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Neuro > CP and GBS > Flashcards

CP and GBS Flashcards

1
Q

What is cerebral palsy

A

non-progressive central motor dysfunction affecting muscle tone, posture, movement

abnormalities of developing fetal/infantile brain (perinatal or post natal)

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2
Q

define muscle tone

A

strength and tension of muscles

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3
Q

define hypotonia

A

decreased muscle tone

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4
Q

define hypertonia

A

increased tightness of muscle tone and reduced capacity to stretch

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5
Q

define paresis

A

weakness

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6
Q

define plegia

A

paralysis

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7
Q

define monoplegia

A

paralysis of one limb

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8
Q

define hemiparesis or hemiplegia

A

paralysis or weakness of one side

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9
Q

define diplegia

A

paralysis of both legs

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10
Q

define quadriplegia

A

paralysis of all limbs

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11
Q

Etiology of CP

A

multifactorial
- no identifiable cause
- can be due to hypoxic event
- damage to developing brain

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12
Q

What are some risk factors of CP

A
  • preterm babies with low birth weight
  • perinatal hypoxia
  • congenital abnormalities
  • genetics
  • stroke or hemorrhage in perinatal period
  • intrauterine infection
  • kernicterus (high bilirubin)
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13
Q

Epidemiology of CP

A
  • most common motor disability in childhood
  • 2 per 1000 children
  • risk among preterm low birth weight
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14
Q

What are the subtypes of CP

A

signs and symptoms more clear after 18-24 mos
- spastic (MC)
- dyskinetic
- ataxic

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15
Q

Describe the positive and negative signs of spastic CP

A
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16
Q

What are the subtypes of spastic CP

A

Spastic hemiplegia/diplegia/quadriplegia

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17
Q

What happens in dyskinetic CP

A

-damage to the basal ganglia

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18
Q

What are the hallmarks of dyskinetic CP

A
  • involuntary movement
  • usually no contractures
  • choreoathetosis
  • dystonia
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19
Q

Define choreoathetosis

A

chorea consisting of rapid irregular contractions of individual muscles and athetosis consisting of slow smooth writhing movements

20
Q

Where is the lesion in spastic CP

A

corticospinal tract or motor cortex

21
Q

Where is the lesion in ataxic CP

A

cerebellum

22
Q

Describe the hallmarks of ataxic CP

A
  • rare
  • motor and language delayed
  • may improve with time
23
Q

What are some of the associated symptoms of CP

A
  • pain
  • intellectual disability
  • SLP disorders
  • epilepsy
  • visual impairment
  • hip displacement
24
Q

what are the clinical features of CP

A
  • nonprogressive but functional ability continue to evolve
  • neurobehavioral signs
  • developmental reflexes
  • motor tone and posture issues
25
Q

What are some of the developmental reflex issues in CP

A
  • tonic labyrinthine reflex
  • tonic neck reflex
  • galant
26
Q

What kind of gait is this

A

scissoring gate

27
Q

What kind of gait is this

A

toe walking

28
Q

What are some of the early signs of CP

A
  • early hand dominance
  • delayed motor milestones
  • primitive reflexes
  • scissored legs below 6 mos
  • floppiness
  • stiffness
29
Q

How is CP diagnosed

A

clinical, no test to confirm or exclude
- typically get a transcranial and/or MRI
- screen for thrombophilia if MRI shows evidence of cerebral infarction
- screen for associated comorbidities
- metabolic and genetic testing

30
Q

Describe the treatment and management of CP

A
  • functional assessments: gross motor function classification or Modified Ashworth scale
31
Q

What meds can be used to treat spasticity in CP

A
  • botulinum toxin
  • oral antispastics (Diazepam, Baclofen)
  • intrathecal baclofen pump
  • DBS or other surgical tx
32
Q

Motor milestones

A
  • 4 mos = rollover
  • 6 mos = sitting
  • 1 year = walking
33
Q

What other treatments may be involved for associated issues with CP

A
  • ortho
  • PT/OT
  • gastrostomy feeding
  • ACh meds for drooling
  • psychosocial support
34
Q

CP prognosis

A
  • most survive to adulthood
  • walking early correlated with better IQ outcomes
  • poor walking prognosis if head control not achieved by 20 mos
  • complications: hip disorders, aspiration pneumonia
35
Q

Define Guillain-Barre syndrome

A

acute, monoplastic, paralyzing illness provoked by preceding infection

36
Q

Etiology of GBS

A

immune response to infection that cross reacts with PNS because of molecular mimicry
- demyelinating
- MC infection = campylobacter jejuni, also EBV, HIV, covid, Zika
- can be triggered by immunization, surgery, trauma, bone marrow transplant

37
Q

What is the general time to illness presentation following viral infection (also Covid)

A

5-16 days

38
Q

Epidemiology of GBS

A

1-2 per 100,000 world wide
- age, M>F

39
Q

Clinical presentation of GBS

A

- progressive symmetric muscle weakness with absent/decreased deep tendon reflexes
- few days-week onset
- starts in legs (10% in face/arms)
- parasthesias in distal extremities
- back pain
- progressive syx for 2 weeks

40
Q

What are the 3 major variants of GBS

A
  • AIDP (acute inflammatory demyelinating polyradiculoneuropathy)(US, Europe)
  • MFS (Miller fisher syndrome)(Japan)
  • AMAN/AMSAN (acute motor sensory/axonal neuropathy) (US)
41
Q

How is GBS diagnosed

A
  • clinical
  • lumbar puncture: elevated CSF protein, normal WBC
  • electrodiagnostics
  • spinal MRI: nerve root enhancement
42
Q

Treatment of GBS

A
  • live threatening! hospital
  • supportive care
  • DVT prophylaxis
  • repositioning
  • bowel/bladder care
  • pain: gabapentin, carbamazepine
43
Q

Describe the autonomic dysfunction of GBS

A
  • dysfunction of nerves that regulate HR, BP, sweating
  • source of mortality
  • occurs in 70%
  • tachy, hypo/hypertensive, urinary retention, orthostatic hypotension
44
Q

Describe the association of vaccines and GBS precautions

A
  • usually no contraindication for routine vax
  • may need avoidance of particular immunizations if received within 6 weeks of onset of GBS
45
Q

GBS prognosis

A
  • full motor recovery after 1 year in 60%, severe motor problems can persist
  • less than 7% die despite ICU
  • complications: resp distress, sepsis, PE, cardiac arrest

Neuro (22 decks)

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