Decreased density of GABA-A receptors in the left sensorimotor cortex in akinetic catatonia: investigation of in vivo benzodiazepine receptor binding. (1/47)

OBJECTIVES: Catatonia is a psychomotor syndrome with concomittant akinesia and anxiety which both respond almost immediately to benzodiazepines such as lorazepam. The benzodiazepine receptor distribution was therefore investigated in akinetic catatonia with single photon emission tomography (SPECT) using iodine-123-iomazenil ((123) I Iomazenil). METHODS: Ten akinetic catatonic patients, 10 psychiatric controls (similar age, sex, medication, and underlying psychiatric diagnosis but without catatonic syndrome), and 20 healthy controls were investigated with SPECT 2 hours after injection of (123) I Iomazenil. To exclude potential effects of cerebral perfusion (r-CBF) r-CBF was additionally investigated with Tc-99mECD SPECT. RESULTS: Catatonic patients showed significantly lower iomazenil binding and altered right-left relations in the left sensorimotor cortex compared with psychiatric (p<0.001) and healthy (p<0.001) controls. In addition, there was significantly lower r-CBF in the right lower prefrontal and parietal cortex in catatonia whereas in the left sensorimotor cortex no differences in r-CBF between groups were found. Catatonic motor and affective symptoms showed significant correlations (p<0.05) with benzodiazepine binding in the left sensorimotor cortex as well as with right parietal r-CBF. CONCLUSIONS: Reduced iomazenil binding suggests decreased density of GABA-A receptors in the left sensorimotor cortex in akinetic catatonia. In addition to reduced GABA-A receptor density in the left sensorimotor cortex the parietal cortex seems to be involved in pathophysiology of catatonic symptoms. It is concluded that, considering results from correlation analyses, both emotional and motor symptoms in catatonia seem to be closely related to left sensorimotor and right parietal alterations.  (+info)

Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal. (2/47)

To describe ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal. Ictal catatonia was documented by concurrent EEG recordings. A catatonic syndrome, first diagnosed as a psychogenic reaction, was found to be an ictal event by EEG recording. De novo absence status and benzodiazepine withdrawal should be considered when a catatonic syndrome suddenly occurs in elderly patients.  (+info)

Catatonia in autistic spectrum disorders. (3/47)

BACKGROUND: The clinical pictures of autistic spectrum disorders include features described in catatonia. AIMS: To examine the severe exacerbation of the catatonic features of autistic disorders in adolescence or early adult life, which occurs in some individuals. METHOD: A semi-structured interview schedule was used to collect information from parents or other care-givers concerning 506 referrals to a specialist clinic for autistic spectrum disorders. Individuals with severe exacerbation of catatonic features were compared with a same-age group of referrals without this type of deterioration in skills and behaviour. RESULTS: Seventeen per cent of referrals aged 15 or over had severe exacerbation of catatonic features. They were significantly more likely than the comparison group to have had, before the onset of the change in behaviour, impaired language and passivity in social interaction. CONCLUSIONS: Catatonia is a later complication of autistic spectrum disorders, which adds considerably to the burden of caring. More research is needed to identify causes, neuropathology, and early signs of vulnerability.  (+info)

Inter-ictal and post-ictal psychoses in frontal lobe epilepsy: a retrospective comparison with psychoses in temporal lobe epilepsy. (4/47)

There have been few studies of the psychopathology of patients with frontal lobe epilepsy (FLE). The majority of studies of both inter-ictal and post-ictal psychoses have strongly suggested the influence of temporal lobe disturbance on psychoses. Patients with organic brain damage or schizophrenia, however, sometimes show frontal lobe dysfunction. The purpose of this study was to better understand the effect, if any, of frontal lobe disturbance and seizure on psychopathology. Patients were divided into four groups based on epilepsy type and preceding seizures; 8 with FLE/inter-ictal psychosis, 3 with FLE/post-ictal psychosis, 29 with temporal lobe epilepsy (TLE)/inter-ictal psychosis, and 8 with TLE/post-ictal psychosis. Psychopathologic symptoms were retrospectively reviewed based on case notes, using a modified brief psychiatric rating scale (BPRS). Psychomotor excitement, hostility, suspiciousness, and hallucinatory behaviour were prominent features in all four groups. Six orthogonal factors were derived by factor analysis from the original data based on the 18 BPRS items. FLE patients with inter-ictal psychosis showed marked hebephrenic characteristics (i.e. emotional withdrawal and blunted effect). Our findings suggest that patients with FLE can exhibit various psychiatric symptoms. However, their psychotic symptoms, hebephrenic symptoms in particular, may often be overlooked.  (+info)

Splitting schizophrenia: periodic catatonia-susceptibility locus on chromosome 15q15. (5/47)

The nature of subtypes in schizophrenia and the meaning of heterogeneity in schizophrenia have been considered a principal controversy in psychiatric research. We addressed these issues in periodic catatonia, a clinical entity derived from Leonhard's classification of schizophrenias, in a genomewide linkage scan. Periodic catatonia is characterized by qualitative psychomotor disturbances during acute psychotic outbursts and by long-term outcome. On the basis of our previous findings of a lifetime morbidity risk of 26.9% of periodic catatonia in first-degree relatives, we conducted a genome scan in 12 multiplex pedigrees with 135 individuals, using 356 markers with an average spacing of 11 cM. In nonparametric multipoint linkage analyses (by GENEHUNTER-PLUS), significant evidence for linkage was obtained on chromosome 15q15 (P = 2.6 x 10(-5); nonparametric LOD score [LOD*] 3.57). A further locus on chromosome 22q13 with suggestive evidence for linkage (P = 1.8 x 10(-3); LOD* 1.85) was detected, which indicated genetic heterogeneity. Parametric linkage analysis under an autosomal dominant model (affecteds-only analysis) provided independent confirmation of nonparametric linkage results, with maximum LOD scores 2.75 (recombination fraction [theta].04; two-point analysis) and 2.89 (theta =.029; four-point analysis), at the chromosome 15q candidate region. Splitting the complex group of schizophrenias on the basis of clinical observation and genetic analysis, we identified periodic catatonia as a valid nosological entity. Our findings provide evidence that periodic catatonia is associated with a major disease locus, which maps to chromosome 15q15.  (+info)

ACUTE CATATONIC REACTION OF ADOLESCENCE. (6/47)

In a study of 21 cases of catatonic schizophrenic reaction of adolescence, sexual conflict situations and stern religious orientation of the family were noted in most cases. Incest was a factor in four of the female patients and masturbatory guilt was a prominent reaction in the remainder. Sex education was mostly misinformation and threats of dire consequences for sexual activity. Fourteen of the cases involved broken homes for significant periods of childhood or adolescence. It was hypothesized that sexual conflict situations grew out of incompatible socio-cultural attitudes and normal adolescent psychological and physiological drives. We formulated the "defined body contact" technique as a means of facilitating the reversal of the catatonic behavior, which we saw as the primary device whereby the patient limited physical contacts. The contacts we used in this technique were defined explicitly and implicitly as non-sexual.The catatonic symptoms remitted in days to several weeks in 13 of the cases. Seven patients required electroshock therapy. Twenty of the 21 patients returned to their homes or to non-institutional residences. The length of hospitalization was materially influenced by the degree of readiness of the outside environment to accept the returnee.  (+info)

ACTIONS OF PROSTAGLANDINS E1, E2 AND E3 ON THE CENTRAL NERVOUS SYSTEM. (7/47)

Prostaglandins E(1), E(2) and E(3), injected into the cerebral ventricles of unanaesthetized cats, produced sedation, stupor and signs of catatonia. The threshold dose was 3 mug/kg. Slight sedation was also observed following an intravenous injection, but a dose of 20 mug/kg was required. In chicks, intravenous injections of prostaglandins (10 to 400 mug/kg) caused respiratory depression, profound sedation, loss of normal posture and, with the higher doses, loss of the righting reflex.  (+info)

SOME PHARMACOLOGICAL PROPERTIES OF THIOPROPERAZINE AND THEIR MODIFICATION BY ANTI-PARKINSONIAN DRUGS. (8/47)

The pharmacological properties of a phenothiazine derivative thioproperazine have been compared with those of chlorpromazine, and the modifications by some anti-Parkinsonian drugs of its actions on the central nervous system have been studied. Thioproperazine was less potent than chlorpromazine in lowering blood pressure and antagonizing adrenaline in the cat, in depressing respiratory rate in the rabbit, in producing hypothermia and analgesia and in reducing the minimum anaesthetic dose of hexobarbitone in mice, and in protecting rats from convulsions induced by tryptamine. It was roughly equipotent to chlorpromazine in reducing locomotor activity of mice. Thioproperazine was more potent than chlorpromazine in protecting grouped mice from the acute toxicity of dexamphetamine, in preventing the acute behavioural disturbances produced by dexamphetamine in the rat, in producing a state of experimental catatonia in the rat and in preventing the emetic action of apomorphine in the dog. Hyoscine, benztropine or promethazine greatly reduced the ability of thioproperazine to prevent behavioural changes due to dexamphetamine in the rat and also abolished symptoms of experimental catatonia produced by thioproperazine. In contrast, the antiapomorphine activity of thioproperazine in the dog was not reduced to any extent by hyoscine or benztropine.  (+info)

• 1
• 2
• 3
• 4
• 5
• 6