Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Stupor”

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 19 recordsLinked to original sources
PubMed1998

Endozepine stupor. Recurring stupor linked to endozepine-4 accumulation.

Recurring stupor can be caused by repeated metabolic, toxic or structural brain disturbances. Recently, cases of recurring stupor, with fast EEG activity were shown to display increased endogenous benzodiazepine-like activity during the episodes of stupor. Patients with recurring stupor underwent extensive metabolic and toxicologic screening, EEG and brain imaging. Endozepines and exogenously administered benzodiazepines were assayed in plasma and CSF by means of mass spectrometry. Flumazenil, a benzodiazepine antagonist was administered and the behavioural and EEG responses monitored. Treatment with oral flumazenil was attempted in selected cases. Twenty patients were found with recurring stupor. Episodes had begun between ages 18 and 67 years, and in nine patients, had disappeared spontaneously after 4-6 years with symptoms. Stupor lasted hours or days. Onset of the episodes and frequency were unpredictable. Patients were normal between attacks. Stupor was characterized by initial drowsiness, staggering and behavioural changes, followed by deep sleep and spontaneous recovery with post-ictal amnesia. Biochemical screening and brain imaging were always normal. Ictal EEG showed fast background activity, and flumazenil transiently awoke the patients and normalized the EEG. In the nine cases examined, endozepine-4 levels were increased during the stupor. Oral flumazenil reduced the frequency of the attacks in three of these nine patients. Recurring episodes of stupor may be due to increased endozepine-4. We propose the term 'endozepine stupor' for such episodes. Endozepine-4 is an endogenous ligand for the benzodiazepine recognition site at the GABAA receptor, with unknown molecular structure.

Adult↗
PubMed1997

Deep venous thrombosis of the leg due to psychiatric stupor.

We report the cases of two patients with psychiatric stupor who developed venous thrombosis. A 29-year-old schizophrenic woman had been hospitalized in psychiatric institutions three times because of stupor associated with auditory hallucinations and thought blocking. These symptoms recurred and she was admitted to our hospital with deep venous thrombosis of her left leg. The other patient was a 67-year-old woman with depression. She had also suffered from insomnia. Following admission to our hospital, she developed a depressive stupor complicated by deep venous thrombosis of her left leg. Both cases were treated with sodium heparin and urokinase, and completely resolved. It is well known that dehydration, infection and decubitus ulcers are important physical complications of psychiatric stupor, but there have been few reports of deep venous thrombosis as a physical complication of stupor.

Adult↗
PubMed1982

Stuporous episodes during treatment with sodium valproate: report of seven cases.

Of 13 patients with complex partial seizures who experienced stuporous states during treatment with sodium valproate (VPA), 4 received VPA only, 4 VPA and phenobarbital (PB) and 5 VPA, PB, and a third anticonvulsant. Seven cases were described in detail. Side effects-stupor or confusion-appeared a few days after efficacious drug plasma levels were attained, persisted until therapy was readjusted, and disappeared 24 to 72 h after VPA withdrawal. Therapeutic trials established the role of VPA in the onset of stuporous states. The adverse effects of VPA were potentiated by the concomitant administration of other anticonvulsants. Stupor was not due to VPA overdoses, and plasma concentration of the drugs were not correlated with the electroclinical signs. The EEG showed spike and wave discharges or continuous sharp theta and delta waves persisting during VPA treatment. The fact that all 13 stuporous, VPA-treated patients were subjected to partial seizures with complex symptomatology, and none were cases of generalized epilepsy, together with the observations that the disturbances of consciousness started with focal symptoms and EEG signs resembling those of spontaneously occurring partial seizures, suggest that VPA given alone or in association with other antiepileptics has a paradoxical epileptogenic effect in certain forms of epilepsy.

Anticonvulsants↗
PubMed1992

Is stupor by itself a catatonic symptom?

Many patients present with stupor or substupor without classical catatonic signs as described by Kahlbaum. The phenomenological literature is not clear as to whether stupor, when it presents alone, constitutes a separate syndrome or is a forme fruste of catatonia. All patients who presented with stupor, (a) partial or total mutism or (b) absent or decreased motor responses (n = 22), were compared with patients who also had classical catatonic signs such as negativism or waxy flexibility (n = 43) over a one-year period (1988), on sociodemographic and clinical variables. There were very few significant differences between the two groups (age, sex, diagnosis, duration of illness, number of ECTs required). The stupor group had a slight excess of patients with manic-depressive psychosis, depression and more frequently positive family histories of mental illness. The current study provides a tentative support to the hypothesis that stupor is a catatonic sign, and even when present alone can be considered to constitute a catatonic syndrome.

Adult↗
PubMed1981

Unusual 'spike-wave stupor' in a patient with manic-depressive psychosis treated with amitriptyline.

'Spike-wave stupor' was observed in a 58-year-old male patient with manic-depressive psychosis. Almost continuous atypical spike-wave activity was seen in conjunction with a stuporous episode with stereotyped automatism. Intravenous diazepam ended both the electroencephalographic epileptiform discharges and the clinical stupor. Before and during this episode the patient was treated with an average-dose amitriptyline monotherapy. There was no family history of epileptic seizures. The patient had had electroconvulsive therapy. The history suggests that the analeptic property of amitriptyline induced the 'spike-wave stupor' in this patient.

Action Potentials↗
PubMed1991

A case of epilepsy characterized by spike-wave stupor followed for long period.

A 34-year-old housewife with nonconvulsive status epilepticus was followed up for 20 years since the initial fit. She maintained some contact with reality during the stupor and recalled the episode to some extent, while the EEG showed continuous spike-wave complexes. During the clinical course, the main type of seizures was spike-wave stupor, of which the maximum frequency was several times a week in the hospital and the duration was many minutes to several hours, and also secondarily generalized convulsive seizures occurred approximately once a month. The lasting control of spike-wave stupor was not achieved in spite of the various medications for the long follow-up period. The ictal EEGs of spike-wave stupor always showed the frontal origin. The meaning of the term "nonconvulsive status epilepticus" in this case was briefly discussed.

Adult↗
PubMed1996

Effective electroconvulsive therapy for stupor in the high risk patient: a report of two cases.

We report two cases of stupor in which the patients were safely treated by electroconvulsive therapy (ECT) despite high risk conditions. Case 1 was a 72 year old schizophrenic woman who had developed catatonic stupor and had joint contractures as a complication of rheumatoid arthritis. Case 2 was a 52 year old woman who developed a stuporous state which was complicated by severe dehydration with hypernatremia. In both cases, psychotic symptoms were improved by ECT without event. Careful application of ECT seemed to be effective and safe even for stupor in high risk patients.

Aged↗
PubMed1979

Stupor following administration of valproic acid to patients receiving other antiepileptic drugs.

Stupor is an unusual complication following the addition of valproic acid to other antiepileptic drugs. We report four such cases. Stupor occurred acutely in 3 patients and insidiously in the fourth. In the cases of acute toxicity, neither toxic levels of valproate nor significant elevations in blood levels of the other drugs occurred. In the fourth patient, stupor occurred concomitantly with a rise in the phenobarbital level. The electroencephalograms of all 4 patients revealed generalized high-amplitude rhythmic bisynchronous delta activity. Recovery occurred following discontinuation of valproic acid or other antiepileptic drugs. These observations suggest that stupor may occur as a result of drug interactions after the addition of valproic acid to other antiepileptic drugs.

Adolescent↗
PubMed1978

[Treatment of reactive stuporous states with L-DOPA].

The paper presents the results of L-dopa use for the treatment of patients with reactive stuporous states. The assumption concerning curability of these patients is based on the similarity of a number of their clinical and biochemical manifestations with an akynetic-rigid form of parkinsonism where L-dopa is very effective. From 25 patients with reactive psychoses 7 demonstrated recovery, 3 patients--significant improvement, 5 patients--improvement and 10 patients--absence of the effect. The drug is the most effective in the stuporous depth of psychomotor inhibition in persons with a monomorphic structure of stuporous syndromes, rather "frequent" depressive disorders and a decrease of a background level of dopamine excreation with urine. Use of L-dopa in schizophrenic stuporous states (5 patients) was ineffective.

Adult↗
PubMed1981

[Stuporous states during treatment with sodium valproate. Pathogenetic hypotheses].

In 11 patients with complex partial epileptic seizures stuporous states were observed during treatment with valproate (VPA) (2 cases), with VPA and phenobarbitone (PB) (4 cases), or with VPA, PB and a third anti-epileptic drug (5 cases). Based on 3 characteristic cases, an attempt is made to define the role of VPA, the nature of the stuporous states, and the origin of digestive disorders which often herald the onset of behavioural disorders. Several clinical studies have suggested the direct responsibility of VPA even if the adverse effects are potentiated by many other anti-epileptic drugs. Stuporous states are not due to VPA overdose and do not depend on the mode of administration. No correlation has been found between electroclinical signs and plasma or CSF levels of the different anti-epileptic drugs. Reported data and the present cases suggest a paradoxical epileptogenic role for VPA on complex partial seizures: there exists a close similarity of electroclinical findings between spontaneous epileptic seizures and stuporous states during DPA treatment. Digestive disorders appear to result from a central mechanism and not from digestive tract intolerance. In some cases, it is likely that partial seizures with digestive symptoms and signs do occur.

Adult↗
PubMed1995

Negative myoclonus during valproate-related stupor. Neurophysiological evidence of a cortical non-epileptic origin.

We retrospectively reviewed clinical and neurophysiological data of 6 epileptic patients who developed negative myoclonus and stupor a few days after introduction of valproate (VPA). Prompt remission of clinical signs and symptoms followed valproate withdrawal. We attempted to elucidate the pathophysiological mechanism of VPA-induced stupor and provide further polygraphic and backaveraging EEG documentation of negative myoclonus. During VPA-induced stupor electroencephalograms revealed posterior background slowing in all patients. Interictal epileptiform discharges were present in 3 patients. In all 6 patients close examination using simultaneous video-polygraphic recording showed negative myoclonus which was not time-related to lateralized spike discharges. In 2 of 3 patients with no spikes on conventional EEG who underwent backaveraged EEG recordings we detected a large (5 microV) cortical positive-negative wave time-locked (30-40 msec) with the postural modification of the contralateral wrist. This cortical potential was similar to that observed in patients with asterixis secondary to metabolic or toxic encephalopathies. In one patient i.v. administration of 10 mg diazepam did not modify this cortical potential and did not reverse the clinical manifestations. In all patients the only abnormal laboratory finding was an increased level of venous ammonemia. Our findings are against an epileptic origin of VPA encephalopathy and provide further argument in favour of a cortical non-epileptic mechanism mediating negative myoclonus. Benzodiazepines should be avoided in the management of this condition.

Adult↗
PubMed1992

Endogenous benzodiazepine receptor ligands in idiopathic recurring stupor.

"Endozepines" are endogenous ligands for the benzodiazepine recognition sites on gamma-aminobutyric acid A receptors in the nervous system. Idiopathic recurring stupor (IRS) is a syndrome of spontaneous stupor or coma that is not associated with known metabolic, toxic, or structural abnormalities but can be reversed by flumazenil, a pure benzodiazepine antagonist. We measured endozepine-2 and endozepine-4 by high-performance liquid chromatography and radioreceptor assay in serum and cerebrospinal fluid from three patients with IRS. During episodes of stupor there was a large (up to 300-fold compared with control patients) increase of endozepine-4 content in cerebrospinal fluid and serum, but a return to normal concentrations between attacks. Endozepine-4 may contribute to, or be the cause of, IRS. The reasons for abnormal concentrations of endozepine in blood and brain are unknown.

Adult↗
PubMed1997

Endozepine stupor in children.

Recurring episodes of stupor in adults have been shown to be related to increased levels of endozepines, which are endogenous ligands for the GABAA receptors. We report here two children presenting with recurrent episodes of stupor associated with fast EEG activity who had increased levels of endozepine-4 in plasma. Mass spectroscopy did not reveal commercially available benzodiazepines. Interictal endozepine-4 levels were normal. In one of the patients, administration of flumazenil (0.25 mg i.v.), a benzodiazepine inverse agonist, induced improvement of consciousness and attenuation of EEG fast activity. In conclusion, children presenting with recurrent episodes of stupor and EEG fast activity should be evaluated for endozepine levels and can be effectively treated with i.v. flumazenil.

Carrier Proteins↗
PubMed1976

Regional levels of glucose, amino acids, high energy phosphates, and cyclic nucleotides in the central nervous system during hypoglycemic stupor and behavioral recovery.

The effects of insulin-induced hypoglycemic stupor and subsequent treatment with glucose on mouse cerebral cortical, cerebellar and brain stem levels of glucose, glycogen, ATP, phosphocreatine, glutamate, aspartate and GABA and on cerebral cortical and cerebellar levels of cyclic AMP and cyclic GMP have been measured. Hypoglycemia decreased glucose, glycogen and glutamate levels and had no effect on ATP levels in all three regions of brain. GABA levels were decreased only in cerebellum. Aspartate levels rose in cerebral cortex and brain stem, and creatine phosphate increased in cerebral cortex and cerebellum. In the hypoglycemic stuporous animals, cyclic GMP levels were elevated in cerebral cortex and depressed in cerebellum whereas cyclic AMP levels were unchanged from control values. Intravenous administration of 2.5-3.5 mmol/kg of glucose to the hypoglycemic stuporous animals produced recovery of near normal neurological function within 45 s. Only brain glucose and aspartate levels returned to normal prior to behavioral recovery. These results suggest that of the several substances examined in this study, only glucose and perhaps aspartate have important roles in the biochemical mechanisms producing neurological abnormalities in hypoglycemic animals.

Adenosine Monophosphate↗
PubMed1981

Regional CNS levels of acetylcholine and choline during hypoglycemic stupor and recovery.

During insulin stupor in mice, acetylcholine levels in cerebral cortex, cerebellum, brainstem, striatum, and hippocampus were unchanged from control values despite brain glucose concentrations 3-10% of normal, whereas choline levels rose 2.4-3.6-fold in all five CNS regions. Brain acetylcholine and choline levels did not change during recovery following glucose injection. The data suggest that, in hypoglycemic stupor, (1) overall rates of acetylcholine synthesis and degradation remain balanced within each of the CNS regions studied; (2) the biochemical mechanism that elevates brain choline levels is unlikely to be related only to cholinergic synaptic processes; and (3) brain choline levels need not rise for stupor to occur.

Acetylcholine↗