58
Seizures and perinatal strokes

Seizures (Table 58.1)

Table 58.1 Recognition, causes, investigation and management of seizures.

Recognition (see video: Seizures)	Seizures may present with clonic or tonic involuntary movements of one or more limbs. Often difficult to recognize with certainty, as manifestations are often subtle: apnea or transient cyanosis, or episodes of oxygen desaturation lip smacking transient eye rolling, altered consciousness, floppiness.
Causes	Cerebral Hypoxic–ischemic: encephalopathy, birth trauma, focal ischemia (arterial/venous) Subarachnoid or subdural hemorrhage Parenchymal hemorrhage in preterm infants Cerebral malformations of the brain, including vascular anomalies	Metabolic Hypoglycemia Hypocalcemia Hypomagnesemia Hyponatremia Hypernatremia Hyperammonemia Inborn errors of metabolism	Sepsis Septicemia Meningitis Encephalitis	Drugs Drug withdrawal: maternal abuse following neonatal narcotic therapy Side-effect of drugs	Others Kernicterus Pyridoxine dependent Benign genetic seizure disorders
Investigations	Always performed Blood glucose (immediate at bedside) Blood urea nitrogen (urea) and electrolytes Calcium and magnesium Complete blood count Blood cultures Lumbar puncture – protein, glucose, gram stain and culture Blood gases Cranial ultrasound to identify hemorrhage or parietal infarcts or cerebral malformation or abnormalities (may miss subarachnoid hemorrhage)	EEG Multichannel EEG (Fig. 58.1) or aEEG (amplitude integrated EEG), preferably with video observation (See Fig. 14.4 for seizures on aEEG and Chapter 80 on aEEG.)		To be considered CT to identify hemorrhage, traumatic injury MRI to identify ischemia, malformations Metabolic screen – plasma for ammonia, amino acids, lactate; urine for amino acids and organic acids Screen for congenital infection Urine for drug toxicology Specific biochemical tests in suspected neurometabolic conditions
Management	Airway, Breathing, Circulation. Check for hypoglycemia. Anticonvulsants: Administer if seizure is prolonged (more than about 5 minutes) or clusters. Controversy about how aggressively to treat electrical seizures (seizures on EEG or aEEG but no clinical manifestations) No drug shown to be superior to others. Those used include phenobarbital (most common first-line drug), phenytoin, levetiracetam, midazolam, clonazepam, lidocaine (lignocaine; with ECG monitoring). Acute seizures often respond poorly. Use as few anticonvulsants as possible. Treat the underlying cause, if possible, e.g. sepsis. If unresponsive to treatment, consider therapeutic trial of pyridoxine.
Prognosis	Depends on cause. Epilepsy in 15–20% and abnormal neurodevelopment in 25%. Poor prognosis – if poor response to initial anticonvulsant treatment, abnormal EEG background and presence of electro-clinical dissociation on EEG. If caused by acute brain insult, most seizures resolve and anticonvulsant therapy can usually be slowly withdrawn. If maintenance anticonvulsant therapy required – is usually with phenobarbital, clonazepam or sodium valproate.

Fig. 58.1 EEG being performed.

Perinatal strokes

Defined as cerebral injury from vascular cause that originates between 20 weeks of gestation and 28 days of life. Occurs in as many as 0.2–1 per 1000 live births.

Types

Perinatal arterial ischemic stroke (PAIS) – the most common site is left middle cerebral artery.
Hemorrhage – may be parenchymal, subarachnoid or intraventricular.
Cerebral sinovenous thrombosis (CSVT) – can cause venous infarction, often with hemorrhage.

Based on neuroimaging, strokes may be classified as fetal if diagnosed before birth, neonatal if diagnosed in the first 4 weeks of life or presumed perinatal ischemic stroke (PPIS) if diagnosed after 28 days of life.

Etiology

Complex and multifactorial. Often no maternal, fetal or neonatal risk factors can be identified.

Perinatal arterial ischemic stroke (PAIS) may be due to thromboembolism. The emboli may originate from thrombosis of placental vessels, from venous thrombi that cross the patent foramen ovale, from right-to-left shunts in congenital heart disease and from thrombi from umbilical vessel catheters. Sepsis or meningitis, trauma and prothrombotic disorders, e.g. protein C or protein S deficiency, may also contribute. Further details of prothrombotic disorders are considered in Chapter 56, Coagulation disorders. The contribution of maternal risk factors and intrapartum events is unclear.

Hemorrhagic stroke may result from intraparenchymal hemorrhage from vascular anomalies or hemorrhage into ischemic infarction; periventricular hemorrhagic infarction is associated with intraventricular hemorrhage in extremely preterm infants.

In cerebral sinovenous thrombosis (CSVT), perinatal complications such as hypoxia or prolonged rupture of membranes or maternal infection may be present. Head trauma during birth and prothrombotic disorders are other risk factors.

Clinical presentation

Most often with seizures within the first 3 days of life, usually focal but can be non-specific. Some present with encephalopathy. Many are asymptomatic in the neonatal period.

Specific investigations

Cranial ultrasound is abnormal in most infants, but is not always diagnostic.
MRI scan for accurate diagnosis and prognosis (Fig. 58.2).
In focal cerebral infarction, investigations to rule out underlying thrombophilic disorders are indicated.

Management

Treatment of seizures with anticonvulsants and supportive therapy. The role of anticoagulation for neonates with cerebral venous thrombosis is controversial.

Prognosis

Nearly 50% of infants with perinatal stroke develop motor disability, often a hemiplegia on the contralateral side presenting in infancy or childhood, and cognitive dysfunction. Occipital lesions may be associated with visual impairment. Large lesions may lead to epilepsy.

Fig. 58.2 MRI scan showing left cerebral infarct (see arrow).

(Courtesy of Dr Frances Cowan.)