HTLV-I associated tropical spastic paraparesis: cerebral spinal fluid evolutive aspects in 128 cases

Moreno-Carvalho, Otávio A.; Nascimento‐Carvalho, Cristiana M.; Galvão–Castro, Bernardo

doi:10.1590/s0004-282x1995000400009

Cited by 13 publications

(5 citation statements)

References 12 publications

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“…CSF examination revealed mild lymphocyte pleocytosis in approximately one-third of cases as well as mildly elevated protein concentration and increased concentrations of inflammatory markers such as neopterin (Nakagawa et al, 1995; Milagres et al, 2002). These abnormalities can persist for as long as 10 years or more after symptom onset (Moreno-Carvalho et al, 1995). …”

Section: Diagnosismentioning

confidence: 99%

Clinical Pathophysiology of Human T-Lymphotropic Virus-Type 1-Associated Myelopathy/Tropical Spastic Paraparesis

Yamano¹,

Sato²

2012

Front. Microbio.

150

131

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Human T-lymphotropic virus type 1 (HTLV-1), a human retrovirus, is the causative agent of a progressive neurological disease termed HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP is a chronic inflammatory disease of the central nervous system and is characterized by unremitting myelopathic symptoms such as spastic paraparesis, lower limb sensory disturbance, and bladder/bowel dysfunction. Approximately 0.25–3.8% of HTLV-1-infected individuals develop HAM/TSP, which is more common in women than in men. Since the discovery of HAM/TSP, significant advances have been made with respect to elucidating the virological, molecular, and immunopathological mechanisms underlying this disease. These findings suggest that spinal cord invasion by HTLV-1-infected T cells triggers a strong virus-specific immune response and increases proinflammatory cytokine and chemokine production, leading to chronic lymphocytic inflammation and tissue damage in spinal cord lesions. However, little progress has been made in the development of an optimal treatment for HAM/TSP, more specifically in the identification of biomarkers for predicting disease progression and of molecular targets for novel therapeutic strategies targeting the underlying pathological mechanisms. This review summarizes current clinical and pathophysiological knowledge on HAM/TSP and discusses future focus areas for research on this disease.

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Section: Diagnosismentioning

confidence: 99%

Clinical Pathophysiology of Human T-Lymphotropic Virus-Type 1-Associated Myelopathy/Tropical Spastic Paraparesis

Yamano¹,

Sato²

2012

Front. Microbio.

150

131

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“…Among routine laboratory tests, moderate pleocytosis and raised protein content represent the most frequent CSF findings in HAM/TSP, especially during recent clinical manifestations, and these parameters tend to gradually decline 32 . Mild CSF mononuclear pleocytosis and discrete increase of CSF protein have been reported 11 .…”

Section: Discussionmentioning

confidence: 99%

Clinical and laboratory features of HTLV-I asymptomatic carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis from the Brazilian Amazon

Takatani

Crispim

Fraiji

et al. 2017

Rev. Inst. Med. trop. S. Paulo

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Clinical and laboratory parameters including blood and cerebrospinal fluid (CSF) neopterin were investigated in human-T-lymphotropic-virus-type-I associated-myelopathy/tropical-spastic-paraparesis-HAM/TSP and in HTLV-I carriers. HAM/TSP (n = 11, 2 males/9 females, median age = 48 years), recently diagnosed HTLV-I carriers (n = 21, 15 females/6 males, median age = 44 years), healthy individuals (n = 20, 10 males/10 females, median age = 34.6 years) from the Brazilian Amazon (Manaus, Amazonas State) were investigated. Neopterin was measured (IBL ELISA Neopterin, Germany) in serum samples of all the participants, in CSF of 9 HAM/TSP patients as well as in 6 carriers. In HAM/TSP patients, CSF cell counts, protein and glucose were measured, the Osame’s motor-disability-score/OMDS was determined, and brain/spinal cord magnetic-resonance-imaging (MRI) was performed. HAM/TSP patients had normal CSF glucose, leukocyte counts; and normal protein levels predominated. Brain-MRI showed white-matter lesions in 7 out of 11 HAM/TSP patients. OMDS varied from 2-8: 9 were able to walk, 2 were wheel-chair-users. The median serum neopterin concentration in HAM/TSP patients was 6.6 nmol/ L; min. 2.8- max. 12.5 nmol/ L); was lower in carriers (4.3 nmol/L; min. 2.7- max. 7.2 nmol/ L) as well as in healthy participants (4.7 nmol/ L; min. 2.7- max. 8.0 nmol/ L) (p < 0.05). CSF neopterin concentrations in HAM/TSP patients were higher than in serum samples, and higher compared to carriers (p < 0.05). Carriers had similar serum-CSF neopterin concentrations compared to healthy participants. Variable clinical and laboratory profiles were seen in HAM/TSP patients, however our results support the neopterin measurement as a potential biomarker of disease activity.

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“…These abnormalities are generally found in the first few years of disease, tending to lessen gradually although they can persist for as long as 10 years after symptom onset 46. Oligoclonal bands are found in the CSF (and also sometimes the serum) in most patients47 but are of little use clinically.…”

Section: Htlv-1-associated Myelopathy/tropical Spastic Paraparesismentioning

confidence: 99%

The neurology of HTLV-1 infection

Cooper

Loeff²,

Taylor³

2009

Practical Neurology

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HTLV-1 is a significant global health problem but remains largely confined to endemic areas and risk groups. However, increasing migration may mean that the virus will be encountered more frequently in areas traditionally thought of as virtually free of HTLV-1. In this review we discuss the epidemiology, transmission, clinical features, diagnosis and treatment of HTLV-1, focussing specifically on the neurological manifestations. We highlight the circumstances in which HTLV-1 should be suspected and outline the current understanding of HTLV-1-associated myelopathy and other neurological presentations.

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HTLV-I associated tropical spastic paraparesis: cerebral spinal fluid evolutive aspects in 128 cases

Cited by 13 publications

References 12 publications

Clinical Pathophysiology of Human T-Lymphotropic Virus-Type 1-Associated Myelopathy/Tropical Spastic Paraparesis

Clinical Pathophysiology of Human T-Lymphotropic Virus-Type 1-Associated Myelopathy/Tropical Spastic Paraparesis

Clinical and laboratory features of HTLV-I asymptomatic carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis from the Brazilian Amazon

The neurology of HTLV-1 infection

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