bubble_chart Overview

Convulsion is a common emergency in children, characterized by sudden onset of generalized or localized muscle group tonic and clonic spasms. Most cases are accompanied by impaired consciousness. The incidence of infantile convulsion is 10 times higher than that in adults, particularly prevalent among infants and young children.

bubble_chart Etiology

The causes of infantile convulsion can be divided into two categories: based on the presence of infection, they are classified as infectious (febrile convulsion) and non-infectious (afebrile convulsion). According to the affected site, they are divided into intracranial and extracranial categories.

(1) Infectious convulsion (febrile convulsion)

1. Intracranial diseases: Viral infections such as viral encephalitis and Japanese encephalitis. Bacterial infections such as purulent meningitis, tuberculous meningitis, brain abscess, and venous sinus thrombosis. Fungal infections such as cryptococcal meningitis. Parasitic infections such as cerebral cysticercosis, cerebral malaria, cerebral schistosomiasis, cerebral paragonimiasis, and toxoplasmosis.
2. Extracranial diseases: Febrile convulsion, toxic encephalopathy (with severe pneumonia, whooping cough, toxic dysentery, or sepsis as the primary disease), tetanus, etc.

(2) Non-infectious convulsion (afebrile convulsion)

1. Intracranial diseases: Craniocerebral injuries such as birth trauma, brain injury, neonatal asphyxia, and intracranial hemorrhage. Brain developmental abnormalities such as congenital hydrocephalus, cerebrovascular malformation, macrocephaly (microcephaly), cerebral palsy, and neurocutaneous syndromes. Intracranial space-occupying lesions such as brain tumors and brain cysts. Epilepsy syndromes such as grand mal seizures and infantile spasms. Brain degenerative diseases such as demyelinating encephalopathy and cerebral macular degeneration.
2. Extracranial diseases: Metabolic disorders such as hypocalcemia, hypoglycemia, hypomagnesemia, hyponatremia, hypernatremia, and vitamin B1 or B6 deficiency. Inherited metabolic diseases such as glycogen storage disease, galactosemia, phenylketonuria, hepatolenticular degeneration, and mucopolysaccharidosis. Systemic diseases such as hypertensive encephalopathy, uremia, arrhythmia, severe anemia, and poisoning from food, drugs, or pesticides.

bubble_chart Pathogenesis

(1) Anatomical and Physiological Factors

Infants and young children are prone to convulsions because their brain development is not yet mature, and the differentiation of cortical nerve cells is incomplete. As a result, the analytical, discriminative, and inhibitory functions of the cortex are weaker. Additionally, the dendrites of neurons are underdeveloped, and the myelination of axons is incomplete, making excitatory impulses prone to generalization and leading to convulsions. When various stimulating factors act on the nervous system, they cause excessive excitation of nerve cells, resulting in excessive repetitive discharge activities. These electrical activities can be localized or generalized, clinically manifesting as localized or generalized spasms.

(2) Generation and Transformation Factors

1. The normal concentration of calcium ions in the blood maintains neuromuscular excitability. When the concentration decreases or intracellular calcium ions are overloaded, the permeability of the nerve and muscle membrane to sodium ions increases, making depolarization more likely and leading to convulsive episodes.
2. γ-Aminobutyric acid (GABA) is an inhibitory neurotransmitter. When vitamin B6 is deficient, it hinders the synthesis of GABA, and a decrease in GABA concentration in the brain can lead to convulsions.
3. Disorders in energy metabolism of brain nerve cells can cause neuronal dysfunction. Hypoxia can generate a large number of free radicals, which act on the unsaturated fatty acids in the phospholipids of nerve cell membranes, producing lipid peroxides that damage and degenerate nerve cells, increasing permeability and causing epileptiform discharges. Lipid peroxides also inhibit sodium-potassium ATPase in synaptic membranes, inactivating them and leading to synaptic membrane depolarization, which triggers convulsions. Hypoglycemia most commonly causes neuronal energy metabolism disorders.
4. The relative concentration of sodium ions inside and outside cells can affect brain function and the seizure threshold. When serum sodium decreases, water moves from outside the cell into the cell, causing nerve cell edema and increased intracranial pressure, which in severe cases can lead to convulsions. When serum sodium increases, the concentration of sodium is directly proportional to neuromuscular excitability, and exceeding a certain concentration can easily cause convulsions. Additionally, high fever overexcites the central nervous system, increasing its responsiveness to internal and external stimuli, or raises the metabolic rate of neurons, increasing oxygen and glucose consumption while reducing their levels, leading to neuronal dysfunction and convulsions.

bubble_chart Clinical Manifestations

(1) Convulsions
The typical manifestations include sudden onset, loss of consciousness, head tilting backward, fixed upward or oblique gaze, foaming at the mouth, clenched teeth, and clonic or tonic spasms of facial or limb muscles. In severe cases, neck stiffness, opisthotonos, irregular breathing, cyanosis, or urinary incontinence may occur. Convulsions last from a few seconds to several minutes or longer, followed by drowsiness or unconsciousness. If the spasms are localized and constant, they often have localizing significance. Neonatal convulsions often present as amorphous and variable abnormal movements, such as apnea, irregular breathing, fixed gaze, or paroxysmal pallor or cyanosis. In infants and young children, convulsions may manifest only as twitching at the corners of the mouth or eyes, unilateral limb twitching, or alternating twitching of bilateral limbs.
(2) Status Epilepticus
This refers to convulsions lasting more than 30 minutes or incomplete recovery of consciousness between two episodes. It is a critical form of convulsion. Prolonged convulsions can lead to high fever, hypoxic brain damage, cerebral edema, or even brain herniation.
(3) Febrile Convulsions
Common in children aged 6 months to 4 years, convulsions often occur early in fever, are short-lived, and rarely recur multiple times during a single febrile illness. They typically occur within 12 hours of fever onset, with rapid recovery of consciousness after the episode and no positive neurological signs. The electroencephalogram (EEG) returns to normal within one 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 presenting as febrile convulsions, they may later occur with low-grade or even no fever after several episodes. Sometimes, they recur multiple times, with each episode lasting longer than 15 minutes. EEG abnormalities persist for more than 2 weeks after convulsions, indicating a poorer prognosis. The likelihood of progression to epilepsy is 15–30%.

bubble_chart Auxiliary Examination

Blood, urine, and stool routine tests; elevated white blood cells in the blood suggest bacterial infection. For high fever convulsions and severe toxic symptoms in summer, cold saline enema should be used to collect stool samples for examination. Tests such as blood glucose, calcium, magnesium, sodium, urea nitrogen, and creatinine should be performed as needed. Cerebrospinal fluid examination is required if intracranial infection is suspected. Skull X-rays, cerebral angiography, and pneumoencephalography can assist in diagnosing brain tumors and cerebrovascular diseases, with a head CT scan performed when necessary. An electroencephalogram (EEG) aids in the diagnosis of epilepsy.

bubble_chart Diagnosis

The cause of infantile convulsion should be emphasized. A detailed medical history must be collected, and a thorough examination, including a neurological examination, should be conducted, combined with necessary laboratory and auxiliary tests for comprehensive analysis.

(1) Age

The causes of convulsions vary at different ages.

1. In newborns, cranial injuries (birth trauma), asphyxia, intracranial hemorrhage, kernicterus, brain malformations, metabolic disorders, tetanus, and purulent meningitis are more common.
2. In infants and young children, febrile seizures, hypocalcemia, intracranial infections, and infantile spasms are more common.
3. In preschool and school-age children, intracranial infections, toxic encephalopathy, epilepsy, cerebral parasitic diseases (e.g., Chinese Taxillus Herb infection), hypertensive encephalopathy, poisoning, and brain tumors are more common.

(2) Season

In winter and spring, meningitis, hand-foot-mouth disease, and febrile seizures are more common, while in summer and autumn, viral encephalitis and toxic dysentery are more prevalent.

During physical examination, attention should be paid to the state of spasm during convulsions (generalized or localized). After the convulsion stops, observe the level of consciousness, pupil size, complexion, respiration, pulse, muscle tone, paralysis, and pathological reflexes. For infants and young children, check the anterior fontanelle, cranial sutures, external auditory canal secretions, and mastoid tenderness, and perform an fundus examination if necessary.

bubble_chart Treatment Measures

General Management of Convulsions

(1) Controlling Convulsions

1. Acupuncture Method: Needle points such as philtrum, Hegu, Shixuan, Neiguan, and Yongquan. If convulsions do not stop within 2–3 minutes, the following medications can be used.
2. Anticonvulsant Medications
   1. Diazepam: 0.2–0.3 mg/kg per dose, maximum dose not exceeding 10 mg, administered intravenously at a rate of 1 mg/min. Effects occur within 1–2 minutes after administration. If intravenous injection is difficult, 0.5 mg/kg per dose can be administered rectally. Diazepam injection is rapidly and directly absorbed in the rectum, typically taking effect within 4–10 minutes. Note that this drug can suppress respiration and heart rate.
   2. Chloral Hydrate: 50–60 mg/kg per dose, prepared as a 10% solution, administered rectally.
   3. Phenobarbital Sodium: 8–10 mg/kg per dose, administered intramuscularly.
   4. Chlorpromazine: 1–2 mg/kg per dose, administered intramuscularly.
   5. Amobarbital Sodium (Sodium Amytal): 5 mg/kg per dose, diluted to a 1% solution with 10% glucose and administered intravenously at a rate of 1 ml/min. Stop administration once convulsions cease.

(2) General Management
Place the child in a lateral position, loosen the collar, and clear secretions and vomitus from the mouth, nose, and throat to prevent aspiration and ensure airway patency. Place a bite block between the upper and lower molars to prevent tongue biting. Administer oxygen if severe. For high fever, use physical cooling methods or antipyretic medications.
(3) Infection Control
For infectious convulsions, appropriate antibiotics should be selected.
(4) Treatment of Underlying Disease
Provide corresponding treatment based on the underlying disease cause.

Management of Status Convulsivus

1. Immediate control of convulsions is the same as general convulsion management.
2. Control high fever using physical cooling (ice cap or cold compress on the head), antipyretic medications, or artificial hibernation combined with cooling.
3. Enhance nursing care and closely monitor the child’s temperature, respiration, heart rate, blood pressure, skin color, pupil size, and urine output.
4. Reduce intracranial pressure: If spasms persist for more than 2 hours, cerebral edema is likely. Use dehydration therapy to lower intracranial pressure. Management principles are the same as for acute intracranial hypertension.
5. Maintain water and electrolyte balance: For those without severe fluid loss, supplement fluids based on basal metabolic needs at 60–80 ml/kg·day, maintaining grade I dehydration and a low-sodium state to help control cerebral edema.
6. Neurotrophic and Antioxidant Therapy: Antioxidants such as vitamins A, E, C, and mannitol can prevent and treat convulsive brain injury. Concurrently, neurotrophic drugs like vitamin B12 and piracetam can be used.