Hypoglycemia is not often in the differential diagnosis for dysesthesias but should be considered when involved in the care of diabetic patients. Such symptoms may herald silent hypoglycemia and resultant nerve injury, as illustrated in the following case.
A 26-year-old female with type 1 diabetes presented with a 2-month history of numbness and tingling in her hands and feet upon waking in the morning. Symptoms began when her treatment was altered from NPH 50 units q 𝒶.𝓂. to NPH 35 and Regular 3 q 𝒶.𝓂. and NPH 8 and Regular 5 at dinner. The patient monitored her glucose more than four times each day and reported three to four glucose values a week that were <60 mg/dl without symptoms. Her morning glucose levels averaged 60 mg/dl. The symptoms were more pronounced in her hands than feet and resolved within minutes. On exam, she showed no objective sensory loss, possessed good muscle tone, bulk, and strength, had intact reflexes (2+) bilaterally, and had no focal neurological signs. HbA1c was 6.8%.
Symptoms were attributed to peripheral neuropathy secondary to hypoglycemia. Her insulin regimen was adjusted to NPH 35 and Regular 3 q 𝒶.𝓂., NPH 4 q HS, and Regular 5 before dinner for glucose >200 mg/dl. One month later, she reported the disappearance of the symptoms and a reduction in the frequency of values <60 mg/dl to once a week.
Hypoglycemia has been proposed to induce nerve injury by several mechanisms. Lack of substrate leads to a reduction in axonal transport, causing an accumulation of intraneural metabolites and neuronal injury (1). Hypoglycemia can induce a reduction in blood flow, leading to neural hypoxia (2–4). These mechanisms may all play a role in nerve injury; disturbance in neural blood flow may be the initial manifestation of hypoglycemia, while prolonged hypoglycemia may induce axonal damage (2).
Peripheral neural injury has been reported in patients with hypoglycemia due to insulinomas (5). These patients displayed paresthesias and/or muscle wasting and weakness. After tumor resection, patients showed resolution of sensory symptoms, while muscle wasting persisted.
We propose that practitioners consider undetected hypoglycemia as a possible cause of paresthesias in diabetic subjects. Frequent episodes of hypoglycemia can hinder patients’ efforts to achieve normoglycemia. Early measures taken to reduce such episodes will promote normoglycemia.