Deep brain stimulation for Parkinson's disease

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative illness with both motor and nonmotor symptoms. Deep brain stimulation (DBS) is an established safe neurosurgical symptomatic therapy for eligible patients with advanced disease in whom medical treatment fails to provide adequate symptom control and good quality of life, or in whom dopaminergic medications induce severe side effects such as dyskinesias. DBS can be tailored to the patient's symptoms and targeted to various nodes along the basal ganglia–thalamus circuitry, which mediates the various symptoms of the illness; DBS in the thalamus is most efficient for tremors, and DBS in the pallidum most efficient for rigidity and dyskinesias, whereas DBS in the subthalamic nucleus (STN) can treat both tremors, akinesia, rigidity and dyskinesias, and allows for decrease in doses of medications even in patients with advanced stages of the disease, which makes it the preferred target for DBS. However, DBS in the STN assumes that the patient is not too old, with no cognitive decline or relevant depression, and does not exhibit severe and medically resistant axial symptoms such as balance and gait disturbances, and falls. Dysarthria is the most common side effect of DBS, regardless of the brain target. DBS has a long‐lasting effect on appendicular symptoms, but with progression of disease, nondopaminergic axial features become less responsive to DBS. DBS for PD is highly specialised; to enable adequate selection and follow‐up of patients, DBS requires dedicated multidisciplinary teams of movement disorder neurologists, functional neurosurgeons, specialised DBS nurses and neuropsychologists.

Role of the subthalamic nucleus in perceiving and estimating the passage of time

“…This study has several limitations. The primary effect of STN DBS is on motor symptoms of PD patients (Hariz and Blomstedt, 2022). In the present study, we assessed basic motor function by using the simple reaction task and found no effect of DBS-STN on it.…”

Nucleus reticularis tegmenti pontis: a bridge between the basal ganglia and cerebellum for movement control

“…Electrical stimulation of the subthalamic nucleus (STN) is an established clinical therapy for reducing motor deficits associated with PD (Benabid et al 2009 ; Hariz and Blomstedt 2022 ), and the STN is considered a potential element in BG connections to the cerebellum. None of our cases labeled more than a few cells in STN, and it is likely that the effects of STN stimulation are mediated by its projections to GPi and SNr.…”

Computational Models in Deep Brain Stimulation : Patient‐Specific Simulations, Tractography, and Group Analysis

“…The patient walks now with great difficulty, and unable any longer to support himself with his stick, he dares not venture on this exercise, unless assisted by an attendant, who walking backwards before him, prevents his falling forwards, by the pressure of his hands against the fore part of his shoulders.' PD is a neurodegenerative disorder that generates both motor dysfunctions as well as other symptoms such as depression, pain, constipation, sleep disorders, cognitive decline and autonomic dysfunction [55]. The cardinal mo-tor symptoms of PD are tremor, ridigity, akinesia (both bradykinesia, slowness of movements, and hypokinesia, small amplitude of movement) and postural instability.…”

“…Dopamine is a neurotransmitter used in the motor circuitry and with its depletion, the projections from the SN to striatum will start to degrade. [55] The symptoms of PD are first treated with levodopa, a dopamine precursor that can cross the blood-brain barrier, and converts to dopamine in the brain [55,58]. In the beginning, this treatment can often satisfactorily control the PD symptoms but with the progression of the disease, many patients experience motor fluctuations from variations in dopamine levels and levodopa-induces dyskinesias (involuntary movements).…”

“…At this stage, DBS surgery an alternative for controlling the dyskinesias together with the PD symptoms and possibly a reduction of the levodopa dose. [55] There are two established targets for PD, the STN and the GPi. Both targets manage all the cardinal PD symptoms, where STN might have a better symptomatic effect but also a higher risk of adverse effects [2].…”