Clinical Approach To Complaints Of Cognitive Dysfunction In Diabetic Patients

The data that are reviewed in this chapter clearly show that diabetes is associated with changes in cerebral function and structure. However, it should be noted that the diagnosis "diabetic encephalopathy" cannot be readily established in individual patients. This is because of the fact that the changes in cognition and in brain structure, as observed on computed tomography or MRI, are not specific to diabetes. There is, for example, considerable overlap with functional and structural changes in the brain that occur with brain ageing, or cerebral changes that occur in association with other vascular risk factors such as hypertension. Because clinically significant cognitive impairments mainly occur in elderly diabetic patients it will be evident that it is difficult to distinguish between the effects of diabetes, ageing, and comorbidity. However, this should not lead to a nihilistic diagnostic approach. The main task of the clinician who is faced with a diabetic patient with cognitive complaints is to assess the severity and nature of the cognitive impairments, to try and classify these impairments and to exclude other (potentially treatable) causes of cognitive deterioration. The next paragraph serves as an illustration of a possible diagnostic approach.

A full disease history should be obtained, focussing on the cognitive and behavioral changes in the patient, their evolution over time, and symptoms suggestive of other medical, neurological, or psychiatric illnesses. The possibility of depression should be considered, as depression may manifest itself primarily in complaints of concentration and/or memory disturbances, particularly in the elderly. Attention should be paid to the assessment of the impact of changes in cognition on day-to-day functioning (for example: problems with such activities as cooking, shopping, managing ones financial affairs, progressive dependence on spouse, social withdrawal, problems with self care, and medication use). Helpful screening lists have been developed to this end (105). Information on the presence of other diabetic complications and vascular risk factors, including blood pressure, is required. Prescription and nonprescription drugs, in particular analgesic, anticholinergic, antihypertensive, psychotropic, and sedative-hypnotic agents, should be reviewed carefully as potential causes of cognitive impairment. Alcohol use should be assessed. Laboratory tests can include a blood count, tests of liver, kidney and thyroid function, vitamin B12 levels, HbA1, and blood lipids. Brain imaging can be used to detect structural lesions (for example, infarction, neoplasm, sub-dural haematoma, and hydrocephalus), but can also contribute to the classification of dementia syndromes in their early stages (62). A neuropsychological examination can help to qualify and quantify the cognitive disturbances, and can help to differentiate between early dementia and depression.

As has been stated in the previous section of this chapter, there are no specific treatments with proven efficacy in preventing cognitive decline in diabetic patients. Still, analogous to the prevention of other diabetic complications, the maintenance of adequate glycemic control while avoiding hypoglycemia, and the treatment of vascular risk factors, appear to be the main targets for the prevention of end-organ damage to the brain.

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