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.
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:
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 Turnbull IM. Surgery for Parkinson’s Disease. NeuroScience News
(1999) 2:44-46.
3. 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 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
There are a number of excellent reviews on the history of neurosurgery for PD.1,2 In British Columbia, the surgical treatment of PD was first performed by Drs. Peter Lehmann and Peter Moyes in the early 1960’s. Before the advent of l-dopa, there was little else to offer patients. Lesions were placed in the thalamus to help PD patients with tremor. The results, however, were variable because of the inconsistency of lesion size and location. After completing a Fellowship in Europe studying stereotaxic surgery, Ian Turnbull returned to Vancouver in 1966 and made many advances to the surgery for PD. He introduced the use of a stereotaxic frame which allowed more accurate target localization. He also switched the method of lesioning the brain from a leucotomy (which cut vessels as well as brain) to radiofrequency lesioning. Radiofrequency lesions are made by heating the uninsulated tip of an electrode to a defined temperature for a specified time. Lesion size can therefore be carefully controlled and adjacent blood vessels are not cut. Further reduction in patient morbidity followed the replacement of ventriculography with computer tomography for preoperative target localization in the1980’s. More recent advances by Dr. Christopher Honey have included MRI guided stereotaxis and a series of new operations utilizing deep brain stimulation.
The most common surgical procedures for PD in British Columbia and around the world are pallidotomy, thalamotomy, and deep brain stimulation (DBS). There are additional experimental procedures including transplantation of dopaminergic neurons (or dopamine secreting cells) and infusion of dopaminergic growth factors that have great promise for the future but are not yet considered standard therapy.3 This review will focus on the current surgical treatment for PD.
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.4 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 and the realization that thalamotomy was better at tremor reduction than pallidotomy. The current era of surgery for PD was heralded by a report of excellent results for PD patients following pallidotomy in the posteroventral pallidum (a slightly different target than the previous standard).5 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.6 A number of well design prospective studies on the effects of pallidotomy have now been published.7-12 One area of controversy in the field is whether or not neurosurgeons need to use microelectrodes when doing pallidotomy. We have published a meta-analysis review of pallidotomies performed with and without microelectrodes around the world to help answer that questions. (see Research below).
Indications
and Outcomes:
The ideal surgical candidate for pallidotomy would have idiopathic Parkinson’s Disease and symptoms refractory to medications. Since the most dramatic improvement after surgery is the reduction in contralateral dyskinesia, most surgeons select patients where this symptom predominates. Improvements are also seen in contralateral tremor, bradykinesia, rigidity, overall balance and pain. Little long-term effect is seen ipsilaterally (on the same side of the body). Patients with motor fluctuations spend less time “off” and their “off” bradykinesia is improved following pallidotomy but their best “on” motor performance does not get much better (except for reduced dyskinesia). At six months post-operative, improvements in off-period UPDRS total motor scores (17 - 46% decrease from baseline) and on-period drug-induced dyskinesia (43 - 92% decrease) have been reported.7-12 Longer trials have demonstrated continued efficacy for off-period signs at two and three year follow-up.13 The potential complications of pallidotomy are infection, seizure, and hemorrhage (common to all stereotaxic operations at approximately 1%) and injury to the internal capsule or optic tract. A number of papers on the neuropsychological effects of pallidotomy have shown subtle changes but no significant permanent detrimental effects.14,15 (see Research below). Patients who are not good candidates for pallidotomy have i) Parkinson Plus Syndromes, ii) or the major problem being speech, autonomic, psychiatric or gait.
Thalamotomy
The results of placing a lesion in the thalamus, or thalamotomy, were first published by Hassler in 1954.16 Throughout the 1960’s different thalamic targets were lesioned until the ventral intermediate (VIM) nucleus emerged as the most effective target for tremor reduction. Since tremor can be quite resistant to medications, the thalamotomy procedure continued to be popular over the years. Unlike the pallidotomy procedure, however, the VIM nucleus thalamotomy has little or no effect on bradykinesia.
Indications
and Outcomes:
Patients with unilateral, tremor dominant PD can benefit from thalamotomy. Reviewing the literature, Tasker found abolition of contralateral tremor in 45-92% of patients and less than 80% in his own series.17 Complications specific to thalamotomy include contralateral weakness, arm and foot ataxia, dysarthria, dysphagia, and cognitive decline. Patients who are not good candidates for thalamotomy have i) cognitive impairment, ii) dysarthria, iii) or PD symptoms other than tremor as the major problem.
References
1. Stereotact Funct Neurosurg 1998;70:114-21.
The fastest growing area of stereotactic surgery is deep brain stimulation
(DBS). The information below is reprinted with permission from an article
we published in New Frontiers April 2002 entitled "Deep Brain Stimulation
for Movement Disorders".
2. Mov Disod 1988;13:582-588.
3. Neurosurg Clin N Am 1995;6:113-125.
4. In: Fields WS (ed) Pathogenesis and Treatment of Parkinsonism.
Springfield: Charles C Thomas, 1958.
5. J Neurosurg 1992;76:53-61.
6. TINS 1990;13:281-285.
7. Ann Neurol1996;40:355-366.
8. Brain1997;120:729-737.
9. J Neurosurg 1997;87:52-59.
10. J Neurosurg 1997;87:358-367.
11. Brain 1997;120:1301-1313.
12. Lancet1995;346:1383-1387.
13. Neurology 1997;48:1273-1277.
14. Neuropsychiatry Neuropsychol BehavNeurol 1998;11:136-145.
15. ArchNeurol 1998;55:1201-1208.
16. Nervenarzt 1954;25:441-447.
17. In: Lunsford LD(ed) Modern Stereotactic Neurosurgery.
Boston: Marinus Nijhoff, 1998:297-314.
Deep Brain Stimulation
The company that makes the deep brain stimulators is Medtronic and they have an extensive website with many pages for patient education.
Most patients with movement disorders are treated effectively with medications. A small portion, however, have refractory symptoms. Some of these symptoms can be treated with neurosurgical techniques. Over the years, the safety and efficacy of these procedures have improved with the introduction of stereotaxis, radiofrequency lesioning, non-invasive imaging, and now DBS. Before the introduction of DBS, neurosurgeons could only destroy the overactive brain regions responsible for movement disorders. These operations (e.g. pallidotomy or thalamotomy) are still done by heating the tip of an electrode and coagulating a small area of the brain. Deep brain stimulation is designed to “turn off” these overactive brain regions without destroying them. The immediate advantage of DBS over conventional destructive neurosurgery is that the ‘lesions’ are titratable and hence reversible.
The Hardware
There are three components to the DBS system. The first is the DBS lead. The tip of this insulated lead has four platinum/iridium electrodes spaced 0.5 or 1.5 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 pulse generator (IPG) is placed in a subcutaneous pocket below the clavicle 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 IPG. 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.
Implantation of the DBS Lead
At the University of British Columbia, we use a MRI compatible head frame (UCLF, Radionics) for patients without tremor and a CT compatible frame (CRW, Radionics) for those with tremor. Frames are placed using local anesthetic and no sedation is given during the procedure. 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 IPG
Early in our experience, this portion of the procedure was often performed several days later. Patients with a temporary external extension from the DBS lead to a hand held pacemaker were monitored for their response to a variety of stimulation settings. If a good response was confirmed, we would then proceed to implantation of the IPG. More recently we have been combining the two procedures following intraoperative confirmation of target localization. During insertion of the IPG, patients receive a general anesthetic. Most patients leave hospital the following day (after 24 hours of antibiotics) although our Multiple Sclerosis patients occasionally need more time. The procedure involves making a subcutaneous pocket for the IPG below the clavicle and tunneling the Extension from the scalp to the chest.
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Brain Targets
The effect of DBS depends on where the electrodes are placed. There are three common target sites for the control of movement disorders: the thalamus, the pallidum, and the subthalamic nucleus. Each target site has different indications, effects and potential complications.
The Thalamus (VIM)
The ventral intermediate nucleus within the thalamus is the target of choice for reducing tremor regardless of the etiology. The most common indications are Essential Tremor and Parkinsonian tremor but other causes such as Multiple Sclerosis (MS), stroke or trauma have 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.2 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.3, 4 Bilateral thalamotomies are well recognized to carry additional risks to cognitive functioning, memory, language, swallowing and speech. Bilateral thalamic DBS can reduce these risks.5 A recent multicenter study showed that thalamic DBS may reduce tremor up to 85% at one year follow-up.4 Both upper and lower limb tremors can be reduced with improvements in the activities of daily living scores.5 We have recently published our results of bilateral thalamic DBS for head tremor (see Research below). 6
The Pallidum (GPi)
The globus pallidus internus (GPi) is the target of choice for symptoms of Parkinsonian dyskinesia. More recently it has been targeted for dystonia from a variety of etiologies. Pallidotomy (the permanent lesioning of 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.7 Similar to the pallidotomy, the most dramatic effect of pallidal DBS is reduction in contralateral dyskinesia.8, 9 Reports of its benefits in dystonia are offering hope in this devastating disease.
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The Subthalamic Nucleus (STN)
The subthalamic nucleus (STN) is the target of choice for the bradykinetic symptoms of Parkinson’s disease. Its overactivity is believed to be a critical abnormality within the Parkinsonian brain. 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.10 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.11 A double blind study done by Kumar et al. yielded similar results.12 They reported a 65% reduction in off-period parkinsonism, 40% improvement in on-period parkinsonism, and an 85% reduction in levodopa induced dyskinesias.
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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. Like any stereotactic procedure, poor results will follow suboptimal target location.
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.
References
1. Am J Health Syst Pharm 2000;57:953-962.
2. Appl Neurophysiol 1987;50:344-346.
3. Surg Neurol 1998;49:145-154.
4. J Neurol Neurosurg Psychiatry 1999;66:289-296.
5. J Neurosurg 1996;84:203-214.
6. J Neurosurg 2002;96:615-618.
7. Neurosurgery 1994;35:1126-1130.
8. J Neurosurg 1998;89:713-718.
9. Can J Neurol Sci 1998;25:300-305.
10. Lancet 1995;345:91-95.
11. N Engl J Med 1998;339:1105-1111.
12. Neurology 1998;51:850-855.
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
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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.
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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
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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
July 2007 - June 2008 Position Filled (Dr. Coenen from Germany)
January 2008 - December 2008 Position Filled (Dr. McMaster from Australia)
Accepting Applications for January 2009 onwards.
There are two funded fellowships in Stereotactic and Functional Neurosurgery
available at the University of British Columbia. Fellows train for a one year period
(January 1 - December 31 or July 1 - June 30).
The positions are both funded (CDN$55,000) and includes coverage from the Canadian Medical
Protective Association. 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 will host the 2010 Winter Olympics!
The American Society for Stereotactic and Functional Neurosurgery will hold 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 (i) a letter outlining why they wish to train in
stereotactic & functional Neurosurgery Christopher
R. Honey, MD, D.Phil., FRCS tel: +1 604 875 5894 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.
For information on how you can help our Research Programme please contact Dr.
Christopher R. Honey.
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
and Multiple Sclerosis. RECENT PUBLICATIONS.
Contact Dr.
Christopher R. Honey for copies of any of these papers.
pallidotomy
thalamotomy
anterior capsulotomy
cordotomy
deep brain stimulation (thalamic, pallidal, subthalamic, hypothalamic, area 25)
motor cortex stimulation
View to UBC from Grouse Mountain
Interested candidates should send:
(ii) two letters of reference (including a letter of support from their Chairman)
(iii) their curriculum vitae (highlighting publications)
(iv) their email address and phone contact numbers to:
Director, Surgical Centre for
Movement Disorders
Suite 8105, 2775 Laurel St.
Vancouver, BC
Canada V5Z 1M9
fax: +1 604 875 4882
RESEARCH
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.
Sayer FT, Vitali AM, Paquette S, Honey CR.
Isolated C3-C4 disc herniations present as a painless myelopathy.
Vitali AM, Sayer FT, Honey CR.
Recurrent trigeminal neuralgia secondary to Teflon felt.
page last updated Jan 23, 2008
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