Brain Infarction (Thalamus and Brainstem)

Central post-stroke pain (CPSP) is a central neuropathic pain condition resulting from lesions of a prior cerebrovascular accident (CVA) mainly affecting the spinothalamocortical tract. About 5%–10% of patients with CVAs develop CPSP. The pain is thought to be secondary to a complex interaction of central disinhibition, central sensitization, and an imbalance of stimuli, although the exact mechanism remains unknown. The pain is located within and associated with sensory dysfunction in a region affected by a prior CVA lesion. The pain is often described as burning, stabbing, and sharp. Allodynia, hyperalgesia, and evoked dysesthesia appear to be major clinical findings for this condition. There are no specific diagnostic criteria for CPSP, and treatment is often difficult. Medications such as tricyclic antidepressants and anticonvulsants are often used. Motor cortex stimulation and deep brain stimulation are active areas of research and offer hope that additional treatment modalities may be identified.

Trigeminal Neuralgia

Trigeminal neuralgia is a rare neuropathic pain condition but can be very disabling. The hallmark is brief episodes of intense, radiating pain within the territory of trigeminal nerve distribution. It is typically unilateral, often accompanied by facial spasms and can be triggered by facial movements in a majority of patients. Microvascular compression of trigeminal ganglion is the etiology for most patients with classical trigeminal neuralgia. Some patients can have continuous facial pain in addition to paroxysms of pain. Trigeminal neuralgia is a clinical diagnosis, but MRI is done to rule out secondary causes or to detect microvascular compression. Pharmacological therapy with first-line agents—carbamazepine or oxcarbazepine—is the preferred treatment. Patients with failed pharmacological therapy are considered for surgical decompression, ablation procedures, or Gamma Knife surgery.

Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) is a neuropathic pain condition classified as type 1 and type 2. The two classifications are distinguished by the presence of documented nerve injury in CRPS type 2. The symptoms of CRPS, including cold, blue, and painful extremities, are believed to occur from vasoconstriction caused by sympathetic dysfunction. Treatment in CRPS focuses on targeting neuropathic and sympathetically maintained pain. Traditional antineuropathic pain medications include membrane stabilizers and serotonin and norepinephrine reuptake inhibitors. Corticosteroids and nonsteroidals target the inflammatory process present in the initial stages of CRPS. Bone resorption has been treated with calcium-modulating drugs. Interventional therapies include sympathetic blockade of the affected extremity, spinal cord stimulation, and intrathecal drug delivery. All these therapies have been implemented in an effort to facilitate functional restoration of the affected limb. Physical and occupational therapies have demonstrated some of the most significant improvements in pain, mobility, and function.

Overview of the Pharmacological Management of Neuropathic Pain

Neuropathic pain refers lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Examples of neuropathic pain include painful polyneuropathy, postherpetic neuralgia, trigeminal neuralgia, and post-stroke pain. Clinically, neuropathic pain is characterized by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. neuropathic pain is treated as a ‘blanket condition’ in this guideline regardless of its aetiologies, unless there is valid and robust clinical and health economics evidence that shows the clinical efficacy and cost effectiveness of a particular treatment for a specific neuropathic pain condition. Management of neuropathic pain requires an interdisciplinary approach, centered around pharmacological treatment. A better understanding of neuropathic pain and in particular of the translation of pathophysiological mechanisms into sensory signs will lead to a more effective and specific mechanism-based treatment approach.