Brain metastasis from prostate carcinoma: antemortem recognition and outcome after treatment.

BACKGROUND: In patients with prostate carcinoma, brain metastasis has most commonly been reported in autopsy series. Symptomatic brain metastasis from prostate carcinoma has occasionally been detected. METHODS: The authors retrospectively studied a series of 38 patients with antemortem intracerebral metastasis found on review of 7994 patients treated over an 18-year period at the University of Texas M. D. Anderson Cancer Center. RESULTS: The mean time from diagnosis of prostate carcinoma to discovery of brain metastasis was 28 months, with a mean survival of 9.2 months after the discovery of the brain metastasis. The brain metastasis was treated only with whole brain irradiation in 29 patients, with craniotomy and irradiation in 8 patients, and with surgery alone in 1 patient. Small cell carcinomas and primary transitional cell carcinomas of the prostate were much more likely to produce brain metastasis than were adenocarcinomas. Also noted among the overall prostate carcinoma cohort was a second group of 16 patients with prostate carcinoma and brain metastasis that had developed from a second primary tumor, which in all was either lung carcinoma or melanoma. CONCLUSIONS: The occurrence of brain metastasis in prostate carcinoma patients is rare, usually signifies a late stage of the disease, and may in some patients be produced by a tandem extraprostatic tumor.

Craniospinal dissemination of central neurocytoma. Report of two cases.

Central neurocytoma was first described in the literature in 1982 and has been noted to be a benign neuronal tumor usually located in the ventricular system. Of the more than 100 reported cases, only seven recurrences have been reported, all of which have been local. The authors report two cases of recurrent central neurocytoma that disseminated through the ventricular system with seeding to the spine, as evidenced by magnetic resonance images and positive cerebrospinal fluid cytology. The histological appearance of these two tumors was typical for the lesion and lacked evidence of malignant change. Central neurocytoma may not be as benign as previously thought, and the recognition of this more malignant behavior has implications for patient follow up and therapy.

Profound arterial hypotension in dogs: brain electrical activity and organ integrity.

To determine whether non-invasive measurement of brain electrical activity can predict ischemic brain damage, we recorded the electroencephalogram (EEG) and somatosensory- (SEP) and auditory- (AEP) evoked potentials before, during, and after trimethaphan-induced profound arterial hypotension in dogs. The authors set out to compare the change in electrical activity with the degree of brain damage, as determined by microscopic examination. Dogs were anesthetized with halothane (1.4 vol % inspired), maintained horizontal (head at the level of the heart), and ventilated mechanically (FIO2 0.50); deviations from normal acid-base status were corrected. Twenty animals received a 1.5-mg/kg intravenous bolus of trimethaphan. Three animals were resistant to the drug. The remaining animals had profound hypotension [mean arterial blood pressure (MABP) at some steady level between 12 and 25 mmHg] for 1 h. Eight of these animals died during or soon after the hypotensive period as a consequence of cardiac arrest (three), intestinal bleeding (three) or unknown causes (two). In all survivors, EEG intensity and the amplitude of the SEP decreased during hypotension; both variables recovered with restoration of MABP. All nine animals surviving hypotension had no apparent neurologic or behavioral deficit nor any histologic evidence of ischemic brain cell injury. We were thus unable to find a MABP threshold for brain with minimal brain injury. Our findings suggest, under the conditions of our experiments, a great margin of tolerance for profound hypotension by the brain in this species. Other organ systems--the heart, gastrointestinal tract, and liver--proved to be more susceptible to ischemic damage. Eight of the nine surviving animals had elevations in serum alanine transaminase (SGPT), aspartate transaminase (SGOT), and alkaline phosphatase. Animals with the greatest increases in these enzymes showed centrilobular hepatocyte degeneration.

Evidence of active regulation of cerebrospinal fluid acid-base balance.

To test the passive transport hypothesis of cerebrospinal fluid (CSF) [H+] regulation, we altered the relationship between plasma [H+] and the electrical potential difference between CSF and blood (PD) by elevating plasma [K+] during 6-h systemic acid-base disturbances. In five groups of pentobarbital-anesthetized dogs, we increased plasma [K+] from 3.5 to an average of 7.8 meq/l. Hyperkalemia produced an increase in the PD of 6.3 mV by 6 h with normal plasma acid-base status (pHa 7.4), of 8.3 mV with isocapnic metabolic acidosis (pHa 7.2), of 5.3 mV with isocapnic metabolic alkalosis (pHa 7.6), of 9.2 mV with isobicarbonate respiratory acidosis (PaCO2 61 Torr) and of 5.7 mV with isobicarbonate respiratory alkalosis (PaCO2 25 Torr). The change in CSF [H+] at 6 h in each group was the same as that observed in normokalemic animals (Am. J. Physiol. 228: 1134-1154, 1975). This result is not consistent with the passive transport hypothesis. The CSF-blood PD is therefore not an important determinant of CSF [H+] CSF [H+] homeostasis must result from some form of active transport control.