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PubMedDate not supplied

Low HTLV-1 seroprevalence in endemic tropical spastic paraparesis in Ethiopia.

Tropical spastic paraparesis (TSP), a chronic progressive myelopathy, occurs in Ethiopia in epidemic form as neurolathyrism, while the endemic form has remained obscure. We describe the clinical features of 22 patients with TSP and the results of screening for HTLV-1 in these patients, 26 patients with other neurological disorders, 14 patients with leukaemia and 66 blood donors. The major manifestations in the patients with TSP were weakness and spasticity of the lower limbs with upper motor neurone signs and minimal sensory loss and bladder dysfunction. Two patients with TSP (9%), 2 patients with other neurological disorders (7.7%) and one patient with leukaemia and deafness were seropositive for HTLV-1. All the 66 blood donors were seronegative. Our results suggest that HTLV-1 may not play a major role in the pathogenesis of TSP in Ethiopia.

Adolescent↗

PubMed2003

Tropical spastic paraparesis in Kerala.

Tropical Spastic Paraparesis (TSP) is an uncommon myeloneuropathy with an insular geographic distribution. In 1985, Human T-lymphotropic virus type I (HTLV-1) was reported to be a possible etiological factor. We did an epidemiological, clinical and virological study of 25 cases of TSP. They were predominantly young adult men, whose duration of illness ranged from 6 months to 15 years. Difficulty in walking, stiffness of legs and paraesthesia of legs were the main symptoms. None had tuberculosis, syphilis, malnutrition or lathyrism. Pyramidal signs of the lower limbs, upper limbs, posterior column involvement and spinothalamic tract dysfunction were the common signs. Laboratory findings and cerebrospinal fluid analysis were normal in most. Myelograms or MRI were normal in all. Only 1 case repeatedly tested positive for HTLV-1 antibodies. None of his relatives had clinical or virological evidence of TSP or HTLV-1 infection. Based on our study, we could not link HTLV-I infection to TSP in Indian cases. Virological testing for HTLV-I infection by polymerase chain reaction may be a better tool to reveal such an association. Our cases were similar to seronegative spinal spastic paraplegia. A related new retrovirus or an altered immune response to HTLV-1 due to environmental or dietary factors are possibilities which require further exploration.

Adolescent↗

PubMed1994

Brazilian studies on tropical spastic paraparesis. A meta-analysis.

Tropical spastic paraparesis (TSP) is a chronic progressive myelopathy and in most of the cases has a retroviral (HTLV-1) etiology, when it is denominated HTLV-1 associated-mielopathy (HAM/TSP). Around 433 cases of TSP have been described in Northeast and Southeast Brazil. Among these cases, 157 (36.2%) are HTLV-1 positive and 276 (63.7%) are negative. Their mean age is 43.8 years with a slight predominance of females and mulattoes, although white patients are also numerous. Clinically all patients exhibit a spastic paraparesis with variable sphincter and sensory disturbance. Pain and autonomic symptoms seem to be expressive in the HTLV-1 positive HAM/TSP Brazilian patients.

Adult↗

PubMed1990

A Dutch family with autosomal dominant pure spastic paraparesis (Strümpell's disease).

Families with "pure" hereditary spastic paraparesis of late onset have rarely been reported. Since the original article by Strümpell in 1880, many "complicated" forms of the disorder have been reported, and the question as to whether a "pure" form exists still arises from time to time. We present a Dutch family with "pure" hereditary spastic paraparesis, involving 15 affected members in three generations. The mode of inheritance was autosomal dominant, with onset of clinical signs in the fourth or fifth decade. Severity of the disease was mild; only a few of them became chairbound in the end. There were no sensory symptoms. Mild sphincter disturbances were mentioned by six patients. A review of the reports on Dutch families is given and arguments in favour of the existence of "pure" hereditary spastic paraparesis are discussed.

Adult↗

PubMed1989

Tropical spastic paraparesis: a model of virus-induced, cytotoxic T-cell-mediated demyelination?

Tropical spastic paraparesis is a neurological disorder that is most commonly seen in certain tropical (mainly Caribbean) areas and that presents as a progressive spastic paraparesis and urinary dysfunction. Recent studies have revealed an association between tropical spastic paraparesis and human T-cell lymphotropic virus type I (HTLV-I) infection. We report the results of a detailed morphological and immunocytochemical study of a patient with tropical spastic paraparesis. Lesions were restricted to the spinal cord and optic nerve, where demyelination, inflammation, and fiber loss were common features. Lymphocytes were seen closely applied to nerve fibers within which were changes resembling those seen in myelinated central nervous system cultures exposed to cytokines. Immunocytochemically, HTLV-I p19 core protein and a predominance of CD8+ (suppressor/cytotoxic) T cells and expression of class I major histocompatibility antigen were demonstrated in spinal cord lesions. It is postulated that cytotoxic T cells, either directly or via cytokines, induce lysis of the myelin sheath and subsequently the axon, resulting in a mixed picture of demyelination and axonal loss with secondary tractal degeneration. Despite this destruction, extensive remyelination was evident within affected areas of spinal cord.

Female↗

PubMed2002

The effect of gamma-aminobutyric acid (GABA) receptor drugs on morphine-induced spastic paraparesis after a noninjurious interval of spinal cord ischemia in rats.

UNLABELLED: We have previously demonstrated that intrathecal morphine given after a noninjurious interval of spinal cord ischemia induced transient spastic paraparesis in a rodent model. However, the mechanism of this paraparesis is unknown. We hypothesized that morphine inhibits gamma-aminobutyric acid (GABA)ergic interneurons that control the tonus of spinal cord alpha-motoneurons and that inhibition of spinal cord interneurons may cause spastic paraparesis. In this study, we investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarified the mechanism of the spastic paraparesis induced by intrathecal morphine. Spinal cord ischemia was induced by aortic occlusion lasting 6 min. We first determined whether intrathecally administered GABA agonists (muscimol or baclofen) improve the spastic paraparesis in this model. GABA agonists did not improve the paraparesis. Next, we examined the effect of GABA antagonists (bicuculline or 5-aminovaleric acid) and determined the interaction between morphine and GABA antagonists. In an isobolographic analysis, the 50% effective dose decreased below the theoretical additive line, indicating a synergistic interaction between morphine and GABA antagonists. These results indicate that the spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors. IMPLICATIONS: The purpose of this study was to investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarify the mechanism of the spastic paraparesis induced by intrathecal morphine. The spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors.

Analgesics, Opioid↗

PubMed2006

[Brain and spinal cord magnetic resonance imaging in spastic paraparesis associated to human T-lymphotropic virus].

BACKGROUND: The spastic paraparesis associated to HTLV-1 causes degenerative pyramidal tract lesions of the spinal cord and affects cortical-nuclear connections in the brain. AIM: To report the findings of magnetic resonance imaging in patients with spastic paraparesis. MATERIAL AND METHODS: A magnetic resonance imaging of the brain and spinal cord was performed in 30 patients (24 females), mean age and evolution of 56 and 12 years respectively, with a clinical and virological diagnosis of tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). RESULTS: No patient had abnormal signals in the spinal cord parenchyma. However, an atrophy of the dorsal segment was observed in 87% of patients. Patients with the highest degree of atrophy showed a higher degree of functional impairment. Eleven patients had spinal cord conus atrophy, associated to neurogenic bladder or impotency. In 80% of patients, hyperintense subcortical white matter images in DP, T2 and Flair, mostly bi frontal, were detected. In half of them, small rounded and isolated images were observed. In the other half, eight or more images, generally larger and occasionally confluent, were found. Ten of 12 patients with confluent brain lesions showed different degrees of cognitive impairment. No patient had lesions in the corpus callosus, periventricular white matter, pons, medulla oblongata or cerebellum. CONCLUSIONS: Most patients with tropical spastic paraparesis have alterations in brain or spinal cord magnetic resonance imaging. The magnetic resonance lesions are concordant with functional impairment. The characteristics of the imaging in TSP/HAM patients can be helpful in the differential diagnosis of patients with paraparesis.

Adult↗

PubMed1992

Recurrent encephalopathy and seizures in a US native with HTLV-I-associated myelopathy/tropical spastic paraparesis: a clinicopathologic study.

A patient with progressive spastic paraparesis originally ascribed to multiple sclerosis developed recurrent encephalopathy and seizures. A diagnosis of HTLV-I-associated myelopathy/tropical spastic paraparesis was established prior to death. Autopsy confirmed chronic inflammatory myelopathy and active inflammation in the white matter of the temporal lobes.

Aged↗

PubMed1995

Tropical spastic paraparesis on the Caribbean coast of Colombia.

Tropical spastic paraparesis (TSP) is a retroviral disease characterized predominantly by a chronic myelopathy and progressive leg weakness. Four patients from the northern coast of Columbia with chronic spastic paraparesis and serum positivity for antibodies to human T cell lymphotropic virus type 1 by enzyme-linked immunosorbent assay and Western blot are reported. All patients had mixed ethnic origins (white, black, and amerindian). This is the first report of TSP on the Caribbean coast of Colombia. This study extends the geographic boundaries of TSP in the Caribbean basin.

Adult↗

PubMed1990

Surveillance of urinary thiocyanate concentration after epidemic spastic paraparesis in Mozambique.

A large epidemic of spastic paraparesis in Mozambique during a drought was attributed to cyanide exposure from cassava. Active surveillance in one of the villages most affected by the epidemic detected four new cases in the first year after the epidemic, and none in the second year. In apparently healthy schoolchildren in the same village, surveillance of urinary thiocyanate concentration, an indicator of cyanide exposure, showed high peak values of 1175 and 673 mumols l-1 in succeeding years, with a gradual return to near-normal values in the third year. A marked seasonal variation in thiocyanate concentration was present, with the highest value coinciding with the dry season, the period of the epidemic, and the cassava harvest. Lower values were found in the neighbouring unaffected semi-urban centre. As cassava cultivation increases in many drought-affected countries, we recommend monitoring urinary thiocyanate concentration to estimate cyanide exposure and identify populations at risk for spastic paraparesis epidemics.

Child↗

PubMed1990

Walking efficiency before and after long-term muscle stretch in patients with spastic paraparesis.

Eight patients with stationary, spastic paraparesis were treated with long-term stretch of the hip adductor muscles to improve walking ability. Gait pattern, walking speed and perceived exertion of walking were assessed. Walking efficiency was assessed before and after treatment by measuring oxygen consumption and blood lactate level. After treatment walking pattern was improved. Perceived exertion decreased but walking speed was unchanged. Oxygen cost directly after treatment was lower in six patients, unchanged in one and higher in one. In the patient with unchanged oxygen cost the blood lactate level decreased, probably due to decreased recruitment of fast, type II muscle fibres. Blood lactate was unchanged in the other patients. When assessing walking ability, measurement of energy cost was found to be a valuable supplement to clinical judgement, but in spastic patients both oxygen cost and blood lactate must be considered.

Aged↗

PubMed1988

The role of HTLV-I in tropical spastic paraparesis in Jamaica.

We report clinical and laboratory investigations of 47 native-born Jamaican patients with endemic tropical spastic paraparesis and of 1 patient with tropical ataxic neuropathy. Mean age at onset was 40 years, with a female-male preponderance (2.7:1). Neurological features of endemic tropical spastic paraparesis are predominantly those of a spastic paraparesis with variable degrees of proprioceptive and/or superficial sensory impairment. Using enzyme-linked immunoabsorbent assay (ELISA), IgG antibodies to human T-lymphotropic virus type I (HTLV-I) were present in 82% of sera and 77% of cerebrospinal fluids. On Western blot analysis, IgG antibodies detected the p19 and p24 gag-encoded core proteins in both serum and cerebrospinal fluid. Titers were tenfold higher by ELISA in serum than in cerebrospinal fluid, and some oligoclonal bands present in fluid were not seen in serum. Serum-cerebrospinal fluid albumin ratios were normal, and IgG indexes indicated intrathecal IgG synthesis. Histopathological changes showed a chronic inflammatory reaction with mononuclear cell infiltration, perivascular cuffing, and demyelination that was predominant in the lateral columns. In 1 patient, a retrovirus morphologically similar to HTLV-I on electron microscopy was isolated from spinal fluid. Our investigations show that endemic tropical spastic paraparesis in Jamaica is a retrovirus-associated myelopathy and that HTLV-I or an antigenically similar retrovirus is the causal agent.

Adolescent↗

PubMed2000

OXPHOS and mtDNA alterations in a family with spastic paraparesis.

OBJECTIVE: To study muscle biopsies in hereditary spastic paraparesis (HSP). METHODS: We analyzed oxidative phosphorylation activities and mtDNA in 3 individuals from an HSP family. RESULTS: We found histochemical evidence for mitochondrial proliferation and cytochrome c oxidase negative fibers. Biochemically, there was an important reduction of the activities of complexes I and IV in 3 patients. In addition, multiple mtDNA deletions (ranging 4.0-7.0 kb) were found in 2 cases by PCR but not by Southern blot. CONCLUSION: We suggest the use of a muscle biopsy when examining HSP patients. HSP can represent a disorder of nuclear-mitochondrial intercommunication.

Adult↗

PubMed1999

Extended extradural spinal arachnoid cyst: an unusual cause of progressive spastic paraparesis.

A 15-year old girl presented with a slowly progressive spastic paraparesis since the age of 12. Creatine kinase was slightly increased. Muscle biopsy carried out during tendon surgery for severe toe-walking showed 'myopathic' changes. Subsequent neurological evaluation and radiological studies revealed a large extradural arachnoid cyst extending from the 11th thoracic vertebra to the first lumbar vertebra. Her condition improved after operation. The 'myopathic' features turned out to be the result of chronic spinal compression. MRI is the method of choice to examine patients with non-hereditary progressive spastic paraparesis. Muscle biopsy and tendon surgery should not be performed, without careful neurological examination.

Adolescent↗

PubMed2004

Reciprocal inhibition and corticospinal transmission in the arm and leg in patients with autosomal dominant pure spastic paraparesis (ADPSP).

The pathophysiological mechanisms underlying the development of spasticity are not clear, but the excitability of the disynaptic reciprocal inhibitory pathway is affected in many patients with spasticity of different origin. Patients with genetically identified autosomal dominant pure spastic paraparesis (ADPSP) develop spasticity and paresis in the legs, but usually have no symptoms in the arms. Comparison of the spinal and supraspinal control of the legs and arms in these patients may therefore provide valuable information about the pathophysiology of spasticity. In the present study, we tested the hypothesis that one of the pathophysiological mechanisms of spasticity in these patients is abnormal corticospinal transmission and that this may lead to decreased reciprocal inhibition. Ten patients and 15 healthy age-matched control subjects were investigated. The patients were all spastic in the legs (with hyperactive tendon reflexes, increased muscle tone and Babinski sign), but had no neurological symptoms in the arms (except for one patient). Disynaptic reciprocal Ia inhibition of flexor carpi radialis (FCR) and soleus (SOL) motoneurons was measured (as the depression of the background FCR and SOL EMG activity and as the short latency inhibition of the FCR and SOL H-reflex evoked by radial and peroneal nerve stimulation). In addition, the latency of motor evoked potentials (MEPs) in the FCR muscle and the tibialis anterior (TA) muscle was measured. In the patients, the mean reciprocal inhibition was normal in the arms, while it was significantly decreased in the leg compared with the healthy subjects. In the patients, the average latency of MEPs in the FCR muscle was normal, while the latency to the MEP in TA muscle was significantly longer than that found in healthy subjects. Four patients, however, differed from the other patients by having significant reciprocal inhibition in the leg and a significantly shorter latency of TA MEPs than found in the other patients. The six patients without reciprocal inhibition in the leg instead had significant short latency facilitation of the SOL H-reflex and a longer TA MEP latency than seen in the healthy subjects and in the four patients with retained reciprocal inhibition. These findings support the hypothesis that disynaptic reciprocal inhibition and short latency facilitation are involved in the development of spasticity and, furthermore, they suggest a positive correlation between impairment of corticospinal transmission and decrease of reciprocal inhibition/appearance of reciprocal facilitation.

Adult↗

PubMed1999

Genetic mapping to 10q23.3-q24.2, in a large Italian pedigree, of a new syndrome showing bilateral cataracts, gastroesophageal reflux, and spastic paraparesis with amyotrophy.

We have recently observed a large pedigree with a new rare autosomal dominant spastic paraparesis. In three subsequent generations, 13 affected individuals presented with bilateral cataracts, gastroesophageal reflux with persistent vomiting, and spastic paraparesis with amyotrophy. Bilateral cataracts occurred in all affected individuals, with the exception of one patient who presented with a chorioretinal dystrophy, whereas clinical signs of spastic paraparesis showed a variable expressivity. Using a genomewide mapping approach, we mapped the disorder to the long arm of chromosome 10 on band q23.3-q24.2, in a 12-cM chromosomal region where additional neurologic disorders have been localized. The spectrum of phenotypic manifestations in this family is reminiscent of a smaller pedigree, reported recently, confirming the possibility of a new syndrome. Finally, the anticipation of symptoms suggests that an unstable trinucleotide repeat may be responsible for the condition.

Abnormalities, Multiple↗

PubMed2004

A boy with spastic paraparesis and dyspnea.

A 4 1/2-year-old boy with signs and symptoms of spastic paraparesis and dyspnea is presented. Biotinidase deficiency was considered and was confirmed by both urine organic acid analysis and biotinidase activity measurement. The child recovered gradually on biotin therapy. Because other systemic signs and symptoms of the disease might not be present initially or might develop later, biotinidase deficiency should be considered in the differential diagnosis of a child presenting with acute or subacute spastic paraparesis.

Biotin↗

PubMed1996

[Effect of the Nucleus CMP forte in 46 patients with progressive spastic paraparesis. Randomized and blind study].

BACKGROUND: Idiopatic or HTLV-1 associated progressive spastic paraparesis does not have a clear etiology or treatment. AIM: To assess the effects of a medication containing cytidinmonophosphate, uridintriphosphate and vitamin B 12 in the treatment of progressive spastic. PATIENTS AND METHODS: Patients with the disease were randomly assigned to receive the Nucleus CMP forte (containing dysodic cytidinmonophosphate 5 mg, trisodic uridintriphosphate 3 mg and hydroxicobalamin 2 Mg) tid or placebo during six months. Gait, spasticity, degree of neurogenic bladder and somatosensitive evoked potentials were assessed during treatment. RESULTS: Forty six patients aged 25 to 79 years old were studied, 24 were female and 29 HTLV-1 positive. Twenty two were treated with the drug and the rest with placebo. Gait and spasticity improved in 7 of 22 patients receiving the drug and 1 of 24 receiving placebo (p < 0.05). Neurogenic bladder improved in 10 of 22 receiving the drug and 4 of 24 receiving placebo (NS) Somatosensitive evoked potentials improved in four of seven patients treated with the drug and in two of seven treated with placebo. CONCLUSIONS: The medication caused a modest improvement in patients with progressive spastic paraparesis and was free of side effects.

Adult↗