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PubMed1985

Antibodies to human T-lymphotropic virus type-I in patients with tropical spastic paraparesis.

10 out of 17 (59%) patients with tropical spastic paraparesis (TSP) had antibodies to human T-lymphotropic virus-I (HTLV-I), as did 5 out of 5 TSP patients with systemic symptoms. Only 13 out of 303 (4%) controls, made up of blood donors, medical personnel, and other neurological patients, had such antibodies. These findings suggest either that HTLV-I is neurotropic or that the virus or a related one contributes to the pathogenesis of TSP.

Adolescent↗

PubMed2004

Cutaneous reflexes from the foot during gait in hereditary spastic paraparesis.

OBJECTIVE: It is known that P2 cutaneous reflexes from the foot show phase-dependent modulation during gait. The role of the motor cortex and the cortico-spinal tract in these reflexes and their modulation is unknown. Patients with hereditary spastic paraparesis (HSP) have a lesion in the cortico-spinal tract and may show deficits in P2 reflexes and/or their modulation. METHODS: Reflex responses of tibialis anterior and biceps femoris after sural nerve stimulation in 10 HSP-patients were compared with those in 10 healthy subjects. The reflexes were studied at two different moments in the step cycle during walking on a treadmill. RESULTS: Both patients and controls showed a phase-dependent modulation of P2 responses. For the individual muscles, no significant difference in reflex activity was observed between HSP-patients and the controls. However, when all muscles were taken together, the reflex activity for the controls was significantly higher than for the patients. CONCLUSIONS: The results of this study suggest that the cortico-spinal tract is involved in the regulation of the amplitude of the P2 responses and their phase-dependent modulation.

Adult↗

PubMed2000

Clinical and pathologic findings in hereditary spastic paraparesis with spastin mutation.

OBJECTIVE: To describe a family with chromosome 2p-linked hereditary spastic paraparesis (HSP) associated with dementia and illustrate the cerebral pathology associated with this disorder. BACKGROUND: HSP comprises a heterogeneous group of inherited disorders in which the main clinical feature is severe, progressive lower limb spasticity. Nongenetic classification relies on characteristics such as mode of inheritance, age at onset, and the presence or absence of additional neurologic features. Several loci have been identified for autosomal dominant pure HSP. The most common form, which links to chromosome 2p (SPG4), has recently been shown to be due to mutations in spastin, the gene encoding a novel AAA-containing protein. RESULTS: The authors report four generations of a British family with autosomal dominant HSP in whom haplotype analysis indicates linkage to chromosome 2p. In addition, a missense mutation has been identified in exon 10 of the spastin gene (A1395G). Dementia was documented clinically in one member of the family, two other affected family members were reported to have had late onset memory loss, and a younger affected individual showed evidence of memory disturbance and learning difficulties. Autopsy of the demented patient confirmed changes in the spinal cord typical of HSP and also demonstrated specific cortical pathology. There was neuronal depletion and tau-immunoreactive neurofibrillary tangles in the hippocampus and tau-immunoreactive balloon cells were seen in the limbic and neocortex. The substantia nigra showed Lewy body formation. The pathologic findings are not typical of known tauopathies. CONCLUSIONS: The authors confirm that chromosome 2p-linked HSP can be associated with dementia and that this phenotype may be associated with a specific and unusual cortical pathology.

Adenosine Triphosphatases↗

PubMed2003

Transcranial magnetic stimulation study in hereditary spastic paraparesis.

The motor-evoked potentials and the cortical excitability by transcranial magnetic stimulation (TMS) were studied in a family with chromosome 2p linked (due to mutations in spastin) and in a family with chromosome 16q linked (due to mutations in paraplegin) hereditary spastic paraparesis (HSP), in order to evaluate the utility of these techniques in identifying the subgroups of the disease. Central motor conduction time and motor treshold to TMS were abnormal in some members of both families; the intracortical inhibition was reduced only in the affected members of the family with chromosome 2p linked HSP, even though the neurological symptoms were sometimes similar and also when clinical features reflecting cortical dysfunction were absent. The motor cortex is differentially involved in the often clinically indistinguishable forms of HSP, and TMS may help in the differential diagnosis.

Adult↗

PubMed1994

Allolymphocytotoxic antibodies in sera from HTLV-I-associated myelopathy/tropical spastic paraparesis patients--putative anti-HLA antibodies.

Thirty-one HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients and 34 asymptomatic carriers were studied in order to investigate the presence of anti-lymphocyte antibodies in their sera. 32% of the patients produced allolymphocytotoxic antibodies reactive to peripheral blood lymphocytes (mainly T cells) as well as to B cells, which belonged to the IgM class, reacted under warm and cold conditions, and showed specificity to multiple HLA antigens, especially HLA A2, A26, A33, B7, B27, B35, B48, B61 and Cw3. Moreover, their reactivities could be absorbed by pooled platelets. Therefore, it may be suggested that either anti-HLA class I antibodies or antibodies cross-reactive to HLA were present. On Western blot analysis, the HAM/TSP cytotoxic sera reacted to the 110 kDa molecules of lymphocyte lysates. In the case of carriers, weak cytotoxic antibodies were detectable in 14% of the sera. No multispecificity to HLA class I antigens was observed and there was no reactivity to the 110 kDa band. The production of allolymphocytotoxic antibodies in HAM/TSP patients may therefore be explained by the presence of allogeneic-like stimuli in this disease. HTLV-I infected cells, expressing altered HLA antigens could possibly account for this stimulation and also contribute to the alteration of immune functions in HAM/TSP, and thus play an important role in its pathogenesis.

Adult↗

PubMed2003

Osteoporosis in HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

Human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) has been associated with changes in extracellular matrix of neural tissue. HTLV-I infection has multiple other systemic effects. Extracellular matrix is important for bone mineral deposition. We examined bone mineral density (BMD) in patients with HAM/TSP. BMD was assessed by ultrasonographic calcaneous densitometry in 24 patients (7 males, 17 females) with HAM/TPS, and 23 healthy HTLV-I-seronegative controls matched by age and sex. Patients with HAM/TPS had a mean BMD T-score of -3.07 +/- 0.64 in males and -2.93 +/- 0.69 in females. Control patients revealed a T-score of -0.77 +/- 1.31 in males and -1.17 +/- 1.08 females. The difference in T-score between HAM/TSP patients and control groups is significant (P < 0.001). Of HAM/TPS patients, 7 of 24 (29.2%) had osteopenia (T-score between -1 and -2.5) and 17 of 24 (70.8%) were diagnosed with osteoporosis (T < -2.5). Respective figures for control patients were 10 of 23 (43.5%) with a normal T-score, 11 of 23 (47.8%) with osteopenia, and 2 of 23 (8.7%) with osteoporosis. After adjustment for age and sex, odds ratio of osteoporosis for HAM/TSP patients was 31.52 (95% confidence interval, 5.07 to 195.88). No correlation was found in HAM/TSP patients between T-score and age, menstrual status, gait functionality, or years of evolution of HAM/TSP. HAM/TSP patients have a significantly diminished BMD of the calcaneous that appears not to be explained by paresis, age, years of disease, menstrual status; may be the result of systemic alterations due to HTLV-1 infection.

Adult↗

PubMed1992

Novel complications with HTLV-1-associated myelopathy/tropical spastic paraparesis: interstitial cystitis and persistent prostatitis.

Lower urinary symptoms associated with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) are common, but have been regarded as 'neurogenic' due to spinal involvements. However, in some cases, these symptoms are persistent, progressive, and not directly correlated with the severity of other neurologic symptoms of the lower spinal cord. These findings prompted us to locate organic lesions in the lower urinary tract and to correlate them with HTLV-1 infection. Among 35 HAM patients with lower urinary symptoms, we found 4 cases with the symptoms persistent and progressive: 3 with contracted bladder and another with persistent prostatitis. Histological or cytological examinations indicated local lymphocytic infiltrations in the lower urinary tract in all cases: 3 by the infiltration in the bladder and the other by a high concentration of lymphocytes in expressed prostatic secretions. Of 3 cases whose urinary samples were available, 2 showed significant increase in the concentration of urinary anti-HTLV-1 antibody of IgA class. The urinary IgA antibody of the third case was not elevated, but the sample had been obtained after resection of the affected bladder. None of the control cases showed significant anti-HTLV-1 IgA antibody in urine except for a case of gross hematuria due to chemotherapy directed against adult T-cell leukemia. We suggest inclusion of these processes into the spectrum of complications for HAM/TSP. The elevated excretion of anti-HTLV-1 of IgA class in urine may be an indicator of these complications.

Adult↗

PubMed1999

The role of human T-lymphotropic virus type 1 (HTLV-1)-infected dendritic cells in the development of HTLV-1-associated myelopathy/tropical spastic paraparesis.

The development of human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is closely associated with the activation of T cells which are HTLV-1 specific but may cross-react with neural antigens (Ags). Immature dendritic cells (DCs), differentiated from normal donor monocytes by using recombinant granulocyte-macrophage colony-stimulating factor and recombinant interleukin-4, were pulsed with HTLV-1 in vitro. The pulsed DCs contained HTLV-1 proviral DNA and expressed HTLV-1 Gag Ag on their surface 6 days after infection. The DCs matured by lipopolysaccharides stimulated autologous CD4(+) T cells and CD8(+) T cells in a viral dose-dependent manner. However, the proliferation level of CD4(+) T cells was five- to sixfold higher than that of CD8(+) T cells. In contrast to virus-infected DCs, DCs pulsed with heat-inactivated virions activated only CD4(+) T cells. To clarify the role of DCs in HAM/TSP development, monocytes from patients were cultured for 4 days in the presence of the cytokines. The expression of CD86 Ag on DCs was higher and that of CD1a Ag was more down-regulated than in DCs generated from normal monocytes. DCs from two of five patients expressed HTLV-1 Gag Ag. Furthermore, both CD4(+) and CD8(+) T cells from the patients were greatly stimulated by contact with autologous DCs pulsed with inactivated viral Ag as well as HTLV-1-infected DCs. These results suggest that DCs are susceptible to HTLV-1 infection and that their cognate interaction with T cells may contribute to the development of HAM/TSP.

Antigen-Presenting Cells↗

PubMed1996

Multiple sclerosis and HTLV-I associated myelopathy/tropical spastic paraparesis are two distinct clinical entities.

Multiple sclerosis (MS) and HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) can overlap in their clinical features and thereby cause difficulties for clinicians in relation to diagnosis and therapy. However, epidemiological biochemical, immunological, virological and radiological studies point to a number of significant differences. Recent comparative neurophysiological data, including blink reflex studies, obtained in these disorders, is briefly reviewed here and provides additional evidence of difference. The abnormal blink reflex in patients with MS consist of prolonged latencies and absences of R1 and R2 responses and are mainly due to demyelinating lesions around the pans. In contrast, in HAM/TSP the blink reflex abnormalities frequently include an unusual early response, R1k, which is probably a consequence of interneuronal hyperexcitability around the brainstem. Thus these findings provide further support for our contention that HAM/TSP and multiple sclerosis are distinctly different both as clinical entities and in their underlying pathomechanisms.

Adult↗

PubMed1995

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP): recent perspectives.

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a well-defined clinicopathological entity, and approximately 1,900 patients with HAM/TSP have been reported in the world. Improved polymerase chain reaction (PCR)-based in situ techniques have allowed a better appreciation of the cellular localization of the virus activation in infected patients, and there is accumulating evidence that HAM/TSP is characterized by a distributional bias of viral activation between the blood flow and central nervous system (CNS). This review summarizes the current status of our understanding of HAM/TSP, and emphasizes the possible pathogenic involvement of cellular interactions between infected cells and responding immunocompetent cells in the CNS of patients with HAM/TSP. In addition, the notable systemic manifestations with or without myelopathy in HTLV-I-infected individuals are described.

Humans↗

PubMed1988

HTLV-I-like viral particles in spinal cord cells in Jamaican tropical spastic paraparesis.

Viral-like particles morphologically identical to human T-lymphotropic virus type I or II, but distinct from human T-lymphotropic virus type III, have been seen by electron microscopy in spinal cord tissue from a Jamaican tropical spastic paraparesis patient who was known to be positive for human T-lymphotropic virus I antibody before death. This is the first electron microscopy report on a patient from an endemic tropical spastic paraparesis region.

Adult↗

PubMed2006

Basilar impression associated with impacted cisterna magna, spastic paraparesis and distress of balance: case report.

We report on a 48 years-old man with basilar impression without syringohydromyelia, in which the cisterna magna was impacted by the cerebellar tonsils. Six months after posterior fossa decompression there was the disappearance of nuchal rigidity, vertigo, spastic paraparesis and improvement of balance. Nevertheless hyperreflexia and diminished pallesthesia of the lower limbs persisted.

Arnold-Chiari Malformation↗

PubMed1984

Mantakassa: an epidemic of spastic paraparesis associated with chronic cyanide intoxication in a cassava staple area of Mozambique. 1. Epidemiology and clinical and laboratory findings in patients. Ministry of Health, Mozambique.

Investigation of an epidemic of more than 1000 cases of spastic paraparesis in a drought-striken cassava staple area of Mozambique strongly suggests an association between this disease (called mantakassa), chronic cyanide intoxication, and cassava consumption. In previous reports of neurological disease with similar associations, the disease affected an older age group with usually a gradual onset, and the predominant clinical feature was an ataxic neuropathy. In mantakassa the onset was acute, and mostly women of reproductive age and children were affected. Serum thiocyanate levels in these patients were much higher than previously reported; while spastic paraparesis of unknown etiology occurs in many tropical countries, it has not previously been linked with raised thiocyanate levels. The present evidence linking cassava consumption to the disease is circumstantial, and dietary deficiency is also probably involved. Cassava is an important food crop and a major source of energy for people in many parts of the world. In these areas, when there is a shortage of food production, e.g., during a drought, the inhabitants may be exposed to the risk of dietary cyanide intoxication. Further research is needed on the causes of mantakassa so that a repetition of this disaster could be prevented.

Adolescent↗

PubMed1989

Viral specific IgG and IgM antibodies in the CSF of patients with tropical spastic paraparesis.

The cerebrospinal fluid (CSF) from seven West Indian migrants to the United Kingdom with tropical spastic paraparesis were studied by antigen immunoblotting for specific anti-HTLV1 oligoclonal IgG and IgM. Eight CSFs from five patients were positive for specific IgG and negative for IgM; three CSFs from two patients were positive for IgM and negative for IgG. No patient had both IgG- and IgM-positive CSF. Those patients with IgM only had disease of the shortest duration. When looking for evidence that neurological damage is caused by HTLV1, both IgM and IgG should be examined.

Adult↗

PubMed2002

Detection of myelin basic protein in cerebrospinal fluid and serum from patients with HTLV-1-associated myelopathy/tropical spastic paraparesis.

BACKGROUND: Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy (HAM)/tropical spastic paraparesis (TSP) is a chronic inflammatory disease that primarily affects the spinal cord and may be a neurological syndrome that is clinically similar to multiple sclerosis (MS). Myelin basic protein (MBP) in the cerebrospinal fluid (CSF) of MS patents is generally measured by radioimmunoassay. We have recently established a sensitive enzyme-linked immunosorbent assay (ELISA) and measured the MBP concentrations in CSF and serum of HAM/TSP patients. METHODS: A sensitive two-site ELISA capable of measuring MBP at a concentration as low as 30 pg/mL in serum and CSF samples was used. RESULTS: Significantly higher CSF MBP concentrations were detected in 61% of HAM/TSP patients than in patients with non-neurological diseases. Serum MBP concentrations were also higher in 9% of HAM/TSP patients compared with patients with non-neurological diseases or healthy controls. CONCLUSIONS: Using our ELISA system, we detected MBP in CSF and serum not only in patients with central active demyelination as in MS, but also in patients with spinal cord demyelination as in HAM/TSP.

Adult↗

PubMed2001

HTLV-I negative tropical spastic paraparesis: a scientific challenge.

We reviewed the historical, clinical and etiological aspects of the progressive chronic spastic myelopathies of unknown etiology, disserting on the clinical similarities between HTLV-I seropositive and seronegative tropical spastic paraparesis (TSP), as well as focusing on the PCR studies of the seronegative TSP.

Diagnosis, Differential↗

PubMed1992

Progressive spastic paraparesis associated with human T-cell leukemia virus type I (HTLV-I).

Patients with progressive spastic paraparesis (PSP), commonly middle-aged women, are distributed throughout the country of Chile. During the three years from 1987 to 1990, we collected 83 cases of PSP from among 225 patients with various neurological diseases. The clinical picture was of a bilateral pyramidal syndrome, with sensory deficits in only 15.5% of the cases, and a slow illness progression in the majority of them. In patients with PSP, antibody to human T-cell leukemia virus type I (HTLV-I) was analyzed by enzyme linked immunosorbent assay (ELISA) and confirmed by western blot analysis. Forty-five (54.2%) patients were anti-HTLV-I antibody positive in cerebrospinal fluid (CSF) and peripheral blood. Among them, 2 patients had leukemia/lymphoma and one had Sjögren syndrome. In the laboratory study of seropositive PSP, mononuclear pleocytosis was found in 35.7%; there was an abnormal increase of the IgG index in 66.6% and an increase in CD2 in blood and CSF, and CD4 in blood. A delayed latency of somatosensory evoked potentials was observed in 90.9%. The neuropsychological study revealed a WAIS with a mean verbal IQ of 80.7 and a mean performance IQ of 84.8. The most impaired items were digit symbol and digit span. Seven subjects (18.9%) with anti-HTLV-I antibody were found among 37 relatives from 19 anti-HTLV-I positive cases of PSP.

Adult↗

PubMed1999

The significance of immune disorder in tropical spastic paraparesis.

The reports of the occurrence of HTLV-1 infection and/or HTLV-1 associated myelopathy (HAM/tropical spastic paraparesis (TSP) in patients with certain organ-specific and nonorgan-specific autoimmune diseases prompted us to assess the relationship between TSP and humoral autoimmunity. Blood samples from 76 TSP patients, 60 asymptomatic HTLV-1 carriers and 100 HTLV-1 seronegative blood donors were examined for the presence of organ-specific and nonorgan-specific autoantibodies, reactive serological tests for syphilis, immunoglobulin and complement concentrations as well as immunecomplexes. High prevalences of autoantibodies (39/76, 51%), reactive serological tests for syphilis (23/76; 30%), hypergammaglobulinaemia (69/76, 90%) and complement fixing immune complexes (44/76, 58%) were found in the TSP patients. These indicators of immunological disorder were found in statistically significantly lower prevalences in asymptomatic HTLV-1 carriers (12/60, 20%; p < 0.001; 6/60, 10%; p < 0.05; 32/60, 53%; p < 0.001 and 8/60, 13%; p < 0.001, respectively) and HTLV-1 seronegative blood donors (8/100, 8%; p < 0.001; 3/100, 3%; p < 0.001; 15/100, 15%; p < 0.001 and 5/100, 5%; p < 0.001, respectively). The profiles of autoimmune phenomena observed in the patient and control groups revealed that they were associated with TSP rather than mere HTLV-1 infection and consequently pathogenetic significance. The array of immunological features present in TSP was suggestive of autoimmune disease resulting from immune dysfunction. Studies which explore the possible existence of HTLV-1 induced autoantibodies with specificity for antigens of the spinal cord in TSP might be useful in elucidating its pathogenesis.

Adolescent↗