Intramedullary spinal cord metastases, mainly of nonneurogenic origin

The clinical data and imaging studies of 12 patients with intramedullary metastases were reviewed retrospectively to see if these lesions had a typical radiographic appearance and to determine the sensitivity of the various radiologic examinations. The lesions were identified antemortem by either myelography, CT, MR, and/or intraoperative spinal sonography (IOSS). Final diagnosis was based on biopsy material from either the spinal cord lesion, another metastatic site, and/or the primary tumor. Ten patients had primary tumors located outside the central nervous system, while only two patients had primary brain tumors. Metrizamide myelography and CT demonstrated a definite intramedullary mass in nine of 11 patients. In five patients the mass was relatively small, well-defined, single, and resembled a primary spinal cord neoplasm. In the other four patients, longer and sometimes several segments of the cord were involved. These appeared irregular and nodular and were often associated with intradural lesions at separate sites. MR detected not only enlargement and abnormal signal in the cord but also clinically unsuspected brain lesions. IOSS localized lesions for biopsy and monitored tumor resection. These various imaging procedures showed that cord metastases were often more extensive than anticipated clinically. Spread of tumor into the spinal and intracranial subarachnoid space was common. Imaging of the entire spinal canal and brain, preferably with MR, is therefore recommended to aid in diagnosis, prognosis, and treatment.     

Salivation from the denervated human parotid gland induced by pirenzepine and telenzepine

Summary In the denervated human parotid gland the non-classical cholinolytic agents pirenzepine and telenzepine induce a similar paradoxical salivatory response to that of atropine, scopolamine and metacine.     

Focal traumatic brain injury causes widespread reductions in rat brain norepinephrine turnover from 6 to 24 h

The effect of right sensorimotor traumatic brain injury (TBI) in male Sprague-Dawley rats on brain norepinephrine (NE) turnover was assessed by measuring the decline of endogenous NE levels following tyrosine hydroxylase inhibition produced with α-methyl-p-tyrosine. Right sensorimotor cortex contusions were produced by a pneumatically driven piston which depressed the dural surface by 2 mm at 3.2 m/s. TBI rats were compared to uninjured, anesthetized controls at 6 h and 24 h after surgery. While NE turnover was not affected at the lesion site at 6 h after TBI, it was either abolished or decreased by 33–75% bilaterally in the hypothalamus and in the cerebral cortex surrounding and rostral to the lesion site. In the cortex caudal to the lesion site, NE turnover was completely abolished. NE turnover in cerebral cortex opposite the lesion site and in the contralateral cerebellum was decreased by 51 and 43%, respectively, at 6 h. At 24 h, NE turnover was either abolished or decreased bilaterally by 45–92% in all cortical areas, in the hypothalamus, cerebellum, locus coeruleus and medulla. Thus, right sensorimotor cortex contusion causes a marked, early and widespread depression of brain NE turnover. Since amphetamine increases NE turnover, this may explain the dramatic improvement in behavioral deficits which occurs following amphatamine administration at 24 h after such lesions.     

Aberrant expression of HLA-DR antigen on valvular fibroblasts from patients with active rheumatic carditis.

Immunofluorescence and immunoperoxidase staining was used to investigate the expression of Class II major histocompatibility antigens in myocardial tissue of 16 patients with acute rheumatic carditis. Aberrant expression of HLA-DR was examined using monoclonal anti-Ia antibodies and was detected on the valvular fibroblasts of those valves with ongoing active carditis. Sections of myocardial and valvular tissue from normal controls or from patients dying of other cardiac diseases did not express HLA-DR. The aberrant expression of HLA-DR on valvular fibroblasts could be important in triggering autoimmune destruction in that these cells could present self-antigens to sensitized T-lymphocytes which could initiate autoantibody production or direct destruction of local tissue.