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 55 records · Page 3Linked to original sources
PubMed2004

Endozepine stupor: disease or deception? A critical review.

Presentation of patients with recurrent stupor associated with apparently elevated levels of an endogenous benzodiazepine-like agent, endozepine-4, has been reported from several centers, and a new syndrome, endozepine stupor has been proposed. We recently reported a case with typical features of this syndrome, which proved to be an example of surreptitious administration of exogenous benzodiazepine. This and other examples of clandestine drug use, together with uncertainties about the validity of tests used to distinguish exogenous and endogenous benzodiazepines, prompted us to undertake a reappraisal of this clinical syndrome.

Benzodiazepines↗
PubMedDate not supplied

Treatment of catatonic stupor with combination of modified electroconvulsive treatment and olanzapine: a case report.

This case report is about the combined use of modified electroconvulsive treatment and an atypical antipsychotic drug, olanzapine, in the treatment of a 20-year-old man with chronic and refractory catatonic stupor. This patient, with a preexisting diagnosis of autism, posturing, nonverbal communication, and contracture of lower extremities, displaying mutism, akinesia, and an extreme level of rigidity, waxy flexibility, and posturing, was diagnosed as with catatonic stupor. After hospitalization, the disease had progressed despite the treatment with an atypical antipsychotic drug, olanzapine. Modified electroconvulsive treatment together with olanzapine caused a dramatic clinical improvement. Follow-up outpatient treatment with olanzapine improved his social functions.

Adult↗
PubMed1994

Idiopathic recurring stupor.

Idiopathic recurring stupor (IRS) is a disease of unknown pathogenesis presenting with recurrent stuporous states. We describe three IRS patients in whom there were no metabolic, toxic, or structural brain dysfunctions. Ictal EEGs were characterized by fast (14- to 16-Hz), unreactive background activity. Flumazenil, a benzodiazepine receptor antagonist, promptly resolved the clinical and EEG picture. In all patients, ictal plasma determination showed a marked increase in benzodiazepine-like activity identified as endozepine-4. IRS may be due to an unexplained excess of endozepine-4.

Adult↗
PubMed2005

Recurrent stupor due to lysinuric protein intolerance.

Recurrent stupor in children is an uncommon clinical problem with a wide differential diagnosis; inherited metabolic disorders account for a vast majority. We report a 9-year-old girl with recurrent episodes of stupor. Initial episode was treated as viral encephalitis and the second episode was managed as non-convulsive status epilepticus. Hyperammonemia was detected in the last episode. Metabolic work-up after dietary protein challenge revealed classical biochemical features of lysinuric protein intolerance. She was managed with protein-restricted diet, which resulted in marked neurological improvement. LPI is a rare inherited metabolic disorder due to membrane transport defect of cationic amino acids.

Amino Acid Metabolism, Inborn Errors↗
PubMedDate not supplied

[Post-traumatic stupor in children: a rare but not exceptional syndrome].

The post traumatic stupor syndrome in children in uncommon, but likely underdiagnosed. In a retrospective review of medical records on all children admitted for acute head injury at the Pediatric Departement of Melegnano between september 1983 and august 1991, we found 459 head trauma: 3 of them (0.65%) showed post traumatic stupor syndrome.

Age Factors↗
PubMed1990

[A case of adult-onset spike-wave stupor associated with hypoparathyroidism and hyperostosis frontalis interna (HFI)].

A 34-year-old women without history of seizures was admitted to our hospital because of the diminished responsiveness and the repeated blinking for two days. Her past history showed neither surgery nor inflammation of the thyroid gland. General physical examination was normal. On neurological examination, the patient was blinking frequently and staring without any responsiveness. However, she occasionally became able to respond correctly to verbal orders, such as "open your eyes", "open your mouth", "stand up" and so on, which occurred abruptly just like the switch-on. She was otherwise normal neurologically. The laboratory data showed hypocalcemia, hyperphosphatemia, decreased level of parathyroid hormone and normal renal function, indicating the presence of idiopathic hypoparathyroidism. EEG showed the continuous generalized 2-4 Hz spike and wave complexes with the maximum intensity on frontal lobes. Skull roentgenograms and MRI CT of the head disclosed hyperostosis frontalis interna (HFI) and the compression of superior medial frontal lobes by the HIF. SPECT also showed the diminished circulation and hypometabolism in the superior frontal lobes. Based on clinical and EEG findings, the diagnosis of spike-wave stupor was made. She was successfully treated with valproic acid and ethosuximide. Spike and wave complexes on EEG completely disappeared after administration of alfacalcidole. It is assumed that both hypoparathyroidism and HFI were deeply involved in the development of spike-wave stupor in this adult case.

Adult↗
PubMed1979

Reversal of neuroleptic-induced stupor by procyclidin. Two case reports and their theoretical implications.

Two case reports and data from literature on the subject are used by the authors to describe characteristics of pathogenetic importance of neuroleptic induced stupor (NIS). The origin of NIS is outlined briefly and some fundamental clinical and experimental facts are presented, all of which stress the importance of the acute blockade of postsynaptic DA-ergic receptors. Emphasis is placed on the significance of the possible relationship and similarity between NIS and catatonic stupor, and on the theoretical possibilities which this offers.

Adult↗
PubMed1977

Sudden catatonic stupor with disastrous outcome.

Catatonic stupor occurred in two psychiatric inpatients, predisposing them to staphylococcal pneumonia, venous thrombosis, and pulmonary embolism. Disastrous outcomes ensued. Catatonic stupor can lead to fatal complications, and aggressive medical and psychiatric therapy is indicated.

Acute Disease↗
PubMed1982

Saturday Conference: stuporous alcoholics: metabolic considerations.

Alcoholics are predisposed to certain metabolic disorders that cause stupor and coma. These entities include acute ethanol intoxication, ethanol-induced hypoglycemia, alcoholic ketoacidosis, ethylene glycol and methanol intoxications, thiamine deficiency, and hepatic encephalopathy. The recognition and management of these entities and the evaluation of stuporous alcoholics are discussed.

1-Propanol↗
PubMed1996

[Depressive stupor--malignant neuroleptic syndrome--serotonin syndrome. A case contribution to a difficult differential diagnosis].

Depressive stupor and malignant neuroleptic syndrome are very well-known problems in clinical psychiatry. The serotonin syndrome, however, a potentially life-threatening side effect of treatment with serotonergic substances, has been included in the clinical differential diagnosis increasingly often in the last few years. The development of new serotonin selective antidepressants and selective reversible inhibitors of monoamine oxidase A has led to the use of more and more substances that can cause these life-threatening complications if they are taken in too high doses or together with other drugs. We present a 61 year old depressed female impatient who developed an abortive malignant neuroleptic syndrome while being treated for depressive stupor. We discuss a possible relation between serotonin syndrome and a highly dosed combination therapy with moclobemide. Owing to the importance of both syndromes, we consider drug monitoring absolutely necessary for patients who are being treated with new antidepressants, and especially for those who develop neurological and psychiatric complications when such preparations are given in combination with other drugs.

Antidepressive Agents, Tricyclic↗
PubMed1997

The treatment of stupor associated with MRI evidence of cerebrovascular disease.

OBJECTIVE: To describe the treatment and outcome of organic stupor associated with MRI evidence of cerebrovascular disease. DESIGN: A case series of three patients. SETTING: An urban mental health of the elderly service in southeast London. PATIENTS: Aged 69 years, 72 years and 78 years. Two had organic catatonic disorder and the third organic depressive disorder. INTERVENTIONS: Diazepam, carbamazepine, antidepressants or electroconvulsive therapy (ECT). MAIN OUTCOME MEASURES: Resolution of symptoms and discharge from hospital. RESULTS: Symptoms resolved between 1 and 10 days. All patients were able to return home but relapsed over the following 12 months. One relapse occurred when a patient stopped diazepam and moclobemide. CONCLUSIONS: It is proposed that the initial treatment of organic stupor associated with cerebrovascular disease should include a benzodiazepine or carbamazepine. If patients fail to respond then ECT should be considered. The safety of ECT is not known, when treating patients with depressive disorder associated with cerebrovascular disease.

Aged↗
PubMed1977

Meningoencephalopathy secondary to infectious mononucleosis. Unusual presentation with stupor and chorea.

We report a case of infectious mononucleosis in which central nervous system involvement was the presenting and sole manifestation of the disorder. The major symptomatology consisted of stupor, chorea, and signs of aseptic meningitis. We also discuss the clinical and laboratory features of the neurological manifestations of infectious mononucleosis and the theories as to its pathogenesis.

Adolescent↗
PubMed1992

Idiopathic recurring stupor: a case with possible involvement of the gamma-aminobutyric acid (GABA)ergic system.

A patient had recurrent spontaneous episodes of stupor or coma in the absence of toxic, metabolic, or structural brain damage. Ictal electroencephalography showed fast 14 Hz background activity; sleep studies excluded narcolepsy. Flumazenil (Anexate), a benzodiazepine antagonist, promptly resolved the episodes and normalized the electroencephalogram. Radioreceptor binding studies showed the presence of a ligand to the central benzodiazepine receptor in plasma and cerebrospinal fluid during the episodes, suggesting a gamma-aminobutyric acid (GABA)ergic system involvement in the origin of the attacks.

Benzodiazepines↗
PubMed1996

Central pontine myelinolysis with stupor alone after orthotopic liver transplantation.

Central pontine myelinolysis (CPM) after orthotopic liver transplantation is frequently diagnosed at autopsy. Its actual prevalence is unknown. We reviewed 386 orthotopic liver transplantations performed at the Mayo Clinic, Rochester, MN, including 39 with autopsy reports. CPM developed in four patients (1%) (found using magnetic resonance imaging in two, at autopsy in two). All four patients lacked typical signs and symptoms of CPM (pseudobulbar palsy and quadriplegia) but had stupor as the main presenting feature. When perioperative plasma osmolality and serum sodium values were compared with those values in patients with transient metabolic encephalopathy but no CPM at autopsy, no consistent association was observed, and values differed greatly. We conclude that CPM in orthotopic liver transplantation frequently is manifested by altered levels of consciousness alone, mimicking metabolic encephalopathy.

Adult↗
PubMed1982

Stuporous states or coma induced by the rapid administration of high doses of sodium valproate.

7 cases of stuporous states or coma induced in epileptic subjects by the rapid administration of high doses of sodium valproate are described. Progressive impairment of consciousness began 2 to 7 days after the administration of sodium valproate and induced a slowing of background EEG activity until the delta activity became of high amplitude, generalized, continuous and areactive. The authors believe that the impairment of consciousness in their patients was related to the rapid administration of high doses and a direct intrinsic action of sodium valproate on the brain, as no increase in plasma levels of the drugs in association with valproate was observed.

Adult↗
PubMed2006

Spike-wave stupor in a patient with metabolic disorder.

We report a 79-year-old woman with a decreased level of consciousness. Investigation revealed an elevated serum ammonia and a portal-systemic shunt on angiography. Thus, her symptoms were thought to be due to metabolic encephalopathy. Her electroencephalogram (EEG) showed bilaterally synchronous runs of three-phase waves consistent with the triphasic waves typically seen in metabolic encephalopathy. However, after intravenous administration of diazepam, the EEG abnormalities improved; indicating that her decreased consciousness was of epileptic etiology, consistent with spike-wave stupor. Therefore, even in the presence of a clearly defined metabolic disorder, triphasic waves on the EEG may not be due to metabolic encephalopathy; they may reflect an epileptic state precipitated by the metabolic disorder.

Aged↗