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At least 307 records · Page 17Linked to original sources
PubMed1996

Differentiation of alpha coma from awake alpha by nonlinear dynamics of electroencephalography.

The electroencephalogram, as a probe of scalp-recorded electrical activity arising from the human cortex, provides useful information because of its temporal and spatial organization. Recent developments in nonlinear dynamics suggest that an object can be constructed in an n-dimensional space out of a temporal sequence of data such as an EEG signal and that its organization is characterized by the dimensionality of the object (in this case, human brain activity). We have carried out an analysis of a set of alpha coma EEG patterns in comparison to the awake alpha EEG patterns of normal volunteers and patients. Alpha coma recorded from a single channel is visually indistinguishable from normal resting alpha due to its similar frequency spectrum (a broad-band spectrum with 1/f characteristics). Our results show that alpha coma dimensionality, however, differs from that of normal alpha in that it has a greater variability over different temporal segments of EEG. Single channel recordings in 7 patients with alpha coma were differentiable from those of 10 subjects with "normal" EEGs. Through dynamic analysis of the EEG, novel methods of signal extraction from EEG may become evident and applicable to clinical practice.

Adult↗
PubMed1986

Alpha coma.

Six personal cases of alpha coma are reported: 3 following a cerebrovascular accident and 3 resulting from cerebral concussion. Two patients survived. On the basis of differences in pathogenesis, EEG characteristics and prognosis, the following classification is proposed: alpha coma resulting from brain stem vascular accident; cerebral concussion; diffuse cerebral hypoxia; drug intoxication. The clinical course of each of the classes of alpha coma is outlined. The alpha coma state is not restricted to cases with structural brain stem lesions c.q. lesions of the pontomesencephalic region.

Adolescent↗
PubMed1989

The effective agent in electroconvulsive therapy: convulsion or coma?

The ability of electrically-induced convulsions to alleviate at least some symptoms of mental illness was first reported in the literature 50 years ago; however, the cerebral mechanisms responsible for such therapeutic effects have thus far escaped elucidation. It is thus interesting to note that those seeking explanations for the therapeutic effects of electroconvulsive therapy (ECT) have focused their attention on the convulsion produced by ECT, as opposed to the coma. The present hypothesis emphasizes the coma following the convulsion as a potential explanation of the effectiveness of ECT and other convulsive therapies. It is postulated that the primary effect of the convulsion is to cause the release of adenosine (ARN) from neuronal tissue and that the subsequent depressant effect of ARN on neuronal activity results in the clinical effect observed. Thus hypothesis suggests that chemically-induced coma, particularly coma induced by benzodiazepines, may offer a safe, effective and more acceptable alternative to ECT.

Adenosine↗
PubMed2006

Minor head trauma-induced sporadic hemiplegic migraine coma.

Familial hemiplegic migraine is a severe, rare subtype of migraine. Gene mutations on chromosome 19 have been identified in the calcium channel, voltage-dependent, P/Q type, alpha-1A subunit gene (chromosome 19p13) for familial hemiplegic migraine. Recently a gene mutation (Serine-218-Leucine) for a dramatic syndrome associated with familial hemiplegic migraine, commonly named "migraine coma", has implicated exon 5 of this gene. The occurrence of trivial head trauma, in such familial hemiplegic migraine patients, may also be complicated by severe, sometimes even fatal, cerebral edema and coma occurring after a lucid interval. Sporadic hemiplegic migraine shares a similar spectrum of clinical presentation and genetic heterogeneity. The case report presented in this article implicates the involvement of the Serine-218-Leucine mutation in the extremely rare disorder of minor head trauma-induced migraine coma. We conclude that the Serine-218-Leucine mutation in the calcium channel, voltage-dependent, P/Q type, alpha-1A subunit gene is involved in sporadic hemiplegic migraine, delayed cerebral edema and coma after minor head trauma.

Calcium Channels↗
PubMed2006

Fulminant hyperammonaemia induced by thiopental coma in rats.

Fulminant hyperammonaemia as a threshold effect of coma-inducing dose of sodium thiopental has been revealed in rats. Blood ammonia content increased progressively after the introduction of 1.0 LD(50) (but not 0.8 LD(50)) of sodium thiopental three times in 3h and five times in 18h. The urinary ammonia excretion was not impaired while the volatilization of ammoniac from the body of ST-treated rats was higher, giving evidence of the augmentation of ammonia production. Blood urea increased by one third despite of insignificant alterations of haematocrit and blood creatinine. Ammonia hyperproduction in the digestive tract could result from gastrointestinal stasis, which has been verified by roentgenography and confirmed by correlation of hyperammonaemia with the stool retardation. In thiopental coma rats the slope of a dose-dependent increase of the blood ammonia and the blood urea after the intraperitoneal injection of ammonium acetate did not exceed that in intact animals. So the ammonia hyperproduction in the digestive tract could be the main contributing cause of fulminant hyperammonaemia in rats with thiopental coma and thus be involved into pathogenesis of the coma.

Acetates↗
PubMed2001

MK801 decreases glutamate release and oxidative metabolism during hypoglycemic coma in piglets.

Hypoglycemic coma increases extracellular excitatory amino acids, which mediate hypoglycemic neuronal degeneration. Cerebral oxygen consumption increases during hypoglycemic coma in piglets. We tested the hypothesis that the NMDA-receptor antagonist dizocilpine (MK801) attenuates the increase in cerebral oxygen consumption during hypoglycemia. We measured EEG, cerebral blood flow (CBF), cerebral oxygen consumption (CMRO(2)) and cortical microdialysate levels of glutamate, aspartate and glycine in pentobarbital-anesthetized piglets during 60 min of insulin-induced hypoglycemic coma. NMDA-receptor distribution was measured by autoradiography. MK801 (0.75 mg/kg i.v.) was given within 5 min after onset of isoelectric EEG. Saline- and MK801-treated normoglycemic control animals were also studied. Brain temperature was maintained at 38.5+/-0.5 degrees C. MK801 prevented the 5--10-fold increase in glutamate and aspartate occurring in saline-treated hypoglycemic animals, and attenuated the increase in CMRO(2). Increases in CBF of 200--400% during hypoglycemic coma were not affected by MK801. MK801 did not alter CBF, CMRO(2) or microdialysate amino acid levels in normoglycemic control animals. Parietal cortex corresponding to microdialysis sites was highly enriched in NMDA receptors, and the density and distribution overall of NMDA receptor binding sites were comparable to that reported in other species. We conclude that NMDA receptor activation plays a central role in hypoglycemia-induced glutamate release, and contributes to increased cerebral oxygen consumption. Neuroprotective effects of MK801 during hypoglycemia in piglets may involve inhibitory effects on glutamate release and oxidative metabolism.

Animals↗
PubMed2000

Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma.

The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.

Aged↗
PubMed1999

Early metabolic acidosis and coma after acetaminophen ingestion.

Metabolic acidosis and coma may develop in patients who experience severe hepatic injury after acetaminophen poisoning. The onset of acidosis and coma soon after acetaminophen overdose, but preceding manifest hepatic injury, contrasts with the typical course of poisoning. This pattern has been reported in a limited number of cases. Coingestions and the rare occurrence of these findings after an overdose have engendered controversy as to whether acetaminophen alone is the cause of early coma and acidosis. We describe 4 separate overdoses among 3 patients who arrived at the emergency department comatose with a metabolic acidosis soon after ingesting large amounts of acetaminophen without evidence of toxic liver injury. Our cases support the view that early metabolic acidosis with coma does indeed occur after acetaminophen poisoning, independent of hepatic failure or its complications.

Acetaminophen↗
PubMed1982

[EEG in the prognosis of toxic coma: reflections apropos of unusual data].

During acute intoxications, the first EEG may show persistence or abolition of cerebral activity, but the possibility of recovery after isoelectric tracing in toxic comas must be emphasized. EEG patterns frequently suggest the probability of hypnotic tranquilizer poisoning; 4 types of EEG are encountered corresponding to different grades of toxic coma. Recurrent periods of electrical silence alternating with bursts of activity are habitually recorded in carus comas with hypothermia due to acute barbiturate intoxication, with good prognosis. The possibility of a neurological disturbance associated with drug overdose must be raised whenever an asymmetric tracing is encountered. Serial recordings may detect complications such as: a localized lesion, anoxia or, very rarely, typical paroxysmal abnormalities reappearing in comitial patients before emergence from a toxic coma. Paradoxical monomorphic delta activity corresponding to improvement must not be considered as an aggravation. Peculiar EEG findings occur after oral trichlorethylene poisoning, with temporary clinical deterioration and intermittent periods of electrical silence; recovery is possible. An alpha-like pattern after cardiac arrest of toxic origin has a poor prognosis. The appearance of alternating patterns suggests the development of irreversible brain damage.

Alpha Rhythm↗
PubMed1982

[Aspects of early somatosensory and auditory evoked potentials in neurologic comas and brain death].

Following stimulation of the median nerve at the wrist, SEPs, BAEPs and EEG activity were recorded during the same session in 20 comatose patients (13 head injuries, 6 comas of vascular origin, 1 anoxic coma). Patients were classified according to clinical data. In traumatic comas with clinically preserved brain stem reflexes (5 patients), BAEPs were all present, with preserved cervical N14 and scalp recorded P15 SEPs; the parietal N20 SEP was either present on both sides or unilaterally absent in case of hemispheric, possibly EEG silent, traumatic lesion. In comas with a reactive EEG and absent brain stem reflexes (8 patients), N14 and P15 SEPs were present when the parietal N20 component was absent on both sides. In these patients various aspects of BAEPs were observed, but in most cases (7 out of 8) either the BAEPs were completely absent or only peaks I or I and II were present. In brain-dead patients (7 cases) the cervical N14 was recorded in all cases, the P15 SEP was inconstant and the parietal N20 component was constantly abolished on both sides; in most cases (5 out of 7) all the BAEPs were absent. The practical use of evoked responses for the survey of comatose patients is discussed.

Adolescent↗
PubMed2002

[Fulminant coma: think hyperammonemia and urea cycle disorders].

The authors report the case of 14-year-old boy admitted for acute coma without neurological focal symptom. The only relevant finding was the death of one uncle after a coma in the year 1992. This coma was associated with an ammonia blood level of 344 mumol l-1 and it rapidly lead to cerebral death despite a symptomatic treatment. The diagnosis of hereditary ornithine transcarbamylase deficiency was confirmed by liver biopsy in the immediate post-mortem period. The authors recommend the measurement of blood ammonia in every coma without diagnosis, whatever patient's age.

Adolescent↗
PubMed1991

[Coma during transurethral resection of the prostate].

Two cases of coma occurring during transurethral resection of the prostate are reported. The 76 and 85-year-old patients lapsed into coma, ranking 9 and 8 on the Glasgow scale, respectively 90 and 120 min after the start of the resection, without any previous haemodynamic alterations. In one patient, coma occurred when the urethral catheter became blocked with fragments of prostates. In the other, coma was initiated by a rupture of the prostatic capsule, with passage of washing fluid (1.5% glycine solution) into the peritoneal cavity. The role played by acute hyponatraemia (128 and 123 mmol.l-1 respectively) and glycine poisoning (10,188 and 11,840 mmol.l-1 respectively) are discussed. These cases underline the interest of regional anaesthetic techniques, allowing an early diagnosis and a rapid surgical procedure which will avoid a worsening of the condition.

Administration, Intravesical↗
PubMed2003

Predictive value of electrophysiology in children with hypoxic coma.

Assessment of prognosis of children in hypoxic coma is difficult. The value of clinical evaluation is often limited. The usefulness of electrophysiologic tests has been documented mostly in adults and neonates and in cases of traumatic coma. We reviewed retrospectively 39 consecutive children with nontraumatic hypoxic coma to assess the prognostic value of EEG, visual, and auditory evoked potentials. Correlation between electrophysiology and neurologic outcome after mean follow-up period of 30 months was significant (r(s) = 0.6, P < 0.001). In contrast there was no correlation between Pediatric Risk of Mortality score (PRISM) and outcome (r(s) = -0.42, P = 0.8). Combining magnetic resonance imaging with electrophysiology further enhanced their prognostic value (r(s) = 0.69, P < 0.001). Neuroimaging was highly sensitive but less specific, and electrophysiologic tests were highly specific but less sensitive. We conclude that early electrophysiology can contribute to predicting outcome in pediatric hypoxic coma.

Adolescent↗
PubMed2003

Use of an anesthesia cerebral monitor bispectral index to assess burst-suppression in pentobarbital coma.

A seven-year-old child with generalized status epilepticus who was placed in a barbiturate coma was monitored with the bispectral index monitor in addition to the standard full channel electroencephalogram. This child had a low bispectral index number and high suppression ratio on the bispectral index monitor when the desired level of pentobarbital coma was induced. There was excellent correlation of the bispectral index monitor to the suppression ratio. The burst rate also correlated well to the bispectral index number and to the suppression ratio. Therefore the bispectral index monitor could allow the patient in barbiturate coma to leave the intensive care unit for diagnostic or therapeutic procedures and may one day replace the full-channel electroencephalogram in the management of patients in barbiturate coma.

Anesthesia↗
PubMed1991

[Alpha coma: rectrospective presentation of 20 cases].

Alpha coma is a relatively rare variety of EEG resulting from diffuse cerebral anoxia, focal brainstem lesions, metabolic disturbances or intoxications. It is a monotonous, unreactive and anteriorly predominant activity of less than 50 microV and of 8 to 13 Hz. Twenty cases of alpha coma are reported: 16 resulting from anoxic encephalopathy, 2 from brain stem strokes, and 2 from metabolic encephalopathy. Cardiac arrest was the main cause of alpha coma (10 cases); a large number of patients (7 cases) died, or have survived with severe neurologic deficits (2 cases). In 2 cases there was a metabolic-toxic cause (benzodiazepines and parathion intoxication). The 2 patients with pontomesencephalic haemorrhage died. The physiopathogenicity of alpha coma, which remains obscure, is also discussed.

Adult↗
PubMed1999

ERPs obtained with the auditory oddball paradigm in coma and altered states of consciousness: clinical relationships, prognostic value, and origin of components.

OBJECTIVE: To study the event related potentials (ERPs) in coma and altered states of consciousness, their relationship with the clinical status and coma outcome. METHODS: ERPs were recorded with a passive auditory oddball paradigm in 103 patients. Their probability of occurrence and the peak latencies and amplitudes were studied as a function of the Glasgow Coma Score (GCS). Their relationship with outcome was studied in a subset of 83 patients examined within the first 4 days, and expressed in terms of sensitivity, specificity, and negative or positive prognostic values. RESULTS: When present, the ERPs to rare stimuli consisted of a fronto-central negativity (N(endog), mean latency: 330 ms) and a fronto-central positivity (P(endog), mean latency: 431 ms) following the exogenous N100-P200 complex. Both their probability of occurrence and their latencies and amplitudes were related with the GCS in anoxic and traumatic comas. The N(endog) and P(endog) had high sensitivity with a negative predictive value of 70% and 100%, respectively, but a low specificity, with a positive predictive value of 44% and 41%, respectively. CONCLUSIONS: ERPs can be recorded in some comatose patients and are likely to reflect implicit orienting processes rather than preserved consciousness. Their presence implies a good prognosis but no conclusion can be drawn from their absence.

Acoustic Stimulation↗
PubMed2000

Clinical correlates and prognosis in early spindle coma.

OBJECTIVE: To determine the prognostic significance of spindle coma (SC) according to etiology and EEG reactivity. METHODS: We reviewed 15 patients with SC due to various causes within 8 days of coma to determine the prognostic significance of this EEG pattern. RESULTS: The outcome among survivors was favorable: among 13 survivors, 9 were independent in all activities of daily living (ADLs) at 6 months; 3 were dependent in all ADLs; and one remained in coma. EEG reactivity to noxious stimuli best predicted outcome: All patients (whatever the coma etiology) with EEG reactivity survived; conversely, not all patients without EEG reactivity died. CONCLUSION: In our patients, EEG reactivity independent of etiology predicted survival, neurological examination did not predict outcome. Most SC survivors had a meaningful recovery achieving all ADLs. From the literature, the cause of SC was predictive of outcome: encephalopathy, seizures and trauma had the best prognosis while hypoxia, CRA and structural lesions carried the worst. Literature review revealed that 23% of patients [56/242] died or remained in a persistent vegetative state (PVS). Best outcomes occurred when SC was due to drugs, encephalopathy or seizures: (0/14 died or were in a PVS). With trauma 15% [25/169] died or were in a PVS). Intermediate outcomes occurred with hypoxia and cardio-respiratory arrest (CRA): 33% [7/21] died or were in a PVS. The gravest outcomes occurred with brain-stem and cerebral infarctions, and tumors: 73% [22/30] died or were in a PVS.

Activities of Daily Living↗
PubMed2000

Myxedema coma of both primary and secondary origin, with non-classic presentation and extremely elevated creatine kinase.

Myxedema coma is a rare, often fatal endocrine emergency that concerns elderly patients with long-standing primary hypothyroidism; myxedema coma of central origin is exceedingly rare. Here, we report a 37-year-old woman in whom classical symptoms of hypothyroidism had been absent. Six years earlier, she had severe obstetric hemorrhage and, shortly after, two subsequent episodes of pericardial effusion. On the day of admission, pericardiocentesis was performed for the third episode of pericardial effusion. Because of the subsequent grave arrhythmias and unconsciousness, she was transferred to our ICU. Prior to the endocrine consultation, a silent myocardial infarction had been suspected, based on the extremely high serum levels of creatine kinase (CK) and isoenzyme CK-MB. However, based on thyroid sonography, pituitary computed tomography, elevated titers of antithyroid antibodies and pituitary stimulation tests, the final diagnosis was myxedema coma of dual origin: an atrophic variant of Hashimoto's thyroiditis and post-necrotic pituitary atrophy (Sheehan syndrome). Substitutive therapy caused a prompt clinical amelioration and normalization of CK levels. Our patient is the first case of myxedema coma of double etiology, and illustrates how its presentation deviates markedly from the one endocrinologists and physicians at ICU are prepared to encounter. In addition, cardiac problems as those of our patient should not discourage from substitutive treatment (using L-thyroxine and the gastrointestinal route of absorption), if the age is relatively low.

Adult↗