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At least 19 recordsLinked to original sources
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↗
PubMed1999

Age-dependent paraparesis in WKA rats: evaluation of MHC k-haplotype and HTLV-1 infection.

Human T-cell leukemia virus type 1 (HTLV-1) infection is shown to be closely associated with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Although the occurrence of HAM/TSP was reported to be associated with MHC class II, the mechanism is still unclear. The WKA(RT1k) strain of rats was reported to develop HAM/TSP-like paraparesis after HTLV-1 infection, and was suggested to be an animal model of HAM/TSP. We asked whether MHC k-haplotype is specifically involved in the pathogenesis of paraparesis of WKA(RT1k) rats. We injected the HTLV-1 producing human T cells (MT-2 cells) intravenously into WKA(RT1k) rats and MHC congenic WKA.1L(RT1l) rats which have MHC l-haplotype of LEW rats on the WKA background. Positive antibody response to HTLV-1 antigens and presence of provirus in peripheral blood mononuclear cells confirmed that MT-2 cell-injected rats were infected with HTLV-1. Two of 13 MT-2 cell-injected WKA(RT1k) rats and five of 13 MT-2 cell-injected WKA.1L(RT1l) rats developed HAM/TSP-like hindlimb paraparesis between 16 and 26 months old. Interestingly, three of 14 MT-2 cell-uninjected WKA(RT1k) rats and four of 13 MT-2 cell-uninjected WKA.1L(RT1l) rats showed similar paraparesis between 15 and 26 months old. MHC k-haplotype is not specific to the development of paraparesis in WKA(RT1k) rats. The role of aging, genetic background, HTLV-1 infection and other factors on the development of HAM/TSP-like paraparesis in rats are discussed.

Age Factors↗
PubMed2000

Non traumatic paraparesis: aetiological, clinical and radiological profile.

AIM OF STUDY: To study the aetiological and clinical profile of non traumatic paraparesis and radiological correlation with newer aids of diagnosis like CT scan, MRI. METHODOLOGY: Forty cases of non traumatic paraparesis admitted at Sri Sayaji General Hospital, Baroda were studied. The clinical, laboratory data and radiological features were analyzed. RESULTS: Spinal tuberculosis was commonest cause (30%) of paraparesis followed by acute transverse myelitis (20%) and then by primary spinal cord tumours (10%). Incidence of paraparesis was highest (32.5%) in third decade. Backache (75%), parasthesias (62.5%) were common symptoms accompanying paraparesis. Spasticity was present in 57.5% patients. Myelography showed block in 58.5% patients. CT scan following myelography exactly delineated the primary spinal cord tumours and confirmed diagnosis in spinal TB, arachnoid cysts and other compressive myelopathies. MRI, showed plaques of demyelination in two patients, and epidermoid cyst in one patient. CONCLUSION: Tuberculosis of the spine was the commonest cause of paraparesis followed by acute transverse myelitis. CT scan and MRI are important diagnostic aids in patients of paraparesis.

Adult↗
PubMed2004

Role of MRI in differentiating various causes of non-traumatic paraparesis and tetraparesis.

OBJECTIVE: To assess the frequency of various causes of non-traumatic paraparesis and tetraparesis in adults based only on the findings of magnetic resonance imaging (MRI). DESIGN: Non-interventional descriptive study carried out from May 2001 to October 2002 at Radiology Department, CMH, Rawalpindi. PATIENTS AND METHODS: A total of 100 adult patients who presented with non-traumatic paraparesis or tetraparesis, were studied. MRI spine of all the patients and MRI brain of selected patients, was carried out. Based on MRI findings alone causes of non-traumatic paraparesis and tetraparesis were categorized. RESULTS: Paraparesis was more frequent than tetraparesis. Cord compression was found in 72% cases. Neoplastic compression, infective spondylitis and non-compressive myelopathies were the main causes of paraparesis while spondylotic myelopathy was the main cause of tetraparesis. CONCLUSION: Based upon MRI findings causes of non-traumatic paraparesis or tetraparesis can be subcategorized into spondylotic, infective or neoplastic cord compression and non-compressive myelopathies. Further subcategorization of neoplastic lesions according to their compartment of origin can also be done.

Adult↗
PubMed2005

Paraparesis associated with ruptured anterior cerebral artery territory aneurysms.

BACKGROUND: Paraparesis is a rare but characteristic manifestation of ruptured anterior communicating artery or anterior cerebral artery (ACA) aneurysms, but the pathogenesis remains unclear. This study investigated the neuroimaging and clinical features of patients with such paraparesis to evaluate possible causes. METHODS: Nine of 178 patients with ruptured anterior communicating artery or ACA aneurysms presented with paraparesis among 462 patients with subarachnoid hemorrhage (SAH) admitted between May 1996 and November 2001. Diffusion-weighted magnetic resonance (MR) imaging was performed within 48 hours of the onset of SAH in 4 of these 9 patients. The clinical course and neuroimaging studies of these 4 patients were retrospectively reviewed. RESULTS: Diffusion-weighted MR imaging revealed -intensity areas in the medial aspects of the bilateral frontal lobes, which were supplied by the ACAs and distal to the aneurysms, in all 4 patients. These high-intensity lesions had normal to subnormal values of apparent diffusion coefficient (ADC). Most of the high-intensity lesions recovered and did not result in the final lesions regardless of the ADC values, but some lesions with subnormal ADC values resulted in cerebral infarction. Paraparesis was transient and almost completely resolved in 3 patients. CONCLUSIONS: Diffusion-weighted MR imaging detected primary brain damage in the ACA territories caused by acute SAH, which was compatible with the clinical paraparesis. Primary brain damage caused by SAH may include 3 types of lesions: reversible with normal ADC value, reversible with subnormal ADC value, and irreversible with subnormal ADC value.

Aged↗
PubMed2004

A novel presenilin-1 mutation (Leu85Pro) in early-onset Alzheimer disease with spastic paraparesis.

BACKGROUND: Early-onset familial Alzheimer disease is caused by mutations in the amyloid precursor protein (APP), presenilin-1 (PSEN1), or presenilin-2 (PSEN2) genes. Phenotypic diversity has been reported to be associated with various mutations in PSEN1. Various mutations of PSEN1 have been reported in cases of early-onset Alzheimer disease with spastic paraparesis. OBJECTIVE: To describe a novel mutation in the PSEN1 gene associated with early-onset Alzheimer disease with spastic paraparesis. PATIENT AND METHODS: The patient was a 27-year-old man who developed early-onset dementia with spastic paraparesis. We examined sequences of the PSEN1, PSEN2, and APP genes from the patient and his family. To detect a possible mutation effect on the production of amyloid-beta peptide (Abeta), transfected HEK293 cells were examined for Abeta42 and Abeta40 production. RESULTS: We found a novel mutation (Leu85Pro) in PSEN1. This mutation influenced the production of Abeta, resulting in a 2-fold elevation of Abeta42 production and of the Abeta42/40 ratio. CONCLUSION: To our knowledge, this is the first report of very early-onset Alzheimer disease with spastic paraparesis and with the visual variant form of the disease, which is associated with visuospatial cognitive disorder. The Leu85Pro mutation in PSEN1 was pathogenic.

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↗
PubMed1993

Spastic paraparesis associated with human T-lymphotropic virus type I: a clinical, serological, and genomic study in Iranian-born Mashhadi Jews.

The Mashhadi-Jewish community originating in Iran is a closed and ethnically segregated population with a unique history and a high rate of intrafamilial marriage among its members. A high risk of infection by human T-lymphotropic virus type I (HTLV-I) and of adult T-cell leukemia associated with such infection was found in this population. HTLV-I is also associated with a syndrome of progressive spastic paraparesis. We therefore evaluated the occurrence of HTLV-I infection and spastic paraparesis in Mashhadi-born Iranian Jews who immigrated to Israel. We examined 83 Mashhadi-born subjects (52 women, 31 men; mean age, 61 +/- 15.5 years) and 73 age-matched non-Mashhadi Iranian-born Jews. Blood samples were tested for HTLV-I antibodies by particle agglutination test. The polymerase chain reaction (PCR) was used to detect HTLV-I proviral DNA sequences from peripheral blood mononuclear cells. Fifteen Mashhadi-born Jews (18%) were both seropositive and PCR-positive for HTLV-I. Four HTLV-I-seronegative subjects were found to be positive for HTLV-I proviral DNA by PCR. Of the 19 HTLV-I-infected subjects (11 women, 8 men; mean age, 59 +/- 16 years), 13 (68%) had spastic paraparesis of varying severity. There were no signs of myelopathy in the Mashhadi-born subjects who were negative for HTLV-I proviral DNA by PCR. None of the non-Mashhadi Iranian Jews was seropositive or PCR-positive for HTLV-I proviral DNA, or had clinical signs of spastic paraparesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

A novel presenilin 1 mutation (Y154N) in a patient with early onset Alzheimer's disease with spastic paraparesis.

Early onset familial Alzheimer's disease with spastic paraparesis (FAD-SP) has been associated with mutations of the presenilin 1 gene (PSEN1). We report a pedigree of FAD-SP due to a novel missense mutation of PSEN1 (Y154N). The symptoms of the proband were characterized by presenile dementia in her 40s, preceded by spastic paraparesis in her 30s, whereas the mother of the proband presented with spastic paraparesis in her 40s, followed by symptoms of dementia in her mid 60s. The mutation was found only in the proband, and not in a normal family member, normal Japanese control subjects, patients with sporadic Alzheimer's disease or patients with familial spastic paraparesis without dementia. Thus, Y154N is a novel PSEN1 mutation responsible for FAD-SP of Japanese origin.

Alzheimer Disease↗
PubMedDate not supplied

Paraparesis due to exacerbation of preexisting spinal pseudoarthrosis following infliximab therapy for advanced ankylosing spondylitis.

BACKGROUND CONTEXT: Recent reports have described the long-term efficacy and safety of infliximab as a treatment for ankylosing spondylitis (AS). The most important adverse effects of infliximab are infections, malignancies, autoimmunities, and hypersensitivity reactions. There has never been a reported case of paraparesis after infliximab therapy for AS. PURPOSE: To describe a case with paraparesis caused by rapid exacerbation of preexisting spinal pseudoarthrosis after infliximab therapy for advanced AS. STUDY DESIGN/SETTING: Case report/Osaka University Graduate School of Medicine, Suita, Japan. PATIENT SAMPLE: A 55-year-old man with a 27-year history of AS. OUTCOME MEASURES: Case report. METHODS: A 55-year-old man with a 27-year history of AS was treated with infliximab, which provided considerable pain relief and improvement of activities of daily living. However, as the patient resumed vigorous daily activity, he felt back pain and subsequently developed paraparesis. Radiographs showed rapid exacerbation of preexisting spinal pseudoarthrosis at the T11-T12 level after infliximab therapy. RESULTS: After laminectomy and posterolateral fusion, the back pain and paraparesis improved sufficiently to allow independent walking, but moderate bladder dysfunction persisted. CONCLUSIONS: Although this patient could have certainly become myelopathic over time without undergoing infliximab therapy, the patient's history and radiographic course suggest that suppression of inflammation by infliximab improved his activities of daily living, which paradoxically exacerbated preexisting spinal pseudoarthrosis and quickened the onset of subsequent myelopathy.

Antibodies, Monoclonal↗
PubMed2003

Alzheimer's disease with spastic paraparesis and 'cotton wool' plaques: two pedigrees with PS-1 exon 9 deletions.

Several pedigrees have recently been reported in which dominantly inherited familial Alzheimer's disease is associated in some family members with spastic paraparesis and non-neuritic 'cotton wool' plaques. Here we report clinical, genetic and neuropathological findings in two further large pedigrees in which this combination of phenotypes is associated with a deletion of exon 9 of the presenilin-1 (PS-1) gene caused by mutations at the splice acceptor site. In both pedigrees, individuals with paraparesis at presentation had a later than average age at onset of symptoms. In addition, one subject with paraparesis had a much less prominent dementia syndrome than his dementia-affected siblings. As PS-1 mutations are almost always associated with a particularly aggressive form of presenile dementia, these findings suggest the existence of a protective or delaying factor in individuals with spastic paraparesis.

Adult↗
PubMed1993

Clinical and demographic features of HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) in Rio de Janeiro, Brazil.

In Rio de Janeiro (RJ) most cases of paraparesis of obscure origin are associated with the human T-cell lymphotropic virus type I (HTLV-I). Thirty-four consecutive patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) from RJ were evaluated. Most patients came from low socio-economic levels. There was no difference in terms of gender. The main affected racial group was white. A history of sexually transmitted diseases was a major risk factor for HAM/TSP and a positive serology for syphilis was found in 26.5% of the patients. The major clinical findings were of a spastic paraparesis with generalized brisk tendon jerks and bilateral Babinki's sign. Sensation was abnormal in 25 patients (73.5%) and five (14.7%) had a sensory level. Three patients (8.8%) had optic atrophy. The cerebrospinal fluid showed a lymphocytic pleocytosis with a mean total protein content of 0.4 g/litre, and an increased intrathecal IgG synthesis in 59.4% of patients. HAM/TSP and multiple sclerosis (MS) occur indigenously in RJ and some HAM/TSP cases can be sometimes confused with MS. Therefore we propose that, in places where MS coexist with HAM/TSP, HTLV-I antibodies should be sought routinely in those MS suspected cases with prominent spastic paraparesis.

Adolescent↗
PubMed2003

Intrathecal administration of morphine, but not small dose, induced spastic paraparesis after a noninjurious interval of aortic occlusion in rats.

UNLABELLED: We sought to investigate the dose-response relationship for the effect of intrathecal morphine on the transient spastic paraparesis after short-lasting spinal ischemia in rats. Spinal ischemia was induced by aortic occlusion for 6 min with a balloon catheter in rats previously implanted with an intrathecal catheter for drug delivery. After ischemia, the animals were allowed to recover, and 3, 10, or 30 microg of morphine or saline was injected intrathecally at 30 min after reperfusion. In a separate group, the quantal bioassay for the effect of intrathecal morphine on neurological function after ischemia was performed to calculate 50% effective dose values for inducing paraparesis at 2 h of reperfusion. Subsequently, histopathology of the spinal cord was assessed at 48 h of reperfusion. Intrathecal injection of 30 or 10 micro g of morphine, but 3 micro g of neither morphine nor saline, caused a progressive development of hindlimb spasticity. The 50% effective dose values for inducing paraparesis were 16.1 +/- 1.5 microg in assessing behavioral analysis at 2 h after intrathecal morphine. Histopathological analysis of spinal cords in the 30- microg group revealed the presence of dark-staining alpha-motoneurons in lumbosacral segments. We conclude that spinal administration of a large dose of morphine after transient aortic occlusion may be associated with a potential risk of paraparesis and the corresponding development of neurological dysfunction. Careful attention should be paid when intrathecal morphine is used for pain control after thoracoabdominal aortic aneurysm repair. IMPLICATIONS: Spinal administration of large-dose morphine after transient aortic occlusion may be associated with a potential risk of irreversible spinal neuronal degeneration and the corresponding development of neurological dysfunction.

Analgesics, Opioid↗
PubMed2000

[Increased activity of metalloproteinases and their inhibitors in cerebrospinal fluid of patients with tropical spastic paraparesis].

BACKGROUND: Proteolytic modifications of neuronal surfaces and the surrounding extracellular matrix are very important in neuronal development and regeneration. Increased activity of matrix metalloproteinases (MMPs) and their tissue inhibitors, due to secretion by macrophages and lymphocytes, occur in inflammatory processes that disrupt the blood brain barrier. However, neurons and microglia can also secrete these enzymes. AIM: To identify the type of MMP present in the cerebrospinal fluid (CSF) and changes in the expression of tissue inhibitors of metalloproteinases (TIMPs) in patients with HTLV-1 associated tropical spastic paraparesis. PATIENTS AND METHODS: CSF samples from 12 patients with HTLV-1 associated tropical spastic paraparesis and 12 healthy controls were obtained by an atraumatic lumbar puncture. The presence of MMPs was measured by zymography and the relative amounts of TIMPs were measured by immunowestern blot. RESULTS: In the CSF of both controls and patients, a similar gelatinolytic band corresponding to proMMP-2 (latent form) was observed. In 83.3% of patients with HTLV 1 associated tropical spastic paraparesis, the MMP-9 was also present. TIMP-1, TIMP-2 and TIMP-3 were elevated 2.24 +/- 0.72, 3.85 +/- 1.38 and 5.89 +/- 3.4 fold, respectively, in the CSF of patients as compared to controls. CONCLUSIONS: Patients with HTLV-1 associated tropical spastic paraparesis have elevated activity of MMP-9 and levels of TIMPs in the CSF, when compared to healthy controls.

Adult↗
PubMedDate not supplied

[Transient paraparesis as a manifestation of left carotid stenosis].

INTRODUCTION: Paraparesis caused by a cerebrovascular disorder is infrequent, although it is seen in infraction of both anterior cerebral arteries (ACA), in vertebrobasilar insufficiency syndromes or in infarction of the border zones of the anterior circulation. CASE REPORT: Male aged 52 years, right handed, with a history of high blood pressure, who visited because of two episodes of transient paraparesis that lasted 5 minutes and 15 hours. During the last episode the presence of paraparesis and left Babinski sign were observed. Complementary explorations conducted to test for medullar pathology were negative. Cranial MRI showed only bilateral lacunar infarctions in deep territories. Four months later, the patient presented an episode of motor aphasia and paresthesia of the right lower limb, which remitted spontaneously in 10 minutes. Echo Doppler exploration of the supra aortic trunks showed significant stenosis of the left internal carotid artery (LICA) and occlusion of the right artery (RICA). Arteriography of the supra aortic trunks revealed a 99% stenosis of the RICA and 95% of the LICA, with vascularisation of both ACA dependent on the LICA. A left carotid endarterectomy was performed and the patient has remained asymptomatic to date. CONCLUSION: In our patient, both ACA depended on the flow from the LICA. We therefore consider that the symptoms of transient paraparesis were secondary to the left carotid stenosis, either due to a haemodynamic or an artery to artery embolic mechanism.

Carotid Stenosis↗
PubMed2004

[Paraparesis, hyperprolactinemia and adynamic ileus in Guillain-Barré syndrome].

A case of Guillain-Barré with unusual autonomic dysfunction at its onset, that consisted of constipation and hypertension, followed by adynamic ileus and flaccid paraparesis with areflexia limited to the lower limbs, is presented. Inappropriate secretion of antidiuretic hormone and hyperprolactinemia were demonstrated, which resolved spontaneously afterwards. The adynamic ileus resolved and the paraparesis improved with gastric aspiration and intravenous immunoglobulin administration, only to worsen eighty days later. Paraparesis worsened, accompanied by hypertension, an abnormal hypotensive response to captopril and limb pain. The whole clinical picture resolved after a second course of intravenous immunoglobulin. Unusual clinical aspects of Guillain-Barré syndrome found in this case are reviewed, such as paraparesis, prolonged adynamic ileus and endocrine abnormalities, comparing them with available data from the neurological literature. Differential diagnosis with myelopathy, metabolic and paraneoplasic neuropathies, POEMS syndrome, chronic inflammatory demyelinating polyneuropathy and recurrent Guillain-Barré syndrome are commented on. Hyperprolactinemia is proposed as a marker, either of adenopituitary denervation or of the autoimmune response, in the course of this disease.

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↗
PubMedDate not supplied

Familial spastic paraparesis: a case of a mitochondrial disorder.

Familial spastic paraparesis is characterized by progressive gait disturbance without associated sensory, cerebellar, or cranial nerve deficits. Mitochondrial disorders are associated with heterogenic clinical presentations, though not with spastic paraparesis. A patient with familial spastic paraparesis had deficiencies of respiratory chain enzyme complex I, III, and IV. Progressive spasticity was arrested after treatment with coenzyme Q, carnitine, vitamin C and K. Familial spastic paraparesis may represent a mitochondrial disorder.

Biopsy↗