But depression is a secondary problem post stroke; solve the primary problem of 100% recovery and all these secondary problems disappear! Does anyone in stroke actually think?
A novel approach to treating post-stroke depression: administration of Botulinum Toxin A via local facial injection
- 1Department of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China
- 2Department of Neurology, Wuxi No.2 People's Hospital, Jiangnan University Medical Center, Wuxi, China
Background: Post-stroke depression (PSD) is a frequent complication following a stroke, characterized by prolonged feelings of sadness and loss of interest, which can significantly impede stroke rehabilitation, increase disability, and raise mortality rates. Traditional antidepressants often have significant side effects and poor patient adherence, necessitating the exploration of more suitable treatments for PSD. Previous researchers and our research team have discovered that Botulinum Toxin A (BoNT-A) exhibits antidepressant effects. Therefore, our objective was to assess the efficacy and side effects of BoNT-A treatment in patients with PSD.
Methods: A total of 71 stroke patients meeting the inclusion criteria were allocated to the two group. 2 cases were excluded due to severe neurological dysfunction that prevented cooperation and 4 cases were lost follow-up. Ultimately, number of participants in the BoNT-A group (n = 32) and Sertraline group (n = 33). Treatment efficacy was evaluated 1, 2, 4, 8 and 12 weeks post-treatment.
Results: There were no significant differences in baseline characteristics between the two groups (p > 0.05). Both groups exhibited comparable treatment efficacy, with fewer side effects observed in the BoNT-A group compared to the Sertraline group. BoNT-A therapy demonstrated significant effects as early as the first week (p < 0.05), and by the 12th week, there was a notable decrease in neuropsychological scores, significantly lower than the baseline level. The analysis revealed significant differences in measurements of the Hamilton Depression Scale (HAMD) (F(770) = 12.547, p = 0.000), Hamilton Anxiety Scale (HAMA) (F(951) = 10.422, p = 0.000), Self-Rating Depression Scale (SDS) (F(1385) = 10.607, p = 0.000), and Self-Rating Anxiety Scale (SAS) (F(1482) = 11.491, p = 0.000).
Conclusion: BoNT-A treatment effectively reduces depression symptoms in patients with PSD on a continuous basis.
Introduction
Stroke is a cerebrovascular event resulting from a sudden interruption of blood supply to the brain, causing irreversible tissue damage. This condition encompasses thrombotic, embolic, or hemorrhagic events. A common complication of stroke is post-stroke depression (PSD), a mood disorder characterized by persistent emotional depression and loss of interest (1). Psychiatrists have observed PSD for nearly a century, and since the 1970s, numerous studies have been conducted to investigate this condition. PSD is a prevalent and manageable complication of stroke (2), with meta-analyses estimating its prevalence to range from 18 to 33% (3, 4). Werheid discovered an intriguing pattern where depressive symptoms in stroke patients tend to worsen in the first 6 months, improve within a year, and then worsen again after the second year (5). PSD can increase disability and mortality rates, reduce rehabilitation efficiency, and lead to a decline in motor function and quality of life, placing a burden on both families and society (6). The clinical manifestations of PSD can be classified into core and non-core symptoms. Core symptoms consist of low mood, anhedonia, and fatigue, while non-core symptoms include cognitive impairment, sleep disturbances, unexplained pain, sexual dysfunction, appetite changes, and gastrointestinal issues. However, due to the diverse and non-specific nature of these symptoms, diagnosis and treatment of PSD are often overlooked or delayed (2).
Research studies have shown that prompt administration of antidepressant therapy after a stroke can prevent the development of PSD (7). Additionally, antidepressant therapy can improve the prognosis of stroke patients, including cognitive and executive functions, thereby enhancing their quality of life (8). It is worth noting that a randomized placebo-controlled trial has established that the benefits of antidepressants can extend beyond emotional symptoms. Patients who received antidepressants demonstrated better motor recovery compared to the control group, leading to a significant increase in the proportion of patients achieving partial or complete living independence (9). As a result, early detection of PSD and timely use of antidepressants are crucial for effective stroke management. However, traditional antidepressants often fail to meet clinical needs due to their slow onset of action and adverse side effects, such as hepatotoxicity, nephrotoxicity, gastrointestinal discomfort, cognitive decline, etc. (10). An increasing number of studies have demonstrated the efficacy of Botulinum Toxin A (BoNT-A) in the treatment of depression. Clinical randomized controlled trials have consistently confirmed the safety and effectiveness of BoNT-A as an antidepressant therapy (11). Building upon this previous research, we recruited PSD patients who met the inclusion criteria to receive BoNT-A for antidepressant treatment, with the traditional antidepressant Sertraline serving as the control group in our study.
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