The cause of infantile epilepsy

Patient's question:

No

Doctor's answer:

Convulsions (convulsio) are a common acute condition in children, characterized by sudden, generalized or focal tonic and clonic muscle contractions. Most are accompanied by impaired consciousness. The incidence of convulsions in children is 10 times higher than in adults, particularly in infants and toddlers.
[Etiology] The causes of pediatric convulsions can be categorized into two types:
1. Infectious (febrile convulsions) and non-infectious (afebrile convulsions) based on the presence or absence of infection.
2. Intracranial and extracranial based on the affected area.
(1) Infectious Convulsions (Febrile Convulsions)
1. Intracranial Diseases:
- Viral infections: such as viral encephalitis, Japanese encephalitis.
- Bacterial infections: such as purulent meningitis, tuberculous meningitis, brain abscess, and cavernous sinus thrombosis.
- Fungal infections: such as Cryptococcus neoformans meningitis.
- Parasitic infections: such as neurocysticercosis, cerebral malaria, cerebral schistosomiasis, cerebral lung fluke disease, and toxoplasmosis.
2. Extracranial Diseases:
- High fever convulsions.
- Toxic encephalopathy (e.g., severe pneumonia, pertussis, toxic dysentery, sepsis).
- Tetanus.
(2) Non-Infectious Convulsions (Afebrile Convulsions)
1. Intracranial Diseases:
- Head trauma: such as birth injury, traumatic brain injury, neonatal asphyxia, intracranial hemorrhage.
- Brain developmental abnormalities: such as congenital hydrocephalus, vascular malformations, macrocephaly/microcephaly, cerebral palsy, and neurocutaneous syndromes.
- Intracranial space-occupying lesions: such as brain tumors and brain cysts.
- Epilepsy syndromes: such as generalized tonic-clonic seizures and infantile spasms.
- Neurodegenerative disorders: such as demyelinating encephalopathy and cerebral macular degeneration.
2. Extracranial Diseases:
- Metabolic disorders: such as hypocalcemia, hypoglycemia, hypomagnesemia, hyponatremia, hypernatremia, and deficiencies of vitamin B1 or B6.
- Inherited metabolic diseases: such as glycogen storage disease, galactosemia, phenylketonuria, Wilson disease, and mucopolysaccharidoses.
- Systemic diseases: such as hypertensive encephalopathy, uremia, arrhythmia, severe anemia, food or drug poisoning, and pesticide poisoning.
[Pathogenesis]
(1) Anatomical and Physiological Factors
Infants and toddlers are prone to convulsions due to underdeveloped brains, incomplete differentiation of cortical neurons, and weaker cortical analysis, discrimination, and inhibitory functions. Additionally, underdeveloped dendrites and incompletely myelinated axons make excitatory impulses more likely to spread, leading to convulsions. When various stimuli affect the nervous system, neurons become excessively excited, resulting in excessive repetitive discharge activity. This electrical activity can be focal or generalized, manifesting as focal or generalized convulsions in clinical practice.
(2) Biochemical Factors
1. Normal calcium ion levels in the blood maintain neuromuscular excitability. When levels drop or intracellular calcium overload occurs, the permeability of nerves and muscle membranes to sodium ions increases, making depolarization more likely and leading to convulsions.
2. Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter. When vitamin B6 deficiency hinders GABA synthesis, reduced GABA levels in the brain can trigger convulsions.
3. Energy metabolism disorders in brain neurons can disrupt neuronal function. Hypoxia can produce large amounts of free radicals, which damage neuronal membrane phospholipids, generating lipid peroxides and increasing membrane permeability, leading to epileptic-like discharges. Lipid peroxides can also inhibit synaptic membrane sodium-potassium ATPase, rendering it inactive and causing synaptic membrane depolarization, resulting in convulsions. Hypoglycemia is the most common cause of energy metabolism disorders in neurons.
4. The relative concentration of sodium ions inside and outside cells affects brain function and seizure threshold. Low serum sodium causes water to shift from the extracellular to intracellular space, leading to cerebral edema and increased intracranial pressure, potentially causing convulsions. High serum sodium increases the excitability of nerves and muscles in proportion to sodium concentration, making convulsions more likely. Additionally, high fever overexcites the central nervous system, increasing responsiveness to external stimuli, or elevates the metabolic rate of neurons, leading to increased oxygen and glucose consumption and reduced levels, disrupting neuronal function and causing convulsions.
[Clinical Manifestations]
(1) Typical Convulsion Manifestations
Sudden onset, loss of consciousness, head retraction, fixed or upward-rolling eyes, frothing at the mouth, clenched teeth, and tonic or clonic muscle contractions in the face or limbs. Severe cases may exhibit nuchal rigidity, opisthotonos, irregular breathing, cyanosis, or incontinence. Convulsions last from seconds to minutes or longer, followed by drowsiness or coma. If the convulsion is localized and persistent, it may indicate a specific lesion. Neonatal convulsions often manifest as various irregular abnormal movements, such as apnea, irregular breathing, staring eyes, intermittent pallor or cyanosis. Infantile convulsions may sometimes only involve twitching of the corners of the mouth or eyes, or unilateral or alternating limb movements.
(2) Status Epilepticus
Convulsions lasting more than 30 minutes or with incomplete recovery of consciousness between episodes. This is a life-threatening condition. Prolonged convulsions can lead to hyperthermia, hypoxic brain damage, cerebral edema, or even herniation.
(3) Febrile Convulsions
Common in children aged 6 months to 4 years, typically occurring early in fever, with short duration and rarely recurring multiple times during a single fever episode. Consciousness recovers quickly after convulsions, with no positive neurological signs. EEG normalizes within a week after fever subsides, indicating simple febrile convulsions with a good prognosis. Complex febrile convulsions can occur at any age, often before 6 months or after 6 years. Initially, they may be febrile convulsions, but later occur during low or even fever-free periods, sometimes with multiple recurrences and prolonged duration (exceeding 15 minutes). EEG abnormalities persist for 2 weeks after convulsions, with a poorer prognosis. The likelihood of developing epilepsy is 15%–30%.
[Diagnosis]
Diagnosing pediatric convulsions requires a thorough search for underlying causes. Detailed history-taking, careful physical examination (including neurological assessment), and combined analysis of necessary laboratory and ancillary tests are essential.
(1) Age
The causes of convulsions vary by age:
1. Neonates: Common causes include head trauma (birth injury), asphyxia, intracranial hemorrhage, kernicterus, brain developmental malformations, metabolic disorders, and tetanus.
2. Infants and Toddlers: Common causes include febrile convulsions, hypocalcemia, intracranial infection, and infantile spasms.
3. Preschool and School-Aged Children: Common causes include intracranial infection, toxic encephalopathy, epilepsy, cerebral parasitic disease, hypertensive encephalopathy, poisoning, and brain tumors.
(2) Season
- Winter and Spring: Common causes include meningococcal meningitis, tetany, and febrile convulsions.
- Summer and Autumn: Common causes include viral encephalitis and toxic dysentery.
During physical examination, attention should be paid to the state of convulsions (generalized or focal) during episodes and neurological signs after convulsions (consciousness, pupil size, complexion, breathing, pulse, muscle tone, paralysis, and pathological reflexes). In infants and toddlers, the anterior fontanelle, cranial sutures, ear canal secretions, and mastoid tenderness should be checked. Fundoscopy may be necessary if indicated.
(3) Laboratory and Ancillary Tests
Complete blood count, urine, and stool tests. Elevated white blood cell count suggests bacterial infection. In severe cases of summer febrile convulsions with prominent toxic symptoms, saline enemas may be used to collect stool for examination. Blood glucose, calcium, magnesium, sodium, urea nitrogen, and creatinine tests may be performed as needed. If intracranial infection is suspected, cerebrospinal fluid examination should be conducted. Skull X-rays, cerebral angiography, pneumoencephalography, and CT scans may assist in diagnosing brain tumors and vascular diseases. EEG is helpful for diagnosing epilepsy.
[Emergency Management]
(1) General Convulsion Management
a. Controlling Convulsions
1. Acupuncture: Stimulate points such as Renzhong (GV26), Hegu (LI4), Shangquang (LI4), Neiguan (PC6), and Yongquan (KD1).
If convulsions do not stop within 2–3 minutes, the following medications may be used:
2. Anticonvulsant Medications
(1) Diazepam: 0.2–0.3 mg/kg per dose, maximum 10 mg, administered intravenously at a rate of 1 mg/min, with effects appearing within 1–2 minutes. If intravenous administration is difficult, 0.5 mg/kg can be retained rectally. Diazepam solution is rapidly absorbed rectally, typically taking effect within 4–10 minutes. Note that this medication can depress respiration and heart rate.
(2) Chloral Hydrate: 50–60 mg/kg per dose, mixed with a 10% solution for rectal retention.
(3) Phenobarbital Sodium: 8–10 mg/kg per dose, administered intramuscularly.
(4) Chlorpromazine: 1–2 mg/kg per dose, administered intramuscularly.
(5) Sodium Amytal (Amobarbital Sodium): 5 mg/kg per dose, diluted with 10% glucose to a 1% solution and infused intravenously at a rate of 1 ml/min. Infusion should stop once convulsions cease.
b. General Management
- Place the child in a side-lying position, loosen clothing, clear oral, nasal, and pharyngeal secretions and vomit to prevent aspiration, and maintain airway patency.
- Place a bite guard between the upper and lower molars to prevent tongue biting.
- Administer oxygen for severe cases.
- Use physical cooling or antipyretic medications for high fever.
c. Controlling Infection
Antibiotics should be used for infectious convulsions.
d. Etiological Treatment
Administer appropriate treatment based on the underlying cause.
(2) Management of Status Epilepticus
1. Immediate Control of Convulsions – Follow general convulsion management.
2. Control Hyperthermia – Use physical cooling (ice cap or cold compress) and pharmacological cooling, or combine with artificial hibernation.
3. Enhance Nursing Care – Closely monitor the child’s temperature, breathing, heart rate, blood pressure, complexion, pupil size, and urine output.
4. Reduce Intracranial Pressure – If convulsions persist for more than 2 hours, brain edema may develop, requiring dehydration therapy to lower intracranial pressure. Refer to principles for acute intracranial hypertension.
5. Maintain Fluid and Electrolyte Balance – For mild fluid loss, supplement fluids based on basal metabolism (60–80 ml/kg/day) to maintain mild dehydration and hyponatremia, which aids in controlling brain edema.
6. Neurotrophic and Antioxidant Agents – Vitamin A, E, C, and mannitol can prevent convulsive brain injury. Simultaneously, neurotrophic drugs such as thiamine, pyridoxine, cyanocobalamin, and Nootropil may be used.