Description

• The term “neuropathic pain” represents a broad spectrum of pain syndromes and encompasses a wide variety of peripheral and central disorders.
• Defined as injury of the nociceptive pathway in the central or peripheral nervous system (CNS and PNS) that result in either impairment, absence, or paradoxically augmentation of pain sensation
• Symptoms are usually burning, tingling, sharp, stabbing, shooting, and electric shock-like quality.
• Often severe and resistant to standard treatments for pain.

Epidemiology

Incidence
There is insufficient evidence on the general incidence rate of neuropathic pain as most studies target a single type of neuropathic pain. In a Dutch study targeted between 1996 and 2003, 9,135 new cases of neuropathic pain out of 362,693 persons contributing to the study were identified, yielding 8.2 new cases per 1,000 person-years (PY). The study approximates an annual incidence of almost 1% of the general population, affecting more women and middle-aged population.

Prevalence
Includes chronic conditions that affect up to 10% of the population, accounting for 20–25% of individuals with chronic pain.

• Malignancy—up to 20% have neuropathic pain from either cancer or treatment
• Post-stroke patients—up to 8%
• Spinal cord injury—60–69%, a large majority of whom present with a syringomyelia
• Herpes zoster—lifetime incidence ~25%. Up to 10% develop chronic postherpetic neuralgia.
• HIV—up to 50% have neuropathic pain
• Diabetes—~50% will eventually develop neuropathy; 34% will develop neuropathic pain.

Etiology and Pathophysiology

• A variety of mechanisms contribute to neuropathic pain and many are still poorly understood.
• One proposed mechanism suggests that damaged primary afferents, including nociceptors, become highly sensitive to mechanical stimuli and may generate impulses in the absence of stimulation. This increase in sensitivity and spontaneous activation without apparent stimulation is thought to be caused by an increase in the density of sodium channels in the damaged nerve fibers, leading to increased excitability and signal transduction.

Genetics
There is growing evidence of genetic factors in neuropathic pain. Human genetics studies have demonstrated that Na_v1.7 and Na_v1.8, two types of voltage-gated sodium channels encoded by the SCN9A and SCN10A genes, respectively, are expressed at high levels on the peripheral nociceptive neurons in the dorsal root ganglion. Thus, therapeutics aimed at these channels with specific genetic mutations can play a role in patient care.

Risk Factors

• General risk factors include older age, female, physical inactivity, and manual occupation.
• Diabetes mellitus I and II, multiple sclerosis, Guillain-Barré syndrome, herpes zoster, trigeminal neuralgia, HIV, Lyme disease, malignancy/chemotherapy, nutrition (B₆ and B₁₂ deficiencies), medications (isoniazid, ethambutol, chloroquine, paclitaxel, cisplatin, amiodarone, vincristine).

General Prevention

• Use of herpes zoster vaccines, which reduces both herpes zoster infections in patients >50 of age and postherpetic neuralgia
• Use of antiviral or analgesic treatment in patients with herpes zoster infection
• Perioperative treatment of surgical patients to prevent chronic postsurgical pain. Use of multimodal analgesia with gabapentin and local anesthetics to prevent acute and chronic pain after breast surgery for cancer
• Proper management of health conditions, such as DM

Commonly Associated Conditions

Depression and anxiety, sleep disturbances, substance abuse, impaired cognition, polypharmacy, and suicidal ideation