Somatosensory Pathology Flashcards
2 tests of THE INTEGRITY OF THE ASCENDING SOMATOSENSORY PATHWAYS
- Quantitative sensory testing (QST)
- Electrical perceptual thresholds (EPT)-
What is an Electrical perceptual thresholds (EPT) test
like QST but semi-automated Electrical current sent to skin and the patient either feels it or doesn’t
What is a Quantitative sensory testing (QST) test
a set of various tools we can use to look into the integrity of all of the different modalities e.g. using a brush to stroke someone’s arm 13 different tests can be done
what causes nociceptive pain?
Tissue damage, typically acute e.g. skin cut
what causes muscle pain?
Lactic acidosis, ischaemia e.g. stretching, fibromyalgia)
what causes somatic pain?
Well-localised e.g. inflammation, infection
what causes visceral pain?
Deep, poorly localised e.g. stomach, colon, IBS
what causes referred pain?
From an internal organ/structure e.g. angina
what causes neuropathic pain?
PAIN CAUSED BY A LESION OR DISEASE OF THE SOMATOSENSORY NERVOUS SYSTEM
How does ACUTE AND CHRONIC PAIN manifest
hyperalgesia and allodynia
What comorbidities can you get with acute and chronic pain
anxiety and depression as secondary comorbidities
What does neuropathic pain feel like
Sharp, burning, electric shocks
Success of analgesic opiated in neuropathic pain?
Poor
3 types of neuropathic pain?
Sciatica (most common)- spinal nerves compressed in intervertebral foramen
Diabetic neuropathy
Post-hepatic neuralgia can be caused by shingles
HIV induced neuropathy
CRPS = pain around the whole body that spreads spontaneously
What types of neuropathic pain can you get (5)
ALLODYNIA Hyperalgesia Sensitisation Hypoalgesia Paraesthesia
What is ALLODYNIA
Pain due to a stimulus that does not normally provoke pain e.g. brush
What is Hyperalgesia
Increased pain from a stimulus that normally provokes pain
What is Sensitisation
Increased responsiveness of nociceptive neurons to their normal input
What is Hypoalgesia
Diminished pain in response to a normally painful stimulus
What is Paraesthesia
Abnormal sensation, whether spontaneous or provoked
How do we diagnose and asses neuropathic pain (2)
Clinically we use a combination of questionnaires and simple sensory tests e.g. brushing etc.
What is central sensitization in chronic pain
Increased amount of pain was found not to just be from sensitization in the periphery but in the spinal cord
What do NMDA receptors do and how does result in central sensitisation and chronic pain
(mechanism for central hypersensitisation) they allow a big post-synaptic depolarisation which allows calcium into the neuron- this activates intracellular signalling and increases synaptic strength and our sensitivity
Persistent activation of NMDA receptor can result in development of chronic pain
What happens in hyperalgesia
Central sensitisation via persistent NMDA activation which causes a lack of inhibitor from interneurons
What happens in allodynia
Almost a rewiring of neurons so mechanoreceptors can stimulate nociceptive fibres
What sort of shape is curve of a stimulus intensity against pain intensity graph
sigmoidal
What is descending modulation of chronic pain
Monoamines released from the brainstem that work to inhibit spinal cord excitability (and thus reduce pain)
What are 2 methods of descending modulation of pain
THE PAG-RVM AXIS LOCUS CERELEUS (LC):
The LOCUS CERELEUS (LC) in descending pain modulation (location, NT,
This is in the pons
This uses noradrenaline as its main neurotransmitter
The PAG-RVM AXIS in descending pain modulation (names of nuclei, locations, NT)
Periaqueductal gray - midbrain
rostral ventral medial medulla - Pons
serotonin (5-HT)
- The PAG and RVM contain high concentrations of X RECEPTORS
Mew opioid
How does the PAG-RVM axis inhibit pain
- The PAG and RVM contain high concentrations of OPIOID RECEPTORS
- Endogenous opioids enhance descending inhibition from the PAG-RVM axis
- Reduce pain transmission from the dorsal horn by inhibiting glutamate release i.e. activation of spinothalamic neurons
- Forms part of an ENDOGENOUS ANALGESIC SYSTEM
Drugs used to target descending pain modulation?
- Opioids
- Antidepressants (Tri-cyclic Antidepressants (TCAs), Serotonin Noradrenaline Reuptake Inhibitors (SNRIs) and Selective Serotonin Reuptake Inhibitors (SSRIs)
Effectiveness of SSRIs as analgesics?
low analgesic efficacy
Effectiveness of SNRI as analgesics?
Effective
MoA of SNRIs in pain inhibition?
- If you give an SNRI e.g. duloxetine, it binds to the presynaptic or postsynaptic terminal in the dorsal horn and inhibits NA reuptake from the synaptic cleft
- This means NA acts on inhibitory 2 receptors for longer and inhibitory influence is increased (pain is reduced)
3 neuropathic pain patient clusters?
- SENSORY LOSS
- THERMAL HYPERALGESIA
- MECHANICAL HYPERALGESIA
