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Lathyrism

Lathyrism a disease caused by eating seeds of species of Lathyrus (the grass pea), mainly L. sativus (the chick pea), L. cicera (flat-podded vetch) and L. clymenum (Spanish vetchling). It affects mostly people in Bangladesh, India, Pakistan, Nepal and Algeria but is sometimes found in France, Italy, Spain and Australia. This disease affects horses and cattle as well as in man. BOAA (beta-oxalyl-amino-L-alanine acid), an excitatory neurotoxin and glutamate agonist, has been identified as the constituent of the chickling pea responsible for the disease. BOAA appears to exert its effects through mitochondrial toxicity.1

The first record of the disease is thought to be an ancient Hindu work called Bhavaprakasa but it was also described by Hippocrates around 400 BC. In the 17th Century, the city of Wuttenberg banned chickling veg. A survey in India in 1833 reported the disease in poor people during a drought but it was not until 1873 that Cantani in Italy named the disease as Lathyrism.

Epidemiology

The chickling pea flourishes in conditions of both flood and drought, when no other food crop survives. It has served as survival food for the poor of certain developing countries. An epidemic in the Gondar region of Ethiopia in the 1970s left 1% of the population permanently crippled.2 Victims of the forced labour camps in the Second World War displayed signs of chronic lathyrism following a wartime daily dietary intake of 400 g of L. sativus peas cooked in water plus 200 g bread made of barley and straw.3 More recently, there has been concern that famine conditions in Afghanistan could produce an epidemic of lathyrism.4
It can be boiled as a vegetable, eaten as gruel, or ground into flour to make bread. In the west and north west of Bangladesh, khesari is a staple part of the diet - agricultural labourers eat rutee or chapatee made of khesari. Signs of disease generally appears whenever a diet consisting of one third to one half of L. sativus seed is consumed for 3 to 6 months. Men are affected more often than women and often those aged 18 to 40, in other words the bread winners.5

Risk factors6

  • Cooking with clay implements
  • Eating green unripe and boiled pea forms
  • Blood group O7

Protective factors6

  • Soaking the green peas prior to cooking
  • Eating with antioxidants or mixed with cereals rich in sulphur-based amino-acids
Presentation
  • The onset of neurolathyrism is usually sudden and coincident with the monsoon season. Early symptoms include:
    • Walking difficulties
    • Unbearable cramps
    • Leg weakness
  • Spastic paralysis develops which becomes irreversible.
  • Pyramidal tract involvement causes:
    • Motor weakness
    • Increased tone
    • A lurching scissoring gait caused by involvement of the thigh extensors and adductors and gastrocnemius
    • Extensor plantar responses
    • Very brisk knee and ankle tendon reflexes, often clonic
    • Hoffmann's sign and exaggerated biceps and/or triceps tendon jerks in the most severely affected
  • There are no objective sensory signs but perverse sensations in the legs are frequently reported at the onset. Walking difficulties often begin suddenly but may also appear subacutely or insidiously. Some people experience partly reversible symptoms suggestive of a diffuse CNS excitation of somatic, motor and autonomic function.8 Spasticity can be more marked than the motor weakness.9
  • Lathyrism is not simply a paralytic syndrome as angiolathyrism causes sudden death. The toxin changes the elasticity of the aorta causing aortic aneurysm that may rupture.
  • Osteolathyrism affects skeletal development, cartilages and bones grow abnormally leaving the body deformed.3 Children suffer skeletal deformity and poor cerebral development.
Differential diagnosis

Other causes of hypertonic paraparesis - for example:

  • Pott's paralysis
  • Konzo
  • HTLV-1 infection
Management

The disease is usually non-progressive but irreversible. Tolperisone, a centrally acting muscle relaxant, has been shown to produce significant reduction in the spasticity in neurolathyrism patients.10 Other than that there is remarkably little in the literature about the drug treatment of the condition with no mention of baclofen or other drugs usually used in spasticity.

Prevention

Education about the dangers of lathyrism is obviously important but the harsh reality is that people may face a choice between lathyrism or starvation.
Food preparation measures can help:

  • Boiling in water or repeated steeping in hot water and discarding the extracts can detoxify the seeds.
  • Roasting the seeds at 140ºC for 15 to 20 minutes results in 80 to 90% destruction of the neurotoxins.
  • Soaking the seeds or dhal overnight and decant the water before cooking eliminates about 90% of the toxin.

The dangers of lathyrism are often known along with knowledge of how to detoxify Lathyrus but drought conditions can lead to fuel and water shortages preventing the necessary steps from being taken.
Obviously, one goal for prevention is to develop a plant with the resilience of chick pea to extreme climatic conditions, with its nutritional content and taste but without toxin ('zero BOAA' strains). This would seem an worthy case for genetic modification of food to feed the world safely and effectively. Some varieties of chick pea that contain a much lower amount of toxin have been developed but they do not seem to have reached the farmers who require them.11


Document references
  1. Ravindranath V; Neurolathyrism: mitochondrial dysfunction in excitotoxicity mediated by L-beta-oxalyl aminoalanine. Neurochem Int. 2002 May;40(6):505-9. [abstract]
  2. Haimanot RT, Kidane Y, Wuhib E, et al; Lathyrism in rural northwestern Ethiopia: a highly prevalent neurotoxic disorder. Int J Epidemiol. 1990 Sep;19(3):664-72. [abstract]
  3. Cohn DF, Streifler M; Intoxication by the chickling pea (Lathyrus sativus): nervous system and skeletal findings. Arch Toxicol Suppl. 1983;6:190-3. [abstract]
  4. FAO; Special Alert number 315:Food and Agriculture Organisation of the United Nations. Crop and food supply assessment mission to Afghanistan. July 2001.
  5. Getahun H, Haimanot RT; Psychosocial assessment of lathyrism patients in rural Estie district of South Gondar, northern Ethiopia. Ethiop Med J. 1998 Jan;36(1):9-18. [abstract]
  6. Getahun H, Lambein F, Vanhoorne M, et al; Neurolathyrism risk depends on type of grass pea preparation and on mixing with cereals and antioxidants. Trop Med Int Health. 2005 Feb;10(2):169-78. [abstract]
  7. Getahun H, Lambein F, Van der Stuyft P; ABO blood groups, grass pea preparation, and neurolathyrism in Ethiopia. Trans R Soc Trop Med Hyg. 2002 Nov-Dec;96(6):700-3. [abstract]
  8. Ludolph AC, Hugon J, Dwivedi MP, et al; Studies on the aetiology and pathogenesis of motor neuron diseases. 1. Lathyrism: clinical findings in established cases. Brain. 1987 Feb;110 ( Pt 1):149-65. [abstract]
  9. Misra UK, Sharma VP, Singh VP; Clinical aspects of neurolathyrism in Unnao, India. Paraplegia. 1993 Apr;31(4):249-54. [abstract]
  10. Haque A, Hossain M, Khan JK, et al; New findings and symptomatic treatment for neurolathyrism, a motor neuron disease occurring in north west Bangladesh. Paraplegia. 1994 Mar;32(3):193-5. [abstract]
  11. Raloff J, Detoxifying desert's manna, Science News July 29th 2000 (from the Free Library)

Internet and further reading Acknowledgements EMIS is grateful to Dr Chloe Borton for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2008.
DocID: 2373
Document Version: 21
DocRef: bgp907
Last Updated: 12 Oct 2007
Review Date: 11 Oct 2009










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