Tremors are a common reason for neurology consultations and can sometimes be a diagnostic challenge. One of the most common causes is essential tremor, which needs to be distinguished from other types of tremors, such as those found in Parkinson’s disease, cerebellar disease or dystonic tremor. This categorisation is important as their treatment and prognosis differ. This review focuses on two main characteristics of tremor to help with its differential diagnosis: ‘The When’, or conditions that enhance the tremor, which include action, postural, intentional components and resting tremor; and ‘The Where’ or the body location, which includes tremor in the upper limbs, head or voice.

Patients with cognitive deficits have a prolonged latency and reduced amplitude of the P300 wave. However, no study has correlated P300 wave alterations with the cognitive performance of patients with cerebellar lesions. We aimed to determine if the cognitive status of these patients was associated with P300 wave alterations. We recruited 30 patients with cerebellar lesions from the wards of the N.R.S. Medical College, Kolkata, in West Bengal (India). The Kolkata Cognitive Screening Battery tasks and the Frontal Assessment Battery (FAB) were used to assess the cognitive status and the International Cooperative Ataxia Rating Scale (ICARS) for cerebellar signs. We compared the results with the normative data of the Indian population. Patients had P300 wave alterations with a significant increase in latency and a non-significant trend in amplitude. In a multivariate model, P300 wave latency was positively associated with the ICARS kinetic subscale (p = 0.005) and age (p = 0.009), regardless of sex and years of education. In the model that included cognitive variables, P300 wave latency was negatively associated with performance in phonemic fluency (p = 0.035) and construction (p = 0.009). Furthermore, P300 wave amplitude was positively associated with the FAB total score (p < 0.001). In closing, patients with cerebellar lesions had an increase in latency and a decrease in the amplitude of the P300 wave. These P300 wave alterations were also associated with worse cognitive performance and some of the subscales of the ICARS, reinforcing that the cerebellum has motor, cognitive, and affective functions.

Toxic oil syndrome (TOS) is a multisystemic disease that emerged in Spain in 1981 due to the ingestion of aniline-adulterated rapeseed oil fraudulently sold as olive oil. Although neurological sequelae, including cognitive deficits, have been documented in long-term survivors, it remains unclear whether TOS leads to chronic or progressive neurodegeneration. In this case-control study, we measured blood concentrations of neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and phosphorylated tau 217 (pTau217) in 50 individuals with clinically confirmed TOS and 50 matched healthy controls. Biomarkers were quantified using ultrasensitive immunoassay platforms (Quanterix SIMOA SR-X and Fujirebio Lumipulse G600II). Group differences were evaluated using non-parametric tests, and multiple linear regression was applied to assess associations between biomarkers and clinical variables. While NfL levels were slightly higher in TOS patients (p = 0.025), no significant group differences were observed for pTau217 or GFAP. Age was a consistent predictor of biomarker levels, particularly for GFAP and pTau217, and female sex was independently associated with higher GFAP concentrations. Lower educational attainment was linked to increased NfL levels. Clinical status (TOS vs. control) did not significantly predict biomarker concentrations in any model. These findings suggest no evidence of overt or ongoing neurodegeneration in long-term TOS survivors as detected by current blood biomarkers. However, the possibility of subtle, compartmentalized, or slowly evolving neurotoxic processes cannot be excluded. Future longitudinal studies incorporating serial biomarker assessments, advanced neuroimaging, and oxidative stress markers are warranted to clarify the long-term neurological consequences of TOS and to detect subclinical trajectories of delayed neurotoxicity in this population.

Background: The association between essential tremor (ET) and mortality risk remains uncertain. This study investigated the impact of episodic memory performance, measured through a word recall task, on mortality risk in ET within the Neurological Disorders in Central Spain (NEDICES) cohort, a population-based study of older adults. Methods: Participants were followed until death or 31 December 2017, and divided into four groups based on ET status and memory performance (errors in the 37-Minimental Examination’s three-word recall task). Cox proportional hazards models estimated mortality hazard ratios (HRs), and the Relative Excess Risk due to Interaction (RERI) assessed additive interactions. Results: Among 3998 participants, 3432 (85.8%) died over a median follow-up of 11.2 years. ET patients with episodic memory impairments had a higher mortality risk (HR = 1.25, 95% CI: 1.06–1.46) compared with controls with similar deficits (HR = 1.19, 95% CI: 1.09–1.28), whereas no significant increase was observed for ET patients without memory impairments (HR = 0.95, 95% CI: 0.74–1.21). RERI analysis revealed no significant additive interaction between ET and memory impairment (fully adjusted RERI: 0.11 [95% CI: −0.19–0.41]). Episodic memory impairments, regardless of ET status, were strongly associated with Alzheimer’s disease as a primary cause of death. Conclusions: These findings highlight the independent contribution of episodic memory impairment to increased mortality risk, with ET modestly amplifying this effect without significant interaction. Further research is needed to explore shared pathophysiological mechanisms between ET and neurodegenerative conditions.

Background: Toxic oil syndrome (TOS) was a major food-borne epidemic that occurred in Spain in May 1981, caused by the ingestion of rapeseed oil adulterated with aniline. While the somatic sequelae of TOS have been well documented, its long-term cognitive consequences remain poorly understood more than four decades after exposure. Methods: In this case-control study, 50 individuals with clinically confirmed TOS were compared to 50 healthy controls matched for age, sex, and education. All participants completed a comprehensive neuropsychological assessment, along with questionnaires evaluating fatigue, anxiety, depression, and health-related quality of life. Multivariate regression models were adjusted for demographic and vascular risk factors, as well as for mood symptoms, fatigue, and use of central nervous system-acting medications. Structural equation modeling was used to explore the potential mediating effects of affective and fatigue symptoms on cognitive performance. Results: TOS survivors showed significantly poorer performance than controls in attention, executive function, processing speed, and global cognition after adjusting for demographic and vascular risk factors. However, these differences were no longer statistically significant after additional adjustment for fatigue, depression, anxiety, and central nervous system-acting medications. Structural equation modeling analyses revealed that affective symptoms—particularly fatigue—substantially mediated the relationship between TOS and cognitive performance. Conclusions: The cognitive profile observed mirrors that of disorders characterized by subcortical dysfunction and impaired neural connectivity, such as multiple sclerosis and vascular cognitive impairment. Although early postmortem studies in TOS did not demonstrate overt white matter lesions, our findings raise the possibility of long-lasting alterations involving both white and gray matter networks. These results emphasize the need to consider mood and fatigue symptoms when evaluating cognition in TOS survivors and point to the potential for widespread, enduring neurobiological effects stemming from the original toxic exposure.