Many conditions lead to neuropathic pain, including multiple sclerosis, post-stroke pain, spinal cord injury, traumatic brain injury, syringomyelia, trigeminal neuralgia, peripheral neuropathy, and post-herpetic neuralgia.
Multiple sclerosis (MS) is commonly associated with pain. It is estimated that 43 percent of MS patients have at least one painful symptom.29 Common painful symptoms include: dysesthetic pain, back pain, spasms, Lhermitte sign, visceral pain, and trigeminal neuralgia.
Central post-stroke pain is experienced as unilateral head/facial pain that starts within six months of a stroke. It affects up to 8 percent of stroke victims.30 The pain is typically persistent but may come and go. The severity of the pain may be variable, and stress often exacerbates the pain.
Treatment of central post-stroke pain includes benzodiazepines; anticonvulsants such as gabapentin, pregabalin, lamotrigine, or carbamazepine; baclofen; antidepressants such as amitriptyline or an SSRIs; and clonidine. When pain is resistant to pharmacotherapy, the use of neuromodulation (deep brain stimulation) and surgery may be considered.
Spinal cord injury (SCI) patients often develop chronic pain after spinal cord injury that affects the quality of life. Pain is often poorly localized and neuropathic in nature (e.g., burning, stabbing). The pain can be evoked or spontaneous. Pain can be at-level pain (pain at the level of the SCI) that is caused by injury to the nerve roots and dorsal gray matter, causing pain at the level of the injury. Pain can also be below the level of the SCI, which is thought to be caused by injury to the spinothalamic tracts and/or thalamic deafferentation.
Pain may be managed with antidepressants (e.g., tricyclic antidepressants), antiepileptics (e.g., gabapentin, lamotrigine, or valproate), and standard analgesic medications (opiates). When medications are not effective, the use of invasive treatments is considered. These may include deep brain stimulation, cordotomy, or motor cortex stimulation.
Syringomyelia is a delayed progressive intramedullary cystic degeneration that affects a small number of patients after spinal cord injury. It is thought to occur from scarring and subsequent obstruction of cerebral spinal fluid flow and altered tissue compliance leading to an extension of the central canal, which presses on the nearby cord tissue.31 In syringomyelia, the patient will present with progressive pain that may include sensory, motor, or bowel problems. Treatment of the condition is mainly surgical.
Post-concussion syndrome can occur days or even weeks after a traumatic brain injury (TBI). This can occur with any degree of head injury from mild to severe. It is characterized by dizziness, vertigo, headache, reduced concentration, apathy, depression, sleep disturbance, confusion, irritability, and anxiety. Headache after TBI typically occurs within seven days of the injury and is typical of the tension-type or migraine type of headache. In those with TBI, many other headache syndromes may be seen.
While the post-concussive syndrome is often reported in athletes, it is more common in older adults. MRIs may be performed for patients who have symptoms that persist in ruling out other problems and provide reassurance.
Treatment options for post-concussive headaches can be variable. Not a lot of research is available on the use of medications in the management of post-concussive headaches. Management involves the treatment of the symptoms, which include analgesics, migraine-specific medication (e.g., tricyclic antidepressants, propranolol), psychotropic medications, and counseling to manage psychosocial symptoms. Most patients have a quick recovery (within weeks), but some patients may have prolonged symptoms.
Trigeminal neuralgia results in head/facial pain coming from one or more of the branches of the trigeminal nerve. Classically the pain is unilateral, brief, stabbing, and/or lancinating that is sudden in onset.
Imaging, typically with an MRI, is sometimes done to distinguish primary from secondary trigeminal neuralgia. The primary disease has no identifiable lesion causing the symptoms. Secondary causes of trigeminal neuralgia include acoustic neuromas, multiple sclerosis, cerebral aneurysms, and trigeminal neuromas. A secondary disease is more common if there is bilateral involvement; it occurs at a younger age; or if there is associated sensory loss.
Conditions that may mimic trigeminal neuralgia include dental pain, multiple sclerosis, herpes zoster, or atypical headaches.
Treatment for the pain of trigeminal neuralgia includes carbamazepine and oxcarbazepine. For those who are intolerant or non-responsive to these agents, baclofen or lamotrigine can be used. Surgical options are sometimes tried for refractory cases.
Peripheral neuropathy can come from many etiologies, including diabetes, cancer, alcohol, and HIV. Peripheral neuropathy typically presents with distal sensory loss, weakness, numbness, and/or burning. The presentation may be variable. Neuropathy due to diabetes is one of the more common types of neuropathies.
Many forms of diabetic neuropathy exist, including symmetric polyneuropathy, radiculopathies, autonomic neuropathy, and mononeuropathies. They typically result in symptoms that begin in the lower extremities. Sensory symptoms are seen first, followed by motor symptoms. Patients complain of a gradual sensory loss, numbness, a burning sensation and pain in the feet, and mild gait abnormalities. Overtime weakness may develop, and a "stocking and glove" distribution of sensory loss may occur. Physical exam findings depend on which nerve fibers are involved.
Diagnostic tests that help define a neuropathy include conduction studies such as electromyogram and/or nerve condition studies. Treatment of neuropathies includes treating the underlying disease (e.g., control blood sugar in diabetes) and medications to treat the symptoms. Medications used to manage the pain of neuropathy include tricyclic antidepressants, duloxetine, gabapentin, pregabalin, carbamazepine, topiramate, tramadol, and NSAIDs.
Post-herpetic neuralgia is pain that presents after a herpes zoster infection, which is caused by the varicella-zoster virus. Certain groups are at higher risk of developing pain after a herpes zoster infection. These include older individuals, those who had higher levels of acute pain during the acute infection and those with a more severe rash.31
Herpes zoster is an infection that starts with a sharp, burning, stabbing pain that follows a dermatome. A rash will be seen a few days later along the same dermatome. Commonly affected dermatomes include the thoracic, cervical, and trigeminal nerves. After the rash abates, some individuals develop pain along the same dermatome that persists longer than four months. Pain may persist for years or even throughout life. Allodynia is often seen in those with post-herpetic neuralgia.
Post-herpetic neuralgia is commonly treated with tricyclic antidepressants, pregabalin, and gabapentin. Topical capsaicin or lidocaine can be used. Opioids are sometimes used but should be used cautiously. They are considered second or third-line options and are sometimes used while the TCAs, pregabalin, gabapentin take effect, then tapered. If all other options are not effective, the use of intrathecal glucocorticoids may be considered.