Anatomic description and clinical relevance of the meningovertebral ligament in dogs.

OBJECTIVE: To determine whether dogs have a meningovertebral ligament (MVL) and to assess the effect that structure may have on pathological lesions within the ventral epidural space. SAMPLE: Cadaveric specimens from 6 neurologically normal dogs and 2 dogs with vertebral neoplasms that extended into the epidural space and MRI sequences and cytologic preparations from 2 dogs with compressive hydrated nucleus pulposus extrusion that underwent decompressive surgery. PROCEDURES: The vertebral column was removed for gross and histologic examination from the cadavers of neurologically normal dogs and dogs with vertebral neoplasms. For dogs with hydrated nucleus pulposus extrusion, MRI sequences to assess lesion location and topography and cytologic preparations of material surgically extirpated from the ventral epidural space were reviewed. RESULTS: All dogs had an MVL, which formed the ventral boundary of the epidural space and consisted of fibrous bands that attached the external ventral surface of the dura mater of the spinal cord to the dorsal surface of the vertebral bodies throughout the length of the vertebral canal. Both vertebral neoplasms had a bilobed appearance as did the extruded nucleus pulposus lesions on MRI sequences. CONCLUSIONS AND CLINICAL RELEVANCE: Results of the present study indicated that dogs have an MVL, which creates an anatomic barrier within the ventral epidural space and causes pathological lesions to adopt a bilobed shape regardless of the pathogenic process. Further anatomic studies of the MVL and vertebral canal of dogs are necessary to elucidate how those structures affect lesion progression within the ventral epidural space.

Schwannosis in Three Foals and a Calf.

Proliferation of ectopic Schwann cells within the central nervous system (CNS) parenchyma (schwannosis) in early life is most commonly associated with human neurofibromatosis type-2 and has been unrecognized in domestic animals. Three foals and a calf, 5 to 11 weeks old, with progressive neurological signs from birth were studied. Histologically, at multiple levels of the spinal cord, all animals had bilateral plaques of proliferative spindle cells, predominantly affecting the white matter adjacent to dorsal and ventral nerve roots and variably extending into the gray matter. Proliferating cells had strong intracytoplasmic immunoreactivity for the Schwann cell markers myelin protein zero and periaxin, highlighting the formation of peripheral nervous system (PNS) myelin within the spinal cord. In all cases, foci of disorganized neural tissue (glioneuronal hamartomas) were present, which in 2 cases formed a mass effect that resulted in syringohydromyelia. Neonatal presentation suggests a congenital maldevelopment of the nervous system, with spontaneous invasion of PNS-derived Schwann cells into the CNS.

A Salivation Abnormality with Trigeminal Nerve Dysfunction in Dogs.

Trigeminal nerve pathology can lead to sensory and motor dysfunction to structures of the head that are easily recognized. The trigeminal nerve is a conduit for the distribution of postganglionic parasympathetic innervation to structures of the head. Parasympathetic innervation to the salivary glands is provided by preganglionic parasympathetic neurons of the facial and glossopharyngeal nerves. Postganglionic axons course with branches of the mandibular branch of the trigeminal nerve to reach the salivary glands. Denervation of the salivary glands impacts glandular function, leading to a reduction in the volume and composition of the saliva produced. Saliva plays an important role in oral health. Poor oral health has widespread systemic implications. This article describes a group of dogs with unilateral or bilateral dysfunction of the trigeminal nerve and/or its branches. In all dogs, an accumulation of thick, foamy saliva was observed accumulating in the dorsal aspect of the caudal oral cavity on the ipsilateral side to the affected nerve. In dogs with magnetic resonance imaging (MRI), there was a reduction in size based on the largest cross-sectional area measurement and an increase in mean signal intensity of the salivary glands ipsilateral to the affected nerves compared to the glands on the normal side. The authors hypothesize that the abnormal saliva and MRI changes observed were consequent to parasympathetic denervation of the salivary glands. The recognition of this clinical observation is the first step in understanding the impact that denervation has on salivation and ultimately on overall oral and systemic health in dogs.

Correlation of MRI with the Neuropathologic Changes in Two Cats with Bromethalin Intoxication.

Two cats were presented with multifocal neurological signs. One cat's signs progressed over 2 wk; the other cat progressed over 5 days. Examinations were consistent with a process involving the prosencephalon, vestibular system, and general proprioceptive/upper motor neuron systems. MRI of the brain and cervical spinal cord reveal widespread T2 hyperintensity of the white matter. Affected areas included the cerebrum, cerebral peduncles, corticospinal tracts of the pons and medulla, and the cerebellum. T2 hyperintensity was present in all funiculi of the spinal cord. Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps were consistent with cytotoxic or intramyelinic edema. Differential diagnosis included toxic or metabolic/degenerative leukoencephalopathies. Necropsies revealed widespread spongy degeneration of the central nervous system white matter. Toxicologic assays of liver specimens revealed desmethylbromethalin, a metabolite of bromethalin. Bromethalin is a rodenticide that causes uncoupling of oxidative phosphorylation. Antemortem diagnosis is challenging. DWI and ADC maps were instrumental in narrowing the differential diagnosis and raised the index of suspicion for bromethalin. Bromethalin intoxication should be considered in all animals with a progressive course of multifocal neurologic deficits. MRI, specifically, DWI and ADC maps, may serve as a biomarker of cytotoxic or intramyelinic edema associated with spongiform leukoencephalomyelopathy.

MASTICATORY MUSCLE MYOSITIS IN A GRAY WOLF (CANIS LUPUS).

A 10-yr-old male, neutered gray wolf ( Canis lupus ) was presented for atrophy of the temporalis and masseter muscles. Clinical signs and magnetic resonance imaging were consistent with a myopathy. Positive serology for antibody titers directed against Type 2M myofibers, and the observation of a mixed mononuclear inflammatory cell infiltrate along with eosinophils and neutrophils within the temporalis muscle, were diagnostic for masticatory muscle myositis. Importantly, protozoal myositis was excluded based on other clinicopathologic data. The case highlights the potential for immune-mediated polymyositis in canids other than the domesticated dog ( Canis lupus familaris). Additionally, awareness of a diet in which raw meat is used should prompt a thorough investigation for an underlying infectious myositis in the gray wolf.

Use of botulinum toxin type A for the treatment of radiation therapy-induced myokymia and neuromyotonia in a dog.

CASE DESCRIPTION A 5-year-old castrated male Maltese was evaluated for intermittent clinical signs of muscle cramping and abnormal movements of the skin of the right pelvic limb at the site where an infiltrative lipoma had twice been resected. After the second surgery, the surgical field was treated with radiation therapy (RT). The clinical signs developed approximately 14 months after completion of RT. CLINICAL FINDINGS When clinical signs were present, the right biceps femoris and semitendinosus muscles in the area that received RT were firm and had frequently visible contractions, and the skin overlying those muscles had episodic vermiform movements. Electromyography of those muscles revealed abnormal spontaneous activity with characteristics consistent with myokymic discharges and neuromyotonia. Magnetic resonance imaging of the affected leg revealed no evidence of tumor regrowth. The myokymia and neuromyotonia were considered secondary to RT. TREATMENT AND OUTCOME 4 U of Clostridium botulinum toxin type A (BoNT-A) neurotoxin complex was injected into the affected muscles at each of 6 sites twice during a 24-hour period (ie, 48 U of BoNT-A were administered). The clinical signs were completely resolved 10 days after BoNT-A treatment and were controlled by repeated BoNT-A treatment every 3 to 4 months for > 1 year. CLINICAL RELEVANCE To our knowledge, this is the first report of myokymia and neuromyotonia secondary to RT in a dog. For the dog of this report, injection of BoNT-A into the affected muscles was safe, effective, and easy to perform.

Embryonic Development of the Central Nervous System.

Ultimately, it is only with an understanding of normal embryologic development that there can be an understanding of why and how a specific malformation develops. Knowing from where and when a specific part of the nervous system develops and what morphogens are at play will enable us to identify undescribed malformation as well as better define causality. The following article reviews the normal embryologic development of the mammalian nervous system and is intended to serve as a foundation for the understanding of the various malformations presented in this issue.

Denervation of the Tensor Veli Palatini Muscle and Effusion in the Tympanic Cavity.

An English springer spaniel was presented for right-sided atrophy of the muscles of mastication, analgesia and paralysis of the face, and vestibular dysfunction. Neurological signs were consistent with a lesion involving the pons and rostral medulla resulting in deficits in the function of the trigeminal, facial, and vestibular nerves. MRI disclosed a right-sided extraparenchymal mass consistent with a trigeminal nerve sheath neoplasm that was compressing and invading the pons and medulla. Atrophy of the muscles of mastication, innervated by the trigeminal nerve, was also observed on MRI. Additionally, effusion was present in the ipsilateral tympanic cavity. Gross and microscopic evaluation of the right tensor veli palatini muscle (TVPM) was consistent with neurogenic atrophy. Effusion in the tympanic cavity was likely the result of an inability to open the auditory tube as a consequence of paralysis of the TVPM. Without the ability to open the auditory tube, gases present within the auditory tube and tympanic cavity may be absorbed, creating a negative pressure environment that leads to fluid transudation and effusion build up. To the authors' knowledge, this is the first report to document neurogenic atrophy of the TVPM with concurrent effusion in the ipsilateral tympanic cavity.

Bilateral Symmetrical Idiopathic Necrotizing Encephalopathy: A New Syndrome in Sprague-Dawley Rats.

This article describes the occurrence of a bilaterally symmetrical encephalopathy in Sprague-Dawley rats, which occurred over the period 2005 to 2012 in our laboratory in both untreated control rats and rats treated with different pharmacologically active compounds. The acute brain lesions consisted of degeneration/necrosis in the ventral areas of the brain mostly with little inflammatory response; in the more rare chronic cases there were numerous lipid-laden macrophages. The areas most consistently affected were the crus cerebri, the ventral midbrain, the pyramids, and the internal capsule. Other areas less frequently affected were the mammillary bodies, the fimbria, the olfactory tubercles, the optic tracts, and the ventral hippocampus. All available data, including clinical signs, gross pathology, clinical pathology, diet, breeding, and housing were collected and are presented. Our investigations did not elucidate the pathogenesis of the lesions, although the infarction-type changes are suggestive of a vascular etiology. To our knowledge, this particular lesion with its consistent distribution pattern has not been reported in the rat literature and its publication is therefore important to the toxicological pathology community, because an unbalanced group distribution in a toxicology study could potentially confound the safety assessment of a compound.

Primary lumbar extradural hemangiosarcoma in a dog.

A 9 yr old castrated male golden retriever weighing 36 kg was presented for evaluation of progressive left pelvic limb paresis and fecal and urinary incontinence. MRI demonstrated an extradural, ovoid mass compressing the lumbar spinal cord. Surgical excision of the mass was performed. Histologically, the mass was consistent with hemangiosarcoma with no involvement of the adjacent vertebrae. The dog underwent a doxorubicin-based chemotherapy protocol with the addition of oral cyclophosphamide. After completion of chemotherapy, the dog was evaluated q 4 mo for restaging. Clinicopathological evidence of primary tumor recurrence or metastatic disease was not detected for 15 mo after initial diagnosis and treatment. To the authors' knowledge, this is the first report of a primary extradural hemangiosarcoma in the lumbar vertebral column in a dog. The clinical presentation, diagnosis, treatment, and outcome are also discussed.

Surgical correction of a sacral meningomyelocele in a dog.

A 15 wk old male unilateral cryptorchid German shepherd dog weighing 18 kg was referred for a nonhealing cutaneous lesion dorsally at the level of the sacrum, urinary incontinence, and a deviated tail. MRI revealed spina bifida and meningomyelocele continuous with the skin surface. Surgical correction of the meningomyelocele involved closure of the open meningeal defect, transection of the abnormal spinal nerves to the skin surface, and closure of the skin defect with a good outcome. Histopathology confirmed a meningomyelocele. This case report describes the MRI findings, surgical procedure, and proposed pathogenesis of spina bifida and meningomyelocele in a dog.

Imaging diagnosis--meningoencephalitis secondary to suppurative rhinitis and meningoencephalocele infection in a dog.

Nasal encephaloceles (meningoceles or meningoencephaloceles) are rare and not reported to be infected or coupled with a facial deformity in dogs. This report describes an older dog with acute worsening of seizures due to suppurative meningoencephalitis with coexisting suppurative rhinitis and infection of a meningoencephalocele. Additionally, the dog had a facial deformity for at least 5 years. The results of necropsy, computed tomography, and postmortem magnetic resonance imaging are compared. The development of nasal encephaloceles is discussed, including the potential role of early trauma, and whether separation of neural ectoderm from the surface ectoderm is part of the pathogenesis.

Insertion of the dorsal oblique muscle in the dog: an anatomic basis for ventral strabismus associated with oculomotor nerve dysfunction.

OBJECTIVE: To describe the insertion of the dorsal oblique (DO) muscle in relationship to the equator of the globe in dogs. PROCEDURE: The study was conducted on 10 fresh cadaver eyes from five dogs, which were euthanized for disease processes unrelated to ocular disease. A manual vernier caliper was used to determine the calculated measurements. RESULTS: The median anterior-to-posterior diameter of the globe was 21 mm. The median length from the vertex of the anterior pole to the anterior point of insertion of the DO tendon was 11.5 mm. The median length from the posterior pole to the posterior point of insertion of the DO tendon was 10 mm. The width of tendon of insertion of the DO tendon was 3.25 mm. CONCLUSIONS: In disorders involving the oculomotor nerve or the oculomotor nerve nucleus in the mesencephalon, the resultant strabismus is directed ventrolaterally. Based on the insertion of the superior oblique muscle in humans, we hypothesized that the DO muscle would likely explain the ventral deviation in disorders of the oculomotor nerve or its nucleus. In this study, the point of the insertion of the DO muscle tendon was posterior to the equator. Based on this anatomic location, unopposed function of the DO muscle would be expected to result in ventral deviation of the globe.

Association of oxidative stress with motor neuron disease in horses.

OBJECTIVE: To investigate the influence of oxidative stress in terms of antioxidant capacity and lipid peroxidation on the probability of motor neuron disease (MND) in horses. ANIMALS: 88 horses with MND (cases) and 49 controls. PROCEDURES: Blood samples were collected from all horses enrolled, and RBCs and plasma were harvested. Activity of the enzyme erythrocytic superoxide dismutase 1 (SOD1) was determined in the RBCs. Plasma concentrations of α-tocopherols and ß-carotenes and activity of glutathione peroxidase were also evaluated. Degree of lipid peroxidation was measured by determining plasma concentrations of lipid hydroperoxides. Differences were evaluated between horse groups. RESULTS: Cases had lower erythrocyte SOD1 activity than did controls, but the difference was not significant. On the other hand, plasma vitamin E concentrations differed significantly between groups, with the cases having lower concentrations. Neither plasma vitamin A concentration nor glutathione peroxidase activity differed between groups; however, cases had significantly higher concentrations of lipid hydroperoxides (18.53µM) than did controls (12.35µM). CONCLUSIONS AND CLINICAL RELEVANCE: Horses with MND differed from those without MND by having a lower plasma concentration of vitamin E and higher concentrations of lipid hydroperoxides. Results parallel the findings in humans with sporadic amyotrophic sclerosis and provide evidence supporting the involvement of oxidative stress in the 2 conditions.