ABR Pain Medicine cheat sheet

Nociceptors are free nerve endings activated by mechanical, thermal, and chemical stimuli; A-delta fibers are thinly myelinated and signal sharp fast pain, while C fibers are unmyelinated and signal slow dull pain.

Dorsal horn laminae I and V receive many A-delta inputs, while lamina II, the substantia gelatinosa, receives many C-fiber inputs and contains interneurons that modulate transmission.

The spinothalamic tract crosses the midline within the spinal cord and ascends to the thalamus, carrying nociceptive and thermal information; the dorsal column-medial lemniscus system carries fine touch and proprioception.

Spinoreticular, spinomesencephalic, and spinoparabrachial pathways project to brainstem and limbic structures and contribute to the affective and motivational dimensions of pain.

Gate control theory holds that non-nociceptive Aβ afferent input can inhibit dorsal horn nociceptive transmission through inhibitory interneurons.

Central sensitization follows repetitive C-fiber input and involves NMDA receptor activation, wind-up, increased synaptic efficacy, and reduced inhibition, producing hyperalgesia and allodynia.

Descending modulation travels from the periaqueductal gray to the rostral ventromedial medulla and then to the dorsal horn; serotonin and norepinephrine contribute to inhibition or facilitation.

Neuropathic pain mechanisms include ectopic discharges, altered sodium and calcium channel expression, loss of inhibitory control, and central somatosensory reorganization.

Sympathetic nervous system contributions are prominent in some complex regional pain syndrome presentations, but sympathetically maintained pain is not universal.

The numeric rating scale asks for pain intensity from 0 to 10, where 0 is no pain and 10 is worst imaginable pain; function and quality of life should be assessed separately.

The DN4 questionnaire suggests neuropathic pain at a score of 4 or more; the LANSS suggests neuropathic pain at a score of 12 or more.

Red flags for serious spinal pathology include fever, unexplained weight loss, cancer history, significant trauma, bowel or bladder dysfunction, saddle anesthesia, and progressive neurologic deficit.

A structured pain history records onset, location, quality, intensity, timing, aggravating and relieving factors, associated symptoms, prior treatments, and functional impact.

Physical examination includes inspection, palpation, range of motion, neurologic testing of strength, sensation, and reflexes, and provocative maneuvers directed by the history.

Diagnostic local anesthetic blocks are interpreted by concordant temporary relief in the expected distribution; controlled or placebo blocks reduce false-positive interpretation.

Psychosocial screening instruments include the PHQ-9 for depression, GAD-7 for anxiety, Pain Catastrophizing Scale, and Oswestry Disability Index for low back disability.

Imaging is not routinely indicated for nonspecific low back pain without red flags or progressive neurologic findings.

Pain mechanisms are commonly classified as nociceptive, neuropathic, or nociplastic; mixed mechanisms are frequent and influence treatment selection.

Acetaminophen is commonly limited to 3,000 to 4,000 mg per day in adults; lower maximum daily doses apply in chronic alcohol use, liver disease, or malnutrition.

NSAIDs inhibit cyclooxygenase and carry gastrointestinal, renal, and cardiovascular risks; risk rises with age over 65, ulcer history, anticoagulants, corticosteroids, chronic kidney disease, and high-dose long-term use.

Opioids can cause respiratory depression, constipation, sedation, tolerance, dependence, and opioid use disorder; naloxone reverses opioid-induced respiratory depression.

Opioid rotation uses approximate equianalgesic potency ratios, calculates a morphine-equivalent dose, and often reduces the new opioid dose by 25% to 50% for incomplete cross-tolerance.

Gabapentin and pregabalin bind alpha-2-delta calcium channel subunits and are used for neuropathic pain; both require renal dose adjustment.

Duloxetine and venlafaxine inhibit serotonin and norepinephrine reuptake and are used for neuropathic pain; duloxetine is FDA-approved for diabetic peripheral neuropathic pain.

Tricyclic antidepressants such as nortriptyline and desipramine have fewer anticholinergic effects than amitriptyline; they are avoided in narrow-angle glaucoma and significant cardiac conduction disease.

Tramadol, meperidine, and other serotonergic analgesics can precipitate serotonin syndrome when combined with serotonergic drugs.

Methadone can prolong the QT interval, and buprenorphine is a partial mu agonist with high receptor affinity that can precipitate withdrawal in opioid-dependent patients.

Epidural corticosteroid injection is considered for radicular pain after conservative care fails and is avoided with local infection, coagulopathy, or progressive neurologic deficit until evaluated.

Medial branch blocks are diagnostic for facet-mediated pain; radiofrequency ablation is considered when concordant diagnostic blocks confirm the target levels.

Stellate ganglion block targets the lower cervical sympathetic chain for upper-limb sympathetically maintained pain; lumbar sympathetic block is used for lower-limb presentations.

Trigger point injection places local anesthetic or saline into a taut muscle band; dry needling is a related technique without injectate.

Intra-articular corticosteroid or local anesthetic injection can treat selected painful joints and is commonly performed with ultrasound guidance.

Spinal cord stimulation delivers electrical pulses to dorsal columns and is used for persistent neuropathic limb pain after appropriate conservative and interventional care.

Anticoagulants and antiplatelet agents are managed before pain procedures according to bleeding risk and procedure-specific interruption guidance.

Procedure complications include bleeding, infection, nerve injury, intravascular injection, vasovagal reactions, and steroid effects; image guidance, aspiration, and contrast help reduce risk.

Informed consent for interventional pain procedures includes the diagnosis, proposed procedure, alternatives, material risks, benefits, and the possibility of failure or repeat treatment.

The biopsychosocial model explains pain and disability through interacting biological, psychological, and social factors rather than tissue pathology alone.

Cognitive behavioral therapy for chronic pain targets unhelpful thoughts and behaviors and teaches coping skills to reduce distress and improve function.

Graded activity and graded exposure gradually increase tolerated movement or activity and reduce fear-avoidance in chronic pain rehabilitation.

Interdisciplinary pain care involves communication among physicians, psychologists, physical therapists, and other clinicians toward shared functional goals; multidisciplinary care may occur with less formal coordination.

Opioid risk mitigation includes prescription drug monitoring program review, urine drug testing when indicated, treatment agreements, and naloxone co-prescribing for high-risk patients.

Under federal U.S. rules, Schedule II prescriptions may not be refilled; Schedule III to V prescriptions may be refilled up to five times within six months of the issue date.

Informed consent requires decision-making capacity, disclosure of relevant information, understanding, voluntariness, and authorization of the treatment.

Functional capacity evaluation and return-to-work planning assess physical tolerances and help align rehabilitation goals with occupational demands.

Professional boundaries, confidentiality, secondary gain, and conflicts of interest are ethical considerations in pain care and disability evaluation.