Imaging features of discospondylitis in cats

ObjectivesThis study describes the imaging features of feline discospondylitis on MRI, comparing them to CT and radiographic findings where available.MethodsThe medical records of cats diagnosed with discospondylitis, presented to three referring institutions, were reviewed. MRI, CT and radiographic features were assessed by two of the authors independently.ResultsFourteen sites of discospondylitis were retrospectively identified in 13 cats. The L7–S1 intervertebral disc space (IVDS) was affected in 7/14 (50%) cases. Characteristic MRI features included a hyperintense nucleus pulposus signal on T2-weighted (T2W) imaging (n = 10/14 [71%]) and short tau inversion recovery (STIR) imaging (n = 11/13 [85%]), with contrast enhancement in all (n = 11/11); involvement of adjacent vertebral endplates (n = 11/14 [79%]) and hyperintense neighbouring soft tissue on T2W (n = 11/14 [79%]) and STIR (n = 10/13 [77%]), with contrast enhancement in all (n = 11/11); and the presence of spondylosis deformans (n = 10/14 [71%]). Other features included narrowed or collapsed IVDS (n = 8/14 [57%]), contrast enhancement of vertebral bodies (n = 5/11 [46%]), epidural space involvement (n = 5/14 [36%]), compression of the spinal cord or nerve roots (n = 5/14 [36%]), paraspinal abscessation (n = 3/14 [21%]) and meningeal signal intensity abnormalities with contrast enhancement (n = 5/6 [83%]). These latter findings may indicate secondary focal meningitis. Radiographs were available covering five sites (in four cats) and CT covering three sites (in two cats). The most common radiological features were collapse or narrowing of the affected IVDS (80%) and endplate erosion (60%). No changes suggestive of discospondylitis were identifiable on radiography or CT in two sites (one cat), despite being identifiable on MRI. Repeated radiography in one case did not reveal complete radiological resolution following 9 months of treatment.Conclusions and relevanceThe results of this study indicate consistent MRI features of feline discospondylitis that should be considered in the diagnosis of this condition

Case report: Necrotizing leukomyelitis and meningitis in a Pomeranian

A 2.5-year-old female entire Pomeranian dog was presented for acute paraparesis progressing within 2 days to paraplegia. General physical examination was unremarkable. Neurological examination showed paraplegia without nociception, a mass reflex upon testing perineal reflexes and withdrawal reflexes in the pelvic limbs and patellar hyperreflexia. Cutaneous trunci reflexes were absent caudal to the level of the 6th thoracic vertebra. Spinal hyperesthesia was present. Neuroanatomical localization was consistent with a T3-L3 myelopathy. Hematological and biochemical blood tests [including C-reactive protein (CRP)] were within reference ranges. MRI of the spinal cord from the level of the 1st thoracic vertebra to the sacrum revealed a patchy, ill-defined, moderate to marked T2W hyperintense, contrast enhancing intramedullary lesion extending from T1 to L4. Medical treatment based on a working diagnosis of meningomyelitis of unknown cause was initiated with corticosteroids and methadone based on pain scores. Prognosis was grave and after 3 days without return of nociception, the dog was euthanized according to the owners’ wishes. Post-mortem histopathological examination of the brain and spinal cord yielded a morphological diagnosis of severe, segmental, bilateral and fairly symmetrical, necrotizing lymphohistiocytic leukomyelitis, with a non-suppurative angiocentric leptomeningitis. Some minor, focal, lymphocytic perivascular cuffing was found in the medulla oblongata as well, but otherwise there were no signs of brain involvement. No infectious causes were identified with ancillary tests. This case report underlines the importance of including meningomyelitis in the differential diagnosis list of dogs presented for acute progressive neurological signs referable to a myelopathy

Neurological signs in 23 dogs with suspected rostral cerebellar ischaemic stroke

Background: In dogs with ischaemic stroke, a very common site of infarction is the cerebellum. The aim of this study was to characterise neurological signs in relation to infarct topography in dogs with suspected cerebellar ischaemic stroke and to report short-term outcome confined to the hospitalisation period. A retrospective multicentre study of dogs with suspected cerebellar ischaemic stroke examined from 2010–2015 at five veterinary referral hospitals was performed. Findings from clinical, neurological, and paraclinical investigations including magnetic resonance imaging were assessed. Results: Twenty-three dogs, 13 females and 10 males with a median age of 8 years and 8 months, were included in the study. The Cavalier King Charles Spaniel (n = 9) was a commonly represented breed. All ischaemic strokes were located to the vascular territory of the rostral cerebellar artery including four extensive and 19 limited occlusions. The most prominent neurological deficits were gait abnormalities (ataxia with hypermetria n = 11, ataxia without hypermetria n = 4, non-ambulatory n = 6), head tilt (n = 13), nystagmus (n = 8), decreased menace response (n = 7), postural reaction deficits (n = 7), and proprioceptive deficits (n = 5). Neurological signs appeared irrespective of the infarct being classified as extensive or limited. All dogs survived and were discharged within 1–10 days of hospitalisation. Conclusions: Dogs affected by rostral cerebellar ischaemic stroke typically present with a collection of neurological deficits characterised by ataxia, head tilt, and nystagmus irrespective of the specific cerebellar infarct topography. In dogs with peracute to acute onset of these neurological deficits, cerebellar ischaemic stroke should be considered an important differential diagnosis, and neuroimaging investigations are indicated. Although dogs are often severely compromised at presentation, short-term prognosis is excellent and rapid clinical improvement may be observed within the first week following the ischaemic stroke

Canine paroxysmal dyskinesia—a review

Paroxysmal dyskinesias (PDs) are a group of involuntary, hyperkinetic movement disorders that recur episodically and may last seconds to hours. An important feature of PD is that there is no loss of consciousness during the episode. Using a clinical classification, three main types of PDs have been distinguished in canine PD: (1) paroxysmal kinesigenic dyskinesia (PKD) that commences after (sudden) movements, (2) paroxysmal non-kinesigenic dyskinesia (PNKD) not associated with exercise and can occur at rest, and (3) paroxysmal exertion-induced dyskinesia (PED) associated with fatigue. Canine PDs are diagnosed based on the clinical presentation, history, and phenomenology. For the latter, a video recording of the paroxysmal event is extremely useful. An etiological classification of canine PDs includes genetic (proven and suspected), reactive (drug-induced, toxic, metabolic, and dietary), structural (neoplasia, inflammatory, and other structural causes), and unknown causes. In this review, an overview of all reported canine PDs is provided with emphasis on phenotype, genotype, and, where possible, pathophysiology and treatment for each reported canine PD

Ischemic stroke can have a T1w hyperintense appearance in absence of intralesional hemorrhage

Magnetic resonance imaging (MRI) signal changes associated with ischemic stroke are typically described as T2w and FLAIR hyperintense, and T1w isointense lesions. Intralesional T1w hyperintensity is generally attributed to either a hemorrhagic stroke, or an ischemic stroke with hemorrhagic transition, and has an associated signal void on gradient echo (GE) sequences. Cases of ischemic stroke with T1w hyperintense signal in absence of associated signal void on GE sequences have been sporadically demonstrated in human stroke patients, as well as in dogs with experimentally induced ischemia of the middle cerebral artery. This multicenter retrospective descriptive study investigates the presence of T1w hyperintensity in canine stroke without associated signal void on GE sequences. High field (1.5 Tesla) MRI studies of 12 dogs with clinical presentation, MRI features, and cerebrospinal fluid results suggestive of non-hemorrhagic stroke were assessed. The time between the observed onset of clinical signs and MRI assessment was recorded. All 12 patients had an intralesional T1w hyperintense signal compared to gray and white matter, and absence of signal void on T2*w GE or SWI sequences. Intralesional T1w hyperintensities were either homogenously distributed throughout the entire lesion (6/12) or had a rim-like peripheral distribution (6/12). The mean time between the recorded onset of clinical signs and MRI assessment was 3 days; however, the age range of lesions with T1w hyperintense signal observed was 1-21days, suggesting that such signal intensities can be observed in acute, subacute, or chronic stages of ischemic stroke. Follow-up was recorded for 7/12 cases, all of which showed evidence of neurological improvement while in hospital, and survived to discharge. Correlation of the age and MRI appearance of lesions in this study with similar lesions observed in human and experimental studies suggests that these T1w hyperintensities are likely caused by partial tissue infarction or selective neuronal necrosis, providing an alternative differential for these T1w hyperintensities observed

Case report: Necrotizing leukomyelitis and meningitis in a Pomeranian

A 2.5-year-old female entire Pomeranian dog was presented for acute paraparesis progressing within 2 days to paraplegia. General physical examination was unremarkable. Neurological examination showed paraplegia without nociception, a mass reflex upon testing perineal reflexes and withdrawal reflexes in the pelvic limbs and patellar hyperreflexia. Cutaneous trunci reflexes were absent caudal to the level of the 6th thoracic vertebra. Spinal hyperesthesia was present. Neuroanatomical localization was consistent with a T3-L3 myelopathy. Hematological and biochemical blood tests [including C-reactive protein (CRP)] were within reference ranges. MRI of the spinal cord from the level of the 1st thoracic vertebra to the sacrum revealed a patchy, ill-defined, moderate to marked T2W hyperintense, contrast enhancing intramedullary lesion extending from T1 to L4. Medical treatment based on a working diagnosis of meningomyelitis of unknown cause was initiated with corticosteroids and methadone based on pain scores. Prognosis was grave and after 3 days without return of nociception, the dog was euthanized according to the owners’ wishes. Post-mortem histopathological examination of the brain and spinal cord yielded a morphological diagnosis of severe, segmental, bilateral and fairly symmetrical, necrotizing lymphohistiocytic leukomyelitis, with a non-suppurative angiocentric leptomeningitis. Some minor, focal, lymphocytic perivascular cuffing was found in the medulla oblongata as well, but otherwise there were no signs of brain involvement. No infectious causes were identified with ancillary tests. This case report underlines the importance of including meningomyelitis in the differential diagnosis list of dogs presented for acute progressive neurological signs referable to a myelopathy

Acetazolamide-responsive paroxysmal dyskinesia in a 12-week-old female golden retriever dog

No abstract available