Mercury Poisoning

Environmental MONDO:0018020 Pathograph 3 Show in embeddings browser

Mercury poisoning is a toxic condition caused by exposure to mercury in its elemental, inorganic, or organic forms, each with a distinct clinical profile. Organic mercury — chiefly methylmercury, bioaccumulated in fish and shellfish — is a potent central neurotoxin and the cause of Minamata disease, the catastrophic 1950s-1960s methylmercury food-poisoning epidemic in Minamata, Japan. Methylmercury crosses the blood-brain and placental barriers and injures specific neuronal populations, producing cerebellar ataxia, constriction of the visual fields, somatosensory disturbance, dysarthria, and, with prenatal exposure, severe congenital neurodevelopmental disease. Inorganic and elemental mercury, by contrast, classically cause peripheral nerve disease and the neuropsychiatric syndrome of erethism ("mad hatter"). An international case-control comparison found no association between mercury exposure from seafood or dental amalgam and amyotrophic lateral sclerosis. Mercury poisoning is a focal/regional neurotoxicity rather than a progressive proteinopathy, and there is no effective disease-modifying treatment for established neuronal injury. SCOPE NOTE: the pathophysiology graph, phenotypes, and exposure sections of this entry currently model only the ORGANIC (methylmercury / Minamata) arm. The elemental and inorganic mercury arms — mercury vapour pneumonitis, erethism, acrodynia, and mercury-associated membranous nephropathy and nephrotic syndrome — are named here for orientation but are not yet curated as pathophysiology nodes or phenotypes. See the attached knowledge gap.

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2
Pathophys.
4
Phenotypes
1
Gaps
3
Pathograph
2
Medical Actions
?

Discussions and Knowledge Gaps

1
What are the pathophysiology nodes, phenotypes, and treatments of the elemental and inorganic mercury arms, which this entry names but does not yet model?
KNOWLEDGE GAP OPEN gap_mercury_inorganic_arm_not_curated
Attached to
pathophysiology#Methylmercury CNS Accumulation and Neuronal Injury
The entry is scoped to mercury poisoning generally and its description contrasts the organic and inorganic clinical profiles, but every pathophysiology node, phenotype, and exposure record curated so far concerns methylmercury and Minamata disease. The inorganic/elemental arm — mercury vapour pneumonitis, erethism, acrodynia, and mercury-associated membranous nephropathy — has a distinct mechanism, a distinct target-organ profile, and (unlike established methylmercury neuronal injury) a chelation-responsive course. Leaving it unmodelled makes the entry read as complete for a disease for which only one arm is represented.
Proposed experiments
Curate the elemental/inorganic mercury arm
exp_mercury_curate_inorganic_arm
Build the inorganic/elemental pathograph from primary literature: vapour inhalation to chemical pneumonitis; mercuric ion binding to renal tubular and glomerular targets to membranous nephropathy and nephrotic syndrome; and CNS deposition to erethism and tremor. Add the chelation treatments (succimer/DMSA, unithiol/DMPS) that apply to that arm and not to established methylmercury injury.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"In contrast, peripheral nerve disease is more characteristic of inorganic mercury intoxication."
Establishes that the inorganic arm has a clinically distinct profile from the methylmercury arm modelled here, which is what makes its absence a gap.
⚙

Pathophysiology

2
Methylmercury CNS Accumulation and Neuronal Injury
Methylmercury readily crosses the blood-brain barrier and accumulates in the central nervous system, where it injures neurons through several converging molecular mechanisms: glutathione/thiol (NPSH) depletion with reactive-oxygen- species overproduction (oxidative stress), intracellular calcium dyshomeostasis, and NMDA-receptor-mediated excitotoxicity. These insults drive neuronal apoptosis and underlie the regional neurodegeneration of the disease.
neuron CL:0000540 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves neuron (CL:0000540). CL:0000540 is a cell type from the Cell Ontology.
response to oxidative stress GO:0006979 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased response to oxidative stress (GO:0006979). GO:0006979 is a biological process from the Gene Ontology. ↑ INCREASED
Downstream
Regional Neuronal Degeneration Oxidative, calcium, and excitotoxic injury drives degeneration of selectively vulnerable neuronal populations.
Show evidence (2 references)
PMID:27538940 SUPPORT In Vitro
"Methylmercury (MeHg) is an extremely dangerous environmental pollutant that induces severe toxic effects in the central nervous system."
Establishes methylmercury as a central neurotoxin acting directly on CNS neurons.
PMID:27538940 SUPPORT In Vitro
"reactive oxygen species (ROS) overproduction showed an obvious oxidative stress in neurons."
Demonstrates the oxidative-stress arm of methylmercury neuronal injury in cultured cortical neurons; the same study implicates calcium dyshomeostasis and NMDA-receptor excitotoxicity.
Regional Neuronal Degeneration
Methylmercury injures characteristic, selectively vulnerable brain regions: cerebellar granule cell neurons (producing ataxia), the calcarine/visual cortex (producing visual-field constriction), and the somatosensory cortex (producing sensory disturbance). This regional pattern of neuronal loss, not a diffuse progressive proteinopathy, defines the neuropathology of Minamata disease.
cerebellar granule cell CL:0001031 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves cerebellar granule cell (CL:0001031). CL:0001031 is a cell type from the Cell Ontology.
neuron apoptotic process GO:0051402 Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased neuron apoptotic process (GO:0051402). GO:0051402 is a biological process from the Gene Ontology. ↑ INCREASED
cerebellum UBERON:0002037 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in cerebellum (UBERON:0002037). UBERON:0002037 is an anatomical location from the Uberon multi-species anatomy ontology. cerebral cortex UBERON:0000956 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in cerebral cortex (UBERON:0000956). UBERON:0000956 is an anatomical location from the Uberon multi-species anatomy ontology.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"Visual field constriction due to involvement of the calcarine cortex, sensory disturbance due to involvement of the somatosensory cortex, and cerebellar ataxia due to involvement of granule cell neurons of the cerebellum are common and characteristic features due to methylmercury poisoning."
Maps the characteristic clinical features of methylmercury poisoning to degeneration of specific brain regions, defining the regional neurodegeneration node.
⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Mercury Poisoning Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
●

Phenotypes

4
Eye 1
Constriction of Visual Fields Constriction of peripheral visual field HP:0001133 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Constriction of peripheral visual field (HP:0001133). HP:0001133 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"Visual field constriction due to involvement of the calcarine cortex"
Visual-field constriction from calcarine cortex involvement is a characteristic feature of methylmercury poisoning.
Nervous System 3
Cerebellar Ataxia HP:0001251 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Ataxia (HP:0001251). HP:0001251 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"cerebellar ataxia due to involvement of granule cell neurons of the cerebellum are common and characteristic features due to methylmercury poisoning."
Cerebellar ataxia from granule-cell degeneration is a cardinal feature of methylmercury poisoning.
Somatosensory Disturbance Somatic sensory dysfunction HP:0003474 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Somatic sensory dysfunction (HP:0003474). HP:0003474 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"sensory disturbance due to involvement of the somatosensory cortex"
Somatosensory disturbance from somatosensory cortex involvement is a characteristic feature of methylmercury poisoning.
Dysarthria HP:0001260 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Dysarthria (HP:0001260). HP:0001260 is a phenotype from the Human Phenotype Ontology.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"Other neurological features include dysarthria, postural and action tremor, cognitive impairment, and hearing loss and dysequilibrium."
Dysarthria is among the recognized neurological features of methylmercury poisoning.
💊

Medical Actions

2
Exposure cessation and source control
Action: therapeutic procedureNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is therapeutic procedure (NCIT:C49236). NCIT:C49236 is a clinical intervention from the NCI Thesaurus. Ontology label: Therapeutic Procedure NCIT:C49236
Identifying and eliminating the mercury source is the primary intervention. For methylmercury this means removing the contaminated dietary source; for the inorganic/elemental arm it means removing the occupational or product exposure. This prevents further accumulation but does not reverse established neuronal injury.
Show evidence (1 reference)
PMID:37372760 SUPPORT Human Clinical
"is a well-known case of food poisoning caused by methylmercury-contaminated fish"
The snippet establishes the contaminated dietary exposure route but does not directly evaluate cessation or source control as an intervention.
Supportive and rehabilitative care for established neurological injury
Action: Supportive CareNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Supportive Care (NCIT:C15747). NCIT:C15747 is a clinical intervention from the NCI Thesaurus. NCIT:C15747
Management of established methylmercury neurological disease is supportive: there is no effective disease-modifying treatment for the neuronal injury once it has occurred. Care targets the resulting ataxia, sensory disturbance, visual field loss, dysarthria, and cognitive impairment.
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"There is no effective treatment."
The source states plainly that no effective treatment exists for chronic neurological disease from methylmercury, which is why management is supportive.
🌍

Environmental Factors

1
Methylmercury-Contaminated Fish and Mercury Exposure
exposure to mercury ECTO:0001571 Environmental Conditions, Treatments and Exposures Ontology (ECTO) Relation: this environmental factor is this exposure This environmental factor is exposure to mercury (ECTO:0001571). ECTO:0001571 is an exposure from the Environmental Conditions, Treatments and Exposures Ontology.
Organic methylmercury bioaccumulates in fish and shellfish; the Minamata epidemic resulted from industrial methylmercury discharge contaminating seafood. Other documented exposures include contaminated waters in Japan and northwestern Ontario and methylmercury-fungicide-treated seed grain in Iraq. Occupational and elemental/inorganic mercury exposures (e.g., the historical felt-hat industry) produce a different, predominantly peripheral and neuropsychiatric syndrome. Notably, an international case-control comparison found no association between mercury exposure from seafood consumption or dental amalgam fillings and amyotrophic lateral sclerosis.
Show evidence (3 references)
PMID:37372760 SUPPORT Human Clinical
"is a well-known case of food poisoning caused by methylmercury-contaminated fish"
Documents the dietary (contaminated-fish) route of methylmercury exposure that caused Minamata disease.
PMID:30278852 SUPPORT Human Clinical
"psychosis is more typical of exposure to inorganic mercury, which has been documented in the felt hat industry"
Distinguishes the neuropsychiatric syndrome of inorganic/elemental mercury exposure (erethism, "mad hatter") from the central syndrome of organic methylmercury.
PMID:30558238 SUPPORT Human Clinical
"this study found no evidence that mercury exposure from eating seafood, or from mercury dental fillings, was associated with the risk of developing ALS"
Sources the negative ALS association stated in these notes and in the disease description. Note the design limits its strength: an online self-report questionnaire case-control study (401 ALS vs 452 non-ALS respondents), so this is absence of an observed association rather than proof of no effect.
Mechanism Target:
TRIGGERS Methylmercury CNS Accumulation and Neuronal Injury — Eating contaminated fish delivers methylmercury that is absorbed from the gut, carried in blood, and crosses the blood-brain barrier before accumulating in the central nervous system, so the exposure reaches this node through known intermediate steps rather than acting on it directly. This edge covers the organic methylmercury arm only; the elemental and inorganic exposures also described in this entry produce a different, predominantly neuropsychiatric syndrome.
Show evidence (1 reference)
PMID:37372760 SUPPORT Human Clinical
"is a well-known case of food poisoning caused by methylmercury-contaminated fish"
Establishes the dietary contaminated-fish route as the source of the methylmercury responsible for the central nervous system disease.
🔬

Diagnosis

2
Blood, hair, and toenail mercury measurement
Mercury concentration in blood, hair, and toenail samples documents exposure and is the standard laboratory approach to suspected mercury poisoning. Interpretation is bounded: in patients presenting with established chronic neurological disease these matrices may not reflect the remote exposure that caused the neuronal injury, so a normal result late in the course does not exclude prior methylmercury poisoning.
Laboratory Procedure NCIT:C25294 NCI Thesaurus (NCIT)
Show evidence (1 reference)
PMID:30278852 SUPPORT Human Clinical
"Laboratory tests (e.g., on blood and hair and toenail samples) are of limited value in the assessment of chronic neurological disease due to mercury poisoning because they may not reflect remote neuronal injury due to mercury."
Names the standard exposure matrices while explicitly bounding their value in chronic disease; marked PARTIAL because the source qualifies rather than endorses the test.
Umbilical cord mercury concentration for prenatal exposure
Archived umbilical cord tissue provides a retrospective measure of in-utero methylmercury exposure and has been used to grade prenatal exposure against neuropsychological outcome in the Minamata population.
Laboratory Procedure NCIT:C25294 NCI Thesaurus (NCIT)
Show evidence (1 reference)
PMID:37372760 SUPPORT Human Clinical
"The average umbilical cord methylmercury concentrations were 1.67 parts per million (ppm) for CMD patients and 0.77 ppm for moderately exposed participants."
Umbilical cord methylmercury concentration is used as the quantitative index of prenatal exposure in this Minamata cohort.
{ }

Source YAML

click to show 
name: Mercury Poisoning
creation_date: "2026-06-11T00:00:00Z"
category: Environmental
categories:
- Toxic Exposure Disorder
- Heavy Metal Poisoning
- Environmental Health Disorder
synonyms:
- Minamata disease
- methylmercury poisoning
- hydrargyria
- mercurialism
disease_term:
  preferred_term: mercury poisoning
  term:
    id: MONDO:0018020
    label: mercury poisoning
description: >-
  Mercury poisoning is a toxic condition caused by exposure to mercury in its
  elemental, inorganic, or organic forms, each with a distinct clinical profile.
  Organic mercury — chiefly methylmercury, bioaccumulated in fish and shellfish —
  is a potent central neurotoxin and the cause of Minamata disease, the
  catastrophic 1950s-1960s methylmercury food-poisoning epidemic in Minamata,
  Japan. Methylmercury crosses the blood-brain and placental barriers and injures
  specific neuronal populations, producing cerebellar ataxia, constriction of the
  visual fields, somatosensory disturbance, dysarthria, and, with prenatal
  exposure, severe congenital neurodevelopmental disease. Inorganic and elemental
  mercury, by contrast, classically cause peripheral nerve disease and the
  neuropsychiatric syndrome of erethism ("mad hatter"). An international
  case-control comparison found no association between mercury exposure from
  seafood or dental amalgam and amyotrophic lateral sclerosis. Mercury poisoning
  is a focal/regional neurotoxicity rather than a progressive proteinopathy, and
  there is no effective disease-modifying treatment for established neuronal
  injury.

  SCOPE NOTE: the pathophysiology graph, phenotypes, and exposure sections of
  this entry currently model only the ORGANIC (methylmercury / Minamata) arm.
  The elemental and inorganic mercury arms — mercury vapour pneumonitis,
  erethism, acrodynia, and mercury-associated membranous nephropathy and
  nephrotic syndrome — are named here for orientation but are not yet curated as
  pathophysiology nodes or phenotypes. See the attached knowledge gap.
pathophysiology:
- name: Methylmercury CNS Accumulation and Neuronal Injury
  conforms_to: "glutamate_excitotoxicity#Glutamate Receptor Overactivation and Calcium Overload"
  description: >-
    Methylmercury readily crosses the blood-brain barrier and accumulates in the
    central nervous system, where it injures neurons through several converging
    molecular mechanisms: glutathione/thiol (NPSH) depletion with reactive-oxygen-
    species overproduction (oxidative stress), intracellular calcium
    dyshomeostasis, and NMDA-receptor-mediated excitotoxicity. These insults drive
    neuronal apoptosis and underlie the regional neurodegeneration of the disease.
  role: trigger
  cell_types:
  - preferred_term: neuron
    term:
      id: CL:0000540
      label: neuron
  biological_processes:
  - preferred_term: response to oxidative stress
    term:
      id: GO:0006979
      label: response to oxidative stress
    modifier: INCREASED
  evidence:
  - reference: PMID:27538940
    reference_title: "Memantine, a Low-Affinity NMDA Receptor Antagonist, Protects against Methylmercury-Induced Cytotoxicity of Rat Primary Cultured Cortical Neurons, Involvement of Ca(2+) Dyshomeostasis Antagonism, and Indirect Antioxidation Effects."
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      Methylmercury (MeHg) is an extremely dangerous environmental pollutant that
      induces severe toxic effects in the central nervous system.
    explanation: >-
      Establishes methylmercury as a central neurotoxin acting directly on CNS
      neurons.
  - reference: PMID:27538940
    reference_title: "Memantine, a Low-Affinity NMDA Receptor Antagonist, Protects against Methylmercury-Induced Cytotoxicity of Rat Primary Cultured Cortical Neurons, Involvement of Ca(2+) Dyshomeostasis Antagonism, and Indirect Antioxidation Effects."
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      reactive oxygen species (ROS) overproduction showed an obvious oxidative
      stress in neurons.
    explanation: >-
      Demonstrates the oxidative-stress arm of methylmercury neuronal injury in
      cultured cortical neurons; the same study implicates calcium dyshomeostasis
      and NMDA-receptor excitotoxicity.
  downstream:
  - target: Regional Neuronal Degeneration
    description: >-
      Oxidative, calcium, and excitotoxic injury drives degeneration of
      selectively vulnerable neuronal populations.
- name: Regional Neuronal Degeneration
  description: >-
    Methylmercury injures characteristic, selectively vulnerable brain regions:
    cerebellar granule cell neurons (producing ataxia), the calcarine/visual
    cortex (producing visual-field constriction), and the somatosensory cortex
    (producing sensory disturbance). This regional pattern of neuronal loss, not
    a diffuse progressive proteinopathy, defines the neuropathology of Minamata
    disease.
  role: effector
  cell_types:
  - preferred_term: cerebellar granule cell
    term:
      id: CL:0001031
      label: cerebellar granule cell
  locations:
  - preferred_term: cerebellum
    term:
      id: UBERON:0002037
      label: cerebellum
  - preferred_term: cerebral cortex
    term:
      id: UBERON:0000956
      label: cerebral cortex
  biological_processes:
  - preferred_term: neuron apoptotic process
    term:
      id: GO:0051402
      label: neuron apoptotic process
    modifier: INCREASED
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Visual field constriction due to involvement of the calcarine cortex,
      sensory disturbance due to involvement of the somatosensory cortex, and
      cerebellar ataxia due to involvement of granule cell neurons of the
      cerebellum are common and characteristic features due to methylmercury
      poisoning.
    explanation: >-
      Maps the characteristic clinical features of methylmercury poisoning to
      degeneration of specific brain regions, defining the regional
      neurodegeneration node.
environmental:
- name: Methylmercury-Contaminated Fish and Mercury Exposure
  exposure_term:
    preferred_term: exposure to mercury
    term:
      id: ECTO:0001571
      label: exposure to mercury
  notes: >-
    Organic methylmercury bioaccumulates in fish and shellfish; the Minamata
    epidemic resulted from industrial methylmercury discharge contaminating
    seafood. Other documented exposures include contaminated waters in Japan and
    northwestern Ontario and methylmercury-fungicide-treated seed grain in Iraq.
    Occupational and elemental/inorganic mercury exposures (e.g., the historical
    felt-hat industry) produce a different, predominantly peripheral and
    neuropsychiatric syndrome. Notably, an international case-control comparison
    found no association between mercury exposure from seafood consumption or
    dental amalgam fillings and amyotrophic lateral sclerosis.
  evidence:
  - reference: PMID:37372760
    reference_title: "Neurological and Neurocognitive Impairments in Adults with a History of Prenatal Methylmercury Poisoning: Minamata Disease."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      is a well-known case of food poisoning caused by methylmercury-contaminated
      fish
    explanation: >-
      Documents the dietary (contaminated-fish) route of methylmercury exposure
      that caused Minamata disease.
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      psychosis is more typical of exposure to inorganic mercury, which has been
      documented in the felt hat industry
    explanation: >-
      Distinguishes the neuropsychiatric syndrome of inorganic/elemental mercury
      exposure (erethism, "mad hatter") from the central syndrome of organic
      methylmercury.
  - reference: PMID:30558238
    reference_title: "A Comparison of Mercury Exposure from Seafood Consumption and Dental Amalgam Fillings in People with and without Amyotrophic Lateral Sclerosis (ALS): An International Online Case-Control Study."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      this study found no evidence that mercury exposure from eating seafood, or
      from mercury dental fillings, was associated with the risk of developing ALS
    explanation: >-
      Sources the negative ALS association stated in these notes and in the
      disease description. Note the design limits its strength: an online
      self-report questionnaire case-control study (401 ALS vs 452 non-ALS
      respondents), so this is absence of an observed association rather than
      proof of no effect.
  influences_mechanisms:
  - target: Methylmercury CNS Accumulation and Neuronal Injury
    environmental_effect: TRIGGERS
    causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
    description: >-
      Eating contaminated fish delivers methylmercury that is absorbed from the
      gut, carried in blood, and crosses the blood-brain barrier before
      accumulating in the central nervous system, so the exposure reaches this
      node through known intermediate steps rather than acting on it directly.
      This edge covers the organic methylmercury arm only; the elemental and
      inorganic exposures also described in this entry produce a different,
      predominantly neuropsychiatric syndrome.
    evidence:
    - reference: PMID:37372760
      reference_title: "Neurological and Neurocognitive Impairments in Adults with a History of Prenatal Methylmercury Poisoning: Minamata Disease."
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: >-
        is a well-known case of food poisoning caused by methylmercury-contaminated
        fish
      explanation: >-
        Establishes the dietary contaminated-fish route as the source of the
        methylmercury responsible for the central nervous system disease.
phenotypes:
- name: Cerebellar Ataxia
  phenotype_term:
    preferred_term: Ataxia
    term:
      id: HP:0001251
      label: Ataxia
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      cerebellar ataxia due to involvement of granule cell neurons of the
      cerebellum are common and characteristic features due to methylmercury
      poisoning.
    explanation: >-
      Cerebellar ataxia from granule-cell degeneration is a cardinal feature of
      methylmercury poisoning.
- name: Constriction of Visual Fields
  phenotype_term:
    preferred_term: Constriction of peripheral visual field
    term:
      id: HP:0001133
      label: Constriction of peripheral visual field
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Visual field constriction due to involvement of the calcarine cortex
    explanation: >-
      Visual-field constriction from calcarine cortex involvement is a
      characteristic feature of methylmercury poisoning.
- name: Somatosensory Disturbance
  phenotype_term:
    preferred_term: Somatic sensory dysfunction
    term:
      id: HP:0003474
      label: Somatic sensory dysfunction
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      sensory disturbance due to involvement of the somatosensory cortex
    explanation: >-
      Somatosensory disturbance from somatosensory cortex involvement is a
      characteristic feature of methylmercury poisoning.
- name: Dysarthria
  phenotype_term:
    preferred_term: Dysarthria
    term:
      id: HP:0001260
      label: Dysarthria
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Other neurological features include dysarthria, postural and action tremor,
      cognitive impairment, and hearing loss and dysequilibrium.
    explanation: >-
      Dysarthria is among the recognized neurological features of methylmercury
      poisoning.
diagnosis:
- name: Blood, hair, and toenail mercury measurement
  description: >-
    Mercury concentration in blood, hair, and toenail samples documents exposure
    and is the standard laboratory approach to suspected mercury poisoning.
    Interpretation is bounded: in patients presenting with established chronic
    neurological disease these matrices may not reflect the remote exposure that
    caused the neuronal injury, so a normal result late in the course does not
    exclude prior methylmercury poisoning.
  diagnosis_term:
    preferred_term: Laboratory Procedure
    term:
      id: NCIT:C25294
      label: Laboratory Procedure
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Laboratory tests (e.g., on blood and hair and toenail samples) are of limited
      value in the assessment of chronic neurological disease due to mercury
      poisoning because they may not reflect remote neuronal injury due to mercury.
    explanation: >-
      Names the standard exposure matrices while explicitly bounding their value
      in chronic disease; marked PARTIAL because the source qualifies rather than
      endorses the test.
- name: Umbilical cord mercury concentration for prenatal exposure
  description: >-
    Archived umbilical cord tissue provides a retrospective measure of in-utero
    methylmercury exposure and has been used to grade prenatal exposure against
    neuropsychological outcome in the Minamata population.
  diagnosis_term:
    preferred_term: Laboratory Procedure
    term:
      id: NCIT:C25294
      label: Laboratory Procedure
  evidence:
  - reference: PMID:37372760
    reference_title: "Neurological and Neurocognitive Impairments in Adults with a History of Prenatal Methylmercury Poisoning: Minamata Disease."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The average umbilical cord methylmercury concentrations were 1.67 parts per
      million (ppm) for CMD patients and 0.77 ppm for moderately exposed participants.
    explanation: >-
      Umbilical cord methylmercury concentration is used as the quantitative index
      of prenatal exposure in this Minamata cohort.
treatments:
- name: Exposure cessation and source control
  description: >-
    Identifying and eliminating the mercury source is the primary intervention.
    For methylmercury this means removing the contaminated dietary source; for
    the inorganic/elemental arm it means removing the occupational or product
    exposure. This prevents further accumulation but does not reverse established
    neuronal injury.
  treatment_term:
    preferred_term: therapeutic procedure
    term:
      id: NCIT:C49236
      label: Therapeutic Procedure
  evidence:
  - reference: PMID:37372760
    reference_title: "Neurological and Neurocognitive Impairments in Adults with a History of Prenatal Methylmercury Poisoning: Minamata Disease."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      is a well-known case of food poisoning caused by methylmercury-contaminated
      fish
    explanation: >-
      The snippet establishes the contaminated dietary exposure route but does
      not directly evaluate cessation or source control as an intervention.
- name: Supportive and rehabilitative care for established neurological injury
  description: >-
    Management of established methylmercury neurological disease is supportive:
    there is no effective disease-modifying treatment for the neuronal injury
    once it has occurred. Care targets the resulting ataxia, sensory disturbance,
    visual field loss, dysarthria, and cognitive impairment.
  treatment_term:
    preferred_term: Supportive Care
    term:
      id: NCIT:C15747
      label: Supportive Care
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "There is no effective treatment."
    explanation: >-
      The source states plainly that no effective treatment exists for chronic
      neurological disease from methylmercury, which is why management is
      supportive.
discussions:
- discussion_id: gap_mercury_inorganic_arm_not_curated
  prompt: >-
    What are the pathophysiology nodes, phenotypes, and treatments of the
    elemental and inorganic mercury arms, which this entry names but does not
    yet model?
  kind: KNOWLEDGE_GAP
  status: OPEN
  attaches_to:
  - pathophysiology#Methylmercury CNS Accumulation and Neuronal Injury
  rationale: >-
    The entry is scoped to mercury poisoning generally and its description
    contrasts the organic and inorganic clinical profiles, but every
    pathophysiology node, phenotype, and exposure record curated so far concerns
    methylmercury and Minamata disease. The inorganic/elemental arm — mercury
    vapour pneumonitis, erethism, acrodynia, and mercury-associated membranous
    nephropathy — has a distinct mechanism, a distinct target-organ profile, and
    (unlike established methylmercury neuronal injury) a chelation-responsive
    course. Leaving it unmodelled makes the entry read as complete for a disease
    for which only one arm is represented.
  proposed_experiments:
  - experiment_id: exp_mercury_curate_inorganic_arm
    name: Curate the elemental/inorganic mercury arm
    description: >-
      Build the inorganic/elemental pathograph from primary literature: vapour
      inhalation to chemical pneumonitis; mercuric ion binding to renal tubular
      and glomerular targets to membranous nephropathy and nephrotic syndrome;
      and CNS deposition to erethism and tremor. Add the chelation treatments
      (succimer/DMSA, unithiol/DMPS) that apply to that arm and not to
      established methylmercury injury.
  evidence:
  - reference: PMID:30278852
    reference_title: "Chronic Neurological Disease Due to Methylmercury Poisoning."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In contrast, peripheral nerve disease is more characteristic of inorganic
      mercury intoxication.
    explanation: >-
      Establishes that the inorganic arm has a clinically distinct profile from
      the methylmercury arm modelled here, which is what makes its absence a gap.