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Thalamic Pain Syndrome
Introduction
Thalamic pain syndrome, also known as central poststroke pain or historically Dejerine-Roussy syndrome, is a common yet challenging consequence of cerebrovascular accidents (CVA). This condition involves centralized, neuropathic pain often exacerbated by temperature changes and is characterized by symptoms, eg, hyperalgesia and allodynia. Although as many as 8% of stroke patients may develop this syndrome, diagnosis can be difficult. The onset of symptoms typically occurs well after the initial stroke event, sometimes delaying significant pain for months or even years. Thalamic pain syndrome specifically pertains to pain that stems from damage to the thalamus area poststroke, a subset of the broader category of central poststroke pain, which involves injury to the spinothalamic tract.
Research on thalamic pain syndrome remains limited, and the diagnosis should be considered in patients with a history of chronic centralized pain and a prior CVA. Treatment options are few and vary in effectiveness, ranging from neuropathic pain medications and opioid analgesics to more invasive techniques, eg, deep brain stimulation, surgery, and neuromodulation. Given the complex nature of thalamic pain syndrome, management typically requires an interprofessional approach involving neurologists, pain medicine specialists, or neurosurgeons. The prognosis for this condition is generally guarded, emphasizing the need for healthcare practitioners to include thalamic pain syndrome in their differential diagnosis when evaluating patients with poststroke neuropathic pain symptoms. Alternative and integrative treatment approaches are also recommended to enhance pain management and improve quality of life.
Etiology
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Etiology
Thalamic pain syndrome commonly develops after a CVA, including ischemic or hemorrhagic strokes. An isolated thalamic infarction, known as a lacunar infarct, or larger strokes involving the middle cerebral artery (MCA), can lead to similar sensory deficits. Thalamic lesions or abscesses can also result in sensory abnormalities, eg, thalamic pain syndrome. The pain from thalamic strokes, which is neuropathic, can manifest acutely or even years poststroke due to damage to the spinothalamic tract, affecting thermoregulation and sensory interpretation.[1][2]
The thalamus serves as a relay station for sensory information, excluding olfactory signals, from the peripheral to the central nervous system (CNS), ultimately reaching the somatosensory cortex for interpretation. In thalamic pain syndrome, this pathway malfunctions, distorting tactile processing and pain perception; normal touch becomes painfully interpreted as allodynia, and typical pain as hyperalgesia, intensified.[3][4][5][6]
Centralized pain, eg, thalamic pain syndrome, originates within the CNS and is marked by central sensitization, where the nervous system remains overly active, reducing action potential thresholds and amplifying neural signals, leading to heightened pain sensitivity or "wind-up" phenomena. Diagnosing thalamic pain syndrome involves identifying central, not peripheral, sources of pain, particularly noting any infarction of the ventral posterior nuclei of the thalamus, often associated with central poststroke pain.[7][8] Additionally, diminished opiate receptors in the thalamus might heighten pain perception, while hypersensitivity along the spinothalamic tract postinfarction could stem from chronic microglial activation.[9][10][11][12][13] Furthermore, autonomic instability can lower skin temperature in affected areas, with stress potentially exacerbating pain symptoms.[14]
Epidemiology
A reported 700,000 CVA cases occur in the United States each year. Of those cerebrovascular infarctions, an estimated 56,000 cases of central poststroke pain occur annually.[15] Thalamic stroke represents 20% to 33% of cases of centralized poststroke pain.[16][17] Central poststroke pain presents in the recovery phase of cerebral infarction.[7] The prevalence of poststroke pain is up to 8% of patients following a CVA and 11% of patients who are older than 80.[4]
Central poststroke pain is more likely to occur from thalamic strokes and lateral medullary infarcts than from any other area.[18][19][20] For thalamic pain syndrome, 17% to 18% of cases occur in the inferior-lateral aspect of the thalamus.[5] Part of what makes the diagnosis of central poststroke pain so difficult is that under 40% of patients develop pain immediately following a stroke.[14] The majority of patients with thalamic pain syndrome develop pain within a month of their stroke. An estimated 18% of patients develop pain within the first 6 months after a stroke, while 18% of patients do not develop symptoms until 6 months following a CVA.[5] Patients develop pain following a stroke up to 1 to 6 years poststroke.
The mechanism of cerebrovascular injury seen in poststroke pain is the same as the percentage of cases of CVAs, with 80% of CVAs being ischemic, and 80% of cases of thalamic pain syndrome secondary to ischemic strokes.[21] According to a 2004 study from the United Kingdom, the incidence of central poststroke pain ranged from 2000 to 6000 patients. The estimated prevalence was closer to 20000 patients.[22]
Central poststroke pain symptoms occur equally in various demographics. Approximately 74% of patients endorse increased pain gradually rather than a sudden onset following a CVA. Furthermore, no significant differences in sex or previous stroke history have been identified between patients with sensory deficits with and without pain.[23][16][24] However, different studies suggest there may be an age discrepancy between patients who develop pain following a stroke and those who do not. One major study did not show an age difference, while 2 studies showed an age discrepancy. Patients who experienced poststroke pain were more than 10 years younger than patients with only sensory deficits.[25][22]
Chronic pain following a stroke is widespread, with over 40% of patients meeting the criteria for the diagnosis of central poststroke pain 4 years after their stroke. Comparatively, only 7.3% of patients diagnosed with chronic pain attribute it to central poststroke pain.[26] Right-sided infarctions are more commonly associated with central poststroke pain than left-sided infarctions. The right hemisphere of the brain is integral for pain mediation.[7]
Pathophysiology
Central imbalance may arise from faulty integration between the functional dorsal-medial lemniscus and damaged spinothalamic tracts or at the level of thalamic projections to cortical regions, though the exact mechanism is unclear. Central disinhibition occurs when a stroke in the lateral thalamus disrupts the thalamic nuclei's intrinsic GABAergic network, leading to pain through cortical activation and possibly cold allodynia due to the loss of inhibition from temperature-sensing fibers. Central sensitization involves increased pain sensitivity and spontaneous pain from suboptimal stimuli, supported by findings of asynchronous electrical activity in thalamic nuclei and the effectiveness of N-methyl-D-aspartate receptor antagonists (eg, ketamine) in animal models, indicating damage resulting from receptor activation.[27] Additionally, the grill illusion theory, first demonstrated in 1896 by Thunberg, produces a sensation of intense, often painful heat when interlaced warm and cool bars are applied to the skin, with neurophysiological studies showing that this effect arises from differential responses of spinothalamic tract neurons to temperature, supporting a model of central disinhibition that integrates pain and temperature sensations.[28]
Diffusion tensor tractography is a noninvasive magnetic resonance imaging (MRI) technique that creates a 3-dimensional view and functional estimation of the spinothalamic tract, where lesions can lead to central poststroke pain.[29] Various etiological theories have been proposed, eg, central imbalance, disinhibition, sensitization, and the grill illusion theory.[30]
History and Physical
The diagnosis of thalamic pain syndrome, often part of broader central poststroke pain, relies primarily on a detailed clinical history and physical examination.
Clinical History
The history should document the onset, description, location, radiation, quality, and severity of the pain. Patients following a thalamic stroke might initially report numbness or tingling contralateral to the injury site, typically involving the entire half of the body.[31] Over time, this can progress to a burning sensation, and patients may experience thermal dysregulation, describing feelings of being frozen or scalded. The severity of this burning pain varies and can significantly impact the patient's quality of life. Pain may be severe, constant, intermittent, and exacerbated by touch or palpation on the side opposite the infarction. Most patients report constant pain, although 15% experience pain only once daily.[4][14]
The pain may be poorly localized and evolve over time.[32] Central pain signs, eg, allodynia, dysaesthesia, and hyperalgesia, suggest the centralization of pain; allodynia is particularly pathognomonic for central poststroke pain, affecting over two-thirds of patients.[14] Approximately 40% of patients may also experience hyperalgesia.[14][33] Other symptoms include unexplained itching, a searing sensation after a stroke, and, after about 12 weeks, symptoms often centralize.[34] Interestingly, thalamic pain syndrome may coexist with anosognosia and somatoparaphrenia—conditions characterized by a denial of the injury or ownership of the injured body parts. Mood changes, fatigue, cognitive disturbances, sleep alterations, and pain catastrophizing are also associated with centralized pain.[35]
Neurologic Examination
A comprehensive neurological evaluation is crucial for patients following a CVA. While gross sensory examination findings are typically normal following an isolated thalamic stroke, patients often have difficulty interpreting temperature, indicating spinothalamic tract dysfunction. An assessment should cover all poststroke sequelae, including muscle strength, sensation, cranial nerve functions, balance, and speech. A comprehensive musculoskeletal exam may also be necessary, depending on the extent of the stroke.
On examination, areas of reported pain may be colder than unaffected areas. The patient's pinprick and temperature sensation may be impaired, yet proprioception and vibration sensation remain intact.[14] The disruption of thermal or pinprick sensation can range from complete to partial.[22] Notably, if a patient's pinprick and temperature sensation are intact, reported symptoms are unlikely due to central poststroke pain.[36][37] Pain correlates with areas of sensory loss, and temperature changes indicate central poststroke pain more than changes in pinprick sensitivity.[16] When normal palpation pressure reproduces the pain, this finding should be documented accordingly.[38]
Imaging
MRI is the gold standard in the recognition of thalamic infarction. MRI is used to identify small, deep ischemic strokes, eg, thalamic small vessel infarcts, that may not be visible on a conventional CT angiogram as part of a normal stroke protocol, and bilateral lesions have been reported.[39][40][39]
Evaluation
According to the International Classification of Headache Disorders, third edition (ICHD-3), the diagnostic criteria for central poststroke pain require the presence of facial and head pain within 6 months of either an ischemic or hemorrhagic stroke. Additionally, an MRI must show a vascular lesion in an appropriate location; no other source should be able to explain the pain. However, contrary to this classification, many cases of central poststroke pain manifest after 6 months from the stroke onset.
Imaging plays a crucial role in excluding other diagnoses and confirming a thalamic stroke, especially in ambiguous cases. MRI is beneficial for identifying and assessing the extent of a thalamic infarction poststroke, with larger infarctions typically resulting in more significant damage and a poorer prognosis.[41] Imaging findings include reduced blood flow in the thalamic area affected by the infarction.[42] If neurological symptoms are chronic and stable with a confirmed history of thalamic stroke, no further specific evaluation is required. However, the presence of new-onset neurological symptoms is indicative of a CVA; therefore, an urgent noncontrast computed tomography (CT) scan of the head is necessary.
In cases where the patient has recently experienced a CVA, repeat CT or MRI of the head may be needed to monitor for changes in brain function, hemorrhagic transformation, and increasing edema. The onset of seizure-like activity poststroke necessitates an electroencephalogram (EEG) and neurological consultation. If a patient presents with symptoms suggestive of thalamic pain syndrome without a known history of stroke, further evaluation for multiple sclerosis is warranted, typically including contrast-enhanced MRI of the brain and spinal cord.
Treatment / Management
Management Approaches
Traditional treatment for chronic pain and centralized pain includes antidepressants, anticonvulsants, and opioid analgesics; however, some novel treatments and case reports exist. A systematic review and meta-analysis showed limited evidence for the use of amitriptyline, opioids, anticonvulsants, transcranial magnetic stimulation, and acupuncture in the treatment of central poststroke pain.[43] Physical therapy should merit consideration as an adjunct treatment following an infarction. Deep brain stimulation is a potential treatment option for patients with refractory cases. Radiation therapy is another viable treatment option for refractory cases of central poststroke pain.[44] Cognitive-behavioral therapy is useful in the prevention of depression in patients following a CVA.[45] Case reports have shown the effectiveness of hyperbaric oxygen therapy in poststroke pain, but no extensive studies have taken place.[46] Additionally, cases of cold water vestibular caloric stimulation have yielded favorable results in the treatment of central poststroke pain.[14](A1)
Pharmacologic therapies
First-line therapy for central poststroke pain includes desensitization of the tactile stimulus, causing pain. Amitriptyline has been the most widely studied drug in the treatment of central poststroke pain. Furthermore, trazodone and venlafaxine are also considerations. Selective serotonin reuptake inhibitors antidepressants are generally ineffective, but results are mixed.[14] Sequellae of immobility, reduced range of motion, decreased forced expiratory volume in 1 second (FEV1), and overall deconditioning are common issues, especially after the depression-pain cycle becomes established. Anecdotally, if failing traditional antidepressants, including serotonin–norepinephrine reuptake inhibitors, a trial of a psychostimulant may be worth considering. The risk/benefit ratio needs careful evaluation in that case.
Second-line treatment includes anticonvulsants. Gabapentin, pregabalin, carbamazepine, phenytoin, and lamotrigine have all been studied for central poststroke pain. Opioid analgesics, clonidine, mexiletine, and beta-blockers have all been used in poststroke pain syndromes.[47] Intravenous infusions of lidocaine, naloxone, and propofol, as well as intrathecal baclofen and ketamine, have also been studied.
Evidence suggests lamotrigine is the most effective anticonvulsant in the treatment of central poststroke pain. Amitriptyline is more effective in patients with spinal cord injury and comorbid depression. Mixed results have been reported in multiple studies regarding the efficacy of pregabalin and gabapentin in central poststroke-related pain and central pain related to spinal cord injuries.[48][49][50][51] Studies have not been performed directly on duloxetine and its effect on central poststroke pain; however, duloxetine is effective in multiple sclerosis-related neuropathies.[52] Similar results were shown with cannabinoids.[53][54] The addition of mexiletine to antidepressants can be part of pharmacological therapy. Relaxation therapy should also be a part of adjunctive treatment.[22] Oral drug therapies have generally been ineffective.[33][32] Modafinil is an option for poststroke fatigue for patients experiencing symptoms for >3 months. Modafinil is effective in both reducing fatigue and improving quality of life.[55] (A1)
Nonpharmacologic therapies
Interestingly, intravenous lidocaine does work as a term analgesia for up to 45 minutes after an infusion in patients with central poststroke pain. A similar injection with naloxone showed mixed results. Sympathetic chain anesthetic blocks can also be complete if less invasive therapies are ineffective. Other nonpharmacologic therapies have shown some benefits, but further study is required, eg, acupuncture, which may play a role in managing thalamic pain syndrome.[56] At least 1 case report involving hyperbaric oxygen therapy showed promising results; however, the sample size consisted of only a single patient.[46] The use of an intrathecal morphine pump for treating thalamic pain syndrome has not been documented in the literature but appears to offer a potentially effective option for controlling this debilitating condition.[JPain](A1)
Anesthetic blocks, eg, a stellate ganglion block, have shown promise in reducing pain symptoms in the upper extremity and face.[57] Infusion of ketamine can significantly reduce pain in patients with central pain.[58][59] Recurring electrical stimulation of the Gasserian ganglion provides up to 50% relief in patients with central poststroke facial pain.[60] Transcutaneous electrical nerve stimulation (TENS) has yielded mixed results, with improvements in pain for some patients and worsening of it for others. One rather involved study on stellatae ganglion block in an animal model could improve CPSP with comorbid anxiety and depression by increasing cerebral blood flow and inhibiting HIF-1α/NLRP3 inflammatory signaling. Not only were pain behaviors decreased, but improvements in maze navigation and even swim tests were noted.[61](A1)
Transcranial magnetic stimulation (TMS) is another treatment option. A single, small study on TMS was conducted in patients with central poststroke pain. The results showed a modest improvement in the patient's pain 4 weeks after the intervention.[62] One study reported a motor cortex stimulation success rate of up to 77%.[63] Motor cortex stimulation is an effective treatment modality, especially in patients with facial pain.[64][65] Deep brain stimulation has yielded conflicting results, whereas motor cortex stimulation has been effective in approximately a third of patients with central poststroke pain.[66][67] Deep brain stimulation is less effective for central neuropathic pain compared to other types of pain. However, deep brain stimulation can be an effective treatment modality in the short term in 50% to 70% of patients with central poststroke pain.[68][69][70][71][72][73](B2)
Surgical therapies
Spinal cord stimulators are less invasive and improve pain in 50% of patients with central poststroke pain. Of the patients who had a spinal cord stimulator installed, about one-third had pain relief 28 months following the procedure.[66] Neurosurgery is often the last resort, but thalamotomy is an option to deactivate the source of the patient's pain. Thalamotomy and mesencephalic tractotomy improve allodynia. Dorsal root entry zone lesioning is also performed in some cases. However, a very high recurrence rate has been observed at 2 years following the procedure.[32] Surgery is most effective if the patient is experiencing paroxysmal shooting-type pains.[74] The effect of pain relief following spinal cord stimulation for central pain disorders decreases over time.[75][76][77](B2)
Differential Diagnosis
Many diagnoses can appear similar to thalamic pain syndrome. However, in the setting of a history and physical suggestive of central poststroke pain, these various diagnoses become less likely. The differential diagnosis for thalamic pain syndrome includes chronic pain syndrome, complex regional pain syndrome, and syringomyelia. The differential also includes:
- Centralized pain syndrome
- Chronic pain syndrome
- Complex regional pain syndrome
- Idiopathic peripheral neuropathy, including small fiber neuropathy
- Lateral medullary infarction Wallenberg's Syndrome)
- Multiple sclerosis
- Brain Mass
- Physiological withdrawal from habit-forming substances
- Syringomyelia
- Somatization
- Malingering
Treatment Planning
Treatment planning, in addition to addressing the underlying etiology behind the CVA, predominantly focuses on symptomatic management and improving quality of life.
Occupational therapy can be of assistance in adaptive equipment, eg, a sock puller and button holder for minimization of the disability caused by impairment from the original stroke, if applicable, to try and maintain independence. Physical therapists can attempt skin desensitization protocols similar to those used for reflex sympathetic dystrophy syndrome, which occupational therapists also use. Everything from music therapy, animal therapy, to meditation/prayer has been attempted to help patients with all pain syndromes, and neuropathic pain from a thalamic infarct is no exception.
Notably, this population, like all chronic pain patients, can become a population vulnerable to scam treatments with nonsensical claims designed around exactly what the patient wants to hear. Ethically legitimate clinicians may find themselves at a disadvantage in trying to get the patient to participate in legitimate therapies (eg, physical therapy, occupational therapy, proper diet, maintenance of normotension) when the patient has a third-party venture capitalist "organization" telling them otherwise.
Toxicity and Adverse Effect Management
Toxicity management will depend on the agents being used, treatments, or procedures being performed; no known toxin specifically causes a thalamic infarct.
Medications, eg, tricyclic antidepressants, may have potential anticholinergic effects that may not be tolerated in older adults, as well as aggravation of cognitive issues. Opiates can cause respiratory suppression, exacerbate cognitive issues, and increase the risk of falls. Caregivers should be trained in administering Narcan and know where this medication is located. The prescribing physician should also prescribe Narcan for emergency use. Care should be exercised, as many older adults or confused patients, if not adequately trained, will go home, find the Narcan in the bag with the other medicine, and self-administer and potentially put themselves into physiologic withdrawal if already on opiates. Caregivers should be supervised and documented as having been supervised while watching the Narcan online video.
Procedures, eg, a stellate ganglion block, can have inadvertent vascular uptake and result in seizure or cardiac rhythm disturbances. Pain pumps, while generally well tolerated, can cause urinary retention and, depending on the drugs, myoclonus in the legs. Pump failure is rare but requires prompt surgical attention.
Prognosis
The prognosis of thalamic pain syndrome is typically poor. Up to 5% of patients experience moderate to severe pain following a cerebral infarction.[4] Once poststroke pain develops, the character, as well as the severity of the patient's pain, will be persistent and often unchanging. Treatment options are limited, and the efficacy of various treatment options is mixed at best. If treatment does not work, unfortunately, symptoms can persist indefinitely.
Early identification of pain following a stroke and initiation of therapy have been shown to have more favorable outcomes. However, this rarely means the resolution of pain. An estimated 50% of patients report some pain relief with medications.[22] A study of central poststroke pain showed significant or complete resolution of patients' pain following antidepressant therapy initiation.[22] However, this is typically not the case. Of patients with sensory changes following a stroke, 18% will have associated pain, specifically with cold and warm stimuli. Following a cerebrovascular infarct, patients endorsing pain and sensory deficits are much more likely to experience allodynia or dysesthesia. Only 3% of patients with only sensory deficits following a CVA experienced allodynia, while 88% of patients with poststroke pain endorsed it.[16]
Complications
Persistent pain can significantly diminish the quality of a patient's life and is often accompanied by an increased incidence of depression. Stroke complications are not limited to thalamic pain syndrome; they also include medical issues, eg, frequent falls, urinary tract infections, and respiratory infections, including pneumonia. Furthermore, pressure sores and depression are common poststroke concerns, with around 29% of patients developing depression after a stroke.[78][79] The risk of major depression notably increases within the first 2 years following a stroke.[80] Outcomes and mortality rates are poorer in stroke patients with comorbid depression, although remission of depression can improve these outcomes.[81][82][83] Additionally, rates of suicide attempts and completions double after a stroke.
When evaluating patients with central poststroke pain, thoroughly assessing their physical disabilities, previous comorbidities, including depression, cognitive impairments, and their level of family and social support is essential.[81] Another significant aspect to consider is poststroke fatigue, which varies widely, affecting 23% to 75% of stroke survivors.[84][85][86] Sequellae of immobility, reduced range of motion, decreased FEV1, and overall deconditioning are common issues, especially after the depression-pain cycle becomes established.
Deterrence and Patient Education
Patients should understand that if they are experiencing pain following a stroke, they should see a primary care clinician. Thalamic pain syndrome, or central poststroke pain, can occur when disruptions of one of the pathways of the brain that affects the sensation of temperature are present. Burning or tingling pain may be noted. Also, significant discomfort with temperature changes is a concern for thalamic pain syndrome following a stroke. Modifiable risk factors, including smoking, diet, and uncontrolled hypertension, should be addressed, and patient education on these risk factors should be provided to prevent increased risk of additional CVA.
Strokes can contribute to the development of chronic pain. Difficulty sleeping, the development of depression, and loss of independence all contribute to poststroke pain. Chronic pain is associated with allodynia or pain to a nonpainful stimulus, as well as hyperalgesia or increased pain with a painful stimulus. Treatment of thalamic pain may require the expertise of a specialist. A single best therapy for thalamic pain syndrome has not been established. Furthermore, to achieve the best treatment results for thalamic pain, therapy should focus on improving the patient’s quality of life.
Pearls and Other Issues
The following factors should be kept in mind when evaluating thalamic pain syndrome:
- Thalamic pain is a form of central pain syndrome.
- Thalamic pain syndrome is the result of CVA in the thalamus (punctate or may be larger) and often results in contralateral pain.
- Thalamic pain syndrome may affect the spinothalamic tract.
- Thalamic lesions or abscesses also result in sensory abnormalities like thalamic pain syndrome. The history should include noting IVDA, prior sepsis, and hemodialysis.
- Risk factors should be identified and, if possible, modified.
- The focus is on the quality of life and functional independence, ie, evaluate for adaptive equipment, treat spasticity if present, and modify home environment.
Enhancing Healthcare Team Outcomes
Managing thalamic pain syndrome demands a highly coordinated interprofessional approach to ensure effective, patient-centered care. Physicians, including primary care clinicians, neurologists, neurosurgeons, and pain medicine specialists, must recognize the often-delayed onset of thalamic pain following a stroke and initiate prompt evaluation with neuroimaging when symptoms arise. Early identification and diagnosis allow for timely intervention. Primary care clinicians play a pivotal role in the initial management and coordination of referrals, ensuring that patients are guided to neurologists or pain specialists when necessary. Pharmacists contribute by selecting appropriate pharmacologic therapies, optimizing dosing, preventing harmful drug interactions, sometimes compounding custom agents either topically or for SA therapies, and educating both patients and team members on medication safety, particularly when opioids are involved. Advanced practitioners and specialty care nurses assist in monitoring for adverse effects, implementing care plans, and maintaining open lines of communication among all team members.
To enhance outcomes and safety, nurses, physical therapists, and occupational therapists must work collaboratively to support functional recovery, mitigate fall risk, and teach adaptive strategies for daily living, such as descending stairs backward or using mobility aids for community navigation. Home health nurses provide essential follow-up care, ensuring continuity and adherence to therapeutic regimens. Mental health professionals, particularly cognitive-behavioral therapists, address the psychological burden of chronic pain and comorbid depression, which are prevalent in patients with central poststroke pain. Effective interprofessional communication is crucial for aligning goals, tracking patient progress, and adjusting strategies in response to evolving needs. Through this team-based, coordinated effort, healthcare professionals can improve patient safety, optimize functional outcomes, and enhance the overall quality of life for individuals living with thalamic pain syndrome.
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