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Parkinson's Disease and Deep Brain Stimulation

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Author:    David Tilton (RN, BSN)

Purpose/Goals

The purpose of this course is to provide information on Parkinson’s disease, the symptoms of Parkinson’s disease, and treatment options for patients with Parkinson’s disease. It is also to provide information on Deep Brain Stimulation and to explain why it should be a serious consideration for treatment of Parkinson’s disease in some patients.

Objectives

At the conclusion of this instructional material, the learner will be able to:

  1. Discuss what is currently known about Parkinson's disease.
  2. List three primary symptoms of Parkinson's disease.
  3. Prioritize when during the course of treatment for Parkinson's that Deep Brain Stimulation should be a serious consideration.
  4. Describe in general terms the procedure for implanting the Deep Brain Stimulation device to an interested patient or patient's family member.
  5. Discuss the need for establishing individual neurostimulator settings.

Introduction

Deep Brain Stimulation (DBS) is rapidly becoming a standard of care in the treatment of those afflicted with significant impairments from Parkinson's disease.

Parkinson's disease does not yet have a cure. Medical treatments, pharmacology, and supportive therapies are, therefore, vital in extending the length of life for sufferers of Parkinson's disease, and more importantly, to increase the quality of that life. Despite efforts for early recognition combined with early and aggressive treatment, some of those afflicted with this devastating disorder are unable to significantly diminish or control disease symptoms using medication and therapies alone. For those clients, procedures invasive to the central nervous system offer a degree of relief that they greatly desire.

DBS is one such alternative. DBS, contrary to older literature that may still be in circulation, is not experimental for the treatment of neuromuscular symptoms in diseases such as Parkinson's. Even mainstream popular press, such as Time Magazine, has featured benefits achieved among patients who have undertaken this procedure for the control of movement related symptoms. According to correspondent, Sora Song, in the July 16, 2006 edition of Time Magazine, “To date, more than 35,000 patients around the world have had DBS electrodes implanted in their brains, and there are 250 centers in the U.S. that perform the operation.”

DBS is a neurosurgical procedure in which an electrode, or stimulator, is planted deep within the nuclei of the brain. The presence of these electrodes allows practitioners to introduce and regulate a flow of stimulating current designed to disrupt and diminish the effects of many of the symptoms that greatly impair quality of life, such as the movement disorders characteristic of Parkinson's disease.

Briefly, we will visit what is known about Parkinson's disease as it relates to DBS. This includes the primary symptoms associated with the disease, as well as the process of early recognition and treatment. We will then look closer at the alternatives available when the disease resists conventional treatment, paying special attention to what is currently the most promising advance for the control of symptoms, an advance that is just now becoming available for use to larger numbers of patients both nationally, as well as around the world, DBS.

What We Know about Parkinson’s

Parkinson's disease is a slowly progressing neurodegenerative condition in which nerve cells in key areas of the brain such as the basal ganglion become damaged and even destroyed.

The Chemicals

Function in our brain and central nervous system results from an intricate interplay of chemicals, nerve impulse, and tissues that, frankly, we do not completely understand. We are learning more each year, however, about how the functions of senses, emotions, thoughts, and movement are coordinated through the use of chemicals, known as neurotransmitters, which allow nerve cells to communicate with each other.

Just to scratch our head in an expression of puzzlement, for example, involves several different chemicals conveying a series of signals from the basal ganglia to the thalamus, and then on to the cerebral cortex, all areas physically located in different regions of our brains.

Movements require many impulse exchanges to flow in set sequences from nerve cell to nerve cell. To accomplish this, the neurotransmitter dopamine must be available. This chemical, dopamine, is produced by special cells located in the brain stem known as the substantia nigra, and the presence of this specific neurotransmitter is essential for normal conduction of the impulses needed for movement. As cells responsible for producing and maintaining an adequate level of dopamine begin to die, as happens when Parkinson's disease progresses, needed instructions that control movement can no longer be reliably communicated.

Ironically, the lack of dopamine should not take exclusive blame for the major movement symptoms associated with Parkinson's. It is actually another neurotransmitter used by the brain, acetylcholine, which is more directly responsible for both the tremors and stiffness of muscles experienced by sufferers of Parkinson's disease. The reason acetylcholine is problematic, however, does circle back to the lack of dopamine in that a very delicate balance between acetylcholine and dopamine must be maintained for proper nerve/muscle function. When dopamine is at low levels, too much acetylcholine is present. Without the correct balance of these neurotransmitters, muscles receive conflicting commands, an excessive amount of commands, or even an absence of, the commands they need for proper function.

Who is Affected

DBS for Parkinson's disease might not seem an important advance to some, yet when you look at the numbers of those affected with this life impairing condition, the impact of the disease can be very shocking. Carefully collected data shows that Parkinson's disease is one of the most common neurological disorders, affecting around one and one half percent to two percent of all adults older than 60 years of age. We also know that around ten percent of those with the disease begin manifesting symptoms before the age of 40, though presence of the disease is uncommon in young adults (Sweeney, 2005).

Estimates concerning how many have this disease at any one time vary between 500,000 and 150,000 individuals in the United States alone. The wide disparity originates from factors such as a high misdiagnosis rate, the masking of symptoms by co-morbid conditions, and the fact that many Parkinson's sufferers present with a profile of symptoms that fails to fall into a commonly recognized pattern. Despite missed or belated diagnosis, each and every year brings reports of approximately 50,000 new cases.

Age is the most consistent factor associated with the onset of Parkinson's disease, with people of advanced age having an increased incidence of disease. Men show a slightly increased chance of suffering from Parkinson's as compared to women (men one and one half percent compared to one percent for women), with a family history of this condition creating a higher risk. Having a first-degree family member (sibling or parent) with Parkinson’s creates an estimated doubling of the chance of manifesting symptoms, though it is uncertain whether shared environment conditions or genetic factors contribute more to this phenomenon (Hauser & Pahwa, 2006).

A limited number of genetic markers have been identified as having a role in increasing the risk of Parkinson's, yet very few individuals can truly be said to have an inherited form of the disease. For most, an increased vulnerability to environmental factors appears to be the most common impact of genetic influences.

When examining environment, the onset of Parkinson's is higher in those individuals with a rural background. There has been speculation that contaminants in well water such as pesticides or fertilizer breakdown particles may be an influential factor.

Environmental influences also seem to protect, to an extent, a person from developing Parkinson's. Surprisingly, the most consistent single factor that has been associated with a decreased chance of developing Parkinson's disease is cigarette smoke. Studies are now looking at just how much smoking effects this disease, and whether the influence is limited to the smoker, or to others living in a smoke-rich environment. Another more recently uncovered surprise is that caffeine consumption is also associated with a reduction in disease incidence.

Early Recognition of Parkinson’s

More and more we are finding that early diagnosis of a neurodegenerative condition combined with early treatment greatly expands the quality of life as well as the length of that life. Significant advances have been made in Alzheimer's, Parkinson's, hypertensive dementias, and well, the list goes on and on. One of the keys to taking advantage of new findings, treatments, and strategies is awareness of risk, of early symptoms, and knowing how to obtain the proper available treatments.

Symptoms

Consideration of DBS is greatly dependant on the type and degree of symptoms present. As with all disease, not every individual who suffers from Parkinson's will exhibit all of the signs or symptoms associated with the condition. For some, the progression of Parkinson’s is very slow, gradual. For others, changes appear with abruptness and decline in functioning is rapid. This disease may also manifest in unusual or atypical manners. For example, one person may show a growing problem with balance while never exhibiting the resting tremors considered a hallmark indication of the disease.

Some of the more common symptoms found with Parkinson's disease are tremor, rigidity, and bradykinesia.

Around two-thirds of Parkinson's sufferers begin to experience mild involuntary tremors early in the disease process. As this tremor typically affects one area of the body first, and to a greater extent than in other areas (i.e. one foot or hand on one side of the body primarily, just the jaw, one cheek exclusively, etc.) it is often regarded early on as more of an annoyance than a condition requiring care.

This tendency for a primary area of affect in tremors becomes an important consideration during DBS planning. In most instances, Parkinson's induced tremors act in a suspicious and consistent manner, which to those aware, call attention to themselves by a tendency to increase during periods of muscular relaxation, hence the term resting tremors.

Rigidity is the inflexibility or stiffness found in most Parkinson's sufferers and is a result of increased muscle tension or tone. For most of us, when our muscles are in movement they possess the ability to stretch and flex, and when not in movement they assume a relaxed state. Not so with Parkinson's. Underlying muscle tension remains present even during periods of rest, leading to increased levels of pain, fatigue, and cramping. This muscular stiffness can be seen in many sufferers when they walk. Note, for example, a tendency to hold the arms still or even partially bent. The absence of arm swings during walking, as well as other observable decreases in range of motion, can give health providers a suspicion of the presence of this disease.

Bradykinesia is the slow movements observed with Parkinson's underlie many of the more commonly discussed symptoms found in individuals with this disease. Bradykinesia leads to festination, the short shuffling steps associated with the pattern of sudden movement stops observed in latter stages of the disease. Combined with the muscular rigidity mentioned above, bradykinesia creates the wax-mask facial appearance that results from an extreme decrease, or even absence, of movement in the muscles which gives us facial expressions. The slowness of muscle response time also contributes to the instability in balance and coordination, difficulties in swallowing and speaking, and the tendency to freeze or stop motion in the middle of a sequence of movements, all symptoms associated with this disease.

Secondary Symptoms

Other symptoms found with Parkinson's disease that manifest in a less consistent fashion are differentiated by using the term secondary symptoms. These include such things as:

  • The tendency towards depression (secondary to neurochemical imbalance)
  • Increase in number of involuntary movements
  • Speech softness or slurring
  • Stooped posture
  • Forward leaning
  • Sialorrhea (drooling)
  • Changes in alertness, memory, or mood
  • Confusion
  • Presence of compulsive behaviors new to that person

As Parkinson's is a progressive disease, additional symptoms can be expected to appear during the course of the disease, and symptoms already present can be seen to intensify. Use of invasive treatments, which include DBS, are rarely considered in the early stages of the disease process. However, once quality of life begins to be seriously compromised, procedures such as these offer options that may provide great benefit.

With Parkinson's, as with all neurodegenerative conditions, early recognition coupled with implementation of treatment aimed at slowing disease progression plays a critical role.

Diagnostic

No specific tests exist for Parkinson's disease. It is, therefore, important to eliminate other possible causes for the symptoms being observed. At the same time, the clinician must use his or her experience with patients to recognize the pattern of symptoms normally demonstrated in the Parkinson’s patient.

An essential part of diagnosis, as well as areas focused on during consideration for the use of DBS, is the presence of the Cardinal Signs of Parkinson's. For diagnostic purposes, two of these three primary symptoms must be present:

  • Tremor
  • Rigidity
  • Bradykinesia

The absence of definitive laboratory testing for Parkinson's increases the need for good clinical judgment in diagnosis, and an essential part of that is the use of laboratory studies to exclude other disease processes. Some of the most frequently ordered lab studies in this process include:

  • CBC
  • Chemistries
  • Liver Function Studies
  • Thyroid Function Studies
  • 24-Hour Urine Copper Study
  • Serum Ceruloplasmin (screening for Wilson Disease)

Imaging studies also play an essential role in narrowing the diagnostic possibilities. This includes brain imaging by means of:

  • MRI
  • CT
  • PET

Results from imaging studies should be negative to allow diagnosis by exclusion from other possible causes of the symptoms observed.

Non-Invasive Treatment of Parkinson’s

Before DBS is seriously considered, less invasive treatments appropriate to that individual should be attempted. These fall within the loose groupings of therapy-oriented treatment, and pharmacological interventions. It is generally held that the best results are obtained with a treatment regimen that utilizes both of these approaches.

Therapies

The rationale that motivates therapy in the Parkinson's sufferer is, perhaps, best attributed to the famous naturalist, Lamarck. A loosely translated quote from Lamarck’s 1801 summation on the way things work is “Use it or Lose it” While Lamarckian theories were most definitely not presented with Parkinson's in mind, the underlying mantra of using abilities in order to retain function, or at least slow the pace of loss, drives many of the interventions we use today.

Occupational Therapies

The need to maximize coordination of the fine motor skills is integral to coping with environmental challenges brought about by stiffness and tremors. By decreasing the amount of energy used during tasks, and maintaining the ability to complete the activities that are part of daily living, Parkinson’s sufferers can function better, and feel better about their ability to function. Interventions include, but are certainly not limited to:

  • Assistance in driving or the use of alternative transportation
  • Adapting existing utensils, articles used in hygiene, or other household items
  • Orthoses or adaptive equipment to assist grasp, grip, or stride
  • Modification of workplace or home environments which may include removing obstacles and increasing accessibility

Physical Therapies

Improvement in balance, coordination, and activity levels does wonders for the individual coping with the changes forced on them by the symptoms of rigidity, bradykinesia, and uncertain gait. To achieve benefit, only the imagination limits health practitioners in arriving at individualized care packages. Some physical therapies to apply are:

  • Exercise that is enjoyable such as golf, dancing, swimming, walks
  • Balance and mobility aids such as stretching, use of exaggerated or patterned movements
  • Range of Motion therapies focused on halting or limiting the postural and motion limitations so common with stiffening, muscle tensions, and joint compromise
  • Practice and training in mobility tasks common to daily living such as walking, or transfer techniques

Swallowing and Speech Therapies

Practice and training are important to offset abilities often diminished during the progression of Parkinson's disease. The tendency toward hypophonia, or low voice volume, is a common accompaniment to this disease. Training programs can be specifically tailored to each person, and many variants are already available for use for those with differing degrees of need. Speech/swallowing therapy can be of great help with such difficulties as:

  • Hypophonia, low voice volume from lessened control over the muscles needed for speech along with chest rigidity
  • Difficulty enunciating clearly
  • Sialorrhea (drooling), an effect secondary to reduced swallowing, not increased saliva production
  • Increasing difficulty with chewing and swallowing

Nutritional Therapies

Quality nutrition is one of the greatest aids during the fight to regain or maintain health. Unfortunately, it is often one of the last ones considered during the treatment of Parkinson's. The following are nutritional therapies to consider.

  • Supplementation of essential dietary nutrients such as the Omega-3 fatty acids, water soluble vitamins, minerals, antioxidants
  • Bowel regimens that decrease constipation – increasing oral fluids, good quality fruits and vegetables, increased fiber intake
  • Mechanical adaptation of food or fluid properties and textures to adjust to changes in swallowing or chewing abilities
  • Maintaining meal appeal to offset the weight loss often accompanying Parkinson's progression

Medications

Pharmacologic treatment of Parkinson's disease can often be decreased following implantation of a DBS device. The use of medication remains important both before and after the more invasive treatment options as such procedures tend to decrease symptoms of the disease without affecting the underlying disease itself.

Medications used for and with Parkinson's are an extensive subject. As many, even most, of the clients considering DBS are on high doses of multiple agents; we will quickly address the high points.

Dopaminergic Agents

Levodopa is a type of amino acid that can be converted in the brain to dopamine, the neurotransmitter involved with movement that is lost as the substantia nigra tissues are destroyed in the course of Parkinson's. Though among the oldest (1960s) of the Parkinson pharmaceuticals, it is still considered to be the most effective pharmacologic treatment that is available for the control of muscle symptoms associated with this disease. Difficulties with absorption combined with side effects from increased systemic levels of dopamine (nausea, vomiting, orthostatic hypotension) limit its use in some individuals. CNS adverse effects (extreme dizziness, paranoia, hallucinations, twitching, shaking) tend to increase as progression of the disease forces administration of doses into higher and higher ranges.

Dopamine agonists are able to mimic some of the effects obtained from Levodopa by directly interacting with the chemical receptors used by the neurotransmitter dopamine. In general, they tend to be less effective than Levodopa, yet provide a valuable alternative as they possess decreased, though still significant side effects. Several types of these agonists are currently in use, offering options regarding duration of action and side effect profiles.

  • Pergolide (Permax®)
  • Pramipexole (Mirapex®)
  • Apomorphine (Apokyn®)
  • Bromocriptine (Parlodel®)
  • Ropinirole (Requip®)

MAO-B Inhibitors

These agents, MAO-B Inhibitors, have the ability to slow the breakdown of the dopamine that is still being produced by the effected persons system. This is a helpful means of decreasing symptoms and, perhaps, may even (trials are not yet clear) slow the progression of Parkinson's disease itself. Unfortunately, effectiveness is limited to the early stages of the disease, so clients considering the use of DBS tend to be past the stage of disease that could have benefited from MAO-B agents.

  • Selegiline (Eldepryl®)
  • Rasagiline

COMT Inhibitors

By prolonging the effect of Levodopa, COMT Inhibitors aid to keep the dosage and side effects at a lower level for a longer period of time in the course of Parkinson's disease. The potential for liver disease and severe diarrhea limit use in some individuals. Even with the ability of COMT Inhibitors to lengthen usefulness of Levodopa treatments, the continuing progression of the underlying neurodegeneration limits the length of effective treatment for many of those who suffer from Parkinson's.

  • Entacapone (Comtan®)
  • Tolcapone (Tasmar®)

Amantadine

This agent provides mild relief from the dyskinesias and motor symptoms associated with Parkinson's for many sufferers. Insomnia, agitation, hallucinations, and some cognitive impairment may occur during use, and up to one-third of those suffering from Parkinson's find it to have little or no benefit in controlling disease symptoms.

  • Amantadine (Symmetrel®)

Anticholinergics

Extensive use of anticholinergic medication is made during the course of Parkinson's disease in an effort to control the effects of the rigidity and tremors found with the disease. Most healthcare providers have experienced the frustration that comes with lessening response to these medications due to disease progression, and it is almost a given that persons seeking relief from symptoms with more invasive procedures, such as DBS, will have a medication history that includes one or more of these agents.

  • Trihexyphenidyl (Artane®)
  • Ethopropazine
  • Benztropine

Invasive Procedures for Parkinson’s

Treating what we once referred to as treatment resistant Parkinson's disease calls for new strategies. We now have that option in the form of invasive procedures aimed at minimizing or mitigating a number of the major symptoms that lead to a reduction in the quality of life.

Pallidotomy

The late 1990s saw a swing away from Pallidotomy, which was until that time the most common invasive procedure for treatment resistant Parkinson's. Though still in use and still effective, the irreversible destruction of portions of the globus pallidus, an area of the brain involved with movement, is leading many of those seeking treatment to consider DBS as a more appealing choice.

In Pallidotomy, a wire probe and radio waves are used to heat surrounding tissue in a carefully controlled reduction of the globus pallidus. The reduction of tissue in this area of the brain serves to greatly decrease the symptoms of dystonia and dyskinesias with an immediate result often observed. Gain is also commonly seen in the areas of rigidity, bradykinesia, and tremor.

One side of the brain (unilateral) or both sides (bilateral) may be the targets for this procedure. Often the unilateral procedure is preferred, as bilateral pallidotomy possesses an increased risk of adverse symptoms affecting cognition, speech, and swallowing. As Parkinson’s disease most frequently affects one side or region of the body more intensely, unilateral pallidotomy is performed on the side of the brain opposite the side of the body targeted for greatest effect.

Hemorrhage, weakness, confusion, speech, and visual deficits are the primary risks associated with pallidotomy, and weight gain is very common (and often desired due to Parkinson's weight loss symptoms) following this invasive procedure.

The underlying disease process is still present. Therefore, clients should anticipate a need to continue both medication and therapy, though often at a significant reduction in medication dosages.

Thalamotomy

The destruction of selected portions of the thalamus has proven very successful for those individuals whose primary symptom is that of tremors. This is due to the role that the thalamus, a structure located deep within the brain, contributes to the control of movements.

Unilateral thalamotomy is again preferred to bilateral due to increasing risk of adverse results, such as speech and visual problems. The process is similar to pallidotomy, and like pallidotomy, thalamotomy is slowly being replaced by DBS, as DBS has shown benefit for the symptoms of not only tremor, but also many other movement related difficulties associated with Parkinson's disease as well, without the need to permanently damage or destroy brain tissues.

Deep Brain Stimulation

DBS is a form of brain surgery. It is an invasive, surgical procedure that is used to treat a variety of neurological symptoms, primarily those that possess muscular components. In Parkinson's disease, the most debilitating symptoms are typically motion related, such as tremor, stiffness, rigidity, slowed movement, gait, or posture problems. This procedure has also found good use in treating the common neurological/movement disorder known as Essential Tremor. At this time, DBS is used primarily for persons with symptoms that both severely decrease quality of life and whose symptoms resist adequate control using medications and therapies.

When considering DBS it is important to determine the amount of benefit that the person might obtain. Experience has shown that in individuals suffering from Parkinson's, the most benefit is gained by:

  • Those persons whose symptoms are partially controlled yet who continue to experience severe motor fluctuations despite trials with differing dosages or combinations of medications (i.e. breakthrough dyskinesia – dystonia – tremor)
  • Those who continue to exhibit motor symptoms that can not be controlled by less invasive means

DBS is not an experimental treatment. In August of 1997 the Food and Drug Administration (FDA) approved DBS for use in the treatment of tremor. Since that time the approved uses have continued to expand as benefit has been seen in many of the movement disorders, including one of the most difficult to treat (FDA approval, 2003), primary dystonia (HHS News, 1997) (FDA Talk, 2003).

The treatment process involves introducing stimulating electric impulses into sensitive motor control areas of the brain through a carefully implanted electrode. In the following section we will take a closer look at the use of this exciting treatment option that is specific for the most difficult to manage symptoms of Parkinson's disease.

DBS works to disrupt abnormal or unwanted motor impulses by means of exciting portions of the brain and has found successful application in three separate brain structures. These are the motor thalamus, the subthalamus, and the globus pallidus, all of which are structures in the brain which affect the control of movement in such a manner as to produce symptoms associated with Parkinson's, such as dystonia and dyskinesia.

More benefit is gained from DBS in the relief of motor symptoms than in those that are primarily non-motor. Particular symptoms improved with use of DBS (in descending rank regarding degree of benefit) according to Dr. Andres M. Lozano, M.D., Ph.D. from the University of Toronto, as recorded in the minutes from the June 2002 Deep Brain Stimulation Consortium Meeting sponsored by the National Institute of Neurological Disorders and Stroke with the National Institute of Aging, are:

  • Levodopa-induced dyskinesias
  • Tremor
  • Rigidity
  • Akinesia
  • Gait and Postural disturbance

While DBS has been shown to be effective in decreasing, and to some extent controlling, motor symptoms in Parkinson's disease, it is not a cure for the disease itself. When used in treatment of other movement disorders, especially Essential Tremor, DBS often shows a dramatic and even instantaneous effect. As tremulousness is the only, and in severe instances disabling, symptom found with Essential Tremor, the use of DBS can produce such a significant degree of relief that many of those treated refer (erroneously) to DBS as a cure.

Although most patients will still need to take medication after undergoing DBS, many patients experience considerable reduction of their movement related symptoms and the amounts of medications can, at times, be greatly reduced.

Looking Inside DBS

The Process

DBS uses a surgically implanted, battery-operated device known as a neurostimulator, or impulse generator (IPG). This device is very similar to the common cardiac pacemaker and is approximately the size of a pocket watch. The neurostimulator is capable of delivering small electrical jolts which serve to stimulate specifically chosen areas within the brain that are responsible for movement. The process of stimulation serves to block the extraneous or abnormal nerve impulses responsible for motor symptoms, such as tremor, in both Essential Tremor and Parkinson's, as well as other motor symptoms stemming from a neurological source.

DBS systems possess three main components. What is referred to as the lead, the extension, and, the neurostimulator. The Lead is a thin insulated wire that is inserted through a small opening in the skull and delicately manipulated into position in a carefully chosen target area of the brain. The Extension is another insulated wire which is maneuvered under the skin of the head, neck, and shoulder. This connecting wire completes a circuit between the lead and the neurostimulator. The Neurostimulator contains both battery and control mechanism and is the final component and may be situated beneath the skin in the chest, abdomen, or even under the skin near the collarbone.

Once placed, these three components form a system allowing electrical impulses from the neurostimulator to travel along the extension wire, to the lead, and from there into the specific target tissue within the brain.

Pre-Procedure Evaluation

Thorough review of symptoms and treatment history must take place before the procedure can occur. When it is determined that the patient may benefit from DBS, the neurosurgeon called on to perform the implantation procedure will use magnetic resonance imaging (MRI) or computed tomography (CT) scanning in order to pinpoint the exact tissues within the brain responsible for the electrical nerve signals that are generating the most problematic symptoms.

In most instances the abnormal motor signals being tracked have a primary source in one (occasionally more) of the following areas:

  • The thalamus
  • Subthalamic nucleus
  • Globus pallidus

One of the exciting things about DBS is that the procedure does not destroy healthy brain tissue. This allows changes to be made in treatment, as the neurostimulator is easily adjustable, and even means that the device can be removed should that be desired.

A neurologist, who will be present alongside the neurosurgeon during implantation of the DBS devise, will perform a detailed cognitive assessment prior to the operation. The assessment allows changes in mentation, cognition, and how that individual responds to his or her environment to be compared in a prior, intra, and post procedure context.

Patient Preparation

DBS placement is a While Awake procedure. This means that it is a surgery in which the person being operated on is not only conscious, they are also expected to assist by taking on an active role throughout the proceedings. This also means that preparation of both patient and family must include extensive counseling and the opportunity to verbally process what is planned during each step of the procedure.

Frequently, the procedure is broken into segments, in part due to the length of the procedure, which is typically around six hours. During the placement segment the patient is awake and actively participating. This is when the implanted electrode, or lead, is maneuvered to the area of best benefit. After lead placement is completed, a light general anesthesia is often used to aid in relaxation during the placement of the subdermal extension and the implantation of the neurostimulator unit. As with all general anesthesia surgical procedures the patient is advised to have no food or drink from twelve hours before the scheduled start. Due to the type and amounts of medication being taken by those with severe Parkinson's symptoms, an individualized schedule must be designed for weaning down, or even off agents that could interfere with the ability to determine the actions and reactions that must be assessed during DBS placement. When significant amounts of medications are to be stopped it is a common practice to admit the patient for careful monitoring at least one day prior to surgery, as rebound effects of discontinuing medication may lead to hypertensive crisis or other undesired effects.

During placement of the lead, the patient will be asked to respond to requests involving movement, memory, and how they are feeling at that specific instant. Due to the impairing effects of Parkinson's symptoms it is necessary to know what that individual is able to do immediately before the procedure. By being aware, sudden changes can be quickly recognized.

Being able to respond to movement commands is especially important, as even though the surgeon will be using real-time imaging techniques, such as fluoroscopy, a better placement of the lead can be gained with active feedback from the patient themselves.

There is an expectation that the person undertaking DBS placement will cut short or even shave off all, or a portion of the hair on their head. Please inform your patient early during discussions of this expectation, just in case an extra bit of processing time is needed.

Procedure

For the person undergoing DBS placement the day starts by, as one person put it, “Having nails screwed into my head!” This is the placement of a stabilization tool known as a stereotactic frame, though typically you will hear it referred to as a halo, due to the encircling appearance it gives. The frame is held in place to the skull using a pair of pins above and slightly to the outside of each eyebrow, with a second pair of pins placed in an oppositional position at the back-sides of the head. The stereotactic frame serves to immobilize the head for the surgeon, and acts as a positional reference by which longitude and latitude within the brain can be determined with consistent accuracy. Local anesthesia is used during the placement of the frame, and if necessary, a light sedation can be administered.

Stereotactic frame fixation is followed by a pre-procedure MRI or CT scan, the results of which are kept present for reference throughout the procedure. For the electrode placement portion of the procedure, the patient is placed in a reclining position, rather like someone leaning back in a recliner to watch television. Once a comfortable position is achieved, the head is firmly immobilized using the stereotactic frame and a light, fast-acting anesthetic is typically administered to achieve sedation. Skin prep is followed by carefully measured markings being placed on the scalp in accordance with the targeted tissue that has been selected using the scan results which are kept close at hand. Adjustments of equipment placement in order to utilize real time radiological scanning (fluoroscopy) are then made to complete the pre-incision preparation. Local anesthesia, a small incision (typically less than one inch long) and the drilling of a small hole (referred to as a burr) allow access to the brain beneath.

Somewhat contrary to logic, very little in the way of sensation, especially of pain, can be felt when the tissue of the brain itself is being manipulated. Therefore, after achieving access to the tissues beneath the skull, sedation is reduced, enabling the patient to rouse and take the active participation needed to gauge reaction and response.

Speech, memory, and motion abilities are all carefully assessed and recorded by the neurologist, who will remain present throughout the lead insertion. Baseline measurements precede lead insertion with the patient being asked to do such tasks as:

  • State their name
  • Count to one-hundred
  • Draw a picture
  • Drink from a glass of water
  • Count backwards from one-hundred

When used, microelectrode recordings are also taken to establish pre-procedure levels. Some practitioners find microelectrode measurements helpful in determining when the tip of the electrode has found the area of greatest nerve activity. Regardless of the decision to use microelectrode recordings or not, the best determination of success is the impact that carefully generated pulses from the neurostimulator has on the patient themselves.

After baselines are taken, the electrode, which will serve as the lead for the neurostimulator, is carefully advanced using the positional coordinates determined earlier. Frequent pauses are taken to see the current position via fluoroscopy, and assess patient reaction and response. As the lead nears its targeted resting place the neurostimulation unit (not yet implanted in the patient's torso) is powered up to determine response to electrical stimulation at current locations of the lead.

During the final positioning it is common for the Parkinson's sufferers to experience significant tremors, at times with movement arcs of five or more inches. The introduction of electrical pulses from the neurostimulator often demonstrates an instant cessation, or great reduction, in these tremors.

Despite considerable excitement on the part of the patient, great patience is an asset as the best results are sought before final placement of the lead. This means questions, answers, tasks, and trials. Understandably, most patients are at this point happy to comply. Once final placement is established, the lead is carefully anchored in the brain. The distal (surface) end is also secured exterior to the skull, and tucked into a pouch formed underneath the skin of the scalp.

At this point, a general anesthesia is administered to ensure patient comfort, while the wire that will form the extension is tunneled beneath the tissue of neck and torso, and the neurostimulator unit itself is implanted using techniques pioneered for cardiac pacemakers.

Recovery

The experiences of patients immediately post DBS implantation differs according to individual factors and neurosurgeon preferences. Some practitioners prefer to utilize traditional post anesthesia recovery, which also allows an interval for CNS settling before turning on the new impulse generator. Other practitioners or situations may call for an extensive period of post procedural stabilization that takes into account the time needed for swelling, irritation, and potential tissue inflammation to resolve. This means that the wait before start-up may stretch out for up to two weeks before active neurostimulation begins.

As with all spectrums, some situations warrant a different path for recovery, occasionally even allowing patients to rouse from anesthesia in the surgery suite with the neurostimulator functioning, and even walk, with assistance, into a post anesthesia recovery setting using their own, newly regained, abilities.

Whether or not active use of the stimulation device begins immediately post implant, some clients exhibit a period of respite in their motor symptoms post electrode implantation. Why this decrease in motor symptoms sometimes occurs is not yet known. Many clinicians speculate that irritation to the over-active neurons of the target area during the physical placement of the lead and the subsequent intra-operative testing of the stimulus generation unit may cause a transient diminishment in aberrant motor impulses.

Whatever the particular needs or practitioner preferences may call for, the excitement runs high during this time in both patient and family. It is important to help ensure that conditions remain safe, as a long, physically exhausting procedure has just occurred. Reminders that motions, movements, and abilities will need time to re-train and adjust to the sudden changes must be stressed, as should reminders that medications to help control residual symptoms are an important part of the total care needed to combat progression of the disease.

Frequent reminders may also be needed that the procedure is not yet finished! With the neurostimulator now implanted the delicate task of determining the correct settings for the best stimulation results are yet to be concluded.

Programming

Despite all that has led up to this point, the job remains only partially complete. Now begins the taxing task of determining neurostimulator programming. The exact sequence of pulsations, pulse rates, intervals between pulses, and voltage levels needed all require managing and will be unique to each person. It is, therefore, acknowledged that when it comes to the intricate task of programming the impulse generator for best response, this, like many things is life, will require a great deal of trial and error.

It is also important to be aware that settings producing good results immediately after implantation will not be those that produce the best results later. The very act of inserting the electrode lead into the brain tissue (i.e. inducing a micro-lesion) has been found to create changes within tissue responsiveness. This means that once tissue stabilization occurs, transmitter settings may require adjusting down, up, or being completely recalibrated.

Informing both patient and family in advance to expect the need for setting adjustments will reduce anxiety all around.

Insertion and post surgical wound care will be managed by the neurosurgeon. It is the neurologist, however, who adds their expertise to managing neurostimulator adjustments.

Once implanted, the neurostimulator settings can be adjusted with the use of a special computer able to send radio impulses to the device. Special magnets are also available which can be held over the site to turn the device off or on. Both computer and magnets are able to function through clothing, and adjusting the settings often takes place while sitting comfortably in the office of the neurologist. Training in the use of the magnet is provided to patient and family, and magnets are sent home with them to allow control in the event of adverse effects.

Complications

The implantation procedure has shown a two to three percent risk for a serious and permanent complication occurring, such as changes in thinking, memory, personality, a new onset or increase in the level of seizures, voice or hearing impairment, and of course, the ever present risks whenever brain tissue is manipulated, of paralysis or infection (Haines, 2005).

Once in place, adverse events such as the stimulation not being effective, migration of the electrode lead, lead fracture, and even shocks or jolts occurring from the control unit have occasionally been reported. There is also a risk of worsening the symptoms already present from the disease process, such as an increase in the level of cognitive difficulties, dyskinesia, dystonia, or speech disorders. Complications associated with any invasive procedure to the brain could include infection, intracranial hemorrhage, headaches, or seizures.

Unwanted interference with the function of the device could also occur, such as electromagnetic interference. The possibility of an undesired effect from external sources warrants ready availability of the supplied magnet, as items or events, including the following, can interfere with proper neurostimulator functioning.

  • Airport screening devices
  • Theft detectors (such as used in shops or stores)
  • Strong magnetic latches (such as some refrigerator doors utilize)

Follow-Up

Appointments to fine tune neurostimulator settings can be expected to be, at least, monthly during the first six months of use. Once the correct adjustments are made, allowing for the best results, following up becomes more of an as needed process with regular checkups being set in accordance with individual patient and health provider desires.

Active therapies focusing on retaining or regaining muscular ability and function should continue, as should medication titration for the relief of symptoms not controlled by use of DBS. Be aware that the disease itself remains active. DBS acts to decrease symptoms only. Patient participation with and between the practitioners working to manage the underlying disease will continue to be essential.

 

Summary

DBS is an effective form of symptom control for many individuals beset by muscular difficulties originating from a neurological disease process. In Parkinson's disease, and especially in those with severe Essential Tremor, clients have shown great benefit from the application of controlled electric impulses directly focused into the deep tissues of the brain where erratic, unfocused motor commands originate.

DBS is not experimental. It is a well-researched, highly-favored treatment option that is available worldwide. Due to the invasiveness of physically implanting an electrode into the tissues of the brain, DBS is currently reserved for those who no longer receive adequate control of their symptoms using medication and therapeutic techniques. Both medication and therapies, therefore, play an important role in the overall treatment of the person considering DBS.

While results from DBS can be dramatic and at times appear instantaneous, DBS only effects symptoms and is not a cure. The underlying disease process remains present and in need of medical control. An awareness and ability to work with patients being treated by DBS is, therefore, a must for every health practitioner. Working together, using all of our skills and resources, we can greatly increase the quality of life for those who seek our care.

References

2002 Deep Brain Stimulation Consortium Meeting. Co-sponsored by the National Institute of Neurological Disorders and Stroke with the National Institute of Aging. June 2002 in Rockville, MD. Accessed on July 6, 2006 at http://accessible.ninds.nih.gov/news_and_events/proceedings/deep_brain_stimulation_2002.htm

FDA Talk Paper. (April 16, 2003). “FDA Grants Expanded Use of Brain Implant for Movement Disorder." U.S. Food and Drug Administration." Accessed on August 14, 2006 at http://www.fda.gov/bbs/topics/ANSWERS/2003/ANS01212.html.

Haines, C. ed. (June 2005). "Parkinson's Disease: Deep Brain Stimulation." Web MD in collaboration with The Cleveland Clinic. Accessed on August 1, 2006 at http://www.webmd.com/content/article/46/1833_50743.htm.

Hauser R., & Pahwa R. (June 8, 2006). “Parkinson's Disease.” eMedicine. Accessed August 2, 2006 at http://www.emedicine.com/neuro/topic304.htm.

HHS News. (August 4, 1997). "FDA Approves Implanted Brain Stimulator to Control Tremors." U.S. Department of Health and Human Services. Accessed on August 14, 2006 at http://www.fda.gov/bbs/topics/NEWS/NEW00580.html.

Song, S. (July 16, 2006). "How Deep Brain Stimulation Works." Time Magazine. Accessed July 18, 2006 from http://www.time.com/time/magazine/article/0,9171,1214939,00.html.

Sweeney, P. (January 19, 2005). “Parkinson’s Disease an Overview.” The Cleveland Clinic. Accessed on June 28th, 2006 at http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/neurology/parkinsons-disease/.