Abstract
It is known that moderate cerebral hypothermia produces excellent neuronal recovery in patients with severe brain injury, but the high incidence of severe systemic infections, DIC and ARDS is a major problem with this treatment. This paper shows how pituitary hypofunction induced by hypothermia leads to an immune crisis. The limited activation of lymphocytes and T-cells with lower growth hormone plays an important role in the occurrence of this immune crisis. The prevention of cerebral ischemia by delivering enough oxygen to maintain the O2ER at 2-23% and CPP>80mmHg was much more important than ICP management within 15-24 hours of surgery. The major mechanisms of neuroprotection by cerebral hypothermia were the prevention of cortical synaptic excitation, NO-induced radicals, brain swelling and synaptic injury of the dopamine nervous system. Based on these findings, a novel treatment using prolonged cerebral hypothermia was developed. The pharmacological activation of dopamine synapses and replacement of LH after prolonged cerebral hypothermia were very useful in neuronal recovery even in patients in a vegetative state. Clinical results were excellent. Resurts in patients rated 3-6 on the Glasgow coma scale (GCS) were as follows: good recovery (n=35 or 47%), mild disability (n=12 or 16%), severe disability (n=4 or 5%), vegetates state (n=5 or 7%) and death (n=19 or 25%). The low incidences of severe disability and vegetative state are especially worthy of attention.
