Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 9

BIOMEDICAL ENGINEERING ASSIGNMENT

DEEP BRAIN STIMULATION

AGENDA

Introduction to Deep Brain Stimulation (DBS)

Instrumentation and working

Parkinsons Disorder

Usage of DBS in Parkinsonism

Risks of DBS

References

DEEP BRAIN STIMULATION

Deep
brain
stimulation (DBS)
is
a neurosurgical procedure involving the implantation
of a medical device called a brain pacemaker, which
sends electrical impulses, through implanted
electrodes, to specific parts of the brain (brain
nucleus) for the treatment of movement and
affective disorders.

DBS in select brain regions has provided


therapeutic benefits for otherwise-treatmentresistant movement and affective disorders such
as Parkinson's
disease, essential
tremor, dystonia, chronic pain, major depression
and obsessivecompulsive disorder (OCD).

Despite the long history of DBS, its underlying


principles and mechanisms are still not clear. DBS
directly changes brain activity in a controlled
manner, its effects are reversible, and it is one of
only a few neurosurgical methods that allow blinded
studies.

INSTRUMENTATION AND WORKING

The deep brain stimulation system consists of


three components: the implanted pulse generator
(IPG), the lead, and the extension.

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 or two different nuclei of the brain.

The lead is connected to the IPG by the


extension, an insulated wire that runs below the
skin, 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.

INSTRUMENTATION AND WORKING

PARKINSONS DISORDER

Parkinson's disease (PD) is the second most common neurodegenerative disorder, with
an estimated 5 million individuals worldwide, living with the disorder.

These estimates correlate to PD affecting approximately 0.3% of the overall population


and 1% to 2% of individuals over the age of 60 years.

PD is associated with a severe loss in function of dopaminergic cells within the substantia
nigra, which project to the striatum, a major component of the basal ganglia.

Progressive degeneration of these nigrostriatal projections leads to the hallmark motor


features of PD such as tremor, rigidity, bradykinesia, and postural instability.

PD is additionally associated with nonmotor symptoms including autonomic dysfunction,


depression, anxiety, and sleep disturbances.

DBS IN PARKINSONISM

An increasingly utilized treatment modality for the management of people with


advanced PD whose disease is complicated by disability from motor
fluctuations and dyskinesias despite an effort to intensify medication therapy
is deep brain stimulation (DBS) surgery.

DBS is the most frequently performed surgical procedure for the treatment of
advanced PD as it can can improve symptoms of tremor, rigidity, bradykinesia,
and dyskinesia.

Symptoms associated with gait, balance, speech, and cognition, in contrast,


do not generally respond well to DBS treatment.

DBS surgery itself involves the implantation of a neurostimulation system that


is composed of two wires (a lead and an extension wire) connected to a
neurostimulator device (implantable pulse generator [IPG]), not dissimilar to a
pacemaker, to control heart rate. The IPG, which is implanted in the patient's
chest, delivers electrical impulses to an electrode located at a target site
within the brain.

The surgical procedure for DBS is typically performed in two stages that are
done approximately 1 week apart. The first surgery involves the implantation
of the lead wire into the brain, and the second surgery involves the
implantation of the neurostimulator and extension wire. Patients can undergo
unilateral or bilateral DBS lead placement depending on whether symptoms
are bothersome on both sides of the body or not.

RISKS OF DBS

REFERENCES

Olanow CW, Stern MB, Sethi K. The scientific and clinical basis for the treatment of Parkinson disease. Neurology. 2009;72(suppl 4):S1-S136.

de Lau LM, Breteler MM. Epidemiology of Parkinson's disease. Lancet Neurol. 2006;5:525-535.

Truong DD, Bhidayasiri R, Wolters E. Management of non-motor symptoms in advanced Parkinson disease. J Neurol Sci. 2008;266:216-228.

Parashos SA, Maraganore DM, O'Brien PC, Rocca WA. Medical services utilization and prognosis in Parkin son disease: a population-based study. Mayo Clin
Proc. 2002;77:918-925.

Guttman M, Slaughter PM, Theriault ME, et al. Burden of parkinsonism: a population-based study. Mov Disord. 2003;18:313-319.

Guttman M, Slaughter P, Theriault M, et al. Parkin sonism in Ontario: comorbidity associated with hospital ization in a large cohort. Mov Disord. 2004;19:49-53.

Pressley JC, Louis ED, Tang MX, et al. The impact of comorbid disease and injuries on resource use and expen ditures in parkinsonism. Neurology.2003;60:87-93.

Tan LC, Tan AK, Tjia HT. The profile of hospitalized patients with Parkinson's disease. Ann Acad Med Singapore. 1998;27:808-812.

Woodford H, Walker R. Emergency hospital admis sions in idiopathic Parkinson's disease. Mov Disord. 2005;20:1104-1108.

Huse DM, Schulman K, Orsini L, et al. Burden of ill ness in Parkinson's disease. Mov Disord. 2005;20:1449-1454.

Louis ED, Henchcliffe C, Bateman BT, Schumacher C. Young-onset Parkinson's disease: hospital utilization and medical comorbidity in a nationwide
survey. Neuroepidemiology. 2007;29:39-43.

Klein C, Prokhorov T, Miniovitz A, et al. Admission of Parkinsonian patients to a neurological ward in a com munity hospital. J Neural Transm.2009;116:1509-1512.

Olanow CW, Watts RL, Koller WC. An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines. Neurology.2001;56:S1-S88.

Benabid AL, Chabardes S, Mitrofanis J, Pollak P. Deep brain stimulation of the subthalamic nucleus for the treatment of Parkinson's disease. Lancet Neurol.2009;8:6781.

Deuschl G, Schade-Brittinger C, Krack P, et al. A randomized trial of deep-brain stimulation for Parkinson's disease. N Engl J Med. 2006;355:896-908.

Limousin P, Krack P, Pollak P, et al. Electrical stimula tion of the subthalamic nucleus in advanced Parkinson's disease. N Engl J Med. 1998;339:1105-1111.

Volkmann J, Allert N, Voges J, et al. Safety and efficacy of pallidal or subthalamic nucleus stimulation in advanced PD. Neurology. 2001;56:548-551.

Benabid AL, Pollak P, Gervason C, et al. Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus. Lancet.1991;337:403-406.

Tasker RR. Deep brain stimulation is preferable to thalamotomy for tremor suppression. Surg Neurol. 1998;49:145-153.

Rehncrona S, Johnels B, Widner H, et al. Long-term efficacy of thalamic deep brain stimulation for tremor: double-blind assessments. Mov Disord.2003;18:163-170.

You might also like