SEARCH · Search PubMed
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.
We present a case of episodic stupor associated with a myriad of neuropyschiatric manifestations that baffled doctors until they were recognized as sleep attacks. Continuous monitoring and recognition of a cyclical pattern of symptoms and signs helped to uncover the underlying cause of a rapidly cycling bipolar disorder. The symptoms abated quickly and persistently when treated by olanzapine and lithium.
Coma and stupor are pathologic neural states whose signs arise from either massive cortical or brainstem disease or toxicity. A variety of pathological processes can cause brain disease. Often one has to begin treatment before the diagnosis of the cause of the problem is made. At all stages of treatment, great care must be taken to avoid precipitating an intracranial crisis. The physiological derangements that may aid in the diagnosis include arousability, pupil reactivity, various reflexes, breathing patterns, and cardiovascular function. The treatment needs to be both specific and general; i.e., the condition itself must be treated, if possible, and the intracranial pressure must be lowered if it has been raised by the condition. Treatments for raised intracranial pressure include hyperventilation, diuretics, corticosteroids, avoidance of jugular vein compression, coughing, and any change of the position of the head and neck from normal. When sedating or anesthetizing these patients, one should avoid drugs that increase cerebral blood flow such as ketamine and inhaled anesthetics, using instead drugs that lower cerebral blood flow such as thiopental, lidocaine, and narcotics (with ventilation).
The case of a patient with reappearing stupor, accompanied by auditory hallucinations and persecutory ideas during the periods and not with alternating excitement, is reported. After 24 years of neuroleptics medication with little effect, the lithium carbonate regimen was started, which showed a remarkable prophylactic effect. The implications of lithium carbonate treatment for recurrent psychosis are discussed.
PURPOSE: To report that acute lamotrigine poisoning may result in severe encephalopathy. METHODS: A 55-year-old woman became stuporous after overdose with lamotrigine (LTG) and valproic acid (VPA) tablets. Evaluation revealed elevated serum LTG levels and no other etiology for encephalopathy. RESULTS: LTG was withheld, and the patient experienced a complete recovery in conjunction with reduced serum levels. CONCLUSIONS: LTG overdose may result in a severe but reversible encephalopathy, a previously undescribed phenomenon. LTG toxicity should be considered in patients taking this drug who have depressed mental status.
Two cases are described in which a dissociative stupor originating from conversion neurosis simulated a coma following a sustained trauma. At first both patients showed no response to being addressed or to pain stimuli. They presented an upward eye gaze deviation, cardiorespiratory functions were stable. Following extensive diagnostic procedures revealing no organic cause for the clinical symptoms, the diagnosis of a hysterical consciousness disorder was stated. Symptoms of conversion neuroses include lacking call response, gait disorder, seizure-like conditions and strength diminution in one or more extremities. In these cases suspicious facts are the absence of injuries (for example by falling down or tongue bite during a dissociative attack), eye gaze deviation and the phenomenon that, when the patient's arm is raised above the head and let fall, it never hits the face but glides down beside the body.
A case history of a man with atypical psychosis who exhibited catatonic stupor is reported. Amytal interview procedures used and the differential diagnosis for catatonia are discussed. Response to Loxitane was excellent, though this was clouded by the patient's belief in root medicine, a source of cultural incongruity between him and his therapist. Distinguishing between psychosis and cultural belief systems is shown to be essential in therapy.
In a single patient suffering from a major depressive episode with melancholia (DSM-III), both severe psychomotor symptoms, such as stupor and mutism, and mood disturbances could be abolished completely and promptly by administration of the benzodiazepine lorazepam. Remission of symptoms was entirely and immediately reversed by the benzodiazepine antagonist Ro 15-1788. These drug effects were constantly reproducible. Possible mechanisms of action and the influence of GABAergic neurotransmission on affective and psychomotor state are discussed.
This review discusses a variety of causes of stupor and coma and associated electroencephalographic (EEG) findings. These include metabolic disturbances such as hepatic or renal dysfunction, which are often characterized by slowing of background rhythms and triphasic waves. Hypoxia and drug intoxications can produce a number of abnormal EEG patterns such as burst suppression, alpha coma, and spindle coma. Structural lesions, either supra- or infratentorial, are reviewed. EEGs in the former may show focal disturbances such as delta and theta activity, epileptiform abnormalities, and attenuation of faster frequencies. In infratentorial lesions, the EEG may appear normal, particularly with a pontine lesion. Some patients may be encephalopathic because of ongoing epileptic activity with minimal or no motor movements. This entity, nonconvulsive status epilepticus (NCSE), is difficult to diagnose in obtunded/comatose patients, and an EEG is required to verify the diagnosis and to monitor treatment. Several EEG patterns and their interpretation in suspected cases of NCSE such as periodic lateralized epileptiform discharges (PLEDs), bilateral independent periodic lateralized epileptiform discharges (BIPLEDs), generalized periodic epileptiform discharges (GPEDs), and triphasic waves are reviewed. Other entities discussed include the locked-in syndrome, neocortical death, persistent vegetative state, brainstem death, and brain death.
Twenty-five cases of stupor referred to a psychiatric teaching hospital over 15 years are reviewed. Ten cases presented with a depressive syndrome, four cases with catatonic phenomena and a further 10 cases with established organic aetiology; one case was considered to be psychogenic in origin. The overall mortality was high (16%), attributable to the basic pathology. Compared with earlier series there was a reduction in cases with catatonic features with a corresponding increase in the proportion of organic cases.
A case is reported of a 32 year old woman with a two year history suggestive of schizophrenia who presented in stupor. This proved to be due to hypercalcaemia with a concomitant high cerebrospinal fluid calcium concentration associated with previously unsuspected lymphosarcoma. Necropsy revealed no significant intracranial abnormality, and mechanisms that may have been involved in the production of the impaired consciousness are discussed.
Two cases of catatonic stupor are described due to presumed encephalitis lethargica. Catatonic and obsessional phenomena in the setting of a depressive psychosis associated with a movement disorder may constitute a post-encephalitic syndrome.
A case of childhood affective disorder with episodes of depressive stupor in a 13-year-old pre-pubertal boy is described. Changes in the patient's clinical state were accompanied by changes in the dexamethasone suppression test. A family history of affective illness on the maternal side, with phenomenological similarities, is noted.
In the development and management of a steroid-induced stupor, in a 17-year-old man, the dose and route of administration of steroid medication were felt to be important aetiological factors. A co-ordinated plan of management involving the physician, surgeon and psychiatrist is needed in such cases.
Stupor is a rare and dramatic presentation of a number of neurological and psychiatric conditions which can cause problems in both diagnosis and management. A case is described which illustrates these difficulties.
We analyzed EEGs performed over a 6-month period on patients with impaired consciousness following acute hypoxia or anoxia. There were 17 EEGs performed on 14 patients. Nine of the 17 records contained spindle activity. Spindles were present in 6/8 EEGs in stuporous patients, in 3/9 EEGs in comatose patients, in 6/10 patients who eventually died, and in 3/3 patients who regained consciousness. When spindle activity or background reactivity were absent, outcome was poor, ie, death or a persistent vegetative state. The presence of EEG spindle activity after hypoxic or anoxic injury did not indicate a favorable prognosis, but the absence of spindles or EEG background reactivity was associated with a poor outcome.
Catatonic stupor is a cluster of symptoms and not necessarily a disease entity. It may be seen not only in schizophrenia, but in major affective disorders, conversion disorders, organic brain syndromes, and atypical psychoses. The dexamethasone suppression test is a valuable tool in the diagnosis of major affective disorders, differentiating them from other types of psychopathology. In a twelve month retrospective study, five patients admitted to Psychiatric Institute of Atlanta were identified as meeting the criteria for catatonic schizophrenia. A dexamethasone suppression test was performed shortly after admission. Four of the five had patterns of inadequate suppression, indicative of a major affective disorder rather than a schizophrenic disorder. The dexamethasone suppression test is simple to administer, relatively painless, free from hazards, easy to interpret, readily available, and reliable. Not only can the dexamethasone suppression test be used in diagnosis, but also as a valuable aid in following the therapeutic progress in resolution of a major affective disorder.
Catatonia is a syndrome with many causes that can be difficult to diagnose. In this report, we describe a case of rapid onset of stupor and loss of consciousness, subsequent evaluation, and treatment of catatonia in an HIV-positive man.
Ocular motor disorders in stupor and coma are important clinical signs which are easily accessible with observation and a few bedside manoeuvres. Although the manifold signs of ocular motor dysfunction may be confusing to most clinicians, many of the signs can be attributed to clear pathophysiological mechanisms. This holds for conjugate eye deviations as well as for most spontaneous eye movements in coma. Using simple methods to elicit reflex eye movements, in most cases a lesion site within or outside the brain stem can be determined. It is stressed that an exact description and documentation of the ocular motor deficit is necessary. The following key aspects should be included in such a documentation: pupil size and reaction, conjugate or disconjugate eye position, spontaneous eye movements and VOR elicited either by head rotation or caloric irrigation. The latter allows assessment of the ocular motor integrator. The VOR may be intact, indicated by full compensatory eye movements, but the gaze-holding mechanism (integrator) can be defective, thus permitting the eyes to drift back to the primary position.