Targeting in DBS - Semantic Scholar · 2017-03-21 · a large therapeutic window between beneficial...

Yurui Gao, BME, Vanderbilt U

Targeting in DBS

Yurui Gao

Department of Biomedical Engineering, Vanderbilt University

CONTENT

WHAT IS DBS? ........................................................................................................................................... 2

History of DBS ....................................................................................................................................... 2

Hardware of DBS ................................................................................................................................... 3

Surgical Procedure of DBS ..................................................................................................................... 4

Mechanisms of DBS............................................................................................................................... 5

DBS vs. ablation ..................................................................................................................................... 7

WHAT ARE THE TARGETS IN DBS? ............................................................................................................ 8

Ventral Thalamic Nuclei ........................................................................................................................ 9

Subthalamic Nucleus ............................................................................................................................. 9

Globus Pallidus pars interna ............................................................................................................... 10

HOW TO TARGETING IN DBS? ................................................................................................................. 11

By brain atlas ....................................................................................................................................... 12

By visible surrounding anatomical landmarks .................................................................................... 14

By direct locating (SWI/7T MRI/DTI) ................................................................................................... 15

By microelectrode recordings ............................................................................................................. 16

By macro stimulation tests ................................................................................................................. 18

References .................................................................................................................................................. 20

Abbreviations

DBS: deep brain stimulation MRI: Magnetic Resonance Imaging CNS: central nerve system PD: Parkinson disease Vim: ventralis intermedius nucleus ET: essential tremor STN: subthalamic nucleus FDA: Food and Drug Administration GPi: globus pallidus pars interna TS: Tourette syndrome GPe: globus Pallidus pars externa OCD: obsessive compulsive disorder SNr: substantia nigra reticulata IPG: internal pulse generator


WHAT IS DBS?

DBS (deep brain stimulation) is a surgical treatment involving the implantation of brain

pacemaker, which sends electrical impulses to target structure deep in the brain for controlling

specific neural activity. The FDA approved DBS as a treatment for ET, PD and dystonia. DBS is

also commonly used to treat chronic pain as well as depression.

History of DBS

The modulation of brain activity by direct electrical stimulation of the brain can be traced to

1870[ (1)]. It was shown that electrical stimulation of the motor cortex in dogs can elicit limb

movement. Four years later, electrical stimulation was introduced as a tool for improving

neurosurgical procedures in humans [ (2)]. The emergence and development of human

stereotaxic devices provided neurosurgeons a chance to investigate the effects of stimulating

deeper cortical structures [ (3)] as well as to identify these deeper structures by observing the

effects of stimulation. Although stimulation had intraoperative use before 1960, its goal

focused on delineating the ‘best’ target for a subsequence lesion.

In the early 1960s, high-frequency (100Hz) stimulation of the ventrolateral thalamus could

diminish tremor [ (4)]. In the early 1970s, it is reported that chronic stimulation was used to

therapeutically treat pain [ (5)], movement disorders, or epilepsy [ (6)]. It took decades of years

to implement combining the implantable pacemaker technology with chronically implanted

deep brain electrode for long-term chronic DBS [ (7)]. Since then, DBS has become increasingly

used for treating a variety of disorders. The first widespread use of DBS in the US and Europe

was for the treatment of ET or the tremor of PD. Also DBS has been reported for treating


Fig.1. DBS hardware in patient http://www.riversideonline.com/source/images/image_popup/r7_deepbrain.jpght

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Lead

IPG

Extension

Lead

Extension

dystonia involved the thalamus [ (8)] and the GPi [ (9)]. There have been a few recent reposts of

DBS for TS [ (10)] and OCD [ (11)]. Furthermore, the advancements in neuroimaging, especially

MRI and intraoperative electrophysiological recordings have increased stereotaxic surgical

targeting accuracy.

Hardware of DBS

Figure 1 displays the major components of DBS hardware: the implanted pulse generator (IPG),

extension and lead (also called electrode). The IPG is a battery-power neurostimulator encased

in a titanium housing, which sends electrical pulses to the brain interfere with neural activity at

the target sites. DBS leads are 4 thin coiled wires insulated in polyurethane. Each wire ends in a

1.5mm platinum iridium electrode, resulting in 4 electrodes ending at the tip of the lead. These

quadripolar leads is implanted in

the brain with the electrodes

positioning at the target cerebral

sites and thus they deliver

stimulation using either one

electrode or a combination of

electrodes. IPG and lead are

connected by extension, an insulated wire that runs from the head, down the side of the neck,

behind the ear to the IPG, which is placed subcutaneously below the clavicle or abdomen. The

stretch coil extension is 15% extensible, which accommodates the natural movement of the

head, neck and shoulders.

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All the hardware of DBS is surgically implanted inside the body. Under local anesthesia, a

hole about 14mm in diameter is drilled in the skull and the electrode is inserted, with feedback

from the patient for optimal placement. The placement of the IPG and lead then occurs under

general anesthesia.

Surgical Procedure of DBS

The surgical procedure of DBS is similar to the ablative stereotactic neurosurgery, except the

final stage of electrode implantation.

First, a stereotactic head frame is fixed to the skull to establish a 3D coordinate system to

allow correlation of the preoperative imaging with each point in the brain and to prevent

intraoperative head movement. Holloway and colleagues [ (12)] proposed frameless stereotaxy

using bone fiducial markers to improve patient comfort. Thereafter CT and/or MRI scanning are

performed to identify the anterior and posterior commissures (also ventriculography). The

target sites of DBS may be or may not be directly indentified in the CT and/ or MRI image due to

the limit of resolution, therefore, direct or indirect targeting methods depending on imaging

process help to locate the target structure in patient’s brain.

Microelectrode recording (MER) and mircostimulation and/or macrostimulation is

performed to determine the best possible location for the DBS electrodes: optimal benefit and

a large therapeutic window between beneficial and adverse effects. After the optimal location

for implantation of the electrode has been decided, the DBS lead (macroelectrode) is secured

to the skull with a plastic cap, metal plate, or cement. The IPG can be implanted the same day.


Fig. 2. Surgical procedure of DBS in MRI [ (36)].

Stimulation settings are adjusted by means of a programmer placed on the skin overlying

the IPG. The adjustable stimulation parameters include frequency (0-185Hz), pulse width (60-

450sµ), voltage (0-10.5V), and stimulating contacts (monopolar or bipolar stimulation).

Mechanisms of DBS

Although the application of DBS has a long history, the therapeutic mechanism of DBS is

currently incompletely understood. In addition, no single mechanism has emerged to account

for the effect of DBS in different brain regions and in different diseases. The effects of DBS have

been well documented to be frequency dependent, with the greatest relief of symptoms at

>100 Hz and no therapeutic relief at <50 Hz. Stimulation pulse width (duration) determines

which neural elements are preferentially affected; longer pulse widths (1-10ms) influence the

cell soma, whereas shorter pulse widths (30-200µs) mainly affect axons. Furthermore, DBS


results in highly localized stimulation because relatively low currents are used which result in

small current spread (about 2-3 mm with an intensity of 2mA) and the intensity of stimulation

decreases proportionally to the square of the distance.

The general therapeutic stimulation parameters of DBS have been derived primarily by

trial and error, from the almost immediate effects on, such as tremor, rigidity, bradykinesia,

paresthesia and chronic pain in patients during surgery. The exact DBS parameters, including

the stimulus amplitude, duration and frequency band, vary with the treatment and with the

targeted brain region. At present, with most commercially available stimulators, these

parameters can be externally changed and fine-tuned over time. However, DBS allows only

open-loop continuous stimulation, which does not take into account the continuous neural

feedback from the individual patient.

It is suggested that the mechanism is reversible inhibition of the target site since the results

and effects are comparable to ablation. Several studies proposed that high-frequency

stimulation increases the excitatory response from the implanted site [ (13)]. GPi stimulation

may result in activation of GPe GABAergic axons [ (14)] that inhibit GPi neurons. A similar

phenomenon may exist with STN DBS. Two additional hypotheses have been proposed as the

mechanisms of DBS: (1) depolarization

blockade of myelinated axons; (2)

‘neuronal jamming’ whereby activation

of fibers transfers non-physiological

and incomprehensible messages to


Fig. 3. Complications of DBS in MRI. Left: Hemorrhagic cortical event. Right: Ischemia

downstream target nuclei, which are then disregarded. It is likely that the neuroanatomical of

various effects of DBS are complex incorporating a combination of various mechanisms (See the

above table: How does DBS work?[ (15)]).

DBS vs. ablation

There are two surgical-based techniques to benefit the affective disorder diseases we

mentioned above: ablation (thalamotomy and pallidotomy) techniques and DBS. DBS appears

to have the same effect as ablation-blocking neuronal transmission in the target nucleus to

improve of tremor and Parkinsonism. However, DBS electrode implantation causes fewer

permanent neurologic adverse effects compared with ablation because much less brain tissue is

destroyed [ (16)]. Radiofrequency ablations may be inadvertently expanded or be misplaced to

involve important structures close to the intended target, which potentially cause permanent

damage of tissue and loss of function. With DBS, stimulation parameters can be finely adjusted

to maximize beneficial results and minimize adverse effects caused by mild current spread to

adjacent structures. DBS electrodes can also be surgically repositioned if they are placed

suboptimally at the first time. Compare to the controllability of DBS, the effects of ablation are

irreversible and unchangeable without additional surgery.

Ablation is usually performed with the patient

awake; however, DBS requires an additional urgery

performed under general anesthesia to implant the IPG

and extension wire. Also, IPG needs to be replaced by

surgery every 2 to 7 years due to the battery out of


Fig.4. Targets in DBS. Left: describes the inhibitory and/or excitatory relationship among the targets in DBS. Right: shows the anatomical location of targets in hand-drawn picture [ (35)].

power. Approximately 25% to 30% of patients with DBS experience hardware complication [

(17)], typically mechanical hardware breakage or skin erosion over the hardware, which usually

require replacement of damaged or infected hardware and treatment with antibiotics. In

patients with severe postural instability and frequent falls, ablative surgery may be preferred

since falls may damage or displace DBS hardware. In addition, DBS is much more expensive

procedure compared than ablation; thus in many regions of the world, ablation is the only

affordable surgical option when medication is not effective to the progress of the disease.

WHAT ARE THE TARGETS IN DBS?

The most popular target sites for DBS are the vertralis intermedius nucleus of the thalamus

(Vim), the subthalamic nucleus (STN), and the globus pallidus pars interna (GPi).


Ventral Thalamic Nuclei

The cerebellar afferent receiving zone of thalamus (human VIM nucleus) has been the primary

target for the treatment of tremor. These nuclei receive excitatory glutamatergic afferents from

the deep cerebellar nuclei, excitatory glutamatergic afferents from the cerebral cortex, and

inhibitory GABAergic inputs from the reticular nucleus of the thalamus. The output from these

nuclei primarily targets motor areas of cerebral cortex but has also been shown to project to

striatum. Thus, although Vim is commonly viewed as a simple relay for information from the

cerebellum to cerebral cortex, the synaptic connections are complex and DBS likely influences

multiple elements.

Anatomically, Vim is a complexly connected structure locating in the ventrobasal thalamus.

Dorsally, Vim is bordered by the dorsal region of the ventral tier nuclei. Posterior to the Vim lies

the principal sensory nucleus ventral caudalis (Vc) or ventral posterior lateral nucleus (VPL).

Anterior to the cerebellar receiving area lies the region that receives afferents from the basal

ganglia (GPi, SNr), incorporating ventro-oralis anterior (Voa), ventral anterior nucleus (VA). The

medial border of Vim is with Vim.i, which is anatomically similar to Vim but receives

proprioceptive afferents with receptive fields in the face region. Laterally, Vim is bordered by

the posterior limb of the internal capsule. Organization within Vim is strictly somatotopic, with

face followed by hand followed by leg from medial to lateral.

Subthalamic Nucleus

The STN has become the most commonly used target for DBS in the treatment o f PD. The STN

is an important node in basal ganglia circuits, serving as major target for cortical afferents and


also receiving multiple inputs from other basal ganglia components. The STN receives

glutamatergic excitatory afferents from the frontal lobe of the cerebral cortex, GABAergic

inhibitory afferents from the GPe, and excitatory afferents from the parafascicular nucleus of

the thalamus. The output from the STN is glutamatergic and excitatory to both segments of the

globus, to the substantia nigra pars reticulata (SNr), and to the pedunculopontine area. Thus

the DBS in the STN has the potential to influence a variety of afferent and efferent targets and

may have different effects on different neurons.

Anatomically, the STN is a complex, biconvex lens-shaped, triply oblique structure. Its

maximal length is 13.2 mm rostrocaudally and 8 to 9 mm mediolaterally. STN is bordered on its

anerior and lateral sides by the corticobulbospinal tract, while posteromedially lies the

prelemniscal radiation and the red nucleus. The dosal border of STN is with the lenticular

fasciculus anteriorly, the thalamic fasciculus posteriorly, with the thalamus dorsal to the latter.

The ventral border is formed by substantia nigra reticulate (SNr).. STN is organized into motor,

limbic, and associative regions. In the axial plane, the STN slopes form anteromedial to

posterolateral, parallel to the cerebral peduncle below. Whereas the limbic region lies in the

anteromedial portion, the sensormotor region of STN lies in the posterolateral portion, and

within this area it lies dorsally. Some mapping strategies are directed toward locating the motor

region by confirming the presence of movement evoked neural responses.

Globus Pallidus pars interna

The GPi is another commonly used DBS target for the treatment of PD and meanwhile is

increasingly targeted for DBS treatment of dystonia. The GPi labeled in figure 4 is one of the


primary output nuclei of the basal ganglia and the main output representation of limb

movements [Mink 1996]. The GPi receives excitatory glutamatergic afferents from the STN,

inhibitory GABAergic afferents form striatum, inhibitory inputs from the GPe, and nigral

dopamine afferents. Due to the size and geometry, the effect of stimulation in the GPi is more

likely to restrict to the nucleus, but the potential remains for the possible spread to adjacent

structures and pathways, especially the GPe.

Anatomically, GPi is the internal segment of globus pallidus (GP) and the motor region of

the GPi is the target for DBS in PD and dystonial. The GPe forms the lateral border of GPi, and

medially, the dorsal border. The posterior limb of internal capsule forms the posteromedial

border. The ansa lenticularis, the main outflow of GPi, lies below GPi coursing medially and

anteriorly. Below this white matter lies the optic tract coursing posterolaterally toward the

lateral geniculate nucleus. GPi is separated from GPe by the internal medullary lamina.

HOW TO TARGETING IN DBS?

Given the small size of DBS targets, targeting is a critical step in the DBS surgical procedure.

Accurate preoperative targeting influences directly and significantly the operating time and

most importantly, the outcome of the surgery. There are directly or indirectly methods

performed preoperatively or intraoperatively.


Fig.5. AC-PC coordinate localization. The anterior and posterior commissures can be identified on this T1-weighted images [ (30)]

Fig.6. AC-PC coordinate localization. The anterior and posterior commissures can be identified on this T1-weighted images [ (30)]

By brain atlas

The targeting based on a standardized brain atlas is also

called ‘indirect targeting’, a common procedure used for

DBS targeting purposes mainly when the targets of DBS is

not clearly visible in MR T2-weighted images. While atlas-

based coordinates are biased by the inherent inaccuracies

of atlases, coordinates can be derived from the experience

of teams and represent the average values of the

coordinates of these best contacts, gathered in a rather

large number of cases. Registering these coordinates to internal landmarks such as AC-PC

length and height of the thalamus above the AC-PC plane provides normalized coordinates less

dependent on individual variations. The registration uses the midcommissural point (MCP) or

the PC as reference, which is calculated after selecting the AC and PC coordinates (Fig.5).

Typical initial anatomical coordinates for the ventral and sensorimotor STN are 11 to 13 mm

lateral to the midline, 4 to 5 mm ventral to the intercommissural plane, and 3 to 4 mm

posterior to the MCP. Coordinates for the

sensorimotor GPi are selected as 19 to 21

mm lateral to the midline, 2 to 3 mm

anterior to the MCP, and 4 to 5 mm

ventral to intercommissural plane. The

Vim is targeted 11 to 12 mm lateral to the


Fig.7. 3D atlas-based targeting. Left:.3D polygonal surface of left thalamus and STN in brain atlas; Right: 3D rendering of the atlas nuclei. [ (33)]

wall of the III ventricle, at the level of the intercommissural plane. Most commonly, the goal is

to target the topography of the upper extremity, which carries the greatest impact for quality

of life. In terms of anterior-posterior position, the Vim is typically located between 2/12 and

3/12 of the AC-PC distance rostral to the posterior commissure. These coordinates may not represent

the ideal location for implantation but are used as initial anatomical targets, which are verified by

physiological recordings. Figure 6 demonstrates a typical digitized version of the Schaltenbrand and

Wahren atlas registered to the MRI space to conform to the patient’s anatomical structures. These atlas-

and-registration-based targets are than cross-correlated with the direct visualization target.

Since the scanning performed in a 3D space, when oblique slices produced by scanner, 2D

registration is not qualified to register atlas to MRI slice by slice. 3D atlas-based targeting may

overcome this difficulty. Briefly, 3D surfaces (fig. 7 left) representing visible subcortical nuclei

were segmented from a high-resolution MRI. These surfaces were then aligned with 2D

Schaltenbrand and Wahren

slices [8] to define outlines

of nonvisible nuclei such as

STN and lofted to create the

additional 3D surfaces.

Atlas-based targeting

has been the traditional method in stereotactic neurosurgery. The limitation of this method is

that it does not take into account the discrete anatomical variations among individuals. Not all

brains correspond to the topographical distribution depicted in a given atlas. Even the

deformable atlases available in computerized planning stations may not conform adequately to


Fig.8. Direct STN targeting in T2-weighted MRI image. (white arrow-> STN anterior; black arrow->lateral to the red nucleus) [ (30)]

the patient’s anatomy. In this sense, direct targeting seems to have obvious benefits over

indirect.

Regarding the registration methods, it is roughly divided into rigid and non-rigid algorithm

according to the characteristic of deformation from source image to reference image. Rigid

registration is referred as primarily affine transformation of source image involving translation,

rotation as well as scaling. Rigid registration is also used as a pre-alignment step for non-rigid

transformation. Non-rigid registration includes intensity-based algorithm (demons/ B-spline/

thin-plate-splin/ adaptive bases algorithm [ (18)]) and segmentation-based registration. Mutual

information [ (19)] is the most commonly used standard for automatically measure the

goodness of the registration result. More details will be skipped in this paper.

By visible surrounding anatomical landmarks

A target within STN can be chosen at the ventral part of the

somatosensory STN, which is the lateral part of the nucleus.

The axial and coronal T2 images are particularly important

for adequate visualization of the STN as a sharp contrast can

often be seen between the nucleus and the surrounding

white matter. The red nucleus can also be clearly seen and

the STN lies anterior and lateral to the red nucleus. The

anterior border of the read nucleus can be used as

landmark for the anteroposterior localization of the STN target [ (20)]. Figure 8 shows the

visualization result in the axial T2 images.


Fig.9.Direct GPi targeting. A: GPi (arrow) is seen on an inversion recovery axial image. B: The optic tract (tip of the trajectory line) can be identified ventral to the GPi and used as a landmark for direct targeting. [11]

Fig.10.Phase image from SWI sequence acquisition in 3T MRI. The STN, SN, and RN are sharply delineated on phase image. [8]

The GPi and the adjacent optic

tract and internal capsule can be

visualized via inversion recovery and

T2 images, Proper windowing of the

images can also provide

visualization of the internal capsule

together with the GPi and GPe. For

GPi DBS, implantation target choice

may be different from that used for pallidotomies, which are typically located at the

posteroventral portion of the nucleus. Implantation at that position may not be optimal for DBS

because the DBS stimulation field may require higher amplitudes and potential spread to the

internal capsule. Thus for DBS, a more anterior and lateral target is preferable, which will allow

the stimulation amplitude to be increased without significant involvement of the descending

white matter fibers. The optic tract courses ventrally to the globus pallidus and can be used as

landmark for the approach (Fig.9).

By direct locating (SWI/7T MRI/DTI)

Since the high iron concentration in the STN causes T2*

shortening and resonance frequency increasing,

susceptibility-weighted imaging (SWI) which exploits the

magnetic susceptibility differences of tissues, provides

additional possible contrast mechanism to visualize STN


Fig.11. In vivo image from 7T MR system with a brain-optimized SENSE coil [ (29)]. 7T MR image reveals detailed structures of the thalamus including STN et al.

without using anatomic landmarks. Using postprocessing techniques, a single SWI acquisition

can generate 3 sets of inherently co-registered images: T2*-weighted maps of signal-intensity

magnitude images phase image and a combination the two. Vertinsky [ (21)] and colleagues

assessed the visibility as well as delimitation of STN using SWI and concluded that STN were

directly visualized on SWI phase image.

Moreover, ultra-high MR system (e.g. 7T MR system) provides an increasing SNR, allowing

much higher spatial and enhanced

susceptibility contrast. Those small

structures which cannot be well delineated

at lower field have opportunity to be seen

and segmented much more exactly.

However, the clinical application of 7T MR

still delayed by many critical problems such

as the regional signal variation resulting

from the inhomogeneous B0 and B1 field.

By microelectrode recordings

A fundamental purpose of microelectrode recording (MER) is to verify the stereotactic location

of the target brain region for the electrode implantation. A neurophysiologist records neural

activity as a microelectrode is advanced through stereotactic brain space and identifies specific

nuclei on the properties of the neural signals recorded [ (22)]. While not performed at all DBS

centers, this verification process can help alleviate two limitations. First, the surgical target


Fig.12. Microelectrode mapping of the STN. A: Serial-track approach, B: Five-simultaneous-track approach. [ (34)]

cannot always be directly identified on preoperative imaging data. Second, the intracranial

pressure changes once the burr hole is drilled, resulting in a possible shift of the subcortical

structures, thereby altering the position of the target point in stereotactic space [ (23)].

MER begins at various distances from the target. Take the target STN as an example, the

distances between recording and STN range from several millimeters (Fig.12B) to up to 40 mm

(Fig. 1A), depending on whether striatal

and/or thalamic activity is recorded.

Findings depend on the obliquity of the

planned tracks. When the entry point is

more lateral, the track misses the striatum

or thalamus, residing completely within the

corona radiate and internal capsule (Fig 1B).

When recording begins more proximally

(~40mm from above target) and with more

medial entry points, the caudate is

encountered with its characteristic pattern

of phasically active units. Below this, the

internal capsule is entered, from which

occasional fibers may be recorded. More

anterior tracks will pass in front of the

thalamus, next encountering the Zona


Fig.13.Semimicroeletrode mapping of the STN.

incerta (ZI), in which small infrequent neurons may be recorded with low tonic firing rates.

More posterior tracks pass into the thalamus, approximately 7mm above the STN. The shell of

the thalamus contains the reticular nucleus with its characteristic bursting pattern discharges

(15±19Hz). The ventral basal complex is

encountered next, the cell of which fire at an

average 28 Hz. These cells are easily

distinguished from the STN itself as their firing

rate is significantly lower, and the overall

background of the thalamus is substantially

quieter. After 1 to 2 mm, the STN is entered,

characterized by an abrupt increase in

background activity. Mean firing rates have been reported in the 34-74 Hz, with standard

deviation is 25Hz [ (24)]. Below the STN, the electrode traverse into SNr whose mean firing rate

in most report is higher[ (25)] than STN but in some notes is lower [ (26)]. Rather, the pattern

of neuronal activity, motor responsiveness, and background activity offer greater reliability in

determining electrode location. These findings are mirrored in semimicroelectrode recordings

[Fig 13], where the overall background of the STN provides a sharp contrast to that of the

internal capsule and ZI above and the SNr below.

By macro stimulation tests

Following mapping via microeletrode recording we described above, macrostimulation is

performed with either the microelectrode using current in the milliamp range, the uninsulated


tip of the inner guide cannula through which the microelectrode was passed, a dedicated

macroelectrode (e.g. a radio-frequency ablation electrode), or DBS electrode.

Within the internal capsule, orofacial and/or appendicular contractions are noted, as are

contraversive eye movements. Within the thalamus, various effects have been reported (e.g.

vegetative effects) in some instances and a mild reduction in distal muscle tone ventrally [13].

Stimulation within zona incerta (ZI) and the fields of Forel can produce a decrease in rigidity at

relatively low voltage thresholds ( (27)). Stimulation in the STN produces the maximal clinical

effects intraoperatively, however, and they are obtained at the lowest thresholds. Stimulation

within SNr is generally without clinical effects, although some have observed decrease in

rigidity and worsening of bradykinesia.

The distance and direction of refinement of initial targeting is related to the accuracy of

the initial imaging and target calculation, as well as the technique and accuracy of the mapping

procedure. One measure of both the inadequacy of the initial imaging, target calculation, and

stereotactic technique, and the subsequent ability of physiological mapping to ‘correct’ these

errors, is the amount of correction of the electrode position following mapping. Both

microelectrode recording techniques and macrostimulation techniques can be used to correct

the electrode position. Some groups relied solely on macroelectrode or microelectrode

mapping to position the electrode optimally while some relied on combination of these two

techniques. Does the use of mapping improve outcome? There are insufficient data available to

determine whether any mapping at all, as opposed to pure anatomical targeting without

modification based on intraoperative evaluation, is necessary for good results from STN DBS.


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