Whether seizure disorders are epileptic seizures or not, there are inconsistent expert opinions. One view is that seizure movement disorder belongs to reflex epilepsy, motion-induced epilepsy, and familial frontal lobe epilepsy, because both epilepsy and seizure movement disorder have recurrent seizures, stereotypy, transient, short seizure duration, and effective AED; while another view is that seizure movement disorder is different from epileptic seizures, because no abnormality is seen in the seizure phase of EEG, clinical seizures are different from epilepsy, no impairment of consciousness, and The other view is that seizure disorder is different from epilepsy because no abnormality is seen in the EEG phase and the clinical seizure is different from epilepsy. Wang Aihua, Department of Neurology, Shandong Qianfo Mountain Hospital Paroxysmal dyskinesia (PD) is a rare group of seizure disorders of the nervous system that manifests as sudden and recurrent abnormal movements with normal interictal performance. It includes: episodic motor-induced dyskinesia (PKD), episodic non-motor-induced dyskinesia (PNKD), episodic hyperkinesia resulting in dyskinesia (PED), and sleep-induced dyskinesia (PHD). It is also known as paroxysmal kinesigenic choreoathetosis (PKC), which is divided into two types: primary and secondary. Primary PKD has a clear family history and is autosomal dominant with gene locus 16q11.2-q12.1; secondary PKD can be seen in basal ganglia infarction, multiple sclerosis, traumatic brain injury, hypoxic encephalopathy, hyperthyroidism, hypoparathyroidism causing hypocalcemia, diabetes mellitus, intracranial infection, intracranial lymphoma, and hypothyroidism. The age of onset of PKD ranges from 4 months to 57 years, mainly in children and adolescents. PKD is characterized by episodes of postural dystonia, choreiform and torsional movements, usually unilateral or asymmetric, or alternating bilaterally, involving the limbs, face, neck and trunk muscles. There is no tongue bite or fecal incontinence during the attack, and there is no amnesia or blurred consciousness after the attack. Triggers: Mostly triggered by sudden changes in movement or posture, especially after a period of rest, such as: standing up from a chair (opening the door, answering the phone, teacher calling on the stage), running (gym class, catching the bus), swimming, walking faster (quickly crossing the sidewalk), getting off the bus, getting off the podium, elevator. It can also be induced by chewing, shock, stress, heat and cold. They last for a few seconds or tens of seconds and rarely last more than 5 min. They occur as often as 100 times/d, usually daily, and can occur at intervals of 1 month or more. Many patients complain of different abnormal sensations before the seizure, called “aura”. Seizures often last from a few seconds to 1 to 2 min and usually do not exceed 5 min. Antiepileptic drug therapy is effective. Seizure paroxysmal nonkinesigenic dyskinesia (PNKD), or paroxysmal dystonias choreoathetosis (PDC), is reported in the literature, PDC). This type occurs spontaneously and is not triggered by sudden movements, but the age of onset is earlier than PKD. It can be triggered by alcohol, coffee, tea, menstruation, fatigue or occur spontaneously, but is not triggered by sudden movements and lasts from a few minutes to a few hours and can last more than a day, usually 5 minutes to 4 hours. The frequency of attacks is low, ranging from a few times a year to several times a day, with a median onset of 12 years (3-30 years) and partial or complete remission with age. Seizures can be unilateral or bilateral, localized or generalized, and speech is often affected, with no loss of consciousness during the seizure. The interictal neurological examination is normal and the EEG is normal. The family history is consistent with autosomal dominant inheritance with gene locus 2q31-36. medication is not effective, but clonazepam may be effective, and Lee suggests that immune mechanisms play a role in MS as a secondary cause of PNKD. other causes include encephalitis, perinatal hypoxia, cystinuria, parathyroid hypo, pseudohypoparathyroidism, hyperthyroidism, thyrotoxicosis, TIA, head trauma, hypoglycemia, basal ganglia calcification, A PNKD, basal ganglia calcification, AIDS, diabetes mellitus, etc. PNKD is difficult to treat and the response to anticonvulsant drugs is poor. Antimuscarinic drugs, benztropine, and minoxidil are effective in combination with phenytoin sodium, and carbamazepine, benzodiazepines, acetazolamide, benzhexol, and haloperidol have been used in trials with varying results. The response to levodopa has been variable. The treatment of paroxysmal exercise-induced dystonia (PED) is also known as paroxysmal exercise-induced chorea. choreoathethosis), occurs after prolonged exercise, 5-15 min of walking or running before the onset. Passive body movements, speech, chewing, stress, heat and cold, menstruation, and alcohol can contribute to the onset. The frequency of attacks ranges from 1-2 times per day to 5 times per month and lasts for 5-30 min. They tend to accumulate bilaterally in the lower extremities, or unilaterally in the face, neck and trunk, but are rare in the upper extremities. The age of onset is 24 months to 30 years, mostly in childhood and equally in both sexes. Antiepileptic drugs are ineffective, levodopa and acetazolamide may be partially effective. Sleep-induced seizure dyskinesia (PHD), also known as nocturnal paroxysmal dystonia (NPD), is a recurrent stereotypic dystonia or dyskinesia that occurs during NREM sleep. NPD is a recurrent episode of stereotypic dystonia or dyskinesia (e.g., throwing or tardive dyskinesia, dance-like movements) during NREM sleep. It is confused with frontal lobe epilepsy and is mostly considered to be an autosomal dominant nocturnal frontal lobe epilepsy. One view is that it is similar to night terrors in abnormal sleep, but the short duration, stereotypy, recurrent nature, and effectiveness with carbamazepine but not with benzodiazepines do not support this view. Another view is that the disease is a manifestation of sleep-related epilepsy. Some believe that it constitutes nocturnal frontal lobe epilepsy with seizure night terrors and seizure nocturnal wanderings, but with different durations. The age of onset ranges from infancy to 50 years, with no difference between men and women, and the duration of short seizures ranges from 15 to 60 s, with prolonged seizures lasting up to 60 min. The duration of short PHD seizures usually does not exceed 1 min, and the seizures usually precede clinical and EEG awakening. The eyes are open, the head is raised, followed by a posture of trunk and limb dystonia, accompanied by throwing or dancing-like or twitchy movements, stereotyped, often accompanied by sounds, and the seizure ends with consciousness and, if undisturbed, sleep. Prolonged PHD episodes are similar to short-lived NPD, but they last longer, up to one hour, and can lead to severe sleep disturbances, often with complaints of insomnia. For short episodes, a small dose of carbamazepine has good therapeutic effect, 200 mg orally at bedtime, and if it is not effective, the dose can be gradually increased until the symptoms are controlled. There is no effective treatment for episodes lasting more than 2 min.