Tropical ataxic neuropathy

Tropical ataxic neuropathy (TAN, also known as Strachan-Scott Syndrome and prisoners of war neuropathy) is a disease or category of diseases that commonly causes disability and increases mortality. The causes of TAN are not understood; there is no generally-accepted treatment, and the reported outcomes are inconsistent.[1] The disease affects poor tropical populations; there aren't good statistics on how many people are affected worldwide, but in some populations, more than a quarter of people are affected.[1]

Classification and signs and symptoms

TAN is one of many tropical myeloneuropathies. It was first described in Jamaica in 1897, by postmortems of 510 cases; in 1959, it was dubbed "tropical ataxic neuropathy".[1] The diagnostic criteria were defined in 1968.[1][2] TAN is defined by "bilateral optic atrophy, bilateral sensory neural deafness, predominant posterior column involvement, and pyramidal tract myelopathy, with ataxic polyneuropathy". The classification of TAN is still not settled, and researchers disagree about it.[1]

There are thought to be two neurological syndromes lumped together as TAN. One affects adolescents, appears with retrobulbar optic neuropathy and evidence of malnutrition, and improves with better nutrition. Half of these adolescents are seen to have spinal ataxia.[1]

The other affects middle-aged and elderly people. They suffer sensory polyneuropathy, including weakness and paresthesic sensations. Paresthesias include sensations of numbness, heat, cold, tightness, crawling motion, tingling, pins and needles, and a feeling of walking on cotton or pebbles. Weaknesses show as gait ataxia (lack of co-ordination). Affected people also suffer optic atrophy and sensory neural deafness, on both sides of the body. There is neurological damage to the pyramidal tract of the spinal cord. For these older patients, evidence of malnutrition is rarer, and improving nutrition does not improve symptoms.[1]

Most have symptoms in their legs, but a third to a half also have arm symptoms. Symptoms tend to worsen during the rainy season (see monsoon, harmattan), and are often worse at night.[1]

Symptoms associated with the lower cranial nerve are rarer; most patients do not show them. These symptoms include dysarthria (difficulty articulating words), dysphagia (difficulty swallowing), shortness of breath, and dysphonia (difficulty speaking); dysphonia is more common in women, and shows as hypophonia (lack of co-ordination in the vocal cords) and an inability to shout.[1]

Risk factors and epidemiology

TAN has only been described as developing in Africa, South-east Asia, and the Caribbean (if Guiana be included). It does not seem to occur in temperate countries.[1] People affected by TAN tend to be poor and live in rural areas.[3] In some areas, more than a quarter of the population are affected. In India and Africa, more women are affected; in Africa, the elderly are most likely to suffer, and in India, people in their thirties. Historical data suggests that, in the 1960s, TAN in Africa was most common in people in their 30s and 40s.[1]

While the areas affected roughly correspond to the areas in which cassava is grown, some people in non-cassava-growing populations get TAN, and some cassava-growing populations do not get TAN.[4][1] It is possible that there are several diseases being categorized as TAN.[1]

It has been estimated that 5% of surviving World War II prisoners of war held in the Far East acquired TAN; while they were held for 3.5 years or less, the TAN symptoms persisted chronically after they returned to temperate climates.[5]

Treatment

Nutritional improvements; supplying nutritional yeast, teaching improved cassava preparation,[1] and ceasing cassava consumption.[3]

Outlook

Unclear, with contradictory reports from different studies.[1]

Research directions

A 2016 review listed twenty-one open research questions.[1] The value of international co-operation on TAN research has also been highlighted.[6]

Other animals

The behaviour and neurology of malnourished and cassava-fed rats has been compared to that of humans with TAN.[1]

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See also

References
  1. Netto, AB; Netto, CM; Mahadevan, A; Taly, AB; Agadi, JB (2016). "Tropical ataxic neuropathy - A century old enigma". Neurology India. 64 (6): 1151–1159. doi:10.4103/0028-3886.193755. PMID 27841178.
  2. "Tropical ataxic neuropathy". British Medical Journal. 3 (5619): 632–3. 14 September 1968. doi:10.1136/bmj.3.5663.178-a. PMC 1986522. PMID 5673206.
  3. Trivedi, S; Pandit, A; Ganguly, G; Das, SK (July–September 2017). "Epidemiology of Peripheral Neuropathy: An Indian Perspective". Annals of Indian Academy of Neurology. 20 (3): 173–184. doi:10.4103/aian.AIAN_470_16 (inactive 2020-04-27). PMC 5586108. PMID 28904445.
  4. Adamolekun, B (March 2011). "Neurological disorders associated with cassava diet: a review of putative etiological mechanisms". Metabolic Brain Disease. 26 (1): 79–85. doi:10.1007/s11011-011-9237-y. PMID 21327546.
  5. Robson, D; Welch, E; Beeching, NJ; Gill, GV (February 2009). "Consequences of captivity: health effects of far East imprisonment in World War II". QJM : Monthly Journal of the Association of Physicians. 102 (2): 87–96. doi:10.1093/qjmed/hcn137. PMID 18854350.
  6. Román, GC; Spencer, PS; Schoenberg, BS (August 1985). "Tropical myeloneuropathies: the hidden endemias". Neurology. 35 (8): 1158–70. doi:10.1212/wnl.35.8.1158. PMID 2991814.
  • Pryse-Phillips, William (2009). "Strachan-Scott Syndrome". Companion to Clinical Neurology. Oxford University Press. p. 966. ISBN 978-0-19-971004-1. Retrieved 12 March 2020.
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