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neuro Flashcards

1
Q

key features of GBS

tpes of microcephaly

whats worse congenital microcephally or post natala

nb formicrophaly epilspesy

A
  1. SUDDEN ONSER
  2. SYMMETERICAL
  3. ASCENDING

symeteircal - everythign low
asymeterical - just head - more common and clincially relavnt

post natal

nb! monogenic

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2
Q

other symptoms of GBS

A

may have pain esp in shoulders, back , thigh
may have cranial nerve involvement
absent deep tendon reflexes vs MG

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3
Q

CAUSE language regression

A

autism
epilepsy
cerebellar mutsism

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4
Q

does gbs affect sensory nerves

A

yes it can affect infect sensory symptoms may be the presenting part of the disease, so patients have report parestheisas

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5
Q

what kind of disease is GBS

A

lower motor neurone

polyneuropathy

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6
Q

what systems does gbs affect

A

sensory motor autonomic

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7
Q

autonomic problems gbs

A

~~~
urinary retention
cardiac arrhythmia
dry eyes
blurred vision
stomach pain
labile hypertension

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8
Q

treatment of gbs

A

plasmapheresis (if severe)

iv immunoglobulin IV 2 G/KG 1st line

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9
Q

when would kerning and brudinzki show

A

after 2 years

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10
Q

signs of increased intracrhail pressure

A

can cause disorders in breathing and heart rate!
vomitting
lethargy
refusal to eat

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11
Q

central facial palsy

A

the opposite lower quadrant

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12
Q

peripheral facial palsy

A

half the face

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13
Q

causes of torticollois

A

tumour
traumatic birth injury
early sign of hemiplegic CP

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14
Q

TESTS FOR MEASURING AXIAL MUSCLES TONE

A

traction

landau

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15
Q

What is contraindicated in GBS

A

corticosteroids

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16
Q

sunset eyes

A

sign of increased ICP such as hydrocephalus and it affects the region of the brain that controls eyes movement as cranial nerves 3, 4, 6 get affected

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17
Q

which muscles affected more in SMA and signs of sma

A

PROXIMAL MORE THAN DISTAL

floppy baby
scarf sign
knee to ear
ventral susupesion
tongue fasiculates +/fingertrtips?
frog leg positon
bell shaped abdomen

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18
Q

which is the disease of anterior horn

A

SMA

POLI

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19
Q

muscles affected more in neuropathy

A

distal

20
Q

dx of GBS

A

POLIO

transverse myelitis

21
Q

POLIO VS GBS

A

POLIO: asymetericl , csf is more inflammatory , autonomic dysfunction not that common like gbs, just supportive treatment , more acute , more likley to cause permanent parylis, can spread via feces , dmaages anterior horn

gbs: csf just protein,has a specific tx , more insisuious,fever is uncommon , immune mediated, cant spread from person to person , damages the myelin , more likley to have sensory abnormalities

22
Q

Sign of botulism

diagnosis

treatment

PATHOPHYS

A

constipation + descending hypotonia , drooling

toxin in stool

immunoglobulin 50mg/kg (human ) not horse

in babies its the ingetsion of sportes and go tht gut and perfom toxins and not the preformed toixn, it affectec the cranial neres (weak cry, weak suck, decreased gag reflex)

23
Q

dx myositis from myopathy

A

myositis : pain upon movement and acute and cause is enterovirus mostly CK only temporary affected for less than a month

myopathy: won’t hurt when you palpate or move

24
Q

dermatomyositis key features

A

PROXIMAL muscle weakenss
heliotrope rash
grottoes papules
elevated creatink kinase
anti JO

25
Q

antibodies in dermatomyositis

features of hsv encephalitis and hwich one is more commone

features of encephalits in older kids
EEG
csf
tx

A

anti jo

but also antinuclear

hemorragic necrotic lesions

hs1 more common but for neonatal period hs2 is common but can also be hs1

anomia (dont know the name of)
aphasia - cant speak
hemiparesis
TEMPORAL LOBE FOCAL seizure which can become genralised

unilateral or bilateral temporal periodic high waves

lymphoctoisis, pleocytosis, erythroctyrachia, proteinrachia

aciclovir IV for 2-3 weeks 30-60mg/kg-

26
Q

are reflexes affected in Dermatomysotis

A

no changes

27
Q

reflexes in collagen laxity

A

normal

28
Q

symptoms of collagen laxity + complications

A

hypotonia
may have transitory motor delay
may have no weakness or slight weakness
tendon reflexes are normal

mitral valve proplapse!
lunation of lens
aneurysms
pneumothorax

29
Q

duchess CK LEVAL

A

VERY HIGH! >1000

30
Q

IS cp congenital or acquired

A

both such as torch infection cmv or acquired during birth delivery

31
Q

most common cause of cp

whoch reflexes persist

a complication of chicken pox

A

ANTENATAL

morro, palmar, fencing

acute cerebelltis - the most common type of cerebellitis

32
Q

what example is hIE in the category of cp

A

perinatal

33
Q

hie more common for

A

TERM BABIES

34
Q

CAUSES OF POST NATAL CP

lennoz gastraut triad (lecture)

A

HSV ENCEPHALITIS

atypical abscences, DROP attacks

slow spik and waves (awake) drop attacks when asleep 10hz
psychomotor retardation

meningitis

35
Q

which CP has has primitive reflexes leading

in hemiplegic what is more affeted

in diplegic what is more affected

A

dyskinetic

upper more affcted

all 4 but the lower limbs more affcted

36
Q

which cp affects arms more than legs

what is paraplagia

A

quads + hemiplegic

legs

37
Q

which cp is associated with epilepsy

A

deffo quadriplegic

but 50% of hemiplegic have focal epilepsy

38
Q

types of dyskinetic cp

ADEM

A

dystonic and choreoathhetoid

acute desiminated encepholitis
after infection oR VACCINATION due to cross reaction
tx methylpredinososle
(multile defcits over the brain)

39
Q

unlikely to be cp if

A 
other family members
have the same “CP”
® no certain etiology
® normal MRI
® regress - motor,
cognitive or other
° multisystem disease
40
Q

signs of hydrocephalus in babies

subactute pan scelrosing

A
  1. bulging fontanelle
  2. prominant scalp veins
  3. sunset eyes
  4. increase HC

after latent measles, memory loss, chnage in behavior then later comes myoconic jerks !!!!lastly persistant vegetative state - die- no cure

41
Q

NMDAR encephalitis

A

antibodies against the receptor in brain
key word is dyseknias and autonomic instablitiys (hypersalvation, hyperthermia)
can come as a result of HSE after recovery so dx from reactivation but you would see NEW SIGNS like the dsykinesia
tx- methylpredisonlone, IVIG, plamapheresis,rituximab

42
Q

how to we treat hydrocephluas

A
  1. shunt- connect from the ventricle of the brain to another area of the body to drain, like peritoneal cavity . risk is that shunt is infected and may have to be changed many time, always suspected meningitis in these kids if they have a fever
  2. Endoscopic third ventriculostomy (ETV) - creating a small hole in the third ventricle of the brain (one of four fluid-filled cavities in the brain) so that the excess fluid can make its way out and relieve pressure.
43
Q

if you had to specifically decribe GBS what woul you say

A

its a lower motor neruon disease and polyneuropathy and demyelinating

44
Q

usual first symptom for gbs

acute necrotiizng encephalopathy

A

tingling sensation in extremities

very fatal, go into coma real fast
tx with methylprednisolone
similar to reyes in that it affects liver enzymes
nb! thalmaus symmetrical lesions on ct

45
Q

compliation os sma

A

willl need feeing help as weak eating and get tired easily from just chewing
resp fialure as muscles fail
freuqnet infectins as weak cough cant clear secrtions

aspirarion pneumonia
scoliois- as the muslces supporting the spine

46
Q

e

examples of prenatal cp

A

TORCH
genetics syndromes
placental insufficnecy

47
Q

clasification of CP accourding to lesion site

reyes syndrome and triggers dx

A

pyrimidal tract

extrapyrimiadal

cerebellar

aspirin + valproate >5-10
hypoglycmeia, fatty liver, elevated transaminase , hyperammonia

ryes like syndrome but no hypoglycmeia you need to check for inborn errors of metabolbilsm s happens <5

peds (26 decks)

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