The use of stereotaxic chemical hypophysectomy in the treatment of thalamic pain syndrome.
Three patients with neurological injuries consistent with cerebral stroke subsequently developed pain over portions of the body contralateral to the injured hemisphere. Stereotaxic chemical hypophysectomy was used in the management of this pain after other surgical procedures and medical management had failed to provide relief. Postoperatively, all patients were treated for hypopituitarism. All developed transient diabetes insipidus, and one patient developed transient right third nerve palsy. No other complications were encountered. All three patients experienced significant pain relief within 48 hours of the procedure. By the date of discharge, two of the three patients reported complete, and the third greater than 80% pain relief. At the initial follow-up visit all patients were essentially pain-free. These patients have now been followed for 58, 39 and 19 months, and remain free of their original pain. During this time the intravenous administration of naloxone has failed to reproduce the preoperative pain. Pituitary function testing 1 year or more following operation demonstrated that none of the patients had an endocrinologically complete hypophysectomy. Recovery from transient diabetes insipidus was not associated with return of the original pain. The mechanism of action of stereotaxic chemical hypophysectomy in the relief of pain related to thalamic lesions remains unknown. The observation that naloxone failed to reproduce the preoperative pain casts doubt on the theory that augmentation of endogenous opiate release is the primary mechanism. Additional observations suggest that pain relief after hypophysectomy may be more directly the result of stimulation of a hypothalamic pain-suppressing mechanism than due to the elimination of pituitary hormones.