Neuro Lecture Flashcards

1
Q

History & Initial Presentation

A

What are you looking for?
-Sudden onset
-Chronic complaints
-Change

What do you see?
-Dysmorphic features
-Abnormal characteristics
-Relative/family features

What does it mean?
-Brain
-Muscle
-Spinal
-Genetic

Where do you start?
-Birth history
-Developmental history
-Childhood illnesses
-Family history

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2
Q

Determinants?

A

Age and willingness to cooperate
Environment
Parental involvement
General health

Complexity of the complete exam
Changing function

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3
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4
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5
Q
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6
Q

At what age does the child sit & places weight on legs?

A

6 months old

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7
Q

At what age does the child walk with help?

A

1 year old

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8
Q

At what age does the child walk independently?

A

18 months old

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9
Q

At what age does the child run, kicks ball & goes up & down the stairs?

A

2 years old

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10
Q

At what age does the child stand on 1 leg & jumps?

A

3 years old

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11
Q

At what age does the child hop on 1 foot?

A

4 years old

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12
Q

At what age does the child hop on either leg?

A

5 years old

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13
Q

What are the neuro dx tests?

A

MRI
Lumbar Puncture
Karyotype - chromosome characteristics of an individual cell or of a cell line
EMG
EEG
Nocturnal Polysomnogram
Apnea
Multiple sleep latency test (MSLT) - a test of the propensity to fall asleep
Narcolepsy

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14
Q

a test of the propensity to fall asleep?

A

Multiple sleep latency test (MSLT)

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15
Q

chromosome characteristics of an individual cell or of a cell line

A

Karyotype test

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16
Q

What are the neuro lab tests?

A

Creatine Kinase (CK)
Complete Blood Count
with differential
Electrolytes
Glucose
Metabolic package
Lactic acid
Lead
Thyroid

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17
Q
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18
Q

What is macrocephaly?

A

-HC more than 2 standard deviations above the mean for age, sex and ethnicity

-Suggestive of increased ICP or can be familial

-Depending on cause – monitoring vs surgical

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19
Q

What is microcephaly?

A

-Primary vs secondary

-Commonly associated with CP, epilepsy, or learning or intellectual disabilities

-Symptomatic care and support

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20
Q

Craniosynostosis?

A

a birth defect that occurs when the skull’s sutures close too early, causing the skull to fuse together and limiting brain growth

Premature closure of the cranial sutures
1 in 2500 births
Surgery typically within the first 6 months of life

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21
Q

Microcephaly

A
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22
Q

Microcephaly

A

Primary vs secondary
Commonly associated with CP, epilepsy, or learning or intellectual disabilities
Symptomatic care and support

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23
Q
A

Tension Type Headaches
Migraines
Secondary Headaches

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24
Q

Acute temporal headache?

A

Single episode of pain without a history of such episodes. The “first and worst” headache raises concerns for aneurysmal subarachnoid hemorrhage in adults,

but is commonly due to febrile illness related to upper respiratory tract infection in children.

Regardless, more ominous causes of acute headache (hemorrhage, meningitis, tumor) must be considered.

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25
Q

Acute recurrent temporal headache?

A

Pattern of attacks of pain separated by symptom-free intervals. Primary headache syndromes, such as migraine or tension-type headache, usually cause this pattern. Recurrent headaches are occasionally due to specific epilepsy syndromes (benign occipital epilepsy), substance abuse, or recurrent trauma.

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26
Q

Chronic progressive temporal headache?

A

Implies a gradually increasing frequency and severity of headache.

The pathologic correlate is increasing ICP.

Causes of this pattern include pseudotumor cerebri, brain tumor, hydrocephalus, chronic meningitis, brain abscess, and subdural collections.

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27
Q

Chronic nonprogressive or chronic daily temporal headache?

A

Pattern of frequent or constant headache.
Chronic daily headache generally is defined as >3-mo history of ≥15 headaches/mo.
Affected patients have normal neurologic examinations; psychologic factors and anxiety about possible underlying organic causes are common

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28
Q

What are different types of headaches?

A

Tension Type Headaches
Migraines
Secondary Headaches

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29
Q

Pediatric migraine criteria

A
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30
Q
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31
Q

What are the triggers for migraine & headaches?

A

-Fever
-Stress
-Foods / additives
-Head injury
-Environmental factors
-Inherited disorders

32
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33
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34
Q

What are the diagnostics for migraines & h/a’s?

A

History
Physical
Neuroimaging

35
Q

What is the treatment for migraines & h/a’s?

A

Intermittent symptomatic analgesics
Dark, quiet room
Tylenol/NSAIDS
Lifestyle modifications
Preventative approaches
Non pharmacologic treatments

Abortive treatment - migraines
Ondansetron
Triptans

36
Q

What is tier 1 treatment for migraines?

A

Tier 1 (analgesics):
Acetaminophen 15 mg/kg per dose, or
Ibuprofen 10 mg/kg per dose, or
Naproxen 5 mg/kg per dose

37
Q

What is tier 2 for migraine treatment?

A

Tier 2 (triptans) for children who weigh > 50 kg (generally >10 yrs):
Sumatriptan 50 mg, or
Almotriptan 6.25 mg, or
Rizatriptan 5 mg (decrease dose with concomitant propranolol)

Tier 2 (triptans) for children 30 to 50 kg (generally 5 to 10 yrs of age):Rizatriptan one-half (2.5 mg) or one (5 mg) tablet (decrease dose with concomitant propranolol), or
Sumatriptan 5 mg nasal spray, or
Sumatriptan 25 mg tablet

38
Q

What is tier 3 for migraine treatment?

A

Combine a triptan with a tier 1 med., take at the same time, and/or
Promethazine 0.25 to 0.5 mg/kg per dose

39
Q

Seizures?

A

One of the most frightening events a parent can witness

5-10% of all children experience one or more seizures

About 1% of all children have epilepsy (seizure disorder)

Most common cause:
Unknown etiology
Febrile illness
Brain damage
Genetic factors
Seizures are an abnormal electrical impulse in the brain

40
Q

What are focal seizures?

A

Simple
Complex
Benign Rolandic
Secondarily generalized

41
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42
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43
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44
Q

Focal seizures with retained awareness : Simple Partial?

A

No loss of awareness
Involuntary movements
Various sensations/feelings/emotion
Can become secondarily generalized

45
Q

Focal seizures with impaired awareness: Complex Partial?

A

Temporal Lobe Epilepsy Psychomotor
Altered consciousness
Automatisms
Lip smacking
Rubbing hands together
Uncharacteristic behavior
Fearfulness
Agitation
Can become secondarily generalized

46
Q

Generalized Seizures?

A

Types
Tonic-Clonic
Absence
JME
Atonic

47
Q

Tonic Clonic Seizures (generalized seizure) what are the phases?

A

May begin with cry
Involves loss of consciousness
Tonic
Clonic
Postictal

48
Q

What is the management for tonic clonic seizure? (generalized seizure)?

A

ABC’s
Lay on side
Nothing in mouth
Clear area
Administer Diastat®

49
Q

Absent seizures?

A

Short lapses of awareness; impaired consciousness only (no LOC)
Most common ages 3-12
Diagnosis frequently months to years after signs and symptoms.
Frequently first noticed by teachers
May cause significant school problems

50
Q

Absent Seizures?

A
51
Q

Absent seizures?

A
52
Q

Juvenile Myoclonic Epilepsy (JME)?

A

Peak onset between 12-18 years

Myoclonic jerks
Arms, shoulders or neck involvement
No loss of consciousness
Mostly occur upon waking
Resemble startle response
Objects are dropped or thrown
Myoclonic - tonic clonic - absence seizures
Usually lifelong
Often inherited

53
Q

What is the peak onset of juvenile myoclonic epilepsy (JME))?

A

12-18 years old

54
Q

Atonic Seizures?

A

Drop attacks
Head drops
Sudden collapse
May need protective head gear
Resistant to AEDs

55
Q

Neonatal seizures?

A

Manifestations
Recurrent apnea
Eye deviation
Jerking movements of one limb or both limbs on the same side
Swimming or bicycling movements
Abnormal EEG
Frequently overlooked due to subtleness of manifestations

56
Q

Neonatal Seizures

A

Etiologies
Hypoxic/ischemic encephalopathy
Intracranial hemorrhage
Central nervous system infection
Cerebral infarction/malformations
Developmental/genetic defects
Drug withdrawal
Trauma
Inborn errors of metabolism
Hypocalcemia
Hypoglycemia
Benign neonatal seizures (familial / non-familial)

57
Q

Infantile Spasms

A

West syndrome - encephalopathy in infancy characterized by infantile spasms, arrest of psychomotor development, and hypsarrhythmia.

Age-dependent
2-7 months peak onset
Flexor and/or extension movement
Cluster series
Hypsarrhythmia - a disorganized, chaotic pattern of brain waves that occurs in children with infantile spasms
Resulting mental retardation
Treatment
ACTH and other antiepileptic drugs (AED’s)

58
Q

West syndrome?

A
  • encephalopathy in infancy characterized by infantile spasms, arrest of psychomotor development, and hypsarrhythmia
59
Q

Infantile spasms?

A

Etiology
Prenatal-microcephaly, polymicrogyria, schizencephaly, encephalopathies, congenital infections

Perinatal -hypoxic-ischemic, meningitis, trauma, intracranial hemorrhages

Postnatal-phenylketonuria, degenerative disease, encephalitis

60
Q

Febrile seizures?

A

3-4% of all children

Fever >38o C
Related to the rapid rate of temperature rise; not just the degree of fever
Typically generalized

Peak at 6-18 months
30-40% recurrence rate
Frequently + family history
3 months to 6 years

61
Q

Febrile seizures?

A

Risk factors
Younger than 12 months of age
Lasting >5 minutes
Partial seizure
Delayed development

62
Q

Treatment for febrile seizures?

A

Fever management
Diastat: 2-5 y/o - 0.5 mg/kg PR x1; Max: 1 tx/5 days up to 5 tx/mo
6-11 y/o - 0.3 mg/kg PR x1; Max: 1 tx/5 days up to 5 tx/mo
IV AED’s
Future fever control

63
Q

Benign Rolandic

A

Begins around ages 5-16 years, often disappears around puberty

Seizures usually occur during sleep or upon wakening

Twitching, numbness, or tingling of the face or tongue; may interfere with speech and cause drooling

AED use optional
EEG may show centro-temporal spikes
Can become secondarily generalized

64
Q

Non-Epileptic Seizures(pseudo-seizures)?

A

Distinguishing characteristics
Occur in adolescence
Females > males (3:1)
Associated with anxiety disorders
Can occur with a seizure disorder
Usually stop after diagnosis

65
Q

Non-Epileptic Seizures?

A

Distinguishing characteristics (cont’d)
Unresponsive to effective AED’s
Appear as atypical generalized clonic or tonic seizure
Jerking from side to side
Wild thrashing
Tonic posturing
Intermittent stopping and starting
Resist eye opening and arm flopping to face
Normal video EEG

66
Q

Status Epilepticus?

A
  1. Convulsive
    Tonic-Clonic
    Tonic
  2. Nonconvulsive
    Absence
    Complex partial
67
Q

Status Epilepticus

A

Description: ?
Seizure > 5 minutes or clusters of seizures without full recovery to base line

10% of first time seizures
Risk
Hypoxia  brain injury  developmental delay  learning difficulties
Death

Sudden Unexplained Death in EPilepsy - SUDEP

68
Q

Sudden Unexplained Death in EPilepsy

A

SUDEP

69
Q

Status Epilepticus Management?

A

ABC
Rectal Diastat
IV access
Draw for glucose, electrolytes, AED levels, LFT’s
Toxic screens as indicated
Urine drug screen
Start infusion
LP
MRI/CT
EEG

70
Q

Status Epilepticus emergency treatement?

A

Benzodiazepines
Diazepam
Lorazepam
Midazolam
Fosphenytoin
Valproic acid
Phenobarbital
Pentobarbital
Levetiracetam

71
Q

Seizure Management?

A

Pharmacological therapy
When to stop medication
Ketogenic diet
3-5:1 fat: carbs & PRO (high-fat, adequate-protein, low-carbohydrate diet)
Brain surgery
Focal resection
Hemispherectomy
Corpus callosotomy
Vagus Nerve Stimulation

72
Q

Ketogenic diet?

A

3-5:1 fat: carbs & PRO (high-fat, adequate-protein, low-carbohydrate diet)

manages seizures

73
Q
A

VNS is sometimes called a “pacemaker for the brain.”

The use of VNS is limited to a select group of individuals who have treatment-resistant epilepsy or treatment-resistant depression.

VNS is approved as add-on therapy for focal (partial) seizures in adults and children four years of age and older when medications haven’t controlled their seizures.

74
Q

School issues related to school?

A

Learning problems
Medication effects
Frequent seizures
Parent/teacher/medical provider communication – vital

75
Q

Patient and family education for seizures?

A

Safety issues
Climbing / heights
Traffic hazards
Bathing
Swimming
Driving
Sleep deprivation
Alcohol
Compliance with treatmen

76
Q
A
77
Q
A