Subject(s)
Brain Ischemia/drug therapy , Brain Ischemia/etiology , Stroke/drug therapy , Stroke/etiology , Thrombolytic Therapy , Animals , Arterial Occlusive Diseases/complications , Arterial Occlusive Diseases/drug therapy , Europe/epidemiology , Fibrinolytic Agents/standards , Fibrinolytic Agents/therapeutic use , Forecasting , Heparin/supply & distribution , Heparin/therapeutic use , Humans , Infusions, Intra-Arterial , Infusions, Intravenous , Middle Cerebral Artery/pathology , Practice Guidelines as Topic , Thrombolytic Therapy/standards , Tissue Plasminogen Activator/standards , Tissue Plasminogen Activator/therapeutic use , Treatment Outcome , United States/epidemiology , United States Food and Drug AdministrationABSTRACT
OBJECTIVES: To describe the occurrence of cerebral venous thrombosis in a 40-year-old man whose cerebral event was induced by a poor golf swing, to review the literature on possible mechanisms producing venous thrombosis, and to compare this case with the literature. BACKGROUND: Headache is the most frequent symptom in patients with cerebral venous thrombosis. However, patients presenting with a headache due to cerebral venous thrombosis are uncommon. The known risk factors for thrombosis include both acquired and genetic factors. When the interaction of these two groups occurs, the magnitude of this interaction is thought to produce a dynamic state that can favor thrombosis. Our case report illustrates that moderate levels of anticardiolipin antibodies together with the mild trauma of a golf swing can induce a cerebral venous thrombosis. This case also suggests that although headache is rarely due to cerebral venous thrombosis, it should be excluded by good medical acumen and testing. RESULTS: Minor trauma induced by a poor golf swing was chronologically related to the development of a progressive cerebral venous thrombosis. The patient had none of the risk factors associated with a predisposition to venous thrombosis: hypercoagulable state, concurrent infection, pregnancy/puerperium, collagen vascular disorder, malignancy, migraine, false-positive VDRL, previous deep vein thrombosis, renal disease, factor V Leiden, or a hematological disorder. There was no anatomical abnormality that would predispose the patient to a cerebral venous thrombosis. The only laboratory abnormality was a moderate anticardiolipin antibody level (25 GPL). The patient was placed on warfarin sodium therapy and is currently without clinical sequela from the venous thrombotic event. CONCLUSIONS: Under certain circumstances, minor trauma can induce cerebral venous thrombosis. A review of the literature indicates that cerebral venous thrombosis in the presence of anticardiolipin antibodies and in the absence of systemic lupus erythematosus is a rare event. Previously, only major traumatic events have been reported to be associated with cerebral venous thromboses. The chronological development of cerebral venous thrombosis after a faulty golf swing strongly indicates that given a background of moderate levels of anticardiolipin antibodies, even minor trauma can induce a venous thrombotic event.
Subject(s)
Golf/injuries , Headache/etiology , Intracranial Thrombosis/etiology , Adult , Antibodies, Anticardiolipin/analysis , Athletic Injuries/complications , Humans , Intracranial Thrombosis/blood , Male , Neck Injuries/complicationsABSTRACT
Aurintricarboxylic acid (ATA), an endonuclease inhibitor, has been shown to protect several cell types from an apoptotic form of cell death. We tested ATA for protective effects against glutamate excitotoxicity in 2-week-old cultured hippocampal neurons. Cell viability was determined 24 h after glutamate exposure either by trypan blue exclusion or by measurement of lactate dehydrogenase release. When ATA was added during exposure to glutamate, there was a dramatic increase in the number of viable neurons compared with cultures that did not receive ATA. If ATA was added after glutamate exposure, the rate of survival approached 100%. Several cellular processes may be the targets for ATA action. If the mechanisms of ATA protection are similar for excitotoxicity and apoptosis, then these distinct forms of cell death may share a common intracellular pathway.
Subject(s)
Aurintricarboxylic Acid/pharmacology , Glutamates/pharmacology , Hippocampus/drug effects , Neurons/drug effects , Neurotoxins/pharmacology , Animals , Cell Count/drug effects , Cells, Cultured , Culture Media , Glutamic Acid , Hippocampus/cytology , L-Lactate Dehydrogenase/metabolism , Neuroglia/cytology , Neuroglia/drug effects , Neurons/cytologyABSTRACT
This study examined the effect of the patient's level of motivation upon process and outcome in short-term psychotherapy. 18 shy, anxious, and depressed male college students received up to 25 sessions of therapy with experienced professional therapists. Analyses of audiotaped samples from four therapy sessions indicated that motivation was a good predictor of a patient's behavior in therapy. These analyses also suggested that the patient's level of motivation may influence the therapist's behavior during treatment. Lastly, ratings of motivation significantly predicted both the therapist's and the clinician's ratings of overall improvement, but not the patient's rating of overall improvement or the residual maladjustment scores derived from the MMPI.