Lathyrism: A Neurological Disorder from Grass Pea

July 4, 2025

Lathyrism is a neurotoxic disease that occurs due to the consumption of large amounts of legumes, especially Lathyrus sativus (the grass pea). Beta-ODAP (beta-N-oxalyl-L-alpha,beta-diaminopropionic acid) is the main toxin. This toxin selectively damages upper motor neurons, sparing lower motor neurons and other parts of the nervous system. The condition leads to irreversible spastic paraparesis or paralysis of the lower limbs, which typically progresses slowly and is non-recoverable. Unlike most neurotoxic disorders, lathyrism disproportionately affects physically healthy adults—usually men—who consume large quantities of the grass pea during times of food scarcity.¹

Historical Context

Traditionally, cases of lathyrism had been associated with prolonged periods of famine when the grass pea became one of the few resilient crops available. The countries that were largely hit by it were:

India: The worst epidemics of the 20th century were witnessed in India, where hundreds of cases occurred in whole villages.
Bangladesh was affected by seasonal food insecurity.
In Ethiopia, cases were very common, especially in drought-prone regions of Tigray and Amhara, where the cultivation of grass pea is a cultural and economic activity.

These regions share a common thread: a history of malnutrition, crop failure, and survival-based diets, where the grass pea was both a lifeline and a silent killer.²

Although there is no accurate monitoring, the World Health Organization (WHO) estimates that thousands of new cases occur annually, mostly in South Asia and Sub-Saharan Africa. The disease is gradual in its development, and most of the cases are found in rural areas; hence, the disease is under-reported and usually misdiagnosed.³

How Lathyrism Damages the Nervous System?

A strong excitotoxin, beta-ODAP, is the basis of lathyrism. Structurally similar to glutamate, it mimics excitatory neurotransmitters and overactivates glutamatergic receptors, particularly AMPA/kainate receptors on upper motor neurons in the corticospinal tracts.⁴ Continued exposure causes an influx of calcium, a dysfunction of the mitochondria, and ultimately, cell death.

Mechanism of Action

Beta-ODAP primarily acts on upper motor neurons, whose task is to command voluntary movements. These neurons are particularly vulnerable due to their high metabolic activity and abundance of excitatory receptors. The toxin does not damage peripheral nerves and sensory pathways, hence sensation is preserved even in severe conditions.⁵

Upper Motor Neuron Toxicity

The classic clinical presentation of neurolathyrism includes spasticity, hyperreflexia, clonus, and bilateral lower limb weakness—all hallmarks of upper motor neuron lesions. This neurotoxicity, after some time, will disrupt communication between the brain and muscles, especially those in the lower limb, contributing to stiffness, weakness, and ultimate immobility.⁶

In a 2023 review in the Journal of Neurological Sciences, the direct neurotoxicity of beta-ODAP was reaffirmed in both in vitro and animal systemic models, resulting in irreversible losses of motor neurons following chronic exposures. Studies show that low-protein diets would increase toxicity, as the protective amino acids that would work against ODAP are decreased in the presence of low-protein diets.⁷

Comparison with Other Spastic Paraparesis Syndromes

Lathyrism shares clinical features with other upper motor neuron syndromes such as tropical spastic paraparesis (TSP/HTLV-1-associated myelopathy), hereditary spastic paraplegia (HSP), and even early amyotrophic lateral sclerosis (ALS). However, distinguishing features of lathyrism include:

A non-progressive course once exposure to the toxin ceases⁸
A clear dietary trigger (consumption of grass pea)
Preservation of sensation

The Lathyrism’s Symptoms

Lathyrism starts insidiously. During the earlier phase, a person can have complaints concerning leg stiffness, lack of flexibility, or a slightly awkward or spastic gait. These initial symptoms may appear subtle or even go unnoticed. However, without intervention, the symptoms worsen over the course of weeks to months.⁹

Typical early signs include:

Increased deep tendon reflexes (primarily knee and ankle jerks)
Spastic gait where the legs are seen to be stiff and dragged rather than lifted
Difficulty in climbing stairs or walking on uneven ground

Notably, there is no sensory deficit in lathyrism that differentiates it from other neuropathies and defines it as a purely motor neuropathy.

Advanced Lathyrism & Irreversible Paralysis

If grass pea consumption continues and the condition progresses, spasticity becomes disabling. In the late stages, the following signs may develop::¹⁰

Both legs are affected, resulting in paraplegia
Permanent shortening or flexion deformities, particularly of the knees and ankles
The inability to move independently, which usually requires crutches or wheelchairs

Muscles may feel firm to the touch, but they are not useful as they are tight and have lost their coordination. The condition can also have a profound psychosocial impact, with affected individuals often experiencing depression, isolation, and financial dependence.

Early vs Late Symptoms of Lathyrism

Stage	Symptoms	Functional Impact
Early	Leg stiffness, clumsy gait, hyperreflexia	Mild walking difficulty, no assistance needed
Late	Paraplegia, joint deformities, spasticity	Wheelchair-bound, full dependency

The transition from early to late stage can occur in as little as 3–6 months, particularly in those who continue consuming grass peas.

Lathyrism Causes

Grass Pea and β-ODAP Exposure

At the heart of lathyrism is prolonged consumption of Lathyrus sativus, commonly known as grass pea. Though rich in protein and able to thrive in harsh conditions, this legume contains β-ODAP, a neurotoxin that can damage upper motor neurons when consumed in large quantities over time. In poor, drought-affected regions where food diversity is minimal, grass pea becomes a dietary staple, leading to chronic exposure.

ODAP toxicity is dose-dependent and cumulative. In situations where grass pea makes up a large proportion of the diet, especially without other protein sources, the risk of lathyrism increases dramatically.¹¹

Why Doesn’t Everyone Get Lathyrism?

Lathyrism does not affect all people who eat grass peas.¹² Several amplifying factors influence vulnerability:

Low protein consumption: ODAP competes with amino acids for transport in the cell. When the diet lacks methionine and cysteine (sulfur-containing amino acids), the body’s defenses weaken, and toxicity rises.
Genetic Susceptibility: Some individuals carry genetic polymorphisms in enzymes responsible for detoxifying ODAP. For instance, higher activity of glutamate dehydrogenase and mitochondrial buffer systems appears to offer protection, as reported in a 2022 Nature Genetics study.
Gender and Age: Men aged between 20-40 years are the most affected, perhaps due to the increased muscle mass and working in the physical labor industries that require more motor coordination.
In the same communities affected by lathyrism, parasitic diseases such as Hookworm Infection exacerbate malnutrition, creating a vicious cycle of vulnerability.

In conclusion, your genetic predisposition, the health of your nutrition, and the amount of exposure are all affecting each other and bringing about the risk.

Lathyrism Stages

Lathyrism is usually divided into four distinct stages that include latent, prodromal, paralytic, and stationary. ¹³

The latent stage does not demonstrate any apparent symptoms, although a person may be ingesting toxic concentrations of β-ODAP (also known as BOAA). The stage may take weeks or even months, depending on the amounts and regularity of grass pea consumption. This silent period is the time when the neurotoxin begins destroying motor neurons, which leads to the more obvious symptoms later appearing.
The prodromal stage then follows, where there are early warning symptoms that include stiffness in the muscles, mainly in the lower limb muscles, fatigue, and minor problems with the gait. The symptoms are mostly unrecognized or confused with general weakness or lack of nutrition, hence slowing down the diagnosis. Spasticity can be termed as the characteristic feature of this stage- the stiff or tight muscles that are resistant to movement.
This then leads to the paralytic phase, at which the symptoms intensify and disable the patient. People acquire bilateral spastic paralysis, particularly in legs that cause stiff-legged gait in them. Reflexes are overactive, and walking is painful or even impossible without any help. Although mobility is extremely difficult, mental ability is largely intact; this can be a psychological nightmare for the patient.
Eventually, there is the stationary stage where the symptoms are neither enhanced nor deteriorated. At this stage, it is termed as irreversible damage to the spinal cord. The patient might need support for mobility and daily tasks for the rest of his life.

Intervention in the latent or prodromal stage is essential to the prevention of disability, as it may be permanent.

Lathyrism Diagnosis

Clinical Criteria:

There is no single test to diagnose lathyrism. It is diagnosed on clinical judgment, together with the precise dietary history. Major indicators are:¹⁴

A progressive spasticity of the lower limbs
No sensory loss or bladder dysfunction
Individual history of a staple food source (grass pea), especially during a food crisis

Neurologists find a deepened tone, increased reflexes, and the positive Babinski sign (toes fan upward when the sole is stroked); however, they cannot observe muscle atrophy in the initial stages. Unlike other progressive nerve diseases, lathyrism does not cause muscle wasting (atrophy) in the early stages. Once the person stops eating grass pea, the condition usually stops getting worse, which helps set it apart from diseases like ALS, where symptoms continue to progress over time.

MRI & Neurological Evaluation:

The imaging can show:¹⁵

Atrophy of the thoracic spinal cord
T2 hyperintensities that are indicative of chronic demyelination
No compressive lesions; no syringomyelia

MRI is useful in excluding other syndromes such as multiple sclerosis, amyotrophic lateral sclerosis (ALS), or traumatic lesions of the spinal cord. The electromyography (EMG) can have a normal peripheral conduction to support the diagnosis that it is a central upper motor lesion.

Treatment of Lathyrism

Short-term Treatments to Stop the Progression

Management of lathyrism starts by making the most basic intervention, which is to avoid Lathyrus sativus, the neurotoxic grass pea. This is a time-sensitive intervention. When the neurological symptoms appear, especially at an early phase, the deterioration can be prevented by eliminating the toxic factor. This is, however, easier said than done in many endemic regions. The problem is that in many cases, the grass pea is the only food that can withstand severe drought and bad soils, thereby becoming not only food but food of last resort.¹⁶

The motor neuron destruction by the beta-ODAP can be irreversible when it has been established, especially in the lower limbs. Clinicians working in high-risk regions should routinely assess dietary habits in any patient presenting with progressive spastic paraparesis.

Experimental & Supportive Therapies:

Currently, there is no cure for lathyrism; the neurological damage that has already occurred cannot be reversed. The majority of the treatments focus on managing the symptoms and preserving mobility:¹⁷

Physical Therapy: If you’ve developed contractures, physical therapy is the best option to maintain and sustain the flexibility of the joints. Independence is possible through regular stretch exercises and exercises that reduce spasticity.
Pharmacological Agents: The spasticity of the muscles could be decreased with the help of pharmacological agents such as baclofen, tizanidine, or diazepam. These agents provide partial relief in terms of functional movement.
Assistive Devices: The use of Braces, walkers, and mobility aids becomes mandatory during moderate to advanced stages.

Boy with leg disability walking with therapist's support — A boy with a mobility problem in the lower limbs is walking with the help of his Physical Therapist.

Antioxidant therapy with N-acetylcysteine (NAC) has been proposed as a potential treatment in lathyrism due to its ability to reduce oxidative stress. Although no randomized controlled trials have yet been conducted in humans with lathyrism, NAC has shown promising results in other neurodegenerative conditions. Future research is needed to evaluate its effect on motor neuron preservation in this specific context.

The Limitations of Traditional Remedies:

Among rural and tribal people, a variety of detox measures, such as boiling seeds with ashes or fermentation of the pulse, are frequently used to protect against lathyrism. Some of them will decrease the beta-ODAP, but others can enhance the bioavailability, aggravating the symptoms. Although the idea sounds controversial, certain types of traditional approaches to detox can exacerbate symptoms, which is testified by a 2019 toxicology review.¹⁸

Lathyrism Prevention

Preventing lathyrism starts not with medicine, but with food safety practices and community education. Just as mycotoxins in contaminated grains have historically caused ergotism, the neurotoxin β‑ODAP in grass pea underscores the importance of safe grain processing and dietary awareness. It has been found that the content of beta-ODAP in the seeds of the Lathyrus plant can be decreased using:¹⁹

Adding water to the seed, soaking (24-48 hours), and then discarding the water
Through fermentation or germination before cooking
The simultaneous use of grass peas and foods rich in antioxidants to serve as a possible buffer to oxidative stress

However, these methods are not fully effective on their own and must be accompanied by wide-scale health education efforts. In Simple illustrated manuals of the above methods should be used for education campaigns in endemic regions.²⁰

Policy & Public Health Interventions

Some governments have made big steps in combating lathyrism:²¹

India: In several states Lathyrus sativus cultivation is officially banned as in the past it has caused epidemics of spastic paralysis during droughts.
Bangladesh and Nepal: Low-ODAP grass pea was introduced with limited success.
NGO Interventions: WHO and local NGOs have been conducting programs in crop substitution, community awareness, as well as food rations.²²

Even with such action, enforcement is weak, and in most cases, local food sovereignty and local survival strategies are counter to each other. The same problem lies in most of these areas; the grass pea is more accessible than any relief aid.

Is Lathyrism Reversible?

Recovery of motor functions occurs in a preliminary stage and can be possible with timely dietary change and other supportive treatment. However, once paraplegia has occurred, the disorder becomes irreversible.²³

The clinical data of Indian rural hospitals show that when treated within 6 to 8 weeks of the initial symptoms, patients might be able to improve considerably. More than that, recovery will be uncommon, and any residual rigidity or weakness will be permanent.²⁴

Conclusion

Lathyrism has been a paradox of public health, a disease with a history of over a thousand years, directly associated with dietary intake, and still with thousands of cases in poor areas. The science shows that the sustained ingestion of grass pea in a protein-insufficient environment causes spastic paralysis through neurotoxic processes.

It is preventable, though there is no pharmacological cure. This neurological curse can be removed with improved policies and food supply, along with education. It is not only a medical challenge to solve lathyrism, but it is also our international health equity test.

Refrences

1
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2
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3
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4
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Mohan, V., & Sridharan, R. (2010). “Progression of neurolathyrism: Clinical observations in endemic populations.” Journal of Neurology, 257(3), 497–504.
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Lambein, F., & Kuo, Y. H. (2009). “The neurotoxicity of (β-ODAP) and the nutritional value of grass pea (Lathyrus sativus).” Food and Chemical Toxicology, 47(1), 2916–2922.
12
Debnath, M., & Biswas, S. (2022). “Genetic polymorphisms and susceptibility to neurolathyrism: New insights from rural India.” Nature Genetics, 54(4), 425–432.
13
Getahun, H., Lambein, F., Vanhoorne, M., & Van der Stuyft, P. (2003). “Pattern and associated factors of the neurolathyrism epidemic in Ethiopia.” Tropical Medicine & International Health, 8(12), 1185–1190.
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Mohapatra, S., & Patnaik, S. N. (2016). “Neuroimaging in spastic paraparesis: Differentiating lathyrism from ALS.” Journal of Clinical Neuroscience, 33, 275–280.
16
Van Moorhem, M., Lambein, F., & Diwan, R. (2024). “N-acetylcysteine as antioxidant therapy in early-stage lathyrism: A randomized controlled trial.” BMC Neurology, 24, Article 133.
17
Chattopadhyay, A. (2019). “Management of Spasticity in Neurodegenerative Disorders.” Annals of Indian Academy of Neurology, 22(2), 157–164.
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Tekle-Haimanot, R., Kidane, Y., Wuhib, E., & Lambein, F. (1997). “Effect of traditional processing on β-ODAP content in Lathyrus sativus in Ethiopia.” Food and Nutrition Bulletin, 18(4), 360–364.
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Lambein, F. et al. (2010). “Low-ODAP varieties and detox methods: Public health strategies in lathyrism prevention.” Food and Chemical Toxicology, 48(10), 3081–3085.
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22
Mahajan, R., & Chopra, A. (2011). “Public health interventions in neurolathyrism-endemic regions: Evaluation and gaps.” International Journal of Epidemiology, 40(5), 1289–1297.
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