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At least 19 recordsLinked to original sources
PubMed1992

Prevalence of tardive dyskinesia, tardive dystonia, and respiratory dyskinesia among Chinese psychiatric patients in Hong Kong.

OBJECTIVE: Only scanty information on the prevalence of tardive dyskinesia in Chinese patients has been available. This study was undertaken to examine the prevalence of tardive dyskinesia, tardive dystonia, and respiratory dyskinesia in Chinese psychiatric patients in Hong Kong. METHOD: All inpatients of a mental hospital in Hong Kong, except those in the admission and children's wards, were surveyed with the Abnormal Involuntary Movement Scale, and standard research criteria were used to establish the diagnosis of tardive dyskinesia. In addition, patients were screened for tardive dystonia, according to published criteria, and for respiratory dyskinesia by physical examination and laboratory tests. RESULTS: Among the 917 patients surveyed, the prevalence rates were 9.3% for tardive dyskinesia, 0.4% for tardive dystonia, and 1.2% for respiratory dyskinesia. With multivariate analysis, greater age and a lower current dose of antipsychotic, but not the presence of mood disorder, were factors found to be significantly associated with tardive dyskinesia. CONCLUSIONS: The prevalence rates were much lower than those found in Western studies. This may indicate that there is an ethnic difference in the prevalence of these conditions. Prospective cross-cultural studies are necessary to explore this possibility.

Adolescent↗
PubMed1986

Anosognosia in tardive dyskinesia: "tardive dysmentia" or "tardive dementia"?

Wilson et al. (1983) called attention to the increasing incidence of affective symptomatology in schizophrenic patients on chronic neuroleptic medication. They designated the emerging syndrome as tardive dysmentia in order to emphasize its connection with the pathophysiology of tardive dyskinesia. The present contribution suggests that the emotional indifference or frank anosognosia of abnormal involuntary movements noted in the great majority (95 percent) of patients with tardive dyskinesia is another possible feature of tardive dysmentia. An attempt was made to explain anosognosia, and some difficulties that mar interpretation of data were pointed out. Anosognosia was proposed to represent a symptom related to some sort of cognitive disorder accompanying tardive dyskinesia, at least in the elderly. It was suggested that dementia may be associated with a predominant impairment of dopaminergic circuitry in the right cerebral hemisphere.

Adult↗
PubMed1993

Central determinants of attention and mood disorder in tardive dyskinesia ("tardive dysmentia").

The typical apathetic state of tardive dyskinesia patients may be punctuated by periods of hyperactivity, vigilance, and tension. Patients may exhibit unusual readiness for contact, even though they remain edgy, loud and loquacious, euphoric, jolly, intrusive, and invasive of the privacy of others. These features designated as "tardive dysmentia" are examined, so as to draw attention to the possibility that the syndrome of dysmentia is comprised of occasional excessive emotional reactivity, enhanced responsiveness to environmental stimuli, and indifference to or reduced awareness of the patient's abnormal involuntary movements. The pathophysiology of tardive dysmentia remains uncertain. It is proposed that behavioral changes in patients with dysmentia may be conceived in terms of a more outward direction of attentional processing. Such an immense change in psychopathology under antipsychotic drugs, from withdrawal to the emotional externalization of behavior, is conceived as reflecting a shift in the approach-avoidance behavior due to alterations in the parieto-frontal balance.

Cognition Disorders↗
PubMed1993

An animal model for coexisting tardive dyskinesia and tardive parkinsonism: a glutamate hypothesis for tardive dyskinesia.

There is now ample evidence for long-term malfunctioning within five different brain GABAergic pathways in a monkey model for tardive dyskinesia (TD). Three of these GABA connections (GPe-STN, CP-SNr, and CP-GPi) are chronically downregulated during neuroleptic treatment and after some years they do not seem to regain their normal activity, even when the neuroleptics are discontinued. The persistent downregulation of these three GABA connections, evidenced by depressions of terminal GAD activity and GABA levels, appears to be a conceivable mechanism behind tardive parkinsonism (TP), often reported to coexist with TD in the clinic. The TD patients' well-known lack of awareness of their symptoms may be due to their parkinsonian "sensory neglect." Another two GABA malfunctioning connections were found in our monkey model: SNr-VA/VL and GPi-VA/VL. These pathways are upregulated during chronic neuroleptic treatment, partly due to an elevated glutamate release within subthalamofugal pathways. This chronic glutamatergic hyperactivity may have acted via an excitotoxic mechanism and consequently both GPi and VA/VL had a low synaptic activity in our dyskinetic monkeys, as measured by 2-deoxyglucose uptake, even 4 months after the last neuroleptic dose. It is hypothesized that TD may be due to an excitotoxic lesion of the inhibitory GABAergic VA/VL afferents, while TP has to do with persistent malfunctioning of downregulated SNr and GPi afferents.

Animals↗
PubMed1980

Oxiperomide in tardive dyskinesia.

Tardive dyskinesia can be suppressed by dopaminergic receptor blockers, but often at the cost of a reciprocal increase in Parkinsonism. Oxiperomide, a dopaminergic antagonist that has been shown to reduce levodopa-induced dyskinesias without producing an equal aggravation of Parkinsonism, was evaluated in a blind placebo-controlled trial in 10 patients with tardive dyskinesia. It decreased tardive dyskinesia significantly (p less than 0.01) without significantly provoking or increasing Parkinsonism. There was no relationship between either tardive dyskinesia or Parkinsonism and eye blinking rates. These results can be interpreted as additional evidence for the existence of more than one population of dopamine receptors involved in controlling extrapyramidal function. Although oxiperomide is only a palliative suppressing agent in tardive dyskinesia, as the symptoms returned when the drug was stopped, it is an interesting agent in the search for selective dopaminergic receptor blockers.

Aged↗
PubMed2003

Oxidative mechanisms and tardive dyskinesia.

Tardive dyskinesia has been and continues to be a significant problem associated with long-term antipsychotic use, but its pathophysiology remains unclear. In the last 10 years, preclinical studies of the administration of antipsychotics to animals, as well as clinical studies of oxidative processes in patients given antipsychotic medications, with and without tardive dyskinesia, have continued to support the possibility that neurotoxic free radical production may be an important consequence of antipsychotic treatment, and that such production may relate to the development of dyskinetic phenomena. In line with this hypothesis, evidence has accumulated for the efficacy of antioxidants, primarily vitamin E (alpha-tocopherol), in the treatment and prevention of tardive dyskinesia. Early studies suggested a modest effect of vitamin E treatment on existing tardive dyskinesia, but later studies did not demonstrate a significant effect. Because evidence has continued to accumulate for increased oxidative damage from antipsychotic medications, but less so for the effectiveness of vitamin E, especially in cases of long-standing tardive dyskinesia, alternative antioxidant approaches to the condition may be warranted. These approaches may include the use of antioxidants as a preventive measure for tardive dyskinesia or the use of other antioxidants or neuroprotective drugs, such as melatonin, for established tardive dyskinesia.

Antioxidants↗
PubMed1988

[The treatment of psychopathologic disorders associated with tardive dyskinesias].

Tardive dyskinesia, an extrapyramidal syndrome consisting of involuntary hyperkinetic movements, is a serious side effect induced by the administration, usually on a long-term basis, of neuroleptic therapy mostly for psychotic disorders. Therefore, psychopathologic disturbances, florid or residual may coexist with the appearance and persistence of tardive dyskinesia. Thus, the exact nature of the psychopathology observed with the presence of tardive dyskinesia and its origin is difficult to delineate and to assess. Indeed, the psychopathological findings observed can possibly originate from the initial psychiatric disorder itself from the intrinsic effect of the neuroleptic medication on psychic processes, may be specifically related to tardive dyskinesia, or be the result of all these factors. Cognitive, thymic or psychotic disturbances have been closely associated with tardive dyskinesia, but their systematic studies is still scarce. Based on these findings, some tentative therapeutic considerations will be outlined, keeping in mind that exact nature and origin of these disturbances still remains to be elucidated, that no really specific and generally effective treatment of tardive dyskinesia has been found.

Cognition Disorders↗
PubMed1979

Sulpiride in tardive dyskinesia.

Tardive dyskinesia can be suppressed by drugs that block dopaminergic receptors, but often at the cost of a concomitant increase in parkinsonism. Sulpiride (400 -- 2100 mg/day), a selective type-2 dopamine receptor antagonist, was evaluated in a blind, placebo-controlled trial in 11 patients with tardive dyskinesia. It significantly (P less than 0.01) reduced tardive dyskinesia without significantly affecting parkinsonism, although three patients had a increase in preexisting parkinsonian hypokinesia and tremor. During the placebo phase, the tardive dyskinesia and parkinsonian scores returned to the pretreatment values. There was no relationship between either tardive dyskinesia or parkinsonism and eye blinking rates. These results are consistent with the hypothesis that more than one population of dopamine receptors are involved in controlling extrapyramidal function. Sulpiride is an important tool for elucidating both the practical and heuristic aspects of subtypes of dopamine receptors and is a lead in the search for compounds that selectively affect dopaminergic mechanisms.

Aged↗
PubMed1979

Normal prolactin responses in tardive dyskinesia.

Tardive dyskinesia has been hypothesized to be caused by a neuroleptic-induced dopamine hypersensitivity in the nigrostriatal system. This study evaluated with dopamine antagonists the possibility that such dopamine hypersensitivity extends to the tuberoinfundibular dopamine (TIDA) system, which regulates, by inhibition, pituitary prolactin secretion. Plasma prolactin concentrations in six patients with tardive dyskinesia were assessed in four conditions: During chronic haloperidol therapy; serially after abrupt haloperidol withdrawal; while unmediated; and in response to an acute dose of 0.5 mg IM haloperidol. In all four conditions, prolactin responses did not differ from those observed in normal subjects and schizophrenic patients without tardive dyskinesia. It is concluded that there is no evidence for post-synaptic dopamine hypersensitivity in the TIDA-pituitary pathway in patients with tardive dyskinesia, consistent with other reports assessing hormonal responses to dopamine agonists in such cases. It is further suggested that neuroleptic-induced dopamine hypersensitivity does not occur in the TIDA-pituitary system in humans, since it was not manifest in these tardive dyskinesia patients who would be thought particularly prone to develop it.

Adult↗
PubMed1981

[Electrophysiological and pharmacological analysis of L-dopa-induced dyskinesia and tardive dyskinesia (author's transl)].

Electrophysiological and pharmacological analysis of L-Dopa-induced dyskinesia and tardive dyskinesia (L.DD) due to neuroleptics was performed on 12 patients with Parkinson's disease and on 12 others with psychotic diseases. This analysis included the examination of spinal reflexes, monosynaptic H reflex, polysynaptic cutaneous reflex of the lower limb, muscular responses to passive movement [stretch reflex and shortening reaction (SR)] and the study of the motor response to a dopaminergic stimulus (I.V. injection of Piribedil (PBD), a dopamine agonist). There was no difference in EMG activity between L.DD and TD. Three EMG patterns can be distinguished: anarchic discharge pattern (ADA), tonic grouping discharge pattern (AST) and rhythmic burst pattern (ABR). PBD effects indicate a possible relationship between the EMG patterns and the sensitivity level of the motor dopamine receptors. During L-Dopa dyskinesia and tardive dyskinesia, the same changes in spinal reflexes were observed. Muscle tone tested by muscular responses to passive movement (shortening and myotatic reaction) was normal. Monosynaptic excitability explored by H/M ratio was within the normal range. In contrast, the polysynaptic nociceptive reflex was increased in every case. In Parkinsonian patients with L-Dopa dyskinesia, this pattern of the spinal reflexes was significantly different in comparison to the rigid phase. Intravenous infusion of PBD suppressed tremor and provoked the occurrence of dyskinetic activity in Parkinsonian patients with L-Dopa dyskinesia during the rigid phase. During the dyskinetic phase, as in tardive dyskinesia, PBD increases these phenomena and changes EMG activity in rhythmic pattern. It is suggested that L-Dopa dyskinesia and tardive dyskinesia can be determined by testing EMG activity, spinal reflexes and dopaminergic reactivity. There is evidence to suggest that the various types of involuntary abnormal movement represent a single entity, and that dopamine receptor supersensitivity may be involved.

Antipsychotic Agents↗
PubMed1984

Variable clinical response to choline in tardive dyskinesia.

Tardive dyskinesia is widely believed to be a state of relative hyperdopaminergic and hypocholinergic imbalance in the striatum of patients chronically treated with neuroleptics. However, not all patients with tardive dyskinesia respond to cholinergic drugs, which theoretically should restore the balance and improve the symptoms. We report a controlled, double-blind, crossover study of choline chloride in 11 patients with persistent tardive dyskinesia. Seven patients showed partial or minimal improvement, while two did not change and two deteriorated. The results are discussed in the light of other similar findings in the literature, and the implications for pharmacological subtypes of tardive dyskinesia using cholinergic probes are explored.

Acetylcholine↗
PubMed2003

Central administration of the neurotensin receptor antagonist SR48692 attenuates vacuous chewing movements in a rodent model of tardive dyskinesia.

Tardive dyskinesia is a movement disorder that develops in 20-30% of patients treated with chronic neuroleptics. Whilst the pathogenesis of tardive dyskinesia remains unclear, altered expression of neuropeptides in the basal ganglia has been implicated in its emergence. The peptide neurotensin is expressed in both dopamine D1 receptor-bearing neurons of the direct striatonigral pathway and dopamine D2 receptor-bearing neurons of the indirect striatopallidal pathway. Increased levels of striatal neurotensin messenger RNA (mRNA) are reported following chronic neuroleptic therapy. Chronic treatment with the typical antipsychotic haloperidol elicits neurotensin immunoreactivity in a large number of striatopallidal and a modest number of striatonigral projection neurons, whilst treatment with the potent dopamine releaser, methamphetamine, induces intense neurotensin immunoreactivity in striatonigral projection neurons. In order to determine whether increased levels of striatal neurotensin mRNA in the direct striatonigral or the indirect striatopallidal pathway play a more influential role in the development of tardive dyskinesia, we explored the effects of a specific neurotensin antagonist in a rodent model (vacuous chewing movements [VCMs] induced by chronic neuroleptics). Three groups of animals received injections of fluphenazine decanoate (25 mg/kg) or its vehicle sesame oil every 3 weeks for at least 18 weeks. They were then surgically implanted with bilateral guide cannulae aimed at the striatum, the substantia nigra pars reticulata, or the globus pallidus respectively. After recovery, animals were infused with 2-[(1-(7-chloro-4-quinolinyl)-5-(2,6-imethoxyphenyl)pyrazol-3-yl)carbonylamino]tricyclo(3.3.1.1.(3.7))decan-2-carboxylic acid (SR48692; 0.25, 0.50, and 1.0 nmol/microl), or its vehicle (10% dimethyl sulfoxide [DMSO] in saline) and observed for 60 min. Intra-striatal, intra-nigral or intra-pallidal infusion of SR48692 attenuated neuroleptic-induced VCMs. These findings lend further support to a role for neurotensin in the development of VCMs but do not clarify which pathway plays a more important role. Thus, treatments that reduce or prevent the effects of increased neurotensin expression and release may be useful in the management of tardive dyskinesia.

Animals↗
PubMed1990

Tardive dyskinesia.

Tardive dyskinesia is a potentially irreversible syndrome of involuntary hyperkinetic movements that occur in predisposed persons receiving extended neuroleptic (antipsychotic) drug therapy. It is usually characterized by choreoathetoid dyskinesias in the orofacial, limb, and truncal regions, but subtypes of this syndrome may include tardive dystonia and tardive akathisia. Although the mechanisms underlying the pathogenesis and pathophysiology of this disorder are unproven, altered dopaminergic functions will likely play a role in any explanation of it. Tardive dyskinesia develops in 20% of neuroleptic-treated patients, but high-risk groups such as the elderly have substantially higher rates. Risk factors include age, female sex, affective disorders, and probably those without psychotic diagnoses, including patients receiving drugs with antidopaminergic activity for nausea or gastrointestinal dysfunction for extended periods. Total drug exposure is positively correlated with tardive dyskinesia risk. Management strategies include a careful evaluation of both the psychiatric and neurologic states, a broad differential diagnosis, and adjustment of neuroleptic agents to the lowest effective dose that controls psychosis and minimizes motor side effects. No drug therapy is uniformly safe and effective for treating this disorder. A favorable long-term outcome of improvement or resolution correlates with younger age, early detection, lower drug exposure, and duration of follow-up.

Antipsychotic Agents↗
PubMed1981

Neural mechanisms of tardive dyskinesia.

Tardive dyskinesia is a disabling movement disorder, caused by antipsychotic medications, that occurs frequently and is not responsive to treatment. It is not known how the brain damage underlying tardive dyskinesia produces abnormal movement. We propose that altered sensory flow to motor systems results in this syndrome. Verification of such a mechanism could lead to early detection and improved treatment of tardive dyskinesia.

Brain↗
PubMed1974

Effect of cholinergic and anticholinergic agents on tardive dyskinesia.

Tardive dyskinesia, like several other choreiform disorders, is felt to be primarily related to dopaminergic activity within the striatum. Physostigmine has been demonstrated to improve the abnormal movements in patients with tardive dyskinesia while scopolamine tends to aggravate abnormal movements and in some cases elicits abnormal movement not previously observed. This evidence supports the hypothesis that anticholinergic therapy in patients prone to develop tardive dyskinesia may increase the incidence of this disorder by lowering the threshold for the appearance of these movements.

Adult↗
PubMed1979

Hyperkinetic dysarthria as an early indicator of impending tardive dyskinesia.

Tardive dyskinesia is a potentially irreversible disturbance of the central nervous system that is associated with the chronic ingestion of neuroleptic medications. Abnormal movements within the oral musculature are characteristic of tardive dyskinesia and are manifested in motor speech production as hyperkinetic dysarthria. Early detection of hyperkinetic dysarthria in patients who have chronically ingested neuroleptic agents may play a critical role in preventing an irreversible condition of tardive dyskinesia.

Dysarthria↗
PubMed2000

Dopamine D(1A) receptor function in a rodent model of tardive dyskinesia.

Tardive dyskinesia develops as a common complication of long-term neuroleptic use. The emergence of such dyskinesias may reflect a shift in the balance of dopamine D(1) and D(2) receptor-mediated activity, with a relative increase in activity in the D(1) receptor-regulated direct striatonigral pathway. In rats, chronic treatment with the antipsychotic fluphenazine triggers a syndrome of vacuous chewing movements, which are attenuated by dopamine D(1) receptor antagonists. A similar syndrome can be seen in drug-naive animals following acute administration of selective dopamine D(1) receptor agonists. However, not all dopamine D(1) receptor agonists elicit these mouth movements. Thus, some investigators have suggested the existence of novel subtypes of the dopamine D(1) receptor. In these studies, we sought to clarify the role of the dopamine D(1A) receptor in vacuous chewing movements induced both by the selective dopamine D(1) receptor agonist SKF 38393, as well as by chronic neuroleptic administration, using in vivo oligonucleotide antisense to dopamine D(1A) receptor messenger RNA. Intrastriatal antisense treatment significantly and selectively attenuated striatal dopamine D(1) receptor binding, accompanied by reductions in SKF 38393- and chronic fluphenazine-induced vacuous chewing movements. These findings suggest that the dopamine D(1A) receptor plays an important role in the expression of vacuous chewing movements in a rodent model of tardive dyskinesia and may contribute to the pathogenesis of the human disorder. This may have important implications for the treatment of tardive dyskinesia in humans.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Diazepam in tardive dyskinesia.

Tardive dyskinesia, a syndrome of involuntary motor movements, can be a permanent consequence of the long-term use of antipsychotic drugs. While there is no well-established drug treatment, case reports and the results of a few clinical studies suggest that drugs that facilitate the GABA-ergic system may decrease the abnormal movements. One such class of drugs is the benzodiazepines. We administered diazepam to 13 subjects in a 24-week, crossover design study. Tardive dyskinesia and psychopathology were assessed by blind raters using the Abnormal Involuntary Movement Scale and the Brief Psychiatric Rating Scale (BPRS). The means of all movement measurements improved from the baseline, with orofacial, subtotal, symptom severity, and total reaching significance. However, we were unable to demonstrate a drug effect; the patients improved to a similar degree whether or not they received diazepam. Their psychiatric disorders did not worsen with diazepam administration and, in fact, improved slightly; the activation factor of the BPRS was significantly improved over baseline. Our results suggest that diazepam is not effective in managing the movements of tardive dyskinesia and that behavior modification strategies be investigated to help patients control symptoms.

Aged↗