tardive dyskinesia
Introduction
Introduction to tardive dyskinesia Delayed dyskinesia (TD), also known as delayed onset dyskinesia, persistent dyskinesia, induced by antipsychotic drugs, is a persistent stereotyped repetitive involuntary movement. Crane (1968) first proposed that it is the most severe and thorny extrapyramidal reaction caused by antipsychotic treatment, and the incidence is quite high. The most common cause is phenothiazines and butyrophenones. The incidence of oral antipsychotic drugs is 20% to 40%, and the incidence of long-acting antipsychotics is about 50%. basic knowledge Prevalence ratio: 20% incidence of long-term use of antipsychotic drugs Susceptible people: no specific people Mode of infection: non-infectious Complications: difficulty swallowing
Cause
Causes of tardive dyskinesia
(1) Causes of the disease
More common in long-term (more than 1 year) high doses of anti-psychotic drugs that block or bind to dopaminergic receptors, especially phenothiazines such as chlorpromazine, perphenazine, butyrylbenzenes such as haloperidol Etc., can cause TD, some dopamine drugs such as levodopa, Madopar, Parkinine, tranquilizers can also cause similar TD involuntary movements, occasionally taking long-term antidepressants, anti-PD drugs, anti-epileptic drugs and In patients with antihistamines, reduction or withdrawal may occur.
Relevant factors include:
1 Age, gender factors: Older people are prone to occur, not easy to recover, more women than men;
2 patients with brain lesions are prone to use antipsychotic drugs, negative symptoms of schizophrenia patients with early onset of TD, high incidence;
3 drug factors: drug dose and duration of treatment are related to TD, more common in patients with Parkinson syndrome in the early stage of treatment.
(two) pathogenesis
The pathogenesis of tardive dyskinesia is unclear. The damage of central dopaminergic neurons is a theory. It has also been reported that the function of GABA energy system is reduced, the neurotoxicity caused by free radicals, and the direct effect of antipsychotics on the nervous system. theory.
It is generally believed that long-term use of high-dose antipsychotic drugs such as phenothiazines and butyrylbenzenes can block post-synaptic dopamine receptors (DR) for a long time, and increase synaptic dopamine (DA) synthesis and release feedback. Post-synaptic DR is more sensitive to DA response, produces DR hypersensitivity, and is in a denervation hypersensitivity. Physiological doses of DA can cause dyskinesia, often induced after levodopa or discontinuation of antipsychotics. To make the symptoms worse, it also supports the refinement of TD symptoms, haloperidol can temporarily cover up the symptoms, DA synergist can make the symptoms worse.
Pathological changes: autopsy revealed degeneration and atrophy of the substantia nigra and caudate nucleus.
Prevention
Delayed dyskinesia prevention
The first thing to do is to avoid risk factors. Clinicians should adhere to the following principles: Only patients who do need antipsychotics (such as schizophrenia) can take it. They should never use antipsychotics to treat neurosis or depression. Antipsychotics should not be used as hypnotics to treat insomnia, because the occurrence of tardive dyskinesia has nothing to do with the size of the drug, even if a small amount is produced. If schizophrenic patients develop tardive dyskinesia, It should be weighed and weighed.
Complication
Delayed dyskinesia complications Complications, difficulty swallowing
Can have tongue bites, oral mucosal erosion, can not wear dentures, food out of the mouth, difficulty swallowing and difficulty breathing, weight loss or fractures.
Symptom
Symptoms of tardive dyskinesia Common symptoms Neck softness can not be raised, body shaking, angulation, angular rhythm, rhythm, stereotype, repetition... Tongue tremor, dyspnea, nausea, hooliganism, involuntary movement, unclear
1. Occurred in elderly patients, especially women, with brain organic lesions mostly, severe symptoms, slow recovery, all kinds of antipsychotics can be caused, fluphenazine, trifluoperazine and haloperidol Fluoride-containing antipsychotic drugs are common, most of which occur after taking antipsychotic drugs for 1 to 2 years, and the shortest 3 to 6 months can occur, the longest is 13 years.
The main clinical manifestations are rhythmic stereotyped repetitive involuntary movements, early manifestations of tongue tremors or salivation, the elderly oral movements are characteristic, young patients have frequent limb involvement, children's oral and facial symptoms are more prominent, the lower muscles are most often involved, performance mouth - Tongue-cheek triad (BLM syndrome) or buccal, tongue, chewing syndrome, showing uncontrollable movements of the lips and tongue, such as involuntary continuous chewing, sucking, tongue, tongue, mouth and drumstick The jaw and the neck, sometimes the tongue involuntarily suddenly protrudes out of the mouth, called the fly-catcher tongue. In severe cases, the articulation is unclear, the dysphagia, the trunk muscles are affected, the body is shaking, and the limbs are far away. The affected side shows the piano finger (toe) sign, the proximal part of the limb is rarely affected, a few show dance-like movements, no purpose flapping, legs jumping, hands and feet, body torsion and torso movements, even performance Gastrointestinal type, stomach discomfort after sudden withdrawal, nausea and vomiting, emotional stress, aggravation of symptoms during agitation, disappearance during sleep, some patients with delayed onset meditation, late onset Dystonia, drug-induced Parkinson syndrome coexist, symptom easily concealed, when exposed withdrawal of medication.
2. Antipsychotics can cause acute specific dystonia or acute sedation. It occurs within 2 days of antipsychotic drugs. It is prone to occur in children and early adulthood. It shows dramatic limbs, trunk, neck, tongue and The twitching or uncomfortable posture of the facial muscles.
3. According to the movement obstacle parts are divided into the following types:
1 abnormal eye movement: performance of blinking, sputum, etc.;
2 facial muscle movement abnormalities: facial muscle convulsions, convulsions and frowning faces;
3 mouth muscle abnormalities: pouting, pouting, chewing, suction and lateral movement of the jaw;
4 abnormal movement of the tongue muscle: stretching the tongue, shrinking the tongue, creeping and licking the lips;
5 abnormal pharyngeal muscle movement: abnormal movement of the ankle affects pronunciation and swallowing;
6 abnormal neck movement: torticollis, neck back, etc.;
7 abnormal trunk movement: the body trunk movement is uncoordinated, in a strange posture, such as shrug and shoulder retraction, horn arch reversal, twisting sputum, diaphragmatic tendon snoring and breathing difficulties, sometimes the whole body swaying, the body repeatedly flexing and stretching, twisting back and forth, Called body-rocking;
8 Abnormal limb movement: continuous flexion and extension of the distal end of the limb, called the piano finger (toe) sign, the proximal end is rarely affected, a few performance dance-like strokes, throwing movements, hand and foot Xu action, hands repeatedly raised or legs Keep jumping, etc.
9 muscle tension is low - paralyzed dyskinesia: involving the head, neck and waist, such as neck soft can not raise the head, waist can not straight up and bulge, walking can not step and lift the legs, foot to the ground.
4. Subtype of TD:
1 Acute withdrawal syndrome: sudden inactivity of antipsychotic drugs, involuntary erratic non-repetitive dance movements, similar to small chorea or Honenting disease, more common in children, can be self-healing; gradually reduce the dance movements gradually disappear ;
2 Delayed dystonia: can occur in children and adults, involuntary exercise similar to torsional dystonia or torsion sputum, persistence, does not show rapid repetitive stereotypes.
Examine
Examination of tardive dyskinesia
Blood electrolytes, drugs, trace elements and biochemical tests help to diagnose and classify the cause.
1. CT or MRI examination is meaningful for differential diagnosis.
2. Positron emission tomography (PET) or single photon emission tomography (SPECT) can show some biochemical metabolism in the brain, which is meaningful for diagnosis.
Diagnosis
Diagnosis and diagnosis of tardive dyskinesia
According to the patient taking antipsychotics or long-term use of antidepressants, anti-Parkinson's drugs, anti-epileptic drugs or antihistamines, dyskinesia occurs during or after 3 months of drug withdrawal, showing rhythmic stereotypes and persistent persistence Involuntary movement.
Differential diagnosis:
1. Drug-induced Parkinson syndrome: Because DR is occupied or blocked by antipsychotic drugs, endogenous DA can not bind to DR, although there is also a history of antipsychotics, but involuntary exercise shows muscle rigidity, exercise reduction and movement Eye crisis and so on.
2. Huntington's disease: According to the genetic history, chorea and dementia and other three main signs, it is not difficult to identify with TD. HD patients also use antipsychotic drugs. If there is sedation, it can't be repeated or stereotyped involuntary movement to prompt TD.
3. Meige syndrome: is a common oral dyskinesia, complete type of mouth, mandibular dystonia, there are eyelids; incomplete type only mouth, tongue, pharynx and mandibular dystonia, or only the primary Sexual eyelids; no history of antipsychotics.
4. Twisting : Involuntary movement with rapid performance, stereotyped repetition, no history of taking antipsychotics.
