Epilepsy and seizure classification in 63 dogs: a reappraisal of veterinary epilepsy terminology

The human definitions of epilepsy and seizure classification were applied rigidly to epileptic dogs to investigate whether the distribution of the seizure types and epilepsies of dogs is comparable to that of human beings. Sixty-three dogs were referred because of recurrent (> 2) epileptic seizures. Only dogs without previous or ongoing antiepileptic treatment were included. All dogs had a physical and neurologic examination and blood work that included a CBC and a biochemical profile. All owners were asked to complete a questionnaire, focusing on seizure development. In addition, video recordings of suspected seizure episodes were analyzed if available. In the majority of dogs where an intracranial lesion was suspected, a computerized tomography scan was performed. Sixty-five percent of the dogs experienced partial seizures with or without secondary generalization and 32% exhibited primary generalized seizures; in 3% of the dogs the seizures could not be classified. Twenty-five percent of these cases were classified as idiopathic, 16% as symptomatic, and 45% as cryptogenic epilepsy; in 14% of these a classification was not possible. Applying human definitions, the distribution of seizure types and epilepsy classifications in these dogs differed widely from those in previous reports of canine epilepsy, where generalized seizures and idiopathic epilepsy were most frequently reported. However, our findings are consistent with the results of several large studies of human epilepsy patients. In dogs with epilepsy, closer attention must be given to the detection of a partial onset of seizures. In this study, detailed questioning of the owners and when possible analysis of video recorded seizures, proved to be sufficient for diagnosing seizures with a partial onset in a significant number of dogs. Partial onset of seizures may be an indication of underlying cerebral pathology. Some adjustments of veterinary epilepsy terminology are suggested.     

RETROSPECTIVE ANALYSIS OF BRAIN SCINTIGRAPHY IN 116 DOGS AND CATS

We performed a retrospective study of 100 dogs and 16 cats with planar brain scintigraphy and histopathologically established diagnoses from a total of 485 studies performed from 1976 to 1992. Necropsy (112) or surgical biopsies (4) diagnoses were categorized in two ways: first as focal brain disease, diffuse brain disease or normal; second as either neoplastic, non-neoplastic or normal. A radiologist reviewed brain scintigrams and categorized the studies as focal areas of increased accumulation, diffuse or poorly localized areas of increased accumulation, or normal. We calculated for this population of 116 animals that focal brain scintigrams had 75% sensitivity and 90% specificity for any focal brain disease. The sensitivity and specificity of a focal scintigraphic lesion for a brain tumor was 72% and 82% respectively. The sensitivity and specificity of a diffuse or poorly localized scintigraphic lesion as a test for diffuse brain disease was 40% and 88% respectively.     

Clinical and pathological findings in a goat with cerebral gliomatosis

This report describes a buck with cerebral gliomatosis. The animal was severely apathetic to somnolent. Neurological examination revealed generalised ataxia and hyper-metria of the fore limbs. There was bilateral mydriasis and severely decreased menace and pupillary light reflexes. Sensitivity to pricking with a needle was markedly reduced over the entire body. There was a delayed response to adduction, abduction and crossing of the limbs and rocking of the animal. Examination of cerebrospinal fluid indicated mild mixed-cell inflammation. Based on all of the findings, an abscess or tumour of the central nervous system with localisation in the cerebrum was suspected. Because of the grave prognosis, the goat was euthanased and a post mortem examination performed. No macroscopic abnormalities were seen in any of the organs including the brain. Histologically, there was extensive diffuse glial cell hyperplasia in the white matter of the cerebral hemispheres and in the brain stem.     

Effects of adrenal gland on the expression of bax and bcl-2 in hippocampus after cerebral ischemia

AIM: To observe the effects of adrenal gland on the hippocampus responses to cerebral ischemia. METHODS: 36 Wistar rats were randomly divided into three groups: sham-operated control group (sham), unilateral adrenalectomy were performed in ADX and GC group, and GC group were injected with 5 mg/per rat of dexamethasone before cerebral ischemia. Fourteen days after the first operation, all animals were performed occlusion of bilateral carotid artery for 15 min, and then reperfusion. 3 rats of each group were sacrificed at 1 h, 4 h, 8 h and 24 h after reperfusion and hippocampus were dissected. The total RNA was rapidly extracted from hippocampus tissue. The expressions of c-fos, bcl-2 and bax gene were quantified with the method of semiquantitive RT-PCR. RESULTS: The expressions of c-fos and bax in three groups showed no statistical differences (P>0.05). The expression of bcl-2 in sham group was significantly higher than that in GC and ADX groups (P<0.05). However, no differences of bcl-2 expression between GC and ADX group (P>0.05) was observed. The ratio of bax to bcl-2 in sham group was significantly lower than that in GC and ADX groups (P<0.05), no significant differences of the ratio displayed between ADX and GC group. CONCLUSION: The expression of c-fos and bax in hippocampus after cerebral ischemia is not affected by adrenal gland. The excision of unilateral adrenal gland downregulates bcl-2 expression and raises the ratio of bax to bcl-2 in rat hippocampus after cerebral ischemia. Dexamethasone treatment does not alter the expression of bcl-2 in ADX and GC groups. The results indicate that the adrenal gland can counteract cell apoptosis in hippocampus tissue induced by cerebral ischemia. Adrenal steroids are not sufficient to enable the compensatory increase in bcl-2 expression in steroid-deficient animal, some other mechanism may exist.     

OX1R expression in chronic ischemic brain tissue of rats

AIM: To study the orexin-1 receptor (OX1R) expression in chronic ischemic brain tissue of rats and the change following the ischemic process.METHODS: The cerebral ischemic model was established by ligating double carotid arteries in rats. The behavior of the models was evaluated by water maze. The OX1R expression was determined by immunohistochemical technique, and the location of OX1R expression was further confirmed by double immunofluorescent staining.RESULTS: The intelligence of rats 15 d after ligating double carotid arteries was impaired obviously, and improved in 1 month and 2 months compared with the model in 15 d. At the same time, the OX1R expression increased obviously from acute phase until 15 d of cerebral ischemia and decreased notably in 1 month compared to the model in 15 d, and then increased significantly for the second time in 2 months of model. From the histology, partial neurons of 15 d model rats got atrophy, and most neurons in 1 month model rats got cytomorphosis and atrophy, however partial neurons in 2-month model rats recovered normally. The OX1R expression was confirmed in neurons definitely by double immunofluorescent staining.CONCLUSION: During the pathologic process of chronic ischemic injury, orexin system has two-way regulatory functions through.     

Neuropathological survey of fallen stock: active surveillance reveals high prevalence of encephalitic listeriosis in small ruminants

This paper describes the prevalence of brain lesions in the Swiss fallen stock population of small ruminants. 3075 whole brains (75% sheep, 25% goats) were collected as part of a year-long active survey of transmissible spongiform encephalopathies (TSEs) in small ruminants conducted by the Swiss authorities between July 2004 and July 2005. All fallen stock brains were systematically examined by histopathology to obtain reliable data on histologically identifiable brain lesions. Lesions were found in an unexpectedly high number of animals (8.1% of all examined brains). A wide spectrum of diseases was detected showing that this approach provides an excellent opportunity to screen for the prevalence of neurological diseases. Encephalitic listeriosis was by far the most frequent cause of CNS lesions in both species and its prevalence was unexpectedly high when compared to notified confirmed cases. In conclusion, the prevalence of listeriosis as estimated by passive surveillance based on the notification of clinical suspects has been underestimated in the past.     

Relationship between FRAS1 protein and brain metastases of NSCLC

AIM: To explore the relationship between FRAS1 protein and brain metastases of non-small cell lung cancer (NSCLC).METHODS: The mRNA expression of FRAS1 in the brain metastatic tumor tissues and primary tumor tissues of NSCLC was detected by qPCR. The protein expression of FRAS1 in the tumor tissues and normal tissues adjacent to tumor tissues of NSCLC was measured by SP method of immunohistochemistry. The protein expression of FRAS1 in NSCLC primary tumor tissues with or without brain metastases was also determined.RESULTS: The mRNA expression of FRAS1 in the brain metastatic zone was nearly 10 times higher than that in the primary tumor tissues, and there was significant difference between the 2 groups (P<0.05). FRAS1 protein was expressed in the NSCLC primary tumor tissues, but was not found in the normal tissues adjacent to primary tumor tissues. The protein expression of FRAS1 in the NSCLC with brain metastases was significantly higher than that without brain metastases (P<0.01).CONCLUSION: FRAS1 protein may be associated with the occurrence of NSCLC. The over-expression of FRAS1 protein may be related to brain metastases with NSCLC.     

Investigation of Known Genetic Mutations of Arabian Horses in Egyptian Arabian Foals with Juvenile Idiopathic Epilepsy

Background

The carrier status of lavender foal syndrome (LFS), cerebellar abiotrophy (CA), severe combined immunodeficiency (SCID), and occipitoatlantoaxial malformation (OAAM1) in foals with juvenile idiopathic epilepsy (JIE) is unknown.

Hypothesis/Objectives

To determine the carrier status of LFS, CA, SCID, and OAAM1 in foals with JIE.

Animals

Ten foals with JIE.

Materials and Methods

Archived DNA samples were tested for known genetic mutations causing LFS, CA, SCID, and OAAM1. The inclusion criteria consisted of having been diagnosed with JIE by ruling out other causes of seizures in foals and supported by electroencephalographic examination.

Results

Ten Egyptian Arabian horses (5 females and 5 males) were phenotyped as foals with JIE by electroencephalography (EEG). All foals were negative for the genetic mutations that cause LFS, CA, SCID, and OAAM1 except for 1 foal that was a carrier of CA.

Conclusions and Clinical Importance

Juvenile idiopathic epilepsy of Egyptian Arabian foals and LFS appear to be phenotypically and genetically distinct disorders. There was no apparent association between JIE and LFS, CA, SCID, and OAAM1.     

Effects of adenosine A1 receptor antagonist DPCPX on cerebral neurons after hypoxia and reoxygenation

AIM: To investigate the effects of adenosine A₁ receptor antagonist DPCPX on the release of cerebral neuronal lactate dehydrogenase (LDH), the activity of calcineurin (CaN) and acetylcholinesterase (AChE), and the level of extracellular amino acid after hypoxia and reoxygenation (H/R).METHODS: Primary cultured rat cerebral cortical neurons were used to establish an H/R injury model. Different concentrations of DPCPX (the final concentrations were as follows: 0, 25, 50 and 100 nmol/L) were added at the same time of hypoxia treatment for 8 h, 12 h or 24 h,followed by reoxygenation for 24 h. The LDH release from the neurons was measured. The effects of DPCPX (100 nmol/L) on the activity of CaN and AChE, and the level of extracellular amino acid in neurons treated with hypoxia for 12 h followed by reoxygenation were observed. RESULTS: Compared to the cells in control groups, the neurons treated with 100 nmol/L DPCPX and exposed to hypoxia for 12 h followed by reoxygenation, showed significantly higher LDH release, higher activity of CaN and AChE, and lower level of extracellular γ-aminobutyric acid.CONCLUSION: These results suggest that DPCPX increases the LDH release and the activity of CaN and AChE, decreases the level of extracellular γ-aminobutyric acid in neurons with H/R.