Syringohydromyelia secondary to foramen magnum overcrowding is described in seven Cavalier King Charles spaniels. Clinical signs were consistent with a central spinal cord lesion. The most common signs were persistent scratching at the shoulder region with apparent neck, thoracic limb, or ear pain and thoracic limb lower motor neuron deficits. The diagnosis was made by magnetic resonance imaging. The syringohydromyelia is postulated to be a consequence of an occipital bone malformation resulting in a small caudal fossa and cerebellar herniation. Clinical signs improved but did not completely resolve when the dogs received treatment with corticosteroids or nonsteroidal anti-inflammatory drugs.

Our model shows that a change in intervertebral disc cell phenotype correlates with the grade of disc degeneration and that the notochordal cells synthesize proteoglycans, which exhibit delayed aggregation than those synthesized by the small nucleus pulposus cells. This implies that the cell type composition of the nucleus pulposus of the chondrodystrophoid and nonchondrodystrophoid dogs produces an extracellular matrix that is assembled in a distinct manner, which may affect tissue integrity.

To describe the signs that may be associated with intracranial inflammatory conditions, magnetic resonance (MR) images of 25 dogs that had inflammatory cerebrospinal fluid (CSF) were mixed with those of a control group of 40 dogs that had CSF negative for inflammatory disease and reviewed without knowledge of the clinical signs or diagnosis. CSF was considered inflammatory if the protein level was > 0.25 g/l and the white cell count was > 5 mm(-3). Abnormalities were found by MR imaging in 19 (76%) dogs with inflammatory CSF. Two dogs had focal lesions, 10 had multifocal lesions, and seven had diffuse lesions. Lesions affected all divisions of the brain. Mass effect was identified in seven (28%) dogs, including one that had a choroid plexus carcinoma. Lesions were hyperintense in T2-weighted images in 18 dogs and hypointense in T1-weighted images in six dogs. Multifocal or diffuse intraaxial lesions that were hyperintense in T2-weighted images were observed in 17 (68%) dogs with inflammatory CSF. Administration of gadolinium resulted in enhancement of intraaxial lesions in nine (36%) dogs and enhancement of meninges in seven (28%) dogs. Six (24%) dogs with inflammatory CSF had images interpreted as normal.