Manganese poisoning is primarily seen in the occupational setting, as numerous industries use manganese ore for the production of batteries, ceramics, steel, etc. The central nervous system is the principal site where manganese causes toxic effects, mainly in the form of a Parkinson's-like disease. Bradykinesia, gait disturbances, rigidity and other extrapyramidal signs constitute the clinical presentation of most patients. A detailed patient history and a full biochemical workup are necessary to make the diagnosis.
Manganese plays an essential role in numerous physiological processes (eg. bone growth, protection from free radicals, protein metabolism, etc.) of humans and other mammalian species [1] [2]. In the setting of excessive exposure, however, toxic effects are exerted in the body. Manganese poisoning can be seen in a wide range of occupations, as the production of steel, batteries and many other electronic devices, as well as ceramics, fertilizers, fungicides, and gasoline mandates the use of this element [3] [4] [5]. In addition to occupational exposure, many studies have confirmed that industrial emissions that contain manganese contaminate air, soil, plants and even water sources, which predisposes a number of individuals to manganese toxicity through inhalation or ingestion, particularly those living in close proximity to these industries [1] [4] [6]. Manganese has a rather short half-life in the circulation, but when it reaches the tissues, such as the bones and the central nervous system (CNS), the half-life is estimated to be around 8-9 years [6]. Signs and symptoms are primarily related to the CNS, as manganese passes through the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier, eventually depositing selectively into the globus pallidus and the basal ganglia [3] [7]. Consequently, the clinical presentation is centered around a Parkinson's-like illness developing years after exposure to high concentrations of manganese - tremor, hypertonia rigidity, micrographia, weakness, and postural instability are main symptoms [3] [4] [8]. Moreover, psychiatric complaints in the form of disorientation, memory and judgment deficits, anxiety, hallucinations, etc. are frequently reported [3] [4] [8]. Apart from nervous system toxicity, the lungs, the heart, the liver and the reproductive system are also described as potential sites where harmful effects of manganese might be seen [3].
The importance of an early diagnosis lies in the fact that symptoms can completely disappear with the cessation of exposure to manganese in the initial stages of the disease, whereas an irreversible clinical course is observed when severe exposure has occurred [8]. For this reason, a detailed patient history and a complete physical examination must be performed in order to include manganese poisoning in the differential diagnosis of Parkinson's-like symptoms and psychiatric complaints. Physicians must ask about the patient's occupation (and to which hazards is he/she exposed on a daily basis) [5], while socioeconomic information (eg. living in proximity to the industrial areas) are also important. As soon as a presumptive diagnosis is made, laboratory confirmation should be attempted. Various procedures have been described in the literature, including the determination of manganese levels in blood, plasma, urine, hair, and nails [5] [6]. Ideally, assessment of manganese levels in bones would provide the most reliable results, and in fact, a non-invasive method has been developed for quantitative detection of manganese in bones [6]. Supplementary to clinical criteria and laboratory studies, magnetic resonance imaging (MRI) of the endocranium shows a specific pattern of bilateral and symmetric hyperintensity of the globus pallidus at T1-weighted studies [7], implying that this procedure is a vital constituent of manganese poisoning workup [6].