CEREBRAL AMYLOID ANGIOPATHY-RELATED INFLAMMATION PRESENTING WITH A STROKE-LIKE EPISODE.

Cerebral amyloid angiopathy (CAA) is characterised by ß-amyloid deposition in the walls of small to medium sized arteries of the cerebral cortex and the leptomeninges. In a significant proportion of patients, CAA is the probable cause of non-traumatic primary cerebral haemorrhage, particularly in those who are over 55 years of age and have controlled blood pressure. Cerebral amyloid angiopathy-related inflammation (CAA-ri) is an uncommon and aggressive subtype of CAA, which is thought to be caused by an immune reaction to the deposits of ß-amyloid. It has a variety of presentations that can mimic other focal and diffuse neurological disorders. Radiographically, its classic presentation is asymmetric cortical or subcortical white matter hyperintense foci due to multiple microhaemorrhages on T2-weighted or fluid attenuated inversion recovery (FLAIR) images. Although definite diagnosis requires brain and leptomeningeal biopsy, diagnostic criteria for probable CAA-ri based on a combination of clinical and radiological features were validated in 2015. We describe a patient with probable CAA-ri mimicking stroke and review the clinical and radiological features important for a proper differential diagnosis between ischaemic stroke (IS) and CAA-ri, and its subsequent appropriate treatment. LEARNING POINTS: MRI is a crucial tool for the diagnostic evaluation of cerebral amyloid angiopathy-related inflammation (CAA-ri).A high index of suspicion and awareness of CAA-ri is necessary for correct diagnosis in stroke-like presentations of the condition.The treatment of choice for CAA-ri is empirical corticosteroid therapy, which is associated with clinical and radiological improvement.

Emerging insights into the genetic basis of canine hip dysplasia.

Canine hip dysplasia (CHD) is the most common inherited polygenic orthopedic trait in dogs with the phenotype influenced also by environmental factors. This trait was described in the dog in 1935 and leads to a debilitating secondary hip osteoarthritis. The diagnosis is confirmed radiographically by evaluating signs of degenerative joint disease, incongruence, and/or passive hip joint laxity. There is no ideal medical or surgical treatment so prevention based on controlled breeding is the optimal approach. The definitive CHD diagnosis based on radiographic examination involves the exposure to ionizing radiation under general anesthesia or heavy sedation but the image does not reveal the underlying genetic quality of the dog. Phenotypic expression of CHD is modified by environmental factors and dogs with a normal phenotype can be carriers of some mutations and transmit these genes to their offspring. Programs based on selection of dogs with better individual phenotypes for breeding are effective when strictly applied but remain inferior to the selection of dogs based on estimation of breeding values. Molecular studies for dissecting the genetic basis of CHD are ongoing, but progress has been slow. In the future, the recommended method to improve hip quality in controlled breeding schemes, which will allow higher selection pressure, would be based on the estimation of the genomic breeding value. Since 2012, a commercial DNA test has been available for Labrador Retrievers using a blood sample and provides a probability for development of CHD but we await evidence that this test reduces the incidence or severity of CHD.