Tropical Myeloneuropathies Clinical Presentation

  • Author: Eliad Culcea, MD; Chief Editor: Karen L Roos, MD   more...
 
Updated: Jan 14, 2011
 

History

TAN

  • Difficulty walking
  • Burning pain in the hands and feet
  • Amblyopia (in some prisoner-of-war camps, as many as two thirds lost vision)
  • Subacute or chronic onset

HAM/TSP

  • Presenting neurological symptoms in 80% of cases - Gradual onset of leg weakness, back pain, paresthesias, and impairment of urinary or bowel function
  • Erectile dysfunction possible - In one case report, the presenting symptom
  • Increased urinary frequency
  • Dermatitis[4] or psoriasis[5]
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Physical

TAN

  • Impaired light touch and vibration sensation and proprioception
  • Gait ataxia
  • Romberg sign
  • Hyporeflexia or areflexia
  • Sensorineural hearing loss
  • Muscle weakness and atrophy that can involve upper extremities
  • Similar symptoms were described among prisoners of war in the tropical and subtropical regions.

HAM/TSP

  • Spastic paraparesis or paraplegia with hyperreflexia, clonus, and extensor plantar responses; weakness of the lower extremities, more marked proximally
  • Decreased touch and pinprick sensation in poorly defined thoracic areas
  • Vibration sensation frequently impaired, especially in the lower extremities, resulting from spinal cord or peripheral nerve involvement[6]
  • Low lumbar pain with radiation to the legs
  • Hyperreflexia of upper extremities frequently associated with Hoffmann sign
  • Less frequent neurological findings - Cerebellar signs (ie, intentional tremor, dysmetria), optic nerve atrophy, deafness, nystagmus, cranial nerve deficits, upper extremities tremor, absent or diminished ankle jerk
  • Increased urinary frequency - Due to detrusor hyperreflexia (ie, neurogenic bladder) associated with increased incidence of urinary tract infection
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Causes

TAN

In many cases, TAN is associated with excessive consumption of cassava, also known as the mandioca or tapioca plant, which is one of the most important sources of calories in the tropical countries. About 300 million people depend on it for subsistence, especially in the tropical regions of the Americas and in Africa. Cassava contains cyanide in the form of a cyanogenic glycoside, linamarin, which releases cyanide by the enzymatic action of linamarinase or by hydrolysis. Chronic cyanide intoxication has been confirmed as the cause of the TAN described in Nigeria and Tanzania. In these patients, treatment with high-dose vitamins was not satisfactory, suggesting that the vitamin deficiencies are not important in the etiology of the disease in these cases.

Processing of the cassava flour removes almost all the cyanide, but during a drought, these procedures tend to be shortened or ignored. Many people, especially women and children, eat the cassava raw or merely sun dried. The cyanide content of cassava increases during a drought, which may lead to a relatively higher incidence of severe cyanide intoxication.

Vitamin deficiencies and tropical malabsorption were the causes of TAN in prisoners of war. In most of the cases, the affected individuals were deficient in group B vitamins.

HAM/TSP

TSP is caused by an infection with HTLV-1.

Cases of TSP have been documented in which HTLV-1 was not detected.

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Contributor Information and Disclosures
Author

Eliad Culcea, MD  Consulting Staff, Department of Neurology, Great Falls Clinic

Eliad Culcea, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Friedhelm Sandbrink, MD  Assistant Professor of Neurology, Georgetown University School of Medicine; Assistant Clinical Professor of Neurology, George Washington University School of Medicine and Health Sciences; Director, EMG Laboratory and Chief, Chronic Pain Clinic, Department of Neurology, Washington Veterans Affairs Medical Center

Friedhelm Sandbrink, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Specialty Editor Board

Carmel Armon, MD, MSc, MHS  Professor of Neurology, Tufts University School of Medicine; Chief, Division of Neurology, Baystate Medical Center

Carmel Armon, MD, MSc, MHS is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American College of Physicians, American Epilepsy Society, American Medical Association, American Neurological Association, American Stroke Association, Massachusetts Medical Society, Movement Disorders Society, and Sigma Xi

Disclosure: Avanir Pharmaceuticals Consulting fee Consulting

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed  Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

Disclosure: Nothing to disclose.

Chief Editor

Karen L Roos, MD  John and Nancy Nelson Professor of Neurology, Professor of Neurological Surgery, Department of Neurology, Indiana University School of Medicine

Karen L Roos, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association

Disclosure: Nothing to disclose.

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Light microscopy of thoracic spinal cord of 2 patients with HTLV-1–associated myelopathy (Klüver-Barrera staining). (Source: Aye et al, 2000, Fig. 1.)
Light microscopy of perivascular inflammatory infiltration in the spinal cord (A, C) and in the brain (B, D) (A, B H&E; C, D Elastica Van Gieson; A, C x400; B, D x200). (Source: Aye et al, 2000, Fig. 2.)
Light microscopy of the middle thoracic spinal cord (A, C, E) and subcortical white matter of the brain (B, D, F). Fibrotic changes are seen even in the capillaries (arrows) (A, B, F H&E; C-E Elastica van Gieson; A, C, D, F x400; B x300; E x100). (Source: Aye et al, 2000, Fig. 3.)
Immunostaining of the infiltrating cells in the thoracic spinal cord (A, C, E) and subcortical white matter of the brain (B, D, F) (A, B UCHL-1 [antibody to CD45RO]; C, D CD8; E, F OPD-4; A-F x150). (Source: Aye et al, 2000, Fig. 4.)
Immunostaining of the infiltrating cells in the thoracic spinal cord (A, C) and subcortical white matter of brain (B, D) (A, B UCHL-1[antibody to CD45RO]; C, D CD8; A-D x160). (Source: Aye et al, 2000, Fig. 5.)
 
 
 
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