Mental disorder at the time of the attack

Introduction Disorder associated with ictal: mental disorders at the time of onset include psychomotor seizures, paroxysmal affective disorders, and transient schizophrenia-like episodes. Also known as psychomotor seizures or temporal lobe epilepsy can be a precursor or can occur separately. It is more common in cortical lesions, and the various symptoms at the time of onset are determined by the location of the lesion. Most lesions are in temporal lobe, and some are in frontal or marginal lobe. It is a transient psychiatric experience at the time of onset, and is often accompanied by a disturbance of consciousness.

Cause

(1) Causes of the disease

Epilepsy is often divided into primary and secondary clinically. Among them, primary epilepsy is also called true epilepsy or idiopathic epilepsy or occult epilepsy, and its etiology is not clear. Secondary epilepsy, also known as symptomatic epilepsy, can be found in the brain, often secondary to brain diseases, brain tumors, craniocerebral trauma, intracranial infections, cerebrovascular diseases, and brain degenerative diseases. It can also occur in systemic diseases such as hypoxia, metabolic diseases, cardiovascular diseases, and toxic diseases.

The pathogenesis of epilepsy is complex and has not yet been elucidated. It is currently attributed to excessive synchronous discharge of neurons. Molecular genetic research has made breakthroughs. For example, the genetic pattern of primary systemic epilepsy and epilepsy with mental retardation is autosomal recessive inheritance, and epilepsy with hallucinatory features is autosomal dominant. Genetics, etc.

Seizures are a clinical manifestation of cerebral cortical neuronal dysfunction. The cause of the first seizure can be:

1. Reactive epileptic seizure caused by acute brain functional disorders such as high fever, metabolic disorders, or structural disorders such as central nervous system infections, cerebrovascular diseases, head trauma or brain tumors ). The prognosis varies according to the cause of seizures. It may be the only time in life, but it may also be epileptic seizures after the acute phase, which is symptomatic epilepsy.

2. Because there have been various types of brain injuries in the past, or congenital brain injury or deformity, although there was no seizure at that time, seizures occurred later, and according to the clinical examination results, it can be speculated that this seizure has a high degree of brain injury in the past. Relevance. There may be only one episode, but the more common one is recurrent epilepsy, which is also symptomatic epilepsy.

3. There has not been any brain damage in the past, and according to clinical data, it is speculated that the first epileptic seizure may be idiopathic epilepsy, which is more related to hereditary factors. The episode may be only one episode, but more common Repeated episodes of epilepsy.

4. Although there has not been any history of brain damage in the past, according to clinical data, it is suspected that there may be hidden brain damage or brain dysfunction causing seizures, called cryptogenic epilepsy.

5. Seizures only occur when directly exposed to external or due to internal stimuli, such as intermittent light stimulation, sound stimulation, etc., such as calculation, thinking, etc., if you can avoid related incentives or receive sensitive treatment, Less recurrence, called reflex epilepsy.

(two) pathogenesis

Neuroelectrophysiology

The underlying cause of seizures is the abnormal discharge of brain neurons, which can occur in the ictal discharge or in the interictal discharge. The causes of this abnormal discharge can vary, but so far, little is known about the nature of abnormal discharges. With the development of science and technology, it is possible to have a clearer understanding of the causes of epilepsy. According to current research, various factors may cause abnormalities in the depolarization of a group of brain cell membranes, and synchronization to form the skinning of peripheral neurons. There are various theories about electrophysiological abnormalities in brain neurons, which are generally thought to be related to ion abnormalities of the mesangial potential. It is also believed that the brain's neuronal mediators are excitatory amino acids (glutamate, etc.) and inhibitory amino acids (GABA, etc.). Balanced. In short, seizures are the result of abnormal, over-discharge of nerve cells in the brain.

2. Neuropathology

The pathogenesis of idiopathic epilepsy is complex and has not yet been fully elucidated. For the pathology of partial symptomatic epilepsy, extensive research has been carried out. In animal experiments, cobalt hydroxide is applied to the brain tissue of monkeys, and glial sputum gradually forms around, and partial seizures appear after 4 to 12 weeks. Epileptic discharges of partial epilepsy usually begin near the site of the epileptic seizure, and also originate from distant sites that are related or completely unrelated to the lesion. If the right amygdala of the cat is damaged, it causes a seizure discharge of the left amygdala. Johnson et al found that in animals with epileptic seizures, the cerebral cortex, subcortical structure, and even the entire brain had a reduced threshold of convulsions. Neurons that are anatomically related to the damage caused by epilepsy may have increased excitability but have no organic damage. This is a very important concept, that is, the scattered spike or rhythmic epileptic discharge on the EEG can be used as a diagnostic evidence for partial epilepsy, but it is not certain that the epilepsy damage is in the same place. It is generally believed that mental disorders associated with epilepsy patients, such as paranoid state, schizophrenia-like state, and aggressive personality disorder, are associated with lesions in the dominant hemisphere of the brain, while depression is associated with non-dominant hemispheric lesions. Clinically manifested as an uncontrollable strong emotional and behavioral disorder called episodic dyscontrol syndrome, which may be associated with abnormal discharge of the amygdala.

an examination

Mental disorders at the time of onset include psychomotor seizures, paroxysmal affective disorders, and transient schizophrenia-like episodes.

Differential diagnosis

(1) Automatic symptoms: refers to the turbid state of consciousness that occurs at the time of attack or just after the attack. At this time, the patient can still maintain a certain posture and muscle tension, and complete simple or complicated actions and behaviors in the unconscious. Automated disease is mainly related to the spontaneous electrical activity of the temporal lobe. Sometimes the discharge of the frontal lobe, the cingulate gyrus and the cortex can also produce an automatic disease. 80% of patients have an automatic syndrome of less than 5 minutes and a few can last up to 1 hour. There are often auras before the onset of autopsy, such as dizziness, salivation, chewing movements, somatosensory abnormalities and strangeness. Suddenly become stunned, confused, unconsciously repeating actions such as chewing, pouting, etc., can even complete more complex technical work. After the event, the patient completely forgot what happened during this time.

(2) Shenyou disease: rarer than automatic disease, which lasts for several hours, summer days or even weeks. The degree of disturbance of consciousness is relatively light, the abnormal behavior is more complicated, and it has a certain ability to perceive the surrounding environment, and can also respond accordingly. It is manifested as roaming without a destination, patients can travel far, and can also engage in coordinated activities, such as shopping, simple conversation. Forgotten or difficult after the attack.

(3) state: sudden onset, usually lasts for 1 to several hours, sometimes as long as more than 1 week. The patient presented with a disturbance of consciousness. Accompanied by emotional and sensory impairments, such as horror, anger, etc. can also express emotional apathy, thinking and slow movements.

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