Lathyrism and Socioeconomic Disparities: A Neglected Public Health Problem in Northeast Ethiopia.

Lathyrism is an incurable neurological disorder, resulting from excessive consumption of grass pea (Lathyrus sativus), which clinically manifests as paralysis of lower limbs. Because of the high production of grass peas, a large number of people are expected to be affected by the disease in Northeast Ethiopia. However, there is no comprehensive study that quantified the magnitude of the problem. Therefore, in this study, we determined the prevalence of lathyrism and socioeconomic disparities in Northeast Ethiopia. A community-based cross-sectional study was used which used a quantitative method of data collection from January to February 2019. Data were collected from a total of 2,307 inhabitants in the study area using structured questionnaires. Lathyrism cases were identified using a case definition of symmetrical spastic leg weakness, and subacute or insidious onset, with no sensory deficit, and with a history of grass pea consumption before and at the onset of paralysis. The majority (56.8%) of participants were male, and 34.7% were aged 45 years or older. Overall, the prevalence of lathyrism was 5.5%, and it was higher in males (7.9%) than in females (2.5%). Moreover, the prevalence was higher among farmers (7.0%) than merchants (0.3%), very poor economic status (7.2%) than very rich (1.1%), who produced (9.6%) grass pea than not produced (0.9%), and those who used clay pottery (6.2%) than metal (4.8%) for cooking. The prevalence of lathyrism in Northeast Ethiopia is remarkably high. Therefore, we recommend lathyrism to be among the list of reportable health problems and incorporated in the national routine surveillance system.

Using Advanced Imaging Methods to Study Neurolathyrism.

BACKGROUND: Neurolathyrism is a toxic nutritional disorder caused by consumption of the grass pea, Lathyrus sativus. The disease, which manifests as an acute or insidiously evolving spastic paraparesis, continues to occur throughout Africa and Asia. Research on this disease is limited, and to our knowledge no imaging studies of patients with neurolathyrism have been published. OBJECTIVES: To better localize the site of damage in neurolathyrism using advanced imaging methods. METHODS: Three male patients, immigrants from Ethiopia, were included in the study. All had a history of arrested spastic paraparesis that had evolved before their emigration from Ethiopia, and a past history of exposure to grass pea without any other cause. Functional magnetic resonance imaging (fMRI) included simple motor tasks to evaluate cortical motor areas. Anatomic scans included diffusion tensor imaging (DTI) to evaluate the corticospinal tracts. RESULTS: In all patients clear activation was found in motor regions, and the patients' activity pattern was qualitatively similar to that in control sublects. In one patient in whom clinical symptoms were asymmetric, an asymmetric activity pattern in Ml was identified. DTI analysis identified intact corticospinal tracts connecting the pons and the primary motor regions, similar to control subjects. CONCLUSIONS: Advanced neuroimaging clearly identified well-functioning motor regions and tracts in neurolathyrism patients, suggesting a spinal etiology.

Bone fracture toughness and strength correlate with collagen cross-link maturity in a dose-controlled lathyrism mouse model.

Collagen cross-linking is altered in many diseases of bone, and enzymatic collagen cross-links are important to bone quality, as evidenced by losses of strength after lysyl oxidase inhibition (lathyrism). We hypothesized that cross-links also contribute directly to bone fracture toughness. A mouse model of lathyrism using subcutaneous injection of up to 500 mg/kg ß-aminopropionitrile (BAPN) was developed and characterized (60 animals across 4 dosage groups). Three weeks of 150 or 350 mg/kg BAPN treatment in young, growing mice significantly reduced cortical bone fracture toughness, strength, and pyridinoline cross-link content. Ratios reflecting relative cross-link maturity were positive regressors of fracture toughness (HP/[DHLNL + HLNL] r(2) = 0.208, p < 0.05; [HP + LP]/[DHNL + HLNL] r(2) = 0.196, p < 0.1), whereas quantities of mature pyridinoline cross-links were significant positive regressors of tissue strength (lysyl pyridinoline r(2) = 0.159, p = 0.014; hydroxylysyl pyridinoline r(2) = 0.112, p < 0.05). Immature and pyrrole cross-links, which were not significantly reduced by BAPN, did not correlate with mechanical properties. The effect of BAPN treatment on mechanical properties was dose specific, with the greatest impact found at the intermediate (350 mg/kg) dose. Calcein labeling was used to define locations of new bone formation, allowing for the identification of regions of normally cross-linked (preexisting) and BAPN-treated (newly formed, cross-link-deficient) bone. Raman spectroscopy revealed spatial differences attributable to relative tissue age and effects of cross-link inhibition. Newly deposited tissues had lower mineral/matrix, carbonate/phosphate, and Amide I cross-link (matrix maturity) ratios compared with preexisting tissues. BAPN treatment did not affect mineral measures but significantly increased the cross-link (matrix maturity) ratio compared with newly formed control tissue. Our study reveals that spatially localized effects of short-term BAPN cross-link inhibition can alter the whole-bone collagen cross-link profile to a measureable degree, and this cross-link profile correlates with bone fracture toughness and strength. Thus, cross-link profile perturbations associated with bone disease may provide insight into bone mechanical quality and fracture risk.

Lessons from neurolathyrism: a disease of the past & the future of Lathyrus sativus (Khesari dal).

Neurolathyrism is past history in India since Lathyrus sativus (khesari dal) is no longer used as a staple. A consensus has evolved that khesari dal is harmless as part of a normal diet. L-ODAP (ß-N-oxalyl-l-α-diamino propionic acid) the neurotoxic amino acid, from this pulse, is detoxified in humans but not in animals but still no laboratory animal is susceptible to it under acceptable feeding regimens. L-ODAP is an activator of protein kinase C and consequential crucial downstream effects such as stabilization of hypoxia inducible factor-1 (HIF-1) could be extremely conducive to humans under a variety of situations. ODAP is gradually finding a place in several patents for this reason. Homoarginine the second amino acid from L. sativus can be a better substrate for endogenous generation of nitric oxide, a crucial signaling molecule associated with the cardiovasculature and control of hypertension. These features could make L. sativus a prized commodity as a functional food for the general cardiovasculature and overcome hypoxic events and is set to change the entire perception of this pulse and neurolathyrism.

Vascular insult accompanied by overexpressed heme oxygenase-1 as a pathophysiological mechanism in experimental neurolathyrism with hind-leg paraparesis.

Neurolathyrism (NL) is a motor neuron disease characterized by spastic paraparesis in the hind legs. ß-N-oxalyl-l-α,ß-diaminopropionic acid (l-ß-ODAP), a component amino acid of the grass pea (Lathyrus sativus L.), has been proposed as the cause of this disease. In our NL rat model, we previously reported that transient intra-parenchymal hemorrhage occurred in the lower spinal cord during the early treatment period. We show here a possible pathological role of the hemorrhage in motor neuron damage and paraparesis pathology. In the lumbo-sacral spinal cord, blood vessel integrity was lost with numerous TdT-mediated dUTP nick end-labeling-positive blood vessel-like structures occurring simultaneously with the hemorrhage. We observed a coincident >10-fold increase in heme oxygenase-1 (HO-1) only in the lower spinal cord. The early period of paraparesis in the lower leg was greatly suppressed by pretreatment with zinc protoporphyrin IX, a HO-1 inhibitor. In vitro, l-ß-ODAP was toxic to human umbilical vein endothelial cells compared to l-glutamate. The present data shed light on the role and the mechanism of vascular insult in causing dysfunction and moribund motor neurons in experimental NL.

Neurolathyrism: two Ethiopian case reports and review of the literature.

Neurolathyrism is a toxic myelopathy caused by ingestion of the Lathyrus sativus grasspea. An irreversible acute to subacute spastic paraparesis or quadriparesis ensues. Despite public education, new cases of this preventable disease still occur. Two Ethiopian cases of neurolathyrism are reported to illustrate the disease, followed by a literature review. Two teenage male farmers from the same village developed irreversible spastic myelopathy following L. sativus ingestion. There was no sensory, sphincter or bulbar dysfunction. Likely causative factors identified were increased consumption of L. sativus prior to and following disease onset, heavy physical exertion and male gender, similar to those reported in the literature. Neurolathyrism is an entirely preventable neurotoxic myelopathy with permanent disability accrued. Treatment is symptomatic. Because of personal disability and subsequent socioeconomic effects, this disease warrants further public health measures to prevent occurrence. Education, avoidance of the grasspea and measures to reduce toxin burden are possible methods.

Lathyrism-induced alterations in collagen cross-links influence the mechanical properties of bone material without affecting the mineral.

In the present study a rat animal model of lathyrism was employed to decipher whether anatomically confined alterations in collagen cross-links are sufficient to influence the mechanical properties of whole bone. Animal experiments were performed under an ethics committee approved protocol. Sixty-four female (47 day old) rats of equivalent weights were divided into four groups (16 per group): Controls were fed a semi-synthetic diet containing 0.6% calcium and 0.6% phosphorus for 2 or 4 weeks and ß-APN treated animals were fed additionally with ß-aminopropionitrile (0.1% dry weight). At the end of this period the rats in the four groups were sacrificed, and L2-L6 vertebra were collected. Collagen cross-links were determined by both biochemical and spectroscopic (Fourier transform infrared imaging (FTIRI)) analyses. Mineral content and distribution (BMDD) were determined by quantitative backscattered electron imaging (qBEI), and mineral maturity/crystallinity by FTIRI techniques. Micro-CT was used to describe the architectural properties. Mechanical performance of whole bone as well as of bone matrix material was tested by vertebral compression tests and by nano-indentation, respectively. The data of the present study indicate that ß-APN treatment changed whole vertebra properties compared to non-treated rats, including collagen cross-links pattern, trabecular bone volume to tissue ratio and trabecular thickness, which were all decreased (p<0.05). Further, compression tests revealed a significant negative impact of ß-APN treatment on maximal force to failure and energy to failure, while stiffness was not influenced. Bone mineral density distribution (BMDD) was not altered either. At the material level, ß-APN treated rats exhibited increased Pyd/Divalent cross-link ratios in areas confined to a newly formed bone. Moreover, nano-indentation experiments showed that the E-modulus and hardness were reduced only in newly formed bone areas under the influence of ß-APN, despite a similar mineral content. In conclusion the results emphasize the pivotal role of collagen cross-links in the determination of bone quality and mechanical integrity. However, in this rat animal model of lathyrism, the coupled alterations of tissue structural properties make it difficult to weigh the contribution of the anatomically confined material changes to the overall mechanical performance of whole bone. Interestingly, the collagen cross-link ratio in bone forming areas had the same profile as seen in actively bone forming trabecular surfaces in human iliac crest biopsies of osteoporotic patients.

Hind-limb paraparesis in a rat model for neurolathyrism associated with apoptosis and an impaired vascular endothelial growth factor system in the spinal cord.

Neurolathyrism is a motor neuron disease characterized by lower limb paraparesis. It is associated with ingestion of a plant excitotoxin, beta-N-oxalyl-L-alphabeta-diaminopropionic acid (L-beta-ODAP), an agonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate-type glutamatergic receptors. Previously, a limited model of neurolathyrism was reported for the rat. To improve upon the model, we stressed rat pups by separation from their mothers, followed by the subcutaneous L-beta-ODAP treatment, resulting in a 4.6-fold higher incidence (14.0-15.6%) of the paraparesis compared with the prior study. The number and size of motor neurons in these rats were decreased only in the lumbar and sacral cord segments, at approximately 13-36 weeks after treatment. Only lumbar and sacral spinal cord tissue revealed pathological insults typical of physical and ischemic spinal cord injury in the surviving motor neurons. In addition, extensive but transient hemorrhage occurred in the ventral spinal cord parenchyma of the rat, and numerous TdT-mediated dUTP-biotin nick end-labeling (TUNEL)-positive cells were also observed. In parallel, vascular endothelial growth factor receptor (VEGFR)-2 (Flk-1) levels were significantly lowered in the lumbosacral spinal cord of the paraparetic rats compared with their controls, suggesting a failure of the VEGF system to protect neurons against L-beta-ODAP toxicity. We propose, based on these data, a novel pathological process of motor neuron death induced by peripheral L-beta-ODAP. For the first time, we present a model of the early molecular events that occur during chemically induced spinal cord injury, which can potentially be applied to other neurodegenerative disorders.

[Describing neurolathyrism. Physicians and the lathyrism epidemic in post-civil war Spain]. / Describiendo el neurolatirismo. Los clinicos ante la epidemia de latirismo en la Espana de la posguerra.

INTRODUCTION: Lathyrism is a chronic disease involving spastic paralysis of the lower limbs caused by the prolonged consumption of large amounts of flour made from grass pea, or almorta as it is known in Spain. In Spain it became an epidemic in the early post-civil war years, and this gave rise to a series of studies and clinical descriptions of unquestionable medical and historical interest. DEVELOPMENT: This paper analyses the clinical reports of patients with lathyrism during the above-mentioned epidemic in order to stress the importance of the symptoms and the neurological examination in identifying new cases and in controlling them. One interesting feature that stands out is how uniform these descriptions are, except in the initial phase of the disease, where certain differences have been reported depending on the epidemic area. Likewise, the (typical and atypical) prodromal symptoms, the classic symptoms of the disease and the so-called residual symptoms are all described. CONCLUSIONS: The lathyrism epidemic that occurred in Spain in the years 1941-1943 resulted in a series of clinical descriptions with very detailed accounts of the signs and symptoms written by the Spanish physicians who treated those patients. These reports constitute a valuable historical and clinical contribution on the subject of a disease that has been eradicated in west but is still endemic in other parts of the world.

Downregulation of glutaredoxin but not glutathione loss leads to mitochondrial dysfunction in female mice CNS: implications in excitotoxicity.

Oxidative stress, excitotoxicity and mitochondrial dysfunction play synergistic roles in neurodegeneration. Maintenance of thiol homeostasis is important for normal mitochondrial function and dysregulation of protein thiol homeostasis by oxidative stress leads to mitochondrial dysfunction and neurodegeneration. We examined the critical roles played by the antioxidant, non-protein thiol, glutathione and related enzyme, glutaredoxin in maintaining mitochondrial function during excitotoxicity caused by beta-N-oxalyl amino-L-alanine (L-BOAA), the causative factor of neurolathyrism, a motor neuron disease involving the pyramidal system. L-BOAA causes loss of GSH and inhibition of mitochondrial complex I in lumbosacral cord of male mice through oxidation of thiol groups, while female mice are resistant. Reducing GSH levels in female mice CNS by pretreatment with diethyl maleate or L-propargyl glycine did not result in inhibition of complex I activity, unlike male mice. Further, treatment of female mice depleted of GSH with L-BOAA did not induce inhibition of complex I indicating that GSH levels were not critical for maintaining complex I activity in female mice unlike their male counterpart. Glutaredoxin, a thiol disulfide oxidoreductase helps maintain redox status of proteins and downregulation of glutaredoxin results in loss of mitochondrial complex I activity. Female mice express higher levels of glutaredoxin in certain CNS regions and downregulation of glutaredoxin using antisense oligonucleotides sensitizes them to L-BOAA toxicity seen as mitochondrial complex I loss. Ovariectomy downregulates glutaredoxin and renders female mice vulnerable to L-BOAA toxicity as evidenced by activation of AP1, loss of GSH and complex I activity indicating the important role of glutaredoxin in neuroprotection. Estrogen protects against mitochondrial dysfunction caused by excitotoxicity by maintaining cellular redox status through higher constitutive expression of glutaredoxin in the CNS. Therapeutic interventions designed to upregulate glutaredoxin may offer neuroprotection against excitotoxicity in motor neurons.

Impact of the gliotoxin L-serine-O-sulphate on cellular metabolism in cultured rat astrocytes.

L-serine-O-sulphate is a member of a group of amino acids collectively called gliotoxins and is a substrate for the high affinity sodium-dependent glutamate transporters. Previous studies have shown that it is toxic to primary cultures of astrocytes but the mode of toxicity is unknown. The current study demonstrates that L-serine-O-sulphate, at a sub-toxic concentration (400 microM), causes significant disruption to glucose and alanine metabolism in cultures of rat cortical astrocytes. More specifically, using (13)C NMR spectroscopy a significant reduction in labelled end products from [1-(13)C]glucose and [3-(13)C]alanine was found in the presence of L-serine-O-sulphate. Additionally, using [2-(13)C]glycine a 27% reduction in de novo glutathione synthesis was observed in the presence of the gliotoxin. Incubation of the cells with L-serine-O-sulphate reduced the activity of alanine and aspartate aminotransferase by 53% and 67%, respectively. Collectively these results show that the gliotoxin, L-serine-O-sulphate, causes major disruptions to metabolic pathways in primary cultures of astrocytes.

Pattern and associated factors of the neurolathyrism epidemic in Ethiopia.

OBJECTIVES: To describe the neurolathyrism epidemic in Ethiopia and to identify associated household factors. METHODS: We interviewed 589 randomly selected heads of household in Debre Sina district of Ethiopia, the area afflicted by the recent neurolathyrism epidemic. Disease information was obtained for 2987 family members. RESULTS: Neurolathyrism patients were detected in 56 (9.5%) households (prevalence rate 2.38%). The mean number of affected family members per household was 1.27 (SD 0.65, range 1-3). Most (77.5%) patients developed the disability during the epidemic (1995-1999). The median age at onset of paralysis was 11 years with a range of 41 (range 3-44). Younger people were more affected during the epidemic than during the non-epidemic period (P=0.01). The presence of a neurolathyrism patient in the family was associated with illiteracy [adjusted OR (95% CI)=2.23 (1.07-5.10)] of the head of household, with owning a grass pea farm [adjusted OR (95% CI)=2.01 (1.04-3.88)] and with the exclusive cooking of grass pea foods using handmade traditional clay pots [adjusted OR (95% CI=2.06 (1.08-3.90)]. CONCLUSION: Males aged 10-14 years were most affected by neurolathyrism. Increased household risk was associated with illiteracy of the head of the household and exclusive cooking of grass pea foods with handmade traditional clay pots.

In vitro toxicological investigations of isoxazolinone amino acids of Lathyrus sativus.

Two non-protein amino acids of Lathyrus sativus, beta-(isoxazoline-5-on-2-yl)-alanine (BIA) and its higher homologue alpha-amino-gamma-(isoxazoline-5-on-2-yl)-alanine (ACI) were tested for excitotoxic potential. BIA (0.5-2.0 mM) but not ACI (2.0 mM) produced a concentration-dependent neurodegeneration in mouse cortical explants. The neuronal damage was prevented by the prior and simultaneous application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), indicating that it was mediated by non-N-methyl-D-aspartate type receptors. BIA (0.5-2.0 mM) activated CNQX-sensitive currents which were significantly smaller than those activated by 3-N-oxalyl-L-2,3-diaminopropanoic acid (beta-ODAP) or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the majority of neurons. In a small number of cells, BIA (2 mM) produced currents which were similar in amplitude to those activated by beta-ODAP (50 microM). These results suggest that Lathyrus sativus plants engineered to block the synthesis of beta-ODAP may accumulate a neurotoxic precursor and therefore must be tested for the presence of both BIA and beta-ODAP.

H reflex studies in neurolathyrism.

Sixteen patients with lathyrism, age ranging between 18 and 55 years and duration of illness between 2 and 25 years, underwent H reflex studies with the aim of studying motor neurone excitability. The patients had marked spasticity (Ashworth score ranging between 2 and 5) and mild to moderate leg weakness. Knee and ankle reflexes were exaggerated in all and the plantar response was extensor in 14 patients. The H reflex abnormalities included increased HM ratio indicating increased motoneurone excitability, significant lack of vibratory inhibition indicating altered transmission in the premotoneuronal portion of the H reflex pathway, and lack of reciprocal inhibition (P < 0.01). These H reflex abnormalities were not related to spasticity, weakness, clonus or plantar response. The H reflex recovery curve in 6 patients revealed increased excitability throughout the recovery curve. The secondary facilitation started and peaked slightly earlier than normal, and the late depression was not marked indicating change in excitability of motoneurones or of interneurones.

Peripheral and central conduction studies in neurolathyrism.

To study the involvement of motor and sensory pathways in neurolathyrism, 19 patients with lathyrism from Unnao, India, where lathyrism is endemic, were studied. The mean age of the patients at the time of the onset of illness was 35.8 (range 18-70) years. The mean duration of illness was 15.6 (range 2-30) years. The clinical picture comprised walking difficulty due to stiffness and mild weakness in all 19 patients, cramps in the legs in five, frequency or urgency of micturition in five, and flexor spasms in three. There was pronounced leg spasticity with a mean Ashworth score of 4.1 (range 2.9-5). Central motor conduction to the tibialis anterior muscle (CMCT-TA) was slow in 14 of the 17 patients (21 sides). Slowing of peripheral motor nerve conduction, although less pronounced, was significant in the upper limb in four and the lower limb in seven sides. The tibial somatosensory evoked potentials were normal and peroneal nerve conduction was marginally impaired. Values for CMCT-TA correlated with the degree of spasticity (p < 0.02) whereas weakness, crossed adductor reflexes, and clonus did not. The wide variability of CMCT-TA in lathyrism may be due to involvement of different types of fibres. Large diameter fibre involvement may cause pronounced slowing. Small diameter fibre involvement could produce appreciable spasticity and mild weakness but a lesser degree of slowing or even normal conduction.

New findings and symptomatic treatment for neurolathyrism, a motor neuron disease occurring in north west Bangladesh.

Neurolathyrism is a form of spastic paraparesis caused by the neuroexcitatory amino acid 3-N-oxalyl-L-2,3-diaminopropanoic acid (beta-ODAP) present in the seeds and foliage of Lathyrus sativus. The disease is irreversible and usually nonprogressive. Tolperisone HCl, a centrally acting muscle relaxant, has been shown to reduce significantly the spasticity in neurolathyrism patients. Sporadic occurrence of HTLV-1 infection (0.9%) and of osteolathyrism was found among the neurolathyrism patients. Osteolathyrism is linked to the consumption of the green shoots of Lathyrus sativus.

Clinical aspects of neurolathyrism in Unnao, India.

To study the clinical picture of lathyrism in Unnao, India and compare it with that reported from other endemic areas, 41 patients from Unnao were studied. Their mean age was 42.9 years (range 22-85) and the mean duration of the illness was 17.1 years (range 2-30). They had been regularly consuming Lathyrus Sativus (LS). The patients complained of walking difficulty due to weakness and leg stiffness (32 each), and of frequency of micturition (4). Gait abnormalities included spastic gait (24), toe walking (18) and the necessary use of walking sticks (13). Weakness was mild to moderate, and was less prominent than was spasticity. In 8 patients the physical signs were asymmetrical. Peripheral neuropathy was present in only one patient, but muscle atrophy and widespread fasciculations were not found. A higher frequency of peripheral neuropathy and lower motor neuron involvement has been reported from Bangladesh and Israel. Severe spasticity in the absence of prominent weakness in lathyrism may be due to the involvement of certain specific groups of corticospinal fibres.

Collagen responsible for tooth eruption? A study of the eruption of rat incisors.

The rate of turnover of collagen in periodontal ligament (PDL) is closely associated with the process of tooth eruption and tissue adaptation allowing good anchorage of the tooth within the socket. Collagen may even be associated with orthodontic relapse. As the collagen protein seems to play a key role in tooth eruption, the investigation concentrated on the presence and maturation of collagen and its possible function in the process of tooth eruption.

Correlation of high-speed tensile strength with collagen content in control and lathyritic rat skin.

Severity of lacerative skin injury depends on the applied load and the resistance of the tissue. At low (static) rates of loading there is a high degree of correlation between skin tensile strength and the degree of collagen crosslinking, with little added strength due to collagen interactions with the glycosaminoglycan matrix. We examined the effects of high (ballistic) rates of loading in order to determine the contributions to strength made by both the degree of collagen crosslinking and the collagen-matrix interaction. Tensile failure experiments were conducted using the dorsal skin of rats 1.5-6 months of age. Test specimen orientations were cut parallel and transverse to the body axis at cephalad and caudad locations on the dorsum. Tensile strength was measured at nominal strain rates of 30%/sec (low speed) and 6000%/sec (high speed) using both control and lathyrogen fed rats. Biochemical analyses were conducted to determine the amount of total and crosslinked (insoluble) collagen. In low-speed tests, there was a significant correlation (r > or = 0.900) between collagen content and skin tensile strength measured both transverse and parallel to the spine. The degree of correlation was higher with insoluble (r = 0.973) collagen content than with total (r = 0.901) collagen. The effect of a lathyrogen diet produced a significant (P < 0.001) reduction (two- to threefold) in tensile strength compared to control. In both high- and low-speed groups, tensile strength was greatest in the transverse samples with a significant correlation to collagen content (r > or = 0.858).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic features in patients with chronic neurolathyrism.

Neurolathyrism is a toxic nutritional disorder induced by the ingestion of the chick-pea "lathyrus sativus" and characterized by a pure motor spastic paraparesis. Eight patients with long-standing disease underwent nerve conduction and electromyographic studies. Two of them (25%) showed electrophysiological signs of lower motor neuron disease in their lower limbs. Subclinical affection of the anterior horn cells occurs probably more frequently than expected in chronic neurolathyrism.