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.

This paper aims at estimating the tremor torque using extended Kalman filter (EKF) applied to a two-link 3-DOF robot with nonlinear dynamics modelled using Lie-group and Lie-algebra theory. Later, it is generalised to d number of links with (d + 1) -DOF. The configuration of each link at any time is described by its rotation relative to the preceding link. Using this formulation, an elegant formula for the kinetic energy of the (d + 1) -DOF system is obtained as a quadratic form in the angular velocities with coefficients being highly nonlinear trigonometric functions of the angles. Properties of the Lie algebra generators and the Lie adjoint map are used to arrive at this expression. Further, the gravitational potential energy and the torque potential energy are expressed as nonlinear trigonometrical functions of the angles using properties of the SO(3) group. The input torque comprises a nonrandom intentional torque component and a highly nonlinear tremor torque component. The tremor torque is modelled as a stochastic differential equation (sde) satisfying Ornstein–Uhlenbeck (OU) process with diffusion and damping coefficients. Further, the tremor is treated as the disturbance. The Euler–Lagrange equations for the angles are derived. These form a system of sdes, and the EKF is used to get a more accurate disturbance estimate than that provided by the usual disturbance observer. The EKF is based on noisy angle measurements and yields as a bonus the angle and angular velocity estimates on a real-time basis. The parameters in the OU process model of the tremor torque, and parameters of the Fourier components of the intentional torque have also been estimated.

Objectives: Essential tremor (ET) is a movement disorder characterized by action tremor which impacts motor execution. Given the disrupted cerebellar-thalamo-cortical networks in ET, we hypothesized that ET could interfere with the control mechanisms involved in regulating motor performance. The ability to inhibit or stop actions is critical for navigating many daily life situations such as driving or social interactions. The current study investigated the speed of action initiation and two forms of action control, response stopping and proactive slowing in ET. Methods: Thirty-three ET patients and 25 healthy controls (HCs) completed a choice reaction task and a stop-signal task, and measures of going speed, proactive slowing and stop latencies were assessed. Results: Going speed was significantly slower in ET patients (649 ms) compared to HCs (526 ms; F(1,56) = 42.37; p <.001; η2 = .43), whereas proactive slowing did not differ between groups. ET patients exhibited slower stop signal reaction times (320 ms) compared to HCs (258 ms, F(1,56) = 15.3; p <.00; η2 = .22) and more severe motor symptoms of ET were associated with longer stopping latencies in a subset of patients (Spearman rho = .48; p <.05). Conclusions: In line with previous studies, ET patients showed slower action initiation. Additionally, inhibitory control was impaired whereas proactive slowing remained intact relative to HCs. More severe motor symptoms of ET were associated with slower stopping speed, and may reflect more progressive changes to the cerebellar-thalamo-cortical network. Future imaging studies should specify which structural and functional changes in ET can explain changes in inhibitory action control. (JINS, 2019, 25, 156–164)

Exactly 200 years ago, the London surgeon-apothecary James Parkinson (1755-1824) published a 66-page-long booklet entitled An Essay on the Shaking Palsy, which contains the first clear clinical description of the shaking palsy or paralysis agitans, which we now refer to as Parkinson’s disease. However, the value of this essay was not fully recognized during Parkinson’s lifetime, which spanned the American Revolution, the French Revolution, and the Napoleonic Wars. James Parkinson was one of the most singular figures of his time and place. He was successively or concomitantly a virulent political activist, a popular medical writer, a scholarly medical contributor, a highly appreciated parish doctor, a prominent amateur chemist, a devoted madhouse doctor, and a renowned paleontologist. It is that branch of geology that brought Parkinson fame during his lifetime. He was an insatiable collector of fossils, minerals, and shells that came to form the core of the museum that he set out at his home in Shoreditch, England. These specimens are beautifully illustrated in his Organic Remains of a Former World (1804-1811), a three-volume treatise that rapidly became a standard paleontology textbook. Parkinson was a founding member of the Geological Society of London, and in recognition of his contribution to the nascent field of paleontology his name was given to many fossils, particularly ammonites (e.g. Nautilus parkinsoni). Hence, we owe much to Mr. Parkinson, the Paleontologist, as he used to be referred to after his death, for such a vast and multifaceted contribution to natural science and medicine.

Objectives: In unpredictable situations, individuals often show tradeoffs between response initiation and inhibition speeds. We tested the hypothesis that Parkinson’s disease (PD) motor subtypes differentially impact tradeoffs between these two action-oriented processes. We predicted that, compared to tremor dominant (TD) patients, predominant postural instability and gait dysfunction (PIGD) patients would show exacerbated tradeoffs between response initiation and inhibition in situations requiring the sudden potential need to interrupt an action. Methods: Fifty-one PD patients (subdivided into PIGD [n=27] and TD [n=24]) and 21 healthy controls (HCs) completed a choice reaction task to establish baseline response initiation speed between groups. Subsequently, participants completed a stop-signal task which introduced an occasional, unpredictable stop stimulus. We measured changes in initiation speed in preparation of an unpredictable stop (i.e., proactive slowing) and inhibition latency (i.e., stop-signal reaction time). Results: Compared to HCs, PD patients showed slower response initiation speeds in the choice reaction task. All groups showed proactive slowing in the stop-signal task but the magnitude was considerably larger in PIGD patients, almost twice as large as TD patients. PD patients, irrespective of motor subtype, showed longer inhibition latencies than HCs. Conclusions: PIGD and TD subtypes both showed exacerbated response inhibition deficits. However, PIGD patients showed much more pronounced proactive slowing in situations with an expected yet unpredictable need to stop action abruptly. This suggests that PIGD is accompanied by exaggerated tradeoffs between response initiation and inhibition processes to meet situational action demands. We discuss putative neural mechanisms and clinical implications of these findings. (JINS, 2017, 23, 665–674)

During the “DBS Canada Day” symposium held in Toronto July 4-5, 2014, the scientific committee invited experts to share their knowledge regarding deep brain stimulation (DBS) management of movement disorders in three domains: (1) the programming algorithms, (2) the necessary team to run a neurosurgery program, and (3) the appropriate scales to better define in a more comprehensive fashion the effect of the brain surgery. Each presentation was followed by an open discussion, and this article reports on the conclusions of this meeting on these three questions. Concerning programming, the role of the pulse width and the switching off of the stimulation at night for thalamic stimulation for the control of tremor have been discussed. The algorithms proposed in the literature for programming in Parkinson’s disease (PD) need validation. In dystonia, the use of monopolar vs bipolar parameters, the use of low vs high frequencies and the use of smaller versus larger pulse widths all need to be examined properly. Concerning the necessary team to run a neurosurgical program, recommendations will follow the suggestions for standardized outcome measures. Regarding the outcome measures for DBS in PD, investigations need to focus on the non-motor aspects of PD. Identifying which nonmotor symptoms respond to DBS would allow a better screening before and satisfaction postoperatively. There is an important need for more data to determine the optimal programming protocol and the standard measures that should be performed routinely by all centers.

Background: Hereditary hemochromatosis (HH) is a genetic disorder causing pathological iron deposition and functional impairment of various organs, predominantly the liver. We assessed patients with HH for the presence of movement disorders. Methods: We reviewed the charts of 616 patients with HH who attended hemochromatosis clinic at London Health Sciences Centre, London, ON, Canada, from 1988 to 2015. Results: We found three HH patients with movement disorders, without any other major systemic manifestation. One had parkinsonism, another had chorea, and the third had tremor. All three patients had evidence of iron deposition in the brain, affecting the basal ganglia in the first two, and the dentate nucleus, red nucleus, and substantia nigra in the third patient. In addition to the C282Y homozygous mutation in the HFE gene, two of our patients had non-HFE gene mutations. Conclusion: HH should be considered in the differential diagnosis of movement disorders with pathological brain iron deposition. We report for the first time chorea in a patient with HH. Non-HFE gene mutations may predispose HH patients to iron deposition in the brain.