This Web Site was created by Dr. Christopher Honey and is designed to provide information about the Stereotactic Neurosurgical operations available at U.B.C. It also provides information on our Fellowship Training Programme and Research activities. Patients must review these procedures with their neurosurgeon because the outcome and complications can vary between patients and institutions.
Members of the Surgical Centre for Movement Disorders: (left to right) Dr. Ahmed Abdel Rahmen (research Fellow), Nicoline Rickard (Clinical Secretary), Mini Sandhu (DBS Clinic Nurse), Dr. Volker Coenen (Clinical Fellow), Dr. Fernando Castro (Clinical Fellow), Dr Charles Dong (Neurophysiologist), Dr. Christopher Honey (Neurosurgeon).
Dr. Honey is Associate Professor of Neurosurgery at the University of British Columbia and Director of Research for the Division of Neurosurgery. He was the President of the Canadian Section of Stereotactic & Functional Neurosurgery for its first seven years. He is on the Board of the World Society of Stereotactic & Functional Neurosurgery and on the Board of the American Societry of Stereotactic & Functional Neurosurgery.
Patient Information
Parkinson's Disease
This information is designed only to help patients
talk with their physicians about Parkinson’s disease (PD) and is not intended
to provide treatment guidelines. Some
peer-reviewed medical papers on the surgery for Parkinson’s Disease are provide
below for background information:
1. Honey CR, Gross, R, Lozano
A. New developments in the surgery for
Parkinson’s Disease. Canadian Journal of Neurological Sciences (1999)
26: Suppl. 2:45-52.
Click on "Download Paper" to get a pdf file of this paper. You can read it if you have Acrobat Reader (goto www.adobe.com to get Reader)
2. Honey CR and Palur RS. Surgery for Parkinson’s Disease. British Columbia Medical Journal (2001) 4:210-213.
Click on the "May" issue of the BCMJ below and then click on the "Surgery for Parkinson's disease" article we wrote in order to get a copy of this paper.
The April and May issues of the BCMJ in 2001 were devoted to Parkinson's Disease. Excerpts from the article we wrote about the surgery for Parkinson's Disease are reprinted below with permission from the Editor.
SURGERY FOR PARKINSON’S DISEASE
A select group of patients with Parkinson’s Disease and symptoms refractory to medication can benefit tremendously from surgery.
Introduction
1. which patients can benefit from surgery
2. the benefit and risk of those surgeriesA word of caution: the benefits and risks of surgery vary with the individual patient and with the centre where the procedure is being performed. Success comes only when the correct patient receives an operation done correctly. Failure follows both the incorrect patient receiving a flawless operation and the ideal patient receiving a flawed operation.
We have found that patients will appreciate the outcome of their operation if their expectations are met. That seems an obvious statement but the goal of the patient and the goal of the (less experienced) surgeon are often different! The patient wants an improvement in their quality of life. The surgeon can only provide an improvement in a specific symptom. Whether a reduction in a specific symptom leads to an improvement in quality of life depends on a great many factors. The ability to make that prediction (“if that symptom is reduced your life will be better”) is the art of medicine. The ability to perform the operation without error is the science of medicine. I have found that most neurosurgeons can perform an operation safely after exposure to about 30 cases (observing and then participating with supervision). I still occasional struggle with the decision for surgery after 300 cases. The art is harder than the science.
Which Patients Benefit from Surgery
There are three symptoms that can be dramatically improved with surgery: tremor, dyskinesia and motor fluctuations. If a patient is suffering from one of those symptoms then alleviating that symptom will improve their quality of life. Tremor is the easiest symptom to understand. It is a rhythmic shaking of the arm (or the leg or jaw) and is a hallmark of Parkinson’s disease. Tremor usually occurs when medications are low, i.e. towards the end of a dose. The tremor in PD is a ‘resting’ tremor – occurring more when the arm is at rest then when moving. If tremor is controlled by medications then surgery is unnecessary. When tremor is not controlled by medications it will begin to interfere with the patient’s quality of life. Initially the tremor is an irritation or embarrassment. If the tremor worsens it will begin to interfere with eating (as well as writing, hobbies, dressing, and cleaning). Once tremor interferes with eating and drinking, patients often feel that their quality of life has been reduced too much and begin to consider surgery. The degree of impairment before an individual considers surgery varies dramatically. It is a personal choice. The same degree of tremor will be considered intolerable by the teacher who must write legibly on the blackboard but considered a minimal nuisance to the retired pensioner.
The surgery for tremor is described below under thalamotomy or thalamic deep brain stimulation. Each operation has its own set of benefits and risks although both can be expected to reduce tremor about 80%.
The second symptom effectively treated by surgery is dyskinesia. Dyskinesia is a side effect of PD medications. It is an uncontrolled excess of movements throughout the body that looks like wiggling, dancing or writhing. Dyskinesia will stop if the medications are stopped (or more commonly just reduced). Unfortunately, when the medications are reduced the other symptoms of PD will worsen – slowness or bradykinesia for example. Some patients are therefore stuck between a metaphorical rock and a hard place: reducing medications helps dyskinesia but makes bradykinesia worse, while increasing medications helps bradykinesia and worsens dyskinesia. If all medication adjustments have failed to provide adequate quality of life then surgery can be considered. Mild dyskinesia is often unnoticed by the patient but will usually be recognized by their partner as wiggling of their hands or neck. More moderate dyskinesia will tend to pull the arm behind the back while walking and severe dyskinesia can produce violent, ballistic movements that can throw the patient off balance or injury bystanders. Any dyskinesia of an arthritic limb will be painful and the constant movement associated with dyskinesia can cause weight loss.
The surgery for dyskinesia is described below under pallidotomy or pallidal deep brain stimulation. Each operation has its own set of benefits and risks although both can be expected to reduce dyskinesia about 90%.
The third symptom of PD that can be dramatically helped with surgery is ‘motor fluctuation’. Motor fluctuation is a term used to describe a condition of advanced Parkinsonism where the patient’s ability to move fluctuates during the day. They typically wake up stiff (we call this ‘rigid’) and slow (we call this ‘bradykinetic’) because they have not had their PD meds overnight. They are “off” – a term we use to describe the state of low medications when patients are rigid, bradykinetic, off balance, stooped in posture and sometimes tremulous. After taking their PD meds (and waiting a variable time for the meds to work) they feel their rigidity melt away and are able to move more normally. Their meds have started to work and they are “on”. At this time, movement is good, balance is fine and they are able to do what they want. As long as the patient is “on” their quality of life is good. Sometimes the medications are too strong and they develop dyskinesia. Unfortunately the meds wear off and the patient slips back into an “off” state. They take another set of medications (usually every 3 hours) and the cycle repeats. They are fluctuating between “on” and “off”. The surgery for motor fluctuation is described below under subthalamic nucleus deep brain stimulation.
The benefits and risks of surgery
Once again, it is very important to know that the benefits and risks of surgery vary tremendously between individual patients and between surgeons. Patients should talk to their surgeons to understand their own personal risks and the success rate (or complication rate) of their own surgeon.
Thalamotomy
The thalamotomy procedure is designed to reduce tremor on the opposite side of the body (i.e. a left thalamotomy reduces tremor in the right hand). If you have ‘tremor dominant’ Parkinson’s disease, then this operation may be ideal. Tremor dominant Parkinson’s disease is a subtype of PD where patients have minimal problems with bradykinesia or rigidity but major problems with tremor. This tremor is interfering with their quality of life and is not controlled by medications.
Download PamphletClick on "Download Pamphlet" to get a pdf file of instructions for our patients having thalamotomy surgery at VGH. You can read it if you have Acrobat Reader (goto www.adobe.com to get Reader)
The results of placing a lesion in the thalamus, or thalamotomy, were first published by Hassler in 1954. Throughout the 1960’s different thalamic targets were lesioned until the ventral intermediate (VIM) nucleus emerged as the most effective target for tremor reduction. Currently, the expectations following thalamotomy is that your tremor (on the opposite side of the body) will be reduced about 80%. We are aiming for the arm – since that will provide the most improvement in quality of life – but leg tremor will also be reduced. Head, jaw and body tremor will not be eliminated after a unilateral procedure since the other side of the body will not be affected. Thalamotomy does not benefit bradykinesia or rigidity. Patients with PD who symptoms of bradykinesia and rigidity are progressing might want to consider STN-DBS instead of thalamotomy since that operation may control bradykinesia and tremor (especially if the tremor responded to medications).
The risks of thalamotomy include but are not limited to contralateral weakness, arm and foot incoordination, difficulty speaking or swallowing and cognitive decline.
Pallidotomy
Before the advent of l-dopa, there was little treatment for PD. Clinicians had recognized that PD patients who developed a stroke in the basal ganglia stroke occasionally had improvements in their Parkinsonian symptoms. Neurosurgeons therefore attempted to induce basal ganglia strokes in PD patients. The results were unpredictable and complications were frequent and severe. Initially the pallidum became the favoured target and the operation, designed to make a small hole in it, was called the pallidotomy. Wycis and Spiegel reported that tremor was reduced in 78 percent of PD patients following pallidoansotomy. Reports of reduced tremor and improved rigidity after pallidotomy followed from the United States, Japan and Sweden. Fewer pallidotomies were performed after the introduction of l-dopa in the 1960s and the realization that thalamotomy was better at tremor reduction than pallidotomy. A Swedish report highlighting their results for PD patients following pallidotomy in the posteroventral pallidum (a slightly different target than the previous standard) was published in 1992. This led to a resurgence of interest in pallidotomy. This new found interest was bolstered by animal models which suggested Parkinson-like symptoms in primates were due to overactivity of the pallidum (inhibiting the motor thalamus) and that lesioning the overactive pallidum improved these symptoms. A number of well design prospective studies on the effects of pallidotomy were published in the 1990s. Pallidotomy was a very common operation in the 1990s (we performed over 250 at Vancouver General Hospital) but has been much less common following the introduction of deep brain stimulation.
Pallidotomy is currently performed at VGH for patients with dyskinesia interfering with their quality of life. A left sided pallidotomy would be expected to reduce dyskinesia on the entire right side of their body by approximately 90%. Following pallidotomy, patients remain on their PD medications to help their bradykinesia. In fact, their medications can be increased (to help their bradykinesia) without causing dyskinesia. There is also some improvement in bradykinesia, PD related pain, sleep and some weight gain after pallidotomy. We have only performed unilateral (one side only) pallidotomy because the risk of complication increases dramatically with bilateral (both sides) procedures.
Download PamphletClick on "Download Pamphlet" to get a pdf file of instructions for our patients having paladotomy surgery at VGH. You can read it if you have Acrobat Reader (goto www.adobe.com to get Reader)
The risks of pallidotomy include a rare chance of stroke (approximately 1%) and a rare chance of one sided weakness or visual field defect (reduced vision towards one side). Although these complications may be mild for the general public, they can be devastating for an already compromised patient with Parkinson’s disease. If patients have bilateral symptoms, they should consider deep brain stimulation (which can be done bilaterally).
Deep Brain Stimulation
Deep Brain Stimulation or DBS is the most common operation for PD performed at Vancouver General Hospital. The information below is reprinted with permission from an article we published in New Frontiers April 2002 entitled "Deep Brain Stimulation for Movement Disorders". Before the introduction of DBS, neurosurgeons could only destroy the overactive brain regions responsible for movement disorders. These operations (see thalamotomy and pallidotomy above) are still performed by heating the tip of an electrode and coagulating a very small area of the brain. Deep brain stimulation is designed to “turn off” these overactive brain regions without destroying them. How DBS works is still debated – the original suggestion was that the neurons around the tip of the electrode were blocked from working, others suggested different neurons were activated and more recently some have suggested that the abnormal rhythms of the PD brain are jammed. Regardless of how DBS works, the immediate advantage of DBS over destructive neurosurgery is that the DBS can be adjusted after surgery to best match an individual patient’s symptoms and can always be turned down if side effects are caused. The DBS ‘lesions’ are therefore titratable and hence reversible.
Download PamphletClick on "Download Pamphlet" to get a pdf file of instructions for our patients having Deep Brain Stimulation surgery at VGH. You can read it if you have Acrobat Reader (goto www.adobe.com to get Reader)
The benefit of DBS surgery depends on where the electrode is placed. Thalamic DBS helps tremor, pallidal DBS helps dyskinesia and subthalamic nucleus DBS helps motor fluctuations. Each operation is detailed below.
The major risks of DBS surgery are the same regardless of the target. Approximately 1% of patients will have a stroke that can be potentially devastating or lethal. Approximately 5% of patients will develop an infection. Infections can be treated with antibiotics but occasionally it means removing the DBS device until the infection has cleared and repeating the operation with a new device. When the DBS is turned after surgery, there can be some stimulation induced side effects. These are always reversible (just turn the stimulation down) but approximately 4% of our STN DBS patients develop stimulation induced behavioural changes that can be very upsetting for their family if not warned. These patients can become hypomanic – saying and doing very inappropriate things. We now only perform this surgery in patients who have reliable supporters (family or friends) who will immediately notify us if the patient is behaving inappropriately. The patient themselves may not notice the changes – or worse, they may enjoy them.
The first company to successfully market the deep brain stimulators was Medtronic and they have an extensive website with many pages for patient education.
The Hardware
There are three components to the DBS system (see diagram below). The first is the DBS lead. The tip of this insulated lead has four platinum/iridium electrodes spaced usually 0.5 mm apart. These electrodes are placed within the target brain region and are used to deliver the high frequency stimulation designed to block or disrupt the function of the surrounding brain. An insulated cable, the Extension, is tunneled subcutaneously from the DBS lead to its power source. The implantable neural stimulator (INS) is usually placed in a subcutaneous pocket below the collar bone and provides both the power for stimulation and the ability to use telemetry to control the stimulation parameters. The final size of the ‘lesion’ is adjusted in the outpatient clinic after surgery by changing these stimulation parameters. The DBS effects can then be tailored to the individual’s symptoms: enlarging the ‘lesion’ to increase beneficial effects or reducing its size to avoid a side-effect.
The Surgery
There are two parts to any DBS operation: implantation of the DBS lead within the brain and insertion of the INS. The details of implantation are beyond the scope of this review but any neurosurgical center with stereotactic experience and appropriate training can perform the operation. Patients should ask their neurosurgeon how many procedures they have done and what their complication rate is. Think about having the procedure done somewhere else if the neurosurgeon has performed less than 30 of that specific operation or has a serious complication rate (stroke or death) over 1%.
Implantation of the DBS Lead
At the University of British Columbia, we typically use a MRI compatible head frame (UCLF, Radionics). Frames are placed using local anesthetic and some sedation may be given especially if the patient has tremor. Patients receive pre-operative antibiotics on transfer to the O.R. The hair is shaved over the coronal suture and the scalp prepared, draped and infiltrated with local anesthetic. A 14 mm burr hole is drilled in the skull and the dura opened. The arc system is then attached to the head ring. The brain target area can be localized with either macrostimulation or microelectrode recording. Once the probe has found the target area, it is replaced by the DBS lead under fluoroscopic guidance. The lead is locked in place with a burr hole button and the scalp temporarily closed.
Insertion of the INS
For the last ten years, this portion of the procedure has been performed immediately after implantation of the DBS lead. During insertion of the INS, patients receive a general anesthetic and are asleep the whole time. The Extension is tunneled under the skin from the scalp to the chest. The Extension s then connected to the DBS lead in the scalp and the INS in the chest.
Post-Operative Care
Most patients stay in hospital for two nights after DBS surgery (some prefer to go home after one day). The wounds must be kept dry for 10 days and then the stitches are removed (typically by the family doctor). Strenuous activity (e.g. lifting a heavy suitcase) should be avoided for 6 weeks. If there is a wound infection (pus in wound or gaping open of the wound edge) call us immediately! All wound infections can be cured with antibiotics but we want to stop the infection from reaching the device.
DBS Clinic
The DBS electrode is just a piece of platinum sitting in the brain. It does nothing until the stimulation is turned on. The benefits of DBS depend on using the right amount of stimulation. Too little stimulation will not improve the PD symptoms enough. Too much stimulation will cause unwanted side-effects. Setting the stimulation requires experience and some trial and error. Patients come to the DBS Clinic 6 weeks after surgery to begin their stimulation trials. The DBS is turned on and patients assess the effects or several days and then return for adjustments. The time required to find just the right amount of stimulation varies between patients from just a few visits to several months of adjustments. In the DBS Clinic your DBS will be adjusted by one of the DBS Clinic nurses. The results will be review by the entire team.
The DBS Clinic will also educate you about your DBS. You will learn how to turn it on and off and also how to check that the internal battery within the DBS is still working. Eventually the INS will run out of power and need to be replaced. This requires an operation to replace the INS. This operation is simple and usually done as an outpatient (you do not stay in hospital) with a local anesthetic (you are not asleep). The brain electrodes are not touched during this operation, only the pacemaker in the chest (INS) is switched. Following this operation the wound must be kept dry for 10 days and then the stitches removed.
Brain Targets
The effect of DBS depends on where the electrodes are placed. There are three common target sites for the control of Parkinson’s disease symptoms: the thalamus, the pallidum, and the subthalamic nucleus. Each target site has different indications, effects and potential complications.
The Thalamus (VIM)
Thalamic DBS will reduce tremor regardless of the cause. The most common cause of tremor requiring surgery in British Columbia is a condition called Essential Tremor. Parkinsonian tremor is also common but other causes such as Multiple Sclerosis (MS), stroke or trauma have also been treated at our institution. We have published our results for the treatment of tremor in patients with MS (see Research below). Benabid was the first to treat Parkinsonian patients with drug resistant tremor using DBS in the thalamus. This procedure has become widely accepted and received FDA approval for the DBS technology August 4, 1997. Retrospective series have shown that DBS is as effective as thalamotomy in tremor control and has less potential complications. Bilateral thalamotomies are well recognized to carry additional risks to cognitive functioning, memory, language, swallowing and speech. Bilateral thalamic DBS can reduce these risks. A multicenter study showed that thalamic DBS may reduce tremor up to 85% at one year follow-up. Both upper and lower limb tremors can be reduced with improvements in the activities of daily living scores. We have published our results of bilateral thalamic DBS for head tremor (see Research below).
The benefit of thalamic DBS is an approximately 80% reduction in tremor in the opposite side of the both. A bilateral procedure (electrodes in the right and left thalamus) will reduce tremor on both sides of the body. The risks are the same for any DBS procedure (approximately 1% chance of a devastating stroke or death and a 8% chance of infection). The stimulation is typically adjusted very quickly in the DBS Clinic with few visits required. Too much stimulation usually causes difficulty speaking or tightness/tingling in the opposite arm. Battery power usually lasts more than four years (sometimes up to seven years).
The Pallidum (GPi)
The globus pallidus internus (GPi) is the target of choice for symptoms of Parkinsonian dyskinesia. We also use this target for patients with dystonia. Pallidotomy (making a permanent lesion within the pallidum) for Parkinson’s disease became very popular again after 1992. This operation dramatically improves contralateral dyskinesia and, to a lesser extent, bradykinesia, tremor, and pain. As the disease progresses, however, the other side of the body is often affected. Most, but not all, neurosurgeons were reluctant to perform the contralateral pallidotomy because of the increased morbidity seen following bilateral thalamotomies. Pallidal DBS provided a solution. Similar to the pallidotomy, the most dramatic effect of pallidal DBS is reduction in contralateral dyskinesia.
The benefit of pallidal DBS for Parkinson’s disease is an approximate 90% reduction in dyskinesia in the opposite side of the body. Patients continue to take their PD medications to help with the bradykinesia but the side effect of their medications (dyskinesia) will be blocked by the surgery. This means they may be able to take even more medications if necessary. A bilateral procedure (electrodes in the right and left thalamus) will reduce dyskinesia on both sides of the body. The risks are the same for any DBS procedure (approximately 1% chance of a devastating stroke or death and a 8% chance of infection). The stimulation is typically adjusted very quickly in the DBS Clinic with few visits required. Too much stimulation usually causes difficulty speaking or tightness/tingling in the opposite arm. Battery power usually lasts more than two years (sometimes up to five years).
The Subthalamic Nucleus (STN)
Subthalamic nucleus (STN) deep brain stimulation (DBS) is the most common neurosurgical procedure for Parkinson’s disease at Vancouver General Hospital. The STN is the target of choice for ‘motor fluctuation’ of Parkinson’s disease. The pathological over-activity of the STN in the Parkinsonian brain is felt to cause symptoms of rigidity and bradykinesia. Blocking this over-activity with DBS can therefore help these symptoms. Unilateral and bilateral STN lesions have been performed but risk permanent dyskinesia or pseudobulbar palsy. The reversible effects of DBS made STN DBS more attractive than permanent lesioning. Unilateral STN stimulation mainly affects the contralateral hemibody. Benabid reported bilateral STN DBS results in improvement of the cardinal features of Parkinson’s disease: bradykinesia, rigidity and tremor. Patients also improved with attenuated motor fluctuations and reduced medication requirements. A double blind study done by Kumar et al. yielded similar results. They reported a 65% reduction in off-period Parkinsonism, 40% improvement in on-period parkinsonism, and an 85% reduction in levodopa induced dyskinesias.
Our experience has shown that the benefit of STN DBS is that the patient will spend more time ‘on’ and less time ‘off’. Their ‘on’ functioning will be the same after surgery as before – they just spend more time ‘on’ than before. The ideal patient is therefore someone who had moments before surgery when they were functioning well. Those good ‘on’ times before surgery may have been ruined by dyskinesia or bad “off” times. After STN DBS, the patient will have less time spent with dyskinesia or “off”. Their best ‘on’ time will be no better than before surgery – they will just spend more of the day ‘on’ and have less motor fluctuations. If a patient is having problems with balance or freezing of gait before surgery it is very important to understand if those problems occur during ‘on’ or ‘off’ times. Balance and freezing of gait occurring ONLY during ‘off’ times can be expected to improve with surgery. Balance and gait problems occurring during ‘on’ times will not improve after surgery.
top of DBS
Complications
Our most common adverse experience with the DBS technology has been infection. Implanting a foreign object under the thin scalp of an elderly patient with borderline nutrition invites potential infection. We have not had a technical malfunction or disconnection but the batteries do wear out in 1.5-5 years depending on usage.
Symptomatic hemorrhage at the electrode target site remains a possibility. Passing an electrode through the brain will cause a hemorrhage (bleeding or stroke) in approximately 1% of patients. Even a small stroke in an advanced PD patient can be devastating.
There can be temporary side effects related to the stimulation spreading outside the target area of the brain and affective other areas of the brain. These side effects depend on what area of the brain is being stimulated and can include tingling, muscle tightness, double vision, hoarse speech, dyskinesia, and behavioural changes. It is very important for the patient totell us about these side effects (and especially important for the family or friends to tell us about any behavioural changes) so we can immediately adjust the stimulation to eliminate those unwanted side effects. This is the main stregth of the DBS system - these side effects can be eliminated by adjusting the stimulation.
There is a possibility that the surgery will not be as effective as hoped. This can be due to suboptimal electrode placement, less than ideal patient selection, or inappropriate patient expectations. In an early survey of 50 patients, 10% were not happy with their results. Over the last ten years, we have improved in all these categories with the experience gained from approximately 300 procedures.
Conclusion
In British Columbia, there has always been a close collaboration between the neurologists and neurosurgeons who treat patients with PD. Patients with symptoms refractory to medications have the potential to benefit from a variety of surgical procedures. In the future, there may be new treatments such as nerve cell transplantation, gene therapy, and growth factor infusion. Each new treatment will provide clinical benefits to our patients and an added understanding of Parkinson’s Disease.
Multiple Sclerosis
This information is designed only to help patients talk with their physicians about Multiple Sclerosis (MS) and is not intended to provide treatment guidelines.
Most of the symptoms caused by MS are well treated with appropriate medications under the guidance of Neurologists. The MS Clinic at the University of British Columbia has an international reputation for the medical treatment and research of this condition. Occasionally there are symptoms that do not respond to medications and patients need to consider the pros and cons of surgical intervention. Three of these symptoms are: 1. trigeminal neuralgia, 2. lower limb spasticity, and 3. tremor.
TRIGEMINAL NEURALGIA is far more common in MS than the general population. We have published our experience with the treatment of trigeminal neuralgia in MS (see Research below). The medical treatments are the same but MS patients seem to suffer more side effects from these medications (e.g. reduced mental quickness or sedation). Patients who continue to have pain despite their medications or those who can not tolerate their medications can consider a surgical treatment. The cause of the pain is thought to be due to a demyelinated plaque in the trigeminal nerve not a vessel compressing it. We therefore recommend percutaneous rhizotomy not microvascular decompression for MS patients with trigeminal neuralgia. These two procedures are described below on the section about trigeminal neuralgia.
LOWER LIMB SPASTICITY can be treated with a variety of oral medications. Occasionally the side-effects of these medications (e.g. sedation) preclude their use and patients need to turn to a surgical option. One option available at the University of British Columbia is an implantable Baclofen pump. These pumps contain a refillable reservoir of this anti-spasticity medication and are connected to a small tube which delivers the drug to the space around the spinal cord. The pump is about the size of a hockey puck and sits under the skin of the lower abdomen. The drug is delivered directly to where it is needed (around the spinal cord) and therefore has less systemic sedative side-effects. The benefits and potential complications of this therapy must be discussed with your surgeon.
TREMOR is rhythmic shaking. Arm tremor can be particularly disabling because the shaking prevents patients from using their arms for the activities of daily living. Tremor can be quite difficult to treat with medications. One option available for patients at the University of British Columbia is thalamic deep brain stimulation. This operation is designed to "turn off" the area of the brain causing the tremors. We have recently published our work with this technique (see Research below).
Tremor
As reviewed above, tremor is rhythmic shaking. It can be caused by Parkinson's disease, Multiple Sclerosis, stroke, trauma, or a genetic condition called Essential Tremor. Patients who have a poor response to their medications or who can not tolerate them have the option of surgical treatment. The procedures 1. thalamotomy or 2. thalamic deep brain stimulation are designed to reduce tremor on the opposite side of the body. We have published our research on bilateral thalamic DBS for head tremor (see Research below).
Dystonia
Dystonia is a condition characterized by abnormal prolonged muscular contractions
in a region of the body. There are many causes including genetic
disorders, stroke, or trauma. There is a growing interest in the surgical
treatment of dystonia. We have had success with
pallidal deep brain stimulation.
When dystonia effects the entire body it is called 'Generalized Dystonia'.
Generalized dystonia can be classified as either Primary (caused by a genetic mutation)
or Secondary (caused by some brain injury such as a stroke). DBS in patients with primary generalized dystonia (e.g. due to the dyt1 gene)
typically results in excellent improvements. DBS in patients with secondary generalized dystonia
has a much more variable response and depends on many factors which your neurosurgeon can discuss with you.
Segmental dystonia involves part of the body (usually an arm or leg). When it involves one side of the body it is called hemidystonia.
Our centre has had variable results in this condition. A number of factors can influence the
results of surgery but many patients have excellent improvement in the function of
their limbs and enjoy a reduction in the associated pain that can accompany the muscle cramps.
Torticollis or cervical dystonia effects the neck and twists the head to one side. Rare cases can pull the head forward
or back. It is often paiful and can lead to arthritis in the neck. This condition has been shown by many centres to respond well to DBS.
This information is designed only to help patients talk with their physicians
about Trigeminal Neuralgia (TN) and is not intended to provide treatment
guidelines. There are some excellent patient support group web sites that you might
wish to review.
Trigeminal Neuralgia Association of Canada http://www.tnac.org
Trigeminal Neuralgia Association http://www.tna-support.org
This painful facial condition has been well described in the medical literature
for over a hundred years. Symptoms are
described as brief stabbing or electric pains on one side of the face. Pain can sometimes be triggered by touching
a particular area on the face, eating, or bushing the teeth. The pain often comes without warning but may
disappear spontaneously. In between
episodes of intense pain, patients can be pain free. If left long enough, however, patients can develop a constant
burning sensation in face. The
condition is often confused with dental pain and many patients have teeth
extracted before the diagnosis is made! The current consensus is that
TN is caused by demyelination of the trigeminal nerve. The trigeminal nerve carries information
about what is touching the face back to the brain. This information is carried in little nerve fibers that are
insulated from each other by myelin (like wires are insulated). If the insulation is lost (demyelination),
then the nerves can “short-circuit”.
Signals coming down one nerve fiber can spread to many nerve fibers and
barrage the brain with signals (felt as the TN pain). The trigeminal nerve can lose myelin in certain diseases such as
multiple sclerosis or more commonly by constant pressure from an abnormally
located artery. The trigeminal nerve
has three branches (hence “tri”-geminal) which join together as the nerves
enter the skull. The first branch (ophthalmic
or V1) controls sensation to the forehead.
The second branch (maxillary or V2) covers sensation from below the eye
to the corner of the lip. The third
branch (mandibular or V3) covers sensation below the corner of the lip to the
angle of the jaw. The pain of TN is
often felt in a single territory (usually V2 or V3) but in severe cases can
include all three division. Most patients with TN can be
treated with medications designed to dampen nerve signals. Medications such as Tegretol, Dilantin, or
Neurontin (used commonly to prevent seizures in epileptics) can reduce or
eliminate the pain. Each medication can
produce side effects of tiredness, dizziness, and slowing of thinking in higher
doses. Surgery is reserved for those
patients who either can not tolerate these side-effects or continue to have
pain despite these medications. Trigeminal
Neuralgia
Introduction
top of TN
Medical
Treatments
Percutaneous
Rhizotomy
Following a rhizotomy, the patient trades their pain for numbness in the corresponding division(s) of the trigeminal nerve. The operation is performed as day surgery (i.e. the patient goes home the same day). The procedure is performed in the sterile conditions of the operating room. A brief pulse of anesthetic is given through an intravenous line and the patient is unconscious for a few minutes. A needle is introduced through the cheek and up through the foramen ovale (the hole in the skull where the trigeminal nerve enters). An electrode is then placed through the needle so that its tip is touching the trigeminal nerve. When the patient wakes up, we confirm that the tip of the electrode is touching the correct division of the nerve. Small pulses of electricity are sent down the electrode until the patient feels “tingling” in one division of the nerve. The electrode is moved slightly until the “tingling” is felt in the same division of the nerve that is causing the pain. Another pulse of anesthetic is given while the electrode is used to burn the offending branch(es) of the nerve. When the patient wakes up, we check that the nerve has been sufficiently lesioned. They will have numbness in the division of the nerve that was lesioned.
Benefits: This operation is quick and effective. It does not have the anesthetic risks associated with the MVD operation and is therefore preferred for patients over 65. The patient goes home the same day and their TN pain is gone. Most people get used to the numbness and do not notice it after a few weeks.
Downside: Patients are urged to speak directly with their surgeons about complication rates, which can vary among institutions. This operation does not fix the cause of TN - only the symptoms are blocked. Patients will have numbness in an area of the face. This numbness is rarely annoying but in 1% of patients their symptoms can worsen into a syndrome called anesthesia dolorosa. Infection is rare. There are potential problems when treating V1 (forehead) TN because the rhizotomy will leave the eye numb. This means a patient would not feel an eyelash or dirt in the eye and this could lead to a corneal ulcer. There is mild post-operative discomfort (where the needle was placed) and patients can complain of soreness or weakness when chewing. The area of numbness usually gets smaller with time because the nerve heals. If the nerve heals sufficiently, it will begin to pass the TN pain signals again. The operation may then need to be repeated.
Microvascular Decompression
If the TN is due to pressure on the trigeminal nerve by a nearby artery, the MVD operation is designed to move the artery away from the nerve. This operation is done under a general anesthetic and takes approximately three hours. Patients go home after several days in hospital. The scalp behind the ear (on the side of the pain) is shaved and an incision made through the skin and muscles. A small hole is drilled through the skull. The surgeon operates around the outside of the brain until the nerve is seen through the microscope. The offending artery or vein is identified and moved away from the nerve. A small patch of padding is placed between the nerve and artery to prevent further compression. The hole in the skull is replaced with acrylic and the muscles and scalp sutured closed.
Benefits: The cause of the TN is fixed and the patient is left with normal sensation in the face (i.e. no numbness like the rhizotomy).
Downside: Patients are urged to speak directly with their surgeons about complication rates, which can vary among institutions. This is a more complex operation and has more potentially serious risks than the rhizotomy. With the general anesthetic and operating close to the brain stem there is the rare chance of death or stroke. Injury to the surrounding nerves could cause facial numbness, deafness, facial droop, double vision, or difficulty swollowing. There is a risk infection or delayed CSF leak (salt water-like fluid escaping from around the brain and draining through the middle ear into the back of the throat). Patient can temporarily complain of discomfort or numbness around the incision.
Hemifacial Spasm
This information is designed only to help patients talk with their physicians about Hemifacial Spasm (HFS) and is not intended to provide treatment guidelines.
Introduction
HFS is a neurologic condition with uncontrolled, repeated contractions of the muscles on one side of the face. It usually begins around the eye and may spread down the face to involve the mouth and neck. The eye can be forced closed and the corner of the mouth can be pulled over to the same side. It is not usually painful but can interfere with vision and social activities. It is usually caused by a blood vessel pinching the facial nerve just as it leaves the brainstem. Rarely it can be caused by a tumor. Most patients are diagnosed by a neurologist and begin non-surgical treatments with them.
top of HFS
Medical Treatment
Some medical treatments include biofeedback training or a trial of a medication. HFS can be very difficult to treat with medications but a variety of drugs can be tried. The choice of these medications and their potential side-effects are best reviewed with your Neurologist.
Botulinum Toxin (Botox) Injections
top of HFS
Microvascular Decompression
The MVD operation is designed to cure the problem. It is very similar to that described above in the trigeminal neuralgia section only in this case, it is the VIIth cranial nerve (the facial nerve) that is decompressed. This operation is done under a general anesthetic and takes approximately three hours. Patients go home after several days in hospital. The scalp behind the ear (on the side of the spasm) is shaved and an incision made through the skin and muscles. A small hole is drilled through the skull. The surgeon operates around the outside of the brain until the facial nerve is seen through the microscope. The offending artery or vein is identified and moved away from the nerve. A small patch of padding is placed between the nerve and artery to prevent future compression. The hole in the skull is replaced with acrylic and the muscles and scalp sutured closed.
At the University of British Columbia, this operation is performed with intraoperative monitoring (IOM) of the facial and acoustic (hearing) nerves. The IOM team is lead by Dr. Charles Dong and provides the surgeons with crucial information about when the facial nerve is adequately decompressed and if the hearing nerve is being compromised. We feel this IOM is essential to the safe performance of this operation.
Benefits: The cause of the HFS is fixed and the patient is left with normal sensation and movement in the face.
Downside: Patients are urged to speak directly with their surgeons about complication rates, which can vary among institutions. This is a complex operation and has potentially serious risks. With the general anesthetic and operating close to the brain stem there is the rare chance of death or disabling stroke. Injury to the surrounding nerves could cause deafness, facial droop, double vision, facial numbness or difficulty swallowing. There is a risk of infection or delayed CSF leak (salt water-like fluid escaping from around the brain and draining through the middle ear into the back of the throat). Patients can temporarily complain of discomfort around the incision or develop chemical meningitis. There is a small chance that the spasms will not be fixed or will recur.
FELLOWSHIP INFORMATION
Accepting Applications for July 2013 onwards.
There is one (or occassionally two) funded fellowships in Stereotactic and Functional Neurosurgery
available at the University of British Columbia. Fellows train for a one year period, usually from
July 1 - June 30.
The position is funded at CDN$55,000. Fellows will
have hands-on participation in all stereotactic & functional procedures at
Vancouver General Hospital. The
Surgical Centre for Movement Disorders is the only neurosurgical facility in
British Columbia (>4 million people) performing:
We also
have a very large referral base for trigeminal neuralgia, hemifacial spasm and spasticity.
Fellows will get hands-on experience with percutaneous trigeminal rhizotomy, microvascular
decompression (V, VII, IX), lumbar rhizotomy, and spinal pump insertion.
Our facilities include microelectrode
recording and Stealth Neuronavigation.
We have a strong collaboration with the four movement neurologists at
U.B.C. and our Neuropsychology team. Fellows will be required to
participate in clinical research and will help run the Deep Brain Stimulation
Clinic. Overview of downtown Vancouver and North Shore Mountains Vancouver is one of the most
beautiful cities in the world and recently hosted the 2010 Winter Olympics!
The American Society for Stereotactic and Functional Neurosurgery held its
biannual meeting here in 2008. The XIIIth International Congress on Parkinson's Disease
was held here in 1999. Vancouver is known for its outstanding
outdoor activities, restaurants, and safe environment. The best ski
resort in North America, Whistler-Blackcomb, is 90 minutes away. The
climate is tempered by the Pacific Ocean. Information about Vancouver,
Canada can be found at www.tourism-vancouver.org
pallidotomy
thalamotomy
anterior capsulotomy
cordotomy
trigeminal tractotomy
deep brain stimulation (thalamic, pallidal, subthalamic, hypothalamic, SCG)
motor cortex stimulation
occipital nerve stimulation
View to UBC from Grouse Mountain
Eligible candidates include:
(i) licenced to practice neurosurgery in home country (Clinical Fellow)
(or) still completing neurosurgery training in home country (Clinical Trainee)
(ii) proficient in English (oral and written)
candidates who did NOT receive their medical training in English,
must submit proof of proficiency in English with a TOEFL-IBT total score of 95 (including 25 for the spoken component)
(iii) planning a career in stereotactic and functional neurosurgery
Interested candidates should send:
(i) a letter outlining why they wish to train in
stereotactic & functional Neurosurgery
(ii) two letters of reference (including a letter of support from their Chairman)
(iii) their curriculum vitae (highlighting publications)
(iv) their email address, fax and phone contact numbers to:
Christopher
R. Honey, MD, D.Phil., FRCS
Director, Surgical Centre for
Movement Disorders
Suite 8105, 2775 Laurel St.
Vancouver, BC
Canada V5Z 1M9
tel: +1 604 875 5894
fax: +1 604 875 4882
There is more general information on Clinical Fellowships at the University of British Columbia web site.
RESEARCH
Our areas of research include the surgical treatment of Parkinson’s Disease, Multiple Sclerosis, Dystonia, and Trigeminal Neuralgia. A list of our recent publications is provided below.
We are particularly grateful to the B.C. Parkinson's Disease Association who generously provided the funds to purchase our (i) Radionics RFG-3C Lesion Generator and (i) Medtronic LeadPoint 4 microelectrode recording system with Stealthdrive™. This equipment has greatly benefited our surgical patients with Parkinson's disease, Tremor and Multiple Sclerosis.
RECENT PUBLICATIONS.
Contact Dr. Christopher R. Honey for copies of any of these papers.
Honey CR and Palur RS:
Surgery for Parkinson's Disease.
BC Medical Journal (2001) 43:210-213.
Laxton AW, Sun MC,
Shen H, Murphy TH, Honey CR: The antioxidant enzyme quinone reductase is up-regulated in vivo
following cerebral ischemia.
NeuroReport (2001) 12:1045-1048.
Murphy TH, Yu J, Ng R,
Johnson DA, Shen H, Honey CR, Johnson JA: Preferential expression of antioxidane response
element mediated gene expression in astrocytes.
Journal of Neurochemistry (2001) 76:1670-1678.
Berk C and Honey CR:
Bilateral thalamic deep brain stimulation for head tremor.
Journal of Neurosurgery (2002) 96:615-618.
Palur RS, Berk C,
Schulzer M, Honey CR: A meta-analysis comparing the results of pallidotomy performed with
microelectrode recording or macroelectrode stimulation.
Journal of Neurosurgery (2002)
96:1058-1062.
Berk C and Honey CR: Percutaneous biopsy through the foramen ovale.
Stereotactic and Functional Neurosurgery (2002) 78:49-52.
Berk C, Carr J, Sinden M, Martzke J, Honey CR:
Thalamic deep brain stimulation for the tremor of multiple sclerosis:
a prospective study of tremor and quality of life.
Journal of Neurosurgery (2002) 47: 815-820.
Sun M-C, Honey CR, Berk C, Wong NLM, Tsui JKC:
Regulation of aquaporin-4 in a traumatic brain injury model.
Journal of Neurosurgery (2003) 98: 565-569.
Carr JAR, Honey CR, Sinden M, Phillips AG, Martzke JS. A waitlist control group study of cognitive, mood, and quality of life outcome from posteroventral pallidotomy in Parkinson's disease.
Journal of Neurosurgery (2003) 99: 78-88.
Berk C, Constantoyannis C, Honey CR. The treatment of trigeminal neuralgia in patients with multiple sclerosis using percutaneous radiofrequency rhizotomy.
Canadian Journal of Neurological Sciences (2003) 30: 220-223.
Heran NS, Berk C, Constantoyannis C, Honey CR. Neuroepithelial cysts presenting
with movement disorders. A report of two cases.
Canadian Journal of Neurological Sciences. (2003) 30: 393-396.
Gusmao S, Oliveira M, Tazinafo U, Honey CR. Percutaneous trigeminal nerve radiofrequency
rhizotomy guided by real time computed tomography: description of a new technique.
Journal of Neurosurgery. (2003) 99: 785-786.
Watts RL, Raiser CD, Stover NP, Cornfeldt ML, Schweikert AW, Allen RC, Subramanian T,
Doudet D, Honey CR, Bakay RAE. Stereotaxic intrastriatal implantation of human retinal pigment epithelial
(hRPE) cells attached to gelatin microcarriers: a potential new cell therapy for Parkinson's disease.
Journal of Neural Transmission (2003) 65: 215-227.
Griesdale D and Honey CR. Aquaporins and brain edema.
Surgical Neurology (2004) 61: 418-421.
Constantoyannis C, Heilbron B, Honey CR. Electrocardiogram artifacts caused by deep brain stimulation.
Canadian Journal of Neurological Sciences (2004) 31: 343-346.
Constantoyannis C, Kumar A, Stoessl J, Honey CR. Tremor induced by thalamic deep brain stimulation in patients with complex regional facial pain.
Movement Disorders (2004) 19: 933-936.
Doudet DJ, Cornfeldt ML, Honey CR, Schweikert AW, Allen RC.
PET Imaging of Implanted Human Retinal Pigment Epithelial (hRPE)
Cells in the MPTP induced Primate Model of Parkinson’s Disease.
Experimental Neurology (2004) 189: 361-368.
Sun DA, Martin L, Honey CR. Percutaneous radiofrequency trigeminal rhizotomy in a patient with an implanted cardiac pacemaker.
Anesthesia & Analgesia (2004) 99: 1585-1586.
Mandat TS, Honey CR, Peters DA, Sharma BR. Artistic assault: an unusual penetrating head injury reported as a trivial facial trauma.
Constantoyannis C, Berk C, Honey CR, Mendez I, Brownstone RM. Reducing hardware-related complications of deep brain stimulation.
Canadian Journal of Neurological Sciences (2005) 32: 194-200.
Mandat TS, Hurwitz T, Honey CR. Hypomania as an adverse effect of subthalamic nucleus stimulation: report of two cases.
Mercado R, Constantoyannis C, Mandat T, Kumar A, Schulzer M, Stoessl J, Honey CR.
Expectation and the placebo effect in Parkinson’s disease patients
with subthalamic nucleus deep brain stimulation.
Mercado R, Mandat T, Moore GRW, Li D, MacKay A, Honey CR.
3T MRI of the ventrolateral thalamus: a correlative anatomical description.
Hurwitz TA, Mandat T, Foster B, Honey CR.
Tract identification by novel MRI signal changes following stereotactic anterior capsulotomy.
Vitali AM, Sayer FT, Honey CR.
Recurrent trigeminal neuralgia secondary to Teflon felt.
Low HL, Honey CR.
Focal childhood-onset, action induced primary hip dystonia treated with pallidal deep brain stimulation.
Coenen VA, Gielen FL, Castro-Prado F, Abdel Rahman A, Honey CR.
Noradrenergic modulation of subthalamic nucleus activity in human: metoprolol reduces spiking activity in microelectrode recordings during deep brain stimulation surgery for Parkinson's disease.
Sayer FT, Vitali AM, Low HL, Paquette S, Honey CR.
Brown-Sèquard syndrome produced by C3-C4 cervical disc herniation: a case report and review of the literature.
Low HL, Sayer FT, Honey CR.
Pathological crying caused by high-frequency stimulation in the region of the caudal internal capsule.
Sayer FT, Vitali AM, Paquette S, Honey CR.
Isolated C3-C4 disc herniations present as a painless myelopathy.
Bürgel U, Mädler B, Honey CR, Thron A, Gilsbach J, Coenen VA.
Fiber tracking with distinct software tools results in a clear diversity in anatomical fiber tract portrayal.
McMaster J, Gibson G, Castro-Prado F, Vitali A, Honey CR.
Neurosurgical treatment of tremor in anti-myelin-associated glycoprotein neuropathy.
Moore GR, Vitali AM, Leung E, Laule C, Kozlowski P, Mackay AL, Honey CR.
Thalamic stimulation in multiple sclerosis: evidence for a 'demyelinative thalamotomy'.
Vertinsky AT, Coenen VA, Lang DJ, Kolind S, Honey CR, Li D, Rauscher A..
Localization of the subthalamic nucleus: optimization with susceptibility-weighted phase MR imaging..
Coenen VA, Honey CR, Hurwitz T, Rahman AA, McMaster J, Bürgel U, Mädler B.
Medial forebrain bundle stimulation as a pathophysiological mechanism for hypomania in subthalamic nucleus deep brain stimulation for Parkinson's disease.
page last updated October 1, 2011
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