NEBOBORN CONVULSIONS
Newborn convulsion, postnatal 0-28. It is the most common clinical sign in neurological diseases of infants. 80% of neonatal seizures occur in the first 2 days of life. The fact that convulsions seen in the neonatal period are generally associated with serious diseases and the need for specific treatment, can disrupt the respiratory-circulatory integrity, and uncontrolled seizures cause serious brain damage and negatively affect the long-term prognosis, necessitates urgent diagnosis and treatment (1,2). Neonatal convulsions etiology They differ from convulsions seen in other age groups in terms of clinical, treatment and prognostic factors (1,3). Although it is not easy to recognize these seizures clinically, there are difficulties in diagnosis and treatment (1,3,4). It is difficult to determine the true frequency of neonatal convulsions due to the uncertainty of their clinical defining features; According to clinical observations, it varies between 2/1000 live births and 50/1000 as birth weight decreases (1).
II.ETIOLOGY
Etiological diagnosis of neonatal convulsions is based on clinical features and laboratory findings. The frequency of etiological causes varies depending on the time of onset of seizures and the gestational ages of the babies.
HIE
Hypoxic ischemic encephalopathy is the most common in the neonatal period. It is a clinical condition known as a common cause of acute neurological disorders and seizures. Despite the advances in antenatal and neonatal care today, acute neonatal encephalopathy following significant intrapartum asphyxia is still the most important cause of acute and chronic morbidity and mortality in these babies. Hypoxia is mostly caused by inadequate feto-maternal gas exchange due to cessation of uteroplacental blood flow or sudden occlusion of the umbilical cord. The fetus responds to this situation by increasing the perfusion of the brain and heart with its stimulated adrenergic system. However, prolonging this situation initiates a chain of biochemical events that will cause cerebral perfusion and oxygenation to deteriorate and the release of neurotoxic mediators. Cell death after hypoxia and ischemia occurs either in the form of apoptosis or necrosis. Beginning If the severity of the event is high, necrosis is observed; if it is low, apoptosis is observed. The negative effect of HIE is mostly on the central nervous system (CNS). Neuropathological lesions associated with hypoxic ischemic encephalopathy differ between term and preterm babies. While damage occurs mostly in the gray matter, cortical and subcortical regions in term babies, intraventricular hemorrhage, white matter damage and some specific neuronal damage are prominent in premature babies (34). Seizures in HIE mostly occur within 4-24 hours after birth, and 60% of patients with this condition have seizures for up to 12 hours (34). Seizures are often isolated at first. They tend to intensify and recur within 12-24 hours after birth and may develop as status. The prognosis of convulsions seen in this period is also quite poor (34).
INTRACRANIAL HEMORRHAGE
It constitutes an important cause of neonatal convulsions. Many studies have reported that intracranial hemorrhage is seen in 15-25% of cases (1,3,10). It often occurs due to birth trauma, and rarely due to bleeding disorders and congenital vascular anomalies. Types of intracranial hemorrhage in newborns: subdural, subarachnoid, intracerebellar, intraventricular and intraparenchymal. Common clinical findings; These are swelling in the fontanelle, decreased sucking, bradycardia, change in respiratory depth and frequency, apnea, hypotonicity, pallor and convulsion. Ultrasonography is required as a screening method, and CT and/or MRI are required to confirm the diagnosis (42). GM-IVH is diagnosed 50% of the time on the first day and 80-90% in the first 3 days. Bleeding continues to progress in 20-40% of these babies. Although clinical convulsions were reported in 17% of GM-IVH cases (40), in studies conducted with electroencephalographic examination, IVC and periventricular hemorrhagic infarction were detected in 45% of babies with EEG findings (44). The most common seizure type seen in these babies is generalized tonic seizures.
INTRACRANIAL INFECTIONS
Bacterial or non-bacterial intracranial infections, newborn It is held responsible for 5%-10% of the convulsions that occur during the period. Meningitis cases due to group B streptococcus and E.coli, among bacterial infections It constitutes the most common group. Convulsions are often observed in these patients after the first 3 days of life. Non-bacterial infections; It includes encephalitis that develops after toxoplasma, herpes simplex virus, rubella and cytomegalovirus. Convulsions in intrauterine toxoplasma and cytomegalovirus infections can be seen within the first 3 days of life (1).
CEREBROVASCULAR DISORDERS
With advanced imaging methods can be shown. It has been detected as a convulsion causative agent at a rate of 5-6%. Thromboembolic events may develop intrauterinely and lead to fetal strokes, especially due to maternal factors, or they may occur secondary to sepsis and dehydration in the neonatal period. In these cases, hereditary coagulation disorders should be considered and the mother and child should be evaluated from this perspective. Vascular malformations and related neurological findings may also occur with convulsions; neuroradiological examinations are guiding.
DEVELOPMENTAL CEREBRAL ANOMALIES
Clinical Findings vary depending on the function of the affected area. Epilepsy, motor-mental retardation and focal neurological problems are the most important clinical findings. Epilepsy is often chronic and consists of partial and generalized attacks depending on the spread of the lesion. Developmental anomalies constitute approximately 50% of the patients sent to epilepsy surgery centers due to unstoppable seizures (46). Seizures often occur in early life and are responsible for 5%-10% of seizures seen in the neonatal period. Although clinically seizures are often observed as myoclonies or infantile spasms, focal clonic seizures or insidious attacks are also observed (5). Electroencephalography (EEG) is useful for the diagnosis of epilepsies caused by cortical dysplasia in 75% of patients, but the findings are nonspecific. Two different EEG patterns have been described. The first is a specific high-amplitude rhythmic fast activity, the second is a low-amplitude focal interictal sharp or spike wave. Although clinical seizures are not described, epileptic disorders can be noted on EEG. For this reason, EEG recording should be done even if there is no clinical seizure (47).
METABOLIC DISORDERS
This general category includes In addition to glucose and serum electrolyte (sodium, calcium, magnesium) disorders, amino acid metabolism disorders (especially nonketotic hyperglycinemia), organic acidemias, mitochondrial (pyruvate dehydrogenase, cytochrome-c oxidase) and peroxisomal (Zellweger syndrome, neonatal adrenoleukodystrophy) diseases, pyridoxine and folinic acid addiction, glucose transport disorder.
a) Hypoglycemia; The most common metabolic disorder in the neonatal period, which can sometimes lead to severe sequelae, is hypoglycemia. Especially babies with low birth weight and gestational age and babies of diabetic mothers are at high risk. Kovisto et al. stated that the most critical determinants in the development of neurological symptoms are the duration of hypoglycemia and the time to start treatment (48). Regardless of the cause, early and recurrent convulsions occur in hypoglycemia. In addition to convulsions, neurological symptoms such as jitteriness, apnea and hypotonia are also common. In a study, it was reported that 80% of under-gestational age babies with hypoglycemia had neurological symptoms and 50% had seizures. Hypoglycemia developed in these babies in the early period (usually on the 2nd day of life) (1,5). Hypoglycemia; It is very difficult to determine the role of hypoglycemia in the seizures of these babies, as it may be associated with clinical conditions such as hypocalcemia, perinatal asphyxia, sepsis and intracranial hemorrhage. Although Volpe explains the frequency of seizures due to isolated hypoglycemia without any other metabolic defect as 9%, this rate has been stated as 3% in recent studies (1,3).
b) Hypocalcemia; It occurs in two different time periods during the neonatal period: early and late hypocalcemia. Early hypocalcemia observed in the first 2nd and 3rd days of life is observed in premature and low birth weight babies; In babies of diabetic mothers; It is a common finding in babies who have experienced neonatal distress for any reason, especially hypoxic damage. Early hypocalcemia therefore depends on other potential etiological factors that play a fundamental role in the occurrence of convulsions and should be considered an additional condition, not the main cause of convulsions (1). As a matter of fact, the failure of calcium treatment alone to stop seizures may lead to babies with early hypocalcemia. The fact that babies with early and late hypocalcemia have a more severe prognosis supports this view (1,5). Late hypocalcemia occurs at the beginning of the 2nd week in term infants fed large amounts of formula containing suboptimal phosphorus-calcium and phosphorus-magnesium ratios. The excessive phosphate load contained in these foods may cause functional hypoparathyroidism due to the limited ability of the immature kidney to excrete phosphorus (5). It is clinically characterized by recurrent, well-formed focal and multifocal seizures in a restless, hyperactive, and often voracious infant. Response to treatment and prognosis are very good in late hypocalcemia (1,5). Although the frequency of hypocalcemia in neonatal seizures was reported to be 13% in the 1970s, the association of hypocalcemia with other etiological factors was emphasized here. Today, the frequency of isolated hypocalcemia in neonatal convulsions has been reported as 3% (3).
It is known that hypomagnesemic convulsions are rare and occur quite late. In addition to magnesium absorption disorder, hypomagnesemia can also be seen with autosomal recessive inheritance (10).
c) Pyridoxine addiction; It is among the rare causes. Decrease in GABA synthesis and increase in the amount of glutamate as a result of abnormal binding of pyridoxal-5-phosphate to glutamic acid decarboxylase are involved in the pathophysiology of cortical excitation and epilepsy (49). Pyridoxine dependence is classically characterized by refractory seizures that begin early and respond dramatically to pyridoxine treatment and may recur within a few days if treatment is discontinued. Seizures usually develop as generalized tonic-clonic and can last for hours. EEG may not always give definitive findings. If an EEG finding appears, it is almost always a chaotic finding in the form of multifocal spikes and slow waves, resembling an infantile spasm. Although the EEG finding is hyssarthmia, the seizure is not in the form of flexion or extension spasm and is almost always generalized clonic, suggesting pyridoxine addiction (10). A response to intravenous 50-100 mg pyridoxine is obtained within minutes. Intravenous pyridoxine should be tried in all resistant cases with unknown cause that present with seizures up to the first 18 months of life outside the neonatal period (5,49).
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