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Seizures

Summary Introduction Differential Diagnosis Investigations Management Areas of Uncertainty in Clinical Practice

Summary
neonatal seizures are relatively common and rarely idiopathic, an underlying cause should be sought and treated there are four different types of clinical seizures seizures must be differentiated from jitteriness and benign neonatal sleep myoclonus treat with anticonvulsants if the seizure is prolonged (longer than 3 minutes), frequent or associated with cardiorespiratory disturbance 70% of seizures will abate with phenobarbitone only

Introduction
Neonatal seizures are paroxysmal alterations in neurological function. This definition allows the inclusion of clinical seizures associated with EEG abnormalities as well as paroxysmal clinical activities (lip smacking, cycling etc.) that are not associated with EEG alterations. Newborn babies have a central nervous system that is vulnerable to epileptogenic activity, and as a result they have a relatively high incidence of seizures (1 2 per 1000 term infants). Seizures represent the brains response to a wide variety of pathological insults. As such, they are often a manifestation of significant neurological disease, they are rarely idiopathic and they are a major predictor of adverse outcome in the newborn. The most common identifiable causes are: hypoxic-ischaemic encephalopathy (49%) cerebral infarction (12%) cerebral trauma (7%) infections (5%) metabolic abnormalities including hypoglycaemia (3%) narcotic drug withdrawal (4%).

Differential Diagnosis
During the neonatal period any unusual repetitive or stereotypic movement may represent a seizure. Alterations in autonomic functions such as blood pressure or heart rate may represent seizure activity. The relationship between a clinical seizure and abnormal electrical activity on an EEG is inconsistent. A clinical classification of neonatal seizures is outlined in the following table:

Type

Clinical manifestation Eye signs: staring, deviation, blinking etc Buccal-oral-lingual: chewing, sucking, lip smacking

Comments

Subtle

Limbs: cycling, swimming rowing Systemic: apnoea, blood pressure alterations

It may be difficult to differentiate subtle seizures from extremes of normal behavior. Many subtle seizures are thought to arise from the basal ganglia as a result of diminished cortical inhibition. Further depression of the cortex with anticonvulsants may not alter these seizures

Clonic

Usually involve one limb or one side of the body jerking rhythmically at 1 4 times per second.

May be a clue to an underlying focal neuropathology e.g. hemorrhage or cerebral infarction

Myoclonic

Rapid isolated jerking of muscles

Seen in drug withdrawal (especially opiates). If it occurs during sleep then it is probably "benign neonatal sleep myoclonus". Can also occur in a very severe form of encephalopathy.

Tonic

Sustained posturing of the limbs or trunk or deviation of the head. It may mimic decerebrate or decorticate posturing. Only 30% have EEG correlates.

Often difficult to treat with anticonvulsants

It is important to distinguish seizures from jitteriness and benign neonatal sleep myoclonus. The following clinical features will help separate jitteriness and benign neonatal sleep myoclonus from seizures:

Movement

Description Symmetrical rapid movements of the hands and feet Stimulus sensitive, and may be initiated by sudden movement or noise. No associated eye movements Bilateral or unilateral jerking during sleep

Jitteriness

Benign neonatal sleep myoclonus

Occurs during active sleep Not stimulus sensitive

Often involve upper > lower trunk

Investigations
A clear history is essential in guiding the choice of investigations. The maternal history e.g. insulin dependent diabetes mellitus and the perinatal history e.g. evidence of fetal distress in labour will provide vital clues to the aetiology of the seizures. Blood glucose, serum electrolytes, calcium and magnesium, full blood examination and packed cell volume should be obtained in all cases even when intrapartum hypoxia appears to fully explain the seizures. Neuroimaging studies are indicated where focal pathology is suspected. Seizures following traumatic delivery particularly if there is significant head trauma or if the seizures are clonic require further investigation with MRI examinations ( or CT if MRI unavailable). If there is any suggestion of infection, then meningitis should be suspected and CSF examination performed. If it is not possible to obtain a sample of CSF then treatment with ampicillin (100 mg/kg 12 hourly) and cefotaxime (50 mg/kg 12 hourly) should be commenced. These drug doses apply to term babies only. If the seizures are difficult to control, and/or require the use of multiple anticonvulsants then an EEG may assist determining the cause of the seizures as well as guiding treatment.

Management
The first step in treatment is to identify and treat the underlying cause e.g. hypoglycaemia. Seizure control will be very difficult unless the underlying cause is addressed. There is some controversy over when to commence anticonvulsants however an anticonvulsant should be commenced if the seizure is prolonged (longer than 3 minutes), frequent or associated with cardiorespiratory disturbance. If a decision is made to initiate treatment, the following medications are generally effective.

Anticonvulsant

Loading dose

Maintenance

% infants controlled

Phenobarbitone

20 mg/kg IV or IM over 30 minutes *

2.5 to 5 mg/kg 12 hourly, 24 hours after the loading dose

70%

Phenytoin

15 to 20 mg/kg IVI over at least 30 minutes

4 to 5 mg/kg/dose 12 hourly in term infants starting 12 hours

85%

after the loading dose

Clonazepam

0.1 to 0.25 mg IV (not per kg)

0.01 mg/kg/dose 8 hourly, 8 hours after the loading dose

90-100%

Paraldehyde

0.3 ml/kg/dose PR. Rectal dosing is preferred. 0.2 ml/kg IV or IM if the rectal route is not feasible.

0.3 ml/kg/dose PR 4 to 8 hourly. 0.1 ml/kg/dose IM or IV 4 to 6 hourly

Pyridoxine **

100 mg IV or IM

50 mg daily

* Some recommend additional loading doses of 5-10 mg/kg up to a total of 50 mg/kg. However such high doses cause CNS depression, which may complicate the assessment of infants with hypoxic ischaemic encephalopathy. They may also cause respiratory depression, which may necessitate endotracheal intubation. ** Pyridoxine may be tried if the aetiology is obscure and the seizures are not responding to the usual medications.

Areas of Uncertainty in Clinical Practice


Routine anticonvulsant therapy following perinatal asphyxia should be restricted to those babies who are having prolonged or frequent clinical seizures. It remains unclear whether the goal of anticonvulsant therapy should be the complete elimination of abnormal EEG activity or the abolition of clinical seizures. The elimination of abnormal EEG activity may require very large doses of anticonvulsants. These may have adverse effects upon the developing brain. Similarly, it is not clear how long therapy should be continued following the initial seizures. There is no indication that prolonged treatment of anticonvulsant therapy reduces the risk for the later development of epilepsy. The only recommendation for continuing anticonvulsant therapy (phenobarbitone 3-4 mg/kg/day) is in the setting of profound neonatal encephalopathy or severe brain injury and then only for 6-8 weeks

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