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From January 1962 to May 1979, 23 patients with biopsy-proved intramedullary spinal cord tumors were treated initially with total resection, subtotal resection, irradiation, or subtotal resection and irradiation. Local control was achieved in 1/2 patients after total resection, 1/3 after subtotal resection, 8/9 after subtotal resection and radiation therapy, and 5/8 after radiation therapy alone. The patients with ependymomas exhibited a radiation dose-response relationship; of eight patients followed five or more years postirradiation, local control was achieved in 2/3 with time dose fraction (TDF) less than 55, 2/3 with TDF 55-65, and 2/2 with TDF greater than 65. The actuarial 5- and 10-year survival rates were 58% and 23% for astrocytoma, and 100% and 73% for patients with ependymoma, respectively. Neurological deficits improved or became totally normal after initial irradiation. Patterns of failure, management of recurrences, and radiotherapeutic techniques and dose recommendations are discussed.

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This study suggests that critical spinal cord ischemia after complete TAASA sacrifice does not occur immediately (intraoperatively), but is delayed 1-5h or longer after clamping, and represents failure to mount a hyperemic response to rewarming and awakening. The short duration of low SCBF associated with spinal cord injury suggests that hemodynamic and metabolic manipulation lasting only 24-72 h may allow routine preservation of normal cord function despite sacrifice of all TAASA secondary to surgical or endovascular repair of large TAAA.

Although the molecular mechanisms underlying GH secreting pituitary tumor formation are not well understood, mutations in the alpha-subunit of the stimulatory G gene, GNAS, have been identified in up to 40%. As these mutations could play a role in tumor growth, we screened 60 GH secreting tumors for GNAS mutations and assessed whether mutation status correlated with their clinical and pathological characteristics. Tumor specimens obtained at surgery were snap frozen. Tumor DNA was extracted, and PCR was used to amplify regions containing 2 sites of recurrent activating somatic mutations in codons 201 and 227 in GNAS. Amplicons were bi-directionally sequenced and analyzed. GNAS mutations were present in 24/60 (40%) of tumors; these were arg201cys(n = 15), arg201ser(n = 2), arg201his(n = 2), gln227leu(n = 4), gln227arg(n = 1). Preoperative IGF-I levels (age-adjusted) were higher (p = 0.01), but GH levels were slightly higher (p = 0.18) in mutation positive vs. negative groups. Mutation positive tumors were somewhat smaller than negative tumors (p = 0.07). The proportion of tumors >2 cm was somewhat less among positive (8.3%) vs. negative tumors (25%) (p = 0.10). Neither mib proliferation index, the proportion of invasive tumors nor surgical remission rates differed in the groups. IGF-I normalization rate with somatostatin analog therapy was similar in positive (3 of 6) vs. negative (3 of 7) patients. GH secreting tumors harboring GNAS mutations had higher preoperative IGF-I levels, somewhat higher preoperative GH levels and tended to be smaller than tumors without mutations. Presence of a GNAS mutation did not predict a difference in a proliferation marker, surgical remission or response to somatostatin analog therapy.

Interruption of all SAs at 32 degrees C in this pig model results in a spectrum of cord injury, with normal function in a majority of pigs postoperatively. The short duration of low SCPP suggests that hemodynamic manipulation lasting only 24-48h may allow routine complete preservation of normal cord function despite sacrifice of all SAs.

SCP provides insufficient SCBF below T8/9 to sustain cord viability. At 28 degrees C, the ischaemic tolerance of the cord may be exceeded enough by 90 min to impair function; by 120 min, SCP at 28 degrees C invariably results in paraplegia.