Manganese Intoxication: The Cause of an Inexplicable Epileptic Syndrome in a 3 Year Old Child

Hernández, Elena Herrero; Discalzi, G; Dassi, Patrizia; Jarre, Laura; Pira, Enrico

doi:10.1016/s0161-813x(03)00026-3

Cited by 34 publications

(20 citation statements)

References 6 publications

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“…It should be stressed that Fe deficiency affects about 2 billion subjects (Garcia et al 2007) and is a risk factor for Mn neurotoxicity even in absence of relevant exogenous exposures. Mn toxicity from various sources has been repeatedly reported in children (Fell et al 1996; Herrero Hernández et al 2003; Komaki et al 1999; Woolf et al 2002), including cognitive effects (Wasserman et al 2006). …”

Section: Occupational Manganismmentioning

confidence: 99%

“…Neurological signs seem to reach a plateau after an initial 5–10 years of progression (Huang et al 2007), but this observation is based on the follow up of four patients only. However, it has been documented, in a few cases and in uncontrolled studies (Discalzi et al 2000; Herrero Hernández et al 2003; Herrero Hernández et al 2006; Ky et al 1992; Ono et al 2002; Penalver 1957; Tuschl et al 2008) that manganism can be reversed if promptly diagnosed and treated with chelating drugs. Manganism frequently appears in young, active workers.…”

Section: Occupational Manganismmentioning

confidence: 99%

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Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

et al. 2009

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The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154, 2007) and Bowman et al. (Metals and neurodegeneration, 2009).

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Section: Occupational Manganismmentioning

confidence: 99%

Section: Occupational Manganismmentioning

confidence: 99%

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

et al. 2009

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“…It should be stressed that Fe deficiency affects about 2 billion subjects (Garcia et al 2007) and is a risk factor for Mn neurotoxicity even in absence of relevant exogenous exposures. Mn toxicity from various sources has been repeatedly reported in children (Fell et al 1996;Herrero Hernández et al 2003;Komaki et al 1999;Woolf et al 2002), including cognitive effects (Wasserman et al 2006). …”

Section: Clinical Aspectsmentioning

confidence: 99%

“…Established irreversible neuronal damage, inadequate treatment duration and/or follow-up period could explain these unsatisfactory results. Several studies (Discalzi et al 2000;Herrero Hernández et al 2003;Herrero Hernandez et al 2006;Ky et al 1992;Ono et al 2002;Penalver 1957) have showed that CaNa2EDTA is clinically effective in the treatment of overt manganism in humans. These observations are consistent with recent therapeutic success in a severe case of genetic hypermanganesemia with extrapyramidal syndrome, polycythemia, and hepatic cirrhosis (Tuschl et al 2008) and possibly in ephedrone-manganic syndrome cases (Selikhova et al 2008).…”

Section: Treatmentmentioning

confidence: 99%

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

et al. 2009

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Abstract:The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147-154, 2007) and Bowman et al. (Metals and neurodegeneration, 2009).

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“…It is generally believed that interactions of environmental factors with genetic and other intrinsic factors play an important role in the etiology of seizures or epilepsy (Kjeldsen et al, 2002; Bener et al, 2006; Todorova et al, 1999, 2006; Nakayama, 2009; Vestergaard and Christenen, 2009; Stewardt, 2010). Exposure to some environmental chemical pollutants such as ozone (Escalantie-Membrillo and Paz, 1997), lead (Krishnamoorthy et al, 1993; Arrieta et al, 2005), nickel (Denays et al, 2005), manganese (Hernandez et al, 2003), teimethyltin (Nishimura et al, 2001), organophosphates (McDonough and Shin, 1997; Solberg and Belkin, 1997; Myhrer, 2007) or domoic acid (Tiedeken and Ramsdell, 2007; Stewardt, 2010) has been shown to initiate or promote the development of seizures or epilepsy. Clinical and epidemiological studies suggest that methylmercury (MeHg), a prominent environmental contaminant, is an important environmental risk factor contributing to epileptogenesis.…”

Section: Introductionmentioning

confidence: 99%

Methylmercury: A potential environmental risk factor contributing to epileptogenesis

Yuan

2012

NeuroToxicology

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Epilepsy or seizure disorder is one of the most common neurological diseases in humans. Although genetic mutations in ion channels and receptors and some other risk factors such as brain injury are linked to epileptogenesis, the underlying cause for the majority of epilepsy cases remains unknown. Gene-environment interactions are thought to play a critical role in the etiology of epilepsy. Exposure to environmental chemicals is an important risk factor. Methylmercury (MeHg) is a prominent environmental neurotoxicant, which targets primarily the central nervous system (CNS). Patients or animals with acute or chronic MeHg poisoning often display epileptic seizures or show increased susceptibility to seizures, suggesting that MeHg exposure may be associated with epileptogenesis. This mini-review highlights the effects of MeHg exposure, especially developmental exposure, on the susceptibility of humans and animals to seizures, and discusses the potential role of low level MeHg exposure in epileptogenesis. This review also proposes that a preferential effect of MeHg on the inhibitory GABAergic system, leading to disinhibition of excitatory glutamatergic function, may be one of the potential mechanisms underlying MeHg-induced changes in seizure susceptibility.

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Manganese Intoxication: The Cause of an Inexplicable Epileptic Syndrome in a 3 Year Old Child

Cited by 34 publications

References 6 publications

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

Methylmercury: A potential environmental risk factor contributing to epileptogenesis

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