- most common motor disability in childhood - 2 per 1000 children - risk among preterm low birth weight

CP and GBS Flashcards by Elizabeth Sager

What is cerebral palsy

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

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

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define muscle tone

strength and tension of muscles

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define hypotonia

decreased muscle tone

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define hypertonia

increased tightness of muscle tone and reduced capacity to stretch

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define paresis

weakness

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define plegia

paralysis

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define monoplegia

paralysis of one limb

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define hemiparesis or hemiplegia

paralysis or weakness of one side

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define diplegia

paralysis of both legs

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define quadriplegia

paralysis of all limbs

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Etiology of CP

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

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What are some risk factors of CP

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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Epidemiology of CP

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

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What are the subtypes of CP

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

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Describe the positive and negative signs of spastic CP

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What are the subtypes of spastic CP

Spastic hemiplegia/diplegia/quadriplegia

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What happens in dyskinetic CP

-damage to the basal ganglia

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What are the hallmarks of dyskinetic CP

involuntary movement
usually no contractures
choreoathetosis
dystonia

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Define choreoathetosis

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

Where is the lesion in spastic CP

corticospinal tract or motor cortex

Where is the lesion in ataxic CP

cerebellum

Describe the hallmarks of ataxic CP

rare
motor and language delayed
may improve with time

What are some of the associated symptoms of CP

pain
intellectual disability
SLP disorders
epilepsy
visual impairment
hip displacement

what are the clinical features of CP

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

What are some of the developmental reflex issues in CP

- tonic labyrinthine reflex - tonic neck reflex - galant

What kind of gait is this

scissoring gate

What kind of gait is this

toe walking

What are some of the early signs of CP

- early hand dominance - delayed motor milestones - primitive reflexes - scissored legs below 6 mos - floppiness - stiffness

How is CP diagnosed

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

Describe the treatment and management of CP

- functional assessments: gross motor function classification or Modified Ashworth scale

What meds can be used to treat spasticity in CP

- botulinum toxin - oral antispastics (Diazepam, Baclofen) - intrathecal baclofen pump - DBS or other surgical tx

Motor milestones

- 4 mos = rollover - 6 mos = sitting - 1 year = walking

What other treatments may be involved for associated issues with CP

- ortho - PT/OT - gastrostomy feeding - ACh meds for drooling - psychosocial support

CP prognosis

- 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

Define Guillain-Barre syndrome

acute, monoplastic, paralyzing illness provoked by preceding infection

Etiology of GBS

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

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

5-16 days

Epidemiology of GBS

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

Clinical presentation of GBS

**- 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

What are the 3 major variants of GBS

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

How is GBS diagnosed

- clinical - lumbar puncture: elevated CSF protein, normal WBC - electrodiagnostics - spinal MRI: nerve root enhancement

Treatment of GBS

- live threatening! hospital - supportive care - DVT prophylaxis - repositioning - bowel/bladder care - pain: gabapentin, carbamazepine

Describe the autonomic dysfunction of GBS

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

Describe the association of vaccines and GBS precautions

- usually no contraindication for routine vax - may need avoidance of particular immunizations if received within 6 weeks of onset of GBS

GBS prognosis

- 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