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Biomedical subjects

R Sandyk

Publications and source records attributed to R Sandyk.

At least 523 records · Page 29Linked to original sources
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The relationship of tardive dyskinesia to positive schizophrenia.

Investigations aimed at identifying the clinical characteristics that discriminate Tardive dyskinesia (TD) from non-TD patients have yielded disparate findings. A number of studies have suggested that TD may be a feature of negative schizophrenia. In particular, the association of TD with high prevalence of "soft" neurological signs, cognitive deficits, and abnormal brain morphology on CT scan in some patients, have led several investigators to propose that negative schizophrenia may be a risk factor for TD. The neurochemical profile of TD, however, is not consistent with this hypothesis. In the following communication, we present our studies which suggest that TD is specific to and an intergral part of positive schizophrenia. The data suggest that schizophrenic patients with predominant positive symptoms may be at increased risk for the development of TD. In addition, we present evidence linking TD with left cerebral hemispheric dysfunction. By comparison, we provide evidence that negative schizophrenia is related to diencephalic damage, and discuss its relevance to negative schizophrenia and to Parkinsonism. We also provide evidence that negative schizophrenia may be a risk factor for acute drug-induced dystonia. Thus, these findings are consistent with our model that negative schizophrenia is a risk factor for Parkinsonism, whereas positive schizophrenia is related to TD. In analogy with the positive/negative dichotomy of schizophrenia, we propose that TD could be considered a "positive," where Parkinsonism a "negative" movement disorder.

Adult↗
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Pineal calcification in relation to menopause in schizophrenia.

I have suggested that critical changes in melatonin secretion, as mediated by the pineal gland, may exert a crucial role in the onset and pathogenesis of schizophrenia. Since pineal calcification (PC) is thought to reflect the metabolic and secretory activity of the gland, I investigated in 29 randomly selected chronic institutionalized female schizophrenic patients the association of PC on CT scan with premenopausal (prior to age 40) versus menopausal (ages 40-55) onset of illness. The premenopausal patients were found to show a significantly higher prevalence of PC than the menopausal patients (55.5% vs. 18.1%; X2 = 3.93, df = 1, p < .05). Since PC was unrelated to historical, demographic, and treatment variables, these findings highlight the importance of the pineal gland for the timing of the onset of schizophrenia, particularly in relation to the female reproductive state. The results carry theoretical implications on the pathogenesis of schizophrenia and suggest that the pineal gland may exert a protective effect against its onset.

Adult↗
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The pineal gland and the mode of onset of schizophrenia.

Recent studies suggest that abnormal melatonin functions may be implicated in the pathophysiology of schizophrenia. Since there is evidence that the presence of pineal calcification (PC) may relate, among other factors, to disturbances in melatonin secretion, I investigated in 23 chronic institutionalized schizophrenic patients the relationship of PC size on CT scan to the mode of onset of schizophrenia which carries both developmental and prognostic significance. Patients with gradual onset schizophrenia had PC size that was significantly larger than those with sudden onset (8.94 +/- 3.96 mm vs. 4.80 +/- 1.75 mm p < .025). These findings suggest that the nature of onset of schizophrenia may be influenced by the activity of the pineal gland, which may exert a role in the development and prognosis of the illness.

Adult↗
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Pineal and habenula calcification in schizophrenia.

Animal data indicate that melatonin secretion is stimulated by the paraventricular nucleus (PVN) of the hypothalamus and that lesions of the PVN mimic the endocrine effects of pinealectomy. Since the PVN lies adjacent to the third ventricle, I propose that periventricular damage, which is found in schizophrenia and may account for the third ventricular dilatation seen on computed tomographic (CT), may disrupt PVN-pineal interactions and ultimately enhance the process of pineal calcification (PC). To investigate this hypothesis, I conducted CT study on the relationship of PC size to third ventricular width (TVW) in 12 chronic schizophrenic patients (mean age: 33.7 years; SD = 7.3). For comparison, I also studied the relationship of PC size to the ventricular brain ratio and prefrontal cortical atrophy. As predicted, there was a significant correlation between PC size and TVW (r pbi = .61, p < .05), whereas PC was unrelated to the control neuroradiological measures. The findings support the hypothesis that periventricular damage may be involved in the process of PC in schizophrenia and may indirectly implicate damage to the PVN in the mechanisms underlying dysfunction of the pineal gland in schizophrenia. In a second study, I investigated the prevalence of habenular calcification (HAC) on CT in a cohort of 23 chronic schizophrenic-patients (mean age: 31.2 years; SD = 5.95). In this sample HAC was present in 20 patients (87%). Since the prevalence of HAC in a control population of similar age is only 15% these data reveal an almost 6-fold higher prevalence of HAC (X2 = 84.01, p < .0001) in chronic schizophrenia as compared to normal controls. The implications of HAC for the pathophysiology of schizophrenia are discussed in light of the central role of the habenula in the regulation of limbic functions.

Adult↗
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L-tryptophan in neuropsychiatric disorders: a review.

Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.

Dopamine↗
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The influence of the pineal gland on migraine and cluster headaches and effects of treatment with picoTesla magnetic fields.

For over half a century the generally accepted views on the pathogenesis of migraine were based on the theories of Harold Wolff implicating changes in cerebral vascular tone in the development of migraine. Recent studies, which are based on Leao's concept of spreading depression, favor primary neuronal injury with secondary involvement of the cerebral circulation. In contrast to migraine, the pathogenesis of cluster headache (CH) remains entirely elusive. Both migraine and CH are cyclical disorders which are characterised by spontaneous exacerbations and remissions, seasonal variability of symptoms, and a relationship to a variety of environmental trigger factors. CH in particular has a strong circadian and seasonal regularity. It is now well established that the pineal gland is an adaptive organ which maintains and regulates cerebral homeostasis by "fine tuning" biological rhythms through the mediation of melatonin. Since migraine and CH reflect abnormal adaptive responses to environmental influences resulting in heightened neurovascular reactivity, I propose that the pineal gland is a critical mediator in their pathogenesis. This novel hypothesis provides a framework for future research and development of new therapeutic modalities for these chronic headache syndromes. The successful treatment of a patient with an acute migraine attack with external magnetic fields, which acutely inhibit melatonin secretion in animals and humans, attests to the importance of the pineal gland in the pathogenesis of migraine headache.

Adult↗
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Nocturnal plasma melatonin and alpha-melanocyte stimulating hormone levels during exacerbation of multiple sclerosis.

The pineal gland has been implicated recently in the pathogenesis of multiple sclerosis (MS). To investigate this hypothesis further, we studied nocturnal plasma melatonin levels and the presence or absence of pineal calcification (PC) on CT scan in a cohort of 25 patients (5 men, 20 women; mean age: 41.1 years; SD = 11.1; range: 27-72) who were admitted to a hospital Neurology service for exacerbation of symptoms. Plasma alpha-melanocyte stimulating hormone (alpha-MSH) estimations were included in the study since there is evidence for a feedback inhibition between alpha-MSH and melatonin secretion. Abnormal melatonin levels were found in 13 patients (52.0%), 11 of whom had nocturnal levels which were below the daytime values (i.e., < 25 pg/ml). Although melatonin levels were unrelated to the patient's age and sex, there was a positive correlation with age of onset of symptoms (p < .0001) and an inverse correlation with the duration of illness (p < .05). PC was noted in 24 of 25 patients (96%) underscoring the pathogenetic relationship between MS and the pineal gland. Alpha-MSH levels were undetectable in 15 patients (60.0%), low in two patients (8.0%), normal in seven patients (28.0%), and elevated in one patient (4.0%). Collectively, abnormal alpha-MSH levels were found in over 70% of patients. These findings support the hypothesis that MS may be associated with pineal failure and suggest, furthermore, that alterations in the secretion of alpha-MSH also occur during exacerbation of symptoms. The relevance of these findings to the pathogenesis of MS are discussed.

Adult↗
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Autonomic functions in the early stages of Parkinson's disease.

Disturbances of autonomic nervous functions are common in patients with Parkinson's disease (PD) and may develop as a result of pathological changes in centers of autonomic regulation such as the hypothalamus, brainstem, and sympathetic ganglia. We examined cardiovascular reflexes using bedside, noninvasive procedures in 20 unmedicated PD patients with early stages of the disease (stages 1 and 2 on the Hoehn and Yahr's scale). Sixteen patients (80%) exhibited some degree of autonomic nervous system dysfunction. These included predominantly cardiovascular functions mediated via the parasympathetic system. Our findings demonstrate: (a) a high prevalence of autonomic disturbances in early stage PD, and (b) that dysregulation of parasympathetic cardiovascular control mechanisms is a major feature of dysautonomia in early, unmedicated PD patients.

Aged↗
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Dysautonomia in Parkinson's disease: relationship to motor disability.

Disturbances of autonomic nervous system functions are common in patients with Parkinson's disease (PD) and may develop as a result of pathology in centers of autonomic regulation such as the hypothalamus, brainstem, and sympathetic ganglia. We examined the relationship between the degree of motor disability, as determined from the Hoehn and Yahr scale (1967), and the presence of pandysautonomia, as determined by the assessment of noninvasive cardiovascular reflexes, in 29 unmedicated PD patients (mean age: 72.0 years, SD = 8.9). In addition, we investigated the relationship of pandysautonomia to CT scan measures of cerebral atrophy and to the presence or absence of pineal calcification. Nine patients (31.0%) were found to have pandysautonomia with deficits in both sympathetic and parasympathetic cardiovascular functions. Pandysautonomia was statistically related only to the degree of motor disability (p < .01). These findings demonstrate a significant association between motor disability and objective impairment of central cardiovascular functions in PD.

Aged↗
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Cocaine addiction: relationship to seasonal affective disorder.

We report a 25 year-old patient with seasonal affective disorder (SAD) and cocaine abuse who experienced cyclical fluctuations in cocaine craving which were concomitant with seasonal alterations in mood. The temporal association of both disorders in this patient suggests that they may share a common underlying pathophysiology. Since disturbances in circadian rhythms and pineal melatonin functions may in part underlie the pathophysiology of SAD and the psychomimetic effects of cocaine are mediated in part through the pineal gland, we propose that dysfunction of circadian rhythms and pineal melatonin functions may partly mediate the association of SAD with cocaine abuse. This hypothesis may have potential clinical and therapeutic implications for a subgroup of cocaine abusers with SAD since light therapy, which is efficacious in the therapy of SAD, may also prove to be beneficial in reducing cocaine addiction. Furthermore, the report illustrates the need for investigations of environmental cues for cocaine abuse with specific attention given to the effects of light on circadian mood changes.

Adult↗
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The role of melatonin in the antipsychotic and motor-side effects of neuroleptics: a hypothesis.

Three phenomena concerning the antipsychotic action of classic neuroleptic drugs have not been adequately explained by the dopamine hypothesis: (1) administration of neuroleptic drugs is commonly associated with an initial period of 3-6 weeks prior to demonstration of antipsychotic effects; (2) similarly, neuroleptic-induced Parkinsonism commonly emerges only after several weeks of neuroleptic therapy; (3) moreover, Parkinsonism may disappear despite continuous neuroleptic treatment. An understanding of these phenomena might shed new light into the nature of the antipsychotic actions of these agents, and hence the pathophysiology of schizophrenia. We propose that the increase in melatonin secretion, which occurs with the initiation of neuroleptic therapy, may be responsible for the delay in the antipsychotic effects of neuroleptics and may also account for the lag in the development of drug-induced Parkinsonism as well as its disappearance. The implications of this hypothesis for the treatment of schizophrenia and the prophylaxis of drug-induced Parkinsonism are discussed.

Antipsychotic Agents↗