more affected than arms
  • facial diapresis
  • pain
  • autonomic involvement -> fluctuation in BP, postural hypotension, cardiac dysrhythmias
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17
Q

subtypes of GBS

A
  • acute inflammatory demyelinating polyneuropathy- most common
  • acute motor axonal neuropathy
  • acute motor sensory axonal neuropathy
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18
Q

pathophys of GBS

A
  • demyelination -> conduction block -> flaccid paralysis and sensory disturbances
  • axonal conduction usu remains in tact
  • if axonal degeneration -> longer recovery and residual disability
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19
Q

diagnosis of GBS

A
  • based on rapidly evolving paralysis with areflexia, absence of fever, systemic sx, hx
  • CSF findings: increased proteins without pleocytosis
  • electrodiagnostics- slowed conduction velocity, conduction block, temporal dispersion
20
Q

treatment of GBS

A
  • IV IG or plasmapheresis
  • steroids not effective
  • 30% require vents
  • most fully recover within few months to a year
  • death secondary to pulm complications
21
Q

cerebral palsy

A
  • neuro dysfunction that occurs in developing brain
  • perm affects body mvmt, muscle coord, posture, balance
  • not progressive
22
Q

what is the most common cause of CP

A
  • antenatal causes
  • cerebral dysgenesis
  • congenital infections (TORCH)
  • substance abuse
  • prematurity
23
Q

other causes of CP

A
  • intrapartum: birth asphyxia, trauma

- post natal: intravent hemorrhage/ ischemia, meningitis, encephalitis, head trauma, hyperbilirubinemia

24
Q

types of CP

A
  • spastic- most common
  • dyskinetic
  • ataxia
25
Q

spastic CP

A
  • produces upper motor neuron type disease
  • d/t cortex damage
  • muscles stiffer than usual
  • may only be present in one part of body, half of body, or one side
  • extensors of UE
  • flexors of LE
  • tip toed walk
26
Q

dyskinetic CP

A
  • d/t basal ganglia damage
  • recurrent uncontrollable mvmnt
  • tone fluctuates
27
Q

ataxic CP

A
  • d/t cerebellum damage
  • least common type
  • generalized hypotonia
  • loss of muscle coord
  • wide gait
28
Q

PE findings for CP

A
  • delayed motor dev
  • persistent or late primitive reflexes
  • spasticity, hyperreflexia, ataxia
  • involuntary mvmt
  • microcephaly
29
Q

other neuro disorders assoc with CP

A
  • most have pain
  • bladder problems
  • seizure disorder
  • sleep disorder
  • varying degree of language, behavioral, vision, and sensory disorders
30
Q

diagnosis of CP

A
  • MRI

- genetic and metabolic testing

31
Q

treatment for CP

A
  • general mgmt- nutrition and proper care
  • pharm mgmt based on sx
  • surgery to relieve muscle tightness
  • physical aids
  • rehab services
  • family services
32
Q

pharm options for CP

A
  • botox, baclofen for muscle spasms and seizures
  • glycopyrrolate- control drooling
  • pamidronate- help with osteoporosis
33
Q

multiple sclerosis

A
  • autoimmune disease of CNS
  • chronic inflammation, demyelination, gliosis, and neuronal loss
  • can be relapsing or progressive
  • course is VERY variable
34
Q

risk factors for MS

A
  • genetic predisposition
  • vit D def
  • EBV exposure after early childhood
  • cigarette smoking
  • high salt diet
35
Q

pathogenesis of MS

A
  • perivenular cuffing by inflammatory mononuclear cells, predom T cells and macrophages
  • BBB gets disrupted
  • demyelination is hallmark
  • spares axons usually
36
Q

si/sx of MS

A
  • optic neuritis
  • exs induced weakness of limbs
  • facial weakness
  • spasticity
  • ataxia
  • vertigo
  • sensory sx: paresthesias, hypesthesia
37
Q

optic neuritis

A
  • often presenting sx of MS
  • diminished visual acuity
  • dimness
  • decreased color perception
  • occurs in central field of vision
38
Q

clinical types of MS

A
  • remission
  • relapsing remitting disease
  • secondary progressive disease
  • primary progressive disease
39
Q

remission of MS

A
  • remodeling of demyelinating axonal plasma membrane

- more Na channels to permit conduction despite myelin loss

40
Q

relapsing remitting disease of MS

A
  • progression with relapses of active disease

- complete recovery during remission

41
Q

secondary progressive MS

A
  • disease becomes more aggressive
  • consistent worsening of function
  • usu progression from relapsing remitting disease
42
Q

primary progressive MS

A
  • sx are progressive from onset
  • early disability
  • only about 15% of pts
43
Q

diagnosis of MS

A
  • 2 episodes of 2 that occur at different points in time
  • absence of other causes
  • MRI shows plaques
  • LP- mild pleocytosis and total protein normal
  • slowed or abnormal conduction in response to visual or auditory stimuli
44
Q

treatment for acute attacks of MS

A
  • IV methylprednisolone 3-5 d

- +/- PO taper over 2 weeks

45
Q

long term tx for MS

A
  • disease modifying therapy
  • spasticity: baclofen, cyclobenzaprine
  • optic neuritis: steroids
  • fatigue: amantidine, anti-depressants
  • pain: gabapentin, pregabalin
  • tremor: propranolol, primodone
46
Q

what are the disease modifying agents for MS

A
  • interferon beta
  • dimethylfumerate
  • natalizumab
  • alemtuzumab

clin med IV (23 decks)

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