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Biomedical subjects

R Sandyk

Publications and source records attributed to R Sandyk.

At least 217 records · Page 12Linked to original sources
PubMed1989

Hypothalamic compensatory mechanisms in Parkinson's disease.

Parkinson's disease (PD) is associated with loss of dopaminergic neurons of the nigrostriatal bundle and to a lesser extent of the mesolimbic and hypothalamic dopaminergic systems. Frank symptoms of the disease usually emerge when at least 70-80% of striatal dopamine (DA) content have been reduced, raising the possibility that the preclinical phase of the disease might be due to compensatory changes that permit residual dopaminergic neurons to subserve functions previously carried out by the entire projection. These neurochemical compensatory mechanisms are known to occur at a striatal level of the rate limiting enzymes of catecholamine synthesis as well as alterations in the sensitivity of the dopaminergic postsynaptic receptors (Zigmond et al., 1984; Bokobza et al., 1984). Compensatory mechanisms, although generally less well recognized, also occur in the hypothalamus and involve endocrine regulation, abnormal neuropeptide release and the emergence of several autonomic and sensory symptoms manifesting prior to or during the course of the disease. Such neurochemical and clinical adaptation mechanisms of the hypothalamus may help to explain the neurobiological events underlying the preclinical phase of Parkinsonism. Moreover, progressive failure of these hypothalamic adaptive mechanisms may be critical in the transition of the disease into the "malignant phase" (Danielczyk et al., 1980).

Endocrine System Diseases↗
PubMed1989

Alpha melanocyte stimulating hormone (MSH) in Tourette's syndrome.

The intermediate lobe of the pituitary is thought to be the primary source of alpha-melanocyte stimulating hormone (alpha-MSH). While the intermediate lobe of the human fetus contains high concentrations of alpha-MSH, the human adult pituitary is devoid of the peptide. Based on evidence implicating the hypothalamus as a site of dysfunction in Tourette's syndrome (TS), and studies suggesting that alpha-MSH may be involved in neuronal maturation, we measured plasma alpha-MSH levels in three unmedicated TS patients (aged 12 to 69), and in three age-matched controls. High plasma alpha-MSH concentrations were detected in all three patients. None of the patients showed any abnormalities in skin coloration. These findings suggest that abnormalities in the synthesis or release of alpha-MSH may be linked to the pathophysiology of TS, and also to the delay in neurodevelopmental maturation.

Adolescent↗
PubMed1989

Dopaminergic supersensitivity factors in Tourette's syndrome: a hypothesis.

Alterations in striatal dopamine receptor functions are thought to underlie the major symptoms of Tourette's syndrome (TS). In this communication, evidence is presented to suggest that the striatal dopamine receptor supersensitivity in TS may be mediated by alterations in the release and function of dopamine supersensitive factors including prolactin, estrogens, beta-endorphin, melanocyte stimulating hormone (MSH), and adrenal corticotrophic hormone (ACTH). It is suggested that treatment of TS should be directed towards rectifying these endocrine and neuropeptide imbalances.

Dopamine↗
PubMed1989

Abnormal opiate receptor functions in Tourette's syndrome.

Opiates and opioids have been shown to modulate the release of pituitary hormones by acting at the hypothalamic level. Since the identification of the various opiate receptors in the human brain, it has been shown that the endocrine modulation of pituitary release by opiates may be differently affected by the various opiate receptors. Our findings in Tourette's syndrome demonstrate a predominant aberrant mu-opiate receptor modulation of anterior pituitary hormonal release, and suggest that endorphins and enkephalins are the predominant group of opioids involved in the pathophysiology of the disease.

Humans↗
PubMed1989

Recurrence of complex motor and vocal tics in an elderly woman responsive to opiates.

A 73-year-old woman experienced recurrence of complex and motor tics in late adult life. Involuntary vocalizations that had a cough-like quality constituted the most distressing feature of her tick disorder. The latter was unresponsive to diverse pharmacological agents including neuroleptics, clonazepam, baclofen, phenytoin, and various nonnarcotic antitussive agents. Low dose oxycodone produced almost complete abolishment of the cough-like involuntary vocalizations. This report implicates derangement in the activity of the endogenous opioid system in the pathophysiology of Tourette's syndrome, and suggest that opiates may be prescribed in the therapy of TS patients otherwise recalcitrant to administration of haloperidol or other dopamine blocking agents.

Aged↗
PubMed1989

Estrogens and the pathophysiology of Parkinson's disease.

Two postmenopausal female Parkinsonian patients experienced exacerbation of symptoms including levodopa-induced "On-Off" following withdrawal or reduction of conjugated estrogen therapy. This report supports animal data implicating female sexual hormones in the pathophysiology of Parkinson's disease and levodopa-induced dyskinesias.

Estrogens↗
PubMed1989

L-tryptophan supplementation in Parkinson's disease.

Two female Parkinsonian patients with levodopa-induced "On-Off" responded dramatically to administration of L-tryptophan supplementation. This report highlights the role of serotonergic deficiency in the pathophysiology of Parkinson's disease and of levodopa-induced motor fluctuations, and suggests that L-tryptophan supplementation may be useful in ameliorating motor complications of chronic levodopa therapy in the disease. The possibility that L-tryptophan supplementation with initiation of levodopa therapy may be useful in preventing levodopa-induced motor complications is discussed.

Aged↗
PubMed1989

Hypothalamic-locus coeruleus mechanisms in the pathophysiology of "on-off" in L-dopa treated Parkinson's disease: a hypothesis.

Fluctuations in motor performance remain a major problem in the longterm management of Parkinson's disease (PD) patients. Although alterations in striatal dopaminergic activity have been initially thought to induce these complications, recent studies failed to support a major role for impaired dopaminergic neuronal or receptor functions in the pathogenesis of the on-off phenomenon. In the following I discuss the possibility that alterations in the activity of norepinephrinergic neurons at the level of the locus coeruleus (LC) associated with dysregulation of descending endorphinergic projections from the arcuate nucleus of the hypothalamus may be intimately involved in the pathogenesis of motor fluctuations in L-dopa treated PD.

Animals↗