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Peds Shelf > Neurology_TN_UW_0823 > Flashcards

Neurology_TN_UW_0823 Flashcards

1
Q

Greatest risk factor for prematurity

A

Cerebral Palsy

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2
Q

EEG of complex partial seizures

A

Normal or brief discharges

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3
Q

What is pseudomotor cerebri

A

idiopathic intracranial hypertension

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4
Q

Homocystinuria?

A

A/R disorder due to cystathionine synthase deficiency results in error in methionine metabolism

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5
Q

What are some of the pathognomoic feature/events in homocystinuria?

A

Intellectual disability and cerebrovascular accidents/thromobosis

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6
Q

Tx for homocytinuria

A

vit supplementation, antiplatelet or anticoagulation to prevent thromboembolic events

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7
Q

Loss of consciousness is seen with what kidn of partial seizures

A

Complex partial and partial seizure with secondary generalization

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8
Q

Infant botulism is caused by? Where can it come from?

A

Clostridium botulinum spores. Honey and also spores from environmental dust/soil.

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9
Q

What is the presentation of infant botulisnism?

A

Descending flaccid paralysis, autonomic symptoms like constipation, drooling, bulbar palsies (ptosis, sluggish pupillary responses, poor suck/gag reflex)

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10
Q

What is the treatment for infant botulism

A

Human derived botulism immune globin

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11
Q

Epidural hematoma clinical ppt

A

Lucid interval and then rapid deterioriation

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12
Q

CT appearance of epidural hematoma

A

Biconvex mass on CT scan

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13
Q

tx for epidural hematoma

A

If patients show deteriorating neurological status or increasing ICP = emergent craniotomy

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14
Q

Ascending polyneuropathy after recent GI infection?

A

Guillan barre

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15
Q

Underlying pathology of guillan barree involves what ?

A

Peripheral motor nerves

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16
Q

Final stage of guillan barre?

A

Flaccid paralysis, absent deep tendon reflexes and nerve conduction abnormalities

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17
Q

What does CSF in guillan barre show?

A

Elevated protein levels and normal cell count

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18
Q

Illnesses that involve anterior horn cells?

A

spinal muscular atrophy (flaccid paralysis in infancy), poliomyelitis, and ALS

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19
Q

What is the best means of monitoring respiratory function in patients with Guillan barre

A

Serial measurements of forced vital capacity

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20
Q

What are important predisposing risk factors for brain abscesses

A

otitis media, mastoiditis, frontal or ethmoid sinusitis, dental infection, bacteremia from other sites of infection, congenital heart disease

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21
Q

Classic triad of brain abscesses

A

Fever, headaches (nocturnal or morning), focal neurological changes. Seizures present in 25% of cases.

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22
Q

What is polycythemia

A

Increased concentration of hemoglobin

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23
Q

Infantile spasms can develop into

A

West syndrome (infantile spasms, psychomotor developmental arrest, hyperarrythmia) or lennox gastuaut

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24
Q

Typical EEG for infantile spasms

A

Hypsarrythmia (high voltage slow waves, spikes and polyspikes, background disorganization)

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25
Q

Infantile spasm onset

A

4-8 months

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26
Q

Tx for infantile spasms

A

Vigabatrin, ACTH, benzodiazepines

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27
Q

Lennox-Gastaut onset?

A

3-5 years

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28
Q

Lennox-Gastaut triad?

A

1) multipe seizure types 2) diffuse cognitive dysfunction 3) slow generalized spike and slow wave EEG

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29
Q

Tx for lennox-gaustaut

A

Valproic acid, benzoes, ketogenic diet; however, response often poor

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30
Q

Juvenile myoclonic epilepsy aka

A

Janz

31
Q

Janz onset?

A

12-16 years of age. A/D with variable penetrance

32
Q

PPT of Janz

A

Myoclonus particularly in morning, frequently presents as generalized tonic-clonic seizures

33
Q

Typical EEG for Janz

A

3.5-6 Hz irregular spike and wave, increased with photic stimulation.

34
Q

Tx for Janz

A

lifelong valporic acid, prognosis is excellent

35
Q

Childhood absence epilepsy. Peak onset?

A

6-7 years. F>M. Strong genetic predisposition

36
Q

Childhood absence epilepsy seizure description

A

Less than 30 seconds, no post-ictal state, may have multiple per day

37
Q

Absence seizure EEG

A

3hz spike and wave

38
Q

Tx for absence seizure

A

Valproic acid or ethosuximide

39
Q

What is the benign focal epilepsy of childhood with centrotemporal spikes onset?

A

5-10 years of age, 16% of all non-febrile seizures

40
Q

What are the seizures like in benign focal epilepsy of childhood with centrotemporal spikes?

A

focal motor seizures invovling tongue, mouth, face, UE usually occuring in sleep-wake transition states

41
Q

typical EEG for benign focal epilepsy of childhood with centrotemporal spikes?

A

repeititve spikes in centro temporal area with normal background.

42
Q

Febrile seizures Epi

A

3-5% of all children, M>F, age 6 months - 6 years

43
Q

Types of febrile seizures

A

Simple and complex

44
Q

Simple vs complex febrile seizures

A

Simple:

45
Q

if febrile seizure lasts >15 minutes, suspect?

A

Meningitis or toxin

46
Q

Migraine Epidemiology

A

4-5% of school children; prevalence F:M = 2:1 after puberty; heterogenous autosomal dominant inheritance

47
Q

Types of migraines

A

Common (without aura) - most common in children. a/w N/V, classic (with aura), complicated (basilar, ophthalmoplegic, confusional, hemiplegic)

48
Q

Migraines clinical features

A

in infants - irritable, sleepy, pallor, vomiting; young child - periodic headaches with n/v, relieved by rest. Usually unilateral throbbing headaches in kids with photofobia and phonofobia

49
Q

What is the pharm prophylaxis for migraines?

A

beta blockers (propanolol), TCAs (amitryptiline), antihistamines, Ca chanel blockkers, anticonvulsants (depakote). Children >12 years can use nasal spray sumitriptan other triptans.

50
Q

What is the ppt for tension headaches

A

bilateral pressing tightness anywhere on cranium, or suboccipital regional, usually frontal, hurting or aching quality not throbbing. Usually lasts more than 30minutes can wax and wane and last for days. No N/V not aggravated by physical activity. Most hcildren have insight into origin (poor self image, fear of school failure)

51
Q

Tx for tension headaches

A

Reassurance explanation. Supportive counseling. Rule out refractory errors in eyesight as cause of tension

52
Q

Organic etiology in headaches usually suggested by?

A

Occipital headache and red flags

53
Q

Characteristics of increased ICP headaches

A

Diffuse early morning headaches, early morning vomiting, headache wornsed by increased ICP (cough, sneeze, valsava). As ICP increases, headache is constant. Child irritable and lethargic

54
Q

What is cerebral palsy

A

nonprogressive central motor impairment syndrome due to insult or anomaly of the immature CNS. Extent of intellectual impairment varies, presentation of the impairment changes with age

55
Q

Etiology of CP

A

association with low birth weight babies, often obscure - no definite cause in 1/3rd cases, only 10% related to intrapartum asphyxia, 10% due to postnatal insults

56
Q

Types of CP

A

1) Spastic (70-80% of cases) 2) athetoid/dyskinetic (10-15%) 3) ataxic

57
Q

What is the clinical ppt of spastic CP

A

truncal hypotonia in 1st year; increased tone, increased reflexes, clonus. Affects one limb (monoplegia), affects one side of body (hemiplegia), affects both legs (diplegia), affects all limbs (quadriplegia).

58
Q

What are the brain areas invovled in spastic CP?

A

UMN of pyramidal tract; diplegia a/w periventricular leukomalaca (PVL) in premature babies; quadriplegia associated with asphyxia

59
Q

What is the clinical ppt of athetoid/dyskinetic CP? What areas of the brain are involved?

A

athetosis (involuntary wrihing movements) +/- chorea (involuntary jerking movements). Can involve face and tongue (dysarthria). Basal ganglia (may be associated with kernicterus)

60
Q

NF-1 incidence

A

1:3000. A/D

61
Q

Mutation of NF-1

A

17q11.2

62
Q

Dx of NF-1 requires

A

2 or more of 1) >=6 café au lait spots (>5mm if prepubertal, >1.5cm if post pubertal) 2)>= 2 neurofibromas of any type or one plexiform neurofibroma 3) >= 2 Llsch nodules 4) optic glioma 5) freckling in axillary or groin area 6) distinctive bony lesion like sphenoid dysplasia or cortical thinning of long bones 7) first degree relative with NF-1

63
Q

NF-2 incidence?

A

1:33000. A/D

64
Q

Dx of NF-2

A

Either bilateral vestibular scwannomas or first degree relative with NF-2 and either a neurofibroma, meningioma, glioma or schwannoma

65
Q

NF-2 a/w

A

posterior subcapsular cataracts

66
Q

Sturge weber syndrome

A

Port-wine nevus syndrome in V1 distribution with associated angiomatous malformations of brain causing contralateral hemiparesis and hemiatrophy.

67
Q

Sturge weber a/w

A

Glaucoma, seizures and mental retardation

68
Q

Tuberous Sclerosis?

A

A/D

69
Q

Findings in TS

A

Adenoma sebaceum (angiokeratomas on face, often in malar distribution) , shagreen patch (isolated plaque over lower back, buttocks), ash leaf hypopigmentation seen with Woods lamp; cardiac rhabdomyomas, kidney angiomyolipoma, mental retardation and seizures

70
Q

What brain findings in TS?

A

Subependymal nodules may evolve into giant cell astrocytomas (may cause obstructive hydrocephalus), cerebral cortex tubers (areas of cerebral dysplasia)

71
Q

What is acute disseminated encephalomyelitis?

A

Immune mediated inflammatory disorder of the CNS, widespread demyelination mostly affecting white matter of brain and spinal cord

72
Q

ADEM usually preceded by

A

Viral infection or vaccination although no clear precedent event in 26% of cases

73
Q

What is the median age/onset of ADEM, m/f ratio, and incidence in NA?

A

5-8 years old, 2:1 male to female ratio and 0.4 per 100,000 children

74
Q

MRI findings of ADEM?

A

large multifocal poorly marginated regions of demyelination affecting bilateral subcortical white amtter and deep grey matter (thalamus, basal ganglia).

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