Background. Factors affecting survival were determined for 109 patients with thoracic spine metastases and cord compression. Lung, prostate, and breast were the most common primary sites (78%). All patients had surgical decompression of the spinal cord, and 99% received radiotherapy. Methods. Survival was determined based on anatomic site of primary carcinoma, preoperative neurologic deficit, extent of disease, number of vertebral bodies involved, tumor location (site of cord compression), and age. The respective compounding weight of the negative prognostic factors also was analyzed in terms of survival. Results. The overall median survival was 10 months. Patients preoperatively ambulatory survived statistically significantly longer than nonambulatory patients or those with sphincter incontinence (P = 3.469 × 10−6). Patients with renal cell carcinoma survived the longest, followed by those with breast, prostate, lung, and colon cancer. Patients with breast cancer survived statistically longer than those with lung cancer (P = 0.039). Patients with one vertebral body involved survived statistically significantly longer than patients with multiple vertebral level involvement (P = 0.027). Extent of disease, age, and tumor location did not significantly influence survival. In patients with vertebral column disease, the presence of two or more poor prognostic indicators (leg strength 0/5‐3/5, lung or colon cancer, multiple vertebral body involvement), had a compounding adverse effect on survival. Conclusions. For patients with spinal metastases and cord compression, the factors found to affect survival include preoperative neurological status, anatomic site of primary carcinoma, and number of vertebral bodies involved. Patients with vertebral column disease and two or more of the poor prognostic indicators have a short life expectancy, and, therefore, radical surgery is not recommended because the benefits may not be substantial.

When a patient with known metastatic cancer develops diabetes insipidus and has radiographic evidence of a pituitary mass, the diagnosis of metastasis is highly probable. Reasonable treatment is palliative with exogenous vasopressin and radiotherapy.

Idiopathic spinal cord herniation should be recognized as a cause of progressive myelopathy that can be managed successfully with microsurgical techniques.

Long-term surface cerebral blood flow (CBF) monitoring was performed to test the hypothesis that temporal lobe epileptogenicity is a function of epileptic cortical perfusion. Forty-three bitemporal 2-hour periictal CBF studies were performed in 13 patients. Homotopic regions of temporal cortex maintained interictal epileptic cortical hypoperfusion and nonepileptic normal cortical CBF. At 10 minutes preictus, a statistically significant, sustained increase in CBF was detected on the epileptic temporal lobe. Two minutes preictus, there was approximation of CBF in the epileptic and nonepileptic temporal lobes. Thereafter, electrocorticographic (ECoG) and clinical seizure onset occurred. The linear relationship between CBF in the two hemispheres (epileptic and nonepileptic) was the inverse of normal (y = -0.347x + 62.767, r = 0.470, df = 95, p < 0.05). The data indicated a direct linear correlation between epileptic cortical CBF and seizure interval (frequency-1), a clinical measure of epileptogenicity (r = 0.610, df = 49, p < 0.05). Epileptogenicity was also found to be a logarithmic function of the difference between nonepileptic and epileptic cortical perfusion (r = 0.564, df = 58, t = 5.20, p < 0.05). The results showed that progressive hypoperfusion of the epileptic focus correlated with a decreased seizure interval (increased epileptogenicity). Increased perfusion of the epileptic focus correlated with an increased seizure interval (decreased epileptogenicity). The fact that CBF alterations precede ECoG seizure activity suggests that vasomotor changes may produce electrical and clinical seizure onset.

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