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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5
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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
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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
Acute recurrent temporal headache?
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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Chronic progressive temporal headache?
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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Chronic nonprogressive or chronic daily temporal headache?
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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What are different types of headaches?
Tension Type Headaches Migraines Secondary Headaches
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Pediatric migraine criteria
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What are the triggers for migraine & headaches?
-Fever -Stress -Foods / additives -Head injury -Environmental factors -Inherited disorders
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What are the diagnostics for migraines & h/a's?
History Physical Neuroimaging
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What is the treatment for migraines & h/a's?
Intermittent symptomatic analgesics Dark, quiet room Tylenol/NSAIDS Lifestyle modifications Preventative approaches Non pharmacologic treatments Abortive treatment - migraines Ondansetron Triptans
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What is tier 1 treatment for migraines?
Tier 1 (analgesics): Acetaminophen 15 mg/kg per dose, or Ibuprofen 10 mg/kg per dose, or Naproxen 5 mg/kg per dose
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What is tier 2 for migraine treatment?
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
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What is tier 3 for migraine treatment?
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
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Seizures?
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
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What are focal seizures?
Simple Complex Benign Rolandic Secondarily generalized
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Focal seizures with retained awareness : Simple Partial?
No loss of awareness Involuntary movements Various sensations/feelings/emotion Can become secondarily generalized
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Focal seizures with impaired awareness: Complex Partial?
Temporal Lobe Epilepsy Psychomotor Altered consciousness Automatisms Lip smacking Rubbing hands together Uncharacteristic behavior Fearfulness Agitation Can become secondarily generalized
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Generalized Seizures?
Types Tonic-Clonic Absence JME Atonic
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Tonic Clonic Seizures (generalized seizure) what are the phases?
May begin with cry Involves loss of consciousness Tonic Clonic Postictal
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What is the management for tonic clonic seizure? (generalized seizure)?
ABC’s Lay on side Nothing in mouth Clear area Administer Diastat®
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Absent seizures?
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
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Absent Seizures?
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Absent seizures?
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Juvenile Myoclonic Epilepsy (JME)?
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
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What is the peak onset of juvenile myoclonic epilepsy (JME))?
12-18 years old
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Atonic Seizures?
Drop attacks Head drops Sudden collapse May need protective head gear Resistant to AEDs
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Neonatal seizures?
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
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Neonatal Seizures
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)
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Infantile Spasms
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)
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West syndrome?
- encephalopathy in infancy characterized by infantile spasms, arrest of psychomotor development, and hypsarrhythmia
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Infantile spasms?
Etiology Prenatal-microcephaly, polymicrogyria, schizencephaly, encephalopathies, congenital infections Perinatal -hypoxic-ischemic, meningitis, trauma, intracranial hemorrhages Postnatal-phenylketonuria, degenerative disease, encephalitis
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Febrile seizures?
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
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Febrile seizures?
Risk factors Younger than 12 months of age Lasting >5 minutes Partial seizure Delayed development
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Treatment for febrile seizures?
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
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Benign Rolandic
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
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Non-Epileptic Seizures (pseudo-seizures)?
Distinguishing characteristics Occur in adolescence Females > males (3:1) Associated with anxiety disorders Can occur with a seizure disorder Usually stop after diagnosis
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Non-Epileptic Seizures?
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
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Status Epilepticus?
1. Convulsive Tonic-Clonic Tonic 2. Nonconvulsive Absence Complex partial
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Status Epilepticus
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
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Sudden Unexplained Death in EPilepsy
SUDEP
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Status Epilepticus Management?
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
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Status Epilepticus emergency treatement?
Benzodiazepines Diazepam Lorazepam Midazolam Fosphenytoin Valproic acid Phenobarbital Pentobarbital Levetiracetam
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Seizure Management?
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
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Ketogenic diet?
3-5:1 fat: carbs & PRO (high-fat, adequate-protein, low-carbohydrate diet) manages seizures
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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.
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School issues related to school?
Learning problems Medication effects Frequent seizures Parent/teacher/medical provider communication – vital
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Patient and family education for seizures?
Safety issues Climbing / heights Traffic hazards Bathing Swimming Driving Sleep deprivation Alcohol Compliance with treatmen
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