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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↗
PubMed1987

Disappearance of tardive dyskinesia during catatonic stupor.

A 61-year-old man diagnosed as having catatonic schizophrenia was treated with neuroleptics for many years. From 1983 he showed tardive dyskinesia on trunk and limbs as well as orofacial dyskinesia. In September 1985 he displayed a catatonic stupor several times. With the outbreak of the stupor the dyskinesia disappeared and vice varsa. This finding induces the hypothesis that the dopaminergic system is suppressed during catatonic stupor in such a way that tardive dyskinesia is no longer visible.

Catatonia↗
PubMed2004

Idiopathic recurrent stupor: a warning.

A proposal that an endogenous benzodiazepine-like agent named endozepine-4 might be responsible for presentations of recurrent stupor has gained wide acceptance. A case of recurrent stupor over two decades is presented with many similarities to previous cases of "endozepine stupor". This case, however, was caused by exogenous benzodiazepine administration and serves as a warning to clinicians to beware of this diagnosis.

Aged↗
PubMed1989

The significance of stupor in the long-term outcome of chronic schizophrenia.

The admission records of 271 long-stay chronic schizophrenic patients, resident in a large psychiatric hospital, were examined in order to identify those who had presented in stupor at the onset of their illness. Twelve patients were found (ten men and two women). When compared, in terms of current mental state and behaviour, with a similar sample of schizophrenics in whom stupor had been absent, significant differences between the two groups were detected, with those presenting in stupor demonstrating a less favourable outcome.

Adult↗
PubMed2005

Postoperative stupor and coma.

OBJECTIVES: To identify predictive factors for postoperative coma or stupor and to examine the value of neuroimaging techniques in elucidating structural brain damage. PATIENTS AND METHODS: We performed a case-control study of surgical patients admitted to a Mayo Clinic-affiliated hospital. We studied preoperative comorbidity, intraoperative hypotension, and postoperative data in patients with postoperative stupor or coma and compared the characteristics with control patients (surgical intensive care unit patients with neurologic consultations for other reasons). RESULTS: A total of 35 patients with stupor or coma after surgery and 31 control patients participated in this study. Comatose patients were older (P=.004) and had significantly more presurgical comorbidity (P<.001), cardiovascular surgical procedures (P<.001), and intraoperative hypotension (P=.03). Adjusted for age and comorbidity, intraoperative hypotension remained statistically significant but not after adjusting for cardiovascular surgery. Of the 34 computed tomograms obtained, 41% showed abnormal results; of the 12 magnetic resonance images obtained, 58% showed abnormal results. Both showed primarily infarctions. In 4 patients with normal computed tomographic results, magnetic resonance imaging showed multiple territorial infarctions. CONCLUSION: Prior comorbidity, older age, intraoperative hypotension, and cardiovascular surgery may predispose patients to postoperative coma. Widespread structural ischemic brain damage was often documented by neuroimaging. Metabolic causes for coma were uncommon.

Adult↗
PubMed2002

[Recurrent idiopathic stupor in a patient: responsibility of exogenous or endogenous benzodiazepines?].

Recurrent transitory consciousness loss represents a neurological diagnostic difficulty. A 56 year old man was hospitalised for recurrent stupor episodes. Explorations allowed to exclude hepatic, renal or respiratory failures, epilepsy or sleep disorder. During a stuporous state, since the patient was clearly awakened by flumazenil administration, the retained diagnosis was idiopathic recurrent stupor, a rare and not well-known disease. The authors discuss the possible effect of a treatment with zolpidem, though its pharmacokinetic characteristics did not correspond to the patient manifestations, and the possible responsibility of endogenous benzodiazepines in the genesis of this trouble.

Benzodiazepines↗
PubMed2003

[A case of dissociative stupor with decorticated posture after neck clipping of brain aneurysm].

We experienced a case of dissociative stupor with decorticated posture in a 71-year-old woman after neck clipping of the brain aneurysm. Decorticated posture is observed with severe midbrain disorder caused by brain herniation. In this case, therefore, severe brain stem damage was suspected, although light reflex was observed and respiration was stable. In addition, in this case, the aneurysm was located at the junction of the internal carotid artery and the posterior communicating artery. Therefore, surgical damage to midbrain was not likely to have happened. Postoperative computed tomography showed no abnormality in this region. Two days later, her symptom disappeared, and she could clearly recollect memory of these two days just after surgery. However, she could not follow directions because of a sense of fear. Thus her symptom might be based on a kind of mental disorder. Patients with conversion disorder react abnormally to stimulus or stress. Stupor was diagnosed as due to defect of reaction to stimulus of sound, light and touch. She was diagnosed as dissociative stupor of the conversion disorder type. In this case, decorticated posture was caused by mental disorder. We have to pay attention not only to brain tissue damage but also to psychological damage of patients.

Aged↗
PubMed1983

[Role of hyperammonemia in stuporous states induced by sodium valproate].

Stuporous states induced by sodium valproate (VPA) are accompanied by an isolated marked hyperammonemia. In reality, hyperammonemia occurs after administration of VPA even in the absence of neurological complications. The hyperammonemia is of purely renal origin and results from modifications in glutamine metabolism, this compound being the main precursor of amino acid neurotransmitters. Combined administration of VPA and phenobarbitone increases the level of hyperammonemia due to lack of detoxification by the liver of the excess of ammonia produced by the kidneys. The anatomical site of origin of the ammoniogenesis, and its intensity, were studied in two patients with a history of stuporous states during combined VPA-phenobarbitone treatment. A single injection of VPA at a later date when they were being treated by combined phenobarbitone-carbamazepine therapy, induced disturbances in ammonia metabolism which did not differ qualitatively from those observed when intolerance to VPA is lacking. It is therefore not possible to rely on simple biological tests to detect patients at risk. Correlation is also lacking between the degree of hyperammonemia and disorders of vigilance. Ammonia does not therefore appear to be the only factor responsible for neurological complications and the role of other factors must be investigated. These include: disturbances of metabolism of inhibitory and excitatory aminoacid neurotransmitters, the condition of the cerebral parenchyma, and the excitatory effect of sodium valproate which could act to varying degrees in synergy with the hyperammonemia to provoke a stuporous state.

Adult↗
PubMed1995

Electroconvulsive therapy for a schizophrenic patient in catatonic stupor with joint contracture.

The successful use of electroconvulsive therapy (ECT) for a patient in catatonic stupor with joint contracture is reported. A 53-year-old woman, who had been diagnosed with schizophrenia, developed a catatonic stupor unresponsive to neuroleptics. Physical emaciation gradually developed under food refusal and poor nutrition. Joint contracture of her extremities resulted from the long period of being bedridden in the same posture. In this case, modified ECT was dramatically effective for catatonic stupor without any complication despite the joint contracture.

Combined Modality Therapy↗
PubMed2003

[Dissociative stupor as a postoperative consequence of general anesthesia].

A 31-year-old woman failed to awaken after an uneventful general anesthesia (propofol, alfentanil and 65% N2O in oxygen) for laparoscopic resection of an ovarian cyst. After the operation she was extubated and vital signs were stable. However, the patient remained unresponsive even to painful stimuli for about 2 h. Just before we performed a computed tomogram of the brain to exclude a cerebral lesion we noticed that she blinked. We hypothesized that unconsciousness was due to a dissociative stupor. After administration of sublingual lorazepam the patient woke up promptly and was alert and normal for the rest of the hospital stay. In conclusion, after exclusion of a pharmacological or organic cause for postoperative unconsciousness, dissociative stupor may be a reason for apparent coma after general anesthesia.

Adult↗
PubMed2005

Prolonged postictal stupor: nonconvulsive status epilepticus, medication effect, or postictal state?

We describe a patient who entered a stuporous state after receiving benzodiazepine treatment for generalized tonic-clonic status epilepticus. A diagnosis of generalized NCSE with tonic seizures was made on the basis of the clinical picture and response to barbiturate anaesthetic, although the EEG pattern was not typical of the changes previously described in tonic seizures-tonic status epilepticus. This report discusses the differential diagnosis of postictal stupor, nonconvulsive status epilepticus with tonic seizures and sedation caused by the emergency treatment of status epilepticus, and summarizes the literature on tonic seizures and tonic status epilepticus.

Adult↗
PubMed1983

Lactate reverses insulin-induced hypoglycemic stupor in suckling-weanling mice: biochemical correlates in blood, liver, and brain.

The recovery of weanling mice from insulin-induced hypoglycemic stupor-coma after injection of sodium -L(+)-lactate (18 mmol/kg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmol/kg). Stimulated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy metabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Ten minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmol/L; plasma glucose levels were unchanged, but the beta-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyruvate (37%), citrate (12%), and malate (19%); the increase in alpha-ketoglutarate (32%) was not significant. Lactate injection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO-3] and pH (examined by injection of 15 mmol/kg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral glycolytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and alpha-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glutamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypoglycemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic intermediates).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

[Treatment of acute schizophrenic stupor: the effect of biperiden (author's transl)].

The study reports about the intravenous application of Biperiden at patients with acute hypokinetic reaction suffering from schizophrenia of the paranoid-hallucinatory type. In all of the six cases examined a fast abolition of the stupor could be observed. The pathophysiological mechanisms deriving from our clinical experiences are discussed. Furthermore, a therapeutic procedure is suggested to treat acute schizophrenic stupor merely with drugs.

Acute Disease↗
PubMed1993

Treatment of catatonic stupor with oral lorazepam in 14-year-old psychotic boy.

The case history of a 14-year-old psychotic boy with catatonic stupor who responded dramatically to 2 mg lorazepam is presented. He had been psychotic for over four weeks and had developed mutism, rigidity, negativism, and posturing (but without fever and without changes in blood and serum parameters) despite neuroleptic therapy, but recovered dramatically from stupor within 40 min. after oral administration of lorazepam.

Adolescent↗