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PubMed1998

[Familial form of tropical spastic paraparesis. Report of 4 families].

We report eight patients with familial tropical spastic paraparesis belonging to four families. The diagnosis was reached by clinical, radiological and electrophysiological studies. Human lymphotropic virus type I infection was confirmed by ELISA, immunofluorescence essays. Western blot and polymerase chain reaction in DNA of peripheral blood mononuclear cells, using primers for tax and 5'ltr genes. In all these families there was a vertical transmission of the disease from the first to the second generation. All patients improved their spastic gait after prednisone treatment. Among patients of the second generation, all had dacrysialoadenitis, three had leukemia like lymphocytes in the blood smear, two had mycosis fungoides and one had hepatic cirrhosis.

Adolescent↗
PubMed1992

Screening of patients with hereditary spastic paraparesis and Addison's disease for adrenoleukodystrophy/adrenomyeloneuropathy.

X-linked adrenoleukodystrophy/adrenomyeloneuropathy presents a wide variation of clinical manifestations and may mimic several diseases. A screening investigation by measuring plasma saturated very long-chain fatty acids was performed in two groups of patients. Among six patients with hereditary spastic paraparesis one woman was detected to be a heterozygous gene carrier. However, in a group of eleven adult men with idiopathic Addison's disease the plasma concentrations of very long-chain fatty acids were all within normal limits. We conclude that X-linked adrenoleukodystrophy and symptomatic heterozygous females should be considered in cases of progressive spastic paraparesis.

Addison Disease↗
PubMed2003

Dermatological findings of human T lymphotropic virus type 1 (HTLV-I)-associated myelopathy/tropical spastic paraparesis.

Dermatological findings for patients with human T lymphotropic virus type 1(HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) were investigated and were compared with dermatological findings for a control group. Only xerosis, cutaneous candidiasis, and palmar erythema were significantly associated with HAM/TSP. Histopathological patterns of cutaneous lymphoma were seen in 25% of 32 patients who underwent biopsy, and, thus, the cutaneous alterations in HAM/TSP can be classified into nonspecific lesions, infectious lesions, immune-inflammatory-mediated lesions, and premalignant or malignant lesions.

Adult↗
PubMed1991

[A case of cerebrotendinous xanthomatosis with spastic paraparesis, epilepsy, and bradykinesia].

A 26-year-old female developed mental deterioration, general convulsion, cataract and spastic gait in order since her entrance into elementary school. A diagnosis of cerebrotendinous xanthomatosis (CTX) was made because of hypercholestanolemia. At the time of admission, cataract, a mild thickening of Achilles tendons, mental deterioration, spastic paraparesis, truncal ataxia, and bradykinesia were noted. Bilateral slowing of 2 to 7 Hz was recorded in EEG, and brain CT and MRI revealed mild cerebellar atrophy. HVA and 5-HIAA levels in CSF were low. Oral administration of chenodeoxycholic acid, 300 mg per day, resulted in improvement of bradykinesia and EEG abnormality, increase of HVA and 5-HIAA levels in CSF, and decrease of serum cholesterol level in two weeks. Bradykinesia observed in the present case is a rare clinical finding of CTX, and the improvement of bradykinesia soon after the treatment with chenodeoxycholic acid has not been reported yet. This case is important for elucidating the mechanism of neurological disorders in CTX.

Adult↗
PubMed1994

Serological tests for Lyme disease in patients with tropical spastic paraparesis and healthy Jamaicans.

The significance of reactive serological tests for Lyme disease in patients with tropical spastic paraparesis (TSP) was assessed by examining serum samples from 128 of these patients and 200 healthy Jamaicans by Lyme indirect immunofluorescent antibody (IFA), enzyme immuno-assay (EIA) and Western blot analyses. Sera were also examined in serological tests for syphilis (STS), an unabsorbed fluorescent treponemal antibody test and leptospira microagglutination test. The prevalence of positive Lyme IFA and EIA results did not differ significantly between sera from TSP patients (12.5%) and healthy controls (10.0%). Western blot analyses showed that the positive Lyme IFA and EIA results observed in this study were due to false positive reactions. Seventy-five per cent of Lyme IFA/EIS positive sera from TSP patients had treponemal antibodies. Eighty per cent of those from healthy controls were negative in standard STS but 85% were positive when tested in an unabsorbed fluorescent treponemal antibody (FTA). These data indicate that reactive serological tests for Lyme disease in Jamaican TSP patients and healthy Jamaicans are false positive reactions due to cross-reactivity with other spirochaetes, notably Treponema pallidum and non pathogenic treponemes.

Adolescent↗
PubMed1997

[Isolated spastic paraparesis disclosing Krabbe disease in adult age].

A 25-year-old woman developed a slowly progressive spastic paraparesis a few weeks after delivering of her first child. A cerebral MRI showed bilateral areas of hyperintensity in T-2 weighted images in the centrum semi-ovale, internal capsule, midbrain and occipital white matter. A profound deficiency of galactosyl/ceramidase activity was demonstrated in leukocytes (< 5 p. 100 of controls) and in cultured fibroblasts. The diagnosis of the adult form of Krabbe's disease was thus retained. We summarize the clinical symptoms and neuroradiological signs of this disorder and discuss the causative factors of its clinical heterogeneity.

Adult↗
PubMed1998

Demonstration of human T lymphotropic virus type I (HTLV-I) tax-specific CD8+ lymphocytes directly in peripheral blood of HTLV-I-associated myelopathy/tropical spastic paraparesis patients by intracellular cytokine detection.

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is an inflammatory neurologic disease caused by HTLV-I infection and has been associated with elevated levels of several proinflammatory cytokines in both serum and cerebrospinal fluid. It is unknown what kind of cells secrete these cytokines and if HTLV-I Ags are associated with this phenomenon. Here, we investigated the expression of cytokines in PBL from eight HAM/TSP patients, nine HTLV-I-infected asymptomatic carriers, and seven healthy controls by flow cytometry combined with intracellular cytokine staining. PBL were cultured with brefeldin A without mitogen and IL-2 for 14 h. Under these conditions, CD8+ cells produced proinflammatory cytokines including IFN-gamma, TNF-alpha, and IL-2, which were significantly elevated in HAM/TSP patients. The proportion of CD8+ cells producing IFN-gamma in HAM/TSP patients, asymptomatic carriers, and healthy controls were, on average, 4.9, 0.4, and 0.3%, respectively. IFN-gamma production by these CD8+ cells was suppressed by anti-HLA-class I Ab. Purified CD8+ cells from an HLA-A2 HAM/TSP patient produced IFN-gamma by cocultivation with autologous CD4 cells, the main reservoir of HTLV-I in vivo, or allogenic HLA-A2+ B cells pulsed with a known immunodominant HTLV-I tax peptide. These data suggest that high levels of circulating HTLV-I-specific CD8+ T lymphocytes have the potential to produce proinflammatory cytokines and may promote inflammatory responses to HTLV-I in HAM/TSP patients.

CD8-Positive T-Lymphocytes↗
PubMed1987

Antibody to human T-lymphotropic virus type 1 in West-Indian-born UK residents with spastic paraparesis.

Of 13 West-Indian-born UK residents with spastic paraparesis of unknown cause, 11 were tested for serum antibody to human T-cell lymphotropic virus type 1 and all were positive. Their magnetic resonance imaging scans were normal or showed only minor abnormalities in the brain, and the spinal cord was normal in the 5 investigated. Of 48 patients with multiple sclerosis, mainly caucasian, none had antibody to HTLV-1 in the blood.

Adult↗
PubMed1988

Tropical spastic paraparesis in Colombia.

A high-incidence focus of tropical spastic paraparesis (TSP) occurs on the South Pacific coast of Colombia. Of 55 patients studied, 52 (94.5%) had IgG antibodies to the human T-cell lymphotropic virus type I (HTLV-I) in serum and/or cerebrospinal fluid. Control groups did not show similar high positivity. Our results suggest that HTLV-I or other antigenically related retroviruses may be the cause of TSP in Colombia. Similar clinical, laboratory, and epidemiological findings have been reported in widely remote geographical regions of the world, with very similar clinical pictures of TSP in all high-incidence regions. The demonstration of IgG antibodies in serum and cerebrospinal fluid of patients with TSP in the Caribbean and Seychelles Islands, southern Japan, and the Ivory Coast indicate that the HTLV-I retrovirus could be the cause of this "tropical" myeloneuropathy.

Adolescent↗
PubMed1997

Influences of muscle stretch reflexes on voluntary, velocity-controlled movements in spastic paraparesis.

We studied voluntary, velocity-controlled knee movements in 22 patients with spastic paraparesis (11 male, 11 female) and 22 healthy controls (11 male, 11 female). Torque and EMG activity of the quadriceps and the hamstring muscles were determined in maximal voluntary concentric (shortening) and eccentric (lengthening) actions of knee extensor and flexor muscles at constant movement velocities of 30, 60, 120 and 180 degrees/s, using an active, isokinetic dynamometer. In the spastic patients, the voluntary strength and the agonist EMG activity were reduced in all movements. The reduction was largest in concentric actions at high velocity. The antagonist EMG activity was reduced in the same proportion as the agonist EMG activity in eccentric actions. In concentric actions when stretch is imposed upon antagonists, the antagonist EMG activity increased with the velocity of stretch, indicating stretch reflex activation. In parallel with the stretch reflex activation of antagonists, there was reduced activation of the agonists compatible with Ia reciprocal inhibition of agonist motoneurons. When agonists were stretched in eccentric actions, stretch reflexes appeared to support the voluntary, agonist activation of knee flexor muscles but not knee extensors.

Adult↗
PubMed1993

Dendritic cells infected in vitro with human T cell leukaemia/lymphoma virus type-1 (HTLV-1); enhanced lymphocytic proliferation and tropical spastic paraparesis.

Evidence supporting a role of the dendritic cell (DC) in stimulating autologous T cell activity in tropical spastic paraparesis (TSP) was sought by studies of cells taken from healthy volunteers and exposed to HTLV-1 in vitro. DC were co-cultured with an HTLV-1-producing cell line (MT-2) at 1:1 or 10:1 ratios. These DC stimulated high levels of proliferation in autologous T cells. This was similar to that seen in an autologous mixed leucocyte reaction (AMLR) using cells from TSP patients. The requirement for both DC and virus was confirmed, since neither DC co-cultured with uninfected MT-2 cells nor addition of infected MT-2 cells directly to T cells caused significant stimulation. DC exposed to the highest dose of HTLV-1 (1:1) for 24 h before addition of T cells caused strong stimulation that increased after 8 h but almost disappeared by 72 h. In situ hybridization showed that approximately 25% of DC became infected in cultured cells after preincubation for 24 h, and over 50% were infected with a 72-h preincubation. We suggest that infection of DC by HTLV-1 may be an initial step in altering the immune system in seronegative patients, and that persistent T cell stimulation in those with genetic susceptibility may underlie the production of neurological disease.

Aged↗
PubMed1994

The transactivator gene of human T-cell leukemia virus type I is more variable within and between healthy carriers than patients with tropical spastic paraparesis.

Human T-cell leukemia virus type I (HTLV-1) causes T-cell leukemia and tropical spastic paraparesis (TSP) in a minority of infected people, whereas the majority remain healthy. No association between a particular HTLV-I sequence and disease manifestation has been found in previous studies. We studied here the sequence variability of the gene for the HTLV-I Tax protein, which is the dominant target antigen of the very strong cytotoxic T-lymphocyte response to the virus. In HTLV-I infection, the intraisolate nucleotide variability is much greater than the variability between isolates. The predicted protein sequence of Tax was significantly more variable in the healthy seropositive individuals' provirus than in those of the patients with TSP. Thus, tax sequence heterogeneity, rather than the presence of particular sequences, distinguishes healthy HTLV-I-seropositive individuals from patients with TSP.

Base Sequence↗
PubMed2000

Immunopathogenesis of HTLV-I-associated myelopathy/tropical spastic paraparesis.

The main pathological feature of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is chronic inflammation of the spinal cord characterized by perivascular cuffing of mononuclear cells accompanied by parenchymal lymphocytic infiltration. Although the exact mechanism of the pathogenesis of HAM/TSP is still obscure, immunological abnormalities arising from a high HTLV-I proviral load in peripheral blood lymphocytes (PBL) play an important role in the pathological process of spinal cord lesions in HAM/TSP patients. The relationship between HLA haplotype and the risk of the occurrence of HAM/TSP will be elucidated by results from studies of HLA allele typing. In addition, recent data indicate that HTLV-I and its expression are localized in infiltrated lymphocytes within the spinal cord lesions of HAM/TSP patients rather than in resident central nervous system (CNS) parenchymal cells. Although a bystander damage of the surrounding CNS tissues, in which CD8+ HTLV-I-specific cytotoxic T lymphocyte (CTL) attack HTLV-I-infected lymphocytes, might be involved in the pathological events of the spinal cords of HAM/ TSP patients as one of the actual pathogenetic mechanisms, heightened transmigrating activity of HTLV-I-infected CD4+ T lymphocytes to the CNS tissues may have a key role in the development of HAM/TSP. Therefore, although the exact mechanism underlying the high HTLV-I proviral load in PBL in HAM/TSP patients is still unknown, we must consider therapeutic approaches in HAM/TSP that eliminate HTLV-I-infected CD4+ T lymphocytes.

Adult↗
PubMed1997

[Clinical and immunological findings of hepatitis B virus associated spastic paraparesis--a comparison with HAM].

We investigated clinical features and immunological parameters in 40 patients with slowly progressive spastic paraparesis including 13 cases (4 men and 9 women, aged 43 to 71, mean 61 years) with positive antibody to hepatitis B virus (HBV), 13 (6 men and 7 women, aged 39 to 75, mean 63 years) with positive antibody to HBV and HTLV-I, and 14 (3 men and 11 women, aged 33 to 71, mean 55 years) with positive antibody to HTLV-I (HAM). None showed obviously organic changes of the spine on magnetic resonance image. Patients with positive antibody to HBV (hepatitis B virus associated myelopathy, HBM) were significantly lower in disability grade and had a fewer incidence of micturition than in the HAM. Furthermore, natural killer (NK) activities were in normal range and peripheral blood lymphocytes did not show autologous proliferation response (APR). Patients with positive antibody to both HBV and HTLV-I showed APR similar to HAM, but in most patients NK activities were within normal range. These results suggest that the mechanism of myelopathy in HBM may be different from that in HAM, and HBV infection may play a role as a cofactor in HAM.

Adult↗
PubMed2006

Portosystemic myelopathy: spastic paraparesis after portosystemic shunting.

Portosystemic encephalopathy (PSE) is a well-known, common complication of portal hypertension. It is thought to be caused by nitrogenous substances such as ammonia, which are normally cleared from the blood stream by the liver. In cirrhosis and other hepatic disorders with portosystemic shunting (PSS)-- either surgical portosystemic anastomoses (PSA) or spontaneous PSS-- the collateral vessels bypass the liver allowing the accumulation of toxic, ammoniacal substances in the blood and tissues. PSE is characterized by encephalopathy; portosystemic myelopathy (PSM) is characterized by paresis of the extremities, Babinski signs and muscle spasticity in patients with cirrhosis and/or PSS. Usually only the lower extremities are involved. This report presents the first case of this syndrome observed 5 years after a transjugular intrahepatic portosystemic shunt. The 31 year old man with chronic Hepatitis B developed complete spastic paraparesis within 4 weeks after onset of clinical/neurological symptoms, accompanied by an episode of severe hepatic encephalopathy. The transcortical magnetic stimulation showed normal motoric stimulation times to the abductor digiti minimi muscles but no stimulation to the tibialis muscles was seen. Lumbar stimulation to the tibialis muscles, however, was normal. This indicates loss of motor neurons in the spinal cord, a characteristic finding in patients with portosystemic myelopathy. We performed a search of the literature for all reported cases of cirrhosis and/or PSS that developed PSM. However, the intervals between the construction of a shunt and the diagnosis of portosystemic myelopathy were shorter in total portacaval shunts (median 16 months) than in partial, non-portacaval shunts (median 60 months, p < 0.01). This suggests that not only the shunt itself but also the shunted volume contributes to the development of the syndrome Sixty-one patients with PSM have been reported in the literature since 1944. PSE had developed before PSM in almost all cases. PSM occurred from 1 month to 10 years after the creation of portacaval anastomoses (PCA) or splenorenal shunts (SRS) or in cirrhotic patients without shunts. No one type of liver disease or type of shunt appears to predispose to PSM. The mechanisms of PSE and PSM are thought to be similar and of nitrogenous origin, but their pathogenesis remains unknown. Lathyrism, a toxic syndrome with similar symptoms and signs, is caused by the ingestion of a legume, Lathyrus sativa, which contains beta-N-oxalo-L amino-L-alanine (BOAA). This animal model with or without BOAA appears to offer a reliable way of studying PSM experimentally.

Adult↗
PubMed2001

Dysautonomia in human T-cell lymphotrophic virus type I-associated myelopathy/tropical spastic paraparesis.

The frequency and importance of dysautonomia in human T-cell lymphotrophic virus type I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) have not been fully investigated. We describe the characteristics of dysautonomia in such patients in a case-control study. Our results indicate that autonomic disturbances are more frequent in HAM/TSP than has been previously suggested, with a predominance of sympathetic nervous system dysfunction. In some of these patients, the symptoms may be severe enough to warrant specific treatment.

Adult↗
PubMed1992

Establishment of T-lymphoid cell lines from Morroccan patients with tropical spastic paraparesis.

Two T-cell lines were established from peripheral blood mononuclear cells of two Moroccan patients with tropical spastic paraparesis and then named PR52 and PR144. The two cell lines showed a T lineage of activated CD4+ with high density of Tac+ (IL2 receptor). No expression of CD8 was observed. The virus particles were detected by reverse transcriptase activity and the viral antigens were also detected by immunofluorescence (IF) and Western blot. After six months of culture greater than 90% of the cells exhibited HTLVI antigen by IF. Lysate virus particles on Western blot analysis revealed p19,p24, and p53 gag protein similar to those detected in C91/PL virus particles from an adult T-cell leukemia (ATL) patient. gp46 and gp61 were also weakly detected. These two T-cell lines established will serve as substrate for further comparative studies on TSP and ATL isolates.

Base Sequence↗