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  • Author or Editor: Ian E. McCutcheon x
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Ian E. McCutcheon and Edward H. Oldfield

✓ The authors report a nulliparous patient presenting with infertility and hyperprolactinemia. She underwent transsphenoidal surgery after radiological investigation disclosed an enlarged pituitary gland which did not respond to bromocriptine therapy. The removed tissue had histological features consistent with adenohypophysitis including a diffuse lymphocytic infiltrate. The lymphocyte subsets present in the infiltrate were characterized by immunohistochemical methods to establish the contribution of different elements of the cellular immune response.

Lymphocytes bearing CD4 antigen (helper-inducer cells) were most prominent and appeared to bear the majority of the interleukin-2 receptor (expressed during lymphocytic activation) present in the pituitary gland. A few B lymphocytes were also observed. The location of the major histocompatibility antigen (classes I and II) and interleukin-2 receptor correlated with the lymphocytes and macrophages rather than with the stromal or parenchymal elements of the pituitary.

Lymphocytic adenohypophysitis is an unusual cause of pituitary enlargement which can mimic a pituitary tumor, and is sometimes associated with hyperprolactinemia. In women of child-bearing age, it almost always occurs during pregnancy or the postpartum stage. The autoimmune disorder reported here has not previously been associated with infertility nor has the lymphocytic infiltrate of the pituitary previously been analyzed in detail by modern immunological methods.

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Ian E. McCutcheon, Bruce D. Weintraub and Edward H. Oldfield

✓ Thyrotropin-secreting pituitary adenomas have been diagnosed more frequently as radiographic techniques and biochemical assays have improved; however, they remain uncommon and are unfamiliar to most neurosurgeons. This report concerns eight patients with hyperthyroidism, inappropriately elevated levels of serum thyrotropin and α-subunit, and radiographic evidence of pituitary tumor. All underwent surgery and had pathological confirmation of a thyrotropin-secreting adenoma, and most had been subjected to prior ablation of the thyroid gland. Only one tumor was a microadenoma; the others ranged in size from 1.4 to 12 cm, and invasion of parasellar structures was common. Thyrotropin, triiodothyronine, thyroxine, and α-subunit were measured preoperatively and at intervals postoperatively. Coexistent hormonal abnormalities (which occurred in all patients) included acromegaly and hyperprolactinemia and were also monitored. All four patients who had tumors less than 2 cm in diameter remain alive. Complete extirpation of tumor in these patients produced rapid correction of all hormonal abnormalities and resolution of clinical hyperthyroidism. The other four patients had larger invasive tumors: two died soon after surgery, one died of disseminated tumor 8 years after presentation, and one remains alive with residual tumor.

Tumors secreting thyroid-stimulating hormone are less easily cured by surgery than are other types of pituitary adenoma because of the large size and invasive features that many attain during the delay to diagnosis; medical therapy can subdue the tumor but not cure it. The experience with these patients establishes the importance of early diagnosis and surgical excision for successful treatment, and demonstrates the utility of modern diagnostic techniques for finding these lesions. As occurs in Nelson's syndrome after adrenalectomy for Cushing's disease, ablation of the target organ may allow the tumor to convert to a more clinically malignant form which is resistant to cure.

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Ian E. McCutcheon, John L. Doppman and Edward H. Oldfield

✓ Although most vascular abnormalities of the spinal cord are now ascribed to an abnormal communication between a dural artery and a medullary vein on the dura near a sensory nerve root, these lesions are too small for their anatomy to be demonstrated directly by spinal arteriography. Thus, it is unknown whether the site of dural arteriovenous shunting is an arteriovenous malformation (AVM), implying a congenital origin, or is a direct arteriovenous fistula (AVF), implying an acquired etiology.

The authors treated six patients by en bloc resection of the involved dural root sleeve, proximal nerve root, and adjacent spinal dura. All of the patients presented with myelopathy and their arteriograms were consistent with a spinal dural vascular malformation. The lesions occurred between T-6 and T-12, levels at which clinical deficits from such resection are minimal. The dural artery or medullary vein associated with the vascular malformation was cannulated and a dilute solution of barium sulfate was injected during sequential fine-grain radiography. In all of the lesions the artery split into daughter vessels that coalesced one to three times to form a skein of arterial loops in the dura that invariably emptied into a medullary vein without an intervening capillary plexus. Several medium-to-small collateral vessels arising from adjacent intercostal or lumbar arteries were commonly present in the dura and converged at the site of the AVF to join a single medullary vein.

These results show that spinal dural AVMs are direct AVFs that link the dural branch of the radiculo-medullarydural artery with the intradural medullary vein. They also provide an anatomical explanation for the presence of a multiple segmental arterial supply and a single draining medullary vein of spinal dural AVFs, and the propensity for reestablishment of flow through the arteriovenous shunt after embolic occlusion.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010