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Biomedical subjects

B Dayrell-Hart

Publications and source records attributed to B Dayrell-Hart.

9 recordsLinked to original sources
PubMed1995

Necrotizing meningoencephalitis of Maltese dogs.

The clinical and pathologic features of five young Maltese dogs with a necrotizing meningoencephalitis were studied and compared with published reports of the necrotizing meningoencephalitis of Pug dogs. The ages of the Maltese dogs ranged from 9 months to 4 years. Four dogs were male, and one was female. The dogs had a history of seizures with or without other neurologic signs for 3 days to 20 weeks prior to death. Cerebrospinal fluid examination in three dogs revealed a pleocytosis and elevated levels of protein. At necropsy, the cerebrum was asymmetrically swollen in four dogs, with a loss of distinction between the gray and white matter and mild to moderate asymmetrical dilation of the lateral ventricles. Histologically, there was extensive necrosis and nonsuppurative inflammation of the cerebral gray and white matter, overlying meninges, and adjacent thalamus and hippocampus. The 4-year-old dog had the longest duration of clinical signs and had little inflammation but extensive atrophy of affected areas, with astrocytosis. The clinical course and pathologic changes in these Maltese dogs are indistinguishable from those in reported cases of necrotizing meningoencephalitis of Pug dogs, indicating that this lesion is probably not unique to Pug dogs.

Animals↗
PubMed1991

Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989).

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.

Animals↗
PubMed1991

Clinical evaluation of gamma-vinyl-gamma-aminobutyric acid for control of epilepsy in dogs.

Gamma-vinyl-gamma-aminobutyric acid is a novel antiepileptic drug that exerts its effects by increasing the concentration of gamma-aminobutyric acid in the brain. The mechanism of action involves irreversible inhibition of the metabolic pathway of gamma-aminobutyric acid. The drug was administered to 14 dogs in conjunction with other anticonvulsants, in an attempt to control refractory epilepsy. Four of these dogs had clinically relevant evidence of decreased seizure frequency. In 4 dogs, response to the drug was no better than response to phenobarbital alone. In 2 dogs, seizure control improved, but gamma-vinyl-gamma-aminobutyric acid was withdrawn because of development of hemolytic anemia. For various reasons, the therapeutic effect in the remaining 4 dogs could not be evaluated. This study of only 14 dogs illustrates some of the problems that confound our ability to judge the efficacy of anticonvulsant treatment.

Aminocaproates↗
PubMed1989

Intracranial dysfunctions: stupor and coma.

Coma and stupor are pathologic neural states whose signs arise from either massive cortical or brainstem disease or toxicity. A variety of pathological processes can cause brain disease. Often one has to begin treatment before the diagnosis of the cause of the problem is made. At all stages of treatment, great care must be taken to avoid precipitating an intracranial crisis. The physiological derangements that may aid in the diagnosis include arousability, pupil reactivity, various reflexes, breathing patterns, and cardiovascular function. The treatment needs to be both specific and general; i.e., the condition itself must be treated, if possible, and the intracranial pressure must be lowered if it has been raised by the condition. Treatments for raised intracranial pressure include hyperventilation, diuretics, corticosteroids, avoidance of jugular vein compression, coughing, and any change of the position of the head and neck from normal. When sedating or anesthetizing these patients, one should avoid drugs that increase cerebral blood flow such as ketamine and inhaled anesthetics, using instead drugs that lower cerebral blood flow such as thiopental, lidocaine, and narcotics (with ventilation).

Anesthesia↗
PubMedDate not supplied

Radiation therapy of canine brain masses.

This article evaluates the responses of 14 dogs with brain masses using orthovoltage irradiation for definitive treatment. Dogs were anesthetized for computed tomography (CT) examination, formation of head immobilization and positioning devices, radiation treatment simulation, and treatments. Total doses of 39 Gy (9 dogs) or 45 Gy (5 dogs) to the tumor were administered over 25 to 41 days. Two or three portals (parallel opposed lateral with or without a dorsal field) were used. Treatment volumes included the tumor and peritumoral edema, as determined by CT scan, and a 1-cm margin. Histopathologic diagnoses were available in 9 of 14 dogs. There were 4 meningiomas, 1 lymphosarcoma, 1 pituitary adenoma, 1 metastatic anaplastic carcinoma, 1 anaplastic oligodendroglioma and 1 dog with granulomatous meningoencephalitis. At the end of radiation therapy, 10 dogs could be evaluated for progression of clinical signs: 3 dogs deteriorated or failed to improve, and 7 dogs improved. At the time of analysis, all dogs were dead. Mean and median survival times, measured from the beginning of radiation, were 345 and 489 days, respectively. This was compared with mean survival times of 30 to 81 days reported in the literature for dogs with brain tumors that did not receive treatment. The median survival time of 9 dogs treated with 39 Gy was 153 days, versus 519 days for 5 dogs that received 45 Gy. It appears that radiation therapy prolongs survival times for dogs with brain masses. Although megavoltage therapy would be optimal, orthovoltage radiation can be applied in total doses of 45 Gy in 3.75 Gy fractions over 28 days without adverse effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Feline cryptococcosis: a retrospective evaluation.

Cryptococcus neoformans causes the most common form of feline systemic fungal disease. Nineteen cats with cryptococcosis were seen at the Veterinary Hospital of the University of Pennsylvania between April 1986 and May 1995. Compared to other studies, these 19 cases showed increased neurological and ophthalmological involvement. Males were affected more often than females. Season and environment appeared to influence time of onset or presentation to the hospital. Clinical pathology did not show typical changes. It is possible that the organism was present frequently in the urine but was mistaken for fat droplets. Treatment with ketoconazole was unrewarding in cases with central nervous system (CNS) involvement.

Animals↗
PubMedDate not supplied

A case of canine central nervous system cryptococcosis: management with fluconazole.

A three-year-old, female Labrador retriever was presented for acute generalized seizures. Disseminated cryptococcosis with central nervous system (CNS) involvement was diagnosed by serum and cerebrospinal fluid (CSF) fungal titers, histopathological examination, and magnetic resonance imaging (MRI). Fluconazole therapy resulted in prolonged, substantial clinical improvement for a period of one year. This report documents the diagnosis of a case of cryptococcal meningoencephalitis and its management with the new antifungal agent, fluconazole.

Animals↗