Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs

Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.     

Computed tomography diagnosis of eight dogs with brain infarction

Objective Medical records of eight dogs presenting with acute onset of neurological signs and a diagnosis of brain infarction as determined by computed tomography (CT) imaging were reviewed. Design Retrospective single-centre case review Results Ischaemic infarction in the territory of the rostral cerebellar artery was identified in three spaniel-breed dogs. All cerebellar infarcts were non-haemorrhagic. Telencephalic infarcts were identified in five dogs, in the territories of the middle cerebral artery (2/5) and rostral cerebral artery (3/5). One of these dogs had an ischaemic infarction, but all other infarctions appeared haemorrhagic. All dogs were geriatric (≥8 years old), with concurrent medical conditions identified in six dogs. One dog was euthanased after diagnosis because of the severity of its neurological signs and one dog was euthanased as a result of associated renal disease 2 months after diagnosis. Six dogs were alive at least 1 year after diagnosis. Conclusions CT is useful in the diagnosis of cerebrovascular accident in dogs, which can present as a spectrum of images with early changes in attenuation and subtle mass effects detected after infarction. CT is particularly sensitive for detecting haemorrhagic infarction, but under-represent ischaemic and lacunar infarctions when compared with MRI.     

Signs consistent with syringobulbia may be detected in dogs undergoing MRI

Syringobulbia is a pathologic condition characterized by one or more fluid‐filled cavities within the brainstem. This retrospective case series describes observations in eight dogs with syringobulbia diagnosed during MRI. All dogs were adult, small‐breed dogs with concurrent syringomyelia and neurologic deficits localized to sites rostral to the spinal cord, which cannot be explained by syringomyelia (eg, six dogs had vestibular signs). On MRI, the fluid‐filled cavities had signal intensity characteristics like cerebrospinal fluid, were in the medulla oblongata, and were solitary in each dog. Initially, the shape of the cavity was a slit in five dogs and bulbous in two dogs. Magnetic resonance imaging was repeated in five dogs (6‐55 months of age). One dog had progression of syringobulbia from slit‐like to bulbous, and four dogs had unchanged slit‐like syringobulbia. One dog developed slit‐like syringobulbia after cranioplasty. A variety of medical and surgical treatments were performed with improvement of some but not all clinical signs. One dog died following surgery due to cardiopulmonary failure and the other seven dogs were alive at least 1 year after the initial diagnosis, which was the least time of follow‐up. One surviving dog developed a unilateral hypoglossal nerve deficit 2 months after the initial diagnosis and megaesophagus 14 months later. In conclusion, detecting a fluid‐filled cavity in the medulla oblongata consistent with syringobulbia is possible in dogs undergoing MRI. The cavity is likely acquired, slit‐like or bulbous, progressive, or static, and might be associated with breed size and neurologic signs localized to the medulla oblongata.     

Presumptive caudal cerebellar artery infarct in a dog: clinical and MRI findings

Clinical signs and magnetic resonance imaging findings of a caudal cerebellar artery infarct are reported for the first time in a dog. Clinical signs were characterised by a peracute, non-progressive, right-sided central vestibular syndrome with paradoxical right-sided head tilt. Magnetic resonance images were consistent with a territorial, non-haemorrhagic, ischaemic lesion affecting the caudo-ventral part of the right cerebellar hemisphere, mainly involving the right paramedian lobe, the ansiform lobe and the caudal cerebellar peduncle. Bloodwork results were suggestive of an underlying hypercoagulable state, although the concomitant presence of a histologically confirmed mammary gland adenocarcinoma could have also been related to the cerebellar vascular obstruction through metastatic emboli formation. Posterior-inferior cerebellar artery infarction is the human equivalent of caudal cerebellar artery infarct in dogs.     

Clinical and magnetic resonance imaging characteristics of quadrigeminal cysts in dogs

BACKGROUND: Quadrigeminal cysts (QC) are the most common intracranial intra-arachnoid cysts in dogs, primarily affecting small breeds. Clinical significance is controversial. HYPOTHESIS: Male, brachycephalic, small breed dogs are predisposed to QC, and objective measurement of parenchymal compression can distinguish clinically relevant QC from incidental findings. ANIMALS: A total of 4,100 client-owned dogs. METHODS: A retrospective study that recorded signalment, history, clinical signs, and magnetic resonance imaging features. The degree of brain compression was evaluated in the presence of relevant clinical signs. The percentage compression of cerebellum and forebrain was calculated by comparing the expected to the actual diameter and longitudinal dimension, respectively. RESULTS: QC were diagnosed in 28 dogs, of which 21 (75%) were small breed dogs. Fifteen dogs (54%) were brachycephalic. Eighteen dogs were male, and 10 were female. Cerebellar, occipital lobe, or compression in both areas occurred in 86% (24/28 dogs). Clinical signs included focal and generalized seizures in 5 dogs and cerebellar signs in 6 dogs. Mean occipital lobe compression was 17% (SD = 4) in clinically affected and 10% (SD = 3) in normal dogs (P = .006). Occipital lobe compression >14% was always associated with clinical signs. The mean cerebellar compression was 18%, but there was no association between compression and clinical signs. The animals were more likely to develop clinical signs if both areas were compressed (P = .04). CONCLUSIONS AND CLINICAL IMPORTANCE: Parenchymal compression by QC can be incidental, and other central nervous system diseases must be excluded when assessing the clinical significance of QC. However, occipital lobe compression over 14% is likely to cause clinical signs.     

Concurrent Diseases and Conditions in Dogs with Splenic Vein Thrombosis

Background: Splenic venous thrombosis (SVT) is usually considered an incidental finding on abdominal ultrasound examination but can indicate the presence of underlying disease. Concurrent disease processes and conditions in dogs with SVT have not been identified previously. Objectives: To identify concurrent diseases and conditions in dogs with SVT. Animals: Eighty dogs with SVT. Methods: Retrospective review. Medical records from 1994 through 2008 were searched for dogs with SVT identified by ultrasound examination. These records were then reviewed for signalment, medical history, clinicopathologic testing, diagnostic imaging, and clinical diagnosis. Results: The most common concurrent conditions were neoplasia (54%), exogenous corticosteroid administration (43%), systemic inflammatory response syndrome (26%), disseminated intravascular coagulation (20%), pancreatitis (18%), and immune‐mediated disease (16%). The most common neoplastic disease was lymphoma, and the most common immune‐mediated disease was immune‐mediated hemolytic anemia. Protein‐losing nephropathy and naturally occurring hyperadrenocorticism were identified in <10% of the dogs. Concurrent splenic infarcts were identified in 33% of dogs, and concurrent portal vein thrombi were found in 18% of dogs. Conclusions: SVT is a sonographic finding of clinical importance, and dogs with SVT can have 1 or more coexisting diseases.     

Concurrent medical conditions and long-term outcome in dogs with nontraumatic intracranial hemorrhage

Nontraumatic intracranial hemorrhage is bleeding originating from the brain or surrounding structures. It results from blood vessel rupture and may be primary or secondary in origin. The magnetic resonance imaging (MRI) characteristics of 75 dogs with nontraumatic intracranial hemorrhage were reviewed to determine signalment; intracranial compartment involved, size and number of lesions; type and prevalence of concurrent medical conditions; and long‐term outcome. Hemorrhagic lesions were intraparenchymal (n = 72), subdural (n = 2) or intraventricular (n = 1). Thirty‐three of 75 dogs had a concurrent medical condition. A concurrent condition was detected in 13 of 43 dogs with a single lesion ≥5 mm and included Angiostrongylus vasorum infection, intracranial lymphoma and meningioma. Of the 20 dogs with multiple lesions ≥5 mm, 7 had A. vasorum infection, 2 had hemangiosarcoma metastasis, 5 had suspected brain metastasis, and 1 was septicemic. Of the 12 dogs with multiple lesions, 2 had hyperadrenocorticism, 2 had chronic kidney disease, and 1 had hypothyroidism. Of these five dogs, all were hypertensive and four died within 12 months. No dog had a single lesion <5 mm. Long‐term outcome was favorable in 26 of 43 dogs with single lesions ≥5 mm, 6 of 20 dogs with multiple lesions ≥5 mm, and 8 of 12 dogs with multiple lesions <5 mm. A. vasorum infection was the most common concurrent condition in dogs with nontraumatic intracranial hemorrhage (16/75), with an excellent outcome in 14 of 16 dogs. Prognosis in nontraumatic intracranial hemorrhage is reported in terms of concurrent medical conditions and the number and size of lesions. © 2012 Crown copyright. This article was written by M. Lowrie, F. Llabrés‐Diaz and L. Garosi of Davies Veterinary Specialists and L. De Risio and R. Dennis of the Animal Health Trust. It is published with the permission of the Controller of HMSO and the Queen's Printer for Scotland     

REGIONAL BRAIN PERFUSION IN 10 NORMAL DOGS MEASURED USING TECHNETIUM-99m ETHYL CYSTEINATE DIMER SPECT

Single photon emission computed tomography (SPECT) of the brain using perfusion tracers allows estimation of regional brain perfusion. This allows in vivo examination of brain function in the setting of neuropsychologic and pathophysiologic changes. However functional imaging data on brain perfusion in dogs are limited. Hence, the aim of this study was to determine the scintigraphic regional perfusion pattern of the normal canine brain. Ten healthy shepherd type dogs were injected with 925 MBq Technetium-99m ethyl cysteinate (ECD) 20 minutes before the examination. Acquisition was performed using a triple head gamma camera equipped with fanbeam collimators. Uniform attenuation correction and triple energy window correction were applied. Computed tomographic images were obtained from the same dogs, reoriented along the orbito-meatal axis and SPECT perfusion data were coregistered to the CT-volume data. Based on morphological and suggested brain divisions, regions-of-interest (ROIs) were defined for the bilateral frontocerebral, temporocerebral, parietocerebral, occipitocerebral, cerebellar, thalamic, and striatal area. Regional count density was normalized on total counts. All dogs had the highest uptake in the thalamic/striatal area compared to a rather homogeneous cerebral uptake. No significant left/right count differences were found, but a rostro-caudal gradient (+12-13%) was present. In this group, age and gender did not influence the perfusion pattern.     

MAGNETIC RESONANCE IMAGING OF BRAIN INFARCTION IN SEVEN DOGS

Magnetic resonance imaging was performed in seven dogs with histopathologically-confirmed brain infarcts. The infarcts were non-hemorrhagic in four dogs and hemorrhagic in three dogs. Six dogs had single infarcts involving the cerebrum and one dog had multiple infarcts involving the cerebrum and brain stem. Non-hemorrhagic infarcts were typically wedge-shaped, hypointense on T1-weighted images, hyperintense on T2-weighted images, and did not enhance with gadolinium-DTPA. Hemorrhagic infarcts had mixed intensity on T1- and T2-weighted images, with variable patterns of enhancement.     

Cerebrospinal fluid analysis and magnetic resonance imaging in the diagnosis of neurologic disease in dogs: a retrospective study

BACKGROUND: Diagnosis of central nervous system (CNS) abnormalities in dogs can be challenging antemortem. Historically, cerebrospinal fluid (CSF) analysis has been used for routine diagnostic evaluation of animals with suspected neurologic disease; however, with increasing availability of magnetic resonance (MR) imaging, the need for concurrent CSF analysis may be questioned. OBJECTIVE: The purpose of this study was to retrospectively assess and compare the diagnostic information contributed from MR imaging and CSF analysis in a population of dogs presenting with neurologic disease. METHODS: Results of concurrent MR imaging and CSF analysis were evaluated in dogs presented for neurologic diseases. Based on clinical diagnosis, the sensitivity of CSF analysis and MR imaging for detecting a nervous system abnormality was calculated. Dogs with diagnoses confirmed by other diagnostic modalities were also evaluated separately. RESULTS: A total of 256 dogs were included in the study. For clinical diagnoses in which abnormalities were expected, MR imaging abnormalities were found in 89% and CSF abnormalities in 75% of dogs; CSF abnormalities were more common than MR imaging abnormalities only in inflammatory CNS disease. The majority of CSF abnormalities were nonspecific; an etiologic diagnosis was determined in only 2% of CSF samples. MR imaging excelled in detecting structural disorders, revealing 98% of vertebral abnormalities. In confirmed cases (n = 55), 76% of MR images and 9% of CSF samples were diagnostic. When intervertebral disk disease (IVDD) and vertebral malformation were excluded from analysis (n = 16 remaining), 25% of MR images and 6% of CSF cytology results were highly indicative of the confirmed diagnoses; CSF titer results provided the diagnosis in 25% of these cases. CONCLUSION: CSF analysis may not be necessary when MR findings of IVDD or vertebral malformation/instability are obvious; however, when the cause of neurologic disorder is uncertain, concurrent MR imaging and CSF analysis provides the greatest assistance in establishing a clinical diagnosis.     

Rostral cerebellar arterial infarct in two cats

A 10-year-old female neutered domestic shorthair (DSH) cat and a 6-year-old female neutered Siamese cat were presented following a peracute onset of decerebellate rigidity and a cerebellar vestibular syndrome, respectively. In both cats, physical examination and routine blood tests were unremarkable, as was routine analysis of cerebrospinal fluid obtained from the DSH cat. Based on the magnetic resonance imaging (MRI) features - focal wedge-shaped lesion in the cerebellum characterised by hyperintensity in T2-weighted, T2( *)-gradient echo and fluid attenuated inversion recovery (FLAIR) images - a presumptive diagnosis of cerebellar infarct was made in both cases. In the DSH cat, the post-mortem examination confirmed the diagnosis of cerebellar infarct and additionally found acute renal infarcts and a pulmonary neoplasia. In the Siamese cat, ultrasonographic evaluation of the heart revealed a probable low-grade chronic valvular endocarditis which was thought to be a potential source of thromboembolism. This paper describes the first two cases - one confirmed and the other suspected - of cerebellar infarct in the cat. The in vivo potential diagnostic value of the MRI study is highlighted. Cerebellar infarcts should be included in the differential diagnosis of cat with a peracute onset of cerebellar signs regardless of the severity of neurological deficits.     

Ischemic Optic Neuropathy in a Dog with Acute Bilateral Blindness and Primary Systemic Hypertension

A 6‐year‐old neutered female Jack Russell terrier was investigated for sudden onset prechiasmatic bilateral blindness, left circling, reduced proprioception in the right pelvic limb and right facial allodynia. Electroretinography was normal. Magnetic resonance imaging (MRI) examination revealed that the right optic nerve and the optic chiasm were hyperintense on diffusion weighted imaging and hypointense on apparent diffusion coefficient map consistent with ischemic optic neuropathy. A concurrent lacunar infarct was detected in the left rostral colliculus. Primary systemic hypertension was diagnosed based on blood pressure measurement and no detectable abnormalities on hematology, comprehensive serum biochemistry, urinalysis including protein/creatinine and cortisol/creatinine ratios and thoracic/abdominal imaging. Prednisolone for 10 days and amlodipine long‐term were administered. Vision was not recovered after 7 months. Repeat MRI supported the diagnosis of ischemic lesions and revealed a recent striatocapsular infarct. Ischemic optic neuropathy is a well‐recognized cause of blindness in humans and should be included as a differential diagnosis for acute prechiasmatic blindness in dogs.     

Chronic pancreatitis in dogs: A retrospective study of clinical,clinicopathological, and histopathological findings in 61 cases

The objective of this study was to characterize the clinical, clinicopathological, and histopathological findings of dogs with chronic pancreatitis. The necropsy database at Texas A&M University was searched for reports of dogs with histological evidence of chronic pancreatitis defined as irreversible histologic changes of the pancreas (i.e. fibrosis or atrophy). A reference necropsy population of 100 randomly selected dogs was used for signalment and concurrent disease comparisons. Cases were categorized as clinical or incidental chronic pancreatitis based on the presence of vomiting, decreased appetite, or both vs. neither of these signs. All archived pancreas samples were scored histologically using a published scoring system.Sixty-one dogs with chronic pancreatitis were included. The most frequent clinical signs were lethargy, decreased appetite, vomiting, and diarrhea. Compared to the reference necropsy population, chronic pancreatitis cases were more likely to be older, neutered, of the non-sporting/toy breed group, and to have concurrent endocrine, hepatobiliary, or neurological disease. Clinical cases had significantly higher histological scores for pancreatic necrosis and peripancreatic fat necrosis, and were significantly more likely to have hepatobiliary or endocrine disease as well as increased liver enzyme activities, or elevated cholesterol and bilirubin concentrations. In conclusion, clinical disease resulting from chronic pancreatitis might be related to the presence of pancreatic necrosis and pancreatic fat necrosis. The signalment, presentation, and concurrent diseases of dogs with chronic pancreatitis are similar to those previously reported for dogs with acute pancreatitis.     

Clinical manifestations of cataracts in small breed dogs

Objective  To determine the incidence, etiology, and concurrent ophthalmic findings in small breed dogs that presented with cataracts.
Animal studied  Five hundred and sixty-one small breed dogs (942 eyes) were presented to the Veterinary Medical Teaching Hospital of Seoul National University between July 2002 and December 2007 with cataract.
Procedure  The medical records of small breed dogs with cataract were reviewed. The reason for presentation, cataract duration, bilaterality, breed, gender, age, vision, etiology, stage of cataract development, concurrent ophthalmic findings, IOP, ocular ultrasonography findings, and scotopic electroretinography (ERG) findings were investigated.
Results  The most frequently presented breeds were the Miniature/Toy Poodle ( n  = 112, 20.0%), Yorkshire Terrier ( n  = 110, 19.6%), and Shih Tzu ( n  = 95, 16.9%). The Miniature/Toy Poodle showed a significantly higher odds ratio for cataract formation (2.6). The proportion of female cataract patients was significantly higher than that of male cataract patients in the overall population ( P  < 0.05). The Miniature/Toy Poodles had significantly higher numbers of females affected with cataract ( P  < 0.01). The mean age for cataract formation was 8.3 ± 3.9 years. The mean age at onset in the Miniature/Toy Poodle and Yorkshire Terrier was significantly higher, whereas that in the Miniature Schnauzer group was significantly lower ( P  < 0.0001). Clinical signs related to lens induced uveitis had a tendency to increase with cataract progression ( P  < 0.05). There were no significant differences in the b-wave amplitude for mixed rod cone response by stage ( P  = 0.137).
Conclusions  Small breed dogs with cataracts had characteristics with regard to age of onset and gender distribution, depending on the breed.     

Cerebellar cortical degeneration with selective granule cell loss in Bavarian mountain dogs

Three Bavarian mountain dogs aged between 18 and 20 months, not related to each other, were presented with chronic signs of cerebellar dysfunction. On sagittal T2-weighted magnetic resonance imaging brain images, the tentative diagnosis of cerebellar hypoplasia was established based on an enlarged cerebrospinal fluid space around the cerebellum and an increased cerebrospinal fluid signal between the folia. Post-mortem examination was performed in one dog and did show an overall reduction of cerebellar size. On histopathologic examination, a selective loss of cerebellar granule cells with sparing of Purkinje cells was evident. Therefore, the Bavarian mountain dog is a breed where cerebellar cortical degeneration caused by the rather exceptional selective granule cell loss can be seen as cause of chronic, slowly progressive cerebellar dysfunction starting at an age of several months.     

Clinicopathological features of canine neuroaxonal dystrophy and cerebellar cortical abiotrophy in Papillon and Papillon-related dogs

Neuroaxonal dystrophy (NAD) was examined in two Papillon dogs and a mix breed dog between Papillon and Chihuahua. In addition, cerebellar cortical abiotrophy (CCA) in a Papillon dog, which had similar clinical and magnetic resonance imaging (MRI) features to those of NAD, was also investigated. The common clinical symptoms of all dogs affected with NAD and CCA, were pelvic limb ataxia and cerebellar ataxia including intention tremor, head tremor, and hypermetria in the early onset. These clinical signs were progressed rapidly, and two dogs with NAD were euthanized by owner's request and the other two died by aspiration pneumonia. MRI examinations and gross observations at necropsy revealed moderate to severe cerebellar atrophy in all cases of NAD and CCA. The most typical histological change of NAD was severe axonal degeneration with marked spheroid-formation in the dorsal horn of the spinal cords, the nuclei gracilis, cuneatus, olivalis and its circumference in the medulla oblongata. The spheroids were characterized as large eosinophilic or granular globes within the enlarged myelin sheaths, sometimes accompanied by moderate accumulation of microglias and/or macrophages. In contrast, such spheroid formation was minimal in the brain of CCA. In the cerebellum, mild to moderate loss of the Purkinje and granular cells were recognized in three dogs with NAD, whereas these changes were more prominent in a dog with CCA. Although the clinical signs and MRI findings relatively resembled between NAD and CCA, the histopathological features considered to be quite differ, suggesting distinct pathogenesis and etiology. Since both NAD and CCA are proposed as the autosomal recessive hereditary disorders, careful considerations might be needed for the breeding of Papillon and Chihuahua dogs.     

Outcome of and postoperative complications in dogs undergoing surgical treatment of laryngeal paralysis: 140 cases (1985-1998).

OBJECTIVE: To compare outcomes of various surgical techniques for treatment of laryngeal paralysis in dogs and determine incidence and risk factors for development of postoperative complications. DESIGN: Retrospective study. ANIMALS: 140 dogs undergoing surgical treatment for laryngeal paralysis at a veterinary teaching hospital between 1985 and 1998. PROCEDURE: Data were analyzed to determine outcome and factors influencing outcome and development of complications. Kaplan-Meier curves were constructed for survival analysis. RESULTS: Postoperative complications were documented in 48 (34.3%) dogs; 20 (14.3%) dogs died of related causes. Aspiration pneumonia was the most common complication (33; 23.6%). Seven dogs died of aspiration pneumonia > 1 year after surgery. Dogs that underwent bilateral arytenoid lateralization were significantly more likely to develop complications and significantly less likely to survive than were dogs that underwent unilateral arytenoid lateralization or partial laryngectomy. Factors that were significantly associated with a higher risk of dying or of developing complications included age, temporary tracheostomy placement, concurrent respiratory tract abnormalities, concurrent esophageal disease, postoperative megaesophagus, concurrent neoplastic disease, and concurrent neurologic disease. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that surgical repair of laryngeal paralysis may be associated with high postoperative complication and mortality rates. Surgical technique and concurrent problems or diseases increased the risk of complications. Dogs appeared to have a life-long risk of developing respiratory tract complications following surgical correction.     

Evaluation of prognostic indicators in dogs with multiple,simultaneously occurring cutaneous mast cell tumours: 63 cases

Sixty‐three dogs with multiple contemporaneous cutaneous mast cell tumours (MCTs) were identified. The aim of this study was to determine the significance of breed, concurrent dermatological condition; number of cutaneous MCTs, size, location, histological grade and mitotic index; completeness of excision (complete, close or incomplete); local recurrence, metastasis and adjuvant therapy for the prognostic evaluation of dogs with a unique disease presentation of multiple, simultaneously occurring cutaneous MCTs. On the basis of multivariable survival analysis, dogs with one recorded grade 3 MCT had shorter progression‐free survival (PFS) times (18.7 versus 2.2 months) and median survival times (MSTs) (24 versus 3 months). Dogs treated with adjuvant vinblastine/lomustine had a 16 times increased risk of dying. MSTs were found to be significantly longer in dogs with one recorded MCT on an extremity. For all dogs, the PFS (range 14–1835 days) and MSTs (range 28–1835 days) were not reached.     

Spongy degeneration of the central nervous system in two canine littermates

Progressive dysmetria was observed at four months and six months of age in two female Labrador retriever littermates. Neurological examinations indicated a cerebellar disorder. Laboratory analyses were normal. The dogs were studied clinically until they were killed for necropsy at nine months and eleven months of age. Both dogs had normal brain size, shape, and calvarial symmetry; the older dog had body weight loss, reduced brain weight, and muscle atrophy. Microscopically, there were vacuoles, hypertrophied fibrous astrocytes, myelin loss, and prominent blood vessels, distributed symmetrically in the subcortical and deep white matter of all lobes of the cerebrum; in the folial and deep white matter of the cerebellum; in the tracts of some cranial nerves; in the thalamic area, midbrain and brainstem; and in the white matter of the spinal cord. There was no significant myelinolysis, inflammation, or axonal degeneration. Ultrastructurally, there were intramyelinic vacuoles with separation of lamellae at intraperiod lines and larger spaces formed by coalescence of ruptured vacuoles. Hypertrophied fibrous astrocytes had abundant glial filaments, edematous cytosol, membrane-bound crystalline inclusions, dilated cytocavitary systems, and abnormal mitochondria. The clinical, histological, and ultrastructural findings resembled those reported for the juvenile form of Canavan's disease (van Bogaert and Bertrand type) in children.