Tremors at Birth and Continue Through Adult
Paediatr Child Health. 2008 Oct; 13(8): 680–684.
Language: English | French
Nonepileptic motor phenomena in the neonate
Richard James Huntsman
1Division of Pediatric Neurology, Department of Pediatrics, University of Saskatchewan, Saskatoon, Saskatchewan
Noel John Lowry
1Division of Pediatric Neurology, Department of Pediatrics, University of Saskatchewan, Saskatoon, Saskatchewan
Koravangattu Sankaran
2Division of Neonatal Medicine, Department of Pediatrics, University of Saskatchewan, Saskatoon, Saskatchewan
Abstract
The newborn infant is prone to clinical motor phenomena that are not epileptic in nature. These include tremors, jitteriness, various forms of myoclonus and brainstem release phenomena. They are frequently misdiagnosed as seizures, resulting in unnecessary investigations and treatment with anticonvulsants, which have potentially harmful side effects. Unfortunately, there is a paucity of literature about many of these phenomena in the newborn, and some of the major textbooks refer to these events as nonepileptic seizures, leading to further confusion for the practitioner. The present paper aims to review these phenomena with special emphasis on differentiating them from epileptic seizures, and offers information on treatment and prognosis wherever possible.
Keywords: Brainstem release phenomena, Hyperekplexia, Jitter, Myoclonus, Tremor
Résumé
Le nouveau-né est prédisposé aux phénomènes moteurs cliniques de nature non épileptique, qui incluent les tremblements, l'agitation, ainsi que diverses formes de myoclonies et de phénomènes de libération du tronc cérébral. Ils sont souvent diagnostiqués à tort comme des convulsions, ce qui entraîne des explorations et un traitement aux anticonvulsivants inutiles qui peuvent avoir des effets secondaires nuisibles. Malheureusement, peu de documents scientifiques portent sur ce sujet chez le nouveau-né, et quelques-uns des principaux manuels médicaux les désignent de crises non épileptiques, ce qui accroît la confusion pour le praticien. Le présent article vise à analyser ces phénomènes, notamment leur différentiation des crises épileptiques, et, dans la mesure du possible, il contient de l'information sur le traitement et le pronostic.
The newborn infant is prone to a variety of motor phenomena that are nonepileptic in nature. Tremor, jitteriness and benign neonatal sleep myoclonus are frequently encountered, while other abnormal movements including neonatal hyperekplexia are less commonly seen. Many of these phenomena are benign and have no bearing on the neonate's eventual neurodevelopmental outcome. However, some phenomena, such as jitteriness, should alert the physician to possible pathology that may require specific investigations and treatment.
Alternately, epileptic seizures in the newborn are frequently associated with significant intracranial pathology and may place the newborn at high risk for poor neurodevelopmental outcome. Differentiating nonepileptic phenomena from epileptic seizures is important to avoid unnecessary parental anxiety, investigations and treatment with potentially harmful medications. While this can often be done clinically, in some circumstances, electroencephalogram (EEG) and other neuroinvestigations are required.
The current paper presents an illustrative case of a neonate with nonepileptic myoclonus, and provides a review of the various nonepileptic motor phenomena seen in neonates. The objectives of the present paper are to provide physicians who care for neonates with a review of these nonepileptic phenomena, with special emphasis on differentiating them from epileptic seizures, and to offer information on treatment and prognosis wherever possible.
ILLUSTRATIVE CASE
A female infant was born vaginally at term after an uncomplicated pregnancy to a healthy 22-year-old primigravida, with no family history of seizures. The delivery was uncomplicated, and the Apgar scores were 8 and 9 at 1 min and 5 min, respectively.
The infant developed recurrent episodes of jerking movements lasting up to 2 min on the first day of life. After a diagnosis of seizure disorder, she was loaded with pheno-barbital (20 mg/kg) for a total of three doses. Because there was no clinical improvement, she was given phenytoin (20 mg/kg). Despite high therapeutic serum levels, she continued the jerking movements. A trial of pyridoxine (50 mg/kg) was given, with no success. She was intubated, given intermittent doses of lorazepam and transported to the neonatal intensive care unit at the Royal University Hospital (Saskatoon, Saskatchewan). On arrival, a complete neurological examination was performed; it was normal, except for the abnormal movements. The infant slept normally between episodes. Her head circumference was 32.5 cm, and her cranial nerve assessment was normal. Whenever handled or even with mildest auditory stimulation, she would develop myoclonic jerks. During these events, she stayed awake and alert with normal eye movements.
Initial investigations including serum glucose, electrolyte and lactate levels were normal. Lumbar puncture revealed normal cerebrospinal fluid analysis. Computed tomography of the head, and magnetic resonance imaging were normal. A metabolic workup consisting of plasma, cerebrospinal fluid amino acids and urine organic acid were normal.
EEG using neonatal montage was performed during many of these events. The interictal background activity was normal. During the events, rhythmical movement artifact, but no epileptiform activity was observed (Figure 1). A diagnosis of stimulus-provoked reflex myoclonus was made.
Electroencephalogram (EEG) recorded during an event using neonatal montage. Note that the high amplitude rhythmical activity due to movement artifact ceases when the event ends. No epileptic activity is identified. AbdResp Abdominal respiration; EKG Electrocardiogram; EMG Electromyograph; LEOG-A1 Left electro-oculogram – A1; REOG-A2 Right electro-oculogram – A2
Her anticonvulsants were stopped, and she was extubated. A low dose of clonazepam was started because the myoclonus interfered with her ability to feed and there was concern of muscle breakdown. The events subsided within three days. She was discharged home shortly after; on neurological follow-up at three months of age, she had no recurrence of the myoclonus nor did she experience any side effects of the medication. Her neurodevelopmental assessment at that time was normal. A trial of withdrawal of the clonazepam is planned when the child reaches six months of age.
The infant had severe stimulus-provoked myoclonus with no apparent cause. Even though she was placed on clonazepam to control the myoclonus, it was believed that this was a benign condition. Although there was no evidence-based knowledge regarding the management of such a case, it was decided that the child should be treated arbitrarily until six months of age, without adjusting the dosage.
TREMOR AND JITTERINESS
Tremor can be defined as an involuntary, rhythmical oscillatory movement of equal amplitude around a fixed axis. It can be either fine with a high frequency (greater than 6 Hz) and low amplitude (lower than 3 cm) or coarse with a low frequency and higher amplitude (1). Jitteriness refers to recurrent tremor (2). In the present review, the terms tremor and jitter are used interchangeably. Tremor is the most common abnormal movement encountered in the neonate. Up to two-thirds of healthy newborns will have some fine tremor in the first three days of life (2); Parker et al (3) reported that up to 44% of newborns were jittery.
Although tremor in older children and adults usually denotes a lesion within the cerebellum, basal ganglia, red nucleus or thalamus, this does not appear to be the case in the neonate (4). One theory is that neonatal tremor is due to immaturity of spinal inhibitory interneurons causing an excessive muscle stretch reflex. As the neonate gets older and the interneurons mature, the tremor resolves (5). Another theory is that elevated levels of circulating catecholamines account for the tremor (6).
Tremor and jitteriness may be benign or pathological. Pathological conditions that may be associated with tremor include hypoglycemia, hypocalcemia, sepsis, hypoxic ischemic encephalopathy, intracranial hemorrhage, hypothermia, hyperthyroid state and drug withdrawal (1–3). In general, fine tremor is usually benign or secondary to metabolic disturbance such as hypoglycemia. Coarse tremor should raise suspicion of intracranial pathology, such as hypoxic ischemic encephalopathy and intracranial hemorrhage. Coarse tremor is frequently associated with the 'neonatal hyperexcitability syndrome' in mildly asphyxiated neonates with increased tendon reflexes and excessive Moro response (1).
The neurological outcome of neonates with tremor is good as long as there are no perinatal complications, such as asphyxia, identified. Two follow-up studies (4, 7) showed that jittery infants without a history of perinatal complications had normal neurodevelopmental outcome, regardless of whether the tremor was fine or coarse. Jittery neonates with a history of perinatal complications were at a 30% risk of adverse neurodevelopmental outcome, in particular, those with coarse tremor as part of the 'neonatal hyperexcitability syndrome' (4, 8).
Tremor can be differentiated from seizure if the following characteristics are observed – the tremor can be brought on with stimuli and can be stopped with gentle passive flexion and restraint of the affected limb; it is not associated with ocular phenomena, such as forced eye deviation; and is not associated with significant autonomic changes such as hypertension or apnea (9).
Investigation of the jittery neonate should depend on the perinatal history and physical examination. If the neonate appears well and has no history of perinatal complications, blood glucose measurement alone will suffice (2). One can determine whether the tremor is benign by placing the neonate supine with hands free at his or her side. A benign tremor will resolve when the neonate is allowed to suck on the examiner's finger (10). Further investigations should be performed in those neonates that appear unwell, have coarse tremor, have a history of perinatal complications and whose tremor does not settle with soothing or suckling. Investigations performed ultimately depend on the clinical situation, but consideration should be given toward doing a septic workup, urine drug screening, neuroimaging, thyroid screening and metabolic workup (2).
Special consideration should be given to tremor as part of a neonatal withdrawal syndrome. Excessive tremor and jitteriness have been reported in newborns of mothers who had been prescribed opiates (11) and selective serotonin reuptake inhibitors (12, 13). Maternal abuse of illicit substances such as marijuana, inhaled volatile substances and cocaine can also cause a withdrawal syndrome in which coarse tremor is prominent (3, 14, 15). Interestingly, tremor does not appear to be more common in neonates of alcohol-or nicotine-dependent mothers (3).
Treatment of neonates with tremor and jitteriness should be aimed at correcting the underlying cause if identified. Those who appear unwell or have a history of perinatal complication should be observed in a neonatal intensive care unit setting. Special care must also be paid to mother-newborn bonding because jittery neonates tend to have decreased visual attention and are more difficult to console (3).
A form of tremor that only involves the perioral muscles is familial trembling of the chin, which is an autosomal dominant condition in which the cutaneous muscles of the chin tremble. In the neonate, it is frequently brought on by crying. Treatment with botulinum toxin injections into the perioral muscles is reserved only for cases in which the trembling causes difficulty eating or drinking, or causes social embarrassment (16).
MYOCLONUS
Myoclonus is a brief shock-like movement of a limb caused by muscle contraction. It can be either localized to one body part or generalized. It can be a single event, but is often repetitive. Unlike tremor, it is irregular and arrhythmic. Myoclonus also tends to have a higher amplitude than tremor. Myoclonus can originate from any level of the central nervous system, in particular, the cortex, brainstem and spinal cord (17). In the neonate, epileptic myoclonus is uncommon and is infrequently associated with synchronous discharges on the EEG. This has provoked much debate whether myoclonus in the absence of synchronous EEG discharges can be epileptic or nonepileptic (9, 18, 19). Epileptic myoclonus should not be provoked by stimulus, and cannot be suppressed by restraining the affected body part (18).
Nonepileptic myoclonus may be benign or may denote severe central nervous sytem pathology. Neonates with pathological nonepileptic myoclonus have abnormal neurological examinations and abnormal EEGs. The most common etiologies are severe intraventricular hemorrhage, hypoxic ischemic injury and glycine encephalopathy (20, 21). Myoclonus has also been reported in premature neonates after receiving intravenous benzodiazepines (22, 23). Nonepileptic pathological myoclonus most likely represents brainstem release phenomena, in which cortical inhibition of normally suppressed brainstem activity is lost due to diffuse cerebral injury (18, 21, 24).
Benign neonatal sleep myoclonus is characterized by rhythmical myoclonic jerks seen only during sleep. It is common and frequently misdiagnosed as seizures. Benign neonatal sleep myoclonus can be distinguished from epileptic myoclonus by the fact that it only occurs in sleep and stops abruptly and consistently when the child is aroused. During myoclonus, the EEG is normal (25). It tends to occur in healthy, full-term newborns. While it can be seen in any stage of sleep, it tends to occur predominantly in quiet sleep (17, 25). Unlike sleep myoclonus in adults, which is usually an asymmetric single jerk, benign neonatal sleep myoclonus is bilateral and repetitive (26). Onset is usually in the first few days of life and usually remits spontaneously by four months of age (17). Unlike tremor and jitteriness, gentle restraint may worsen the myoclonus. Because myoclonus can last up to 1 h, it can be mistaken for status epilepticus, leading to treatment with anticonvulsants, which provide no benefit and often worsen the myoclonus (27).
Often EEG is used to confirm the diagnosis. Rocking the neonate in a head-to-toe direction starting at a slow frequency and gradually speeding up until myoclonus occurs can be used to bring out the myoclonus while recording with EEG (28). The underlying mechanism behind benign neonatal sleep myoclonus is poorly understood. One proposed mechanism is immaturity of serotonergic pathways within the brainstem, which normally suppresses movement during sleep (17, 26).
Benign myoclonus of early infancy, which has usual onset between three to nine months, has also been reported in the neonatal period (29). In this condition, the infant will have recurrent clusters of myoclonic jerks when awake. Typically, they are not provoked stimulus. They resemble infantile spasms, but are not associated with developmental decline; the EEG is normal even during events. Resolution is by nine months of age, and there is no apparent effect on neurodevelopment. The underlying etiology is unknown (30, 31).
NEONATAL HYPEREKPLEXIA
Also known as startle disease, hyperekplexia is a rare disorder characterized by generalized muscle rigidity in the neonate, nocturnal myoclonus and an exaggerated startle reaction to auditory, tactile and visual stimuli. The startle reaction is a normal response to stimuli that consists of facial grimace and blinking followed by flexion of the trunk. The startle response is exaggerated when it interferes with normal activities, and causes apnea and frequent falls (32).
There are two forms of hyperekplexia. The minor form has an exaggerated startle response only. The exaggerated startle response can consist of a generalized tonic spasm with tonic flexion of the limbs and trunk and clenching of the fists. The eyes often remain open in an anxious stare. Apnea is common during the spasms due to chest wall rigidity. The exaggerated startle response can be elicited by tapping the nasal bridge, thus differentiating it from seizures for which it is often mistaken. In the major form, there is also a generalized muscle rigidity seen only when the infant is awake in addition to nocturnal myoclonus (32, 33).
During the first two years of life, the affected infant is at an increased risk of sudden infant death syndrome due to central apnea secondary to brainstem dysfunction, as well as apnea during tonic spasms. Although the muscle rigidity resolves by approximately three years of age, the exaggerated startle persists, resulting in frequent falls and injury. Clonazepam can be helpful in controlling the startle episodes (32).
Hyperekplexia is, for the most part, a familial condition inherited in an autosomal dominant fashion with variable expression. The genetic defect is linked to chromosome 5q33–35. This results in defective chloride conduction through the alpha-1 subunit of the glycine receptor in the caudal pontine reticular formation, resulting in defective neuronal inhibition (32).
OTHER TRANSIENT MOVEMENT DISORDERS
A movement disorder results from dysfunction within the basal ganglia circuitry. While many are transient and benign, some may result from permanent basal ganglia injury. Up to one-third of the transient benign movement disorders of childhood can be seen in the first three months of life. Benign paroxysmal torticollis is characterized by episodes of painless lateral neck flexion or torticollis often associated with pallor, emesis and abnormal eye movements. The attacks may last up to several days. Fernandez-Alvarez (30) reported that two of 13 patients had attacks in the first month of life.
A hyperkinetic movement disorder resulting in choreiform movements of the extremities and abnormal mouth and tongue movements similar to those seen in oral-buccal dyskinesia has been reported in premature infants with severe bronchopulmonary dysplasia. These movements seemed to worsen during periods of respiratory failure and are attenuated during sleep. The proposed pathophysiology is chronic hypoxic injury to the basal ganglia. The neurodevelopmental outcome of these infants was poor (34).
SUBTLE SEIZURES AND BRAINSTEM RELEASE PHENOMENA
The neonate is prone to a variety of epileptic seizures including 'subtle' and tonic seizures. Volpe (9) defines subtle seizures as paroxysmal alterations in the neonate's behaviour or motor and autonomic functions that are not associated with tonic, myoclonic or clonic activity. Frequently associated changes include abnormal eye movements (random, nystagmoid or sustained lateral gaze) and oral-buccal lingual movements, such as sucking, chewing or tongue protrusions. Tonic seizures can either consist of tonic extension of all four extremities mimicking decerebrate posturing, or tonic flexion of the arms and extension of the legs mimicking decorticate posturing (9).
These events are frequently not associated with epileptic changes on the EEG, and respond poorly to standard anticonvulsants. This has led to the debate of whether they represent epileptic seizures or nonepileptic brainstem release phenomena (9, 18, 19). Volpe (9) believes that these may represent seizures that are not detectable on standard EEGs because they arise from deep subcortical structures such as the diencephalon or from deep within the limbic structures (9). While there is evidence derived from animal studies to support this theory, it has not been shown in humans. Two studies (18, 19) argued that if these events are not associated with epileptic changes in the EEG and they have features of reflexive behaviour, such as being provoked by stimulation and suppressed by gentle restraint, then they are not epileptic and represent brainstem release phenomena. Single photon emission computed tomography imaging obtained in a neonate with severe hypoxic ischemic injury with recurrent episodes of tonic posturing (21) showed that the posturing originated in the brainstem, thus supporting the above studies argument.
Both seizures and brainstem release phenomena occur in neonates who have abnormal neurological functioning; they can occur concurrently in the same patient (18, 19, 21). Differentiating between the two can be very difficult on clinical grounds alone, making video EEG necessary. Electrographic seizure activity in the neonate tends to be localized most commonly to the temporal and central head regions. Seizures arising from the occipital and frontal lobes are very uncommon. The EEG features of a seizure in the neonate can be quite subtle, with features very different from those seen in adults or older children, making them easy to miss (35). Therefore, the recording must be read by an electroencephalographer with experience in neonatal EEG. To optimize detection of seizure activity and interictal discharges, the neonatal montage should be used when recording the EEG. This montage maximizes recording in the temporal, central and vertex head regions (35). To assist in interpretation of the EEG, the technologist needs to record changes in head position, state changes or movement.
A common interictal discharge encountered in the neonate is the sharp transient, which is a sharply contoured wave that is clearly distinguished from the underlying background activity. These can be benign or pathological depending on their location, frequency and persistence. Whether pathological sharp transients should be used to determine that an event is epileptic or not is controversial (19, 35, 36).
CONCLUSION
Differentiating epileptic seizures from nonepileptic motor phenomena is extremely important. While neonatal seizures are usually a sign of serious intracranial pathology, nonepileptic motor events may be benign. If they are pathological, the underlying cause may be different from those that cause seizures, requiring a different treatment approach.
While the neonatal brain may have an innate resistance to injury from a prolonged seizure, recurrent brief seizures are more common and may result in further brain injury in an already neurologically compromised neonate (9, 37, 38). This has to be balanced with the fact that the standard anticonvulsants used in neonates have potentially harmful side effects. Acute anticonvulsant administration can cause hypotension, bradycardia and respiratory depression, all of which can lead to further hypoxic or ischemic brain injury. There is also concern about the long-term effects of anticonvulsants on the developing brain. Animal studies have shown that the most commonly used anticonvulsants, including phenobarb, phenytoin and diazepam, cause apoptic neurodegeneration at therapeutic levels. This, however, has not been extrapolated to humans, and their effect on long-term neurodevelopmental outcome is debatable (19).
Consequently, anticonvulsants should only be used in the neonate when the likelihood that the events are truly epileptic is high. Features that increase the likelihood that the events in question are epileptic would be the presence of associated autonomic changes, abnormal ocular phenomena, and whether they can be brought on by stimulating the neonate and suppressed by restraining the affected body part. In the case of benign neonatal sleep myoclonus, the events should cease when the neonate is awoken. If there is any clinical uncertainty, an EEG recorded in the neonatal montage and interpreted by an experienced electroencephalographer is vital.
Acknowledgments
The authors thank Dr Allan Ross for his assistance in reviewing and editing the present article.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2606074/
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