Mais um trabalho sobre tape cinesiológico!

J Orthop Sports Phys Ther. 2008 Jul;38(7):389-95. Epub 2008 May 29.

The clinical efficacy of kinesio tape for shoulder pain: a randomized, double-blinded, clinical trial.

Thelen MD, Dauber JA, Stoneman PD.

Source

Physical Therapy Service, Winn Army Community Hospital, Fort Stewart, GA, USA. mark.thelen@us.army.mil

Abstract

STUDY DESIGN:

Prospective, randomized, double-blinded, clinical trial using a repeated-measures design.

OBJECTIVES:

To determine the short-term clinical efficacy of Kinesio Tape (KT) when applied to college students with shoulder pain, as compared to a sham tape application.

BACKGROUND:

Tape is commonly used as an adjunct for treatment and prevention of musculoskeletal injuries. A majority of tape applications that are reported in the literature involve nonstretch tape. The KT method has gained significant popularity in recent years, but there is a paucity of evidence on its use.

METHODS AND MEASURES:

Forty-two subjects clinically diagnosed with rotator cuff tendonitis/impingement were randomly assigned to 1 of 2 groups: therapeutic KT group or sham KT group. Subjects wore the tape for 2 consecutive 3-day intervals. Self-reported pain and disability and pain-free active ranges of motion (ROM) were measured at multiple intervals to assess for differences between groups.

RESULTS:

The therapeutic KT group showed immediate improvement in pain-free shoulder abduction (mean +/- SD increase, 16.9 degrees +/- 23.2 degrees ; P = .005) after tape application. No other differences between groups regarding ROM, pain, or disability scores at any time interval were found.

CONCLUSION:

KT may be of some assistance to clinicians in improving pain-free active ROM immediately after tape application for patients with shoulder pain. Utilization of KT for decreasing pain intensity or disability for young patients with suspected shoulder tendonitis/impingement is not supported.

LEVEL OF EVIDENCE:

Therapy, level 1b-.

Estudo mostra que abordagem fisioterapêutica na capsulite adesiva do ombro é eficaz e que um pequeno grupo de pacientes está eleito à cirurgia.

Bratisl Lek Listy. 2011;112(4):204-7.

The efficacy of supervised physiotherapy for the treatment of adhesive capsulitis.

Ulusoy H, Sarica N, Arslan S, Olcay C, Erkorkmaz U.

Source

Gaziosmanpasa University, Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Tokat, Turkey. ulusoyh@mynet.com

Abstract

OBJECTIVES:

The aim of this study was to evaluate the efficacy of supervised physiotherapy supplemented with non-steroidal antiinflammatory drugs (NSAIDs) for treating adhesive capsulitis.

BACKGROUND:

Even though adhesive capsulitis is a common disorder, literature on its treatment is still limited.

METHODS:

Forty-five patients with adhesive capsulitis treated between 2004 and 2007 were reviewed retrospectively and 29 patients were enrolled in the study. All patients received a supervised physiotherapy program supplemented with NSAIDs. The outcome variables were determined as passive range of motion (ROM) values and intensity of shoulder pain. The clinical assessment was performed at the initial visit and immediately after physiotherapy. One to four years after the supervised physiotherapy, the resolved patients were reevaluated.

RESULTS:

The mean age of patients was 55.4+/-9.2 years. Fifteen patients (51.7 %) were women and 14 (48.3 %) were men. The average length of supervised physiotherapy was 3.5+/-0.5 weeks. After physiotherapy, the shoulder flexion, abduction and external rotation significantly increased (p<0.001) compared with the initial values. Additionally, shoulder pain significantly decreased (p<0.001). In the follow-up, 25 (86.2 %) of 29 patients were resolved with physiotherapy, whereas 4 (13.8 %) patients required capsular release operation because of residual functional impairment. As to long-term results of patients resolved with physiotherapy, 45.4 % of cases were cured with less than a 10 % loss in total passive ROM of the shoulder, 22.7 % of cases with a total ROM loss between 10 and 20 %, 18.1 % of cases with a total ROM loss from 20 to 30 %, and lastly, 13.6% of cases with a total ROM loss up to 40 %.

CONCLUSIONS:

Supervised physiotherapy supplemented with NSAIDs improves the ROM values in most of patients with adhesive capsulitis. A small percentage of patients may require operative treatment (Tab. 2, Fig. 1, Ref. 23). Full Text in free PDF www.bmj.sk.

Trabalho mostra a necessidade de intervenção fisioterapêutica nos pacientes com baixa resolutividade nas cirurgias da coluna.

Revista da Associação Médica Brasileira

version ISSN 0104-4230

Rev. Assoc. Med. Bras. vol.57 no.3 São Paulo May/June 2011

doi: 10.1590/S0104-42302011000300010 

ORIGINAL ARTICLE

Failed back surgery pain syndrome: therapeutic approach descriptive study in 56 patients


Manoel Jacobsen Teixeira^I; Lin Tchia Yeng^II; Oliver Garcia Garcia^III; Erich Talamoni Fonoff^IV; Wellingson Silva Paiva^V; Joaci O Araujo^VI
ILecturer; Chair Professor in Neurosurgery, School of Medicine, Universidade de São Paulo (USP), São Paulo, SP, Brazil
^IIPh.D. in Science; Pain Center Coordinator, Division of Physical Medicine, Clinical Hospital of the School of Medicine, USP, São Paulo, SP, Brazil
^IIIM.D.; Residence in Neurosurgery; Medical Trainee, Pain Center, Clinical Hospital of the School of Medicine, USP, São Paulo, SP, Brazil
^IVPh.D. in Neurology; Pain Center Coordinator, Department of Neurology, Clinical Hospital of the School of Medicine, USP, São Paulo, SP, Brazil
^VPh.D. Student in Neurology; Attending Physician, Pain Center and Functional Neurosurgery, Clinical Hospital of the School of Medicine, USP, São Paulo, SP, Brazil
^VIM.D.; Residence in Orthopedics; Musculoskeletal Outpatient Clinic Coordinator, Pain Center, Clinical Hospital of the School of Medicine, USP, São Paulo, SP, Brazil
Correspondence to

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SUMMARY
OBJECTIVE: The authors show the clinical evaluation and follow-up results in 56 patients diagnosed with a failed back surgery pain syndrome.
METHODS: Descriptive and prospective study conducted over a one-year period. In this study, 56 patients with a failed back surgery pain syndrome were assessed in our facility. The age ranged from 28 to 76 years (mean, 48.8 ± 13.9 years). The pain was assessed through a visual analog scale (VAS).
RESULTS: Postoperative pain was more severe (mean VAS score 8.3) than preoperative pain (7.2). Myofascial pain syndromes (MPS) were diagnosed in 85.7% of patients; neuropathic abnormalities associated or not with MPS were found in 73.3%. Drug therapy associated with physical medicine treatment provided > 50% pain improvement in 57.2% of cases; trigger point injection in 60.1%, and epidural infusion of morphine with lidocaína in 69.3% of refractory cases.
CONCLUSION: In patients with a post-laminectomy syndrome, postoperative pain was more severe than preoperative pain from a herniated disk. A miofascial component was found in most patients.
Keywords: Low back pain; intervertebral disk displacement; post-laminectomy syndrome.

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Introduction
According to the International Association for the Study of Pain (IASP), the post-laminectomy syndrome is defined as a "low back pain of unknown origin, persisting at the same location as the original pain despite operative interventions or with a post-surgery onset. The low back pain may be associated with a referred or radiating pain"¹. This definition applies to all surgeries designed to treat pain arising from the low back spine, including those aiming to treat a herniated disk. Surgical management applied to herniated disks is a hemilaminectomy with a flavectomy, nerve root dislocation and a hernia excision. The many clinical manifestations of the post-laminectomy pain often overlap and have a low back pain as a common expression. The term "unknown origin" in the definition should not be strictly used, as although the post-laminectomy syndrome is complex and the pain can arise from various nosological entities affecting varied anatomical elements in the spine or away from the spine or even being a result from systemic conditions, its origin can be found in many cases².
Low back pain causes are varied and differential diagnosis is wide. The structure causing the pain is identified in less than 20% of cases³. The herniated disks are the most common indication for laminectomy to treat low back pain. Over 300 thousand laminectomies are estimated to be carried out in the United States, with a failure rate higher than 40%⁴. Misinterpretation of pain origin as resulting from a herniated disk seen in imaging studies⁵, misidentification of spine instability and other mechanical causes, including incomplete removal of the herniated disk⁶, and operative complications are blamed for the poor surgical results². Pain can also result from articular facet instability or from reduced intervertebral space due to structure abnormalities or intervertebral disk removal, with consequent change in the articular facet angle⁷. Among non-mechanical causes for the failed back surgery pain syndrome, disk infection, peridural "fibrosis", arachnoiditis and psychosocial factors should be mentioned⁸. In this study, we aimed to assess the clinical features and the non-surgical management outcome in patients with a failed back surgery pain syndrome seen in a pain center.

Methods
Fifty-six patients diagnosed with a failed low back surgery pain syndrome were prospectively followed over one year at the Neurological Clinic Pain Center of the Clinical Hospital of Universidade de São Paulo in a descriptive study. The design was approved by the Institutional Ethics Board (213/05). Every patient signed an informed consent form. Patients with a persisting low back pain or an early relapse within less than three months of a surgical herniated disk procedure were selected. The patients were admitted into a specific postoperative low back pain outpatient clinic according to a spontaneous demand in the unit. Patients with evidence of metabolic, inflammatory, and oncological diseases or a radiological segmental instability picture were excluded. No patients experienced a cognitive impairment. Out of 73 patients admitted into our unit, 14 were excluded by exclusion criteria and the follow-up was lost in three cases. We obtained data from history, general physical exam, neurological and physiatric evaluation in addition to pre- and postoperative imaging studies. Laboratory tests to rule out rheumatic or metabolic diseases (ANA, RF, ESR, CRP, blood cell count) were performed.

The pain magnitude, characteristic, nature and location, as well as the radiating course in pre- (retrospectively) and postoperative periods. The pain intensity was assessed according to a visual analog scale (VAS) before and after treatment. The physiatric exam aimed specially to assess low back spine and paravertebral, low back, gluteal and lower limb muscle groups, consisting of muscle power assessment, miofascial trigger point presence, spasms, sensitivity, cutaneous changes, and trophism. Data collection was performed by using a standard protocol. The statistical analysis used Sigmastat 4 software.
For all patients, a drug therapy with a rehabilitation program using kinesiotherapy and muscle stretching was adopted and if a rehabilitation refractory myofascial component (MPS) was associated, these patients underwent needling with a 1% lidocaine injection. MPS was identified in 48 (85.7%) patients. Drug therapy consisted of amitriptyline 25 to 150 mg/day (mean, 64 mg/day), chlorpromazine 20 to 100 mg/day (mean, 48 mg/day), naproxen 1000 to 1500 mg/day (mean = 1150 mg/day), acetaminophen 2 to 4 g/day (mean = 2.4 g/day) and codeine phosphate 120 to 240 mg/day (mean = 184 mg/day) according to the requirements and tolerability in each case. All patients underwent physiatric follow-up.
In case there was not > 50% original pain improvement (VAS) all over the follow-up, the patients were considered frankly refractory, undergoing a 2 mL infusion containing morphine 1 mg/mL and 2% lidocaine by catheter placement into the low back peridural compartment bid over two weeks.

Results
Overall, 37 (60.5%) patients were male and their ages ranged from 28 to 76 years (mean, 48.8 years ± 13.9 years). The patients' mean age at the original pain onset ranged from 22 to 66 years (mean = 37.2 years). The patients had undergone from one up to four low back laminectomies (mean = 1.5) to treat low back pain or lumbosciatic pain. The mean symptomatology length was 96 months.
The length of the low back pain or lumbosciatic pain complaints ranged from 8 to 168 months (mean = 36 months). Regarding the pain intensity, the patients with a radiculopathy persisting postoperatively were found with a higher pain score by the pain analog scale. Those with a postoperative root pain diagnosed had a mean score of 8.7, compared with 6.6 for those with no radiculopathy (p = 0.001).
In 17 (30.3%) patients, the preoperative pain history was consistent with a root origin, in 9 (16.1%) with referred pain in musculoskeletal conditions in both lower limbs, in 22 (39,3%) with referred pain in one lower limb, in 2 (3.6%), the pain location was only the lower back region and in 6 (10.7%) the pain had polyneuropathy characteristics. Three (5.4%) patients who did not experience pain with root characteristics preoperatively had undergone a diskectomy and spinal fixation.
X-ray studies disclose a one- or two-lumbar-segment hemilaminectomy unilaterally (L4 or L5) in 53 (94.6%) patients and bilateral lumbar laminectomy in 3 (5.4%). The lumbar spine dynamic study did not show instability in any patient. The computed tomography (CT) scan or magnetic resonance (MR) imaging did reveal a periradicular scar at the operative site in 32 (57.1%) cases.
The pain intensity before the operations ranged from moderate to severe, according to the VAS, scoring from 5 to 10 (mean = 7.2); the pain intensity at the first attendance to the Pain Center, Clinical Hospital, Universidade de São Paulo was severe, scoring from 7 to 10 (mean = 8.3).
Thirty-six patients (64.9%) had undergone physical therapy, 53 (94.6%) had been on nonsteroidal anti-inflammatory drugs (NSAIDs), and 17 (30.4%) had been on corticosteroids alone or in combination with B complex vitamins, four (7.1%) had been on opiates, and five (8.9%) had been on tricyclic antidepressive agents before and after the surgery. All of the patients had stayed at rest and those exerting an occupational activity had been put away from work.
In 38 (67.9%) patients, uniradicular (53.7%) or multiradicular (14.3%) syndromes were shown. Ten (17.9%) patients had muscle pain and myofascial painful points in several body regions, sleep disturbances and depression, suggesting the fibromyalgia syndrome.
Trigger points characteristic of MPSs were identified in 48 (85.7%) patients. Out of 17 (30.3%) patients with preoperative nerve root pain, 15 (88.2%) had lumbar or gluteal MPSs (Table 1).

Satellite or secondary trigger points were found in 29 (51.8%) patients (Table 2).

The treatment outcome was rated as excellent (> 75% improvement over the original pain according to the VAS), good (50% to 75% improvement), fair (25% to < 50% improvement) and poor (< 25%).
Drug therapy combined with physical rehabilitation measures provided an excellent outcome in 5 (16.1%) patients, a good outcome in 23 (41.1%), a fair outcome in 16 (28.6%) and a poor outcome in 12 (21.4%).
In 48 patients, MPS was found and trigger point injections were performed by using 1% lidocaine 0.5 mL. By comparing the pain improvement scores, patients with MPS had worse outcomes over post-laminectomy syndrome without MPS. The immediate results were excellent in 5 (10.4%), good in 17 (35.4%), fair in 18 (37.5%) and poor in 8 (17.8%). The results were satisfactory for 68.75% of patients with MPS versus 75% in patients without MPS, but the difference was not statistically significant (p = 0.2).
At the end of treatment, significant improvement (excellent and good outcomes) occurred in 34 (60.1%) patients, while 13 (23.2%) had a fair outcome. However, the outcome was considered poor in 8 (17.5%) patients. Regarding the pain intensity at the final follow-up, we found a reduced general mean in the visual analog scale from 7.2 to 4.7 (p = 0.01).
A peridural catheter for spinal infusion of a morphine and lidocaine solution was placed in thirteen patients; all of them had a MPS, being considered refractory after a rehabilitative treatment attempt. The outcome was excellent in 4 (30.8%) patients, good in 5 (38.5%), and poor in 4 (30.8%), meaning the outcome was excellent or good in 9 (69.2%) patients treated with a peridural infusion.

Discussion
Low back pain is present at some point in life and constitutes a serious public health problem in 40% to 85% of individuals². Treatment cost, compensation, and lost productivity are high. The patients' mean age at pain onset was 37.2 years, with the individuals within this age group usually exercising their occupational activity to a very great extent.
In most cases, the course is favorable, even when no care measures are taken. However, low back pain becomes chronic in 15% to 20% of individuals⁹. In 13.8% of patients studied by Frymoyer¹⁰, the pain lasted more than two weeks and in 22% it was severe. In 21.2% of Deyo and Tsiu's patients⁹, the pain was mild; in 43.4%, it was moderate and in 35%, severe; in 40% of cases, the low back pain irradiated to lower limbs and in only 1% a true sciatic pain could be found. In our series, preoperative pain was severe, with a 7.2 score according to the VAS; 45.4% had a low back pain and referred pain to lower limbs history before the surgery. In only 30.3%, the history suggested a true sciatic pain, and these findings indicate selection criteria for the surgery were likely inappropriate in most cases.
According to Hanley et al.¹¹, the operative treatment outcome of herniated disks is poor in 14% of cases. The numbers of spine surgeries to relieve pain have steadily grown in the United States, with 170 thousand operations in 1974, 300,413 in 1994 reaching 392,948 in 2000¹², with 80 thousand cases of failed back surgery pain syndrome per year¹³. According to Deyo and Tsiu⁹, the main reason for an increasing number of laminectomies is the growing number of surgeons operating the spine in each country. In different countries and different regions, the frequency of operation indications is variable, and this is not explained only by the different prevalence of low back pain or lumbosciatic pain; in 3% or 4% of individuals, herniated disk surgeries are indicated in the USA, but only in 1% of individuals in Sweden and Denmark.
Poor outcome of operative treatment might result from an incorrect diagnosis. Among the identified causes for low back pain, the following could be highlighted: rheumatic conditions, primary or secondary spine tumors, vascular conditions, hematological abnormalities, endocrine conditions, pelvic or abdominal viscus diseases (endometriosis, ovarian cyst torsion, pelvic inflammatory disease, prostatitis, cystitis, pancreatopathy, nefropathy, kidney disease, peptic ulcer, urinary tract, biliary or duodenal conditions), mechanical abnormalities (herniated intervertebral disk, articular facet injury, segmental instability or sacroiliac joint instability), systemic conditions (fibromyalgia, myositis, autoimmune or immune-allergic diseases), psychiatric diseases and other conditions (hip joint disease, trochanteric bursa injury, polyradiculoneuritis, meningeal irritation signs)¹⁴. Because of the great number of possibilities, the high surgical therapeutic failure rate is justifiable in care provided to these patients, but it also indicates there must be a more judicious semiologic evaluation.
Surgeries that do not meet the indication criteria to treat a herniated disk can result in maintenance or worsening of pain and preoperative deficits. A herniated disk misinterpreted as a cause for low back pain is the most common reason for indicating spine surgeries that progress to a post-laminectomy chronic pain syndrome with an early onset postoperatively. This is partly due to overvaluing the anatomical findings not related to the low back pain that are shown in imaging studies, but those usually do not warrant the pain and the surgical intervention¹⁴. In 35% of asymptomatic individuals studied by Hitselberg and Wihen¹⁵, the x-ray imaging revealed abnormalities suggesting a herniated disk. In 35% of asymptomatic individuals studied by Wiesel et al.¹⁶, a spine CT scan found abnormalities; in 20.2% of cases, there was a herniated disk evidence. Boden et al.¹⁴ observed 60% of asymptomatic individuals had a herniated disk on magnetic resonance imaging. Therefore imaging studies can confirm a herniated disk clinical diagnosis, but they are not the main determinants for indicating a surgery, since asymptomatic herniated disks are so commonly seen².
Even in symptomatic conditions, there is a progressive absorption of the herniated disk fragment, a phenomenon accompanied by symptom improvement in most cases¹⁷. Hakelius¹⁸ observed 38% of patients with a herniated disk not undergoing a surgery, but having been on medical treatment, were clinically improved within a month, 52% within two months, and 73% within three months. Saal and Sall¹⁹ conducted a retrospective study involving 58 patients with a radiculopathy resulting from a herniated disk; 52 underwent a conservative treatment, resulting in improvement in over 90% of cases; only in three cases surgical ablation of extruded fragments was required. This means the indication criteria for diskectomy, represented by a cauda equina syndrome, marked acute or progressive motor deficit or lumbosciatic pain occurrence and evident radiculopathy, characterized by sensory, motor and deep tendon reflexes deficits over one or more nerve root territory, nerve root irritation evidence, translated as a positive straight leg raising maneuver and consistent imaging study findings²⁰ in patients achieving no improvement after symptomatic drug therapy with physical medicine measures during a period of over 6 to 12 weeks^20,21, are not always met. Only 64.9% of patients included in the current casuistry had undergone physical medicine treatment and only 8.9% had undergone a tricyclic antidepressant therapy before the operations, suggesting medical methods had not been adopted in most cases.
Mechanical causes are responsible for 90% of post-laminectomy pain cases⁶. Among them, residual or relapsed herniations, spinal instability, post-vertebral fixation pseudarthrosis, articular facet abnormalities, spinal canal stenosis, meningocele and pseudomeningocele are highlighted²². In no patient of ours a spinal instability or residual herniation was found. In addition to the diskectomy, a spinal fixation and fusion was proposed²³. However, there is little evidence the spinal fusion is useful in patients with no actual spinal instability⁷. This occurred in 5.4% of study subjects. Postoperative imaging of a residual disk herniation does not imply this is necessarily the cause for a persisting pain, as postoperative imaging studies often show similar abnormalities in individuals whether they are symptomatic or not²⁴. Peridural scar occurring after a laminectomy is a frequent postoperative finding. Newly formed tissue can involve, distort and/or compress the nerve root. However, epidural fibrosis is often shown on CT scan or MRI postoperatively in cases there is no pain⁸. In 57.1% of patients in this study, a periradicular scar was found.
The patients included in our study had undergone up to 4 surgical lumbar spine surgical procedures with no improvement; the mean was 1.5 operations per patient. Many patients undergoing further operations to treat persisting or residual pain get frustrated. The improvement rate in reoperations is low, around 30% after the second surgery, 15% after the third surgery and 5% after a fourth procedure with up to 20% of worsening¹³.
Out of 56 patients analyzed in the present study, 85,7% had MPS not found previously on physical exam. There is evidence that MPS is involved in low back pain genesis or maintenance²³. However, MPS diagnosis is frequently disregarded²⁵. Many lumbar muscles affected by MPS and the operative injury would result in pain worsening. Although physiatrically speaking lumbar and gluteal muscle MPS is considered the most important cause for low back pain, bone, tendinous, nerve, disk and bursa conditions are still valued as symptom causes²⁶. The muscle fiber injury is not necessarily a cause for pain, since in patients with primary degenerative conditions, as in Duchenne muscular dystrophy, there is a disruption in a large amount of myofibrils and the sarcoplasmic reticulum, but there is no pain, suggesting MPS symptoms result from nonstructural muscle fiber changes or dysfunctions²⁶. The main electrophysiological abnormality seems to be a neuromuscular dysfunction in the motor endplate.
The energy crisis theory postulates there is an increased calcium concentration in the sarcoplasm due to a sarcoplasmic reticulum, sarcolemma and or muscle cell membrane disruption. The sarcoplasmic reticulum function is storing and releasing ionized calcium, which activates contractile elements and causes sarcomere shortening. Sustained sarcomere contraction results in increased metabolism, causes localized ischemia and generates a localized energy crisis. The combination of electrophysiological and histopathological theories generated the neuromuscular endplate multiple dysfunction concept. The potentials recorded as spontaneous activity or spikes in trigger points would result in abnormal acetylcholine release by the nervous ending. Acetylcholine release would accentuate depolarization and calcium release from the sarcoplasmic reticulum, causing sarcomere contraction and small-caliber vessel compression. Increased depolarization due to acetylcholine release and sarcomere contraction would cause increased energy demand, which, if associated with hypoxia resulting from reduced muscle blood flow, would then cause the energy crisis. This energy crisis generates metabolites which sensitize nociceptores and referred pain from trigger points²⁶. The abnormalities in nerve fibers responsible for supplying the muscle could cause localized muscle contraction and MPS²⁷. The referred pain from the trigger point is due to a sensory neuron sensitization in the spine cord posterior horn and may have a distribution similar to that in the radiculopathic pain. This referred pain associates with tingling and numbness²⁶. In 88.2% of 17 patients with preoperative nerve root pain history, lumbar and gluteal MPS was identified.
The ages of patients included in the study when firstly seen at the Pain Center ranged from 28 to 76 years (mean age, 48.8 years). The mean symptom length was 96 months and the mean pain intensity was 8.3, showing the magnitude and the extended distress the patients went through. The postoperative pain was also shown more severe than the preoperative pain.
The chronic pain treatment should involve a multidisciplinary team and pharmacological, physiatric, psychotherapeutic, and neuroanesthesic procedures; functional neurosurgical procedures should be performed if required²⁸. The treatment with analgesic drugs, whether they are anti-inflammatory drugs or not, psychotropic drugs and physical medicine provided > 50% original pain improvement in 57.2% of patients evaluated in this study. Myofascial trigger point treatment consists of using analgesic drugs, psychotherapeutic agents, muscle relaxant drugs, refrigerant vapor, dry needling, local anesthetic injection and stretching, as well as correction of causal or perpetuating factors²⁹.
In 69.4% of patients undergoing administration of a morphine and lidocaine solution via peridural route in our study, the original pain had > 50% improvement.
The pain in patients with failed back surgery pain syndrome is severe, affects individuals in the fullness of their activities, is often found as a lumbar and/or gluteal MPS and, less frequently, has a neuropathic pattern alone or associated with MPSs²⁹.

Conclusion
The failed back surgery pain syndrome evaluation and management is challenging for the medical team. Analgesic drugs and physical medicine provide major improvement in most cases. The pain intensity in post-laminectomy syndrome is worse than the herniated disk preoperative pain. The injection of myofascial trigger points and opiate infusion into the lumbar spine compartment can be required in refractory pain cases.

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Um pouco da História da Fisioterapia no Brasil

Muito interressante este post nesse blog.

A FISIOTERAPIA NO BRASIL: LINHAS GERAIS
“A história da fisioterapia mostra que a criação da profissão se deu principalmente em virtude da demanda que no contexto mundial se referia às grandes guerras e, no Brasil, aos acidentes de trabalho e epidemias, como a poliomielite. Antes de fundamentar bases sólidas como área de conhecimento, esteve sob a coordenação de departamentos médicos, tanto em serviços público/privados quanto em universidades. Sempre ligada à medicina, com características de subárea, seu corpo de conhecimentos acabou por acompanhar, de forma dependente e estreita, as mesmas áreas de estudo e campos de atuação profissional (REBELATTO; BOTOMÉ, 1999).
Perceber as concepções teóricas que nortearam o saber fisioterapêutico como uma cultura específica, porém em interação com outras realidades, pode encaminhar para uma reflexão mais crítica. Apesar de a fisioterapia e de a medicina serem áreas de conhecimento diferentes, ambas se apóiam e são baseadas em um paradigma mecanicista, no qual a perspectiva unicausal, não obstante ser percebida como insuficiente, não possibilitou a incorporação do contexto social como fundamental para a análise dos fenômenos de doença e saúde.
Essa condição definiu para a fisioterapia as formas de assistência que poderia oferecer, ou seja:
[...] as formas de assistência às condições de saúde novamente ficaram reduzidas ao atendimento de uma população já lesada, já acometida de males que necessitavam ser “controlados”, não no sentindo de “não ocorrência”, mas de “mantê-los em níveis” que não perturbassem o sistema social. Partindo do pressuposto de não perturbação do sistema social vigente e predominante, o desenvolvimento das profissões no campo da Saúde, por muitas vezes, parece ter sido orientado a trilhar caminhos sem mesmo levar em conta os conhecimentos científicos já produzidos e disponíveis (REBELATTO; BOTOMÉ, 1999, p. 46).
A re-inserção social dependia muito mais de uma habilidade adaptativa do paciente do que a realidade de suas redes sociais ou do seu itinerário terapêutico. A saúde como um todo se restringia somente ao ato curativo, abandonando de uma forma incisiva a iniciativa de uma possibilidade de medicina social, na qual a relação saúde–doença e as condições econômico-sociais deveriam ser submetidas à investigação científica (KOIFMAN, 2001).
A perspectiva de uma medicina social remonta ao século XIX, onde na França e na Alemanha já se concebia a medicina como uma ciência social. Contudo, em oposição a essa perspectiva, Bering, médico alemão, pontuou que tais concepções mereciam restrições, porque, de acordo com a teoria das doenças infecciosas de Pasteur, o médico poderia trabalhar na sua “especificidade sem a necessidade de um desvio para considerações e reflexões sociais” (ROSEN, 1980, apud KOIFMAN, 2001, p. 55).
Várias teorias sobre a doença surgiram posteriormente, e uma negava a outra; o que as unia era somente a negação da medicina como ciência da sociedade, pois
a medicina como ciência social implicava compromisso e redirecionamento econômico do Estado; as novas concepções, por sua vez, além de desonerar o Estado, responsabilizando o indivíduo por suas doenças, necessitavam do desenvolvimento de equipamentos e medicamentos muito mais compatíveis com a lógica capitalista de desenvolvimento (KOIFMAN, 2001, p. 56).
De acordo com tal lógica, em 1910, nos Estados Unidos, foi realizado um estudo sobre a educação médica, liderado pelo médico Abraham Flexner. Tinha como objetivo geral dar ao ensino médico e à medicina uma base científica sólida. Para isso, buscava contemplar um grande número de temas, que variavam desde os aspectos mais específicos da educação, passando pela questão da participação feminina no trabalho médico, até a discussão sobre a inclusão de minorias na assistência médica (LAMPERT, 2002; KOIFMAN, 2001).
A enorme força que teve esse relatório fez com que ele, além de disciplinar o aparato formador dentro dos Estados Unidos, incluindo a redução do número de instituições de ensino existente na época, influenciasse não apenas a formação, mas também a prática médica, tanto naquele país com em todo o mundo.Embora tenha reformulado e modernizado o ensino médico, nele foram descritas características mecanicistas, biologicistas, individualizantes e de especialização da medicina, com ênfase na medicina curativa e exclusão das práticas alternativas. Consolidou-se, então, o paradigma da medicina científica que orientou o desenvolvimento das ciências médicas, do ensino e das práticas profissionais em toda a área da saúde ao longo do século XX.
Assim, as características ainda hoje tão marcantes da educação superior nessa área, quais sejam a segmentação em ciclos básico e profissional, o ensino baseado em disciplinas ou especialidades e ambientado predominantemente no hospital, têm origens no relatório Flexner, que assume, segundo Lampert (2002), as seguintes características:
1. Predominância de aulas teóricas, expositivas/demonstrativas, nas quais o processo de ensino–aprendizagem está centrado no professor;2. Prática desenvolvida predominantemente no hospital;3. Capacitação docente centrada unicamente na competência técnico-científica;4. Mercado de trabalho referido apenas pelo tradicional consultório, no qual o médico domina os instrumentos diagnósticos e os encaminhamentos e cobra seus honorários sem intervenções de terceiros.
A prática empírica, já suprimida, é praticamente diluída em especializações e subespecializações e dá lugar à prática indissociável da investigação científica. A profissão médica, pelo avanço técnico alcançado, diferenciou-se pelo processo contínuo de obtenção de informação, reforçou a idéia de poder, constantemente, definir e redefinir os limites entre o normal e o anormal fisiológico. Conseqüentemente, para garantir esse domínio, desenvolveu-se a necessidade de divisão técnica do trabalho no interior do corpo profissional (LAMPERT, 2002).
No Brasil, segundo Rebelatto e Botomé (1999), o primeiro serviço de fisioterapia propriamente dito foi instalado em 1929, dentro do Hospital Central da Santa Casa de Misericórdia de São Paulo, pelo médico Waldo Rolim de Morares, que, posteriormente, também organizou o Serviço de Fisioterapia do Hospital das Clínicas de São Paulo, iniciando o primeiro curso para a formação de técnicos em fisioterapia em 1951 até 1956, o qual possuía a duração de 2 anos.
O primeiro Parecer Oficial (n.º 388/63) sobre a profissão no Brasil apresentou limitações em relação à construção de uma identidade com bases sólidas. O que atrasou a definição do objeto de trabalho e as discussões sobre a busca de autonomia profissional. O texto do Parecer (BRASIL, 1963) é significativo:
A referida Comissão insiste na caracterização desses profissionais como auxiliares médicos que desempenham tarefas de caráter terapêutico sob a orientação e responsabilidade do médico. A este cabe dirigir, chefiar e liderar a equipe de reabilitação, dentro da qual são elementos básicos: o médico, o assistente social, o psicólogo, o fisioterapeuta e o terapeuta ocupacional. [grifo nosso]
[...] Não compete aos dois últimos o diagnóstico da doença ou da deficiência a ser corrigido. Cabe-lhe executar, com perfeição, aquelas técnicas, aprendizagens e exercícios recomendados pelo médico, que conduzem à cura ou à recuperação dos parcialmente inválidos para a vida social. Daí haver a Comissão preferido que os novos profissionais paramédicos se chamassem Técnicos em Fisioterapia e Terapia Ocupacional, para marcar-lhes bem a competência e atribuições. [grifo nosso]
Segundo uma visão mais atual, percebe-se que o problema não foi solucionado completamente. Um estudo realizado por Rebelatto e Botomé (1999) sobre a grade curricular de 15 universidades de fisioterapia no Brasil acabou po revelar as seguintes perspectivas profissionais. Observa-se que não existe uma homogeneidade das disciplinas e que os objetivos apresentados não definem claramente o que o aluno deverá absorver como essencial no exercício da profissão. Há uma ausência de graus ideais de unificação [interação] das matérias, o que remete a uma identidade profissional influenciada por campos profissionais já existentes e mais ‘consolidados’ e decorrentes de definições estabelecidas em outras realidades sociais.
Até 1969, ano de regulamentação da profissão, existiam seis escolas de reabilitação para a formação de fisioterapeutas no país. Nos 12 anos seguintes, entre 1969 a 1981, foram registrados aproximadamente 14 novos cursos de fisioterapia. Em 1984 subiu para 22 escolas, em 1998 para 115, em 2002 estava em torno de 141 cursos (SCHMIDT, 2002).
Em 1975, por intermédio da Lei 6.316, foram criados os Conselhos Federal (COFFITO) e Regionais (CREFITOS) de Fisioterapia e Terapia Ocupacional. Em decorrência do número insuficiente de fisioterapeutas na época da criação dos conselhos, e considerando os vínculos anteriores mantidos, a união com os terapeutas ocupacionais foi necessária para que a criação dos Conselhos fosse aprovada. Assim, a profissão se fortalecia por meio de um órgão de classe que assumia a função de legislar, estabelecendo o Código de Ética Profissional, normatizando a profissão e a atuação do fisioterapeuta (SCHMIDT, 2002).”

---Fonte:
ALBERTO SUMIYA: “O CORPO NA HISTÓRIA E O PARADIGMA BIOMÉDICO NA MUDANÇA CURRICULAR DA FISIOTERAPIA”. (Dissertação apresentada ao Programa de Pós-Graduação em Ciências Sociais da Universidade Estadual de Londrina, como requisito parcial à obtenção do título de Mestre em Ciências Sociais. Orientadora: Profª. Drª. Leila Sollberger Jeolás). Universidade Estadual de Londrina – UEL. Londrina, 2007

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Iba Mendes

Bandas Terapêuticas: Trabalho randomizado mostra eficácia!

Short-Term Effects of Cervical Kinesio Taping on Pain and Cervical Range of Motion in Patients With Acute Whiplash Injury: A Randomized Clinical Trial

Javier González-Iglesias, Maria del Rosario Gutiérrez-Vega, César Fernández-de-las-Peñas, Peter Huijbregts, Joshua A. Cleland

DOI: 10.2519/jospt.2009.3072

DESIGN: Randomized clinical trial. OBJECTIVES: To determine the short-term effects of Kinesio Taping, applied to the cervical spine, on neck pain and cervical range of motion in individuals with acute whiplash-associated disorders (WADs). BACKGROUND: Researchers have begun to investigate the effects of Kinesio Taping on different musculoskeletal conditions (eg, shoulder and trunk pain). Considering the demonstrated short-term effectiveness of Kinesio Tape for the management of shoulder pain, it is suggested that Kinesio Tape may also be beneficial in reducing pain associated with WAD. METHODS AND MEASURES: Forty-one patients (21 females) were randomly assigned to 1 of 2 groups: the experimental group received Kinesio Taping to the cervical spine (applied with tension) and the placebo group received a sham Kinesio Taping application (applied without tension). Both neck pain (11-point numerical pain rating scale) and cervical range-of-motion data were collected at baseline, immediately after the Kinesio Tape application, and at a 24-hour follow-up by an assessor blinded to the treatment allocation of the patients. Mixed-model analyses of variance (ANOVAs) were used to examine the effects of the treatment on each outcome variable, with group as the between-subjects variable and time as the within-subjects variable. The primary analysis was the group-by-time interaction. RESULTS: The group-by-time interaction for the 2-by-3 mixed-model ANOVA was statistically significant for pain as the dependent variable (F = 64.8; P<.001), indicating that patients receiving Kinesio Taping experienced a greater decrease in pain immediately postapplication and at the 24-hour follow-up (both, P<.001). The group-by-time interaction was also significant for all directions of cervical range of motion: flexion (F = 50.8; P<.001), extension (F = 50.7; P<.001), right (F = 39.5; P<.001) and left (F = 3.8, P<.05) lateral flexion, and right (F = 33.9, P<.001) and left (F = 39.5, P<.001) rotation. Patients in the experimental group obtained a greater improvement in range of motion than thosein the control group (all, P<.001). CONCLUSIONS: Patients with acute WAD receiving an application of Kinesio Taping, applied with proper tension, exhibited statistically significant improvements immediately following application of the Kinesio Tape and at a 24-hour follow-up. However, the improvements in pain and cervical range of motion were small and may not be clinically meaningful. Future studies should investigate if Kinesio Taping provides enhanced outcomes when added to physical therapy interventions with proven efficacy or when applied over a longer period. LEVEL OF EVIDENCE: Therapy, level 1b.
J Orthop Sports Phys Ther 2009;39(7):515-521, Epub 24 February 2009. doi:10.2519/jospt.2009.3072
KEY WORDS: cervical spine, neck, taping, WAD


The authors determine the short-term effects of Kinesio Taping, applied to the cervical spine, on neck pain and cervical range of motion in individuals with acute whiplash-associated disorders (WADs).

Aerobic capacity and skeletal muscle function in children with asthma.

Autores: Villa F,Castro AP,Pastorino AC,Santarém JM,Martins MA,Jacob CM,Carvalho CR

Revista: Arch Dis Child (Archives of disease in childhood). Idioma: Inglês

Volume: Páginas: Data: 2011 Mar 23

Background Peripheral muscle strength and endurance are decreased in patients with chronic pulmonary diseases and seem to contribute to patients exercise intolerance. However, the authors are not aware of any studies evaluating peripheral muscle function in children with asthma. It seems to be implied that children with asthma have lower aerobic fitness, but there are limited studies comparing the aerobic capacity of children with and without asthma. The present study aimed to evaluate muscle strength and endurance in children with persistent asthma and their association with aerobic capacity and inhaled corticosteroid consumption. Methods Forty children with mild persistent asthma (MPA) or severe persistent asthma (SPA) (N=20 each) and 20 children without asthma (control group) were evaluated. Upper (pectoralis and latissimus dorsi) and lower (quadriceps) muscle strength and endurance were assessed, and cardiopulmonary exercise testing was performed. Inhaled corticosteroid consumption during the last 6 and 24 months was also quantified. Results Children with SPA presented a reduction in peak oxygen consumption (VO(2)) (28.2±8.1 vs 34.7±6.9 ml/kg/min; p<0.01) and quadriceps endurance (43.1±6.7 vs 80.9±11.9 repetitions; p<0.05) compared with the control group, but not the MPA group (31.5±6.1 ml/kg/min and 56.7±47.7 repetitions respectively; p>0.05). Maximal upper and lower muscle strength was preserved in children with both mild and severe asthma (p>0.05). Finally, the authors observed that lower muscle endurance weakness was not associated with reductions in either peak VO(2) (r=0.22, p>0.05) or corticosteroid consumption (r=-0.31, p>0.05) in children with asthma. Conclusion The findings suggest that cardiopulmonary exercise and lower limb muscle endurance should be a priority during physical training programs for children with severe asthma

TENS: Além da Teoria do Gate Control

Release of GABA and activation of GABA_A in the spinal cord mediates the effects of TENS in rats

Y. Maeda, T.L. Lisi, C.G.T. Vance, and K.A. Sluka^*

Physical Therapy and Rehabilitation Science Graduate Program, Neuroscience Graduate Program, Pain Research Program, 1-242 MEB, University of Iowa, Iowa City, IA 52242, USA

^*Corresponding author. Fax: +1 319 335 9707. E-mail address: kathleen-sluka@uiowa.edu (K.A. Sluka).

 The publisher's final edited version of this article is available at Brain Res

 See other articles in PMC that cite the published article.

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Abstract

Transcutaneous electrical nerve stimulation (TENS) is a commonly utilized non-pharmacological, non-invasive treatment for pain. GABA is a neurotransmitter in the dorsal horn of the spinal cord that mediates analgesia locally, and also through activation of supraspinal sites. TENS reduces hyperalgesia through activation of receptor-mediated pathways at the level of the spinal cord, and supraspinally. The current study tested the hypothesis that either high or low frequency TENS applied to the inflamed knee joint increases GABA in the spinal cord dorsal horn and activates GABA receptors spinally. We utilized microdialysis to sample the extracellular fluid before, during and after TENS and analyzed GABA in dialysates with high performance liquid chromatography. We analyzed the extracellular GABA concentrations in animals with and without knee joint inflammation induced by intra-articular injection of kaolin and carrageenan. We further tested if spinal blockade of GABA receptors prevents the antihyperalgesia produced by TENS in rats with joint inflammation. We show that high frequency TENS increases extracellular GABA concentrations in the spinal cord in animals with and without joint inflammation. The increases in GABA do not occur in response to low frequency TENS, and there are no increases in glycine in response to low or high frequency TENS. However, the reduction in primary hyperalgesia by both high and low frequency TENS is prevented by spinal blockade of GABA_A receptors with bicuculline. Thus, high frequency TENS increases release of GABA in the deep dorsal horn of the spinal cord, and both high and low frequency TENS reduce primary hyperalgesia by activation of GABA_Areceptors spinally.

Keywords: Pain, Electrical stimulation, Microdialysis, Bicuculline, Hyperalgesia

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1. Introduction

Transcutaneous electrical nerve stimulation (TENS) is the application of surface electrodes to the skin for pain relief. Clinically, TENS is applied at varying frequencies of stimulation, high (>50 Hz) or low (<10 Hz). Previously, we show different mechanisms of action for the ability of low and high frequency TENS to reduce hyperalgesia. Specifically, low frequency TENS activates mu-opioid, serotonin, and cholinergic receptors in the spinal cord and mu-opioid receptors supraspinally (Sluka et al., 1999; Kalra et al., 2001; Radhakrishnan and Sluka, 2003;Radhakrishnan et al., 2003). On the other hand, antihyperalgesia produced by high frequency TENS activates delta-opioid receptors and cholinergic receptors spinally, and delta-opioid receptors suprapspinally (Sluka et al., 1999; Kalra et al., 2001;Radhakrishnan and Sluka, 2003; Radhakrishnan et al., 2003).

Activation of descending inhibitory pathways from the periaqueductal gray relays through the RVM and utilizes opioids to produce analgesia (see Fields and Basbaum, 1999). Stimulation of the PAG inhibits spinothalamic tract cells through activation of GABA_A receptors in the spinal cord (Lin et al., 1994). Supraspinal activation of mu-opioid receptors increases release of GABA in the spinal cord that is prevented by 5-HT₃ receptor antagonists (Kawamata et al., 2002). Indeed, dorsal column stimulation at high frequency (100 Hz), which would activate large diameter sensory afferents like TENS, also increases spinal release of GABA in normal animals and those with nerve injury (Linderoth et al., 1994; Stiller et al., 1996), and reduces glutamate release through activation of GABA_B receptors (Cui et al., 1997). These data suggest that analgesia mediated by supraspinal μ-opioid receptors releases serotonin in the spinal cord that in turn activates 5-HT₃ receptors on GABAergic neurons resulting in release of GABA. We suggest a similar pattern for effects of low frequency TENS: supraspinal μ-opioid receptors releases serotonin in the spinal cord that in turn activates 5-HT₃ receptors on GABAergic neurons resulting in release of GABA that subsequently decreases activity of dorsal horn neurons (Fig. 1A). We suggest that high frequency TENS activates supraspinal delta-opioid receptors that releases GABA and enkephalins in the spinal cord resulting in decreased release of glutamate and decreased activity of dorsal horn neurons (Fig. 1B). We are therefore testing the hypothesis that either high or low frequency TENS applied to the inflamed knee joint increases GABA in the spinal cord dorsal horn and activates GABA receptors spinally. The hypothesis will be tested by 1) using in vivo microdialysis of the dorsal horn to examine the time course of neurotransmitter release in response to TENS and 2) using behavioral tests to examine if blockade of GABA_A receptors spinally prevents the antihyperalgesia produced by TENS.

Fig. 1 Schematic diagram representing potential pathways involved in low (A) or high (B) frequency TENS antihyperalgesia. RVM=rostra ventral medulla; Endo=endomorphin-2; Glu=glutamate; STT=spinothalamic tract; SRT=spinoreticular path; 5-HT=serotonin.

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2. Results

2.1. GABA

Baseline concentrations for GABA in the spinal cord were 2.9 pg/ml ± 0.3 (mean ± S.E.M.). GABA concentrations increased in the dorsal horn of the spinal cord in the sample beginning after the termination of high frequency TENS but not during application of high frequency TENS. For the changes in GABA concentrations there was a significant effect for time (F_5,115 =4.6, p=0.001, repeated ANOVA) and for frequency (F_2,23=4.1, p=0.03, repeated ANOVA). The high frequency TENS group was significantly higher than the no TENS group (p=0.02; Tukey’s post hoc) (Fig. 2). However, there was no significant difference between the inflamed and the non-inflamed groups with similar increases in GABA occurring in response to high frequency TENS for both the inflamed and the non-inflamed groups. For analysis of the area under the curve, there was an overall effect for time for the period after TENS (F_5,41=4.3, p=0.03), but not during TENS with increases in concentrations of GABA in the group treated with high frequency TENS (p=0.01) when compared to the animals that did not receive TENS (Fig. 3).

Fig. 2 Time course of changes in extracellular concentrations of GABA during (10–20 min) and after (30–60 min) treatment with low frequency (middle panel), high frequency (bottom panel), or no TENS (top panel) for animals with (open circles) (more ...)

Fig. 3 Summary of the responses during and after TENS for changes in GABA and glycine. The average increase after treatment with high frequency TENS was signicantly greater than the group that did not receive TENS or the group that received low frequency TENS. (more ...)

2.2. Glycine

Baseline concentrations for glycine in the spinal cord were 46.8±2.4 pg/ml. No significant differences in glycine either during or after treatment with either high or low frequency TENS, in inflamed or non-inflamed animals (Figs. ​(Figs.33 and ​and44).

Fig. 4 Extracellular concentrations for glycine during and after high frequency (bottom panel), low frequency (middle panel) or no TENS (top panel) treatment in animals with (closed circles) and without (open symbols) inflammation. No changes in glycine were (more ...)

2.3. Primary hyperalgesia

Induction of knee joint inflammation reduced the compression withdrawal threshold of the knee on the side of inflammation 24 h later. Application of high (p=0.001) or low (p=0.004) frequency TENS, with ACSF infusion, increased the compression withdrawal threshold of the knee joint when compared to ACSF infusion with sham TENS (Fig. 5). Pretreatment with bicuculline prior to either high or low frequency TENS significantly prevented the reduction in hyperalgesia by both high and low frequency TENS (F_10,42=7.8, p=0.0001, time*group effect). Post hoc testing showed that the high frequency TENS+bicuculline group was significantly less than the high frequency TENS+ACSF group (p=0.02; Tukey’s test) and the low frequency+bicuculline group less than the low frequency+ACSF group (p=0.03, Tukey’s test). The sham TENS+ACSF group was not different with the sham TENS+bicuculline group. The percent inhibition by TENS was also significantly different between groups (F_5,26=7.1, p=0.001, one-way ANOVA) with the high frequency+bicuculline group less than the high frequency+ACSF group (p=0.01; Tukey’s test) and the low frequency+bicuculline group less than the low frequency+ACSF group (p=0.03, Tukey’s test). There was no difference between the rats treated with ACSF and sham TENS when compared to ACSF and bicuculline. There were no changes for the compression withdrawal threshold of the contralateral hindlimb after inflammation, or after TENS with ACSF or TENS with bicuculline.

Fig. 5 Graphs represent the compression withdrawal threshold for groups of rats that received high frequency TENS or low frequency TENS with ACSF (open squares) or with bicuculline (closed circles). Twenty-four hours after inflammation there was a decrease in (more ...)

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3. Discussion

3.1. GABA and high frequency TENS

The current study shows that high frequency TENS increases extracellular concentrations of GABA in the L3/L4 spinal segments, and these increases in extracellular concentration of GABA begin after removal from the stimulus. The current study also shows that blockade of GABA_A receptors in the spinal cord prevents the antihyperalgesia produced by high frequency TENS. Similarly, prior studies show increased extracellular concentrations of GABA in the spinal cord during dorsal column stimulation, at high frequency, also begins after removal of the stimulation and utilizes GABA receptors in the spinal cord to produce analgesia (Linderoth et al., 1994; Stiller et al., 1996). Dorsal column stimulation, delivered at sensory intensity and high frequency, would activate large diameter afferent fibers similar to TENS delivered at sensory intensity and high frequency (Radhakrishnan and Sluka, 2005). Thus, high frequency stimulation at intensities that activate large diameter afferents results in increases in GABA in the spinal cord dorsal horn.

The time course of changes in extracellular GABA differs from that observed in prior studies examining the release of neurotransmitters and TENS (Sluka et al., 2005,2006). For high frequency TENS, decreases in glutamate occur during TENS and return to baseline concentrations after removal of TENS (Sluka et al., 2005). Further the inhibition of extracellular glutamate by TENS only occurs in animals with joint inflammation, and not those without (Sluka et al., 2005). Since GABA increases are delayed in relation to the time of stimulation in the current study, GABA is likely not increased in direct response to the stimulation, but rather indirectly as a result of other long-lasting neurotransmitter and/or cellular mechanisms.

The current study also shows equivalent increases in extracellular GABA during high frequency TENS in animals with and without joint inflammation that begins after removal of TENS. It is thus, unlikely that the increases in GABA are responsible for the decreases in glutamate by high frequency TENS observed in a prior study (Sluka et al., 2005). Further, we show that the decreases in glutamate are prevented by prior treatment with naltrindole, a delta-opioid receptor antagonist, suggesting that endogenous opioid release mediates the decreases in glutamate (Sluka et al., 2005). We hypothesize that the increases in extracellular GABA are a parallel, spinal inhibitory system that enhances the antihyperalgesia produced by TENS. In support, early work shows that spinal transection reduces, but does not eliminate, the analgesic effects of TENS in animals without tissue injury (Woolf et al., 1980). Approximately 50% of the analgesic effect of high frequency TENS remains after spinal transection. The delayed increases in extracellular GABA in the spinal cord in response to TENS parallel the timing of TENS antihyperalgesia testing in prior studies (Sluka et al., 1998). In addition to antihyperalgesia occurring after removal of TENS, inhibition of dorsal horn neuron sensitization also continues after removal of TENS (Ma and Sluka, 2001). Thus, delayed increases in GABA follow the time course of effectiveness of high frequency TENS for reduction in hyperalgesia and thus likely represent one mechanism by which TENS reduces pain.

3.2. GABA and low frequency TENS

In the current study we show that low frequency TENS, unlike the results with high frequency TENS, had no effect on extracellular GABA concentrations in the L3/L4 dorsal horn of the spinal cord, which does not support our initial hypothesis. However, in the current study, blockade of GABA_A receptors in the spinal cord reduced the antihyperalgesia produced by low and high frequency TENS, supporting our initial hypothesis. One explanation for this discrepancy between release and behavior data for low frequency TENS could be that there was an increase in GABA extracellularly in animals with joint inflammation in other spinal segments such as the L5 or L6 segments. Alternatively, increases in GABA could occur in the superficial dorsal horn that we were unable to measure in the deep dorsal horn by microdialysis. Bicuculline, delivered by microdialysis, is expected to diffuse at least 2–4 mm in the rostrocaudal direction and dorsoventral directions. Thus, while sampling the extracellular environment is restricted to the area surrounding the microdialysis fiber, drug delivery would encompass multiple spinal sections and the superficial dorsal horn. Further the release studies were performed while the rat was anesthetized with sodium pentobarbital. The behavioral studies, on the other hand, were performed with the animal awake except for the short duration when TENS was applied under light halothane anesthesia (1–2%). Thus, the effects of blockade of GABA receptors spinally during low frequency TENS could be to reduce the binding to GABA_Areceptors in the L5/L6 spinal cord and/or superficial dorsal horn, or related to use of anesthetic during collection.

Prior studies support a role for GABA in analgesia that involves suprspinal stimulation and serotonin. Specifically, these prior data show 1) electrical stimulation of supraspinal sites (PAG) decreases dorsal horn neuron activity through activation of GABA receptors (Lin et al., 1994; Peng et al., 1996; Lin et al., 1996a), 2) the analgesia and reduction in dorsal horn neuron activity as a result of stimulation of supraspinal sites (PAG and RVM) utilizes serotonin (Lin et al., 1996b; Cui et al., 1999; Hammond et al., 1985, 1998; Sorkin et al., 1993; Bowker and Abhold, 1990), 3) activation of 5-HT3 receptors in the spinal cord increases the release of GABA in the spinal cord (Kawamata et al., 2002), and 4) low frequency TENS increases release of serotonin and activates 5-HT2 and 5-HT3 receptors in the spinal cord (Sluka et al., 2006; Radhakrishnan et al., 2003).

3.3. Neurotransmitter mechanisms of TENS

The differential changes in extracellular GABA concentrations in response to low and high frequency TENS has been shown previously for other neurotransmitters and receptors (Sluka et al., 1999; Kalra et al., 2001; Radhakrishnan et al., 2003; Sluka et al., 2005, 2006). Specifically, in the spinal cord serotonin is increased in response to low frequency TENS, but not high frequency TENS. The reduction in hyperalgesia by low frequency TENS is prevented by spinal blockade of mu-opioid, or 5-HT2 and 5-HT3 receptors, and supraspinal blockade of mu-opioid receptors. Spinal blockade of delta-opioid or serotonin receptors has no effect on the reduction in hyperalgeisa by high frequency TENS. In contrast, for high frequency TENS we previously show that there is a reduction in glutamate release in the spinal cord, and the antihyperalgesia is prevented by spinal or supraspinal blockade of delta-opioid receptors, but not mu-opioid receptors. Thus, different frequencies of stimulation produce antihyperalgesia through distinct mechanisms in the spinal dorsal horn and supraspinal pathways.

3.4. Extracellular GABA release mechanisms

The increased extracellular concentrations of GABA that occur in response to TENS could be a result of increased neuronal release, decreased reuptake, and/or increased glial release (see del Arco et al., 2003; Timmerman and Westerink, 1997). Basal concentrations of GABA likely reflect metabolic or glial release since these basal concentrations are independent of calcium mechanisms and tetrototoxin-insensitive (Timmerman and Westerink, 1997). However, increased extracellular concentrations evoked by peripherally applied electrical stimulation are less clear. Traditionally, it was thought that extracellular GABA was supplied by spillover from the synaptic cleft. However, GABAergic synapses are surrounded a large number of high and low affinity transporters in both neurons and glia. These GABA transporters tightly regulate GABA and blockade of these transporters increases extracellular GABA as measured by microdialysis (Schousboe, 2003). Further, glia can release GABA into the extracellular fluid, and increases in GABA concentrations extracellularly are likely to effect both neurons and glia though receptors located on astrocytes and extrasynaptically on neurons (Sykova, 2004). This general increase in GABA in the extracellular fluid has been hypothesized to modulate neuronal excitability and gene expression by modifying membrane potential and intracellular cascades through extrasynaptic receptors (del Arco et al., 2003).

4. Summary

In summary, increases in extracellular GABA in the L3/L4 spinal cord occur in response to high frequency TENS, but not low frequency TENS. The increases in extracellular GABA occur in both the inflamed and the non-inflamed animals. These increases in GABA are delayed in onset with respect to the time of application of TENS, and parallel the time in which antihyperalgesia occurs in response to TENS. In parallel, blockade of GABA_A in the spinal cord reduced the antihyperalgesia produced by both low and high frequency TENS. Thus, these data suggest that increased spinal release of GABA activates GABA_A receptors in the spinal cord to reduce hyperalgesia.

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5. Experimental procedures

All experiments were approved by the Animal Care and Use Committee at the University of Iowa. A total of 69 male Sprague—Dawley rats (Harlan, St. Louis, MO, 250–350 g) were used for this study.

5.1. Injection of kaolin and carrageenan into the knee joint

Male Sprague—Dawley rats were injected with a mixture of 3% kaolin and 3% carrageenan (0.1 ml in sterile saline, pH 7.2–7.4) into the knee joint while the rat was anesthetized with halothane, 2–5% (Sluka and Westlund, 1993). For release of neurotransmitters knee joints were injected bilaterally since the microdialysis fiber encompasses both dorsal horns. For the behavioral studies, one knee joint was injected.

5.2. Measurement of compression withdrawal threshold of the knee

The compression withdrawal threshold of the knee was measured as previously described (Skyba et al., 2005). Rats were acclimated to the restraining device for 5 min 3 times per day for 2 consecutive days. On the day of testing, the experimenter extended one hind limb and the knee joint was compressed using measuring device. The measuring device consists of two strain gauges attached to the inner arm of a forceps. Compression was stopped when the animal withdrew the limb forcefully or when the animal vocalized. The maximum force applied at withdrawal was recorded as the threshold in grams as an average of 3 trials for each time period. A reduction in withdrawal threshold of the knee is interpreted as primary hyperalgesia.

5.3. Application of TENS

TENS was applied to the inflamed knee(s) for 20 min while the rat was anesthetized with 1–2% halothane (Sluka et al., 1999). Electrodes were placed on the medial and lateral aspects of the joint and high frequency (100 Hz), low frequency (4 Hz), or placebo TENS was applied. All other parameters were kept constant as follows: pulse width, 100 μs; amplitude/intensity, sensory level (just below motor contraction). Previously we demonstrated that reduction of secondary mechanical or heat hyperalgesia was equivalent with high or low frequency TENS at sensory intensity (Sluka et al., 1999; King and Sluka, 2001).

The TENS units used in these studies are utilized clinically (EMPI Eclipse⁺). The waveform is a balanced asymmetrical biphasic square wave. Amplitude is adjustable from 0–60 mA; pulse width is adjustable from 30 to 250 μs; pulse rate (frequency) is adjustable from 2–125 Hz. Electrodes are 0.5″ diameter round pregelled and used clinically for TENS treatment (of small areas such as the hand/fingers). The size of electrodes used in these experiments compares to the area of tissue that would be covered by electrodes in human subjects receiving TENS to the knee joint.

5.4. Placement of microdialysis fibers

Microdialysis fibers (200 μm o.d., Hospal Filtral AN69) were covered with epoxy except for a 2 mm gap (Sluka and Westlund, 1992) and placed the day before the experiment while the rat was anesthetized with halothane (2–4%). Specifically, the T13 vertebra was cleared of muscle and small holes drilled into the lateral aspect on each side to expose a small portion of the spinal cord. Microdialysis fibers were inserted transversely across the dorsal horn of the spinal cord through the two holes and then fixed to the bone with dental cement. The free ends of the microdialysis fiber were inserted into PE20 tubing and the connection secured with epoxy. The incision was sutured closed and animals recovered for 24 h.

5.5. Analysis of glycine and GABA

Samples from microdialysis experiments were analyzed for glycine and GABA using fluorescent detection after derivitization with o-phthaldialdehyde (OPT; Sigma)(Zahn et al., 2002)⁴. All samples were stored at −70 °C until analysis. Aliquots of 20 μl of the sample were diluted with 160 μl ACSF, and 20 μl 10 ng/ml of the internal standard homoserine. Samples underwent pre-column derivitization with OPT and injection with an auto-injector. A Supelcosil LC-18 HPLC column (5 μmparticle diameter, 4.6 mm i.d., 15 cm long) and a mobile phase composed of 17% methanol and 0.05 M sodium acetate was used with a pumping rate of 1.0 ml/min. The fluorescence detector was set at 330 nm for excitation and 420 nm for emission. Standards were dispersed through the run so that there were 3 standards at the beginning of the run, one standard every 5 samples, and two standards at the end of the run. The limit of detection for glycine is 0.25 ng/ml, the limit of quantification is 0.77 pg/ml, and precision is 4%. The limit of detection for GABA is 0.01 ng/ml, the limit of quantification is 0.02 ng/ml and precision is 4%. Peak areas were first normalized to the internal standard homoserine and concentrations calculated based on normalized peak areas with external standards run simultaneously. With the current techniques glycine and GABA are well above the levels of detection for samples collected from the spinal cord.

5.6. Experimental protocol

5.6.1. Microdialysis

The day after placement of the microdialysis fiber, rats were anesthetized with sodium pentobarbital (50 mg/kg, i.p.). An intravenous line was inserted to maintain anesthesia throughout the sampling period with sodium pentobarbital (2–4 mg/kg/h, i.v.). TENS electrodes were placed on the knee joint prior to collection of samples. Artificial cerebrospinal fluid (ACSF) was infused through the microdialysis fiber at 5 μl/min. All samples were collected on ice, immediately frozen on dry ice, and stored at −70 °C until analysis. After 1 h of washout, 4, 10 min baseline samples were collected. TENS was then applied for 20 min to the knee joint and 2, 10 min samples collected during TENS treatment. TENS was then stopped and 4, 10 min samples collected.

Animals were divided into the following groups as follows: 1) Inflammation, no TENS (n=6); 2) Inflammation, high frequency TENS (n=4); 3) Inflammation, low frequency TENS (n=10); 4) Normal, no TENS (n=7); 5) Normal, high frequency TENS (n=9); 6) Normal, low frequency TENS (n=6). At the end of the experiment, rats were euthanized with an overdose of sodium pentobarbital, the spinal cord removed, fixed in 10% formalin and analyzed for microdialysis fiber placement. Fifteen animals were removed from the study due to placement in L5 or L6 spinal segments. The animals included in this manuscript had microdialysis fibers were placed in the L3/L4 spinal segments and the deep dorsal horn (laminae III—VI).

5.6.2. Behavior

Prior to placement of microdialysis fibers the compression withdrawal threshold of the knee was measured (baseline, pre-inflammation). After baseline testing one knee joint was injected with a mixture of 3% kaolin and 3% carrageenan under halothane anesthesia (4%) and the rats were returned to their cage. After 2–3 h, the rats were re-anesthetized with halothane (2–4%) and a microdialysis fiber was placed in lumbar enlargement of the spinal cord at the level of the T13 vertebra.

The next day, the compression withdrawal threshold of the knee was assessed after inflammation to ensure development of hyperalgesia (post-inflammation). Rats were then randomly divided into the following groups as follows: 1) ACSF (n=5)+high frequency TENS, 2) bicuculline+high frequency TENS (n=5), 3) ACSF+low frequency TENS (n=4), 4) bicuculline+low frequency TENS (n=4), 5) ACSF+sham TENS (n=4) and 6) bicuculline+sham TENS (n=5). Preliminary experiments in an additional four animals determined that 1 h infusion of 0.1 mM bicuculline blocked the analgesic effects of the GABA agonist muscimol, and thus we utilized 0.1 mM bicuculline to block GABA_A receptors in the spinal cord.

ACSF or 0.1 mM bicuculline was infused with the animal awake for 30 min. The rats were then lightly anesthetized with 1–2% halothane and TENS was applied to the inflamed knee joint for 20 min. ACSF or bicuculline was infused throughout the application of TENS for a total infusion time of approximately 1 h. Approximately 10–15 min after application of TENS and recovery from anesthesia the compression withdrawal threshold of the knee joint was re-assessed. Total testing time was 10–15 min. Rats were euthanized and the spinal cord was removed to confirm placement of microdialysis fibers in the lumbar enlargement.

5.7. Statistical analysis

For GABA and glycine data was converted to a percent of baseline. Data were analyzed with a repeated measures ANOVA for time and frequency of stimulation. The area under the curve for the GABA and glycine release data was analyzed for the period during the application of TENS, and for the time period after application of TENS. A one-way ANOVA compared differences between groups. Post hoc testing was done with Tukey’s test. For behavioral experiments, data was analyzed with a repeated measures ANOVA for time and for group. Post hoc testing with a Tukey’s test compared differences between groups. Behavioral data were also converted to a percent of baseline so that 100% inhibition resulted in a full reversal of hyperalgesia, 0% inhibition was no change in hyperalgesia, and >100% was analgesic. Analysis with a one-way ANOVA compared differences between groups.

Acknowledgments

Funded by the Arthritis Foundation, National Institutes of Health K0202201.

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