The symptoms of hypoglycaemia are fundamental to the early detection and treatment of this side-effect of insulin and oral hypoglycaemic therapy in people with diabetes. The physiology of normal responses to hypoglycaemia is described and the importance of symptoms of hypoglycaemia is discussed in relation to the treatment of diabetes. The symptoms of hypoglycaemia are described in detail. The classification of symptoms is considered and the usefulness of autonomic and neuroglycopenic symptoms for detecting hypoglycaemia is discussed. The many external and internal factors involved in the perception of symptoms are reviewed, and symptoms of hypoglycaemia experienced by people with Type 2 diabetes are addressed. Age-specific differences in the symptoms of hypoglycaemia have been identified, and are important for clinical and research practice, particularly with respect to the development of acquired hypoglycaemia syndromes in people with Type 1 diabetes that can result in impaired awareness of hypoglycaemia. In addition, the routine assessment of hypoglycaemia symptoms in the diabetic clinic is emphasized as an important part of the regular review of people with diabetes who are treated with insulin.

OBJECTIVE -To examine the effects of acute insulin-induced hypoglycemia on short-term, delayed, and working memory in individuals with type 1 diabetes. RESEARCH DESIGN AND METHODS-A hyperinsulinemic glucose clamp was used to maintain arterialized blood glucose level at either 4.5 mmol/l (euglycemia) or 2.5 mmol/l (hypoglycemia) on two separate occasions in 16 adults with type 1 diabetes. The participants completed tests of immediate and delayed verbal memory, immediate and delayed visual memory, and working memory during each experimental condition. Two other mental tests, the Trail Making B Test and the Digit Symbol Test, were also administered.RESULTS -Performance in tests of immediate verbal and immediate visual memory was significantly impaired during hypoglycemia. The effect of hypoglycemia on working memory and delayed memory was more profound. Performance in the nonmemory tests, the Trail Making B Test, and the Digit Symbol Test also deteriorated during hypoglycemia.CONCLUSIONS -All of the memory systems examined in the present study were affected significantly by acute hypoglycemia, particularly working memory and delayed memory. Mild (self-treated) hypoglycemia is common in individuals with insulin-treated diabetes; therefore, these observed effects of hypoglycemia on memory are of potential clinical importance because they could interfere with many everyday activities.

OBJECTIVE -Experimentally induced hypoglycemia in humans causes progressive but reversible cognitive dysfunction, but it is not known to what extent neuropsychological tests index abilities of cognitive functioning that are important in everyday life. This study examines the effects of acute insulin-induced hypoglycemia on attention and intelligence in nondiabetic humans. RESULTS -Hypoglycemia induced a significant deterioration in tests sensitive to both visual and auditory selective attention. During hypoglycemia, attentional flexibility deteriorated and speed of information processing was delayed. Sustained attention was preserved and intelligence scores did not deteriorate during hypoglycemia. RESEARCH DESIGN AND METHODSCONCLUSIONS -During hypoglycemia, a significant deterioration occurs in attentional abilities, whereas fluid intelligence is preserved. On the basis of these results, it can be surmised that many complex attention tasks relevant to everyday life are impaired during moderate hypoglycemia.

The effects of acute insulin-induced hypoglycemia on short-term, delayed, and working memory were examined in healthy adults. A hyperinsulinemic glucose clamp was used to maintain arterialized blood glucose at either 4.5 (euglycemia) or 2.5 (hypoglycemia) mmol/L on 2 separate occasions in 16 healthy volunteers. Tests of immediate and delayed verbal memory, immediate and delayed visual memory, and working memory were administered during each experimental condition. All memory systems were impaired during acute hypoglycemia, with working memory and delayed memory being particularly susceptible. These findings are informative concerning the metabolic basis of adequate memory function and are of practical importance to people with insulin-treated diabetes, in whom hypoglycemia is common.

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A 42 year old man presented with glutenresponsive coeliac disease and secondary pancreatic insuYciency. Subsequently his symptoms relapsed and repeat small intestinal biopsy showed villous atrophy and infiltration by leukaemic cells, despite continuation of a gluten-free diet. Serious causes of relapse and non-responsiveness in coeliac disease include enteropathyassociated T-cell lymphoma, ulcerative jejunitis and an end-stage hypoplastic mucosa. This is the first report of nonresponsiveness due to infiltration by leukaemia. (Postgrad Med J 2000;76:227-229) Keywords: coeliac disease; villous atrophy; gluten sensitivity; leukaemia Most patients with coeliac disease respond satisfactorily to a gluten-free diet. A small number fail to respond, either initially or after a period of treatment. There are many causes for this. [1][2][3] In such a situation the diagnosis should be carefully reviewed and a search made for serious causes of the non-responsiveness. Case reportA 42 year old man presented with a 6-month history of severe watery diarrhoea, dehydration and weight loss of 6.4 kg. He had previously been well, although had always had loose stools since childhood. Investigation revealed a macrocytic anaemia with a low serum folate, and subtotal villous atrophy on duodenal biopsy (figure, A). Coeliac disease was diagnosed and a gluten-free diet (GFD) was started.Seven months later a repeat duodenal biopsy showed significant histological improvement (figure, B), suggesting mucosal glutenresponsiveness and supporting the diagnosis of coeliac disease. However, the diarrhoea was still present and failed to improve, despite the subsequent addition of a lactose-free diet, prednisolone and metronidazole. The macrocytic anaemia had progressed, despite folic acid replacement, and splenomegaly had developed. Bone marrow examination revealed chronic myelomonocytic leukaemia (CMML). He required monthly blood transfusions.At that stage, 18 months after his initial symptoms and 11 months after starting a GFD, he was referred to us for further assessment of his diarrhoea. He still had watery diarrhoea up to 10 times per day. He was lethargic and had lost a further 6.4 kg in weight. There was no rectal bleeding or abdominal pain. On examination he was thin and wasted, with splenomegaly and mild peripheral oedema.Investigations directed towards finding the cause of his diarrhoea included: haemoglobin 10.6 g/dl, white cell count 34 × 10 9 /l, platelets 46 × 10 9 /l, mean corpuscular volume 108 fl, monocytosis and leucoerythroblastic blood film; prothrombin time 23.8 s, albumin 22 g/l, alkaline phosphatase 679 IU/l, vitamins A and E decreased, ferritin 2310 µg/l, IgA antigliadin positive. Enteroscopy showed ulceration in the second and third parts of the duodenum. Colonoscopy and small bowel enema were normal. Abdominal computed tomography (CT) scan revealed hepatosplenomegaly and low volume inguinal lymphadenopathy. Pancreolauryl test was low at 18.5% (normal >30%). A SeHCAT scan showed severe bile salt malabsorption.The ...

In people with Type 1 diabetes, hypoglycaemia causes a significant deterioration in attentional abilities, while non-verbal reasoning is preserved. It is likely therefore that many complex cognitive tasks which involve attention will be impaired during moderate hypoglycaemia during everyday life.

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