Konzo: The Paralysis Linked to Poorly Processed Bitter Cassava

Table of Contents

1. What Konzo Is
2. How It Begins and What It Does to the Body
3. Who Is Affected
4. Where Outbreaks Have Been Reported
5. Drought, War and Food Shortage as Reported Circumstances
6. Bitter Cassava Cyanogens and How Processing Removes Them
7. The Wetting Method and Its Reported Results
8. Protein, Sulfur Amino Acids and Cyanide Detoxification
9. The Exact Toxin Remains Unsettled
10. Thinking, Learning and Development in Affected Communities
11. Tropical Ataxic Neuropathy, a Related but Different Condition
12. Care and Daily Life After Konzo
13. Limits of the Evidence
14. Key Research Papers
15. Connections
16. Featured Videos

What Konzo Is

The word comes from the Yaka people of the Democratic Republic of Congo. One 2026 report gives its meaning as "tired legs" and records the local name buka-buka in the Bandundu region (Kamate and colleagues, 2026). A 2013 review instead says the disease was named after a Yaka fetish (Tshala-Katumbay and colleagues, 2013). In Nampula Province, Mozambique, the local name is mantakassa, "that which breaks legs" (Raimundo and colleagues, 2026). The first description dates from 1938, in what is now the Democratic Republic of Congo (Banea and colleagues, 2014).

Doctors call the pattern a spastic paraparesis: weakness of both legs with tight, stiff muscles. It comes from selective damage to the upper motor neurons, the nerve cells that carry movement signals from the brain down the spinal cord (Nzwalo and Cliff, 2011).

The World Health Organization uses three epidemiologic criteria, as summarized in the 2013 review (Tshala-Katumbay and colleagues, 2013):

• An abrupt onset of leg weakness, in under one week, with a course that does not progress, in a person who was previously healthy.
• A symmetrical spastic abnormality when walking or running.
• Exaggerated knee or ankle jerks on both sides, without signs of disease of the spine.

How It Begins and What It Does to the Body

The classic account comes from a drought-affected part of Tarime district in northern Tanzania, where 39 people aged 4 to 46 were studied. Their findings were uniform: abrupt, symmetric, isolated and permanent damage to the upper motor neurons that did not progress (Howlett and colleagues, 1990). Later reviews describe no sensory loss and no bladder or genital problems in the main picture. People affected most severely can have weakness in all four limbs and pseudobulbar signs, which involve the muscles of speech and swallowing (Tshala-Katumbay and colleagues, 2013).

Tests point to the motor pathways specifically:

• Two Tanzanian patients, severely disabled six years after onset, had normal magnetic resonance imaging of the brain and spinal cord. Yet motor signals could not be evoked by magnetic brain stimulation, even in their slightly affected arms (Tylleskär and colleagues, 1993).
• In a study using magnetic stimulation, 13 of 14 people with konzo had no signal response in a leg muscle. A hand muscle gave no resting response in 9 of the 14, even though their arms appeared preserved on examination (Tshala-Katumbay and colleagues, 2002).
• Damage may exist without visible paralysis. Among schoolchildren in communities of northern Mozambique previously affected by konzo, ankle clonus, a repetitive reflex jerk that signals upper motor neuron damage, was found in 8 to 17% (Ernesto and colleagues, 2002).

Konzo has been confused with other conditions. In 1996, cases reported as poliomyelitis in Kahemba, Democratic Republic of Congo, were reviewed and reassigned to konzo (Bonmarin and colleagues, 2002). Blood tests have not supported a retroviral cause (Kashala-Abotnes and colleagues, 2019).

Not every report fits the purely motor picture. A survey of 81 cases in the Central African Republic listed tremor in 88.9%, slurred speech in 67.9%, loss of visual sharpness in 65.4% and heightened skin sensitivity in 66.7% (Mbelesso and colleagues, 2009). One of the two Tanzanian patients above also had central visual field defects (Tylleskär and colleagues, 1993).

Who Is Affected

Children and women of childbearing age carry most of the burden across reports. Specific findings give the pattern more detail:

• Zambia: an outbreak investigation found 32 cases, in children aged 6 to 14 and, among older people, mostly women. Of the 15 cases aged 15 or older, 14 were female, and 11 of those women were breastfeeding when symptoms began (Siddiqi and colleagues, 2020).
• Mozambique: konzo mostly affects women of childbearing age and children over 2 years old (Cliff and colleagues, 2011). In the 1981 outbreak, raw and dried uncooked cassava was eaten mostly by women and children (Ministry of Health, Mozambique, 1984).
• Kahemba, Democratic Republic of Congo: women after childbirth were especially affected (Bonmarin and colleagues, 2002).
• Popokabaka, Democratic Republic of Congo: among 487 households surveyed in an area with a prevalence of 1.4%, higher prevalence was associated with being female, being unmarried, not being able to read, farming as main occupation and eating cassava from one's own land (Diasolua Ngudi and colleagues, 2011).

Cases cluster in families, which a recent review attributes to shared diets and shared economic hardship (Raimundo and colleagues, 2026).

Where Outbreaks Have Been Reported

Konzo has been reported in the Democratic Republic of Congo, Mozambique, Tanzania, the Central African Republic, Angola, Cameroon and, most recently, Zambia (Kashala-Abotnes and colleagues, 2019). A sample of the published record:

• Democratic Republic of Congo: a survey of 6,764 people in Bandundu found 110 living and 24 deceased people affected, with annual outbreaks from 1974 (Tylleskär and colleagues, 1991). In Kahemba, a survey found 237 people affected, 101 of them with onset in 1996 (Bonmarin and colleagues, 2002). Six villages in Boko Health Zone had 144 cases among 4,588 people, with prevalence between 2.0 and 5.2% (Banea and colleagues, 2015). In South Kivu, surveys in 2003 and 2005 identified 41 people (Chabwine and colleagues, 2011).
• Mozambique: over 1,100 cases in 1981, over 600 in 1992 to 1993 and over 100 in 2005 (Cliff and colleagues, 2011). Rehabilitation centers treated 384 patients in the war-related epidemic, with a prevalence of 30 per 1,000 in a badly affected area (Cliff and colleagues, 1997).
• Tanzania: four outbreaks between 1985 and 2002/2003, with 363 cases in total (Mlingi and colleagues, 2011).
• Central African Republic: 81 cases identified in a month of surveillance in 2007 in one health region, a prevalence of 10 per 100,000 (Mbelesso and colleagues, 2009).
• Cameroon: 469 patients in eastern villages, 80% of them refugees from the Central African Republic (Ciglenečki and colleagues, 2011).
• Zambia: 32 cases in Mongu District, the first documented in the country (Siddiqi and colleagues, 2020).

These counts almost certainly understate the total. A 2011 review put published cases at 6,788 up to 2009, against unofficial reports estimating at least 100,000 by 2000 (Nzwalo and Cliff, 2011). During outbreaks, up to 10% of the population in some regions can be affected (Kocher and colleagues, 2022).

Drought, War and Food Shortage as Reported Circumstances

Reports repeatedly describe konzo arriving when families have few options left. Bitter cassava survives conditions that destroy other crops, and it can become almost the only food available.

Drought. In 1981 in northern Mozambique, a prolonged drought had exhausted all food resources except cassava, especially bitter varieties. Investigators found unusually high cyanide levels in the plant and estimated daily intakes of 15 to 31.5 milligrams of hydrogen cyanide. Sun-drying was inadequate because of the general food shortage (Ministry of Health, Mozambique, 1984). In Tarime, Tanzania, drought raised the natural level of cyanogenic compounds in the roots, and processing was shortened because of food shortage (Howlett and colleagues, 1990). An analysis of climate and case records in the Democratic Republic of Congo found repeating cycles of 3 to 6 years, with a strong match between rainfall variation and konzo epidemics. Its author concluded that public health control of konzo will require food and water programs during droughts (Oluwole, 2015).

War and displacement. In Mozambique, war led communities to turn to bitter cassava as their staple and take shortcuts in processing, and they continued to depend on it after the war ended (Cliff and colleagues, 1997). In South Kivu, where cassava had been eaten safely for decades, konzo appeared amid long conflict, and the report concluded that food shortages from insecurity triggered it, with new bitter varieties a contributing factor (Chabwine and colleagues, 2011). In eastern Cameroon, around 60,000 people fleeing the Central African Republic sought refuge between 2005 and 2007, and most konzo patients seen there were refugees (Ciglenečki and colleagues, 2011).

Markets and money. In Bandundu, annual outbreaks began in 1974, when a new paved road to the capital made cassava the main cash crop. Heavy sales encouraged families to eat roots that had not been adequately processed (Tylleskär and colleagues, 1991). A later qualitative study of 131 women in Kwango, Democratic Republic of Congo, found they knew about safe processing. The barriers they described were access to water and lack of money: carrying water was burdensome, roots soaking in the river could be stolen, and processing was shortened to reach the market quickly (Bokundabi and colleagues, 2023).

Season and soil. Cases tend to cluster in the dry season (Kamate and colleagues, 2026; Banea-Mayambu and colleagues, 1997). Soils in Mtwara, Tanzania, were short of several nutrients, and some soil conditions were associated with more cyanogens in roots or more cases of cassava poisoning (Imakumbili and colleagues, 2019). Farmers interviewed in the same region named soil characteristics and plant age at harvest among the things they connect to more bitter roots (Imakumbili and colleagues, 2019).

Bitter Cassava Cyanogens and How Processing Removes Them

Cassava contains cyanogenic glucosides, mainly linamarin (Kashala-Abotnes and colleagues, 2019). An enzyme called linamarase breaks these down into cyanohydrins, which then break down to toxic cyanide (Bradbury and colleagues, 2011). The body converts cyanide largely into thiocyanate, so thiocyanate in urine is the usual marker of exposure. Bitterness is a rough guide used by farmers, since increased root bitterness is often associated with higher levels of these compounds (Imakumbili and colleagues, 2019).

Processing lets these compounds break down and escape. Time is the critical variable in the reports:

• Soaking length: in one comparison, an affected population ate flour from roots soaked for one day and had urinary thiocyanate of 757 micromoles per liter in children. An unaffected population whose cassava was soaked for three days had 50 micromoles per liter (Tylleskär and colleagues, 1992).
• Short soaking in practice: in Boko Health Zone, high flour cyanide of 50 parts per million was attributed to soaking for 1 to 2 days instead of 3 to 4 (Banea and colleagues, 2013).
• Other methods: programs in Mozambique have promoted grating and flour wetting, along with less toxic cassava varieties (Cliff and colleagues, 2011).

A commonly cited World Health Organization cut-off for cassava flour is 10 parts per million. Household flour in one Congolese community study averaged 52.18 parts per million (Kashala-Abotnes and colleagues, 2018). Mean flour levels in northern Mozambique ranged from 26 to 186 parts per million (Ernesto and colleagues, 2002).

Cassava cyanide can also cause sudden poisoning, separate from konzo, and it can cause death (Bradbury and colleagues, 2011). In Kasese District, Uganda, in 2017, 33 people were admitted to hospital with diarrhea, vomiting and abdominal pain after eating a dish made with cassava flour later found to have a high cyanogen content (Alitubeera and colleagues, 2019). Food sold far from these regions is not automatically free of the issue. A survey in Melbourne, Australia, against that country's 10 parts per million limit for ready-to-eat products, found a mean of 95.9 parts per million in imported ready-to-eat products, compared with 1.0 in locally made ones; following packet instructions significantly reduced cyanide in frozen products (Quinn and colleagues, 2022). The European Food Safety Authority's contaminants panel found that available data do not allow a long-term safe intake value for cyanide to be set (EFSA Panel on Contaminants in the Food Chain, 2019).

Plant science offers another route. Gene editing that knocked out two genes in the first step of cyanogen production eliminated cyanide in leaves and storage roots of the three cassava lines tested (Gomez and colleagues, 2022). That is a laboratory-stage result; it says nothing yet about konzo in people.

The Wetting Method and Its Reported Results

Soaking removes cyanogens from roots. The wetting method adds a further step at the flour stage. Developed in 2005, it involves wetting the flour, spreading it in a thin layer in the shade for 5 hours and using it the same day to make the traditional thick porridge. Exposing wet flour in a thin layer in the sun for 2 hours was reported as equally effective. Its developers report a 3- to 6-fold reduction in total cyanide, with no additional equipment or water needed (Bradbury and colleagues, 2011). A community program in Tanzania measured about a 4-fold reduction (Mlingi and colleagues, 2011).

Published village interventions report the following:

• Kay Kalenge, Democratic Republic of Congo (1.5 years): flour cyanide fell below 10 parts per million, children's mean urinary thiocyanate fell from 332 to 130 micromoles per liter, and the number of 100 school children above 350 fell from 26 to 0. No new cases occurred, across two dry seasons when konzo peaks (Banea and colleagues, 2012).
• The same village 14 months later: women still used the method, there were no new cases, flour averaged 9 parts per million and the method had spread by itself to three adjacent villages (Banea and colleagues, 2014).
• Three villages in Boko Health Zone (1 year): flour cyanide fell from 50 to 14 parts per million, children's mean urinary thiocyanate fell from 930 to 150 micromoles per liter, and no new cases occurred (Banea and colleagues, 2013).
• Six villages in Boko Health Zone (9 months): no new cases, with flour cyanide reaching World Health Organization safe levels. The authors estimate at least 60 to 70% of women need to use the method regularly to prevent konzo, and report a cost of $16 per person across four interventions covering nearly 10,000 people in 13 villages (Banea and colleagues, 2015).
• Three villages in Mozambique: the share of children with urinary thiocyanate above 350 micromoles per liter fell from 52, 10 and 6% to 17, 0 and 4%. Uptake was only 30 to 40% of households in two villages and lower in the third (Nhassico and colleagues, 2016).

A cost-effectiveness analysis from the Democratic Republic of Congo reported that the method was a cost-effective way to improve children's cognitive development (Chen and colleagues, 2021). Authors of these studies recommend that the method be taught in all konzo areas of East Africa (Nhassico and colleagues, 2016). The Kwango study concluded that knowledge alone is not enough to change practice under severe resource limits (Bokundabi and colleagues, 2023).

Protein, Sulfur Amino Acids and Cyanide Detoxification

The body detoxifies cyanide largely through a sulfur-dependent enzyme called rhodanese, which turns it into thiocyanate. The sulfur comes from amino acids in protein, such as methionine and cystine (Tor-Agbidye and colleagues, 1999). This may explain why many reports find cyanide exposure and low protein together.

• Mozambique, 1985: children from the epidemic area had high thiocyanate and low inorganic sulfate in urine, indicating high cyanide and low sulfur amino acid intake. Children in a neighboring cassava-eating area with no cases had less thiocyanate and more sulfate (Cliff and colleagues, 1985).
• Popokabaka: a median of 304 grams of cassava flour per person per day was used in stiff porridge, and main foods were poor in protein, especially sulfur amino acids (Diasolua Ngudi and colleagues, 2011).
• Zambia: cases ate cassava a median of 14 times a week and protein-rich foods less than once a week (Siddiqi and colleagues, 2020).
• Case-control study of 122 children with konzo and 87 without: konzo was associated with stunting (odds ratio 5.8) and higher urinary thiocyanate. After adjustment, a defined increase in cyanide detoxification rate was associated with 63% lower odds of konzo (Kambale and colleagues, 2017).
• Eastern Democratic Republic of Congo, 2021: people with konzo had a high prevalence of wasting (54.5%), stunting (72.7%) and cyanide poisoning (81.8%). Unaffected people in two nearby areas also had high cyanide poisoning (50.0% and 63.0%) but far less wasting (3.3% and 6.5%). The authors conclude that malnutrition may be a key factor in whether disease occurs (Baguma and colleagues, 2021).
• Trace minerals: 123 children with konzo had lower selenium, copper and zinc than 87 children without it. Selenium correlated with motor scores, but these deficiencies were not associated with cognition (Bumoko and colleagues, 2015).

Rat studies give a possible explanation. In rats fed a diet lacking cystine and methionine and given oral cyanide for up to 4 weeks, plasma cyanate rose exponentially, consistent with the idea that low sulfur intake diverts cyanide toward cyanate (Tor-Agbidye and colleagues, 1999). A separate review proposes that low methionine and cystine could deplete glutathione in the central nervous system, a feature it suggests konzo may share with neurolathyrism from grass pea (Nunn and colleagues, 2011). That remains a hypothesis.

Nutrition does not explain every case. In the 1981 Mozambican outbreak, investigators wrote that the population's general nutritional status was not very poor and that advanced undernutrition was rare (Ministry of Health, Mozambique, 1984).

The Exact Toxin Remains Unsettled

Almost a century after the first description, a 2021 systematic review states that the causative agent and underlying mechanisms remain unknown. Cyanide poisoning and protein malnutrition are the two well-documented risk factors, yet observational studies have failed to demonstrate a causal relationship between konzo and cyanide. The review also notes that thiocyanate may understate true exposure when protein is short, because more cyanide then goes through other routes (Baguma and colleagues, 2021).

Candidates under discussion include:

• Thiocyanate: one review of epidemics names it the most likely neurotoxicant (Oluwole, 2015).
• Cyanate: in mouse and human nerve-derived cell lines and rat spinal cord neurons grown in culture, cyanate was toxic at 0.3 to 3 millimolar, while thiocyanate toxicity appeared at around 30 millimolar, leading the authors to favor cyanate (Baguma and colleagues, 2024). In 40 Congolese children, konzo was associated with higher levels of carbamoylated peptides, the protein change cyanate produces (Rwatambuga and colleagues, 2021).
• Linamarin itself: a 1997 study found urinary linamarin more closely associated with konzo than cyanide exposure (Banea-Mayambu and colleagues, 1997).
• Nitriles: one review proposes that compounds containing cyano groups could explain konzo, lathyrism and tropical ataxic neuropathy, based largely on animal data (Llorens and colleagues, 2011).

Biological studies have opened other directions, none of them proof of cause. Plasma glutathione peroxidase 3, an antioxidant enzyme, was markedly reduced in people with konzo in two Congolese groups of 60 and 204 people sampled 10 years apart (Bramble and colleagues, 2024). A study of 180 people identified gut bacteria and functions that the authors suggest could modify susceptibility (Bramble and colleagues, 2021). An analysis of 16 people with konzo and matched controls found 117 differentially methylated DNA sites (Kocher and colleagues, 2022). A marker of oxidative damage was linked to cognitive scores in 40 children (Makila-Mabe and colleagues, 2014).

Thinking, Learning and Development in Affected Communities

Recent work has widened the question from paralysis to child development, including in children who are not paralyzed.

• First neuropsychological findings (2013): children with konzo did worse than unaffected neighbors on visual-spatial processing and an overall mental processing score, and much worse on motor proficiency. Both groups scored below children from a non-outbreak area on memory and overall mental processing (Boivin and colleagues, 2013).
• Four-year follow-up (2017): 123 children with konzo and 87 without were enrolled. Motor scores remained lower in both boys and girls with konzo at 2 and 4 years. Cognitive differences appeared only in boys at 2 years, might have been related to stunting, and were not significant at 4 years. Urinary thiocyanate was linked to lower motor scores in boys but was not linked to cognitive scores in either sex (Boivin and colleagues, 2017).
• Young children (2018): in children aged 12 to 48 months, cyanide in household flour was associated with fine motor skill and overall neurodevelopment even without visible paralysis, after adjusting for other factors (Kashala-Abotnes and colleagues, 2018).
• Other associations: in 40 children, female sex was linked to lower cognitive scores after adjustment, and low blood albumin in an unadjusted analysis (Bumoko and colleagues, 2014).
• Emotional wellbeing: in interviews with parents of 210 children in affected areas, 46.0% of children had irritability, 30.2% physical violence and 18.7% inhibition, with or without sadness (E-Andjafono and colleagues, 2018).

A 2024 burden estimate for the Democratic Republic of Congo modeled a median loss of 2.37 intelligence quotient points at a median cassava cyanide level of 12.5 milligrams per kilogram, and gave a burden of 13,862 disability-adjusted life years per 100,000 children, or 3.01 million for all children under 5 (Chen and Wu, 2024). This is a model built on a concentration-effect relationship, not a count of examined children. The paper's reported 95% interval for the per-100,000 figure runs from 0 to 14,773, so the estimate is uncertain.

Tropical Ataxic Neuropathy, a Related but Different Condition

Tropical ataxic neuropathy is another neurological condition reported in cassava-eating regions. First described in Jamaica in 1897 and named in 1959, it combines loss of sensation and coordination with changes in vision and hearing, such as optic atrophy and nerve deafness (Netto and colleagues, 2016). One 2013 konzo review groups the two terms together (Tshala-Katumbay and colleagues, 2013), but direct comparisons treat them as separate:

• The 1984 Mozambique report contrasted the two: earlier cassava-linked disease affected older people, usually with gradual onset and ataxic neuropathy, while mantakassa began acutely in women of reproductive age and children (Ministry of Health, Mozambique, 1984).
• In Ososa, Nigeria, prevalence among 3,428 people screened was 6.0%, reaching 24% in women aged 60 to 69. The authors found features unlike those of konzo (Oluwole and colleagues, 2000).
• In Odeda, Nigeria, 39 cases among 2,392 adults gave a prevalence of 16.3 per 1,000 (Otubogun and colleagues, 2019).
• In Kerala, India, most of 40 patients ate a diet heavy in tapioca (another name for cassava); 90% had decreased hearing and 50% decreased vision. Most improved after they stopped eating cassava and ate better overall (Madhusudanan and colleagues, 2008).

The cause is even less settled than for konzo. A two-year cohort in Ososa found no link between cassava intake or cyanide exposure and new cases, and its authors wrote that the findings do not suggest cyanide as the cause (Oluwole and colleagues, 2003). A review implicates chronic thiamine deficiency and cites a placebo-controlled trial with improvement in ataxia (Adamolekun, 2010). A genetic study of 65 patients found variants in nuclear genes in 36 of the 45 who had exome sequencing, along with signs of mitochondrial dysfunction in some, and offered this as preliminary evidence that differs from the dietary toxin hypothesis (Sharma and colleagues, 2024).

Care and Daily Life After Konzo

No curative treatment exists, and the lifelong effects fall on individuals and their communities (Kamate and colleagues, 2026). Published care is supportive. In southern Tanzania, 214 people were screened and supplied with crutches and wheelchairs where needed (Mlingi and colleagues, 2011). In eastern Cameroon, patients received nutritional supplements, and selected cases were referred for physiotherapy (Ciglenečki and colleagues, 2011). Cognitive rehabilitation has yet to be tested (Kashala-Abotnes and colleagues, 2019).

How a community explains the illness matters for care. A review from Nampula Province found that narratives often link konzo to spiritual causes, while health workers noted low diagnostic accuracy and limited knowledge of the condition. Traditional healers are often the first source of care in rural areas, and their understanding remains poorly documented (Raimundo and colleagues, 2026).

Authors writing from Mozambique have asked for attention to agricultural development and food security in regions dependent on bitter cassava (Cliff and colleagues, 2011). A 2019 review describes prevention as of paramount importance because there is no cure (Kashala-Abotnes and colleagues, 2019).

Limits of the Evidence

• Causation is not proven. The link rests on observational studies. The 1984 Mozambique report itself called the evidence linking cassava to the disease circumstantial (Ministry of Health, Mozambique, 1984), and the 2021 systematic review reached a similar view of cyanide (Baguma and colleagues, 2021).
• Exposure is measured indirectly. Urinary thiocyanate is an indirect marker and may understate exposure in protein-deficient people (Baguma and colleagues, 2021). In one epidemic, values were lower than earlier reports, probably because samples were taken before the harvest peak (Cliff and colleagues, 1997).
• Wetting method studies are village before-and-after reports. None of those read for this page describes a randomized comparison, and most come from a connected group of investigators, including the method's developers. Follow-up ran from 9 months to under three years. Konzo also varies by season and year, so an absence of new cases over a short period is informative but not conclusive.
• Case counts are incomplete. Published counts fall far below unofficial estimates, and outbreaks occur in remote areas with limited diagnosis (Nzwalo and Cliff, 2011; Raimundo and colleagues, 2026).
• Cognitive studies have real constraints. The four-year study retained 55 of 123 children with konzo and 33 of 87 without. Stunting, poverty and other exposures are hard to separate from cyanide (Boivin and colleagues, 2017). The burden figures are modeled.
• Biomarker and microbiome studies are small and associative. They cannot show whether a difference comes before the disease or after it.
• Animal and cell findings do not transfer directly. The cyanate and low-sulfur results come from rats and cultured cells.

Key Research Papers

1. Kamate DP, Neumayr A, Blum J. Konzo: a nutrition-related tropical spastic paraparesis. BMJ Case Rep. 2026;19(4):e270728. PubMed PMID: 42031371
2. Kashala-Abotnes E, Okitundu D, Mumba D, Boivin MJ, Tylleskär T, Tshala-Katumbay D. Konzo: a distinct neurological disease associated with food (cassava) cyanogenic poisoning. Brain Res Bull. 2019;145:87-91. PubMed PMID: 29981837
3. Nzwalo H, Cliff J. Konzo: from poverty, cassava, and cyanogen intake to toxico-nutritional neurological disease. PLoS Negl Trop Dis. 2011;5(6):e1051. PubMed PMID: 21738800
4. Baguma M, Nzabara F, Maheshe Balemba G, Malembaka EB, Migabo C, Mudumbi G, Bito V, Cliff J, Rigo JM, Chabwine JN. Konzo risk factors, determinants and etiopathogenesis: What is new? A systematic review. Neurotoxicology. 2021;85:54-67. PubMed PMID: 33964344
5. Siddiqi OK, Kapina M, Kumar R, Ngomah Moraes A, Kabwe P, Mazaba ML, Hachaambwa L, Ng'uni NM, Chikoti PC, Morel-Espinosa M, Jarrett JM, Baggett HC, Chizema-Kawesha E. Konzo outbreak in the Western Province of Zambia. Neurology. 2020;94(14):e1495-e1501. PubMed PMID: 32127386
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1. PubMed: konzo
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Connections

• Neurology — the parent section
• Peripheral Neuropathy — nerve damage outside the brain and spinal cord
• Subacute Combined Degeneration — a nutritional spinal cord disease
• Amyotrophic Lateral Sclerosis — another motor neuron disease
• Goiter — a thyroid condition also discussed with cassava
• Methionine — a sulfur amino acid
• Vitamin B1 — thiamine, proposed in tropical ataxic neuropathy
• Laetrile and Amygdalin — another cyanide-releasing plant compound

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