Does surgical timing affect the rapidity of recovery in deep pain-entire non-ambulatory dogs with thoracolumbar intervertebral disk extrusion?

OBJECTIVE: To investigate whether the delay between onset of neurological signs and spinal cord decompression affects the time to recovery in non-ambulatory paraparetic/paraplegic dogs with deep pain perception affected by thoracolumbar intervertebral disc extrusion. MATERIALS AND METHODS: Data on non-ambulatory dogs with preserved deep pain perception in both hindlimbs and surgically treated for thoracolumbar intervertebral disc extrusion were prospectively collected from three referral hospitals. Cox proportional hazards regression was used to explore the relationship of time until restoration of independent ambulation with age, weight, preoperative use of anti-inflammatory drugs, delay between onset of inability to walk and arrival at the clinic, time between presentation and spinal surgery and surgery time. RESULTS: One hundred and fifty-one dogs were included. Median time from admission to surgery, including imaging, was 180 (interquartile range, 65.4 to 240) minutes. All dogs were operated within 72 hours. Follow-up was available for all 151 dogs and ranged from 1 to 21 months. All but three dogs, which were all grade IV at presentation, recovered the ability to ambulate. In both univariable and multivariable models, only duration of surgery and neurological (Frankel) grade at presentation were significantly associated with the rapidity of recovery of ambulation. CLINICAL SIGNIFICANCE: Delay between onset of clinical signs and presentation and time between presentation and spinal surgery was not associated with the rapidity of recovery of ambulation in dogs surgically treated for thoracolumbar intervertebral disc extrusion. These results should be evaluated in the context of a limited range of delay since only 14.5% dogs had a delay ≥6.5 hours. Duration of surgery and neurological grade at presentation were significantly associated with rapidity of recovery of ambulation.

ABCB1 c.-6-180T>G polymorphism and clinical risk factors in a multi-breed cohort of dogs with refractory idiopathic epilepsy.

Epilepsy is the most common chronic neurological disorder in dogs. Approximately 20-30% of dogs do not achieve satisfactory seizure control with two or more anti-epileptic drugs at appropriate dosages. This condition, defined as refractory epilepsy, is a multifactorial condition involving both acquired and genetic factors. The P glycoprotein might play and important role in the pathophysiological mechanism and it is encoded by the ABCB1 gene. An association between a single nucleotide variation of the ABCB1 gene (c.-6-180T>G) and phenobarbital resistance has previously been reported in a Border collie population with idiopathic epilepsy. To date, the presence and relevance of this polymorphism has not been assessed in other breeds. A multicentre retrospective, case-control study was conducted to investigate associations between ABCB1 c.-6-180T>G, clinical variables, and refractoriness in a multi-breed population of dogs with refractory idiopathic epilepsy. A secondary aim was to evaluate the possible involvement of the ABCB1 c.-6-180T>G single nucleotide variation this population. Fifty-two refractory and 50 responsive dogs with idiopathic epilepsy were enrolled. Of these, 45 refractory and 50 responsive (control) dogs were genotyped. The G allele was found in several breeds, but there was no evidence of association with refractoriness (P=0.69). The uncertain role of the c.-6-180T>G variation was further suggested by an association between the T/T genotype with both refractoriness and responsiveness in different breeds. Furthermore, high seizure density (cluster seizure) was the main clinical risk factor for refractory idiopathic epilepsy (P=0.003).

Clinicopathological features of globoid cell leucodystrophy in cats.

Clinical and pathological findings consistent with globoid cell leucodystrophy (GLD) were evaluated in two domestic shorthaired cats, aged 3 and 4 months. Both showed neurological signs mainly characterized by progressive pelvic limb ataxia, paraplegia with loss of deep pain perception in the pelvic limb, and intentional tremors of the thoracic limbs. Pathological changes affecting the central and peripheral nervous systems were characterised by diffuse, bilateral and symmetrical myelin loss, and marked astrogliosis. In the leucodystrophic areas there was perivascular accumulation of large PAS-positive, non-metachromatic macrophages (globoid cells), with intracytoplasmic accumulation of crystalloid tubular aggregates. Peripheral nerves showed demyelinating features with thin myelin sheaths, myelin splitting, and ballooning; the nerve fibres had bizarre shapes due to the presence of pale inclusions in the Schwann cells. GLD in cats shares clinical and pathological features with the disease described in other animals and human beings. The neurological signs differed from those of other feline inborn neurometabolic diseases and cerebellar hypoplasia.