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At least 19 recordsLinked to original sources
PubMed1976

The blink reflex in coma and after recovery from coma.

Comparative studies of the blink reflex in a series of head injuries through the stages of coma and recovery from coma in a series of miscellaneous hemispheral lesions, and in a normal series, reveals that, although the principal centre for the R1 component of the blink reflex seems to be localised in the upper pons, the seat of the R2 late component is in the reticular system. The reappearance of this late component of the blink reflex in our cases of coma although seeming to depend on the integrity of the mesencephalic formation, correlates with the recovery of the patient's alertness. On the other hand, habituation of this reflex depends on the integrity of global cognitive function, rather than on any localised centre. The roles of the cortex, selective attention, and emotional factors, are discussed. The recovery of the normal habituation of the blink reflex obtained by glabellar tapping was found to be a useful sign in the follow up of patients recovering from concussion and other lesions, such as subdural haematomas and brain tumours, with global mental impairment.

Adult↗
PubMed1976

[Acute hepatic coma. Experimental study on the predictive value of clinical-chemical findings for the prognosis of acute hepatic coma].

In order to determine the validity of clinical-chemical parameters for the prognosis of hepatic failure, 28 pigs were subjected to liver ischemia for 40--160 minutes duration. The following parameters were studied: GOT, GPT, gamma-GT, LAP, LDH, GlDH, AP and isoenzymes, total bilirubin, potassium, sodium and chloride. In a statistical comparison in the surviving animals, an unexplainable increase in GlDH activity was observed. In the other clinical-chemical parameters none was seen to be of use for the prognosis for either life or death in acute hepatic failure.

Acute Disease↗
PubMed1979

Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units.

In 181 patients resuscitated from cardiac arrest, the prevalence and duration of coma were registered and related to the site of occurrence of cardiac arrest, cardiac rhythm during arrest, age and clinical outcome of the patients. Coma was most frequent after cardiac arrest outside the hospital, as 84% of these patients were comatose for more than 1 h and 56% for more than 24 h; the corresponding values for patients with cardiac arrest in general wards were 63% and 30%, respectively, and for patients with cardiac arrest during ambulance transport, 80% and 44%. Permanent brain damage was extremely rare if the coma lasted less than 6 h (1 out of 62 patients), and relatively rare with a coma duration between 6 and 24 h (5 out of 34 patients). Of the patients, 85 remained comatose for more than 24 h and only 7 of them were discharged alive, all with cerebral impairment of a severity increasing with the duration of the coma. None regained consciousness after more than 7 days' coma, and a total of 80 patients died in coma, 20 with signs of cerebral death. Older patients were more vulnerable to coma than younger ones, but coma as such was not more frequent. We found no differences in coma after asystole and ventricular fibrillation. Problems concerning the selection of patients who have a chance of survival, although comatose after cardiac arrest, are discussed.

Adolescent↗
PubMed1978

Brain monoamines in hepatic encephalopathy and other types of metabolic coma.

Tyrosine (Tyr), tyrosine hydroxylase (TH), tryptophan (Trp), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed spectrofluorometrically and radioenzymatically in various regions of post-mortem brains of human patients with hepatic, uremic, and diabetic coma, liver cirrhosis without coma, and hepatic coma treated with parenteral administration of L-valine, a branched-chain amino acid. The results were as follows: In both hepatic and diabetic coma Tyr was increased as compared to non-comatose cirrhosis and controls, while TH acitivity was within normal limits, indicating sufficient oxygen supply of the brain in both types of coma. Brain DA showed a mild decrease in all types of metabolic coma. Brain Trp was not considerably changed in non-comatose cases of liver cirrhosis and after L-valine treatment of hepatic encephalopathy, but was significantly increased in hepatic coma, with highest elevation in the brainstem tegmentum. Both 5-HT and 5-HIAA were not significantly changed in non-comatose cirrhosis, while a general increase with prevalence for the brainstem was obvious in all types of metabolic coma. After L-valine treatment of hepatic coma, 5-HT levels were usually decreased below control values, while 5-HIAA levels were at or below controls. These results in human post-mortem brains confirm previous CSF and brain findings in experimental and human hepatic and uremic encephalopathies, indicating derangement of brain monoamine neurotransmitter metabolism which is attributed to imbalance of aromatic and branched-chain amino acids in plasma and brain. Increased cerebral 5-HT turnover, particularly in the ascending serotonergic brainstem systems, due to derangement of brain uptake of Trp is suggested to represent an important biochemical substrate of disorders of consciousness in hepatic failure and other types of metabolic encephalopathies. Clinical improvement of hepatic encephalopathy and of the underlying neurotransmitter derangements by administration of L-valine and the possible role of this competitive amino acid on intermediary metabolism and ammonia detoxification are discussed.

Aged↗
PubMed1977

[Hepatic coma--causes, recognition, treatment].

The name of the disease coma hepaticum is a collective notion for etiologically, pathologo-anatomically and biochemically different kinds of a failure of the function of the liver. A demarcation of different forms of the liver coma is necessary above all for prognostic and therapeutic reasons: hepatic disintegration coma, coma in hepatic failure, mixed coma, false hepatic coma, ferment block coma. Despite certain progress the therapeutic possibilities in hepatic coma cannot satisfy in recent years. Also the use of different, partly very expensive methods of the so-called liver substitute (exchange function and plasmapheresis, heterologous and homologous extracorporal liver perfusion, parasymbiotic crossed circulation, haemoperfusion with encapsulated activated charcoal, liver transplantation) up to now did not lead to a decisive improvement of the nearly infaust prognosis of the hepatic disintegration coma. Therefore preventing measures and careful control of endangered patients deserve particular attention.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Significance of epileptic seizures occurring during the first week of traumatic coma (author's transl)].

Clinically evident epileptic seizures were observed in 145 patients during the first week of traumatic coma. They frequently occurred during the first day in young subjects in reactive coma, and were often isolated attacks. When ssen at a later stage they are more common in adults with non-reactive coma. The partial or generalised nature of the seizures, the depth of the coma, and the chronological order in which the seizures appear have no bearing on the etiology; the only positive finding was that recurrent seizures were more frequent in patients with intracranial hematoma (18,6% of the patients). The early appearance of seizures does not worsen the prognosis of reactive coma or non-reactive coma in young people. Critical discharges without clinical manifestations were present in 37 patients with traumatic coma during the first week. The average age of these injured patients was higher, and the prognosis for non-reactive coma worse in this group. The comatous state does not modify the clinical aspects or the etiological significance of these early post-traumatic discharges.

Adolescent↗
PubMed1978

[Differences in plasma aminograms in hepatic and diabetic coma].

In hepatic coma as well as diabetic coma severe disturbances occur in the amino acid metabolism. The defect lies in completely different levels which result two different plasma aminograms (PAG). In 24 patients with hepatic encephalopathy stage III-IV (7 patients with acute and 17 with chronic liver failure) the PAG were evaluated. The determination of the plasma amino acids (PAA) was carried out on Multichrom B (Beckmann, Munich). In hepatic coma high concentrations of Met, Tyr, Ala, Lys and Arg are found. The deviations of PAA from normal controls show between acute and chronic hepatic failure no qualitative but only quantitative differences. In diabetic coma the three branches chain AA (Val, Leu and Ile) were elevated upon 3--5 times of normal. Near normal concentrations are found for the AA Thr, Ser, Gly, Ala, Met and the aromatic AA (Phe and Tyr). The quotient between the branched chain and aromatic AA lies for hepatic coma at a mean of 1.18 and by diabetic coma at 7.18 (p less than 0.001). In hepatic coma a correlation exists between the level of the AA-quotient improvement and the decrease with a deterioriation of the metabolic encephalopathy. The high level of the AA-quotient in the patients of diabetic "coma" gives therefore a good explanation for the rare unconscious state of these patients.

Adult↗
PubMed1977

Clinical course and prognosis of one hundred and two patients with hepatic coma 1958 through 1975.

The clinical course and prognosis of hepatic coma were examined in 102 patients treated in the period from 1958 to 1975. The diagnoses included 9 fulminant hepatitis, 7 subacute hepatitis, 53 liver cirrhosis without liver carcinoma (40 cases of the acute type, 10 cases of the chronic type and 3 cases of another type, according to Sherlock's classification of hepatic coma) and 33 liver cirrhosis with primary liver carcinoma. Four of 9 fulminant hepatitis patients gained consciousness within 1 week and recovered completely. Seven subacute hepatitis patients died within 2 weeks after onset of hepatic coma. In the period from 1958 to 1969, 20% of liver cirrhosis patients with the acute type of coma recovered from coma, and in the period from 1970 to 1975, 45% of patients recovered. Seven of 10 patients with the chronic type of coma died between 4 months and 9 years after the onset of coma. Three other patients are presently still alive. The median survival time was 2.5 years. Nine primary liver carcinoma patients with coma were hospitalized from 1958 to 1969 and 24 from 1970 to 1975. Hepatorenal syndrome was present in 31 of 71 examined patients. Twenty-three patients with hepatorenal syndrome were in the period from 1970 to 1975.

Adolescent↗
PubMed1975

Correlation between brain monoamine levels and postictal coma following electroshock.

Duration of postictal coma following maximal electroshock seizure and monoamine levels in the whole brain were measured in mice. Pretreatment with intraperitoneal alpha-methyl-p-tyrosine (alpha-MT), 5-hydroxytryptophane (5-HTP), or intraventricular 6-hydroxydopamine (6-OHDA) prolonged the coma duration, whereas p-chlorophenylalanine (PCPA) did not affect the coma, and L-DOPA tended to shorten the coma and counteracted the effect of alpha-MT. When the shock was repeated five times with one hour intervals, the duration of coma was progressively increased being accompanied by elevated serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) levels in the brain. In alpha-MT treated group, a striking parallelism was remarked between coma prolongation and norepinephrine (NE) or dopamine (DA) reduction. These data suggest that prolongation of postictal coma is correlated with reduced NE and DA levels and/or with elevated 5-HT and 5-HIAA levels in the brain.

Animals↗
PubMed1992

[The type of coma as prognostic indicator in severe cranial trauma in childhood].

Various methods are used by neurologists to evaluate posttraumatic brain damage. The most important and reliable are the length of posttraumatic amnesia and coma. In previous papers we have already described the value of the type of coma in the prognosis of serious head injury in childhood (Baracchini-Muratorio et al. 1985; Pruneti et al. 1985). In this study, 30 children (aged 6-12 years) with serious closed head injury and subsequent coma were evaluated. The children were divided into two groups according to the type of coma, using the Plum and Posner coma classification (1966) modified by Pagni et al. (1974). The children were followed up for at least two years (9 for five years) after the trauma by means of neurological, physical, EEG, CT scan and neuropsychological examinations. The neuropsychological test results confirm the hypothesis of a different evolution of sequelae in relation to the type of coma, independently of length of coma and site of brain damage.

Adolescent↗
PubMed1979

Hyperammonemic coma after hepatectomy in germ-free rats.

Current theories on the pathogenesis of hepatic coma indicate that intestinal bacteria produce cerebral toxins, such as ammonia, mercaptans, and short-chain fatty acids. To test the hypothesis that elimination of anaerobic and aerobic intestinal bacteria retards the onset and alters the biochemical profile of acute hepatic coma, we determined the onset of coma and the ammonia concentration in blood and cecal contents in 7 germ-free and 10 normal dehepatized rats. Ammonia levels were also determined in a further group of 7 germ-free and 12 normal rats 24 hr after hepatic vascular exclusion was accomplished. Onset of coma for germ-free rats (x: 34 hr) was identical to that of normal rats (x: 36 hr). Arterial ammonia was equally elevated in germ-free rats (x: 834 mumol/liter) and in normal rats (x: 854 mumol/liter), although the ammonia concentration in the cecal contents was significantly lower in germ-free rats (x: 1762 mumol/liter) than in normal rats (x: 5572 mumol/liter). In germ-free animals, portal venous blood contained more ammonia than arterial blood (x A-V difference: -87 mumol/liter), indicating nonbacterial intestinal ammonia release. We conclude that intestinal bacteria toxins are of minor importance in the mechanism of acute hepatic coma of the liverless rat and that presumably bacterial toxins, such as ammonia, can be products of nonbacterial metabolism. Since hyperammonemia could be considered an important determinant of coma in our model, prevention of hyperammonemia in functionally anhepatic animals should be the next objective in unraveling the pathogenesis of acute hepatic coma.

Ammonia↗
PubMed1978

[Hormone and metabolic profile in diabetic hyperosomolar coma. Plasma insulin response to intravenous tolbutamide (author's transl)].

Fifteen patients with non-ketotic hyperosmolar diabetic coma were investigated and compared with ketoacidotic patients. Basal plasma insulin levels were low in all patients (14.8 +/- 1.0 micronU/ml in hyperosmolar coma, 11.0 +/- 1.3 in keto-acidosis), but insulin level increased after intravenous tolbutamide (between 30 and 105 micronU/ml) in eight hyperosmolar comas. Insulin showed no increase in seven hyperosmolar comas and in none of the ketoacidotic patients. In hyperosmolar coma plasma free fatty acids (1710 +/- 197 micronEq/1), triglycerides (3,4 +/- 0,4 g/1) and cortisol levels (49,7 +/- 9,0 microgram/100 ml) were increased, must as in keto-acidosis. Growth hormone (1,7 +/- 0,1 ng/ml) was normal, unlike the case in keto-acidosis. Plasma lactate concentrations were elevated and account for the frequent mild acidosis found in hyperosmolar coma. In spite of the low peripheral "insulin/glycemia ratio", the positive response to tolbutamide in half of the hyperosmolar cases suggests a less complete pancreatic deficiency than in keto-acidosis. The plasma high free fatty acid and triglyceride levels suggest that the lack of ketosis is not due to inhibition of lipolysis but could be a consequence of inhibition of hepatic ketogenesis.

Adult↗
PubMed1976

Head injury in children and teenagers; functional recovery correlated with the duration of coma.

Residual impairments and mortality were assessed in 48 patients under 20 years of age at least two years after a traumatic head injury had caused coma lasting more than seven days. In this study the duration of coma was defined as the period of time when it is impossible to establish intellectual contact with the patient. A classification of functional levels 1 to 8 was used to identify the residual impairment and relate this impairment to the duration of coma for each patient. Of 30 patients who remained in coma less than three month, only one did not have independent ambulation with or without equipment at the time of his last follow-up evaluation. This was one parameter among others to show that the prognosis for recovery in this age group is much better than expected following severe head injury. These follow-up data, correlated with the duration of coma, can assist rehabilitation personnel in the prognostic planning for younger people with severe head injuries. Rehabilitation medicine needs to be involved in patient care during the period of coma to prevent contractures and other complications which often interfere with and delay later rehabilitation programs, making them more costly and less successful.

Adolescent↗