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At least 721 records · Page 40Linked to original sources
PubMed1988

Central somatosensory conduction time and acoustic brainstem transmission time in post-traumatic coma.

Short-latency evoked potentials (SEPs) of the scalp and neck after median nerve stimulation and acoustic brainstem evoked potentials (BAEPs) were recorded in 85 patients in post-traumatic coma with clinical signs of brainstem impairment between days 2 and 6 after trauma. The central somatosensory conduction time (CCT), the amplitude ratio (AR) N20:N13, the interpeak latencies (IPL) I-III, III-V, I-V, and the ARs between waves I and V (I:V) and between wave I and the wave IV/V complex (I:IV/V) were calculated and related to the outcome of the patients. In cases of coma due to supratentorial lesions, CCT and ARs of SEPs were close to normal in patients with good outcome: CCT increased and ARs decreased with worsening of outcome. In cases of primary brainstem injury, a significant prolongation of CCT was also seen in patients with good recovery, whereas normal CCTs could be found in patients with severe disability and death outcome. In this case, unilateral absent scalp SEPs were frequently found. The IPLs I-III, III-V, I-V, and the ARs of BAEPs increased with worsening of outcome. Significant differences of IPL I-V and III-V (brainstem transmission time) were seen between patients with good recovery or moderate disability outcome and the patients with severe disability or death outcome. There was no difference in BAEPs between patients with primary brainstem lesion and patients with secondary brainstem lesion. Patients with bilateral absent SEPs and bilateral absent BAEPs not related to traumatic or preexisting hearing disorders died or survived severely disabled. Unilateral absence of scalp SEPs and unilateral absence of BAEPs were frequently found in patients who died or who had severe disability. Asymmetries in scalp SEPs appeared to be distributed equally to all outcome categories, but asymmetries in BAEPs increased with worsening of outcome too. In most of the patients who died or survived disabled, both SEPs and BAEPs were abnormal.

Adolescent↗
PubMed2000

The EEG in coma.

The EEG allows insight into thalamocortical function in comatose patients when this is inaccessible clinically. A single EEG can help with broad diagnostic categorization whereas continuous or serial EEG provides monitoring for unstable and potentially treatable conditions and for monitoring the effects of therapy. The EEG plays a supplemental role in establishing the prognosis in disease states that are capable of causing neuronal death. The most prevalent and problematic of these conditions involves survivors of cardiac arrest who are initially in coma with intact brainstem reflexes. In such patients single EEGs are of 100% specificity for no possibility of recovery of consciousness only for essentially complete generalized suppression (<10 microV) after the first day of the arrest. Several other generalized patterns, including less marked suppression, burst-suppression, epileptiform activity, periodic complexes, and alpha-theta coma patterns, usually but not invariably indicate a poor outcome. Serial EEGs, continuous raw and automated "trending," testing of reactivity, and the inclusion of multiple variables hold promise for an improved role in the prognostic determination in these patients.

Brain Diseases, Metabolic↗
PubMed1987

Correlation of cerebral perfusion pressure and Glasgow Coma Scale to outcome.

Cerebral Perfusion Pressures (CPP) and Glasgow Coma Scale (GCS) scores were monitored to guide the management of severely head-injured patients. These measures were correlated to outcome (Glasgow Outcome Scale-GOS) in 136 consecutive patients at least 1 year after injury. The GOS showed highly significant positive correlations to either CPP or GCS assessments (p less than 0.001). Two parameters that are correlated with subsequent death in most patients include 1) highest (h) GCS = 3 or 4 (Day 1: 31 of 32 patients died, and Day 2: 19 of 19 patients died), and 2) CPP less than or equal to 60 mm Hg more than 33% of the hourly measures during Day 2 (36% of all subsequent deaths; 11% overlap with the highest Glasgow Coma Scale). The Day 2 measures identifying two groups that have a greater than 75% incidence of "good outcome" or GOS = 4 or 5 include 1) hGCS greater than or equal to 6 (N = 45) and 2) the average (a) CPP greater than or equal to 90 mm Hg (N = 26). Of the 45 patients with a GOS = 4 or 5 who had both CPP and GCS recorded on the third day, 44 were identified by these "good outcome" parameters.

Blood Pressure↗
PubMed1987

Early coma in intussusception: endogenous opioid induced?

A decreased level of consciousness with little abdominal pain or gastrointestinal symptoms is an uncommon, but well described, presentation of infantile intussusception. Its etiology is unclear. We describe a 10-month-old male who presented with coma and miosis, reversible with bolus injections of naloxone on three separate occasions. No opiates were involved and an intussusception was subsequently found. We speculate that the coma and miosis were induced by an endogenous opioid which could also mask the abdominal pain, thus explaining this presentation of intussusception. If so, miosis would be a valuable clue for diagnosing such children.

Coma↗
PubMed1989

Ingestion of cannabis: a cause of coma in children.

Previous reports of accidental ingestion of cannabis by children are rare. None has reported coma, although one described a stuporous state that required assisted ventilation. Over the past four years, the staff of British Columbia's Children's Hospital has managed six children with cannabis toxicity, three of whom presented in coma, including one with airway obstruction. Recurring diagnostic features included rapid onset of drowsiness, moderate pupil dilation, hypotonia, lid lag, and the presence of small granules or leaves in the mouth. Confirmation was obtained by positive urine screening for cannabinoids. The six cases described emphasize the need for emergency physician awareness of possible diagnostic criteria, the potential severity of intoxication, and the need for prevention through parent education.

Airway Obstruction↗
PubMed2006

Coma due to cannabis toxicity in an infant.

In young children, cannabis ingestion resulting in coma is very rare. Only nine cases have been reported in the literature and most have occurred in inquisitive toddlers. We review the cases to date and report the youngest recorded case of coma due to cannabis ingestion in an 11-month-old girl. This case highlights the importance of considering toxicological causes and the parental recreational drug history in young children who present with an altered level of consciousness. Child protection considerations are also discussed.

Cannabis↗
PubMed1988

Glasgow Coma Scale scores in the patient post cardiopulmonary resuscitation.

This study was conducted to examine the difference in pre- and post-resuscitation Glasgow Coma Scale (GCS) scores in patients who suffered a cardiopulmonary arrest. Patients who arrested in an acute hospital setting were compared in terms of Glasgow Coma Scale scores with patients who arrested outside an acute hospital setting. The subjects for this study were 39 patients who arrested in the hospital and 16 patients who arrested outside the hospital setting. Data were collected over a period of one year using chart review. The data for this study included: GCS scores at one, two, four, twelve, and twenty-four hours post-arrest; age of the subjects; sex; site of arrest; and etiology of arrest. Results indicated that hospitalized arrest subjects had significantly higher GCS scores than out-of-hospital arrest subjects. Results further indicated that younger patients and those with myocardial infarctions had significantly higher GCS scores post-arrest. This study has implications for serial neurological assessment of the patient post-arrest.

Adult↗
PubMed1996

Quantitative EEG analysis as a supplement to the clinical coma scale RLS85.

BACKGROUND: The aim of the study was to investigate the correlation between EEG indicators and clinical scores based on the RLS85 (Reaction Level Scale 85) in comatose patients. The results of a simple visual assessment of the EEG, using an arbitrary scale with typical EEG patterns, were compared with those obtained by quantitative electroencephalography (qEEG). METHOD: The RLS85 scores were examined in 34 patients with impaired consciousness due to brain tumours, vascular lesions or head injuries. The EEG was recorded shortly before or after the clinical examination. The semiquantitative assessment was made by visual inspection of the tracings, using an arbitrary scale where 12 EEG patterns with increasing proportion of slow activity were displayed. Parallel to the visual analysis, the EEGs were processed by means of EEG spectrum analysis and the power/amplitude in slow frequency bands was used as an indicator. The results were based on correlation between various types of EEG variables and the RLS scores which were obtained in the same patients. RESULTS: The correlation between the visual EEG indicators and coma scores ranged between 0.53 and 0.57 (P < 0.01). As regards the computerised EEG analysis, the correlation between the clinical scores and various EEG spectrum values did not exceed 0.45 (P < 0.01). A higher correlation could be obtained by combining eight EEG variables; the multiple correlation coefficient was then 0.68. CONCLUSIONS: The amount of EEG slow activity is significantly correlated to the RLS85 score. This means that the EEG also provides information on the level and not only on the changes of the coma degree. Surprisingly, the indicators based on quantitative EEG, as used in commercially available instruments, did not give better results than the visual assessment. However, the results of the computerised analysis could be improved using multivariate statistical methods. The study also showed a way to improve communication between the neurophysiologist and clinician by presenting the EEG findings in terms similar to those used in the clinical scales. However, the clinician should be aware of the fact that the "EEG score" and the clinical score is not the same: the intention is to supplement rather than to simulate the clinical observation.

Adolescent↗
PubMed1997

Case report: interferon induced coma in Sheehan's syndrome.

A 54-year-old woman who was being treated with 10 million units (mu) of natural interferon (IFN)-alpha per day for chronic active hepatitis C at a local clinic, developed coma on the fourth day of treatment. On admission to Yamagata University Hospital, she was still in a state of semicoma with severe hyponatraemia (122 mEq/L) and hypochloraemia (89 mEq/L). After the administration of electrolytes, her condition improved remarkably. Endocrinological loading tests showed a hypofunction of the anterior pituitary gland. In consideration of these results, and her past experiences of haemorrhage during childbirth and subsequent amenorrhoea, we diagnosed her illness as a coma as a result of Sheehan's syndrome which had become overt during IFN therapy. She recovered completely after treatment with hydrocortisone and l-thyroxine.

Adrenocorticotropic Hormone↗
PubMed1996

Cannabis cookies: a cause of coma.

Despite the prevalence of cannabis use in the community, reports of adverse effects in young children are rare. Two cases of cannabis-induced coma are reported following accidental ingestion of cannabis cookies. The possibility of cannabis ingestion should be considered in cases of unexplained coma in a previously well young child if signs of conjunctival hyperaemia, pupillary dilatation and tachycardia are present and other causes such as CNS infection or trauma are unlikely. Specific screening for cannabinoids should be undertaken.

Cannabis↗
PubMed1998

Horner's syndrome resulting from a prolonged abnormal posture during a coma.

BACKGROUND: Horner's syndrome results from the impairment of the sympathetic nerve supply to the eye and orbit. Other nerve palsies from prolonged unchanged posture are well described, but Horner's syndrome following prolonged lateral flexion has only twice been seen previously and these cases were in association with anaesthesia. METHODS/RESULTS: A case is described of Horner's syndrome resulting from a prolonged period of unchanged posture from an alcohol-induced coma. A review of the anatomy of Horner's syndrome is presented. CONCLUSION: To my knowledge, this is the first reported case of Horner's syndrome resulting from a coma.

Adult↗
PubMed1977

A case of myxoedema coma successfully treated by low dose oral triiodothyronine.

Myxoedema coma is fortunately rare and is probably rarer in a warm climate such as Australia. It carries a high mortality rate. Its correct management is still a controversial issue. A case of severe myxoedema coma who was successfully treated is described. Thyroid hormone was replaced in the form of triiodothyronine given orally in doses of 20-40 microng/day. There was an improvement in body temperature within six hours of the first dose; this was accompanied by a brisk fall in serum CPK and cholesterol with a rapid rise of plasma T3 into the euthyroid range. There was a defect in water excretion which was rapidly reversed as renal function returned to normal. Review of the literature suggests that low dose oral therapy with T3 is a satisfactory form of initial management.

Aged↗
PubMed1990

Practical management of diabetic ketoacidosis and hyperosmolar coma.

In diabetic ketoacidosis (DKA) and particularly in hyperosmolar coma, rapid normalisation of the measured extracellular fluid abnormalities cannot be equated with optimal management. In both disorders there are complex imbalances between extra- and intracellular compartments that are best corrected in a series of rational steps, based on an understanding of pathophysiology. Fluid administration in DKA can generally be divided into three successive phases: (i) a short period of rapid isotonic saline infusion, (ii) slower infusion of isotonic saline with potassium chloride, and (iii) glucose-potassium infusion until oral food intake is well established. In severe cases, there is a definite place for judicious use of isotonic sodium bicarbonate in small amounts. While insulin infusion is desirable, intramuscular insulin remains a satisfactory alternative. Biochemical monitoring is mandatory and management must be reviewed and modified every three to four hours on the basis of the clinical and biochemical response. In the management of hyperosmolar coma, insulin and fluid therapy are more conservative, with the aim of achieving complete rehydration and normoglycaemia only after 36 to 72 hours. Pulmonary complications and the effects of tissue ischaemia, as well as thromboembolic events, remain important causes of death in both disorders. The frequent recurrences of DKA that occur in a group of psychiatrically-unstable young patients remain an unsolved problem.

Diabetic Coma↗
PubMed1980

Vegetative state following coma in childhood: evolution and outcome.

The data have been analysed for 17 children who showed features of the vegetative state following an acute illness that resulted in coma. 15 were under three years of age. Diffuse anoxia/ischaemia (N=12) and meningitis (N=4) were the most common causes of the comatose state. Seven children died, and nine of the 10 survivors have remained severely neurodevelopmentally handicapped, with no cognitive function (follow-up two months to five years). One child became ambulant a year after the initial insult and is moderately retarded. The findings suggest that children who develop the vegetative state following an illness resulting in coma have a poor prognosis and that decorticate or decerebrate responses, roving eye-movements and spontaneous blinking may be early indicators of its emergence.

Brain↗
PubMed1998

Prolonged coma and severely attenuated EEG after a single seizure.

A 63-year-old woman presented with a comatose state after a fall. Results of cranial computed tomography (CT) and magnetic resonance imaging (MRI) scans were normal. An EEG recorded 5 h after admission was very severely attenuated and slowed. Consciousness and EEG were improved the next day. No cause was detected initially. After sleep deprivation, the patient had a generalized seizure followed by a similar coma and EEG. Even a single seizure may cause a prolonged coma with a very severely attenuated and slowed EEG.

Accidental Falls↗
PubMed1984

Prediction of outcome in non-traumatic coma in childhood.

The data in 104 comatose children were analysed, neonates and those with head injury being excluded. The median age was 30 months, with a range of one month to 17 years. 50% were normal, 32% died and the remainder had handicaps ranging from mild to severe. A number of individual clinical variables related with outcome. Stepwise multivariate discriminate analysis individually classified 75% of 102 cases correctly into one of 5 outcome groups, using clinical information obtained at the time of initial assessment within 12 hours of the onset of coma; 67% of 66 cases could be classified correctly on the basis of information available at 24 hours after the onset of coma. There were, respectively, 8% and 3% serious misclassification errors for the 2 time periods. Our data suggest that the stepwise procedure may be a useful method for the early prediction of outcome in comatose children. Classification errors may be minimized by enlarging the data base, by using alternate statistical methods and by taking into account information from investigative variables, the most promising of which seems to be multimodality evoked potentials.

Child↗
PubMed1992

Carbamyl phosphate synthetase-1 deficiency discovered after valproic acid-induced coma.

Valproic acid induced coma is presented in an adult patient without a history of metabolic disease. Liver biopsy revealed a reduction in activity of carbamyl phosphate synthetase-I, an enzyme obligated for transformation of ammonia to urea in the urea cycle. After recovery CT scan follow-up showed marked cerebral atrophy which did not exist prior to the state of coma. Risk factors are discussed.

Adult↗
PubMed1993

Enhanced endogenous ornithine concentrations protect against tonic seizures and coma in acute ammonia intoxication.

Pretreatment of mice with 5-fluoromethylornithine (5FMOrn), a selective inactivator of ornithine aminotransferase, diminishes the accumulation of ammonia in the brain after administration of ammonium acetate, and antagonizes ammonia-induced fatal tonic extensor convulsions. In about 50% of the treated animals the loss of the righting reflex and coma is prevented. Presumably these effects are based on the enhancement of urea formation by the increased liver ornithine concentrations. However, since brain ornithine concentrations are greatly enhanced by 5FMOrn, it is not excluded that ornithine has direct effects on cellular events involved in ammonia-induced seizure generation, even though 5FMOrn had no anticonvulsant properties in a series of established animal seizure models, including N-methyl-D,L-aspartate-induced convulsions. NMDA receptor antagonists are capable of preventing death, but do not protect against the generation of coma and tonic extensor convulsions in ammonium acetate intoxicated mice. Since no evidence was found for ammonia-induced glutamate release from rat hippocampus, there is no convincing evidence for the idea that the tonic convulsions are mediated by NMDA receptors. L-Methionine-D, L-sulfoximine (MSO)-induced seizures can be partially antagonized by pretreatment with 5FMOrn. However, the effect is considerably smaller than against ammonia-induced convulsions, although at the time of seizure onset brain ammonia levels of MSO-intoxicated mice were lower than in the animals receiving ammonium acetate. This suggests that MSO-convulsions are not entirely due to the elevation of brain ammonia concentrations, even though MSO administration mimics effects of ammonia on cortical inhibitory neuronal interactions.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Mercaptopropionic Acid↗