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Biomedical subjects

R Sandyk

Publications and source records attributed to R Sandyk.

At least 163 records · Page 9Linked to original sources
PubMed1991

Neuroradiological facets of cognitive abnormality in schizophrenia.

Cognitive abnormality has long been regarded as a core feature of schizophrenia, but its nature and etiopathology have been poorly understood. Predicated on new tests that characterize fundamental cognitive impairments, we investigated their relationship to four neuroradiological markers that have been previously implicated in schizophrenia: choroid plexus calcification, cerebellar atrophy, third ventricle enlargement, and pineal calcification. Twenty-three chronic schizophrenic inpatients meeting RDC and DSM-III diagnostic criteria were stabilized on chlorpromazine and assessed independently on a cognitive battery and on CT scan. The results indicated that all four neuroradiological variables were independent of one another and of demographic, historical, and general intellectual measures. The neuroradiological assessments, however, correlated significantly with different cognitive parameters, implying separate pathophysiological bases for distinct profiles of cognitive abnormality. The findings support a "dual-process model" of cognitive dysfunction that posits developmental and arousal-related components which may, more generally, underlie the positive-negative dimension of schizophrenia.

Adult↗
PubMed1991

Risk factors for neuroleptic-induced movement disorders.

Chronic neuroleptic therapy may be associated with the development of diverse movement disorders including Tardive dyskinesia (TD), Parkinsonism, dystonia, and akathisia in a subset of schizophrenic patients. It is presently unknown why only a proportion of neuroleptic-treated patients develop these movement disorders. In the following communication, we present a series of studies which demonstrate that the development of these movement disorders may be facilitated by certain risk factors including disturbances in pineal melatonin functions, diabetes mellitus, cognitive deficits, suicidal behavior, and disturbances in the functions of the choroid plexus. Recognition of these biological factors may prove useful in: (a) further understanding of the pathophysiology of these disorders, and (b) identifying patients at risk for these movement disorders.

Antipsychotic Agents↗
PubMed1991

Relevance of the habenular complex to neuropsychiatry: a review and hypothesis.

Since the initial observation by Brown (1914) that electrical stimulation applied to the habenular efferent bundle in the chimpanzee evoked a pattern of respiration which closely resembled the act of laughter, the habenular complex has remained a mysterious structure. The anatomy of the habenular complex is well delineated (Jones, 1985) forming a major component of the dorsal diencephalic conduction system. Data derived mainly from animal experimentation over the past decade point to the fact that the habenular complex functions as an important link between the limbic forebrain and the midbrain-extrapyramidal motor system. The elucidation of the functions of the habenular complex may thus significantly increase the current insight into the understanding of the interaction between behavioral and motor functions. Clearly, such information would be of great relevance for further understanding of neuropsychiatric disorders such as schizophrenia, Parkinson's disease, Tardive dyskinesia, and Tourette's syndrome in which behavioral and motor impairments are interfaced. This review summarizes anatomical, functional, and pharmacological aspects of the habenular complex and discusses its potential contribution to the pathophysiology of selected neuropsychiatric and movement disorders.

Afferent Pathways↗
PubMed1991

The relationship of pineal calcification to cortical atrophy in schizophrenia.

Several recent computed tomographic (CT) studies have provided evidence for structural cerebral abnormalities in schizophrenia. CT scan findings included enlargement of the lateral cerebral ventricles, cortical atrophy, third ventricular dilatation, ventricular asymmetry, and cerebellar atrophy. In addition, there is increasing data to suggest that abnormal pineal melatonin functions are associated with the pathophysiology of schizophrenia. To explore further the relationship of the pineal gland to the pathophysiology of schizophrenia and its specific association with structural abnormalities, we investigated: (a) the relationship of pineal calcification (PC) to computerized tomographic (CT) scan measurements of cortical and subcortical atrophy in 41 chronic schizophrenic patients, and (b) the relationship of PC size to CT scan measurements and cortical and subcortical atrophy in 51 chronic schizophrenic patients. Results of the first study revealed that the presence of PC was significantly associated with measurements of prefrontal cortical atrophy (p less than .01), while there was no association with measurements of parieto-occipital atrophy, sulcal prominence, or ventricular brain ratio (VBR). These findings support the notion that the various structural brain abnormalities in schizophrenia may reflect different pathological processes and that abnormal pineal melatonin functions may be associated with the pathophysiology of prefrontal cortical atrophy. In addition, since some clinical facets of schizophrenia covary with frontal lobe dysfunction, our findings highlight the significance of abnormal pineal functions for the pathophysiology of schizophrenia. In the second study we found a significantly higher prevalence of pathologically enlarged PC (i.e., greater than 1 cm in diameter) in schizophrenia as compared to controls of similar age. In addition, we found a significant association between CT scan measurements of cortical atrophy and pathologically enlarged PC size (p less than .05). By contrast, PC size was unrelated to VBR. These findings demonstrate a specific association between pathologically enlarged PC and cortical atrophy in schizophrenia. The implications of these findings to the pathophysiology of schizophrenia and, specifically, to the morphological abnormalities that accompany the disease are discussed.

Adult↗
PubMed1991

Atrophy of the cerebellar vermis: relevance to the symptoms of schizophrenia.

Degeneration of the cerebellar vermis is a common pathological and neuroradiological feature of chronic schizophrenia, but its relationship to symptoms of the disease are poorly understood. We investigated the relationship of vermal cerebellar atrophy on CT scan to features of positive (productive) and negative (defect) dimensions of schizophrenia as well as to symptoms of general psychopathology in a sample of 23 chronic schizophrenic patients. For comparison, we also studied the relationship of third ventricular width (TVW), which reflects periventricular and diencephalic atrophy, to these features of schizophrenic symptomatology. Vermal cerebellar atrophy was found in 43.5% of patients and correlated significantly with general psychopathology and, more specifically, with feelings of guilt and disturbance of volition. It was unrelated to global positive or negative features of schizophrenia. By contrast, TVW was uniquely associated with global negative syndrome. These observations indicate that degeneration of the cerebellar vermis and enlargement of the third ventricle are integral aspects of schizophrenia, and that each contributes independently to specific clinical aspects of the disease.

Atrophy↗
PubMed1991

Tobacco addiction as a marker of age at onset of schizophrenia.

Schizophrenia is a heterogenous disorder, with diversity in symptoms, course, prognosis, and probably etiology. The timing of its onset (i.e., early vs. late) not only predicts outcome of illness, but also corresponds to fundamental neurochemical and neuroendocrine distinctions. There is recent evidence that early age at onset of schizophrenia is associated with more prominent negative symptoms, which are associated with decreased dopaminergic functions in the limbic system. Since addictive behaviour may be related to decreased dopamine activity in the mesolimbic reward circuitry, we predict a higher prevalence of tobacco addiction in patients with an earlier age at onset of schizophrenia. To investigate this hypothesis, we studied the association of cigarette smoking to age at onset of illness in a sample of 142 chronic schizophrenic inpatients, 73 of whom were smokers. We found that patients who smoked had a significantly earlier age at onset of psychiatric illness as compared to the nonsmokers (p less than .01). Since damage to dopaminergic systems at the lateral hypothalamic level of the medial forebrain bundle and in the ventral tegmental reward system produces the strongest indication of reward, our data suggest that alterations in dopaminergic functions in these systems may be linked to the timing of onset of schizophrenic symptoms.

Aged↗
PubMed1991

Magnetic stimulation in the treatment of partial seizures.

We have recently demonstrated that Magnetoencephalographic (MEG) brain measurements in patients with seizure disorders show significant MEG activity often in the absence of conventional EEG abnormalities. We localized foci of seizure activity using the mapping technique characterized by the ISO-Spectral Amplitude (ISO-SA) on the scalp distribution of specified spectral components or frequency bands of the emitted MEG Fourier power spectrum. In addition, using an electronic device, we utilized the above recorded activity to emit back the same intensity and frequency of magnetic field to the presumed epileptic foci. Using this method we were able, over the past two years, successfully to attenuate seizure activity in a cohort of over 100 patients with various forms of epilepsy. We now present in more detail three randomly selected patients with partial seizures in whom application of an external artificial magnetic field of low intensity produced a substantial attenuation of seizure frequency during an observation period extending from 10 to 14 months. All patients had previously obtained only partial response to conventional anticonvulsant therapy. Attenuation in seizure frequency was associated with normalization of the MEG activity. These cases demonstrate that artificial magnetic treatment may be a valuable adjunctive procedure in the management of partial seizures. The possible mechanisms underlying the anticonvulsant properties of magnetic stimulation at both cellular and systemic levels are discussed. Specifically, since the pineal gland has been shown to be a magnetosensitive organ which forms part of a combined compass-solar clock system, and since it exerts an inhibitory action on seizure activity in both experimental animals and humans, we discuss the potential pivotal role of the pineal gland in the long term anticonvulsant effects of external artificial magnetic stimulation.

Adult↗
PubMed1990

The hypothalamus in MPTP-induced parkinsonism.

1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) has been shown to produce a parkinsonian syndrome in humans and other primates. Recent studies have demonstrated that in humans the hypothalamus has the highest binding density for (3H) MPTP, which corresponds to monoamine oxidase type B (MAO-B). There is evidence that the conversion of MPTP to the toxic compound MPP+ takes place in the hypothalamus; subsequently, MPP+ is transported to the striatal system, where destruction of nigrostriatal dopamine neurons occurs. Thus, the hypothalamus appears to be a primary target organ of MPTP toxicity. This assumption is supported by the observation that monkeys exposed to MPTP exhibit extensive pathological lesions in the hypothalamus which are manifested clinically by the development of life-threatening anorexia requiring forced feeding to overcome. We discuss the clinical implications of MPTP-induced hypothalamic damage to the pathophysiology of MPTP-induced parkinsonism and to Parkinson disease. It is suggested that consideration of hypothalamic involvement in MPTP-induced parkinsonism may provide a broader understanding of the pathophysiology of parkinsonism and may, in addition, account for the preliminary observations that MAO-B inhibitors retard the progression of Parkinson disease and possibly prolong life expectancy.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1990

Relationship of neuroleptic-induced akathisia to drug-induced parkinsonism.

Akathisia refers to subjective inner restlessness and a feeling of the need to move. Its occurrence in association with Parkinson disease suggests a common underlying pathophysiological mechanism. We investigated the relationship of neuroleptic-induced akathisia to drug induced parkinsonism in a group of 123 neuroleptic-treated elderly chronic schizophrenic inpatients (mean age: 63.9 +/- 8.9 years). In addition, since neuroleptic-induced akathisia has been noted to be more common in females, we studied the severity of akathisia separately by gender. Akathisia was present in 40 patients (32.5%). We found no significant differences in the severity of akathisia between patients with and these without parkinsonism. Although a significantly larger proportion of females than males had akathisia, there were no significant differences in respect of parkinsonism. Our findings do not support a major role for the dopaminergic system in the pathophysiology of akathisia might be related to dysfunction of nondopaminergic systems.

Aged↗
PubMed1990

Neuroleptic-induced "painful legs and moving toes" syndrome: successful treatment with clonazepam and baclofen.

The syndrome of "painful legs and moving toes" is characterised by spontaneous causalgic pain in the lower extremities associated with peculiar involuntary movements of the toes and feet. It has been observed after a variety of lesions affecting the posterior nerve roots, the spinal ganglia and the peripheral nerves. The pathophysiology of the syndrome is unknown. I report a patient who developed the syndrome during treatment for schizophrenia with the antipsychotic agent molindone hydrochloride. The patient's response to the combination of clonazepam and baclofen suggests that the pathophysiology of the "painful legs and moving toes" may be linked to impairment of spinal serotonergic and GABA functions.

Baclofen↗
PubMed1990

Pineal melatonin in schizophrenia: a review and hypothesis.

It has long been suggested that abnormal functions of the pineal gland may be implicated in the pathophysiology of schizophrenia. We present evidence proposing that diminished melatonin secretion may be associated with the pathophysiology of a subgroup of schizophrenic patients characterized by cerebral atrophy and ventricular enlargement, negative symptoms, impaired cognitive and psychosexual development, onset at pubescence, poor response to neuroleptic medication, and possible increased risk of extrapyramidal symptoms. This view holds that a subnormal plasma melatonin level may be a marker of a subgroup of schizophrenia and may also denote a specific genetic susceptibility.

Dyskinesia, Drug-Induced↗