Proprioceptive Ataxia Research Articles

Clinical presentation, diagnostic findings and short-term outcome in French bulldogs with presumptive spinal only meningoencephalomyelitis of unknown origin: 15 cases (2016-2023).

To describe clinical presentation, diagnostic findings and outcome of presumptive spinal only meningoencephalomyelitis of unknown origin in French bulldogs, and to compare clinical presentation between intervertebral disc herniation and spinal only meningoencephalomyelitis of unknown origin in this breed. Medical records of French bulldogs diagnosed with presumptive spinal only meningoencephalomyelitis of unknown origin in seven referral centres were reviewed. Clinical presentation was compared to a group of French bulldogs with intervertebral disc herniation. Fifteen French bulldogs were included. Median age at presentation was 31 months. Most dogs were presented with a chronic onset (54%), and the median duration of clinical signs before diagnosis was 21 days. The most common presentation was ambulatory paresis and proprioceptive ataxia (80%). Spinal pain was uncommon (20%). There was no preferential location between the cervical and thoracolumbar segments. In all but one case, magnetic resonance imaging revealed broad focal or multifocal, poorly defined, intramedullary lesions that typically appeared hyperintense on T2W images and isointense on T1W images with parenchymal and/or meningeal contrast enhancement in 12 dogs (80%). Median total nucleated cell count in cerebrospinal fluid was 15 cells/mm3 with predominance of mononuclear cells in all cases. Follow-up (available for 12 dogs, ranging from 1 month to 1 year) indicated initial positive response to various immunosuppressive treatments in all but one case, with subsequent suspected relapse in three cases. Dogs with spinal only meningoencephalomyelitis of unknown origin had longer clinical sign duration compared to intervertebral disc herniation cases (60 dogs) (21 days compared to 3 days, respectively) and less frequent spinal pain during examination (20% compared to 75%, respectively). Spinal only meningoencephalomyelitis of unknown origin is an uncommon cause of myelopathy in French bulldogs that should be particularly considered in young adults with non-acute and non-painful presentation.

A utilização da ozonioterapia no tratamento de hérnia de disco em cão

Herniated disc is an affection of the intervertebral disc that often affects dogs of all breeds, ages and sex, and may have higher incidence in the breeds Dachshund, Pug, Cocker Spaniel and Pekinese. There are predisposing causes for the development of these discopathies, such as obesity, anatomical peculiarities of the spine of some breeds, falls, or trauma. The affected patients usually present pain, resistance to locomotion, proprioceptive ataxia, urinary and fecal incontinence or urinary retention, loss of sensation in the extremities, and may evolve to paresis or paralysis. The diagnosis is made by imaging exams, most commonly magnetic resonance and/or tomography, which indicate disc protrusions and extrusions causing spinal cord compression and dehydration/degeneration of the intervertebral disc. The treatment acquired depends on the clinical condition that the animal is in, and may be drug treatment, integrative medicine such as ozone therapy, physiotherapy, acupuncture, or in more severe cases such as disc extrusion, the treatment may be surgical. In this report the case of a 07-year-old pug dog that underwent ozone therapy sessions as a treatment for disc herniation will be discussed. The animal presented a great recovery after 10 sessions of ozone therapy through paravertebral, trigger point and rectal insufflation techniques. Because it is a very common diagnosis in the clinical routine, it is of utmost importance the investigation of the clinical signs and complementary exams to reach the correct diagnosis, and to have anatomical knowledge and the ozone therapy techniques to obtain success in the integrative treatment.

Uniparental IsoDisomy: a case study on a new mechanism of Friedreich ataxia.

Friedreich's Ataxia (FRDA) is the most common hereditary ataxia and is mainly caused by biallelic GAA repeat expansion in the FXN gene. Rare patients carrying FXN point mutations or intragenic deletions are reported. We describe the first FRDA patient with a chromosome 9 segmental Uniparental isoDisomy (UPiD) unmasking a homozygous FXN expansion initially undetected by TP-PCR. The child presented with a progressive proprioceptive ataxia associated with peripheral sensory neuronopathy and severe scoliosis. Whole genome sequencing (WGS) identified a maternal segmental Uniparental Isodisomy (UPiD) encompassing FXN. Short tandem repeats analysis on WGS showed a biallelic FXN expansion. The identification of a deletion in the primer-annealing region of the TP-PCR explained the initial TP-PCR failure. This is the first documented case of FRDA caused by segmental UPiD. This case highlights the complexity of the molecular diagnosis of FRDA, and emphasises the importance of integrating results from various technical diagnostic approaches.

Desmoid fibromatosis following surgery of an intradural spinal lipoma in a young cat

BackgroundIntradural lipomas have been previously reported in individuals with spinal dysraphism; however, they have not been reported in cats with an intact spinal canal. Desmoid tumors are a rare finding in veterinary medicine, and there is no prior description of these tumors invading the spinal cord. Furthermore, the etiopathogenesis remains debated, with trauma, such as surgical intervention of an intradural structure, potentially contributing to its development.Case descriptionA 10-month-old domestic shorthair cat was presented initially with progressive proprioceptive ataxia. The MRI identified an intradural compressive lesion at the cranio-cervical junction, confirmed as a lipoma by histopathology. Despite surgical removal, postoperative complications led to the cat's euthanasia. Postmortem examination revealed invasion of a desmoid tumor at the surgical site.ConclusionsThis case highlights the rarity of intradural lipomas in this location and the unusual complication of desmoid tumor invasion. It underscores the need for further research into the underlying mechanisms and potential diagnostic and therapeutic strategies for similar cases and suggests that these findings may be added to the list of potential post-surgical complications.

Effects on Gait and Balance of VIM Gamma Knife Radiosurgery in Essential Tremor

Introduction: Essential tremor (ET) is the most common movement disorder, characterized by an action tremor in the upper limbs. Neurosurgical techniques targeting the thalamic ventrointermediate nucleus (VIM) including thermocoagulation demonstrated a potential risk for gait and posture worsening. This study evaluates the potential effect of VIM Gamma Knife radiosurgery (GKR) in ET on gait and posture performances. Methods: We conducted a prospective study to quantitatively assess gait and balance in severe ET patients before and 1 year after unilateral GKR. Seventy-three patients were included in this series. Results: First, we confirmed the unilateral GKR efficacy in severe ET patients: global tremor score and impairments in activities of daily living improved, respectively, by 67% and 71.7%. The global gait and posture analysis found no significant differences before and 1 year after GKR. Three patients (4.1%) developed mild to moderate gait and posture impairment with proprioceptive ataxia. All of these AEs were induced by a hyper-response to radiosurgery. Conclusions: Gait and posture performances were not statistically significant at the population. Nevertheless, gait and posture worsened in 4% of patients after GKR, all in the setting of hyper-response. This study shows that GKR may be a safe neurosurgical alternative to improve ADL in a population of patients with TE.

Primary phenotypic features associated with caudal neck pathology in warmblood horses.

Detailed descriptions of clinical signs associated with radiological findings of the caudal cervical vertebral column are not available. Describe the clinical features associated with neck pain or stiffness, neck-related thoracic limb lameness, proprioceptive ataxia consistent with a cervicothoracic spinal cord or nerve lesion, and their frequency of occurrence compared with control horses. A total of 223 Warmblood horses. Case-control study. Controls and cases were recruited prospectively. All horses underwent predetermined lameness and neurologic examinations. The frequency of occurrence of each clinical feature was compared between cases and controls and relative risk (RR) were calculated. Ninety-six cases and 127 controls were included. Forty-seven (49%) of the cases were classified as neurologic, 31 (32.3%) had thoracic limb lameness, and 18 (18.7%) had neck stiffness or pain or both. Focal caudal cervical muscle atrophy (46, 47.9%), hypoesthesia (38, 39.6%), patchy sweating (16, 16.7%), hyperesthesia (11, 11.5%), and pain upon firm pressure applied over the caudal cervical articular process joints and transverse processes (58, 60.4%) were only observed in cases (P < .001). Sideways flexion of the neck was restricted in a higher proportion of cases (47/96, 49%) compared with controls (40/127, 31.8%; P = .009, RR 1.5). Hopping-type thoracic limb lameness was only observed in cases, (30, 31.6%). Deterioration in lameness after diagnostic anesthesia occurred in 13/31 (41.9%) cases. Systematic clinical evaluation using the methods described should enable clinical differentiation between horses with caudal cervical lesions and horses with other causes of gait abnormalities.

Perioperative epidural catheter analgesia as a component of a multimodal analgesic approach in a dog with thoracic hemivertebrae and kyphosis undergoing thoracic vertebral stabilisation

AbstractA 4‐year‐old, male, neutered French bulldog weighing 13.5 kg presented with urinary and faecal incontinence, progressive, non‐painful paraparesis and pelvic limb proprioceptive ataxia. Magnetic resonance imaging revealed a T12 constrictive myelopathy in association with multiple thoracic vertebral malformations, and mildly impinging thoracic intervertebral disc protrusions. Additionally, there was a sacral axial defect and degenerative lumbosacral stenosis. Surgical treatment comprised bilateral dorsal vertebral stabilisation of T9–T13. This case report summarises the peri‐anaesthetic management, which included an ‘in‐plane’ ultrasound‐guided placement of an epidural catheter at the level of L3–L4 and advancement cranially to T12 as a component of a multimodal analgesic regimen. Following the cessation of postoperative epidural bupivacaine administration, the patient remained comfortable without requiring rescue analgesia, and was discharged within 24 hours of surgery. At the latest recheck 5 months after surgery, the dog's neurological status remained static. This technique and application remain unexplored in existing veterinary literature.

Surgical Outcomes of Laminectomy, Durotomy and a Non-Synthetic Dura Substitute Application in Ten Dogs with a Spinal Subarachnoid Diverticulum.

This retrospective study aimed to report the surgical treatment and outcomes of laminectomies followed by durotomy and the application of a non-synthetic collagen matrix dura substitute (DurepairTM) in ten dogs with a spinal subarachnoid diverticulum (SAD). The medical records of these ten client-owned dogs with SAD diagnosed by magnetic resonance imaging (MRI) were reviewed. All patients had chronic and progressive deficits. At presentation, common neurological signs were proprioceptive ataxia, ambulatory spastic paraparesis or tetraparesis, and faecal incontinence. Dorsal thoracolumbar laminectomy was performed in eight dogs; one dog underwent cervical dorsolateral laminectomy, and one patient had thoracic hemilaminectomy. Laminectomies were followed by durotomy, allowing the dissection of the pia-arachnoid adhesions. A rectangular patch of a non-synthetic dura substitute was applied as an onlay graft over the durotomy site before routine closure. Proprioceptive ataxia, paraparesis, and tetraparesis improved in all patients. Faecal incontinence in one patient resolved postoperatively. Laminectomy, durotomy, and the application of a non-synthetic dura substitute was a safe procedure facilitating postoperative improvement over a long-term follow-up period (from 9 to 40 months).

Vitamin deficiencies in children: Lessons from clinical and neuroimaging findings

Background and aimsWater-soluble vitamins play an essential coenzyme role in the nervous system. Acquired vitamin deficiencies are easily treatable, however, without treatment, they can lead to irreversible complications. This study aimed to provide clinical, laboratory parameters and neuroimaging data on vitamin deficiencies in an attempt to facilitate early diagnosis and prompt supplementation. MethodsFrom July 1998 to July 2023, patients at Necker-Enfants-Malades Hospital presenting with acute neurological symptoms attributed to acquired vitamin deficiency were included. Clinical data were extracted from Dr Warehouse database. Neuroimaging, biochemical and electrophysiological data were reviewed. ResultsPatients with vitamin B1 deficiency exhibited abnormal eye movements (n = 4/4), fluctuations in consciousness (n = 3/4), and ataxia (n = 3/4). Brain MRI showed alterations of fourth ventricle region (n = 4/4), periaqueductal region (n = 4/4), tectum (n = 3/4), and median thalami (n = 3/4). Patients with vitamin B2 deficiency presented with early onset hypotonia (n = 3/4), hyperlactatemia (n = 4/4), and hyperammonemia (n = 4/4). Plasma acylcarnitines revealed a multiple acyl-coA dehydrogenase deficiency-like profile (n = 4/4). In vitamin B12 deficiency, young children presented with developmental delay (n = 7/7) and older children with proprioceptive ataxia (n = 3/3). Brain MRI revealed atrophy (n = 7/7) and spinal MRI hyperintensity in posterior cervical columns (n = 3/3). Metabolic findings showed elevated methylmalonic acid (n = 6/7) and hyperhomocysteinemia (n = 6/7). Patients with vitamin C deficiency exhibited gait disturbances and muscle weakness (n = 2/2). ConclusionsAcquired vitamin deficiencies may display reversible clinical symptoms mimicking inherited metabolic disorders. Some situations raise suspicion for diagnosis: concordant clinical presentation, suggestive neuroimaging findings, and/or biochemical evidence. Any acute neurological condition should be treated without waiting for definitive biochemical confirmation.

Homozygous CNP Mutation and Neurodegeneration in Weimaraners: Myelin Abnormalities and Accumulation of Lipofuscin-like Inclusions.

A progressive neurological disorder was observed in a male neutered Weimaraner. Clinical signs included fecal incontinence, lethargy, moderate paraparesis, proprioceptive pelvic limb ataxia, falling, cognitive decline, incoordination, decreased interest in food, changes in posture, and episodes of trance-like behavior. Neurologic signs were first observed at approximately 4 years, 10 months of age and progressed slowly. Magnetic resonance imaging showed generalized brain atrophy with areas of white matter pathology. Humane euthanasia was elected at 6 years, 7 months of age due to increasing severity of the neurological signs. Autofluorescent intracellular granules were observed in the cerebral and cerebellar cortexes, optic nerve, and cardiac muscle of the affected dog. These abnormal inclusions in the cerebral cortex and cardiac muscle immunolabeled with antibodies to mitochondrial ATP synthase subunit c protein, like that observed in the neuronal ceroid lipofuscinosis group of lysosomal storage diseases. Immunolabeling also demonstrated pronounced neuroinflammation in brain tissues. The ultrastructural appearances of the disease-related inclusion bodies in the brain and optic nerve were quite variable. The ultrastructure and locations of many of the inclusions in the nervous tissues suggested that they were derived, at least in part, from the myelin surrounding axons. The storage bodies in the cardiac muscle were located in mitochondria-rich regions and consisted of parallel arrays of membrane-like components interspersed with electron-dense flocculent material. The disease was characterized by pronounced abnormalities in the myelin of the brain and optic nerve consisting of distinctive areas of ballooning between the layers of myelin. The whole genome sequence generated from the affected dog contained a homozygous G-to-A missense mutation in CNP, which encodes proteins with CNPase enzyme activity and a structural role in myelin. The mutation predicts a Thr42Met amino acid sequence substitution. Genotyping of archived Weimaraner DNA samples identified an additional G > A variant homozygote with a clinical history and brain lesions similar to those of the proband. Of 304 Weimaraners and over 4000 other dogs of various breeds, the proband and the other Weimaraner that exhibited similar signs were the only two that were homozygous for the CNP missense variant. CNPase immunolabeling was widespread in brain tissues from normal dogs but was undetectable in the same tissues from the proband. Based on the clinical history, fluorescence and electron-microscopy, immunohistochemistry, and molecular genetic findings, the late-onset Weimaraner disorder likely results from the missense mutation that results in CNPase deficiency, leading to myelin abnormalities, accumulation of lysosomal storage bodies, and brain atrophy. Similar disorders have been associated with different CNP variants in Dalmatians and in human subjects.

Measurement of 8-hydroxy-2'-deoxyguanosine in serum and cerebrospinal fluid of horses with neuroaxonal degeneration and other causes of proprioceptive ataxia.

Eight-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of oxidative damage evaluated in human neurodegenerative disease, has potential to correlate with postmortem diagnosis of neuroaxonal dystrophy/degenerative myeloencephalopathy (NAD/DM) in horses. We hypothesized that 8-OHdG will be higher in CSF and serum from NAD/DM horses compared with horses with other neurologic diseases (CVSM, EPM) and a control group of neurologically normal horses. We also hypothesized that 8-OHdG will be higher in CSF compared with serum from NAD/DM horses. Fifty client-owned horses with postmortem diagnoses: 20 NAD/DM, 10 CVSM, 10 EPM, and 10 control horses. Serum and CSF samples were obtained between November 2010 and March 2022. Case-control study using biobanked samples was performed and commercial competitive ELISA kit (Highly Sensitive 8-OHdG Check ELISA) utilized. Concentration of 8-OHdG was quantitated in both CSF and serum and compared between groups. No correlation was established between the measures of 8-OHdG in serum and CSF and group. CSF median [8-OHdG] for NAD/DM was 169.9 pg/mL (IQR25-75 : 67.18-210.6), CVSM 157.1 pg/mL (IQR25-75 : 132.1-229.1), EPM 131.4 pg/mL (IQR25-75 : 102.1-193.2), and control 149.8 pg/mL (IQR25-75 : 113.3-196.4). Serum median [8-OHdG] for NAD/DM was 130 pg/mL (IQR25-75 : 51.73-157.2), CVSM 125.8 pg/mL (IQR25-75 : 62.8-170.8), EPM 120.6 pg/mL (IQR25-75 : 87.23-229.7), and control 157.6 pg/mL (IQR25-75 : 97.15-245.6). Poisson regression analysis showed no difference established once confounding variables were considered. Eight-OHdG did not aid in antemortem diagnosis of NAD/DM in this cohort of horses. At the time of diagnosis horses with NAD/DM do not have ongoing oxidative stress.

Atypical magnetic resonance imaging findings of a vertebral melanotic melanoma in a dog

AbstractAn 8‐year‐8‐month‐old whippet was investigated by magnetic resonance imaging for acute thoracolumbar discomfort and pelvic limb stiffness, which had progressed to severe ambulatory paraparesis and proprioceptive ataxia of the pelvic limbs in the 24 hours before presentation. An aggressive, extradural T10 vertebral mass‐like lesion was identified, with resultant marked compression of the spinal cord. The lesion was heterogeneously T2‐weighted hyperintense and moderately T1‐weighted hyperintense relative to the adjacent vertebrae and paravertebral musculature. Cytological analysis of the lesion was consistent with a melanotic melanoma, which was confirmed by histopathological analysis and immunohistochemistry. The vertebral column is an uncommon location for either primary or metastatic melanomas in both humans and veterinary species. This lesion was particularly unusual in that its imaging characteristics were not typical for melanotic melanoma. This case report illustrates the unusual anatomical and imaging features of this tumour and outlines the diagnostic considerations pertinent to this case.

Transcriptome analysis in a humanized mouse model of familial dysautonomia reveals tissue-specific gene expression disruption in the peripheral nervous system

Familial dysautonomia (FD) is a rare recessive neurodevelopmental disease caused by a splice mutation in the Elongator acetyltransferase complex subunit 1 (ELP1) gene. This mutation results in a tissue-specific reduction of ELP1 protein, with the lowest levels in the central and peripheral nervous systems (CNS and PNS, respectively). FD patients exhibit complex neurological phenotypes due to the loss of sensory and autonomic neurons. Disease symptoms include decreased pain and temperature perception, impaired or absent myotatic reflexes, proprioceptive ataxia, and progressive retinal degeneration. While the involvement of the PNS in FD pathogenesis has been clearly recognized, the underlying mechanisms responsible for the preferential neuronal loss remain unknown. In this study, we aimed to elucidate the molecular mechanisms underlying FD by conducting a comprehensive transcriptome analysis of neuronal tissues from the phenotypic mouse model TgFD9; Elp1Δ20/flox. This mouse recapitulates the same tissue-specific ELP1 mis-splicing observed in patients while modeling many of the disease manifestations. Comparison of FD and control transcriptomes from dorsal root ganglion (DRG), trigeminal ganglion (TG), medulla (MED), cortex, and spinal cord (SC) showed significantly more differentially expressed genes (DEGs) in the PNS than the CNS. We then identified genes that were tightly co-expressed and functionally dependent on the level of full-length ELP1 transcript. These genes, defined as ELP1 dose-responsive genes, were combined with the DEGs to generate tissue-specific dysregulated FD signature genes and networks. Within the PNS networks, we observed direct connections between Elp1 and genes involved in tRNA synthesis and genes related to amine metabolism and synaptic signaling. Importantly, transcriptomic dysregulation in PNS tissues exhibited enrichment for neuronal subtype markers associated with peptidergic nociceptors and myelinated sensory neurons, which are known to be affected in FD. In summary, this study has identified critical tissue-specific gene networks underlying the etiology of FD and provides new insights into the molecular basis of the disease.

Clinical and histopathological features in horses with neuroaxonal degeneration: 100 cases (2017-2021).

Adult horses with proprioceptive ataxia and behavior changes that have histologic lesions consistent with neurodegenerative disease have been increasingly recognized. Describe the history, clinical findings and histopathologic features of horses presented to a referral institution with neuroaxonal degeneration. One hundred horses with a necropsy diagnosis of neuroaxonal degeneration compatible with neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM). Retrospective study of horses presented to the University of Pennsylvania, New Bolton Center, between 2017 and 2021 with a necropsy diagnosis of eNAD/EDM. Affected horses had a median age of 8 years (range, 1-22), and the majority were Warmbloods (72). Sixty-eight horses had behavioral changes, and all 100 had proprioceptive ataxia (median grade, 2/5). Fifty-seven horses had abnormal findings on cervical vertebral radiographs, and 14 had myelographic findings consistent with compressive myelopathy. No antemortem diagnostic test results were consistently associated with necropsy diagnosis of neurodegenerative disease. All 100 horses had degenerative lesions characteristic of eNAD in the brainstem gray matter, and 24 had concurrent degenerative features of EDM in the spinal cord white matter. Clinical and histopathologic findings in this large group of horses with neurodegenerative disease were most consistent with eNAD/EDM, but with a different signalment and clinical presentation from earlier descriptions. The increasing occurrence of neurodegenerative disease in horses and the safety risk posed emphasize the importance of focused research in affected horses.

Computed tomography myelography description of pneumorrhachis secondary to a degenerative intervertebral disk disease in a cross‐breed dog

AbstractA 9‐year‐old, male, neutered, cross‐breed dog was presented for a 6‐month history of spinal pain, mild pelvic limbs proprioceptive ataxia and discrete ambulatory paraparesis. Computed tomography myelography identified focal gas accumulation in the left aspect of the vertebral canal at the level of T11–T12, resulting in moderate extradural spinal cord compression. Minor chronic intervertebral disk protrusion was also identified at this level with no evidence of spinal cord compression. An encapsulated space‐occupying gas accumulation was identified and removed during a left‐sided T11–T12 hemilaminectomy. On histopathological analysis, the capsule was formed by connective and inflammatory tissue. Early neurological deterioration following surgery was observed due to persistent extradural material causing spinal cord compression. Widening of the previous hemilaminectomy window was performed to remove the compressive material, and progressive improvement was noted during the following weeks. This is the first case of computed tomography myelography description of pneumorrhachis in a dog.

A female Bullmastiff with calvarial hyperostosis syndrome and concurrent hyperostotic changes affecting the mandible and cervical vertebrae

AbstractAn immature female Bullmastiff presented for assessment of swelling of the right dorsal orbital region, causing discomfort. Computed tomography showed osseous proliferation of the calvarium, frontal bone and concurrent unilateral osseous changes at the level of the left mandible. Ventral new bone formation and remodelling changes were noted between vertebrae C7 and T1. The vertebral bodies of C5, C6 and C7 were fused. Histopathology was consistent with calvarial hyperostosis syndrome. Subsequently, the dog developed neurological signs: proprioceptive ataxia and lower motor neuron ambulatory tetraparesis. Magnetic resonance imaging showed mild osseous spinal cord compression at C7 level. Calvarial hyperostosis syndrome described in this report is the first recorded case of a dog having concurrent hyperostotic changes affecting the calvarium, mandible and cervical vertebrae in a dog.

Case report: Surgical treatment of an astrocytoma in the thoracic spinal cord of a cat

A 15-year-old spayed female domestic shorthaired cat was evaluated for chronic progressive paraparesis and proprioceptive ataxia. Neurological examination was consistent with a T3–L3 myelopathy. Plain thoracolumbar vertebral column radiographs and CT without intravenous contrast or myelography performed at another facility did not highlight any abnormalities. MRI of the thoracolumbar spinal cord identified an intraparenchymal space-occupying lesion extending from T10–T12. Surgery was performed to remove as much of the mass as possible, and to submit samples for histopathology. A dorsal laminectomy was performed over T9–T13. A midline myelotomy provided access to the mass, which was debrided with an intraoperative estimate of 80% removal. Histopathologic examination was consistent with a diagnosis of an astrocytoma. Post-operative treatment consisted of amoxicillin clavulanic acid, prednisolone, gabapentin, and additional analgesic medications in the direct post-operative period. Over the following 4 months, slow recovery of motor function was seen with continued physiotherapy. During the following 2 months, renal and cardiopulmonary disease were diagnosed and treated by other veterinarians. The cat was also reported to have lost voluntary movement in the pelvic limbs during this period, suggesting regression to paraplegia. Finally, 6 months post-surgery, the owner elected humane euthanasia. This is the second documentation of surgical treatment and outcome of an astrocytoma in the spinal cord of a cat.

Clinical-imaging aspects of the spinal arachnoid diverticulum in dog

Spinal arachnoid diverticulum is a focal, dilatative lesion of the arachnoid membrane, filled with cerebrospinal fluid and which can cause spinal cord compression of varying degrees. It can present as a primary or secondary, single or multiple lesion. Commonly, it affects the cervical segment in large dogs and the thoracolumbar segment in small dogs. The clinical picture is dominated by progressive proprioceptive ataxia with varying degrees of tetraparesis or paraparesis. The diagnosis of the lesion involves the use of myelography or CT-myelography to identify and locate the intradural arachnoid diverticulum. However, the gold standard method is represented by the MRI exam that determines the degree of damage to the spinal cord, as well as the identification of associated conditions.

Head tilt as a clinical sign of cervical spinal or paraspinal disease in dogs: 15 cases (2000-2021).

To characterise head tilt as a rare clinical sign of cervical spinal or paraspinal disease in dogs. Retrospective single-centre case-series study of dogs with head tilt and cervical spinal or paraspinal disease in the absence of intracranial abnormalities. Descriptive statistics were used. Fifteen dogs met the inclusion criteria of this study. Median age at onset was 6 years (range 2.5 to 12 years). Onset of neurological signs was mainly chronic (9/15, 60%). Most common presenting complaints included head tilt (9/15, 60%) and cervical hyperaesthesia (8/15, 53%). Most common neurological findings included head tilt (15/15, 100%), generalised proprioceptive ataxia and tetraparesis (6/15, 40%) and cervical hyperaesthesia (8/15, 53%). Diagnoses included post-operative complication of C2 spinal nerve root mass removal (2/15, 13%), C3-C4 intervertebral disc extrusion (2/15, 13%), cervical paraspinal myositis (2/15, 13%) and one of each: C2 vertebral malformation, C2 spinal nerve root mass, C1-C2 meningioma, C2 vertebral fracture, C4-C5 intervertebral disc extrusion, C4 vertebral body mass, C5-C7 osseous-associated cervical spondylomyelopathy, and concurrent C5-C6 and C6-C7 intervertebral disc protrusions. Two dogs were euthanased shortly after diagnosis and two of 15 were dogs lost to follow-up. No post-mortem examination was performed for these cases. For the 11 of 15 remaining dogs, head tilt resolved in eight of 15 (53%) dogs after treatment of the underlying condition and in three of 15 (20%) dogs, it remained static. Head tilt can be a rare clinical sign of cervical spinal or paraspinal disease in dogs.

Proprioceptive and tactile processing in individuals with Friedreich ataxia: an fMRI study.

Friedreich ataxia (FA) neuropathology affects dorsal root ganglia, posterior columns in the spinal cord, the spinocerebellar tracts, and cerebellar dentate nuclei. The impact of the somatosensory system on ataxic symptoms remains debated. This study aims to better evaluate the contribution of somatosensory processing to ataxia clinical severity by simultaneously investigating passive movement and tactile pneumatic stimulation in individuals with FA. Twenty patients with FA and 20 healthy participants were included. All subjects underwent two 6 min block-design functional magnetic resonance imaging (fMRI) paradigms consisting of twelve 30 s alternating blocks (10 brain volumes per block, 120 brain volumes per paradigm) of a tactile oddball paradigm and a passive movement paradigm. Spearman rank correlation tests were used for correlations between BOLD levels and ataxia severity. The passive movement paradigm led to the lower activation of primary (cSI) and secondary somatosensory cortices (cSII) in FA compared with healthy subjects (respectively 1.1 ± 0.78 vs. 0.61 ± 1.02, p = 0.04, and 0.69 ± 0.5 vs. 0.3 ± 0.41, p = 0.005). In the tactile paradigm, there was no significant difference between cSI and cSII activation levels in healthy controls and FA (respectively 0.88 ± 0.73 vs. 1.14 ± 0.99, p = 0.33, and 0.54 ± 0.37 vs. 0.55 ± 0.54, p = 0.93). Correlation analysis showed a significant correlation between cSI activation levels in the tactile paradigm and the clinical severity (R = 0.481, p = 0.032). Our study captured the difference between tactile and proprioceptive impairments in FA using somatosensory fMRI paradigms. The lack of correlation between the proprioceptive paradigm and ataxia clinical parameters supports a low contribution of afferent ataxia to FA clinical severity.