Björn Karlsson avlade akademisk avhandling 970321 vid samhällsvetenskapliga fakulteten vid Lunds Universitet. Han berör i sin litteraturgenomgång en viktig fråga. Följande är inscannat från hans ramberättelse. Den är läsvärd.

A number of cross-sectional studies have shown neuropsychological impairment in adult IDDM patients compared with non-diabetic control subjects, although the magnitude of the impairemnt has generally been found to be only mild to moderate, also when compared with test norms. In addition, there is a certain inconsistency of different studies with respect to whether or not IDDM show impairment on specific cognitive functions or cognitive tasks. Impairment gave been found for most cognitive domains, such as lowered performance IQ, and in impairments in such measures as those of learning abilities and memory, psychomotor speed and mental flexibility, spatial information processing and problem solving and abstract reasoning. The functions most usually found to be impaired in type 1 diabetic patients are psychomotor efficiency and mental flexibility, such as measured by the Tactual Performance Test, Grooved Pegboard and by Digit Vigilance.

Cerebral effects at an electropgysiological and a structural level
In addition to these emperical findings, there are indications of cerebral effects at an electrophysiological and a structural level in diabetic patients, providing good reasons to believe that cognitive impairment can occur in IDDM. Electrophysiologically, an increase in P300 wave latency, refelcting information processing speed and associated with attention and short-term memory, has been demonstrated in IDDM patients. Also, in examing brain stem auditory evoked potentials in IDDM patients, a measure of the efficiency of nerve conduction, showed there to be aconduction delay combined with a reduced responsivity in the central nervous system in these patients. It was suggested that such alterations be termed "central diabetic neuropathy". The alterations were not related to clinical symtoms of peripheral neuropathy but to subclinical measures of peripheral conduction velocity. Later Ryan et al showed psychomotor slowing to be predicted by peripheral neurpathy, suggested as being a marker for central neuropathy, although functional relationship between the two is unclear.

"Diabetic encephalopathy"
In a structural sense, the degeneration of grey and white matter are among the changes that have been described. More severe changes of this sort has given rise to the term "diabetic encephalopathy", a concept which has later been supported by magentic-resonance findings of abnormal plaques in long-term diabetic patients with peripheral neuropathy and microangiopathy.

The risk of hypo- and hyperglycaemia
For adults, the major risk factors for the occurence of more dnuring cognitive deficits that have been focused upon are hypoglycaemia and hyperglycaemia, as well as late diabetic complications associated with the latter, such as retinopathy and peripheral neuropathy. Poor metabolic control increases the risk of changes in the small blood vessels (microangiopathy), which is common in diabetes and is a risk factor for the development of all the late diabetic complications. Macrovascular diseases, including cerebral macrovascular disorders, are more commin in diabetic patients than in the general population, and may be a cause of cognitive impairment. Another major risk factor that has been examined in regard to the aetiology of cognitive impairment is that of recurrent severe hypoglycaemic episodes, such episodes tending to increase when metabolic control is improved. In experimentally induced hypoglycaemia, transient disruptions of cogntive functioning, as measured both neurophysiologically and neurophycologically, have been demonstrated in both diabetic and non-diabetic patients. Neuropathological studies have demonstrated hypoglycaemia-associated damage in the cortex, the basal ganglia and the hippocampus. Various cross-sectional studies have shown cognitive impairemnt in patients with a history of repeated episodes of sever hypoglycaemia, whereas two recent prospective longitudinal studies were unable to demonstrate any cogntiive detoriation when intensified insulin treatment produced an increased frequency of hypoglycaemic episodes. Thus, there is remaining controversy concerning the enduring effects of hypoglyaemia.

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Red DiabetologNytt 970227