neurology Flashcards

1
Q

rate of epilepsy occurrence in canada

A

1-2% of canadians

40 000 people in BC

associated with cerebral palsy, autism, intellectual impairment

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2
Q

what is an epileptic seizure

A

paroxysmal interference of brain function due to abnormal electrical discharge in the brain

sudden disruption of the brains normal electrical activity

this may result in motor activity, sensory symptoms, behavior changes and/or altered consciousness depending on which areas of the brain are involved

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3
Q

how common are seizures

A

1 in 12 people will have a seizure

50% of people who do, have only 1

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4
Q

define epilepsy

A

2 or more unprovoked seizures

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5
Q

name the generalized seizures

A
tonic
atonic
absence
clonic
tonic-clonic
myoclonic
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6
Q

name the focal seizures

A

dyscognitive

bilateral convulsive seizures

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7
Q

what are the 5 questions to ask about a first afebrile seizure?

A
  1. was the episode an epileptic seizure
  2. what was the cause of the seizure
  3. what investigations should i do
  4. does the child require treatment
  5. what else should i think about
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8
Q

how do you determine if a seizure was an epileptic seizure

A

clinical hx is key

detailed description of the event and circumstances around the event

  • -setting in which it occurred
  • -observation at onset of the event
  • -how did the patient feel just prior to the event
  • -other important factors like development, febrile seizures, family hx of epilepsy, history of brain injury/infection
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9
Q

what are the factors that favor an epileptic seizure

A

aura

brief

post ictal confusion

automatisms

amnesia of event

incontinence

tongue biting

events in sleep

eyes open

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10
Q

what are some non epileptic paroxysmal events

A
  1. syncope and reflex anoxic seizure
  2. day dreaming
  3. steroetypies
  4. panic/anxiety attacks
  5. psychogenic nonepileptic seizures
  6. sleep disorders
  7. migraine, complex
  8. transient ischemic attack/stroke
  9. paroxysmal movement disorder
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11
Q

what are some examples of syncope/reflex anoxic seizure episodes

A

vasovagal syncope
breath holding spells
orthostatic hypotension
cardiogenic (i.e prolonged QT, other arrhythmia)
Gastroesophageal reflux (sandifer syndrome)

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12
Q

what causes syncope

A

sudden decrease in oxygen availability to the brain (via reduced cerebral blood flow or oxygen content of blood)–> reflex anoxic seizures

NOT epileptic seizures

can result in LOC, GTC, incontinence

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13
Q

what causes epileptic seizures in childhood (categories)

A

50% genetic

30% structural-metabolic

10% unknown

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14
Q

what are the genetic causes of epileptic seizures in childhood

A

childhood and juvenile absence epilepsy

benign Rolandic epilepsy of childhood

juvenile myoclonic epilepsy

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15
Q

what are the structural-metabolic causes of epileptic seizures in childhood

A

malformation of brain development

neurocutaneous syndromes like tuberous sclerosis

vascular malformations

congenital or acquired CNS infections

hypoxic ischemic brain injury

stroke

traumatic brain injury

tumour

inborn error of metabolism

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16
Q

how do you distinguish between idiopathic and symptomatic epilepsy

A

idiopathic–> norma development, neuro exam. no family hx of epilepsy. no hx brain injury. characteristic EEG abnormalities

symptomatic–> developmental delay, hx brain injury, abnormal neuro exam, other congenital malformations

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17
Q

what investigations should be done in a child presenting with first epileptic seizure

A

a child presenting immediately after this first seizure should have a blood glucose checked

further labs should be guided by clinical judgement at the time i.e vomiting, fever, illness

consider toxicology

ECG with QTc interval (may be syncopal episode)

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18
Q

what is the most useful investigation for seizures

A

EEG

assessing risk of recurrent seizures

epileptic syndrome or seizures that may be associated with a structural lesion

can guide anticonvulsant meds

helps ID prognosis

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19
Q

when should you do the EEG

A

does not need to be done in ER

order an outpatient sleep deprived EEG

(may need sedation i.e autism)

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20
Q

does a normal EEG exclude epileptic seizures?

A

no

in patients with epilepsy, 1st EEG displays epileptiform activity only 50% of the time –> if you suspect epilepsy but EEG is normal, repeat EEG increases yield

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21
Q

what is the significance of an abnormal EEG in the setting of a seizure

A

if it is true epileptiform activity, there is a two fold increase in tendency to seizure

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22
Q

can epileptiform discharges alone dx epilepsy

A

no–not diagnostic without appropriate clinical history

certain epileptiform discharges are seen in 4% of children without epilepsy

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23
Q

what kids should get neuroimaging

A

children who have had more than 1 afebrile seizure

exception is if the clinical history and EEG findings are consistent with genetic etiology

**neuroimaging abnormalities occur in up to 1/3 of children with a first afebrile seizure, but only 2% will demonstrate a clinically significant abnormality that will influence management

**seizures are an uncommon presenting symptom of a brain tumour in kids

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24
Q

what are the indications for a pediatric neurologist

A

focal lesion on neuroimaging

uncertainty as to seizure type and/or epilepsy syndrome

seizure associated with developmental delay/regression

multiple seizure types

infantile spasms

failed appropriate therapy with two or more AEDs

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25
Q

how do behavioral problems in kids with epilepsy compare to those with diabetes

A

much more common in kids with epilepsy

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26
Q

how does a new epilepsy diagnosis in a kid affect the mom

A

1/3 of mothers of kids with newly dx epilepsy exhibit sx of PTSD or MDD

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27
Q

define benign febrile seizures

A

an idiopathic (inherited) epilepsy

tendency to seizures associated with fever or an intercurrent infection in normal children aged 6 mo-5 years (most 1-2 years)

occurence 2-4%–> most common inherited form of seizures

NOT associated with meningitis, encephalitis or toxins…

normal CT scan, often family history, usually developmentally normal

most common seizure type is generalized tonic-clonic

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28
Q

describe a typical febrile seizure

A

1 seizure in 24 hours

less than 5 min duration

no focal features

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29
Q

describe an atypical febrile seizure

A

2 or more seizures in 24 hours

last longer than 5 min

focal seizures

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30
Q

what are the recurrence risks of febrile seizures

A

1/3 will have 1+ seizure

1/11 will have 3+ seizures

75% of the recurrence happen within 12 mo

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31
Q

what puts a kid at increased risk of a recurrent febrile seizure

A

family hx

younger than 12 mo

low temp at seizure

*no increased risk of recurrence with atypical febrile seizures

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32
Q

what are the risk factors for developing Afebrile seizures after febrile seizures

A

developmentally abnormal prior to febrile seizure

atypical febrile seizure

positive family history of epilepsy

risk depends on number of risk factors–> 0 risk factors is less than 2% risk, 3 risk factors is 10% risk

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33
Q

do you start treatment after a single, brief febrile seizure?

A

no–> since the majority of kids will not have recurrent seizures

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34
Q

when should you give medication for a kid who had febrile seizures?

A

if the kid had a prolonged febrile seizure, teach parents to give VALIUM or buccal MIDAZOLAM to abort a seizure lasting longer than 5 min

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35
Q

what parental counseling should be done after a febrile seizure

A

first aid management of a seizure at home

safety precautions around water/bathing

risk of recurrence of febrile seizures

risk of recurrence of epilepsy

risks of brain damage (none for seizures lasting less than 30 min)

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36
Q

list primary headaches

A

migraine headaches–with and without aura, migraine equivalents

tension headaches

trigeminal autonomic cephalagias (TACs)

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37
Q

list secondary headaches

A

structural (tumour, Chiari etc)

infectious

hemorrhagic

traumatic

vascular

altered ICP without intracranial lesion (pseudotumour cerebri/idiopathic intracranial hypertention, post LP headache)

med overuse

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38
Q

what should you ask about on hx for headaches

A
  1. course
    - -onset (new vs old)
    - -frequency
    - -duration
    - -course (worsening, improving, stable, fluctuating)
  2. onset and timing
    - -triggers (sleep deprivation, illness, food)
    - -timing (nocturnal, first thing in the morning, later in the day)
    - -episodic vs continuous
    - -rate of onset (sudden, gradual)
    - -warning signs (aura)
    - -exacerbating factors (valsalva, position)
  3. characterstics
    - -severity
    - -quality (throbbing, pounding, pressure, squeezing, stabbing, burning, dull)
    - -location (unilateral vs bilateral, generalized vs localized)
  4. associated features
    - -N/V
    - -photo or phonophobia
    - -neuro features/auras
  5. systems review
    - -loss of skills or developmental regression
    - -neuro sx and signs
    - -systemic illness (weight changes, fevers etc)
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39
Q

what should you pay attention to in the physical exam for a kid with headache

A

head circumference

high ICP? papilledema on fundoscopy or CN palsies

evidence of focal neuro abnormalities (hemiplegia, ataxia, vision or movement abnormalities, abnormal reflexes)

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40
Q

in what cases should you consider imaging in the setting of a headache

A
  1. recent onset of severe headache
  2. change in type of headache
  3. neuro dysfunction
  4. focal findings
  5. signs of increased ICP
  6. altered consciousness
  7. co existence of seizures
41
Q

when is imaging not indicated in the setting of a headache

A

recurrent headaches

normal exam

42
Q

are routine bloodwork or EEG indicated in evaluation of headache?

A

no not really

43
Q

what are the headache red flags (12)

A
  1. sudden, worst, thunderclap headache
  2. progressive headache
  3. occipital headache
  4. positional
  5. worse with valsalva, exertion
  6. present first thing upon waking up
  7. wakes patient at night
  8. neuro or devel regression
  9. seizures
  10. systemic illness
  11. focal findings on exam
  12. findings suggestive of increased ICP
44
Q

what are migraines

A

paroxysmal headaches separated by pain free episodes

45
Q

what are associated features of migraine

A
aura
nausea
abdo pain
throbbing quality
unilateral 
family history
46
Q

what are the diagnostic criteria for migraine without aura

A
  1. at least 5 attacks fulfilling the next 3 criteria
  2. headache lasts 2-72 hours
  3. headache has at least two of–> unilateral location (may be bilateral or frontotemporal but not occipital), pulsating quality, moderate or severe pain, aggravation by or causing avoidance of routine physical activity
  4. during headache at least 1 of–> nausea and/or vomiting, photophobia and/or phonophobia which may be inferred from behavior
  5. not attributable to another disorder
47
Q

what is an aura

A

attacks of reversible focal neuro sx

usually develop gradually over 5-20 min

lasts less than 60 min

migraines usually follow but may be absent

most commonly visual–> binocular scotoma, distortion/hallucinations, monocular

48
Q

what are the diagnostic criteria for migraine with aura

A
  1. at least two attacks fulfilling the next 2 criteria
  2. one or more of the following fully reversible aura symptoms
    - -visual, sensory, speech and/or language, motor, brainstem, retinal
  3. at least two of the following 4 characteristics–>
    - -at least one aura symptoms spreads gradually over more than 5 minutes and/or two or more symptoms occur in succession
    - -each individual aura symptom lasts 5-60 minutes
    - -at least one aura symptom is unilateral
    - -the aura is accompanied or followed within 60 min by a headache
  4. not better accounted for by another ICDH-3 diagnosis and TIA has been excluded
49
Q

what are other types of migraine with aura

A

brainstem aura

hemiplegic migraine

retinal migraine

alice in wonderland syndrome

50
Q

describe a basilar migraine

A

typically younger (mean age 7y)

posterior fossa involvement

vertigo, dizzyness, ataxia, nausea, diplopia, tinnitus, hearing loss etc

  • *neuroimaging to rule out structural posterior fossa lesion recommended
  • *seizures and ingestions are also on the ddx
51
Q

describe a hemoplegic migraine

A

aura has “stroke like” quality–typically hemiplegia

may also include hemisensory changes, aphasia, visual field deficits

several familial forms

  • *neuroimaging and other tests to rule out vascular, intracranial etiologies
  • *ddx is stroke, TIA, seizure (post ictal todd’s paresis), demyelinating disease, tumour, hemorrhage, metabolic disturbance
52
Q

what is alice in wonderland syndrome

A

visual distortions, may be bizarre/vivid

macropsia–> object appear larger
micropsia–> objects appear smaller
metamorphopsia–> objects appear distorted
teleopsia–> objects appear far away

53
Q

what are “childhood periodic syndromes” and why do we care about them

A

commonly precursors of migraine

cyclical vomiting, abdo migraine, benign paroxysmal vertigo of childhood

54
Q

what is the pathophysiology of migraine generally

A

inherent vulnerability with hyperexcitable cortex

often inherited

inherited vulnerability plus triggering events cause attacks

55
Q

what happens in the brain to cause a migraine

A
  1. cortical spreading depression
    - -neuronal event of neuronal depolarization, spreading across the cortex–> pathophysiologic correlate of migraine aura
  2. accompanied by oligemia, later followed by hyperemia
  3. extravasation of proteins (sterile inflammation) into dural vessels–> activation of meningeal afferents–> trigeminal activation–> pain
  4. role of central brainstem structures in modulating pain (locus ceruleus–adrenergic, dorsal raphe–serotoninergic)
  5. sensitivity to activities and cutaneous allodynia due to sensitization of trigeminal afferents
56
Q

what are the principles of migraine treatment

A

parents must recognize “typical” headaches

best to treat headache at ONSET of pain
–delay makes it harder to treat and more likely to have chronic or status migrainosus

use adequate dosing for age and weight

goal to relieve symptoms as best as possible and enable patient to return to normal function within 1-2 hours

tx encompasses lifestyle mods/prevention, meds (abortive and prophylactic meds) and non pharma intervention

57
Q

what lifestyle mods can be used to manage migraine

A

ID and eliminate triggers

improve sleep

ensure adequate food and fluid intake

avoid stressors

58
Q

what is used for abortive therapy in migraines

A
  1. ibuprofen (10mg/kg/dose)
    - -FIRST line, superior to acetaminophen
    - -may use up to 15mg/kg/dose
  2. acetaminophen (15mg/kg/dose)
    - -possible faster than ibuprofen
    - -use in those with poor tolerance to ibuprofen or contraindications
    - -avoid exceeding 60mg/kg/day due to hepatotoxicity
  3. triptans
    - -recommended in patients whose headaches respond poorly to NSAIDs or acetaminophen
59
Q

what are triptans

A

migraine specific agents

selective serotonin receptor AGONIST at 5-HT1B and 1D sites

4 recommended for pediatric use

  • -almotriptan (12 and older)
  • -rizatriptan (6-17 years old)
  • -sumatriptan
  • -zolmitriptan
60
Q

what are the contraindications to triptans

A
  1. vascular disorders
    - -stroke, TIA, HTN, angina pectoris, MI, peripheral artery occlusive disease, reynaulds
  2. vascular risk factors
  3. MAOI use within two weeks
  4. ergotamine use
  5. impaired renal or liver function
  6. pregnancy
  7. lactation
61
Q

what is the emergency treatment for a migraine

A
  1. analgesics (naproxen, diclofenac, ketorolac… IV or IM)
  2. dopamine antagonists (help N/V, specific antimigraine)
  3. triptans
  4. ergots (i.e DHE)

**do not use ergots and triptans together

62
Q

why do you admin dopamine antagonists in migraine emergency

A

help with N/V

interferes with dopaminergic system–> specific antimigraine effect

example: metoclopramide, chlorpromazine

risk of EPS (dytonia, hyperkinesis)… can give diphenhydramine prophylaxis

63
Q

why do you administer ergots in migraine emergency

A

i.e DHE

are 5-HT agonists wth wide range of effects

side effects are N, dizziness, paresthesias, abdominal/chest pain, rebound

contra-indications are pregnancy, HTN, renal and hepatic failure

DO NOT USE WITH TRIPTANS

little pediatric data

64
Q

when should you use prevention meds for migraines

A
  1. frequent (more than 1-2 per week or 3-4 a month)
  2. headache related disability that interferes with school attendance, daily routine, daily activities

also if…
acute tx options are ineffective or not tolerated or overused, or if the patient has extremely intensive, prolonged (more than 48 hour), hemiplegic or basilar type migraines or severe aura

65
Q

what natural products can prevent migraine

A
  1. riboflavin (vitamin B2)
  2. magnesium
  3. coenzyme Q10–expensive with questionable efficacy
  4. butterbur
    - -currently not recommended due to risk of liver toxicity
66
Q

what are the preventative migraine meds

A
  1. amitriptylline
    - -TCA with antichoinergic SEs and need to rule out long QT before starting
  2. propanolol
    - -beta blocker… avoid in patients with asthma and heart block and in highly athletic patients
  3. flunarazine
    - -calcium channel blocker, efficacy high in hemiplegic migraine
  4. cyproheptadine
    - -FIRST LINE in less than 6 years old…often useful for migrain equivalents, but causes sedation adn weight gain
  5. valproic acid
    - -causes weight gain, risk of hepatotoxicity, plately dysfunction, teratogen
  6. topiramate
    - -can cause anorexia, renal stones, cognitive slowing
67
Q

what are tension type headaches

A

may be similar pathophysiologic spectrum as migraine

bilateral, pressing/tightening quality

mild to moderate severity

not exacerbated by activity

no N/V usually

photophobia OR phonophobia may be present but NOT BOTH

tx with simple analgesics; risk of med overuse and rebound

68
Q

what is another name for idiopathic intracranial HTN

A

pseudotumour cerebri or benign intracranial HTN–not not benign

69
Q

what is idiopathic intracranial HTN

A

raised pressure (above 2oo mm/water) in absence of intracranial lesions

caused by/associated with obesity, endocrinopathies (hypothyroid, addisons), meds (tetracycline, contraceptives, oral steroids), vitamin A intox, SLE

if untreated can lead to vision loss

70
Q

how do you treat idiopathic intracranial HTN

A

acetazolamide

optic neuronal sheath fenestration

therapeutic LP

71
Q

name the trigeminal autonomic cephalagies

A

cluster headaches

paroxysmal hemicrania

72
Q

what are cluster headaches

A

uncommon in kida/adolescents
m:f is 3:1

severe unilateral retroorbital pain lasting 15-180 minutes

ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, edema, sweating, miosis, ptosis

may have attacks that last weeks to months

73
Q

how do you treat cluster headaches

A

inhaled oxygen

sumatriptan SC or IM

verapamil, valproic acid, lithium

74
Q

what is paroxysmal hemicrania

A

intense periorbital or temporal unilateral pain for 2-30 min

up to dozens of times a day

may also have ipsilateral autonomic features

75
Q

tx of paroxysmal hemicrania

A

responsive to indomethacin

76
Q

what is an ice pick headache

A

momentary (seconds)

sharp/jabbing

once or several times a day at irregular intervals

periorbital or temporal

more common in patients with migraine or cluster headaches

77
Q

treatment of ice pick headache

A

indomethacin

78
Q

what are the two components of conciousness

A

wakefulness and awareness

79
Q

what is obtundation

A

mild to mod reduction in alertness

decreased interest in environment

appear sleepy, may sleep if left alone

80
Q

what is stupor

A

unresponsiveness with little to no spontaneous movement

aroused only by vigorous stimulation

81
Q

what is coma

A

unrousable, sustained unconsciousness

dysfunction of ascending reticular activating system and/or both cerebral hemispheres

82
Q

what is a vegetative state

A

complete unawareness of self

sleep wake cycle present though irregular

some preservation of autonomic functions

cannot interact with environment

irregular periods of wake that cycle with sleep

may exhibit spontaneous sounds or emotional expressions–but sustained response to enviro stimuli is lacking

no visual tracking

83
Q

what is a minimally conscious state

A

minimal awareness of self or environment but CAN interact with the environment

may follow simple commands

yes and no answers

purposeful behavior in respnose to stimuli like smiling, vocalization, reaching

84
Q

what is brain death

A

permanent, irreversible absence of all brain function

includes brainstem functions

no respiratory drive

hypothermia, anesthesia, sedatives may mimic this though the brainstem responses and respiratory drive are often present in comatose patients

85
Q

how is the glasgow coma scale adjusted for children

A
  1. eye opening–> out of 4. 4–spontaneous, 3–to SOUND (rather than command)
  2. verbal–> out of 5
    5–age appropriate verbalization
    4–cries but consolable
    3–irritable, uncooperative, aware of environment
    2–irritant persistent cry, inconsistently inconsolable
    1–unaware of environment/parents, inconsolable
  3. motor–> out of 6
    6–obeys or has spontaneous movement
86
Q

dilated, symmetric pupils suggests…

A

hypoxic ischemic injury

87
Q

dilated, asymmetric pupils suggests..

A

compression (i.e herniation)

88
Q

small, reactive pupils suggests…

A

drug ingestions, metabolic disorders, hypothalamic injury

89
Q

midposition and unresponsive pupils suggests…

A

midbrain lesion

90
Q

what does decorticate (flexion) posturing suggest

A

higher lesions (midbrain and above)

91
Q

what does decerebrate (extensor) posturing suggest

A

lower brainstem lesion (midbrain or below)

tends to carry poorer prognosis

92
Q

what is tone

A

resistance to passive muscle stretch

93
Q

how is tone controlled

A

mediated by elements of both central and peripheral nervous systems

facilitators and inhibitors–> sum total results in clinically observed and measured tone

lesion localization results from functional anatomy

94
Q

what are you looking at in particular in the exam of a floppy infant

A
dysmorphic features
other affected systems (cardiomyopathy etc)
joint contractures
pectus excavatum
flat occiput
hip subluxation
95
Q

by what age should head track with body when being lifted by the arms from supine position (traction response)

A

by one month

96
Q

what are some causes of hypotonia in the infant

A
  1. brain–>benign congenital hypotonia, genetic (i.e prader willi, trisomy), HIE, malformation, inborn error of metabolism
  2. spinal cord–> ischemia, trauma
  3. anterior horn cell–> SMA
  4. peripheral nerve–> hereditary neuropathy
  5. NMJ–> infantile botulism, transient neonatal MG, congenital MG
  6. muscle–> congenital myopathy, congenital muscular dystrophy, congenital myotonic dystrophy, metabolic myopathy
97
Q

what signs would suggest a central cause of hypotonia

A

impaired consciousness or seizures

dysmorphic features

fisting of hands/scissoring of legs

presence or exaggeration of moro reflex

norma or brisk tendon reflexes

98
Q

what signs would suggest lower motor neuron cause of hypotonia

A

absent or decreased tendon reflexes

absent moro

fasciculations

muscle atrophy