Complications Cerebral Dysfunction In

Cerebral abnormalities may occur in the setting of hyperglycemia and ketoacidosis. When compared to those with T1DM and normoglycemia, patients with diabetic ketoacidosis demonstrate increased levels of tryptophan and 5-hydroxyindoleacetic acid in the cerebrospinal fluid (CSF) (21). Plasma tyrosine and CSF tyrosine and homovanillic acid concentrations are typically normal. Similar findings are demonstrated in those with uremia and hepatic encephalopathy, as well as in rodents with diabetes and DKA secondary to streptozotocin administration. Magnetic resonance (MR) spec-troscopy studies in children with DKA have demonstrated possible neuronal injury and/or dysfunction. In one study, 29 children underwent MR spectroscopy and were evaluated with brain ratios of N-acetylaspartate (NAA) to creatinine (Cr) during therapy and after recovery from DKA (22). NAA/Cr levels were significantly lower during DKA therapy in the basal ganglia suggesting compromised neuronal function.

In the presence of DKA, confusion and headache may occur. Patients with new or pre-existing T1DM and acute ketoacidosis may have abnormal electroencephalograms (EEG). In a study of 39 patients aged from 11 months to 16 years who underwent serial EEGs at 1, 12, 24 h, and 5 days after initiation of treatment for DKA, 30 patients were found to have abnormal studies initially (23). EEG severity correlated with serum glucose, osmolality, bicarbonate, ^-hydroxybutyrate and acetoacetate levels, but did not correlate with pH and glycosylated hemoglobin. Abnormal EEG findings were resolved in 20 of 30 patients in 5 days. EEGs were repeated 2-5 months after treatment; five of seven patients undergoing repeat EEG had persistent abnormalities despite DKA resolution.

Neuropsychological testing profiles have yielded mixed results in patients with diabetes with and without DKA. In one study, chronically elevated glucose without ketoacidosis portended negative changes in neuropsycho-logical profiles (24). While a second study found no correlation between negative neuropsychological profiles and variables such as age at diabetes onset, poor chronic control, or major metabolic crises such as hypoglycemia and ketoacidosis (25).

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