Implications of the neuroanatomy of the equine thoracolumbar vertebral column with regional anaesthesia and complications following desmotomy of the interspinous ligament.

Impinging/overriding dorsal spinous processes (DSPs) of the thoracolumbar vertebrae are a common cause of poor performance in horses. In the last five decades, numerous surgical treatments have been reported on, from transverse transection of the affected DSPs, and endoscopic resection of the affected DSPs, to transection of the interspinous ligament. Until recently, cosmetic outcomes have been reported as good to excellent in studies. However, a previously unreported complication of neurogenic atrophy of the contralateral epaxial muscle following desmotomy of the interspinous ligament has been recently reported. The authors hypothesised that this was because of a more lateral approach than previously described, resulting in the scissors being too far across midline and transecting a nerve in the region. Considering this finding, we have reviewed the literature on the neuroanatomy of the thoracolumbar region in the horse. Literature on the neuroanatomy of the horse is lacking when compared with that of humans and companion animals, with most of the work extrapolated from companion animals. Based on the current literature, we hypothesise that transection of an intermediate branch of the dorsal spinal nerve supplying the m. longissimus is potentially the cause of the post-operative neurogenic atrophy. The lack of detailed knowledge of the neural anatomy of the equine back has resulted in the role of local anaesthesia in localising pain in the equine back being poorly understood. The wide variation in techniques used for localising back pain may explain why some horses suffering from poor performance or an abnormal gait because of back pain improve to local anaesthesia of the back while others do not. This review article highlights a lack of anatomical knowledge regarding the equine thoracolumbar region in the literature despite diagnostic local anaesthesia, medication, and surgery in this area being relatively common.

A study of residual lesions in horses that recovered from clinical signs of chronic equine dysautonomia.

BACKGROUND: Equine dysautonomia (ED) causes degeneration and loss of autonomic neurons. Approximately 50% of chronic cases recover, but it is unclear how they survive neuronal loss. OBJECTIVES: To assess lesions, autonomic neuron numbers, interstitial cells of Cajal (ICC), and neurodegeneration in recovered cases. ANIMALS: Thirteen cases (group ED), euthanized 10.3 ± 5.2 (1-16) years from diagnosis and 6 age-matched controls (group C). METHODS: Prospective, case control; routine post mortem examination, neuron counts in peripheral and enteric ganglia and immunohistochemical assessment of neural networks (Protein gene product [PGP] 9.5), ICC (c-kit), and neurodegeneration (beta-amyloid precursor protein and ubiquitin) in intestine. RESULTS: Postmortem findings in group ED were small intestinal dilation (4/12, 33%) and muscular hypertrophy (4/12, 33%), and gastric mucosal hypertrophy (3/11, 27%) and ulceration (4/11, 36%). Neuron density was lower in group ED (mean 39% lower for cranial cervical ganglion [P < .001], median 44% lower in celiacomesenteric ganglion [P = .01]). In intestine, neuronal depletion was worst in ileum (median 100% lower in submucosal plexus [P < .001], 91% lower in myenteric plexus [P = .004]). Group ED had less PGP 9.5 staining in ileal myenteric plexus (mean 66% lower [P = .04]) and circular muscle (median 75% lower [P = .006]). In ileum, there was less c-kit staining in myenteric plexus (median 57% lower [P = .02]) but not muscularis externa. Beta-amyloid precursor protein and ubiquitin results were not indicitive of neurodegeneration. CONCLUSIONS AND CLINICAL IMPORTANCE: Intact ICC in muscularis externa might help maintain motility after neuronal loss. Treatment supporting ICC function warrants investigation.

Assessment of the utility of using intra- and intervertebral minimum sagittal diameter ratios in the diagnosis of cervical vertebral malformation in horses.

Cervical vertebral malformation is one of the most common causes of ataxia in horses. The most important factor in the diagnosis of cervical vertebral malformation is the identification of cervical vertebral canal stenosis, but published data for minimum sagittal diameter ratios in adult horses are only available for C4-C7 intravertebral sites. Intra- and intervertebral sagittal diameter ratios at C2-C7 were evaluated in 26 ataxic horses, for which a complete clinical and neuropathological evaluation was undertaken. Eight of these horses were diagnosed with cervical vertebral malformation. In these horses the majority of compressive lesions were intervertebral. The mean sagittal diameter ratios of horses with cervical vertebral malformation were significantly smaller than those of horses without cervical vertebral malformation, and for an individual horse in our study, the site with the smallest intervertebral sagittal diameter ratio was always the site at which the spinal cord was compressed. Mean sagittal diameter ratio intravertebral site measurements of horses with cervical vertebral malformation were smaller than those of horses without cervical vertebral malformation; however, the site of compression could not be predicted from the data. For our dataset, horses with a sagittal diameter ratio of < or = 0.485 at any inter- or intravertebral site could be correctly classified as having cervical vertebral malformation, and sagittal diameter ratio measurements were an effective tool to identify at least one site of compression in an individual case.

CNS gene therapy applications of the Semliki Forest virus 1 vector are limited by neurotoxicity.

The Semliki Forest virus (SFV) 1 vector system is highly efficient at gene transduction in a broad range of host cells, including neurons. To determine the potential of SFV1-based vectors to mediate gene expression in substantia nigra neurons, we inoculated d1EGFP-expressing SFV virus-like particles stereotaxically into the mouse brain. This system selectively and extensively mediated gene expression in dopaminergic neurons of the substantia nigra. Continual reporter gene expression was evident in neuronal cell bodies for up to 3 weeks postinoculation and d1EGFP-positive neuronal processes were apparent for 12 weeks. There was no evidence of an apoptotic response to infection, but with time cell degeneration and an axonopathy, indicative of neuronal loss, were increasingly apparent. This system has potential for experimental studies requiring efficient transient gene transduction of mouse CNS neurons. The current SFV1 vector system is, however, limited in its potential for CNS gene therapy by neurotoxicity.