PET imaging is increasingly recognized as an important diagnostic tool to investigate patients with cognitive disturbances of possible neurodegenerative origin. PET with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG), assessing glucose metabolism, provides a measure of neurodegeneration and allows a precise differential diagnosis among the most common neurodegenerative diseases, such as Alzheimer’s disease, frontotemporal dementia or dementia with Lewy bodies. PET tracers specific for the pathological deposits characteristic of different neurodegenerative processes, namely amyloid and tau deposits typical of Alzheimer’s Disease, allow the visualization of these aggregates in vivo. [18F]FDG and amyloid PET imaging have reached a high level of clinical validity and are since 2022 investigations that can be offered to patients in standard clinical care in most of Canada.

This article will briefly review and summarize the current knowledge on these diagnostic tools, their integration into diagnostic algorithms as well as perspectives for future developments.

Parkinson’s disease (PD) is a complex disorder with a significant genetic component. Genetic variations associated with PD play a crucial role in the disease’s inheritance and prognosis. Currently, 31 genes have been linked to PD in the OMIM database, and the number of genes and genetic variations identified is steadily increasing. To establish a robust correlation between phenotype and genotype, it is essential to compare research findings with existing literature. In this study, we aimed to identify genetic variants associated with PD using a targeted gene panel with next-generation sequencing (NGS) technology. Our objective was also to explore the idea of re-analyzing genetic variants of unknown significance (VUS). We screened 18 genes known to be related to PD using NGS in 43 patients who visited our outpatient clinic between 2018−2019. After 12−24 months, we re-evaluated the detected variants. We found 14 different heterozygous variants classified as pathogenic, likely pathogenic, or VUS in 14 individuals from nonconsanguineous families. We re-evaluated 15 variants and found changes in their interpretation. Targeted gene panel analysis with NGS can help identify genetic variants associated with PD with confidence. Re-analyzing certain variants at specific time intervals can be especially beneficial in selected situations. Our study aims to expand the clinical and genetic understanding of PD and emphasizes the importance of re-analysis.

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.

Clozapine is the least likely anti-psychotic to induce extrapyramidal symptoms (EPS). We present a surprising case of a woman schizophrenic patient treated with clozapine suffering from EPS. Single photon emission computed tomography (SPECT) revealed a low density of presynaptic dopamine transporters in our patient's brain. A comorbid diagnosis of Parkinson's disease in schizophrenia was confirmed in this way. This helped us to find a proper therapeutic strategy for our patient.

In the present open prospective study the effects of quetiapine were investigated in two elderly patients with parkinsonism and psychosis. Treatment induced a marked antipsychotic effect that coincided with an improvement of general motor functioning. These findings support the idea that quetiapine may be preferentially of use in the elderly with parkinson’s disease and psychotic symptoms.

Akathisia, dystonia, dyskinesia and parkinsonism, the four main categories of neuroleptic-induced extrapyramidal syndromes (EPS), represent major disadvantages in antipsychotic therapy. In vulnerable patients, acute EPS may progress into potentially irreversible forms such as tardive dystonia and tardive dyskinesia. In the psychiatric clinic, these EPS are often insufficiently recognised or permitted to exist without treatment. In order to ensure a better EPS diagnosis, a simple examination procedure is described. EPS rating scales may serve as an aid in this process. Guidelines are given to prevent and treat EPS. Thus, EPS are best prevented by a course of neuroleptic medication involving as little antidopaminergic D2 effect as possible, including the use of the lowest effective dose (sometimes obtained by addition of a benzodiazepine or carbamazepine) and with antipsychotic drugs which produce low D2 receptor blockade. Treating EPS also consists of using the lowest effective dose and antipsychotics with a low D2 dopamine receptor occupancy. At present, clozapine is the only drug that produces antipsychotic benefits at doses that cause far less D2 receptor antagonism in the basal ganglia of the brain than that seen with standard neuroleptics; however, newer drugs, such as olanzepine, seroquel and sertindole, are on the way.

This naturalistic, observational pan-European study assessed the safety and early effectiveness of intramuscular (IM) psychotropic treatments in patients with acute agitation suffering from schizophrenia or bipolar mania. One thousand nine hundred and forty of 1945 patients completed the 24-hour observation period after initial IM treatment. Patients from 12 European countries were included (mean age 39 years; 58% male, 66% schizophrenia). IM treatment was at the physician's discretion. The primary objective was to describe the acute tolerability of IM psychotropic therapies in clinical practice, with particular emphasis on EPS. At baseline, 68% of the patients received IM monotherapy, with IM olanzapine most commonly prescribed (36%). During the first 24hours, 190 (9.8%) patients experienced EPS. The occurrence of EPS was statistically significantly lower in patients treated with IM olanzapine compared to those treated with other IM psychotropic medications (mainly typical antipsychotics and benzodiazepines): acute dystonia: 1.1%, 95% CI 0.5–2.3 and 2.9%, CI 2.0–4.0; akathisia: 2.3%, CI 1.3–3.7 and 5.5%, CI 4.3–6.9; Parkinsonism: 2.9%, CI 1.8–4.4 and 7.8%, CI 6.4–9.4, respectively. Anticholinergic treatment was given to 12% IM olanzapine versus 31% non-olanzapine treated patients. Acute agitation after 24hours was reduced by 1.68 (95% CI 1.46–1.91) points on the Clinical Global Impression of Severity (CGI-S) in IM olanzapine patients and 1.51 (95% CI 1.30–1.73) points in non-olanzapine patients. Additional psychotropic medication was required for 90% of the patients during the first 24hours of treatment. Results provide naturalistic evidence for low EPS rates and improvement of agitation with IM psychotropic medications during acute states of patients suffering from acute mania or schizophrenia.

Tardive dyskinesia (TD) was first described in 1964, but treatment for this sometimes poorly characterized condition lagged decades as it was labored by medico-legal implications. TD has often been lumped with other medication-induced disorders and incorrectly classified as extrapyramidal symptoms. TD is likely to be under-recognized for many of these reasons. Though diverse in its presentations, TD is distinct in terms of time course, pathophysiology, and phenomenology.

Objectives: We assessed trends in the incidence, prevalence, and post-diagnosis mortality of parkinsonism in Ontario, Canada over 18 years. We also explored the influence of a range of risk factors for brain health on the trend of incident parkinsonism. Methods: We established an open cohort by linking population-based health administrative databases from 1996 to 2014 in Ontario. The study population comprised residents aged 20–100 years with an incident diagnosis of parkinsonism ascertained using a validated algorithm. We calculated age- and sex-standardized incidence, prevalence, and mortality of parkinsonism, stratified by young onset (20–39 years) and mid/late onset (≥40 years). We assessed trends in incidence using Poisson regression, mortality using negative binomial regression, and prevalence of parkinsonism and pre-existing conditions (e.g., head injury) using the Cochran–Armitage trend test. To better understand trends in the incidence of mid/late-onset parkinsonism, we adjusted for various pre-existing conditions in the Poisson regression model. Results: From 1996 to 2014, we identified 73,129 incident cases of parkinsonism (source population of ∼10.5 million), of whom 56% were male, mean age at diagnosis was 72.6 years, and 99% had mid/late-onset parkinsonism. Over 18 years, the age- and sex-standardized incidence decreased by 13.0% for mid/late-onset parkinsonism but remained unchanged for young-onset parkinsonism. The age- and sex-standardized prevalence increased by 22.8%, while post-diagnosis mortality decreased by 5.5%. Adjustment for pre-existing conditions did not appreciably explain the declining incidence of mid/late-onset parkinsonism. Conclusion: Young-onset and mid/late-onset parkinsonism exhibited differing trends in incidence over 18 years in Ontario. Further research to identify other factors that may appreciably explain trends in incident parkinsonism is warranted.