Professor: Dr.Towhidkhah Presented by: Kayvan Mojtahedi

Deep Brain Stimulation(DBS)

Introduction

Components & Placement

Surgery

Advantages of Deep Brain Stimulation

Possible Disadvantages

Potential Complications & Side Effects

Anatomical Targeting

PD:DBS

PD

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. Post-operative 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 leadiii. 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

non-Parkinsonian 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.

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).

Anatomical Targeting

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).

Kinds of Treatments(4.1,P.P of YasharSarbaz):

1-1. Medical treatment

1-2. Deep Brain Stimulation

Parkinson’s Disease

PD & it’s symptomsReason 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 symptomsSymptoms of PD:HypokinesiaAkinesia: lack of slowness of spontaneous and

associative movement Rigidity: increased tone on passive

manipulation of jointsTremor:rhythmic,involuntary,oscillatorymovement around 4-6 Hz

PD:DBSTarget of

Stimulation: GPi: The Globus Pallidus Internal

STN:The Subthalamic Nucleus

Vim: The Ventro-Intermediate nucleus Thalamus

Characteristics of the common DBS signal:

1. Frequency greater than 100 2. Pulse width about 90 3. Amplitude of stimulation voltage nearly

3 v

Effects of low-frequency stimulation of the subthalamic nucleus on movement in Parkinson's

diseaseI. AbstractII. IntroductionIII. Materials and methods:

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).

Patients and surgery:

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.

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.

Task

Statistics5. 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)

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.

iv. Result

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).

Referencei. 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

iii. Deep brain stimulation - Wikipedia, the free encyclopedia.mht

ii. Deep Brain Stimulation on MedicineNet_com.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