Laurent S. Garosi

Treatment with gabapentin of 11 dogs with refractory idiopathic epilepsy

Eleven dogs diagnosed with refractory idiopathic epilepsy were treated orally with gabapentin for a minimum of three months at an initial dose of 10 mg/kg every eight hours. They were all experiencing episodes of generalised tonic-clonic seizures and had been treated chronically with a combination of phenobarbital and potassium bromide at doses sufficient to reach acceptable therapeutic serum levels without causing significant side effects. In each dog, the number of seizures per week, the average duration of the seizures and the number of days on which seizures occurred were compared for the three months before and after they were treated with gabapentin. A minimum 50 per cent reduction in the number of seizures per week was interpreted as a positive response to gabapentin, and six of the dogs showed a positive response. After the addition of gabapentin, both the number of seizures per week (P= 0·005) and the number of days with any seizures in a one-week period (P=0·03) were significantly reduced. Mild side effects of ataxia and sedation were observed in five of the dogs, but they were not severe enough to warrant the treatment being discontinued during the trial.

Cerebrovascular Disease in Dogs and Cats

Cerebrovascular disease is defined as any abnormality of the brain resulting from a pathologic process affecting its blood supply. Stroke or cerebrovascular accident (CVA) is the most common clinical manifestation of cerebrovascular disease, and can be broadly divided into ischemic stroke and hemorrhagic stroke. Ischemic stroke results from occlusion of a cerebral blood vessel by a thrombus or embolism, depriving the brain of oxygen and glucose, whereas hemorrhagic stroke results from rupture of a blood vessel wall within the brain parenchyma or subarachnoid space. Previously considered uncommon, CVA is being recognized with greater frequency in veterinary medicine since magnetic resonance imaging has become more readily available. Once the diagnosis of ischemic or hemorrhagic stroke is confirmed, potential underlying causes should be sought after and treated accordingly.

L-2-hydroxyglutaric aciduria in a West Highland white terrier

A five-year-old, neutered male West Highland white terrier was presented to the Neurology Unit at the Animal Health Trust, Newmarket, for investigation of a long-standing history of a gait abnormality affecting all four limbs, impaired vision, inappropriate behaviour (loss of obedience training and staring at walls) and recent episodes of severe head tremor when stressed. The clinical signs had an insidious onset and progressively became more severe. Neurological examination demonstrated mild dementia and moderate ataxia of all four limbs, with the additional finding of thoracic limb hypermetria. Severe postural deficits were evident in all four limbs, as shown by the dog’s impaired ability to perform hopping and placing tests, but its segmental spinal cord reflexes were intact. Cranial nerve examination demonstrated a decreased menace response, in the presence of normal pupillary light reflexes. The neuroanatomic localisation was consistent with a diffuse and symmetrical intracranial lesion affecting the forebrain, brainstem and cerebellum. Based on the neurolocalisation and clinical history, the most likely differential diagnoses included inflammatory and degenerative central nervous system diseases and metabolic encephalopathy. Initial diagnostic evaluations, including a complete blood count, serum biochemistry and preand postprandial bile acid concentrations, were all within normal limits. A MRI scan of the brain was performed under general anaesthesia with a 1·5 T superconducting magnet (1·5 T Signa Echospeed system; General Electric Medical Systems) and an extremity coil. The following pulse sequences were used: T1-weighted preand postcontrast after intravenous administration of 0·1 L-2-hydroxyglutaric aciduria in a West Highland white terrier

Dystrophin-deficient muscular dystrophy in an old English sheepdog

MUSCULAR dystrophies are a heterogeneous group of inherited, degenerative, mostly non-inflammatory disorders characterised by progressive muscle weakness and wasting (Braund 1997, Shelton and Engvall 2002). In companion animals, dystrophies associated with an absence of or abnormality in dystrophin, dystrophin-associated proteins and laminin α2 have been recognised (Cooper and others 1988, O’Brien and others 2001, Shelton and others 2001). Dystrophin-deficient muscular dystrophy, resulting from mutations in the dystrophin gene, is the most common and best studied form in dogs, and is known to be X-linked (Shelton and Engvall 2002). It has been reported in several breeds, including the golden retriever (Kornegay and others 1988, Sharp and others 1992), rottweiler (Winand and others 1994), German shorthaired pointer (Schatzberg and others 1999), Irish terrier (Wentink and others 1972), Belgian Groenendaeler shepherd dog (Van Ham and others 1993), samoyed (Presthus and Nordstoga 1993), miniature schnauzer (Paola and others 1993), Brittany spaniel (Van Ham and others 1995), rat terrier (Wetterman and others 2000), Pembroke Welsh corgi (Woods and others 1998), labrador retriever (Bergman and others 2002) and Japanese spitz (Jones and others 2004). Specific mutations have been identified for the golden retriever (Sharp and others 1992), rottweiler (Winand and others 1994) and German shorthaired pointer (Schatzberg and others 1999). This short communication describes, to the authors’ knowledge, the first case of dystrophin-deficient muscular deficiency in an old English sheepdog. A three-month-old, male old English sheepdog was presented to the neurology/neurosurgery department of the Animal Health Trust, for evaluation of a three-week history of difficulty in eating, excessive salivation, mild exercise intolerance and impaired growth. The littermates and parents were apparently unaffected. The animal weighed 8·2 kg; physical examination confirmed a poor body condition, with atrophy of the temporalis, paraspinal and distal limb muscles. Marked swelling of the tongue and pharyngeal region was evident, accompanied by excessive salivation. Neurological findings included a stiff gait with an increased muscle tone of both pelvic limbs, decreased to absent withdrawal reflexes on all four limbs, decreased tongue movement and absent gag reflex. A generalised myopathic disorder was suspected, with an inflammatory, infectious, dystrophic or other congenital myopathy as the primary differential diagnoses; the possibility of a neuropathy was also considered. The results of a complete blood count and serum biochemistry revealed a marked elevation of serum creatine kinase (CK) (53,396 iu/l, reference range 21 to 56 iu/l), suggesting muscle disease. Serum antibody titres for Toxoplasma gondii and Neospora caninum were negative. Electrodiagnostic testing was performed under general inhalational anaesthesia. Concentric needle electromyography of the major muscle groups of the foreand hindlimbs and paraspinal, tongue and laryngeal muscles, as well as the temporalis and masseter muscles, revealed fibrillation potentials, positive sharp waves and complex repetitive discharges. Cardiac ultrasound was normal, as were thoracic and abdominal radiographs. A barium swallow revealed poor laryngeal motility. Muscle biopsies were taken from the right cranial tibial, right temporalis and left myohyoideus muscles, and unfixed and fixed (immersed in 10 per cent buffered formalin) biopsies from each site were submitted under refrigeration to the Comparative Neuromuscular Laboratory, University of California, San Diego, USA, by a courier service. Upon receipt, the fixed muscle specimens were embedded in paraffin, and the unfixed, refrigerated specimens were flash frozen in isopentane precooled in liquid nitrogen and stored at –80°C before further processing. Cross-sections 8 μm thick were cut using a cryostat, and stained and reacted with a standard panel of histological and histochemical stains and enzyme reactions, including the general stains haematoxylin and eosin and modified Gomori trichrome for morphological abnormalities, periodic acid-Schiff for glycogen, myofibrillar ATPases at pH 9·8 and 4·3 for fibre typing, esterase for localisation of motor endplates and macrophage activity, nicotinamide adenine dinucleotide dehydrogenase for oxidative activity, acid phosphatase for macrophages, oil red O for neutral triglycerides, and the alizarin and von Kossa stains for calcium (Dubowitz 1985, Dickinson and LeCouteur 2002). Degeneration and regeneration were the predominant pathological changes, including variability in myofibre size, with large groups of necrotic fibres, and clusters of small basophilic regenerating fibres (Figs 1a, b, c). Multifocal areas of myofibre mineralisation were present with both the alizarin and von Kossa stains for calcium (Fig 1d). Cellular infiltrates were limited to macrophages within necrotic fibres, without overt lymphocytic infiltration. Fibrosis was not a feature. A non-inflammatory myopathy with a distinctly dystrophic phenotype was diagnosed based on the pathological changes. Immunohistochemical staining was performed on frozen muscle specimens from the affected dog and a control dog (a young adult dog that had been euthanased because of trauma, Veterinary Record (2006) 158, 270-273

Porencephaly and hydranencephaly in six dogs

A retrospective study was performed to identify dogs with cerebrospinal fluid-filled cavitatory lesions on MRI. Six dogs were included and the lesions were classified. In the three dogs in the present study with hydranencephaly, unilateral but complete loss of the temporal and parietal lobes was noted and had almost complete loss of the occipital and frontal lobes of a cerebral hemisphere. In the three dogs with porencephaly, there was unilateral incomplete loss of the parietal lobe and one dog had additional partial loss of the temporal and frontal lobes. Two of the dogs with porencephaly had seizures; the third showed no associated clinical signs. The dogs with hydranencephaly had mentation changes and circled compulsively. The two porencephalic dogs with seizures were treated with phenobarbitone. One of the dogs with hydranencephaly showed increased frequency and duration of circling; one dogs clinical signs did not progress and the third dog was euthanased due to increasing aggression. The dog with increased circling had ventriculoperitoneal shunt placement and the circling frequency reduced.

Bilateral, hypertrophic neuritis of the brachial plexus in a cat: magnetic resonance imaging and pathological findings

A 9-year-old Burmese cat was presented for investigation of a subacute onset of bilateral forelimb paresis. Magnetic resonance imaging of the cervico-thoracic vertebral column and brachial plexus revealed a bilaterally symmetrical, severe and diffuse swelling of the spinal nerves forming the caudal part of the brachial plexus. Histopathology of the abnormal nerve roots, spinal nerves and brachial plexi showed inflammatory and marked proliferative changes with similar features to that of hypertrophic neuritis of man. Hypertrophic neuritis in man is a rare, tumor-like, chronic inflammatory peripheral nerve disorder of unknown origin most frequently involving the brachial plexus.

Dysplasia of the caudal vertebral articular facets in four dogs: results of radiographic, myelographic and magnetic resonance imaging investigations

Congenital anomalies of the vertebral column associated with aberrations of one of the primary vertebral ossification centres have been frequently described in the veterinary literature, but clinically significant abnormalities of secondary vertebral ossification centres, particularly involving the caudal articular processes, are much less frequently reported. This paper describes three dogs with aplasia and one dog with hypoplasia of the caudal vertebral articular processes. Thoracolumbar spinal cord compression and ataxia was evident in the three dogs with aplasia but no clinical signs were evident in the dog with hypoplasia. The radiographic appearance was similar in all four cases, with aplasia or hypoplasia of the caudal articular facets at one or more intervertebral joints in the thoracolumbar region. Bone proliferation was evident secondary to an associated degenerative joint disease. Compensatory hyperplasia of the adjacent cranial articular facets and ligamentum flavum protruded into the vertebral canal, resulting in a compressive myelopathy observed by myelography and magnetic resonance imaging.

Corpus callosal abnormalities in dogs

Background Corpus callosal abnormalities (CCA) in dogs have been only sporadically reported and are poorly characterized. Hypothesis/Objectives To describe the clinical presentation and magnetic resonance imaging (MRI) characteristics of dogs with CCA. Animals Fifteen client‐owned dogs. Methods Retrospective study. Records of the contributing institutions were reviewed to identify dogs diagnosed with malformations affecting the corpus callosum (CC); cases in which the CCA was thought to be secondary were excluded. Results The most represented breeds were Staffordshire Bull Terriers (5/15) and Miniature Schnauzers (3/15; n = 3, 20%) and the mean age at time of presentation of 19 months (range 3–81 months). The clinical signs most commonly reported were adipsia/hypodipsia with associated hypernatremia (12/15), tremors (6/15), and seizures (6/15). Review of the MR images revealed that 10 dogs had absence of the rostral CC and hypoplasia of the caudal portion, 4 dogs had a diffusely hypoplastic and dysplastic CC, and 1 dog had a diffusely hypoplastic CC. In 14 cases, there was abnormal cortical development with fusion of the ventral frontal lobes and part of the diencephalon, indicating lobar holoprosencephaly. Conclusions and Clinical Importance Previous literature has mainly associated CCA with adipsia and only 12 of 15 dogs in the current series demonstrated this abnormality. There are different degrees of the malformation but in 10 dogs the rostral portion of the CC is most severely affected. Fourteen dogs have simultaneous fusion of the midline structures rostral to the CC; this region has several structures involved in thirst regulation and might explain this derangement.