Cognitive dysfunction syndrome
Cognitive dysfunction syndrome (CDS) is a neurobehavioural syndrome affecting older dogs characterized by neurological changes.
This syndrome umbrellas a wide range of under-diagnosed cognitive deficits associated with the aging brain including learning deficits or degeneration, loss of memory and spatial awareness, aimless or changes in behaviour, loss of curiosity directed toward novel stimuli, inappropriate incontinence and sleep irregularities.
Cognitive dysfunction is exacerbated in dogs with concurrent hypothyroidism, hyperlipidemia, hypercholesterolemia and/or atherosclerosis which collectively result in microvascular ischemia, increased viscosity and hypercoagulability, with subsequent greater risk of thromboembolism.
Each dog with cognitive dysfunction has unique clinical presenting signs (designer disease) but common underlying neuropathology. Although the rate of onset and severity are individual within each dog, once cognitive decline begins it is generally a progressively predictable disorder.
CDS is a degenerative process of beta-amyloid plaque deposition within the basal forebrain (parietal cortex and hippocampus), with subsequent loss of cholinergic system activity (increased sensitivity to scopolamine impairment and decreased muscarinic receptor density) and coordination, similar to what is seen with Alzheimer's disease in humans.
The plaque deposition (akin to canine amyloidosis) is primarily due to inflammatory deposition of Aβ1-42 and Aβ42/40 amyloid protein in the parietal cortex and hippocampus of aged dogs, resulting in neuronal dysfunction. The underlying causes of oxidative stress which leads to neuronal amyloidosis are manifold, including chronic exposure to environmental pollutants, dietary chemicals and other, often unrelated, chronic inflammatory diseases.
The consequences of these neuropathic changes include thickening and calcification of the meninges, decreased cerebral blood flow and glucose utilization, reduced frontal lobe volume and demyelination of neurones and glial cells, leading to overt neurological and behavioral changes which can be observed clinically.
Typical clinical signs include anxiety, confusion, disorientation, reduced activity, changes to sleep patterns, loss of appetite (despite any obvious underlying disease process), inappropriate elimination, inappropriate vocalization, forgetting familiar people in the dog's home. A canine cognitive rating scale is often employed to assess canine patients clinically.
A ready reckoner is also available online to assist in individual cases.
Diagnosis of CDS is based on presenting clinical size, age of dog and breed, and elimination of any underlying metabolic disease, neoplastic or musculoskeletal disease that may be attributed to the symptoms.
The physical size of the dog (referable to breed) is not a reliable indicator of disease onset, although there is a suggestion that brain pathology, including the age of onset and extent may vary across breeds.
In humans, the use of statins to lower blood cholesterol has shown increased cognitive function in the early stages of Alzheimer disease and this has been mirrored in canine models, emphasizing the importance of minimizing cerebral amyloidosis as a preventative measure against age-related cognitive disorders. However, in geriatric dogs with existing amyloid plaques, statins and statin-immunotherapy have been shown to decrease cognitive function and although they do reduce circulating cholesterol in dogs, may not play an important role in management of this disease in dogs
Nutritional supplementation is an important aspect of management of this condition, as it is with other age-onset diseases (e.g. obesity, arthritis). The use of antioxidants (vitamins E and C, fruits and vegetables), mitochondrial cofactors (e.g. Co-Q10, S-adenosylmethionine, lipoic acid and carnitine) and nutriceuticals such as pyridoxine, Ginkgo biloba and vitamin E have been shown to significantly improve cognitive function in aged dogs.
Pharmacotherapy with ergot-drivative drugs such as selegiline, and possibly nicergoline, have shown anecdotal benefits in clinical settings and should be considered as an adjunct therapy in advanced clinical cases.
Quality of life is essential in the treatment and maintenance of this generally progressive disease, and compassion must be directed to a dog which is neurologically challenged but often strongly bonded to its owner(s) and lifestyle.
Euthanasia is not recommended unless other disease(s) accompany this condition and consequently result in rapidly diminishing, poor or absent quality of life parameters.
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