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23 Cards in this Set
- Front
- Back
Define neuropathic pain |
Pain that is initiated or caused by a lesion or disease affecting the somatosensory system in the peripheral or central nervous system |
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Definition of postherpetic neuralgia |
Neuropathic pain that persists beyond 4 months in the setting of reactivated shingles |
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Highest risk of PHN |
1. Trigeminal involvement 2. Thoracic dermatomes 3. Lower risk, other regions |
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Ways to minimize risk of PHN |
1. Zoster vaccine for all patients older than 50 (regardless of whether they have had shingles previously) 2. A small RCT showed that amitriptyline may decrease the risk of PHN if the drug is administered when the shingles rash appears and is used for 3 months 3. Acyclovir used within 72 hours have a modest effect |
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Treatment of PHN? |
Topicals, including lidocaine patch and a single application of a high-concentration (8%) capsaicin patch (after anesthesizing the region of PHN) are effective without systemic side effects 2. Oral neuropathic and analgesic medications are used, although only gabapentin and pregabalin are FDA approved for PHN 3. Spinal cord stimulation has been used for refractory cases |
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Small fiber neuropathy is |
limited to A delta and unmyelinated C fibers |
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Primary treatment of painful peripheral neuropathy (4) |
1. Treat underlying cause 2. When the underlying cause is treated, the hope is that the associated pain syndrome may improve 3. Primary goal is to prevent or slow further progression 4. Neuropathic pain is usually worse in the evenings when the distractions of the day are absent and the patient's positive sensory phenomenon and pain are no longer masked |
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Treatment of painful peripheral neuropathy? (2) |
1. Pregabalin 2. Duloxetine |
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Chemotherapy-induced peripheral neuropathy is most commonly caused by which chemotherapeutic agents? (3) |
1. Vinca alkaloids 2. Taxanes 3. Platinum agents |
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Pathophysiology of CIPN? |
Disruption of axonoplasmic flow (necessary to maintain the axon) through microtubule disruption, mitochondrial dysfunction, or cytotoxic effects on DNA |
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Prognosis of CIPN? |
Clinical neuropathic pain may improve and in some cases resolve, but in most cases CIPN is only partially reversible and is often permanent |
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Management of CIPN? |
1. Prevention would be ideal, however, most drugs have proven ineffective in trials 2. Common practice is to extrapolate evidence-based recommendations for the treatment of other neuropathic pain conditions to painful CIPN. This approach is rational, but well-designed RCTs of commonly used neuropathic agents have failed to show an effect in patients with painful CIPN |
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What is erythromelalgia? (5) |
Triad of: 1. Erythema 2. Heat (subjective and objective) 3. Severe pain usually affecting the distal limbs (feet more common than hands) 4. May be precipitated by heat and exercise, and is 5. due to a gain of function mutation in SCN9A |
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Diagnostic testing for erythromelalgia (3) |
1. Distal small-fiber features 2. Vasculopathy shown with vascular testing 3. Increase in temperature, increase in blood flow, and, paradoxically, no increased skin oxygenation |
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Treatment of erythromelalgia? (4) |
1. Defined by case and cohort reports 2. Aspirin, anticonvulsants, and antidepressants 3. CCBs and beta-blockers 4. Topical lidocaine or compounded creams of amitriptyline and ketamine |
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Define complex regional pain syndrome |
Neuropathic pain disorder in which pain is within a region (e.g., foot or leg) but outside an individual nerve territory |
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Treatment of CRPS? (4) |
1. Mobilization of the affected limb through physical therapy; all other treatments are symptomatic and aimed at facilitating mobilization 2. Desensitization is important 3. Sympathetic blocks for LE and stellate ganglion block for UE 4. Topical and oral neuropathic and analgesic pain medications are necessary in almost all cases |
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Subgroups of CRPS? |
CRPS 1 - no identifiable injury CRPS 2 - identifiable nerve injury |
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Central neuropathic pain refers to? |
Processes in which the primary lesion or dysfunction (not the secondary effects of it) occurs within the CNS; ventroposterior thalamic strokes are the quintessential central neuropathic pain syndrome, but strokes elsewhere can have the same consequences |
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Critical factor for the development of a central neuropathic pain syndrome is what+ |
That the neurologic lesion causes dysfunction of the spinal-thalamic-cortical pathways, which is clinically evident as impaired pain (pinprick) and temperature sensation |
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What are the three most common central neuropathic pain syndromes? |
1. Central poststroke pain (CPSP) (25% within 6 months after the stroke) 2. Spinal cord injury (SCI) 3. MS-related pain |
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Temporal relationships in central pain syndromes |
1. CPSP: usually within first month, although for some patients it begins later, even a year after the original stroke 2. MS: Occurs with the presentation of the demyelinating plaque (classic example - trigeminal neuralgia in a young patient with paroxysmal neuralgiform pain that heralds a pontine demyelinating plaque) 3. SCI: below the lesion - years to develop, at level - within months |
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Treatment of central pain |
Pregabalin is the only one approved; other treatments include typical oral neuropathic and analgesic medications. Medical literature is evolving on the role of cannabinoids in the treatment of central neuropathic pain syndromes |