Complex Regional Pain Flashcards
What is complex regional pain syndrome (CRPS)?
CRPS is characterized by pain associated with sensory, autonomic, trophic, and motor abnormalities. CRPS is triggered by noxious stimuli (type I) or by nerve injury (type II). It is not limited to the distribution of a single peripheral nerve and is disproportionate to the inciting even
RSD, causalgia, algodystrophy, Sudeck atrophy, and various other conditions are all grouped under CRP
What are the two types of CRPS?
CRPS-I is defined as a clinical syndrome triggered by a noxious stimulus that is not limited to the distribution of a single peripheral nerve; no nerve lesion can be identified.
CRPS-II is defined as a clinical syndrome that is due to a nerve injury and is mostly limited to the distribution of the injured nerve. The diagnostic criteria are the same for CRPS-I and II.
What are the diagnostic criteria for CRPS? What is the incidence of this disease?
Orlando criteria or a modified version referred to as the Budapest criteria. Abnormal function of the sympathetic nervous system (vasomotor changes, skin color changes) Swelling Movement disorder Changes in tissue growth (dystrophy and atrophy) Sensory disturbances (hyperalgesia or allodynia)
The main features include pain that is continuous, burning in nature, independent of type and severity of injury, and not limited to a dermatomal distributionPatients may complain of allodynia, dysesthesia, or hyperalgesia. Movement or stress exacerbates pain. Edema is usually present. Abnormal sudomotor activity, limb discoloration, and local temperature changes are common but inconsistent.
Define allodynia
hyperalgesia
hyperesthesia
dysesthesia.
What are the stages of CRPS?
What are the possible etiologies of CRPS?
Inflammatory conditions (e.g., fasciitis, tendonitis, bursitis, and arthritis)
Immobilization as a result of injury or cast application
Inflammatory conditions (e.g., fasciitis, tendonitis, bursitis, and arthritis) Immobilization as a result of injury or cast application Peripheral nerve injury resulting from direct compression or ischemia (e.g., brachial plexopathy, postherpetic neuralgia, and nerve root injury
Peripheral nerve injury resulting from direct compression or ischemia (e.g., brachial plexopathy, postherpetic neuralgia, and nerve root injury
Explain the pathophysiology of the development of CRPS.
More than one sequence of events likely take place in a patient, giving rise to a mixed clinical picture. A dynamic change in the physiology and structure of central pain projecting neurons mediated through the N-methyl-D-aspartate (NMDA) receptor. Injury initiates and maintains a state of central sensitization in the central pain pathways, resulting in a lower threshold to fire pain transmission neurons and an increase in their receptive fields. This may involve disinhibition of spinal and trigeminal nociceptive neurons. This often precedes thermal and mechanical allodynia and spontaneous pain. Finally, the psychological component and neuromodulation cannot be discernibly separated.
- Abnormal discharges in sympathetic and nociceptive afferents produced by trauma
- Sensitization of peripheral sensory receptors produced by sympathetic hyperactivity Formation of ephapses (artificial synapses) after peripheral nerve injury
- Spontaneous neuronal ectopy at the site of demyelination or axonal injury Central reorganization of pain processing (central sensitization)
Define sympathetically maintained pain (SMP
The pain that is maintained by sympathetic innervation or circulating catecholamines is defined as SMP. It describes a pain mechanism, not a clinical syndrome. Therefore, by definition, patients with CRPS who report pain relief after a sympathetic block (e.g., stellate ganglion block) have SMP