I. Typology of complex localized pain syndrome (CRPS): Type I CRPS (RSD) Type I CRPS or RSD is a syndrome that is usually secondary to an initial noxious stimulus and is not confined to a single peripheral nerve distribution area, often incompatible with the stimulus condition. It is accompanied by marked edema, altered skin blood flow, abnormal sweating behavior, sensory abnormalities and/or nociceptive hypersensitivity. Common complaints of patients are hyperalgesia to cold pain and abnormal sensation to mechanical stimuli, and on examination, significant thermal hyperalgesia and abnormal vibratory sensation may be found. Type II CRPS (burning neuralgia) Type II CRPS or burning neuralgia is a burning pain, sensory abnormalities, and nociceptive hypersensitivity that often occurs after injury to a major peripheral nerve portion of the hand or foot. The most common injuries that accompany type II CRPS are injuries to the median and sciatic nerves. The typical cause of CRPS is traumatic injury to the limb such as sprains, dislocations, fractures, crush injuries and lacerations or surgery, or peripheral nerve injury. It has also been reported to occur from minor injury processes such as routine venipuncture or epidural injections of steroids. There is no association between the severity of the injury and the intensity of the final patient’s symptoms. It is also associated with other diseases such as diabetic neuropathy, multiple sclerosis, cerebrovascular accident, myocardial infarction and cancerous infiltration of the nerve plexus. Sometimes no cause can be identified. The true incidence of CRPS is unknown because of its variable clinical presentation and frequent misdiagnosis. There are few published data to assess the epidemiology of CRPS. In the United States, many clinical studies have confirmed a high prevalence of the disease in middle-aged adults, but it is present in all age groups, including children. The high prevalence in people of working age reflects the association of this disease with injury at work. The disease affects all ethnic groups, although it shows a high prevalence in women, Caucasians, and Northern Europeans. The etiology and pathogenesis of CRPS Despite the many theories, the definitive etiology and pathogenesis of CRPS remain elusive. 1. enhanced sympathetic activity 2. sensitization of peripheral mechanical and nociceptive receptors 3. altered central afferents 4. neurogenic inflammation 5. altered central processing 6. initiation and maintenance of WDR neuronal sensitization 4. clinical manifestations of CRPS The main clinical symptoms, the triad of sensory, autonomic and motor dysfunctions, vary greatly in their manifestations and course. 1. Abnormalities in sensory neuron function: Pain: Pain associated with CRPS is the most prominent and disabling symptom. Pain is usually constant and spontaneous, but often worsens paroxysmally under physical or psychological stress. Its severity can range from mild discomfort to severe and unbearable pain, with the pain being worst at night. The nature of the pain can be described as burning, aching, tearing, squeezing, stabbing, or cutting pain. In most patients, the pain is of multiple natures. Initially, pain may be confined to the site of injury, but later manifests as a non-anatomic distribution that does not follow a single peripheral nerve distribution. The pain is often described as a glove or sock-like distribution. Over time, the pain may extend to encompass the entire limb. The following phenomenon has also been described: the pain extends beyond the end of the affected limb to the contralateral limb, sometimes to the ipsilateral limb or to the side of the entire torso. Sensory changes: Sensory hypersensitivity (increased sensitivity to stimuli) is an almost constant component of CRPS. The patient is characteristically protective of the affected limb. If the attending physician attempts to touch the affected limb, the patient will intentionally withdraw the limb and refuse any contact. Patients with CRPS may also complain of unpleasant or uncomfortable, but not painful, sensations when cold (ice, halothane), vibration (tuning fork), or light touch is applied to the affected limb. There is also a delayed nociceptive hypersensitivity, which is a delayed overreaction to stimuli and sensory legacy. 2. Autonomic symptoms: Autonomic dysfunction is commonly present in patients with CRPS. It may manifest as either vasoconstriction, producing pale, cyanotic and chilled skin, or vasodilation, resulting in warmth and erythema of the extremities, and commonly marked edema and abnormal sweating (hyperhidrosis or hypohidrosis). As the disease progresses, progressive nutritional changes occur, including changes in skin thickness and luster; atrophy of muscles; bone decalcification; thickened and brittle nails; dull hair; and slower growth of hair and nails. 3. motor dysfunction: muscle stiffness is the most frustrating physical examination finding for patients with CRPS, and it manifests more severely than in patients with trauma, surgery, and other common conditions. patients with CRPS are often unable to initiate movement. Without treatment, muscle stiffness can worsen as the disease progresses. Other signs and symptoms of kinetic abnormalities include muscle spasms, intentional or postural tremor, decreased muscle strength, and hyperreflexia. 4. Other Another group of clinical findings includes reactive psychological disorders. These include anxiety, depression, and despair. Although most cases of CRPS have been reported to occur in the extremities, facial pain syndromes have also been reported following maxillofacial tumor surgery, bullet penetrating wounds, head injury, and treatment of difficult dental disease. The clinical manifestations of facial CRPS may be similar to those of extremity CRPS. V. Diagnostic studies There are no specific tests or diagnostic maneuvers that can be applied optionally to CRPS. The following studies can help to make a correct diagnosis or develop a final treatment plan. 1.Thermometry 2.Thermogenic imaging 3.X-ray plain film 4.Radionuclide imaging (three-stage radionuclide bone scan) 5.Sweat test 6.Sympathetic nerve block