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We Are Specialized in Treating |
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- Back Pain
- Cervicogenic Headache
- Pain after Motor Vehicle Accident
- Arm pain
- Cancer pain
- Complex Regional Pain Syndrome
- Disc herniation
- Facial pain
- Headache
- Hip pain
- Knee pain
- Leg pain
- Muscle pain
- Nerve pain
- Pain due to other injuries
- Peripheral neuropathy
- Post back surgery pain syndrome
- Post herpetic neuralgia
- Shoulder pain
- Trigeminal neuralgia
- Other difficult pain conditions
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COMMON PAIN SYNDROMES
Low back pain
Low back pain (LBP) is the most common pain condition seen in pain clinics. Approximately 60% to 80% of the Unites States population will experience back pain at some point time during life. Neurologists are often consulted for the diagnosis and treatment of LBP. It is critical for clinicians to appropriately examine the patients and make a diagnosis before treatment is rendered. Common causes of LBP include muscle strain, lumbar disc herniation, lumbar radiculopathy, lumbar facet joint syndrome, sacroiliac joint syndrome and lumbar spinal stenosis.
Patients with acute muscle strain in the low back often have histories of acute injury. Physical examination may reveal tenderness or muscle spasms. Non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, massage therapy, physical therapy or acupuncture often provide effective pain relief. However, many times muscle pain in the low back is secondary to injuries in deeper tissues such as lumbar disc herniation or lumbar radiculopathy.
Acute lumbar disc herniation after injury may cause severe low back pain. Patients often complain of severe, shooting, or stabbing pains in the low back with frequent radiation pain down the dorsomedial part of the foot when the L5 nerve root is involved, or the lateral part of the foot or the small toe when the S1 nerve root is involved. Straight leg raising test is often positive. Detail neurological examinations may find decreased sensation to pin prick in the area innervated by L5 and/or S1 nerve root(s). Patient may also have mild weakness on the tibialis anterior (L5), or peroneous longus and brevis muscles (S1). These patients usually have severe tenderness and spasm over the lumbar paraspinal muscles. Lumbosacral MRIs may reveal disc herniation at L4-5 and/or L5-S1 level(s). EMG/NCV tests may not detect a lumbar radiculopathy. NSAIDs, muscle relaxants, and physical therapy may help some of patients with acute disc herniation and lumbar radiculopathy. If patients fail these treatments, lumbar epidural corticosteroid injections may offer fast and effective pain relief if the nerve roots are not severely mechanically compressed. Open surgeries are suggested for those with severe focal weakness of relevant muscles or incontinence. Surgery may also be indicated for severe pain that lasts for more than 3 months and does not respond to aggressive pain management if disc herniation is demonstrated by MRI or CT studies.
Lumbar facet joint syndromes are found in up to 35% of patients with LBP. It is frequently associated with arthritis or injuries in lumbar facet joints. Patients may complain of pain in the low back, often on one side only. Pain may radiate down the back or front of the thigh. Physical examination may find positive tenderness over the lumbar paraspinal muscles and facet joints. Back extension and lateral rotation to the side of the pain often increases the back pain. Results of a straight leg raising test should be negative. Neurological examination should be normal unless there is a coexistent lumbar radiculopathy or other neurological condition. Diagnosis of facet joint syndrome is clinical. MRI and CT reports of facet joint arthropathy are not well correlated with clinical findings. Often, these changes are age-related. NSAIDs should be tried for those with lumbar facet joint syndromes before the patients are considered for diagnostic medial branch blocks or intra-joint corticosteroid injections.
Sacroiliac (SI) joint syndrome is another major source of low back pain. The patient may have pain in one side of the low back with pain radiation down to the hip or thigh. Pain is often increased when the patients try to walk upstairs. Physical examination may find tenderness over the SI joint. Patrick’s test or single leg standing test often exacerbates the SI joint pain. NSAIDs are the first line mediation for SI joint inflammation. SI joint corticosteroid injection can provide temporary pain relief. Radiofrequency lesions to denervate the SI joint have been reported to be effective, however, more studies are needed to confirm this.
Lumbar spinal stenosis is a common age-related change. The majority of senior citizens over 60 years old have varying degrees of spinal stenosis due to disc herniation, osteophytes or degenerative spondylolisthesis. Pre-existing congenital lumbar canal stenosis predisposes to the development of this syndrome. Fortunately, less than 30% of those with spinal stenosis have clinical pain. Patients often have pain in the low back with pain radiation down the back of both legs. Standing or walking may make the pain worsen. Patients often walk with a hunched back and sit down after walking a short distance to relieve pain (neurogenic claudication). The pain usually takes minutes to disappear, compared to the seconds with vascular claudication. On physical examination, patients often have less tenderness over the lumbar spine than those with acute lumbar disc herniation. A straight leg raising test may be normal. The condition must be separated from vascular claudication. Patients may try NSAIDs first. Lumbar corticosteroid injections may provide pain relief for this group of patient for weeks or to months. If a patient has severe pain and does not wants surgery, chronic narcotic treatment often provides adequate pain control, but runs a risk of the development of tolerance and addiction.
Cervicogenic headache
Cervicogenic headache refers to head pain originating from the pathology in the neck. The term cervicogenic headache was first introduced by Sjaastad and colleagues in 1983. However, the concept of cervicogenic headache is controversial and not well accepted by the majority of neurologists. The International Headache Society published its first diagnostic criteria in 1998 and revised it 2004. Patients with cervicogenic headache often have histories of head and neck trauma. Pain may be unilateral or bilateral. Pain is frequently localized in the occipital area. However, pain may also be found in the frontal, temporal or orbital regions. Headaches may be triggered by neck movement or sustained neck postures. This headache is constant with episodic throbbing attacks, like a migraine. Patients may have other symptoms mimicking a migraine, such as nausea, vomiting, photophobia, phonophobia, and blurred vision. Cervicogenic headache is often misdiagnosed as migraine(10). History of head injury and detail physical examination on the occipital and upper cervical area often can help differential diagnosis. Patient with cervicogenic headache may have tenderness over the suboccipital, C2, C3, or C4 regions, or over the third occipital nerve. Cervicogenic headache does not respond well to migraine medications. Treatment should be focused on the removal of pain source from the occipital-cervical junction. Initial therapy is directed to physical therapy modalities and NSAIDs. Interventional treatment, such as greater occipital nerve block, cervical facet joint block, and botulinum toxin injections, often provides effective pain relief.
Complex regional pain syndrome (CRPS)
Terminology describing the complex regional pain syndromes has evolved over the last century. The term causalgia was first coined by Weir Mitchell in the 1870s for severe progressive distal limb pain with major nerve injury. In 1946, Evans introduced the term reflex sympathetic dystrophy (RSD). It was late defined by the International Association for Study of Pain (IASP) as "continuous pain in a portion of an extremity after trauma, which may include fracture but does not involve a major nerve, associated with sympathetic hyperactivity". In 1994, the IASP introduced the term Complex Regional Pain Syndrome (CRPS), describing a painful condition that includes regional pain, sensory changes (e.g. allodynia), abnormalities of temperature, abnormal sudomotor activity, edema and abnormal skin color changes that occur after an initiating noxious event such as trauma. Two types of CRPS have been recognized: CRPS I corresponds to RSD, in which no definable nerve lesion is found. CRPS II refers to a case with a definable nerve lesion and corresponds to the earlier term of causalgia.
The mean age of CRPS patients ranges from 36-46 years with women predominating (60-81%). It is caused typically by an injury, such as a fracture (16-46%), strain or sprain (10-29%), post-surgery (3-24%), and contusion or crush injury (8-18%). Clinical features of CRPS often include pain, edema, autonomic dysfunction such as change in temperature, color in the involved limbs, motor dysfunction and psychological abnormalities such as depression. Schwartzman and Maleki reported the pattern of spreading of CRPS in three stages. In the early stage, CRPS often involves only one limb with pain, minor edema and increased skin temperature. CRPS may spread from one limb to the others. In the later stage, CRPS could involve the full body and the four extremities with severe pain, edema, cold and cyanotic limbs, joint contracture, and atrophy of muscles and bones.
Excruciating pain is the cardinal feature of CRPS. Pain is often described as burning, aching, pricking or shooting. Severity of pain is not proportional to the initial injury and pain is not limited to the area of the injury or a specific nerve distribution. Patients may feel severe pain to minor pain stimulation such as a safety-pin prick (hyperalgesia). A light touch to skin (innocuous stimulation) may cause severe long-lasting pain (mechanical allodynia). A cooling stimulus such as a drop of alcohol may be perceived as painful (thermal allodynia). Decreased temperature and pinprick sensations in the affected limb are common.
Edema of the affected limb is present in the majority of patients. It could be very mild in the early stage of CRPS, mimicking mild cellulitis. However, in the late stage, edema may be so severe that a Doppler test is needed to rule out the possibility of deep vein thrombosis.
Autonomic dysfunction may be manifested by changes of skin color and temperature, as well as sweating abnormalities. The affected area may be reddish at one time and then become blue, purple or pale over a course of minutes to hours. Livedo reticularis is common in CRPS. Livedo is a descriptive term used to describe the red, non-blanchable (i.e. it does not turn white when pressed) network-pattern (reticulated) in the skin. About 60 % of patients may report excessive sweating in the affected limbs. Temperature asymmetry between the affected and unaffected sides may exceed 1 °C .
Motor dysfunctions in CRPS include mild weakness, decreased range of motion, tremor, dystonia and myoclonus. Dystrophic manifestations are seen in the form of increased or decreased nail and hair growth in the affected extremity, hyperkeratosis or thin, glossy skin, and osteoporosis of the underlying bones.
Diagnosis of CRPS is clinical. According to IASP (1994), if a patient has the above-mentioned features, a diagnosis of CRPS may be made if other clinical conditions, such as infection or DVT, are ruled out. EMV/NCV tests are not sensitive to CRPS and frequently cause severe pain to patients. A triple-phase bone scan may reveal abnormal absorption in the affected limbs (increased or decreased), though it is not a primary diagnostic procedure for CRPS.
The pathophysiology of CRPS is not completely understood. Multiple mechanisms are considered in the generation and maintenance of CRPS. Increased systemic calcitonin gene-related peptide (CRGP) levels may contribute to neurogenic inflammation, edema, vasodilatation and increased sweating. Elevated neuropeptide concentrations may lead to pain and hyperalgesia. Immunological mechanisms (such as altered expressions of HLA, substance P, cytokines, and interleukins) are believed to contribute to the pathogenesis of clinical symptoms, such as edema. Up-regulation of adrenergic receptors and functional coupling between sympathetic efferent and sensory afferent fibers may provide the basis of the sympathetic nervous system abnormalities in the pathogenesis of CRPS. The central mechanisms in CRPS may include central sensitization in the spinal cord, brainstem or thalamus, cortical reorganization in the primary somatosensory cortex, as well as disinhibition of the motor cortex.
The goals of treatment for CRPS are pain relief, functional recovery and psychological improvement. However, treatment of CRPS remains a challenge. There is little, if any, evidence for the efficacy of any treatment modality. In the early stages of CRPS treatment, occupational and physical therapies are often used. Occupational and physical therapies are supported by anecdotal data, and have not been validated by randomized prospective trials.
Patients diagnosed with CRPS for over 2 months should also receive a psychological evaluation, which includes psychometric testing, to identify and treat psychological disorders, such as anxiety, depression, or personality disorders. Counseling, behavioral modification, biofeedback, relaxation therapy, group therapy, and self-hypnosis should be considered. The goal of psychotherapy is to improve patient motivation and coping skills.
Tricyclic antidepressants, antiepileptics, and narcotics such as methadone are commonly used empirically for CRPS, even though clinical controlled studies have not proven their efficacy. Corticosteroids have proven to be effective analgesics in several trials with early CRPS patients. However, this is not widely used, possibly due to the side effects of corticosteroids. Subcutaneous calcitonin and intravenous phentolamine studies have had conflicting results. NMDA receptor modulation is a major interest of current research. A recent study indicated that sub-anesthetic infusions of ketamine might offer a promising therapeutic option in the treatment of appropriately selected patients with intractable CRPS. However, more studies are needed to further establish the safety and efficacy of this novel approach.
Minimally invasive techniques have been used extensively for the treatment of CRPS. These techniques include sympathetic block, intravenous regional block (IVRB), somatic nerve block, epidural drug administration, intrathecal drug delivery, and neurostimulation. Stellate ganglion blocks in the early stage CRPS may significantly decrease pain and hasten clinical recovery. It may also prevent the recurrence of CRPS after re-operation of the affected extremity. In a double blind study, IVRB with bretylium provided significantly longer analgesia than lidocaine. Epidural delivery of clonidine and ketamine, intrathecal baclofen and morphine have reported to provide good pain relief. A randomized trial, with a two-year follow-up of 36 patients, suggested that spinal cord stimulation results in a long-term pain reduction and improvement in health-related qualities of life.
Trigeminal neuralgia
Trigeminal neuralgia (TN), tic douloureux, is characterized by paroxysmal lancinating attacks of severe facial pain. TN has an incidence of approximately 4/100,000 with a large majority of cases occurring spontaneously. Both genders experience TN with a slight female predominance, and the diagnosis is most common over the age of 50. Classic TN is characterized by abrupt onset and termination of unilateral brief electric shock-like pain. Pain is often limited to the distribution of one or two (commonly the second and third) divisions of the trigeminal nerve. Trivial stimuli, including washing, shaving, smoking, talking and/or brushing the teeth (trigger factors) can evoke the pain. Some areas in the nasolabial fold and/or chin may be particularly susceptible to stimulation (trigger areas). In individual patients, pain attacks are stereotyped, recurring with the same intensity and distribution. Most TN patients are symptom-free between attacks and clinical examination is usually normal. Attacks of TN occur in clusters and remissions can last for months.
The cause of TN pain attacks is unknown. Compression of the trigeminal nerve by benign tumors and vascular anomalies may play a role in the development of clinical symptoms. Studies of surgical biopsy specimens from TN patients who had presumed vascular compression, demonstrate evidence of inflammation, demyelination, and close apposition of axons (leading to the possibility of ephaptic transmission between fibers). The “ignition hypothesis” of Devor, proposes that a trigeminal nerve injury induces physiologic changes that lead to a population of hyperexcitable and functionally linked trigeminal primary sensory neurons. The discharge of any individual neuron in this group can quickly spreads to activate the entire population resulting in a sudden synchronous discharge and a sudden jolt of pain characteristic of a TN pain attack.
The diagnosis of TN is based primarily on a history of characteristic paroxysmal pain attacks. The White and Sweet criteria are still commonly used worldwide (Table 1). In the majority of TN patients, the clinical examination, imaging studies, and laboratory tests are unremarkable (“classic TN”). In a smaller group, TN is secondary to another disease process affecting the trigeminal system (“symptomatic TN”). Because a significant percentage of patients have symptomatic TN resulting from another disease process, diagnostic brain imaging studies should be part of the initial evaluation of any patient with TN symptoms. MRI is better than CT to visualize the trigeminal (Gasserian) ganglion and the cerebello-pontine angle. Special attention should be paid to MS plaques, tumor and subtle vascular anomalies that may be the source of root compression.
“White and Sweet criteria” for TN:
1. The pain is paroxysmal.
2. The pain may be provoked by light touch to the face (trigger zones).
3. The pain is confined to the trigeminal distribution.
4. The pain is unilateral.
5. The clinical sensory examination is normal.
Carbamazepine is the first choice for treatment of TN. Both controlled and uncontrolled studies confirm its clinical efficacy. Carbamazepine monotherapy provides initial symptom control in as many as 80% of TN patients. Of those initially responding to the drug, approximately 75% will continue to have long-term control of pain attacks. Controlled studies demonstrate that baclofen, and lamotrigine are superior to the placebo for treatments of TN (7). In the experience of many clinicians, baclofen is just as effective as carbamazepine and often better tolerated. Baclofen could be an alternate choice for initial drug therapy. Other medications that may be effective include oral gabapentin, clonazepam, oxcarbazepine, topiramate and phenytoin. If a patient is not satisfied with single medication therapy adding another oral medication may offer additional benefits. Intravenous lidocaine or phenytoin may be effective for some severe refractory cases of TN. However, these treatments carry additional risks and require close cardiovascular monitoring. Opioid analgesics have not been proven effective for TN and should be avoided.
Posterior fossa exploration and microvascular decompression (MVD) is assumed to directly treat the cause of TN. However, this is a complex and invasive therapy with a possibility of death. With the availability of other less invasive procedures, MVD is infrequently used and is only reserved for younger and healthier patients. Several studies demonstrated trigeminal radiofrequency rhizotomy successfully controls symptoms in over 85% of TN cases. The technique is minimally invasive. To heat the Gasserian ganglion, a radiofrequency needle is inserted through the foramen ovale under the guidance of fluoroscopy. The procedure can be finished in less than 30 minutes in experienced hands. A few patients experience sensory loss and dysesthesia (analgesia dolorosa) in the distribution of the damaged trigeminal fibers with this procedure. Stereotactic radiosurgery employs computerized stereotaxic methods to concentrate ionizing radiation on the trigeminal root entry zone. Several studies have demonstrated the high clinical efficacy and the relative safety of this new technique. It is currently recommended as a first line noninvasive surgical technique in many pain centers, especially for frail or elderly patients.
Post-stroke pain syndrome
Lesions at any level of the neuroaxis (generally affecting spinothalamocortical afferent sensory pathways) including the medulla, pons, midbrain, thalamus, subcortical white matter, and the cortex may produce central pain. However, the thalamus and the brainstem are common sites for central post-stroke pain.
Thalamic post-stroke pain syndrome (Dejerine-Roussy syndrome) was first described in 1903. Eight to sixteen percent of thalamic stroke may lead to chronic pain. The frequency of pain after a geniculothalamic artery stroke is relatively higher (13% to 59%). Pain is the cardinal symptom and is described as spontaneous, severe, paroxysmal, and burning. Patients with thalamic pain syndrome also have hyperalgesia and allodynia in the affected limbs. Right-sided lesions predominate among reported cases of the thalamic pain syndrome.
Patients reporting pain due to brainstem infarction usually have involvement of pontine or medullar. Patients with midbrain infarction seldom complain of pain. Transient eye and nose pain may be manifested as an initial symptom of pontine infarction. About 25% patients with dorsolateral medullary infarction develop ipsilateral facial pain, especially when the lesion involves the spinal trigeminal tract. Facial allodynia is also common. Some patients may experience pain in the contralateral limbs and trunk.
Treatment of central post-stroke pain remains a challenge. Tricyclic antidepressants are still a choice of treatment. Gabapentin and lamotrigine have been used to treat central post-stroke pain syndrome in open labeled studies. Selective posterior rhizotomy has been reported to decrease painful spasticity in the lower limbs of hemiplegic patients after a stroke. It has been reported that chronic motor cortex stimulation therapy provides pain relief for some post-stroke patients. Thiamylal- and ketamine-sensitive and morphine-resistant cases may have more long-lasting pain reduction after chronic motor cortex stimulation therapy. Stereotactic radiosurgery of the pituitary has been used to treat thalamic pain syndrome with some success.
Forty to sixty percent of patients may develop shoulder pain after a stroke. The mechanism of shoulder pain is not clear. However, there is a strong association between pain and an abnormal shoulder joint examination, ipsilateral sensory abnormalities and arm weakness. These patients usually have significant tenderness over the shoulder joint. It is postulated that the pain is due to inflammation in the joint, secondary to immobilization and joint contracture (frozen shoulder syndrome). The majority of shoulder pain may be resolved or improved for 6 months following a stroke with intensive physical/occupational therapy. Anti-inflammatory medications may be used. Suprascapular nerve or brachial plexus block can provide temporary pain relief to prepare for physical therapy. Proper positioning of the shoulder, range of motion activities, and avoidance of immobilization may further help prevent or alleviate shoulder pain.
Spinal cord injury and pain
There are about 240,000 patients with spinal cord injuries (SCI) in the Unites States; 86% of individuals with SCI report pain at 6 months post-discharge, with 27% of these individuals reporting pain that impacts most of their daily activities. Patients can have pain both at the level of spinal injury and at the level below the injury. Pain intensity is not associated with the magnitude of the spinal lesion, location of the lesion, occurrence of myofascial pain syndrome or the onset of pain. However, pain is usually more severe in patients with gunshot injuries.
Pain after SCI may be from different sources. These sources include neuropathic, musculoskeletal and visceral pain. Neuropathic pain after SCI is further divided into central and segmental pain. Central neuropathic pain often begins within weeks or months after injury. It is generally described as a burning, sharp or shooting pain. Patients feel pain at or below the level of injury in areas where there is partial or complete loss of sensation to the touch. Central pain is believed due to deafferentation caused by spinal cord injury. Astrocytic activation in the spinal cord, upregulation of chemokines, and hyperexcitability of wide dynamic range neurons in the spinal dorsal horn rostral to the lesion have been suggested to cause the neuropathic pain after SCI. Segmental pain often occurs around the border of injury. It usually develops within the first few months following an injury. Allodynia and hyperalgesia are common. Nerve root entrapment could lead to severe segmental pain. Patients may describe stabbing or sharp pain or a band of burning pain at the level of injury. Syringomyelia, with a cyst ascending from the level of the SCI, may occasionally cause central pain.
Musculoskeletal pain in this group of patients may be due to muscle spasms below the level of SCI and arthritis in disused joints. Pain is generally described as dull or aching. It is usually worsened by movement and eased with rest. Visceral pain may begin a short time following SCI. It could be related to the constipation and urinary retention due to sphincter dysfunction. It may occur in the abdomen, above or below the level of injury. The pain is often described as cramping, burning and constant.
Pain management after SCI is difficult. Pharmacological and rehabilitative procedures are effective in only about 38% of patients. However, the initial work up should be aiming at identifying the pain source. Different kinds of pain may respond differently to treatments. For neuropathic pain, medications such as gabapentin, amitriptyline and nortriptyline, may ease the pain in some patients. Intravenous lidocaine may provide temporary pain relief. Intrathecal baclofen therapy may reduce chronic musculoskeletal pain associated with spasticity and improve the patient’s quality of life. Intrathecal morphine and clonidine offer limited help to relieve the pain. Thalamic stimulation and motor cortex stimulation have been reported to be effective in some cases. Use of the spinal cord stimulator lacks long-term efficacy for the relief of spasticity and pain in the SCI and is believed not to be cost-effective. Dorsal root entry zone lesions and dorsal rhizotomy have also been used with limited success. Appropriate management of bowel or bladder dysfunction may help ease visceral pain. If an ascending syrinx is present, surgical drainage may be effective in relieving the pain.
Pain in multiple sclerosis
Pain is more common in MS than has been recognized previously. The rates of pain vary in different studies, from 44% to 80%, depending on the sample and specific questions used to assess the incidence and severity of pain. Osterberg et al (18) studied pain syndromes in 429 patients with definite MS; 58% of the patients reported pain during the course of their disease. One hundred patients (28%) had central pain, including 18 patients (5%) with trigeminal neuralgia. The majority of patients (87%) with central pain had symptoms located in the lower extremities, while 31% were in the upper extremities. It was mostly bilateral (76%) and constant. Aching, burning, and pricking were common qualities. Other reported pain syndromes in MS include, Lhermitte's sign, dysesthetic pain, back pain, headache and painful tonic spasms. Chronic pain in MS was found to have no significant relationship to gender, age of onset, disease duration or disease course. Chronic pain can have a significant negative impact on functions in persons with MS, such as the ability to engage in household work and psychological functioning. Chronic pain is significantly related to anxiety and depression in females. In the long-term care facility, residents with MS are more physically disabled and have more frequent pain. There also is a higher prevalence of pressure ulcers and depression than residents without MS.
Though pain is common, it is frequently overlooked in MS patients, and only one-third of MS pain patients are treated for pain. The following principles are recommended for treatment of MS related pain: 1) For pain directly related to MS, such as trigeminal neuralgia, carbamazepine is the first choice. Lamotrigine, gabapentin, oxcarbazepine and other anticonvulsants may also be used. Painful "burning" dysesthesia may be treated with tricyclic antidepressants or carbamazepine. Further options include gabapentin or lamotrigine. 2) Pain related to spasticity may improve with adequate physiotherapy. Drug treatment includes antispastic agents like oral baclofen or tizanidine. In severe cases, intrathecal baclofen and botulinum toxin injections merit consideration. 3) Pain due to subcutaneous injections of beta interferons or glatiramer acetate may be reduced by optimizing the injection technique and by local cooling. Systemic side effects of interferons like myalgias could be reduced by paracetamol or ibuprofen.
Even though cannabis is not legally used in the USA to treat pain, European studies indicate that cannabis-based medicines are effective in reducing pain and sleep disturbance in patients with multiple sclerosis-related central neuropathic pain and are mostly well tolerated. Oral ketamine, an NMDA receptor antagonist, has also been reported to be effective in the treatment of pain and allodynia associated with MS.
Phantom limb pain and stump pain
Weir Mitchell coined the term phantom-limb pain in 1872. It describes the pain in the body part that is no longer present, which occurs in 50–80% of all amputees. Pain can have several different qualities, such as stabbing, throbbing, burning, or cramping. It seems to be more intense in the distal portions of the phantom limb. This pain may be related to a certain position or movement of the phantom and may be elicited or exacerbated by a range of physical factors (e.g., changes in weather or pressure on the residual limb) and psychological factors (e.g., emotional stress). It is more likely to occur if the individual had chronic pain before the amputation. Pain in the phantom is often similar to the pain felt in the limb before amputation. Phantom pain is most common after the amputation of an arm or leg, but it may also occur after the surgical removal of other body parts, such as breast, rectum, penis, testicle, eye, tongue, or teeth. About 30% of persons with amputation report the feeling of telescoping, i.e., the retraction of the phantom towards the residual limb and in many cases, the disappearance of the phantom into the limb. This may be accompanied by a shrinking of the limb. Recent evidence suggests that telescoping is associated with more phantom-limb pain.
Phantom-limb pain is commonly confused with pain in the area adjacent to the amputated body part. This pain is referred to as residual-limb or stump pain. Patients may report severe, knife stabbing or sharp pain in at the end of the amputated limb. Formation of neuroma or pressure-lesions of the stump may exacerbate the stump pain. Physical examination may reveal the existence of a neuroma. It is usually very sensitive to touch or pressure. However, stump pain may coexist with phantom limb pain. .
Changes along the neuroaxis may contribute to the experience of phantom-limb pain. Spinal mechanisms are characterized by increased excitability of the dorsal-horn neurons, reduction of inhibitory processes, and structural changes at the central nerve endings of the primary sensory neurons, interneurons, and the projection neurons. Supraspinal changes related to phantom-limb pain involve the brainstem, the thalamus, and the cortex. Reorganization of the somatosensory cortex of the human cerebral cortex in amputees has been supported by findings from several imaging studies. People with arm or hand amputations show a shift of the mouth into the hand representation in the primary somatosensory cortex. Studies in human amputees have shown that reorganizational changes also occur at the thalamic level and are closely related to the perception of phantom limbs and phantom-limb pain. Neuroma in the stump may be more responsible for stump pain than phantom limb pain. However, abnormal input originated from a neuroma in the residual limb may increase the amount of central reorganization, enhancing the chance of phantom-limb pain. Psychological factors also play a role in the modulation of phantom-limb pain. Phantom-limb pain may also be exacerbated by stress. Patients who lack coping strategies, fear the worst, or receive less social support, tend to report more phantom-limb pain.
Treatment for phantom limb pain has been difficult. Although tricyclic antidepressants and sodium-channel blockers are treatments of choice for neuropathic pain, there have been no controlled studies of these agents for phantom-limb pain. Opioids, calcitonin, and ketamine have been proven to be effective in reducing phantom-limb pain in controlled studies. Transcutaneous nerve stimulation (TENS) may have a minor effect on phantom-limb pain. A maximum benefit of about 30% has been reported from treatments such as local anesthesia, sympathectomy, dorsal-root entry-zone lesions, cordotomy, rhizotomy, neurostimulation methods, or pharmacological interventions such as anticonvulsants, barbiturates, antidepressants, neuroleptics, and muscle relaxants. Use of a myoelectric prosthesis may alleviate cortical reorganization and phantom-limb pain. Deep brain stimulation also has been reported to treat phantom limb pain.
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