Computer-assisted magnetic resonance imaging brain morphometry in American Staffordshire Terriers with cerebellar cortical degeneration

BACKGROUND: Cerebellar cortical degeneration exists in American Staffordshire Terriers. Magnetic resonance imaging (MRI) can be suggestive, but a definitive diagnosis requires histopathology. HYPOTHESIS: Computer-assisted MRI morphometry can be used to distinguish between American Staffordshire Terriers with or without cerebellar cortical degeneration. ANIMALS: Normal American Staffordshire Terriers (n = 17) and those with clinical signs of cerebellar cortical degeneration (n = 14). METHODS: This was a partly retrospective and partly prospective study. Causes of cerebellar disease were ruled out with brain MRI, cerebrospinal fluid (CSF) analysis, CBC, blood biochemistry, and clinical follow-up. On T2-weighted midsagittal MR images, the following parameters were calculated: size of the cerebellum relative to the entire brain, size of the CSF space surrounding the cerebellum relative to the cerebellum, and 2 threshold-dependent cerebellar CSF indices (with and without surrounding CSF). RESULTS: Statistical analyses indicated a significantly lower relative cerebellar size (P < .001) and a larger relative cerebellar CSF space (P < .001) in dogs with cerebellar cortical degeneration. The measurement of relative cerebellar size could distinguish between affected and nonaffected dogs with a sensitivity and a specificity of 93 and 94%, respectively, using a cut-off of 13.3%. Using a cut-off of 12.8%, the measurement of relative CSF space could distinguish between both groups with a sensitivity of 93% and a specificity of 100%. There was a significant difference in 1 of the 2 CSF indices between affected and normal dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: Relative cerebellar size and relative CSF space calculated from MRI are effective in American Staffordshire Terriers to differentiate between normal animals and those with cerebellar cortical degeneration.     

Cerebellar cortical degeneration in an American Staffordshire terrier

Most diseases affecting the cerebellum are congenital and three groups can be distinguished on pathogenetic grounds. In the first group, diseases are caused by intrauterine or neonatal viral infections, in the second group by malformations of genetic or unknown origin, and in the third group by degenerative disease, or abiotrophies. Familial late-onset cerebellar abiotrophy has been reported in the Gordon Setter the Old English Sheepdog, the Brittany Spaniel and more recently the American Staffordshire Terrier. This case report describes the clinical, diagnostic and pathological changes in an American Staffordshire Terrier with cerebellar cortical degeneration. This is the first case diagnosed in the Netherlands.     

Late onset cerebellar cortical degeneration in a koala

A 10-year-old male koala started to fall from the tree while sleeping. Subsequently, the koala often fell down while walking and showed a gait abnormality, abnormal nystagmus and hypersalivation. At 12 years of age, the koala became ataxic and seemed blind. At 13 years of age, the koala exhibited signs of dysstasia and was euthanased. Necropsy revealed marked symmetrical atrophy of the cerebellum. Histopathologically, a severe loss of Purkinje and granule cells was evident in the cerebellum, while the molecular layer was more cellular than normal with cells resembling small neurons, which were positively stained with parvalbumin immunohistochemistry. Reactive Bergmann glial cells (astrocytes) were present adjacent to the depleted Purkinje cell zone. The very late onset and slow progression of the cerebellar cortical degeneration in this case is particularly interesting and appears to be the first report in the koala.     

Diagnosis of laryngeal dysplasia in five horses using magnetic resonance imaging and ultrasonography

Reasons for performing study: Laryngeal dysplasia due to suspected maldevelopment of the fourth branchial arch has been reported previously in the horse and has been associated with rostral displacement of the palatopharyngeal arch and/or right laryngeal dysfunction. These studies all described the endoscopic and/or anatomical post mortem identification of the disease, but ultrasonography or magnetic resonance imaging (MRI) of this disease have not been described. Hypothesis: MRI and ultrasound findings accurately reflect the anatomical features of presumptive fourth branchial arch abnormality and allow accurate ante mortem diagnosis of this condition and, therefore, appropriate management. Methods: Between February 2008 and January 2009, all horses examined at Rood and Riddle Equine Hospital diagnosed with rostral displacement of the palatopharyngeal arch and/or right laryngeal dysfunction using upper airway endoscopy (n = 5) underwent ultrasonography and MRI of the laryngeal region. Results: All 5 horses that met the inclusion criteria were identified and all underwent laryngeal MRI and ultrasound examinations. Features consistent with laryngeal dysplasia, including lack of the cricothyroid articulation, dorsal extension of the thyroid cartilage lamina, and absence or hypoplasia of the cricopharyngeus muscle, were seen in all cases using both types of imaging. Conclusions and potential relevance: MRI and ultrasonography permit definitive premortem diagnosis of laryngeal dysplasia. Upper airway abnormalities identified using endoscopy can be more fully characterised using MRI and ultrasonography allowing more appropriate recommendations to be made. Preoperative imaging may also prevent inappropriate surgical intervention.     

Cerebellar degeneration in a mature Staffordshire terrier

A 5-year-old Staffordshire terrier exhibited slowly progressive signs of cerebellar disease, including nystagmus and dysmetria. After a 30-month course, the dog was euthanized. Grossly, the cerebellum was small and comprised only 5% of the brain weight. Histopathological examination of the brain documented diffuse degeneration. Purkinje cells were most depleted, but granular cells and the molecular layer of cerebellum were also depleted. The history and necropsy examination were evidence of late-onset primary cerebellar degeneration.     

Multisystemic chromatolytic neuronal degeneration in a Cairn terrier pup

In a four-month-old female Cairn terrier with mild episodic paraparesis, a multisystemic chromatolytic degeneration affected widespread neuronal populations in the brain and spinal cord as well as spinal, autonomic, and enteric ganglia. There was little axon degeneration or cell body loss, and the latter findings may explain the mild clinical signs. Among affected perikarya the extent and distribution of chromatolysis varied. While peripheral lysis of Nissl substance occurred often in spinal motoneurons, central chromatolysis was frequent in brain stem nuclei, and patchy Nissl loss appeared in some neurons including those in the cerebral cortex and spinal dorsal horns. Although prior studies of various chromatolytic neurodegenerations often have demonstrated characteristic massings of neurofilaments, the major, and invariable ultrastructural finding in this study was dispersion and loss of ribosomes. Neurofilamentous accumulations were observed less consistently. The clinical and pathologic findings in this pup were compared and constrasted with those made in prior studies of chromatolytic neurodegenerations.     

Diagnosis of suspected hypovitaminosis A using magnetic resonance imaging in African lions (Panthera leo)

Vitamin A deficiency is described in captive lions. Ante mortem diagnosis can either be made by serum analysis or liver biopsy, both of which may be problematic. This study utilised magnetic resonance imaging to identify vitamin A deficiency in lions with relatively mild clinical signs, which could otherwise be attributed to numerous other neurological conditions. Magnetic resonance imaging is a non-invasive, reliable diagnostic tool to demonstrate pathology typically associated with this condition. To accommodate varying lion ages and sizes, a number of cranium and brain measurements were compared with that of the maximum diameter of the occular vitreous humor. Occular ratios of the tentorium cerebelli osseum and occipital bone were most reliable in diagnosing the thickened osseous structures characteristic of hypovitaminosis A. The ratio of maximum:minimum dorsoventral diameter of the C1 spinal cord was also of value.     

Adult-onset cerebellar cortical abiotrophy and retinal degeneration in a domestic shorthair cat.

A 4-year-old, neutered male domestic shorthair cat presented for evaluation of ataxia and visual deficits. Neurological examination revealed severe cerebellar ataxia with symmetrical hypermetria and spasticity, a coarse whole-body tremor, positional vertical nystagmus, and frequent loss of balance. A menace response was absent bilaterally, and the pupils were widely dilated in room light. A funduscopic examination revealed markedly attenuated to absent retinal vessels and pronounced tapetal hyperreflectivity, findings consistent with end-stage retinal degeneration. Blood work evaluation included retroviral testing, a complete blood count, serum biochemistry analysis, taurine levels, and toxoplasma immunoglobulin G and immunoglobulin M titers. All were within reference ranges. The patient was euthanized, and a necropsy was performed. Microscopically, lesions of the nervous system were confined to the cerebellum and were consistent with cerebellar cortical abiotrophy. Selective photoreceptor degeneration was seen on histopathological examination of the retina with a reduction in the number of rods and cones. The combination of clinical findings and histopathological lesions seen here has not been previously reported in the cat.     

Angiostrongylus vasorum infection in a Scottish terrier associated with gastric dilation

A case of Angiostrongylus vasorum infection in an eight-month-old Scottish terrier associated with gastric dilation is reported,     

Conventional and functional magnetic resonance imaging features of late subacute cortical laminar necrosis in a dog

Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1‐weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3‐year‐old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three‐Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2‐weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W‐hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion‐weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia‐related brain hypoxia. Three‐Tesla MRI enabled identification of the laminar pattern of the cortical lesions.     

Verminous pneumonia due to Filaroides hirthi in a Scottish terrier in Spain

A previously healthy Scottish terrier developed verminous pneumonia due to Filaroides hirthi. The disease was diagnosed on the basis of cytology of a transtracheal wash, which contained 17 per cent eosinophils and a large number of parasite larvae. Treatment with 50 mg/kg bodyweight fenbendazole daily for three weeks eliminated the parasites and improved the clinical condition of the dog.     

Myeloencephalopathy with eosinophilic refractile bodies (Rosenthal fibers) in a Scottish terrier

Myeloencephalopathy with diffuse Rosenthal fiber formation (Alexander's disease) was detected in a 9-month-old Scottish Terrier with progressive tetraparesis. Additional abnormalities included an electroencephalogram characteristic of an encephalopathy and a narrowed intervertebral disk space at C2-3. The diagnosis of Alexander's disease is uncommon in human and veterinary medicine. Results from this case and previous reports suggest that this disease in the dog may have a congenital or genetic basis.