Benign Neonatal Convulsions

Updated: Oct 17, 2018
Author: Nitin C Patel, MD, MPH, FAAN; Chief Editor: Amy Kao, MD 



Benign neonatal convulsions are defined as seizures with onset after birth through day 28 in an otherwise healthy child with no other known medical or neurologic problems. Such cases may be familial or isolated. Psychomotor development should be normal for a full-term or near full-term infant with benign convulsions. Between seizures, findings on neurologic examination should be normal. Clinically, the seizures are frequent and brief, occasionally occurring many times within a day. The brief seizures are followed by a short or no postictal state. The episodes usually resolve within days but may continue for several months and have no neurologic sequelae.

The occurrence of status epilepticus is common in benign idiopathic neonatal convulsions (BINC) but is uncommon in benign familial neonatal convulsions (BFNC). Because the condition benign idiopathic neonatal convulsions is a diagnosis of exclusion, it is nearly always made in retrospect, when the seizures spontaneously resolve and the infant is found to have neurologically normal development.[1, 2, 3, 4]

At the outset, considering how broadly to define benign neonatal convulsions is important: for example, whether to include those with myoclonic or partial onset components or those with a known or treatable etiology. Certainly, multiple presentations of seizures that may have a benign long-term outcome are possible in the neonatal period.[3, 5] Definite advantages exist in approaching the subject from each position. Too broad a definition in a research situation can lead to confusion when searching for a common pathology. Too narrow a definition in the clinical setting may result in confusion about a clinical diagnosis. Later, when the mechanisms are better defined, broader groups not meeting the initial criteria may exist.

Clinically, the more important considerations are taking an appropriate approach to the patient and family, making the correct diagnosis, and pursuing treatment options concordant with the situation. Sometimes, the correct clinical plan may include a decision not to treat a benign condition with medications that often are not so benign. It should also be emphasized that a definitive diagnosis may take some time, given the often retrospective nature of the diagnosis.

For the purposes of this article, myoclonic and partial onset seizures of the neonatal period are considered separate entities; they are mentioned briefly during the discussion on differential diagnosis. See Juvenile Myoclonic Epilepsy, Myoclonic Epilepsy Beginning in Infancy or Early Childhood, Partial Epilepsies, and Complex Partial Seizures for more information on these topics.

For more information, see the following:

  • Benign Childhood Epilepsy

  • First Pediatric Seizure

  • Epilepsy and Seizures

  • Pediatric Status Epilepticus


The genetics of benign familial neonatal convulsions (BFNC) is currently an area of active investigation; inheritance of this condition is autosomal dominant.[6]

M-type potassium channel mutation

Loci on chromosome arm 20q have been identified for most families, and at least one family was identified to have a locus on chromosome arm 8q. Some of these loci have been identified further as specific mutations in the KCNQ2 and KCNQ3 M-type potassium channel proteins.[7, 8, 9, 10, 11, 12, 13, 14] Both mutations encode voltage-gated potassium channel subunits.[15] The specific location of the mutation appears to vary from family to family and at least 1 family has been noted to include an increased incidence of rolandic epilepsy.[16]

Several additional genes have been associated with benign familial neonatal convulsions in single families, including KCNQ5 M-type potassium channel in one family.[17] Another family has been noted to have abnormalities in the acetylcholine alpha-4 receptor subunit, which also has been associated with autosomal dominant, nocturnal frontal lobe epilepsy.[18, 19]

Expression of the mutated genes in xenopus oocytes has provided some insight into how the potassium channel mutation leads to lowering of the seizure threshold. The potassium current was reduced in the channel expressed by the mutated gene to 5% of that in the channel expressed by the normal gene. However, voltage sensitivity and kinetics were not affected. The effect is therefore to impair repolarization of the neuronal cell membrane, leading to hyperexcitability of the central nervous system (CNS).[20, 21]

Given the severity of the impairment to the M-type potassium channel, that these seizures are difficult to treat is not surprising, because no currently used antiepileptic medications are known to increase the efficiency of the potassium channel. What is surprising is the self-remitting nature of the condition, that many individuals never have another seizure, and that the profound abnormalities of the voltage-gated potassium channel do not appear to compromise the nervous system in any other way. Possibly, some intrinsic method exists for upregulating expression of the normal potassium channel genes, or the neurons may find other ways of normalizing the hyperexcitability, but these theories remain to be demonstrated.[22, 23, 24]

A KCNQ2 mutation was identified in a family with seizure onset between 2-4 months of age, which may fulfill the diagnosis of BFNIS (benign familial neonatal-infantile seizures). Genomic deletion of KCNQ2 causes neonatal onset, whereas a point mutation in KCNQ2 causes delayed-onset epilepsy. This indicates the role of KCNQ2 beyond a typical neonatal period. A small portion of affected patients suffer afebrile seizures later in their childhood or adulthood. A new mutation is responsible for the malignant form up to and including epileptic encephalopathy.[25]

Epilepsy predisposition/susceptibility

A number of cases have been reported in which benign idiopathic or familial neonatal convulsions have preceded the development of epilepsy later in life. Similarly, perhaps, febrile seizures early in life may predispose to later development of epilepsy. Given the polygenic etiology of susceptibility to epilepsy, it is not surprising that an abnormality in part of the system maintaining homeostasis within the neuron should render the neuron more prone to dysfunction.[26, 27, 28, 29]

A complicating factor is that in neonates the action of the gamma-aminobutyric acid (GABA)–A receptor is excitatory rather than inhibitory in the brain.[30, 31, 32, 33]

GABA is initially excitatory as a result of a high intracellular concentration of chloride ([Cl-]). Then, GABA-releasing and glutamatergic synapses are formed sequentially. There is a primitive network-driven pattern of electrical activity in all developing circuits: the giant depolarizing potentials (GDPs), which are generated in part by the excitatory actions of GABA. This pattern allows the generation of large oscillations of intracellular calcium, even in neurons that have few synapses and an activity-dependent modulation of neuronal growth and synapse formation. Later on, once a sufficient density of glutamate and GABA synapses has been generated and inhibition becomes necessary, a chloride-excluding system becomes operative, an event that is activity dependent. As a result, chloride is efficiently pumped from the intracellular milieu, GABA begins to exert its conventional inhibitory action, and the primitive pattern is replaced by more diverse and elaborate patterns of activity.[34]

The pathophysiology of benign idiopathic neonatal convulsions (BINC) has been less well defined and remains somewhat elusive. One issue is that the neonatal brain is more prone to seizures, which has been demonstrated in a number of experimental systems.[30, 31, 32, 33]

Ion channel dysfunction

Ion channels regulate the flow of ions into and out of the cell and are absolutely critical for a wide range of biological processes, including the transmission of signals in the nervous system. Disrupting ion channel function can have disastrous consequences.[35]

Several etiologies have been proposed as a result of isolated findings of lowered zinc level in the cerebrospinal fluid and low levels of vitamin B-6.[36] Both of these compounds are important cofactors in ligand-gated ion channel function. However, these findings have not been robust, and the search continues. These seizures are likely also linked in some way to ion channel dysfunction as is found in the familial seizures, but they may be caused by multiple etiologies or occur as a multigenomic entity.[37, 38, 39] These sorts of multifactorial etiologies are more difficult to define precisely. More research is needed in this area, and apparent monogenic diseases, such as benign familial neonatal convulsions, provide important insight into more complex etiologies.


Several causes have been proposed for benign idiopathic neonatal convulsions (BINCs), including rotavirus infection, low central nervous system (CNS) zinc levels, and vitamin B-12 deficiency. None of these causes has been confirmed. The more likely explanation is the presence of a self-limited malfunction in one of the ligand-gated or voltage-gated ion channels.[3]

Potassium channel abnormalities

Most families in which benign familial neonatal convulsions occurs have abnormalities in the genes coding for the KCNQ2 and KCNQ3 potassium channels.[40, 41] The gene for this disorder has been localized to 2 chromosomes in many, but not all, of the families: BFNC 1, locus on band 20q13.3 (voltage-gated potassium channel gene, KCNQ2) and BFNC 2, band 8q24 (potassium channel gene, KCNQ 3).[42]

This defect leads to abnormal repolarization of the neuronal membrane and likely causes the neonatal seizures. The real puzzle is why this profound abnormality in membrane polarization does not lead to more problems in later life or persistent seizures extending from the neonatal period. This may be evidence that the drive toward homeostasis in the brain is strong, with redundant systems capable of maintaining a seizure-free state until more than one system is affected, or that systems are affected that do not have the redundancy of the voltage-gated potassium channels. Moreover, the normal potassium channels may be upregulated to accommodate for the deficiency in function of the abnormal channels.

Abnormal neurotransmitter development

Clearly, the immature infant brain is different electrophysiologically during early development. Gamma-aminobutyric acid (GABA) has a seemingly paradoxical excitatory effect.[30] Glutamate synapses are slow to develop, and there is delayed expression of the K+/Cl- cotransporter KCC2 and NKCC1.[31] The primary inhibition in the neonatal brain is presynaptic rather than postsynaptic. As the brain matures and expression of postsynaptic inhibitory and excitatory processes develop, the maintenance of neuronal homeostasis as well as postsynaptic excitatory postsynaptic responses (EPSPs) and inhibitory postsynaptic potentials (IPSPs) gradually approach the adult state. Because all of these processes are under development at the same time as neonatal convulsions appear, it is likely that neonatal seizures are affected by the normal developmental sequence of the other neurotransmitter systems.


Benign neonatal convulsions in the United States and internationally are uncommon; that is, not rare but not common, either. Underreporting is likely an issue. Seizures that resolve in the early months of life without sequelae and normal neonatal development are often lost to follow-up. Exact frequencies are undetermined. Families identified with the familial form thus far have been primarily of western European origin, although reports from Japan and China exist.[43, 44, 6] This is certainly an artifact of observation rather than occurrence. Part of the reason for this is likely the stability of reporting resources in European countries.

In benign idiopathic neonatal convulsions (BINCs), males are affected somewhat more frequently than females (62%) in examined cases,[36] whereas in benign familial neonatal convulsions (BFNCs), the frequency in males is equal to that in females, compatible with simple autosomal dominant inheritance.[36] With such a small number of cases reported, this may be due to reporting bias or simple sampling error, or it may represent a real difference in frequency.

There is also a slight age difference between the 2 conditions. In benign idiopathic neonatal convulsions, patients are aged 1-7 days at onset, with day 5 the most frequently reported day of onset; the frequent onset on the fifth day of life is responsible for the term fifth day disease or fifth day fits, which continues to be used in the pediatric literature. However, in actuality, fifth day fits are most likely seizures that were reportedly linked to the use of hexachlorophene (pHisoHex), which now has been discontinued.[45]

Patients may be slightly older at onset in benign familial neonatal convulsions, with some patients in previously identified families several weeks old. Characteristically, the onset of benign familial neonatal convulsions occurs when neonates are aged 2 days.[1, 2, 4]

Interestingly, unaffected family members of patients with benign familial neonatal convulsions have a higher-than-expected risk of developing epilepsy in later life. Presently, family studies have not clarified whether these relatives always share the genetic defect in the potassium channel.[3, 36]


The risk of seizures later in life is 11-16% in benign familial neonatal convulsions (BFNCs) and somewhat less in benign idiopathic neonatal convulsions (BINCs), perhaps as low as 2%. Other reported problems have been sporadic and within the incidence range expected for the general population.[36]

Overall, as the name implies, benign neonatal convulsions have an excellent prognosis and resolve without neurologic sequelae.

Patient Education

Inform families with the syndrome of the risk of affected siblings, but reassure them as to the benign nature of the syndrome. Also alert them to the possible development of epilepsy in later life in affected as well as apparently unaffected children. Furthermore, inform them that the incidence of minor neurologic problems is the same as expected in the general population.

For patient education information, see the Brain and Nervous System Center, as well as Seizures in Children.




The history of a patient with benign neonatal convulsions should be free of suspicion of causative elements for neonatal seizures, such as prenatal or perinatal stroke, perinatal asphyxia, fever, persistent lethargy, pertinent maternal illness or drug abuse, signs of metabolic dysfunction, or neurologic abnormalities.

Other criteria that have been noted but may be of limited value are a lack of neurologic or genetic abnormalities in siblings or other family members or metabolic dysfunction of any cause. A 5-minute Apgar score less than 9 (see the Apgar Score calculator) has also been suggested but is almost certainly too stringent to require for diagnosis.

Diagnostic criteria have been suggested by Miles and Holmes[36] as well as Plouin[3] for both benign idiopathic neonatal convulsions (BINCs) and benign familial neonatal convulsions (BFNCs).

Suggested diagnostic criteria for benign idiopathic neonatal convulsions include the following[3, 36] :

  • Infants born after 39 weeks' gestation

  • Apgar score of 9 or more at 5 minutes, greater than 7 at 1 minute: Lower scores should not exclude the diagnosis if other criteria are met.

  • Presence of a seizure-free interval between birth and the onset of seizures

  • Clonic and/or apneic seizures

  • Negative findings on evaluation for alternative etiology

  • Normal developmental and intellectual outcome: These are largely determined in retrospect.

  • Lack of seizures beyond the neonatal period

  • Normal laboratory findings (including but not limited to metabolic studies, neuroimaging, and lumbar puncture)[46]

Suggested diagnostic criteria for benign familial neonatal convulsions are as follows[3, 36] :

  • Normal neurologic examination findings

  • Negative findings on evaluation for alternative etiology

  • Normal developmental and intellectual outcome: These are largely retrospective criteria.

  • Positive family history of newborn or infantile seizures

  • Onset of seizures during neonatal period or early infancy

Physical Examination

The physical examination findings should be normal during the interictal period. The neurologic examination should also be normal during this period.



Diagnostic Considerations

Before diagnosing an infant with benign neonatal convulsions, other conditions should be ruled out as causative factors, including prenatal or perinatal stroke, perinatal asphyxia, fever, persistent lethargy, pertinent maternal illness or drug abuse, signs of metabolic dysfunction, or neurologic abnormalities. See the differentials list below.

Although a "shotgun" approach is wasteful and unreasonable, it is also important not to miss a diagnosis of a treatable meningoencephalitis in the early stages or intracranial hemorrhage. Both of these conditions in neonates lack the typical findings observed in older infants and children, and the only early symptom may be seizures.

Also, entertain a healthy suspicion for child abuse in neonates, who often have just arrived home from the hospital following delivery.

Other Problems to Be Considered

Vitamin B-6 deficiency, maternal drug abuse, arteriovenous malformations, and tuberous sclerosis should also be considered during the evaluation of an infant for benign neonatal convulsions.

Differential Diagnoses



Approach Considerations

The reason for ordering tests in benign familial and idiopathic neonatal convulsions is to exclude the presence of any etiology for the seizures. The diagnosis of benign infantile convulsions of either type requires that no other explanation exist for the seizures. Order tests for individual patients with a plan for that patient in mind.

Review of basic screening laboratory studies performed at delivery may also be helpful.

Routine Laboratory Studies

The following studies may provide a starting point in the laboratory workup of benign neonatal convulsions:

  • Chemistry studies: Obtain a basic metabolic panel plus calcium, magnesium, phosphorus levels; thyroid function tests; and possibly B vitamin levels.

  • Basic hematologic tests: Obtain a complete blood cell (CBC) count, prothrombin time (PT), and activated partial thromboplastin time (APTT).

  • Lumbar puncture: A cerebrospinal fluid examination may be indicated to exclude neonatal meningoencephalitis or occult blood.

Any abnormalities found that are inconsistent with a diagnosis of benign neonatal convulsions require the appropriate further workup and treatment.

CT Scanning and/or MRI of the Brain

Perform brain computed tomography (CT) scanning, magnetic resonance imaging (MRI), or both of these studies in every patient with neonatal seizures to exclude structural lesions and intracranial hemorrhage. An argument can be made that both studies are needed, because CT scanning yields better information on acute hemorrhage and skull fracture, and MRI shows better brain structural detail.


The classic electroencephalogram (EEG) observed in 60% of patients with benign idiopathic neonatal convulsions (BINCs) is nonreactive, focal, rhythmic activity in the theta (4-7 Hz) frequency, which may be mixed with sharp waves. This activity is discontinuous and may alternate between hemispheres. This pattern is often termed theta pointu alternant.[3, 5, 36] Although clinical seizures may spontaneously resolve within a short time, it has been reported that the theta pointu alternant EEG pattern may persist for up to 2 weeks.[46]

The remaining patients with benign idiopathic neonatal convulsions have either a normal interictal EEG or focal abnormalities. The EEG during seizures is most often high-voltage (200-400 µV) generalized discharges, which may appear to have a focal onset.

In benign familial neonatal convulsions, the interictal EEG is most commonly normal (50-70% of patients). The theta pointu alternant pattern is also observed—but only in approximately 25% of patients. In a small percentage of patients, focal, often rolandic, discharges or spikes may be present.[3, 47, 48]

Video EEG

In selected patients, continuous video-EEG can be used to confirm behavioral events concordant with abnormal EEG and to confirm that treatment is effective. The state of the patient and improvement or deterioration can make decision making easier and facilitate accurate communication with an often anxious family.[5]



Approach Considerations

Although the seizures are benign, general agreement exists that they should be treated, particularly benign idiopathic neonatal convulsions (BINCs).

Patients should be observed in the inpatient unit, until the physician is satisfied that the patient's condition is stabilized and that the infant is feeding well and is free of seizures that compromise feeding or sleeping. In some situations, patients may be seizure free at discharge, but this is not a requirement. Exclude reasonable alternative diagnoses before discharge.

The choice to continue or discontinue any medications that were started can be tailored to each patient. Consider each of the following:

  • Have the seizures abated to the point that they are no longer interfering with function?

  • What is the family's level of comfort? Fully inform the patient's family of the situation and address their questions and concerns before the infant’s discharge.

  • Is the electroencephalogram (EEG) improved? A normal EEG is not required, but improvement in the EEG indicates that the diagnosis is more likely to be benign and that the prognosis is good for continued improvement at home. Likewise, the typical pattern (ie, theta pointu alternant) indicates a benign course. Conversely, deterioration of the EEG background or development of a less benign pattern may indicate a less benign prognosis.

It is important to keep in mind that other seizure types are often intermixed in families with inherited seizure disorders. This is also observed in families with benign neonatal convulsions. Children (and apparently unaffected siblings) who have benign neonatal convulsions are at an increased risk of seizures in later life.

Medical Management

Treatment with antiepileptic medications may prevent the occurrence or reduce the length of the period of status epilepticus. Continuing antiepileptic treatment for more than 10 days may not be necessary in benign idiopathic neonatal convulsions. Keep in mind that during treatment although the seizures may abate, the electroencephalogram (EEG) may remain abnormal. In some cases, the EEG may change appearance but remain abnormal nevertheless.

No known antiepileptic medications alter the behavior of the potassium channel. Other drugs known to have an effect on potassium transporters are currently being considered for investigation. No studies have revealed any medications that have any advantage over other medications. Select medications on the basis of the following 2 factors:

  • Appropriateness of the drug in neonates

  • Lack of significant serious adverse effects

The most important consideration in choosing an antiepileptic medication in these patients is to remember that the syndrome is benign. Therefore, any medication chosen should have no risk of serious adverse effects.

The medications used most frequently are benzodiazepines, phenobarbital, levetiracetam, and fosphenytoin, but no particular reason exists for the preferential use of these drugs rather than some of the newer drugs, except for their current availability in intravenous (IV) formulations and the long-term experience with their use in neonates.

The disadvantages of phenobarbital and benzodiazepines are that they are overdosed easily in the neonate and can be very sedating. In addition, ample evidence shows that GABA-A agonists may not be a good choice in the immature brain. Phenobarbital has potential long-term effects on neurocognitive development.[49]

Fosphenytoin may be used acutely, but phenytoin is absorbed unpredictably in the neonate and should not be used as an oral preparation.

Levetiracetam is rapidly absorbed and is eliminated through the renal system. The most reported adverse effects are somnolence and behavior problems.[50]

Valproate and phenytoin are less appropriate choices. Generally, valproate in very young patients is reserved for serious conditions that do not respond to therapy with other medications, because the high risk of hepatic complications must be outweighed by the risk of the seizures themselves, a situation that normally is not under consideration in a benign condition. Phenytoin is less appropriate because of an unpredictable decreased absorption in the neonate when administered orally (PO) and a high possibility of IV extravasation in neonates.

When IV and liquid formulations become available, some of the newer drugs may prove to be of greater benefit in the future, owing to their multiple mechanisms of action and their neuromodulatory/neuroprotective effects.

Special concerns

Gamma-aminobutyric acid (GABA)–A agonists (barbiturates and benzodiazepines) should be used with caution in the neonate.

Use caution when treating status epilepticus with phenobarbital in neonates. Mistaking a normal deep anesthesia EEG in this age group with a burst suppression pattern of status epilepticus is easy.

Do not treat neonates in whom benign convulsions are suspected with valproate because of the increased risk of liver failure with the drug and the benign nature of the syndrome.


Patients with benign familial neonatal convulsions have an increased risk of developing seizures in later life; depending on the study, 11-20% of patients develop epilepsy in later life. Some families examined have also demonstrated an increased risk of epilepsy in apparently unaffected siblings.

Long-Term Monitoring

Follow-up care should consist of a visit soon after discharge to confirm that the patient is physically and neurologically healthy. Perform a repeat electroencephalogram (EEG) at that time.

Provide later follow-up care spaced at intervals consistent with the physician's and parents' level of comfort. In general, at least 2 serial assessments spaced several months apart should demonstrate a normal EEG, normal developmental milestones, and normal findings on neurologic examination.

Currently, the most appropriate medications for neonates that can be given in both intravenous (IV) and oral (PO) formulation after discharge remain phenobarbital and levetiracetam. In the future, other medications may prove more appropriate.



Medication Summary

No specific antiepileptic medication is preferred for the treatment of benign neonatal convulsions. In general, most epileptologists agree that status epilepticus should be treated when it occurs. Most neonates are best treated at this time with phenobarbital because of long experience with the drug, convenient monitoring, and adequate intravenous (IV) and (PO) absorption in the neonate or levetiracetam for its low adverse effect profile and ease of use with either parenteral (IV) or liquid (PO) formulations.[51] However, treatment has not been shown unequivocally to have an effect, except possibly to decrease the duration or severity of the seizures. By definition, the seizures resolve in days (benign idiopathic neonatal convulsions [BINCs]) to weeks (benign familial neonatal convulsions [BFNCs]).

Limit the choice of antiepileptic drug to those with no serious potential adverse effects. Most notably, avoid valproate in this age group if benign convulsions are suspected, because neonates are at the highest risk for liver failure due to valproate. Avoid phenytoin because of cardiac adverse effects, the high possibility of extravasation in neonates, and problems with reliable absorption if administered PO. A trial off the antiepileptic drug(s) should begin soon after the seizures stop and the electroencephalogram (EEG) is normal.

An important factor to remember when treating neonates is that pharmacokinetics and pharmacodynamics are very different than in infants. Do not use infant loading dosages, as they may lead quickly to toxic levels that resolve slowly.

Neonatal pharmacology is complex. Maturation of general liver and renal function is in a period of transition from the fetal to infant state. Stresses or lack of stress on the systems in utero greatly affect the function and maturation of both systems.

Normal glomerular filtration rate (GFR) in the neonate varies in individuals from 1 to 4 mL/min and can increase rapidly as maturation of the renal cortex progresses. Adult values for GFR are not reached before the infant is aged 2.5-5 months.

Blood flow within the hepatic portal system changes at birth with closing of the ductus venosus. Maturation of the glucuronidation pathway is often slowed. Neonates whose mothers have been exposed to drugs (both prescribed and otherwise) may have active cytochrome P-450 enzymes, and unexposed neonates have initial low activities that usually increase rapidly with the introduction of drugs such as phenobarbital.


Class Summary

Anticonvulsants prevent seizure recurrence and terminate clinical and electrical seizure activity.

Phenobarbital (Luminal)

Phenobarbital is the drug of choice for treatment of neonatal seizures. Use care in the dosing of this agent, as toxicity can occur quickly and resolve slowly. Also note doses that are initially adequate may need to be increased quickly as cytochrome P-450 becomes more active.

Fosphenytoin (Cerebyx)

Fosphenytoin may initially be used to control status epilepticus in patients with benign neonatal convulsions; however, this agent is unsuitable for long-term therapy.

Topiramate (Qudexy XR, Topamax, Trokendi XR)

Topiramate is a sulfamate-substituted monosaccharide with a broad spectrum of antiepileptic activity that may have state-dependent sodium channel blocking action. This agent potentiates the inhibitory activity of the neurotransmitter gamma-aminobutyric acid (GABA) and may block glutamate activity.

Levetiracetam (Keppra, Keppra XR, Spritam)

The exact mechanism of action is unknown. Stereoselective binding of levetiracetam is confined to synaptic plasma membranes in the central nervous system with no binding occurring in peripheral tissue. Levetiracetam inhibits burst firing without affecting normal neuronal excitability, which suggests it may selectively prevent hypersynchronization of epileptiform burst firing and propagation of seizure activity.


Class Summary

Alternative intravenous medications used in treating benign neonatal convulsions include benzodiazepines. The disadvantages of benzodiazepines are that they are overdosed easily in the neonate and can be very sedating.

Lorazepam (Ativan)

Lorazepam is a benzodiazepine with a short onset of effects and relatively long half-life. By increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, it may depress all levels of the CNS, including limbic and reticular formation.

Diazepam (Valium)

Diazepam is a benzodiazepine that is an extremely lipid-soluble agent and enters brain very quickly in first pass and often will stop seizures in 1-2 min. It modulates the postsynaptic effects of GABA-A transmission, resulting in an increase in presynaptic inhibition. It appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect.