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PubMed1998

Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment.

Intensive insulin treatment of IDDM is associated with increased frequency of hypoglycemic coma. The extent of possible cerebral sequelae after recovery is still unknown. We studied the impact of previous hypoglycemic coma on neurophysiological measures of cognitive brain function in 108 patients with adult-onset IDDM receiving intensive insulin treatment. In the study, 55 IDDM patients (age 38 +/- 14 years, mean +/- SD) who had a history of > or =1 (median 3, range 1-35) comatose hypoglycemic event were compared with 53 IDDM patients (age 34 +/- 12 years) with no history of hypoglycemic events using P300 event-related potentials and psychometric tests (the Mini-Mental State Exam and trailmaking test, part A). Findings on these patients were compared with those from 108 matched healthy control subjects. No difference was observed in P300 latencies and psychometric tests between patients with and without a history of hypoglycemic coma (P300 latency, 346 vs. 342 ms; trailmaking test, 31 vs. 30 s; Mini-Mental State Exam, 29.5 vs. 29.6; NS). In diabetic patients, however, P300 latencies were delayed compared with those of healthy control subjects (344 vs. 332 ms; P < 0.001) and were correlated to diabetes duration but not to total hypoglycemic episodes. Scores on the Mini-Mental State Exam (29.5 vs. 29.6; P = 0.59) and trailmaking test (31 vs. 28 s; P = 0.10) were not different between patients and control subjects. In conclusion, previous episodes of hypoglycemic coma are not associated with permanent impairment of cognitive brain function in patients with adult-onset IDDM receiving intensive insulin treatment compared with patients without such episodes. Cognitive brain function, however, is subclinically impaired in relation to duration of diabetes.

Adult↗
PubMedDate not supplied

Coma associated with flaccidity produced by fluid-percussion concussion in the cat. II: Contribution of activity in the pontine inhibitory system.

In the preceding paper we reported that concussive levels of fluid-percussion head injury can produce transient flaccidity of postural muscles associated with other indices of coma. This reversible coma associated with flaccidity follows an initial period of generalized areflexia and occurs in the absence of EEG slow waves. The present study investigated the physiological mechanisms underlying the flaccidity following concussive head injury be recording dorsal and ventral root potentials of the spinal cord. Studies indicated that, during the initial period of generalized areflexia, afferent input transmission was depressed although the excitability of motoneuronal pools was increased. In contrast, during periods of flaccidity, spinal cord somatomotor functions were depressed while transmission of afferent inputs was recovering. Systematic transection of the brain stem showed that activity within structures lying between collicular and midpontine levels is necessary to produce this latter condition. Cholinergic activation of pontine inhibitory areas within this same region of the rostral pons can produce profound descending inhibitory influences on postural somatomotor function in conjunction with other features of coma including suppression of eye-opening responses. Such effects occur without EEG slow waves. Moreover, other data indicate that local rates of glucose utilization within this pontine inhibitory area increase following concussive head injury. Thus, it is possible that a predominance of activity within the pontine inhibitory area could provide at least one neural basis for the reversible comatose state following concussive head injury characterized by close association between flaccidity and other indices of coma. Possible relationships of these data to clinically observed features of concussion are discussed.

Animals↗
PubMed1978

Hypothalamic hypothyroidism and hypogonadism in prolonged traumatic coma.

Prolonged coma afterhead trauma is associated with depletion of 3', 5' cyclic adenosine monophosphate (cAMP) in the cerebrospinal fluid (CSF). Because cAMP has previously been implicated in neurorendocrine secretion, this study examines the pituitay-hypothalamic function in 15 adult male patients (to exclude the effects of puberty and menses) with traumatic coma lasting longer than 2 weeks. Ventricular CSF cAMP was measured at 2- to 4-day intervals for 10 to 25 days. Simultaneously, plasma hormone concentrations were also determined. In all 15 cases, CSF cAMP and plasma levels of thyroid-stimulating hormone (TSH), thyroxine (T4), free T4, triiodothyronine (T3), luteinzing hormone (LH), follicle-stimulating hormone (FSH), and testerone became subnormal. In 11 patients whose level of consciousness fluctuated, the reduction in plasma T4 and testerone were proportional to both severity of coma ( r greater than 0.81, p less than 0.05) and depletion of CSF cAMP (r greater than 0.81, p less than 0.05). In four patients who remained deeply comatose for 17 to 25 days, the hypothyroidism and hypogonadism persisted. In six patients who regained consciousness, both endocrine defects improved partially or completely. Injection of 1) thyrotrophic-releasing hormone and 2) gonadotrophic-releasing hormone elicited normal or supernormal increases in plasma concentrations of 1) TSH, and 2) LH and FSH, reduced, respectively, suggesting a suprahypophyseal deficiency. These observations demonstrate that suprahypophyseal hypothryoidism and hypogonadism may occur regularly in patients with traumatic coma lasting longer than 2 weeks.

Adult↗
PubMed1981

Barbiturate-induced coma therapy for focal cerebral ischemia. Effect after temporary and permanent MCA occlusion.

The authors have studied the therapeutic effect of barbiturate coma following middle cerebral artery (MCA) occlusion in primates. The relationship of the efficacy of barbiturate protection to the presence or absence of recirculation was examined. Barbiturate therapy was begun 30 minutes after MCA occlusion. The findings were as follows: 1) barbiturate-induced coma, with its attendant monitoring, was safely tolerated by primates for 96 hours; 2) 6 hours of MCA occlusion followed by recirculation resulted in a neurological deficit that was worse than the neurological deficit produced by permanent MCA occlusion; 3) barbiturate-induced coma for 96 hours, initiated 30 minutes after the onset of MCA occlusion, in the absence of reperfusion, was in fact detrimental; 4) barbiturate-induced coma for 96 hours, initiated 30 minutes after MCA occlusion, with the establishment of reperfusion at 6 hours, provided nearly complete protection from ischemic damage.

Animals↗
PubMed1982

The effects of deep barbiturate coma on multimodality evoked potentials.

The authors report their investigation of the effects of high-dose barbiturates on the multimodality evoked response in 9 cats. After baseline evoked responses were obtained, boluses of pentobarbital were infused intravenously at regular intervals, amounting to cumulative total doses of 9, 18, 27, 45, 63, 123, and 183 mg/kg at respective infusions. This resulted in gradually increasing serum pentobarbital levels, reaching therapeutic coma levels (4 to 5 mg/dl) after the fifth infusion. At this point, the electroencephalogram was flat, and pressor agents were required to maintain cardiovascular stability. Evoked responses were obtained 15 minutes after each infusion. Brain-stem auditory evoked response (BAER) showed little change in wave latencies at therapeutic coma levels of pentobarbital. Further barbiturates resulted in delay of the late components of this response. In the somatosensory evoked responses (SER), early brain-stem components were relatively unaffected by therapeutic coma levels. Late brain-stem components and the initial cortical response showed progressive latency increase. Late cortical (association cortex) waves were abolished at relatively low doses. The central conduction time was relatively unaffected. The late waves of the visual evoked responses (VER) were abolished with low-dose barbiturates (9 mg/kg). A single positive-negative complex persisted despite massive infusions. It is concluded that evoked responses may prove useful in monitoring patients in deep barbiturate coma, but barbiturate effects must be kept in mind.

Animals↗
PubMed1988

Acute epidural hematoma: an analysis of factors influencing the outcome of patients undergoing surgery in coma.

Mortality due to epidural hematoma is virtually restricted to patients who undergo surgery for that condition while in coma. The authors have analyzed the factors influencing the outcome of 64 patients who underwent epidural hematoma evacuation while in coma. These patients represented 41% of the 156 patients operated on for epidural hematoma at their centers after the introduction of computerized tomography (CT). Eighteen patients (28.1%) died, two (3.1%) became severely disabled, and 44 (68.8%) made a functional recovery. The mortality rate for the entire series was 12%, significantly lower than the 30% rate observed when only angiographic studies were available. A significant correlation was found between the final result and the mechanism of injury, the interval between trauma and surgery, the motor score at operation, the hematoma CT density (homogeneous vs. heterogeneous), and the hematoma volume. The patient's age, the course of consciousness before operation (whether there was a lucid interval), and the clot location did not correlate with the final outcome. The mortality rate was significantly higher in patients operated on within 6 hours or between 6 and 12 hours after injury than in those undergoing surgery 12 to 48 hours after injury. Compared with the patients operated on later, the patients undergoing surgery in the early period were, on the average, older and had more rapidly developing symptoms, more pupillary changes, lower motor scores at surgery, larger hematomas, a higher incidence of mixed CT density clots, more severe associated intracranial lesions, and higher postoperative intracranial pressure (ICP). The mechanism of trauma seems to influence the course of consciousness before and after surgery. Passengers injured in traffic accidents had a lower incidence of a lucid interval and longer postoperative coma than patients with low-speed trauma, suggesting more frequent association of diffuse white matter-shearing injury. The duration of postoperative coma correlated with the morbidity rate in survivors. Forty-eight patients (75%) had one or more associated intracranial lesions, and 70% of these required treatment for elevation of ICP after hematoma evacuation. An ICP of over 35 mm Hg strongly correlated with poor outcome; administration of high-dose barbiturates was the only effective means for lowering ICP in nine of 15 patients who developed severe intracranial hypertension after surgery. This study attempts to identify patients at greater risk for presenting postoperative complications and to define a strategy for control CT scanning and ICP monitoring.

Acute Disease↗
PubMed1999

The ciliospinal reflex in pentobarbital coma.

OBJECT: This study was conducted to delineate the ciliospinal reflex (CSR), which is defined as pupillary dilation caused by a noxious stimulus to the face or head. The authors anecdotally observed that patients in a pentobarbital coma have a CSR that can mimic pathological conditions. A pentobarbital coma obscures the results of the neurological examination in patients with potentially life-threatening cerebral edema; pupil size and reactivity are the only readily monitored signs. Any condition that incorrectly suggests evolving intracranial pathological processes can lead to unnecessary clinical actions. METHODS: The authors evaluated six consecutive patients in the neurointensive care unit in whom a pentobarbital coma had been induced, documenting the presence and duration of the CSR. The CSR was always bilateral and symmetrical, manifesting as enlarged (6-8 mm), seemingly nonreactive pupils continuing from 1 to 6 minutes and was usually seen after routine nursing maneuvers. The pupils appeared nonreactive to short flashes of direct light but did react if longer flashes were used. CONCLUSIONS: Recognition of the CSR can potentially lead to reduction of unnecessary transportation and complicating medical interventions in critically neurologically ill patients in whom a pentobarbital coma has been induced.

Adult↗
PubMed1981

Prognosis in nontraumatic coma.

We conducted serial neurologic examinations on 500 patients in nontraumatic coma to identify factors predicting recovery. Overall, 81 patients (16%) led an independent life at some point within the first year; the remainder either died without recovery from coma (61%), never improved beyond the vegetative state (12%), or regained consciousness but remained dependent on others for daily activities (11%). Functional recovery did not depend on age but was to some degree related to the cause of coma (subarachnoid hemorrhage and other cerebrovascular disease having the worst recovery; hypoxia-ischemia, intermediate; and hepatic and miscellaneous causes, best) and especially to early clinical signs of brain dysfunction. Even within hours of the onset of coma, only one of 120 patients lacking two of corneal, pupillary, and oculovestibular responses ever regained independent function. The study identifies clinical features of comatose patients that appear within the first week and that are important for predicting recovery and designing future therapeutic trials.

Adult↗
PubMed2000

Myxedema coma: diagnosis and treatment.

Myxedema coma, the extreme manifestation of hypothyroidism, is an uncommon but potentially lethal condition. Patients with hypothyroidism may exhibit a number of physiologic alterations to compensate for the lack of thyroid hormone. If these homeostatic mechanisms are overwhelmed by factors such as infection, the patient may decompensate into myxedema coma. Patients with hypothyroidism typically have a history of fatigue, weight gain, constipation and cold intolerance. Physicians should include hypothyroidism in the differential diagnosis of every patient with hyponatremia. Patients with suspected myxedema coma should be admitted to an intensive care unit for vigorous pulmonary and cardiovascular support. Most authorities recommend treatment with intravenous levothyroxine (T4) as opposed to intravenous liothyronine (T3). Hydrocortisone should be administered until coexisting adrenal insufficiency is ruled out. Family physicians are in an important position to prevent myxedema coma by maintaining a high level of suspicion for hypothyroidism.

Coma↗
PubMed2000

The usefulness of EEG, exogenous evoked potentials, and cognitive evoked potentials in the acute stage of post-anoxic and post-traumatic coma.

Three-modality evoked potentials (TMEPs) have been used for several years in association with the EEG as a diagnostic and prognostic tool in acute anoxic or traumatic coma. Cognitive EPs have been recently introduced. EEG and cognitive EPs provide functional assessment of the cerebral cortex. TMEP parameters can be described by two indices: the index of global cortical function (IGCF) and the index of brainstem conduction (IBSC). Although it remains a unique tool for epilepsy assessment, the value of EEG is largely limited by its high sensitivity to the electrical environmental noise, its dependence on sedative drugs, and its inability to test the brainstem. Major TMEP alterations (absence of cortical activities more than 24 hours after the onset of post-anoxic coma, major pontine involvement in head trauma) are associated in all cases with an ominous prognosis (death or vegetative state). However, even if mild TMEP changes are associated with a good prognosis in 65% (post-anoxic coma) to 90% (head trauma) of cases, some patients never recover despite exogenous TMEPs that are only mildly altered in the acute stage. Thus, cognitive EPs can usefully complement exogenous EPs as a prognostic tool in coma. Indeed, even if the absence of cognitive EPs in comatose patients does not have any prognostic value, their presence implies a very high (more than 90%) probability of consciousness recovery. The major technical challenge for the future will be the development of reliable tools for continuous EEG and TMEP monitoring.

Acute Disease↗
PubMedDate not supplied

The Glasgow Coma Scale in intensive care: a study.

This study reviewed neurological assessment and therapeutic intervention records of adult, intubated, sedated and ventilated patients who had sustained a severe cerebral insult. The purpose of the study was to determine whether the Glasgow Coma Scale detected neurological change in the ventilated, sedated patient. In addition the study aimed to establish whether changes to therapeutic intervention took place in response to an alteration in Glasgow Coma Scale parameters. A retrospective analysis of patient observation records was conducted and descriptive statistics presented. The study found that the Glasgow Coma Scale did not predict or correlate with a sustained rise in intracranial perfusion pressure (ICP) in ventilated and sedated patients. Changes in therapeutic intervention appear to be initiated in response to changes in a number of differing parameters. It is suggested that it may not be appropriate to use the Glasgow Coma Scale as a neurological assessment tool in ventilated and sedated patients.

Adolescent↗
PubMed1992

Diabetic ketoacidosis and hyperosmolar coma.

DKA-hyperosmolar coma is a readily diagnosed and easily treated, potentially catastrophic emergency that regularly occurs in both Type I and Type II diabetics. This review emphasized that diabetic ketoacidosis and hyperosmolar coma can, and very frequently do, occur concurrently, but it is the hyperosmolar state rather than the DKA that is the primary cause of coma and death in this condition. One must therefore vigorously treat the hyperosmolarity and resulting dehydration, especially when total calculated osmolarity exceeds 230 to 240 mOsm/L. The major aim of treatment is to rapidly replace the major water loss that is responsible for this clinical condition and to stimulate glucose metabolism with insulin. The diagnosis of this dangerous condition is relatively simple. The therapy, in most regards, is equally apparent. There are good data demonstrating that the prompt recognition of DKA-hyperosmolar coma and the simple institution of rapid rehydration have continued to reduce the mortality and complications of this potentially disastrous complication of diabetes mellitus.

Diabetes Complications↗
PubMed1992

[Early rehabilitation of coma patients on the neurosurgical intensive care station. On the philosophy and practice of interdisciplinary cooperation].

The concept of early rehabilitation is an important task of humanity for neurosurgical intensive care patients emerging from coma. In Germany only little experience in this field has been reported, although the concept of early rehabilitation is well known in the other western European countries and the USA. In connection with the author's teaching activities at the pedagogical and psychological departments of the University of Oldenburg, an interdisciplinary concept of communicative "cooperative dialogues" was established for early rehabilitation, beginning in the earliest phases of coma at the neurosurgical intensive care unit. Although the results could not be evaluated statistically yet, the clinical course and outcome of emergence from primary or postoperative coma have improved rapidly by single patients, based on mobilization of neuronal plasticity and self-organized processes. Because of a significant lack of possibilities of early rehabilitation in the northwestern part of Germany, especially for young head injured adults, our efforts will continue. The philosophy and practice of early rehabilitation propose a new interpretation of neurosurgical patients emerging from coma, i.e. a dynamic process of a "second human creation". Early rehabilitation is an important task for the neurosurgically working doctor. Also for the neurosurgical profession the concept of early rehabilitation has to be integrated interdisciplinary to medical teaching at university level as soon as possible.

Activities of Daily Living↗
PubMed2006

New coma scale offers option to Glasgow.

A new coma scale called the FOUR Score may provide ED managers with an alternative to the Glasgow Coma Scale. Here are some of the advantages it offers: the ability to test brainstem reflexes to obtain a clearer picture of neurological status, according to the scale's developer; greater simplicity. In the new scale, every component has a maximal score of 4. In the Glasgow Coma Scale, the maximal number varies with each component; the ability to learn more about the condition of intubated patients than you can with the Glasgow Coma Scale.

Coma↗
PubMed1977

[Comas of realimentation].

Parenteral realimentation in the patient with severely impaired nutrition is sometimes associated with the development of a metabolic encephalopathy with coma. The onset of this complication is sudden. The coma is deep, accompanied by signs of neuromuscular hyperexcitability and very marked hyperventilation. It generally regresses rapidly, without sequellae. The onset of such a realimentation coma should be feared in the presence of a certain combination of conditions : severely impaired nutrition, parenteral alimentation with a high level of nitrogen and calories, transfer to the anabolic phase (perfect carbohydrate utilisation, fall in blood phosphate levels with hypophosphaturia, sometimes very marked positivisation of nitrogen balance) and, sometimes, mild premonitory clinical signs. The relationship between this type of complication and hypophosphoraemia is quite definite, but the fall in serum phosphates would not appear to be directly responsible for the coma. The exact mechanism is not known. In order to avoid such complications, great caution should be observed in both the quality as well as the quantity of the intake, as well as in the clinical and laboratory surveillance of the malnourished patient undergoing realimentation.

Coma↗
PubMed1989

[Coma and cerebral death].

The concept of cerebral death is universally accepted. It rests on a panel of signs which must all be present and constant, and provided this is the case no error is possible. No authentic case throwing doubt on this statement has ever been reported. It has been said that the term "coma dépassé" which we chose in 1959 could lead to confusion with the different degrees of coma and for this reason, be an obstacle to organ donation. I do not consider this a satisfactory explanation. In favour of the appellation "coma dépassé" are the originality of its first description and its use in the French medical language. It does not matter if "cerebral death" is preferred, both terms being synonymous. The individualization of "coma dépassé" and the possibility of grafting organs with success are acquisitions separated by only a few years. They have made it possible to obtain the remarkable successes known to every one, they have given medical thinking a new dimension and placed upon doctors an increased responsibility.

Brain Death↗
PubMed1989

Validity of a revised EEG coma scale for predicting survival in anoxic encephalopathy.

A revised EEG grading scale in coma has been introduced previously. This scale is based on the internationally accepted 5 grade scale but also contains uncommon patterns such as spindle, alpha and theta pattern comas. By defining 15 separate grades and subgrades it was possible to reduce the number of patterns of uncertain prognostic significance for survival to 4 out of the 15 possible patterns. It is also hoped that by a clear definition of individual grades and subdivisions the scale will assist electroencephalographers who lack experience of coma cases. The validity of the scale has been tested in a group of 63 patients who suffered cardiac arrest in excess of 7 minutes' duration. The EEG was performed 24 to 36 hours after the onset of coma. The accuracy of prediction for survival was 98.4%, a rate higher than in previously published studies. The mortality rate was 70%, 19 patients surviving. There was a statistically significant correlation between mortality rate and duration of cardiac arrest and also between mortality rate and increasing age. Four suggested scale subdivisions did not occur in the material studied but these subdivisions are more common in traumatic encephalopathies. This study shows that an EEG performed 24 to 36 hours after cardiac arrest provides significant information for the prediction of survival. No specific patterns of microscopic changes in the brain were found to correlate with individual EEG abnormalities in fatal anoxic encephalopathies.

Adult↗
PubMed1987

Causes and early prognosis of non-traumatic coma in Tanzania. Muhimbili Medical Centre experience.

150 patients admitted in medical coma at Muhimbili Medical Centre were studied prospectively to determine the causes and early prognosis. 89 (60%) patients had potentially treatable causes (60 cerebral malaria, 16 meningitis, 7 diabetic ketoacidosis and 6 drug over dosage). Other causes were 20 (13%) with cerebrovascular diseases, 30 (20%) hepatic failure and 11 (8%) were of miscellaneous and obscure causes. The cause of coma was an important indicator of prognosis. Good recovery was achieved in 42 (70%) with cerebral malaria, 4 (57%) diabetic ketoacidosis, 4 (25%) meningitis and 1 (16%) drug overdosage. Other indicators were the Glasgow Coma Score on admission and subsequent scores, early neurological signs and complications that arose. The Glasgow Coma Scale was found useful and easy to perform. Further studies are needed to confirm its usefulness in developing countries.

Adolescent↗