Phantom pain is a complex of sensation related to the removal of a part of the body. This phenomenon typically occurs after a limb amputation, but may also develop after radical surgery of other parts of the body, such as tongue, eyes, penis, or breast, after nerve or brachial plexus avulsion or spinal cord injury [28]. It has been described in about 20 % of children with congenital limb aplasia.

The pathophysiology of phantom limb remains unclear [29]. Central and peripheral mechanisms [28, 30] have been suggested to be determinant for the development of the disorder, which occurs in the majority of patients after an amputation and encompasses a wide range of symptoms.

About 70 % of patients can experience phantom pain (e.g., shooting, stabbing, squeezing, or burning) immediately after the amputation, whereas 84 % of patients experience phantom sensations, namely, sensory illusions of the removed limb in the form of cold or warm feelings, itch, or tingling. These are part of the large spectrum of symptoms, which includes kinetic (movement) and kinesthetic (positional orientation) sensations. Patients can experience phantom movement (often referred to as painful spasm) and some are able to move the phantom at will. The phantom limb can assume unnatural positions in the space, such as outstretch in front, behind, or sideways. Telescoping is another perception reported as the phantom limb seems shortened and it feels like only the digits remain on the stump.

Treatment of phantom pain is based on a multidisciplinary approach including neuropathic pain drugs (antidepressants, anticonvulsant, and opioids), physical therapies (acupuncture, ultrasound, TENS, motor, cortex, and spinal cord stimulation), rehabilitation programs, and, in a very limited number of critical patients, surgical treatments (revision of the stump, dorsal column tractotomy, dorsal root entry zone lesions) [31].

Phantom limb pain can spontaneously improve or resolve, but it persists over 2 years in 60 % of patients and is referred as severe in 0.5–5 %.

The abnormal growth of Schwann cells and nerve fibers that can occur after a peripheral nerve injury is known as traumatic neuroma. It represents the ineffective attempt of regeneration and can develop in any nerve. Typical examples are Morton’s neuroma (usually affecting the common digital nerve in the third planter space) or amputation neuroma (involving the distal stump of the truncated nerve). Pain has the features of neuropathic pain and the efficacy of the pharmacological treatments is often poor [32].

Neuroma formation should be prevented in the case of predetermined surgical nerve injury (e.g., amputation) or surgical revision. Surgical approaches include relocating the nerve stump into an environment (such as bone, muscle, or vein) far from the original injury site and protecting the nerve from further injuries. In these cases, success rate with partial pain relief is 50–60 % [33].

Central post-stroke pain (CPSP) is a condition arising as a consequence of a cerebrovascular disease. In the past, this condition was known as “Dejerine–Roussy syndrome” and strictly related to a thalamic stroke. The definition of CPSP has been currently extended and includes the whole somatosensory pathway as a possible site of injury.

CPSP shows a neuroanatomic distribution that corresponds to the damaged central nervous system (CNS) area. It should not be confused with other common post-stroke pain syndromes, such as shoulder pain, headache, or painful spasticity. The estimated prevalence of CPSP varies between 11 and 55 %, a wide range likely due to the lack of well-defined diagnostic criteria. Most commonly, CPSP occurs a few months after the CNS injury, although it can develop either immediately after the cerebrovascular event or years later.

CPSP is difficult to treat and has a poor outcome.

Pharmacological treatments have limited efficacy despite multi-drug therapy (e.g., antidepressants, anticonvulsant, and opioids).

Neurostimulation targeting the sensory thalamus has shown a success rate of 45–50 % at 1-year follow-up [34]. The factors predisposing to the development of central pain after stroke are still unknown. A recent study found that patients with a lesion in the posterior and lateral thalamus have an increased risk to develop CPSP than those with anterior-medial lesions [35].

Postherpetic neuralgia (PHN) is the most common complication of Herpes Zoster (HZ) infection and is defined as pain in the territory of a cranial nerve or dermatome lasting more than 3 months after skin rash onset.

The overall incidence of HZ infection ranges between 1.2 and 3.4 per 1,000 persons per years. Its frequency increased with aging from 2 cases per 1,000 persons under 50 years to 10 cases per 1,000 between 70 and 80 years. About 50 % of individuals who reach age 85 years may have had at least one episode of Herpes Zoster. Elderly and immunocompromised patients are at higher risk. PHN shows a similar age-related increase of incidence, from 5 % in subjects younger than 60 years to 10 % in those aged 60–69 years and up to 20 % in those aged 80 years or older [36].