Ataxia and cranial neuropathies from subcutaneously injected elemental mercury

Malkani, Roneil G.; Weinstein, Jill M.; Kumar, Neeraj; Victor, Thomas A.; Bernstein, Lisa

doi:10.3109/15563650.2011.566881

Cited by 9 publications

(3 citation statements)

References 12 publications

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“…11,12 Existence in liquid form makes it possible for the metal to be injected subcutaneously, intradermally, intramuscularly, and intravenously. 8, [12][13][14] Following entry into the bloodstream, metallic mercury and its vapors undergo rapid oxidation to mercuric and mercurous ions which cannot cross the blood-brain barrier and bind to serum proteins to exert cumulative effect. 13 The metal and its vapors, however, readily cross the blood-brain barrier and accumulate in the brain since oxidation to mercury ions is not rapid enough to prevent their considerable uptake by the central nervous system (CNS).…”

Section: Casementioning

confidence: 99%

Clinical Spectrum of Mercury Poisoning in India: Case-series from a Poison Control Center

Balachandran¹,

Jambugulam²,

George³

et al. 2023

JAPI

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Background: Mercury is a naturally occurring heavy metal that finds wide application in industrial and household settings. It exists in three chemical forms which include elemental (Hg0 ), inorganic mercurous (Hg+) or mercuric (Hg++) salts, and organic compounds. All forms are highly toxic, particularly to the nervous, gastrointestinal, and renal systems. Common circumstances of exposure include recreational substance use, suicide or homicide attempts, occupational hazards, traditional medicines, and endemic food ingestions as witnessed in the public health disasters in Minamata Bay, Japan and in Iraq. Poisoning can result in death or long-term disabilities. Clinical manifestations vary with chemical form, dose, rate, and route of exposure. Aims and objectives: To summarize the incidence of mercury poisoning encountered at an Indian Poison Center and use three cases to highlight the marked variations observed in clinical manifestations and long-term outcomes among poisoned patients based on differences in chemical forms and routes of exposure to mercury. Materials and methods: A structured retrospective review of the enquiry-database of the Poison Information Center and medical records of patients admitted between August 2019 and August 2021 in a tertiary care referral center was performed. All patients with reported exposure to mercury were identified. We analyzed clinical data and laboratory investigations which included heavy metal (arsenic, mercury, and lead) estimation in whole blood and urine samples. Additionally, selected patients were screened for serum voltage-gated potassium ion channels (VGKC)— contactin-associated protein-like 2 (CASPR2) antibodies. Three cases with a classical presentation were selected for detailed case description. Results: Twenty-two cases were identified between August 2019 and August 2021. Twenty (91%) were acute exposures while two (9%) were chronic. Of these, three representative cases have been discussed in detail. Case 1 is a 3.5-year-old girl who was brought to the emergency department with suspected elemental-mercury ingestion after biting a thermometer. Clinical examination was unremarkable. Chest and abdominal radiography revealed radiodense material in the stomach. Subsequent serial radiographs documented distal intestinal transit of the radiodense material. The child remained asymptomatic. This case exemplifies the largely nontoxic nature of elemental mercury ingestion as it is usually not absorbed from the gastrointestinal tract. Case 2 is a 27-year-old lady who presented with multiple linear nodules over both upper limbs after receiving a red intravenous injection for anemia. Imaging revealed metallic-density deposits in viscera and bones. Nodular biopsy was suggestive of mercury granulomas. A 24-hour urine mercury levels were elevated. She was advised chelation therapy with oral dimercaptosuccinic acid (DMSA). Case 3 is a 22-year-old lady who presented with acrodynia, neuromyotonia, tremulousness, postural giddiness, tachycardia, and hypertension for 2 months, associated with intractable, diffuse burning pain over the buttocks and both lower limbs, 1 month after completing a 3-week course of traditional medications for polycystic ovarian syndrome. A 24-hour urine normetanephrine levels and mercury levels were markedly elevated. Serum anti-VGKC antibodies were present. She was treated with glucocorticoids and oral DMSA with a favorable clinical response. Conclusions: The clinical manifestations of mercury toxicity are highly variable depending on the source, form, and route of mercury exposure and are related to its toxicokinetics.

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Section: Casementioning

confidence: 99%

Clinical Spectrum of Mercury Poisoning in India: Case-series from a Poison Control Center

Balachandran¹,

Jambugulam²,

George³

et al. 2023

JAPI

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“…29 Malkani et al have reported the development of limb and gait ataxia, dysdiadochokinesia, nystagmus, dysarthria along with multiple cranial nerve palsies from subcutaneous injection of elemental Hg ("quick silver pellets") with the cultural belief of protection against sickness. 30 A study in Brazilian gold traders exposed to Hg vapor have measured tremor frequency mainly in high-frequency windows (6.6-10.0 Hz). 31 Motor deficits in the form of tremor, incoordination and poor fine motor control, and subtle cognitive changes have been noted among dentists exposed toHg.…”

Section: Other Movement Disordersmentioning

confidence: 99%

“…[53][54][55][56][57] Similarly, Malkani et al noted anti-Purkinje cell cytoplasmic-type Tr antibody positivity in a case of elemental mercury toxicity presenting with cerebellar ataxia. 30 In a developing country like India, ayurvedic drugs containing Hg are still being used abundantly and the physician should never forget to take detailed drug history when a patient presents with such phenotype.…”

Section: Mercury and Autoimmune Movement Disordersmentioning

confidence: 99%

Mercury and Movement Disorders: The Toxic Legacy Continues

Ganguly

Kulshreshtha

Jog

2021

Can. J. Neurol. Sci.

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Mercury (Hg) exists in the environment as inorganic (metallic Hg vapor, mercurous and mercuric salts) or organic (bonded to a structure containing carbon atoms) forms. Neurotoxic effect of Hg is known for years. While the organic form (methylmercury (meHg)) led to the Minamata incidence in Japan and “wonder-wheat” disaster in Iraq, the “mad hatters” and “Danbury shakes” were related to the inorganic elemental form (Hg vapor). Human exposure to toxic Hg continues in the modern world to a large extent by artisanal gold mining, biomass combustion, chloralkali production, and indigenous medicine use to name a few. Heavy industrial use of Hg contaminates air and landfills, affecting the aquatic ecosystem and marine food chain. A detailed social and occupational history with a high index of clinical suspicion is required to not miss this toxic etiology for movement disorders like ataxia, tremor, or myoclonus. In this review, we have discussed the past and present global health impact of Hg from a movement disorder perspective. The connection of Hg with neurodegeneration and autoimmunity has been highlighted. We have also discussed the role of chelating agents and the preventive strategies to combat the neurotoxic effects of Hg in the modern world.

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Chelation Treatment During Acute and Chronic Metal Overexposures—Experimental and Clinical Studies

Andersen¹

2016

Chelation Therapy in the Treatment of Metal Intoxication

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Ataxia and cranial neuropathies from subcutaneously injected elemental mercury

Cited by 9 publications

References 12 publications

Clinical Spectrum of Mercury Poisoning in India: Case-series from a Poison Control Center

Clinical Spectrum of Mercury Poisoning in India: Case-series from a Poison Control Center

Mercury and Movement Disorders: The Toxic Legacy Continues

Chelation Treatment During Acute and Chronic Metal Overexposures—Experimental and Clinical Studies

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