Objectives: To define the role of magnetic resonance imaging (MRI) and intraoperative electrophysiological recording in targeting the subthalamic nucleus (STN) in Parkinson's disease and to determine accuracy of electrode placement. Patients and methods: We implanted 54 electrodes into the STN in 27 patients. Target planning was done by coordinate guidelines and visualising the STN on MRI and defined in relation to the mid-point of the AC-PC line. Intraoperative microelectrode recording was used. We adjusted electrode positions for placement in the centre of the STN electrical activity and verified this on postoperative MRI in 16 cases, which were fused to the preoperative images to measure actual error in electrode placement in the three axes.Results: Based on coordinate calculation and MRI localisation, the mean of the target was 11.5 mm lateral, 2.5 mm posterior and 4.1 mm inferior to the mid-point of the AC-PC line. Fifty good electrophysiological recordings of the STN (average length 4.65 mm) were achieved and target point adjusted in 90% of lead placements. The mean of the final target after electrophysiological correction was 11.7 mm lateral, 2.1 mm posterior, and 3.8 mm inferior to the mid-point. The distance from the centre of the electrode artefact to the final target used after electrophysiological recording on the fused images was 0.48 mm, 0.69 mm, and 2.9 mm in the x, y, and z axes, respectively. No postoperative MRI related complication was observed. Conclusion: Both direct visualisation of the STN on MRI and intraoperative electrophysiological recording are important in defining the best target. Individual variations exist in the location of the STN target. Fewer tracks were required to define STN activity on the side operated first. Our current stereotactic method of electrode placement is relatively accurate.

BackgroundA number of epidemiologic studies show a decreased risk of non-melanoma cancer in Parkinson's disease (PD). Cigarette smoking is less prevalent in PD and hence the risk of smoking related neoplasia such as lung and colon would be expected to be decreased in PD. A link is shown between decreased physical activity and colorectal cancer. Increased dietary intake of iron increases colorectal cancer risk and iron deposition in the basal ganglia is a feature of PD. Thus common mechanisms may be involved in both disorders. Our study looks at a cohort of surgically treated PD patients to see if there is an altered risk of colorectal cancer among them.MethodIn our population of patients fitted with a deep brain stimulator between 2002 and 2010, we searched for causes of death confirmed against death certificates and a histological diagnosis of colorectal cancer in the patient records.ResultsOf 22 patients who had died, 3 had a diagnosis colorectal cancer. 1 more died of a carcinoembryonic antigen positive cancer of unknown origin.DiscussionFrom UK national statistics, colorectal cancer accounts for between 2.7 and 3.2% of all deaths. Although the small number of deaths in our cohort requires careful interpretation of the results, 14% of our cohort having a diagnosis of colorectal cancer suggests that the lifetime risk of colorectal cancer is not reduced in PD patients. This observation merits further investigation in a larger cohort of PD patients.

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Lambert Eaton Myasthenic Syndrome (LEMS) is an autoimmune disorder affecting the neuromuscular junction caused by antibodies against voltage gated calcium channel antibodies. The neurophysiological hallmark of LEMS is incremental response to repetitive nerve stimulation, especially at high frequency stimulation.A 54-year-old gentleman presented to the Neurology clinic with a 9-month history of progressive walking difficulty. He had difficulty standing up from a sitting down position and the symptoms were worse towards the end of the day. He had a transient history of dry mouth when the symptoms started, but denied any postural dizziness, sweating or bowel/bladder symptoms. He denied having any double vision, droopy eyelids, speech or swallowing symptoms. He had lost 1.5 stones in weight over the preceding 7–8 months. Examination showed proximal muscle weakness with reduced reflexes, which could not be potentiated. A clinical suspicion of LEMS was made, but the neurophysiological examination (repeated on three occasions) showed consistently decremental response at low and high frequency stimulations.The VGCC antibody was positive (293, normal 0–45), confirming the clinical suspicion of LEMS. The AChR and MuSK antibodies were negative.This is an unusual neurophysiological finding of a decremental response in a patient with clinical and immunological evidence of LEMS.