ISCHEMIA DURING DBS IMPLANTATION

Two Cases of Ischemia
Associated With Subthalamic
Nucleus Stimulator Implantation
for Advanced Parkinson’s Disease
Kevin E. Novak, PhD,1,2*
Emmanuel K. Nenonene, DSci, PhD,1,2
Lawrence P. Bernstein, MD,1,2 Sandra Vergenz, RN,1
Gina Medalle, RN,1 Jordan M. Prager, MD,3
Theodore W. Eller, MD,4 Jeffrey W. Cozzens, MD,5,6
and Michael Rezak, MD, PhD1,2
1

Department of Neurology, at Evanston Northwestern
Healthcare, Evanston, Illinois, USA; 2Department of
Neurology, at Northwestern University, Feinberg School of
Medicine, Chicago, Illinois, USA; 3Department of Radiology,
at Evanston Northwestern Healthcare, Evanston, IL, USA;
4
Department of Neurosurgery, Rockford Memorial Hospital,
Rockford, Illinois, USA; 5Department of Neurosurgery, at
Evanston Northwestern Healthcare, Evanston, Illinois, USA;
6
Department of Neurosurgery, at Northwestern University,
Feinberg School of Medicine, Chicago, Illinois, USA
Abstract: Deep brain stimulation is generally a safe and
effective method of alleviating motor impairment in advanced-stage Parkinson’s disease patients. However, adverse events of surgery have been noted, such as hemorrhage, infection, seizures, and device failure. In this report,
we describe 2 cases of the unusual adverse event of ischemia
associated with subthalamic nucleus stimulator implantation. We present the intraoperative neurological symptoms,
microelectrode recording data, imaging findings, and other
correlated events. In the first case, the clinical effects of
ischemia were evident intraoperatively and coincided with
silence during microelectrode recording from the ischemic
region. In the second case, the timing of the ischemic event
could not be determined precisely but also was associated
with a difficult mapping. Subcortical ischemia may be an
underrecognized event that confounds neurophysiological
mapping of deep brain structures and affects clinical
outcomes. © 2006 Movement Disorder Society
Key words: Parkinson’s disease; deep brain stimulation;
subthalamic nucleus; complications; ischemia; microelectrode
recording

The motor impairment in Parkinson’s disease (PD) is
often disabling and diminishes quality of life.1 In the past

*Correspondence to: Dr. Kevin Novak, Evanston Northwestern
Healthcare, Department of Neurology, 2650 Ridge Avenue, Searle
4995E, Evanston, IL 60201. E-mail: k-novak@northwestern.edu
Received 2 August 2005; Revised 22 November 2005; Accepted 24
January 2006
Published online 23 May 2006 in Wiley InterScience (www.
interscience.wiley.com). DOI: 10.1002/mds.20947

1477

decade, surgical treatment for PD has gained acceptance
as an effective method to control the medically refractive
motor symptoms of PD.2,3 Destructive radiofrequency
lesioning has been superseded by deep brain stimulation
(DBS) of the globus pallidus interna (GPi)4 and subthalamic nucleus (STN).5 DBS for advanced PD is very
effective, particularly in patients whose therapeutic window (the balance between beneficial and undesirable side
effects) has narrowed. STN DBS currently is the preferred surgical option for treating the three major PD
symptoms: tremor, rigidity, and bradykinesia.6 This procedure also allows levodopa doses to be reduced considerably,7 reducing motor fluctuations and dyskinesias.
Although the benefits of movement disorder surgery
on patient quality of life are substantial, the morbidity
and mortality associated with invasive surgery can also
be significant. A report of adverse events from one DBS
case series8 included a meta-analysis of seven other
studies totaling over 900 patients. Adverse events occurred in 115 patients (12.7%), including intracranial
hemorrhage (ICH, 4.1%), infection or erosion (4.2%),
seizures (1.1%), and death (0.6%). Although ICH is
known to occur in 1 to 4% of cases,9,10 and its risk factors
have been studied recently,11,12 nonhemorrhagic lesions
induced by movement disorders surgery (and other stereotactic surgery involving intraparenchymal penetration
such as biopsy or depth electrode placement for epilepsy
surgery) commonly are not reported. Although there was
one report of cerebral venous infarction8 and 9 cases of
cerebral contusion,13 there were no reports of subcortical
ischemia in the review of DBS surgical complications in
900 patients.
Because it is seldom reported and its symptoms may
not be apparent immediately, ischemia may be an underrecognized problem that contributes to failed localization
and poor outcomes. We encountered 2 cases of new
ischemic lesion along the electrode trajectory, discovered
on diffusion-weighted imaging after surgery to implant
subthalamic stimulators. We present the clinical, neurophysiological, neurological, and neuroradiological findings of these 2 cases.
PATIENTS AND METHODS
Patients with late stage, poorly controlled idiopathic
Parkinson’s disease were evaluated by a movement disorders specialist and elected to have surgery for placement of STN stimulators. Preoperative evaluation included the use of several clinical rating scales for PD,14
including the Unified Parkinson’s Disease Rating Scale
(UPDRS) and Hoehn & Yahr (H&Y) staging; the “stepsecond test” of gait, which measures the number of steps
and time required to walk 15 feet and back; neuropsy-

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K.E. NOVAK ET AL.

chological testing; and brain magnetic resonance imaging (MRI). Patients were excluded if they had central
nervous system (CNS) pathology such as stroke, tumor,
or other CNS disease; severe cognitive or behavioral
impairment; significant medical illnesses; or who were
judged unable to tolerate the procedure.
Stereotactic surgery was performed with Radionics
(Burlington, MA) halo base-plate, MRI localizing frame,
and Cosman–Roberts–Wells stereotactic frame. Standard
MRI-based targeting of STN was performed on T2 axial
images. Based on the Schaltenbrand and Wahren (S&W)
anatomical atlas,15 STN was targeted at a point 12 mm
lateral and 4 mm posterior to the mid-commissural point
(MCP) in an axial section 4 mm ventral to the anterior
commissure–posterior commissure (AC-PC) line. During
some cases, the surgeon would choose a target visually
from T2 coronal sections (Fig. 2A). In the operating
room, a 10-mm burr hole was drilled anterior and lateral
to the coronal suture for passing electrodes into the brain
along a superior–anterolateral to inferior–posteromedial
trajectory. Microelectrode recording was performed for
localization of the STN. The angle of microelectrode
penetration in the sagittal plane was typically 50 to 55
degrees up from the AC-PC line and 10 to 20 degrees
from vertical in the coronal plane. Multiple penetrations
were made orthogonal to the first one by adjusting the
position of the x–y stage in either the anteroposterior or
mediolateral direction with respect to the frame.
Microelectrode recordings were made with commercially available equipment (ARS Neurosystem-2, Atlantic Research Systems, Atlanta, GA; or Axon Guideline
3000A, Fred Haer Corp., Bowdoinham, ME). Glasscoated, platinum iridium microelectrodes with an impedance of approximately 1.0 M⍀ were used (Fred Haer
Corp.). MER tracks were reconstructed with marker on
transparencies and overlaid onto parasagittal S&W sections,15 or with a computerized drawing program and
digitized atlas. Because the penetrations were made with
a 10- to 15-degree coronal angle and, thus, passed
through multiple parasagittal planes, using the S&W
parasagittal sections could lead to inaccuracies in mapping. To generate a more accurate brain atlas in the plane
of the recording, the S&W atlas was digitized and manipulated to generate oblique parasagittal sections. Each
S&W section was colored in grayscale tones and placed
into a three-dimensional (3D) volume, using interpolation in the mediolateral direction to generate the volume
between S&W sections. This volume was resliced according to the electrode trajectory. Figure 1 shows a
10-degree oblique parasagittal slice from this volume,
passing through 11.0 mm lateral at the level of the
AC-PC axial plane. Essentially, the top of the plane uses

Movement Disorders, Vol. 21, No. 9, 2006

FIG. 1. Four MER tracks from Case 1 were reconstructed on a
digitized atlas. Thalamic units (dark lines or circles along the MER
track) were encountered above the area of infarct, but the infarcted area
(gray circle) was atypically silent.

relatively lateral S&W parasagittal sections, whereas the
bottom uses medial ones.
Intraoperative neurological testing of the patients included periodic communication and examination during
the recording, and more extensive neurological examination after every track. Additional testing during the
recording involved examining the somatomotor responses of neurons. Receptive fields of cells were examined by passively manipulating the patients’ joints on the
contralateral side.
Per our protocol, after the STN was localized with
microelectrode recording, the quadripolar stimulating
lead (Model 3389, Medtronic, Inc., Minneapolis, MN)
was placed such that the bottom electrode was at the
ventral border of the STN. We aimed for the center of the
STN in the AP direction, and slightly lateral in the ML
direction, usually choosing the track with the longest
stretch of active, sensorimotor cells.
The lead was tested intraoperatively for relief of
symptoms and possible adverse events using a Medtronic
Model 3628 test stimulator with the following parameters: 0.0 to 5.0 V, 130 to 185 Hz., and 90 to 120 ␮sec
pulse width, using monopolar cathodal stimulation of
each electrode individually, with scalp as anode. As the
voltage was slowly increased, the awake patient was
asked to report any unusual sensations, and the patient
was examined for capsular responses (contralateral arm,
leg, and face contraction) and eye movements. We asked

ISCHEMIA DURING DBS IMPLANTATION
the patient to repeat a phrase and listened for dysarthria.
Surface electromyogram (EMG) and accelerometers or
velocity sensors were used to measure the benefits (i.e.,
speed of rapid alternating pronation–supination movements or reduction in tremor on EMG and movement
sensors) and adverse events (i.e., tonic contraction) of
test stimulation. If the patient experienced serious adverse events at low voltages, such as dysarthria or capsular response, the lead was moved to another location
away from the area of unwanted stimulation, according
to the mapping and known anatomy of the region. If
results were satisfactory (the patient had no serious adverse events at low voltages, and ideally the patient
showed some immediate improvement of motor symptoms), the lead was permanently secured in place. Fluoroscopy was used to ensure that the lead did not move
during attachment to the burr-hole cap. The pulse generator (Medtronic Soletra) was typically implanted the
same day, with the lead tunneled subcutaneously and
connected to the generator.
Postoperative imaging included same day computed
tomography (CT) and MRI the following morning to
look for complications and to verify the location of the
stimulating electrode. The bottom electrode of the quadripolar lead was identified as the most ventral artifact on
images (MRI hypointensity). Laterality of the bottom
electrode from midline was measured using the GE distance tool on axial or coronal sections. Anterior–posterior and dorsal–ventral location of the bottom electrode
was measured with a computer drawing program. The
most medial parasagittal T1 MRI section showing the
lead was overlaid onto the midsagittal section showing
the AC and PC, and the drawing program measured the
distance from this midsagittal point. More recently, postoperative 3D spoiled gradient MRI data were imported
into the computer software program AFNI16 for measurement of lead location. AFNI was used to transform the
images into AC-PC coordinates by selecting AC, PC,
and several midsagittal points, and subsequently to measure the bottom electrode in this coordinate system.
RESULTS
Case Series
During the first 5.5 years we offered STN DBS as a
treatment option for advanced-stage PD, 41 patients underwent surgery to implant 87 leads. Although surgery
was beneficial, complications did occur, such as ICH
(n ⫽ 2), subdural hematoma (n ⫽ 2), infection (n ⫽ 3),
device failure (n ⫽ 2), seizures (n ⫽ 1), failed mapping
(n ⫽ 1), lead relocation because of unsatisfactory results
(n ⫽ 5), and subcortical ischemic infarction (n ⫽ 2).

1479

Permanent deficits were present in 4 patients and consisted of cognitive and behavioral deterioration. Below,
we report the details of the 2 cases of ischemia.
Case Report 1
A 53-year-old man with severe tremor, bradykinesia,
and rigidity, predominantly on the right side, had symptoms refractory to medical management (800 mg of
L-dopa and 6 mg of ropinirole per day). Gait, posture,
and balance were intact, and the patient was in H&Y
stage 2. The patient completed the step-second test in 16
seconds, using 22 steps. Speech was hypophonic and
mildly dysarthric. UPDRS Motor scores in the off and on
medication states were 22 and 20.5, respectively. Vascular risk factors were negative for hypertension and
diabetes, positive for obesity (body mass index [BMI] of
33), mitral valve disorder, and prior ischemic events (as
seen in periventricular and subcortical white matter on
FLAIR images in Fig. 2D), and unknown for other risk
factors. The patient elected to receive bilateral STN
DBS, implanted in a staged manner, beginning with the
left brain.
Five MER tracks were made in this patient, along a
trajectory angled 50 degrees in the sagittal plane, and 12
degrees in the coronal plane. Track 1 was toward the
target, as chosen on T2 coronal MRI (Fig. 2A). Four
additional tracks were made: 2 mm anterior, 5 mm anterior, 2.5 mm posterior, and 2 mm lateral to target.
Figure 1 shows the reconstruction of the first four MER
tracks, overlaid on a 10 degree (coronal angle) oblique
parasagittal section based on the Schaltenbrand and
Wahren atlas. The areas where thalamic cells were encountered are highlighted in black. The quiet area with
no cells, presumably from the ischemic infarction, is
shaded with a gray, 10-mm diameter circle. The reconstruction in Figure 1 reveals a targeting error, in which
the initial track went 8 mm behind the intended target of
4 mm posterior to the MCP.
All five tracks showed the same overall pattern of
extracellular neuronal activity. Low rate, bursting thalamic units were encountered over a 10-mm region from
roughly 20 to 10 mm above target. Immediately after this
typical thalamic activity, during the first three tracks,
activity was faster and more regular for 1 to 3 mm.
Below this region, neural activity was extremely depressed, presumably due to ischemia.
The patient was noted to have slurred speech and mild
right-side weakness following the fifth microelectrode
recording track. The surgical procedure was aborted, and
the patient was brought to the CT suite in stable condition. Same-day postoperative CT scan revealed a small,
hypodense abnormality in the thalamus, shown in Figure

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K.E. NOVAK ET AL.

FIG. 2. Case 1 images. A: T2 image used for targeting subthalamic nucleus preoperatively. B: Computed tomography scan 30 minutes after surgery
shows decreased density in the left thalamus. C: Diffusion-weighted magnetic resonance imaging (MRI) scan later that day depicts acute infarct. D:
Fluid-attenuated inversion recovery (FLAIR) MRI scan at 6 weeks after surgery demonstrates encephalomalacia.

2B. The diffusion-weighted MRI scan in Figure 2C
shows a hyperintensity in the left thalamus indicative of
acute ischemic stroke. The signal abnormality persisted 6
weeks later on the FLAIR image, shown in Figure 2D.
Repeat imaging 2.5 years after surgery (not shown) demonstrated an area of encephalomalacia.
On follow-up, the patient experienced no cognitive or
behavioral disturbances. The patient obtained relief of
his tremor for 2 years after the event, with a 60% improvement in his rigidity and bradykinesia on the effected side. In the past 6 months, the patient’s tremor has
progressed slightly, and the patient’s mild dysarthria has
persisted. To date, no stimulator has been implanted in
this patient.
Case Report 2
The patient was a 67-year-old man with tremor predominant idiopathic PD who was no longer responsive to
medical therapy without experiencing significant adverse
effects. He was treated with 600 mg of L-dopa daily but
could not tolerate a higher dose without nausea, and his

symptoms remained inadequately controlled. UPDRS
Part III score was 48.5 in the medication off condition,
and 43.0 in the medication on state. He had no dyskinesias on or off medication, and because medication was
not particularly helpful, had no motor fluctuations. Preoperative MRI scans revealed enlarged perivascular
spaces in the basal ganglia bilaterally (not shown). In
addition, multiple, scattered, small foci of increased T2
signal nonspecific for ischemia in the basal ganglia,
thalamus, and periventricular and subcortical white matter, were found on FLAIR images (Fig. 3A). Vascular
risk factors were negative for hypertension, diabetes, and
valvular heart disease; positive for hypercholesteremia,
obesity (BMI of 35) and prior ischemia; and unknown
for other factors. The patient elected to receive staged
bilateral STN DBS implantation. Prior left STN DBS
insertion provided excellent benefit, including a reduction in tremor and other right-sided symptoms. Two
months after left brain implantation, surgery was undertaken to implant the right side, as described below.

FIG. 3. Case 2 images. A: Fluid-attenuated inversion recovery magnetic resonance imaging before surgery. B: T2 image after left brain implantation.
C: Next-day imaging shows increased T2 signal in the right caudate/periventricular white matter. D: Eight-day imaging shows diffusion weighted
abnormality indicative of ischemia.

Movement Disorders, Vol. 21, No. 9, 2006

ISCHEMIA DURING DBS IMPLANTATION
Seven recording tracks were made in this patient,
along trajectories angled 49 degrees in the sagittal plane
and 16 degrees in the coronal plane. The first track
passed through the posteromedial edge of the globus
pallidus externa, the anterolateral edge of the subthalamic nucleus, and into the substantia nigra. Subthalamic
nucleus was identified from 2.2 mm above target to 4.0
mm below, followed by substantia nigra 1.0 mm later.
None of the STN units were modulated by passively
manipulating the contralateral joints. Track 2, made 1.5
mm anterior to the target, traversed more of the pallidum
and missed in front of the STN. Pallidal units were
recorded from 14.3 to 4.6 mm above target. STN was
traversed on the edge, with two units present at 1.2 mm
above target. During electrode pass 3, located 2 mm
medial to target, the only activity was a small train of
potentials at 3.9 mm below target. There was a surprising
absence of neuronal discharge above this area. Equipment-related technical problems were ruled out, and the
electrode’s impedance remained stable at around 750
k⍀. The fourth electrode pass was 1.5 mm posterior. It
was also extremely quiet, with only seven sparsely
spaced, small units from 9 to 6 mm above target. Below
this area, only a single, small, pulse-bursting cell was
found at 0.5 mm below target. No active STN was found.
During track 5, 1.5 mm lateral to target, again only a
few scattered units were recorded. Cells from what
seemed to be pallidum were encountered from 9 to 5 mm
above target, and a few small STN cells were recorded
from 3 mm above to 2 mm below target. Track 6 was
made 1.5 mm lateral and 1 mm posterior to target.
Pallidal units were encountered at the top of the penetration, and STN from 4.7 mm to 0.4 mm above target.
The first cell in STN was a tremor unit, with a peak on
the firing rate frequency spectrum at 4.4 Hz. The final
track was made 1.5 mm anterior and 1.5 mm medial to
target. Eight GPi cells were recorded from 10.2 to 5.1
mm above target, all with faster, more regular firing. No
other neuronal activity was encountered.
After exploring the subthalamic area in several directions and encountering an unexplained absence of activity in many areas, the stimulating electrode was ultimately placed in Track 1, the track with the longest
extent of STN activity. During test stimulation at each of
the electrodes, no benefits or adverse events were noted.
During surgery, the patient had no observable deficits.
The motor system was intact, and the patient had no
language or speech problems.
Same-day postoperative CT scan showed implanted
leads and associated artifact, but no abnormalities. Nextday MRI showed increased T2-weighted signal due to
edema and/or ischemic changes, seen posterior and me-

1481

dial to the right-sided electrode on axial MRI scan in
Figure 3C. The 7-day CT images again were normal, but
8-day MRI scans showed a persistent T2 hyperintense
and gadolinium-enhancing lesion (not shown). The diffusion-weighted image (Fig. 3D) at 8 days was also
abnormal, consistent with the notion that the lesion was
ischemic. The right brain lead was measured on MRI to
be placed slightly anterior and lateral to the desired
location, with measured coordinates of electrode 0 at 1
mm posterior, 14 mm lateral, and 5 mm below the MCP.
Furthermore, the patient developed a right-sided subdural fluid collection, which spontaneously reabsorbed
over several weeks.
The patient was stable when discharged to home 2
days after surgery. Approximately 3 to 6 days after
surgery, the patient became confused and had short-term
memory loss. Electroencephalogram testing 10 days after
surgery was mildly abnormal with slight slowing, but at
3 months, slowing was more pronounced and focal to the
right side. In addition, bilateral epileptiform activity was
noted during sleep. The patient was treated with anticonvulsants, and there was improvement in confusion, despite some persistent short-term memory problems.
Tremor remains effectively controlled with bilateral
DBS implants. UPDRS Motor score at 9 months after
surgery was 15.5 with the patient’s stimulator ON and
L-dopa dosage was cut to 300 mg. Current stimulator
settings for the left brain lead are 1-, 2-, case ⫹, 1.5 V at
185 Hz, and 120-␮sec pulse width. For the right brain,
stimulator settings are electrode 3-, case ⫹, 3.9 V at 185
Hz, and 180-␮sec pulse width.
DISCUSSION
We report 2 cases from a series of 41 consecutive
patients in which microelectrode recording and subthalamic stimulator implantation resulted in subcortical,
nonhemorrhagic lesions. These hyperintense T2 lesions
show restricted diffusion, evolved into encephalomalacia
and, thus, are best described as ischemic infarcts. A
review of the literature revealed only a few other reports
of subcortical ischemic infarction related to movement
disorders surgery. Sutton reported two instances of thalamic infarct during STN DBS,17 which were not apparent perioperatively but resulted in persistent language
deficits. The other report was of a lesion in the internal
capsule during a unilateral pallidotomy adjacent to the
radiofrequency lesion.18 It is possible that other patients
may have experienced ischemic events intraoperatively
or perioperatively, but these events went unrecognized,
due to delayed clinical manifestation and inconsistent
follow-up with MRI, or have not been reported.

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Although much attention has been given to risk factors
and the frequency of ICH in movement disorders surgery,11,12 not much is known about the frequency, clinical significance, and risk factors for ischemic infarction.
One study reported 3 cases of delayed infarction of the
posterior limb of the capsule after pallidotomy.19 These
authors showed a significantly higher incidence of infarction in patients with pre-existing vascular disease
(3/11) compared to those with vascular disease risk factors (0/11) and those with neither disease nor risk factors
(0/20). That both of our cases of surgically induced
infarction had small vessel disease or pre-existing areas
of ischemia (Figs. 2D and 3A) supports that this condition may be a risk factor for intraoperative ischemic
infarct. Other positive risk factors for stroke20 were obesity in both patients, hypercholesteremia in 1, and mitral
valve disease in the other. It is important to consider the
possibility that pre-existing vascular disease may increase risk of ischemic stroke during movement disorder
surgery.
There are several potential obstacles to successful
implantation of subthalamic stimulators, including targeting errors, technical problems with equipment, misinterpretation of MER, and adverse events due to MERinduced brain injury. We encountered an apparent
targeting error in Case 1, as the initial penetration went 8
mm more posterior than planned. Some of this inaccuracy may result from choosing the target on a coronal
section, with seven fiducial markers, and not using the
standard atlas-based coordinates chosen on axial images
(with nine markers). Our current practice with axial
targeting has resulted in accuracy of over 90%, with
success defined as recording STN activity from the first
track.
Although it is possible we misinterpreted the MER
activity in Case 1 and had silence because we recorded
from noncellular areas, the majority of the evidence
supports that we recorded from a cellular area (thalamus)
that was abnormally silent because of ischemia. As
shown in Figure 1, Tracks 1, 2, and 4 should have
traversed 20 mm of thalamus, yet only 10 mm was
encountered at the top. The unexplained quiet area on the
bottom 10 mm of thalamus corresponds directly with the
location of the infarct on MRI. The hypothesis that
ischemia caused MER silence and that unexplained MER
silence may indicate ischemia is supported in Case 1 by
the appearance of clinical signs of stroke after five MER
tracks and immediate postoperative imaging findings.
In Case 2, however, the timing of the ischemic event
could not be determined with certainty, as the patient
displayed no obvious signs during surgery and the immediate imaging findings were inconclusive. Thus, the

Movement Disorders, Vol. 21, No. 9, 2006

hypothesis that ischemia caused unexplained MER silence in this patient is not supported. It can only be
suggested that a dorsal ischemic infarct occurred intraoperatively, blocking afferent excitatory input to STN by
means of cortico-subthalamic and striato-subthalamic
pathways, and reducing STN activity. Although other
arguments support the hypothesis that ischemia may
have caused unexplained STN silence, such as that the
lead looks mostly well placed in or near STN on MRI,
that we isolated a STN cell that fired at tremor frequency
on Track 6 and that the patient receives clinical benefit
from this stimulator, it cannot be proven that an ischemic
event occurred during the MER to cause unexplained
MER silence in STN. Another explanation for STN
silence, such as anterolateral targeting, may be correct
instead. Nonetheless, whenever unexpected silence is
encountered and other explanations are ruled out, an
acute ischemic insult should be considered. It is important to note that during Case 1, ischemia appeared to
change the activity of neurons before it could be clinically recognized.
One possible mechanism of ischemic stroke during
movement disorders surgery is vasospasm induced by
electrical stimulation, edema, or mechanical irritation. In
our Case 2, the area of edema may have compressed
small penetrating arteries, leading to ischemia. Christoforidis and colleagues18 suggested thrombosis or spasm
of a lenticulostriate artery in their case of ischemic infarct in the internal capsule. The mechanisms of surgically induced ischemia, vasospasm, and small perforating vessel ischemia (“lacunar infarct”) in general remain
poorly understood.21,22 One can speculate that a small
amount of blood product from a minor vessel rupture
could induce spreading depression, which, in the presence of the nitrous oxide scavenger hemoglobin, could
lead to vasoconstriction.23 This hypothesis seems to be
supported by the neurophysiological recordings of Case
1 (Fig. 1), in which there was increased thalamic single
unit activity just above the silent area, which could be the
expected result of a spreading depolarization wave.
Thus, neurons in the core of the infarct may be inactive,
but surrounding areas hyperactive, perhaps in the process
of dying.
CONCLUSION
Subcortical ischemic infarction can occur during implantation of DBS leads into subthalamic nucleus and
may occur more frequently than realized, especially in
apparently higher-risk patients that have pre-existing
vascular disease. It is important to recognize that, if
cellular activity suddenly disappears during MER map-

NEUROPSYCHOLOGICAL DEFICITS AND VH IN PD
ping, ischemia must be suspected, even without the immediate appearance of clinical symptoms.
Acknowledgment: The Evanston Northwestern Healthcare
movement disorders surgical program acknowledges the generous support of the Parkinson’s Disease Research Society.

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Neuropsychological Deficits in
Parkinson’s Disease Patients With
Visual Hallucinations
Blanca Ramı́rez-Ruiz, MSc,1,2* Carme Junqué, PhD,1,2
Marı́a-José Martı́, MD, PhD,2,3
Francesc Valldeoriola, MD,2,3
and Eduardo Tolosa, MD2,3
1

Department of Psychiatry and Clinical Psychobiology,
University of Barcelona, Barcelona, Spain; 2Institut
d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS),
Barcelona, Spain; 3Parkinson’s Disease and Movement
Disorders Unit, Neurology Service, Institut Clinic de
Neurociències, Hospital Clı́nic Universitari, University of
Barcelona, Barcelona, Spain
Abstract: Recent neuropathological and neuroimaging studies suggest the involvement of several temporal regions in
Parkinson’s disease (PD) patients with visual hallucinations
(VH). We examined 24 nondemented PD patients with VH,
21 PD patients without VH, and 21 healthy controls using a
battery of tests assessing different aspects of temporal lobe
function. PD patients with VH showed poorer performance
in language, verbal learning, semantic fluency, and visuoperceptive functions compared to controls and PD patients
without VH. Differences in verbal learning and visuoperceptive functions were independent of general cognitive
status, disease severity, and depression. We suggest that a
wide range of neuropsychological deficits can contribute to
the emergence of VH in PD. © 2006 Movement Disorder
Society
Key words: Parkinson’s disease; visual hallucinations; language; memory; visuoperceptive

Visual hallucinations (VH) belong to the most frequent neuropsychiatric symptoms of Parkinson’s disease

*Correspondence to: Dr. Carme Junqué, Departament de Psiquiatria
i Psicobiologia Clı́nica, Universitat de Barcelona, IDIBAPS, Casanova
143, 08036 Barcelona, Spain. E-mail: cjunque@ub.edu
Received 16 November 2005; Revised 20 January 2006; Accepted
24 January 2006
Published online 16 May 2006 in Wiley InterScience (www.
interscience.wiley.com). DOI: 10.1002/mds.20965

Movement Disorders, Vol. 21, No. 9, 2006