Prevalence, clinical presentation, and etiology of myelopathies in 224 juvenile dogs.

BACKGROUND: Intervertebral disc herniation is widely recognized as the most common cause of myelopathy in dogs older than 2 years; however, the prevalence of various causes of myelopathy in younger dogs has not been reported. HYPOTHESIS/OBJECTIVES: To describe the prevalence, clinical presentation, and etiology of myelopathy in dogs aged 18 months or less. Secondarily, to investigate which clinical features were associated with each of the most common etiologies. ANIMALS: Two hundred twenty-four dogs aged 18 months or less with myelopathy were included in the study. METHODS: Retrospective review of clinical records from 4 referral institutions. Multivariable logistic regression analyses assessed which clinical features were associated with each diagnosis. RESULTS: French bulldogs (n = 51, 22.8%), pugs (n = 18, 8.0%), crossbreeds (n = 12, 5.4%), and English bulldogs (n = 11, 4.9%) were the most frequently affected breeds. Overall, 31 diagnoses were reached. The 5 most frequent diagnoses were vertebral malformation (VM; n = 42, 18.8%), spinal arachnoid diverticulum (SAD; n = 28, 12.5%), traumatic fracture of the vertebral column (n = 22, 9.8%), atlantoaxial instability (n = 18, 8.0%), and osseous-associated cervical spondylomyelopathy (n = 17, 7.6%). Intervertebral disc extrusion (IVDE) accounted for 4.5% of cases (n = 10). A final diagnosis of VM was associated with younger, screw-tailed, and pug breeds with chronic signs of T3-L3 myelopathy. SAD was associated with screw-tailed and pug breeds with nonpainful clinical signs. Intervertebral disc extrusion was associated with older, screw-tailed, and pug breeds with shorter duration of clinical signs. CONCLUSIONS AND CLINICAL IMPORTANCE: Prioritization of differential diagnoses for dogs presenting with signs of myelopathy when aged 18 months or less should differ to those for older dogs, with IVDE not the most common cause in the former.

Vertebral and spinal malformations in small brachycephalic dog breeds: Current knowledge and remaining questions.

Small brachycephalic dog breeds, such as the French bulldog, English bulldog and pug have become increasingly popular. These breeds are predisposed to a variety of vertebral and spinal malformations, including hemivertebra, caudal articular process dysplasia, transitional vertebra, cranial thoracic vertebral canal stenosis, spinal arachnoid diverticulum and meningeal fibrosis. Recent studies have provided new insights into the prevalence, anatomical characteristics, pathophysiology and treatment of these conditions. Thoracic hemivertebra, caudal articular process dysplasia, transitional vertebra, and cranial thoracic vertebral canal stenosis occur commonly in neurologically normal dogs. Although the clinical relevance of these vertebral anomalies has therefore been questioned, severe kyphosis and hemivertebra in pugs have been associated with an increased likelihood of neurological signs. Meningeal fibrosis is characterised by the formation of dense intradural fibrotic adhesions, constricting the spinal cord. This condition has been heavily associated with the pug breed. It is in pugs further common to observe multiple concurrent spinal disorder in association with chronic progressive pelvic limb gait abnormalities. This clinical presentation has been referred to as 'pug dog thoracolumbar myelopathy' and potential genetic risk factors have recently been identified. Despite our increased knowledge, many questions remain currently unanswered. This review discusses our current understanding and controversies surrounding vertebral and spinal malformations in small brachycephalic dog breeds.

NDUFS7 variant in dogs with Leigh syndrome and its functional validation in a Drosophila melanogaster model.

Two Jack-Russell Terrier × Chihuahua mixed-breed littermates with Leigh syndrome were investigated. The dogs presented with progressive ataxia, dystonia, and increased lactate levels. Brain MRI showed characteristic bilateral symmetrical T2 hyperintense lesions, histologically representing encephalomalacia. Muscle histopathology revealed accumulation of mitochondria. Whole genome sequencing identified a missense variant in a gene associated with human Leigh syndrome, NDUFS7:c.535G > A or p.(Val179Met). The genotypes at the variant co-segregated with the phenotype in the investigated litter as expected for a monogenic autosomal recessive mode of inheritance. We investigated the functional consequences of the missense variant in a Drosophila melanogaster model by expressing recombinant wildtype or mutant canine NDUFS7 in a ubiquitous knockdown model of the fly ortholog ND-20. Neither of the investigated overexpression lines completely rescued the lethality upon knockdown of the endogenous ND-20. However, a partial rescue was found upon overexpression of wildtype NDUFS7, where pupal lethality was moved to later developmental stages, which was not seen upon canine mutant overexpression, thus providing additional evidence for the pathogenicity of the identified variant. Our results show the potential of the fruit fly as a model for canine disease allele validation and establish NDUFS7:p.(Val179Met) as causative variant for the investigated canine Leigh syndrome.

Idiopathic and structural episodic nonintentional head tremor in dogs: 100 cases (2004-2022).

BACKGROUND: Although idiopathic episodic head tremor (IEHT) in dogs is well-known, little is known about structural brain lesions causing structural episodic head tremor (SEHT). HYPOTHESIS/OBJECTIVES: Describe semiology, magnetic resonance imaging (MRI) findings and outcome of dogs with IEHT or SEHT. We hypothesized that structural lesions affecting the middle cranial fossa or mesencephalic aqueduct could lead to SEHT. ANIMALS: One hundred dogs with IEHT (n = 71) or SEHT (n = 29). METHODS: Retrospective, multicenter, study of dogs with episodic (nonintentional) head tremor and brain MRI between 2004 and 2022. RESULTS: Lesions on MRI in SEHT dogs were localized to the middle cranial fossa (15/29), cerebrocortex (3/29), brainstem (2/29), fourth ventricle (1/29) or multifocal (8/29) with thalamus involvement (6/8). Secondary compression of the mesencephalic aqueduct (19/29), third ventricle or interthalamic adhesion or both (14/29) was common. The most common underlying condition in dogs with SEHT was a pituitary mass. Dogs with SEHT were older, had additional neurological signs and were more likely to be euthanized after diagnosis (P < .001 for all) compared to IEHT dogs. Two SEHT dogs had only tremor. In IEHT dogs, 8/10 owners reported that the tremor decreased or abated over time (range, 106-2315 days) without treatment. Tremor remission occurred in SEHT dogs treated for underlying meningoencephalitis. CONCLUSIONS AND CLINICAL IMPORTANCE: Presence of additional neurological signs and older age may indicate an underlying structural cause for episodic (nonintentional) head tremor involving the mesencephalic aqueduct, third ventricle, interthalamic adhesion or some combination of these. An intracranial structural abnormality cannot be excluded in dogs with normal neurological examination.

Demographics, clinical findings and diagnoses of cranial thoracic myelopathies (T1-T6 vertebrae) in cats.

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.

MRI and clinical findings in 133 dogs with recurrent deficits following intervertebral disc extrusion surgery.

BACKGROUND: Recurrence of neurological signs following surgery for intervertebral disc herniation (IVDH) is reported, yet many cases lack MRI-confirmed diagnosis. This study describes the MRI and clinical findings in dogs presenting with recurrence of neurological signs following surgical treatment of IVDH. METHODS: Medical records of dogs that underwent decompressive surgery for IVDH followed by a subsequent MRI within 12 months were retrospectively reviewed. RESULTS: One hundred and thirty-three dogs were identified, all of which initially presented with intervertebral disc extrusion (IVDE). Of these, 109 (81.9%) had a recurrent IVDE, and 24 (18.1%) had an alternative diagnosis that included haemorrhage (n = 10), infection (n = 4), soft tissue encroachment (n = 3), myelomalacia (n = 3) or other (n = 4). Same-site IVDE recurrence or alternative diagnoses were significantly more likely to present within 10 days postoperatively. Thirty-nine percent of dogs presenting with 'early recurrence' had an alternative diagnosis. Type of surgery, fenestration, neurological grade or IVDE site was not significantly associated with the subsequent MRI diagnosis. LIMITATIONS: Limitations include the retrospective study design, the exclusion of conservatively managed recurrences, the variable length of follow-up and differences in the clinicians' surgical experience. CONCLUSION: The most common cause for the recurrence of neurological signs following decompressive spinal surgery was IVDE. Just over one-third of dogs presenting with early recurrence had an alternative diagnosis.

A TNR Frameshift Variant in Weimaraner Dogs with an Exercise-Induced Paroxysmal Movement Disorder.

BACKGROUND: Some paroxysmal movement disorders remain without an identified genetic cause. OBJECTIVES: The aim was to identify the causal genetic variant for a paroxysmal dystonia-ataxia syndrome in Weimaraner dogs. METHODS: Clinical and diagnostic investigations were performed. Whole genome sequencing of one affected dog was used to identify private homozygous variants against 921 control genomes. RESULTS: Four Weimaraners were presented for episodes of abnormal gait. Results of examinations and diagnostic investigations were unremarkable. Whole genome sequencing revealed a private frameshift variant in the TNR (tenascin-R) gene in an affected dog, XM_038542431.1:c.831dupC, which is predicted to truncate more than 75% of the open read frame. Genotypes in a cohort of 4 affected and 70 unaffected Weimaraners showed perfect association with the disease phenotype. CONCLUSIONS: We report the association of a TNR variant with a paroxysmal dystonia-ataxia syndrome in Weimaraners. It might be relevant to include sequencing of this gene in diagnosing humans with unexplained paroxysmal movement disorders. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Clinical and MRI findings of a suspected cortical malformation presented as a giant cerebral pseudomass in a German Shepherd dog.

A 5-month-old German Shepherd dog was presented with cluster seizures. MR imaging showed a large irregular pseudomass in the central region of the cranial cavity, compatible with a malformation of cortical development. Despite the extensive changes, the patient was neurologically normal interictally 1 year following diagnosis.

Signalment and C-reactive protein values in dogs with immune-mediated polyarthritis and steroid responsive meningitis arteritis.

Introduction: This retrospective multicentric study aims to evaluate the ability of CRP concentration to differentiate between dogs diagnosed with IMPA and SRMA. C-reactive protein (CRP) is a marker of inflammation widely used in two of the most commonly diagnosed immune-mediated diseases in dogs-Immune-mediated polyarthritis (IMPA) and steroid responsive meningitis arteritis (SRMA). Materials and methods: Data collected from medical records of 167 client-owned dogs included age, breed, gender, neuter status, body weight, body temperature, CRP concentration, month and season of diagnosis. CRP was measured quantitatively in 142 dogs (84%) and semi-quantitatively in 27 dogs (16%). Results: SRMA was diagnosed significantly more often in dogs < 12 months old and IMPA in dogs ≥12 months old (P < 0.001). Dogs diagnosed with SRMA had higher CRP concentration than dogs diagnosed with IMPA (P = 0.02). This difference was influenced by the dog's age-when a dog was <12 months old, a higher CRP concentration indicated IMPA (P = 0.02), whereas when a dog was ≥12 months old, a higher CRP concentration indicated SRMA (P = 0.02). Discussion: CRP concentration as a sole diagnostic modality showed only fair discriminatory potential to differentiate between SRMA and IMPA (area under ROC curve close to 0.7). CRP concentration varied depending on patient age and definitive diagnosis. It may play some role in differentiating between SRMA and IMPA but should not be used as the sole diagnostic modality, given it has been demonstrated to only have fair discriminatory potential.

A novel missense variant in the L2HGDH gene in a cat with L-2-hydroxyglutaric aciduria and multicystic cerebral lesions.

CASE DESCRIPTION: A 9-month-old intact male domestic shorthair cat was evaluated for increasing frequency of generalized tonic-clonic seizures. CLINICAL FINDINGS: The cat was reported to have had episodes of circling between the seizures. Upon examination, the cat had bilateral inconsistent menace response but otherwise normal physical and neurological examinations. DIAGNOSTICS: Magnetic resonance imaging (MRI) of the brain identified multifocal, small, rounded intra-axial lesions within the subcortical white matter containing fluid with similar characteristics as cerebrospinal fluid. Evaluation of urine organic acids showed increased excretion of 2-hydroxyglutaric acid. An XM_023255678.2:c.397C>T nonsense variant in the L2HGDH gene encoding L-2-hydroxyglutarate dehydrogenase was identified using whole genome sequencing. TREATMENT AND OUTCOME: Levetiracetam treatment was initiated at 20 mg/kg PO q8h, but the cat died after a seizure 10 days later. CLINICAL RELEVANCE: We report the second pathogenic gene variant in L-2-hydroxyglutaric aciduria in cats and describe for the first time multicystic cerebral lesions on MRI.

SCN9A variant in a family of mixed breed dogs with congenital insensitivity to pain.

BACKGROUND: Congenital insensitivity to pain (CIP) and hereditary sensory and autonomic neuropathies (HSANs) are a rare group of genetic disorders causing inability to feel pain. Three different associated variants have been identified in dogs: 1 in Border Collies, 1 in mixed breed dogs, and 1 in Spaniels and Pointers. OBJECTIVES: To clinically and genetically characterize CIP in a family of mixed breed dogs. ANIMALS: Two mixed breed dogs from the same litter were independently presented: 1 for evaluation of painless fractures, and the other for chronic thermal skin injuries. METHODS: Physical, neurological, and histopathological evaluations were performed. Whole genome sequencing of 1 affected dog was used to identify homozygous protein-changing variants that were not present in 926 control genomes from diverse dog breeds. RESULTS: Physical and neurological examinations showed the absence of superficial and deep pain perception in the entire body. Histopathological evaluations of the brain, spinal cord and sensory ganglia were normal. Whole genome sequencing identified a homozygous missense variant in SCN9A, XM_038584713.1:c.2761C>T or XP_038440641.1:(p.Arg921Cys). Both affected dogs were homozygous for the mutant allele, which was not detected in 926 dogs of different breeds. CONCLUSIONS AND CLINICAL IMPORTANCE: We confirmed the diagnosis of CIP in a family of mixed breed dogs and identified a likely pathogenic variant in the SCN9A gene. The clinical signs observed in these dogs mimic those reported in humans with pathogenic SCN9A variants causing CIP. This report is the first of a spontaneous pathogenic SCN9A variant in domestic animals.

Serum anti-GM2 and anti-GalNAc-GD1a ganglioside IgG antibodies are biomarkers for immune-mediated polyneuropathies in cats.

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-Barré 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.

MRI ischemic and hemorrhagic lesions in arterial and venous territories characterize central nervous system intravascular lymphoma in dogs.

Intravascular lymphoma (IVL) is characterized by the proliferation of large malignant lymphocytes within the lumen of blood vessels. This retrospective, multi-center, case series study aimed to describe the MRI features of confirmed central nervous system IVL in dogs and compare them with histopathological findings. Medical record databases from seven veterinary centers were searched for cases of histologically confirmed IVL. Dogs were included if an MRI was performed. The MRI studies and histopathology samples were reviewed to compare the MRI changes with the histopathological findings. Twelve dogs met the inclusion criteria (12 brains and three spinal cords). Imaging of the brains revealed multifocal T2-weighted/FLAIR hyperintense and T1-weighted iso-hypointense lesions, with variable contrast enhancement; areas of abnormal diffusion both in arterial and venous territories in diffusion-weighted imaging; and meningeal enhancement. On gradient echo images (GRE), the changes comprised tubular susceptibility artifacts, consistent with the "susceptibility vessel sign", and additional variably sized/shaped intraparenchymal susceptibility artifacts. Spinal cord lesions presented as fusiform T2-weighted hyperintensities with scattered susceptibility artifacts on GRE and variable parenchymal and meningeal contrast enhancement. On histopathology, subarachnoid hemorrhages and neuroparenchymal areas of edema and necrosis, with or without hemorrhage, indicating ischemic and hemorrhagic infarctions, were found. These lesions were concurrent with severely dilated meningeal and parenchymal arteries and veins plugged by neoplastic lymphocytes and fibrin. Due to the unique angiocentric distribution of IVL, ischemic and hemorrhagic infarcts of variable chronicity affecting both the arterial and venous territories associated with thrombi formation can be detected on MRI.

Otitis media and interna with or without polyps in cats: association between meningeal enhancement on postcontrast MRI, cerebrospinal fluid abnormalities, and clinician treatment choice and outcome.

OBJECTIVES: The aim of this study was to evaluate the association between meningeal enhancement (MgE) and cerebrospinal fluid (CSF) analysis results, their individual association with bacteriology results from affected ear samples and whether these test results influenced clinicians' therapeutic choice in cats with otitis media and interna (OMI). METHODS: This was a multicentre retrospective study carried out over an 8-year period. Cats diagnosed with OMI, with or without a nasopharyngeal polyp, leading to peripheral vestibular signs were included. Only cats for which MRI with postcontrast T1-weighted sequences and CSF analyses available were included. Cats with intra-axial MRI lesions or empyema were excluded. RESULTS: Fifty-eight cats met the inclusion criteria. MgE was reported in 26/58 cases, of which nine had an abnormal CSF result (increased total nucleated cell count [TNCC] or total protein); 32/58 cases had no MgE, of which 10 showed abnormal CSF results. There was no association between bacteriology results (external ear canal or bulla) and MgE or abnormal CSF results. CSF abnormalities were statistically significantly more common in acute cases (n = 16/37) than in chronic cases (n = 3/21; Fischer's test P = 0.04). Prednisolone was prescribed in 10/16 cases with increased TNCC. Among the 42 cases with normal TNCC, 15 received prednisolone and 13 received non-steroidal anti-inflammatory drugs. Various antimicrobial drugs were prescribed in 53/58 cats. Duration of antimicrobial treatment was similar, regardless of positive bacterial culture (5.58 vs 4.22 weeks), abnormal CSF (5.83 vs 4.76 weeks) or MgE (5.33 vs 4.90 weeks). CONCLUSIONS AND RELEVANCE: No association was found between the CSF and MgE results. Furthermore, no association was found between MgE, CSF or bacteriology findings. In addition, abnormal CSF results might lead the clinician to treat with corticosteroids, but they did not have any impact on duration of antimicrobial treatment. CSF abnormalities were seen significantly less frequently in chronic cases. The outcome tended to be poorer when MgE was detected on MRI.

Cranial thoracic myelopathies (T1-T6 vertebrae): Retrospective evaluation of the signalment, clinical presentation, and, presumptive or final diagnoses in 84 dogs.

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.

Mitochondrial fission factor (MFF) frameshift variant in Bullmastiffs with mitochondrial fission encephalopathy.

Familial cerebellar ataxia with hydrocephalus in Bullmastiffs was described almost 40 years ago as a monogenic autosomal recessive trait. We investigated two young Bullmastiffs showing similar clinical signs. They developed progressive gait and behavioural abnormalities with an onset at around 6 months of age. Neurological assessment was consistent with a multifocal brain disease. Magnetic resonance imaging of the brain showed intra-axial bilateral symmetrical focal lesions localised to the cerebellar nuclei. Based on the juvenile age, nature of neurological deficits and imaging findings, an inherited disorder of the brain was suspected. We sequenced the genome of one affected Bullmastiff. The data were compared with 782 control genomes of dogs from diverse breeds. This search revealed a private homozygous frameshift variant in the MFF gene in the affected dog, XM_038574000.1:c.471_475delinsCGCTCT, that is predicted to truncate 55% of the wild type MFF open reading frame, XP_038429928.1: p.(Glu158Alafs*14). Human patients with pathogenic MFF variants suffer from 'encephalopathy due to defective mitochondrial and peroxisomal fission 2'. Archived samples from two additional affected Bullmastiffs related to the originally described cases were obtained. Genotypes in a cohort of four affected and 70 unaffected Bullmastiffs showed perfect segregation with the disease phenotype. The available data together with information from previous disease reports allow classification of the investigated MFF frameshift variant as pathogenic and probably causative defect of the observed neurological phenotype. In analogy to the human phenotype, we propose to rename this disease 'mitochondrial fission encephalopathy (MFE)'.

Idiopathic generalised tremor syndrome in dogs.

BACKGROUND: Idiopathic generalised tremor syndrome (IGTS) causes tremor and often vestibulocerebellar signs. Previous publications on IGTS in dogs are restricted to case reports or lack exclusion of structural causes. METHODS: Medical records of 75 dogs diagnosed with IGTS that had undergone magnetic resonance imaging (MRI) of the brain were collected retrospectively. RESULTS: Crossbreeds were affected most commonly (41.3%), followed by West Highland white terriers (14.7%) and cocker spaniels (10.7%). A higher proportion of females were affected than males (68.0%). Median age of the affected dogs was 17 months (range 6-121 months), and median bodyweight was 9.15 kg (range 2.9-26 kg). All dogs presented with tremors and most experienced concomitant neurological signs (93.3%). Seventeen (22.7%) were hyperthermic and 31 (41.3%) had gastrointestinal signs. MRI of the brain was normal in most of the cases, and cerebrospinal fluid analysis frequently revealed mild pleocytosis. All animals were treated with prednisolone, and 39 (51.3%) also received diazepam. Median follow-up time was 13 months (range 0-134 months). The overall outcome was good, although 16 (21.3%) patients were reported to have relapsing clinical signs and 10 (13.2%) patients experienced persistent mild clinical signs. CONCLUSIONS: IGTS should be suspected in any dog with generalised tremor and vestibulocerebellar signs with younger and smaller dogs more commonly affected.