Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain.
Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D001929:Brain Edema / Q000209:etiology; D002490:Central Nervous System / Q000378:metabolism; D002555:Cerebrospinal Fluid; D048909:Diabetes Complications; D003926:Diabetic Coma / Q000188:drug therapy / Q000378:metabolism; D016883:Diabetic Ketoacidosis / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia; D006973:Hypertension / Q000209:etiology; D007328:Insulin / Q000009:adverse effects; D009461:Neurologic Manifestations; D011312:Pressure; D012640:Seizures / Q000209:etiology; D012964:Sodium / Q000378:metabolism
D007328:Insulin; D012964:Sodium; D005947:Glucose