Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The experience of 500 transcranial Doppler (TCD) sonographies at Siriraj Hospital between April 1988- June 1989 were reported. The indications for TCD study were hemiplegia 156 (31.20%), vertigo 119 (23.80%), transient ischemic attack (TIA) 26 (5.20%), hemihypalgesia 14 (2.80%), dysarthria-dysphagia syndrome 13(2.60%), visual problem 13(2.60%), syncope 10(2.00%), memory loss 8(1.60%), aphasia 6(1.20%), carotid bruit 6(1.20%), miscellaneous (artereovenous malformation, aneurysm, arteritis, carotico-cavernous fistula, tinnitus, etc) 25(5.00%), and healthy subjects 92(18.4%). Abnormal TCD studies were found in various conditions of different percentages, i.e. 91.03 per cent in hemiplegia, 76.47 per cent in vertigo, 65.38 per cent in TIA, 71.43 per cent in hemihypalgesia, 61.54 per cent in dysarthria - dysphagia syndrome, 38.46 per cent in visual problem and 30.43 per cent in normal subject. TCD is noninvasive, safe and painless. It is a useful screening test for prophylaxis of cerebrovascular disease in the elderly.
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PMID:Transcranial Doppler ultrasonography: experience of 500 patients. 228 86

At presentation the history of an 87-year-old woman included progressive memory loss, repeated transient ischaemic attack, increasing fatigue, dizziness, palpitations and frequent falls. Investigations revealed erythrocytosis, leukocytosis, thrombocytosis, normal arterial oxygen concentration and an increased red cell volume. Polycythaemia vera was diagnosed and was successfully managed by phlebotomy with half a unit twice a week and rechecks of her haematocrit, initially; she reported marked improvement after 2 weeks of treatment. The alternative treatments for polycythaemia vera are discussed; in addition to venesection, conventional treatments include bone-marrow depressive agents such as phosphorus-32 and chemotherapy with agents such as hydroxyurea. More recent developments include isovolumic erythrocytophoresis, alpha-interferon and ticlopidine. All of the treatments are associated with complications, or other disadvantages, thrombotic complications in the case of phlebotomy, malignancies in the case of most myelosuppressive treatments, and problems of compliance in others. The optimal treatment for polycythaemia vera is a judicious combination of the alternatives, depending on the phase of the disease, the age of the patient, and other prognostic factors.
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PMID:Primary polycythaemia vera in the elderly. 802 Jun 39

Transient global amnesia (TGA) is a transient, benign neurological syndrome, characterized by global loss of memory, preserved consciousness and self-awareness, associated with some behavioral changes (in particular, repetitive questioning). It generally resolves within 24 h. Mild brain stem symptoms can often be demonstrated during the attack, but major neurological abnormalities never occur. The only sequel is a permanent amnesic gap for the duration of the episode. The episode is often preceded by typical precipitating events, such as physical activity, emotional stress, acute pain, comprising haemodynamic changes of the body. The diagnosis is easy provided one is acquainted with the syndrome. The prevalence of vascular risk factors is low and the risk for stroke is not increased. Although much evidence indicates the possibility of a causative ischaemia in the inferomedial parts of the temporal lobes, an atherothrombo-embolic TIA is not the cause of TGA, and TGA is unrelated to cerebrovascular disease in general. In the author's view, the cause of TGA is a transient ischemic attack (TIA) but a haemodynamic one of the vertebrobasilar system, producing a transient dysfunction of inferomedial parts of the temporal lobes, regions that are particularly sensitive to impaired blood supply. For a full pathogenetic explanation of TGA, clarification of the underlying mechanisms is a prerequisite. This touches on the genesis of migraine and Leao's spreading depression phenomenon. The term 'amnesic TIA' would reflect the pathogenesis more appropriately.
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PMID:Transient global amnesia. 829 84

Our understanding of the pathophysiology of ITP owes to pioneering work of W J Harrington in 1951, delineating the immunologic nature of platelet destruction. In ITP, antibody-coated platelets are destroyed by macrophages of RES. However, other mechanisms are also implicated: C-mediated platelet lysis and newly described C-independent peroxide injury. Both induce platelet fragmentation and lysis, generating procoagulant platelet microparticles (PMP). A third mechanism of platelet consumption in the microvasculature is proposed, based on overlapping syndromes of ITP and TTP in some patients. In assessing hemostasis in ITP, platelet counts alone is not sufficient. Evaluation of platelet clumping, giant platelets, and platelet activation, marked by increased PMP is useful. Patients with platelet activation or giant platelets bleed less and detection of clumping prevents unwarranted therapy. Thrombotic complications may develop in ITP. A syndrome, characterized by recurrent TIA-like symptoms, progressive memory loss due to ischemic small vessel disease is described. The management of ITP should include the search for and elimination of underlying causes and careful evaluation of hemostasis. Therapy is divided into definitive vs symptomatic measures. The former including splenectomy, danazol, chemotherapy offers lasting remission after therapy was stopped, while the later including glucocorticoids, gammaglobuin, antiD antibodies and others increases platelet counts but seldom sustains remission upon withdrawal. Danazol therapy is up-dated since it is an effective and safe definite measure in ITP.
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PMID:Idiopathic thrombocytopenic purpura: pathophysiology and management. 1243 Sep 12