Emad N. Eskandar, MD,
Leslie Shinobu, MD PhD and G. Rees Cosgrove, MD, FRCS (C)
Address for Correspondence:
N. Eskandar, M.D.
Massachusetts General Hospital
15 Parkman St. ACC # 331
Boston, MA 02114
Patient Appointments: 617.724.6590
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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
Essential tremor (ET) is one of the
most common movement disorders and is characterized by disabling
intentional tremor which is not secondary to Parkinsons 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
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 Parkinsons 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
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 patients
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.
Thalamotomy and Thalamic Stimulation
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.
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)
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
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.
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 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.
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.
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.
The general finding that thalamotomy is an effective treatment
for tremor in patients with tremor-predominant Parkinsons
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 Parkinsons 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)
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 Frenchays
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
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
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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