Impact of Subthalamic Nucleus Deep Brain Stimulation on Bradykinesia and Rigidity in Parkinson’s disease

Bronkhorst Cann^*
*Correspondence: Bronkhorst Cann, Department of Psychiatry, University of Toronto, Toronto, ON M5T 1R8, Canada, Email:

Introduction

Parkinson’s Disease (PD) is a progressive neurodegenerative disorder that primarily affects movement control. It is characterized by the classic motor symptoms of bradykinesia (slowness of movement), rigidity (muscle stiffness), tremor, and postural instability. These symptoms result from the degeneration of dopaminergic neurons in the substantia nigra, which leads to a disruption in the basal ganglia's complex network that regulates voluntary motor movements. While pharmacological treatments, particularly levodopa, remain the cornerstone for managing Parkinson’s disease, their effectiveness diminishes over time, and motor fluctuations (such as wearing-off effects and dyskinesias) become problematic [1].

In this context, Deep Brain Stimulation (DBS) has emerged as a viable therapeutic option for patients with advanced PD who no longer respond adequately to medication. DBS involves the implantation of an electrode into specific brain regions to modulate abnormal neural activity. One of the most commonly targeted regions for DBS in PD is the Subthalamic Nucleus (STN), a key structure within the basal ganglia circuitry. The impact of STN DBS on motor symptoms such as bradykinesia and rigidity has been extensively studied, and this article aims to explore the mechanisms behind this effect, the clinical outcomes, and the long-term impact of STN DBS in the management of these symptoms in Parkinson’s disease [2].

Description

The Subthalamic Nucleus (STN) is part of the indirect pathway of the basal ganglia, playing a crucial role in the modulation of motor control. The basal ganglia itself is a group of nuclei involved in regulating voluntary movement, and dysfunction in this network underlies the motor symptoms observed in Parkinson’s disease. In PD, the degeneration of dopaminergic neurons leads to an imbalance between the direct and indirect pathways of the basal ganglia, which in turn causes excessive inhibition of the thalamus and, ultimately, abnormal motor output. The STN, through its connections with other basal ganglia structures such as the Globus Pallidus Internus (GPi), Substantia Nigra pars reticulata (SNr), and the motor cortex, plays a pivotal role in the regulation of movement. Hyperactivity of the STN, often seen in PD due to dopaminergic loss, contributes to motor dysfunction, including bradykinesia and rigidity. DBS of the STN aims to normalize this excessive neuronal activity, thereby alleviating motor symptoms. Deep Brain Stimulation (DBS) is a neurosurgical procedure that involves the implantation of a stimulator electrode into a targeted brain region. The electrode is connected to a pulse generator, typically implanted in the chest, which delivers continuous electrical impulses to the brain. In PD, the target for DBS is commonly the STN, though other structures like the Globus Pallidus Internus (GPi) may also be considered depending on the patient’s specific symptoms and response to treatment [3].

Normalization of Abnormal Basal Ganglia Activity: In Parkinson’s disease, the loss of dopamine leads to excessive firing in the STN and a subsequent increase in inhibitory output from the GPi and SNr. This abnormal pattern of activity results in the motor impairments characteristic of PD. STN DBS has been shown to reduce this excessive neuronal firing, which in turn normalizes the flow of information through the basal ganglia network. This is thought to alleviate the motor symptoms of bradykinesia and rigidity. Restoration of Cortical Output: The basal ganglia communicate directly with the motor cortex, which is responsible for initiating voluntary movement. In PD, the abnormal activity in the basal ganglia disrupts this communication, leading to motor dysfunction. By modulating the STN, DBS may help restore more efficient communication between the basal ganglia and the motor cortex, improving the initiation and execution of movement and reducing rigidity. Beyond the direct effects on the STN, DBS is also thought to influence other regions of the basal ganglia, including the GPi, thalamus, and cortex. This broader modulation of neural circuitry is believed to contribute to the alleviation of motor symptoms, improving not only bradykinesia but also rigidity [4].

Numerous clinical studies have demonstrated the efficacy of STN DBS in reducing bradykinesia, which is one of the most disabling motor symptoms of Parkinson’s disease. Bradykinesia refers to the gradual slowness of movement and difficulty in initiating voluntary movements. It can affect both fine and gross motor skills, including tasks such as walking, handwriting, and self-care. Research consistently shows that STN DBS leads to significant improvements in bradykinesia, with patients experiencing faster movement initiation, improved motor coordination, and greater ease in performing daily activities. The improvement in bradykinesia following STN DBS is often seen within days or weeks of implantation and can be sustained long-term. In fact, studies have reported that up to 50-70% of patients experience a marked reduction in bradykinesia after undergoing DBS, resulting in a better quality of life and a greater degree of independence. One of the most well-established outcomes of STN DBS in PD patients is the reduction in the need for dopaminergic medications. Because DBS directly modulates the basal ganglia, it can help reduce the reliance on levodopa and other dopaminergic drugs, which can cause undesirable side effects like dyskinesia. This has the dual benefit of improving motor function while reducing medication-related complications. Rigidity, characterized by increased muscle tone and resistance to passive movement, is another hallmark motor symptom of Parkinson’s disease. It often coexists with bradykinesia and can be particularly disabling for patients, affecting their range of motion and causing discomfort or pain. STN DBS has been shown to have a profound impact on rigidity in PD patients. Similar to its effects on bradykinesia, STN stimulation modulates abnormal basal ganglia activity and leads to a reduction in muscle tone. Patients undergoing STN DBS report significant improvements in muscle stiffness and resistance, with more fluid and coordinated movements. Rigidity may decrease substantially, allowing patients to experience a greater range of motion and reduced discomfort during movement. The improvement in rigidity following STN DBS has been observed both in the upper and lower extremities, and it plays a critical role in enhancing overall mobility and functional independence in PD patients. As with bradykinesia, the impact of STN DBS on rigidity is often sustained over time, contributing to long-term improvements in motor function and quality of life [5].

Conclusion

Subthalamic Nucleus Deep Brain Stimulation (STN DBS) represents a transformative treatment option for patients with Parkinson’s disease who experience refractory motor symptoms, particularly bradykinesia and rigidity. By modulating abnormal neural activity in the basal ganglia, STN DBS can significantly improve motor function, reduce reliance on medications, and enhance the quality of life for many patients. The impact of STN DBS on bradykinesia and rigidity is supported by a substantial body of clinical evidence, with studies showing marked improvements in both symptoms. These benefits are often sustained over time, although long-term follow-up is required to monitor for potential complications or changes in stimulation parameters.

Acknowledgement

None.

Conflict of Interest

None.

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