A 7-year-old male neutered Miniature Schnauzer was assessed due to an acute and progressive history of pelvic limb weakness and incoordination. At the examination, the dog was non-ambulatory paraparetic, the postural reaction were abscent in both pelvic limbs, with intact withdrawal and patellar reflexes and increased pelvic limb muscle tone, which lead into paraplegia with intact nociception in the follow 24 h. A T3-L3 myelopathy was suspected, and an MRI of the thoracolumbar vertebral column was performed under general anaesthesia. An ill-defined, solitary, T2W hyperintense and strongly contrast enhancing intramedullary lesion was found, extending from the caudal endplate of T12 to the midbody of T13 and associated with severe spinal cord oedema and meningeal enhancement. A lumbar CSF analysis revealed a severe mononuclear pleocytosis (309 cells/μL) and markedly increased protein level; serology against Neospora caninum and Toxoplasma gondii was negative, and treatment with steroids for a suspected focal meningomyelitis of unknown origin was started. The patient deteriorated over the following days, becoming paraplegic with reduced nociception in the right pelvic limb. An exploratory surgery was carried out via T12-T13 right-sided hemilaminectomy, durotomy and myelotomy, and a well-defined, firm intramedullary mass was removed and sent for histopathology. The mass was consistent with an inflammatory pyogranuloma with intralesional fungal hyphae. Panfungal PCR was negative. Treatment with fluconazole was started, and a follow-up MRI was performed 6 months after surgery. At this time the dog was ambulatory paraparetic and MRI revealed complete resolution of the previous mass. Repeat CSF analysis revealed a mild mononuclear pleocytosis (6 cells/μL) and a mild increase in protein. Fluconazole treatment was continued for another 12 months; during all this time, the patient remained ambulatory with a mild paraparesis. The patient died for unrelated reasons 18 months after surgery when under general anaesthesia for routine removal of a subcutaneous lipoma.

[This corrects the article DOI: 10.3389/fvets.2024.1390971.].

BACKGROUND:Humans with peripheral vestibular disorders can suppress nystagmus through visual fixation, a capability often compromised in those with central vestibular disorders. Bedside tests that exploit this difference can aid neurolocalization in humans. These tests remain unexplored in veterinary medicine. HYPOTHESIS:Removal of visual input will reveal or enhance nystagmus in animals with peripheral vestibular disease, while animals with central vestibular disease would show little change. ANIMALS:Twenty-one dogs and cats with peripheral vestibular lesions and 16 with central vestibular lesions. Diagnosis was confirmed by MRI. METHODS:A prospective study was conducted using a modified penlight-cover test. Because animals cannot be easily instructed to fixate on a visual target, removal of visual input was used as a substitute for eliminating visual fixation, based on the assumption that visual fixation also occurs spontaneously. A 0.5-W LED penlight was shined into one eye while covering the other to eliminate visual input. Nystagmus beat frequency (BF) and subjective evaluation of slow phase velocity (SPV) were recorded before and during penlight application. RESULTS:In animals with peripheral lesions, BF increased in 33% and SPV in 24% of cases after removal of visual input. Among those with central lesions, only one of 16 showed an increase in BF, and none exhibited an increase in SPV. CONCLUSIONS:When used alongside the neurological examination, the modified penlight-cover test, could raise suspicion of a peripheral vestibular lesion if it reveals increased BF or SPV.

Myokymia is a form of peripheral nerve hyperexcitability that can be focal or generalized. Information regarding focal myokymia in veterinary medicine is currently limited, resulting in a need for a better understanding of this clinical sign. Describe the clinical presentation, diagnostic findings, treatment, and outcomes in dogs and cats with facial myokymia (FM). Seven dogs and two cats with clinically confirmed FM. Retrospective study. Clinical records from six referral institutions were reviewed to identify cases with FM. Signalment, clinical presentation, diagnostic test results, treatment, and outcome were recorded and evaluated for each patient. Facial myokymia was detected before referral in 6/9 cases. Concurrent vestibular signs were present in 7/9 cases, whereas signs of facial nerve dysfunction other than FM were present in three cases. The diagnoses in the seven dogs were facial and vestibular neuropathy of unknown etiology (n = 2), extra-axial neoplasia (n = 1), otitis media-interna with intracranial extension (n = 1), otitis interna with associated facial and vestibulocochlear neuropathy (n = 1), meningoencephalitis of unknown origin (n = 1) and neoplasia or hypertrophic neuritis (n = 1). The two cats were diagnosed with retrobulbar adenosquamous carcinoma with intracranial extension and traumatic orofacial injury. When prednisolone was used (6/9 cases) FM improved or resolved, although relapses were common. Facial myokymia is an uncommon and nonspecific clinical sign in dogs and cats, associated with a range of structural disorders affecting the facial motor nucleus, nerve, or both. Control of FM is variable, and treatment and outcome depend on the underlying cause.

Idiopathic generalized tremor syndrome is a disorder characterized by an acute onset of full-body tremors, sometimes accompanied by vestibulo-cerebellar signs, that is responsive to treatment with corticosteroids. Although considered to have an overall good outcome, relapsing and persistent mild clinical signs have been described. So far, little is known about the etiopathology of this syndrome, but it is believed to have an immune-mediated origin. In human medicine, description of numerous autoantibodies involved in certain non-infectious neurologic disorders has revolutionized understanding of their pathophysiology, diagnosis and treatment. In this multicenter retrospective study, we aimed to describe the clinical signs, course, and outcome of dogs with idiopathic generalized tremor syndrome and correlate potential findings with the presence or absence of autoantibodies associated with autoimmune cerebellar syndromes in humans. Information regarding signalment, history, clinical signs, laboratory findings, diagnostic imaging and testing for regional infectious diseases was gathered and the remaining serum and CSF samples were then analyzed for neural antibodies against targets associated with autoimmune encephalitic diseases of humans. Thirty-three dogs were included, and screening for neural antibodies was performed in 30 of those dogs. The analysis showed an increased titer of mGluR1 antibodies in two dogs, GFAP and later in the course of disease mGluR1 antibodies in one dog and an increase in unspecific autoantibodies which could not be further classified in two dogs. Dogs with detectable neural autoantibodies always had cerebrospinal fluid abnormalities in the form of a pleocytosis, with or without increased protein concentration, and tended to present with hyperthermia, potentially indicating a more severe clinical form of idiopathic generalized tremor syndrome in these cases. In conclusion, idiopathic generalized tremor syndrome is proposed to be an immune-mediated disorder potentially mediated by neural autoantibodies in a subgroup of dogs.

Metabolic/neurodegenerative encephalopathies encompass a wide list of conditions that share similar clinical and magnetic resonance imaging (MRI) characteristics, challenging the diagnostic process and resulting in numerous tests performed in order to reach a definitive diagnosis. The aims of this multicentric, retrospective and descriptive study are: (I) to describe the MRI features of dogs and cats with metabolic/neurodegenerative encephalopathies; (II) to attempt an MRI recognition pattern classifying these conditions according to the involvement of grey matter, white matter or both; and (III) to correlate the MRI findings with previous literature. A total of 100 cases were recruited, comprising 81 dogs and 19 cats. These included hepatic encephalopathy (20 dogs and three cats), myelinolysis (five dogs), intoxications (seven dogs and one cat), thiamine deficiency (two dogs and seven cats), hypertensive encephalopathy (three dogs and two cats), neuronal ceroid lipofuscinosis (11 dogs and one cat), gangliosidosis (three dogs and two cats), fucosidosis (one dog), L-2-hydroxyglutaric aciduria (13 dogs and one cat), Lafora disease (11 dogs), spongiform leukoencephalomyelopathy (one dog) and cerebellar cortical degeneration (four dogs and two cats). None of the hepatic encephalopathies showed the previously described T1-weighted hyperintensity of the lentiform nuclei. Instead, there was involvement of the cerebellar nuclei (8/23), which is a feature not previously described. Dogs with myelinolysis showed novel involvement of a specific white matter structure, the superior longitudinal fasciculus (5/5). Thiamine deficiency affected numerous deep grey nuclei with novel involvement of the oculomotor nuclei (3/9), thalamic nuclei, subthalamus and cerebellar nuclei (1/9). Cats with hypertensive encephalopathy had a more extensive distribution of the white matter changes when compared to dogs, extending from the parietal and occipital lobes into the frontal lobes with associated mass effect and increased brain volume. Lysosomal storage disease showed white matter involvement only, with neuronal ceroid lipofuscinosis characterised by severe brain atrophy when compared to gangliosidosis and fucosidosis. All patients with L-2-hydroxyglutaric aciduria had a characteristic T2-weighted hyperintense swelling of the cerebral and cerebellar cortical grey matter, resulting in increased brain volume. Lafora disease cases showed either normal brain morphology (5/11) or mild brain atrophy (6/11). Dogs with cerebellar cortical degeneration had more marked cerebellar atrophy when compared to cats. This study shows the important role of MRI in distinguishing different metabolic/neurodegenerative encephalopathies according to specific imaging characteristics.

Recent work identified anti-GM2 and anti-GalNAc-GD1a IgG ganglioside antibodies as biomarkers in dogs clinically diagnosed with acute canine polyradiculoneuritis, in turn considered a canine equivalent of Guillain-Barre syndrome. This study aims to investigate the serum prevalence of similar antibodies in cats clinically diagnosed with immune-mediated polyneuropathies. The sera from 41 cats clinically diagnosed with immune-mediated polyneuropathies (IPN), 9 cats with other neurological or neuromuscular disorders (ONM) and 46 neurologically normal cats (CTRL) were examined for the presence of IgG antibodies against glycolipids GM1, GM2, GD1a, GD1b, GalNAc-GD1a, GA1, SGPG, LM1, galactocerebroside and sulphatide. A total of 29/41 IPN-cats had either anti-GM2 or anti-GalNAc-GD1a IgG antibodies, with 24/29 cats having both. Direct comparison of anti-GM2 (sensitivity: 70.7%; specificity: 78.2%) and anti-GalNAc-GD1a (sensitivity: 70.7%; specificity: 70.9%) antibodies narrowly showed anti-GM2 IgG antibodies to be the better marker for identifying IPN-cats when compared to the combined ONM and CTRL groups (P = .049). Anti-GA1 and/or anti-sulphatide IgG antibodies were ubiquitously present across all sample groups, whereas antibodies against GM1, GD1a, GD1b, SGPG, LM1 and galactocerebroside were overall only rarely observed. Anti-GM2 and anti-GalNAc-GD1a IgG antibodies may serve as serum biomarkers for immune-mediated polyneuropathies in cats, as previously observed in dogs and humans.

A 10-month-old, 3 kg, female spayed Domestic Shorthair cat was presented with a chronic, infected wound at the level of the proximo-lateral left pelvic limb. General physical examination revealed a weight-bearing lameness of the left pelvic limb, which was moderately and circumferentially swollen and edematous proximal to the tarsal joint. On the lateral aspect of the proximal thigh, there was a chronic wound of 1 cm in diameter and an additional exudative skin lesion was present throughout the whole length of the caudo-lateral thigh. Complete blood count and serum biochemistry profile revealed mild anemia, increased serum amyloid A, hyponatraemia, hypochloraemia, hypocalcaemia, hyperkalaemia, hypermagnesaemia, hyperglycaemia, increased creatine kinase, and increased liver parameters. Surgical exploration of the wound was performed, and necrotizing fasciitis was suspected. The affected limb was amputated and swabs for bacterial culture were taken from both the skin lesions and surgical site before wound closure. One day after surgery, mild muscular contractions on the forehead and an increased muscle tone of the right pelvic limb were evident. One day later, the cat developed a generalized increase in extensor tone, with intermittent opisthotonos, resulting in lateral recumbency. Based on these clinical signs, a diagnosis of generalized tetanus was made and treatment with midazolam, methocarbamol, and metronidazole was started. Despite an improvement of all blood parameters, the cat progressively deteriorated and 4 days after surgery, it developed episodes of tetanic convulsions, associated with hyperthermia and ventricular arrhythmias. Despite intensive care and medical management, the cat died following a cardio-respiratory arrest 3 days later. This case report describes a rare case of severe generalized tetanus in a young cat.

Background The chondrodystrophic body type predisposes miniature dachshunds to thoracolumbar intervertebral disc extrusion (IVDE). However, the relationship between thoracolumbar IVDE and the relative lengths of the thoracic and lumbar vertebral columns has not yet been evaluated. Methods This prospective multicentre study included 151 miniature dachshunds with ( n = 47) and without ( n = 104) thoracolumbar IVDE. All dogs had their thoracic and lumbar vertebral columns measured with a tape measure. Detailed descriptions were provided to facilitate consistent measurement. A thoracic to lumbar vertebral column ratio was calculated. Thoracolumbar IVDE was confirmed by magnetic resonance imaging or computed tomography. Results The thoracic to lumbar vertebral column length ratio and absolute thoracic vertebral column length were significantly smaller in miniature dachshunds with IVDE than in those without IVDE ( p < 0.0001 for both). There were no significant differences in lumbar vertebral column length, age, sex or neuter status between the two groups. Limitations The dogs without IVDE did not undergo a neurological examination and the thoracic and lumbar vertebral column measurements were not validated. Conclusions The relative lengths of the thoracic and lumbar vertebral column segments could contribute to the development of thoracolumbar IVDE in miniature dachshunds. Further studies are needed to evaluate ideal thoracic to lumbar vertebral column length ratios in miniature dachshunds.

Objectives The aim of the study was to describe the patient demographics, clinicopathological features and presumptive or final diagnoses in cats with myelopathies between the T1 and T6 vertebrae. Methods This retrospective multicentre case study enrolled cases between 2015 and 2022 that were diagnosed with myelopathies between the T1 and T6 vertebrae as the primary cause for the presenting clinical signs. Results A total of 21 cases matched the inclusion criteria, 13 males (11 castrated and 2 entire) and 8 spayed females (median age 93 months; range 5–192). Most of the cases presented with a chronic and progressive history (76% and 86%, respectively), with a median duration of 29 days (range 1–2880). At the time of presentation, 90% of the cases were localised to the T3–L3 spinal cord segments based on neurological examination. The most common underlying pathology was neoplasia (42.9%), followed by inflammatory (24%), anomalous (19%), degenerative (9.5%) and vascular (4.8%) disorders. The most common location was T3–T4 (29%), followed by T2–T3 and T5–T6 (19% each). The cutaneous trunci reflex was normal in 86% of the cases and most of the cases (71%) did not show spinal discomfort upon admission. Conclusions and relevance Neoplasia was the most common cause of cranial thoracic myelopathy in this study. The lack of pathognomonic clinical signs for this specific region highlights the importance of assessing the entire thoracolumbar region up to and including at least the T1 vertebra when investigating cases with signs consistent with a T3–L3 myelopathy.

AbstractBackgroundKCNJ10 and CAPN1 variants cause “spinocerebellar” ataxia in dogs, but their association with generalized myokymia and neuromyotonia remains unclear.ObjectiveTo investigate the association between KCNJ10 and CAPN1 and myokymia or neuromyotonia, with or without concurrent spinocerebellar ataxia.AnimalsThirty‐three client‐owned dogs with spinocerebellar ataxia, myokymia neuromytonia, or a combination of these signs.MethodsGenetic analysis of a cohort of dogs clinically diagnosed with spinocerebellar ataxia, myokymia or neuromyotonia. KCNJ10 c.627C>G and CAPN1 c.344G>A variants and the coding sequence of KCNA1, KCNA2, KCNA6, KCNJ10 and HINT1 were sequenced using DNA extracted from blood samples.ResultsTwenty‐four Jack Russell terriers, 1 Jack Russell terrier cross, 1 Dachshund and 1 mixed breed with spinocerebellar ataxia were biallelic (homozygous) for the KCNJ10 c.627C>G variant. Twenty‐one of those dogs had myokymia, neuromyotonia, or both. One Parson Russell terrier with spinocerebellar ataxia alone was biallelic for the CAPN1 c.344G>A variant. Neither variant was found in 1 Jack Russell terrier with ataxia alone, nor in 3 Jack Russell terriers and 1 Yorkshire terrier with myokymia and neuromyotonia alone. No other causal variants were found in the coding sequence of the investigated candidate genes in these latter 5 dogs.ConclusionThe KCNJ10 c.627C>G variant, or rarely the CAPN1 c.344G>A variant, was confirmed to be the causal variant of spinocerebellar ataxia. We also report the presence of the KCNJ10 c.627C>G variant in the Dachshund breed. In dogs with myokymia and neuromyotonia alone the reported gene variants were not found. Other genetic or immune‐mediated causes should be investigated to explain the clinical signs of these cases.

The aim of the study was to describe the signalment, clinical presentation and presumptive or final diagnoses of dogs with cranial thoracic spinal cord lesions identified on advanced imaging. Retrospective evaluation of the databases of three veterinary specialty centres, between 2009 and 2021, was performed to identify dogs with a lesion affecting the cranial thoracic vertebral column (T1-T6 vertebrae) as the primary cause for presenting signs of myelopathy and/or spinal pain. Eighty-four dogs were included in the study, with the majority (n = 76) presenting with a progressive history of over 4-weeks' duration. On neurologic examination, most dogs were ambulatory (n = 64), and the most common neuroanatomic localisation was the T3-L3 spinal cord segments (n = 63). Twelve dogs (14%) showed a short-strided thoracic limb gait on clinical examination. The most common diagnosis was neoplasia (n = 33), followed by anomalies (n = 22, including vertebral body malformations in 14 dogs) and degenerative disorders (n = 16, with intervertebral disc protrusion diagnosed in 9 dogs). The most common vertebrae affected were T3 and T5. Most dogs with degenerative conditions showed asymmetric clinical signs, and the majority of dogs with neoplasia showed signs of spinal hyperaesthesia on examination. The findings of this study describe the clinical signs and presumptive or final diagnoses associated with lesions affecting the cranial thoracic spinal cord. When combined with the signalment and clinical history, this information can assist in both the recognition of and problem-based approach to these cases.

AbstractBackgroundAcquired narcolepsy has rarely been reported in veterinary medicine.ObjectiveTo describe the presentation, clinicopathological features, diagnostic imaging findings, and management of dogs with suspected‐acquired narcolepsy.AnimalsEight dogs with clinical features consistent with acquired narcolepsy.MethodsA call for suspected cases of acquired narcolepsy was made online, followed by a retrospective review of detailed medical records of potential cases. Dogs were included if episodes consistent with cataplexy were present during examination by a board‐certified veterinary neurologist and diagnostic work‐up included magnetic resonance imaging of the brain and analysis of cerebrospinal fluid.ResultsSeven French Bulldogs and 1 Chihuahua (age range, 9‐66 months) were included. Meningoencephalitis of unknown origin was diagnosed in 2 dogs, extracranial foci of inflammation were identified in 2 dogs (aspiration pneumonia, esophagitis, otitis media), and no abnormalities were found on diagnostic investigations in 4 dogs. Prednisolone was used in the management of all dogs, 6 dogs received imipramine, and 2 received cytosine arabinoside. An initial remission of signs was observed in all dogs, but a subsequent relapse of clinical signs was recorded for 4 dogs, of which 3 responded to adjustment or resumption of treatment.Conclusions and Clinical ImportanceThe presence of cataplexy episodes should prompt a thorough diagnostic work‐up to exclude the presence of intracranial (and extracranial) pathology. The potential for both remission and relapse of signs in suspected acquired cases is important for clinicians and owners to be aware of.

Acquired narcolepsy has rarely been reported in veterinary medicine. To describe the presentation, clinicopathological features, diagnostic imaging findings, and management of dogs with suspected-acquired narcolepsy. Eight dogs with clinical features consistent with acquired narcolepsy. A call for suspected cases of acquired narcolepsy was made online, followed by a retrospective review of detailed medical records of potential cases. Dogs were included if episodes consistent with cataplexy were present during examination by a board-certified veterinary neurologist and diagnostic work-up included magnetic resonance imaging of the brain and analysis of cerebrospinal fluid. Seven French Bulldogs and 1 Chihuahua (age range, 9-66 months) were included. Meningoencephalitis of unknown origin was diagnosed in 2 dogs, extracranial foci of inflammation were identified in 2 dogs (aspiration pneumonia, esophagitis, otitis media), and no abnormalities were found on diagnostic investigations in 4 dogs. Prednisolone was used in the management of all dogs, 6 dogs received imipramine, and 2 received cytosine arabinoside. An initial remission of signs was observed in all dogs, but a subsequent relapse of clinical signs was recorded for 4 dogs, of which 3 responded to adjustment or resumption of treatment. The presence of cataplexy episodes should prompt a thorough diagnostic work-up to exclude the presence of intracranial (and extracranial) pathology. The potential for both remission and relapse of signs in suspected acquired cases is important for clinicians and owners to be aware of.

Cutaneous and renal glomerular vasculopathy (CRGV) is an emerging disease in the UK, but its aetiology remains unclear. It is considered a thrombotic microangiopathy (TMA) in which the kidney and skin are the most commonly affected organs. We now document two cases of CRGV with brain lesions, which may have accounted for neurological signs displayed by these animals. The histopathological brain lesions were similar to TMA lesions in humans with thrombotic thrombocytopaenic purpura (TTP) and complement-mediated haemolytic uraemic syndrome (CM-HUS), in which the neurological signs are more associated with TMA than with any systemic disease or electrolyte imbalance. Fibrinoid necrosis in brain arterioles and associated lesions in these dogs were similar to those in human CM-HUS, indicating that the alternative complement pathway may play an important role in the pathophysiology of CRGV.

Knowledge regarding the etiology and prognosis for canine megaesophagus (ME) is currently limited to small case series that may now be out of date in light of recent advances in the understanding of neurological syndromes and the availability of advanced diagnostic testing. Ninety-nine dogs diagnosed with nonstructural ME were included. Congenital idiopathic ME was present in 10 cases, with complete resolution of clinical signs in a single case. Eighty-nine cases were considered acquired, with most cases being either idiopathic (42.7%) or associated with myasthenia gravis (38.2%). Idiopathic cases represented a smaller percentage of acquired ME than previously reported. Death or euthanasia directly related to ME occurred in almost 50% of acquired cases, whereas clinical signs persisted in ∼20% of cases and resolved in 30% of cases. A diagnosis of an underlying etiology, in particular myasthenia gravis, was associated with a better outcome in acquired ME. ME continues to be a challenging condition to manage, with a guarded-to-poor prognosis, particularly when an underlying etiology is not identified. Thorough diagnostic testing for an underlying neurological disorder is important in cases with ME as this may allow institution of appropriate treatment and the potential for a better prognosis.