RESUMEN

BACKGROUND: Deep Brain Stimulation (DBS) is FDA-approved for several movement disorders; such as Parkinson's disease, dystonia, and neuropsychiatric disorders. There are various reports of Body mass index (BMI) changes following different DBS targets in various disorders. AIM: A comprehensive systematic review and meta-analysis were conducted to investigate the impact of DBS on patients' Body Mass Index (BMI) and provide an in-depth overview of its underlying mechanisms. MATERIALS AND METHODS: We conducted research according to PRISMA guidelines. Our study assessed comprehensively electronic databases, including Pubmed, Scopus, Embase, web of science, and the Cochrane Library, up to May 2024. The random-effect model analysis was performed by the Comprehensive Meta-analysis software (CMA) version 3.0. As well, Cochran's Q test was used to determine the statistical heterogeneity of included studies. RESULT: This systematic review ultimately included 49 studies, 46 of which entered the meta-analysis. The total number of patients was 1478, consisting of Parkinson's disease (PD), dystonia, and the obsessive compulsive disorder (OCD) patients. The most common DBS target was subthalamic nucleus, followed by globus pallidus internus (GPi). Our meta-analysis depicted the BMI of participants significantly mount after DBS electrode implantation (SMD = -0.542, 95%CI: -0.678 to -0.406, and P-value < 0.001). However, moderate to high heterogeneity was detected among the studies (I2 = 67.566%). Additionally, the Daily energy intake (DEI) of patients significantly decreased after DBS (SMD: 0.457, 95%CI; 0.205 to 0.709, and P-value < 0.001). CONCLUSION: STN and GPi DBS can lead to weight gain through distinct central pathways in various movement and neuropsychiatric disorders, posing a potential risk for obesity, insulin resistance, and metabolic syndrome.

Asunto(s)

RESUMEN

BACKGROUND: Migraine affects one in ten individuals worldwide and is the second leading cause of disability. Studies have shown an association between migraine and the musculoskeletal system, and myofascial trigger points (MTrPs) play an essential role. Additionally, those with myofascial pain have been proven to experience higher levels of depression and anxiety. Understanding the association between MTrPs and migraine is crucial for developing targeted treatment strategies. Additionally, recognizing the link between MTrPs and migraine-related depression and anxiety underscores the importance of a holistic approach to migraine management. By addressing both musculoskeletal and neurological factors, healthcare providers can provide more effective and personalized care for migraine patients. This study aims to determine the association between MTrPs with migraine-related disability, anxiety, depression, and migraine characteristics. METHODS: This cross-sectional study included 68 migraine patients from an outpatient neurology clinic. The number of MTrPs was determined through examination by an experienced neurologist during a migraine-free period using the recommended international criteria. We evaluated anxiety and depression with the Hospital Anxiety and Depression Scale (HADS) and disability with the Migraine Disability Assessment Scale (MIDAS). RESULTS: We enrolled 68 patients (22 males) with a mean age of 36.23 ± 9.63 years. The mean number of MTrPs was 2.75 ± 2.934. MTrPs were positively correlated with severity (CC: 0.576, P-value < 0.001). There was no association between MTrPs and HADS-D or MIDAS, but migraine patients with abnormal HADS-A scores had more MTrPs than patients with normal HADS-A scores (0.6 ± 0.84 vs 3.56 ± 3.11, P-value:0.013). CONCLUSIONS: The number of MTrPs is associated with higher anxiety levels and headache intensity. Further research could investigate the impact of MTrP-based therapies on anxiety among individuals suffering from migraines.

Asunto(s)

RESUMEN

PURPOSE: Cognitive impairment can begin in the early stages of multiple sclerosis (MS). No medicine has been approved for treating cognitive impairment in MS patients. There is a lack of data on the role of rituximab in managing cognitive impairment in MS patients. Using minimal assessment of cognitive function in MS (MACFIMS), this study aims to investigate the effect of rituximab on the cognitive status of relapsing-remitting MS (RRMS) patients. METHODS: In this pre-post interventional trial, 28 eligible RRMS patients participated. They were administered rituximab for a year. Cognitive tests (MACFIMS), MS neuropsychological questionnaire (MSNQ), and Beck depression inventory-fast screen (BDI-FS) scores were evaluated at baseline, six, and 12 months following rituximab administration. FINDINGS: Eighteen participants with a mean age of 40.5 ± 12.91, 7 men, completed all three follow-ups. There was no statistically significant change in BDI-FS, MSNQ, Paced Auditory Serial Addition Test (P: 0.743), Symbol Digit Modalities Test (P: 0.711), Brief Visual Memory Test (BVMT) (P: 0.426), learning BVMT (P: 0.268), and delayed recall BVMT (P: 0.394) scores. However, the California Verbal Learning Test (CVLT), CVLT learning, and Controlled Oral Word Association Test scores significantly improved by 45.2% (P < 0.001), 12.3% (P: 0.013), and 26.7% (P: 0.011), respectively, 6-month follow-up rituximab treatment. There was a significant improvement in CVLT (+55.7%, P < 0.001), CVLT learning (+15.9%, P: 0.011), and delayed recall CVLT (+28%, P: 0.022) scores 12-month follow-up rituximab treatment. IMPLICATIONS: Rituximab prevents cognitive deterioration and improves some cognitive functions. Further investigations with a larger sample size, longer follow-ups, and inclusion of a placebo or another treatment arm are recommended.

RESUMEN

Background: Treatment-resistant epileptic seizures are associated with reduced quality of life (QoL). As polypharmacy with routine antiseizure medications has many side effects, novel add-on treatments are necessary. Recent research showed the efficacy of add-on therapy by cannabidiol (CBD) on refractory epilepsy. We attempted to extend data on the efficacy and safety profile of CBD in patients with frontal lobe treatment-resistant epilepsy. Methods: A total of 27 patients were recruited into two CBD (n = 12) and placebo (n = 15) groups. The CBD group received a highly purified liposomal preparation of the drug in addition to routine antiseizure medications. The placebo group only received antiseizure medications. This experiment followed a triple-blinding protocol. Outcome measures were seizure frequency, the Chalfont seizure severity scale (CSSS), and the quality of life questionnaire score (QOLIE-31) assessed at baseline, 4 weeks, and 8 weeks. Results: At 4 weeks, results indicated that a higher fraction of patients in the CBD group (66.67%) showed improvement in seizure, compared to the placebo group (20.00%). Before-after comparison revealed that CBD, unlike routine ADEs, was effective in reducing the occurrence of seizures at the study's final timepoint [mean difference 45.58, 95% CI (8.987 to 82.18), p = 0.009]. Seizure severity was not affected by study groups or time intervals (repeated-measures ANOVA p > 0.05). Post-hoc tests found that the QoLI-31 score was improved at 8 weeks compared to baseline [mean diff. -5.031, 95% CI (-9.729 to -0.3328), p = 0.032]. The difference in cases who experienced enhanced QoL was meaningful between the CBD and placebo groups at 8 weeks [RR: 2.160, 95% CI (1.148 to 4.741), p = 0.018] but not at 4 weeks (p = 0.653). A positive finding for QoL improvement was associated with a positive finding for seizure frequency reduction [r = 0.638, 95% CI (0.296 to 0.835), p = 0.001]. Interestingly, limiting the correlation analysis to cases receiving CBD indicated that QoL improvement was not linked with seizure parameters such as severity and frequency (p > 0.05). Conclusion: The present study suggests the benefit of a purified and highly efficient preparation of CBD for seizure frequency reduction and improvement of QoL in refractory frontal lobe epilepsy. Further study with longer follow-ups and larger sample size is advised. Clinical trial registration: https://www.irct.ir/trial/56790, identifier: IRCT20210608051515N1.