Parkinson’s Disease & Deep Brain Stimulation (DBS)

What is Parkinson’s disease in simple terms?

A movement disorder that begins deep within the brain’s “control hubs.”

Parkinson’s disease is a chronic, progressive disorder of the nervous system. It primarily affects movement and typically presents with:

• bradykinesia (slowness in initiating and executing movement)
• rigidity (stiffness or resistance in the joints)
• gait instability and increased risk of falls
• resting tremor (shaking when the limb is relaxed)

Symptoms usually begin on one side of the body (e.g., in one hand) and gradually spread. Parkinson’s disease affects more than movement—it can influence sleep, mood, blood pressure regulation, cognition, and overall daily independence.

Why does it occur—what happens in the brain?

Loss of dopaminergic neurons and disruption of motor control circuits.

In Parkinson’s disease, neurons that produce dopamine in the pars compacta of the substantia nigra progressively degenerate. Dopamine is essential for the proper function of the basal ganglia, the neural “circuits” that regulate and refine voluntary movement.

When approximately 70–80% of these neurons are lost, motor circuits shift toward overactivity of the indirect pathway (via GPe, STN, GPi), leading to:

• suppression of normal movement
• “freezing,” small steps, and difficulty initiating motion
• the emergence of resting tremor.

In a minority of patients, Parkinson’s disease is associated with specific genetic mutations (PARKIN, PINK, LRRK2, SNCA, among others). In most cases, it is considered multifactorial, reflecting a combination of age, environmental factors, and genetic susceptibility.

What are the key symptoms and how do they progress?

From mild unilateral tremor to falls and dependence on assistance.

Motor symptoms include:

• Bradykinesia – small, slow movements and delayed changes in direction
• Rigidity – a sensation of stiffness in limbs and trunk
• Resting tremor – characteristic shaking of the hand
• Postural instability – shuffling gait, imbalance, falls

Non-motor symptoms may include:

• sleep disturbances, fatigue
• depression, anxiety, apathy
• constipation, orthostatic hypotension, urinary dysfunction
• mild cognitive impairment in some patients.

Disease severity is often summarized using the Hoehn & Yahr scale (1–5), ranging from mild, unilateral symptoms to severe disability with frequent falls and need for continuous assistance.

How is Parkinson’s diagnosed and how is “atypical” Parkinsonism excluded?

Clinical diagnosis supported by levodopa response and targeted imaging when necessary.

The diagnosis of Parkinson’s disease is primarily clinical:

• presence of bradykinesia with resting tremor and/or rigidity
• characteristic response to levodopa (substantial improvement when medication is “on”).

The neurologist must exclude:

• secondary parkinsonism (drug-induced—e.g., antipsychotics, SSRIs; metabolic causes; Wilson’s disease)
• atypical parkinsonian syndromes (e.g., PSP, MSA, dementia with Lewy bodies), which usually show poor levodopa response and a different clinical course.

Brain MRI is used to exclude alternative diagnoses (vascular lesions, hydrocephalus, etc.). DaT–SPECT, when indicated, can demonstrate reduced dopaminergic uptake in the nigrostriatal pathway and help differentiate Parkinson’s disease from essential tremor.

What medications are used and when do they reach their limits?

From neuroprotective agents and dopamine agonists to levodopa-based therapy.

Pharmacologic treatment is individualized based on age, symptoms, and lifestyle, but typically includes:

• MAO-B inhibitors (selegiline, rasagiline) – mild benefit, possible neuroprotective effect in early stages.
• Dopamine agonists (pramipexole, ropinirole) – often in younger patients to delay early reliance on levodopa.
• Carbidopa–levodopa – the most effective therapy for motor symptoms, available in immediate- or extended-release formulations.
• Adjunctive agents (amantadine, COMT inhibitors, etc.) as needed.

After several years, many patients develop:

• “wearing-off” – shorter duration of medication benefit
• dyskinesias – involuntary, excessive movements at peak medication effect
• unpredictable on–off fluctuations throughout the day.

When fluctuations and dyskinesias significantly impair daily life despite optimized medical therapy, the discussion about DBS becomes appropriate.

What is Deep Brain Stimulation (DBS)?

A “brain pacemaker” that modulates abnormal motor circuits.

DBS is a functional, invasive yet reversible therapy. Ultra-thin electrodes are implanted into specific deep brain nuclei and connected to a pulse generator (IPG) placed subcutaneously beneath the clavicle.

The electrodes deliver electrical impulses that modulate basal ganglia activity, improving:

• bradykinesia
• rigidity
• tremor
• dyskinesias, in combination with medication adjustments.

DBS does not cure Parkinson’s disease and does not halt neurodegeneration, but it can provide substantially better symptom control and reduce time spent in the “off” state.

Who is considered a good candidate for DBS?

Typical Parkinson’s disease with a strong levodopa response. In general, a patient is a good candidate if:

• they have a confirmed diagnosis of idiopathic Parkinson’s disease for several years
• they demonstrate at least ~30% improvement in motor symptoms with levodopa (UPDRS on/off testing)
• despite optimal therapy, they experience significant fluctuations, wearing-off, or bothersome dyskinesias
• there is no established dementia or severe depression/psychosis
• there are no major medical contraindications to surgery.

Most importantly, DBS replicates your best medication-“on” state. If you never experience meaningful improvement with levodopa, you are generally not an appropriate candidate for deep brain stimulation.

What are the targets (STN, GPi, VIM) and how are they chosen?

Different neural “pathways” can be modulated—at Neuroknife, target selection is individualized.

The principal DBS targets in Parkinson’s disease are:

• Subthalamic Nucleus (STN): highly effective for bradykinesia, rigidity, and tremor; often allows greater medication reduction, but may affect mood or behavior in vulnerable patients.
• Globus Pallidus internus (GPi): excellent for dyskinesias and effective for bradykinesia/rigidity; often chosen when medication reduction is not a priority or when psychiatric side-effects are a concern.
• Ventral Intermediate Nucleus (VIM) of the thalamus: primarily for resting tremor when tremor is the dominant symptom or when cognitive reserve is limited.

Target selection is determined by a multidisciplinary team, considering:

• which symptoms are most disabling
• the importance of medication reduction
• psychiatric and cognitive profile
• MRI findings and neuropsychological testing

How is DBS surgery performed in practice?

Stereotactic, sub-millimetric accuracy using combined imaging and physiology.

The procedure typically includes:

1. Preoperative planning: high-resolution MRI 1–2 weeks prior, target localization using anatomical landmarks (AC–PC line, red nucleus, human atlas).
2. Day of surgery—electrode placement: a frameless stereotactic system is used with CT–MRI fusion. Patients are usually under conscious sedation and off antiparkinsonian medication for ~12 hours.
3. Microelectrode recording (MER) & macrostimulation: neural activity is recorded as the electrode advances toward the target. Test stimulation identifies the site with the best clinical benefit and fewest side effects.
4. Permanent lead fixation: the electrode is secured to the skull. For bilateral procedures, the process is repeated on the opposite side.
5. Pulse generator (IPG) implantation: typically performed in a second stage a few days later, beneath the clavicle, with subcutaneous connection to the leads.

In selected cases, intraoperative MRI may be used instead of MER. Both approaches aim for millimetric precision.

What are the risks, complications, and realistic benefits?

Surgical risks versus the risks of a progressively restricted daily life.

The main risks of DBS include:

• Hemorrhage (intracerebral) in a small percentage of cases
• Infection of implanted hardware (lead or generator)
• Lead migration or fracture (rare)
• Transient effects such as confusion in the early postoperative period, paresthesias, or dyskinesias at higher stimulation settings.

Realistic benefits in properly selected patients include:

• substantial improvement in bradykinesia, rigidity, and tremor
• reduction in “off” time and dyskinetic “on” periods
• potential reduction in levodopa dosage (especially with STN-DBS)
• a more stable and predictable daily life.

Importantly, DBS offers limited benefit for speech impairment, freezing of gait, advanced postural instability, or significant cognitive decline. Therefore, timing is critical—not too early after diagnosis, but not when disease has already reached an advanced stage.

What should you expect after surgery and programming?

Meaningful improvement occurs months after surgery, following repeated visits with a movement-disorders neurologist and optimization of stimulator settings.

After surgery:

• hospital stay is typically 1–3 days
• fatigue, mild headache, or local discomfort near the generator may occur
• medications are initially continued as before.

DBS programming begins days to weeks later, performed wirelessly in the outpatient clinic using specialized software:

• selection of active contacts
• adjustment of voltage, pulse width, and frequency
• gradual medication optimization in collaboration with the patient.

Typically, multiple visits over up to 6 months are required to achieve optimal benefit. Long-term follow-up is essential, with less frequent adjustments thereafter.