Midori Okada

Magnetic resonance imaging features and clinical signs associated with presumptive and confirmed progressive myelomalacia in dogs: 12 cases (1997-2008).

OBJECTIVE To characterize clinical signs and findings from magnetic resonance imaging (MRI) and CSF analysis for dogs with progressive myelomalacia (PM) diagnosed on the basis of clinical and histologic features. DESIGN Retrospective case series. ANIMALS 5 dogs with confirmed PM and 7 with presumptive PM evaluated from 1997 through 2008. PROCEDURES Medical records of study dogs were reviewed, and clinical signs and MRI and CSF findings were evaluated. A clinical diagnosis of PM was made on the basis of detection of disk-associated spinal cord compression via MRI and progression of clinical signs from initial paraparesis or paraplegia to thoracic limb lower motor neuron paresis to tetraplegia associated with cranial migration of the extent of cutaneous trunci reflex extinction and analgesia, terminating in death due to respiratory paralysis. RESULTS All dogs were paraplegic and had signs of lower motor neuron lesions. As revealed by MRI of the vertebral column, the length of abnormal signal intensity was more than 6-fold, compared with the body length of L2. In some dogs, these abnormal MRI findings were observed before PM was clinically diagnosed. The CSF examination revealed hemorrhagic xanthochromia. CONCLUSIONS AND CLINICAL RELEVANCE A hyperintense region of the spinal cord > 6 times the length of L2 on T2-weighted imaging might be a characteristic MRI finding of PM. In some dogs, such MRI findings were observed before PM was clinically diagnosed. Progressive myelomalacia may thus be diagnosable at the early stage through MRI and CSF examination before signs of PM develop.

Diagnosis of olfactory neuroblastoma in a dog by magnetic resonance imaging

FIG 1: Olfactory neuroblastoma in a dog, showing isointensity on (a) a T1-weighted (TR 350 TE 15 FA 90 NEX 2·5) dorsal image (arrow), and (b) a T2-weighted (TR 4000 TE 120 FA 90 NEX 2·5) dorsal image (arrow). (c) The tumour is enhanced by the contrast medium gadoteridol (arrow). (d) The cyst compressing the frontal lobe can be seen caudal to the tumour; on the contrast T1-weighted parasaggital image, the tumour can be seen extending into the intracranial cavity (a) (b)

Identification of ventrolateral intramedullary intervertebral disc herniation in a dog

A 10-year-old male cross-breed dog was brought to Nihon University Animal Hospital with a history of acute onset of paralysis in the pelvic limbs 13 days previously. Magnetic resonance imaging revealed an intramedullary linear tract in the spinal cord at the thoracic vertebrae 12-13 region, which appeared hyperintense on T2-weighted images, but was hypointense and isointense on T1-weighted images when compared with normal parenchyma of the spinal cord. A hemilaminectomy was performed and a blob of what appeared to be fibrous tissue was found adhering to the surface of the dura mater. The diameter of the blob was about 4 mm. A durotomy was performed over the affected area and chondroid material was found within the spinal cord. Material from the nucleus pulposus penetrated the dura mater from the ventral aspect of the spinal cord in previously reported intramedullary intervertebral disc herniation cases, but, in this case, penetration occurred from the left ventrolateral aspect and progressed through to the right lateral aspect, forming a visible blob of what appeared to be fibrous tissue on the surface of the dura mater at the exit point. To the best of our knowledge, this was the first case report of an intramedullary intervertebral disc herniation originating from the ventrolateral aspect of the spinal cord in a dog.

Dystrophin-deficient muscular dystrophy in an Alaskan malamute

DYSTROPHIN-deficient muscular dystrophy is an X-linked inherited degenerative myopathy. It is the most common form of muscular dystrophy seen in dogs, and is similar to that termed Duchennes muscular dystrophy in human medicine (Shelton and Engvall 2002, Schatzberg and Shelton 2004). Dystrophin-deficient muscular dystrophy has been reported in several breeds, summarised in Table 1 (Shelton and Engvall 2002, Schatzberg and Shelton 2004, Wieczorek and others 2006, Baltzer and others 2007, Klarenbeek and others 2007, Walmsley and others 2010). This short communication reports a confirmed case of dystrophin-deficient muscular dystrophy in an Alaskan malamute, which has only previously been suspected in this breed (Cardinet and Holliday 1979). View this table: Table 1 Breeds of dog confirmed to be affected by dystrophin-deficient muscular dystrophy A four-month-old, 12.9 kg, intact male Alaskan malamute was presented to the Animal Medical Center at Nihon University with a one-month history of anorexia, excessive salivation, exercise intolerance, dysphagia and impaired growth. In addition to these clinical signs, the owner had also observed abnormal movement of the tongue and difficulty when drinking water. The owner reported no deficits in mentation or in behaviour, learning or house training compared with its littermates. Rectal temperature was slightly elevated (39.9°C). Physical examination revealed hypertrophy of the tongue and laryngopharyngeal muscles, but other muscles appeared relatively unaffected and without pain on palpation. Postural reactions and spinal reflexes were normal, but the swallowing reflex was poor and abnormal movement of the tongue was also apparent. In addition, there was a reduced menace reaction with normal palpebral reflex and nasal sensation. Complete blood count was unremarkable but serum biochemistry indicated elevated creatine kinase (CK) activity …