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Mucocele of the Sphenoid Sinus

Report of a Case with Autopsy Findings

F. H. Linthicum, Carl W. Rand and David L. Reeves

attention as a possible explanation of the cause. Congenital narrowing of the duct rendering a catarrhal inflammatory obstruction is also given as a likely cause as well as septal deviation, and too, congenital absence of a communication from the nose and the frontal sinus. Other writers 1, 5 have inclined to the theory of a cystic dilatation of one or more mucous glands, or a cystic degeneration of the mucosa of the polyps therein. Schüller 18 pointed out the possibility of the development of an hypophyseal cyst from the inner or under half of the sella turcica

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Loyal Davis, John Martin, Stanton L. Goldstein and Moses Ashkenazy

, revealing extensive necrosis, and a secondary type, revealing comparatively small or no necrosis, usually with some small areas of cystic degeneration. From his description, we believe that these strongly resembled our angiothrombotic and angioproliferative groups respectively. His latter group were also those with “long clinical evolution,” whereas his primary glioblastomas did not live beyond 6 to 12 months. Busch and Christensen 4 subdivided their glioblastomas into three main pathological groups. These groups were: (1) angionecrotic , characterized by

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Homer S. Swanson and Edgar F. Fincher

displaced downward into the vertebral canal (Type II, Chiari). Fig. 1. Photograph of operative findings, (a) Occipital-cervical junction, (b) Caudally displaced and distorted cerebellar tonsils, (c) Third cervical level of spinal cord. Inspection of the site of junction of the medulla oblongata and the cervical cord disclosed a small area of cystic degeneration in the midline and a distinct cleft in the cervical cord corresponding to the level of the similar indenture noted in the dura. This cystic area corresponded to the lowermost portion of the 4th

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Syringo-Encephalomyelia

Discussion of Related Syndromes and Pathologic Processes, with Report of a Case

Homer D. Kirgis and Dean H. Echols

the central canal of the spinal cord (which might be more correctly termed hydromyelia) to cystic degeneration within a glioma, have been discussed under the term syringomyelia . An insufficient number of cases that might be termed true syringomyelia and in which treatment consisted of establishing a permanent communication between the cavity of the cyst and the subarachnoid space has been followed to reach definite conclusions regarding the neoplastic significance of the proliferation of glial cells which has generally been reported to be present about the cyst

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Studies on the Sacral Reflex Arc in Paraplegia

I. Response of the Bladder to Surgical Elimination of Sacral Nerve Impulses by Rhizotomy

Arnold M. Meirowsky, C. David Scheibert and Thomas R. Hinchey

11, T12 and L1 (AMM) on Oct. 30, 1947 revealed a yellowish discoloration with cystic degeneration of the cord at the level of the 11th thoracic vertebra with atrophy below. Novocaih block of the left 1st lumbar nerve relieved the root pain. Automatic bladder function without residual urine or incontinence, as well as relief of pain, resulted under the influence of low spinal anesthesia. After anterior and posterior rhizotomy of T11 to S5 (AMM) on Sept. 1, 1948, the patient had relief of pain and automatic bladder function. Bladder status before and after

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Loyal Davis, John Martin, Frank Padberg and Robert K. Anderson

and cystic degeneration with some fibrotic repair and numerous thickened, tortuous blood vessels. Mitotic figures were not seen. The longest survival period following this type of radiation therapy was 123 months and the average was 36.5 months, with no correlation between the number of mg. hours of radiation and survival time. Seven of these 114 patients received x-ray therapy postoperatively varying from 1,600 r in air to 14,438 r in air. In most instances the factors were as follows: 200 kV.; 1 mm. copper and 1 mm. aluminum filters; distance 50 cm.; 3 to 5

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Colloid Cyst of the Fourth Ventricle

Report of a Case of Two Colloid Cysts of the Fourth Ventricle

Dwight Parkinson and A. E. Childe

necessarily mean that they can arise only from the paraphysis. This structure and the remaining ependymal lining all have a common origin from the embryonic ectoderm. The cystic masses 11 covered with epithelium that resembles choroid plexus, probably begin as papillomata whose supporting stromal core undergoes cystic degeneration. These may be related but are certainly not the same as the cysts in this report which are lined, not covered, with epithelium, which epithelium is embryonic in nature. SUMMARY A case of two colloid cysts of the 4th ventricle is presented

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Paul C. Bucy and L. Willard Freeman

improvement. 25 It must be borne in mind that with progression of the disease, the dura mater may become densely adherent to the leptomeninges and the spinal cord making satisfactory separation impossible or very difficult and that eventually changes within the spinal cord, softenings and cystic degeneration, may become irremediable. The first operation for this disease, according to Kment and Salus, 14 was performed by Schede in 1901 (reported by Schultze 28 ). Since then a number of patients with this condition have been operated upon. In 1931, Kment and Salus

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Oscar A. Turner

marked herniation of brain through the operative site with adhesions between the fungating cerebral tissue, the scalp, and the edge of the bone defect. The base of the brain was covered with an abundant translucent greenish-yellow gelatinous exudate and a marked pressure cone involved the tonsils of the cerebellum and the brain stem. There was a purulent ependymitis which had extended to involve the right temporal lobe, where an area of inflammatory softening and cystic degeneration communicated with the inferior portion of the right temporal horn. Sections through the

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N. Malamud, E. B. Boldrey, W. K. Welch and E. J. Fadell

millimeters in size, were found in the putamen and substantia nigra on the right side. These showed central areas of necrosis which were bounded by round cells with hyperchromatic nuclei and frequent mitoses, and pervaded by a network of reticulin, characteristic of sarcoma ( Fig. 4 ). The most conspicuous change, however, was widespread degeneration of both cerebral hemispheres. In the cerebral cortex, the changes were patchy and varied from areas of cystic degeneration of the tissue which was held together by glial fibers ( Fig. 5 ) up to foci of diffuse depletion of