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Deep Brain Stimulation(DBS)
Introduction
Components & Placement
Surgery
Advantages of Deep Brain Stimulation
Possible Disadvantages
Potential Complications & Side Effects
Anatomical Targeting
PD
PD:DBS
Effects of low-frequency stimulation of the
subthalamic nucleus on movement in
Parkinson's disease
Deep Brain Stimulation
In
neurotechnology
deep
brain
stimulation (DBS) is a surgical treatment
involving the implantation of a medical
device called a brain pacemaker, which
sends electrical impulses to specific parts
of the brain.
The Food and Drug Administration (FDA)
approved DBS as a treatment for essential
tremor in 1997, for Parkinson's disease in
2002, and dystonia in 2003. DBS is also
routinely used to treat chronic pain and
has been used to treat various affective
disorders, including major depression.
A) DBS systems are permanently implanted with a
pulse generator in the chest and a four contact
electrode stereotactically placed in the brain. Postoperative MR is used to identify STN and local
structures, as well as electrode location.
Deep Brain Stimulation
Components & Placement
i. The implanted pulse generator (IPG)
ii. The lead
iii. The extension
Electrodes are placed in the thalamus (for essential
tremor and multiple sclerosis) or in the globus
pallidus (for Parkinson's disease).
DBS leads are placed in the brain according to the
type of symptoms to be addressed. For nonParkinsonian essential tremor the lead is placed in
the ventrointermedial nucleus (VIM) of the thalamus.
For
dystonia
and
symptoms
associated
with
Parkinson's disease (rigidity, bradykinesia/akinesia
and tremor), the lead may be placed in either the
globus pallidus or subthalamic nucleus.
Deep Brain Stimulation
The IPG is a battery-powered neurostimulator
encased in a titanium housing, which sends
electrical pulses to the brain to interfere with
neural activity at the target site.
The lead is a coiled wire insulated in
polyurethane with four platinum iridium
electrodes and is placed in one of three areas
of the brain.
The lead is connected to the IPG by the
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 in some cases, the
abdomen.[
Pacemaker device (called an impulse generator,
or IPG) implanted under the skin of the chest,
below the collarbone.
Deep Brain Stimulation
(Surgery)
All three components are surgically implanted inside the
body:
Under local anesthesia, a hole about 14 mm in diameter
is drilled in the skull and the electrode is inserted, with
feedback from the patient for optimal placement.
(The right side of the brain is stimulated to address
symptoms on the left side of the body and vice versa.)
The installation of the IPG and lead occurs under
general anesthesia.
Insertion of electrode during surgery
a: Variation of the lead position in the xz-plane: Position A is along the symmetry axis
of the scanner, position C is along the RF coils, and position B is in between. In each
case the lead is parallel to the z-axis.
b: Variation of the lead position in the xy-plane: after the lead exits the phantom, it is
fixed at the tunnel wall of the scanner under different angles. From there it is led
outside the scanner parallel to its z-axis.
Photographs illustrating the consecutive steps in the described DBS-electrode anchoring technique for
patients. After satisfactory DBS-electrode placement the dura is sealed with a drop of fibrin glue (A and
B). A 20mm long piece of a ventricular catheter cut slit open is fitted around the electrode (C). The burr
hole is filled with BioGlue® fixating the electrode to the burr hole, and the applied electrode cover to the
electrode and the burr hole (D). The electrode stiletto is removed and the electrode released from the
stereotaxic device (E). The covered electrode is fixated to the calvarium with a 3×4 hole Lorentz titanium
microplate placed over the burr hole and screwed onto the skull by four 4mm titanium screws (F).
a: Experimental setup. The lead connects the pulse generator outside the scanner room and the
electrode inside the phantom. The phantom is positioned at the isocenter of the scanner. Induced
voltage is measured at the connecting lead outside the scanner room. Measurement points for the
temperature are equally spaced along the electrode and the lead.
b: Percutaneous placement of the lead before the final implantable pulse generator (IPG) is
implanted into the patient’s chest. The lead penetrates the scalp and is coupled to the test stimulator
by the connector.
What Are the Advantages of Deep Brain Stimulation?
i.
It does not require purposeful destruction of any part of the brain and therefore, has fewer
complications than thalamotomy and pallidotomy.
ii.
The electrical stimulation is adjustable and can be changed as the person's disease changes or his
or her response to medications change. No further surgery is necessary to make the adjustments.
iii.
Another significant advantage of deep brain stimulation relates to future treatments. Destructive
surgery, such as thalamotomy or pallidotomy, may reduce the persons potential to benefit from
future therapies. For example, future brain cell transplantation may be of great help to people with
Parkinson's disease. There is concern that a pallidotomy or thalamotomy may prevent patients
from benefiting from brain cell transplantation. This would not be the case with deep brain
stimulation, as the stimulator could be turned off.
iv.
Deep brain stimulation is a relatively safe procedure.
v.
The procedure can treat all the major symptoms of Parkinsons disease.
vi.
Daily living tasks and quality of life are also improved.
vii.
With subthalamic nucleus stimulation, medications can usually be reduced.
viii. The stimulator can also be turned off at any time if deep brain stimulation is causing excessive
side effects.
Possible Disadvantages
i.
Potential complications and side effects: Increased risk of infection. The
implantation of any foreign object carries that risk.
ii.
Additional surgery may be needed if the equipment stops working or for battery
replacement
iii.
Additional time on the part of the patient and health care provider to program device
and adjust medications
iv.
Device may interfere with antitheft devices, refrigerator door magnets.
Potential Complications & Side Effects
a.
The possibility of apathy, hallucinations, compulsive gambling, hypersexuality,
cognitive dysfunction, and depression. However, these may be temporary and
related to correct placement and calibration of the stimulator and so are
potentially reversible. (There is a 2%-3% risk of a serious and permanent
complication such as paralysis, changes in thinking, memory and personality,
seizures, and infection.)
b.
Because the brain can shift slightly during surgery, there is the possibility that
the electrodes can become displaced or dislodged. This may cause more
profound complications such as personality changes, but electrode misplacement
is relatively easy to identify using CT or MRI. There may also be complications of
surgery, such as bleeding within the brain.
Anatomical Targeting
Pallidum and putamen are shown. Stimulation has varying effects
on different symptoms in internal globus pallidus (GPi) and
external globus pallidus (GPe) (Bejjani et al., 1997; Krack et al.,
1998; Yelnik et al., 2000).
Fig. 3. (a) Model of the DBS lead with four contacts centered in the STN, surrounded by white fiber tracts (zona
incerta (ZI), Fields of Forel (FF), and internal capsule (IC)) and grey matter. Distribution of (1) electric potential (V);
(2) electric field (ΔV); and (3) the activating function (ΔV^2) generated in the subthalamic nucleus and the
surrounding fiber tracts during (b) monopolar stimulation (V=-1) applied through Contact 1, (c) bipolar stimulation
(Contact 1 at V=-0.5; Contact 2 at V=0.5); (d) bipolar stimulation (Contact 1 at V =0.5 V, Contact 2 at V=-0.5 V), and
(e) tripolar stimulation (Contacts 0 and 2 at V =0.05, Contact 1 at V=-0.5). ΔV and ΔV^2 have both positive and
negative components, but the magnitudes are shown here. Positive ΔV^2 results in depolarization and negative ΔV^2
results in hyperpolarization of the surrounding neural elements. CNS gray matter has a conductivity of 0.2 S/m (Li et
al., 1968; Ranck, 1963). CNS white matter has conductivities of 1 S/m in the direction parallel to the fibers and 0.1
S/m in the direction perpendicular to the fibers (Nicholson, 1965).
Parkinson’s Disease
Kinds of Treatments(4.1,P.P of YasharSarbaz):
1-1. Medical treatment
1-2. Deep Brain Stimulation
PD & it’s symptoms
Reason of PD:
Loss of nerve cells in substantia nigra pars compacta
Low level of Dopamine in patient’s brain
Changing activity of other blocks
PD and it’s symptoms
Symptoms of PD:
 Hypokinesia
Akinesia: lack of slowness of spontaneous and
associative movement
Rigidity: increased tone on passive manipulation of
joints
 Tremor:rhythmic,involuntary,oscillatory
movement around 4-6 Hz
PD:DBS
Target of Stimulation:
 GPi: The Globus Pallidus Internal
 STN:The Subthalamic Nucleus
 Vim: The Ventro-Intermediate nucleus Thalamus
Characteristics of the common DBS signal:
1.
2.
3.
Frequency greater than 100
Pulse width about 90
Amplitude of stimulation voltage nearly 3 v
Effects of low-frequency stimulation of the subthalamic
nucleus on movement in Parkinson's disease
I.
Abstract
II. Introduction
III. Materials and methods:
Patients and surgery:
1. The DBS electrode used was model 3389 (Medtronic Neurological
division, Minneapolis, USA) with four platinum–iridium cylindrical surfaces
(1.27 mm diameter and 1.5 mm length) and a centre-to-centre separation
of 2 mm.
Contact 0 was the most caudal and contact 3 was the most rostral. The
intended coordinates at the tip of contact 0 were 10–12 mm from the
midline, 0–2mm behind the midcommissural point and 3–5mm below the
anterior commissural–posterior commissural line.
2. Correct placement of the DBS electrodes in the region of the STN was
further supported by: [1] effective intra-operative macrostimulation; [2]
post-operative T2-weighted MRI compatible with the placement of at least
one electrode contact in the STN region; [3] significant improvement in
UPDRS motor score during chronic DBS off medication (22.7±3.0) compared
to UPDRS off medication with stimulator switched off (52.6±4.8; p‹0.00001,
paired t-test).
Protocol:
3. All patients were assessed after overnight withdrawal of antiparkinsonian
medication.
They were studied when the stimulator was switched off and during bilateral STN
stimulation at 5 Hz, 10 Hz and 20 Hz.
Task
4. Tapping was performed in two runs of 30 s, separated by ∼30-s rest and each
hand tested separately (giving four runs per condition).
The number of taps made with the index finger in 30 s was recorded.
Statistics
5. The results of the tapping task in patients were analyzed according to their
baseline performance (e.g. without stimulation).
The lower limit of normal baseline performance was obtained by testing ten
healthy age matched control subjects (20 sides, 4 males, mean age 57 years,
range 52–64 years) using the same tapping task. The mean tapping rate in this
control group was 162 taps/30 s.
6. The lower limit of the normal range (e.g. mean−[2×standard deviation]) in
this control group was 127 taps per 30 s. The 35 tapping sides studied in the 18
patients were accordingly divided into those with baseline performance within
normal limits (n=17; the mean tapping performance across this group, 157
taps/30 s, was still lower than the mean tapping performance in healthy subjects)
and those with baseline tapping rates lower than normal limits (n=18; mean
tapping performance 58 taps/30 s).
7. Greenhouse–Geisser corrections: Means±standard error of the means(SEM)
iv.
Result
Fig. 1. Effects of stimulation frequency on tapping rate off medication. Mean (±SEM)
tapping rate off (‘0 Hz’) and on stimulation at 5, 10 and 20 Hz on those sides (n=17) with
baseline tapping performance within normal range (tapping off DBS›127 taps in 30 s) (A)
and below normal range (n=18) (B).
In those patients with baseline performance within normal limits, tapping rate was
significantly slower during stimulation at 5 and 20 Hz than without stimulation and there
was a similar trend for the 10-Hz stimulation. On those sides with baseline performance
below normal limits no significant differences between the different stimulation frequencies
were found.
Fig. 2. Effects of stimulation frequency on variability of tapping rate off medication.
Mean (±SEM) coefficient of variation (CV) of the intervals between taps off (‘0 Hz’)
and on stimulation at 5, 10 and 20 Hz in patients with baseline tapping performance
within normal range. CV of tap intervals during stimulation at 5 and 10 Hz significantly
increased compared to no stimulation.
V.
Discussion
8. We have shown that STN DBS at a variety of low frequencies can slow distal
upper limb movements in PD patients with relatively preserved baseline tapping
function at the time of study.
The effect was present with DBS at 5 Hz and 20 Hz in line with previous studies
(Chen et al., 2007; Fogelson et al., 2005; Moro et al., 2002), and there was a trend
towards a similar effect with stimulation at 10 Hz (Timmermann et al., 2004).
9. The susceptibility of basal ganglia–cortical loops to the effects of excessive
synchronization may be elevated across a broad low-frequency band in parkinsonian
patients.
10. Only DBS at 5 and 10 Hz increased temporal variability, whereas DBS at 20 Hz
selectively decreased tapping rates without changing tapping variability.
VI.
Acknowledgments
11. This work was supported by research grants from the Medical Research Council
(UK),Wellcome Trust (UK), Fondation pour la RechercheMedicale (France), Chang
GungMemorial University Hospital (Taipei, Taiwan) and Parkinson Appeal (UK).
Reference
i.
Effects of low-frequency stimulation of the subthalamic nucleus on movement in Parkinson's disease
Alexandre Eusebio a,1, Chiung Chu Chen a,b,1, Chin Song Lu b, Shih Tseng Lee c, Chon Haw Tsai d, Patricia
Limousin a,e, Marwan Hariz a,e, Peter Brown a,
a Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, 8-11 Queen
Square, WC1N 3BG London, UK
b Department of Neurology, Chang Gung Memorial Hospital and University, Taipei, Taiwan
c Department of Neurosurgery, Chang Gung Memorial Hospital and University, Taipei, Taiwan
d Department of Neurology, China Medical University Hospital, Taichung, Taiwan
e Unit of Functional Neurosurgery, Institute of Neurology, London, UK
Received 13 July 2007; revised 29 August 2007; accepted 5 September 2007 Available online 18 September 2007
ii.
Deep Brain Stimulation on MedicineNet_com.mht
iii. Deep brain stimulation - Wikipedia, the free encyclopedia.mht
iv. Powerpoint of Yashar Sarbaz
v. Other CNF & Papers & Journals
Thanks for your attention
1-1.Origion of PD (BG)
The basal nucleii (ganglia) have an inhibitory role in motor control
The basal nucleii (ganglia) have an inhibitory role in motor control