Parkinson deep brain stimulation neurosurgery inselspital bern

Historical drawing on Parkinson's symptoms. In 1888, British neurologist William Gowers published A Manual of Diseases of the Nervous System with many excellent illustrations like this one of the core symptoms of Parkinson's: akinesia, rigor and tremor, and postural instability. Image: Handbook of Clinical Neurology, Volume 95, 2009. Used with the kind permission of Elsevier.

Bradykinesia, hypokinesia, akinesia

At Bradykinesis one understands a Slowing of voluntary motor activity. Affected patients are less able to switch quickly between different motor tasks or movements and activities are generally slowed down. Practically, the gait pattern becomes small-stepped, handwriting smaller and less peppy, speech softer, swallowing less frequent, etc. Patients first notice this during activities with the hands, such as writing or playing a musical instrument. This symptomatology increases in the course of the disease. The Lack of movement or. decreased mobility is called Hypokinesia. A high-grade expression of the symptoms up to the immobilize is described as Akinesia designated.

Tremor

The tremor is typically a Resting tremor of the extremities – a trembling without voluntary movement during physical relaxation. The typical rhythmic tremor movement of the fingers is similar to the movement of the fingers when turning pills and is therefore often called a "tremor" Pill tremor Designated. The tremor decreases as soon as the affected limbs are moved in a targeted manner. Typically, tremor is intensified during emotional or mental exertion.

Rigor

Parkinson's syndrome permanently increases muscle tone throughout the entire range of movement. Because of this Muscle rigidity patients have the impression that their limbs are "as if paralyzed" and also often suffer from painful cramps. Walking upright. The balance are disturbed. Straight posture therefore becomes increasingly difficult as the condition progresses. For this reason, falls are a possible dangerous consequence of Parkinson's disease.

Freezing of gait

Patients may also suffer from a specific gait disorder called "freezing of gait". In this case, the walking Parkinson's patient suddenly experiences. Without notice to a blockage. Sufferers appear frozen or frozen in place. Due to the forward-leaning posture of most Parkinson's patients, loss of balance and falls can occur * .

Non-motor symptoms

Although Parkinson's is considered a classic movement disorder and motor symptoms are paramount in patients, there are other non-motor accompanying symptoms of Parkinson's:

vegetative disorders: Disturbances in urination, blood prere disturbances, temperature regulation disturbances, sleep disturbances

mental disorders:Depression, anxiety

cognitive disorders: Behavioral disorders, dementia

sensory disturbances: Visual disturbances, olfactory disturbances, sensory disturbances

The cognitive difficulties often manifest themselves in the advanced stages of the disease and, in the worst case, end in dementia. This Parkinson's dementia differs clinically from the most commonly known form of dementia, Alzheimer's dementia. While Alzheimer's dementia is mainly characterized by memory disorders, Parkinson's dementia is mainly characterized by behavioral disorders such as apraxia. This means that the affected patient is able to perform complex movements, such as making coffee, dressing, etc., in the same way. no longer perform properly.

What are the different forms of Parkinson's disease?

Depending on which main symptoms are particularly pronounced, a distinction is made between different types of Parkinson's disease:

akinetic-rigid type: Lack of movement and rigor are in the foreground

tremor-dominant type: pronounced tremor, less rigor and postural instability

Equivalence type: the classic main symptoms akinesia, rigor and tremor are about equally pronounced

Parkinson's symptoms can also occur in the context of other diseases of the nervous system. The prognosis here is different, and the affected patients also do not respond or respond inadequately to current therapies (drug treatment or neuromodulation). The diagnosis of these atypical Parkinson's syndromes is therefore important both prognostically and therapeutically.

Atypical Parkinson's syndromes are:

– Multisystem atrophies (MSA) – Lewy body dementia – Progressive supranuclear gaze palsy (PSP) – Corticobasal ganglionic degeneration (CBD)

How is Parkinson diagnosed?

The Parkinson's diagnosis is made clinically. In this History of the patient and the clinical-neurological examination findings of central importance. Individual symptoms can be clinically graduated and are used for staging purposes. This so-called Staging is done by means of the Hoehn and Yahr scale (Hoehn 1967) and the Unified Parkinson's Disease Rating Scale (UPDRS). Additional examinations such as magnetic resonance imaging (MRI or engl. Magnetic Resonance Imaging), dopamine transporter scintigraphy SPECT (DAT scan), cerebrospinal fluid diagnostics, etc. are used only as a supportive measure to exclude non-idiopathic Parkinson's syndromes for which the cause is known.

What therapy options are available for Parkinson's patients?

For successful treatment of PD, close collaboration between multiple disciplines is critical. The drug therapy is of primary importance and is performed by neurologists with special knowledge in the field of movement disorders. Surgical procedures such as lesional procedures or deep brain stimulation, respectively. Deep brain stimulation (DBS) can play an important supporting role in therapy. These procedures are highly specialized and require in-depth training in functional neurosurgery. The close interdisciplinary collaboration between neurologists and functional neurosurgeons at Inselspital ensures a competent and, above all, individually tailored holistic treatment for each of our patients.

Drug therapy

Due to the demise of the nerve cells of the substantia nigra, which release dopamine as a neurotransmitter, there is an imbalance in the finely tuned transmitter system of the basal ganglia. As a result, in very simplified terms, there is a deficiency of dopamine and an excess of acetylcholine in signal transmission between neurons in the basal ganglia area. Drug treatment is primarily aimed at restoring dopaminergic signal transmission. The simultaneous inhibition of acetylcholine transmission as of. L-dopa is a precursor of dopamine. Is converted to dopamine in the brain by the enzyme DOPA decarboxylase (DDC). L-dopa is the most effective and tolerable drug for the treatment of Parkinson's symptoms and is currently the drug of choice. It mainly improves akinesia and rigor, less tremor. Long-term observations have shown that L-DOPA therapy over several years leads to a gradual decline in efficacy and that the effect is subject to significant fluctuations (so-called fluctuations in efficacy) during the course of the day.

Dopamine agonists

The dopaminergic agonists such as z. B. Pramipexole, ropinirole, rotigotine, piribedil have a direct effect on the dopamine receptors. These are u. a. Used to reduce the amount of L-DOPA needed and in cases where patients no longer respond reliably to L-DOPA. Advantages of dopamine agonists include having fewer fluctuations in effect as well as hypermobility (called dyskinesia) as a side effect. Disadvantages are that behavioral problems such as obsessive-compulsive disorder or decreased impulse control have been observed in 15% of patients during treatment. This manifests itself, for example, in gambling addiction, spending sprees, money problems, hypersexuality, etc.

Inhibitors of monoamine oxidase type B (IMAO-B)

IMAO-B (rasagiline) has a small dopaminergic effect by inhibiting dopamine degradation. Mostly used as an adjunct to enhance the effect of L-DOPA and reduce fluctuations in the effect of L-DOPA therapy.

Anticholinergics

For example, benserazide. This longest-known therapy inhibits acetylcholine signaling. These drugs continue to be important in cases where tremor or vegetative disturbances are predominant. The effect on akinesia. The rigor is in the background. Possible side effects include memory impairment. Can be a problem in advanced Parkinson's.

The list, of drugs listed here does not claim to be exhaustive. The drugs can be used individually or in combination.

Injection therapy

In addition to the listed medications, the dopamine agonist apomorphine can also be administered as an injection under the skin or in the form of a Apomorphine Pump are used for continuous administration into the duodenum. This therapy comes into play when drug treatment with tablets no longer helps sufficiently.

Surgical therapy

Surgical therapy for Parkinson's disease is a subset of the functional neurosurgery. The history of functional neurosurgery in Parkinson's therapy dates back to the second half of the 20th century. Twentieth century. The development of neurosurgical procedures at that time, based on so-called stereotaxic frames, made it possible to place probes in specific target areas of the brain with millimeter precision.

Classically, the probes inserted in this way were used to heat and thus obliterate surrounding nerve tie * . Furthermore, Parkinson's disease was treated by placing smaller lesions in the area of the globus pallidus internus (GPi) and the nucleus subthalamicus as well as in the area of the motor thalamus (nucleus ventralis intermedius, VIM) in case of tremor being in the foreground. Pioneering work in the 1990s by French neurosurgeon Alim Louis Benabid showed that inserting radiofrequency stimulation electrodes in these brain regions achieved the same effect with the advantage that side effects could be better avoided by adjusting the stimulation intensity.

This new therapy was called deep brain stimulation or deep brain stimulation (DBS) and is now the standard surgical therapy at Inselspital * . There are Three possible structures in the brain for deep brain stimulation in patients with Parkinson's disease:

– the subthalamic nucleus (STN) – the globus pallidus internus (GPi) – the ventral intermediate nucleus of the thalamus (Vim)

These potential targets must be discussed as alternatives in each patient individually in the expert board. Stimulation in the area of the subthalamic nucleus (STN) is the target of first choice because akinesia and rigor can be successfully treated by stimulation and the dosage of medication can usually be considerably reduced. Potential disadvantage is the worsening of pre-existing postural instability. According to studies, GPi stimulation is currently equivalent * .

3D image of a DBS electrode. Shown is the reconstruction of two DBS electrodes in the area of the subthalamic nucleus (orange) and the modeled electric field induced around the electrode (light-red). Other nuclei of the basal ganglia are shown as well. Image: Department of Neurosurgery, Inselspital Bern © CC BY-NC 4.0

What can a Parkinson's patient expect from deep brain stimulation??

Symptoms before and after DBS surgery

The following two graphs show the percentage of sleep, poor mobility (blockages), good mobility and dyskinesia before surgery and six months after surgery. The duration of poor mobility is reduced from an average of six and three-quarters hours to two hours per day (adapted from Deuschl et al. NEJM 2006).

What are the side effects of deep brain stimulation??

Are all Parkinson's disease patients suitable for deep brain stimulation?

Not all patients are suitable for surgical therapy. Suitable candidates meet the following criteria:

– Patient exhibits severe motor impairments despite good drug treatment (e.g. B. dyskinesia) or a strong tremor. – The patient's drug therapy is subject to strong fluctuations and sudden loss of effect during the course of the day (wearing-off, fluctuations in effect). – Patient does not have severe cognitive problems (dementia), behavioral problems or depression.

Tremor, fluctuations in effect, and relief of dyskinesias respond best to surgical therapy. Autonomic symptoms (blood prere fluctuations, micturition disorders, salivation, etc) are not suitable for surgical treatment.) and cognitive symptoms (Parkinson's dementia) cannot be improved at the present stage. However, several studies are currently underway. Mixed success is provided by deep brain stimulation of the pedunculopontine nucleus in freezing of gait * . The decision must be made on a case-by-case basis. The indication for DBS is generally made jointly by neurologists and neurosurgeons after time-consuming examinations (neurological examinations, neuropsychological tests, psychiatric evaluation, surgical evaluation) to ensure that only patients with a high chance of success in improving their symptoms are selected for the procedure.

At Inselspital, patients are discussed individually within the framework of our interdisciplinary board for movement disorders in order to find the best therapeutic options for each patient. We combine modern technology with humanity, always focusing on the patient and his individual needs.

References

Deuschl G, Schade-Brittinger C, Krack P et al. A Randomized Trial of Deep-Brain Stimulation for Parkinson's Disease. New England Journal of Medicine. 2006;355:896-908.

Nowacki A, Galati S, Ai-Schlaeppi J, Bassetti C, Kaelin A, Pollo C. Pedunculopontine nucleus: an integrative view with implications on deep brain stimulation. Neurobiology of disease. 2019;128:75-85.

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