W
Waddell Signs
Non-Organic Symptoms and Signs
Wage Replacement
Definition
The wage replacement benefit is the ratio of the expected disability benefit to the preinjury wage.
Pain in the Workplace, Risk Factors for Chronicity, Workplace Factors
Walking Epidural
Definition
Walking epidural is a term used to describe an epidural technique whereby a woman in labor has analgesia but is also able to ambulate. The medication used to confer epidural analgesia typically causes lower extremity mo- tor weakness. With the “walking epidural” technique, a small concentration of local anesthetic with an opioid
Wallerian Degeneration, Figure 1 Intact (a) and injured (b) PNS. (a) Intact axons are surrounded by myelin forming Schwann cells, and fibroblasts are scattered between nerve fibers. (b) Axotomy is followed by rapid-WD throughout distal to and remote from the lesion site. Amongst others, axons degenerate, Schwann cells reject their myelin, macrophages are recruited, and macrophages and Schwann cells are activated to phagocytose myelin. In complete PNS injury all axons undergo rapid-WD. In partial PNS injury, lesioned axons and non-neuronal cells participating in rapid-WD are situated next to intact axons and their associated non-neuronal cells and receptors (envisage axons a and b next to each other).
is used to achieve analgesia while maintaining lower extremity motor function. There is no scientific evi- dence demonstrating a benefit with respect to obstetric outcome, but women are more satisfied when they can move their legs during labor.
Analgesia During Labor and Delivery
Wallerian Degeneration
S
HLOMOR
OTSHENKERDepartment of Anatomy & Cell Biology, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel
rotsh@md.huji.ac.il
Definition
Wallerian degeneration (WD) defines the array of
cellular events that follow injury to peripheral nervous
system (PNS)
axons (Waller 1850). They take place
throughout the nerve segment situated distal to a lesion
site: anterograde degeneration. Notably, the term WD is
sometimes used in reference to injury to central nervous
system (CNS) axons, although cell types and cellular
events differ substantially.
2660 Wallerian Degeneration
Characteristics
In intact PNS (Fig. 1a),
Schwann cells surround ax- ons and form myelin sheaths around the larger diameter sensory and motor axons. In between intact nerve fibers,
fibroblasts and a few mast cells and macrophages are scattered. Endothelial cells are present within walls of capillaries that nourish the PNS tissue. In WD (Fig. 1b), amongst others, axons disintegrate, Schwann cells reject the myelin portion of their membrane and proliferate, fibroblasts proliferate, and as of the third day after injury numerous monocytes/macrophages are recruited from the circulation. Activated macrophages and Schwann cells complete the removal of degenerated myelin by phagocytosis within 8 to 12 days, which is signifi- cant to successful regeneration since myelin contains molecules that inhibit axonal growth. The simplistic view that WD emanates from the loss of metabolic sup- port of axons due to disconnection from their cell bodies, is at most partial since in mutant C57/BL/Wld mice axon/myelin degeneration,
monocyte/macrophage recruitment and myelin removal are delayed for many days after the injury. Thus, C57/BL/Wld mice display abnormal slow progression of WD (slow-WD) com- pared to the normal rapid progression of WD displayed, for example, by normal strain C57/BL mice described above (Brown et al. 1991, Reichert et al. 1994). Normal WD will be referred to as WD or rapid-WD.
Wallerian Degeneration, Figure 2 The cytokine-network of WD. The cel- lular elements depicted are a resident Schwann cell surrounding an axon, a resident fibroblast and a recruited monocyte/macrophage. Solid lines represent induction/up-regulation and dotted lines represent production down-regulation of cytokine proteins. Axotomy induces the production of TNFα and IL-1 α in resident Schwann cells first. Sequentially thereafter follow IL-6 and GM-CSF production in resident fibroblasts and IL-1β pro- duction in resident Schwann cells. Monocytes/macrophages, which are recruited as of the third day after injury, produce the inflammatory cy- tokines TNFα, IL-1 α, IL-1 β and IL-6, and the anti-inflammatory cytokine IL-10. IL-10 down-regulates the production of all inflammatory cytokines and itself in all non-neuronal cells. Not shown are low functionally in- significant levels of IL-10 produced by fibroblasts, and the ability IL-6 to down-regulate TNFα production. After Shamash et al. 2002.
WD can be viewed as the inflammatory response of the PNS to injury. The production of cytokines, the mediator molecules of inflammation, and the involve- ment of monocytes/macrophages, which are inflamma- tory/immune cells, indicate this. Detailed examinations of cytokine-mRNA expression and cytokine-protein synthesis and secretion in C57/BL mice, which dis- play rapid-WD, indicate that cytokine production is orchestrated in time and magnitude, thereby forming the cytokine-network of WD (Fig. 2) (Rotshenker et al. 1992; Reichert et al. 1996; Saada et al. 1996; Be’eri et al. 1998; Shamash et al. 2002; Mirski et al. 2003).
The producing of non-neuronal cell types, their spa- tial distribution in the PNS tissue, and the timing of monocyte/macrophage recruitment determine timing and magnitude. Schwann cells are the first to respond rapidly to axotomy, by producing the inflammatory cy- tokines
TNF Alpha(α) followed by IL-1α. The rapid response of Schwann cells is possible since: (1) they form intimate contact with axons and are thus the first among the non-neuronal cells to ”sense” axonal injury, (2) they normally express TNFα and IL-1α mRNAs, and (3) they normally contain low levels of TNFα protein.
Fibroblasts follow by producing IL-6 and GM-CSF within 2 and 4-hours after injury, respectively. IL-6 and GM-CSF production can be induced by diffusible TNFα and IL-1α synthesized and secreted by Schwann cells. IL-1β, whose onset of production by Schwann cells is delayed by 5 to 10-hours after injury, can further contribute to IL-6 and GM-CSF production. Schwann cell-derived TNFα,IL-1αandIL-1βcontributetomono- cyte/macrophage recruitment directly and indirectly by inducing monocyte chemoattractant protein-1 (MCP-1) production in Schwann cells, fibroblasts and mast cells (Subang and Richardson 2001). These cytokines further induce recruited monocytes/macrophages to synthe- size mostly IL-6, but also TNFα, IL-1α and IL-1β.
TNFα, IL-1α and IL-1β further induce the production
of anti-inflammatory cytokine IL-10 in fibroblasts and
recruited monocytes/macrophages. Indeed, the onset
of IL-10 production by fibroblasts is rapid, but levels
of production are low and insignificant. High levels of
IL-10 are produced by, and therefore concomitant with,
monocyte/macrophage recruitment from the fourth
day of WD. IL-10 then down-regulates the produc-
tion of the inflammatory cytokines and itself, thereby
down-regulating the inflammatory aspects of WD. Re-
markably, all cytokines augment myelin phagocytosis
by macrophages. The inflammatory nature of WD and
the role of cytokines are supported by observations of
deficient cytokine production in slow-WD in mutant
C57/BL/Wld mice. Notably, TNF α and IL-1α pro-
tein production fails in injured PNS of C57/BL/Wld
mice, although their mRNAs are expressed, which
suggests differential regulation between mRNA ex-
pression and protein synthesis. It is likely, therefore,
that TNF α and IL-1α play a critical role in setting the
W
Wallerian Degeneration 2661
normal cytokine-network and rapid-WD in-motion, and the failure of their production results in an abnormal deficient cytokine-network and slow-WD.
Neurotrophic factors are an additional class of molecules whose expression is altered after PNS injury (e. g. reviewed in (Terenghi 1999)). For ex- ample,
nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT-4), glial-derived neurotrophic factor (GDNF), and leukemia inhibitory factor (LIF) expressions are up-regulated in WD. In contrast, ciliary neurotrophic factor (CNTF) and NT-3 expressions are down-regulated in WD.
Cytokines and neurotrophic factors are closely asso- ciated. For example, NGF production up-regulation is integrated into the cytokine-network of WD. NGF mRNA expression and protein synthesis is efficient in rapid-WD but deficient in slow-WD (Brown et al.
1991). This discrepancy can be partially explained by:
(1) efficient versus deficient TNFα, IL-1α and IL-1β production in rapid- and slow-WD, respectively (see above), and (2) the induction of NGF production in fibroblasts by these cytokines (Hattori et al. 1994). Fur- thermore, some molecules display both neurotrophic factor and cytokine properties; for example, IL-6, LIF and CNTF (Patterson 1994, Stahl and Yancopoulos 1994).
Delayed and reduced neuropathic pain in C57/BL/Wld mice that display slow-WD (Myers et al. 1996), and the ability to provoke neuropathic pain by inducing in- flammation without axonal injury (Safieh-Garabedian et al. 1995, Woolf et al. 1997, Eliav et al. 2001), suggest that the molecular events associated with WD play a major role in the development of neuropathic pain (e. g. IL-1β, TNFα, and NGF). There are several po- tential sites of action for molecules produced in WD.
First, secreted/diffusible molecules may act upon the producing and neighboring non-neuronal cells in an autocrine/paracrine fashion. For example, TNFα and IL-1α secreted from Schwann cells may induce pro- ductions, amongst others, of IL-6, GM-CSF, MCP-1 and NGF in nearby fibroblasts. Second, in instances of partial PNS injury, some axons are cut but others remain intact (Fig. 1; envisage axons a and b next to each other). Molecules (e. g. TNFα and NGF) secreted from the non-neuronal cells that participate in WD may affect neighboring intact axons, myelinated and non-myelinated, their surrounding Schwann cells and sensory receptors/endings to alter electrical properties and thresholds, mechanisms suggested to be instrumen- tal in the pathophysiology of neuropathic pain (e. g.
Wu et al. 2002). Third, at the neuroma site, the region immediately proximal to the injury site (<1 mm in length), non-neuronal cells may produce cytokines and neurotrophic factors (e. g. documented for IL-1 α, IL-6, IL-10, and NGF), which, in turn, may affect properties of lesioned axons and surrounding non-neuronal cells (Zimmermann 2001). Fourth, secreted molecules (e. g.
NGF, BDNF, NT-3/4, CNTF and LIF, Curtis et al. 1998) can be taken up by lesioned axons, and reach sensory and motor nerve cell bodies by retrograde axonal trans- port, where they may affect cell survival and phenotype.
It is unclear to what extent this mechanism replaces target-derived retrograde transport of neurotrophic factors occurring under normal conditions.
Cytokines, Upregulation in Inflammation Neuro- pathic Pain Model, Chronic Constriction Injury
Dorsal Root Ganglionectomy and Dorsal Rhizotomy
Neuropathic Pain Model, Diabetic Neuropathy Model
Painless Neuropathies
Viral Neuropathies
References
1. Be’eri H, Reichert F, Saada A, Rotshenker S (1998) The Cytokine Network of Wallerian Degeneration: IL-10 and GM-CSF. Eur J Neurosci 10:2707–2713
2. Brown MC, Perry VH, Lunn ER, Gordon S, Heumann R (1991) Macrophage Dependence of Peripheral Sensory Nerve Regen- eration: Possible Involvement of Nerve Growth Factor. Neuron 6:359–370
3. Curtis R, Tonra JR, Stark JL, Adryan KM, Park JS, Cliffer KD, Lindsay RM, DiStefano PS (1998) Neuronal Injury Increases Retrograde Axonal Transport of the Neurotrophins to Spinal Sen- sory Neurons and Motor Neurons via Multiple Receptor Mech- anisms. Mol Cell Neurosci 12:105–118
4. Eliav E, Benoliel R, Tal M (2001) Inflammation with No Axonal Damage of the Rat Saphenous Nerve Trunk Induces Ectopic Dis- charge and Mechanosensitivity in Myelinated Axons. Neurosci Lett 311:49–52
5. Hattori A, Iwasaki S, Murase K, Tsujimoto M, Sato M, Hayashi K, Kohno M (1994) Tumor Necrosis Factor is Markedly Syner- gistic with Interleukin 1 and Interferon-Gamma in Stimulating the Production of Nerve Growth Factor in Fibroblasts. FEBS Lett 340:177–180
6. Mirski R, Reichert F, Klar A, Rotshenker S (2003) Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) Activity is Regulated by a GM-CSF Binding Molecule in Wallerian Degen- eration Following Injury to Peripheral Nerve Axons. Journal of Neuroimmunology 140:88–96
7. Myers RR, Heckman HM, Rodriguez M (1996) Reduced Hy- peralgesia in Nerve-Injured WLD Mice: Relationship to Nerve Fiber Phagocytosis, Axonal Degeneration, and Regeneration in Normal Mice. Exp Neurol 141:94–101
8. Patterson PH (1994) Leukemia Inhibitory Factor, a Cytokine at the Interface Between Neurobiology and Immunology. Proc Natl Acad Sci USA 91:7833–7835
9. Reichert F, Levitzky R, Rotshenker S (1996) Interleukin 6 in Intact and Injured Mouse Peripheral Nerves. Eur J Neurosci 8:530–535
10. Reichert F, Saada A, Rotshenker S (1994) Peripheral Nerve In- jury Induces Schwann Cells to Express Two Macrophage Pheno- types: Phagocytosis and the Galactose-Specific Lectin MAC-2.
J Neurosci 14:3231–3245
11. Rotshenker S, Aamar S, Barak V (1992) Interleukin-1 Activity in Lesioned Peripheral Nerve. J Neuroimmunol 39:75–80 12. Saada A, Reichert F, Rotshenker S (1996) Granulocyte
Macrophage Colony Stimulating Factor Produced in Lesioned Peripheral Nerves Induces the Up-Regulation of Cell Surface Expression of MAC-2 by Macrophages and Schwann Cells. J Cell Biol 133:159–167
13. Safieh-Garabedian B, Poole S, Allchorne A, Winter J, Woolf CJ (1995) Contribution of Interleukin-1 Beta to the Inflammation- Induced Increase in Nerve Growth Factor Levels and Inflamma- tory Hyperalgesia. Br J Pharmacol 115:1265–1275
14. Shamash S, Reichert F, Rotshenker S (2002) The Cytokine Network of Wallerian Degeneration: Tumor Necrosis Factor-
2662 Warm Allodynia
alpha, Interleukin-1alpha, and Interleukin-1beta. J Neurosci 22:3052–3060
15. Stahl N, Yancopoulos GD (1994) The Tripartite CNTF Receptor Complex: Activation and Signaling Involves Components Shared with Other Cytokines. J Neurobiol 25: 1454–1466
16. Subang MC, Richardson PM (2001) Influence of Injury and Cy- tokines on Synthesis of Monocyte Chemoattractant Protein-1 mRNA in Peripheral Nervous Tissue. Eur J Neurosci 13:521–528 17. Terenghi G (1999) Peripheral Nerve Regeneration and Neu-
rotrophic Factors. J Anat 194 (Pt 1):1–14
18. Waller A (1850) Experiments on the Section of the Glossopha- ryngeal and Hypoglossal Nerves of the Frog, Observations of the Alterations Produced Thereby in the Structure of their Primitive Fibers. Phil Transact Royal Soc London 140:423–429 19. Woolf CJ, Allchorne A, Safieh-Garabedian B, Poole S (1997)
Cytokines, Nerve Growth Factor and Inflammatory Hyperalge- sia: The Contribution of Tumour Necrosis Factor Alpha. Br J Pharmacol 121:417–424
20. Wu G, Ringkamp M, Murinson BB, Pogatzki EM, Hartke TV, Weerahandi HM, Campbell JN, Griffin JW, Meyer RA (2002) Degeneration of Myelinated Efferent Fibers Induces Spon- taneous Activity in Uninjured C-Fiber Afferents. J Neurosci 22:7746–7753
21. Zimmermann M (2001) Pathobiology of Neuropathic Pain. Eur J Pharmacol 429:23–37
Warm Allodynia
Definition
Allodynia evoked by a warm stimulus.
Neuropathic Pain Model, Tail Nerve Transection Model
WDR Neurons
Wide Dynamic Range Neuron
Wegener’s Granulomatosis (WG)
Definition
A rare systemic necrotizing vasculitis associated with antineutrophile cytoplasm antibodies (c-ANCA) lead- ing to affections of the lung and kidney.
Headache Due to Arteritis
Weighted Scores Technique
Definition
The weighted scores technique identifies four distinct categories (0 = injected paw is not favored, 1 = injected paw has little or no weight on it, 2 = injected paw is el- evated and not in contact with any surface, 3 = injected paw is licked, bitten or shaken). A weighted pain score (which ranges from 0 to 3) is calculated by multiplying the time spent in each category by the category weight,
summing these products and dividing by the total time in a given time interval.
Formalin Test
Weight-Lifter’s Headache
Primary Exertional Headache
Well Behaviours
Definition
Behaviors that are pain-incompatible and related to health.
Operant Treatment of Chronic Pain
Wernicke-Korsakoff Syndrome
Definition
This consists of two distinct syndromes caused by the same pathology. Wernicke syndrome describes opthal- moparesis, ataxia and global confusion. Korsakoff syn- drome affects cognitive function, and is dominated by both anterograde and retrograde amnesia often associ- ated with confabulation and impaired insight.
Metabolic and Nutritional Neuropathies
West Haven-Yale Multidimensional Pain Inventory
Synonyms WHYMPI Definition
The West Haven-Yale Multidimensional Pain Inventory (WHYMPI) is a multidimensional self-report instru- ment that consists of 52 questions, and is designed to measure psychosocial and behavioral aspects of chronic pain across a variety of clinical populations.
Pain Inventories
WGA-HRP
Definition
Wheat germ agglutinine coupled with horseradish per-
oxidase. This protein is extracted from wheat and cou-
pled to an enzyme that has a high affinity for the soma
and axon of a neuron. It migrates in both retrograde (an-
tidromic) and anterograde (orthodromic) directions. It
W
Whiplash 2663
labels somata of afferent projections and, less effectively than PHA-L, efferent axonal projections.
Parabrachial Hypothalamic and Amydaloid Projec- tions
Whiplash
M
ICHELEC
URATOLO1, N
IKOLAIB
OGDUK2 1Department of Anesthesiology, Division of Pain Therapy, University Hospital of Bern Inselspital, Bern, Switzerland
2
Department of Clinical Research, Royal Newcastle Hospital, Newcastle, NSW, Australia
michele.curatolo@insel.ch
Synonyms
Whiplash syndrome; acceleration-deceleration injury;
Whiplash-Associated Disorders
Definition
The term
whiplash, is used to describe both an event and an injury. The whiplash event is the movement ex- perienced by the head and neck during a motor vehicle accident in which no force is directly exerted onto the head. The whiplash injury is the injury that may occur to the neck as a result of this movement. The symptoms that arise from either the event or the injury are described as a whiplash-associated disorder (WAD).
Characteristics
AetiologyClassically, whiplash occurs during a rear-end collision.
However, only about 45 % of cases of WAD arise from rear-end collisions. The remainder occur in front-end, side-impact, and combined collisions (Bogduk 2000).
Clinical Features
Not all patients involved in a whiplash event suffer, or seek treatment for, symptoms. In those that do, the symptoms typically arise within 24 hours of the event.
Patients who do develop symptoms in this period are three times more likely to suffer chronic neck pain than members of the general community, or individuals who do not develop symptoms after a motor vehicle accident (Berglund et al. 2000).
In the acute phase, the most frequent symptoms are neck pain and headache. Other features that can occur in a minority of patients include anxiety, sleep disturbances, back pain, visual disturbances, dizziness, inability to concentrate, and other cognitive disturbances (Barns- ley et al. 2002). In patients who do not recover, these same symptoms persist, but with greater prevalence in affected individuals, together with psychological distress (Radanov et al. 1995). In the chronic phase, patients display
hyperalgesia to stimuli applied to
both painful and non-painful areas of the body (Banic et al. 2004).
Natural History and Prognostic Factors
Most patients who suffer a whiplash-associated disor- der recover. Two years after injury, 82 % of patients are asymptomatic (Radanov et al. 1995). For those who do not recover, increasing age, injury-related cognitive dis- turbances, and the severity of initial neck pain predict the persistence of symptoms at 6 months (Radanov et al. 1991). The chance of spontaneous recovery after two years is minimal.
Mechanisms
During the whiplash event, the torso is thrust upwards and forwards, and compresses the neck from below.
Initially, the cervical spine undergoes a sigmoid defor- mation, but subsequently the head drops into extension, and later rebounds into flexion (Bogduk and Yoganan- dan 2001). At no time does the head and neck exceed normal physiologic range of motion. The offending insult is the initial compression and sigmoid defor- mation of the cervical spine. During this motion, the lower vertebrae undergo an abnormal pattern of exten- sion, in which anteriorly, the intervertebral discs are strained; and posteriorly, the zygapophysial joints are impacted (Bogduk and Yoganandan 2001). Injury to these structures may or may not occur, depending on the severity of impact, and the morphology and strength of the vertebrae and their joints and ligaments.
Most patients suffer no substantive or lasting injury, but a minority does. Tears of the
annulus fibrosus and con- tusion or small fractures of the zygapophysial joints have been demonstrated in postmortem studies, but these defy resolution by current medical imaging techniques (Yo- ganandan et al. 2001); giving the false impression that no injury is present.
The frequent absence of evident tissue damage has led to the hypothesis that psychosocial factors are the main determinants of symptoms. However, psycholog- ical disturbances do not predict the clinical course of whiplash patients (Radanov et al. 1991), and there is no evidence that therapies aiming at correcting these dis- turbances consistently produce resolution of symptoms.
The persistence of pain, and the legal and economic consequences that often follow a whiplash-associated disorder, may cause psychological distress, which may contribute to the pain complaints. However, there is no evidence that psychological factors per se cause persistent pain.
Hypersensitivity of central nociceptive pathways in
chronic whiplash patients has been demonstrated ob-
jectively using electrophysiological measurements
(Banic et al. 2004). This central hyperexcitability may
amplify the nociceptive signal arising from areas of
minimal and undetectable tissue damage, which could
partly explain the discrepancy between objective clini-
2664 Whiplash
cal findings and extent of pain and disability that occurs in these patients. Importantly, these data indicate that increased pain sensitivity at non-painful areas does not necessarily imply hysteria, a conclusion that is still made by too many physicians.
In summary, the most likely cause of persistent pain and disability after a whiplash trauma is an occult injury to a zygapophysial joint or an intervertebral disc, caused by the acute distortion of the spine. The resulting psy- chological distress, as well as central neural hypersen- sitivity, is likely to amplify symptoms.
Physical Examination
Both in the acute phase and in patients with chronic pain, physical examination may detect areas of ten- derness and impaired range of movement of the neck.
These signs, however, are not reliable, lack
validity (Bogduk 2003), and do not permit a patho-anatomic diagnosis to be made.
Neurological examination is usually normal, but a small proportion of patients may suffer cervical disc prolapse and nerve root compression as a result of whiplash.
These patients will exhibit signs of
radiculopathy.
Investigations
Medical imaging is not indicated for patients with just neck pain after whiplash. According to the Canadian C- Spine Rule, radiography is not justified in a patient who has been in a motor-vehicle collision and can rotate their neck at least 45˚ to the left and right (Stiell et al. 2001).
Magnetic resonance imaging is of no diagnostic value for most patients (Bogduk 2003). It is indicated only in those patients with neurological signs.
In patients with chronic neck pain after whiplash, the zy- gapophysial joints are the single most common source of pain (Lord et al. 1996), but zygapophysial joint pain cannot be diagnosed by physical examination or medical imaging (Bogduk 2003). It requires controlled diagnos- tic blocks performed under fluoroscopic guidance. Even if performed correctly, these diagnostic blocks cannot pinpoint the painful joint (or joints) in over 50 % of pa- tients (Bogduk 2003).
Treatment
Given the favourable prognosis of acute pain after whiplash, the first imperative is for the physician to reassure the patient of the high likelihood of complete recovery. Passive therapy is not indicated and, indeed, the evidence shows that conventional interventions do not work (Bogduk 2003). The evidence supports only reassuring the patient, encouraging them to resume normal activities, and to keep the neck moving through simple exercises that the patient can do regularly, them- selves, at home (Bogduk 2003). Analgesics may be prescribed to reduce pain, but no evidence supports their efficacy.
For patients with acute neurological symptoms, one study has shown that high-dose intravenous
methyl- prednisolone was effective in reducing the number of sick days (Pettersson and Toolanen 1998); but this treatment may not apply for patients who do not have radiculopathy.
For patients with chronic neck pain after whiplash, few treatments have been vindicated by controlled stud- ies. There are no data on the efficacy of short-wave diathermy, collars, traction, transcutaneous electrical nerve stimulation (TENS), laser therapy, neck school, spray and stretch or trigger point therapy. Magnetic necklaces, acupuncture, and physiotherapy are no bet- ter than sham therapy (Bogduk 2003). Manual therapy is no more effective than using salicylates while on a waiting list. Intensive exercises are no more effective than less intensive exercises; both achieve only modest improvements (25 %) in pain and disability (Bogduk 2003). Intra-articular injections of corticosteroids for cervical zygapophysial joint pain offer no long-term and little short-term benefit (Barnsley et al. 1994).
Multidisciplinary biopsychosocial rehabilitation pro- grams are widely used. However, these treatment pro- grams are expensive and still lack convincing evidence of effectiveness (Karjalainen et al. 2001). One uncon- trolled study attests to the efficacy of a four-week, multimodal treatment program involving graded return to activity, abolishing pain behavior, and restoring mus- cle strength and endurance (Vendrig et al. 2000). At six months follow-up, cognitive and behavioral complaints were eliminated in some 90 %; 65 % of patients returned to work, 58 % ceased to use drugs; and 81 % ceased to pursue medical care; pain was reduced to “healthy”
levels in 46 % of patients; disabilities were reduced to normal levels in 38 %.
A further option for pain-relief may be the long-term use of analgesics. Unfortunately, however, there is no evi- dence of their efficacy. Opioids may be required for se- vere, persistent pain; but these need to be prescribed and monitored carefully.
Radiofrequency denervation of painful zygapophysial joints is the only treatment that has been vindicated by a randomized, double-blind, placebo-controlled trial (Lord et al. 1996), and subsequent, long-term follow-up studies (Bogduk 2003). This procedure is indicated only in those patients in whom controlled diagnostic blocks have identified the joint responsible for the patient’s pain. Successful treatment of the pain also results in resolution of the psychological distress suffered by these patients (Bogduk 2003).
Discussion
Pain after whiplash injury is a temporary experience for most patients: spontaneous healing is almost the rule.
Patients with persistent symptoms, however, constitute
an important medical and social problem.
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WHO System on Impairment and Disability 2665
As patients with persisting pain lack conventional, ob- jective signs of organic lesions, they are often treated in a pejorative manner. Resources, such as zygapophysial joint blocks, by which the source of pain can be deter- mined, are not readily available or are not implemented.
Conventional therapies have been found to have little or no effect, and few practitioners are able to implement those few interventions that have been shown to be ef- fective. As a result of these factors, patients continue to suffer pain and disability. Beyond the misfortune of get- ting an illness that changes their life, patients are con- fronted with the new experience of having to fight in- surance companies, employers and doctors, to convince them that they really “do have something wrong with their neck” The resulting psychological distress is an ob- vious consequence of this state of affairs, but is not the cause of the problem.
Patients with acute neck pain after whiplash have the advantage of a favorable prognosis. Being reassured and resuming normal activities is all that they may require for recovery. For patients with persisting pain after whiplash, two main problems apply. First is the lack of reliable diagnostic tools to identify the source of pain.
The most honest approach by the physician is to declare and explain this deficiency, as opposed to insisting that there is nothing wrong. The second problem is the lack of proven treatments. This too should be explained, rather than causing unrealistic hopes. Radiofrequency denervation is the only proven treatment, but is provided by very few practitioners.
References
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12. Radanov BP, Sturzenegger M, Di Stefano G (1995) Long-Term Outcome after Whiplash Injury. A 2-Year Follow-Up Consider- ing Features of Injury Mechanism and Somatic, Radiologic, and Psychosocial Findings. Medicine 74:281–297
13. Stiell IG, Wells GA, Vandemheen KL et al. (2001) The Cana- dian C-Spine Rule for Radiography in Alert and Stable Trauma Patients. Jama 286:1841–1848
14. Vendrig AA, van Akkerveeken PF, McWhorter KR (2000) Results of a Multimodal Treatment Program for Patients with Chronic Symptoms after a Whiplash Injury of the Neck.
Spine 25:238–244
15. Yoganandan N, Cusick JF, Pintar FA et al. (2001) Whiplash Injury Determination with Conventional Spine Imaging and Cryomi- crotomy. Spine 26:2443–2448
Whiplash-Associated Disorders
Whiplash
WHO Analgesic Ladder
World Health Organization (WHO) Analgesic Ladder
WHO System on Impairment and Disability
J
ENNYS
TRONGUniversity of Queensland, Brisbane, QLD, Australia j.strong@uq.edu.au
Synonym
World Health Organisation International Classification of Functioning; Disability and Health (ICF)
Definition
The World Health Organisation’s (WHO) International Classification of Functioning, Disability and Health (ICF) (WHO 2001), replaces the earlier WHO Interna- tional Classification of Impairments, Disabilities and Handicaps (WHO 1980). The ICF provides a frame- work for health practitioners to evaluate the impact of health conditions upon particular individuals. Against the background of contextual, personal and environ- mental factors, the impact of the health condition upon the person is considered in terms of the interaction between body structures and functions, activities, and participation (Gibson and Strong 2003; WHO 2001).
The ICF model conceptualizes the functional aspects of
health, moving from an impairment focused or deficit
focused framework to a participative framework. This is
in contrast to the old ICIDH (WHO 1980) that focused
upon impairments, activity limitations, and handicaps.
2666 WHO System on Impairment and Disability
WHO System on Impairment and Disability, Figure 1 Interaction of Concepts ICF 2001 (World Health Organisation 2001), reproduced with permission.
The WHO ICF model is illustrated in Figure 1. Instead of focusing on impairments, which are problems in body function such as significant deviation or loss, attention is given to not only the difficulties the person may have in executing activities but also to the problems the person has being involved in life situations.
Characteristics
The ICF (http://www.who.int) was developed to pro- vide a unified and universally understood language to describe the outcomes of all health conditions (Gray and Hendershot 2000). It provides a useful framework for considering the impacts of chronic pain upon the individual client or patient. It is also suggested as a useful framework for considering the outcomes of pain rehabilitation programs. The ICF particularly directs the health practitioner to be clear as to the level at which they are measuring outcomes, viz, are they confining their outcome assessment to body structures and impairment based systems (e.g. active and passive range of motion, allodynia and presence of vasomotor and sudomotor changes); or are they considering outcomes in terms of activity limitations or participation restrictions (e.g.
ADLs, and life roles) (Unsworth 2000). Furthermore, are the individual patient’s particular personal and en- vironmental factors being considered in such outcome measurement (e.g. financial pressures upon the family unit, and fear of failure).
WHO System on Impairment and Disability, Table 1 Assessment Matrix, based upon the WHO ICF 2001
Body function and structures Activities Participation
Muscle testing ADL assessment Home assessment
Range of Motion testing Functional Capacity Evaluation Work-place assessment*
NB Psychosocial assessment of personal factors
* Ergonomic assessment of environmental factors
Personal factors to be considered may include sex, age, co-morbidities, usual coping style, social background and education, job, past experiences, and type of person- ality. Patients with chronic pain are embedded within contexts that can facilitate or hinder their rehabilitation.
Environmental factors may be familial, work-related, cultural, political, societal, or of the built environment (WHO 2001).
Use of the ICF framework can assist in the mea- surement of outcomes of relevance for the individual client/patient, the health care provider and the insurer or employer. The patient will most probably be concerned with the elimination of pain, an increase in function, and a return to work. The health care professional will be concerned with pain control, assisting the patient to gain an increase in function, and a decrease in suffering.
The insurer or employer will primarily be concerned with return to work.
The value of the ICF framework is illustrated by con- sidering the case of a 42-year old man who sustained a soft tissue injury at work, and developed complex re- gional pain syndrome Type I (CRPSI). The patient was a miner and sole provide for the family. He was married with 2 children. Assessment using a body structures and impairment framework revealed he had no active range of motion of his right hand (guarding), a reduced passive range of motion of his right hand, allodynia, and marked vasomotor and sudomotor changes.
Considering the patient’s ability to engage in activities, he reported limitations in all functional activities that required bilateral upper limb involvement, including personal activities of daily living, e.g. pushing, lift- ing, using controls (driving), handling, and carrying tasks. He was fearful of increased pain, and therefore self-limited many of his instrumental activities such as walking near other people, or going out of the house to shop or socialize. He reported reduced participation in all home-based activities, and was currently off work.
There were significant financial pressures upon his family. This was combined with self-esteem problems he faced, having been ‘transformed’ from a strong, in- dependent, successful miner to a weak, disabled person.
His employer and fellow workers did not understand his pain problem, and suspected he was malingering.
His current problems with body function would pre-
clude him from working with heavy machinery in an
underground mine.
W
Wide Field Radiation 2667
The ICF provides a useful framework for evaluating such patients with chronic pain, and highlights the multidi- mensional nature of assessment, enabling a matrix of outcome measurements to be identified for use in a pain rehabilitation program. A possible matrix is illustrated in Table 1.
By using an assessment matrix such as the one in Ta- ble 1, which is based upon the WHO ICF, it is easier for health practitioners working with patients with pain, and pain clinics in general, to ensure that the focus of assess- ment is not only focused upon the impairment, or body function and structures level. Good outcomes for pain treatments should be focused upon the activities and par- ticipation levels as indicated by the WHO ICF classifi- cation. It is the outcome at these levels that are of most salience to patients and to insurers, and surely to health practitioners.
References
1. Gibson L, Strong J (2003) A Conceptual Framework of Func- tional Capacity Evaluation for Occupational Therapy in Work Re- habilitation. Australian Occupational Therapy Journal 50:64–71 2. Gray DB, Hendershot GE (2000) The ICIDH-2: Developments for a New Era of Outcomes Research. Arch Phys Med Rehabil 81 (Suppl 2):S10–S14
3. Unsworth C (2000) Measuring of Outcome of Occupational Therapy: Tools and Resources. Australian Occupational Therapy Journal 47:147–158
4. World Health Organisation (1980) International Classification of Impairments, Disabilities, and Handicaps. World Health Organ- isation, Geneva
5. World Health Organisation (2001) The International Classifica- tion of Functioning, Disability and Health (ICF). World Health Organisation, Geneva
Whole Body Receptive Fields
Definition
Stimulation anywhere on the body activates these neu- rons.
Spinothalamocortical Projections to Ventromedial and Parafascicular Nuclei
Whole-Brain/Partial Brain Coverage
Definition
The most common forms of functional imaging employ whole-brain coverage. This means that signal changes are measured throughout the whole brain. However, to achieve greater spatial resolution, e.g. for a study of differences between hippocampus and entorhinal cortex processing (or if faster acquisition of data is required), one option is to acquire a signal from a smaller section of the brain only (partial brain coverage).
Hippocampus and Entorhinal Complex, Functional Imaging
Whole Cell Patch Clamp Recordings
Definition
Recording of membrane currents in an intact cell by ap- plying gentle suction to a micropipette patched onto the cell membrane to create an opening.
Amygdala, Pain Processing and Behavior in Animals
WHYMPI
West Haven-Yale Multidimensional Pain Inventory
Wide Dynamic Range Neuron
Synonym WDR neuron
Definition
Wide dynamic range (WDR) neurons are nociceptive neurons that respond with small responses to innocu- ous pressure to deep tissue, and stronger and graded re- sponses to noxious mechanical stimulation of peripheral tissues. They often also respond to noxious, thermal and chemical stimuli. This type of neuron is defined physio- logically by its response properties and can be found at spinal thalamic and cortical sites important in the pro- cessing of noxious information.
Alternative Medicine in Neuropathic Pain
Arthritis Model, Kaolin-Carrageenan Induced Arthri- tis (Knee)
Encoding of Noxious Information in the Spinal Cord
Freezing Model of Cutaneous Hyperalgesia
Functional Changes in Sensory Neurons Following Spinal Cord Injury in Central Pain
Human Thalamic Nociceptive Neurons
Lateral Thalamic Pain-Related Cells in Humans
Nick Model of Cutaneous Pain and Hyperalgesia
Referred Muscle Pain, Assessment
Spinothalamic Input, Cells of Origin (Monkey)
Thalamic Nuclei Involved in Pain, Human and Mon- key
Thalamus, Nociceptive Cells in VPI, Cat and Rat
Trigeminal Brainstem Nuclear Complex, Physiology
Wind-Up of Spinal Cord Neurons
Wide Field Radiation
Definition
Radiation of a large area.
Cancer Pain Management, Radiotherapy
2668 Wind-Up (Phenomenon)
Wind-Up (Phenomenon)
Definition
Repetitive stimulation of unmyelinated C–fibers can result in prolonged discharge of dorsal horn cells, termed “wind–up” It is characterized by a progressive increase in the number of action potentials elicited, per stimulus, which occurs in dorsal horn neurons.
“Wind–up” is a short-lived process, however, repetitive episodes may precipitate long-term potentiation (LTP), which involves a long lasting increase in the efficacy of synaptic transmission and thus alters synaptic plasticity.
Both “wind–up” and LTP are believed to be important components of central sensitization.
Acute Pain Mechanisms
Brainstem Subnucleus Reticularis Dorsalis Neuron
Encoding of Noxious Information in the Spinal Cord
Hyperpathia, Assessment
Neuropathic Pain Models, CRPS-I Neuropathy Model
Opioids in the Spinal Cord and Central Sensitization
Opioid Modulation of Nociceptive Afferents In Vivo
Postoperative Pain, Pre-Emptive or Preventive Anal- gesia
Psychiatric Aspects of Pain and Dentistry
Quantitative Sensory Testing
Somatic Pain
Spinothalamic Tract Neurons, in Deep Dorsal Horn
Visceral Nociception and Pain
Wind-Up of Spinal Cord Neurons
Wind-Up of Spinal Cord Neurons
J
UANF. H
ERRERODepartment of Physiology, Edificio de Medicina, University of Alcalá, Madrid, Spain
juanf.herrero@uah.es
Synonyms
Frequency-Dependent Nociceptive Facilitation
Definition
Progressive and frequency-dependent facilitation of the responses of a spinal cord neuron observed on the ap- plication of constant and high intensity repetitive elec- trical stimuli. It is a phenomenon that shares some com- mon mechanisms with central sensitization and is me- diated by
NMDA receptors and
NK1 receptors, al- though cyclooxygenases, nitric oxide, TRH, adenosine and other systems are also involved in its generation or maintenance.
Characteristics
Wind-up is a phenomenon described in terms of neu- ronal responses to repetitive electrical stimulation. It can be defined as a progressive and frequency-dependent facilitation of the responses of a spinal cord neuron ob- served on the application of constant and high intensity repetitive electrical stimuli. It was first described by Lorne Mendell (Mendell and Wall 1965) as a frequency- dependent facilitation of spinal cord neuronal responses mediated by afferent C-fibers, suggesting that it might be due to a reverberatory activity evoked by C-fibers in interneurons of the spinal cord. Systematic studies of the in vivo activity of spinal cord neurons (Schouenborg and Sjölund 1983) established that under normal con- ditions, wide dynamic range or class 2 neurons showed the most pronounced wind-up, whereas classes 1 and 3, equivalent to low threshold and high threshold neurons, showed a very weak response. Wind-up is also observed in nociceptive withdrawal reflexes recorded as single motor units (SMU), spinal cord field potentials, isolated in vitro spinal recordings from immature rats (see for review Herrero et al. 2000) or even dorsal horn neurons in cell culture (Vikman et al. 2001). The generation of wind-up depends critically on the frequency of stimula- tion of afferent C-fibers. The greatest wind-up is seen at frequencies of around 1–2 Hz. It is not observed below frequencies of 0.2–0.3 Hz. Above frequencies of 20 Hz, rather than observing wind-up, the usual observation is a habituation of the response or wind-down. This is due to a progressive slowing of the conduction velocity of afferent C-fibers when stimulated at high frequency, resulting in a conduction blockade and a reduction in the number of impulses reaching the spinal cord with sufficiently high frequencies.
The generation of wind-up does not only depend on the frequency of stimulation, it also depends on other param- eters such as the duration and the intensity of the stim- uli used. The level of excitability of spinal cord neurons and the integrity of spinal cord connections to the brain are also crucial in the generation of wind-up. Prolonged noxious stimulation, peripheral injury and inflammation evoke an enhancement of the excitability of spinal cord neurons and an increase in the degree of wind-up, as well as a reduction in the threshold for the generation of wind- up, which has been interpreted as a result of loss of in- hibitory modulation.
In hyperalgesic states induced by peripheral injury or
inflammation, wind-up is also evoked by stimulation of
A β-fibers. This new phenomenon has been described
either in isolated preparations of the spinal cord from
newborn rats (Thompson et al. 1995) or in adult in
vivo preparations (Herrero and Cervero 1996). Re-
flex wind-up facilitation and a novel A-fiber mediated
wind-up evoked in arthritic animals were, however,
only observed in intact, not in spinalized, preparations
(Herrero and Cervero 1996). The enhancement of the
W
Wind-Up of Spinal Cord Neurons 2669
Wind-Up of Spinal Cord Neurons, Figure 1 Wind-up of a single motor unit recorded in an in vivo preparation. Sixteen stimuli of 2 ms of duration, at an intensity of 6 mA, twice the threshold for C-fiber activation, were applied at 1 Hz frequency in the cutaneous receptive field. Note how the number of spikes recorded increase progressively despite a constant stimulus intensity.
reflex wind-up observed during hyperalgesia, therefore required an intact spinal cord and might be explained as the consequence of a direct descending excitatory influ- ence on spinal cord neurons. Supraspinal modulation is also evidenced by the reduction of wind-up in deep dorsal horn class 2 neurons observed after applying a re- mote noxious mechanical stimulation to the nose of the rat (Schouenborg and Dickenson 1985), showing that wind-up is also affected by diffuse noxious inhibitory controls (DNIC).
The mechanisms underlying the generation of wind-up are still unresolved. Multiple factors may contribute to wind-up: network properties, pre-synaptic mech- anisms, post-synaptic receptors and post-synaptic membrane properties. Glutamate NMDA receptors are intimately involved in the generation of wind-up, as demonstrated by experiments showing that the adminis- tration of NMDA antagonists, such as ketamine, D-AP5 (2-amino-5-phosphonopentanoate) or kynureic acid, abolished wind-up (Davies and Lodge 1987, Dickenson and Sullivan 1987). At normal resting membrane poten- tial, NMDA receptors are blocked by Mg
2+ions. During repetitive stimulation, each stimulus leaves the neuron at a more depolarized membrane potential, which in turn may contribute to the removal of the Mg
2+block from the NMDA receptors. The progressive release
of the Mg
2+block would act as an amplifier mech- anism, boosting the summation of EPSPs and hence potentiating subsequent afferent input. Furthermore, as a consequence of NMDA receptor over-activity, an increase in intracellular Ca
2+may activate protein ki- nase C and this, in turn, would increase the probability of NMDA receptor channel opening and reduce the voltage-dependence of the Mg
2+block of the receptor (Chen and Huang 1992).
Blockade of wind-up by NMDA receptor antagonists is, however, only partial and, based on this observation, other modulators have been proposed to contribute to the long latency depolarization and to the hyperactivity observed during wind up. Substance P, a member of the tachykinin family of peptide neurotransmitters, was proposed to be involved in wind-up and this was con- firmed in NK1 knockout mice by De Felipe et al. (1998).
Some
Cyclooxygenases inhibitors, especially nitric
oxide derivatives such as nitroparacetamol, are very
effective inhibitors of wind-up (for review see Herrero
et al. 2000); two complementary mechanisms of action
have been proposed to explain this effect. On the one
hand, nitric oxide seems to inhibit the reuptake of some
monoamines like serotonin. The enhancement of the
amount of monoamines in the synaptic space would
reduce the release of glutamate (Kiss and Vizi 2001).
2670 Winging Scapula
On the other hand, the cyclooxygenase inhibition would reduce the level of circulating prostaglandins, which have been shown to enhance the release of glutamate and aspartate in the spinal cord (Nishihara et al. 1995).
Wind-up results from a synchronous electrical (and therefore artificial) stimulation of a peripheral nerve, producing a pattern of input distinct from the asyn- chronous discharge evoked by natural stimulation.
Thus, it is not clear if this represents a genuine physi- ological response or is simply an artificially generated phenomenon. However, since nociceptive neurons re- spond in a very characteristic way to this specific pattern of artificial stimulation, it seems probable that there is a physiological correlate. Further, repetitive natural stimuli in human subjects can induce a temporal sum- mation of pain sensation very similar, if not identical, to that induced by repetitive electrical stimuli.
Wind-up is also similar in many respects to the process that evokes short-term potentiation, i.e. an increase in hippocampal excitability that lasts for a few seconds to up to an hour. Wind-up may underlie the continuation of pain sensation in response to prolonged or repetitive stimuli, despite a reduction in the number of action potentials in afferent C-fibers and may represent an am- plification mechanism or even a ‘pain memory’ in spinal cord neurons. In addition, wind-up-inducing stimuli evoke some of the manifestations of
central sensitiza- tion in spinal neurons, such as enlarged receptive fields and enhanced responses to input from afferent C-fibers.
NMDA receptors are involved in the generation of both phenomena. However, it has been shown that whilst stimuli that evoke wind-up may be sufficient to induce central sensitization, wind-up is not essential for the induction of central sensitization (Woolf 1996). There is no doubt that wind-up is a useful tool in the study of spinal cord-processing of somatosensory information and provides an experimental correlate of spinal cord hyperexcitability, sharing some common mechanisms with central sensitization or hyperalgesia.
References
1. Chen L, Huang LYM (1992) Protein kinase C reduces Mg block of NMDA-receptor channels as a mechanism of modulation. Nature 356:521–523
2. Davies SN, Lodge D (1987) Evidence for the involvement of N-methylaspartate receptors in ‘wind-up’ of class 2 neurons in the dorsal horn of the rat. Brain Res 424:402–406
3. De Felipe C, Herrero JF, O’Brien JA et al. (1998) Altered nocicep- tion, analgesia and aggression in the mice lacking the substance P receptor. Nature 392:394–397
4. Dickenson AH, Sullivan AF (1987) Evidence for a role of the NMDA receptor in the frequency dependent potentiation of deep rat dorsal horn nociceptive neurons following C fiber stimulation.
Neuropharmacol 26:1235–1238
5. Herrero JF, Cervero F (1996) Supraspinal influences on the facilitation of rat nociceptive reflexes induced by carrageenan monoarthritis. Neurosci Lett 209:21–24
6. Herrero JF, Laird JMA, Lopez-Garcia JA (2000) Wind-up of spinal cord neurons and pain sensation: much ado about some- thing? Prog Neurobiol 61:169–203
7. Kiss JP, Vizi ES (2001) Nitric oxide: a novel link between synaptic and nonsynaptic transmission. TiNS 24:211–215
8. Mendell L M, Wall PD (1965) Responses of single dorsal cells to peripheral cutaneous unmyelinated fibers. Nature 206:97–99 9. Nishihara I, Minami T, Watanabe Y et al. (1995) Prostaglandin E2 stimulates glutamate release from synaptosomes of rat spinal cord. Neurosci Lett 196:57–60
10. Schouenborg J, Dickenson AH (1985) The effects of a distant noxious stimulation on A and C fiber evoked flexion reflexes and neuronal activity in the dorsal horn of the rat. Brain Res 328:23–32
11. Schouenborg J, Sjölund BH (1983) Activity evoked by A- and C-afferent fibers in rat dorsal horn neurons and its relation to a flexion reflex. J Neurophysiol 50:1108–1121
12. Thompson SWN, Dray A, McCarson KE et al. (1995) Nerve growth factor induces mechanical allodynia associated with novel A fiber-evoked spinal reflex activity and enhanced neurokinin-1 receptor activation in the rat. Pain 62:219–231
13. Vikman KS, Kristensson K, Hill RH (2001) Sensitization of dorsal horn neurons in a two-compartment cell culture model:
wind-up and long-term potentiation-like responses. J Neurosci 21:RC169
14. Woolf CJ (1996) Windup and central sensitization are not equiv- alent. Pain 66:105–108
Winging Scapula
Definition
Winging of the scapula is a protrusion of the scapula away from the thorax when the patient attempts to raise the arm above the shoulder level. The serratus anterior muscle keeps the scapula close to the ribs while stabi- lizing the scapula for shoulder abduction, overhead use of the hand, and push-up type work. Any injury or com- pression of the long thoracic nerve, which innervates this muscle, will cause scapular winging. A neurolysis of the long thoracic nerve in the thoracic inlet can resolve this problem.
Thoracic Outlet Syndrome
Withdrawal
Definition
Withdrawal is a reflex reaction (the rat withdraws its limb or tail).
Randall-Selitto Paw Pressure Test
Withdrawal Symptoms
Definition
Withdrawal symptoms are a result of abrupt discontinu- ation of a drug, and in the case of opioid analgesics can include diarrhea, sweating, insomnia and goosebumps.
Opioids, Clinical Opioid Tolerance
W
World Health Organization (WHO) Analgesic Ladder 2671
Work Capacity
Definition
Work capacity is the client’s ability to experience, un- derstand and learn to perform job tasks/occupations re- sulting in production that is at least comparable with the industrial standard for that product or service. In choos- ing a suitable occupation, work capacity is understood as the client’s valuable and useful quality and skills, indi- cating that he/she is specially matched for a certain type of work.
Vocational Counselling
Work Fitness
Definition
Work fitness is a capacity to successfully meet the present and potential challenges of work requirements with vigor, and to demonstrate the traits and capacities that will prevent occupational injuries.
Vocational Counselling
Work Samples
Definition
Work samples are designed to appraise whether an indi- vidual’s ability to perform actual work matches the job description and skills required for that job. The client’s vocational aptitudes (physical and mental), skills and occupational behavior are exposed. In a therapeutic environment, the client performs well-defined simu- lated work activities, involving tasks, materials and tools resembling those in actual job tasks, occupations or cluster of occupations. A work sample simulates factors that are required in thousands of specific jobs.
One example is the VALPAR Component Work Sam- ple (VCWS), which covers 21 individual criterion- referenced work samples. Each VCWS job requirement corresponds to the classification and analysis system of the Dictionary of Occupational Titles (DOT) and the Worker Qualification Profile (WQP). Ability to perform a cluster of VCWS demonstrates whether the client has met the WQP. The WQP is rated in a time-standard known as Methods-Time Measurement (MTM) scores.
MTMs represent the standards of time a well-trained worker would be expected to perform tasks like those of the Valpar’s VCWS within a typical industrial setting during an eight-hour working day.
Disability Functional Capacity Evaluations
