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PubMed1988

Immunological findings in neurological diseases associated with antibodies to HTLV-I: activated lymphocytes in tropical spastic paraparesis.

A retrovirus involvement in the etiology of certain neurological diseases is currently an area of intense interest. Tropical spastic paraparesis and other chronic progressive myelopathies have been clearly associated with increased serum and cerebrospinal fluid antibody titers to human T-lymphotropic virus type I; however, little is known about the cellular immune response. In the present study, activated T-lymphocytes were found in the peripheral blood of patients with this disorder. There were increased numbers of large CD3-positive cells that also expressed histocompatibility leukocyte Class II (DR) and interleukin 2-receptor molecules. In addition, a significantly elevated spontaneous lymphoproliferative response was demonstrated in all patients. This is consistent with the known in vitro effects of human T-lymphotropic virus type I. In one patient, a defect in the generation of measles virus-specific cytotoxic T cells was identified. These observations indicate abnormalities of the cellular immune response in tropical spastic paraparesis.

Antibodies, Viral↗

PubMed1996

Tropical spastic paraparesis and HTLV-I infection: clinical and epidemiological study in Lima, Peru.

A descriptive study was performed to investigate the epidemiology and clinical features of 50 patients with tropical spastic paraparesis (TSP) associated with HTLV-I infection acquired in Peru. Cases seen at two reference centers in Lima (Alexander von Humboldt Tropical Medicine Institute and Guillermo Almenara National Hospital) between August 1989 and December 1995 are reviewed. All patients had serologic evidence of infection with reactive ELISA tests for HTLV-I, confirmed by positive Western blot assays. The male-female ratio of cases was 1.0:1.78. The mean age at the time of diagnosis was 52.4 years (range: 29 to 73, SD:11.3). A considerable proportion of patients (68%) had lived in Andean regions: this basically due to their native places (48%) because only 8% of cases were referred from these regions. The mean duration of symptoms prior to diagnosis was 4.95 years (range 0.5-22 years). The clinical features at diagnosis included progressive spastic paraparesis (100%) associated with sphincter disturbances (77.7%), paresthesia (61.1%) or lumbar pain (44%). The functional status of all patients was impaired at the time of evaluation: 44.1% walked unaided with a 'scissors-like' gait, 38% used assist devices for walking, 10% used wheelchairs and 8% were bedridden.

Adult↗

PubMedDate not supplied

[Tropical spastic paraparesis and HTLV-I associated myelopathy in infancy. A case report and review of the literature].

INTRODUCTION: HTLV-I associated myelopathy is characterised by a clinical picture of slowly progressive spastic paraparesis that generally presents when the patient is at an age somewhere between his or her thirties and sixties; few cases have been reported involving children. It is a pathology that is prevalent in tropical regions that are endemic for HTLV-I (southern Japan, the Caribbean, Central and South America, and some areas of Africa). CASE REPORT: The authors report the case of a 9-year-old child from Guinea who was admitted to the Paediatric Neurology Unit in the Hospital de Santa Maria with a two-year-old clinical history of spastic paraparesis. Computerised tomography and magnetic resonance imaging did not show any alterations to the spinal cord. Somatosensory evoked potentials revealed a lesion in the posterior dorsolumbar spinal cord. The exclusion of other (infectious, metabolic and demyelinating) pathologies and the confirmation of infection by HTLV-I (by means of PCR) led to a diagnosis of myelopathy associated to this virus. Therapy was established with interferon alfa, but no appreciable significant improvement was observed. DISCUSSION: This case stands out because of the uncommonness of this pathology at the paediatric age. We review the most relevant aspects of this disorder at the earliest ages, above all with regard to its epidemiology, transmission, clinical symptoms and complementary diagnostic examinations. Known therapeutic options (corticoids, interferon alfa, antiretroviral agents, among others) and prognosis are also discussed.

Black People↗

PubMedDate not supplied

[Spastic paraparesis due to long term consumption of wild cassava (Manihot esculenta): a neurotoxic model of motor neuron disease].

INTRODUCTION: Cassava (Manihot esculenta) is the basic foodstuff of more than 500 million persons in developing countries. Its edible root contains a glucoside with a high cyanogenic content, linamarina, which is hydrolysed in the human intestinal tract by the resident microbial flora, with liberation of HCN. Inadequate preparation and cooking followed by consumption whilst half-raw, especially in diets based almost exclusively on cassava for a long period of time, may lead to a neurological syndrome of damage to the upper motor neuron and the appearance of spastic paraparesia. CLINICAL CASE: We present the case of a 44 year old male agricultural worker from the Amazon region who had a predominantly crural spastic paraparesis which had been present for four years. His main food was 'mandioca brava' or wild cassava which was insufficiently cooked. Study of the CSF ruled out infection by HTLV and neurosyphilis. On magnetic resonance there was slight thoracic atrophy. CONCLUSIONS: In patients with spastic paraparesis, normal neuroimaging and CSF findings, and a normal family history, one should specifically investigate exposure to potentially toxic plants and foods, especially in regions in which nutrition is based on potentially cyanogenic roots or plants. It is necessary to improve the methods of processing and cooking cassava, and to avoid diets based almost entirely on this root, in order to reduce the potential neurotoxic damage which may be caused by this plant.

Adult↗

PubMed2002

A case of paroxysmal kinesigenic dyskinesia with spastic paraparesis.

We report the first case of paroxysmal kinesigenic dyskinesia (PKD) with spastic paraparesis. A 17-year-old male began to show a dystonic posture in both his upper limbs when walking at age 12 years. Neurological examination revealed bilateral talipes cavus, spasticity in all extremities with general hyperreflexia and pathological reflexes. On starting to walk, he showed a dystonic posture in bilateral maniphalanx, wrists, elbows, and toes. Magnetic resonance imaging (MRI) revealed high T2-weighted signal intensity in bilateral pyramidal tract. Although the combination of pyramidal and the basal ganglia disorders is very rare, the present case suggests an inter-relation of the pyramidal and the basal ganglia systems.

Adolescent↗

PubMed1995

Contralateral early blink reflex in patients with HTLV-I associated myelopathy/tropical spastic paraparesis.

Thirty-two Japanese patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) were studied by means of the electrically elicited blink reflex and three responses (R1, R2, R3) were registered. 69% of the patients displayed a uni- or bilateral crossed R1 response (R1k) as compared to 11% in the control group. A positive correlation between R1k and an exaggerated jaw jerk reflex was found in the patients. Central abnormalities of the nervous system with diminished presynaptic inhibition acting in the interneuronal input of the brainstem of HAM/TSP patients was the most likely cause. It could lead to the unmasking of crossed trigemino-facial pathway reflex which is present in the normal population from birth. These results strongly support the supraspinal involvement of the central nervous system (CNS) in HAM/TSP more than usually thought.

Action Potentials↗

PubMed2004

HTLV-1-associated myelopathy/tropical spastic paraparesis accompanied with psoriasis.

Two adult females developed HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and psoriasis. Both showed chronic progressive paraparesis and sharply demarcated erythematous scaling plaques on their extremities and trunk. One patient had polymyositis while in the other anti-thyroid antibodies, antinuclear antibodies and SS-A antibody, all autoantibodies, were positive. Both patients were treated by intramuscular injections of interferon-alpha for 2 to 4 weeks, resulting in amelioration of paraparesis. After the therapy psoriasis and polymyositis markedly improved in one patient without any additional therapy, while in the other simultaneous use of topical corticosteroids was effective. This is the first report to describe occurrences of psoriasis in HAM/TSP patients. Although there are several reports indicating interferon-alpha induces or exacerbates psoriasis, our experience suggests that psoriasis associated with HAM/TSP can be successfully managed even during interferon-alpha therapy.

Adult↗

PubMed2002

Polygenic control of human T lymphotropic virus type I (HTLV-I) provirus load and the risk of HTLV-I-associated myelopathy/tropical spastic paraparesis.

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is one outcome of infection with HTLV-I. A population association study of 229 patients with HAM/TSP and 202 healthy carriers of HTLV-I in southern Japan showed that this outcome of HTLV-I infection and the HTLV-I provirus load are under polygenic control. Of 58 polymorphic sites studied in 39 non-HLA candidate gene loci, 3 new host genetic factors that influenced the risk of HAM/TSP or the provirus load of HTLV-I were identified. The promoter TNF -863A allele predisposed to HAM/TSP, whereas SDF-1 +801A 3'UTR, and IL-15 191C alleles conferred protection. Knowledge of HTLV-I-infected individuals' ages, sex, provirus load, HTLV-I subgroup, and genotypes at the loci HLA-A, HLA-C, SDF-1, and TNF-alpha allowed for the correct identification of 88% of cases of HAM/TSP in this Japanese cohort.

Alleles↗

PubMed2005

Human T lymphotropic virus type I (HTLV-I) proviral load in cerebrospinal fluid: a new criterion for the diagnosis of HTLV-I-associated myelopathy/tropical spastic paraparesis?

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is associated with accumulation of HTLV-I-infected T cells in the central nervous system (CNS). However, data on HTLV-I proviral load in the CNS at the asymptomatic stage are still lacking. We measured HTLV-I proviral load in cerebrospinal fluid (CSF) cells from 17 patients with HAM/TSP and 25 asymptomatic carriers. The percentage of HTLV-I-infected cells in CSF cells and the CSF cell : peripheral blood mononuclear cell HTLV-I proviral load ratio were always >10% and >1, respectively, in the patients with HAM/TSP but were always <10% and <1, respectively, in the asymptomatic carriers. We propose that determination of HTLV-I proviral load in CSF cells should be included as a new parameter for the diagnosis of HAM/TSP.

Adult↗

PubMed2004

Clinical characteristics of patients in Peru with human T cell lymphotropic virus type 1-associated tropical spastic paraparesis.

BACKGROUND: Human T cell lymphotropic virus type 1 (HTLV-1) is associated with tropical spastic paraparesis (TSP). Peru is an area of endemicity for HTLV-1. METHODS: All patients with suspected cases of TSP referred to our institute (Institute of Tropical Medicine Alexander von Humboldt, Lima, Peru) from 1989 through 2002 were interviewed and tested for HTLV-1. All patients with positive results were evaluated by an expert physician. Disease progression was defined as "rapid" if the time between TSP onset and inability to walk unaided was <2 years. RESULTS: Among 165 patients enrolled, the symptoms and signs most frequently found were spasticity (in 97.5% of patients), hyperreflexia (95.4%), lower limb paresthesia (90.2%), pyramidal signs (82.6%), urinary complaints (82.0%), and lumbar pain (79.0%). Rapid progression was present in 21.5% of patients; mean age at TSP onset was higher among these patients than among slow progressors (P<.001). Severe spasticity, diminished vibratory sensation, and tremor were found more frequently among rapid progressors, compared with slow progressors. CONCLUSIONS: HTLV-1--associated TSP is frequently diagnosed in areas of HTLV-1-endemicity. A subgroup of patients experiences rapid disease progression.

Adolescent↗

PubMed1993

Isolation of HTLV-II from a patient with chronic, progressive neurological disease clinically indistinguishable from HTLV-I-associated myelopathy/tropical spastic paraparesis.

An increasing spectrum of diseases has been shown to be associated with the human T-cell lymphotropic virus type I (HTLV-I), most notably a chronic, progressive myelopathy termed HTLV-I--associated myelopathy/tropical spastic paraparesis and adult T-cell leukemia. HTLV-II is a close relative of HTLV-I and is structurally similar but molecularly distinct. This virus is endemic in Amerindian populations and a high seroprevalence rate has been observed in intravenous drug abusers. Here, for the first time, we have identified a patient with a chronic, progressive neurological disease clinically indistinguishable from HTLV-I--associated myelopathy/tropical spastic paraparesis from whom we have isolated and characterized HTLV-II in the absence of any other detectable human retrovirus. Antibodies to HTLV were detected in both serum and cerebrospinal fluid, with typical HTLV-II banding patterns on Western blots. HTLV-II viral sequences were detected in high copy number from peripheral lymphocytes by polymerase chain reaction techniques, and cloning and sequencing of this virus revealed a 99.5% homology with prototype HTLV-II. These results serve to alert the medical community to the possibility that in addition to HTLV-I, HTLV-II may be associated with a neurological disorder.

Brain↗

PubMed2002

The prevalence of "pure" autosomal dominant hereditary spastic paraparesis in the island of Ireland.

OBJECTIVES: Hereditary spastic paraparesis (HSP) is clinically and genetically heterogeneous. "Pure" autosomal dominant (AD) HSP is most common and eight genetic loci are identified to date. Previous studies have included autosomal recessive and sporadic cases in prevalence calculations. This study aimed to determine the prevalence and features of pure ADHSP in the island of Ireland. METHODS: Index cases were identified from a 5 year survey of all adult and paediatric neurologists, clinical geneticists, hospital records, and hospital inpatient enquiry system data in Ireland, north and south. Families were examined by two neurologists and classified as affected or unaffected according to specific criteria. The prevalence date was set at 1 June 2000 and the midyear population estimate for the previous year was 5.436 million. RESULTS: Eighty two patients with pure ADHSP and a further 12 obligate carriers from 19 families were identified. In total 69 patients with pure ADHSP were alive and resident in Ireland at the prevalence date. Twenty nine per cent of these were asymptomatic but with signs of paraparesis. CONCLUSIONS: The prevalence of ADHSP in Ireland to estimated to be 1.27/100 000 population. The high proportion of asymptomatic cases and obligate carriers means that this condition is likely to be underdiagnosed.

Adolescent↗

PubMed2000

Effect of intrathecal baclofen on gait control in human hereditary spastic paraparesis.

The covariation between thigh, shank and foot elevation angles during locomotion was analysed by means of orthogonal planar regression in a patient with pure hereditary spastic paraparesis before and after an intrathecal bolus of baclofen and in seven healthy subjects. The size, shape and spatial orientation of the loop defining patient's planar covariation (thigh angle vs. shank angle vs. foot angle) significantly differed from the controls' before baclofen, whereas these features resumed normal characteristics after baclofen injection. This shows that alteration of the control of phase coupling for the co-ordination of lower limb segments in human gait by increased spinal reflexes can be reversed by intrathecal baclofen injection.

Adult↗

PubMed2006

Impacted cisterna magna without syringomyelia associated with spastic paraparesis: case report.

We report on a 49 year old man with impacted cisterna magna without the presence of syringohydromyelie (SM). The clinical picture was characterized by spastic paraparesis. Magnetic resonance imaging depicted a cisterna magna filled by the cerebellar tonsils. Six months after osteodural-neural decompression of the posterior fossa there was resolution of neurological symptoms and signs with the exception of hyperactive patellar and Achilles reflexes.

Arnold-Chiari Malformation↗

PubMed2005

A prospective uncontrolled trial of fermented milk drink containing viable Lactobacillus casei strain Shirota in the treatment of HTLV-1 associated myelopathy/tropical spastic paraparesis.

Ten patients with human T-cell lymphotropic virus type-1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) were treated in an uncontrolled preliminary trial by oral administration of viable Lactobacillus casei strain Shirota (LcS) containing fermented milk. HTLV-1 provirus load, motor function, neurological findings, and immunological parameters were evaluated after 4 weeks. Although LcS did not change the frequencies or absolute numbers of all the examined cell surface phenotypes of peripheral blood mononuclear cells, NK cell activity was significantly increased after 4 weeks of oral administration of LcS preparation. Improvements in spasticity (modified Ashworth Scale scores) and urinary symptoms were also seen after LcS treatment. No adverse effect was observed in all the 10 patients throughout the study period. Our results indicated that LcS may be a safe and beneficial agent for the treatment of HAM/TSP; therefore randomized controlled studies are warranted.

Adult↗

PubMed1996

Cutaneous T-cell lymphoma, tropical spastic paraparesis, cerebral vasculitis, and protein S deficiency in a patient with HTLV-I.

The clinical spectrum of retroviruses is expanding rapidly. Human T-cell lymphotropic virus type I (HTLV-I) was the first retrovirus to be described, and its role had been established in adult T-cell leukemia/lymphoma and tropical spastic paraparesis. We report the case of a 35-year-old woman with HTLV-I and the unusual combination of cutaneous T-cell lymphoma, tropical spastic paraparesis, cerebral vasculitis, and protein S deficiency. We discuss the relationship of all her diseases to HTLV-I.

Adult↗

PubMed1991

Amplifications of multiple regions of the HTLV-I genome from DNA of an Italian spastic paraparesis patient but not from DNA of multiple sclerosis patients.

We searched for evidence of infection by the human T-cell lymphoma/leukemia virus type I (HTLV-I) in patients with multiple sclerosis (40 cases); brainstem encephalitis (1 case); Friedreich's ataxia (1 case); spastic paraparesis of unknown etiology (1 case). All patients were from the region of Abruzzo, Italy. Sera were all negative for anti-HTLV-I reactivity by the Western blotting (WB) analysis. DNAs from peripheral blood mononuclear cells were amplified using the polymerase chain reaction (PCR) technique with primers specific for the HTLV-I gag, pol, and env proviral regions. HTLV-I sequences were amplified only in the patient with spastic paraparesis of unknown etiology. In this case, HTLV-I infection might have been related to blood transfusions received 2 years prior to the onset of the neurologic symptoms. Members of the patient's family were negative for HTLV-I by PCR and WB. These data indicate that HTLV-I associated myelopathy is present also in Italy, but fail to substantiate an association of HTLV-I with multiple sclerosis.

Adolescent↗

PubMed1985

Association of high cyanide and low sulphur intake in cassava-induced spastic paraparesis.

Urinary excretion of sulphur compounds was studied in children from a population in Mozambique that had been affected, during a drought, by an epidemic of spastic paraparesis attributed to cyanide exposure from cassava. The children had increased thiocyanate and decreased inorganic sulphate excretion, indicating high cyanide and low sulphur-containing amino-acid intake. Children from a neighbouring cassava-eating area, where no cases of spastic paraparesis had occurred, had lower thiocyanate excretion but higher inorganic sulphate excretion. These results support the hypothesis that the epidemic was due to the combined effects of high dietary cyanide exposure and sulphur deficiency.

Child↗