The occurrence of pain was investigated in 118 patients with posttraumatic brachial plexus injuries (BPI). Ninety-five patients were operated upon by the same surgeon. Three to 14 years after BPI and reconstructive surgery, 91% of the patients experienced permanent pain that was severe in 40% and mild in 51% of cases. When early reconstructive surgery was successful, a significant decrease in pain occurred more frequently. For 57% of patients with pain, a plurimodal medical treatment with tricyclic antidepressants, antiepileptic drugs, and behavioral therapy efficiently reduced pain. For the patients with unbearable paroxystic pain, when medical treatment failed, the destruction of deafferented dorsal horns at the level of avulsion (Nashold procedure) could produce pain relief. In all cases psychosocial management produced early rehabilitation.Pain after injury of the brachial plexus has not received much attention. However, the increasing frequency of motorcycle accidents makes the relief of pain a more immediate challenge.' 1~1 3~1 8 , 2 4Incomplete reports of lesion patterns and inadequate evaluations of pain disqualify most studies for quantitative comparison. Taylor" reported a series of 50 patients with brachial plexus injury (BPI), including 13
Background. The authors describe the clinical and morphologic patterns in four patients with acquired immune deficiency syndrome (AIDS) who developed intracranial glial tumors.
Methods. This retrospective study reports 70 patients at various stages of human immunodeficiency virus‐1 (HIV‐1) infection who underwent stereotactic brain biopsy for an intracerebral space‐occupying lesion.
Results. Of these patients, four had glial tumors: one astroblastoma, two astrocytomas, and one glioblastoma. Glial tumors probably arise from a complex interplay of factors; possibilities include the activation of a dominant oncogene or viral inactivation of a tumor suppressor gene by a viral promoter (like the tat protein), impairment of immune defenses (which facilitates the growth of astrocytomas in acute lymphoblastic leukemia), production fo cellular growth factors, cytokines, possible infection of glial cells by HIV, and the potentiation of a coinfectious agent.
Conclusions. These cases illustrate that glial tumors should be considered in the differential diagnosis of brain masses in HIV‐1 infection, especially because specific treatment for these tumors is available. Moreover, the occurrence of glial tumors in AIDS patients is not only an important event from a clinical point of view, but may also have implications for the pathogenesis of tumors in AIDS. Cancer 1994; 74: 686‐92.
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