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Biomedical subjects

R Sandyk

Publications and source records attributed to R Sandyk.

At least 199 records · Page 11Linked to original sources

Tardive dyskinesia associated with depression in a bipolar patient: possible role of melatonin.

Several clinical studies have suggested that patients with affective disorder are at high risk for developing tardive dyskinesia (TD). An intriguing aspect of the relationship between TD and affective disorders involves mood dependent alterations in the severity of TD in bipolar patients. In most reported cases, depressive episodes have been reported to be associated with exacerbation of TD, while manic episodes were accompanied by attenuation of TD. Current neurochemical hypotheses of TD do not explain adequately the relationship of TD to depression or mania in bipolar patients. A patient with bipolar illness is presented in whom TD emerged concurrently with the onset of depression that developed during management of an acute manic episode. It is suggested that decline in melatonin secretion with onset of the depression was associated with the emergence of TD. Thus, the increased incidence and risk of TD in bipolar patients may in part be related to decreased melatonin secretion, while increased melatonin secretion during manic episodes may have protective effect against the development of TD.

Adult↗

Possible role of pineal melatonin in the mechanisms of aging.

The pineal gland has captured man's attention as early in recorded history as the Greeks when philosophers considered it the "seat of the soul". Descartes, in the Middle Ages, furthered this concept naming it "esprits animaux" or, in current language, the psychic and somatic activating principle. These notions about the pineal gland were initially purely speculative and unsupported by scientific facts. However, with the development of a sound knowledge base concerning the pineal gland over the past twenty years, evidence has accumulated to suggest a pivotal role for the pineal in the 'fine tuning' and integrating of various neural and endocrine functions. The secretion of pineal melatonin has been shown to decline progressively with age. Recent hypotheses of aging have suggested that cumulative neuronal insults associated with free radical production may be associated with the process of aging. There is evidence to suggest that melatonin may protect against the age processes in part by attenuating the effects of free radical-induced neuronal damage. Other studies derived mainly from observations on pinealectomized rats also suggest that diminished melatonin secretion may be associated with acceleration of the aging process. Thus, pineal melatonin may be a natural anti-aging hormone.

Aging↗

Melanocyte-stimulating hormone and persistent tardive dyskinesia: a hypothesis.

An increased incidence of abnormal perioral movements has recently been reported in drug-naive pinealectomized rats with further accentuation of these movements following administration of haloperidol. Analysis of the temporal course of the development of the perioral dyskinetic movements revealed that the onset of these movements occurred within 4 days postoperatively and peaked at 3 weeks to plateau over the following 4-6 weeks. Increased pituitary Melanocyte-stimulating hormone (MSH) content has been reported in pinealectomized rats. Elevation of MSH content in the pinealectomized rats occurred within 3 days of surgery and was followed by normalization within 4 weeks. These findings suggest that compensatory mechanisms involving hypothalamic-pituitary MSH release must have been activated to induce normalization of pituitary MSH levels. Moreover, reduction of pituitary MSH levels may have coincided with attenuation in the severity of the perioral dyskinetic movements. It is possible that the development of tardive dyskinesia (TD) may in part be associated with increased brain and plasma MSH levels and that impaired hypothalamic-pituitary regulatory mechanisms of MSH release may be associated with persistent TD. The pineal gland may be implicated in this process as diminished melatonin secretion may be associated with disinhibition of MSH release. Thus, the above hypothesis complements and extends the recently presented "melatonin hypothesis" and suggests that research of pineal-hypothalamic interactions may be crucial to the further understanding of TD.

Animals↗

The significance of eye blink rate in parkinsonism: a hypothesis.

Alterations in blink rate have been reported in several neuropsychiatric disorders presumed to result from abnormal central dopaminergic functions. Increased blink rate in schizophrenia, Tardive dyskinesia, Tourette's syndrome and Meige's disease are associated with enhanced dopaminergic functions. Parkinson's disease is associated with reduced dopaminergic functions and decreased blink rate. Thus, blink rate may reflect striatal and mesolimbic dopaminergic activity. Since acute light exposure suppresses melatonin production and darkness stimulates melatonin secretion, blinking may serve to regulate light-dark exposure to the pineal gland and thus to 'fine tune' melatonin production. As there is evidence to suggest that melatonin inhibits the release of dopamine in the striatum and limbic system, increased blink rate may serve to reduce light exposure, increase melatonin secretion and attenuate dopaminergic functions. Conversely, decreased blinking (as is observed in patients with Parkinson's disease) could reflect a compensatory mechanism to increase light exposure, reduce melatonin production and ultimately increase dopamine functions. This model is novel in that for the first time it suggests a functional link among blink rate, melatonin secretion and striatal dopaminergic functions in movement disorders.

Blinking↗

Pyridoxine improves drug-induced parkinsonism and psychosis in a schizophrenic patient.

Drug-induced Parkinsonism is a common serious side-effect of neuroleptic therapy. In cases of irreversible drug-induced Parkinsonism, pharmacological management is notoriously difficult. A schizophrenic patient with severe neuroleptic-induced Parkinsonism and Tardive Dyskinesia is presented in whom administration of pyridoxine (vitamin B6) (100 mg/d) resulted in dramatic and persistent attenuation of the movement disorders as well as reduction of psychotic behavior. Since pyridoxine deficiency is associated with marked reduction of cerebral serotonin concentrations and pineal melatonin production in rats, the effects of pyridoxine on the movement disorder and psychosis may have been mediated largely by enhancing serotonin and melatonin functions. An additional effect of excess pyridoxine administration on GABA and dopamine activity cannot be excluded. Pyridoxine has been reported to attenuate the severity of levodopa-induced dyskinesias in patients with Parkinson's disease and it is suggested that pyridoxine supplementation should be considered in psychiatric patients with drug-induced movement disorders including persistent Parkinsonism. An underlying pyridoxine deficiency in these patients may exacerbate the psychotic behavior and additionally, potentially increase the risk of drug-induced movement disorders.

Adult↗

Tardive dyskinesia in bipolar disorders: possible role of pineal melatonin.

Several clinical studies have suggested that patients with affective disorders, are at high risk for developing tardive dyskinesia (TD). An intriguing aspect of the relationship between TD and affective disorders involves mood dependent alterations in severity of TD. In most reported cases, depressive episodes are associated with exacerbation of TD, while manic episodes are accompanied by attenuation of TD. Current neurochemical hypotheses of TD do not explain adequately the relations of TD to depression or the mood dependent variations in the severity of TD. I propose that alterations in the secretory activity of pineal melatonin during manic and depressive episodes may explain better both the higher risk of TD in patients with affective disorders and the mood-dependent fluctuations in severity of TD. Consideration of pineal melatonin functions may further our understanding of the pathophysiology of TD in patients with affective disorders.

Bipolar Disorder↗

Pineal melatonin and sensory symptoms in Parkinson disease.

Sensory symptoms have been reported in 40-60% of patients with Parkinson's disease, and in at least 10% of patients these symptoms precede the onset of the motor disorder. The pathophysiology of these symptoms remains unknown. Diminished brain serotonin concentration has been reported to be associated with sensory symptoms. Serotonin metabolism is regulated by pineal melatonin. The secretory activity of the pineal gland may be diminished in Parkinson's disease. In experimental animals pineal melatonin has been shown to exert analgesic effects by interacting with opiate receptors. In addition, since opioid peptides mediate the analgesic effects of melatonin, decreased opioid peptide functions in Parkinson's disease may be associated with disruption of the "fine-tuning" pain modulatory functions of melatonin and possibly indirectly facilitate the emergence of sensory symptoms.

Animals↗

Persistent tardive dyskinesia and neuroleptic effects on glucose tolerance.

The relations of persistent tardive dyskinesia (TD) to glucose tolerance and family history of type 2 diabetes mellitus (FH-NIDDM) were examined in 22 schizophrenic patients. All patients underwent a standard oral glucose tolerance test (GTT) while receiving haloperidol, and 15 patients also underwent a GTT when drug free. Fasting blood glucose (FBS) was significantly higher in the TD group than in the non-TD group in the medicated condition, but not in the drug-free state. TD and non-TD groups did not differ significantly in postload glucose levels either in the drug-free or in the medicated condition. However, relative to the drug-free state, haloperidol-treated TD patients showed decreased glucose tolerance while non-TD patients showed increased glucose tolerance. Seven (32%) of the 22 patients had an FH-NIDDM. A positive FH-NIDDM was significantly associated with the presence of TD and with higher drug-free FBS. A possible role of melatonin in mediating the TD-augmenting effects of FH-NIDDM and the neuroleptic-induced decrease in glucose tolerance has been proposed.

Adult↗