Neuro Flashcards
tension HA
emotional distress, fatigue, lack of sleep, stressors.
eipsodic, worsen throughtout day, band around head, tenderness of posterior M of neck
migraine
can be atypical: cyclical vomiting, abd migraine, paroxysmal vertigo.
throbbing, photophobia, phonophobia, N/V
precipitate by stress, light, odor, food
relieved by sleep
RF: fx
classic- has aura - visual sx, speech changes, sensory abn like paresthesias
common- w/o aura. most common type in children. unilateral, usually frontal or temporal.
basilar artery migran or hemiplegic migrane cause acute ataxia
concerning sx of HA
- relieved by vomiting after lying down- incr ICP
- sudden onset- intracranial hemorrhage
- awaken from sleep- incr ICP
- fever + photophobia- infection
- worsen with cough or valsava- incr ICP
- progressively worsen- serious
ataxia DD
post infectious cerebellitis, infectious cerebellitis, medication or toxin, IC mass, opsoclonus- myoclonus syndrom, migraine HA, hydrocephalus, metabolic disease, neurodegen disease, psych illness
post infectious cerebellitis aka acute cerebellar ataxia
most common cause of ataxia in kids. only in 1-3yo. AI - cerebellar demyelination
occur wks after viral infection
onset- sudden + ataxia, vomit, nystagmus in 50%, dyarthria in some
CSf normal or pleocytosis, protein elevated
most recover in few mo
usually no fever or systemic sx
infectious cerebellitis
viral or bacterial. often febrile, AMS, maps, enterovirus EBV or bacteria that cause meningitis
ataxia localizing tumor
most likely in cerebellum or frontal lobe
opsoclonus-myoclonus syndrome
paraneoplastic syndrome- neuroblastoma. 6mo-3yo. ataxia + myoclonus + opsoclonus( jerky conjugate mvt of eyes)
hydrocephalus ataxia
insidious onset, chronic decr in coordination. HA/V
cerebellar mass
coordination, precision and balance impacted. no impact on initiation of mvt. bc close to 4th ventricle, cause obstructive hydrocephalus.
1) vermis- dysarthria, truncal ataxia, gait abn
2) cerebellar hemispheric lesion-IL lim abn, nystagmus, tremor/ dysmetria, spares speech
fall/look toward side of lesion
3) deep cerebellar nuclei- tremor, myoclonus, opsoclonus
LP + incr ICP
LP is CI bc cause brain herniation
infratentorial lesion
cerebellar signs, incr ICP
brain tumor
most common solid tumor in children and 2nd most common form of childhood ca behind leukemia. highest ca childhood death.
most common 10 is supratentorial.
RF: radioation exposure, genetic syndrome (tuberous sclerosis, NF)
most common medulloblastoma and juvenile pilocytic astrocytoma are each 20%.
brain stem glioma
resection for low grade. prog variable
ependymomas
from 4th ventricle. cause hydrocephlus. resection + rad. 50% 5y survival
astrocytoma of cerebellum
best prog of infratentorial tumor in kids. often cystic. resection. rad if high grad, 90% 5y survival with complete resection
medulloblastoma
most common pediatric tumor. malig that spread through CNS - metastasize to extra cranial site. resection + rad+ chemo.
prog dep on size and spread
hypotonic infant types and PE
1) central hypotonia- dysfunc of UMN
2) peripheral hypotonia- dysfunc of LMN
PE: weak cry, decr spontaneous mvt, frog leg posture, M contractures
peripheral hypotonia
associated with decr fetal mV and breech presentation.
consciousness unaffected. M bulk and DTR decr
etio
1) serum CK
2) DNA test for SMA
3) EMG - myathenic D
4) M bx
central hypotonia
associate with sz in neonatal period, altered lvl of consciousness, incr DTR, ankle clonus
etio:
1) CT to r/o CNS injury or congenital malformation
2) electrolyte: Ca, Mg, MH3, lactate, pruvate to r/o metabolic D
3) high resolution chromosome studies- FISH for genetic D(prader willi)
acute life threatening causes of hypotonia etio
sepsis, meningitis, acute metabolic D
spinal muscular atrophy (SMA)
anterior horn cell degeneration
P: hypotonia, weakness, weak cry, tongue fasiculations, bell shaped chest, frog leg posture, nomral extraocular mvt and sensory
type I-infantile 3yo
etio: AR -C5-survivial MN gene SMN1 mut –> degeneration and loss of anterior horn MN
dx: DNA test -90%, M bx show atrophy
tx: supportive. no cure. gastrotomy tube feeding. physical therapy
prog: survive till type I- 1yo. II-adolescent III-adult.
infantile botulism
bulbar weakness and paralysis. 2/2 ingest C. botulinum spore and absorption of botulinum toxin-in contaminated honey
toxin prevent presynaptic release of ach.
time line
1) onset 12-48 post ingestion.
2) consitmation = 1st sx
3) neuro sx follow- weak cry suck, loss of previous motor milestones, ophthalmoplegia, hyporeflexia
4) paralysis symmetric and descending. diaphragmatic paralysis sometimes
dx: hv, neuro exam, EMG-ancremental response during high freq stimulation
tx: supportive NG feed, ventilation. botulism ig improve course. ab CI = worsen course
prog- excellent
congenital myotonic dystrophy
can’t relax contracted M
AD- C19-trinucleotide repeat, transmit though affected mother in 90% cases
P: antenatal hx- poyhydramnios+ poor swallowing, neonatal-weakness, hypotonia, poor feeding and respiratory problem
PE: facila diplegia (bl weakness), hypotonia, areflexia, arthrogyrposis
myotonia dev after 5yo.
adult-myotonic facies, can’t release rip after handshaking, ptosis