NEUROLOGIC PROBLEMS IN THE NEWBORN INFANT
Saturday, August 16, 2008
SEIZURES
Newborns rarely have well-organized tonic-clonic seizures because of their incomplete cortical organization and a preponderance of inhibitory synapses. The most common type of seizure is characterized by a constellation of findings, including horizontal deviation of the eyes with or without jerking; eyelid blinking or fluttering; sucking, smacking, drooling, and other oral-buccal movements; swimming, rowing, or paddling movements; and apneic spells. Strictly tonic or multifocal clonic episodes are also seen.
Clinical Findings
The differential diagnosis of neonatal seizures is presented in Table 1–28. Most neonatal seizures occur between 12 and 48 hours of age. Later-onset seizures suggest meningitis, benign familial seizures, or hypocalcemia. Information regarding antenatal drug use, the presence of birth asphyxia or trauma, and family history (regarding inherited disorders) should be obtained. Physical examination focuses on neurologic features, other signs of drug withdrawal, concurrent signs of infection, dysmorphic features, and intrauterine growth. Screening workup should include blood glucose, ionized calcium, and electrolytes in all cases. Further workup is dependent on diagnoses suggested by the history and physical examination. If there is any suspicion of infection, a spinal tap should be done. Hemorrhages and structural disease of the CNS can be addressed with real-time ultrasound and CT scan. Metabolic workup should be pursued when appropriate. EEG should be done; the presence of spike discharges must be noted and the background wave pattern evaluated. Not infrequently, correlation between EEG changes and clinical seizure activity is absent.
Treatment
Adequate ventilation and perfusion should be ensured. Hypoglycemia should be treated immediately with a 2 mL/kg infusion of D10W followed by 6 mg/kg/min of D10W (100 mL/kg/d). Other treatments such as calcium or magnesium infusion and antibiotics are indicated to treat hypocalcemia, hypomagnesemia, and suspected infection. Electrolyte abnormalities should be corrected. Phenobarbital, 20 mg/kg intravenously, should be administered to stop seizures. Supplemental doses of 5 mg/kg can be used if seizures persist, up to a total of 40 mg/kg. In most cases, phenobarbital controls seizures. If seizures continue, therapy with phenytoin, sodium valproate, or lorazepam may be indicated. For refractory seizures, a trial of pyridoxine is indicated.
Prognosis
Outcome is related to the underlying cause of the seizure. The outcomes for hypoxic-ischemic encephalopathy and intracranial hemorrhage have been discussed earlier in this chapter. In these settings, seizures that are difficult to control carry a poor prognosis for normal development. Seizures resulting from hypoglycemia, infection of the CNS, some inborn errors of metabolism, and developmental defects also have a high rate of poor outcome. Seizures caused by hypocalcemia or isolated subarachnoid hemorrhage generally resolve without sequelae.
HYPOTONIA
One should be alert to the diagnosis of congenital hypotonia when a mother has polyhydramnios and a history of poor fetal movement.
INTRACRANIAL HEMORRHAGE
1. SUBDURAL HEMORRHAGE
Subdural hemorrhage is related to birth trauma; the bleeding is caused by tears in the veins that bridge the subdural space. Prospective studies relating incidence to specific obstetric complications are not available.
The most common site of subdural bleeding is rupture of superficial cerebral veins with blood over the cerebral convexities. These hemorrhages can be asymptomatic or may cause seizures, with onset on days 2–3 of life, vomiting, irritability, and lethargy. Associated findings include retinal hemorrhages and a full fontanelle. The diagnosis is confirmed by CT scan.
Specific treatment entailing needle drainage of the subdural space is rarely necessary. Most infants survive; 75% are normal on follow-up.
2. PRIMARY SUBARACHNOID HEMORRHAGE
Primary subarachnoid hemorrhage is the most common type of neonatal intracranial hemorrhage. In the term infant, it can be related to trauma of delivery, whereas subarachnoid hemorrhage in the preterm infant is seen in association with germinal matrix hemorrhage. Clinically, these hemorrhages can be asymptomatic or can occur with seizures and irritability on day 2 or, rarely, a massive hemorrhage with a rapid downhill course. The seizures associated with subarachnoid hemorrhage are very characteristic—usually brief, with a normal examination interictally. Diagnosis can be suspected on spinal tap and confirmed with CT scan. Long-term follow-up is uniformly good.
3. NEONATAL STROKE
Focal cerebral ischemic injury can occur in the context of intraventricular hemorrhage in the premature infant and hypoxic ischemic encephalopathy. Neonatal stroke has also been described in the context of underlying disorders of thrombolysis and maternal drug use (cocaine). In some cases, the origin is unclear. The injury often occurs antenatally. The most common clinical presentation of an isolated cerebral infarct is with seizures, and diagnosis can be confirmed with CT scan. The most frequently described distribution is that of the middle cerebral artery.
Treatment is directed at controlling seizures. Long-term outcome is variable, ranging from normal to hemiplegias and cognitive deficits.
Newborns rarely have well-organized tonic-clonic seizures because of their incomplete cortical organization and a preponderance of inhibitory synapses. The most common type of seizure is characterized by a constellation of findings, including horizontal deviation of the eyes with or without jerking; eyelid blinking or fluttering; sucking, smacking, drooling, and other oral-buccal movements; swimming, rowing, or paddling movements; and apneic spells. Strictly tonic or multifocal clonic episodes are also seen.
Clinical Findings
The differential diagnosis of neonatal seizures is presented in Table 1–28. Most neonatal seizures occur between 12 and 48 hours of age. Later-onset seizures suggest meningitis, benign familial seizures, or hypocalcemia. Information regarding antenatal drug use, the presence of birth asphyxia or trauma, and family history (regarding inherited disorders) should be obtained. Physical examination focuses on neurologic features, other signs of drug withdrawal, concurrent signs of infection, dysmorphic features, and intrauterine growth. Screening workup should include blood glucose, ionized calcium, and electrolytes in all cases. Further workup is dependent on diagnoses suggested by the history and physical examination. If there is any suspicion of infection, a spinal tap should be done. Hemorrhages and structural disease of the CNS can be addressed with real-time ultrasound and CT scan. Metabolic workup should be pursued when appropriate. EEG should be done; the presence of spike discharges must be noted and the background wave pattern evaluated. Not infrequently, correlation between EEG changes and clinical seizure activity is absent.
Treatment
Adequate ventilation and perfusion should be ensured. Hypoglycemia should be treated immediately with a 2 mL/kg infusion of D10W followed by 6 mg/kg/min of D10W (100 mL/kg/d). Other treatments such as calcium or magnesium infusion and antibiotics are indicated to treat hypocalcemia, hypomagnesemia, and suspected infection. Electrolyte abnormalities should be corrected. Phenobarbital, 20 mg/kg intravenously, should be administered to stop seizures. Supplemental doses of 5 mg/kg can be used if seizures persist, up to a total of 40 mg/kg. In most cases, phenobarbital controls seizures. If seizures continue, therapy with phenytoin, sodium valproate, or lorazepam may be indicated. For refractory seizures, a trial of pyridoxine is indicated.
Prognosis
Outcome is related to the underlying cause of the seizure. The outcomes for hypoxic-ischemic encephalopathy and intracranial hemorrhage have been discussed earlier in this chapter. In these settings, seizures that are difficult to control carry a poor prognosis for normal development. Seizures resulting from hypoglycemia, infection of the CNS, some inborn errors of metabolism, and developmental defects also have a high rate of poor outcome. Seizures caused by hypocalcemia or isolated subarachnoid hemorrhage generally resolve without sequelae.
HYPOTONIA
One should be alert to the diagnosis of congenital hypotonia when a mother has polyhydramnios and a history of poor fetal movement.
INTRACRANIAL HEMORRHAGE
1. SUBDURAL HEMORRHAGE
Subdural hemorrhage is related to birth trauma; the bleeding is caused by tears in the veins that bridge the subdural space. Prospective studies relating incidence to specific obstetric complications are not available.
The most common site of subdural bleeding is rupture of superficial cerebral veins with blood over the cerebral convexities. These hemorrhages can be asymptomatic or may cause seizures, with onset on days 2–3 of life, vomiting, irritability, and lethargy. Associated findings include retinal hemorrhages and a full fontanelle. The diagnosis is confirmed by CT scan.
Specific treatment entailing needle drainage of the subdural space is rarely necessary. Most infants survive; 75% are normal on follow-up.
2. PRIMARY SUBARACHNOID HEMORRHAGE
Primary subarachnoid hemorrhage is the most common type of neonatal intracranial hemorrhage. In the term infant, it can be related to trauma of delivery, whereas subarachnoid hemorrhage in the preterm infant is seen in association with germinal matrix hemorrhage. Clinically, these hemorrhages can be asymptomatic or can occur with seizures and irritability on day 2 or, rarely, a massive hemorrhage with a rapid downhill course. The seizures associated with subarachnoid hemorrhage are very characteristic—usually brief, with a normal examination interictally. Diagnosis can be suspected on spinal tap and confirmed with CT scan. Long-term follow-up is uniformly good.
3. NEONATAL STROKE
Focal cerebral ischemic injury can occur in the context of intraventricular hemorrhage in the premature infant and hypoxic ischemic encephalopathy. Neonatal stroke has also been described in the context of underlying disorders of thrombolysis and maternal drug use (cocaine). In some cases, the origin is unclear. The injury often occurs antenatally. The most common clinical presentation of an isolated cerebral infarct is with seizures, and diagnosis can be confirmed with CT scan. The most frequently described distribution is that of the middle cerebral artery.
Treatment is directed at controlling seizures. Long-term outcome is variable, ranging from normal to hemiplegias and cognitive deficits.
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