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*Only for medical professionals to read for reference.
Delayed dyskinesia is the most serious and troublesome extrapyramidal reaction caused by antipsychotic treatment today, with a very high incidence
.
Tardive dyskinesia, also known as tardive hyperactivity, is more common in patients who have been treated with antipsychotics for a long time.
It is most likely to occur when the dose is reduced or stopped, and it is manifested as a persistent and repetitive involuntary movement
.
According to statistics, up to 30% of people who take antipsychotics for a long time will develop tardive dyskinesia.
Therefore, neurologists should improve their understanding and master coping strategies
.
At the 24th National Neurology Conference of the Chinese Medical Association to be held on September 24-26, 2021, Professor Chen Lei from the Department of Neurology, Huanhu Hospital, Tianjin, gave us a lecture "Recognition of Delayed Dyskinesia And processing", let us see it! 012 definitions to understand ▌ Tardive Dyskinesia (TD) TD was originally used to describe the rhythmic, repetitive (stereotypical), continuous movement that occurs after prolonged exposure to antipsychotic drugs
.
Initially, “tardive” was long-term exposure to dopamine receptor blockers (DRBA) before involuntary movements, but persistent dyskinesias were quickly observed, but it may also appear very early, even a few days after using DRBA Appeared
.
TD usually refers to classic repetitive and complex movements, which may occur in the limbs, torso, or pelvis
.
▌ Delayed onset syndrome (TS) TS refers to the persistent hyperactivity, hypoactivity and sensation caused by all DRBA exposures for 3 months or more
.
TS must meet two requirements at the same time: 1) These abnormal movements are due to exposure to DRBA; 2) Dyskinesia still exists after stopping the drug
.
It is very important to recognize and be able to distinguish between TD and TS in clinical practice.
Persistence is a key feature of TS, which distinguishes it from other similar acute disorders caused by DRBA
.
TS does not include acute disorders, such as drug-induced Parkinson's syndrome, acute dystonia, and acute akathisia
.
023 hypotheses should be known that the pathogenesis of TD is still unclear.
The mainstream hypotheses include dopamine receptor hypersensitivity hypothesis, neurodegeneration hypothesis and abnormal synaptic plasticity hypothesis.
These hypotheses are of great significance for the exploration of the pathogenesis of TD and the treatment of TD
.
▌ Dopamine receptor hypersensitivity hypothesis Traditional antipsychotic drugs work by blocking D2 receptors in the central limbic system.
Chronic D2 dopamine receptor blockade leads to the gradual up-regulation of D2 receptors and post-synaptic dopamine receptor hypersensitivity
.
▌ Neurodegeneration hypothesis long-term use of DRBA will produce neurotoxicity, such as the formation of lipid peroxides and the production of free radicals, which may lead to neuronal damage and degeneration
.
Patients with schizophrenia treated with DRBA have a 15% decrease in dopamine neuron transporter every 10 years, and a natural decrease of 5% in normal people every 10 years
.
▌ The hypothesis of abnormal synaptic plasticity Synaptic plasticity refers to the increase or decrease of transmission of intersynaptic nerves based on previous experience
.
Synaptic plasticity is regulated by cholinergic, GABAergic and dopaminergic systems
.
DRBA is thought to impair the synaptic plasticity of the neocortex.
Long-term use of DRBA can lead to maladaptive neocortex and abnormal output of the basal ganglia, resulting in abnormal movements and TD symptoms
.
03 Many risk factors should be clear.
There are many risk factors for TD, including: DRBA type, course of disease, dose and length of exposure to DRBA, diabetes, smoking, alcohol and cocaine abuse, intermittent antipsychotic medication, anticholinergic therapy, Old age, female, ethnicity, etc.
.
Among them, the age factor is an important factor in the occurrence of TD and an important factor affecting its recovery.
The elderly are prone to occur and are not easy to recover.
The dosage of drugs and the duration of treatment are related to the occurrence of TD.
The drugs that are likely to cause TD are summarized in the table.
One
.
Table 1: Common drugs that can cause tardive dyskinesia.
044 clinical manifestations.
Keep in mind the involuntary, rhythmic repetitive stereotyped exercise
.
The earliest manifestation is tongue tremor or drooling.
The elderly are characterized by oral movement: slight tremor of the lips when not speaking or tongue twitching back and forth or left and right movement in the slightly opened mouth.
Limb involvement is common in young patients
.
The most common one is mouth-tongue-buccal triad: it manifests as repetitive and uncontrollable movements of the lips and tongue, such as sucking, tongue turning, tongue licking, chewing, pouting, bulging cheeks, neck turning, etc.
Sometimes the tongue involuntarily Suddenly sticking out of the mouth, this sign is called the fly-catcher tongue sign.
In severe cases, there may be dysarthria and swallowing disorders
.
Other symptoms include involuntary movement of the limbs, purposeless twitching, dancing finger strokes, hand rubbing movements, slight shaking of the lower limbs when sitting, foot movement or torsion movement of the limbs and trunk
.
It may also involve muscles in other parts, occasionally gastrointestinal-type tardive dyskinesia, stomach discomfort, nausea and vomiting after sudden withdrawal
.
Its severity is fluctuating, aggravating when emotionally stressed or excited, and disappearing during sleep.
Some patients can coexist with delayed akathisia, delayed dystonia, drug-induced Parkinson's syndrome, etc.
, and the symptoms are often It is covered up and exposed when the drug is reduced or discontinued
.
Table 2: Clinical manifestations of TD at different locations 05 Treatment should be cautious.
TD is an important clinical problem.
It is the most serious and troublesome extrapyramidal reaction caused by antipsychotic treatment today, with a very high incidence, especially Patients using long-acting antipsychotics
.
Some patients with TD have extremely severe symptoms that affect their basic functions and are highly disabling, but there is currently no exact treatment for TD
.
The occurrence of this disease is closely related to the long-term use of antipsychotics.
Therefore, reasonable and cautious use of antipsychotics under the guidance of a doctor is very important to prevent the occurrence of TD.
The medication should be used in small amounts and short-term.
If TD occurs, it should be targeted at the disease.
The mechanism adopts comprehensive treatment measures
.
Summary: Patients with long-term use of DRBA have a high prevalence of TD and TS, and abnormal movements can survive long-term or even life-long after withdrawal
.
The occurrence of TD may be related to genetic background, dopamine receptor hypersensitivity, neurodegeneration and abnormal synaptic plasticity
.
Currently, there is no specific treatment, prevention first, comprehensive treatment
.
Delayed dyskinesia is the most serious and troublesome extrapyramidal reaction caused by antipsychotic treatment today, with a very high incidence
.
Tardive dyskinesia, also known as tardive hyperactivity, is more common in patients who have been treated with antipsychotics for a long time.
It is most likely to occur when the dose is reduced or stopped, and it is manifested as a persistent and repetitive involuntary movement
.
According to statistics, up to 30% of people who take antipsychotics for a long time will develop tardive dyskinesia.
Therefore, neurologists should improve their understanding and master coping strategies
.
At the 24th National Neurology Conference of the Chinese Medical Association to be held on September 24-26, 2021, Professor Chen Lei from the Department of Neurology, Huanhu Hospital, Tianjin, gave us a lecture "Recognition of Delayed Dyskinesia And processing", let us see it! 012 definitions to understand ▌ Tardive Dyskinesia (TD) TD was originally used to describe the rhythmic, repetitive (stereotypical), continuous movement that occurs after prolonged exposure to antipsychotic drugs
.
Initially, “tardive” was long-term exposure to dopamine receptor blockers (DRBA) before involuntary movements, but persistent dyskinesias were quickly observed, but it may also appear very early, even a few days after using DRBA Appeared
.
TD usually refers to classic repetitive and complex movements, which may occur in the limbs, torso, or pelvis
.
▌ Delayed onset syndrome (TS) TS refers to the persistent hyperactivity, hypoactivity and sensation caused by all DRBA exposures for 3 months or more
.
TS must meet two requirements at the same time: 1) These abnormal movements are due to exposure to DRBA; 2) Dyskinesia still exists after stopping the drug
.
It is very important to recognize and be able to distinguish between TD and TS in clinical practice.
Persistence is a key feature of TS, which distinguishes it from other similar acute disorders caused by DRBA
.
TS does not include acute disorders, such as drug-induced Parkinson's syndrome, acute dystonia, and acute akathisia
.
023 hypotheses should be known that the pathogenesis of TD is still unclear.
The mainstream hypotheses include dopamine receptor hypersensitivity hypothesis, neurodegeneration hypothesis and abnormal synaptic plasticity hypothesis.
These hypotheses are of great significance for the exploration of the pathogenesis of TD and the treatment of TD
.
▌ Dopamine receptor hypersensitivity hypothesis Traditional antipsychotic drugs work by blocking D2 receptors in the central limbic system.
Chronic D2 dopamine receptor blockade leads to the gradual up-regulation of D2 receptors and post-synaptic dopamine receptor hypersensitivity
.
▌ Neurodegeneration hypothesis long-term use of DRBA will produce neurotoxicity, such as the formation of lipid peroxides and the production of free radicals, which may lead to neuronal damage and degeneration
.
Patients with schizophrenia treated with DRBA have a 15% decrease in dopamine neuron transporter every 10 years, and a natural decrease of 5% in normal people every 10 years
.
▌ The hypothesis of abnormal synaptic plasticity Synaptic plasticity refers to the increase or decrease of transmission of intersynaptic nerves based on previous experience
.
Synaptic plasticity is regulated by cholinergic, GABAergic and dopaminergic systems
.
DRBA is thought to impair the synaptic plasticity of the neocortex.
Long-term use of DRBA can lead to maladaptive neocortex and abnormal output of the basal ganglia, resulting in abnormal movements and TD symptoms
.
03 Many risk factors should be clear.
There are many risk factors for TD, including: DRBA type, course of disease, dose and length of exposure to DRBA, diabetes, smoking, alcohol and cocaine abuse, intermittent antipsychotic medication, anticholinergic therapy, Old age, female, ethnicity, etc.
.
Among them, the age factor is an important factor in the occurrence of TD and an important factor affecting its recovery.
The elderly are prone to occur and are not easy to recover.
The dosage of drugs and the duration of treatment are related to the occurrence of TD.
The drugs that are likely to cause TD are summarized in the table.
One
.
Table 1: Common drugs that can cause tardive dyskinesia.
044 clinical manifestations.
Keep in mind the involuntary, rhythmic repetitive stereotyped exercise
.
The earliest manifestation is tongue tremor or drooling.
The elderly are characterized by oral movement: slight tremor of the lips when not speaking or tongue twitching back and forth or left and right movement in the slightly opened mouth.
Limb involvement is common in young patients
.
The most common one is mouth-tongue-buccal triad: it manifests as repetitive and uncontrollable movements of the lips and tongue, such as sucking, tongue turning, tongue licking, chewing, pouting, bulging cheeks, neck turning, etc.
Sometimes the tongue involuntarily Suddenly sticking out of the mouth, this sign is called the fly-catcher tongue sign.
In severe cases, there may be dysarthria and swallowing disorders
.
Other symptoms include involuntary movement of the limbs, purposeless twitching, dancing finger strokes, hand rubbing movements, slight shaking of the lower limbs when sitting, foot movement or torsion movement of the limbs and trunk
.
It may also involve muscles in other parts, occasionally gastrointestinal-type tardive dyskinesia, stomach discomfort, nausea and vomiting after sudden withdrawal
.
Its severity is fluctuating, aggravating when emotionally stressed or excited, and disappearing during sleep.
Some patients can coexist with delayed akathisia, delayed dystonia, drug-induced Parkinson's syndrome, etc.
, and the symptoms are often It is covered up and exposed when the drug is reduced or discontinued
.
Table 2: Clinical manifestations of TD at different locations 05 Treatment should be cautious.
TD is an important clinical problem.
It is the most serious and troublesome extrapyramidal reaction caused by antipsychotic treatment today, with a very high incidence, especially Patients using long-acting antipsychotics
.
Some patients with TD have extremely severe symptoms that affect their basic functions and are highly disabling, but there is currently no exact treatment for TD
.
The occurrence of this disease is closely related to the long-term use of antipsychotics.
Therefore, reasonable and cautious use of antipsychotics under the guidance of a doctor is very important to prevent the occurrence of TD.
The medication should be used in small amounts and short-term.
If TD occurs, it should be targeted at the disease.
The mechanism adopts comprehensive treatment measures
.
Summary: Patients with long-term use of DRBA have a high prevalence of TD and TS, and abnormal movements can survive long-term or even life-long after withdrawal
.
The occurrence of TD may be related to genetic background, dopamine receptor hypersensitivity, neurodegeneration and abnormal synaptic plasticity
.
Currently, there is no specific treatment, prevention first, comprehensive treatment
.
