Differentiation of vascular dementia from AD on neuropsychological tests.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to G C Roman.
Explore the source record for details and available documents.
Vascular dementia (VaD) incorporate different vascular mechanisms and changes in the brain, and have different causes and clinical manifestations. Variation in defining the cognitive syndrome, in vascular etiologies, and allowable brain changes in current clinical definitions of VaD have resulted in variable estimates of prevalence, of groups of subjects, and of the types and distribution of putative causal brain lesions. Thus current criteria for VaD select an etiologically and clinically heterogeneous group. This definitional heterogeneity may have been a factor in "negative" clinical trials. An alternative for clinical drug trials is to focus on a more homogeneous group, such as those with subcortical (ischemic) VaD. This designation incorporates two small vessel clinical entities "Binswanger's disease" and "the lacunar state". It comprises small vessel disease as the primary vascular etiology, lacunar infarct(s) and ischaemic white matter lesions as the primary type of brain lesions, and subcortical location as the primary location of lesions. The subcortical clinical syndrome is the primary clinical manifestation, a definition which still requires additional empirical data. We expect that subcortical VaD show a more predictable clinical picture, natural history, outcome, and treatment responses. We propose a modification of the NINDS-AIREN criteria as a new research criteria for subcortical VaD.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Nucleus pulposus embolism causing spinal cord infarction is exceptional. A 16-year-old girl was seen with sudden onset of interscapular pain and paraplegia from fatal ischemic transverse myelopathy due to arterial and venous occlusions by fibrocartilaginous embolism. In 32 cases of nucleus pulposus embolism, females predominated (69%) and age distribution was bimodal with peaks at 22 and 60 years (median, 38.5). Embolization was either arterial and venous (50%) or purely arterial (50%). Myelopathy predominated in cervical (69%) and lumbosacral (22%) segments. Schmorl's nodes, larger volume and vascularization of nucleus pulposus in the young, and spinal arteriovenous communications, trauma, and degenerative changes in older patients could be important pathogenetic factors. Diagnosis requires histopathologic confirmation. Nucleus pulposus embolism may be an underlying cause in cases diagnosed as transverse myelitis and ischemic infarction of spinal cord.
Accepted approaches to therapy for the different forms of neurocysticercosis are reviewed. Therapy must be individualized according to the level of disease activity and the location of the parasite. Patients with inactive disease should receive only symptomatic treatment. In contrast, patients with parenchymal brain cysts must receive a course of anticysticercal drugs. Both albendazole and praziquantel are useful; however, recent evidence favors the former as the drug of choice for this form of the disease. Albendazole (but not praziquantel) is also effective in the treatment of giant subarachnoid cysts; such medical treatment obviates surgery in some cases. Patients with ventricular cysts may also benefit from medical therapy; however, surgery is the current approach to this type of lesion, as it is to spinal cysticercosis. Although intraocular cysts have classically been resected by surgery, a recent study indicates that albendazole is equally effective. For patients with mixed forms of neurocysticercosis, therapeutic measures related to--but not directly targeting--the disease (i.e., steroid administration for brain edema or shunt placement for hydrocephalus) should be contemplated before therapy with anticysticercal drugs is instituted.
Explore the source record for details and available documents.
Several authors have demonstrated the presence of antibodies against the HTLV-I retrovirus in patients with MS. Considerable controversy exists regarding the etiologic significance, if any, of this finding, but the presence of these antibodies in the blood or CSF of MS patients has led to reconsideration of that diagnosis in certain cases. It is recommended that, before the diagnosis of MS is changed to that of HTLV-I-associated chronic myelitis, at least 2 of the following abnormalities be present: (1) clinical or electrophysiologic involvement of peripheral nerve or muscle; (2) the presence of oligoclonal bands in the serum; (3) the presence in blood or CSF of lymphocytes with multilobed nuclei; (4) a positive serologic test for syphilis; (5) the presence of a sicca syndrome; and (6) the presence of pulmonary lymphocytic alveolitis.
Human T-Cell Leukaemia Virus (HTLV) has been found to be endemic in the Caribbean Islands. So-called spastic paraplegia of unknown origin, described in Martinique (named tropical spastic paraplegia in other countries) was found to be associated with signs of HTLV-l infection in 1984-1985. This association has since been found in non-tropical countries, particularly in Japan where HTLV-l is endemic. Numerous questions about the physiopathology of the neurological involvement and the systemic symptoms and signs remain unanswered. The identification of the retrovirus and of the diseases is only beginning.
Explore the source record for details and available documents.
To investigate the possible occurrence of human immunodeficiency virus (HIV) or human T-cell lymphotropic virus, type I (HTLV-I) infections in the United States prior to 1979-1981, when acquired immune deficiency syndrome (AIDS) was first recognized, we tested sera from 310 pregnant women who participated in the Collaborative Perinatal Project during the period 1959-1964 for HIV and HTLV-I antibody. These samples included sera from 53 pregnant women who were intravenous drug users. The remainder were from women who had cervical epithelial abnormalities, who developed cervical carcinomas, who had had children with erythroblastosis fetalis, who had had children that developed malignant neoplasms early in life, or normal pregnant women. None of the 310 women had confirmed HIV or HTLV-I antibody. The rate of false-positive reactions with the HIV enzyme-linked immunosorbent assay (ELISA) antibody test in these long-frozen samples was similar to that observed in fresh sera. HIV antibody was detected in homosexual patients with AIDS; HTLV-I antibody was not detected in any of these sera. HTLV-I antibody was detected in 17 of 20 patients with tropical spastic paraparesis (TSP) and in two of seven patients with other neurological diseases diagnosed as transverse myelopathy and multiple sclerosis, and in none of nine normal controls; HIV antibody was not detected in any of these sera patients. Thus, we conclude that there was no serological evidence of infection with HIV or HTLV-I in the pregnant women studied; however, HIV antibody was present in all AIDS patients tested, and HTLV-I antibody was found in the majority of patients with TSP.