Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CATATONIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2000

Splitting schizophrenia: periodic catatonia-susceptibility locus on chromosome 15q15.

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.

Catatonia↗
PubMedDate not supplied

Consistency of symptoms in recurrent catatonia.

This study examined the consistency of symptom profiles across episodes of catationia. A recently developed standardized examination and symptom scale systematically rates 23 motor signs of catatonia, permitting symptom analysis of recurrent illness. Patients from the emergency room or inpatient unit were prospectively examined using the 23-item Bush-Francis Catatonia Rating Scale (BFCRS), both on initial presentation and during a later episode of catatonia. Five cases were identified, with a variable interval (mean, 10.7 months; range 4.5 to 20) between episodes. All five met DSM-IV motor criteria for catatonia (293.89) and research criteria of more than two BFCRS signs. They showed a mean of 9.6 (range, 7 to 15) catatonic signs in the first episode, and 9.6 (range, 4 to 14) signs in the second. Of the 23 individual BFCRS motor signs, a mean of 16.6 (range, 13 to 21) showed agreement of signs (absence or presence) between the two episodes. The catatonic syndrome shows consistency of motor symptoms on recurrent episodes and the BFCRS facilitates the systematic study of catatonia.

Adult↗
PubMed1992

Catatonia on the consultation-liaison service.

Catatonia is a syndrome that requires both nonpsychiatric medical and psychiatric evaluation. The authors report on six patients with catatonia that were seen by a psychiatric consultation-liaison service. Five of these patients had medical conditions reported to cause catatonia. Treatment recommendations included the following: 1) subcutaneous heparin for deep venous thrombosis prophylaxis, 2) a trial of lorazepam, and 3) transfer to a medical/psychiatric unit or locked psychiatric unit. Catatonia was most parsimoniously attributed to the primary psychiatric illness in five of the patients and to corticosteroid treatment in the sixth patient. These findings suggest that clinicians should use the proposed criteria, past psychiatric history, physical exam, and laboratory and radiological studies when evaluating patients with symptoms of catatonia.

Adrenal Cortex Hormones↗
PubMed2006

Towards a valid nosography and psychopathology of catatonia in children and adolescents.

Paraphrasing Taylor and Fink (2003), catatonia needs "a home of its own" in child and adolescent psychiatry. Limited but expanding literature supports that catatonia in children and adolescent can be identified reliably among other childhood conditions, is sufficiently common, treatable with the same specific treatments as adult catatonia (e.g., sedative drugs and electroconvulsive therapy), and can be worsened by other treatments (e.g., antipsychotics). Other findings in child and adolescent catatonia suggest that sex ratio and associated disorders may differ, and the proposed classification of Taylor and Fink (2003) needs modification. Adopting a broader diagnostic schedule may accommodate both child, adolescent, and adult catatonia. A psychomotor automatism variant should be included as a diagnosis, as well as specifiers for associated disorders such as acute nonpsychotic anxious state and pervasive developmental disorder. Duration of illness should be specified as acute or chronic. Regardless of associated psychiatric disorders, this chapter describes a new psychopathological model. Three main modalities of movement dysfunction in catatonic subjects are listed: (1) adherence to delusional ideas leading to a psychomotor automatism (De Clérambault, 1927); (2) resistance to delusional thinking or conviction; and finally (3) hyperanxious states. Case-vignettes illustrate the model, and future research directions are identified.

Adolescent↗
PubMed2002

What catatonia can tell us about "top-down modulation": a neuropsychiatric hypothesis.

Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called "conflict of paradigms." Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting "horizontal modulation" of cortico-cortical relation. Furthermore, alteration in "top-down modulation" reflecting "vertical modulation" of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered "bottom-up modulation" between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation--"vertical" and "horizontal" modulation, respectively.

Affective Symptoms↗
PubMed1983

Rat brain sites responsive to etorphine: analgesia and catatonia.

One hundred forty-two rats given intracerebral microinjections of 1 microgram of etorphine hydrochloride were observed for subsequent analgesia (flinch-jump technique) and catatonia (bar test). Neuroanatomical specificity of effect was demonstrated to the extent that behavioral effects did not result from injections into areas of low opiate receptor binding affinity, such as medial cerebral cortex and hippocampus, nor were positive results obtained from injections into fiber bundles, such as the corpus callosum and internal capsule. Positive results were obtained in a large number of areas, ranging from brain stem to telencephalon. Injections eliciting analgesia without catatonia were limited in number (9 animals) and were widely scattered throughout neuroanatomical loci. Microinjection more frequently elicited catatonia only (29 animals), and site of injection was limited to posterior cerebral cortex, posterior amygdala, dorsal reticular formation, and cerebral aqueduct. Dual behavioral effects were elicited in 28 of the animals and occurred most frequently upon injection into the periaqueductal gray, inferior colliculus, and cerebral aqueduct. (Injection into cerebral aqueduct produced 50% catatonia only and 50% dual effects). The study suggests that opiate-elicited analgesia and catatonia may be neuroanatomically distinct phenomena.

Animals↗
PubMed2004

"Scared stiff": catatonia as an evolutionary-based fear response.

Catatonia, long viewed as a motor disorder, may be better understood as a fear response, akin to the animal defense strategy tonic immobility (after G. G. Gallup & J. D. Maser, 1977). This proposal, consistent with K. L. Kahlbaum's (1874/1973) original conception, is based on similarities between catatonia and tonic immobility ("death feint") as well as evidence that catatonia is associated with anxiety and agitated depression and responds dramatically to benzodiazepines. It is argued that catatonia originally derived from ancestral encounters with carnivores whose predatory instincts were triggered by movement but is now inappropriately expressed in very different modern threat situations. Found in a wide range of psychiatric and serious medical conditions, catatonia may represent a common "end state" response to feelings of imminent doom and can serve as a template to understand other psychiatric disorders.

Animals↗
PubMed2003

Incidence of catatonia in children and adolescents in a paediatric psychiatric clinic.

OBJECTIVE: To investigate the incidence and phenomenology of catatonia in a child and adolescent population. METHOD: Children and adolescents who had attended a paediatric psychiatric outpatient clinic between April and July 2001 were examined for catatonic signs with a formal catatonia rating scale, and patients who had at least two catatonic signs were included. RESULTS: Eleven patients met the criteria (5.5% of the entire sample and 17.7% of the patients with affective and nonaffective psychotic disorder); of them eight had an affective disorder and three a nonaffective disorder. The mean catatonic scores were significantly high for males and patients with mental retardation. CONCLUSION: This study shows that catatonia occurs in children and adolescents. Further studies are essential to clarify the distribution of catatonia across various diagnoses and the outcome of paediatric catatonia.

Adolescent↗
PubMed2001

Kahlbaum's catatonia revisited.

Modern psychiatric nosologies separate catatonia along the lines of presumed etiology: bipolar, major depression, schizophrenia and due to a general medical condition. The presence of catatonia has always held diagnostic and prognostic value. Kahlbaum's description of catatonia includes careful documentation of phenomenology and the course of the illness. Since there were no effective treatments in his time, Kahlbaum was documenting the natural history of the illness. A review of classic studies of the natural history of catatonia demonstrates that the syndrome is episodic, may have few other psychotic signs, may have periods of remission and may, in some cases, be associated with the disorganized subtype of schizophrenia. The literature of the past 100 years supports the validity of Kahlbaum's description for a subset of patients with catatonia.

Bipolar Disorder↗
PubMed1995

Catatonia mimicking nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) and catatonia share many clinical features and distinguishing between them on the basis of the physical examination may be difficult and even impossible. Although several reports have been made of NCSE simulating catatonia, there are no published cases of catatonia mimicking NCSE. We report a 24-year-old woman whose initial examination was notable for a fixed stare, no response to voice or command, gaze preference, tonic head posturing, constant stereotypic chewing movements, profuse foamy salivation, and dramatic response to the parenteral administration of benzodiazepines (BZDs). She was initially misdiagnosed as having NCSE. EEG, however, was normal. We believe this is the first published report of catatonia simulating NCSE. The EEg may be more useful than the clinical examination in distinguishing NCSE from catatonia.

Adult↗
PubMed1996

Catatonia. I. Rating scale and standardized examination.

To facilitate the systematic description of catatonic signs, we developed a catatonia rating examination, rating scale and screening instrument. We constructed a 23-item rating scale and a truncated 14-item screening instrument using operationalized definitions of signs ascribed to catatonia in published sources. Inter-rater reliability was tested in 44 simultaneous ratings of 28 cases defined by the presence of > or = 2 signs on the 14-item screen. Inter-rater reliability for total score on the rating scale was 0.93, and mean agreement of items was 88.2% (SD 9.9). Inter-rater reliability for total score on the screening instrument was 0.95, and mean agreement of items was 92.7% (SD 4.9). Diagnostic agreement was high based on criteria for catatonia put forth by other authors. Seven per cent (15/215) of consecutively admitted patients to an academic psychiatric in-patient facility met criteria for catatonia. It is concluded that catatonia is a distinct, moderately prevalent neuropsychiatric syndrome. The rating scale and screening instrument are reliable and valid. Their use facilitates diagnosis, treatment protocols, and cross-study comparisons.

Catatonia↗
PubMed1996

Catatonia. II. Treatment with lorazepam and electroconvulsive therapy.

Case material and retrospective studies support the use of both lorazepam and ECT in treating catatonia, but few prospective investigations exist and none employ quantitative monitoring of response. In this study we test their efficacy in an open, prospective protocol, and define a "lorazepam test' with predictive value for treatment. Twenty-eight patients with catatonia were treated systematically with parenteral and/or oral lorazepam for up to 5 days, and with ECT if lorazepam failed. Outcome was monitored quantitatively during the treatment phase with the Bush-Francis Catatonia Rating Scale (BFCRS). In 16 of 21 patients (76%) who received a complete trial of lorazepam (11 with initial intravenous challenge), catatonic signs resolved. A positive response to an initial parenteral challenge predicted final lorazepam response, as did length of catatonic symptoms prior to treatment. Neither demographic variables nor severity of catatonia predicted response to lorazepam. Four patients failing lorazepam responded promptly to ECT. It is concluded that lorazepam and ECT are effective treatments for catatonia. The rating scale has predictive value and displays sensitivity to change in clinical status.

Adult↗
PubMed1999

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

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.

Adult↗
PubMed1974

The mechanism of the potentiating effect of antidepressant drugs on the protective influenc oe of diphenhydramine in experimental catatonia. The role of histamine.

The anticatatonic action of various antidepressants in moderate doses and their combination with sub-effective doses of diphenhydramine was correlated with brain histamine levels. The catatonia was induced by perphenazine with a concomitant and remarkable increase in the brain histamine level. Diphenhydramine partially protected the animals from the increase in brain histamine and mitigated the catatonia. The antidepressants, i.e. monoamine oxidase inhibitors and tricyclic antidepressants, partially protected animals both the increase in brain histamine and also the catatonia. The tricyclic antidepressants were, however, found to be more potent in both respects. The combination of sub-effective doses of monoamine oxidase inhibitors and diphenhydramine was effective in terminating experimental catatonia and the elevation of brain histamine while tricyclic antidepressants failed. A relationship between the duration of protection against catatonia and brain histamine level due to antidepressants alone and their combination with diphenhydramine was observed.

Animals↗
PubMed1999

Progressive catatonia.

We present the case of a young man with a diagnosis of a childhood-onset pervasive developmental disorder who developed a progressive neurologic deterioration with persistent catatonia and right hemiparesis. On his initial evaluation approximately three years after the onset of mutism, he manifested right hemiparesis and catalepsy. Two years later, although catalepsy had subsided, motor function had deteriorated so that he could not use his hands to feed or dress himself. Oral-facialbuccal dyskinesia manifested by blepharospasm and grimacing were present constantly during waking hours. Quantitative electroencephalography demonstrated markedly decreased amplitude, a finding associated with catatonia. Left sural nerve biopsy indicated large axon cylinder degeneration. Left deltoid biopsy demonstrated perimysial fibrosis and type II fiber predominance. Although magnetic resonance imaging of the head without contrast was normal, positron emission tomography indicated hypometabolism of the right cerebral and the right cerebellar hemispheres. The patient continues to deteriorate despite a course of 25 electroconvulsive treatments. He continues to manifest criteria for catatonia including motoric immobility, mutism, and peculiarities of voluntary movement such as prominent grimacing. We suspect an inherited neurodegenerative disorder. Since catatonia is a treatable condition frequently associated with medical and neurological diseases, examination for the features of catatonia must be included in the assessment of patients with progressive brain degeneration. This report is an attempt to clarify the traits of a serious variant of progressive brain degeneration.

Activities of Daily Living↗
PubMedDate not supplied

Suppression of catatonia-like signs by lorazepam in nonconvulsive status epilepticus without seizure termination.

Nonconvulsive status epilepticus (NCSE) cannot be reliably distinguished from catatonia by signs or symptoms. The authors report on a 68-year-old man with endogenous major depression who displayed catatonia-like psychopathology, which temporarily disappeared with lorazepam. An EEG then revealed NCSE. Presumably, lorazepam suppressed seizure in areas where it had caused clouding of consciousness, but it did not suppress all seizure activity. When lorazepam was stopped, the catatonia-like delirium returned; it disappeared again with valproate administration. This case illustrates that the reduction of signs consistent with catatonia by benzodiazepines does not by itself confirm catatonia, even in patients with endogenous depression.

Aged↗
PubMedDate not supplied

[Catatonia de novo, report on a case: immediate vital prognosis and psychiatric prognosis in longer term].

We report on the case of a 20 year old woman with no previous psychiatric history, who displayed a first episode of catatonia with acute onset. Symptoms started plainly with sudden general impairment, intense asthenia, headache, abdominal pain and confusion. After 48 hours, the patient was first admitted to an emergency unit and transferred to an internal medicine ward afterwards. She kept confused. Her behaviour was bizarre with permanent swinging of pelvis, mannerism, answers off the point and increasingly poor. The general clinical examination was normal, except for the presence of a regular tachycardia (120 bpm). The paraclinical investigations also showed normal: biology, EEG, CT Scan, lumbar puncture. Confusion persisted. The patient remained stuporous, with fixed gazing and listening-like attitudes. She managed to eat and move with the help of nurses but remained bedridden. The neurological examination showed hypokinaesia, extended hypotonia, sweating, urinary incontinence, bilateral sharp reflexes with no Babinski's sign and an inexhaustible nasoorbicular reflex. The patient was mute and contrary, actively closed her eyes, but responded occasionally to simple instructions. For short moments, she suddenly engaged in inappropriate behaviors (wandering around) while connecting back to her environment answering the telephone and talking to her parents. The patient's temperature rose twice in the first days but with no specific etiology found. During the first 8 days of hospitalization, an antipsychotic treatment was administered: haloperidol 10 mg per os daily and cyamemazine 37.5 mg i.m. daily. Despite these medications, the patient worsened and was transferred to our psychiatric unit in order to manage this catatonic picture with rapid onset for which no organic etiology was found. On admission, the patient was stuporous, immobile, unresponsive to any instruction, with catalepsy, maintenance of postures, severe negativism and refusal to eat. A first treatment by benzodiazepine (clorazepate 20 mg i.v.) did not lead to any improvement. The organic investigations were completed with cerebral MRI and the ruling out of a Wilson's disease. Convulsive therapy was then decided. It proved dramatically effective from the first attempt; 4 shocks were carried out before the patient's relatives ask for her discharge from hospital. The patient revealed she had experienced low delirium during her catatonic state. The clinical picture that followed showed retardation with anxiety. She was scared with fear both for the other patients and the nursing team. She kept distant and expressed few affects. The treatment at the time of discharge was olanzapine 10 mg per os. She was discharged with a diagnosis of catatonia but with no specific psychiatric etiological diagnosis associated. She discontinued her follow-up a few weeks later. After one year, we had no information about her. Catatonia has now become rare but remains a problem for clinicians. We reviewed data concerning short term vital prognosis and psychiatric long term prognosis in catatonia. Lethal catatonia is associated with acute onset, both marked psychomotor and neurovegetative symptoms. In the light of literature, there is no proband clinical criterion during the episode that is of relevant diagnostic value to ascertain the psychiatric etiology.

Acute Disease↗
PubMed1994

Lorazepam treatment of acute and chronic catatonia in two mentally retarded brothers.

BACKGROUND: Acute catatonia of the retarded type responds rapidly to treatment with lorazepam. There is little information about (1) the efficacy of benzodiazepines in patients with longstanding catatonic syndrome; (2) the effect of longer-term lorazepam therapy in catatonic patients who do not respond to a brief trial of the medication; and (3) the development of catatonic syndromes in family members. METHOD: We gave lorazepam to two mentally retarded brothers with catatonia. One had become catatonic 2 weeks before starting treatment while the other had been hospitalized in a catatonic state for 5 years. RESULTS: The brother with acute catatonia recovered slowly but completely within 2 weeks of starting lorazepam. The brother with long-standing catatonia responded gradually during the first 5 months of treatment and required higher doses of lorazepam but did eventually recover and was discharged from the hospital on a regimen of lorazepam after 1 year of treatment. CONCLUSION: (1) Lorazepam may be effective even in patients who have been catatonic for years. (2) Catatonic patients who do not recover immediately with lorazepam may respond to a longer course or higher doses of the medication. (3) There may be a familial predisposition to developing catatonia in response to stressful situations.

Adult↗