Visualised manganese ion within the basal ganglia and long axonal tracts

Abstract

Acknowledgements: We are grateful to M Mario Coriasco for technical assistance.Competing interests: None. Patient consent: Obtained. REFERENCES 1. Dalmau J, Graus F, Rosenblum MK, et al. Anti-Hu-associated paraneoplastic encephalomyelitis/sensory neuronopathy. A clinical study of 71 patients. Medicine (Baltimore) 1992;71:59-72. 2. Pittock SJ, Lucchinetti CF, Lennon VA. Anti-neuronal nuclear autoantibody type 2: paraneoplastic accompaniments. Ann Neurol 2003;53:580-7. 3. Dietl HW, Pulst SM, Engelhardt P, et al. Paraneoplastic brainstem encephalitis with acute dystonia and central hypoventilation J Neurol 1982;227:229-38. 4. Gómez-Choco MJ, Zarranz JJ, Saiz A, et al. Central hypoventilation as the presenting symptom in Hu associated paraneoplastic encephalomyelitis. J Neurol Neurosurg Psychiatry 2007;78:1143-5. 5. Voltz R. Paraneoplastic neurological syndromes: an update on diagnosis, pathogenesis and therapy. Lancet Neurol 2002;5:294-305. Visualised manganese ion within the basal ganglia and long axonal tractsA 53-year-old male was admitted to our ward because of recurrent generalised tonic-clonic seizures. He had consumed 700-1300 ml of Japanese sake (16% alcohol) daily since the age of 19 years, and had suffered from liver cirrhosis and varices in both the oesophagus and stomach since the age of 40 years. The seizures were successfully treated with oral diazepam (15 mg daily) and nitrazepam (5 mg daily). After recovering from the seizures, he exhibited no neurological abnormalities other than a slight intention tremor. His EEG was normal. A T1-weighted MRI study showed strongly high signal areas in the globus pallidus and red nuclei as well as high signal areas throughout the subcortical white matter and internal capsules, whereas T2-weighted pictures did not (fig 1). These signals are known to represent manganese ion, 1 which had accumulated in neurons and was transported downward within the axons 2 ; the values of serum manganese and iron were 3.9 mg/dl and 30 mg/ dl, respectively. Thereafter, the patient began to attend psychoeducational meetings and behavioural therapy for alcoholism. He was discharged home after 45 days. REFERENCE 1. Spampinato MV, Castillo M, Rojas R, et al. Magnetic resonance imaging findings in substance abuse: alcohol and alcoholism and syndromes associated with alcohol abuse. Top Magn Reson Imaging 2005;16:223-30. 2. Pautler RG. In vivo, trans-synaptic tract-tracing utilizing manganese-enhanced magnetic resonance imaging (MEMRI). NMR Biomed 2004;17:595-601.Figure 1 Magnetic resonance images recorded on the second hospital day of the case. The upper two pictures clearly show the distribution and the density of manganese ion.

Serum iron, Magnesium, Copper, and Manganese Levels in Alcoholism: A Systematic Review

“…It is essential for proper bone growth. In higher concentrations, manganese can act as a neurotoxin which is then deposited in the brain, in particular the basal ganglia, affecting proper function [4]. Chronic alcohol consumption leads to structural changes in the brain [5,6,7].…”

Transcranial Magnetic Stimulation and Deep Brain Stimulation in the Treatment of Alcohol Dependence

“…Excessive accumulation of manganese in the brain causes early psychotic symptoms usually followed by a syndrome similar to idiopathic Parkinson’s disease, associated with neuronal loss and gliosis in the globus pallidus, the substantia nigra pars reticulata and the striatum (67). Since on the one hand manganese is the sole trace element to accumulate in the brain of alcoholics (68), and on the other hand manganese deposition in the habenula provides an ideal contrast signal in T1 weighted MRI images (69,70), the habenula may be clearly visible (and therefore amenable to direct targeting) in the context of deep brain stimulation for alcoholism.. Further neuroimaging studies in alcohol patients should investigate the impact of manganism on T1 quality images.…”