According to the definition made by the International Association for the Study of Pain in 1997, neuropathic pain is "pain that occurs due to primary lesion or dysfunction of the nervous system". Although its clinical course may vary depending on the region of origin, it begins with a disorder related to pain processing in the central and peripheral nervous system and develops secondary to this disorder. On the other hand, while no pathological findings can be observed in the central nervous system in many patients diagnosed with neuropathic pain, neuropathic pain may not be observed in many patients with nervous system pathology. Symptoms may persist after years.
Classification:
Neuropathic pain can be classified as central or peripheral neuropathic pain depending on where it originates. The autonomic nervous system is also affected in neuropathic pain. This type of neuropathic pain is defined as Complex Regional Pain Syndromes.
Etiology:
In the etiology of peripheral neuropathic pain, damage to peripheral nerves for different reasons plays a role. Factors that play a role in this damage:
Focal nerve damage
- Trauma (crushing, avulsion, incision, stretching)
- Tumor (neuroma)
- Infection (postherpetic neuralgia)
- Ischemia
- Compression
- Injury (heat, cold, electricity, radiation)
Generalized nerve damage
- Toxins
- Metabolic effects (Diabetes mellitus)
- Nutritional disorders (Vit B12 deficiency)
Schwann cell damage
- Multiple sclerosis
- Guillaine Barre syndrome
Epidemiology:
Incidence of neuropathic pain in the general population %1-2. However, this incidence may be higher in some patient groups. For example, while 8% of stroke patients may develop central neuropathic pain within 1 year, 10-15% of patients with HIV infection may develop neuropathic pain. It has been reported that 22% of patients with multiple sclerosis may experience moderate to severe pain.
20%after acute herpes zoster infection, especially in patients over 60 years of age. Deafferentation pain may develop at > rate. This rate reaches 34% over the age of 80. Neuropathic pain is observed in 50% of diabetic patients, especially if the duration of the disease is over 25 years. br />
Pathophysiology:
The pathophysiology of neuropathic pain is not well known. As a matter of fact, experimental studies on non-traumatic neuropathic pain are quite few. However, it is thought that peripheral and central sensitization mainly play a role in the pathogenesis of chronic neuropathic pain.
Following a peripheral nerve injury, inflammatory and growth factors are released. As a result, nociceptive neurotransmitters such as substance P and brain-derived neurotropic factor (BDNF) are released. These released neurotransmitters affect the adrenergic, TrpV1, P2Xand m opioid receptors, sodium and calcium channels associated with Ad and C fibers.
The resulting ectopic discharges occur with peripheral sensitization. . A. b fibers also play a role, especially in the mechanical allodynia process. It is emphasized that central sensitization is a reason for the continuation of neuropathic pain and the development of pain as a result of painless stimuli. Factors that play a role in this sensitization occurring in the spinal cord:
- Increase (upregulation) in N-methyl-D-aspartate (NMDA)receptors
- Intracellular calcium ion changes
- Reduction of inhibitory control
Although the underlying mechanisms have not been fully elucidated, sensitization of C fibers, partial denervation, ectopic activity, endogenous Nerve growth factor (NGF) and damaged and undamaged neurons are thought to play a role in pathogenesis. While a symptom may occur through several mechanisms (peripheral and central sensitization in touch allodynia), more than one mechanism may play a role in the pathogenesis of a syndrome (postherpetic neuralgia). /> DIAGNOSIS:
History:
It should be questioned whether there is any abnormal feeling in the history. Hyperalgesia, dysaesthesia, allodynia, hyperpathy, hyperesthesia and chronic burning pain may occur. In examining the underlying pathology, it should be known whether there is infection, metabolic disorders, autoimmune diseases and malignancy. Pain intensity should be evaluated and paroxysmal attacks of pain should be asked. The patient's quality of life, emotional and psychological state should also be evaluated. Sleep disorders and physical limitations are also parameters that should be emphasized in the history.
Previous treatments the patient has received and his response to them should also be known.
Symptoms:
Neuropathic In patients with pain, clinical findings manifest themselves with persistent pain. r. Pain may occasionally show a paroxysmal course. Its character can be sharp and stinging, but it can also be flammable. Abnormal sensations after the stimulus, sleep disorders, emotional and psychological disorders, physical restriction and autonomic symptoms may accompany the pain. While pain may not always be well localized, some patients may have symptoms in an anatomically appropriate area.
The abnormal sensation manifests itself as hyperalgesia or allodynia. Hyperalgesia is defined as an increased pain response to painful stimuli. It can be classified as mechanical, thermal or chemical hyperalgesia. Allodynia is a pain response to a non-painful stimulus. It is classified as dynamic and cold allodynia.
Physical examination:
Determining the boundaries of the affected area of the patient guides the monitoring during the treatment. In the superficial nerve examination, the presence of abnormal sensation is tested with cotton, brush hair, thread, needle pricking and touch. Skin temperature measurement can give insight into autonomic changes. Edema, color change, sweating disorder, skin atrophy and nail changes are important in the evaluation of sympathetic pain. Evaluation of tactile and vibration thresholds are helpful parameters in both diagnosis and monitoring.
Advanced examinations:
Quantitative Sensory Test (QST), for diagnosis. Verification is an important test in monitoring the treatment by determining baseline values. Magnetic Resonance Examination (MRI) to show the pathology and electromyography to determine the location of the nerve lesion are the tests that can be applied. Positron Emission Tomography (PET) and Functional MRI (fMRI) There are future prospects for explaining the mechanisms of neuropathic pain and directing the treatment.
Post herpetic neuralgia (PHN) develops in approximately 10% of cases. The rate is higher in the elderly. Diabetes mellitus is a predisposing factor for herpes zoster and increases the likelihood of developing postherpetic neuralgia. If pain persists for 4-6 weeks after healing of dermatomal vesicles, PHN is diagnosed. PHN pain is a constant, burning, aching pain and sometimes stabbing pain. It may start spontaneously or be triggered by gentle stimulation of the skin. Skin hyperesthesia and hyperalgesia are usually observed, but rarely analgesia may also occur. It may often be accompanied by dysesthesia and paresthesia. Especially in patients over 60 years of age, PHN can be very prolonged.
Diabetic Neuropathy:
The most common cause of neuropathic pain is diabetic neuropathy. Different mechanisms play a role in the formation of diabetic neuropathy. It is the one related to the “sorbitol pathway” that is most emphasized and studied. Glucose is converted to sorbitol by the enzyme aldose reductase. Excessive functioning of this pathway due to hyperglycemia leads to sorbitol accumulation within the cell. This accumulation leads to a decrease in myoinositol and taurine within the cell, and as a result, cell metabolism is disrupted. It has been reported that the decrease in taurine and myoinositol within the cell leads to a decrease in Na+-K+ATPase activity and a decrease in nerve conduction velocity. The second mechanism is a decrease in endoneural blood flow velocity and nerve ischemia. Decreased nerve blood flow leads to a decrease in nerve conduction velocity. There have been findings that disorders related to neurotrophic factors may be responsible for diabetic neuropathy.
In the development of diabetic neuropathy. Views on the role of autoimmune mechanisms have begun to gain importance in recent years. There are many studies showing the presence of microscopic vasculitis in nerve biopsies of patients with diabetic lumbosacral radiculoplexopathy. These findings have brought to the agenda the application of immune modulatory treatments, especially intravenous immunoglobulin, in the treatment of diabetic neuropathy.
Diabetic neuropathy appears clinically as mononeuropathy or polyneuropathy. Third cranial nerve neuropathy is frequently seen in diabetes. Additionally, median ulnar, peroneal, femoral and lateral cutaneous nerves are also involved. Pain is expressed by the patient as throbbing, burning, cramping and aching in the distal areas.
Sensory symmetric polyneuropathy is observed in a high rate of 35% of diabetic patients. In addition, the complaint of burning pain may be accompanied by numbness, paresthesia and autonomic dysfunction.
Phantom Extremity Pain:
Phantom extremity pain (FEA) 50-75%, and in some cases it may occur several months or years later. It has been suggested that preamputation pain plays a role in the basis of phantom limb pain. However, this relationship is not clear. Post-amputation factors also play a big role in FEA.
The severity of pain varies from patient to patient. Severe pain is often accompanied by paresthesia. It may be continuous or intermittent. Pain quality also varies widely. Sharp pain that is burning, crampy, aching and explosive It is described as �. Pain is localized in the phantom(non-existent)distal part of the extremity(hands and feet). In stump pain, there is usually a palpable neuroma in the incision area.
Touch and pressure on the stump, emotional tension, weather change, autonomic and reflex movements, stimulation of other body parts.
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