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Although dermal lesions in patients with drug poisoning have been widely documented, similar oral conditions are seldom reported. A case of cutaneous and oral mucosal necrosis related to barbiturate-induced coma is reported.
The low pressure reactions of sulfur dioxide, carbon disulfide, and hydrazine with H2O+ and H3O+ were studied by the ion cyclotron resonance technique. These reactions are potentially important for sulphur chemistry in cometary comae. Rate coefficients and branching ratios of product channels are presented.
Alterations in several neurotransmitter systems in brain have been implicated in the pathophysiology of hepatic coma (HC). Studies on human autopsy material are few. We investigated 3H-quinuclidinylbenzilate (QNB), 3H-spiperone, 3H-imipramine, 3H-PN-200-110, 3naloxone, 3H-flunitrazepam, 3H-muscimol, 35S-t-butylbicyclophosphothionate and 3H-cyclohexyladenosine binding sites in frontal cortex from seven patients with HC and five controls. The density of 3H-QNB binding sites was significantly decreased and the affinity slightly increased in HC. The functional significance of these selective changes in muscarinic receptor binding sites is unclear. Further studies evaluating cholinergic function in HC are indicated. Acute studies in animals point to an increase in GABA and BZ binding sites in HC. The present results show that the BZ/GABA-receptor-chloride-ionophore complex is unchanged in HC in man. Serotonergic (5HT-2), adenosine (A-1), imipramine (5HT uptake sites), opiate (naloxone) and calcium channel antagonist binding sites are unchanged in HC.
A 64-year-old Turkish male is described with recurrent hepatitic (pre-)coma resulting from a spontaneous porto-spleno-renal shunt, portal hypertension and hepatic insufficiency. In cases of chronic encephalopathy resulting from hepatic insufficiency that may be due to liver cirrhosis, the presence of a spontaneous porto-spleno-renal shunt should be considered as a distinct possibility, not only in the absence of apparent oesophageal varices and splenomegaly, but also when there is hepatopetal flow in the portal vein.
The study has been carried out in order to investigate the effects of some drugs in coma doses on the concentration in brain of some amino acids involved in brain function. Six groups of 25 guinea pigs each were utilized. In each of the five groups a subcutaneous dose of diazepam, flunitrazepam, phenobarbital, phenytoin or alfaxalone, was injected and one group was utilized as control. Some neurotransmitter amino acids (glutamate, aspartate, glycine and taurine) and precursors of neurotransmitters (phenylalanine and tyrosine) were determined in brain preparations. The results are discussed.
Decompensation in the cirrhotic patient is typically manifested as hepatic encephalopathy or coma. This may be precipitated by azotemia, gastrointestinal bleeding, infection, hypokalemic alkalosis, excess dietary protein, or the use of sedative, tranquilizer, or analgesic medications. The pathogenesis of hepatic encephalopathy associated with portal-systemic shunting is unknown, but theories purporting major roles for ammonia, AAAs, false neurotransmitters, and GABA have been advanced. Treatment is aimed at removing precipitating factors and eliminating nitrogenous substances from the gastrointestinal tract.
It is proposed that severe impairment of liver function in cirrhosis or portacaval shunt results in unrestricted entry of insulin into the peripheral circulation. The ensuing high level of insulin promotes excessive removal of the branched-chain aminoacids by muscle, thereby lowering the plasma levels of these aminoacids. In consequence, the competitive action of the branched-chain aminoacids on the entry of tryptophan into the brain is reduced, more tryptophan enters the brain, and serotonin is synthesised in excess, thus facilitating hepatic coma.
The human COMA cell line has been established from a storiform pleomorphic malignant fibrous histiocytoma (MFH). As expected for this tumor type, a very complex karyotype was observed after R-banding analysis. An extensive analysis by 24-color painting, comparative genomic hybridization (CGH), and fluorescence in situ hybridization (FISH) was performed. Twelve complex marker chromosomes recurrently observed were clearly identified; among them, three were systematically present in all analyzed metaphases. Amplifications detected by CGH were refined by FISH with probes specific for various candidate loci. A significant aneuploidy and numerous micronuclei were observed, which could be related to the anomalies of centriole numbers detected in a proportion of cells. Such an analysis, performed on a series of MFH cell lines, would allow the delineation of the genomic alterations specific for the oncogenesis or progression of this complex tumor type or both.
It is reported a case of quadriplegia occurring in a 67-year-old women after she commits suicide with flunitrazepam. The patient stayed during around twenty hours unconscious, in the sitting position, with an extreme flexion of the neck on the left side. After injection of flumazenil the patient's consciousness was restored. Nevertheless a complete sensitive and motor deficit at the C4 and C5 level was then observed. Several diagnosis such as peripheral neuropathy, infectious disease, or arterial occlusion were eliminated and we finally postulated that the regulation of the spinal blood flow had likely been disturbed by the prolonged flexion of the neck, the hypotension and the putative respiratory depression. The fact that the patient suffered from cervicarthrosis would have already impaired the spinal blood flow regulation and consequently had probably damaged the spinal cord. No clinical improvement of the quadriplegia was noticed and the patient died in the intensive care unit thirteen days after admission. Such an exceptional complication after a toxic coma remind us the necessity to avoid long lasting vicious position of the cervical spine in anaesthesia and emergency practice.
We review the nosological criteria and functional neuroanatomical basis for brain death, coma, vegetative state, minimally conscious state, and the locked-in state. Functional neuroimaging is providing new insights into cerebral activity in patients with severe brain damage. Measurements of cerebral metabolism and brain activations in response to sensory stimuli with PET, fMRI, and electrophysiological methods can provide information on the presence, degree, and location of any residual brain function. However, use of these techniques in people with severe brain damage is methodologically complex and needs careful quantitative analysis and interpretation. In addition, ethical frameworks to guide research in these patients must be further developed. At present, clinical examinations identify nosological distinctions needed for accurate diagnosis and prognosis. Neuroimaging techniques remain important tools for clinical research that will extend our understanding of the underlying mechanisms of these disorders.
[reaction: see text] Dialkylmagnesiums react with chiral secondary amines to form chiral organomagnesium amides (COMAs). These reagents alkylate aldehydes to form secondary alcohols with enantioselectivities up to 91:9 er.
Chiral organomagnesium amides (COMAs), readily prepared from dialkylmagnesiums and chiral secondary amines, can reduce trifluoromethyl ketones to form secondary alcohols with excellent enantioselectivities (up to 98:2 er) and chemical yields (typically >95% conversion, >85% isolated yields). These MPV-type reductions use an achiral hydride source, and the chiral amine is readily recovered. [reaction: see text]
Two patients in hepatic coma were treated with L-dopa. The first patient showed clear clinical improvement, but the second patient did not. Analyses of urinary metabolites indicated that L-dopa was not absorbed by the second patient. There was evidence that L-dopa had the following beneficial effects in the first patient: (1) increased production of urine, which could have been accompanied by increased excretion of toxins; (2) displacement of tyramine from transmitter sites (because increased excretion of p-hydroxyphenylacetic acid, a major metabolite of tyramine, occurred during L-dopa treatment in patient 1); (3) replenishment of dopamine, and to a much lesser extent, norepinephrine, at central or peripheral neuroeffector junctions; and (4) scavenging of methyl groups by L-dopa, because ratio of methylated amines to catecholamines was higher than normal in both comatose patients before L-dopa treatment, and this ratio decreased during L-dopa treatment in patient 1.
Significant gas-phase chemistry occurs in the comae of bright comets, as is demonstrated here for the case of Comet Hale-Bopp. The abundance ratio of the two isomers, hydrogen cyanide and hydrogen isocyanide, is shown to vary with heliocentric distance in a way that is consistent with production of HNC by ion-molecule chemistry initiated by the photoionization of water. Likewise, the first maps of emission from HCO+ show an abundance and an extended distribution that are consistent with the same chemical model.
It has been previously reported that following severe brain damage, a deficit of cellular immunity could be detected in the early phase after the occurence of the lesion. We report here the results of a cross-sectional study on long term effects of severe brain damage on immunological and neuro-endocrine changes in patients who recovered from prolonged coma caused by head injury. Results obtained from post-comatose (PC) patients were compared with those obtained from two control groups made up of spinal-cord injury (SCI) patients and healthy subjects, respectively. The following parameters were studied: lymphomonocyte subsets; interleukin 2 (IL-2) production; natural killer (NK) activity and serum levels of adrenocorticotrophic hormone (ACTH), cortisol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, tri-iodothyronine (T3) and thyroxine (T4). With respect to healthy controls the PC1 subgroup, i.e. patients examined 3-6 months after injury, showed a statistically significant decrease in IL-2 production, NK activity and CD25+ lymphocytes. Similar immunological disturbances were observed in SCI but not in the PC2 subgroup, i.e. patients examined later than 6 months after injury. The same sub-group of PC1 patients showed high serum levels of cortisol and PRL. These results could be related to the immunological status and may be interpreted as a transient but prolonged condition of chronic stress or "chronic alarm reaction". Copyright Rapid Science Ltd
Using the model of galactosamine-induced fulminant hepatic failure in the rat, the effects of multisorbent plasma perfusion over Asahi uncoated spherical charcoal, Plasorba (BR-350) resin, and an endotoxin removing adsorbent (polymyxin B-sepharose) were determined in Grade III hepatic coma animals by studying survival as influenced by timing, duration, and frequency of treatment. The effects of treatment on liver cell proliferation and endotoxin removal also were examined. The results demonstrate that duration and frequency of treatment are major contributing factors in the successful application of nonbiological membrane-based multisorbent liver support systems. Examination of the regenerative activity in the liver indicates an enhanced proliferative response following multisorbent plasma perfusion compared with untreated fulminant hepatic failure (FHF) paired controls. Utilizing an endotoxin removal adsorbent alone, a marked reduction in systemic levels of endotoxin in FHF was demonstrated compared with nonperfused FHF paired controls. Despite current emphasis on bioartificial liver support systems, plasma purification by multisorbent systems offers a simple method for the removal of circulating toxic metabolites in general together with specific toxin removal.
Fulminant hepatic failure is an extremely rare coma syndrome resulting from massive necrosis of liver cells. A wide variety of etiologic agents have been identified, including viruses, drugs, and other toxic agents. Treatment focuses on reducing the ammonia load presented to the liver and on preventing or controlling complications, including sepsis, bleeding, cerebral edema, renal failure, and respiratory failure. With further research and identification of the specific toxins or metabolic derangements underlying the pathophysiology of this syndrome, more effective therapeutic measures may be devised.
We present 1-20 micrometers photometry of P/Giacobini-Zinner obtained at the NASA Infrared Telescope Facility, during 1985 June-September (r = 1.57-1.03 AU). A broad, weak 10 micrometers silicate emission feature was detected on August 26.6; a similar weak emission feature could have been hidden in the broadband photometry on other dates. The total scattering and emitting cross section of dust in the inner coma was similar to that in other short-period comets, but a factor of 10 (r = 1.56 AU) to 100 (r = 1.03 AU) lower than the amount of dust in Comet Halley. The thermal emission continuum can be fit with models weighted toward either small or large absorbing grains. The dust production rate near perihelion was approximately 10(5) g/s (small-grain model) to approximately 10(6) g/s (large-grain model). The corresponding dust/gas mass ratio on August 26 was approximately 0.1-1. A silicate-rich heterogeneous grain model with an excess of large particles is compatible with the observed spectrum of Giacobini-Zinner on August 26. Thus, weak or absent silicate emission does not necessarily imply an absence of silicates in the dust, although the abundance of silicate particles < or = 1 micrometer radius must have been lower than in Comet Halley.