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At least 235 records · Page 13Linked to original sources
PubMed2000

Is neuronal injury caused by hypoglycemic coma of the necrotic or apoptotic type?

In this study, we explored if a 30 minute period of hypoglycemic coma yields damage which shows some features associated with apoptosis. To that end, we induced insulin-hypoglycemic coma of 30 min duration, and studied brain tissues after the coma period, and after recovery period of 30 min, 3 h, and 6 h. Histopathological data confirmed neuronal damage in all of the vulnerable neuronal populations. Release of cytochrome c (cyt c), assessed by Western Blot, was observed in the neocortex and caudoputamen after 3 and 6 h of recovery. In these regions, the caspase-like activity increased above control after 6 h of recovery. By laser-scanning confocal microscopy, a clear expression of Bax was observed after 30 min of coma in the superficial layers of the neocortex, reaching a peak after 30 min of recovery. Punctuate immunolabeling surrounding nuclei in soma and dendrites in cortical pyramidal neurons likely represents mitochondria, which suggests that Bax protein assembled at the surface of mitochondria in vulnerable neocortical neurons. It is concluded that although previous morphological data have suggested that cells die by necrosis, neuronal damage after hypoglycemic coma shows some features of apoptosis.

Animals↗
PubMed1990

Extracellular pH in the rat brain during hypoglycemic coma and recovery.

It has previously been shown that hypoglycemic coma is accompanied by marked energy failure and by loss of cellular ionic homeostasis. The general proposal is that shortage of carbohydrate substrate prevents lactic acid formation and thereby acidosis during hypoglycemic coma. The objective of the present study was to explore whether rapid downhill ion fluxes, known to occur during coma, are accompanied by changes in extra- and/or intracellular pH (pHe and/or pHi), and how these relate to the de- and repolarization of cellular membranes. Cortical pHe was recorded by microelectrodes in insulin-injected rats subjected to 30 min of hypoglycemic coma, with cellular membrane depolarization. Some rats were allowed up to 180 min of recovery after glucose infusion and membrane repolarization. Arterial blood gases and physiological parameters were monitored to maintain normotension, normoxia, normocapnia, and normal plasma pH. Following depolarization during hypoglycemia, a prompt, rapidly reversible alkaline pHe shift of about 0.1 units was observed in 37/43 rats. Immediately thereafter, all rats showed an acid pH shift of about 0.2 units. This shift developed during the first minute, and pHe remained at that level until repolarization was induced. Following repolarization, there was an additional, rapid, further lowering of pHe by about 0.05 units, followed by a more prolonged decrease in pHe that was maximal at 90 min of recovery (delta pHe of approximately -0.4 units). The pHe then slowly normalized but was still decreased (-0.18 pH units) after 180 min when the experiment was terminated. The calculated pHi showed no major alterations during hypoglycemic coma or after membrane repolarization following glucose administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1976

Concentration of 3', 5' cyclic adenosine monophosphate in ventricular cerebrospinal fluid of patients with prolonged coma after head trauma or intracranial hemorrhage.

A previous study showed that cerebrospinal fluid from the lateral ventricle of patients without disturbance of sensorium or intracranial pressure contains 15 to 30 nm 3', 5' cyclic adenosine monophosphate. We measured the concentration of this cyclic nucleotide by radioimmunoassay in cerebrospinal fluid from the lateral ventricle of six patients with prolonged coma (20 days or longer) after head trauma (four), or spontaneous intracranial hemorrhage (two). Coma was graded IV to I in order of decreasing severity. Fluid was removed at intervals of six to 72 hours from a Rickham reservoir placed in the lateral ventricle. Concentration of the cyclic nucleotide (mean +/- S.E.M.) in coma of Grades IV, III, II and I was 2.1 +/- 0.3, 4.6 +/- 0.5, 6.3 +/- 1.4 and 12.5 +/- 2.4 nM respectively. After sensorium became normal, cAMP was 21.0 +/- 1.4 nM. Correlation between grade of coma and concentration was -0.89 (P less than 0.01). Thus, prolonged coma appears to be associated with a disturbance of cyclic AMP metabolism within the central nervous system.

Adult↗
PubMed1996

Scalp, earlobe and nasopharyngeal recordings of the median nerve somatosensory evoked P14 potential in coma and brain death. Detailed latency and amplitude analysis in 181 patients.

Median nerve somatosensory evoked potentials (SEPs) were recorded in a total of 181 patients in coma and brain death. Special attention was paid to derivation of P14 (the positive potential occurring approximately 14 ms after median nerve stimulation) with different electrode montages, using midfrontal scalp (Fz), linked earlobe (A1/2), median nasopharyngeal (Pgz) and non-cephalic reference (NC) electrodes. The P14 amplitude (and, to a lesser extent, latency) were invariably lower in brain death than in coma. The potential was preserved in coma in all patients, but lost in brain death in 9.8% in Fz-NC and Pgz-NC recordings, in 23.2% in Fz-A1/2, and in 100% in Fz-Pgz. Thus, Fz-Pgz was the derivation yielding the most reliable results with respect to the distinction between coma and brain death and is therefore recommended as a confirmatory test, when other diseases interrupting the lemniscal pathway (isolated brainstem death, high cervical transverse cord lesion and focal bilateral lemniscal lesion) are excluded. Theoretical considerations lead to the hypothesis of different (rostral and caudal) segments of the P14 generator dipole being recorded by the different electrode montages. It is assumed that Fz-Pgz picks up the most rostral part of P14 (rP14) that is invariably lost in brain death and preserved in coma.

Adolescent↗
PubMed2003

Neuroanatomical correlates of brainstem coma.

The brainstem tegmentum, including the reticular formation, contains distinct nuclei, each of which has a set of chemical, physiological and anatomical features. Damage to the brainstem tegmentum is known to cause coma, the most radical disturbance of consciousness. However, it has remained unclear which nuclei within the tegmentum are crucial for the maintenance of consciousness in humans. Accordingly, we initiated a retrospective study of MRIs obtained from 47 patients with brainstem stroke. The lesion boundaries were charted on patient MRIs and transferred onto a corresponding series of 4.7 T MRIs obtained from a control brainstem specimen that later was cut on a freezing microtome and analysed histologically. In addition, medical charts and available post-mortem materials were used to obtain relevant clinical and anatomical data to verify the MRI readings in each case. We found that in the 38 patients who did not have coma, brainstem damage either was located outside the tegmentum (n = 29) or produced a very small and unilateral compromise of the tegmentum (n = 9). In contrast, in patients who had coma (n = 9), the lesions in the tegmentum were mostly bilateral (n = 7) and were located either in the pons alone (n = 4) or in the upper pons and the midbrain (n = 5). The maximum overlap territory of the lesions coincided with the location of the rostral raphe complex, locus coeruleus, laterodorsal tegmental nucleus, nucleus pontis oralis, parabrachial nucleus and the white matter in between these nuclei. We also found that four coma subjects developed hyperthermia and died in the absence of any infections. In these cases, the maximum lesion overlap was centred in the core of pontine tegmentum. Our findings suggest that lesions confined to the upper pons can cause coma in humans even in the absence of damage to the midbrain. The findings also point to the brainstem nuclei whose lesions are likely to be associated with loss of consciousness and fatal hyperthermia in humans.

Adult↗
PubMed1988

Prognostically important EEG coma patterns in diffuse anoxic and traumatic encephalopathies in adults.

Because of the paucity in the English literature of a detailed and universally accepted EEG grading scale relating to survival after diffuse traumatic and anoxic brain insults, prognostically oriented EEG patterns including recently described abnormalities are presented and discussed. The significance of these patterns may also apply in cases of coma of other etiologies, which can present morphologically similar features. EEG patterns have been classified into five major grades based on an internationally accepted scale. Individual patterns have been more clearly defined on the basis of the morphology of dominant activities, their distribution, persistence, and reactivity to external stimulation. Favorable outcome with survival seems to occur with both grade 1 and the "reactive type" of grade 2 abnormalities, with preservation of normal sleep features, and with frontal monorhythmic delta activity. Prognostically uncertain patterns are "nonreactive" grade 2 abnormalities, diffuse delta activity with grade 3 abnormality, and the "reactive type of alpha pattern coma." The following patterns are suggested to be prognostically malignant if persistent: grade 3 abnormality with small amplitude, diffuse, irregular delta activity; grade 4 ("burst suppression pattern"), in particular when epileptiform discharges are present and with "low-output EEG"; and grade 5 ("isoelectric EEG"). Fatal outcome is also common with the "nonreactive type of alpha pattern coma" and the recently reported "theta pattern coma." These patterns are presented in the illustrations. It is intended that this more detailed subdivision will promote understanding between electroencephalographers using visual EEG assessment in cases of coma.

Brain Damage, Chronic↗
PubMed1994

Decerebrate posturing in alcoholic coma.

Two cases of alcoholic coma are presented where extensor responses to noxious stimuli are demonstrated. Decerebrate posturing normally indicates severe structural or functional depression of midbrain function but can be caused by depressant drugs. Blood alcohol measurements are a vital test in the comatose patient as the clinical picture may be caused, or temporarily significantly worsened, by severe alcohol intoxication. The preservation of pupillary light reflexes in the presence of deep coma with decerebrate posturing should alert the clinician to a possible metabolic cause for the coma, including alcohol. Nevertheless, a diagnosis of alcoholic coma should not be made unless the blood alcohol concentration is grossly elevated and other causes of coma have been excluded by careful physical examination, blood glucose and electrolyte measurement, skull radiography and, in the absence of a rapid improvement, computerized tomography.

Adult↗
PubMed1979

Reversal of ammonia coma in rats by L-dopa: a peripheral effect.

Ammonia coma was produced in rats within 10 to 15 minutes of an intraperitonealinjection of 1.7 mmol NH4CL. This coma was prevented with 1.68 mmol L-dopa given by gastric intubation 15 minutes before the ammonium salt injection. The effect of L-dopa was correlated with a decrease in blood and brain ammonia, an increase in brain dopamine, and an increase in renal excretion of ammonia and urea. Intraventricular infusion of dopamine sufficient to raise the brain dopamine to the same extent did not prevent the ammonia coma nor affect the blood and brain ammonia concentrations. Bilateral nephrectomy eliminated the beneficial effect of L-dopa on blood and brain ammonia and the ammonia coma was not prevented. Thus, the reduction in blood and brain ammonia and the prevention of ammonia coma after L-dopa, can be accounted for by the peripheral effect of dopamine on renal function rather than its central action. These results provide a reasonable explanation for the beneficial effects observed in some encephalopathic patients receiving L-dopa.

Ammonia↗
PubMed1980

Neurophysiological assessment of alpha pattern coma.

Somatosensory evoked potentials, blink reflexes, and H wave reflexes, were recorded on several days from three patients with alpha pattern coma. Coma was secondary to cardiac arrest in two cases and to brainstem infarction in one. Results are compatible with damage to the brainstem reticular formation with sparing of thalamo-cortical circuits as the main physiopathological characteristic of alpha pattern coma. This condition should not be regarded as a discrete entity when establishing the prognosis of patients in coma, since they only differ from other patients in coma from the point view of the EEG record.

Aged↗
PubMed1989

Non-traumatic coma in Zambia.

A series of 170 patients with non-traumatic coma seen over a 16-month period is reported. The Glasgow coma scale significantly correlated with outcome (P less than 0.001). The diagnosis was also important in determining outcome. Hospital mortality was lowest in patients with cerebral malaria (22.7%), eclamptic coma (36.4%), and organophosphorous poisoning (30.4%). A diagnostic approach to non-traumatic coma is outlined and the management of the different causes is discussed. Most hospitals in tropical Africa should be able to diagnose up to 90% of cases with non-traumatic coma and simple therapy is likely to be effective in the majority of cases.

AIDS Serodiagnosis↗
PubMed1990

Value of a revised EEG coma scale for prognosis after cerebral anoxia and diffuse head injury.

The prognostic validity for survival of a recently devised EEG grading scale was tested in anoxic and post-traumatic coma. This scale divides EEG in coma into five major grades and ten subdivisions with emphasis on the presence of dominant activities, their amplitude, persistence, distribution and reactivity. In this scale, patterns previously not allocated, such as "spindle pattern coma," "alpha pattern coma," and "theta pattern coma" are also included. The prognostic power of the revised scale was tested retrospectively without knowledge of clinical data in a group of patients with cerebral anoxia after cardiac arrest lasting more than seven minutes and in a group of diffuse head injuries. The validity of the scale was found to be higher than those used in previously published studies, reaching 98.4% prognostic accuracy in anoxic encephalopathies and was very high in head injuries.

Coma↗
PubMed1990

Spindle coma: observations and thoughts.

The occurrence of physiological patterns of NREM sleep ("spindle coma") is well known since the first major study of Chatrian et al who--like most of the authors of subsequent studies--placed particular emphasis on the etiological role of CNS trauma. Further work showed that nontraumatic causes may also result in spindle coma. This study is based upon 11 observations of spindle coma extracted from 861 patients with acute severe CNS conditions. The age of the patients ranged from 6 months to 46 years. Metabolic, infectious and hypoxic problems were the most common etiologies; there was no case of CNS trauma. It is assumed that spindle coma represents a combination (i.e. coexistence) of true sleep and coma, the latter accounting for the failure of arousal that is attributed to impairment of the activating ascending reticular formation (midbrain level). The presence of spindles (and also vertex waves and K complexes) indicates relative integrity of the cerebral hemispheres. Such a constellation is more likely to occur in CNS trauma but--as our nontraumatic patient population shows--may also materialize in other types of CNS pathology.

Adult↗
PubMed1994

Post-anoxic theta and alpha pattern coma.

Theta pattern coma is a rare EEG finding, described in the course of post-anoxic or post-traumatic coma and interpreted as a "malignant" variant of alpha pattern coma. A case of isolated theta pattern coma, followed by alpha pattern coma is reported. Short temporal succession of such patterns would seem to confirm the hypothesis of a close relationship between them. Possible physiological mechanisms involved in the generation of the patterns are discussed.

Alpha Rhythm↗
PubMed1999

Metabolic acidosis and coma following a severe acetaminophen overdose.

OBJECTIVE: To report a case of metabolic acidosis and coma in a severe acetaminophen overdose. CASE SUMMARY: A 29-year-old white woman was admitted to the emergency department with a diminished level of consciousness and metabolic acidosis. The toxicology screen revealed a serum acetaminophen concentration of 1072 microg/mL, and she was consequently treated with intravenous acetylcysteine. Despite the elevated concentration, the patient did not manifest signs of hepatotoxicity. DISCUSSION: Metabolic acidosis and coma are rare manifestations in acetaminophen overdoses. In published case reports, severe acetaminophen ingestion independently causes metabolic acidosis and coma in the absence of hepatotoxicity. The mechanism by which metabolic acidosis occurs is not clearly defined. Studies conducted on animals demonstrated that in severe overdoses, acetaminophen may cause lactic acidosis by inhibiting mitochondrial respiration. The mechanism by which acetaminophen can cause coma is still unknown. CONCLUSIONS: Severe acetaminophen overdoses can independently cause metabolic acidosis and coma in the absence of hepatotoxicity.

Acetaminophen↗
PubMed2005

Acute hyperammonemic coma with chronic valproic acid therapy.

OBJECTIVE: To report a case of dose-related hyperammonemic coma without liver failure in a patient receiving chronic valproate therapy. CASE SUMMARY: A 56-year-old woman with poorly controlled epilepsy, receiving valproate at subtherapeutic levels for 6 years, developed a life-threatening hyperammonemic coma following a moderate dosage increase. DISCUSSION: Hyperammonemic coma without associated liver failure is an extremely rare complication of valproate therapy, described primarily in patients with inborn errors of metabolism and occurring idiosyncratically during initial stages of therapy. In our case, family history was suggestive of an X-linked disorder, raising the possibility that our patient may have been an asymptomatic carrier of a urea cycle enzyme deficiency unmasked by valproate therapy. To our knowledge, as of October 24, 2005, only one prior case of hyperammonemic coma in the context of chronic valproate monotherapy has been described. Application of the Naranjo probability scale score suggests that a causal relationship between valproic acid and hyperammonemic coma was probable. CONCLUSIONS: The widespread use of valproic acid emphasizes the need to maintain a high degree of suspicion with respect to this rare but potentially fatal adverse effect at all times, regardless of therapy duration.

Anticonvulsants↗
PubMed2005

Postoperative stupor and coma.

OBJECTIVES: To identify predictive factors for postoperative coma or stupor and to examine the value of neuroimaging techniques in elucidating structural brain damage. PATIENTS AND METHODS: We performed a case-control study of surgical patients admitted to a Mayo Clinic-affiliated hospital. We studied preoperative comorbidity, intraoperative hypotension, and postoperative data in patients with postoperative stupor or coma and compared the characteristics with control patients (surgical intensive care unit patients with neurologic consultations for other reasons). RESULTS: A total of 35 patients with stupor or coma after surgery and 31 control patients participated in this study. Comatose patients were older (P=.004) and had significantly more presurgical comorbidity (P<.001), cardiovascular surgical procedures (P<.001), and intraoperative hypotension (P=.03). Adjusted for age and comorbidity, intraoperative hypotension remained statistically significant but not after adjusting for cardiovascular surgery. Of the 34 computed tomograms obtained, 41% showed abnormal results; of the 12 magnetic resonance images obtained, 58% showed abnormal results. Both showed primarily infarctions. In 4 patients with normal computed tomographic results, magnetic resonance imaging showed multiple territorial infarctions. CONCLUSION: Prior comorbidity, older age, intraoperative hypotension, and cardiovascular surgery may predispose patients to postoperative coma. Widespread structural ischemic brain damage was often documented by neuroimaging. Metabolic causes for coma were uncommon.

Adult↗
PubMedDate not supplied

[Coma associated with migraine].

INTRODUCTION: Basilar migraine is a particular form of migraine with an aura in which crises of headache are accompanied by symptoms of dysfunction in the vertebro-basilar territory, including alteration of consciousness in the form of stupor or coma. CLINICAL CASES: We report four patients, three men of 14, 17 and 83 years of age and one woman of 21. All had previous histories of migraine and presented with transitory episodes of coma. During the coma, the woman woke up spontaneously with intense bulimia. In the three men, it was seen, on injecting flumazenil, that the state of consciousness and the EEG returned to normal transiently. Neuroimaging studies (CT and MR) were normal in all patients. CONCLUSIONS: Migraine-coma is an exceptional, emergency condition in which structural, infectious, toxic and metabolic pathology of the Central Nervous System should be ruled out. As well as in patients with basilar migraine, the association of migraine and coma may also be seen in patients with familial hemiplegic migraine and CADASIL and MELAS syndromes. It may be that gabaergic mechanisms are involved in the theoretical dysfunction of the ascending reticular activating system causing alteration of consciousness, since in the three patients in whom flumazenil was injected, there was a response.

Adolescent↗
PubMedDate not supplied

[The importance of fluid perfusion for the outcome of the disease in malarial coma due to Plasmodium falciparum in adult Africans].

Malaria coma induced by P.falciparum was diagnosed in 51 of 390 adult African patients who had been admitted to the therapeutical unit of the Donk Central Hospital and were receiving parenteral quinine at day 1 of the onset of coma. Examining some clinical and laboratory manifestations of malaria coma indicated that fatal outcome was significantly recorded among the patients with severe concomitant anemia and among the patients who had not or had received inadequate liquid parenterally on the first day of coma. The occurrence of acute renal failure in 4 patients with malaria coma resulted in 3 deaths. No great impact on the prognosis of malaria "hyperparasitemia", the severity of fever, the values of blood pressure was found. Whether it is advisable to use the parameters characterizing the opportuneness and scope of health care delivered to patients with severe malaria is discussed.

Adolescent↗