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Deep Brain Stimulation - Anatomy and Physiology 2012

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Brandon Tyler

on 25 October 2012

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Transcript of Deep Brain Stimulation - Anatomy and Physiology 2012

Introduction to
DBS Deep brain stimulation
High frequency stimulation
Mimics lesions Treats motor symptoms
Stimulates the basal nuclei, specifically the:
Subthalamic nucleus
Globus pallidus Basic Principles Q = a + bt "b" is the rheobase "a/b" is the chronaxie The shape of the electric pulse is irrelevant Factors to consider Complex factors:
Anisotropic tissues
Heterogeneous electrophysiological cellular and structural properties of stimulated elements Large myelinated fibres Chronaxie of 30–200 ms Cell bodies & dendrites Chronaxie of 1 - 10 ms In 6-8 weeks, Extracellular fluid
around electrode Cell and microglia formation Shape and size of electric field is altered

Extracellular potential is stronger due to conductive properties Placebo effects appear to have an effect
Patients said they felt better before the simulation was turned on Outcome of stimulation depends on expectation Implantation alone appears to have a therapeutic benefit The main aspects of
designing an electrode
are as follows Size Shape Area Electrode Design Factors Electrode polarizes and tissue can undergo hydrolysis Design will affect tissue
reactivity and potential
degree of damage Tissue pH change Production
of gas Works Cited:
Diagrams:
Coronal view of deep brain - Andrew Gillies (GFDL)

Gubellini, P., Salin, P., Kerkerian-Le Goff, L., Baunez, C. (2009). Deep brain stimulation in neurological diseases and experimental models: From molecule to complex behavior. Progress in Neurobiology, 89 : 79-123

Pollanen, M. S., Dickson, D. W., & Bergeron, C. (1993). Pathology and biology of the Lewy body. Journal of Neuropathology & Experimental Neurology, 52(3), 183-191.

Doering, L. (2012). Parkinson’s Disease [PowerPoint slides]. Retrieved from https://avenue.cllmcmaster.ca/d2l/lms/content/viewer/main_frame.d2l?ou=89830&tId=777384

Dickson, D. W., Feany, M. B., Yen, S. H., Mattiace, L. A., & Davies, P. (1996). Cytoskeletal pathology in non-Alzheimer degenerative dementia: new lesions in diffuse Lewy body disease, Pick's disease, and corticobasal degeneration. Journal of neural transmission. Supplementum, 47, 31.

de Lau, L. M., & Breteler, M. (2006). Epidemiology of Parkinson's disease. The Lancet Neurology, 5(6), 525-535.

Weaver, F. M., Follett, K. A., Stern, M., Luo, P., Harris, C. L., Hur, K., ... & Franks, R. (2012). Randomized trial of deep brain stimulation for Parkinson disease Thirty-six-month outcomes. Neurology, 79(1), 55-65.

Benabid, A. L., & Torres, N. (2012). New targets for DBS. Parkinsonism & related disorders, 18, S21-S23.

Weaver, F. M., Follett, K., Stern, M., Hur, K., Harris, C., Marks Jr, W. J., ... & Huang, G. D. (2009). Bilateral deep brain stimulation vs best medical therapy for patients with advanced Parkinson disease. JAMA: the journal of the American Medical Association, 301(1), 63-73.

Clements, Isaac Perry. (2008). How Deep Brain Stimulation Works. Retrieved October 24, 2012, from http://science.howstuffworks.com/environmental/life/inside-the-mind/human-brain/deep-brain-stimulation.htm

National Parkinson’s Foundation. (2009). Deep Brain Stimulation. Retrieved October 24, 2012 from http://www.parkinson.org/Parkinson-s-Disease/Treatment/Surgical-Treatment-Options/Deep-Brain-Stimulation.aspx

Radiology Info. (2012). MRI of the Head. Retrieved October 25 from http://www.radiologyinfo.org/en/info.cfm?pg=headmr

D. Hellwig , H. Freund, M. Giordano, F. Sixel-Döring. (2012). Deep Brain Stimulation for Treatment of Parkinson’s Disease Deep brain stimulation, Parkinson’s disease, subthalamic nucleus, stereotactic surgery. Retrieved October 24, 2012 from The Internet Journal of Neuromonitoring. 2012 Volume 7 Number 1

Nordqvist, Christian. (2009). What is a CAT Scan? Retrieved October 24, 2012 from http://www.medicalnewstoday.com/articles/153201.php.

Mandybur, George. (2010). Deep Brain Stimulation Surgery. Retrieved October 25, 2012 from http://www.mayfieldclinic.com/PE-DBS.htm Commonly
Used Lead in
Humans Optimal design entails a low diameter/height ratio to maximize the volume of tissue that can be activated Signal Types Monophasic Biphasic Two types: Current diffusion is minimized
due to inverse-square and Coulomb’s laws Biphasic is preferred Minimizes damage The Basal Ganglia Procedural Memory Regulation of Motor
Output Applications to PD 1950's Brain Lesions 1970's Levodopa The Basal Ganglia Store
Procedural Memories Swinging a racket Turning
around Going up and down stairs Standing up
from a chair When the Motor Cortex wants
to complete a task, it has to
ask the Basal Ganglia how to
do it. In order to access these memories,
signals have to be sent through the
main relay of the brain - the
Thalamus Subthalamic Nucleus Primarily PD Preferred target Treatments Dystonia
Epilepsy
OCD STN becomes hyperactive in PD Response of DBS is frequency dependent Targets 1980's Frequency increases with age What is Parkinson's Disease? Globus Pallidus
interna (GPi) areas of the brain were removed
damaging side effects
can not be undone 100 Hz L-dihydroxyphenylalanine
precursor to dopamine
relieves symptoms
patients become immune to drugs Deep Brain Stimulation Effects like brain lesions
pulses of electricity
reversible effects
localized stimulation Deep Brain Stimulation Device Electrodes 125 Hz Extension Wire Pulse Generator 166 Hz 10% Mutagenic
PARK1: autosomal dominant; responsible for alpha-synuclein protein 90% Sporadic
Heavy metals, pesticides?
Cigarettes, coffee, Advil: neuroprotective effects Epidemiology PD triad of symptoms immediately reversible lower drug dosage by 65% Mechanism Where are they
placed? Does not rely on: Activation of GABA Ionotropic glutamate receptors Secondary location for PD treatment Reduces Similar results from STN Sodium & calcium voltage-gated currents Does not allow reduction in medication Ranges Other Locations 100-130 Hz Silence AP failures Soletra Neurostimulator
55mm x 60 mm
42 g Placed near the clavicle Battery Life:
3-7 years The Facts Thalamus High frequency
spiking Burst
activity Pedunculopontine nucleus Anterior Hypothalamus Symptoms - ventromedial
- lateral 70-90 Hz Tremor Rigidity Is it successful? AP failures Akinesia Both GPi and STN
improve motor function Postural Instability Burst
activity Difficulties Improvement was comparable by
target. Fine Movement Facial expressions Remaining fixed for long periods of time Speech volume Slanted and jagged writing Improvements were stable through
24 months. UPDRS-III Third section of widely used scale
for the evaluation of PD Evaluates motor function Maximum score of 56 Reduced dopamine in the nigrostriatal pathway Unfavourable motor symptoms Reduced dopamine in the striatum Reduced dopamine in the basal nuclei Dopamine-rich neurons die in the substantia nigra The therapeutic range is from 80 - 185 Hz Where is the electrode
placed? Some studies showed decreased improvements over time Could be attributed to
natural disease
progression ? Follow-up showed stable improvements
36 months out Two Main Paths SNc neurons innervate predominantly the striatum, one primary input station of the BG, a richly interconnected group of brain nuclei playing a key role in the subtle regulation of voluntary and purposive movements. Direct InDirect CT Scans MRI Computer Tomography
X-Rays and Computer Imaging Magnetic Resonance Imaging
Strong magnetic field, Radio Frequency, Computer Imaging Replaces spontaneous firing with stimulus-driven firing Suppresses burst activity Imposes a tonic pattern Disrupts abnormal synchronized activity in
the BG-thalamocortical loops Excitatory Inhibitory 3D Imaging Lewy Bodies Spherical mass made of alpha-synuclein
Displaces cell components
Associated with degenerative diseases
Pick's disease
Corticobasal degeneration
Dementia Striatum single spike burst mixed burst Stereotactic Planning SNc (Substantia Nigra pars compacta) sends
DA (Dopamine) to Striatum to regulate which
path is activated at a given time. SNr and GPi Thalamus Cortex GPe STN SNr and GPi Thalamus Inhibitory Excitatory Motor
Activation Cortex Motor
Inhibition Target Path One large study:

STN - 42.5 to 29.7 --> -31%
GPi - 41.1 to 27.1 --> -43% Medication and DBS work
synergistacly Entry point at the Cortical Surface Avoids loss of CSF Avoid the brain sulci Would lead to damage of vessels Avoid Ventricles Would cause electrode dislocation Normally, the STN has an excitatory effect on the SNr/GPi complex. single spike burst mixed burst Practice Tonic firing Globus Pallidus
(i)nternal
(e)xternal SubThalamic Nucleus Substantia Nigra Essentially a normal action potential 1 2 3 Single spikes with brief quiescent periods Burst firing Depolarizes and stays depolarizes Blocks of rapid spiking Mixed firing A mix of bursts and single spikes When should DBS be used? PET scan showing fluorodopa (FDOPA) Normal Parkinson's Had PD for > 5 years
non-invasive treatments are not effective
Positive L-Dopa response (30% improvement)
Age below 75 years
Little to no cognitive dysfunction Progressive degenerative disorder of the central nervous system Movement disorder Second most common neurodegenerative disorder next to Alzheimer’s Disorder Affects 1% of people over 60 Affects over 100,000 Canadians Surgery Plan trajectory of electrode Test stimulation
& Programming Implant
electrodes Test Placement MRI and CT Scan Ben Kinsella
Gareth Chan
Matt Stone
Brandon Tyler
Emily Au Parkinson's Disease and Deep Brain Stimulation BN-Thalamocortico Loop in PD STN is not regulated,
because it is not receiving regular
input from striatum
It loses its own rhythm
Enters hyperactivity Causes the SNc to become further damaged
SNc reduces dopamine production
Striatum becomes further confused Lack of DA sent to the striatum
from the SNc
Causes striatum to become disorganized
Selection of paths becomes disorganized as a result Brain computer interfaces allow external stimulation and control of neural circuits. Deep Brain stimulation has been used to treat movement disorders such as Parkinson's Disease (Lega et al, 2011). How is deep brain stimulation performed, where is the ideal location for electrode implantation, what are the electrical characteristics of the stimulus and why are they chosen? How successful has this technique been? THANK YOU Periodic oscillatory neuronal activity at low frequency (which in humans is highly correlated with tremor) is present in a large proportion of STN neurons.
These oscillatory patterns are in the low (beta) frequency range are commonly recorded in PD patients. What does it mean for the STN to be unregulated? spike are info- deficient
bursts have uch more info fidelity and flexibility
when the STN is hyperactive - incoherent, disorganised
constant burst is outputted
DBS imposes silence on STN - lessens its negative impact on motor
systems
as STN recovers from DBS, enters temporary "spike" mode - much
less destructive and more manageable for the motor sytem than
the disorganised bursts.
Combined with LDOPA, which helps restore regular striatum fn,
the patient's basal ganglia system resumes an almost-normal
state, which is reflected in the huge motor improvement
of patients. Recall that burst output from the STN is a high-density form of data transmission When the STN is hyperactive, a constant, incoherent and overwhelming signal is outputted. DBS imposes silence on STN - lessens its negative impact on motor systems STN recovery - Temporary spike mode -> less destructive Combine with LDOPA for
"Miracle Cure"
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