What are convulsions, specifically neonatal convulsions, their types, common causes, and diagnostic workup?

Convulsions and Neonatal Convulsions: Definition, Types, Causes, and Diagnostic Workup

What Are Convulsions?

Convulsions are uncontrolled electrical discharges of neurons in the brain that manifest as violent contractions of muscles, typically with generalized movements and unresponsiveness reflecting excessive synchronous cortical electrical activity 1. The term "convulsions" is best reserved for epileptic seizures, distinguishing them from other paroxysmal events 1.

• A seizure is defined as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain 1
• Convulsive seizures affect large areas or both sides of the brain and manifest as full-body rhythmic jerking with alterations in consciousness 1
• The mere presence of myoclonic movements (brief jerking) does not confirm epileptic seizures, as these can occur in syncope; the distinction depends on synchrony, rhythmicity, and number of movements (many movements in seizures vs. few in syncope) 1

What Are Neonatal Convulsions?

Neonatal convulsions are the most common neurological emergency in the early period after birth, occurring in 1.5 to 3 per 1000 live births, with a lower seizure threshold due to immature neonatal neurons and differences in neurotransmitters 2.

• The neonatal period (0-28 days of life) is the most vulnerable time for seizure development, particularly in the first weeks after birth 3
• These seizures often signify serious malfunction or damage to the immature brain and constitute a neurological emergency requiring urgent diagnosis and management 3

Types of Neonatal Convulsions

Neonatal seizures are classified into four distinct clinical types, with subtle (undefined) seizures being the most common presentation 2, 4:

1. Subtle Seizures (Most Common - 42%)

• Undefined or difficult-to-classify movements 4
• May include oral automatisms (chewing, smacking), eye movements, or cycling movements 2

2. Clonic Seizures

• Multifocal clonic (64.3%): Jerking movements affecting multiple body parts 4
• Focal clonic (10.7%): Rhythmic jerking confined to one body part or side 4

3. Tonic Seizures (33.9%)

• Sustained stiffening or posturing of limbs or trunk 4

4. Myoclonic Seizures (16.1% multifocal)

• Brief, shock-like jerks of muscle groups 4

Important clinical note: 55.4% of infants present with two or more types of clinical convulsions simultaneously, and 25% develop status epilepticus 4.

Non-Epileptic Paroxysmal Movements (Must Be Distinguished)

The following movements should NOT be confused with seizures and do not require anticonvulsant treatment 2, 5:

• Jitteriness: Tremulous movements that stop with passive flexion
• Benign neonatal sleep myoclonus: Myoclonic jerks during quiet sleep without EEG discharges 5
• Hyperekplexia: Exaggerated startle response

Most Common Causes of Neonatal Convulsions

Hypoxic-ischemic encephalopathy (HIE) is the dominant cause of neonatal seizures, accounting for 46-65% of cases, with 90% of these seizures occurring within the first 2 days of life 6, 7, 2.

Timing-Based Etiologic Framework:

First 48 Hours (Days 0-2):

• Hypoxic-ischemic injury (46-65%): The primary etiology, predominantly presenting in the first 48 hours after birth 6, 7
• Intracranial hemorrhage and perinatal ischemic stroke (10-12% combined): Second most common category 6, 7

Days 3-7:

• Metabolic derangements become more prominent:
  • Hypoglycemia 6
  • Hypocalcemia 6
  • Hypomagnesemia 6
  • Hyponatremia 6

Beyond Day 7 (Late-Onset):

• Infection: More likely with late presentation 7
• Genetic disorders: Congenital metabolic diseases (13.1% in one series, particularly in populations with consanguinity) 3
• Malformations of cortical development: Structural brain abnormalities 7

Additional Causes by Category:

Prenatal factors (16%) 8:

• Cerebral malformation (6%)
• Tuberous sclerosis (2%)
• Congenital heart disease (1%)

Natal factors (12%) 8:

• Birth asphyxia and trauma

Postnatal factors (38%) 8:

• Purulent meningitis (4%)
• Brain tumors (1%)

Diagnostic Workup

The diagnostic approach must prioritize immediate stabilization, rapid exclusion of treatable metabolic causes, and systematic evaluation to identify the underlying etiology in approximately 95% of cases 6, 7.

Immediate Stabilization (First Minutes):

Step 1: Ensure ABCs and continuous monitoring 6:

• Patent airway, adequate breathing, and circulation
• Continuous monitoring of heart rate, blood pressure, temperature, and oxygen saturation
• Establish IV/IO access immediately 6

Step 2: Point-of-care glucose testing (MANDATORY) 6:

• Check glucose immediately to exclude hypoglycemia
• If hypoglycemic, correct with D10%-containing isotonic IV solution at maintenance rate 6

Laboratory Evaluation:

Essential immediate labs 6:

• Electrolytes: Sodium, calcium, and magnesium must be monitored
• Correct hypocalcemia and hypomagnesemia BEFORE initiating anticonvulsants 6
• Blood gas analysis
• Complete blood count
• Blood culture if infection suspected

Metabolic screening 3:

• Indicated when congenital metabolic disease suspected (family history of consanguinity, late-onset seizures, or atypical presentation)
• Ammonia, lactate, amino acids, organic acids

Neuroimaging:

Imaging algorithm based on clinical stability 6, 7:

1. Head ultrasound: Initial bedside imaging if infant is unstable or MRI unavailable 6
2. MRI with diffusion-weighted imaging: Gold standard for identifying etiology 6
   • Should be performed when infant is stable
   • Superior for detecting HIE, stroke, malformations, and metabolic disorders

Electroencephalography (EEG):

Continuous video-EEG monitoring is essential 2, 4:

• Confirms clinical seizures (only 56 of 74 suspected cases had EEG-confirmed seizures in one study) 4
• Detects subclinical seizures (unexpectedly high number) 5
• Identifies electroclinical dissociation (42.9% of cases) 4
• Amplitude-integrated EEG (aEEG): Burst suppression pattern detected in 56.7% of monitored cases, indicating severe brain dysfunction 3

Critical EEG prognostic patterns 4:

• Multifocal discharges (64.3%): Associated with worse pharmacological control and unfavorable outcome
• Moderately abnormal background: 72.2% unfavorable outcome
• Markedly abnormal background: 100% unfavorable outcome
• Normal or mildly abnormal background: Only 15.4% unfavorable outcome

Infection Workup:

When infection is suspected 6:

• Treat with empirical antibiotics immediately
• Blood culture, urine culture
• Lumbar puncture: DO NOT perform in comatose infants without experienced physician evaluation due to risk of herniation 6

Critical Pitfalls to Avoid

Clinical diagnosis alone is insufficient 4, 5:

• EEG confirmation is necessary before and after establishing anticonvulsant treatment
• Clinical control of convulsions was achieved in >80% of cases, but electrical seizure control only in 62.5% 4
• Subclinical seizures and atypical seizures are common and require EEG detection 5

Do not delay metabolic correction 6:

• Hypocalcemia and hypomagnesemia must be corrected BEFORE anticonvulsants
• Hypoglycemia requires immediate correction

Avoid lumbar puncture in unstable infants 6:

• Risk of herniation in comatose infants
• Requires experienced physician evaluation first

Do not confuse benign paroxysmal movements with seizures 2, 5:

• Benign neonatal sleep myoclonus does not require anticonvulsant therapy
• Jitteriness and hyperekplexia are not seizures