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Movement disorders are a heterogeneous group of clinical syndromes in humans and animals characterized by involuntary movements without changes in consciousness. Canine movement disorders broadly include tremors, peripheral nerve hyperexcitability disorders, paroxysmal dyskinesia, and dystonia. Of these, canine paroxysmal dyskinesias remain one of the more difficult to identify and characterize in dogs. Canine paroxysmal dyskinesias include an array of movement disorders in which there is a recurrent episode of abnormal, involuntary, movement. In this consensus statement, we recommend standard terminology for describing the various movement disorders with an emphasis on paroxysmal dyskinesia, as well as a preliminary classification and clinical approach to reporting cases. In the clinical approach to movement disorders, we recommend categorizing movements into hyperkinetic vs hypokinetic, paroxysmal vs persistent, exercise-induced vs not related to exercise, using a detailed description of movements using the recommended terminology presented here, differentiating movement disorders vs other differential diagnoses, and then finally, determining whether the paroxysmal dyskinesia is due to either inherited or acquired etiologies. This consensus statement represents a starting point for consistent reporting of clinical descriptions and terminology associated with canine movement disorders, with additional focus on paroxysmal dyskinesia. With consistent reporting and identification of additional genetic mutations responsible for these disorders, our understanding of the phenotype, genotype, and pathophysiology will continue to develop and inform further modification of these recommendations., (© 2021 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC. on behalf of the American College of Veterinary Internal Medicine.)

Background: Optical neuronavigation-guided intracranial surgery has become increasingly common in veterinary medicine, but its use has not yet been described in horses., Objectives: To determine the feasibility of optical neuronavigation-guided intracranial biopsy procedures in the horse, compare the use of the standard fiducial array and anatomic landmarks for patient registration, and evaluate surgeon experience., Animals: Six equine cadaver heads., Methods: Computed tomography images of each specimen were acquired, with the fiducial array rigidly secured to the frontal bone. Six targets were selected in each specimen. Patient registration was performed separately for 3 targets using the fiducial array, and for 3 targets using anatomic landmarks. In lieu of biopsy, 1 mm diameter wire seeds were placed at each target. Postoperative images were coregistered with the planning scan to calculate Euclidian distance from the tip of the seed to the target., Results: No statistical difference between registration techniques was identified. The impact of surgeon experience was examined for each technique using a Mann-Whitney U test. The experienced surgeon was significantly closer to the intended target (median = 2.52 mm) than were the novice surgeons (median = 6.55 mm) using the fiducial array (P = .001). Although not statistically significant (P = .31), for the experienced surgeon the median distance to target was similar when registering with the fiducial array (2.47 mm) and anatomic landmarks (2.58 mm)., Conclusions and Clinical Importance: Registration using both fiducial arrays and anatomic landmarks for brain biopsy using optical neuronavigation in horses is feasible., (© 2020 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Musladin-Lueke syndrome (MLS), previously termed Chinese Beagle syndrome, is an autosomal-recessive connective tissue disorder characterized by extensive fibrosis of the skin and joints that was first identified in Beagles in the 1970s. Recent research identified a founder mutation (c.660C>T; p.R221C) in the ADAMTSL2 gene in Beagles with MLS. Here, we report the detailed clinical phenotype and laboratory findings in 2 Beagles affected with MLS. We discuss these findings in relation to the human disorder geleophysic dysplasia (GD), which also arises from recessive ADAMTSL2 mutations, and recent findings in Adamtsl2-deficient mice., (Copyright © 2017 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Background: Increased D-lactate concentrations cause neurological signs in humans with gastrointestinal disease., Hypothesis/objectives: To determine if serum D-lactate concentrations are increased in cats with gastrointestinal disease compared to healthy controls, and if concentrations correlate with specific neurological or gastrointestinal abnormalities., Animals: Systematically selected serum samples submitted to the Gastrointestinal Laboratory at Texas A&M University from 100 cats with clinical signs of gastrointestinal disease and abnormal gastrointestinal function tests, and 30 healthy cats., Methods: Case-control study in which serum D- and L-lactate concentrations and retrospective data on clinical signs were compared between 30 healthy cats and 100 cats with gastrointestinal disease. Association of D-lactate concentration with tests of GI dysfunction and neurological signs was evaluated by multivariate linear and logistic regression analyses, respectively., Results: All 100 cats had a history of abnormal gastrointestinal signs and abnormal gastrointestinal function test results. Thirty-one cats had definitive or subjective neurological abnormalities. D-lactate concentrations of cats with gastrointestinal disease (median 0.36, range 0.04-8.33 mmol/L) were significantly higher than those in healthy controls (median 0.22, range 0.04-0.87 mmol/L; P = .022). L-lactate concentrations were not significantly different between the 2 groups of cats with gastrointestinal disease and healthy controls. D-lactate concentrations were not significantly associated with fPLI, fTLI, cobalamin, folate, or neurological abnormalities (P > .05)., Conclusions and Clinical Importance: D-lactate concentrations can be increased in cats with gastrointestinal disease. These findings warrant additional investigations into the role of intestinal microbiota derangements in cats with gastrointestinal disease, and the association of D-lactate and neurological abnormalities., (Copyright © 2012 by the American College of Veterinary Internal Medicine.)

Background: Paroxysmal dyskinesias are episodes of abnormal, involuntary movement or muscle tone, distinguished from seizures by the character of the episode and lack of seizure activity on ictal EEG., Hypothesis: Paroxysmal dyskinesia is an inherited, autosomal recessive disorder in Chinook dogs., Animals: Families of Chinook dogs with paroxysmal dyskinesia., Methods: Pedigrees and medical histories were reviewed for 299 Chinook dogs. A family of 51 dogs was used for analysis. Episodes were classified as seizures, paroxysmal dyskinesia, or unknown, and segregation analysis was performed., Results: Paroxysmal dyskinesia was identified in 16 of 51 dogs and characterized by an inability to stand or ambulate, head tremors, and involuntary flexion of 1 or multiple limbs, without autonomic signs or loss of consciousness. Episode duration varied from minutes to an hour. Inter-ictal EEGs recorded on 2 dogs with dyskinesia were normal. Three dogs with dyskinesia also had generalized tonic-clonic seizures. One of 51 dogs had episodes of undetermined type. Phenotype was unknown for 6 of 51 dogs, and 28 dogs were unaffected. Segregation was consistent with an autosomal recessive trait., Conclusions and Clinical Importance: This movement disorder is prevalent in the Chinook breed, and consistent with a partially penetrant autosomal recessive or polygenic trait. Insufficient evidence exists for definitive localization; episodes may be of basal nuclear origin, but atypical seizures and muscle membrane disorders remain possible etiologies. The generalized seizures may be a variant phenotype of the same mutation that results in dyskinesia, or the 2 syndromes may be independent., (Copyright © 2010 by the American College of Veterinary Internal Medicine.)