To the Editor:
I read with great interest the study by Hyllienmark et al. [1] on the risk factors for EEG abnormalities in adolescents with type 1 diabetes. Recurrent severe hypoglycaemia and poor metabolic control contribute to EEG abnormalities characterised by an increase in slow activity (delta and theta) and a reduction in alpha peak frequency.
We reported similar results 26 years ago [2], even though the methods we used were simplistic in comparison with those employed by Hyllienmark et al. We found that the incidence of abnormal EEGs was higher in patients with poor metabolic control. Moreover, using fluorescein angiography, which has high sensitivity, we demonstrated a clear correlation between incipient retinal angiopathy and EEG abnormalities. Eighty percent of our patients who experienced more than five severe hypoglycaemic attacks showed evidence of abnormal EEG. On the other hand, minor hypoglycaemic episodes had no effect on the EEG. The EEG abnormalities were classified as diffuse or focal. Paroxysmal sharp waves, spikes and spike-and-wave forms, as well as bursts of slow wave activity (theta or delta), were regarded as paroxysmal. Among the abnormal EEG patterns, six were diffuse (non-rhythmic, slowing) and nine were paroxysmal (spike-and-wave in five, spikes in one, sharp waves in one, and bursts of delta waves in two). There were no focal abnormalities.
These EEG abnormalities are not necessarily related to cognitive dysfunction or impaired intellectual development in children and adolescents. Schoenle et al. [3] showed that long-term bad glycaemic control, rather than hypoglycaemic attacks, is a risk factor for impaired intellectual development. According to the DCCT [4], to avoid long-term complications, patients with type 1 diabetes must maintain blood glucose concentrations close to the normal range; this increases their risk of severe hypoglycaemia, but without changes in neurophysiological function. Thus, fear of hypoglycaemic attacks is not a good argument to stay in a bad metabolic control, even in children. Moreover, the Hvidore Study Group on Childhood Diabetes has shown that some centres are more successful than others at preventing severe hypoglycaemia, independent of the prevailing average HbA1c level at the respective centre [5]. We have reported that in 144 unselected diabetic children and adolescents aged <18 years, with a mean HbA1c level of 6.6% (upper normal limit: 5.5%) [6], the yearly incidence of severe hypoglycaemia was 0.2, which is three times less than in the intensive-therapy group of the DCCT [3].
References
Hyllienmark L, Maltez J, Dandenell A, Ludvigsson J, Brismar T (2005) EEG abnormalities with and without relation to severe hypoglycaemia in adolescents with type 1 diabetes. Diabetologia 48:412–419
Haumont D, Dorchy H, Pelc S (1979) EEG abnormalities in diabetic children. Influence of hypoglycemia and vascular complications. Clin Pediatr 18:750–753
Schoenle EJ, Schoenle D, Molinari L, Largo RH (2002) Impaired intellectual development in children with type 1 diabetes: association with HbA1c, age at diagnosis and sex. Diabetologia 45:108–114
The Diabetes Control and Complications Trial Research Group (1993) The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 329:977–986
Danne T, Mortensen HB, Hougaard P et al. For the Hvidore Study Group on Childhood Diabetes (2001) Persistent differences among centers over 3 years in glycemic control and hypoglycemia in a study of 3,805 children and adolescents with type 1 diabetes from the Hvidore Study Group. Diabetes Care 24:1342–1347
Dorchy H, Roggemans M-P, Willems D (1997) Glycated haemoglobin and related factors in diabetic children and adolescents under 18 years of age: a Belgian experience. Diabetes Care 20:2–6
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Dorchy, H. Comment. Diabetologia 48, 2191–2192 (2005). https://doi.org/10.1007/s00125-005-1898-9
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DOI: https://doi.org/10.1007/s00125-005-1898-9