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PubMed1999

Antibodies to cardiolipin and beta2-glycoprotein-1 in HTLV-1-associated myelopathy/tropical spastic paraparesis.

Anticardiolipin and anti-beta2GP1 antibodies were measured in 50 patients with HTLV-1-associated Myelopathy-Tropical Spastic Paraparesis (HAM-TSP) and the results were compared with those obtained for 34 HTLV-1-positive and 35 HTLV-1-negative controls, as well as 128 SLE patients. aCL but not anti-beta2GP1 was associated with HTLV-I infection. aCL was more prevalent than anti-beta2GP1 (32% vs. 8%) and was not associated with anti-beta2GP1 in HAM-TSP. IgA was the dominant isotype of aCL and anti-beta2GP1. The data suggest that tin HAM-TSP, IgA aCL are frequent and are associated with HTLV-1 infection.

Antibodies, Anticardiolipin↗

PubMed1997

A prospective survey of the causes of non-traumatic spastic paraparesis and tetraparesis in 585 patients.

OBJECTIVE: To ascertain the relative frequencies of the causes of non-traumatic paraparesis and tetraparesis in adults. DESIGN: Survey of patients enrolled prospectively over a 3 year period between 1986 and 1989 and review of their case notes 1 year after enrollment ceased (mean duration of follow up 30 months). SETTING: Regional neurosciences centre in the UK serving over three million people in Merseyside and North Wales. PATIENTS: Experienced clinicians from the centre saw most patients in the region with non-traumatic spastic paraparesis or tetraparesis. Primary investigation of patients was by myelography, for which patients were admitted to the centre. 585 consecutive patients with spastic paraparesis or tetraparesis were identified by daily screening of all 2104 patients undergoing myelography or radiculography during the 3 year period, ie selection by the intention to investigate them for myelopathy. EXCLUSIONS: age under 15 years, previous myelography for myelopathy. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Numbers and proportions of patients with each condition or category of disease. RESULTS: Commonest diagnoses were cervical spondylotic myelopathy (23.6%), extrinsic neoplastic or developmental tumour (16.4%), multiple sclerosis (9.1% rising to 17.8% after MRI of a selected group), and motor neurone disease (4.1%). Diagnosis was uncertain in 27.4%, falling to 18.6% after MRI. CONCLUSIONS: This survey shows the pattern of diseases producing non-traumatic myelopathy in the Mersey Region and in North Wales. Changing patterns of referral, investigation in peripheral hospitals and by non neurologically trained practitioners, and increasing use of outpatient MRI for primary investigation may make comparable surveys impossible in the future.

Adolescent↗

PubMed1985

Tropical spastic paraparesis: a neuroepidemiological study in Colombia.

A geographic isolate of tropical spastic paraparesis (TSP) in Tumaco, Colombia, is described. Fifty confirmed cases were identified (29 men, 21 women) with an estimated prevalence ratio of 98 cases per 100,000 population. Patients with identified cases ranged in age from 24 to 75 years (mean, 46.5). TSP begins with burning feet, leg stiffness, spastic bladder, and, in men, impotence. Patients exhibited leg weakness, spasticity, hyperreflexia, and scissoring gait. Babinski, Chaddock, and Hoffmann signs could be elicited. Ankle reflexes and vibratory sensation of the feet were decreased. Intellectual function, coordination, and cranial nerves remained normal. TSP is a slowly progressive disorder but so far there have been no deaths from it. Forty cases in this report began between 1971 and 1980; the earliest documented case began in 1952. Living conditions and occupations of the patients were typical for the region. Yaws had occurred in 74% of confirmed cases. No likely etiological neurotoxic or nutritional factors were identified. TSP also has been described in India, Africa, the Seychelles, and Jamaica.

Adult↗

PubMed1998

Reduction in HTLV-I proviral load and spontaneous lymphoproliferation in HTLV-I-associated myelopathy/tropical spastic paraparesis patients treated with humanized anti-Tac.

Human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neurological disease that results from an interaction of retroviral infection and immune activation. In this study, five doses (1 mg/kg) of humanized anti-Tac antibody were administered to 9 HAM/TSP patients at weeks 0, 2, 6, 10, and 14. Preliminary immunological studies on HAM/TSP patients treated with humanized anti-Tac indicate that there is a selective down-regulation of activated T cells and a decrease in the HTLV-I viral load in peripheral blood lymphocytes, most likely through the selective removal of HTLV-I-infected, activated CD4+ lymphocytes.

Antibodies↗

PubMed1988

Tropical spastic paraparesis. A clinical study of 50 patients from Tumaco (Colombia) and review of the worldwide features of the syndrome.

Tropical spastic paraparesis (TSP) is a chronic and slowly progressive endemic myelopathy occurring in geographical isolates in the Caribbean, South India, South Africa, the Seychelles, and Colombia. A detailed clinical and laboratory study was performed on 50 TSP patients from the island of Tumaco (Colombia), in a tropical rain forest area. Most patients were middle-aged blacks, 29 (58%) men and 21 women. In every case, neurological examination confirmed the presence of pyramidal signs in the lower limbs, plus, in 58%, moderate decrease in vibratory perception distally in the feet, bilaterally and symmetrically. Absent ankle jerks were found in 28%. Slow onset and chronic progression were documented in most patients. Positive treponemal serology, from yaws infection in childhood, was found in the serum in 92%, and in 19% also in the cerebrospinal fluid (CSF). No pleocytosis was documented on 27 CSF samples, but increased protein content occurred in 86%, with elevation of gamma-globulins in 78%. Treatment of 20 patients with high doses of penicillin produced no change in the clinical picture. TSP emerges from this review of the literature as a remarkably homogeneous clinical entity worldwide. A retrovirus-human T-lymphotropic virus type 1 (HTLV-1)--has been recently implicated as a possible etiology of the syndrome.

Adult↗

PubMed1996

Study of lower limb somatosensory evoked potentials in 96 cases of HTLV-I-associated myelopathy/tropical spastic paraparesis.

Lower limb somatosensory evoked potentials (LSEPs) were performed along with neurological evaluation in 96 HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients. The N20 latencies were abnormal in 5 cases. Central sensory conduction time (CSCT) was abnormal in 42 cases. A highly significant correlation (p < 0.001, r = 0.418) was found between CSCT and disability score. Such a correlation was not found between CSCT and other clinical findings, onset of illness, illness duration, serum and CSF antibody titer to HTLV-I and vibratory sensation. There was no difference of the mean of CSCT between the cases with sensory impairment and those without it. This shows that LSEPs are useful to estimate the disability of HAM/TSP. Also the cases with delayed CSCT and normal sensation suggest that LSEPs are capable of detecting subclinical lesions of the spinal cord in HAM/TSP.

Adult↗

PubMed2001

HTLV-1-associated myelopathy/tropical spastic paraparesis with pseudohypoparathyroidism.

In many short-stature patients with human T-lymphotrophic virus type I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), signs and symptoms were manifested during childhood. Successive investigations revealed 12 of 14 short-stature patients with pseudohypoparathyroidism (PHP) from the findings of short metacarpi, parathyroid hormone infusion test, immunoblotting of erythrocyte membrane, or lymphocytic Northern blotting of Gsalpha. Patients with PHP probably showed HAM/TSP based on their modified immunologic status. Human T-lymphotrophic virus type I infection did not induce PHP, but PHP may be a risk factor for the occurrence of HAM/TSP.

Adolescent↗

PubMed1996

Therapeutic trials in 200 patients with HTLV-I-associated myelopathy/ tropical spastic paraparesis.

We report here the results of therapeutic trials in 200 patients with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP) conducted in our department between 1986 and 1993. Motor disability grades were improved by more than one grade in 69.5% (91/131) of patients by oral administration of prednisolone, 50% (3/6) by eperisone hydrochloride only, 43.8% (7/16) by blood purification (lymphocytapheresis and plasmapheresis), 40.0% (2/5) by intrathecal injection of hydrocortisone, 30.0% (3/10) by intravenous injection of high-dose methylprednisolone, 23.3% (10/43) by interferon-alpha (intramuscular injection and inhalation), 22.2% (2/9) by azathioprine, 20.0% (4/20) by high-dose vitamin C, 16.0% (4/25) by erythromycin, 12.5% (3/24) by salazosulfapyridine, 11.8% (2/17) by mizoribine, 7.1% (1/14) by fosfomycin, and 6.3% (1/16) by thyrotropin releasing hormone. No critical side effects of these therapies were seen with the exceptions of one patient with adult respiratory distress syndrome due to cytomegalovirus infection and one patient with drug-induced hepatitis/hepatic failure. Selection of these treatments for patients with HAM/ TSP must be considered on the basis of age, sex, disease severity and complications to reduce adverse events and to improve quality of life. Although the results were a synopsis of different treatments given to 200 patients with HAM/ TSP as an open trial, we consider this the first report of a large-scale therapeutic trial in patients with HAM/TSP. The results of this study indicate that immunomodulatory therapies have some beneficial effects in HAM/TSP, and the functions of these agents are related to the pathophysiology of this disease.

Administration, Oral↗

PubMed1997

Human T cell lymphotropic virus type-1-associated myelopathy/tropical spastic paraparesis in Sao Paulo, Brazil: association with blood transfusion.

Human T cell lymphotropic virus type-1 (HTLV-1) associated myelopathy/tropical spastic paraparesis (HAM/TSP) has been epidemiologically linked to prior blood transfusion. The prevalence of transfusion as a risk factor for infection varies among endemic areas. Here we report the relative frequency of reported history of blood transfusion among 52 patients evaluated in Sao Paulo, Brazil. A patient reported history of blood transfusion prior to the onset of symptoms, found in 15 (28.8%) of the patients, was the most important risk factor identified in this group of patients when compared with a history of sexually transmitted diseases, homo/bisexuality, sexual promiscuity (three or more sexual partners a year), and intravenous drug use. The mean time between reported transfusions and the onset of symptoms was longer than previously reported. There was no trend toward a more severe evolution to motor inability among the HAM/TSP patients with a history of previous transfusion.

Adult↗

PubMed1993

Reactive serological tests for syphilis in tropical spastic paraparesis: a dilemma.

The prevalence of reactive serological tests for syphilis (STS) was investigated in 183 Jamaican patients with tropical spastic paraparesis (TSP) and 200 age and sex matched controls. A significantly higher prevalence of reactive STS was found in TSP patients (34.9%) compared with controls (14.0%, P < 0.001). The biological false positive (BFP) rate was also significantly higher in TSP patients (P < 0.01) as well as controls (P < 0.001) over 40 years of age. However, these findings do not imply a pathogenetic role for treponemal disease in TSP. The high prevalence of reactive STS in Jamaican TSP patients may be multifactorial, and include biological false positives (BFP), previous childhood yaws and concurrent syphilis.

Adult↗

PubMed1997

Dominantly inherited leukodystrophy showing cerebellar deficits and spastic paraparesis: a new entity?

We studied a dominant hereditary disorder showing progressive spastic paraparesis. The symptoms began in early childhood, with cerebellar deficits and mild mental deterioration, and the subsequent appearance of limb spasticity resulted in severe disability in the 3rd-4th decades of life. None of the patients were associated with any somatic abnormalities. Brain MRI showed diffuse white-matter involvement in all affected patients, but not in unaffected siblings. Although dominant, recessive, or X-linked leukodystrophies cause similar clinical features, our family did not show any known biochemical or gene deficits characteristic of these disorders. The clinical, radiological, and biochemical findings of this family are reported and suggest a possible novel genetic disorder.

Adult↗

PubMed1991

Leukoencephalopathy in HTLV-I-associated myelopathy/tropical spastic paraparesis: MRI analysis and a two year follow-up study after corticosteroid therapy.

Magnetic resonance imaging (MRI) of the brain was studied in 35 patients with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP), 19 HTLV-I seropositive carriers without HAM/TSP (non-HAM/TSP carriers), 18 patients with HTLV-I seronegative spastic spinal paraparesis (SSP), and 82 HTLV-I seronegative controls with other neurological disorders. The incidence of white matter lesions was significantly higher in HAM/TSP (66%) than in the controls (23%) and SSP (11%). HAM/TSP exceeded non-HAM/TSP carriers significantly in the incidence of multiple white matter lesions (37% vs 10%). HAM/TSP affected the deep and subcortical cerebral white matter multifocally, sparing the periventricular regions. None of the lesions were enhanced by gadolinium-DTPA. HAM/TSP patients with the white matter lesions had both a longer duration of disease and a greater disability than did those without lesions. The white matter lesions gradually increased in number, as the disability status became worse, in spite of the high dose corticosteroid treatment. All these observations suggest that the MRI abnormalities of the HAM/TSP brain may reflect the chronic perivascular inflammation with progressive gliosis (chronic disseminated encephalomyelitis). We propose that brain MRI can be successfully utilized as a reliable and non-invasive measure for following the disease progression in HAM/TSP.

Age Factors↗

PubMed1991

Cellular immune surveillance against HTLV-I infected T lymphocytes in HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP).

To investigate the cellular immune surveillance against HTLV-I infected T lymphocytes in HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP), we studied the cytotoxic T lymphocytes (CTL) activity against an HTLV-I infected human T cell line (MT-2) and the natural killer (NK) cell activity in 15 HAM patients, 6 HTLV-I carriers, and 15 controls. The activity of CTL against MT-2 cells was found to be significantly elevated in HAM compared with that in the controls. This cytotoxicity in HAM was higher than in HTLV-I carriers, although the difference was not statistically significant. There was an HLA class I restriction in this CTL activity against MT-2 cells in HAM. On the other hand, NK cell activity was significantly lower in HAM than in controls. Cold target inhibition studies suggested that NK cells could not lyse MT-2 cells effectively. There was a positive correlation between the CTL activity against MT-2 cells and the serum antibody titers to HTLV-I in HAM.

Adult↗

PubMed2005

Differences in viral and host genetic risk factors for development of human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis between Iranian and Japanese HTLV-1-infected individuals.

Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neurological disease observed only in 1-2 % of infected individuals. HTLV-1 provirus load, certain HLA alleles and HTLV-1 tax subgroups are reported to be associated with different levels of risk for HAM/TSP in Kagoshima, Japan. Here, it was determined whether these risk factors were also valid for HTLV-1-infected individuals in Mashhad in northeastern Iran, another region of endemic HTLV-1 infection. In Iranian HTLV-1-infected individuals (n=132, 58 HAM/TSP patients and 74 seropositive asymptomatic carriers), although HLA-DRB1*0101 was associated with disease susceptibility in the absence of HLA-A*02 (P=0.038; odds ratio=2.71) as observed in Kagoshima, HLA-A*02 and HLA-Cw*08 had no effect on either the risk of developing HAM/TSP or HTLV-1 provirus load. All Iranian subjects possessed tax subgroup A sequences, and the protective effects of HLA-A*02 were observed only in Kagoshima subjects with tax subgroup B but not in those with tax subgroup A. Both the prevalence of HTLV-1 subgroups and the host genetic background may explain the different risks levels for HAM/TSP development in these two populations.

Genetic Predisposition to Disease↗

PubMed1992

Evidence of preferential female prevalence of HTLV-I associated tropical spastic paraparesis in Bahia-Brazil.

In order to evaluate the prevalence of HTLV-I infection and its association with tropical spastic paraparesis (TSP) in Bahia, a Northeastern State of Brazil, CSF and sera from TSP patients and CSF and/or sera from some selected groups of individuals were studied. The results seem to indicate a higher prevalence of HTLV-I infection in women than men with TSP and among individuals of HIV risk groups. Some alterations of routine analysis of CSF can suggest HTLV-I infection in TSP patients.

Adult↗

PubMed1997

Discrepancy, coincidence or evidence in chronic idiopathic spastic paraparesis throughout the world. A meta-analysis on 2811 patients.

HTLV-I has been associated with a chronic idiopathic spastic paraparesis (CHISPA) in man; however, a complete understanding of this association is still debated. We selected the most comprehensible papers on this topic between 1985 and 1996, and found that 1261 out of 2811 patients (44.9%) reported, throughout the world, were HTLV-I positive. The mean age was 39.5 years and there was a female predominance of 1.9:1. These results do not exclude the causality of HTLV-I as a germen associated to CHISPA; however, other causes (e.g., toxic, immunosuppressors) must be considered as participating in the multistep neurodegeneration observed in CHISPA throughout the world.

Adolescent↗

PubMed1995

Detection of human T-lymphotropic virus type I (HTLV-I) tax RNA in the central nervous system of HTLV-I-associated myelopathy/tropical spastic paraparesis patients by in situ hybridization.

Autopsy specimens from 3 patients with human T-lymphotropic virus (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) were examined for the presence of HTLV-I in the central nervous system (CNS). In situ hybridization using an HTLV-I tax RNA probe detected cells containing HTLV-I RNA in spinal cord and cerebellar sections. HTLV-I infected cells were located within the white matter and, in particular, within the anterior and lateral funiculi of the spinal cord. Consistent with previously described HAM/TSP pathology, there were perivascular infiltrates in these CNS specimens. Significantly, HTLV-I RNA was not localized to these infiltrates but was detected deeper within the neural tissue. Furthermore, phenotypic analysis demonstrated that at least some of the infected cells were astrocytes. While previous polymerase chain reaction studies have demonstrated the presence of proviral HTLV-I in CNS specimens, here we provide evidence for the in situ expression of HTLV-I RNA in the CNS of HAM/TSP patients.

Aged↗

PubMed1998

Expression of FAP-1 (Fas-associated phosphatase) and resistance to Fas-mediated apoptosis in T cell lines derived from human T cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis patients.

Human T cell leukemia virus type 1 (HTLV-I) is the etiologic agent of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) with an autoimmune condition. We examined the sensitivity of HTLV-I-infected T cell lines to Fas-mediated apoptosis, which plays a critical role in the elimination of self-reactive T cells. Among 13 human T-cell lines, all 4 HAM-derived T cell lines and 4 of 6 non-HAM/HTLV-I T cell lines were resistant to apoptosis induced by anti-Fas antibody, whereas only 1 of 3 uninfected cell lines was resistant to apoptosis. The cell lines resistant to apoptosis expressed the viral tax gene and/or the cellular FAP-1 (Fas-associated phosphatase) gene, both of which inhibit Fas-mediated apoptosis in T cell lines. Although Tax is a transcriptional activator of a number of cellular genes, the expression of Tax in a T cell line did not induce the expression of FAP-1, suggesting that these two antiapoptotic proteins independently function in HTLV-I-infected cells. Seven of 10 HTLV-I-infected cell lines, compared with only 1 of 3 virus-negative cell lines, expressed FAP-1. All four HAM cell lines expressed the FAP-1 gene, and its level in these cells was higher than in other T cell lines. Our results suggest that virus-infected T cells escape Fas-mediated immune surveillance by the function of Tax and FAP-1, and this escape may be involved in the autoimmune condition observed in HAM/TSP patients.

Apoptosis↗