Tardive dyskinesia


Tardive dyskinesia

Description, Causes and Risk Factors:

Abbreviation: TD.

Tardive dyskinesia is a neurological disorder caused by the long-term use of neuroleptic drugs, or antipsychotic medications. Neuroleptic drugs are generally prescribed for psychiatric disorders, as well as for some gastrointestinal and neurological disorders. The prevalence of tardive dyskinesia is estimated to be 10 to 20 percent of individuals treated with antipsychotic medications. The elderly are more susceptible to persistent and irreversible tardive dyskinesia than younger people.

Tardive dyskinesia can be classified according to its severity and chronicity, into at least three types:

    Withdrawal tardive dyskinesia.

  • Transient tardive dyskinesia.

  • Persistent tardive dyskinesia.

Despite considerable research efforts, the pathophysiology and neuroanatomic picture of tardive dyskinesia remain largely unknown. Although dopaminergic supersensitivity may be an essential component in the emergence of tardive dyskinesia, recent hypotheses involving other neurotransmitters (e.g., ?-aminobutyric acid, norepinephrine, serotonin, acetylcholine), iron metabolism, diminished melatonin secretion, and free-radical neurotoxicity have been advanced. Neuropathological studies of tardive dyskinesia patients have reported increased nigral degeneration and gliosis. Pineal-gland calcification has also been reported and suggested as a potential neuroradiologic marker of persistent tardive dyskinesia in schizophrenic and bipolar patients.

On the basis of incidental observations and findings from pilot studies, researchers earlier hypothesized that impaired glucose metabolism is associated with increased risk for tardive dyskinesia. That view was based on the following observations: (1) In two separate studies, the proportion of tardive dyskinesia patients also diagnosed as having non-insulin-dependent diabetes mellitus (NIDDM) was considerably higher than would have been expected on the basis of the known rates of NIDDM in the general population. (2) On average, fasting blood glucose concentrations were found to be significantly higher in patients with tardive dyskinesia than in patients without tardive dyskinesia, an effect that remained significant after controlling for variance due to age and gender.

Recently, hereditary susceptibility to tardive dyskinesia has been the subject of much discussion. Researchers suggested that blue-eyed men are more prone to develop tardive dyskinesia than brown-eyed men, although researchers could not confirm that finding, nor could it be confirmed in women. In a study of six pairs of twin patients (four monozygotic and two dizygotic) treated with high-dosage neuroleptics, researchers found that the specific type of neurological side effect was not determined genetically, inasmuch as the identical twins showed distinctly different reaction patterns. Moreover, in a study of 50-year-old female schizophrenic quadruplets on neuroleptic treatment, found that only one of the four had definite tardive dyskinesia. However, reported the presence of tardive dyskinesia in two schizophrenic brothers treated with neuroleptics.

The classic explanation of the pathogenesis of tardive dyskinesia is the dopamine-hypersensitivity theory. According to this theory, chronic blockade of the postsynaptic dopamine receptors by neuroleptics results in adaptive dopamine-receptor hypersensitivity and cholinergic hypofunction, changes that result in chronic dyskinesia. Acute dyskinesia, on the other hand (i.e., dyskinesia occurring at the onset of dopamine blockade), has been believed to be a direct result of the dopamine blockade itself (i.e., acute dopamine hypofunction and cholinergic hyperfunction). Because further development of the dopamine-hypersensitivity theory has focused mainly on the examination and manipulation of dopamine D2 receptors in rodents, it could more properly be termed the dopamine D2-hypersensitivity theory of tardive dyskinesia. In recent years, this theory has been criticized for lack of confirmation of its postulates in humans.

A number of factors increase the risk of developing tardive dyskinesia. Not all people with risk factors will get tardive dyskinesia. Risk factors of tardive dyskinesia may include:

    Advanced age.

  • Female gender.

  • Substance abuse.

  • Use of neuroleptic drugs.

Symptoms:

Tardive dyskinesia causes repetitive movements. Movements usually occur in the face, mouth, limbs, or trunk. The movements are involuntary and serve no purpose. They may occur occasionally or all of the time. They may be barely noticeable or very pronounced. Symptoms may begin while on the drug or within weeks of stopping it.

They can worsen with stress, moving other parts of the body, taking certain drugs

General symptoms may include the following:

    Facial tics.

  • Smacking lips.

  • Puckering lips.

  • Blinking eyes.

  • Grimacing.

  • Sticking out the tongue

  • Twisting the tongue.

  • Chewing.

  • Sucking.

  • Foot tapping.

  • Moving fingers as if playing the piano.

  • Rapidly moving arms, legs, or body.

  • Writhing movements.

  • Pelvic thrusts.

  • Grunting.

  • Sighing.

  • Noisy breathing.

Diagnosis:

Differential diagnosis may include multiple tics, Gilles de la Tourette's syndrome, Parkinsonism, akathisia, the rabbit syndrome, mannerisms and stereotyped motor behavior of psychotic patients, senile dyskinesia, Huntington's chorea, Wilson's disease, torsion dystonia and movements disorders resulting from brain damage, metabolic disorders and drug intoxication.

The importance of a careful assessment of a patient with tardive dyskinesia cannot be overrated. Assessment of both the intensity and frequency of the disordered movements is necessary for a diagnosis of tardive dyskinesia. Measuring the severity of movements is important for documenting the course of the movement disorder and for evaluating the response to treatment, and sometimes even for prognosis. In fact, many clinical and medicolegal decisions are based solely on the findings in a thorough assessment. Unfortunately, reliable assessment of the severity of tardive dyskinesia presents a challenge. Noted that the absence of reliable, precise methods for assessment may be contributing to our inability to delineate the syndrome, to determine its prevalence, and to evaluate the efficacy of treatments; but the ability to monitor the severity and course of tardive dyskinesia is critical to our understanding and management of this disorder. A better understanding of the pathophysiology and pharmacology of tardive dyskinesia inevitably will depend on precise assessment of the distribution and variations of dyskinetic movements.

The doctor will ask about your symptoms and medical history. He/she will also do a physical exam. Other disorders can cause symptoms similar to those of TD. The doctor will rule out other disorders before making a diagnosis. There is no specific test for TD.

Tests may include:

    Blood tests to check electrolytes and blood chemistry.

  • CT scan—a type of x-ray that uses a computer to make pictures of structures inside the head.

  • MRI scan—a test that uses magnetic waves to make pictures of structures inside the brain.

Treatment:

There is no single satisfactory treatment for tardive dyskinesia. The main treatment is prophylaxis. Psychiatrists should be made more aware of the condition, its early diagnosis and the risk factors with the aim to prevent its development. This could be achieved by:

    Proper selection of antipsychotic drugs e.g. low potency drugs like thioridazine, sulpiride, clozapine.

  • Supplementing antipsychotic treatment with lithium, benzodiazepines or carbamazepine for high risk groups e.g. the aged, females, and presence of organic factors like alcoholism.

  • Reducing the antipsychotic drugs to a minimal effective dose and avoiding high doses and drug holidays (more than one week).

  • Slow reduction (one third of total dose per month) when antipsychotic medication can be withdrawn.

  • Reduction and withdrawal of anticholinergic (antiparkinsonian) drugs early.

  • Periodic (3 monthly) reviews for early signs including a trial period of drug withdrawal (less than one week).

  • Stopping the offending drugs as soon as tardive dyskinesia (or tardive dystonia) is detected.

  • Informing the patient (and relatives) about the condition and the choice of subsequent treatment (as a medico-legal precaution).

Specific drug treatment has not been found to be satisfactory. Dopamine blockers like thioridazine, haloperidol, pimozide, sulpiride and oxiperomide, can be used to produce immediate and temporary suppression of symptoms. This apparent improvement will be followed by a more severe tardive dyskinesia unresponsive to other therapies. Dopamine-depleting agents were also used in past regimes. Side effects were hypotension, parkinsonism, drowsiness, confusion and depression. Agents that preferentially block the dopamine D2 (non-adenylate cyclase-linked) receptors have been found to decrease tardive dyskinesia. These were metoclopramide, tiapride. sulpiride, oxiperomide and remoxipride. Side effects positive.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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