Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pets, or companion animals, are said to be good for people. Until recently there has been little serious study of the effects on people's health of their interactions with companion animals. This is in spite of the fact that they have shared human lives for centuries and their beneficial effects have been known for at least 200 years. This paper reviews the ways in which companion animals have favourable effects on human health and behaviour, for example, as guides for blind and deaf people, for enriching the lives of long stay patients and for providing physical activity like horse riding for the severely disabled. Current knowledge of the effects of animals on human psychological, behavioural, physiological and social development is reviewed, including the use of animals in prison programmes. New findings in Australia show that pet owners had marked reduction in risk factors related to cardiac disease compared with non-owners. Other recent work has indicated that companion animals are able to act as 'early warning systems' for acute human conditions such as epileptic seizures.
Vet Rec 1992 Apr 04
PMID:Companion animals and human health. 153 28

Fifty dogs showing clinical signs of spinal disease were investigated by myelography, using iopamidol. In 27 cases the technique was considered worthwhile. Of the 19 dogs not subjected to surgery or euthanasia as a result of the findings, three suffered seizures during recovery from anaesthesia, eight deteriorated in neurological condition and one suffered permanent respiratory arrest as a result of extensive subarachnoid haemorrhage.
Vet Rec 1992 May 23
PMID:A review of the usefulness of myelography in 50 dogs. 162 55

Three blonde d'Aquitaine calves (one male and two females) about four months old, exhibited skin lesions just after birth, the site and nature of which suggested photosensitisation. Their porphyrin metabolism indicated a marked decrease in the activity of lymphocytic ferrochelatase, leading to a diagnosis of congenital erythrocytic protoporphyria. The associated nervous disorders of the 'recurrent epileptiform seizure' type are discussed in the light of complementary histological and biochemical tests.
Vet Rec 1991 Nov 02
PMID:Observation on bovine congenital erythrocytic protoporphyria in the blonde d'Aquitaine breed. 176 83

We have identified three examples of female Wistar rats exhibiting the tremor and seizures characteristic of the X-linked myelin deficiency (md) mutation, which is ordinarily seen only in males. Cytogenetic study of two of these animals has shown them to have 41 chromosomes instead of the normal 42. The missing chromosome was identified as an X chromosome by G-banding analysis. These animals thus have an XO genotype comparable to that in Turner's syndrome. Anatomically, one of the animals, which was studied in detail, showed no abnormality of the uterus, and the ovaries, although somewhat smaller than normal, were histologically indistinguishable from those in a normal female rat. No evidence of endocardial fibroelastosis was detected, nor was there any anomaly of the aorta. The myelin deficiency in the central nervous system was comparable to that in hemizygous mutant male rats. XO monosomy in the Wistar rat thus has little effect on phenotype and is more comparable to that in mice than to Turner's syndrome in man. The myelin-deficient rat is useful for studies of X-chromosome monosomy since XO females can readily be identified by the neurological syndrome characteristic of the md mutation.
Anat Rec 1990 Mar
PMID:X-chromosome monosomy in the myelin-deficient rat mutant. 232 8

The results presented were derived from an anticonvulsant monitoring service, provided for two years to practising veterinary surgeons, in which samples of serum were taken from dogs treated with either primidone or phenobarbitone. Of the 19 patients assessed, 13 were controlled after the recommended changes in dose had been made. Of the six patients not completely controlled after changes in dose, four had a much lower incidence of seizures but two did not respond to treatment in spite of having high serum phenobarbitone levels. There were large variations between the doses of anticonvulsant drugs required to reach therapeutic serum levels; these variations underlined the value of routine monitoring for improving the control of canine seizures.
Vet Rec 1988 Apr 09
PMID:Effectiveness of a therapeutic drug monitoring service as an aid to the control of canine seizures. 338 49

The anticonvulsant profile of N-[beta-[4-(beta-phenylethyl)phenyl]-beta-hydroxyethyl]imidazole hydrochloride (denzimol, Rec 15-1533) has been evaluated in mice, rats and rabbits in comparison with some standard antiepileptic drugs. Denzimol suppressed electrically and chemically induced tonic seizures but did not prevent the clonic ones. In mice and rabbits the anticonvulsant activity of denzimol against maximal electroshock seizures was almost equal to that of phenytoin and phenobarbital with more rapid onset of action, whereas in rats the compound resulted in being the most potent and the less toxic one showing a longer duration of anticonvulsant activity than phenytoin. In the maximal pentetrazol seizures test in rats denzimol showed a profile similar to that of phenytoin and carbamazepine, but different from that of barbiturates and benzodiazepines so that it is suggested that its clinical application would be that of "grand mal" and psychomotor type seizures therapy.
 ...
PMID:Denzimol, a new anticonvulsant drug. I. General anticonvulsant profile. 668 93

Cholesterinic granulomas have been previously reported as an incidental post mortem in horses. Three adult horses with diencephalic dysfunction due to cholesterinic granulomas are described. All the horses exhibited profound depression, somnolence and reluctance to move. One horse experienced generalised seizures. Cerebrosinal fluid was xanthochromic with an elevated total protein in two of the cases evaluated. The large cholesterinic granulomas caused expansion of the lateral ventricle and secondary hydrocephalus due to the build up of cerebrospinal fluid behind the mass. Cholesterinic granulomas are believed to result from choroid plexus congestion and haemorrhage.
Vet Rec 1994 Sep 03
PMID:Neurological manifestation of cholesterinic granulomas in three horses. 781 10

The acute polymyopathy in a seven-year-old German shepherd dog was attributed to the muscular hypertonia, tremors and seizures which developed during the acute phase of carbamate poisoning. After two days of generalised muscular rigidity, the dog adopted a characteristic fetal position which could be explained by the imbalance between the injuries to the extensor and flexor muscles. The polymyopathy resolved gradually over the course of a week.
Vet Rec 1994 Jul 23
PMID:Acute polymyopathy after carbamate poisoning in a dog. 797 95

The history, clinical signs and radiographic and ultrasonographic findings in 16 dogs with pancreatic neoplasia were reviewed retrospectively. Thirteen of the dogs had islet cell carcinoma compatible with insulinoma, one had a pancreatic adenocarcinoma and two had secondary invasion of the pancreas, one by a gastric carcinoma and one by an intestinal lymphoma. The clinical signs in the 13 dogs with insulinoma included collapse in 10 dogs, ataxia in seven, weakness in five, and seizures in two. Two of the 16 dogs had jaundice due to biliary obstruction by the primary tumour or metastases. The sensitivities for pancreatic neoplasia were three of 16 (19 per cent) for radiography and 12 of 16 (75 per cent) for ultrasonography; the sensitivities for metastasis were two of 11 (18 per cent) for radiography and six of 11 (55 per cent) for ultrasonography. Biliary obstruction was detected by ultrasonography in both affected dogs.
Vet Rec 1995 Jul 15
PMID:Ultrasonography of pancreatic neoplasia in the dog: a retrospective review of 16 cases. 853 34

Severe, repetitive ("binge") ethanol intoxication in adult rats (intragastric delivery 3 times daily for 4 days in a modification of the Majchrowicz method) precipitates neuronal degeneration in selected cerebral cortical regions involved in memory and olfaction, confirming the results of Switzer and colleagues (Anat. Rec. 202: 186a, 1982). Neuronal damage was visualized with the de Olmos cupric silver technique for degenerating neurons and processes (argyrophilia), and was quantitated by total counts and densities of argyrophilic cells/fields. The specificity of the degeneration provides a neuropathological basis for the olfactory memory deficits in chronic alcoholics. In highly intoxicated rats, argyrophilia was most extensive among hippocampal dentate gyrus granule cells, pyramidal neurons in layer 3 of the entorhinal cortex, and olfactory nerve terminals in the olfactory bulb. Degenerating pyramidal neurons were also consistently seen in the insular cortex and olfactory cortical regions, such as the piriform and perirhinal cortices. There were few argyrophilic neurons in the CA regions of the hippocampus and none in the cerebellum--regions generally shown to have cell loss in long-term ethanol feeding models--but degenerating mossy fibers in the CA2 region were observed. Degeneration was maximal before the peak period of abstinence symptoms in this model, because argyrophilic densities were no greater 36 hr, compared with 8 hr after the last ethanol dose. High blood ethanol levels were required, because argyrophilia, absent from isocaloric controls, also was only evident in ethanol-intoxicated rats with mean blood ethanol levels for days 2 to 4 above 300 mg/dl; however, it increased substantially between 350 and 550 mg/dl. The resemblance of the argyrophilic distribution to the regional neuropathology that occurs in experimental seizures indicates that the ethanol-induced degeneration may have an excitotoxic basis. Progressive reductions in the seizure threshold (e.g., kindling phenomena that have been documented during binge ethanol intoxication) might be associated with excitotoxic hyperactivity during the repetitive nadirs between high blood and brain ethanol peaks. However, direct toxic actions of ethanol or its metabolites could also be involved. Overall, the model should be useful for studying mechanisms of ethanol-induced selective cortical and olfactory brain damage.
 ...
PMID:Neuronal degeneration in rat cerebrocortical and olfactory regions during subchronic "binge" intoxication with ethanol: possible explanation for olfactory deficits in alcoholics. 873 Feb 19


1 2 3 4 5 Next >>