Deep Brain Stimulation Flashcards

1
Q

What is the procedure for deep brain stimulation

A
  • This is the procedure in which stimulating electrodes are placed sterotatically into certain deep Brain structures
  • the electrodes are connected to an implanted pulse generator which is batter powered
  • the electrodes are then secreted to the skull and a cable tunnelled around th year down to the neck to the pulse generate situated in front of the chest
  • battery replacements happen every 3-4 years whereas rechargeable systems have been developed to have a lifespan of 10 years
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2
Q

How much does deep brain stimulation cost

A
  • Device £12,200
  • £7,800 for surgery
  • So total cost is around £20,000
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3
Q

What is currently NICE approved for deep brain stimulation

A
  • Parkinson’s disease (hypokinetic movement)
  • essential tremor (hyperkinetic movement)
  • dystonia (hyperkinetic movement)
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4
Q

What type of movement is essential tremor and dystonia

A

Hyperkinetic

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5
Q

Define essential tremor

A
  • Brain disorder causing part of the body such as the head and forearms to tremor uncontrollably
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6
Q

Define dystonia

A
  • Brains disorder with sustained or repetitive muscle contractions resulting in twisting and repetitive movements or abnormal fixed postures
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7
Q

In what diseases can you get deep brain stimulation if you ask for individual funding requests

A

Epilepsy
chronic neuropathic pain
- this is when the consultant has to put forward a case as to why you should get it

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8
Q

describe and name the different types of tremor

A

there are two main categories these are resting tremor and action tremor

Resting Tremor
- this is when you have a tremor while resting

Action tremor

  • either postural, kinetic and intention
  • a postural tremor is a tremor when you life a limb such as an arm - holding something against gravity
  • Kinetic - occurs with voluntary movement
  • Intention - occurs with goal directed movement and worsens as approaching the target
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9
Q

resting tremor indicates….

A

parkinsons disease unless proven otherwise

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10
Q

what are the 4 classical symptoms of Parkinson

A

tremor
bradykinesia
rigidity
postural instability

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11
Q

What is the criteria for parkinsons patients in order to get deep brain stimulation

A
  • Idiopathic Parkinson’s disease 4 classical symptoms – tremor, bradykinesia, rigidity, postural instability
  • Do not have sensory issues such as numbness and tingling
  • Do not get weakness or hyperreflexia
  • Require an MRI scan – check for no abnormalities in brain such as brain tumour
  • No mental disorders
  • Still Levodopa responsive (DBS will not work as patient is burnt out with no DA neurones to have an effect)
  • Physically fit for surgery
  • Realistic expectation of surgery (not a cure but to help with motor symptoms, PD will eventually catch up)
    age
  • Younger patients benefit more from DBS but older patients can still be treated
  • DBS only treats the motor symptoms and no the non-motor symptoms (such as gait or balance, cognitive problems and depression)
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12
Q

what does the basal ganglia do

A
  • Nuclei in our brain to decide to make movements and stop unwanted movements
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13
Q

What does the thalamus do

A
  • Central control unit, as everything is leaving the brain and coming up from spinal cord to pass through the thalamus
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14
Q

What are the targets in Parkinson’s for deep brain stimulation

A

 Subthalamic nuclei. = targets tremor
 Thalamus. = targets dystonia and tremor
 Globus pallidus interna. = targets dystonia and tremor

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15
Q

Describe how deep brain stimulation works

A
  • Patients are not on medication for this procedure so stiff and slow when arrive at hospital
  • Using MRI scan to work out the target site
  • Connect a stereotaxic frame on a patients head
  • Drill a 4cm hole in the skull and then insert the microelectrode tip to the presumptive target site
  • Each brain structure as a distinct neurophysiological spiking and spike background patterns
  • Once the target site has been located microelectrode is removed and the stimulating electrode is inserted
  • Cap hole, close wound, MRI scan to check electrode at correct site, then general anaesthesia for neuro-stimulator implant
  • Return home next day then return to the clinical 1 month alter to programme DBS and adjust drug dosage
  • Patient is awake
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16
Q

What does deep brain stimulation do to Parkinson’s

A
  • Increase on time
  • Decrease bradykinesia and rigidity
  • Reduces medication dose 1/3 less
  • Improves dyskinesia as less drug required
  • Effectively treats tremor (L dopa not good with tremor)
17
Q

Describe how deep brain stimulation improves the on and off effect of parkinsons

A
  • When L dopa kicks in this is the on time and you can walk normally
  • Then drug disappears and then if you want to walk and move again then take L dopa again
  • Become tolerant to it the one time becomes shorter
  • Then eventually when you take it you get dyskinesia after a short on time – cant really control your movement
  • DBS rises the line of bradykinesia up therefore you need a smaller amount of the dose of L dopa for its effect to last longer
18
Q

describe how deep brain stimulation can be used for epilepsy

A
  • treatment for epilepsy when medications are inadequate
  • electrode is implanted into the anterior nucleus of the thalamus as this is the part of the brain that causes then seizure to spread
  • this reduces seizure frequencies but does not eliminate them
19
Q

Describe how deep brain stimulation can be used to treat neuropathic pain

A
  • Surgery via lesion brain regions related to the pain pathway is more invasive than DBS
  • Only reduce not eliminate pain experience
  • Benefit 15-20% of pain patients
20
Q

what are the pros of DBS

A
  • Proven safe
  • More than 140,000 patients have been implanted with DBS systems
  • Can improve tremor that are l dopa resistant
  • The effects are reversible and can be tailored to a patients clinical status
  • Provides continuous symptom control 24 hours a day for years
  • Patients who have undergo DBS are still candidates for other treatment options such as stem cell or gene therapy when they become available
  • Allows a decrease in medication
21
Q

What are the cons of DBS

A
  • 2-3% risk of brain haemorrhage that can cause paralysis, stroke and speech impairment
  • A small risk of cerebrospinal fluid leakage causing headaches and meningitis
  • 15% risk of temporary problems with transplantation (infection, allergy to implant)
  • May experience temporary tingling in the face or limbs, loss of balance, dizziness, concentration issues
  • Migration of electrode from original implantation site
  • Temporary rebound in worsening of tremor when stimulation is stopped
  • No guarantee DBS surgery will benefit patients even though large percentage report significant improvement
22
Q

Name the brain region where DBS is targeted for

  • tremor
  • dystonia
  • pain
  • epilepsy
  • depression
  • anorexia
  • addiction
  • alzheimers
  • tourettes syndrome
A

Other Uses:
 Tremor - subthalamic nuclei and thalamus targeted.
 Dystonia (uncontrollable muscle contraction) – globus pallidus interna.
 Pain – Sensory thalamic nuclei, anterior cingulate gyrus.
 Epilepsy - Anterior thalamic nuclei.
 Depression – Nucleus accumbens, subcallosal cingulate (brodmann area 25)
- anorexia - hypothalamus
- addiction - nucleus accumbens
- Alzheimers disease - anterior of the fornix
- Tourette syndrome - thalamic centromedian

23
Q

what are the 4 hypothesis for the mechanism of action of DBS

A
  • Inhibition hypothesis
  • Excitation hypothesis
  • Disruption hypothesis
  • Neuro-network modulation hypothesis
24
Q

Describe Inhibition hypothesis theory

A
  • This is the idea that Parkinson’s disease is due to overactive basal ganglia neurones in the STN and or/GPi
  • DBS can block this and remove spontaneous discharge from GPi neurones
  • This hypothesis agrees with anatomical lesioning and pharmacological intervention (GABA agonists)
  • DBS inhibits the local neuronal firing removing the spontaneous discharge from GPi
25
Q

Describe excitation hypothesis

A
  • DBS excites afferent axons antidromically resulting in jamming the spontaneous activity
  • DBS inhibits the local neuronal firing removing the spontaneous discharge from thalamus
26
Q

Describe disruption hypothesis

A
  • The GPI receive input from the direct(GABA) and indreict(GABA) and hyperdirect pathway (glutamate)
  • DBS can activate axon terminals causing extensive release of NTs such as GABA and glutmate
  • DBS dissociates inptus and outputs in the stimulated nucleus thus disrupting and blocking the abnroaml information flow through the GPi
  • DBS disrupts abnormal information flow through the GPi
27
Q

Describe Neuro-network modulation hypothesis

A
  • Far more complex
  • Suggest that there are other things such as neuroprotection release of astrocytic gliotransmitters, electrotaxis and cortical plasticity
  • They suggest this as if the other hypothesis were true we would see the changes straight away but we don’t and DBS takes time to work (days)therefore these things must be involved