Abstract
During insulin shock induced therapeutically there is a progressive depression of nervous functions, in a gradient manner, from the highest (cortical) levels to lower subcortical levels (striatum, mid-brain, medullary) which is temporary and reversible. 1 , 2 It was decided to demonstrate this gradient effect clinically with the production of animal preparations showing permanent, irreversible lesions at progressively lower levels in the nervous system by prolonging the period of hypoglycemia.
Cats, fasted 18 hours, were given 15 to 20 units of insulin per kilo body weight. When clinical signs indicated early medullary decompensation, small amounts of glucose were given intraperitoneally to prevent death and still maintain a marked degree of hypoglycemia. Hypoglycemia was terminated after 12 to 20 hours. Persistent brain damage was observed in 17 animals. Group I consisted of 5 animals with variable degrees of cortical damage. Group 2 totaled 8 animals with cortical plus subcortical injury (“thalamic preparations”?). Group 3 included 4 cats with loss of function at the midbrain level or lower.
The decorticate preparations (Group 1) showed impairment of vision, impairment of placing and hopping reactions (Bard), slight impairment of righting reactions, difficulty in feeding self, impairment of cleaning habits, restlessness and absence of rage reaction when confronted by a dog. They were able to walk and maintained normal body temperature. These preparations were kept alive from 6 to 90 days.
Preparations in Group 2 showed in addition to the above, inability to walk, decerebrate rigidity, increased tonic neck reflexes and mock rage. These animals were also able to maintain body temperature. These signs point to loss of function at the “thalamic level.” The animals lived 19 to 48 hours after the hypoglycemia was terminated.
Animals in Group 3 were not studied as carefully as the above, but are added because they showed inability to maintain body temperature.
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