Vestibular disease in dogs: association between neurological examination, MRI lesion localisation and outcome.

OBJECTIVES: To determine whether the neurological examination correctly distinguishes between central and peripheral vestibular lesions in dogs. MATERIALS AND METHODS: Retrospective study on dogs with vestibular disease presenting to two referral clinics in Germany. RESULTS: Ninety-three dogs were included; neurological examination suggested central vestibular disease in 62 and a peripheral lesion in 31. MRI diagnosis was central vestibular disease in 68 dogs and peripheral in 25. Of the 62 dogs with a lesion localisation diagnosed as central vestibular by neurological exam, 61 were correctly identified (98.4%). Twenty-four of the 31 dogs diagnosed with a peripheral lesion by neurological exam had a consistent lesion on MRI (77.4%). CLINICAL SIGNIFICANCE: The neurological examination is efficient at identifying lesions in the central vestibular system but less so for peripheral lesions. Therefore it is prudent to recommend imaging in dogs that show signs of peripheral vestibular syndrome but do not rapidly respond to treatment.

Cervical myelopathy due to complex Atlanto-axial malformation including partial atlantal dorsal arch aplasia in a domestic rabbit.

A 1-year-old dwarf rabbit was presented with sub-acute progressive tetraparesis. Radiography, CT and MRI revealed compressive cervical myelopathy secondary to a complex atlanto-axial malformation including partial aplasia of the atlantal dorsal arch, dens malformation, malarticulation and lateral atlanto-occipital displacement. Owners decided against surgical treatment and elected conservative treatment including analgesia with non-steroidal anti-inflammatory drugs, cage rest and physiotherapy. Within 2 months clinical signs deteriorated and the owner elected euthanasia. Subsequent necropsy confirmed imaging findings. Similar cases described in humans and dogs suggest that partial aplasia of the dorsal arch of the atlas might often be an asymptomatic radiologic finding in these species. In contrast, this first description of a similarly affected rabbit demonstrates that complex atlanto-axial malformations can cause severe clinical signs.

Spontaneous acute and chronic spinal cord injuries in paraplegic dogs: a comparative study of in vivo diffusion tensor imaging.

STUDY DESIGN: Prospective observational-analytical study. OBJECTIVES: Description of diffusion tensor imaging (DTI) metrics obtained from the spinal cord (SC) of dogs with severe acute or chronic spontaneous, non-experimentally induced spinal cord injury (SCI) and correlation of DTI values with lesion extent of SCI measured in T2-weighted (T2W) magnetic resonance imaging sequences. SETTING: Hannover, Germany. METHODS: Forty-seven paraplegic dogs, 32 with acute and 15 with chronic SCI, and 6 disease controls were included. T2W and DTI sequences of the thoracolumbar spinal cord were performed. Values of fractional anisotropy (FA) and apparent diffusion coefficient (ADC) were obtained from the epicentre of the lesion and one SC segment cranially and caudally and compared between groups. Pearson's correlation coefficient was calculated between DTI and T2W metrics. RESULTS: During acute SCI, FA values were increased (P=0.0065) and ADC values were decreased (P=0.0099) at epicentres compared to disease controls. FA values obtained from dogs with chronic SCI were lower (P<0.0001 epicentres and caudally; P=0.0002 cranially) and ADC showed no differences compared to disease control values. Dogs with chronic SCI revealed lower FA and higher ADC compared to dogs with acute SCI (P<0.0001 for both values at all localisations). FA values from epicentre and cranially to the lesion during chronic SCI correlated with extent of lesion (r=0.5517; P=0.0052 epicentres and r=0.6810; P=0.0408 cranially). CONCLUSION: Using DTI, differences between acute and chronic stages of spontaneous canine SCI were detected and correlations between T2W and DTI sequences were found in chronic SCI, supporting canine SCI as a useful large animal model.

Comparison of Preoperative Quantitative Magnetic Resonance Imaging and Clinical Assessment of Deep Pain Perception as Prognostic Tools for Early Recovery of Motor Function in Paraplegic Dogs with Intervertebral Disk Herniations.

BACKGROUND: Prognostic tools to predict early postoperative motor function recovery (MFR) after thoracolumbar intervertebral disk herniation (IVDH) in paraplegic dogs represent an opportunity to timely implement novel therapies that could shorten recovery times and diminish permanent neurological dysfunctions. HYPOTHESIS: Fractional anisotropy (FA) values obtained using diffusion tensor imaging have a higher prognostic value than a lesion extension ratio in T2-weighted images (T2W-LER) and clinical assessment of deep pain perception (DPP) for MFR. ANIMALS: Thirty-five paraplegic dogs with diagnosis of acute or subacute thoracolumbar IVDH. METHODS: Prospective, descriptive observational study. At admission, absence or presence of DPP, T2W-LER, and FA values was evaluated. MFR was assessed within 4 weeks after decompressive surgery. Values of T2W-LER and FA of dogs with and without MFR were compared using t-tests. All 3 methods were evaluated for their sensitivity and specificity as a prognostic factor. RESULTS: No differences were found between groups regarding T2W-LER. FA values differed statistically when measured caudally of lesion epicenter being higher in dogs without MFR compared to dogs with MFR (P = .023). Logistic regression analysis revealed significance in FA values measured caudally of the lesion epicenter (P = .033, area under the curve = 0.72). Using a cutoff value of FA = 0.660, the technique had a sensitivity of 80% and a specificity of 55%. Evaluation of DPP had a sensitivity of 73.3% and specificity of 75% (P = .007). CONCLUSIONS AND CLINICAL IMPORTANCE: Evaluation of DPP showed a similar sensitivity and a better specificity predicting early MFR than quantitative magnetic resonance imaging.

Correlation between severity of clinical signs and transcranial magnetic motor evoked potentials in dogs with intervertebral disc herniation.

Transcranial magnetic motor evoked potentials (TMMEPs) can assess the functional integrity of the spinal cord descending motor pathways. In intervertebral disc herniation (IVDH), these pathways are compromised to varying degrees reflected by the severity of neurological deficits. The hypotheses of this study were as follows: (1) TMMEPs differ in dogs with IVDH and healthy control dogs; (2) TMMEPs reflect different severities of neurological signs; and (3) TMMEPs can document functional motor improvement and therefore monitor recovery of function. TMMEPs were recorded in 50 dogs with thoracolumbar IVDH. Clinical signs ranged from spinal hyperesthesia to non-ambulatory paraparesis in 19 dogs and paraplegia with/without deep pain sensation in 31 dogs. In these 31 paraplegic dogs, transcranial magnetic stimulation (TMS) was repeated during follow-up examinations. Ten healthy Beagle dogs served as controls. There was a significant increase in onset latency and decrease in peak-to-peak amplitude in the pelvic limb TMMEPs of dogs with spinal hyperesthesia to severe paraparesis compared to control dogs. Waveforms in dogs with IVDH were predominantly polyphasic in contrast to the biphasic waveforms of the control dogs. TMMEPs could not be generated in the pelvic limbs of paraplegic dogs. However, TMMEPs with markedly increased onset latencies and decreased peak-to-peak amplitudes reappeared in the pelvic limbs of dogs that were paraplegic before surgery and showed functional motor improvement during follow-up. The severity of neurological deficits was reflected by TMMEP findings, which could be used to document functional motor recovery in IVDH. TMS could therefore be used as an ancillary test to monitor response to therapy in dogs during rehabilitation.

Transcranial magnetic stimulation with acepromazine or dexmedetomidine in combination with levomethadone/fenpipramide in healthy Beagle dogs.

The aim of this study was to evaluate the influence of two sedation protocols on transcranial magnetic motor evoked potentials (TMMEPs) after transcranial magnetic stimulation in medium sized dogs. Onset latencies and peak-to-peak amplitudes, elicited in the extensor carpi radialis and cranial tibial muscles, were analysed in 10 healthy Beagles that received either acepromazine or dexmedetomidine in combination with levomethadone/fenpipramide, in a crossover design. Similar TMMEP recordings could be made using both sedation protocols at 80-90% stimulation intensity; however, there were significantly shorter onset latencies with the acepromazine-levomethadone/fenpipramide protocol at 100% stimulation intensity. Reference values were established and it was concluded that both drug combinations are feasible for measuring TMMEPs in medium sized dogs.

Vertebral and spinal dysplasia: A novel dominantly inherited congenital defect in Holstein cattle.

Monitoring and surveillance strategies are imperative for managing genetic defects in livestock populations in order to avoid detrimental effects on animal welfare and productivity. Recently, a number of previously unknown defects have been described in cattle, fostered by the huge progress in genome analysis and genomic selection. In response to reports about a potentially new defect in Holstein cattle, case-control studies were carried out to confirm a genetic background of the defect and to evaluate its phenotypic relevance. Eighty-five potentially affected offspring of a suspected carrier sire for the defect and 41 matched control calves were subjected to clinical and epidemiological monitoring on 39 farms. Forty-one animals, all offspring of the suspected carrier sire, showed pathognomonic tail malformations providing highly significant evidence for a congenital inherited defect, which was subsequently termed vertebral and spinal dysplasia (VSD). The defect is characterised by vertebral (specifically tail) deformities and neurological dysfunctions with gait abnormalities of the hind limbs. The deformities and neurological dysfunctions varied from very mild (only tail deformities) to severe (paraparesis). Detailed epidemiological monitoring provided no indication of environmental factors affecting VSD. The malformations and dysfunctions associated with VSD, as well as its mode of inheritance and the genotyping of the suspected carrier sire, indicated that VSD is a defect previously not described in cattle. VSD is inherited in a dominant mode, but shows incomplete penetrance of the phenotype, which impedes unequivocal identification of VSD carriers. A direct diagnostic genetic test for VSD is available.

[Porencephaly in a female Greater Swiss Mountain Dog]. / Porenzephalie bei einer Großen Schweizer Sennenhündin.

A 15-month-old female Greater Swiss Mountain Dog was presented after an epileptic episode. In addition, the owner had noticed a recent marked change in the animal's behaviour. Because of the progressive nature of the neurological signs, a magnetic resonance imaging scan of the brain was performed and porencephaly in the parietal lobe of the right hemisphere was diagnosed. The dog was euthanized and submitted for pathology. Because of the histopathological findings and the history of a craniocerebral injury whilst a puppy, a traumatic genesis of this rare cystic lesion is discussed.

Dynamic changes of Foxp3(+) regulatory T cells in spleen and brain of canine distemper virus-infected dogs.

Canine distemper virus (CDV) infection causes immunosuppression and demyelinating leukoencephalitis in dogs. In viral diseases, an ambiguous function of regulatory T cells (Treg), with both beneficial effects by reducing immunopathology and detrimental effects by inhibiting antiviral immunity, has been described. However, the role of Treg in the pathogenesis of canine distemper remains unknown. In order to determine the effect of CDV upon immune homeostasis, the amount of Foxp3(+) Treg in spleen and brain of naturally infected dogs has been determined by immunohistochemistry. In addition, splenic cytokine expression has been quantified by reverse transcriptase polymerase chain reaction. Splenic depletion of Foxp3(+) Treg was associated with an increased mRNA-expression of tumor necrosis factor and decreased transcription of interleukin-2 in the acute disease phase, indicative of disturbed immunological counter regulation in peripheral lymphoid organs. In the brain, a lack of Foxp3(+) Treg in predemyelinating and early demyelinating lesions and significantly increased infiltrations of Foxp3(+) Treg in chronic demyelinating lesions were observed. In conclusion, disturbed peripheral and CNS immune regulation associated with a reduction of Treg represents a potential prerequisite for excessive neuroinflammation and early lesion development in canine distemper leukoencephalitis.

Intervertebral disk degeneration in dogs: consequences, diagnosis, treatment, and future directions.

Evidence of intervertebral disk degeneration (IVDD) is extremely common in dogs, and its prevalence increases with age. It has many important consequences because degeneration of the intervertebral disks often is a prelude to disk herniation, which can injure the spinal cord, spinal nerves, or both. This review summarizes the advances in diagnosis and treatment of IVDD that have been made since the 1950s when the first detailed description of the degenerative changes was published. It also discusses new approaches to treatment of the associated spinal cord injury and new methods by which to classify injury severity that are currently under development.

Peripheral primitive neuroectodermal tumour in a dog.

A 1-year-old German shepherd dog was presented with paraparesis quickly progressing to paraplegia. Magnetic resonance imaging revealed a large mass beneath the thoracolumbar vertebral column infiltrating the spinal canal and resulting in severe extradural compression of the spinal cord. Microscopically, this comprised a cell-rich unencapsulated tumour supported by fine bands of a fibrovascular stroma and occasionally forming primitive rosettes. Immunohistochemistry showed the tumour cells to express synaptophysin and neuron-specific enolase. Ultrastructurally, the neoplastic cells had low to moderate numbers of intracytoplasmic neurosecretory granules. A peripheral primitive neuroectodermal tumour was diagnosed. This is a rare embryonal tumour of neural origin that may have arisen from adrenal medulla, autonomic ganglia or peripheral nerves.

Cerebrospinal fluid tau protein as a biomarker for severity of spinal cord injury in dogs with intervertebral disc herniation.

Intervertebral disc herniation (IVDH) is a common cause of spinal cord injury (SCI) in dogs. Microtubule-associated protein tau derives predominantly from neurons and axons, making it a potential marker of neuronal injury. A retrospective study, including 51 dogs with thoracolumbar or cervical IVDH and 12 clinically normal dogs, was designed to describe associations between cerebrospinal fluid (CSF) tau concentration, degree of neurological signs and motor functional recovery in dogs with IVDH. Signalment, degree of neurological dysfunction and outcome were recorded. Cisternal CSF tau values were determined by ELISA. Associations between CSF tau concentration and various clinical parameters were evaluated. Receiver-operating characteristics curve (ROC) analyses were performed to assess the validity of protein tau measurements. CSF tau concentrations were significantly higher in dogs showing plegia (median, 79.9 pg/mL; range, 0-778.7 pg/mL; P=0.016) compared to healthy dogs and dogs with paresis (median, 30.1 pg/mL; range, 0-193.1 pg/mL; P=0.025). Plegic dogs that improved by one neurological grade within 1 week had significantly lower tau protein levels compared to plegic dogs that needed more time for recovery or did not show an improvement (P=0.008). A CSF tau concentration >41.3 pg/mL had a sensitivity of 86% and specificity of 83% to predict an unsuccessful outcome in plegic dogs based on ROC analysis (area under the curve, 0.887; P=0.007, 95% confidence interval [CI] 0.717-1.057). CSF protein tau levels are positively associated with the severity of spinal cord damage and may serve as a prognostic indicator in dogs with IVDH.

Impact of Theiler's virus infection on hippocampal neuronal progenitor cells: differential effects in two mouse strains.

AIMS: Disease-associated alterations in hippocampal neurogenesis are discussed as an important factor contributing to long-term consequences of central nervous system diseases. Therefore, the study aimed to determine the impact of Theiler's murine encephalomyelitis virus infection on hippocampal cell proliferation, neuronal progenitor cells and neurogenesis as well as the influence of microglia on respective disease-associated alterations. METHODS: The impact of the infection was evaluated in two mouse strains which differ in the disease course, with an acute polioencephalitis followed by virus elimination in C57BL/6 mice and a chronic demyelinating disease in SJL/J mice. RESULTS: Infection with the low neurovirulent BeAn strain did not exert significant acute effects regardless of the mouse strain. In the chronic phase, the number of neuronal progenitor cells and early postmitotic neurones was significantly reduced in infected SJL/J mice, whereas no long-term alterations were observed in C57BL/6 mice. A contrasting course of microglia activation was observed in the two mouse strains, with an early increase in the number of activated microglia cells in SJL/J mice and a delayed increase in C57BL/6 mice. Quantitative analysis did not confirm a correlation between the number of activated microglia and the number of neuronal progenitor cells and early postmitotic neurones. However, flow cytometric analyses revealed alterations in the functional state of microglial cells which might have affected the generation of neuronal progenitor cells. CONCLUSIONS: Theiler's murine encephalomyelitis virus infection can exert delayed effects on the hippocampal neuronal progenitor population with long-term alterations evident 3 months following infection. These alterations proved to depend on strain susceptibility and might contribute to detrimental consequences of virus encephalitis such as cognitive impairment.

Distemper virus encephalitis exerts detrimental effects on hippocampal neurogenesis.

AIMS: Despite knowledge about the impact of brain inflammation on hippocampal neurogenesis, data on the influence of virus encephalitis on dentate granule cell neurogenesis are so far limited. Canine distemper is considered an interesting model of virus encephalitis, which can be associated with a chronic progressing disease course and can cause symptomatic seizures. METHODS: To determine the impact of canine distemper virus (CDV) infection on hippocampal neurogenesis, we compared post-mortem tissue from dogs with infection with and without seizures, from epileptic dogs with non-viral aetiology and from dogs without central nervous system diseases. RESULTS: The majority of animals with infection and with epilepsy of non-viral aetiology exhibited neuronal progenitor numbers below the age average in controls. Virus infection with and without seizures significantly decreased the mean number of neuronal progenitor cells by 43% and 76% as compared to age-matched controls. Ki-67 labelling demonstrated that hippocampal cell proliferation was neither affected by infection nor by epilepsy of non-viral aetiology. Analysis of CDV infection in cells expressing caspase-3, doublecortin or Ki-67 indicated that infection of neuronal progenitor cells is extremely rare and suggests that infection might damage non-differentiated progenitor cells, hamper neuronal differentiation and promote glial differentiation. A high inter-individual variance in the number of lectin-reactive microglial cells was evident in dogs with distemper infection. Statistical analyses did not reveal a correlation between the number of lectin-reactive microglia cells and neuronal progenitor cells. CONCLUSIONS: Our data demonstrate that virus encephalitis with and without seizures can exert detrimental effects on hippocampal neurogenesis, which might contribute to long-term consequences of the disease. The lack of a significant impact of distemper virus on Ki-67-labelled cells indicates that the infection affected neuronal differentiation and survival of newborn cells rather than hippocampal cell proliferation.

Pathogenetic factors for excessive IgA production: Th2-dominated immune response in canine steroid-responsive meningitis-arteritis.

Canine steroid-responsive meningitis-arteritis (SRMA) is a systemic inflammatory disease with a predominant manifestation within the cervical meninges, increased immunoglobulin A (IgA) levels in serum and cerebrospinal fluid (CSF), and a shift of the B:T cell ratio towards a higher percentage of B cells. A Th2-dominated immune response associated with SRMA was therefore hypothesised. Pellets of peripheral blood mononuclear cells (PBMNCs) and CSF white blood cells (CSF WBCs) from dogs in the acute phase of SRMA (n=16) and under glucocorticoid treatment for SRMA (n=16) were investigated for interleukin (IL)-2, interferon (IFN)-γ, IL-4, IL-5 and IL-10 mRNA expression by means of reverse-transcriptase real-time polymerase chain reaction. Results were compared with those of dogs with other inflammatory (n=9) and neoplastic disorders (n=10) of the central nervous system. A tendency towards low levels of Th1 response related cytokines (IL-2, IFN-γ) and high IL-4 expression was observed indicating a Th2-skewed immune response. The pronounced IL-4 production may be an important pathogenetic factor for excessive IgA production in the acute phase of SRMA and for those cases under glucocorticoid treatment.

Age-dependent decline of blood-brain barrier P-glycoprotein expression in the canine brain.

The efflux transporter P-glycoprotein serves as a major molecular gatekeeper at the blood-brain barrier. It has been suggested that a reduction of P-glycoprotein activity with aging might enhance exposure of brain tissue to exogenous and endogenous compounds thereby contributing to the development of neurodegenerative diseases. Brain tissue from owner-kept dogs renders an excellent tool to study the impact of aging on the background of variable environmental and genetic influencing factors. Therefore, we determined expression rates of P-glycoprotein in canine post-mortem tissue from 23 non-laboratory dogs. P-glycoprotein expression in the parahippocampal cortex exhibited a negative correlation with age. Analysis of the area labeled for P-glycoprotein in dogs aged >100 months revealed a 72% drop in P-glycoprotein expression as compared to young adults aged 23-36 months. Respective data from the dentate hilus and dentate gyrus indicated an earlier drop with a reduction by 77 and 80% in dogs aged 37-99 months in comparison with younger individuals. In contrast to the decline observed with aging in dogs without plaques, P-glycoprotein expression rates rather tended to increase with further aging in dogs with plaque formation. In conclusion, the thorough analysis of P-glycoprotein expression rates in non-laboratory dogs revealed a significant decline with aging. The data strongly support the concept that age-dependent changes might predispose to neurodegenerative diseases. In the early pathogenesis of Alzheimer's disease which is modelled by diffuse plaques in the canine brain, an up-regulation of P-glycoprotein might act as a compensatory mechanism to enhance Abeta efflux from the brain. Future studies are necessary to further evaluate the correlation between Abeta deposits and P-glycoprotein expression in different phases of the disease.

Marked MMP-2 transcriptional up-regulation in mononuclear leukocytes invading the subarachnoidal space in aseptic suppurative steroid-responsive meningitis-arteritis in dogs.

Canine Steroid-Responsive Meningitis-Arteritis (SRMA) is a suitable animal model for studies on the development of neutrophilic pleocytosis in aseptic meningitis. Samples of dogs in the acute phase of SRMA (n=16) were examined for gene expression of matrix metalloproteinases (MMP)-2 and -9 and tissue inhibitors of metalloproteinases (TIMP)-1 and -2. Results were compared to those of dogs under glucocorticosteroid treatment for SRMA (n=16) and dogs with other inflammatory and neoplastic diseases of the central nervous system (CNS) (n=19). Samples included mononuclear (PBMCs) and polymorphonuclear cells (PBPMNs) of peripheral blood and cerebrospinal fluid white blood cells (CSF WBCs). In the acute phase of SRMA CSF WBCs showed mRNA expression for MMP-2 and -9 and TIMP-1 and -2, highlighting a contribution of these cells to the overall content of MMPs and TIMPs in CSF. MMP-2 mRNA levels in CSF WBCs were significantly up-regulated in comparison to PBMC expression levels, suggesting that MMP-2 is relevant for PBMC invasion into the subarachnoidal space and that the expression is influenced by migratory activity through the blood-CSF-barrier.

Barbiturate intoxication in two dogs confirmed by toxicological urinalysis.

Two dogs were presented within 24 hours to the Department of Small Animal Medicine and Surgery at the University of Veterinary Medicine Hannover for investigation of the sudden onset of neurological abnormalities following a walk in the same park. One dog was observed ingesting a piece of meat. Analysis of urine by gas chromatography-mass spectrometry from each of the dogs identified the presence of barbiturates. Both dogs recovered with supportive treatment. This is the first report to describe the use of toxicological urinalysis with gas chromatography-mass spectrometry for the diagnosis of barbiturate intoxication in dogs.

A new cell culture protocol for enrichment and genetic modification of adult canine Schwann cells suitable for peripheral nerve tissue engineering.

Easily applicable techniques are presented to obtain high numbers of enriched canine Schwann cells (cSC) in a short time-window. The potential of adult SC for tissue engineering of peripheral nerves and ex vivo gene therapy is obvious from physiological events taking place after peripheral nerve transection [Haastert, K., Grothe, C., 2007. Gene therapy in peripheral nerve reconstruction approaches. Curr. Gene Ther. 7, 221-228]. The presented techniques were modified from a protocol for cultivation and expansion of adult cSC by others [Pauls, J., Nolte, C., Forterre, F., Brunnberg, L., 2004. Cultivation and expansion of canine Schwann cells using reexplantation. Berl. Munch. Tierarztl. Wochenschr. 117, 341-352] and own experiences in rodent and human SC cultivation and transfection [Haastert, K., Mauritz, C., Chaturvedi, S., Grothe, C., 2007. Human and rat adult Schwann cell cultures: fast and efficient enrichment and highly effective non-viral transfection protocol. Nat. Protoc. 2, 99-104]. A purity of about 80% cSC achieved by immunopanning techniques and selective culture conditions is 2.5 fold higher as previously reported (Pauls et al., 2004). Additionally, highly enriched cSC populations are available in 3-4 weeks, only half the time period reported previously (Pauls et al., 2004). Furthermore, electroporation and genetic modification of cSC is reported for the first time.

Magnetic resonance imaging findings in acute canine distemper virus infection.

Demyelination is the prominent histopathological hallmark in the acute stage of canine distemper virus infection. Magnetic resonance imaging is an important diagnostic tool in human beings to determine demyelination in the brain, for example in multiple sclerosis. Five young dogs with clinically suspected canine distemper virus infection were subjected to magnetic resonance imaging of the brain and histopathological and immunohistochemical examinations. Hyperintense lesions and loss of contrast between grey and white matter were detected in T2-weighted images in the cerebellum and/or in the brainstem of three dogs, which correlated with demyelination demonstrated in histopathological examination. Furthermore, increased signal intensities in T2-weighted images were seen in the temporal lobe of four dogs with no evidence of demyelination. Magnetic resonance imaging seems to be a sensitive tool for the visualisation of in vivo myelination defects in dogs with acute canine distemper virus infection. Postictal oedema and accumulation of antigen positive cells have to be considered an important differential diagnosis.