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Transcript of Surgical movement disorders
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Surgical Treatment ofMovement Disord ers
Benzi M. Kluger, MDa,*, Olga Klepitskaya, MDa, Michael S. Okun, MDb,c
The past 2 to 3 decades have been marked by a resurgence in surgical approaches for
the treatment of movement disorders, specifically the creation of neuroanatomical
lesions and deep brain stimulation (DBS). This renewed interest has been spurred
on by several factors including (1) improvements in our understanding of the neuro-
physiology and anatomy of movement disorders, (2) the refinement of DBS as
a surgical approach, (3) improvements in neurosurgery and neuroimaging, which
have enhanced our ability to localize brain structures, and (4) an increasing role for
surgical interventions, especially in circumstances in which current pharmacologic
treatments have reached their limits. Appropriate patient selection for surgery can
result in a compelling treatment option for a variety of movement disorders, with themost common to date including Parkinson’s disease (PD), dystonia, and essential
tremor.
HISTORY
Surgical treatments for movement disorders can be traced to the late 1800s and early
1900s where applications included lesions placed in the motor cortex,1 the corticospi-
nal tracts,2 and the cerebral peduncles.3 Early attempts at therapy were focused
mainly on treating hyperkinetic movement disorders, including tremor. Not surpris-
ingly, these early treatments had an unacceptable rate of side effects, particularly of motor weakness. With the introduction of the stereotactic head frame technology in
This work was supported by an American Academy of Neurology Foundation Clinical ResearchTraining Fellowship (B.M.K.), and the National Parkinson Foundation Center of Excellence,Gainesville, FL.a University of Colorado Denver and Health Sciences Center, Academic Office 1 mailstop B185,PO Box 6511, Aurora, CO 80045, USAb Department of Neurology, University of Florida, 100 S. Newell Dr, Room L3-100, PO Box
100236, Gainesville, FL 32610, USAc University of Florida Movement Disorders Center, McKnight Brain Institute, 100 S. Newell Dr.Room L3-100, PO Box 100236, Gainesville, FL, USA* Corresponding author.E-mail address: [email protected] (B.M. Kluger).
KEYWORDS
Movement disorders Surgical treatment Deep brain stimulation Parkinson’s disease Dystonia Essential tremor
Neurol Clin 27 (2009) 633–677doi:10.1016/j.ncl.2009.04.006 neurologic.theclinics.com0733-8619/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
mailto:[email protected]://neurologic.theclinics.com/http://neurologic.theclinics.com/mailto:[email protected]
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the late 1940s by Spiegel and colleagues,4 targeting very small subcortical structures
became a more realistic possibility. However, there was still a paucity of basic or clin-
ical scientific evidence to know which nodes of this circuitry would be most appro-
priate for surgical interventions. A breakthrough in our understanding came in 1953,
when Cooper accidentally ligated the anterior choroidal artery during a pedunculotomy,
and this dramatically improved his patient’s tremor. The ligation interrupted the main
blood supply to many structures in the basal ganglia, including the globus pallidus,
a finding confirmed by pathologic examination of some of Cooper’s5 similar but later
cases. Although this procedure was abandoned as a result of unacceptable side
effects, and because of difficulty in reproducing Cooper’s success, it was followed
by more refined surgical approaches that focused largely on many subcortical struc-
tures. In 1955, Hassler6 reported that thalamotomy was more effective than pallidot-
omy for tremor. Cooper subsequently endorsed this surgical approach, adding that
results of thalamotomy were more consistent than those of pallidotomy. In 1960,
Svennilson and colleagues7 reported that the clinical results of pallidotomy were loca-
tion dependent, with posterior lesions demonstrating superior results to anterior
lesions. Although this article demonstrated that posteroventral pallidotomy improved
all the cardinal motor signs of PD, this research did not influence general clinical prac-
tice, which continued to favor the thalamotomy. In 1963, a few authors published
results suggesting that subthalamotomy may obtain tremor improvement similar to
that with thalamotomy.8 However, the fear of inducing hemiballism and subsequent
reports showing clinical improvements in only a minority of patients with subthalamot-
omy led to thalamotomy being the procedure of choice.9 The introduction of levodopa
in 1967 for the treatment of PD provided a remarkable therapeutic benefit, which
initially threatened to make all surgical approaches to PD obsolete.10
The 1980s brought a renewed interest in surgical approaches for movement disor-
ders, beginning with the use of thalamotomy for severe drug-resistant tremor.11 In
1992 Laitinen and colleagues12 replicated Leksell’s benefits for posteroventral pallidot-
omy in all cardinal PD motor signs, and in 1997, Gill and Heywood13 reported their
results of bilateral subthalamotomy. This renewed interest in surgery was driven largely
by an increased recognition of the limitations of long-term levodopa therapy. Equally
important were advances made in our understanding of basal ganglia circuitry and
physiology,14 including the emergence of animal models of basal ganglia disease.15
In 1987, Benabid and colleagues16 observed that high-frequency electrical stimu-
lation to the ventral intermediate (VIM) nucleus of the thalamus, usually performed aspart of neurosurgical localization, could be left in place and have dramatic chronic
effects in improving tremor. This observation fueled the further development of
DBS as a means of treating basal ganglia disorders. Although there are no
adequately powered trials published to date comparing DBS to lesion therapy,
DBS has virtually supplanted surgical lesions mainly due to its reversibility, flexibility
in changing settings, and its improved tolerability in patients requiring bilateral
surgical treatment (eg, avoiding speech and swallowing problems). We focus on
DBS in this review, recognizing that the efficacy and general principles of lesion
therapy are similar and that there may be cases in which ablative surgery may be
advantageous.18
MECHANISMS OF ACTION
Ablative brain lesions seem to achieve their functional improvement through the
disruption of aberrant network activity. The pioneering work of Delong14 and Albin
and Young17 in describing the direct and indirect pathways as well as the parallel
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circuitry of the basal ganglia circuitry has laid the foundation for identifying potential
regions where surgical interventions may improve symptoms. PD is known to result
in increased firing rates and changes in the pattern of activity of both the globus pal-
lidus interna (GPi) and subthalamic nucleus (STN).19 These patterns have been
confirmed in humans by physiologic recordings from PD patients undergoing DBS
or ablative surgery.20 Moreover, ablative lesions within the GPi and STN appear
to somewhat normalize this abnormal physiologic activity and are associated with
functional improvements.15
Although DBS appears to produce an informational lesion (a term coined by Grill)
that may mimic many of the effects from ablative surgery, the physiologic mechanisms
are thought to be more complex.21 In simple terms, DBS is thought to work by inhibit-
ing cells close to the stimulating electrode and by exciting passing fiber tracts, but this
simplistic model does not consider many of the complex changes that may contribute
to DBS effects. There is currently evidence to support the existence of several poten-
tial sites of action including the following:
1. Inhibition of neuronal cell bodies in close proximity to the electrode. Evidence from
primate recordings demonstrates a reduction in firing rates of cells adjacent to
stimulation electrodes during therapeutic stimulation of both STN and GPi.22 This
reduction in firing rate may be due to a depolarization block through alterations
of potassium or sodium channels and/or alterations in the balance of presynaptic
excitatory and inhibitory afferents.23 Depolarization blockade as a singular mecha-
nism has fallen out of support of most experts in the field.
2. Stimulation of axons in close proximity to the electrode. In fact, studies have shown
increased output from an inhibited nucleus, which is believed to be due to action
potentials initiated via axonal stimulation.24 This activity is time locked to the stim-
ulator frequency. Computer models have further suggested that the therapeutic
efficacy of STN is strongly linked to axonal activation.25
3. Stimulation of fiber tracts passing through the field of stimulation. DBS currents
sufficient for axonal activation may spread beyond the anatomic target to adjacent
fiber tracts. Several tracts important to basal ganglia functioning pass in close
proximity to the STN and have been hypothesized to contribute to the clinical effect
of DBS, including cerebellothalamic fibers (tremor reduction), nigrostriatal tracts
(increase striatal dopamine release), and the zona incerta (all cardinal motor
symptoms).23
4. Alterations in neurotransmitter release and synthesis. As noted above, activation of
the nigrostriatal tract may increase striatal dopamine release. Other microdialysis
studies of STN DBS in rats have demonstrated modulatory effects on both gluta-
mate and g-aminobutyric acid release within basal ganglia circuits.26
5. Alterations in network dynamics. DBS may interrupt pathologic neural output by
providing stimulation greater than a neuron’s spontaneous activity and thus pre-
empting intrinsic firing. This has been referred to as an ‘‘informational lesion,’’
because it replaces irregular pathologic activity with regular but ‘‘informationally’’
neutral output.21 Functional imaging studies have demonstrated changes in
multiple nodes of the motor circuitry, including the motor cortex, supplementarymotor area (SMA) and cerebellum with symptom improvement following DBS.
6. Chronic network changes. As discussed in the section on dystonia, many clinical
improvements take days to weeks, suggesting that they are dependent on neuro-
plastic changes. Consistent with this concept, studies have demonstrated long-
term changes in synaptic plasticity following DBS.27 There is also preliminary
evidence to suggest that DBS may confer some neuroprotective effects.28
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These mechanisms are not mutually exclusive, and it appears likely that the thera-
peutic effects of DBS are the result of multiple mechanisms.26 Moreover, there is
evidence that the mechanisms of DBS may not be identical across disease states,29
subcortical targets,30 or stimulation parameters.31
SELECTION OF SURGICAL CANDIDATES
The evolution of DBS therapy has resulted in the acceptance that selection of appro-
priate patients is critically important to the therapeutic benefit. In fact, only a small
subset of patients (10%–20%) may be appropriate at any one time.32 Currently,
patients with PD, dystonia, and essential tremor (ET) may be considered surgical
candidates after they have failed medical management (DBS is Food and Drug Admin-
istration approved for these indications in the United States). Patients must be moti-
vated and have the resources available to participate in the extensive follow-up
required to program and monitor the DBS device. In addition, potential candidatesmust have an acceptable risk benefit ratio favoring surgery. All indications (PD, ET,
and dystonia) for DBS carry risks, especially with comorbidities such as age, cognitive
dysfunction, frailty, psychiatric disease, cerebral atrophy, blood thinners, and espe-
cially hypertension. Among dystonia patients, primary and/or tardive dystonia seems
to have the best response, whereas patients with other forms of secondary dystonia,
including structural changes or neurometabolic diseases, tend to have less-predict-
able responses to DBS.33 However, an increasing number of successes may be
seen in these secondary dystonias with appropriate selection of target and stimulus
parameters.34 In PD, patients and clinicians should be aware that DBS will potentially
benefit only symptoms that are levodopa responsive.35
DBS can improve ‘‘on’’ time,reduce on-off fluctuations, and decrease dyskinesias but, with the exception of
tremor, does not provide motor benefits that exceed the patient’s best ‘‘on’’ medica-
tion state (with the current available targets of STN or GPi). It is thus critical for poten-
tial PD DBS candidates to have the Unified Parkinson disease rating scale (UPDRS)
completed in both the practically defined ‘‘on’’ and ‘‘off’’ states. In general, clinics
should follow the Core Assessment Program for Surgical Intervention Therapies in
PD criteria, which include a minimal disease duration of 5 years, a diagnosis of idio-
pathic PD, screening for depression and cognitive decline, and assessment for
minimal motor improvement of 30% based on UPDRS scores.35 One exception to
this 30% rule is medically refractory tremor in PD, which may occur in 20% or morepatients. There is currently insufficient evidence to support the use of ‘‘early’’ DBS
in any movement disorder, although considerations are being explored in research
arenas, including effects on quality of life (QOL), decreased surgical mortality (vs de-
layed operations ), cost savings, and the possibility that DBS may have a disease-
modifying effect.36 Caution is required in how we define ‘‘early’’ disease, particularly
in patients without significant disability, patients who have not received adequate trials
of standard medications, and in patients with short disease duration who may not have
a definitive diagnosis.
Although potential surgical candidates may be identified by general neurologists,
the decision to proceed through surgery is in the best circumstances made by anexperienced multidisciplinary/interdisciplinary team typically including a movement
disorders neurologist, neurosurgeon, psychiatrist, neuropsychologist, and, in some
circumstances, a social worker, speech therapist, occupational therapist, and/or
physical therapists ( Fig. 1 ).37 Each member of the multidisciplinary team should
have a specific role in this evaluation and should contribute to a discussion by the
team regarding the diagnosis, scale changes, expectations of benefit, risk, financial
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issues, QOL, target choice, staged versus simultaneous implantation if bilateral
devices may be required, and the ability of the patient to meet the schedule of
follow-up appointments. The neurologist must ensure that patients have beencorrectly diagnosed and that they present with symptoms likely to respond to DBS.
They must have exhausted medical options and their symptoms carefully quantified
with appropriate disease-specific scales (eg, on/off UPDRS for PD, tremor rating scale
[TRS] for ET, and Burke-Fahn-Marsden dystonia rating scale [BFMDRS]). In the case
of PD, it is recommended that the patient have at least 5 years of symptoms as it is
frequently difficult to distinguish levodopa-responsive parkinsonian syndromes that
may be manifesting in early stages. The Florida Surgical Questionnaire for Parkinson’s
Disease (FLASQ-PD) was developed as a screening questionnaire to aid in the iden-
tification of surgical candidates with PD ( Box 1 ).37 It is important that the neurologist
appropriately educates the patient, because unrealistic expectations regarding the
benefits and convenience of DBS are a frequent cause of patient’s perception of
DBS failure. As discussed later, significant nonmotor complications, including
mood, cognition, and speech, may occur following DBS and may be in part prevent-
able through the appropriate screening of high-risk patients.38 There is some evidence
that younger patients (younger than 70 years) may have less risk of cognitive compli-
cations; however, this is not an absolute rule, and many older patients have excellent
outcomes following DBS.
STIMULATOR PLACEMENT AND PROGRAMMING
The accurate localization of DBS targets requires a combination of high-quality neuro-
imaging, stereotactic localization (frameless or frame-based), and physiologic record-
ings. The superior resolution of subcortical structures evident on magnetic resonance
imaging (MRI) has resulted in its use as the primary imaging modality at most centers.
Many centers fuse computed tomography with MRI images to save time on the day of
surgery (by performing the MRI the day before) and postoperatively to localize lead
Fig.1. Multidisciplinary team.
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Box1
FLASQ-PD
A. Diagnosis of idiopathic Parkinson’s disease
Diagnosis 1: Is Bradykinesia present? Yes/No (Please circle response)
Diagnosis 2: (check if present):
—Rigidity (Stiffness in arms, leg, or neck)
—4–6 Hz resting tremor
—Postural instability not caused by primary visual, vestibular, cerebellar, proprioceptivedysfunction
Does your patient have at least 2 of the above? Yes/No (Please circle response)
Diagnosis 3: (check if present):
—Unilateral onset
—Rest tremor
—Progressive disorder
—Persistent asymmetry affecting side of onset most
—Excellent response (70%–100%) to levodopa
—Severe levodopa-induced dyskinesia
—Levodopa response for 5 y or more
—Clinical course of 5 y or more
Does your patient have at least 3 of the above? Yes/No (Please circle response)
(‘‘Yes’’ answers to all 3 questions above suggest the diagnosis of idiopathic PD)
B. Findings suggestive of Parkinsonism due to a process other than idiopathic PD
Primitive reflexes
1- RED FLAG—presence of a grasp, snout, root, suck, or Myerson’s sign
N/A—not done/unknown
Presence of supranuclear gaze palsy
1- RED FLAG—supranuclear gaze palsy present
N/A—not done/unknownPresence of ideomotor apraxia
1- RED FLAG—ideomotor apraxia present
N/A—not done/unknown
Presence of autonomic dysfunction
1- RED FLAG—presence of new severe orthostatic hypotension not due to medications,erectile dysfunction, or other autonomic disturbance within the first year or 2 of diseaseonset
N/A—not done/unknown
Presence of a wide-based gait
1- RED FLAG—wide-based gait present
N/A—not done/unknown
Presence of more than mild dementia
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more research is needed to determine if staged or simultaneous procedures have
distinct advantages and in which populations they should be applied.
SURGICAL AND DBS COMPLICATIONS
DBS complications may be divided into risks associated with the surgical procedure
and chronic complications of therapy that may or may not be device related. The
most serious complications associated with DBS surgery are cerebrovascular acci-
dents (including transient ischemic events) (0.9%), intracranial hemorrhage (1.2%),seizure (1.2%), device infection (4.4%), lead fracture (3.8%), and device movement
or misplacement (3.2%),42 and the risks vary from study to study depending on
many factors. Many centers do not prospectively assess adverse events, and this
may lead to under-reporting.43 These risks may be somewhat attenuated by appro-
priate screening and treatment of comorbid conditions, including hypertension,
which increases hemorrhage risk during MER; diabetes, which increases the risk
of infection; psychiatric disease, which increases the risk of depression and suicide;
cognitive deficits, which increase the risk of postoperative confusion; and obesity or
other significant cardiopulmonary diseases, which may increase the general risk of
surgery.44,45Complications of DBS may also occur following the acute operative period. These
complications may occur from problems in triage, screening, inadequate patient
counseling/unreasonable patient expectations, operative procedure (including DBS
misplacement), medication adjustments, or device programming difficulties. In a series
of patients seeking further management after suboptimal DBS outcomes, the most
common reasons for poor DBS outcome/DBS failure included inadequate screening
(no movement disorder neurologist or documented neuropsychological testing)
(66%), inappropriate or missed diagnosis (22%), suboptimally placed electrodes
(46%), inadequate programming follow-up (17%) or suboptimal DBS parameters
(37%), and suboptimal medication management (73%).38 Of the patients seen inthis series, two-thirds had good outcomes (51%) or modest improvement (15%) after
receiving appropriate interventions. Chronic side effects may occur in patients even
when the device has been appropriately placed, and lead settings may be optimized
for the greatest symptomatic benefit. Side effects may be stimulation related and may
be reversible with a simple change in settings. However, some side effects may be due
to microlesional effects of the DBS placement and thus not amenable to changes in
Table1
(continued )
Summary of Adverse Events
Event No. of Patients (%)
Psychogenic tremor 2 (0.6)
Urinary incontinence 2 (0.6)
Blepharospasm 1 (0.3)
Emotional lability 1 (0.3)
Insomnia 1 (0.3)
Metallic taste 1 (0.3)
Suicide 1 (0.3)
Data from Kenney C, Simpson R, Hunter C, et al. Short-term and long-term safety of deep brainstimulation in the treatment of movement disorders. J Neurosurg 2007;106:621–5.
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Table 2
(continued )
Author, Year N Type Target
Duration
(mo) UPDRS II ADL
UPDRS III
Motor LE
Jahanshahiet al., 2000115
7 NC (on/off) STN 2–26 62.7/25.160.0%
6 GPi 54.2/27.249.8%
Molinuevoet al., 2000116
15 Prosp NC STN 6 N/A 26.7/7.571.9%
N/A 49.6/16.965.9%
13380.4
Pillon, 2000117 48 NC STN 12 N/A N/A N/A 55.4/18.167.3%
11168.6
15 STN 6 N/A N/A N/A 56.1/19.465.4%
10656.3
8 GPi 12 N/A N/A N/A 55.4/37.133.0%
74417
5 GPi 6 N/A N/A N/A 41.6/27.035.1%
85013.
Alegret, 2001118 15 Prosp STN 3 N/A 29.9/10.9
63.6%
N/A 53.6/23.2
56.7%
57.9
Capus, 2001119 7 Prosp NC STN 6 N/A N/A 20.3% 50.6% 40.7
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DBS/PD studygroup, 2001120
96 Prosp DBlCrossover
STN 6 11.2/10.28.9%
28.4/16.043.7%
23.6/17.824.6%
54.0/25.752.4%
12137.3
38 Same GPi 6 12.7/8.830.7%
17.9/17.90.0%
24.1/16.531.5%
50.8/33.933.3%
109-2.8
Dujardin et al.,2001121 9 Prosp NC STN 3 8.66/7.6711.4% 31.55/13.7856.3% 22.44/13.4440.1% 62.9/32.648.2% NA
6 ProspNC
STN 12 9.2/7.518.5%
31.2/14.354.2%
21.6/17.220.4%
65.0/40.537.7%
NA
Faist et al.,2001122
8 Prosp NC STN 15 N/A N/A N/A 49.8/7.485.1%
N/A
Lopiano et al.,
2001123
16 Prosp NC STN 3 8.8/7.7
12.5%
28.3/9.1
67.8%
20.3/14.8
27.1%
59.8/25.9
56.7%
116
72.4Lopiano et al.,
200112420 Prosp NC STN 12 N/A N/A 19.8/16.8
5.0%58/25.156.7%
95476.
Volkmann et al.,2001125
16 Prosp NC STN 12 13.7/11.019.7%
28.8/12.656.3%
15.1/16.4-8.6%
56.4/22.460.3%
2.73
11 GPi 12 12.1/5.852.1%
21.0/12.142.4%
30.2/16.744.7%
52.5/16.768.2%
2.0/80.0
Durif et al.,2002126
6 GPi 6 N/A N/A Unchanged 36% N/A
6 GPi 12 N/A N/A Unchanged 26% N/A6 GPi 24 N/A N/A Unchanged 38% N/A
6 GPi 36 N/A N/A Unchanged 32% 14113.4
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Simuni et al.,2002134
12 Prosp NC STN 12 N/A N/A 19.3/19.82.6%
43.5/23.047.1%
1946/8755.0%
Thobois et al.,2002135
18 Prosp NC STN 6 5.3/8.152.8%
26.9/12.752.8%
17.9/15.215.1%
44.9/20.255.0%
1045/3635.5%
14 Prosp NC STN 12 5.3/7.541.5%
26.9/10.760.2%
17.9/1327.4%
44.9/1762.1%
same
Vesper et al.,2002136
38 Prosp NC STN 12 N/A N/A 27.7/17.437.2%
48.3/24.948.4%
900/58035.5%
Vingerhoetset al., 2002137
20 Prosp NC STN 21 N/A 21.0/13.337%
N/A 48.8/26.944.8%
1135/2379.7%
Voges et al.,2002138
15 Prosp NC STN 6–12 N/A NA N/A 55.3/22.758.9%
909/37458.9%
Welter et al.,2002139
41 Prosp NC STN 6 10.4/6.636.5%
29/11.161.7%
14.7/10.627.9%
51.4/18.564.0%
1459/4867.1%
Chen et al.,2003140
7 Prosp NC STN 6 N/A N/A 39.0/19.151.0%
65.7/32.850.0%
N/A
Daniele et al.,2003141
20 Prosp NC STN 12 10.1/6.238.6%
31.8/8.872.3%
24.0/22.17.9%
58.8/30.947.5%
1395/5064.2%
9 STN 18 12.4/5.456.5%
33.1/7.477.6%
25.0/17.330.8%
60.8/27.055.6%
1185/5354.8%
Funkiewiez et al.,2003142
50 Prosp NC STN 12 N/A N/A N/A N/A N/A
Herzog et al.,2003143
48 Prosp NC STN 6 N/A 22.6/10.752.6%
18.7/14.721.4%
44.2/21.750.9%
1425/7348.8%
32 STN 12 N/A 21.6/10.749.2%
18.1/12.431.5%
43.9/18.757.4%
42.4%
20 STN 24 N/A 23.4/13.243.2%
19.3/12.435.8%
44.9/19.257.2%
67.8%
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Table 2
(continued )
Author, Year N Type Target
Duration
(mo) UPDRS II ADL
UPDRS III
Motor LE
Kleiner-Fismanet al., 2003144
25 Prosp NC STN 12 12.1/10.513.2%
25.8/17.432.6%
22.8/19.414.9%
50.1/24.650.9%
38
Krack et al.,2003145
49 Prosp NC STN 60 (5 y) 7.3/14.091.8%
30.4/15.648.7%
14.3/21.147.6%
55.7/25.853.7%
140963.2
Pahwa et al.,2003146
33 Prosp NC STN 12 N/A 21.1/14.332.2%
N/A 43.8/26.539.5%
10.444.2
19 STN 24 11.6/12.810.3%
21.1/15.327.5%
26.2/24.18.0%
41.3/29.827.8%
12.457.3
Varma et al.,2003147
7 Prosp NC STN 6 15/146.7%
38/25 34.2% 61% 206749.0
Volkmann et al.,2004148
9 Prosp NC Gpi 36 11.3/7.137.2%
20.9/15.525.8%
30.8/13.954.9%
52.8/26.849.2%
870/3.1
6 60 8.8/10.317.1%
19.5/19.81.5%
22.2/18.715.8%
49.5/38.023.2%
961/20.9
Liang et al.,2006149
27 Prosp NC STN 12 10.0/9.46.0%
26.0/17.333.5%
17.6/19.711.9%
38.4/23.937.8%
136436.4
33 10.0/17.272.0%
26.0/22.314.2%
17.6/22.125.6%
38.4/26.531.0%
136424.6
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Portman et al.,2006150
20 Prosp NC STN 12 N/A N/A 23/2013.0% NS
46/3328.3%
124239.5
Derost,2007151
53 Prosp NC STN 24 3.7/8.51.3%
18.0/15.613.3%
N/A 45.0% 124628.9
34 STN 24 5.6/11.198.0%
18.8/16.711.2%
N/A 41.0% 130841.9
Gan et al.,2007152
36 Prosp NC STN 12 4.5/8.588.9%
23.7/12.547.3%
14.1/12.511.3%
42.2/21.050.2%
122861.7
36 4.5/12.5177.8%
23.7/13.941.4%
14.1/12.511.3%
42.2/19.354.3%
122848.6
Rodriqueset al., 2007153
11 Prosp NC Gpi 7 N/A N/A 12.5/10.416.8%
40.6/21.846.3%
11822.9
Schüpbachet al., 2007154
10 Prosp NCComp BMT
STN 18 2.3/5.1121.7%
19.2/12.932.8%
NA 69.0% 57.0
Tir et al.,2007155
100 Prosp NC STN 12 9.5/815.8%
27.5/1930.9%
20/14.428.0%
50/2942.0%
122241.0
Vesper et al.,2007156
73 Prosp NC STN 24 N/A N/A 30/2613.3%
50/2550.0%
45.0
Witjas et al.,2007157
40 Prosp NC STN 12 8.8/4.746.6%
23.7/13.343.9%
11.8/6.941.5%
38/12.467.4%
109157.8
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Table 2(continued )
Author, Year N Type Target
Duration
(mo) UPDRS II ADL
UPDRS III
Motor LE
Zibetti et al.,2007158
36 Prosp NC STN 12 N/A 25.3/9.960.9%
N/A 54.5/25.852.7%
24 N/A 25.3/10.359.3%
N/A 54.5/24.155.8%
Wider et al.,2008159
50 Prosp NC STN 6 10.0/11.515.0%
N/A 24.3/26.79.9%
47.2/24.847.5%
24 10.0/12.828.0% N/A 24.3/27.714.0% 47.2/24.947.3%
60 10.0/18.989.0%
N/A 24.3/30.625.9%
47.2/33.229.7%
Abbreviations: BDI, Beck’s Depression Inventory; BMT, Best medical treatment; DRS, Mattis Dementia rating scale; complication) or AIMS (abnormal involuntary movements scale); FBA, frontal battery assessment scale; GPi, Globuorrage; IVH, intraventricular hemorrage; LD, Levodopa dose only; LE, Levodopa equivalent (the method of calculaLID, levodopa induced dyskinesias; MADRS, Montgomery and Asberg depression rating scale; MDRS, Mattis Demestatus Examination; NS, nonsignificant; Off and On, applies to the medication state; Off time, Hours per day spent iParkinson disease quality-of-life questionnaire, total score; Prosp., NC, prospective noncontrolled clinical trial; Ssubdural hemorrage; STN, Subthalamic nucleus; Th, Thalamus; TIA, transient ischemic attack; UPDRS II—ADL, ac
motor subscore, maximum 108. Results are represented as Preoperative/Postoperative, with the percentage chantive)/Preoperative] 100.Data from Kenney C, Simpson R, Hunter C, et al. Short-term and long-term safety of deep brain stimulation in the
2007;106:621–5.
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Table 3
Summary of VIM thalamic DBS outcomes for ET
Study Sample Size Study Type Tremor Improvement
Pahwa et al., 2006160 26 Prosp NC 46% (unilateral) and 78%(bilateral) FTM TRS
Lee and Kondziolka, 2005161 18 Case series 75% improvement FTM TRS
Putzke et al., 2005162 22 Case series 81% improvement FTM TRS
Putzke et al., 2004163 52 Case series 45% improvement FTM TRS
Kumar et al., 2003164 5 Case series 62% improvement in FTM TRS
Bryant et al., 2003 165
16 Case series 34% FTM TRS Fields et al., 2003166 35 Case series 56% FTM TRS improvement
Rehncronaet al., 2003167
19 Prosp NC 46% improvement FTM TRS
Hariz et al., 200259 27 Prosp NC 47% improvement FTM TRS
Koller et al., 2001168 49 Case series 78% improvement FTM TRS
Obwegeser et al., 2001169 31 Case series 6-point reduction in FTM TRS
Pahwa et al., 2001170 17 Case control(vs thalamotomy)
50% improvement FTM TRS
Krauss et al., 2001171 42 Case series 57% excellent outcome, 36%marked improvement
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Troster et al., 199957 40 Prosp NC 51% reduction in FTM TRS
Limousin et al., 1999110 37 Prosp NC 55% reduction in FTM TRS
Pahwa et al., 1999 172 9 Case series 57% improvement in FTM TRS
Kumar et al., 1999173 9 Case series 61% improvement FTM TRS
Koller et al., 1999174 38 (headtremor)
Case series Head tremor improved in 75% patients
Hariz et al., 1999175 36 Case series 48% improvement in FTM TRS
Lyons et al., 1998176 22 Case series 39% improvement in FTM TRS
Ondo et al., 1998177 14 Case series 83% improvement in FTM TRS
Koller et al., 1997178 29 Prosp NC > 50% improvement in FTM TR
Hubble et al., 1996179 10 Prosp NC >50% improvement in bothpatient and clinician FTM TRSratings
Blond et al., 1992180 4 Case series Sustained improvement in 75%patients
Abbreviations: ADLs, activities of daily living; FTM TRS, Fahn Tolosa Marin tremor rating scale; MMSE, Folstein mini m
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Yianni et al.,2003188
12 Generalized GPi 4–184 BFMDRS (m) 79.7 45.3
7 Cervical GPi 2–12 TWSTRS (t) 57.8 23 Yianni et al.,
20031892 Primary DYT11 GPi 12 BFMDRS (m) N/A N/A 11 Primary DYT1 GPi 12 BFMDRS (m) N/A N/A 7 Cervical GPi 12 TWSTRS (s/d/p) 21.3/21.7/
15.110/14/8
Cif et al.,2004190
1 Myoclonus-dystoniasyndrome
GPi 20 UMRS 69 13
BFMDRS (m/d) 9.5/9 1.5/1
Coubes et al.,2004191
17 Primary DYT11 GPi 24 BFMDRS (m) 62.6 12.4 14 Primary DYT1 GPi 24 BFMDRS (m) 56.3 13.4
Detante et al.,2004192
13 Primary generalized STN 3 N/A N/A N/A 3 Secondary PKAN STN 3 N/A N/A N/A
Eltahawy et al.,200433
1 Primary DYT11 GPi 6 BFMDRS (m) 88 66
1 Primary DYT1 GPi 6 BFMDRS (m) 48 16 3 Cervical GPi 6 TWSTRS (t) 37.7 16
Krause et al.,2004193
4 Primary DYT11 GPi 12–66 BFMDRS (m) 72 34 6 Primary DYT1 GPi 12–66 BFMDRS (m) 73.9 50
1 Cervical GPi 12–66 BFMDRS (m) 6 6 Trottenberg et al.,
20051945 Secondary
tardiveGPi 6 BFMDRS (m/d) 32/8 N/A
Vayssiere et al.,2004195
19 Primarygeneralized
GPi N/A BFMDRS N/A N/A
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Starr et al.,2006201
6 Primary DYT11 GPi 13 BFMDRS (m) 59.6 24.2 3 Segmental GPi 22 BFMDRS (m) 22.6 12 1 Cranial-cervical (MS) GPi 9 BFMDRS (m) 30 3 1 Secondary PKAN GPi 12 BFMDRS (m) 30 6 1 Secondary
cerebral palsyGPi 33 BFMDRS (m) 82 51
1 Secondary
posttraumatic
GPi 32 BFMDRS (m) 54 49.5
4 Secondarytardive
GPi 20 BFMDRS (m) 46.5 24.6
2 Generalized GPi 11 BFMDRS (m) 83 72.8
Zhang et al.,2006202
1 Secondary tardivedystonia
STN 3 BFMDRS (m) 98.8 8
1 Secondaryantiemetics
STN 3 BFMDRS (m) 26.5 2
2 Secondaryneonatalanoxia
STN 6 BFMDRS (m) 76 7
5 Other secondary STN N/A N/A N/A N/A
Alterman,2007203
12 Primary DYT11 GPi 12 BFMDRS (m/d) 35/8 4/2
3 Primary DYT1 GPi 12
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Table 4
(continued )
Author N Type of Dystonia Target
Follow-up
Period (mos) Scale
Preoperative
Score
Postopera
Score Damier et al.,
200720410 Secondary tardive GPi 6 ESRS 73.1 27.8
AIMS 25 31.1
Evidente et al.,2007205
1 X-linkeddystoniaParkinsonism
GPi 12 UPDRS-III 21 8
BFMDRS (t) 32.5 9.5
Grips et al.,2007206
8 Segmental GPi N/A UDRS 36.9 16.1
GPi BFMDRS 25.6 13.1 GPi GDS 29.3 10.3
Hung et al.,200762
10 Cervical GPi 12–67 TWSTRS (s/d/p) 21.9/18/11.7 9.9/7.4/5.8
Kiss et al.,2007207
10 Cervical GPi 12 TWSTRS (s/d/p) 14.7/14.9/26.6 8.4/5.4/9.2
Kleiner-Flisman
et al., 2007208
1 Cervical STN 12 BFMDRS (m/d) 36.5/5 29/10
TWSTRS (s/d/p) 31/27/14 23/20/5.5 1 Cervical STN 12 TWSTRS (s/d/p) 21/16/17 12/5/14.31 Cervical STN 12 BFMDRS (m/d) 53/14 59/17
TWSTRS (s/d/p) 26/27/15.3 28/24/18.31 Primary
generalizedSTN 12 BFMDRS (m/d) 23/5 12/3
Novak et al.,2007209
1 Primarygeneralized
STN 29 BFMDRS (m/d) N/A N/A
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Ostrem et al.,200767
6 Cranial-cervical GPi 6 BFMDRS (m/d) 22/6 6.1/3.7 GPi 6 TWSTRS (t) 39 17
Sun et al.,200766
12 Primarygeneralized
STN 6–42 BFMDRS N/A N/A
2 Secondary tardive STN 6–42
Tisch et al.,
2007210
7 Primary DYT11 GPi 6 BFMDRS (m/d) 38.9/9.0 11.9/4.1
8 Primary DYT1 GPi 6
Vidailhet et al.,2007211
7 Primary DYT11 GPi 36 BFMDRS (m/d) 46.3/11.6 19.3/6.3
15 Primary DYT1 GPi 36
Loher et al.,2008212
4 Cervical GPi 36 TWSTRS (s/d/p) 20.5/40.5/6 14.7/15.7/2 Primary generalized GPi 36 BFMDRS (m/d) 81/18.5 28.3/7.5
Magarinos-Asconeet al., 200864
10 Primary generalized GPi 12 BFMDRS (m/d) 57.8/18.1 20.0/8.6
Sako et al.,2008213 6 Secondary tardive GPi 21 BFMDRS (m/d) N/A N/A
This table is an expanded version of that published in the work of Ostrem, 2007, with full permission from Elsevie Abbreviations: BFMDRS (m/d), Burke-Fahn-Marsden dystonia rating scale (motor subscore, maximum 120/disabil
Fahn-Marsden dystonia rating scale, total score; PKAN, pantothenate kinase associated neurodegeneration; TWSTrating scale (severity, maximum 35/disability, maximum 30/pain, maximum 18); UDRS, Unified dystonia rating scascale, motor subscore (maximum 108); UMRS, Unified myoclonus rating scale; ESRS, Extrapyramidal symptoms raments scale; GDS, Global dystonia scale; Primary generalized, Primary generalized dystonia of an unknown etDYT1 gene positive dystonia; Primary DYT1 -, Primary; generalized DYT1 gene negative dystonia, Percentage of cherative)/Preoperative]x100. For generalized and cervical dystonia, only reports with 5 or more cases were included. Fwere included.
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Ackermans et al.,2006218
2 Case study TS One patient GPi,other CM
85%–90% reductionin tics/minute bothpatients
Flaherty et al.,2005219
1 Case study TS Anterior IC 25% improvementin YGTSS
Diederich et al.,2005220
1 Case study TS GPi 46% improvementin YGTSS
Houeto et al.,2005221
1 Case study TS CM-Pf and GPi 65% improvementin YGTSS with eitheor both sites
Visser-Vandewalleet al., 2003222
3 Case series TS CM 82% reductiontics/minute
Vandewalle et al.,1999223
1 Case study TS CM 901% reductiontics/ minute
Fasano et al.,200897
1 Case study HD GPi Complete resolutionof chorea
Hebb et al.,200698
1 Case study HD GPi Significant improvemein total UPDRS andchorea
Moro et al.,2004224
1 Case study HD GPi 44% and 37% improvein chorea anddystonia
Freund et al.,200799
1 Case study SCA-2 VIM STN Improved tremor
Shimojima et al.,2005100
1 Case study SCA (negativegenetictesting)
VIM 45% improvement inFTM TRS
Foote and Okun,200596
1 Case study TraumaticHolmestremor
VIM, VOAand VOP
40% improvement inFTM TRS
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Table 5
(continued )
Study
Sample
Size Study Type Dx Target Motor Improvement
Nikkhah et al.,200469
2 Case series Holmes tremor VIM Improved tremor andystonia
Kudo et al.,2001225
1 Case study Holmes tremor VIM Improved tremor
Plaha et al.,200892
13 Case series PD, MS, ET,Holmes,dystonictremor
Zona Incerta 60%–90% improvemin all tremors
Lim et al.,200779
2 Case studies MS and stroke VIM/VOA andGPi (stroke
only)
40% improvement MS with VIM/VOA
in stroke with GPFoote et al.,
2006854 Case series MS 1 Trauma 3 VIM VOA/VOP 23%–66% improvem
in TRS, trend towmore improvemedual leads in 2 pa
Moringlane et al.,200490
1 Case study MS VL Improved tremor
Wishart et al.,200395
4 Case series MS VIM Improved tremor
Schulder et al.,200393
9 Case series MS VIM 68% improvement Bain-Finchley TRS
Bittar et al.,200583
10 Case series MS VOP/ZI 64% and 36%improvement ofpostural and intetremor on 10-poiscale
Berk et al.,200282
12 Case series MS VIM Overall tremor redu63% on Fahn ratiscale
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several months or even longer, suggesting that GPi DBS in dystonia may have both
direct effects from stimulation and also induce longer-term neuroplastic changes or
disease-modifying benefits.23
The potential chronic side effects of GPi DBS for dystonia are similar to those seen
in PD. With regard to mood disturbances, a careful neuropsychiatric evaluation,
particularly in patients with tardive dystonia, is strongly recommended.58 Patients
with dystonia appear to have a lower risk of cognitive side effects after GPi DBS,
possibly because they are younger and the underlying disease may be associated
with less cognitive dysfunction and fewer comorbidities.72 However, suicides in
patients, particularly those with premorbid depression, have been reported following
GPi DBS for dystonia.73 Another side effect noted in a small case series of patients
with Meige syndrome was the development of a subjective sense of clumsiness and
slowness in previously unaffected body parts.67 Although these symptoms were often
not evident on examination, they were persistent and present only when DBS was
turned on. Side effects from field spread into pallidal and surrounding regions are
similar to what is seen in GPi DBS for PD.
OTHER MOVEMENT DISORDERS
There have been several case series demonstrating the potential for DBS in Tourette
syndrome (TS). These case series have used multiple separate targets and combina-
tions of targets, including the centromedian thalamus-parafascicular complex
(including the ventralis oralis complex of the thalamus),74 GPi,75 the anterior limb of
the internal capsule,76 and the nucleus accumbens.77 As a side benefit, many of these
patients also noted improvements in comorbid psychiatric symptoms, including anxiety
and obsessive-compulsive disorder. Principles of patient selection are similar to thosein other movement disorders, namely, the use of a multidisciplinary team to carefully
screen patients and failure to achieve adequate symptom control despite maximal
medical management. The Tourette Syndrome Association has now published general
guidelines for Tourette DBS.78 There are several small case series showing improve-
ment in poststroke tremor,79,80 posttraumatic tremor,79,80 and multiple sclerosis (MS)
tremor with DBS.79–95 These treatments typically target the VIM, although some authors
have used multiple simultaneous thalamic or GPi and thalamic targets.79,85,96 VIM in
complex tremors may not be the target of choice, and other areas of thalamus will
need to be explored ventralis oralis anterior, ventralis oralis posterior and centromedian
(Voa, Vop, CM). In these patients, one must be careful to determine how much disability
is due to tremor, which may improve with DBS, versus ataxia or weakness, which will not
improve with DBS. Three case reports suggest that chorea in Huntington’s disease (HD)
may be reduced with bilateral GPi DBS.97,98 Case reports of efficacy in some of the
spinal cerebellar ataxias have also been reported.99,100 In Table 5 we provide a review
of the literature on DBS outcomes in other movement disorders for motor, mood, QOL,
and cognitive outcomes. In studies of mixed populations, we included only studies
where specific outcome information was available for each diagnosis.
SUMMARY
DBS is an efficacious treatment option for appropriately selected patients with PD, ET,
and dystonia. Indications and options for DBS continue to expand rapidly. There are
important side effects and benefits that may influence target selection for individual
patients. Advances in our understanding of the pathophysiology of movement disor-
ders combined with technological advances in our ability to precisely target neuroan-
atomical structures continue to push improvements in the efficacy and safety of DBS
Surgical Treatment of Movement Disorders 665
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for basal ganglia disorders. Basic science advances need to be combined with well-
designed clinical trials to define rational treatment algorithms to improve motor, mood,
cognitive, and QOL outcomes.
ACKNOWLEDGMENT
The authors would also like to acknowledge Leah Gaspari for her assistance in the
preparation of this manuscript.
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