Cushing's syndrome and acute lymphoblastic leukemia.

Cushing's disease developed in a 5-year-old girl with acute lymphoblastic leukemia 18 months after her last therapeutic exposure to adrenal glucocorticosteroids. Obesity, hyperpigmentation, striae, osteoporosis, and hirsutism were accompanied by elevated levels of plasma cortisol. These showed no diurnal fluctuation and they were not suppressed by dexamethasone. At autopsy, the adrenal glands were enlarged and the pituitary gland showed increased numbers of basophils of the adrenocorticotropic hormone (ACTH)/melanocyte-stimulating hormone secreting type. Leukemic infiltrates in brain tissue were prominent in the hypothalamus and in the limbic system. It is postulated that the destructive leukemic infiltrate of the limbic system removed a restraining influence on pituitary function, with basophilic hyperplasia, ACTH hypersecretion, adrenocortical hypertrophy, and clinical Cushing's disease the consequences.

Central functional changes after facial-spinal-accessory anastomosis in man and facial-hypoglossal anastomosis in the cat.

A left facial-spinal-accessory anastomosis was performed for peripheral facial paralysis in an 8-year-old boy. By the fourth postoperative year, the corneal reflex showed a normal latency, and left arm and face movements could be executed independently. The possibility of neural plasticity playing a role in establishing new central relationships which enable the achievement of a "normal" latency corneal reflex and independent face and arm movements is discussed. The latency of the corneal reflex recorded as electrical response of the orbicularis oculi muscle to electrical stimulation of the ipsilateral cornea was measured in normal cats and cats which had undergone a facial-hypoglossal anastomosis 12 to 14 months previously. The latency of the reflex was 8 to 22 msec in normal animals and 200 to 300 msec in the operated cats, while conduction times in the regenerated hypoglossal nerve fibers were found to be within normal limits. This suggests that the long latency of the corneal reflex following the cross anastomosis is due to the time required for transmission across newly-formed connections between the trigeminal terminals and the hypoglossal neurons.