Neonatal seizures Flashcards

1
Q

Neonatal seizures incidence

A

Incidence is~1.5–5.5/1000 live births;

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2
Q

When do neonatal seizures occur?

A

In the first week of life and are a sign of acute brain injury

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3
Q

What are risk factors for neonatal seizures?

A

There are two main specific risk factors:

Conceptional age: <30 weeks—higher incidence ~3.9% 30 weeks—1.5%

Birth weight:
<1500 gm → 57/1000 live birth
1500–2499 gm → 5/1000 live birth
2500 gm → 3/1000 live birth.

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4
Q

What are semiology’s of neonatal seizures?

A

Semiology:
Focal and multifocal clonic (25%)
Focal and generalized tonic (5%)
Myoclonic (20%)
Subtle seizure pattern (50%) ​– ​Apnea ​– ​Tonic deviation of the eyes ​– ​Eyelid fluttering – ​Drooling, sucking, and chewing ​– ​Swimming movements of the arm ​– Pedaling movements of the legs ​– ​Paroxysmal laughing.

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5
Q

What are etiologies for neonatal seizures?

A

Metabolic disorders have poor prognosis
10% of neonatal seizures are of unknown etiology

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6
Q

Pyridoxine-Dependent and Folinic Acid Responsive Seizures

A

Age of onset: Neonatal type—presents soon after birth; Atypical type: Late onset between 1 and 3years in pyridoxine-dependent seizures.

Seizure features: intractable seizures not controlled with antiepileptic medications which respond both clinically and electrographically to daily pyridoxine or folinic acid.

Variable seizure semiology seen.

Prolonged seizures and status epilepticus common.

Testing: Elevated—α-aminoadipic semialdehyde (α-AASA) in urine and plasma. Elevated—pipecolic acid in plasma and cerebrospinal fluid. Mutations in ALDH7A1cause pyridoxine-dependent epilepsy.

Management: Response seen with IV pyridoxine 100–500mg or daily PO pyridoxine 30mg/kg/d for at least 2weeks Prior to the administration of folinic acid, CSF neurotransmitters studies are obtained Response seen within 24h with folinic acid started at 4mg/k/D divided BID.

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7
Q

Benign neonatal seizures

A

Benign neonatal seizures represent two rare genetically mediated syndromes with seizures in the newborn period.

The long-term outcome for both seizures and development is generally good. In this, they resemble the spectrum of benign focal epilepsies of childhood.

However, interictal EEGs are not helpful.

These disorders are often a diagnosis of exclusion in the acute setting. The two well-characterized benign neonatal seizure syndromes are described in Table4.3.

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8
Q

Neonatal Non-epileptic Events

A

Benign nocturnal myoclonus
Jitteriness
Opisthotonus
Pathological myoclonus
Apneic spells

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9
Q

When is electrical seizure activity rare?

A

Rare before 34weeks;

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10
Q

Generalized EEG activity in neonates?

A

Infantile spasm and myoclonic jerks

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11
Q

BIRDS

A

Brief ictal rhythmic discharges of unclear significance

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12
Q

What special condition is burst suppression seen in?

A

Burst suppression is seen in metabolic diseases and has poor prognosis

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13
Q

Alpha seizures

A

Seen in severe HIE and has poor prognosis

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14
Q

Neonatal seizures management

A

Neonatal seizures always require urgent treatment.

First-line phenobarbital—82% → lorazepam—9% → phenytoin—2% Second-line therapy: lorazepam 50% → phenytoin (39%) → phenobarbital (20%)

~58% continued to have EEG seizures after the administration of AED and cessation of clinical seizures.

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15
Q

Neonatal seizures outcomes

A

~20% neonatal seizures survivors develop postnatal epilepsy.

Neonates with seizures due to perinatal asphyxia and cerebral dysgenesis develop postnatal epilepsy about~30 and 80%, respectively. Neonatal seizures due to acute encephalopathy usually improve in 7–14days.

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