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Methyl iodide rhombencephalopathy: clinico-radiological features of a preventable, potentially fatal industrial accident
  1. Ivan Iniesta1,
  2. Mark Radon2,
  3. Colin Pinder1
  1. 1Department of Neurology, The Walton Centre Foundation Trust, Liverpool, Merseyside, UK
  2. 2Department of Neuroradiology, The Walton Centre Foundation Trust, Liverpool, Merseyside, UK
  1. Correspondence to Dr Ivan Iniesta, Department of Neurology, The Walton Centre Foundation Trust, Lower Lane, Fazakerley, Liverpool, Merseyside CH64 9RS, UK; iniesta.ivan{at}gmail.com

https://doi.org/10.1136/practneurol-2013-000565

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    Introduction

    Methyl iodide or ‘Mel’ is a dense, colourless, volatile monohalomethane, which is rapidly metabolised in man (Ofigures 1 and 2); the organically bound iodine is converted to inorganic iodide and excreted in this form in the urine.1 It is used as a pesticide in the USA and in a variety of organic chemical reactions and for dye-works and detergents in the UK. Although methyl iodide is a rare intoxicant, its manifestations are similar to those of poisoning with the other more common monohalomethane agents. Indeed, methyl iodide intoxication resembles that of methyl bromide and methyl chloride. Characteristics of the poisoning include a delay between exposure and onset of symptoms with early systemic toxicity, including congestive changes in the lungs and oliguria; metabolic acidosis; prominent cerebellar and extrapyramidal neurological features; and in severe cases, seizures and coma. Psychiatric disturbances may persist for years.

    Figure 1
    Figure 1

    Molecular structure of methyl iodide (CH3I).

    Figure 2
    Figure 2

    Ball and stick model of methyl iodide.

    Presentation

    A previously healthy 40-year-old man employed in a chemical factory manufacturing methyl iodide for detergents was admitted to the intensive care unit in status epilepticus. The previous day he had inhaled an unspecified amount of methyl iodide. On returning home his wife described him as ‘out of character’, incoherent at times and with visual hallucinations of ‘wallpaper monkeys coming towards him in 3-D’. The next morning, he woke with headache, nausea and giddiness but went to work, where he had the first of a succession of generalised tonic–clonic seizures before being transferred to hospital.

    Investigations

    Plasma iodine on admission was 539 µmol/L with a urine level of 1809 µmol/L (normal being zero for both). Initial CT scan of head and CSF results were normal. MR scans of brain taken within a week (Ofigure 3) and 2 weeks of admission showed progressive bilateral symmetrical signal abnormality in the globus pallidus nuclei, substantia nigra, periaqueductal grey matter, dorsal brainstem tracts (notably the medial longitudinal fasciculus), middle cerebellar peduncles, dentate nuclei and inferior olivary nuclei; there was a microhaemorrhage in the left side of the medulla. Follow-up MR scans after 1 and 6 months (Ofigure 4) showed the signal changes had resolved.

    Figure 3
    Figure 3

    Initial MR brain scan 7 days after admission. (A) Axial T2 image at the level of the basal ganglia showing subtle increased signal in the globus pallidus nuclei (arrows). (B) Axial T2 image at the level of the middle cerebellar peduncles showing increased signal bilaterally in the dentate nuclei (white arrows), subtle increased signal in the middle cerebellar peduncles (arrowheads) and signal abnormality in the dorsal brainstem (black arrow).

    Figure 4
    Figure 4

    MR brain scan after 6 months. (A) Axial T2 image at the level of the basal ganglia showing normalisation of the signal from the globus pallidus nuclei. (B) Axial T2 image at the level of the middle cerebellar peduncles showing resolution of the signal abnormalities.

    Clinical progress

    Early systemic complications included severe metabolic acidosis, oliguria, deep venous thrombosis and both pulmonary and peripheral arterial embolisms. Although no longer sedated after 48 h, he remained in a deep coma state (Glasgow coma scale score of 3) for a further 3 weeks. He then started to react slowly to pain stimuli and within a week he could respond to simple verbal commands and to tactile stimuli. After 6 weeks, he could sit up and communicate, despite severe dysarthria. By 6 months, his speech had improved significantly and could walk with two sticks. He continued to experience olfactory hallucinations, resembling a ‘smell of diesel’.

    Discussion

    Since Jaquet's first description in 1901,2 there have only been seven other reported cases of methyl iodide poisoning.3–8 Garland and Camps (1940) reported a 38-year-old man employed in a UK factory manufacturing methyl iodide, who became severely encephalopathic and subsequently died. As with our patient, the symptoms at onset included unsteadiness, drowsiness and incoherent speech, accompanied by oliguria, followed by vomiting, restlessness, incontinence and irreversible coma within 3 days. His urinary iodine concentration was 90 mg/L (708 μmol/L).3 Exposure routes of Mel include lungs, eyes and skin; it can also be ingested. The main organs damaged are the eyes, skin, lungs and central nervous system. Once absorbed, Mel is rapidly converted to S-methylglutathione in the liver. Intracellular glutathione depletion may start a chain of events leading to neuronal death; glial cells may be more sensitive than neurones to this primary effect. Mel's depleting effect on intracellular glutathione probably causes the cellular (glial and neuronal) damage found in neural cell cultures.9

    In mild cases of methyl iodide intoxication, patients report gait instability, dizziness and headache, followed the next day by anorexia, nausea and vomiting; these are not usually severe enough to prevent men from working. In the most severe cases, patients may have acute symptomatic seizures, potentially causing death. The differential diagnosis includes acute demyelination, meningoencephalitis or poisoning by other toxic agents, particularly other monohalomethanes. Methyl iodide poisoning can mimic a posterior circulation stroke.4 Clearly, the occupational and clinical history are the key to the diagnosis.

    Health and safety

    As Garland and Camps had rightly pointed out, prevention is crucial,3 since there is no antidote. Poisoning in factories can be prevented by adequate exhaust ventilation and appropriate personal protective equipment. Above all, however, is an increased awareness of the dangers of methyl iodide, which is an almost odourless, non-irritating, yet life-threatening poisonous gas.

    Conclusions

    This case raises awareness of the risks of the poisonous industrial agent, methyl iodide, with the first clinico–radiological description of its acute intoxication. Intensive care and support should be maintained even despite ominous clinical signs, given the potential reversibility of methyl iodide encephalopathy. Preventing exposure through adequate health and safety measures to methyl iodide is paramount.

    Acknowledgments

    We thank our patient, who discovered the poisonous action of methyl iodide by bitter experience, for his pursuit in raising awareness about methyl iodide intoxication in preventing future cases.

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    Footnotes

    • Contributors II has written this article, MR has contributed with the MRI images and legends and CP contributed with useful comments on following this patient from a neurorehabilitation perspective.

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval This case report did not require ethics approval.

    • Provenance and peer review Not commissioned; externally peer reviewed. This paper was reviewed by Mark Manford, Cambridge, UK.

    • Data sharing statement We confirm that this article is an original contribution. As such, Dr I Iniesta (Consultant Neurologist) has been the main author and Dr M Radon (Consultant Neurorradiologist) and Dr C Pinder (Consultant in Neurorehabilitation) the collaborators. Yours faithfully, Ivan Iniesta (On behalf of all the authors).

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