T
Tabes Dorsalis
Definition
A late complication of neurosyphilis. It results in gait impairment, joint deformity, pain, lack of coordination, sensory loss, as well as autonomic dysfunction and oc- ular symptoms. Pain is felt mostly in the legs and is de- scribed as lightning and lancinating. Abdominal colicky pain is also reported.
Central Nervous System Stimulation for Pain
Tachykinin
Definition
Tachykinins are a family of structurally-related pep- tides, widely scattered in vertebrate and invertebrate tissues. Mammalian tachykinins are substance P (SP), neurokinin A (NKA), and neurokinin B (NKB). All mammalian tachykinins share a common C-terminal amino acid sequence, i.e. Phe-x-Gly-Leu- MetNH, which is the minimal structural motif for the activation of tachykinin receptors (NK1, NK2 and NK3). Phar- macologically, they all cause hypotension in mammals, contraction of gut and bladder smooth muscle, and secretion of saliva.
Neuropeptide Release in the Skin
NGF, Regulation during Inflammation
Visceral Nociception and Pain
Tachyphylaxis
Nociceptor, Fatigue
Tactile Allodynia
Definition
Tactile allodynia refers to touch-evoked pain, i.e. pain due to a mechanical stimulus that does not normally pro- voke pain.
Opioids in the Spinal Cord and Modulation of Ascend- ing Pathways (N. gracilis)
Tactile Allodynia Test
Definition
The plantar aspects of intact and neuropathic legs of rats are probed with Von Frey hairs of different calibers or strengths. The number of paw withdrawals per 10 trials is counted. In general, a number of 5/10 withdrawals is observed with hairs of strength > 20 g in rats with intact legs, and in rats with mononeuropathy, a hair of 2 g can produce a score of > 5/10 withdrawals.
Thalamotomy, Pain Behavior in Animals
Tactile Stimuli
Definition
Stimuli of light touch applied to the skin.
Causalgia, Assessment
Dysesthesia, Assessment
Tail Immersion
Definition
Submersion of the tail in hot water may be used as the nociceptive stimulus in the Tail-Flick Test.
Tail-Flick Test
Tail Skin Temperature Recording
Definition
Thermocouples, thermistors or infrared sensors may be used.
Tail-Flick Test
2392 Tail-Flick Latency
Tail-Flick Latency
Definition
Tail-Flick latency is the time from the start of the noxious stimulus until the animal flicks its tail.
Tail-Flick Test
Tail-Flick Latency Correction
Definition
The tail-flick latency may be corrected for influences of tail skin temperature using a regression analysis or anal- ysis of covariance. Linearity of the data can be assumed only for a limited range of skin temperatures. In some experiments preheating of the tail to a certain tempera- ture may be used.
Tail-Flick Test
Tail Flick Test
K
JELLH
OLE, A
RNET
JØLSENUniversity of Bergen, Bergen, Norway kjell.hole@fys.uib.no, arne.tjolsen@fys.uib.no Definition
The tail–flick test is a test of nociception used in rats and mice. The noxious stimulus is usually
radiant heat on the tail or
tail immersion in hot water, and the response is a flick of the tail.
Characteristics
The tail–flick test is an extensively used test of nocicep- tion in rats and mice, and is the nociceptive test most frequently used in animals (Le Bars et al. 2001), first described in 1941 (D’Amour and Smith 1941). In the standard method, radiant heat is focused on the tail, and the time it takes until the animal flicks the tail away from the beam is measured. This
tail–flick latency is a mea- sure of the nociceptive sensitivity of the animal, and is prolonged by opioid analgesics, for instance. A spinal transection above the lumbar level does not block the tail–flick response. Thus, in this test, a spinal nocicep- tive reflex is measured, and pain is not measured directly.
Still, this is considered a very useful test of “phasic pain”, both in basic pain research and in pharmacological inves- tigations of analgesic drugs. The relevance of the test as a measure of pain has been discussed (Le Bars et al. 2001).
The test stimulus is noxious heat. In addition to the test with radiant heat (e.g. focused light from a light bulb), the stimulus may be applied by e.g. direct contact with a heated surface, such as a Peltier element, or by sub- mersion of part of the tail in hot water. The test may be
performed in lightly anaesthetized rats or mice, as well as in animals that are awake.
Several tail–flick apparatuses are commercially avail- able, and many laboratories have made their own appa- ratus. The main requirements are stable functioning and proper focus of the light beam on the tail. The tail–flick latency may be recorded by means of a photocell, which is activated when the animal flicks the tail. When a photo- cell is used, one should be aware that the reflex response may involve retracting the tail, without immediately re- moving the tail from the light beam. Thus the rats’ be- haviour should always be observed.
The tail–flick test may be a good and useful test of noci- ception, but only if it is carefully performed and possible sources of error are taken into account. One requirement, particularly in rats, is that the animals are well handled.
This may require daily handling for up to a week, includ- ing adaptation to the test apparatus. Some researchers confine the animals in a plastic tube during testing. If this is used, it is necessary that the animals are so well handled that they freely walk in and out of the tube. We find it better and faster not to use a tube, but to hold the well-adapted animal by hand.
A particular problem with tests that use thermal stimu- lation is the possible confounding influence of the skin temperature. In electrophysiological studies in animals, it has been reported that changes in the temperature or blood flow of the skin (Duggan et al. 1978) alter the re- sponse to cutaneous heat stimulation. More recently, it has been found that the tail skin temperature affects the tail–flick latency as well. This has been described using radiant heat stimulation (Ren and Han 1979; Berge et al. 1988; Roane et al. 1998; Sawamura et al. 2002) as well as with hot water immersion of the tail (Milne and Gamble 1989). For an extensive review see Le Bars et al. (2001). However, in many laboratories the tail–flick test is still performed without taking the tail skin temper- ature into account. This is probably a main confounding factor, and therefore needs special consideration in the following.
We have investigated the relationship between skin sur- face temperature and tail–flick latency in rats in a setup with a radiant heat apparatus, stimulating the distal part of the tail (10–15 mm from the tip), with a stimulated area of 15–20 mm
2(Fig. 1). Using control latencies of approximately 4s, we regularly find a clear and repro- ducible relationship between tail skin temperature and tail–flick latency, with a slope of the regression equa- tion of –0.3 – 0.4s/˚C (Tjølsen et al. 1989). With similar methodology, the same relationship has been found in mice, with a very similar slope (Eide et al. 1988).
The tail is the most important thermoregulatory organ of
the rat. The heat loss is regulated by an on–off regulation
of blood flow in the tail, which leads to rapid variations in
skin temperature (Milne and Gamble 1989, Tjølsen and
Hole 1992). The amount and duration of vasodilation is
partly determined by the relationship between the am-
T
Tail Flick Test 2393
Tail Flick Test, Figure 1 Simple test equipment for concomitant record- ing of tail skin temperatures and tail–flick latencies. A standard tail–flick apparatus can easily be modified to enable recording of tail skin temper- atures. The temperature is measured by means of a small thermocouple mounted on a plastic arm, 65 mm long, which rests on the tail with a force corresponding to approximately 1g. For a thorough description see Tjølsen et al. (1989).
bient temperature and the acclimatization temperature.
In rats at rest, the ambient temperature where vasodila- tion occurs is lower after acclimatization to cold, than after acclimatization to a warmer environment. When animals are lightly stressed and activated due to exper- imental procedures, a considerable increase in tail skin temperature is regularly observed (Tjølsen et al. 1989).
Rats restrained in tubes for a short time may show a con- siderable increase in the temperature of the tail (Tjølsen and Hole 1992), probably due to vasodilation.
The relationship between skin temperature and response latency (Fig. 2) would be expected to vary with different experimental conditions. The most reliable values for the slope are obtained in experiments where data from re- peated measures are not pooled, but analysed separately
Tail Flick Test, Figure 2 The relationship between tail–flick latency and tail skin temperature. Data were obtained from eight measurements in each of 12 rats. Tail skin temperature was controlled by means of a heating blanket. Adapted from Sawamura et al. (2002), with permission.
for each time point (Tjølsen et al. 1989). In fact, if re- peated measures on the same animals are pooled in a re- gression analysis, an error in the calculated slope may be introduced. A possible cause of error is the effect of re- peated testing on nociception itself, whether due to stress or to local effects in the skin if the same site is stimu- lated repeatedly. The time required for heating the tissue to a critical response temperature will depend on the ini- tial skin temperature, which is determined by local blood flow within the limits given by deep body and ambient temperatures. Measuring subcutaneous tissue tempera- tures during a radiant heat stimulus, we found that the rate of increase in tissue temperature was independent of initial skin temperature, and the time required to reach a hypothetical threshold temperature was strongly depen- dent on the initial temperature (Hole and Tjølsen 1993).
As a consequence, the tail–flick latency is negatively cor- related to the ambient temperature (Berge et al. 1988) and to skin temperature when the heating intensity is kept constant.
The temperature of the tail skin of rats during an ex- periment may rise as much as 8˚C in untreated animals (Tjølsen and Hole 1992). It is reasonable to consider this is the maximal possible difference in skin temper- ature due to changes in vasodilation. With a change in tail–flick latency of 0.3–0.4 s/˚C, it would imply a potential difference in tail–flick latency of up to approximately 3s. In a group of rats, not all animals would show this degree of vasodilation, and hence the mean difference in latency would be somewhat smaller.
However, this shows that increased vasoconstriction
or inhibition of vasodilation may cause differences in
2394 Tail Flick Test
tail–flick latency that easily could be misinterpreted as analgesia.
The potential for treatment–induced vasodilation to cause reduction of the tail–flick latencies is approx- imately the same size. Under circumstances when control animals are relatively vasoconstricted, vasodi- lation may lead to an increase in tail skin temperature from about ambient temperature to above 30˚C. The ef- fect of vasodilation is particularly important, as smaller changes in the tail–flick latency are required to interpret the results as hyperalgesia than as analgesia. Even a modest increase in the mean tail skin temperature of about 3.5˚C, due to lesioning of descending serotoner- gic systems, leads to a reduction of the tail–flick latency from 4–4.5s to about 3s (Hole and Tjølsen 1993). If the change in skin temperature were not taken into consideration, a reduction of the tail–flick latency of this size would have been considered an indication of a hyperalgesic state.
Many experimental treatments affect blood flow and thereby the tail skin temperature. This may by itself influence the tail–flick latency, and lead to erroneous conclusions with regard to nociception. An increase in tail skin temperature may shorten tail–flick latencies and may be interpreted as hyperalgesia (Urban and Smith 1994; Roane et al. 1998; Sawamura et al. 2002).
Even a reduction in tail skin temperature compared to untreated animals may occur, and may be interpreted as analgesia. Desipramine reduced tail skin temperature and increased tail–flick latencies at an ambient tem- perature of 24–25˚C, while no significant change was observed at 21–22˚C (Hole and Tjølsen 1993). This difference in temperature is well within the variation in ambient temperature between laboratories, and even within the range of ambient temperatures that may occur in a laboratory with insufficient control of room tem- perature. In the experiments at 24–25˚C, desipramine inhibited vasodilation so that the skin temperatures in the drug–treated group were close to the ambient temperature, while control animals showed higher skin temperatures and hence shorter response latencies.
Stress, due to a new environment, handling or injection procedures, may influence peripheral blood flow and tail temperature. In rats, stress causes motor activation, in- creased heat production, increased core temperature and an increased frequency and duration of the periods of va- sodilation and increase in skin temperature of the tail. It has been shown (Tjølsen et al. 1992) that immobiliza- tion may cause a considerable increase in core tempera- ture and tail vasodilation, while small doses of morphine (0.5–1mg/kg) completely abolish the vasodilation.
The importance of the skin temperature for the ordinary use of the tail–flick test has been discussed (Roane et al. 1998). Clearly, when high doses of potent analgesics like opioids are used, the relative influence of the skin temperature may be small. However, when the temper- ature influence is not known, this will always be an un-
predictable confounding factor. As discussed above, this has, in several instances, lead to erroneous conclusions.
Possible Remedies
The temperature of the tail skin should always be con- sidered a possible confounding factor when performing the tail–flick test. A minimal requirement should be that the tail skin temperature is measured before testing, e.g.
by means of thermocouples (Fig. 1), thermistors or in- frared sensors, and the possible influence of the temper- ature evaluated.
It is obviously necessary to take the effects of skin temperature into account when investigating factors, or using drugs that may influence autonomic activity and thermo – or cardiovascular regulation. Recording the tail skin temperature and correcting the tail–flick latency data for changes in the temperature may reduce the problem. In some cases, a regression analysis or an analysis of covariance may be performed for this pur- pose. Methods for tail–flick testing with measurement of skin temperature and for correction of tail–flick data (see
tail-flick latency correction)have been described (Tjølsen et al. 1989; Roane et al. 1998; Sawamura et al. 2002). However, there are some limitations when using this type of statistical analysis on tail–flick data.
In these statistical methods, linearity of the relationship is supposed. It seems to be a reasonable approximation to suppose linearity over a normal, limited range of skin temperatures in untreated animals, e.g. 20–30
oC.
In studies where drug administration causes a large in- crease in tail–flick latency due to changes in nociception, the assumption of linearity may not be correct. Above all, these methods for statistical evaluation cannot ad- equately handle cut-off values for tail–flick latencies.
This should be considered in each experiment, and even when limitations as above are applicable, the tempera- ture of the skin of the tail should be measured and the possible influence on the results should be evaluated.
As a number of factors may possibly influence the rela-
tionship between skin temperature and response latency,
it seems ideal to adjust data from one experiment accord-
ing to the regression slope calculated from that experi-
ment. However, this will not always be possible, in that a
regression analysis requires an adequate number of mea-
surements to allow calculation of a reliable regression
coefficient, and the spread of the independent variable
(skin temperature) must be sufficiently large. If these re-
quirements are not fulfilled, the results of the regression
analysis will be inconclusive. With an increasing number
of measurements in the analysis, there is an increasing
probability that a reliable regression coefficient may be
calculated. In many cases, it may be a problem to ob-
tain a reliable correction of tail–flick data based on the
same experiment, due to a limited number of animals
measured. An alternative method for correction of la-
tencies is to establish the relationship between skin tem-
perature and tail–flick latency in an adequate number of
T
Targeting 2395
animals under similar experimental conditions, and sub- sequently to correct tail–flick latencies according to the calculated regression factor (Ren and Han 1979). This method should be used with caution, because it must be assumed that the experiment is performed under the same conditions as when the correction factor was de- termined. This is of course an approximation.
Another alternative that has been used is local preheat- ing of the tail to a certain temperature before measuring the tail–flick latency. If the temperatures of the skin and subcutaneous tissue in the stimulated area are constant before the start of stimulation, this may abolish the con- founding effect of varying tissue temperatures. In elec- trophysiological experiments in anaesthetized cats, pre- heating has been used with a heating lamp and a feedback control system, with a thermocouple on the area of skin to be heated (Duggan et al. 1978). This procedure seemed to reduce the confounding effect of differences in blood flow. For tail–flick reflex recordings, this technique may be used in experiments in lightly anaesthetized animals for instance (Haws et al. 1990), or when the rat is placed in a restrainer and the tail is fixed (Carstens and Dou- glass 1995). It may probably be more difficult to use this method in animals that are awake when little restraint of the animal is required to minimize stress.
When performed as described here, the tail–flick test is a reliable and useful test of nociception in rodents.
References
1. Berge O-G, Garcia-Cabrera I, Hole K (1988) Response Latencies in the Tail–Flick Test Depend on Tail Skin Temperature. Neurosci Lett 86:284–288
2. Carstens E, Douglass DK (1995) Midbrain Suppression of Limb Withdrawal and Tail–Flick Reflexes in the Rat: Correlates with Descending Inhibition of Sacral Spinal Neurons. J Neurophys- iol 73:2179–2194
3. D’Amour FE, Smith DL (1941) A Method for Determining Loss of Pain Sensation. J Pharmacol Exp Ther 72:74–79
4. Duggan AW, Griersmith BT, Headley PM, Maher JB (1978) The Need to Control Skin Temperature when Using Radiant Heat in Tests of Analgesia. Exp Neurol 61:471–478
5. Eide PK, Berge O-G, Tjølsen A, Hole K (1988) Apparent Hyperalgesia in the Mouse Tail–Flick Test due to Increased Tail Skin Temperature after Lesioning of Serotonergic Pathways.
Acta Physiol Scand 134:413–420
6. Haws CM, Heinricher MM, Fields HL (1990)α-Adrenergic Re- ceptor Agonists, but not Antagonists, Alter the Tail–Flick La- tency when Microinjected into the Rostral Ventromedial Medulla of the Lightly Anesthetized Rat. Brain Res 533:192–195 7. Hole K, Tjølsen A (1993) The Tail–Flick and Formalin Tests in
Rodents: Changes in Skin Temperature as a Confounding Factor.
Pain 53:247–254
8. Le Bars D, Gozariu M, Cadden SW (2001) Animal Models of Nociception. Pharmacol Rev 53:597–652
9. Milne RJ, Gamble GD (1989) Habituation to Sham Testing Pro- cedures Modifies Tail–Flick Latencies: Effects on Nociception rather than Vasomotor Tone. Pain 39:103–107
10. Ren MF, Han JS (1979) Rat Tail–Flick Acupuncture Analgesia Model. Chin Med J 92:576–582
11. Roane DS, Bounds JK, Ang C-Y, Adloo AA (1998) Quinpirole- Induced Alterations of Tail Temperature Appear as Hyperalgesia in the Radiant Heat Tail–Flick Test. Pharmacol Biochem Be- hav 59:77–82
12. Sawamura S, Tomioka T, Hanaoka K (2002) The Importance of Tail Temperature Monitoring during Tail–Flick Test in Evalu- ating the Antinociceptive Action of Volatile Anesthetics. Acta Anaesthesiol Scand 46:451–454
13. Tjølsen A, Hole K (1992) The Effect of Morphine on Core and Skin Temperature in Rats. NeuroReport 3:512–514
14. Tjølsen A, Lund A, Berge O-G, Hole K (1989) An Improved Method for Tail–Flick Testing with Adjustment for Tail-Skin Temperature. J Neurosci Meth 26:259–265
15. Urban MO, Smith DJ (1994) Nuclei within the Rostral Ventro- medial Medulla Mediating Morphine Antinociception from the Periaqueductal Gray. Brain Res 652:9–16
Talairach Coordinates
Definition
Initially developed for a specific stereotactic frame;
based on one single brain; frequently used as a common coordinate system; X: left-right, Y: anterior-posterior, Z: superior-inferior; the reference point (0, 0, 0) is the anterior commissure (Talairach and Tournoux 1988).
Nociceptive Processing in the Secondary Somatosen- sory Cortex
Tampa Scale for Kinesiophobia
Synonyms TSK
Definition
The Tampa Scale for Kinesiophobia is a questionnaire aimed at the assessment of fear of (re)injury due to move- ment, consisting of 17 items with 4–point likert-scales.
Disability, Fear of Movement
Tapotement
Massage and Pain Relief Prospects
Targeting
Trafficking and Localization of Ion Channels
2396 Tarsal Tunnel
Tarsal Tunnel
Definition
The anatomic structures that the tibial nerve passes through at the medial ankle are termed the tarsal tun- nel. Within this tunnel, the tibial nerve divides into the medial and lateral plantar and the calcaneal nerves, each of which has its own separate tunnel as it goes from the ankle to its final destination. These tunnels represent sites of anatomic narrowing in which nerves can become entrapped, and which can give symptoms of chronic nerve compression in the foot. These can be present in the patient with a systemic neuropathy, such as that due to diabetes.
Painful Scars
Ulceration, Prevention by Nerve Decompression
Task Force on Promotion and Dissemination of Psychological Procedures
Definition
In 1993, Division 12 (Clinical Psychology) of the Amer- ican Psychological Association appointed a Task Force, with the goal of identifying and disseminating psycho- logical interventions that could be considered as empir- ically validated. In its 1995 report, this Task Force pub- lished criteria that allowed the classification of psycho- logical treatments as “well-established” and “probably efficacious” In 1999, for its special issue on empirically validated treatments in pediatric psychology, the Journal of Pediatric Psychology defined an additional category of “promising interventions” A treatment was consid- ered to be well-established if there were at least two good between-group design experiments (or well-controlled single case studies) by at least two different investigators that demonstrated the treatment’s efficacy over placebo, or at least equal efficacy as compared to an already es- tablished treatment. In addition, a treatment manual or a well defined treatment protocol needed to be available.
A treatment was considered as “probably efficacious” if there were at least two experiments showing its superior- ity to a wait-list control, or if there was at least one study (or a small series of single-case designs) that met the well-established treatment criteria. Finally, an interven- tion was considered “promising” if there was at least one well-controlled and another less well controlled study by separate investigators, or a small number of single case experiments, or at least two well-controlled studies by the same investigator.
Modeling, Social Learning in Pain
Psychological Treatment of Pain in Children
Task Force on Vicarious Instigation
Definition
Vicarious instigation describes the phenomenon that, possibly mediated by empathy, mere observation of another person’s response to a stimulus or a situation (e.g. a pain response) can induce a similar response in the observer in the absence of any direct experience with the eliciting stimulus or situation. In the context of pain, it is still a matter of debate whether observing another person in pain can induce a pain-like vicarious response in the observer or whether it elicits a more generalized emotional response in the observer.
Modeling, Social Learning in Pain
TAUT
Definition
TAUT is a plasma membrane GABA transporter, which transports taurin with higher affinity than GABA.
GABA and Glycine in Spinal Nociceptive Processing
Taut Band
Definition
A taut band is a string- or cord-like structure in striated muscle that extends the length of the muscle fibers. It consists of a number of fascicles that are most palpable across (at a right angle to) the fiber direction in the region of fiber midpoints, where the myofascial trigger point is located. The taut band is the responsive part of the muscle in a local twitch response.
Myofascial Trigger Points
Taxonomy
N
IKOLAIB
OGDUKRoyal Newcastle Hospital, Department of Clinical Research, University of Newcastle, Newcastle, NSW, Australia
nbogduk@mail.newcastle.edu.au
Synonyms
Classification; Catalogue; List of Diagnoses and their
Definitions
T
Taxonomy 2397
Definition
A
taxonomy is a catalogue that lists and classifies en- tities and provides definitions of them. It is like a dic- tionary restricted to a particular field of scholarship. It is designed to standardize the meaning and use of par- ticular terms. In relation to pain medicine, a taxonomy lists, classifies, and defines terms used to describe pain, and provides criteria for the use of diagnostic labels.
Characteristics
Two taxonomies have been produced for use in pain medicine. One, developed by the International Associa- tion for the Study of Pain (IASP), covers pain in general (Merskey and Bogduk 1994). The other, developed by the International Headache Society, relates exclusively to headache (Headache Classification Subcommittee of the International Headache Society 2004). A related taxonomy – the Diagnostic and Statistical Manual of Mental Disorders (
DSM, DSM-IV, DSM-IVR), was developed by the American Psychiatric Association and is designed to cover mental disorders, but includes some entries that potentially relate to pain (American Psychiatric Association 2000).
IASP Taxonomy
The taxonomy of the IASP (Merskey and Bogduk 1994) consists of a short, introductory section devoted to the definition of terms used to describe pain, its different forms, (such as
somatic pain,
Visceral Nociception and Pain,
referred pain, and
radicular pain), and its associated clinical features, such as
hyperalgesia,
allodynia, and
hyperpathia). The longer, more substantive section lists various entities that constitute possible diagnoses for patients with
chronic pain.
For each entity, criteria for making the
diagnosis are stipulated. The entities are catalogued and listed according to the region of the body that they affect.
Conditions that affect the whole body, or which may occur in any region of the body, are described first, followed by conditions that affect the head, the neck and cervical spine, the upper limbs, the thoracic region and thoracic spine, the abdomen and pelvis, the lumbar spine, and the lower limbs.
The IASP Taxonomy was developed because it was rec- ognized that particular terms were being used indiscrim- inately by practitioners. Different practitioners were us- ing the same term to apply to different conditions, and different terms were used to apply to the same condition.
Practitioners were also applying different diagnostic la- bels to what were essentially the same patients, or were applying labels to patients that were not appropriate. In effect, the use of terms and diagnostic labels was arbi- trary. In 1979, Bonica likened the terminology for pain syndromes in use at that time to the “tower of Babel”
(Bonica 1979).
The first edition of the Taxonomy of the IASP (Merskey 1986) listed common and rare conditions associated with
chronic pain, and provided defining descriptions of each.
It allowed each condition to be described along five axes:
The axis system, however, pertained mainly to the six- digit alphanumeric code ascribed to each condition. The conditions themselves were classified largely according to Axis I, with only parenthetical mention of pathology, aetiology and other features, if these were known.
The first edition of the Taxonomy was not intended to be, or expected to be, comprehensive or fixed. Indeed, readers were invited to submit revisions (Merskey 1986).
The second edition of the Taxonomy (Merskey and Bogduk 1994) addressed many of the shortcomings of the first edition. Some descriptions were modernized, and involved a name change, e.g.
Reflex Sympathetic Dystrophy and
causalgia became
complex regional pain syndrome Type I and Type II. Some entries were deleted (e.g. prolapsed disc, osteophyte, spondylolysis, arachnoiditis, acute low back strain, recurrent low back strain, and chronic mechanical low back pain) and were replaced by more generic or alternative entries. Some new entries were added, e.g. cervicogenic headache, xiphoidalgia, carcinoma of the lung, proctalgia fugax, piriformis syndrome, and peroneal muscular atrophy.
The greatest revision pertained to entries on spinal pain.
Some 96 new entries replaced all previous entries on neck pain, back pain, and other spinal pain. Moreover, the new entries were systematic and rigorous. They were designed to eliminate the problems of content validity and of former entries.
The new entries covered standard conditions such as spinal pain attributable to tumour, infection, metabolic disease, and arthritis. Radicular pain, due to osteophyte, disc prolapse, cysts, tumours, etc, was strictly distin- guished and segregated from spinal pain on the grounds that, although radicular pain might have a spinal aeti- ology, it was pain perceived in the limbs or trunk wall rather than in the spinal region.
Perhaps the most comprehensive change was the intro- duction of the rubric – “spinal pain of unknown origin”.
Users were invited, if not directed, to use this rubric wherever an alternative could not be legitimately, or honestly, applied. Providing this rubric encouraged physicians to avoid other poorly defined, invalid, or arbitrary rubrics, in an effort to reduce confusion and false labelling of patients.
Nevertheless, other rubrics were offered. They cov- ered emerging entities, such as discogenic pain and zygapophysial joint pain, as well as classical entities, such as ligament strain and muscle strain, and allopathic entities such as segmental dysfunction. In providing these entries, however, the Taxonomy stipulated strin- gent, essential diagnostic criteria, in order to avoid the rubrics being applied on intuitive or presumptive grounds.
Thus, for “ligament strain” the ligament had to be spec-
ified, and the diagnosis had to be proven with a test that
explicitly showed that the ligament in question was the
2398 Taxonomy, Orofacial Pain
Taxonomy, Table 1 Taxonomy
Axis I Region Referred to the anatomical region in which the pain was perceived (e.g., head, abdomen, lower limb).
Axis II System Referred to the body system that ostensibly was affected by pathology to produce pain (e.g. nervous system, vascular system, musculoskeletal system
Axis II Temporal Described whether the pain was continuous, recurring, paroxysmal, etc.
Axis IV Intensity and Duration
Stated if the pain was mild, medium or severe; and lasted less than one month, between one and six months, or longer than six months.
Axis V Aetiology Stated the nature of the cause of the pain (e.g. infectious, inflammatory, and neuropathic).
source of pain. Similar criteria were applied for “muscle strain”. For “segmental dysfunction” the essential crite- ria required clinical tests of proven reliability, and estab- lished validity to implicate the specified segment as the source of pain.
These rigorous criteria were stipulated quite deliberately in the full knowledge that the tests required to make the diagnosis did not (yet) exist. In effect, therefore, it was impossible to make the diagnosis in practice; yet it ap- peared in the Taxonomy. The purpose of this action was to indicate to proponents of specific, but ill–defined, yet perhaps popular, diagnoses, that research was required in order for the entity to satisfy the standards of a responsi- ble Taxonomy, and for the diagnosis to be reliable, valid and, therefore, respectable.
IHS Taxonomy
The taxonomy for headache catalogues the many forms of
headache according to mechanism or cause. Diag- nostic criteria are stipulated for each form of headache.
These are designed to ensure that practitioners use a par- ticular diagnostic label only in those patients who exhibit the prescribed criteria.
The taxonomy describes and defines those headaches whose mechanism is not known but which have well- defined clinical features, such as
migraine,
cluster headache, and
paroxysmal hemicrania. It contin- ues with descriptions and definitions of headaches associated with particular circumstances (such as the headaches of analgesic abuse, and rebound headache), headaches due to particular causes (such as raised or lowered pressure of cerebrospinal fluid, cerebral tu- mours, aneurysms, infections and granulomas), and headaches associated with other disorders (such as disorders of the ear, nose, and throat, or the cervical spine) (see essay
headache).
The headache taxonomy is complemented by a textbook, now in its second edition (Olesen et al. 2000), with a third edition in preparation. The textbook follows the format of the taxonomy, but provides descriptions, in detail, of the entities and their diagnosis and treatment.
References
1. American Psychiatric Association (2000) DSM-IV-TR. Diagnos- tic and Statistical Manual of Mental Disorders, 4thedn, Text Revision. American Psychiatric Association, Washington DC
2. Bonica JJ (1979) The Need for a Taxonomy. Pain 6:247–252 3. Headache Classification Subcommittee of the International
Headache Society (2004) The International Classification of Headache Disorders, 2ndedn. Cephalalgia 24 Suppl 1:1–160 4. Merskey H (ed) (1986) Classification of Chronic Pain. Descrip-
tions of Chronic Pain Syndromes and Definition of Pain Terms.
Pain Suppl 3:S1–S225
5. Merskey H, Bogduk N (1994) Classification of Pain. Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms, 2nd edn. International Association for the Study of Pain, Seattle, pp 64–65
6. Olesen J, Tfelt-Hansen P, Welch KM (2000) The Headaches, 2nd edn. Lippincott Williams & Wilkins, Philadelphia
Taxonomy, Orofacial Pain
Orofacial Pain, Taxonomy/Classification
TCAs
Tricyclic Antidepressants
TCD
Thalamocortical Dysrhythmia
Team Approach
Physical Medicine and Rehabilitation, Team-Oriented Approach
Technique of Ultrasound Application
Definition
The most common technique is the stroking technique.
Ultrasound Therapy of Pain from the Musculoskeletal
System
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Temporomandibular Joint 2399
Tegretol
Synonyms
Generic carbamazepine Definition
Tegretol (Generic Carbamazepine) is an anti-epileptic drug acting at non-voltage dependent sodium channels, which is so effective in the treatment of cranial neural- gias that lack of a (at least transient) response to this med- ication raises a significant question about the diagnosis.
Trigeminal, Glossopharyngeal, and Geniculate Neu- ralgias
Telemetric
Definition
Telemetric means the transmission of data by radio or other means from a remote source.
Opioid Therapy in Cancer Pain Management, Route of Administration
Temperament
Personality and Pain
Temporal Arteritis
Definition
Temporal arteritis is an arterial disease with inflam- mation of the temporal arteries characterized by fever, anorexia, loss of weight, leukocytosis, and tenderness over the scalp and along the temporal vessels. The giant cell arteritis most often attacks the external arteries in the anterior skull region – branches from the arteria cerebri externa.
Cancer Pain, Assessment in the Cognitively Impaired
Muscle Pain in Systemic Inflammation (Polymyalgia Rheumatica, Giant Cell Arteritis, Rheumatoid Arthri- tis)
Temporal Association
Definition
Temporal association between two disorders or clinical problems refers to their hypothesized relationship in terms of time of onset, most often inferring a causal or contributory relationship.
Depression and Pain
Temporal Resolution
Definition
The value indicates how reliable the results are in terms of the time period. The higher, the better, and EEG and MEG are much higher than fMRI and PET.
Magnetoencephalography in Assessment of Pain in Humans
Temporal Summation (Windup)
Definition
When synaptic potentials overlap in time, they add to- gether. In this case, repeated administration of the same stimulus, at a given interval of time, produces a progres- sively increased painful response. Temporal summation is probably the initial part of wind-up, which is the in- creased neuronal firing to a train of stimuli recorded in animals.
Encoding of Noxious Information in the Spinal Cord
Exogenous Muscle Pain
Opioids and Muscle Pain
Opioids, Effects of Systemic Morphine on Evoked Pain
Pain in Humans, Electrical Stimulation (Skin, Muscle and Viscera)
Temporomandibular Disorder
Synonyms TMD Definition
A collective term embracing a number of clinical prob- lems that involve the masticatory musculature, the tem- poromandibular joint and associated structures, or both.
Temporomandibular disorders have been identified as a major cause of nondental pain in the orofacial region, and are considered to be a subclassification of muscu- loskeletal disorders.
Orofacial Pain, Movement Disorders
Orofacial Pain, Taxonomy/Classification
Psychological Aspects of Pain in Women
Temporomandibular Joint
Definition
The jaw joint. The joint formed between the condylar
process of the mandible and the mandibular fossa and
articular tubercle of the temporal bone.
2400 Temporomandibular Joint and Muscle Pain Dysfunction
Nociceptors in the Orofacial Region (Temporo- mandibular Joint and Masseter Muscle)
Psychiatric Aspects of Pain and Dentistry
Temporomandibular Joint Disorders
Temporomandibular Joint and Muscle Pain Dysfunction
Temporomandibular Joint Disorders
Temporomandibular Joint Disorders
C
HRISTIANS. S
TOHLERBaltimore College of Dental Surgery, University of Maryland, Baltimore, MD, USA
cstohler@dental.umaryland.edu
Synonyms
Temporomandibular joint disorders (TMJDs); Tem- poromandibular disorders (TMDs); Craniomandibular Disorders; Previously used diagnostic labels; Tem- poromandibular Joint and Muscle Pain Dysfunction;
TMJD Definition
Temporomandibular disorders (TMJDs) comprise of a family of musculoskeletal conditions that involve deep ache or pain in the area of the temporomandibular joint(s) and/ or adjacent tissue structures. These conditions con- stitute a major source of non-dental pain in the cranio- facial complex.
Characteristics
Etiology and Pathogenesis
Although the etiology of these musculoskeletal pain disorders is not established and various pathogenetic constructs have been proposed, these conditions are believed to develop from the combined action of many genes, risk-conferring behaviors and environmental factors. The fact that pain originates in deep tissue appears to be relevant to understanding the clinical phenomenon because, unlike superficial pain, deep pain is poorly localized and frequently associated with pronounced autonomic reactions. Genetic vulnerability is attributed to differences in the genetic makeup that enhance, directly or indirectly, pro-nociceptive and/ or attenuate anti-nociceptive signalling (Fig. 1).
Earlier etiological constructs have placed significant weight on the dental occlusion as a causal factor in the etio-pathogenesis of TMJDs. However, low strengths
Temporomandibular Joint Disorders, Figure 1 Etiological construct.
of association between occlusal features and TMJDs, inconsistent findings from study to study regarding the role of a given occlusal attribute, and the absence of any gradient effect of occlusal factors put these earlier theories in question.
Case Assignment
Although research in this subject matter has been in- tensified in recent years, no biomarkers of exposure or effect are established for valid and reliable TMJD case ascertainment. TMJD case assignment occurs on the basis of clinical features, which consist of symptoms like pain and limited range of mandibular motion. Fa- cial pain reports focus on anatomical regions such as the temples, cheeks, pre-auricular area, or inside the ear and vary in intensity and spatial distribution, both inter-individually and intra-individually, with time.
With respect to corresponding clinical signs, allody- nia in the form of tenderness to palpation is linked to painful topographical sites. Limited range of motion is often noted and attributed to factors such as the ar- ticular disc preventing smooth gliding movement of the mandibular condyle along the articular eminence, constraining mandibular excursion, and/ or the recruit- ment of jaw closing muscles during their function as antagonists, limiting mandibular side-to-side excur- sions and the capacity to open the jaw fully. However, under no circumstances should observable signs be used in isolation to define a TMJD case, because of insufficient diagnostic validity due to high sensitivity and low specificity.
Classification Systems
Important in directing clinical research in the past decade
were efforts to produce a dual axes taxonomy for the ma-
jor types of TMJDs (Dworkin and LeResche 1992). Fo-
cusing on the craniofacial domain, Axis I distinguishes
three main diagnostic subsets (Fig. 2):
T
Temporomandibular Joint Disorders 2401
Temporomandibular Joint Disorders, Figure 2 Overview of the diagnostic construct adopted by the Research Diagnostic Criteria for temporomandibular disorders.
(For detail see Dworkin and LeResche 1992).
Temporomandibular Joint Disorders, Figure 3 Overlap of TMJDs with regional and systemic disorders.
1. Group I: Masticatory myofascial pain 2. Group II: TMJ internal derangements 3. Group III: TMJ arthritides
Axis II criteria assess pain intensity, pain-related disabil- ity, and the presence and severity of depressive and anx- iety symptoms. Using this classification scheme, about half of all TMJD cases are identified as Group I disorders (List and Dworkin 1996).
Due to the overlap with regional myofascial pain, tension-type headache, fibromyalgia, polyarthritides and possibly connective tissue disorders with impaired collagen makeup, shortcomings of available TMJD tax- onomies are becoming increasingly recognized (Fig. 3).
The fact that persistent TMJDs are rarely limited to a single topographical domain underscores the need to assess these conditions in the broader context.
Phenomenology
General Characteristics
Poorly localizable ache or pain unrelated to dental pathology, constitute the chief complaint of all major
forms of TMJDs. The sensory experience is captured by pain descriptors, such as “aching”, “tight”, “throb- bing” and “tender” (Turp et al. 1997). Besides pain, (a) inability to freely move the jaw due to pain and/ or soft or hard tissue interference, (b) sounds originating from the jaw joint, and (c) the disturbing perception of teeth not fitting properly constitute the other shared concerns.
With respect to clinically observable signs, pressure
allodynia, the experience of pain in response to defined
pressure that is rarely identified as painful by subjects
without TMJDs, represents the clinical hallmark fea-
ture of this family of pain conditions. Inability to move
the jaw freely is determined by measurements of the
mandibular range of motion and expressed by the clini-
cally observable maximum mandibular excursions in all
directions. Joint sounds are often linked to mechanical
events between moving articular structures, such as the
temporal component of the TMJ, the articular disc and
the condyle. With respect to age, prevalence rates are
lower among older subjects, and initial care-seeking in
both men and women is more likely to occur before age
50 than later in life.
2402 Temporomandibular Joint Disorders
Temporomandibular Joint Disorders, Figure 4 Cases (in %) reporting pain in a given dermatome. Adapted from (Turp, Kowalski, O’Leary, and Stohler, 1998).
Spatial Characteristics
Not only can temporomandibular joint (TMJ) arthridites be part of an existing polyarthritis that affects additional joints other than the TMJs, those TMJDs that involve muscle differ in the extent of their bodily involvement as well. Distinction of local and widespread phenomena is important, because cases with widespread pain are more likely in pain on follow-up examination than cases with localized pain (Raphael et al. 2000).
In contrast to TMJD, muscle pain conditions that involve the face and adjacent head or neck regions, fibromyalgia (FMS) is understood as a clinical entity characterized by persistent widespread pain and tenderness to 4 kilograms of pressure at 11 of 18 anatomically defined body sites (Wolfe et al. 1990). Overlap between TMJDs and FMS has been demonstrated in a number of studies (Plesh et al. 1996; Hedenberg- Magnusson et al. 1997; Korszun et al. 1998). According to Plesh and coworkers, 75% of their FMS patients had TMJDs, while, on the other hand, 18% of cases with TMJDs met the diagnostic criteria for FMS. Epidemiological studies also report high as- sociations between TMJDs and the two most common types of headache, tension-type headache and migraine headache (Agerberg and Carlsson 1973). In fact, per- sistent TMJD pain is associated with co-morbid pain in body parts other than the face at much greater rates than the condition is limited to the face (Fig. 4) (Turp et al.
1998).
Temporal Characteristics
Complaints of pain range from a local response to simple injury to complaints of persistent widespread bodily involvement without obvious cause. From a
phenomenological point of view, it needs to be em- phasized that the overwhelming case majority seen in the primary care setting exhibits episodic forms, while cases encountered in the tertiary care environment are more likely affected by persistent conditions. The fact that the personally most devastating and clinically most challenging TMJD presentations occur in females in greater numbers than males, results in up to 90% of tertiary care cases being women (Figure 5). Among women, prevalence rates are higher for subjects of reproductive age than those in postmenopausal years without hormone replacement therapy (LeResche et al.
1997).
TMJD pain is characterized as non-progressive and fluctuating in intensity, which is often translated into
“good” and “bad” days. What is applicable to a wide range of pain disorders seems also to be the case for TMJDs. As a generalization, infrequent pains of even high intensity are more likely perceived as a nuisance when compared to persistent pain of lesser intensity.
On the other hand, persistent pain disrupts the lifestyle,
causing functional limitations and restrictions in daily
activities. In this context, it is increasingly understood
that time in pain influences the subject’s physiological
state and response behavior. Initial pain constitutes a
warning signal, causing the subject to stop the ongoing
activity and to take actions to alleviate the pain. If pain
persists, longer lasting effects on neuronal excitability,
such as the up-regulation of NMDA-mediated effects
and changes in the CNS “hardwiring” occur via a series
of events and involve alterations in intermediate and
late gene expressions. Binding of c-fos and c-jun to
DNA alters the transcription of intermediate and even-
T
Temporomandibular Joint Disorders 2403
Temporomandibular Joint Disorders, Figure 5 Comorbid conditions and male-to-female ratios in different observational settings.
tually late effector genes, which in turn affect enzymes, growth factors, peptides, and even the phenotype.
Pain Affect
Prolonged and persistent pain can induce significant pain affect, which in itself constitutes an integral part of the TMJDs. Pain affect is captured by pain descrip- tors, such as “tiring”, “exhausting”, “frightening” and
“fearful”. Great variations are observed with respect to the degree to which pain affect is expressed from patient to patient, even within a given TMJD subset (Ohrbach and Dworkin 1998). Much of the variability in response to pain is believed to be of genetic origin.
Consequently, intense research is beginning to iden- tify the allelic variants that underlie these response differences. For example, a 3- to 4-fold reduction in the activity due to a valine-methionine polymorphism of catechol-O-methyltransferase (COMT), an enzyme that catalyzes the O-methylation of compounds with a catechol structure, results in less or greater than normal availability of catecholamines at the site of neurotrans- mission, which in turn significantly shapes the sensory and affective experience of facial pain (Zubieta et al.
2003).
Management
Because the causal sequence of events that leads to pain and dysfunction is not known, therapeutic inter- ventions focus on symptom management rather than on the elimination of the cause. Patients who seek care for the first time, report symptom relief of TMJD by 65- 95%. Treatments include thermal packs, non-steroidal anti-inflammatory drugs (NSAIDs) and/or muscle re- laxants, inter-occlusal appliances, physical therapy, relaxation and stress management, and acupuncture
and diet counselling to mention the most common interventions. There are little differences among the various types with respect to symptom relief. Those patients that do not get a satisfactory outcome, which happen to constitute a clear case minority in the primary care setting, are characterized by persistent pain and dysfunction for which all current forms of treatment fall short. Given the questionable superiority of one type of intervention over another, the choice of care is more influenced by unwanted effects attributable to the intervention, and/or the greater cost for care that does not translate into a justifiable improvement of the therapeutic efficacy. Consequently, case management tends to be “conservative” and “reversible”.
References
1. Agerberg G, Carlsson GE (1973) Functional Disorders of the Masticatory System. II. Symptoms in Relation to Impaired Mo- bility of the Mandible as Judged from Investigation by Ques- tionnaire. Acta Odontol Scand 31:337–347
2. Dworkin SF, LeResche L (1992) Research Diagnostic Criteria for Temporomandibular Disorders: Review, Criteria, Examinations and Specifications, Critique. J Craniomandib Disord 6:301–355 3. Hagberg C, Hagberg M, Kopp S (1994) Musculoskeletal Symptoms and Psychosocial Factors Among Patients with Craniomandibular Disorders. Acta Odontol Scand 52:170–177 4. Hedenberg-Magnusson B, Ernberg M, Kopp S (1997) Symptoms and Signs of Temporomandibular Disorders in Patients with Fi- bromyalgia and Local Myalgia of the Temporomandibular Sys- tem. A comparative study. Acta Odontol Scand 55:344–349 5. Korszun A, Papadopoulos E, Demitrack M, Engleberg C, Crof-
ford L (1998) The Relationship Between Temporomandibular Disorders and Stress-Associated Syndromes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 86:416–420
6. LeResche L, Saunders K, Von KM, Barlow W, Dworkin SF (1997) Use of Exogenous Hormones and Risk of Temporo- mandibular Disorder Pain. Pain 69:153–160
7. List T, Dworkin SF (1996) Comparing TMD Diagnoses and Clin- ical Findings at Swedish and US TMD Centers using Research
2404 Temporomandibular Pain
Diagnostic Criteria for Temporomandibular Disorders. J Orofac Pain 10:240–253
8. Ohrbach R, Dworkin SF (1998) Five-Year Outcomes in TMD:
Relationship of Changes in Pain to Changes in Physical and Psy- chological Variables. Pain 74:315–326
9. Plesh O, Wolfe F, Lane N (1996) The Relationship Between Fi- bromyalgia and Temporomandibular Disorders: Prevalence and Symptom Severity. J Rheumatol 23:1948–1952
10. Raphael KG, Marbach JJ, Klausner J (2000) Myofascial Face Pain. Clinical Characteristics of those with Regional vs.
Widespread Pain. J Am Dent Assoc 131:161–171
11. Turp JC, Kowalski CJ, O’Leary TJ, Stohler CS (1998) Pain Maps from Facial Pain Patients Indicate a Broad Pain Geography. J Dent Res 77:1465–1472
12. Turp JC, Kowalski CJ, Stohler CS (1997) Pain Descriptors Char- acteristic of Persistent Facial Pain. J Orofacial Pain 11:285–290 13. Wolfe F (1997) The Relation Between Tender Points and Fi- bromyalgia Symptom Variables: Evidence that Fibromyalgia is not a Discrete Disorder in the Clinic. Ann Rheum Dis 56:268–271 14. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P et al. (1990) The American College of Rheumatology 1990 Cri- teria for the Classification of Fibromyalgia. Report of the Mul- ticenter Criteria Committee [see comments]. Arthritis Rheum 33:160–172
15. Zubieta JK, Heitzeg MM, Smith YR, Bueller JA, Xu K, Xu Y, Koeppe RA, Stohler CS, Goldman D (2003) Genotype Affects Mu-Opioid Neurotransmitter Responses to a Pain Stressor. Sci- ence 299:1240–1243
Temporomandibular Pain
Definition
Chronic pain in the jaw muscles and TM joint, often as- sociated with malocclusion; also referred to as cranio- mandibular or temporo-mandibular dysfunction.
Jaw-Muscle Silent Periods (Exteroceptive Suppres- sion)
Tender Points
M
ICHAELS
PAETHFriedrich-Baur-Institute, University of Munich, Munich, Germany
spaeth.m5@t-online.de
michael.spaeth@lrz.uni-muenchen.de
Synonyms TePs
Formerly often used as synonymous: trigger points (but nowadays clearly discriminated)
Definition
If an individual reports local pain when a site is palpated with standardized pressure, this is considered a positive
“tender point” (TP).
Characteristics
AnatomyThe anatomic TP sites do not appear to represent a sin- gle type of anatomical structure, but rather can include ligaments, tendons, skeletal muscles and bursae. The TP hurts at the site where pressure is applied, only, whereas pain induced by pressure at a myofascial pain syndrome (MPS) “trigger point“ causes both local pain and pain at a more distant area of reference (“referred pain“). Several efforts have been made to find a pri- mary origin of fibromyalgia (FM) pain at the anatomic sites themselves (Bengtsson et al. 1986; Drewes et al.
1993; Henriksson et al. 1982; Yunus and Kalyan Ra- man 1989). In fact, most of these investigations studied skeletal muscle exclusively and did not report any find- ings on other anatomical structures composing the TP regions. Morphological findings in skeletal muscle tis- sue specimens from FM patients are rather non-specific and presumably secondary to pain-related reduction of activity. Results of image analysis quantification of substance P immunoreactivity in the trapezius mus- cle of patients with fibromyalgia and myofascial pain syndrome pointed to a peripheral hyperactivity of the peptidergic nervous system in FM as well as in MPS (De Stefano et al. 2000). Recently reported ultrastructural changes in fibromyalgic muscle fibers may contribute to the induction and / or chronicity of nociceptive trans- mission from muscle to the central nervous system (Sprott et al. 2004). But, these alterations could not be identified as a primary cause of hyperalgesia in FM TP areas.
Clinical Characteristics
Application of pressure on each of the TPs often induces patient’s involuntary withdrawal. After the examination of all 18 TPs, patients may report a persisting “deep ache“, similar to that of bone pain. Some patients may show the symptoms with either one half (upper or lower) or one side (right or left) of the body preponderating.
For standardization and for research purposes, pressure gauges are available. A dolorimeter is commonly used and can further help to standardize the amount of pres- sure (e.g. 4 kg) applied by the examining finger of each investigator.
Recent Objections
Despite the lack of information on what TPs really do measure, research over the last few years has brought up some interesting findings about these points. There is evidence from different studies, that FM patients are tenderer in both TP and non-TP regions than healthy con- trol subjects and that these TP regions represent areas, where anyone is tenderer. TPs were revealed not to be specific to FM (Granges and Littlejohn 1993b; Tunks et al. 1995).
TPs were studied in a random sample from adults in the
general population. As a result, tenderness to pressure
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Tendon Sheath Inflammation 2405
was found to occur both in people without widespread pain and in people without any pain. The investigators found that TP counts were increased in people who had other symptoms (i.e. poor sleep and / or fatigue), even if they did not complain about pain at all (MacFarlane et al.
1996). Data suggest that TP counts can discriminate be- tween tender and non-tender individuals and can there- fore be considered as a clinically useful measure of ten- derness (Gracely et al. 2003). From another study, it was concluded that the tender point count was associated not only with the extent of rheumatic pain, but also indepen- dently with the extent of bodily complaints (Schochat and Raspe 2003). Significant correlations were found between TP count and psychological distress, evaluated by analyzing somatic and depressive symptoms (Croft et al. 1994). Another study found that TP pain severity ratings produced higher correlations with symptoms of FM and predicted distress better than TP counts (Mc- Carberg et al. 2003).
Since the TP count seems to be a composite measure of at least tenderness and psychological distress, it is of limited value in research settings but useful in a clinical setting in order to recognize the tenderness-distress na- ture of FM (Gracely et al. 2003). Furthermore, the TP count does not reflect differences in distress or pressure- pain sensitivity or provide help in subgrouping FM pa- tients (Giesecke et al. 2003). Another study replicated previous findings in population-based samples showing that dolorimeter determinations are less influenced by psychological factors than TP counts (Croft et al. 1994;
Granges and Littlejohn 1993a), but there was still an im- pact of distress even on dolorimetry results (Petzke et al.
2003).
Most of these data-based objections were followed by recommendations: (1) to re-consider the current defi- nition of FM, (2) to be aware of the tenderness-distress nature of both FM and TPs and (3) to re-evaluate chronic widespread pain (CWP) in further population-based studies both to potentially discriminate between CWP and FM and to emphasize FM characteristics.
Muscle Pain, Fibromyalgia Syndrome (Primary, Sec- ondary)
References
1. Bengtsson A, Henriksson KG, Larsson J (1986) Muscle biopsy in primary fibromyalgia. Light-microscopical and histochemical findings. Scand J Rheumatol 15:1–6
2. Croft P, Schollum J, Silman A (1994) Population study of tender point counts and pain as evidence of fibromyalgia. Bmj 309:696–699
3. De Stefano R, Selvi E, Villanova M et al. (2000) Image analysis quantification of substance P immunoreactivity in the trapezius muscle of patients with fibromyalgia and myofascial pain syn- drome. J Rheumatol 27:2906–2910
4. Drewes AM, Andreasen A, Schroder HD et al. (1993) Pathology of skeletal muscle in fibromyalgia: a histo-immuno-chemical and ultrastructural study. Br J Rheumatol 32:479–483
5. Giesecke T, Williams DA, Harris RE et al. (2003) Subgrouping of fibromyalgia patients on the basis of pressure-pain thresholds and psychological factors. Arthritis Rheum 48:2916–2922
6. Gracely RH, Grant MA, Giesecke T (2003) Evoked pain mea- sures in fibromyalgia. Best Pract Res Clin Rheumatol 17:593–609 7. Granges G, Littlejohn G (1993a) Pressure pain threshold in pain- free subjects, in patients with chronic regional pain syndromes, and in patients with fibromyalgia syndrome. Arthritis Rheum 36:642–646
8. Granges G, Littlejohn GO (1993b) A comparative study of clin- ical signs in fibromyalgia / fibrositis syndrome, healthy and ex- ercising subjects. J Rheumatol 20:344–351
9. Henriksson KG, Bengtsson A, Larsson J et al. (1982) Muscle biopsy findings of possible diagnostic importance in primary fi- bromyalgia (fibrositis, myofascial syndrome). Lancet 2:1395 10. MacFarlane GJ, Croft PR, Schollum J et al. (1996) Widespread
pain: is an improved classification possible? J Rheumatol 23:1628–1632
11. McCarberg B, Barkin RL, Wright JA et al. (2003) Tender points as predictors of distress and the pharmacologic management of fibromyalgia syndrome. Am J Ther 10:176–192
12. Petzke F, Gracely RH, Park KM et al. (2003) What do tender points measure? Influence of distress on 4 measures of tenderness.
J Rheumatol 30:567–574
13. Schochat T, Raspe H (2003) Elements of fibromyalgia in an open population. Rheumatology (Oxford) 42:829–835
14. Sprott H, Salemi S, Gay RE et al. (2004) Increased DNA fragmen- tation and ultrastructural changes in fibromyalgic muscle fibres.
Ann Rheum Dis 63:245–251
15. Tunks E, McCain GA, Hart LE et al. (1995) The reliability of ex- amination for tenderness in patients with myofascial pain, chronic fibromyalgia and controls. J Rheumatol 22:944–952
16. Yunus MB, Kalyan Raman UP (1989) Muscle biopsy findings in primary fibromyalgia and other forms of nonarticular rheuma- tism. Rheum Dis Clin North Am 15:115–134
Tenderness
Definition
Tenderness describes a feeling of discomfort or pain caused by pressure that would normally be insufficient to cause such sensations.
Headache, Episodic Tension Type
Tendinitis
Definition
Tendinitus is a painful tendon, usually resulting from un- accustomed physical activity. Classified as a localized STP. Fraying and thickening of the tendon may be ob- served.
Ergonomics Essay
Muscle Pain, Fibromyalgia Syndrome (Primary, Sec- ondary)
Tendon Sheath Inflammation
Definition
Tendon sheaths have synovial lining cells, which are in-
cluded in the inflammation in rheumatoid arthritis.
2406 Tenosynovitis
Muscle Pain in Systemic Inflammation (Polymyalgia Rheumatica, Giant Cell Arteritis, Rheumatoid Arthri- tis)
Tenosynovitis
Definition
Tenosynovitis refers to inflammation of the tendon sheaths, through which the tendons slide when the muscle length changes. Excessive fluid accumulation can cause swelling and pain in the affected areas.
Ergonomics Essay
TENS
Transcutaneous Electrical Nerve Stimulation
TENS, Mechanisms of Action
K
ATHLEENA. S
LUKAPhysical Therapy and Rehabilitation Science Graduate Program, University of Iowa, Iowa City, IA, USA kathleen-sluka@uiowa.edu
Synonyms
PES; electrical stimulation analgesia; transcutaneous electrical nerve stimulation
Definition
Electrical stimulation applied to the skin for pain relief.
Characteristics
The mechanisms of action of
TENS primarily involve central mechanisms and have been extensively reviewed (see Sluka and Walsh 2003 for more details and refer- ences). There are generally two types of TENS applied clinically, low frequency (<10 Hz) and high frequency (>50 Hz). These can be applied at either a sensory inten- sity that produces a tapping or tingling sensation or at motor intensity that produces an additional motor con- traction. The mechanisms of action for TENS appear to be frequency, not intensity, dependent.
High Frequency (50–100 Hz) TENS
Effects on Behavior and Dorsal Horn Neurons Early studies utilizing acute pain tests show that high frequency, motor intensity TENS increases the tail flick latency to heat (i.e. analgesia) and decreases the flexion reflex response to noxious stimuli (reviewed in Sluka and Walsh 2003). Recording from spinothalamic tract cells, stimulation at an intensity activating A β fibers (3 × the threshold) has no effect on the spontaneous firing
rate. However, increasing the intensity so as to also ac- tivate Aδ nociceptors reduces spontaneous activity and responses to noxious heat or pinch (Lee et al. 1985). Sim- ilarly, studies by Garrison and Foreman (1997) and by Sjolund (1985) both show that increasing intensity in- creases inhibition of dorsal horn neurons and the flexion reflex response to noxious stimuli. These data suggest that high and low frequency TENS are effective and that increasing intensity increases inhibition.
Utilizing an animal model of joint inflammation re- veals that high frequency, sensory intensity TENS has long-lasting effects on both primary and secondary heat and mechanical
hyperalgesia (reviewed in Sluka and Walsh 2003) (Fig. 1). In fact, these studies show that high frequency, sensory intensity partially reverses the primary hyperalgesia and completely reverses the secondary hyperalgesia associated with
carrageenan inflammation for 24 h. Importantly, modulation of frequency (4 Hz vs. 100 Hz), intensity (sensory vs.
motor) or pulse duration (100 μs vs. 250 μs) shows a frequency, but not intensity or pulse duration, de- pendent effect on primary hyperalgesia to mechanical and heat stimuli in animals with carrageenan paw in- flammation. The increased responsiveness of dorsal horn neurons to innocuous and noxious mechanical stimuli that occurs after inflammation is completely reduced following high frequency, sensory intensity TENS treatment applied to the inflamed paw (Ma and Sluka 2001). Utilizing a
model of neuropathic pain, Somers and Clemente (1998) demonstrated that high frequency, sensory intensity TENS stimulation over the paraspinal musculature reduced the heat but not the mechanical hyperalgesia that normally occurs in this model. This inhibition of heat hyperalgesia only occurs if TENS was started the first day after injury but not if it was started 3 days after injury.
Pharmacology
In animals that were spinalized to remove descending inhibitory pathways (Fig. 2), inhibition of the tail flick by high frequency, motor intensity TENS still occurs but is reduced by about 50% (Woolf et al. 1980). Thus, these studies suggest both spinal and
descending inhibition are involved in the analgesia produced by high frequency, motor intensity TENS. Later studies prevented the antihyperalgesia, by blockade of δ-opioid receptors in the rostral ventral medial medulla (RVM), further supporting a role for descending inhibitory systems in the inhibition produced by TENS.
Pharmacologically, opioid peptides mediate the ef-
fects of high frequency TENS. Concentrations of
beta-endorphins increase in the bloodstream and cere-
brospinal fluid and methionine-enkephalin increases in
the cerebrospinal fluid of human subjects, following ad-
ministration of high frequency, sensory intensity TENS
(reviewed in Sluka and Walsh 2003). High frequency,
motor intensity TENS is blocked by systemic block-
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TENS, Mechanisms of Action 2407
TENS, Mechanisms of Action, Figure 1 Effects of TENS on primary and secondary, mechanical and heat hyperalgesia induced by carrageenan inflammation. High, but not low, frequency TENS partially reverses primary hyperalgesia to heat and mechanical stimuli induced by carrageenan paw inflammation (left panels). In contrast, both high and low frequency TENS reverse secondary hyperalgesia induced by carrageenan knee joint inflammation (right panels).
TENS, Mechanisms of Action, Figure 2 Schematic drawing demonstrating that TENS applied to the periphery at the site of injury activates primary afferent fibers.
This information is transmitted to the spinal cord and results in inhibition both locally and from descending inhibitory pathways. Descending inhibition from the rostral ventral medial medulla (RVM) involves 5-HT and opioids and can be activated by the periaqueductal gray (PAG).
Previous studies show that opioid receptors in the spinal cord and RVM and serotoninergic and muscarinic receptors in the spinal cord mediate the reduction in hyperalgesia by TENS.
