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T G Bolwig

Publications and source records attributed to T G Bolwig.

At least 37 records · Page 2Linked to original sources
PubMed1998

Clinical definitions of sensitisation in affective disorder: a case register study of prevalence and prediction.

The observation of a progressive recurrence in affective disorder has been interpreted as a process of sensitisation. The clinical applicability of such a theoretical model was investigated using the Danish case register, which includes all hospital admissions with primary affective disorder in Denmark from 1971 to 1993. A total of 8,737 patients admitted to a psychiatric hospital at least twice constituted the study sample. Information on treatment intervention was not available. Measures describing the initial course of admission episodes were defined in three different ways: 1) a short period between initial episodes 2) decreasing intervals between initial episodes or 3) a combination of 1) and 2). Socio-demographic variables such as gender, age at onset and marital status differentiated between the three types of measures and the measures also demonstrated different effects in predicting the risk of further recurrence. In unipolar disorder, patients with a decreasing interval between episodes had the greatest risk of further recurrence, whereas for bipolar patients, a short period between episodes played a more important role than the sequence of episodes in itself.

Bipolar Disorder↗
PubMed1998

Clinical consequences of sensitisation in affective disorder: a case register study.

Clinically derived measures of the initial course of episodes might reflect a process of sensitisation in affective disorder. However, the clinical consequences of such measures have not been investigated. The predictive effect of measures of the initial course of episodes was investigated in relation to the subsequent risk of alcoholism, dementia, death and suicidal attempts/suicide in a case register study including all hospital admissions with primary affective disorder in Denmark from 1971 to 1993. A total of 8737 patients with more than one episode were included in the analyses. A short period between initial episodes of the illness, reflecting a great intensity of illness, predicted increased risk of subsequent development of dementia, and for unipolar patients, decreased risk of subsequent alcoholism. Surprisingly, a progressive course, with decreasing intervals between initial episodes of the illness, had no predictive effect. Similarly, no predictive effects on the risk of death or suicidal acts could be demonstrated with any measure of the initial course of episodes.

Aged↗
PubMed1998

The efficacy of psychotherapy in non-bipolar depression: a review.

A review of efficacy studies on psychotherapy of depression is made. Based on the available literature, there is evidence of effectiveness of cognitive and interpersonal therapy in the treatment of mild to moderate depression. To a lesser degree, the effect of psychoanalytically oriented and behavioural therapy has been documented. The effectiveness of psychotherapy among in-patients and patients with severe depression has not been documented. No studies have documented a preventive effect of psychotherapy on future recurrent depressive episodes. In recurrently depressive patients who respond to a combination of imipramine and interpersonal psychotherapy, maintenance treatment with interpersonal psychotherapy may prevent new episodes, but not as effectively as maintenance therapy with imipramine.

Antidepressive Agents, Tricyclic↗
PubMed1998

Crime in Huntington's disease: a study of registered offences among patients, relatives, and controls.

OBJECTIVES: Criminal behaviour has been described as a problem in Huntington's disease, but systematic studies including control groups have been missing. Based on information from Danish registries, rates and types of crime committed by patients with Huntington's disease, non-affected relatives, and controls were studied. METHODS: 99 males and 151 females with Huntington's disease were compared with 334 non-affected first degree relatives (134 men and 200 women) and to matched control groups as to frequencies and types of registered criminal convictions. Due to specific age criteria, the group of relatives comprised only about 9% carriers of the gene coding for Huntington's disease. RESULTS: In male patients, crime rates were significantly increased compared with first degree relatives (RR=2.8) and controls (RR=2.3). All types of crime occurred more often in male patients; more severe crimes (murder, rape, arson) were not reported. Rates of drunken driving were significantly increased compared with relatives (RR=3.8) and controls (RR=7.1). Crime rates were neither increased in female patients nor in male and female first degree relatives. CONCLUSION: The results indicate increased prevalence of criminal behaviour in males carrying the gene for Huntington's disease. The crimes committed seem to be of relatively minor severity and are probably closely linked to the personality changes often seen as a result of the disease process, although depressive reactions to the disease, with secondary alcohol misuse, may also play a part. Environmental and familial factors shared by patients and non-affected at risk persons seem to be of less aetiological importance.

Adult↗
PubMed1998

Recurrence in affective disorder. I. Case register study.

BACKGROUND: In recent years, studies of the risk of recurrence in affective disorder in relation to the number of prior episodes have given contradictory results. METHOD: Survival analysis was used to calculate the rate of recurrence after successive episodes in a case register study including all hospital admissions with primary affective disorder in Denmark during 1971-1993. A total of 20,350 first-admission patients were discharged with a diagnosis of affective disorder, depressive or manic/cyclic type. RESULTS: The rate of recurrence increased with the number of previous episodes in both unipolar and bipolar disorder. Initially, the two types of disorders followed markedly different courses, but later in the course of the illness the rate of recurrence was the same for the two disorders. CONCLUSIONS: The course of severe unipolar and bipolar disorder seems to be progressive in nature despite the effect of treatment.

Adult↗
PubMed1997

Reduction of neuropeptide Y binding sites in the rat hippocampus after electroconvulsive stimulations.

Repetitive electroconvulsive stimulations (ECSs) increase neuropeptide Y (NPY) synthesis in hippocampal neurons, but whether NPY release and the density of NPY receptors are affected is unknown. In rats exposed to 14 daily ECSs, the concentration of NPY specific binding sites in hippocampal membranes was reduced by about 75% compared with sham, but was unchanged in membranes isolated from the cerebral cortex and the thalamus. In accordance with this, in vitro autoradiography revealed a similar reduction in binding in the dentate gyrus and the CA1 and CA3 regions, but not in the parietal cortex, the entorhinal cortex or the thalamus. These results show significant changes in NPY receptor binding after repeated ECSs, suggesting that NPYergic neurotransmission, most likely within the hippocampus, is strongly affected by ECSs.

Animals↗
PubMed1997

[Psychiatry].

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Denmark↗
PubMed1997

[Depression].

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Comorbidity↗
PubMed1997

Powerful inhibition of kainic acid seizures by neuropeptide Y via Y5-like receptors.

Neuropeptide Y (NPY) is widely distributed in interneurons of the central nervous system (CNS), including the hippocampus and cerebral cortex, in concentrations exceeding those of any other known neuropeptides. Sequence data comparing different species show that NPY is highly conserved. This suggests a critical role in regulation of regional neuronal excitability. Kainic acid, a glutamate agonist at kainic acid receptors, causes severe limbic motor seizures culminating in status epilepticus. We here report that NPY administered into the lateral ventricle is a powerful inhibitor of motor as well as electroencephalographic (EEG) seizures induced by kainic acid. This effect was mediated via receptors with a pharmacological profile similar to the recently cloned rat Y5 receptor. The present study is the first to demonstrate that NPY possesses anticonvulsant activity. This is consistent with the concept that NPY is an endogenous anticonvulsant and suggests that agonists acting at Y5-like receptors may constitute a novel group of drugs in antiepileptic therapy.

Animals↗
PubMed1996

Neuropeptide Y inhibits hippocampal seizures and wet dog shakes.

The effects of intracerebroventricular neuropeptide Y (NPY) or somatostatin were studied upon hippocampal EEG seizures elicited by electrical stimulation of the rat dentate gyrus or subiculum. At doses of 6 and 12 nmol, the latter dose being more effective, NPY reduced the primary afterdischarge duration (1.ADD) and almost completely abolished the secondary afterdischarge. The reduction in 1.ADD resulted from an increase in afterdischarge threshold. The reduction in secondary afterdischarge duration was independent of a reduction in 1.ADD. This implies that NPY not only exerts antiepileptiform effects in the dentate gyrus and subiculum, but also in areas to which epileptiform EEG activity spreads before reverberating. In addition, NPY strongly reduced seizure-related 'wet dog shakes' (WDS). This is consistent with previous studies showing that the dentate gyrus is essential for the generation of WDS. However, NPY inhibited WDS even when 1.ADDs were evoked which did not differ from those of vehicle rats, indicating extra-dentate inhibition by NPY as well. No effects were seen with somatostatin. These results show that NPY exerts antiepileptiform effects in vivo, suggesting that increased NPY in the hippocampal formation observed after seizures is a compensatory anti-seizure response.

Animals↗
PubMed1996

No loss of hippocampal hilar somatostatinergic neurons after repeated electroconvulsive shock: a combined stereological and in situ hybridization study.

Electrically induced seizures with anesthesia and muscle relaxation (ECT) is commonly used in the therapy of psychotic depression in humans. Unmodified electroshock (ECS) is used as a model for epilepsy in the rat. In several seizure models of epilepsy, in particular the dentate hilar somatostatin-containing (SSergic) neurons have been found to undergo degeneration. To assess the potential loss of SSergic hilar neurons after repeated ECS, 10 rats were given 110 ECS, one per day, 5 days a week. One day after the last ECS the rats were anesthesized, perfused, the brains cut on a vibratome and prepared for nonradioactive in situ hybridization for somatostatin along with five control rats. Like rats given 10-36 ECS in earlier studies, the ECS-treated rats displayed a markedly increased neuronal hybridization labeling when compared with control rats. The total number of dentate hilar SSergic neurons of each rat was estimated using the optical disector technique. The mean number of hilar SSergic neurons in the ECS-treated rats was 12,785, compared to 12,392 in the control rats. The total number of hilar SSergic neurons in ECS-treated versus control rats was not significantly different (Student's t test; t value = .35; p = .74). We conclude that repeated ECS treatment does not cause loss of hilar SSergic neurons.

Animals↗
PubMed1996

Prolonged induction of c-fos in neuropeptide Y- and somatostatin-immunoreactive neurons of the rat dentate gyrus after electroconvulsive stimulation.

Induction of c-fos mRNA and Fos was studied in the hilus and granular layer of the dentate gyrus at various times up to 24 h after single electroconvulsive stimulation (ECS) using in situ hybridization and immunocytochemistry. In both areas of the dentate gyrus, a prominent induction of c-fos mRNA and Fos was observed. Compared to the granular layer, however, c-fos mRNA and Fos in hilar cells reached maximum later and remained elevated considerably longer. Several neurochemically distinct populations of hilar neurons have been described, some of which contain neuropeptide Y (NPY) and/or somatostatin (SS). Using double-labelling immunocytochemistry, we examined to what extent Fos was induced in these hilar neurons after ECS. Although a minor population of non-NPY non-SS cells displayed Fos induction early after ECS, prolonged induction of Fos almost exclusively occurred in NPY or SS neurons. The Fos-immunoreactive NPY or SS neurons only amounted to about 50% of the total hilar population of NPY or SS neurons. The present observations suggest that a subpopulation of hilar NPY and SS neurons may be central to the actions of electroconvulsive seizures in the dentate gyrus.

Animals↗
PubMed1996

[Abnormal neurological findings at first admission in patients with schizophrenia or schizophreniform disorders. Results of computer tomography and measurement of regional cerebral blood flow].

Forty-five patients with schizophrenia or schizophreniform disorder admitted to hospital for the first time had a neurological examination, including integrative sensory and complex motor acts, by a trained neurologist. The patients were studied by CT and regional cerebral blood flow as well. A control group of 24 healthy volunteers was included. The patients had significantly more neurological abnormalities (NA) than the healthy volunteers. Medication did not explain the discrepancy. The NA were associated with sulcal enlargement and smaller brains as visualized by CT but not with ventricular enlargement. There was no association between the regional flow values and NA.

Adolescent↗
PubMed1996

Synaptic degeneration and remodelling after fast kindling of the olfactory bulb.

Kindling of the olfactory bulb using a novel fast protocol (within 24 h) was studied in rats. In target brain regions, the effects of kindling were measured on the concentration of glial fibrillary acidic protein (GFAP) by dot-blot and on the concentrations of neural cell adhesion molecule (NCAM) and the 25 kDa synaptosomal associated protein of the D3 immunoprecipitate (D3(SNAP-25)) by crossed immunoelectrophoresis. Bilateral increases in the levels of GFAP, indicating activation of astrocytes, were detected in primary olfactory cortical projection areas, including the piriform cortex, and also in the basolateral amygdala and dentate gyrus, suggesting that these regions may be functionally altered during the kindling process. In the piriform cortex and dentate gyrus increased NCAM/D3(SNAP-25) ratios found ipsilaterally at seven days after kindling probably reflect an elevated rate of synaptic remodelling. At this time, however, an overall pattern of ipsilateral decreases in the synaptic marker proteins NCAM and D3(SNAP-25) indicated that this remodelling occurred on a background of synaptic degeneration. These results confirm previous studies showing that kindling is associated with synaptic remodelling and neuronal degeneration in the hippocampal formation and extends the area of plasticity to include the piriform cortex which is believed to be central to the kindling process.

Animals↗
PubMed1996

No loss of somatostatin-immunoreactive neurons in the hippocampal dentate hilus of alcohol-withdrawal-kindled rats.

The neuropeptide somatostatin has been suggested to play a role in seizure genesis, electrical kindling and the neurotoxic effects of alcohol. The purpose of the present experiment was to study somatostatin-immunoreactive (SS-IR) neurons in hippocampus during alcohol-withdrawal kindling. Alcohol-withdrawal kindling was performed by subjecting male Wistar rats to seven weekly episodes consisting of 2 days of severe alcohol intoxication and 5 days of alcohol withdrawal. Then the kindled animals (multiple withdrawal group) and a single withdrawal group, which was fed isocalorically with the kindled animals during episodes 1-7, were exposed to 4 days of severe alcohol intoxication (episode 8). During the following withdrawal, the seizure activity was observed 9-15 h after last alcohol dose, in order to subdivide the animals from these two groups into groups with and without seizures. Subsequently, SS-IR neurons were visualized immunocytochemically and counted in the hilus of the dentate gyrus (hippocampus). The number of SS-IR neurons per unit area of the hilus was neither affected by a single nor by multiple episodes of alcohol withdrawal. We therefore concluded that a loss of these neurons is not involved in the development of alcohol-withdrawal-kindled seizures.

Alcohol Withdrawal Delirium↗