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Neurology Oski > Nelson Essentials Neuro > Flashcards

Nelson Essentials Neuro Flashcards

1
Q

Skin features of tuberous sclerosis

A
  1. adenoma sebaceum - fibrovascular lesions that look like acne on nose and male regions
  2. nail fibromas
  3. ash-leaf spots - hypo pigmented macules
  4. Shagreen patches
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2
Q

What is Broca aphasia

A

anterior, expressive aphasia

sparse, confluent language

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3
Q

What is Wernicke aphasia

A

receptive, posterior aphasia

inability to understand language, with speech that is fluent but nonsensical

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4
Q

What is vision in newborns? in older infants?

A

should be able to follow face in a dark room

20/200 in newborns, 20/20 in 6 month olds

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5
Q

What is an afferent pupillary defect

A

swinging flashlight test - light on the abnormal eye, both pupils dilate inappropriately; on the normal eye, they both constrict

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6
Q

What is Horner syndrome

A

meiosis
anhydrosis
ptosis

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7
Q

What is the doll’s eye maneuver?

A

rotate the infant’s head - > if brainstem is okay, then moving the head of newborn or comatose patient, eyes will move to the left and vice versa
in awake, older patients, voluntary eye movements mask the reflex

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8
Q

What does the eye look like in oculomotor 3rd CN palsy?

A

eye will be down and out with ptosis and dilated pupil

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9
Q

CN IV palsy?

A

weakness of downward eye movement

vertical diplopia

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10
Q

CN VI palsy

A

can’t move the eye outward - therefore the eye will be inward
has a long intracrnial route - a frequent sign of increased ICP (but nonspecific)

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11
Q

Which cranial nerves are tested by corneal reflex?

A

V opthalmic division and VII at agy age

facial sensation

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12
Q

weakness of a patient’s face, only affects the lower face and mouth? where is the lesion?

A

consider upper motor neuron lesion - tumor/stroke abscess

-

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13
Q

weakness of an entire side of the face?

A

CN 7 palsy - Bell palsy -

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14
Q

True or false - very premature neonates should have a gag reflex

A

very immature neonates may not have but all other ages should have a brisk gag

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15
Q

atrophy and fasciculation of the tongue, what type of lesion to think of?

A

anterior horn cell problem - i.e. in SMA
most reliable when baby asleep
tongue will deviate toward the weak side in unilateral lesions

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16
Q

Conditions with decreased muscle bulk

A

lower motor neurone conditions - neuropathies, SMA

muscle bulk is diminished or atrophic

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17
Q

Conditions with increased muscle bulk

A
  1. myotonia congenita

pseudo hypertrophy of calves - muscular dystrophy

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18
Q

Ways to access cerebellar dysfunction?

A
  1. ataxia
  2. intension tremor
  3. dysmetria
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19
Q

When should the Babinski be down going?

A

12-18 months

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20
Q

DTRs in lower motor neurone vs upper?

A

decreased in LMN, increased in UMN

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21
Q

What does muscle fibrillation/fasciculation indicate?

A

indicates denervation of muscles/nerves

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22
Q

Abnormal muscle response to repetitive nerve stimulation, Differential?

A
  1. abnormal response to repetitive stimulation of nerve: Neuromuscular conditions: M. gravis and botulism
  2. lower amplitude and duration of muscle action potentials - in primary muscle diseases
  3. slowed nerve conduction velocities - demyelinating nerve conditions - i.e. GBS
  4. lower amplitude of signal - decreased in axonal neuropathies
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23
Q

new onset of complex partial seizures, what type of imaging to do?

A

MRI - may not see areas of focal cortical dysplasia or other subtle lesions , may not be apparent on CT

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24
Q

Most common type of recurrent primary headache in children and teens

A

tension types headaches - most common type of recurrent primary headaches in children and teens
pain is global and squeezing
can last hours to days
no associated nausea, vomiting, phono phobia or photophobia

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25
Q

Migraine headaches

A

stereotyped attacks of frontal, bitemporal or unilateral moderate to severe, pounding or throbbing pain aggravated by activity
lasts 1-72 hours
associated symptoms: nausea, vomiting, pallor, photophobia, phono phobia, desire to seek a quiet dark room for rest
can be associated with auras
complex, atypical symptoms with migraine - i.e. hemiparesis, monocular blindness, ophthalmoplegia or confusion need investigations

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26
Q

Most common causes of secondary headaches -

A
  1. head trauma
  2. intercurrent viral illness
  3. sinusitis
  4. medication overuse headaches
  5. increased ICP - if worse h/a lying down or when awake , worse when coughing/valsalva, or pending over
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27
Q

which pattern or headache most concerning

A

chronic progressive
need to image
MRI is the best - since better to detect posterior fossa lesions

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28
Q

Treatment of migraines:

A

symptomatic or abortive tretament - early analgesia, rest and sleep
acetaminophen/NSAID
hydration and anti-emetics
if these don’t work, then consider triptans - serotonin receptor agonists

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29
Q

contraindications to triptans

A

focal neuro deficits with migraine

signs consistent with basilar migraine - syncope - because of risk of stroke

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30
Q

Preventative treatments for migraines

A

can consider when >1 disabling headache per week
TCAs - ie amitriptylline, nortriptyline
anticonvulsants - topiramate, valproic acid
antihistamines - cyproheptadine
beta-blockers - propanolol
calcium channel blockers - flunarizine, verapamil

before these; lifestyle modification : sleep, routines, exercise, identify precipitating factors (i.e. caffeine, foods, stress, meals missing, dehydration
psych/stress management/biofeedback are other things to consider

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31
Q

EEG pattern in absence seizure

A

3hz spike and wave
can have multiple in one day
should be back to self ASAP

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32
Q

what age does absence seizure usually start

A

4-6 year old

can provoke with lights and/or hyperventilation

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33
Q

BECTs

A

usually age 5-10 year old
seizures usually during sleep or on awakening in most patients
focal motor seizures involving face and arm - abnormal movement/sensation, drooling, guttural sound
may have speech arrest/swallowing problem
sometimes get secondary generalization

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34
Q

BECTS - EEG findings and , do you need imaging?

A

imaging (interictal _ bilateral centrotemporal sharp waves but otherwise nomal
if otherwise normal neuro exam - then don’t need imaging
intellectual outcome normal, resolves after puberty

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35
Q

BECT comorbidities

A

ADHD/learning difficulties

36
Q

Absence epilepsy - if doesn’t remit, what type of epilepsy might they develop

A

juvenile myoclonic epilepsy

37
Q

patient with absence epilepsy and tonic - clonic seizures, 1st choice treatment?

A

valproic acid, can help with both

38
Q

classic treatment for juvenile myoclonic epilepsy

A

valproic acid (but other meds also have been showed
most common generalized epilepsy among teens and young adults
myoclonic jerks in the AM
generalized tonic-clonic seizures
absence seizures

39
Q

when do infantile spasms happen and how long do they last usually?

A

usually <2 seconds
most when awakening or going to sleep
often have clusters
West syndrome: infantile spasms, developmental regression, abnormal EEG pattern (hypsarrhthmia)
age of onset: 3-8 months is the peak **may be

40
Q

Differential for infantile spasms

A
  1. tuberous sclerosis
  2. malformations of cortical development
  3. genetic syndromes - i.e. trisomy 21
  4. acquired brain injury - i.e. stroke, HIE
  5. metabolic disorders - ie PKU
41
Q

better prognosis for symptomatic infantile spasms or from cryptogenic?

A

cryptogenic somewhat better than symptomatic (i.e. those who have an underlying aetiology)

42
Q

Treatment of infantile spasms

A

ACTH treatment, steroids, vigabatrin

for patients with tuberous sclerosis - whose vigabatran

43
Q

What is Lennox-Gastaut syndrome

A

severe spilepsy syndrome
most kids present before 5 years old
multiple seizure types - including atonic, focal, atypical absence, generalized tonic, clonic or tonic-clonic varieties
big Nelson says:
between age 2-10 years, developmental delay, multiple seizure types
tonic seiuzures occur while awake or while asleep
EEG findings: 1-2 Hz spike and slow waves
most are left with significant MR

44
Q

What is Landau-Kleffner syndrome

A

abrupt loss of previously acquired language
EEG highly epileptiform
peak area of abnormality in dominant perisylvian region
should consider in kids who have clear autistic regression
Big nelson:
rare condition of unknown cause
hearing is nona
have behavioural problems
lots of types of seizures
EEG findings more apparent in sleep- if you suspect this, need to do EEG during sleep
Treatment: valproic acid
onset at early age - poor prognosis

45
Q

What are benign neonatal convulsions

A

autosomal dominant genetic disorder - abnormal neuronal potassium channels
otherwise well newborns - focal seizures towards 5 days of age - “fifth-day fits”
usually have good response to treatment , favourable long-term outcome

46
Q

focal seizures - best drugs

A

oxcarbaepine, carbamazepine (big nelson)

little nelson also says phenytoin, lacosamide

47
Q

best med for absence seizures

A

ethosuximide

48
Q

juvenile myoclonic epilepsy - best med

A

valproate and lamotrigine

49
Q

best drug for lennox-gastaut

A

valproate topiramate, lamotrigine

50
Q

generalied epilepsy

A

valproate has been shown to be effective

51
Q

main side effect of vigabatrin

A

retinal toxicity

52
Q

baby nelson says for generalized seizures

A

clobazam, felbamate

53
Q

for both focal and generalized

A

lamotrigine, levetiractam, phenobarbital, topiramate, valproic acid, zonisamid, ketogenic diet

54
Q

side effects of valproate therapy

A

main one is liver toxicity in kids < 2year old, on polytherapy or with metabolic disorders , need to rule out metabolic disease

55
Q

baby with tongue fasciculations, absent DTRs, rapid/shallow/abdominal breathing -likely diagnosis

A

SMA type 1
(the other types of SMA present later and more gradually)
inheritance if autosomal recess

56
Q

how to diagnose SMA 1

A

diagnosis by genetic testing
CK may be normal or mildly elevated
EMG - fasciculations, fibrillations, other signs of denervation
muscle biopsy show grouped atrophy

57
Q

Treatment of SMA

A

minimize contractures, prevent scoliosis, maximizing nutrient, avoiding infections

58
Q

Most classic presentations of peripheral neuropathy in childhood

A
  1. GBS
  2. chronic inflammatory demyelinating polyneuropathy
  3. hereditary motor sensory neuropathy
  4. tick paralysis
59
Q

Most common cause of acute flaccid paralysis in children

A

gbs
Mycoplasma and Campylobacter cause it
post infectious autoimmune peripheral neuropathy
symptoms: areflexia, flaccidity and symmetrical ascending weakness
progression in hours, or over weeks
weakness can ascend to involve the arms, trunk and bulbar muscles
DTRs ABSENT (even if have some strength)
can get autonomic dysfunction

60
Q

what is miller fischer variant of Guillain-Barre?

A

ataxia
partial opthalmoplegia
areflexia

61
Q

What is the classic CSF finding in Guillain barre?

A

can be normal early in illness
elevated protein levels without significant pleocytosis
MRI - may show enhancement of spinal nerve roots

62
Q

Treatment of Guillain Barre

A

IVIG ; alternatives are plasma exchange dna immunosuppressive therapies

63
Q

When does Guillain Barre resolve

A

80% back to normal in 1-12 months

can have relapse

64
Q

Charcot Marie Tooth

A

start with frequent tripping/ankle weakness
will have pea caves deformity
eventually get weakness and atrophy of lower legs and hands, get mild to moderate sensory loss in hands and feet
no specific treatment

65
Q

Treatment of juvenile M. gravis?

A

pyridostigmine - inhibits acetylcholinesterase

if severe, may need immunosuppression

66
Q

Treatement of neonate born to mother with myasthenia gravis - who presents with ptosis, opthalmoplegia, weak facial movements, poor feeding, hypotonia, respiratory difficulty, variable extremity weakness

A

cholinesterase inhibitors, supportive care

67
Q

Congenital M. Gravis vs. juvenile

A

juvenile - variable ptosis, diplopia, ophthalmoplgia, facial weakness
worse when tired, with repetitive activity
some kids, never advances, others will have effect on resp and swallowing
vs. congenital - is a gene mutation in the neuromuscular junction ; might have resp problems, can have lifelong problems - some will respond to pyridostigment

68
Q

Diagnosis fo M. gravis

A

electrodecrement with 3hz repetitive stimulation
most will have antibodies to the acetylcholine receptor
“Tensilon” test - edrophonium chloride - cholinesterase inhibitor - can lead to transient improvement i strength (especially of ptosis)

69
Q

infantile botulism

A

presentation - constipation and poor feeding
then get hypotonia and weakness, CN dysfunction
can get resp failure

70
Q

Treatment of infantile botulism:

A

botulism IVIG

71
Q

Symptoms of muscular dystrophy

A
  1. awkward gait, +ve Gower sign
  2. cardiomyopathy
  3. scoliosis
  4. resp decline
  5. some boys have cognitive and behavioural dysfunction
72
Q

Labs in Muscular dystrophy?

A

elevated CK
genetic testing of dystrophin gene
can do prenatal diagnosis
1/3 of cases are new mutations

73
Q

inheritance of myotonic dystrophy

A

autosomal dominant genetic disease - progressive expansion of triplet repeat
genetic anticipation - each generation is worse than the previous

74
Q

Clinical features of myotonic dystrophy

A
  1. weakness - progressive facial and DISTAL extremity weakness
  2. myotonia: muscles have a hard time relaxing after contraction
  3. characteristic facial appearance
  4. cardiac muscle - arrythmias (can have second wave of arrythmias in teens, can kill ya)
  5. endocrinopathies
  6. immunologic deficiencies
    7 cataracts
  7. intellectual impairment

*severe congenital myotonic dystrophy - can also have some atony of uterus, present with HIE makes diagnosis even harder

75
Q

prenatal features which can suggest intrauterine neuromuscular disease

A

contractures
clubfoot
poor fetal movements

76
Q

Malignant hyperthermia

A
  1. increase temperature, muscle rigidity, metabolic and respiratory acidosis, hypotension, arrythmias, convulsions
  2. can have increase in CK then myoglobinuria, result in ATN, acute renal failure
    Diagnosis: genetic or in vitro muscle contraction
77
Q

Treatment of malignant hyperthermia

A

IV dantrolene
bicarb
cooling

78
Q

most common cause of hypotonia

A

HIE

79
Q

most common genetic causes of neonatal hypotonia

A

PWS, trisomy 21
failure to thrive, small hands and feet
in boys, small penis, small testicles and cryptorchidism

80
Q

What is benign congenital hypotonia

A

age 6-12 months, delay gross motor
family history
seem floppy from birth
usually catch up by age 3

81
Q

pediatric stroke management

A

thrombolytic not proven

anticoagulation if progressive

82
Q

most common causes of acute ataxia in children

A

drug intoxication
post infectious acute cerebellar ataxia
other causes: tumours, MS, strokes, bleeds , BPPV, head trauma, seizures, postictal states, migraine, paraneoplastic opsoclous-myoclonus syndrome with neuroblastoma, inborn errors of metabolism

83
Q

Ingestions for ataxia with lethargy and without?

A

ataxia with lethargy : sedative-hypnotic agent

without lethargy: ethanol or anticonvulsant intoxication

84
Q

What is the difference between truncal and appendicular ataxia?

A

truncal ataxia: disturbance of midline cerebellar vermis - ie medulloblastoma, acute postinfectius cerebellar ataxia, ethanol ingestion
Appendicular ataxia: disturbance of the ipsilateral cerebellar hemisphere

85
Q

usual symptoms of ataxia

A

broad based unsteady gait (truncal ataxia)
intention tremor or dysmetria
usually from cerebellar pathways, but CAN have from peripheral nerve lesions which cause loss of proprioceptive inputs to cerebellum (i.e. GBS)

86
Q

mitochondrial diseases which can present with ataxia and somnolence?

A 
Harnup
maple syrup urine
mitochondrial
abetalipoproteinemmia
vitamin E deficiency

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