Convulsions and convulsions

Introduction to convulsions and convulsions Twitching refers to the involuntary contraction of abnormalities of the whole body or local skeletal muscles, and causes joint movements, mostly systemic and symmetrical. The synonym is spasm. If accompanied by loss of consciousness, it is called convulsion. Forms can be tonic (sustained muscle contraction), clonic (intermittent muscle contraction), and mixed (several tonic and clonic muscle contractions). Twitching can occur from muscles, peripheral nerves, and any part of the central nervous system. basic knowledge The proportion of sickness: 0.2--0.5% Susceptible people: no specific people Mode of infection: non-infectious Complications: disturbance of consciousness, intracranial hypertension syndrome

Causes of convulsions and convulsions

Intracranial lesions (35%)

Congenital diseases such as brain penetrating malformations, craniocerebral trauma, brain infections such as meningitis and brain abscess, cerebrovascular diseases such as cerebral embolism and subarachnoid hemorrhage, intracranial tumors, central demyelinating diseases and other brain diseases can be Cause the disease.

Metabolic abnormalities (20%)

Metabolic endocrine diseases: 1 abnormal amino acid metabolism, such as phenylketonuria. 2 lipid metabolism disorders, such as lipid accumulation. 3 sugar metabolism diseases, such as hypoglycemia, galactosemia. 4 water, electrolyte disorders, such as hyponatremia, hypernatremia, water poisoning, hypokalemia, hypomagnesemia, hypercapnia and so on. 5 vitamin D deficiency, hypoparathyroidism. 6 vitamin deficiency and dependence, such as vitamin B6, vitamin B12 and folic acid deficiency.

Cerebral hypoxia (15%)

Cerebral hypoxia can induce the disease, such as suffocation, shock, acute hemorrhage, carbon monoxide poisoning, inhalation anesthesia.

Poisoning (8%)

Poisoning can often cause convulsions common types of poisoning are: 1 drug poisoning: such as central stimulant (nicaramide, pentylenetetrazol, camphor) excess; antipsychotics (chlorpromazine, trifluoperazine, chloropyrazine Etc.) The dose is too large; sudden withdrawal of anticonvulsants or central nervous system inhibitors. 2 heavy metal poisoning, such as lead, mercury poisoning. 3 food poisoning, pesticide poisoning and alcohol withdrawal.

Other factors (15%)

Cardiovascular diseases: such as Adams-Stokes syndrome, hypertensive encephalopathy. Hysteria and high fever can also cause convulsions, which are common in infants and young children.

Pathogenesis

The mechanism of convulsions is extremely complicated. It can be a central nervous system function or structural abnormality, or it can be an abnormality of peripheral nerves and even effectors, or both. According to the source of abnormal electrical excitation signals, it can be divided into two types. Happening:

1. Normal physiological function and structural abnormalities of the brain, the well-developed brain neurons have a certain self-stabilizing effect, and their excitation and inhibition systems are in a relatively balanced state. Many brain or systemic diseases destroy this balance, leading to neurons. The threshold of excitability is reduced and the over-synchronized discharge causes convulsions.

(1) Decreased neuronal excitation threshold: The membrane potential of neurons is stable depending on the polar distribution and structural integrity of the ions inside and outside the membrane. Many diseases inside and outside the skull can affect the stability of membrane potential through different pathways, such as hyponatremia, high potassium. Hypertension directly causes a decrease in membrane potential (a decrease in neuronal excitation threshold), which causes auto-depolarization of neurons to produce action potentials; ischemia, hypoxia, hypoglycemia, hypomagnesemia and digitalis poisoning affect energy metabolism, or high fever Excessive consumption of oxygen, glucose, and adenosine triphosphate can cause a decrease in membrane potential; in addition, toxins in brain infection or extracranial infection directly damage the membrane of the neuron to increase its permeability, and hypocalcemia causes the cells to be sodium. Increased ion permeability can cause extracellular sodium influx and auto-depolarization of neurons.

(2) Impaired brain neurons and their surrounding structures: various brain organic diseases (such as hemorrhage, tumor, contusion, encephalitis, brain abscess, etc.) can lead to sparse neurons, impaired membrane structure, and tree mutations. Shape, glial cell proliferation and astrocyte dysfunction, leading to the loss of potassium ions, making it difficult for neuronal membranes to maintain a relatively stable polarization state, easy to form spontaneous, long-term potential fluctuations.

(3) Neurotransmitter changes: When there are too many excitatory neurotransmitters, such as organophosphate poisoning, cholinesterase activity is inhibited, and excitatory transmitter acetylcholine accumulates too much, so that convulsions can occur, and vice versa. Lack of neurotransmitters, such as vitamin B6 deficiency, lack of coenzyme of glutamate decarboxylase, affecting the decarboxylation of glutamate into the formation of the inhibitory transmitter -aminobutyric acid; in the early stage of hepatic encephalopathy, due to brain tissue The detoxification of ammonia requires glutamic acid, resulting in a decrease in the precursor glutamate synthesis of -aminobutyric acid, which results in convulsions.

(4) Mental factors: trauma can cause temporary dysfunction of cerebral cortex function, loss of regulation and inhibition of the subcortical central, leading to convulsions, such as convulsions.

(5) genetic factors: febrile seizures and idiopathic epilepsy have significant family aggregation, which suggests that genetic factors play a role in the occurrence of seizures, that is, the hereditary neuron excitability is reduced.

2. Non-brain dysfunction: mainly the movement of the spinal cord or peripheral nerves, such as tetanus exotoxin selectively acting on the synapse of the central nervous system (mainly the spinal cord, the lower motor neurons of the brainstem), leading to persistent muscles Tonic convulsions, strychnine poisoning caused excessive excitability of the anterior horn cells of the spinal cord, and a tetanus-like convulsion occurred.

In addition to increasing the permeability of neuronal membranes, hypocalcemia or alkalosis often exacerbates the excitability of peripheral nerves and sarcolemma by increasing the permeability of sodium ions, causing hand and foot spasms.

In addition, tumors of the posterior cranial fossa, cerebellum, etc. or cerebellar tonsils affect brainstem function, and intermittent cortical tonicity may occur.

Convulsion and convulsion prevention

1. Active prevention of primary disease for the cause. For example, patients with epilepsy need to take the medicine according to the doctor's advice. If the drug is suddenly stopped, even 1 day to 2 days, it will lead to the onset of epilepsy cramps. Another example is that children with high heat and easy cramps, timely fever can prevent cramps; tetanus can cause cramps, so to break the cold vaccine to prevent tetanus; rabies can cause cramps, prevention of dog bites is very important, in case of dog bites, You should go to the hospital immediately for treatment; the animals with rabies should be killed immediately; calcium deficiency can cause cramps, so children should make up the calcium (eat more calcium-containing foods, if necessary, take calcium gluconate, calcium tablets, etc.), and at the same time The sun, taking cod liver oil and so on.

2. To prevent gastrocnemius cramps, it is necessary to prepare for exercise and warm-up before strenuous exercise or before swimming. In order to prevent cramps at night when sleeping, do not get too tired during the day, do not let the legs get cold at night.

Convulsions and convulsion complications Complications, disturbance of consciousness, intracranial hypertension syndrome

Complications mainly depend on the cause, such as encephalitis, meningitis may lead to subdural effusion, cerebral ependymitis, hydrocephalus, sputum, mental retardation and epilepsy; neonatal hypoxic ischemic encephalopathy may lead to the brain Sexual paralysis, developmental backwardness, and epilepsy; only 7% of febrile seizures may develop into epilepsy; while seizures caused by electrolyte disorders are mostly prognostic, with few complications.

Symptoms of convulsions and convulsions Common symptoms Anterior angulation, convulsions, convulsions, systemic infection, severe symptoms, severe pain, closed jaw, loss of consciousness, intracranial hypertension, repeated convulsions, convulsions

1. Types of convulsions: Due to different causes, the form of convulsions is different.

(1) systemic convulsions: for the body skeletal muscle contraction, such as epileptic seizures manifested as tonic-clonic convulsions; tetanus is continuous tonic convulsions.

(2) localized convulsions: continuous twitching of a part of the body or face, such as localized sports epilepsy often manifested as repeated convulsions of the mouth, eyelids, hands or feet; if convulsions start from one place, according to the cerebral cortex The arrangement of the sports area gradually expands, that is, from the side of the thumb, the extension and wrist, arm, shoulder, is Jackson epilepsy, while the hand and foot sputum is intermittent limbs (the most significant of the upper limbs) myotonic muscle Hey, the typical person is a "midwife" hand.

2. Symptoms associated with convulsions: There are many diseases causing convulsions in the clinic, and some types of convulsions are similar. Therefore, analysis of the accompanying symptoms is of great significance for the diagnosis of etiologies. Epileptic seizures are often accompanied by loss of consciousness and incontinence; tetanus has Angle bow reversal, closed jaw, bitter face and severe muscle pain; infectious diseases are often accompanied by symptoms of systemic infection; brain tumors are often accompanied by symptoms of intracranial hypertension and local brain dysfunction; cardiovascular, renal lesions, endocrine and metabolism Disorders, etc. have corresponding clinical signs.

Convulsions and convulsions

According to the medical history and physical examination to provide clues to choose laboratory tests, in addition to hematuria and fecal routine, blood biochemistry (blood sugar, electrolytes, etc.), blood gas analysis, heart, liver, kidney function determination and endocrine examination, cerebrospinal fluid routine, biochemistry And cytology to help the etiology of central infection with convulsions.

1. Internal medicine: When the clinical suggestion that convulsion is caused by systemic diseases, the corresponding examination should be selected according to the provided clues, including toxicant analysis, electrocardiogram, echocardiography, B-ultrasound, etc.

2. Nervous system: Once the neurological disease is suspected, the corresponding examination should be selected according to the location and nature of the disease.

Suspected epileptic seizures, EEG, SPECT scan and PET scan can be selected. Intracranial space-occupying lesions can be localized and qualitatively diagnosed by X-ray, brain CT and MRI; cerebrovascular disease can be selected for cerebrovascular function test, transcranial Doppler and angiography (qi brain, ventricle, brain) Angiography).

Electromyography and spinal canal angiography can be used to diagnose the spinal cord or peripheral nerve with twitching. Somatosensory evoked potentials, brainstem evoked potentials (auditory, visual evoked potentials) are important for the localization diagnosis of brain, spinal cord or peripheral nerves and muscle lesions.

Diagnosis of convulsion and convulsion

Twitching is not a disease, but a serious clinical sign of the disease, or the main manifestations of certain diseases (epilepsy, febrile seizures, hypocalcemia, etc.), which should be comprehensively analyzed to determine the cause.

1. Identify the nature of convulsions and analyze the cause of convulsions

(1) The type of convulsion.

(2) Symptoms associated with convulsions.

(3) Past history: Past history has important reference value for diagnosis. Repeated episodes often suggest epilepsy, while trauma, infection and disease of internal organs help to find the primary disease of convulsion.

2. Physical examination

There are many causes of convulsions, often involving clinical subjects, so detailed physical examination is very important, usually focusing on internal medicine and nervous system examinations.

(1) Internal examination: almost all diseases of important internal organs can cause convulsions, so it must be checked according to the system. For example, cardiac convulsions can have heart sounds and pulse disappearance, blood pressure drops or can not be measured, or arrhythmia; kidney There are clinical signs of uremia in convulsions; convulsions caused by hepatic encephalopathy often have clinical manifestations of cirrhosis; common signs of hypocalcemia are Chvostek sign and Trousseau sign.

(2) Neurological examination: Many diseases of the nervous system can cause convulsions. Through careful neurological examination, it is helpful to judge the lesions that cause convulsions. When there are focal signs, such as hemiplegia, hemianopia, aphasia, etc., brain damage The positioning is more valuable.

The examination of mental state has reference value for the determination of functional convulsions.

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