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PubMed2000

CACNA1A gene de novo mutation causing hemiplegic migraine, coma, and cerebellar atrophy.

Familial hemiplegic migraine is caused by CACNA1A missense mutations in 50% of families, including all families with cerebellar ataxia. A patient with healthy parents, who experienced prolonged attacks of migraine with hemiplegia, coma, and seizures, is reported. The patient also had mental retardation, permanent cerebellar ataxia with cerebellar atrophy, and right-sided brain atrophy. This patient carried a de novo Tyr 1385 Cys mutation in the CACNA1A gene and illustrates a novel phenotype associated with CACNA1A mutations.

Adult↗
PubMed1981

Galactorrhea after prolonged traumatic coma: case report.

A 17-year-old girl suffered a traumatic acute subdural hematoma and rib fractures after a motor vehicle accident. Prolonged coma resulted, and significant galactorrhea began 4 weeks after the accident. The galactorrhea was treated successfully by the administration of 2-bromoergocryptine. The pathophysiology of this condition is discussed.

Adolescent↗
PubMed1983

Effects of therapeutic pentobarbital coma on multimodality evoked potentials recorded from severely head-injured patients.

We sought to determine whether pentobarbital (PB) coma compromises the use of evoked potentials (EPs) in the assessment of brain dysfunction and of the prognosis of severely head-injured patients. Therefore, the effects of therapeutic PB on somatosensory (SEPs, BSEPs), visual (VEPs), and auditory (BAEPs) evoked potentials recorded from 20 patients early after injury were analyzed. Seventeen head-injured patients served as controls. EP studies were obtained shortly after admission (Mean Day 2, PB present) and approximately 2 weeks after injury (Mean Day 15, PB absent). The mean serum level of PB in the treatment group was 1.9 mg/100 ml. The drug effect was assessed by comparisons between the PB and the control groups. Statistical analyses were based on differences observed between two studies in the same patient. Analyses of covariance (F tests) were performed on data from all modalities. Wave form complexity was minimally affected by the drug. Middle and long latency components of the SEP were depressed by PB, and latencies of BSEP peaks and the early components of the SEP were delayed. The amplitude of some VEP peaks was reduced by PB. The BAEP was not significantly altered. All of the observed effects of PB were determined to be due to the hypothermia exhibited by PB-treated patients (mean temperature, 36.1 degrees C), which was not seen in the control group (mean, 37.8 degrees C). It is concluded that, with appropriate interpretation, EPs can be used to monitor brain function in head-injured patients when PB therapy is used.

Adult↗
PubMed1994

Outcome prediction after penetrating craniocerebral injury in a civilian population: aggressive surgical management in patients with admission Glasgow Coma Scale scores of 3, 4, or 5.

In an attempt to evaluate the response of patients who have low admission Glasgow Coma Scale scores (GCS) after a penetrating craniocerebral injury to aggressive management, we evaluated a series of 190 patients with penetrating injuries who presented with a GCS score of 3, 4, or 5 during a 6-year period. Entrance criteria required replicable neurological examinations that were not altered by the presence of hypotension, drugs/toxins, or systemic injury. The surgical patients included 21 patients with an admission GCS score of 3, 24 with an admission GCS score of 4, and 15 with an admission GCS score of 5. All patients underwent surgical intervention and aggressive perioperative management in the neurosurgical intensive care, including resuscitative protocols. Five of the patients with a GCS score of 3 survived, all with poor outcomes. Seven of the patients with a GCS score of 4 survived, although only one had a good outcome. Eleven of the patients with a GCS score of 5 survived. Five had a Glasgow Outcome Score of 2, five had a Glasgow Outcome Score of 3, and one had a Glasgow Outcome Score of 4. We have devised a prospective model of outcome based on our series in an attempt to predict nonsurvivors at admission (while overpredicting for survivors). The variables most predictive of mortality include admission GCS score and subarachnoid hemorrhage in one model and admission GCS score and pupillary changes in a second, when pupillary response was definitive at admission (P < or = 0.00005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Using the Glasgow Coma Scale: analysis and limitations.

This article addresses the gap between the literature and practice in relation to the use of the Glasgow Coma Scale (GCS). It will explore level of consciousness and the GCS. The instigation of both central and peripheral painful stimuli is analyzed in an effort to prevent ritualistic practice. Attention is also given to the importance of including vital signs when using the GCS, as these can tell a lot, if not more, about the patient's neurological condition. Finally, the limitations of the GCS are examined to assist in a more accurate and consistent assessment tool for neurologically impaired patients.

Aphasia↗
PubMed2006

Prolonged coma from refractory status epilepticus.

OBJECTIVE: Status epilepticus is a life-threatening medical condition. In its most severe form, refractory status epilepticus (RSE) seizures may not respond to first and second-line anti-epileptic drugs. RSE is associated with a high mortality and significant medical complications in survivors with prolonged hospitalizations. METHODS: We describe the clinical course of RSE in the setting of new onset lupus in a 31-year-old male who required prolonged barbiturate coma. RESULTS: Seizure stopped on day 64 of treatment. Prior to the resolution of seizures, discussion around withdrawal of care took place between the physicians and patient's family. Medical care was continued because of the patient's age, normal serial MRI studies, and the patient's reversible medical condition. CONCLUSION: Few evidence-based data exist to guide management of RSE. Our case emphasizes the need for continuous aggressive therapy when neuroimaging remains normal.

Adult↗
PubMed1982

Hyponatremia without inappropriate secretion of vasopressin in a case of myxedema coma.

A 45-year-old woman with myxedema coma due to primary hypothyroidism manifested hyponatremia, impaired water excretion, and elevated urine osmolarity as well as natriuresis suggestive of a syndrome of inappropriate antidiuretic hormone secretion. However, plasma vasopressin was undetectable or very low and plasma aldosterone levels were suppressed in the presence of hyponatremia. Subsequent replacement therapy with levothyroxine caused a rapid decline in sodium clearance which was independent of the change in glomerular filtration rate, and corrected the impaired water excretion and hyponatremia. Plasma vasopressin levels returned to the normal range after the correction of hyponatremia. Thus, the results indicate that neither vasopressin nor aldosterone plays a dominant role in the pathogenesis of the hyponatremia in this patient. It appears that thyroid hormone deficiency itself caused the derangement of tubular cell function, which resulted in the development of the impaired water excretion and hyponatremia.

Coma↗
PubMed2005

Hemorrhagic pituitary apoplexy in an 18 year-old male presenting as non-ketotic hyperglycemic coma (NKHC).

Pituitary apoplexy is an acute clinical event usually caused by hemorrhage or infarction in a pituitary adenoma. We report the unusual case of hemorrhagic pituitary apoplexy in an 18 year-old male with previously undiagnosed type 2 diabetes mellitus who presented with unexplained hyperglycemia (glucose 49.2 mmol/l [887 mg/dl]) and obtundation and in whom an initial diagnosis of non-ketotic hyperglycemic coma (NKHC) was made. MRI revealed a heterogeneous mass arising from an expanded sella turcica into the suprasellar cistern. Despite well-controlled glucose levels on continuous insulin infusion, dexamethasone, and initiation of bromoergocriptine (parlodel) therapy, the patient's vision and pupillary responses deteriorated acutely. Following emergency transphenoidal surgery, the patient's vision and mental status improved. Data confirmed preoperative panhypopituitarism; serum prolactin was 396 ng/ml (microg/l). Immunostudies demonstrated tumoral labeling for prolactin, but not for ACTH, GH, TSH, LH, FSH, or P53.

Adenoma↗
PubMed1978

[Prognostic-evolutive evaluation of patients in coma based on ocular reflexes].

The ocular reflexes (ciliospinal, photomotor, oculocephalic, vestibulo-ocular, corneal) were studied in 84 comatose patients. The scope of the investigation was the assessment of each reflex in terms of its resistance according to the degree of depth of the coma. From the statistical viewpoint it was possible to emphasize the photomotor, corneal and vestibulo-ocular as the most resistant ones. The periodic evaluation in short time intervals of these five reflexes, observing their extinction or their re-appearance, permits a better prognostic assessment in a longitudinal viewpoint of the comatose patient.

Coma↗
PubMed1990

[Neurophysiological evaluation using multimodal sensory evoked potentials in patients in coma: general aspects].

Noninvasive sensory evoked potentials (SEP) performed at bedside in the Intensive Care Unit for patients in coma can be helpful in establishing both a diagnosis and a prognosis. Based on a more than 6-year experience on this subject, the authors discuss general aspects concerning these EP, their probable known generators, and propose a classification depicting different aspects observed for flash visual EP (F-VEP), brainstem auditory EP (BAEP), and median nerve somato-sensory EP (SSEP). Isolated, SSEP shows the best diagnostic and prognostic performance. Nevertheless, the authors consider that multimodality SEP are even better than any isolated EP study; cross-correlating information generated through a horizontal (F-VEP), a vertical (SSEP), and a pathway focusing brainstem in greater detail (BAEP) allows the neurophysiological establishment of the level of lesion in the CNS from a better perspective; besides, SEP can help setting the diagnosis of brain (encephalic) death, and the diagnosis of particular problems concerning each pathway. Notwithstanding, most important is prognosis definition, and the findings are summarized. Abnormal BAEP implies bad prognosis, as would be expected considering the severity of a brainstem lesion; on the other hand, a normal BAEP per se does not allow a precise definition, resting on other EP the role prognosis characterization. SSEP if bilaterally normal or only mildly abnormal imply good prognosis; bilateral absence of SSEP thalamo-cortical components has always carried a bad prognosis, since younger patients may at best evolve into a persistent vegetative state; SSEP intermediary results are more often accompanied by variable evolution. FVEP results parallel those of SSEP.

Coma↗
PubMed1998

[3-Hydroxy-3-methyl-glutaryl-CoA-lyase deficiency as coma etiology in the neonatal period: case report].

We report a patient that presented two episodes of coma in the neonatal period, with severe metabolic acidosis and hypoglycemia, without ketosis. The urinary organic acid analysis showed increased amounts of 3-hydroxy-3-methyl-glutaric, 3-methylglutaconic, 3-methylglutaric and 3-hydroxyisovaleric acid. The deficiency of 3-hydroxy-3-methylglutaryl-CoA lyase was diagnosed by the clinical and metabolic features. This disease shows autosomal recessive inheritance and the treatment is done by a diet with restriction of protein (mainly leucine) and lipids, high in carbohydrate content, and the avoidance of fasting and carnitine supplementation.

Coma↗
PubMed2003

[Hyponatremic coma induced by oxcarbazepine: case report].

We report a rare case of severe hyponatremia with coma induced by the use of oxcarbazepine after one month of treatment, in pos-operatory of neurosurgery. We discuss the importance of this condition and its differential diagnosis.

Anticonvulsants↗
PubMed1997

Acidosis and coma after hemodialysis.

Ethylene glycol poisoning is a rare yet potentially fatal illness seen most commonly in association with ingestion by alcoholics or in suicide attempts. It is characterized by an elevated anion gap metabolic acidosis, osmolal gap, calcium oxalate crystals in the urine, and a well-defined clinical picture. Prompt treatment is crucial because effective intervention can prevent the neurologic, cardiac, pulmonary, and renal sequelae associated with ethylene glycol poisoning. Hemodialysis offers rapid clearance of ethylene glycol and its toxic metabolites. In this article, the case of a hemodialysis patient who suffered contamination of the dialysate solution with ethylene glycol, leading to altered mental status, coma, and severe anion gap metabolic acidosis, is reported. Despite prolonged dialysis and correction of the acidosis, the patient remained comatose and subsequently died.

Acidosis↗
PubMed1983

Epidemiologic characteristics of mortality from diabetes with acidosis or coma, United States, 1970-78.

Deaths due to diabetes with acidosis or coma (DAC) in the United States from 1970 through 1978 were analyzed to determine epidemiologic characteristics associated with mortality likely to be due to diabetic ketoacidosis (DKA), a complication of diabetes mellitus considered largely preventable. Annual age-adjusted rates for DAC deaths decreased during the study period, and the secular trend was significant in all regional, race, and sex groups examined. General population-based mortality rates increased linearly with age, were higher in non-Whites than in Whites among persons aged greater than 14, were higher in females, and increased significantly with age in both races and both sexes. By region, rates were lowest in the West. DAC mortality rates specific to estimated diabetic populations decreased annually from 1970 to 1978 in all race and sex groups, and were highest at age greater than or equal to 65, but did not show significant linear increases with age, except in non-Whites. These results indicate declining secular trends, as well as age, race, sex, and regional differences in the risk of such deaths. Further studies are warranted to determine factors contributing to these differences.

Adolescent↗
PubMed2002

Hyperosmolar hyperglycaemic nonketotic coma associated with acute myocardial infarction: report of three cases.

Diabetes mellitus is one of the most commonly associated diseases of patients suffering an acute myocardial infarction. Although the coexistence of acute myocardial infarction with other clinical manifestations of diabetes have been well described, extremely few data exists about the concomitant occurrence of hyperosmolar hyperglycaemic nonketotic coma and myocardial infarctions. This article presents three patients with this association and aimed to discuss the clinical course and treatment strategies of this rare condition.

Aged↗
PubMed1996

Anorexia nervosa with recurrent hypoglycemic coma and cerebral hemorrhage.

A 22-year-old woman with anorexia nervosa showed recurrent hypoglycemic coma and cerebral hemorrhage (Weber's syndrome). She also showed marked liver dysfunction. However, the liver damage was unlikely the main cause of these complications, because liver function tests were improved, and platelet count and prothrombin time were normal when cerebral bleeding occurred. These complications could be induced by her severe malnutrition. Although she rejected any nutritional support before cerebral hemorrhage, she began to accept glucose infusion after the episode, and psychiatric and nutritional states were apparently improved. Cerebral hemorrhage was a turning point in her disease.

Adult↗
PubMed2001

Cerebral atrophy and convulsive seizures after recovery from cerebral edema and coma in a patient with fulminant hepatitis B.

We report a 48-year-old woman who developed convulsive seizures and cerebral atrophy after recovery from fulminant hepatitis B with coma and cerebral edema at the acute stage. Neurological disturbances and cerebral signs are rare sequelae of fulminant hepatic failure (FHF); only a few cases have reported in the literature. Cortical laminar necrosis secondary to cerebral edema or delayed neuronal death due to toxic substances may have caused delayed brain atrophy and epileptogenesis.

Atrophy↗
PubMed2005

Recovery process of immediate prolonged posttraumatic coma following severe head injury without mass lesions.

The recovery process of immediate posttraumatic coma was investigated in 24 patients with severe head injury. The correlation between poor outcome in the recovery process and magnetic resonance (MR) imaging findings was analyzed. MR imaging was performed within the first 7 days for all patients. The recovery process was classified into phase 1 for recovery to moderately disabled and phase 2 to good recovery (GR) according to the Glasgow Outcome Scale. The median of phase 1 was 21.0 days. Four patients did not recover to GR and had poor outcome. Twenty patients recovered to GR. Thirteen patients had short phase 2 of under 10 days and seven patients had long phase 2 of over 60 days. All patients had abnormal lesions on MR imaging considered to be diffuse axonal injury. The number of lesions ranged from two to 10, with a mean of five. Lesions in the dorsal upper brainstem were significantly associated with poor outcome (p < 0.05). The combination of focal lesions in the callosal splenium and dorsal upper brainstem was most common in patients with poor outcome. Patients with long phase 2 had significantly more lesions than patients with short phase 2.

Adolescent↗