w8 Flashcards
what are some common causes of chronic patin
trauma: external injury, nerve compression, inflammation
genetic predisposition: inhereted neurodegeneration, metabolic or endocrine abnormailities.
therapeutic intervention (most common): surgery, chemotherapy, irradiation
disease process: infection/inflammation, neurotoxicity, tumor infiltration, metabolic abnormality.
describe the process for peripheral nerve regeneration
when a nerve is severed, schwann cells proliferate to attempt to recover the nerve.
could regenerate and remyelinate, or it could cause problems such as neuromas or lack of long distance regeneration
For the following types of nerve fibres, what is the information carried,
A-alpha
A-beta
A-delta
C
note that in reality, nerves are not this distinct, there is a alot of overlap between classes.
A-alpha: proprioception
A-beta: touch
A-delta: pain (mechanical and thermal)
C: pain (mechanical, thermal and chemical)
describe the difference between
normal nociceptor responses
normal low-threshold mechanoreceptor responses
and central sensitization (Hyperalgesia / Allodynia) responses
Normal nociceptor => pain
Normal mechanoreceptor => touch.
Hyperalgesia: nociceptors have increased response i.e. more pain is experienced than normally
Allodynia: mechanoreceptors trigger nociception. i.e. pain response is triggered from stimuli that do not normally provoke pain.
what are some first line treatments for neuropathic pain
Cognitive and Behavioural Modifications
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Transcutaneous Electrical Nerve Stimulation (TENS)
Biofeedback
OTC Pain Medications / Rehabilitative Therapy
what are some second line treatments for neuropathic pain
Systemic Opioids
Nerve Blocks
what are some third line treatments for neuropathic pain
Neurostimulation
Implantable Drug Pumps
Neuroablation
what is the gate control theory of pain and describe its biological mechanism.
what is the gate control theory mechanism of action for spinal cord stimulation
The theory that the spinal cord contains a neurological “gate” that blocks pain signals or allows them to pass on to the brain. The “gate” is opened by the activity of pain signals traveling up small nerve fibres and is closed by activity in larger fibres or by information coming from the brain.
Activates inhibitory interneurons by stimulating myelinated a-beta nerves in the dorsal column, thus preventing the transmission of nociception to the brain. The inhibititory interneurons mediate GABA release into the neuron pool, which leads to analgesia.
Where was the first spinal cord stimulator prototype implanted
Subarachnoid space (in Cerebrospinal fluid)
Describe the placement of the spinal cord stimulator devices over time
Started in CSF, lead to infections
Then sub-dural space
Now in epi-dural space (safest placements)
why does the Nevro device stimulate at high frequency (~10kHz)
patients don’t preceive stimulation (paraesthesia free)
At high frequencies, the stimulus current required to generate an action potential drops
but also reduces excitability over time (needs resting period to get same response)
where are the electrodes (leads) of SCS implanted
Electrodes are placed in thoracic region (around T7) to stimulate lower back and lower limbs
where is the pulse generator of SCS implanted
on lower back between ribs and pelvis
what is a Dermatome map
Diagram of the areas of skin innervated by a single spinal nerve
Anecdotally SCS is said to work for 65% of
people who achieve 50% or better pain relief.
what are the 3 main issues with SCS products
Unpredictable Benefit: trial stimulation is needed to assess benefit
Unstable Therapy: patient movement produces over-stimulation. long term electrode migration
Invasive Process: long procedure time, paraesthesia and side effects