Surgery for Intractable Tremor
Emad N. Eskandar, MD, Leslie Shinobu, MD PhD and G. Rees Cosgrove, MD, FRCS (C)

Address for Correspondence:
Emad N. Eskandar, M.D.
Massachusetts General Hospital
15 Parkman St. ACC # 331
Boston, MA 02114

E-mail: eeskandar@partners.org
Patient Appointments: 617.724.6590
FAX: 617.724.0339

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Introduction

Tremor is defined as an involuntary rhythmical movement and is often categorized in three positions: hands in repose (rest ), hands held up with arms outstretched (postural ), and during movement (intention ). The amplitude, frequency and severity of the tremor vary from patient to patient, but at its worst, tremor can cause severe functional disability.

Essential tremor (ET) is one of the most common movement disorders and is characterized by disabling intentional tremor which is not secondary to Parkinson’s disease (PD) or other neurologic disroders. It is an idiopathic disorder that involves a 4-12 Hz tremor of the extremities that is most prominent during purposeful movement. About half of the cases are familial and transmitted in an autosomal dominant mode with variable penetrance.(21) This disorder has been termed "benign essential tremor" since tremor is the only major symptom but it can produce significant disability including inability to feed or drink, control hand movements, or even talk on a telephone. The onset is insidious and can occur at any age but has a bimodal distribution with peak incidence in the second and sixth decades. The disease has a variable progression and most often affects the upper extremities. Recent studies have supported the finding that both thalamotomy and thalamic stimulation can be quite effective in controlling medically refractory essential tremor.(3, 4, 5, 9, 13, 14, 17, 19, 25, 27, 38)

Essential tremor must be differentiated from Parkinsonian tremor because PD may be better treated by other techniques. Parkinsonian tremor is generally present at rest with a frequency of 3 - 5 Hz and is suppressed by movement. It can however be both postural and intentional and is often quite resistant to dopamine replacement therapy. PD patients with unilateral disease or marked asymmetry in their symptoms and in whom tremor is the predominant cause of disability may benefit from thalamotomy or thalamic stimulation.(3, 4, 5, 8, 14, 15, 16, 17, 19, 20, 22, 24, 26, 27, 29, 41) However, the effects of thalamotomy or thalamic stimulation on the other cardinal symptoms of PD are much less predictable and may in some cases cause worsening of symptoms. Therefore, patients in whom the symptoms of dyskinesia, bradykinesia, or rigidity predominate should be considered for other treatment modalities such as pallidotomy, pallidal stimulation, or subthalamic stimulation. In addition, since PD is a progressive disease, it is reasonable to expect that even patients with tremor-predominant PD will eventually develop the more disabling symptoms of akinesia and rigidity.

Tremors secondary to other underlying neurological conditions must also be differentiated from ET. These disorders include disabling intention tremor due to damage of the cerebellum or cerebellar tracts from cerebrovascular accidents, trauma or multiple sclerosis (2, 6, 10, 14, 18, 23). These conditions often imply more diffuse CNS pathology and therefore the outcome of thalamic surgery is less predictable and complication rate may be higher.

Anatomy and Pathophysiology

The role of the ventro-lateral thalamus in movement disorders and the optimal location for therapeutic lesions have been the subject of debate. Part of the difficulty lies in the fact that numerous anatomic classification schemes are in use. The most widely used schemes are the Anglo-American Terminology and the Hassler terminology. In the Anglo-American Terminology the ventro-lateral nuclei are divided from anterior to posterior into the ventralis anterior (VA), ventralis lateralis (VL), and ventralis posterior (VP) while in the Hassler terminology the same nuclei are divided into lateral polaris (LPO), ventralis oralis anterior (Voa), ventralis oralis posterior (Vop), Ventralis intermedius (Vim) and ventralis caudalis (VC) (FIGURE 1). The Hassler nomenclature will be used in this discussion as it appears to correlate with the relevant anatomy and physiology.

The main pallidal output pathways terminate in the ventrolateral thalamus particularly the Voa nucleus, which in turn projects back to the premotor cortex. In contrast the Vop and Vim nuclei receive multiple inputs including afferents from the contralateral cerebellum through the brachium conjunctivum. The Vop and Vim nuclei then project to the motor and premotor cortices. The VC nucleus is the primary thalamic relay for the medial lemniscal and spinothalamic tracts and projects to the somatosensory cortex. Microelectrode recordings in the area of Vim reveal neurons which respond to kinesthetic stimulation, i.e. movement of the joints and squeezing of muscle bellies, while neurons in VC respond to tactile stimulation.(8, 38) Furthermore, neurophysiological recordings have also revealed cells which fire synchronously with the observed tremor (tremor cells) further implicating the Vim in the pathology of tremor.(38) Whether the presence of these cells indicates that the genesis of tremor lies within Vim or that Vim is simply part of a larger loop mediating tremor is not clear. In either case, there is a considerable amount of clinical evidence that Vim lesions are quite effective in alleviating tremor. Lesions placed more anteriorly, in the Vop nucleus, or large lesions including both Vim and Vop lead to improvement in tremor and rigidity although bradykinesia is either unaffected or possibly worsened by such lesions.(18, 34, 39, 43) These findings support the contention that thalamotomy is best reserved for patients with Parkinson’s disease in whom tremor is the predominant complaint or in patients with intractable essential or intention tremor.

In patients with ET, the goal of thalamotomy is to permanently abolish tremor by placing a small lesion in the Vim nucleus of the thalamus. In thalamic stimulation, the goal is to place the probe 2-3 mm anterior to the junction of Vim and VC so that the stimulating current inactivates a portion of Vim while avoiding stimulation of the VC nucleus or other nearby structures such as the internal capsule.

Indications for Thalamic Surgery

The indications for thalamotomy or thalamic stimulation are similar. Patients should have tremor that is refractory to medical therapy and represents the predominant form of disability. The best candidates for thalamic surgery are patients with incapacitating benign essential tremor and those with tremor-predominant PD that is unilateral or asymmetric. Patients with PD who have other motor signs should be considered for surgery aimed at other targets such as the globus pallidus internus (Gpi) or the subthalamic nucleus (STN). Thalamic surgery may also be useful for patients with tremor secondary to multiple sclerosis or trauma although the results are less predictable due to the associated injury to other brain structures inherent in these afflictions.

Patients being considered for thalamic surgery should be evaluated by an experienced movement disorders team to ensure that they are good candidates for surgery and that all appropriate medical therapies have been tried. Medical therapy for patients with ET should include adequate trials of propanolol, mysoline, and clonazepam while therapy for patients with PD should include Sinemet, dopamine agonsists, etc. An essential element of this evaluation is to determine the major cause of the patient’s disability so that realistic goals and expectations can be agreed upon prior to surgery.

It is important to confirm the clinical diagnosis of benign essential tremor or idiopathic PD since a variety of neurodegenerative diseases can present with tremor in their early stages. Patients with these other neurodegenerative diseases appear to have a much poorer prognosis after thalamotomy. Evidence of dementia or other cognitive decline, speech disorders, serious systemic disease, and advanced age are also considered contraindications to surgery. As a final point, bilateral thalamotomies are generally associated with a prohibitively high complication rate and should not be undertaken.

Operative Technique – Thalamotomy and Thalamic Stimulation

Anesthetic Considerations

Patients are kept NPO on the evening before surgery and are generally advised to withhold their anti-parkinsonian and anti-tremor medication on the morning of surgery to ensure that the tremor will be evident throughout the surgery. Thalamic surgery is performed under local anesthesia and requires the full cooperation of the patient therefore the intraoperative use of sedating agents should be avoided.

Stereotactic Imaging

An MRI compatible stereotactic frame is affixed to the cranial vault after infiltration of the pin insertion sites with 1% lidocaine with 1/200,000 epinephrine. Following frame placement, the patient is taken to the MRI scanner where sagittal T1-weighted images are obtained first. These images are used to identify the anterior commissure (AC) and the posterior commissure (PC) and measure the AC-PC length. Next T1-weighted (TR 400, TE 12/Fr, FOV 30x30, 2 NEX, 3mm thickness) axial images are obtained through the basal ganglia and thalamus so that these images are parallel to the AC-PC plane. Additional images in the coronal plane with fast spin echo inversion (FSE IR) recovery sequences to accentuate the gray-white matter borders of the thalamus and internal capsule can be utilized depending on the experience of the center. Alternatively, 3-dimensional volumetric acquisition series can be acquired which allow thinner sections and reconstruction in any plane but these series generally require 10 - 11 minutes and are thus subject to movement artifacts. While a variety of MR sequences can be used for targeting, it is imperative that each center verify the spatial accuracy of their stereotactic frame in their scanner with phantoms. At our center we prefer to complement the MRI targeting with CT. After MR imaging, the patient is taken to the CT scanner and after the appropriate localizer is placed, axial CT images (DFOV, 1.0 - 1.5 mm thickness) parallel to the intercommissural line and through the area of interest are obtained. CT images, although geometrically accurate, do not provide the intrinsic anatomical details that MR images provide and should not be used alone for targeting purposes. In most cases however, the AC/PC line can be identified and used for initial target identification. The target coordinates from the MRI and CT images are then compared for accuracy. Some centers have continued to use the classical method of ventriculography to localize the target, however, recent studies have shown that surgery guided by CT/MRI alone is just as effective and may have a lower complication rate.(1, 17, 44)

Target Selection

A variety of stereotactic atlases are available with detailed anatomic representations of thalamic and basal ganglia anatomy. Although there is some controversy regarding optimal target location, the following parameters are generally agreed upon. The initial target is located at a point about 4 - 5 mm posterior to the mid AC-PC plane, 13.5 - 15 mm lateral to the midline, and 0 - 1 mm above the level of the intercommissural plane. When the third ventricle is dilated, it is wise to add 1 - 2 mm to the lateral dimension. Although the spatial resolution of modern MRI and CT scanners continue to improve, the detailed nuclear anatomy of the thalamus is still impossible to discern. Therefore, intraoperative physiologic confirmation of the lesion location through stimulation or a combination of stimulation and microelectrode recording remains essential.

Surgical Technique

The patient is placed in a comfortable position and the frame is fixed to the operating table with the head slightly elevated above the chest. After infiltration of the scalp with 1% lidocaine, a 2 - 3 cm parasagittal incision is made and a burr hole is placed 2.5 cm from the midline at the level of the coronal suture. The dura is coagulated and opened and a small pial incision is made avoiding any cortical veins to allow for atraumatic introduction of the electrode. At this point the stereotactic arc is brought into position and the electrode guide tube is lowered into the burr hole directly over the pial incision. The skin is then temporarily closed around the guide tube with nylon sutures to prevent excessive loss of CSF and brain settling.

Physiologic Recording

There are two techniques available for microelectrode recording in the thalamus. Some centers use true microelectrodes, usually made of tungsten, which allow for the discrimination of single neurons. Other centers use semi-microelectrodes, which are less delicate and potentially easier to use in the electrically hostile environment of the operating theater, but cannot record from single units. These concentric bipolar electrodes have low impedance but can record useful subcortical electrical activity. Both kinds of electrodes are then connected via short leads to a preamplifier. The signal from the preamplifier is then filtered, amplified, and passed through a window discriminator.

Microelectrode recordings in the ventrolateral thalamus reflect the connectivity of the various nuclei as reviewed by Tasker.(34) Recordings in the Vop nucleus frequently reveal voluntary cells that are less noisy than those in Vim or VC. These cells change their firing rate in advance or at the beginning of their related movements.(28) Some cells may increase their firing shortly before the movement while others may show a decreased rate or become rhythmic at the onset or completion of a movement. Recordings in Vim reveal moderately noisy high voltage neurons which respond to contralateral passive joint movement, squeezing of muscle bellies, or pressure on deep structures such as tendons. In patients with tremor, kinesthetic cells fire rhythmically at tremor frequency. Recordings in VC reveal very noisy spontaneous activity and many high voltage cells. These cells generally respond to superficial light tough such as light brushing of the skin or a puff of air. These cells respond faithfully without fatigue. The largest volume of VC is occupied by tactile cells representing the face and manual digits. The floor of the thalamus can be identified by the sudden loss of spontaneous neuronal activity as the microelectrode leaves the gray matter of the thalamus and enters the white matter of the zona incerta. A careful analysis of the neuronal activity of these various cell types can confirm that the appropriate target in Vim thalamus is selected.

Macrostimulation

Macrostimulation can also be used to delineate the optimal lesion location. A commercially available lesion generator (Radionics, Burlington, MA) is used for impedance monitoring, stimulation and lesioning. Stimulation is performed with square wave pulses at 0.5 - 2.0 volts with a frequency of 2 Hz to obtain motor thresholds and at 50 - 75 Hz to assess for amelioration of symptoms or sensory responses.

The typical thalamotomy target is the Vim nucleus and occasionally, the mere introduction of the electrode reduces the tremor indicating that the electrode is in good position. More often, due to individual variation and the small size of Vim, the electrode may be in a suboptimal position and require adjustment. The goal is to place a lesion within Vim, directly anterior to the appropriate somatotopic area in VC and medial to the internal capsule without encroaching on either structure.

If the electrode is placed too anteriorly in the Vop nucleus, low frequency stimulation may induce movement in the contralateral limbs. This movement is focal at threshold, beginning at one joint and involving greater parts of the contralateral limbs as stimulation intensity is increased.(34) Since Vim is thought to be the relay nucleus for kinesthetic sensation and VC the relay nucleus for superficial tactile sensation, high frequency stimulation can generally reflect this difference. The threshold (0.25 - 0.5 volts) for inducing parasthesias in the VC nucleus is usually much lower than that of the Vim nucleus. Consequently, low threshold parasthesias of the fingertips or mouth indicate that the electrode is too posterior and needs to be moved anteriorly.

An indication that the electrode is in good position relates to tremor response. Low frequency (2 Hz) stimulation within Vim usually causes driving of the tremor whereas high frequency (50 Hz) stimulation causes amelioration of the tremor. Suppression of tremor with 0.5 - 2.0 volts is the goal and indicates accurate targeting. In addition to the anterior-posterior differences between the nuclei, there is also a clear medial-to-lateral somatotopy within both Vim and VC. Neurons in VC representing the face are found most medial, those representing the lower limbs more lateral near the internal capsule, and those representing the upper extremity and hand intermediate (FIGURE 3). The definition of this somatotopic distribution is important as the lesion or the stimulating electrode in Vim should be placed directly anterior to the appropriate site in the VC nucleus.(7, 15) Thus lesions for tremor involving the upper extremity should be placed more medially whereas lesions for tremor involving the lower extremities should be placed more laterally.

If the electrode is correctly positioned at the physiologic target site, the mere presence of the electrode in Vim, or more typically, high frequency stimulation causes a reduction in the tremor. In addition, stimulation should be used to ensure that there is no evidence or neurologic impairment with particular attention being paid to speech and motor difficulties.

Lesion Generation

Once the target has been confirmed, a test lesion is made at 46 ^o C for 60 seconds. During this time, the patient is tested neurologically for contralateral motor dexterity and sensation along with verbal skills. If there is improvement in tremor and no neurologic problems then a permanent lesion is made at 75 degrees for 60 seconds. During the lesioning, the neurological status of the patient is continuously monitored and lesioning is halted if any impairment or change is noted. If complete abolition of the tremor has not been accomplished, then the lesion may be enlarged as guided by the intraoperative physiologic responses and recordings.

Stimulator Placement

Once the target coordinates have been performed, the stimulating electrode is introduced to the appropriate depth. By temporarily connecting the lead to an external stimulator the inhibitory effect on tremor can be assessed as can the presence of side effects. If all is well, the probe is secured in place using the supplied cap or bone cement. The primary incision is closed and the patient is then placed under general anesthesia. The infraclavicular pocket for the stimulator is made and the leads are tunneled and connected. Some groups use fluoroscopic guidance to ensure that the electrode has not migrated during the procedure.

RESULTS

Thalamotomy

The general finding that thalamotomy is an effective treatment for tremor in patients with tremor-predominant Parkinson’s disease has been known for some time (Table 1).(8, 14, 15, 16, 16, 24, 26, 30, 36, 39). In a study of the long term effects of thalamotomy on sixty patients, Kelly and Gillingham found that contralateral tremor was abolished in 90% of patients undergoing unilateral thalamotomy at the first postoperative evaluation.(16) Subsequent evaluations revealed that the effect diminished somewhat over time so that at 4 years 86% of patients remained tremor free while at 10 years 57% of surviving patients remained tremor free. Rigidity was also improved by thalamotomy in 88% of patients initially and in 55% of patients at 10 years. There was no effect of thalamotomy on bradykinesia or other manifestations of Parkinson’s disease such as mental deterioration or gait disturbance. More recent series reflect a similar distribution. Jankovic et al. reported a series of 42 patients who underwent thalamotomy for intractable tremor.(14) Of these patients, 72 percent had complete abolition of tremor while an additional 14% had significant improvement in tremor. There was a small but statistically insignificant effect on rigidity and no effect on bradykinesia. In another series reported by Fox et al., 34 out of 36 (94%) PD patients had complete abolition of contralateral tremor while 29 out of 34 (85%) remained tremor free at one year.(8)

Similar results are obtained in patients with intractable essential tremor with 80-100% of patients having marked or moderate improvement (Table 1).(9, 14, 25) In a series of 8 patients with ET treated with thalamotomy reported by Goldman et al., tremor was absent or markedly reduced in all patients at a mean follow-up of 17 months. Jankovic et al , treated six ET patients with thalamotomy. Overall, 5 of 6 or 83% of patients had moderate to marked improvement in their tremor at a mean follow-up of 59 months. Patients with intractable cerebellar intention tremor respond at somewhat lower rates with 60-80% of patients having significant improvement in tremor.(10, 14, 23)

Thalamic Stimulation

There are few long-term studies on thalamic stimulation but as expected the results are largely comparable to thalamotomy. Patients with tremor-predominant PD have sustained response rate of 80-95% while patients with essential tremor have a response rate of 70-85%.(3, 4, 5, 13, 17, 19, 27, 29, 38) There have been two recent large series looking at thalamic stimulation for the treatment of intractable tremor. In a multicenter American trial, reported by Koller et al., 29 patients with ET and 24 patients with Parkinsonian tremor were treated with high frequency unilateral thalamic stimulation.(17) Moderate to marked improvement occurred in 90% of ET patients and 71% of PD patients. The effects were largely maintained at one year. The results of a multicenter European trial were similar. In this study, a total of 74 patients with Parkinsonian tremor and 37 patients with ET were treated with thalamic stimulation.(19) Overall, there was a moderate to marked improvement in 85% of treated sides in patients with PD, and in 89% of patients with ET.

There are few studies directly comparing thalamotomy and thalamic stimulation in the modern era. The best recent study was a prospective randomized trial of 68 patients from an experienced group in the Netherlands.(29) A total of 68 patients with either PD ( n = 45) , ET (n = 13), or MS (n = 10) were randomized to receive either thalamotomy or thalamic stimulation. The primary outcome measure was functional improvement as measured by the Frenchay’s Activity Index. Secondary outcome measures included the severity of residual tremor, adverse effects of intervention and patient self-assessment of functional outcome. All measure were obtained at 6 months after surgery. As expected, tremor was either completely abolished or greatly suppresed in 27 /34 or 79% of thalamotomy patients and in 30/33 (91%) of thalamic stimulation patients. However the improvement in functional status was significantly greater in the thalamic stimulation group than in the thalamotomy group. Over twice as many patients undergoing deep brain stimulation reported that their functional status had improved as compared to those undergoing thalamotomy. Although one patient died post-operatively from an intracranial hemorrhage following thalamic stimulation (a risk inherent to both techniques) the overall neurologic complication rate was better for the stimulator patients (6/34 - 18%) than the thalamotomy patients (16/34 – 47%).

This well designed study confirms the prevailing clinical impression that thalamic stimulation appears equally effective in controlling tremor as thalamotomy and may be associated with fewer side effects. However, this study also demonstrated that tremor control is not necessarily equivalent to functional improvement. The greater functional improvement in the thalamic stimulation group as compared to the thalamotomy group my be attributable to reduced side effects, to the fact that the amount of current can be titrated in the stimulation group to maximize benefit while avoiding side-effects, or to a different mechanism of action of stimulation. The limitations of this study include the fact that assessments were not blinded. Furtthermore, the duration of the study is short and more long-term studies will be needed before definitive conclusions can be reached regarding the duration of benefit.

Complications of Thalamic Surgery

Thalamotomy shares the same general risks associated with other stereotactic procedures namely hemorrhage and infection which occur in about 2-5% of patients. The mortality rate is between 0.5-1%. Other specific complications of thalamotomy are due to inaccurate lesion placement or overly large lesions. Lesions placed too laterally may result in contralateral weakness due to injury of the posterior limb of the internal capsule. Many patients, about 25%, have transient contralateral facial weakness presumably secondary to edema involving the internal capsule.(8) The percentage of patients suffering from transient contralateral arm weakness ranges from 3-30% and 1-15% of patients go on to suffer mild but persistent contralateral weakness.(8, 14, 20) Another major source of morbidity, particularly in bilateral lesions, relates to difficulties with speech. About 30% of patients have transient dysarthria or dysphasia while about 10% go on to have persistent deficits.(8, 14) Lesions placed too posterior may cause contralateral hemisensory deficits due to injury of the VC nucleus. Correspondingly, there may be numbness or parasthesias of the mouth or fingers in 1-5% of patients.(7, 35) Transient confusion occurs in about 10-20% of patients and mild cognitive and memory deficits may persist in about 1-5% of patients.(14, 35) Older patients and patients with preexisting cognitive deficits or evidence of tissue loss on CT scan appear to be at a higher risk for impaired postoperative cognition.(7) Left thalamic lesions are associated with an increased risk for deficits in learning, verbal memory and dysarthria while right thalamic lesions are associated with impaired visuospatial memory and nonverbal performance abilities.(40) Bilateral thalamotomies are associated with deficits in memory and cognition in up to 60% of patients along with increased risk of hypophonia (decreased speech volume), dysarthria, dysphasia, and abulia.(7)

The risks of thalamic stimulation are similar to those of thalamatomy. There is a risk of intracerebral hemorrhage which ranges between 2-5%.(29) In addition there are specific risks associated with implanting hardware which are familiar to neurosurgeons such as infection, migration, and hardware malfunction. In the multicenter American study of 53 patients the complications included 2 peri-operative hemorrhages which resolved without sequelae, 1 peri-operative seizure, 2 wound infections, 1 stimulator malfunction, and 1 instance of hardware erosion.(17) In the mutlicenter European trial of 111 patients treated with thalamic stimulation complications related to the surgery included 3 subdural hematomas, 1 thalamic hematoma (which resolved without sequelae), 2 infections, and 1 patient with transient cognitive deficits.(19) Although there are few studies directly comparing the two techniques, as mentioned above the recent study by Schurman et al. suggests that there may be fewer neurologic complications with thalamic stimulation.(29)

DISCUSSION: Thalamotomy or Thalamic Stimulation

The decision to employ thalamotomy or thalamic stimulation is not clear-cut. There are several potential advantages of thalamotomy. It is an established technique with which there is considerable experience. The surgery is relatively more straightforward and is shorter. Once the surgery is complete there are no further concerns about hardware infection, migration, or malfunction. Furthermore, once the lesion is made there are no adjustments to be made to the stimulator. This can be an important consideration for patients who live in remote areas or, for example, international patients for whom frequent visits for adjustments are not practical. There are, however, a number of potential disadvantages. Thalamatomy has the potential to cause more neurologic complications because an irreversible lesion is created. If the lesion is too large or is not placed properly there is no recourse. Of course, in experienced hands and with careful attention to detail the neurologic risk should be minimal. Thalamotomy can not be performed bilaterally due to the increased risk of neurologic complications such as hypophonia, dysarthria and cognitive deficits.

Although thalamic stimulation been available for a relatively short period of time it is rapidly becoming an established technique. An increasing number of studies thalamic stimulation appears to be at least as effective as thalamotomy for the alleviation of tremor. One major advantage is that stimulators can be placed bilaterally with less risk of neurologic complications. Since the stimulators are adjustable it should at least in theory be possible to titrate the magnitude of stimulation to achieve the maximal possible benefit while avoiding side effects. Since no lesion is made the technique is easily reversible thereby leaving the door open for new restorative therapies that may become available in the near future. In the only recent study prospectively comparing the two techniques, patients undergoing thalamic stimulation had similar tremor control, a better functional outcome, and fewer neurologic complications when compared to patients undergoing thalamotomy. Nevertheless, thalamic stimulation has a number of disadvantages. The surgery is more complex and requires general anesthesia for the internalization if the pulse generator. Patients with implanted stimulators require a good deal more follow-up for adjustments, battery replacement, repair of malfunctions and so on. As with all implanted hardware the stimulator is subject to infection, migration, and malfunction. Finally, since the technique has been available for less time, the long term efficacy is unknown.

Both thalamotomy and thalamic stimulation can impart useful functional improvement in selected patients with intractable essential tremor or tremor-predominant PD. At the present time, based on the available evidence, the best recommendation that can be given is that for patients in whom thalamic surgery is indicated stimulation should be considered as the first option because it appears to provide good relief from tremor with potentially fewer side effects and because it does not create an irreversible lesion. However, thalamotomy is still an effective and well-proven technique that can be used that can be used when patients decide against a stimulator or when other considerations mitigate against the placement of a stimulator. Given the rapid advances in functional neurosurgery, it is likely that these treatment strategies will continue to evolve. The optimal management of patients with intractable tremor will continue to require a combined approach with medical therapy providing the first line of treatment and thalamic surgery providing an option for selected patients who can no longer be adequately managed with medical therapy alone.

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