Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A herd of 15 mature riding horses with a history of anorexia, weight loss, and lethargy was examined. The animals had been fed a 50/50 mixture of commercial sweet feed and corn screenings contaminated with a heavy growth of Fusarium moniliforme. Thirteen of the horses had one or more neurologic signs. The most characteristic signs were profound depression and mild ataxia. Over the 19-day course of the epizootic, the horses had increasing severe neurologic deficits, including unilateral blindness and delirium. Despite the clinical appearance of dehydration, 12 horses had low PCV (16 to 27%), hematocrit (21.2 to 31.0%; determined by automated cell counter), and RBC counts (3.76 to 5.5 x 10(6) RBC/microliters). White blood cell counts were variable (4,900 to 17,000 WBC/microliters). Necropsy findings included diffuse malacia of the white matter of the frontal cortex and severe multifocal perivascular hemorrhage in the white matter of the temporal cortex, basal ganglia, anterior medulla, and pons. One horse had a hepatic lesion consisting of a mixed inflammatory cell infiltrate and bile duct proliferation. The attack rate of this epizootic was 100%. The course of disease was unusually long in some animals. In an experiment, the fusarium-infected corn screenings were fed to horses and did not cause clinical signs or alterations in blood or serum biochemical values.
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PMID:Clinical and epidemiologic features of an epizootic of equine leukoencephalomalacia. 204 19

We report a 54-year-old woman who revealed right hemiparesis and ataxia in her right extremities due to a lesion which was suggested to be cavernous hemangioma located in the left side of pons in 1971, and showed remarkable crossed cerebellar atrophy (CCA) by computed tomography and magnetic resonance imaging in 1985 and 1989. Angiography showed no abnormality but made iatrogenic embolism in left thalamus which developed severe pain in her right side. Single-photon-emission-computed-tomography (SPECT) with I123-IMP in 1989 showed reduction of right cerebellar hemispheric blood flow (crossed cerebellar diaschisis: CCD) and left cerebral hemispheric blood flow. Our case was thought to have revealed persisting CCD. Although there are many reports about CCD and CCA following cerebral damage, CCD and CCA due to brain stem lesion has not been described yet. This might be explained by the persisting functional depression of cerebro-ponto-cerebellar pathways at the pons' level by cavernous hemangioma. It was assumed that the left cortical hypometabolism was result from damage to thalamo-cortical pathways due to ipsilateral thalamic lesion.
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PMID:[Crossed cerebellar diaschisis and crossed cerebellar atrophy in a patient with a lesion in brain stem]. 204 4

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pharmacologic profile of protirelin tartrate]. 212 84

Cats are susceptible to poisoning by insecticidal products containing D-limonene, linalool, and crude citrus oil extracts. Signs of toxicosis include hypersalivation, muscle tremors, ataxia, depression, and hypothermia.
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PMID:Toxicology of selected pesticides, drugs, and chemicals. D-limonene, linalool, and crude citrus oil extracts. 218 Jan 84

Acute poisoning with organic solvents and other volatile compounds now usually follows deliberate inhalation (volatile substance abuse) or ingestion of these compounds. Solvents from adhesives, typewriter correction and dry cleaning fluids, cigarette lighter refills (butane) and aerosol propellants are commonly abused. The major risk is that of sudden death. Arrhythmias leading to cardiac arrest are thought to cause most deaths, but anoxia, respiratory depression and vagal stimulation leading to cardiac arrest may also contribute, as may indirect causes such as aspiration of vomit or trauma. In the United Kingdom (UK), 3.5 to 10% of young people have at least experimented with volatile substance abuse and mortality is more than 100 per annum. The products abused are cheap and readily available despite legislation designed to limit supply. Volatile substance abuse is not illegal and only a minority of abusers are known to progress to heavy alcohol or illicit drug use. Prevention of abuse by education, not only of children but also of parents, teachers, retailers and health care workers, is important in limiting the problem. However, volatile substance abuse-related deaths are still increasing in the UK despite many measures aimed at prevention. Clinically, volatile substance abuse is characterised by a rapid onset of intoxication and rapid recovery. Euphoria and disinhibition may be followed by hallucinations, tinnitus, ataxia, confusion, nausea and vomiting. It is important not to further alarm the patient if signs of serious toxicity are present, since a cardiac arrest may be precipitated. Further exposure should be prevented and the patient resuscitated and given supplemental oxygen if necessary. Cardiac arrhythmias should be treated conventionally and respiratory failure managed supportively. Long term exposure to n-hexane is associated with the development of peripheral neuropathy, while prolonged abuse (notably of toluene or chlorinated solvents) can cause permanent damage to the central nervous system, heart, liver, kidney and lungs. Knowledge of the routes of absorption, distribution and excretion of volatile compounds, and of the rates governing these processes, is important in understanding the rate of onset, intensity and duration of intoxication, and rate of recovery after volatile substance abuse. In addition, such knowledge is helpful when the clinician is attempting to interpret the results of toxicological analyses performed on samples (blood, other tissues, urine) from such patients. Many volatile substances are partly metabolised, the metabolites being eliminated in exhaled air or in urine. Although metabolism normally results in detoxification, enhanced toxicity may also result as with carbon tetrachloride, chloroform, dichloromethane, n-hexane, trichloroethylene and possibly halothane.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An introduction to the clinical toxicology of volatile substances. 222 69

There are no reports of xylene/amitraz ingestion in children. Studies have characterized the adverse reactions caused by dermal applications in dogs, but the mechanisms involved were undetermined Accidental ingestion of the product by a child prompted a retrospective search of the medical records of the Georgia Animal Poison Information Center to profile the signalment, clinical signs, route of exposure and target sites of the suspected toxicosis in dogs. Clinical signs of depression, ataxia, stupor, and coma were most attributable to the xylene and propylene oxide components. Hyperglycemia, hypotension, and bradycardia were probably attributable to the alpha-2 adrenoceptor agonist action of amitraz. Most reports were initiated by owners, using the prescription product at home.
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PMID:Xylene/amitraz: a pharmacologic review and profile. 223 43

Two hundred forty-one elderly depressed patients entered the 8-week, double-blind phase of this parallel-group, multicenter study; 161 patients were randomized to receive sertraline (50-200 mg/day) and 80 were randomized to receive amitriptyline (50-150 mg/day). Among evaluable patients, there were no statistically significant differences between treatments in any of the primary efficacy variables: change in total Hamilton Rating Scale for Depression (HAM-D) score (17 items), percentage change in HAM-D score, change in HAM-D Item 1, change in Clinical Global Impressions (CGI) Severity score, change in the Depression Factor of the 56-item Hopkins Symptom Checklist, and the CGI Improvement score at the last visit. Similar results were obtained using data from all patients (intention-to-treat analysis), except that amitriptyline was superior in HAM-D Total score (p = .044). The two drugs produced a similar degree of response: on the basis of the HAM-D criterion, 69.4% of sertraline patients and 62.5% of amitriptyline patients responded, and, on the basis of CGI criterion, 79.5% of sertraline and 73.4% of amitriptyline patients responded. Twenty-eight percent of the sertraline patients withdrew from the study because of a treatment-related side effect and 2.5% (4) because of a laboratory abnormality. In comparison, 35% of the amitriptyline patients withdrew because of treatment-related side effects. Sertraline was associated with a statistically lower frequency of somnolence, dry mouth, constipation, ataxia, and pain and a higher frequency of nausea, anorexia, diarrhea/loose stools, and insomnia; thus, anticholinergic effects were less common and gastrointestinal effects were more common with sertraline than with amitriptyline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double-blind, multicenter comparison of sertraline and amitriptyline in elderly depressed patients. 225 79

Twenty-six cases of accidental 5-fluorouracil (5-FU) ingestions by dogs were reviewed from phone calls to the Illinois Animal Poison Information Center. Cases were collected from January 1, 1987 to December 31, 1988. Of the 26 calls involving 5-FU exposures, 12 were classified as "toxicosis," 13 as "suspected toxicosis," and one as "exposure." Dogs were the only species involved in 5-FU cases received during this time. Accurate estimates of the amount of 5-FU ingested by dogs could be made in 17 cases. Ingestion of more than 20 mg/kg of 5-FU was associated with the development of toxicosis. None of the 12 dogs that ingested oral doses in excess of 43 mg/kg (estimated) survived. Clinical signs associated with 5-FU poisoning in the dog were death, seizures, vomiting (with and without blood), tremors, diarrhea (with and without blood), ataxia, and depression. Clinical signs generally developed within 45 to 60 minutes after exposure, and deaths occurred 6 to 16 hours after ingestion.
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PMID:5-Fluorouracil toxicosis in the dog. 226 27

Toxicosis attributable to fenvalerate and N,N-diethyl-m-toluamide (Deet) exposure was suspected in 2 cats. Clinical signs of toxicosis developed within 4 to 6 hours of dermal application of the pesticide. Clinical signs of toxicosis seen in both cats included hypersalivation, ataxia, and depression. In addition, seizures were seen in 1 cat. Both cats died. Analysis of skin, kidney/urine, liver, and brain tissues confirmed the presence of fenvalerate and Deet. The pyrethroid fenvalerate and the insect repellent Deet are used for the control of fleas and ticks on cats. Suspected fenvalerate/Deet toxicosis in cats is associated with tremors, hypersalivation, ataxia, vomiting, depression, and seizures.
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PMID:Fenvalerate/N,N-diethyl-m-toluamide (Deet) toxicosis in two cats. 229 39

Propylene glycol (1,2-propanediol) is a solvent in numerous pharmaceuticals and a major preservative and source of carbohydrates in processed foods. In mammals, propylene glycol is metabolized similar to ethanol, proceeding via hepatic alcohol and aldehyde dehydrogenases to lactate, which can then enter gluconeogenesis. We observed that cats ingesting 1.6 gm of propylene glycol/kg body weight/day developed increased anion gap. To investigate this further, we measured D- and L-lactate concentrations in these cats; we also measured D-lactate in cats ingesting high doses of propylene glycol (8.0 gm/kg). While L-lactate actually decreased throughout the 35-day course of propylene glycol feeding, D-lactate levels were significantly increased on a dose-dependent basis and correlated positively with anion gap. In cats ingesting the high dose of propylene glycol, D-lactate concentrations were as high as 7 mmol/liter, levels associated with encephalopathy in humans. Indeed, this group of cats developed depression and ataxia, consistent with intoxication by D-lactate. These findings are significant not only for animals ingesting diets which contain propylene glycol, but for humans who receive propylene glycol-containing medications.
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PMID:Propylene glycol ingestion causes D-lactic acidosis. 229 57


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