CHAPTER I
INTRODUCTION
One
of the well established surgical treatment for medication-refractory movement
disorders is Deep brain stimulation (DBS), DBS enabling people to regain
control of their motor function (Perlmutter and Mink, 2006) and now being
explored for a variety of neurological and psychiatric disorders (Tierney et
al., 2011), providing new possibilities to manage conditions that become
refractory to conventional medical therapy.
In
this chapter, we cover the physiological mechanisms underlying DBS therapy,
positing that, although general principles exist, DBS threating the disorder
and the therapeutic mechanism(s) of action may depend on the site of
stimulation
The
use of electrical stimulation to modulate brain function has been around for
some time, evolving from a predictive tool for ablative outcomes to its
modernday therapeutic application. Through the 1950s, Hassler and colleagues
were one of the first groups to use intraoperative electrical stimulation to
alleviate or exacerbate contralateral tremor when applied to the globus
pallidus (GP) at what was considered at that time high (25–100 Hz) and low
(<25 Hz) frequency, respectively (Hassler et al., 1960). They suggested that
high-frequency electrical stimulation could be used as a tool to identify brain
regions that would reduce motor symptoms when lesioned.In the following years
numerous studies reported the use of high-frequency electrical stimulation to
treat movement disorders ranging from dyskinesia (Alberts et al., 1966) to
cerebral palsy (Bergstrom et al., 1966),
psychiatricdisorders(Heath1954),autonomicdisorders(SemJacobsen 1968),
convulsive disorders (Cooper 1973), and pain syndromes (Hosobuchi et al.,
1977). Yet, it was not until the 1980s, with the development of fully
implantable pulse generators and the pioneering work of Benabid and colleagues
(1987), that DBS was introduced as a feasible alternative to lesioning
procedures, with the added benefit of reversibility and titration to maximize
therapeutic effects while minimizing sideeffects. Since then, DBS systems have
been implanted in nearly 100 000 patients with medication-refractory
neurological and psychiatric disorders.
We
also cover electrophysiological experiments, biochemical analyses, computer
modeling, and imaging studies related to DBS to support the hypothesis that the
mechanism(s) of action depend on both the site of stimulation and the
neurological disorder being treated. Specifically, we address the questions of
(1) how DBS affects neuronal tissue surrounding the electrode through an
overview of experimental studies related to DBS for Parkinson’s disease, and
(2) how these neurophysiological effects translate into clinical benefit for a
range of neural targets and disorders.
CHAPTER II
CONTENT
2.1.
Definition
Deep Brain Stimulation (DBS) is a surgical procedure
that use a high frequency electrical stimulation through chronically implanted
electrodes into a specific target in the subcortical structures (Chiken and Nambu,
2016). Nowadays it’s been widely used as an effective treatment for movement
disorders, such as Parkinson’s Disease (PD), essential tremor, and dystonia,
and it is now under investigation as for it to be used for a wide variety of
neurological and psychiatric conditions such as, epilepsy, Obsessive-Compulsive
Disorder (OCD), and major depression (Herrington, Cheng and
Eskandar, 2016).
2.2.
History of
Deep Brain Stimulation
The
account of DBS is an entrancing case of the transaction amongst fundamental and
clinical science as a two-way process. A possibility clinical perceptions
identified with tranquilize manhandle prompted the production of a monkey
demonstrate for PD, and serious examination of this model drove inside four
years to a handy approach in PD patients
(Bergman H,
1990).
Some
the turning points in this specific improvement were:
a.
1983 The compound MPTP
was found to be the wellspring of Parksinson-like manifestations in youthful architect
tranquilize addicts
b.
1983 Injection of MPTP
into monkeys caused a Parkinson-like
state.
c.
1983-1990 Recordings in
the basal ganglia of both ordinary and MPTP-treated monkeys characterized the
operational standards of basal ganglia-thalamocortical circles, and appeared
interestingly articulated over-movement in a piece of the basal ganglia called
the subthalamic core (STN). These papers have given the reasonable structure to
quite a bit of work on the basal ganglia and development issue over the previous
decade or something like that. They depended on the two chronicles from single
neurons in alert, carrying on monkeys, yet additionally utilized metabolic
markers to delineate of over-and under-action (Bergman H,1990).
d.
1990 Lesions of STN in
monkeys were appeared to totally and forever turn around the impacts of MPTP
e.
1993 The principal
report from Benabid's facility of the utilization of DBS in the STN to treat
Parkinson's Disease. Benabid's gathering had first utilized DBS in the thalamus
as ahead of schedule as 1987. This was completed in three patients, with DBS
anodes embedded on the two sides of the cerebrum, which is currently the
standard approach in PD patients (Svjetlana
Miocinovic, MD, PhD, 2013)
f.
1997 FDA endorsement
given for DBS in the thalamus.
g.
2001 FDA endorsement
given for DBS in the STN.
h.
(387 references from
2001-2003) It is observable that
in this illustration, both the calculated system and the exploratory
confirmation to help clinical trials in PD patients originated from the
creature display . Quite a bit of this exploratory work was done in the UK (Buckner RL, 2005)
2.3.
Components and placing
The
Deep Brain Stimulation system consists of three major components, the first
being the lead, which is also called the electrode, is essentially a coiled
wire insulated in polyurethane with four platinum-iridium electrodes and is
placed in one or two different nuclei of the brain (Drew S. Kern, 2017). This component is inserted through a small
opening in the skull and implanted in the brain. The tip of the electrode is
positioned within the targeted brain area. The second component is the
extensions, an insulated wire that is passed under the skin of the head, neck,
and shoulder, connecting the lead to the third component, which is the
neurostimulator or sometimes also called the “battery pack” or the implanted pulse generator (IPG) – the equivalent of a pacemaker.
The IPG is a battery-powered neurostimulator encased in a titanium housing,
which sends electrical pulses to the brain that interferes with neural activity
at the target site. This component is usually implanted under the skin near the
collarbone, and in some cases it may be implanted lower in the chest or under
the skin over the abdomen (J.S. Perlmutterand, 2006).
2.4.
Method
Since 1997, a lot of Parkinson’s Disease patients have
been treated with DBS, as surgical technique as I already said before that
involves the implantation of ultra-hin wire electrodes. The Implanted device,
sometimes referred to as a ‘brain pacemaker’, delivers electrical pulses to a
structure called the subthalamic nucleus, located near the center of the brain,
and effectively alleviates many of the physical symptoms nof the disease, such
as tremor, muscle rigidity, and slowed movements. The most common use DBS
system uses a four contact stimulating electrode stereo tactically implanted in
the target and connected via a subcutaneous wire to pacemaker-like unit called
an Implantable Pulse Generator (IPG) that is placed on the chest wall
underneath the collarbone. Electrodes are typically placed bilaterally,
although clinical needs sometimes dictate unilateral stimulation. Most targets
are deep brain structures (include deep white matter tracts) rather than
cortical areas. A clinician uses a handheld device to wirelessly communicate
with with the IPG to adjust the parameters of stimulation, tuning stimulation
to maximize symptom relief and minimize side effects (Umemura A,, 2017).
DBS is actually safe, but still like any other
surgical procedure, comes with some risks. First of all, it is highly invasive,
it requires small holes to be drilled in the patient’s skull, through which the
electrodes are inserted. Potential complications of this include infection,
stroke, and bleeding on the brain. The electrodes which are implanted for long
periods of times also sometimes move out of place ; they can also cause
swelling at the implantation side and the wire connecting them to the battery,
typically placed under the skin of the
chest, can erode , all of which require additional surgical procedures (C. C.
McIntyre, 2004)
Now, researchers at the Massachusetts Institute of
Technology have a developed a new method that can stimulate cells deep inside
the brain non-invasively, using multiple electric fields applied from outside
the organ. In a study published today in the journal Cell, they show that the
method can selectively stimulate deep brain structures in live mice, without
affecting the activity of cells in the overlying regions, and also that it can
be easily adjusted to evoke movements by stimulation of the motor cortex (T.M.
Choiand, 2009).
The
new method, called “temporal interference”, exploits the fact that neurons do
not respond to electric fields with frequencies of around 1,000 Hertz (Hz, or
cycles per second) or more. Thus, high frequency electric fields applied to the
brain pass through it without affecting neuronal activity. If, however, two
fields are applied to the brain, at high frequencies that differ by small
amounts corresponding to the frequencies to which neurons can respond, they
interfere with each other to produce an ‘envelope’ electric field that excites
the cells within it (Grossman et al., 2017).
2.5.
Neurophysiology
of Deep Brain Stimulations
Electrical stimulation of the brain has
been shown to influence a variety of mechanisms involved in neuronal function
and signaling. The effect of DBS on neurons in different nuclei may be quite
different. Different types of central nervous system (CNS) neurons possess
different types of ion channels that may have different voltage-sensitive
activation and inactivation properties. Nonetheless, the net effect resulting
from different mechanisms may be comparable (Christine
CW, 2009).
There are many primary principles of CNS
elements affected by DBS under the usual clinical conditions; one of the most
important principles is the relationship between stimulus amplitude and
duration. As current amplitude decreases, duration must increase to produce a
constant effect. Similarly, as duration decreases, amplitude must increase to
produce the same effect. The form of the amplitude-duration curve is usually an
exponential decay. The amplitude asymptote (threshold) at very long durations
is called the rheobase. The chronaxie distinguishes different types of neural
tissues or elements. The larger the chronaxie, the higher the current or pulse
width (duration) must be to activate the neuronal element (Vesper
Fe Marie L Ramos, 2015).
The chronaxie is substantially different,
large myelinated CNS fibers have chronaxies of 30–200 μs, whereas the chronaxie
of dendrites and cell bodies may be in the 1–10-ms range. In rat visual cortex,
the chronaxie was 271 μs for subcortical white matter, 380 μs for cortical gray
matter, and 15 ms for cortical cell bodies. With usual stimulation parameters,
postsynaptic responses from electrical stimulation of the cortical gray matter
result primarily from the activation of efferent axons (initial segments or
branches) rather than from cell bodies.
The orientation of the cell body and axons
in relation to current flow is an important determinant of responsiveness. For
axons, the voltage gradient parallel to the axon is most important for
eliciting a response. Gray matter and white matter have different resistivities
as do myelinated and unmyelinated fibers. Thus the response to stimulation in a
nucleus containing a mixture of elements is likely to be complex depending on
the geometry of the neural elements, the stimulating electrode configuration,
and the nucleus (Alexander GE, 1990).
A final factor in determining
responsiveness is the distance of the neural element from the electrode.
Rheobase and chronaxie rise in proportion to the distance from the electrode.
Furthermore, currents from monopolar cathodes more than eight times threshold
may block action potentials in axons. Thus, at high currents, nearby elements
may be blocked, and distant elements may not receive sufficient stimulation,
but elements in an intermediate “shell” will be activated.
The response to high-frequency stimulation
in the context of therapeutic DBS has been studied mostly in the ventral tier
nuclei of the thalamus, the STN, and the globus pallidus. Studies have
suggested the physiologic response to high-frequency stimulation may differ
across nuclei.
Ventral Thalamic Nuclei
The cerebellar afferent receiving zone of
the 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
it is common to view VIM as a simple relay for information from the cerebellum
to cerebral cortex, the synaptic connections are complex and DBS likely
influences multiple elements.
To investigate the cellular mechanism by
which DBS might work, studies have used a slice preparation from rat thalamus.
The rat homologues of human VIM are the ventrolateral and ventroposterior
nuclei. Using simulated DBS (sDBS) with variables comparable with that used in
human DBS, the effect of stimulation of ventral lateral ventral posterior
thalamic nuclei (VL-VP) on neurons is both amplitude and frequency dependent.
Response to stimulation was seen at frequencies above 20 Hz, it increased with
increasing stimulation frequency, and it reached a maximum at 200 Hz. This is comparable
with the frequency response characteristics of VIM DBS for ET. When rhythmic
pulse trains were injected into VL-VP neurons to simulate tremor-like bursting,
sDBS eliminated the rhythmic firing. At moderate currents, the rhythmic firing
was replaced by nonrhythmic firing, but higher currents induced block and
eliminated firing.
In addition to activating excitatory
presynaptic terminals, sDBS in rat thalamic slice also produced increased
excitability of thalamic neurons. The threshold for triggering Na+-dependent
action potentials was decreased by sDBS, even in the presence of ionotropic
glutamate blockade, causing a 30% increased probability of firing action
potentials in response to injected depolarizing currents. The decreased
threshold was not a result of changes in membrane resistance. These nonsynaptic
effects were dependent on current and distance from the stimulating electrode.
Thus, regardless of presynaptic effects, the increased excitability of cell
bodies suggests there also may be increased excitability of efferent axons (Rosa
M, 2012).
Subthalamic Nucleus
The STN has become the most commonly used
target for DBS in the treatment of PD. The STN is an important node in basal
ganglia circuits, serving as a major target for cortical afferents and also
receiving multiple inputs from other basal ganglia components. DBS in the STN
has the potential to influence a variety of afferent and efferent targets and
may have different effects on different neurons (Limousin
P, 1995).
The effect of high frequency stimulation
has been studied in rat STN slices by several investigators. The two most
frequently encountered neuron types were (a) tonically active neurons
that had a round soma and extensive radial dendritic field (68%) and (b)
bursting neurons with a triangular soma and less extensive dendritic field
(25%). Tonically active cells followed 130 Hz stimulation for 5–15 s, then
developed a bursting pattern, before ceasing to fire after 25 s of stimulation.
Bursting cells responded to stimulation trains with a brief burst of action
potentials followed by prolonged silence. However, the stimulation current was
low and primarily affected presynaptic axons rather than cell bodies,
suggesting that presynaptic driving of STN neurons may fail at sustained high
frequencies.
A prolonged inactivation of STN neurons
also has been reported. The post-stimulation silence was a result of changes in
membrane properties and not synaptic effects. Prolonged post-stimulation
silencing occurred only at frequencies higher than those that produce maximum
benefit from STN DBS in PD patients (Aziz TZ, 1991).
The pattern of response varied among
neurons but did not depend on the distance from the stimulating electrode. The
blockade of ionotropic or metabotropic glutamate receptors or of GABA receptors
had no effect on the stimulus-driven firing. The stimulation-driven firing
appeared to be a result of the activation of voltage-sensitive Na+ and
L-type Ca2+ channels. Combinations in the therapeutic range replaced
baseline firing with stimulus-driven spikes in a stable oscillatory pattern
time locked to the stimuli.
In the absence of STN stimulation, motor
cortex stimulation typically elicits a triphasic response in SNr neurons with
early excitation, inhibition, then late excitation. The early excitation is
mediated by the activation of the excitatory projection from the STN to the SNr
and the inhibition by the activation of inhibitory striatonigral neurons
(“direct pathway”), and the late excitation is mediated by the disinhibition of
subthalamonigral neurons (“indirect pathway”). High-frequency STN stimulation
blocks the transmission of information through the STN. This implies that STN
stimulation can activate multiple pathways but also that high-frequency STN
stimulation activates excitatory projections from the STN to the SNr.
Furthermore, STN stimulation blocks the flow of information through the STN,
potentially preventing aberrant signals from being propogated in disease states
(Mitchell IJ,
1989).
Globus Pallidus
The GPi is the second most commonly used
DBS target for the treatment of PD and is increasingly targeted for DBS
treatment of dystonia. The GPi is one of the primary output nuclei of the basal
ganglia and is considered the main output representation of limb movements. The
GPi receives excitatory glutamatergic afferents from the STN, inhibitory
GABAergic afferents from striatum, inhibitory inputs from the GPe, and nigral
dopamine afferents. The inhibitory GABAergic output of the GPi projects to the
ventral anterior and ventral lateral thalamus, intralaminar thalamus, and the
pedunculopontine area. Owing to its size and geometry, the effect of stimulation
in the GPi is more likely to be restricted to the nucleus, but the potential
remains for the possible spread to adjacent structures and pathways, especially
the GPe and internal capsule.
In human subjects undergoing the
implantation of GPi DBS electrodes, studies recorded the response of GPi
neurons to low-frequency (5–50-Hz), that low-amplitude stimulation delivered
250–600 μm from the recording site. The response in 22 of 23 cells was
inhibition lasting 15–25 ms after each pulse, consistent with the activation of
presynaptic inhibitory terminals. At higher frequencies up to 300 Hz, stimulus
trains produced decreased firing but did not completely block firing (Manuela
Rosa, 2012).
Release of neurotransmitters by deep brain stimulation
An early study stated that high-frequency
stimulation of the STN in rodents increases extracellular glutamate in the GPi
and a downstream target of STN projections, and that release may be dependent
upon stimulation frequency. Although a similar increase was not found in humans
with PD, there was an increase in cyclic guanosine monophosphate (cGMP) in the
GPi. Other studies also support the notion that STN DBS drives output neurons.
A similar effect may be important for other sites of stimulation. For example,
the effects of high-frequency stimulation of thalamic slices were blocked by
glutamate receptor antagonists (Manuela Rosa, 2012).
Synthesis of Neurophysiologic data
Differences in techniques, anatomy, cell
type, and experimental setting limit the ability to make direct comparisons
across the studies reviewed above. However, several conclusions are possible. (a)
High-frequency stimulation affects multiple elements, including afferent axons,
cell bodies, efferent axons, and fibers of passage. (b) The stimulated
elements may differ depending on the anatomy of the target (e.g., the VIM
thalamus, STN, GPi, or others). (c) The effects may vary depending on
the intrinsic physiologic properties of the targeted cells. (d) The
effects vary with frequency, amplitude, pulse width, and duration of the spike
trains. (e) Stimulation of the STN releases glutamate from excitatory
efferent neurons. (f) The net effect on distant targets, whether
monosynaptic or polysynaptic, may be independent of local effects. Thus local
cells may be inhibited by the activation of inhibitory afferents or by the
effects on intrinsic ion conductances, but the efferent axons may still be
activated. The high-frequency stimulation effect on downstream targets is
consistent with the activation of efferent axons either directly or through
activation of local cell bodies to axon initial segments. This conclusion is
also supported by computer models and by human functional imaging work (Vesper
Fe Marie L Ramos, 2015).
DBS has the potential to provide
substantial benefit for a variety of neuropsychiatric conditions. Physiologic
and imaging studies support the notion that the net effect of DBS is to
increase the firing of neurons projecting from the site of stimulation. This
may be mediated primarily via the stimulation of axons rather than cell bodies.
DBS seems to mimic the effect of
destructive lesions, suggesting that despite the activation of efferent axons,
there is interruption of information flow or processing. Experiments using rats
and monkeys indicate that high-frequency stimulation can prevent the normal
pattern activity whether driven by electrical cortical stimulation or related
to a limb-movement task. If normal circuits are disrupted in this way, it makes
sense that abnormal circuit activity also would be disrupted. Indeed, STN DBS
has been shown to eliminate abnormal rhythmic oscillation of GPi local field
potentials, and impairing abnormal firing patterns may be more critical than
changing net firing rates.
Future
studies may continue to distinguish variations in the effects of DBS on
different nuclei and different neuronal cell types. Furthermore, patients with
implanted DBS electrodes afford an outstanding opportunity to investigate
behavioral effects of functional circuits (Greenberg,
B. D., 2010).
2.6.
Application of Deep Brain Stimulation
Deep brain stimulation (DBS) is a surgical treatment
that effective for medication-refractory hypokinetic and hyperkinetic disorder.
It’s also being explored for a variety of other psychiatric and neurological
diseases. Deep brain stimulation has been Food and Drug Administration–approved
for essential tremor and Parkinson disease and has a humanitarian device
exemption for dystonia and obsessive-compulsive disorder.
There are some application of Deep Brain Stimulation.
Deep brain stimulation can be an alternative to surgery for the management of
tremor. Thalamic DBS has been shown to be efficacious in the treatment of
essential and parkinsonian tremor, with excellent long-term outcomes and an
acceptable adverse effect profile The main adverse effects of the stimulation
are paresthesias, headache, dysarthria, paresis, gait disturbance, and ataxia.
Adverse effects are usually mild and effectively managed by stimulation
parameter adjustment (S.Y. Chen, 2017).
One of the primary clinical uses of DBS is for the
treatment of Parkinson Disease. A robust motor response to levodopa is
generally considered a prerequisite for successful DBS outcome in Parkinson
Disease (except for tremor-predominant PD), and stimulation may be considered
once patients develop disabling motor fluctuations and dyskinesias while
receiving medical therapy (Michael S. Okun, M.D, 2012). Studies of DBS for PD have reported
significant improvement in cardinal motor signs, including tremor, bradykinesia,
and rigidity, with variable response in medication-refractory gait freezing,
postural instability, and gait mechanics. Adverse effects are typically
transient and reversible (Langston JW, 1983).
Deep brain stimulation has also been useful for treatment
of primary dystonia. Unlike tremor and PD, there is typically a gradually
increasing clinical response to stimulation over weeks to months of therapy.
The shorter disease duration has been reported to lead to better result
Overall, DBS for essential and parkinsonian tremor has been successful, while
treatment of other causes of tremor has been more limited (Burns
RS, 1983).
This surgical procedure can be done to Anorexia
Nervosa patient. After surgery, average follow-up period was 38months (range, 9
–50 months). Average BMI at last follow-up was 19.6 kg/m2 (range,
18.4 –22.1 kg/m2), an average increase of 65% in body
weight. All patients weighed greater than 85% of expected body weight and
thus no longer met the diagnostic criteria of AN. Israel et al. reported a
52-year-old female patient suffering from severe refractory depression with
concomitant recurrent AN (AN age of onset: 17 years of age) who underwent
bilateral DBS at subgenual cingulate cortex in 2005. She was able to maintain
her BMI at an average of 19.1 kg/m2 for more than two years
postoperatively. The nature of this procedure, however, remains investigational
andshould not be viewed as a standard clinical treatment option. Further
scientific investigation is essential to warrant the long-term efficacy and
safety of DBS for AN (Hemmings Wu, 2013).
Deep brain stimulation (DBS) has emerged as a
treatment for severe cases of therapy-refractory obsessive-compulsive disorder
(OCD). The latest results from the procedure have shown a 50% reduction of OCD
scores, depression, and anxiety. There is a clinical trial that using DBS as a
treatment for Alzheimer Disease and Dementia. Evidence for the use of DBS to
treat dementia is preliminary and limited. Further investigation into the
potential clinical effects of DBS for dementia is warranted (Patric Blomstedt,
2012).
DBS can also used as a treatment for Resistant Major
Depression. After the procedure was done. all patients showed strikingly
similar intraoperative effects of increased appetitive motivation (Thomas E.
Schlaepfer, 2013).
This study first reviews clinical outcomes and mechanisms of Deep
Brain Stimulation (DBS) for OCD then discusses these results in an overview of
current and future psychiatric applications which is including DBS for
Parkinson's disease, mood disorders, Tourette's syndrome, addiction, anorexia
nervosa, autism, schizophrenia and anxiety disorders. Deep brain stimulation,
implantation surgery is an established treatment modality for a variety of
medical refractory movement disorders such as Parkinson's disease and many
more. Following the success of DBS in these movement disorders with a high rate
of safety and efficacy, there is a resurgence of interest in the utility of
this modality in other medical refractory disorders. Consequently,
neuromodulation has been explored for a variety of refractory conditions such
as neuropsychiatric disorders (major depressive disorders and
obsessive-compulsive disorders), eating disorders including obesity, traumatic
brain injury, post-traumatic stress disorders (PTSD), dementias and chronic
pain. This review provides an overview of the emerging applications of DBS in
these disorders. DBS does not cures Parkinson's but it can help to manage some
of it's symptoms whose medications has severe side effects. It's the direct
effect on the physiology of brain cells and neurotransmitters are currently
debated but by sending high frequency of electrical impulses into specific
areas of the brain, it can diminish the side effects produced by Parkinson's
medications which allows a decrease in medications. Parkinson's disease is one
of the example that application of DBS works on to reduce the side effects (Yamamoto T, 2010).
2.7.
Prognosis
Profound
cerebrum incitement successfully eases engine side effects of therapeutically
stubborn Parkinson's illness, and furthermore alleviates numerous other
treatment-safe development and full of feeling issue. Regardless of its
relative accomplishment as a treatment choice, the premise of its viability
stays slippery. In Parkinson's infection, expanded practical availability and
oscillatory movement happen inside the basal ganglia because of dopamine
misfortune. A correlative connection between obsessive oscillatory action and
the engine manifestations of the illness, specifically bradykinesia,
inflexibility, and tremor, has been set up. Concealment of the motions by
either dopamine supplanting or DBS likewise relates with a change in engine
side effects. DBS parameters are at present picked experimentally utilizing an
"experimentation" approach, which can be tedious and expensive. The
work exhibited here amalgamates ideas from speculations of neural system
displaying with nonlinear control building to portray and break down a model of
synchronous neural action and connected incitement. A hypothetical articulation
for the ideal incitement parameters important to smother motions is determined.
The impact of changing stimulation parameters on incited motions is examined in
the model. Expanding either incitement beat span or plentifulness improved the
level of concealment. The anticipated parameters were found to concur well with
clinical estimations detailed in the writing for singular patients. It is
expected that the disentangled model portrayed may encourage the advancement of
conventions to help ideal incitement parameter decision on a patient by quiet
premise (Hamani
C, 2008).
Deep
brain stimulation (DBS) is a final resort treatment for neurological and mental
disarranges that are recalcitrant to standard treatment. In the course of the
most recent decades, the advance of DBS in psychiatry has been slower than in
neurology, to some extent inferable from the heterogenic symptomatology and
complex neuroanatomy of mental issue. In any case, for over the top urgent issue
(OCD) DBS is presently an acknowledged treatment. This examination initially
audits clinical results and instruments of DBS for OCD, and after that talks
about these outcomes in a diagram of present and future mental applications,
including DBS for disposition issue, Tourette's disorder, dependence, anorexia
nervosa, extreme introvertedness, schizophrenia, and nervousness issue.
Likewise, it will concentrate on novel procedures that may improve the
utilization of DBS in psychiatry
(C. R. Butson, 2006).
Deep
brain stimulation (DBS) has created amid the previous 20 years as an
exceptional treatment alternative for a few distinct issue. Advances in
innovation and surgical methods have basically substituted ablative methodology
for the greater part of these conditions. Incitement of the ventralis
intermedius core of the thalamus has unmistakably been appeared to uniquely
enhance tremor control in patients with basic tremor and tremor identified with
Parkinson malady. Manifestations of bradykinesia, tremor, walk unsettling
influence, and inflexibility can be fundamentally enhanced in patients with
Parkinson malady. As a result of these upgrades, a lessening in prescription
can be instrumental in diminishing the debilitating highlights of dyskinesias
in such patients. Essential dystonia has been appeared to react well to DBS of
the globus pallidus internus. The accomplishment of these methods has prompted
use of these systems to various other crippling conditions, for example,
neuropsychiatric clutters, recalcitrant agony, epilepsy, camptocormia, cerebral
pain, fretful legs disorder, and Alzheimer ailment (Adrian W. Laxton, 2013).
Deep brain stimulation (DBS) has been found
as a more highly effective and less morbidity-producing alternative to other
surgeries in the treatment of medically intractable movement disorders , but
the exact incidence of morbidity and mortality associated with the procedure is
not well known.
A study was done to assess
the surgical morbidity in 140
consecutive patients with various disease entities of movement disorders,
epilepsy and obsessive-compulsive disorders that underwent deep brain
stimulation (DBS) in a single DBS center of Taiwan. From Feb 2002 to Feb 2015,
a total of 140 patients in the institute were included . All patients underwent
standard DBS procedures with intra-operative microelectrode recordings, and
were followed for at least 6 months.
The results shows that among surgical morbidity,
symptomatic hemorrhage 2.8%(4/140), lead mal-positioned 3.6%(5/140) and
hardware infection 1.4%(2/140). There had no surgical related mortality.
Post-operative morbidity within 6 months was 40.7% (57/140), which included:
weight gain (more than 5 kg) 28.6% (40/140), mania/hypophonia 8.6%(12/140),
transient confusion 7.9% (11/140), depression 4.3%(6/140) and pulmonary edema
2.1%(3/140). Stimulation related morbidity was 47.8% (66/140), which included
hypophonia 18.1%(n=25/138), dyskinesia 13.8%(19/138), dysarthria 13.8%(19/138),
sialorrhea 12.3%(17/138) and decreased memory 11.6% (16/138). The comorbidity
of these patients within the follow-up period up to 13 years was 73%(86/118,
loss follow=20), which included patients who expired, demented, received
bone/spine surgery and diagnosed as cancer (Sorin
Breit, 2014).
The associated morbidity and comorbidity is
significant in DBS patients. Stimulation related morbidity was high,
nevertheless, most of these was transient, and could be improved after change
in stimulation parameters. Though the incidence is low, intracranial hemorrhage
remains as a high risk in DBS surgery.There
is also a significant incidence of adverse events associated with the DBS
procedure. Nevertheless, DBS is clinically effective in well-selected patients
and should be seriously considered as a treatment option for patients with
medically refractory movement disorders (Lancioni GE, 2010).
CHAPTER III
SUMMARY
Deep Brain Stimulation (DBS) is a surgical procedure
that use a high frequency electrical stimulation through chronically implanted
electrodes into a specific target in the subcortical structures. The Deep Brain
Stimulation system consists of three major components, the first being the
lead, which is also called the electrode, is essentially a coiled wire
insulated in polyurethane with four platinum-iridium electrodes and is placed
in one or two different nuclei of the brain. The second component is the
extensions, an insulated wire that is passed under the skin of the head, neck,
and shoulder, connecting the lead to the third component, which is the
neurostimulator or sometimes also called the “battery pack” or the implanted
pulse generator (IPG) – the equivalent of a pacemaker.
The most common use DBS system uses a four contact
stimulating electrode stereo tactically implanted in the target and connected
via a subcutaneous wire to pacemaker-like unit called an Implantable Pulse
Generator (IPG) that is placed on the chest wall underneath the collarbone.
Electrodes are typically placed bilaterally, although clinical needs sometimes
dictate unilateral stimulation. Most targets are deep brain structures (include
deep white matter tracts) rather than cortical areas. The
effect of DBS on neurons in different nuclei may be quite different.
DBS can be an alternative to surgery for the management of tremor, Parkinson
Disease (PD), primary dystonia, Anorexia Nervosa, treatment for OCD and aslo
for Resistant Major Depression. Deep brain stimulation (DBS) has been found as a more
highly effective and less morbidity-producing alternative to other surgeries in
the treatment of medically intractable movement disorders , but the exact
incidence of morbidity and mortality associated with the procedure is not well
known.
REFERENCES
Adrian W. Laxton, Andres M. Lozano. Deep Brain
Stimulation for the Treatment of Alzheimer Disease and Dementias. 2013.
Division of Neurosurgery, Toronto Western Hospital, University of Toronto,
Toronto, Ontario, Canada
Alexander
GE, Crutcher MD and DeLong MR. (1990) Basal ganglia-thalmocortical circuits:
parallel substrates for engine, oculomotor, prefrontal and limbic capacities.
Advance in Brain Research 85: 119-146
Aziz
TZ, Peggs D, Sambrook MA and Crossman AR. (1991) Lesion of the subthalamic core
for the mitigation of 1-methyl-4-phenyl1,2,3,6tetrahydropyridine
(MPTP)- instigated parkinsonism in the primate. Development Disorders 6:
288-292
Bergman
H, Wichmann T, DeLong M. (1990) Reversal of trial parkinsonism by sores of the
subthalamic core. Science 249: 1436-1438.
Buckner RL, Snyder AZ, Shannon BJ, et al. Molecular,
structural, and functional characterization of Alzheimer's disease: evidence
for a relationship between default activity, amyloid, and memory. J Neurosci.
2005;25(34):7709-7017
Burns RS, Chieuh CC, Markey SP, Eberet
MH, Jacobwitz DM and Kopin IJ (1983) A primate model of parkinsonism:
particular decimation of dopaminergic neurons in the standards compacta of the
substantia nigra by MPTP. PNAS 80, 4546-4550
Chiken, S. and Nambu, A. (2016) ‘Mechanism of Deep
Brain Stimulation : Inhibition , Excitation , or Disruption ?’.
Christine CW, Langston JW, Turner RS, Starr PA. The
neurophysiology and effect of deep brain stimulation in a patient with
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism. J. Neurosurg. 2009 Feb;110(2):234-8. doi:
10.3171/2008.8.JNS08882
C. C. McIntyre, et al. “Uncovering the mechanism(s) of
deep brain stimulation: activation, inhibition, or both” Clinical
Neurophysiology, vol. 115, pp. 1239-1248, 2004
C. R. Butson, et al. “Sources and effects of electrode
impedance during deep brain stimulation” Clinical Neurophysiology,vol. 117, no.
2, pp. 447-454, 2006
Drew S. Kern, MS, Rajeev Kumar, MD, FRCPC. Deep Brain
Stimulation. The Neurologist • Volume 13, Number 5, (2017)
Greenberg, B. D.; Rauch S. L.; Haber, S. N.; “Invasive
Circuitry-Based Neurotherapeutics: Stereotactic Ablation and Deep Brain
Stimulation for OCD”Neuropsychopharmacology(2010) 35,317–336; 16 September 2009
Grossman, N. et al. (2017) ‘Noninvasive Deep Brain
Stimulation via Temporally Interfering Electric Fields’, Cell. Elsevier Inc.,
169(6), p. 1029–1041.e16.
Hamani C, McAndrews MP, Cohn M, et al. Memory
enhancement induced by hypothalamic/fornix deep brain stimulation. Ann Neurol.
2008;63(1):119-123
Hemmings Wu, Pieter Jan Van Dyck-Lippens, Remco
Santegoeds, Kris van Kuyck, Loes Gabriëls et all. Deep-Brain Stimulation for
Anorexia Nervosa. World Neurosurg. (2013) 80, 3/4:S29.e1-S29.e10, alvaible
http://dx.doi.org/10.1016/j.wneu.2012.06.039
Herrington, T. M., Cheng, J. J. and Eskandar, E. N.
(2016) ‘Mechanisms of deep brain stimulation’, Journal of Neurophysiology,
115(1), pp. 19–38.
J.S. Perlmutterand J. W. Mink “Deep Brain Stimulation”
Annual Review of Neuroscience, vol. 29, pp. 229-257, 2006
Lancioni GE, Bosco A, Belardinelli MO, Singh NN,
O'Reilly MK, Sigafoos J. An overview of intervention options for promoting
adaptive behavior of persons with acquired brain injury and minimally conscious
state. Res Dev Disabil. 2010;31(6):1121-1134
Langston
JW, Ballard P, Tetrud JW, Irwin I. (1983) Chronic Parkinsonism in people
because of a result of meperidine-simple combination. Science, 219:979-80.
Limousin P, Pollak P, Benazzouz A,
Hoffmann D, Le Bas JF, Broussolle E, Perret JE, Benabid AL (1995). Impact of parkinsonian
signs and indications of two-sided subthalamic core incitement. Lancet, 345,
91-95
Manuela Rosa, Gaia Giannicola, Sara
Marceglia, Manuela Fumagalli, Sergio Barbieri, Alberto Priori. Neurophysiology
of Deep Brain Stimulation. International Review of Neurobiology, Vol. 107, Burlington:
Academic Press, 2012, pp. 23-55.
Michael S. Okun, M.D. Deep-Brain Stimulation for
Parkinson’s Disease. N Engl J Med 2012;367:1529-38.
Mitchell
IJ, Jackson A, Sambrook MA and Crossman AR. (1989) The part of subthalamic core
in trial chorea-prove from 2deoxyglucose metabolic mapping and
horseradish-peroxidase following examinations. Mind 112: 1533-1548.
Patric Blomstedt, Rickard L. Sjo¨ berg, Maja Hansson,
Owe Bodlund, and Marwan I. Hariz. Deep Brain Stimulation in the Treatment of
Obsessive-Compulsive Disorder. World Neurosurg. (2012). Available
http://dx.doi.org/10.1016/j.wneu.2012.10.006
Rosa M, Giannicola G, Marceglia S, Fumagalli M,
Barbieri S, Priori A. Neurophysiology of deep brain stimulation. Int Rev Neurobiol. 2012;107:23-55.
doi: 10.1016/B978-0-12-404706-8.00004-8
Sorin Breit, Jörg B. Schulz, Alim-Louis Benabid. Deep
Brain Stimulation. Cell Tissue Res (2014) 318: 275–288
Svjetlana Miocinovic, MD, PhD; Suvarchala Somayajula,
MD; Shilpa Chitnis, MD, PhD; Jerrold L. Vitek, MD, PhD. History, Applications,
and Mechanisms of Deep Brain Stimulation. JAMA Neurol. 2013;70(2):163-171
S.Y. Chen, Y.H. Pan, S.H. Lin. Morbidity and
comorbidity of deep brain stimulation for Parkinson’s disease – A
thirteen-years retrospective cohort study [abstract]. Mov Disord.2016; 31
(suppl 2). http://www.mdsabstracts.org/abstract/morbidity-and-comorbidity-of-deep-brain-stimulation-for-parkinsons-disease-a-thirteen-years-retrospective-cohort-study/.
Accessed September 14, 2017.
Thomas E. Schlaepfer, Bettina H. Bewernick, Sarah
Kayser, Burkhard M¨adler, and Volker A. Coenen. Rapid Effects of Deep Brain Stimulation
for Treatment-Resistant Major Depression. Biol psychiatry. 2013
T.M. Choiand Y.T. Lee, “Modeling Deep Brain
Stimulation” IFMBE Proceedings, vol. 23, no. 1, pp. 619-621, 2009
Umemura A, e. (2017). Deep brain stimulation for
movement disorders: morbidity and mortality in 109 patients. - PubMed - NCBI.
[online] Ncbi.nlm.nih.gov. Available at:
https://www.ncbi.nlm.nih.gov/pubmed/12691402 [Accessed 15 Sep. 2017].
Vesper Fe Marie L Ramos, Ajay S Pillai, Codrin
Lungu, Jill Ostrem, Philip Starr, and
Mark Hallett. Intraoperative neurophysiology in deep brain surgery for
psychogenic dystonia. Ann Clin Transl Neurol. 2015 Jun; 2(6):
707–710.
Yamamoto T, Katayama Y, Kobayashi K, Oshima H, Fukaya
C, Tsubokawa T. Deep brain stimulation for the treatment of vegetative state.
Eur J Neurosci. 2010;32(7):1145-1151
