1 1.1 Neural Tension Background

1.1.1 Tests for Neural Tension

Test procedures are required for abnormal neural tension in the lower

quadrant. This is not a new concept. In 1864 sciatica was recognised by

Lasègue and his student. Forst published a description of the Lasègue test

now known as the straight-leg-raise (SLR) test (Woodhall & Hayes, 1950).

The SLR test is performed with the patient lying and the leg is raised with the

knee straight until pain is felt (Woodhall & Hayes, 1950). This test is

recognised as a good diagnostic test of lumbar intervertebral disc and nerve

root lesions (Farhni, 1966).

Petren (1909) presented the earliest description of a sitting lower limb neural

tension test based on extension of the knee in sitting (Woodhall & Hayes,

1950). Cyriax, (1942) also described neural tension tests in sitting whereby

the knee was extended passively or cervical flexion was performed (Cyriax,

1942). The modern form of these sitting SLR tests known as the ‘slump test’

combines trunk and neck flexion with the SLR (Maitland, 1979). Both the SLR

and the slump tests include sensitising movements. Remote testing

procedures such as neck flexion, medial rotation of the hip or ankle

dorsiflexion can be added to the base neural tension test to further tension

the neural system from either the distal or proximal segment (Butler &

Gifford, 1989a; Troup, 1981). Troup (1981) described these qualifying tests

of the SLR test as sensitive diagnostic and predictive tests that indicated the

severity of episodes of back pain or sciatic pain (Troup, 1981). This

emphasises the importance of adding sensitising manoeuvres to the base

neural tension test.

The diagnostic value of neural tension tests is well recognised but their use as

treatment techniques is a more recent development (Butler & Gifford, 1989b).

Physiotherapists have modified clinical examination and treatment techniques

designed to assess the mechanosensitivity of the major nerve trunks in the

upper and lower limbs (Butler & Gifford, 1989a; Butler & Gifford, 1989b;

Elvey, 1992a; Maitland, 1979; Shacklock, 1995l). The slump test is one such

test designed to produce movement of the pain-sensitive neuromeningeal

structures within the vertebral canal and was first described by Maitland

(1979) in the current form (Maitland, 1979).

1.1.2 Slump Test

The slump test is a neural tension test of the lower quadrant that tests neural

tissue in the spine and lower limb and it combines the sitting SLR tests

described above with the addition of trunk flexion and neck flexion (Maitland,

1979). The test is widely used by physiotherapists to test for suspected

involvement of the peripheral nervous system (PNS) in many lower quartile

conditions including low back pain, hamstring strains, calf strains and ankle

sprains (Kornberg & Lew, 1989; Maitland, 1985; Pahor & Toppenberg, 1996).

The slump test applies tension to neural tissue through the full range of spinal

and extremity motions (Louis, 1981; Maitland, 1985). It is often more

applicable to functional situations such as slouched sitting, getting in and out

of a car and raising one leg with the trunk flexed when dressing than the SLR

test. The slump test has been shown to be consistent with high inter-

therapist reliability when the patients symptoms form the criterion for a

positive or negative test (Philip, Lew, & Matyas, 1989). Figure 1.1 provides a

pictorial description of the slump test. The amount of knee extension gained

during the test and the impact that knee extension has on pain along with the

effect of neck flexion are the main factors of interest during the slump test.

Tension applied to neural tissue during the slump test can be divided into

three levels:

• Slight tension of neural tissue is produced by neck flexion performed in

sitting with the trunk upright.

• Moderate tension of neural tissue is produced by trunk flexion performed in

sitting with the head up.

• Maximum tension of neural tissue is produced by trunk flexion with the

addition of neck flexion performed in sitting.

The assumption that these positions place tension on neural tissue is based

on the anatomy of neural tissue being the major structure that is a

continuous tract from the head to the foot. Anatomical and biomechanical

studies provide evidence that neck flexion, trunk flexion and combined trunk

and neck flexion in a sitting position with the hip flexed and the knee

extended creates movement and tension in neural tissue (Breig, 1978; Breig

& Marions, 1962; Ishida, Suzuki, & Ohmori, 1988; Louis, 1981; O'Connell,

1951; Reid, 1960; Tencer, Allen, & Ferguson, 1985).

Figure 1.1: Slump test.

Stage One: Full cervical, thoracic and

lumbar flexion with overpressure from

the therapist.

Stage Two: Knee extension with the ankle

dorsiflexed (maximum slump).

Stage Three: Cervical flexion is released and

the neck is extended relative to the thoracic

spine (moderate slump).

2 1.2 Restriction of Movement in Neural Tension Tests

The term neural tension implies reduced mobility of the nervous system but

evidence has been provided that there is normal compliance in the neural

system with neural tension tests until the onset of protective muscle activity

(Hall et al., 1998). The focus on the mechanical aspect of stretch on neural

tissue does not address the importance of the central nervous system (CNS)

and neurophysiological changes that may be occurring in response to

movement of a nerve trunk. Neurophysiological changes in the CNS are

considered to contribute to the mechanism where reflex muscle spasm limits

the neural tension test (Zusman, 1998).

1.2.1 Muscle Activity during Lower Limb Neural Tension Tests

Recent research has indicated muscle activity as the factor that restricts

movement during neural tension tests. In an attempt to identify the cause of

the restriction to movement during neural tension tests studies to date have

used electromyography (EMG) to measure muscle activity in lower limb

neural tension tests (Fidel, Martin, Dankaerts, Allison, & Hall, 1996; Goeken &

Hof, 1994; Hall et al., 1995; Hall et al., 1998; Hall et al., 1993; Lew &

Puentedura, 1985). The majority of studies relating to neural tension tests of

the lower limb have been performed during the straight leg raise (SLR) test.

These studies along with those assessing the slump test support the

argument for a reflex muscle contraction being the restricting factor of neural

tension tests.

Slump Test

Changes in EMG activity recorded from the hamstring muscle group during

the slump test were inconclusive. EMG activity during the slump test

demonstrated that hamstring muscle activity was generally present during

knee extension in normal subjects (Fidel et al., 1996; Lew & Briggs, 1997).

There was no consistency in whether EMG activity accompanied the first or

second point of pain during the knee extension movement in the slump

position (Fidel et al., 1996) and readings fluctuated within baseline levels

irrespective of whether the neck was flexed or extended (Lew & Briggs,

1997). When the knee was flexed and extended in the slump position as it

would be during a neural mobilisation treatment technique, the EMG

amplitude was reduced with each repetition of knee extension (Fidel et al.,

1996). This may indicate neurophysiological accommodation with the

mobilisation technique and suggests that the tension evoked on neural tissue

during the slump test may influence the motoneuron pool. Substantive

evidence that the slump test can influence α-motoneurons, however, has not

been provided with these studies.

Straight Leg Raise Test

Studies performed on the SLR test also show conflicting results as to the

presence and amount of EMG activity recorded, and the effect of the

sensitising manoeuvres of cervical flexion and ankle dorsiflexion on activity

(Goeken & Hof, 1994; Hall et al., 1995; Hall et al., 1998; Hall et al., 1993;

Lew & Puentedura, 1985). When active and passive straight leg raising was

measured in normal subjects with the ankle in relaxed plantar flexion and

then dorsiflexed, the angle of SLR with the ankle dorsiflexed was less than

with the ankle relaxed (Gajdosik, LeVeau, & Bohannon, 1985). The loss of

motion, however, was unrelated to the EMG activity of the hamstring muscles

(Gajdosik et al., 1985). Other authors have also found that a passive SLR

elicited negligible EMG in the hamstring muscle group (Norton & Sahrmann,

1981).

EMG activity recorded in the hamstring muscles during SLR coincided with the

onset of pain in normal subjects. The onset of pain associated with SLR was

most rapid in subjects that were inflexible (Goeken & Hof, 1993). These

authors suggested that the evoked EMG activity may be considered a

physiological phenomenon that protects the connective tissue from too much

tension (Goeken & Hof, 1994). The variation in muscle activity measured by

EMG recordings of the hamstring muscles during SLR testing indicates there is

a difference between a SLR test that provokes pain in normal subjects

compared with a non-pain provoking test (Gajdosik et al., 1985; Goeken &

Hof, 1993; Norton & Sahrmann, 1981).

Subjects with abnormal neural tension demonstrated an increase in muscle

activity with neural tension tests (Hall & Quinter, 1996; Hall et al., 1995; Hall

et al., 1998). The type of muscle activity that occurred during the neural

tension test was important and in particular the differentiation between

normal and abnormal muscle contractions limiting the test (Goeken & Hof,

1994). Abnormal muscle contractions occurred in subjects who had low back

and leg pain and was evidenced by early onset contractions in one or more

muscles during the SLR test (Goeken & Hof, 1994).

Hall et al (1998), found that abnormal muscle activity was present in all

subjects with radiculopathy when SLR was tested (Hall et al., 1998). These

subjects demonstrated normal through range neural tissue compliance until

the onset of muscle activity. Further support for the production of muscle

activity with neural tension tests in subjects with abnormal neural tension was

demonstrated in subjects with cervical spine radiculopathy where palpation

over major nerve trunks and tendon reflexes elicited a widespread increase in

EMG activity often in muscles unrelated to the spinal level affected (Hall &

Quinter, 1996). In contrast, palpation over normal peripheral nerve trunks

produced no pain and no EMG activity in muscles (Hall & Quinter, 1996).

The increase in EMG activity in the SLR test and upper limb tests in normal

subjects when pain was provoked and in subjects with abnormal neural

tension suggests that a protective reflex muscle contraction occurs which

prevents movement of sensitive neural structures (Goeken & Hof, 1994; Hall

& Quinter, 1996; Hall et al., 1998). The onset of muscle activity during

neural tension tests rather than an increased stiffness of neural tissue more

accurately represents neural pathophysiology (Hall et al., 1998).

There appears to be contrasting EMG responses to neural tension tests in

normal subjects and subjects with abnormal neural tension. No studies have

assessed muscle activity during the slump test in abnormal neural tension

subjects. The questions remain as to whether normal subjects exhibit muscle

activity during the slump test and to what extent muscle activity occurs in

abnormal subjects during the slump test.

3 1.3 Neurophysiology of Neural Tension

The consequences of abnormal neural tension cannot be explained solely by

the anatomy and biomechanical behaviour of neural tissue when it is placed

under tension. Neurophysiological influences of tension are of great

importance especially with regard to abnormal neural tissue.

1.3.1 Peripheral Nerve Damage

Neurogenic pain is described by the International Association for the study of

Pain as “pain initiated or caused by a primary lesion, dysfunction or transitory

perturbation in the peripheral or central nervous systems” (Merskey &

Bogduk, 1994). Pain that has its origin in nerve tissue is easily identified

when the damage to the nerve is great enough to impair axonal conduction,

the resultant sensory loss and motor weakness presents no obstacle to

diagnosis (Greening & Lynn, 1998). Neuropathic pain creates permanent

changes in the nervous system (Woolf, 1987) and it is doubtful that physical

treatment of nerve injuries with associated morphological changes are

appropriately treated with physical techniques (Elvey, 1998).

Minor peripheral nerve injuries under the category of neurogenic pain that do

not show changes to nerve function present a greater challenge to diagnosis.

These injuries are capable of responding to physical treatment, however, and

can be usefully assessed and treated using neural tension techniques (Hall &

Elvey, 1999; Klingman, 1999; Kornberg & Lew, 1989; Uth, 1999; Wise,

1994). Ashbury and Fields, (1984), hypothesised that a pain state of neural

origin without the loss of axonal conduction was probably mediated by the

nervi nervorum (Ashbury & Fields, 1984).

1.3.2 Nervi Nervorum

The nervi nervorum supply local innervation of the connective tissue of nerve

trunks (Hromada, 1963). Hromada (1963) made observations on the

innervation of peripheral nerve trunks and identified the unmyelinated nervi

nervorum with mainly free nerve endings and some encapsulated endings in

the epineurium, perineurium and endoneurium. The nervi nervorum take

origin from the perivascular plexuses and nerve bundles within the sheath

they are in and have a vasomotor innervation function (Hromada, 1963).

Bove and Light (1995) in a study on rats confirmed that these nerve fibres

were nociceptors that responded to mechanical, chemical and thermal

stimulus (Bove & Light, 1995). The nervi nervorum were found to respond to

longitudinally applied stretch on the nerve. These authors also found that the

nervi nervorum had receptive fields in deep structures like muscle or tendon.

This finding indicates that pain stemming from the nervi nervorum may not

be restricted to one area, stimuli from the muscle or tendon in the

corresponding receptive fields could be transmitted by the nervi nervorum.

It has been theorised that the nervi nervorum mediated local nerve

inflammation where there was no axonal damage (Zochodne & Ho, 1993). A

local inflammatory reaction that was independent of central connections was

demonstrated in peripheral nerves. Capsaicin application to the epineurium

of rat sciatic nerve resulted in the release of substance P and calcitonin gene-

related peptide along with other neuropeptides from ‘capsaicin-sensitive’

afferents and resulted in vasodilation and plasma extravasation (Zochodne,

1993; Zochodne & Ho, 1993). The nervi nervorum may also be an ongoing

generator and ‘refresher’ of the central changes associated with central

sensitisation (Bove & Light, 1997).

1.3.3 Central Sensitisation – Influence on the Ventral Horn

Nociceptive input from the nervi nervorum may initiate sensitisation of central

neurons but this remains to be established (Zochodne & Ho, 1993). Injury to

any of the structures of the spinal motion segment would, however, initiate

sensitisation of central neurons. Sensitised dorsal horn neurons abnormally

process mechanical input from nerve, muscle, cutaneous or joint afferents

(Dubner & Ruda, 1992). The known correlates of central sensitisation are a

lowered threshold to firing, increased frequency in background firing,

increased responsiveness to noxious and innocuous stimuli and increased

receptive field size in the periphery so that a larger area in the periphery

would be capable of triggering central neurons (Dubner & Ruda, 1992).

Changes to the flexor reflex demonstrated that sensitised dorsal horn

neurones are able to generate an increase in the excitability of α-

motoneurons in the ventral horn (Woolf, 1984; Woolf & McMahon, 1985;

Woolf & Wall, 1986). Thus afferent input into the sensitised dorsal horn of

the spinal cord will more readily activate α-motoneurons producing aberrant

muscle activity. Receptors within neural tissue capable of responding to

tension have been identified and the influence of central sensitisation on

motoneuron excitability has also been recognised. The question remains,

however, as to whether tension applied to neural tissue is capable of

influencing motoneuron excitability, thus causing an alteration in muscle

activity during a neural tension test.

1.3.4 Receptors that may Influence Alpha-Motoneuron Excitability

Aside from receptors within the nerve there are many other receptors that

may be activated by the slump positions and thereby influence the α-

motoneuron pool. Muscle afferents would be activated by stretch on

paravertebral muscles (Burke, Gandevia, & Macefield, 1988) in the moderate

slump position and this stretch may be increased with cervical flexion by the

attachments of the thoraco-lumbar fascia (Macintosh, Bogduk, &

Gracovetsky, 1987; Vleeming, Pool-Goudzwaard, Stoeckart, van Wingerden,

& Snijders, 1995). Joint afferents would be activated by end range stretch on

the lumbar spine joints (Burke et al., 1988; Gandevia, DI, & Burke, 1992) in

the moderate slump position but this stretch would not increase with the

addition of neck flexion in the maximum slump as the lumbar spine joints

would remain unchanged. Cutaneous receptors are likely to be activated with

stretch in both the moderate and maximum slump positions and are capable

of modulating the motoneuron pool (Burke et al., 1988; Walk & Fisher, 1993).

4 1.4 Methodology Used to Measure Muscle Activity

The use of EMG to record changes in muscle activity during neural tension

tests has had mixed results. Several studies have shown that normal

subjects did not show an increase in EMG activity during the Slump or SLR

test (Fidel et al., 1996; Gajdosik et al., 1985; Goeken & Hof, 1993; Lew &

Briggs, 1997; Norton & Sahrmann, 1981) and sometimes no EMG activity was

measurable (Gajdosik et al., 1985; Goeken & Hof, 1993; Norton & Sahrmann,

1981). This indicates that either the muscles were inactive or an inhibitory

effect of the neural tension test may have occurred in these normal subjects.

When pain was provoked with the neural tension test in normal subjects

(Goeken & Hof, 1993) and in pathological subjects where pain was a feature,

an increase in EMG activity was recorded (Goeken & Hof, 1994; Hall &

Quinter, 1996; Hall et al., 1998).

Surface EMG measures muscle activity occurring directly below the surface

electrode in primarily in superficial muscles (De Luca, 1997; Gilmore &

Meyers, 1983). One of the limitations of measuring EMG during neural

tension tests is that in asymptomatic subjects a reduction in EMG cannot be

measured. When using EMG recording during neural tension tests EMG

activity was typically calibrated as a percentage of an isometric contraction of

the muscle being recorded (Gajdosik et al., 1985; Goeken & Hof, 1993).

Therefore, a positive EMG activity level must be present before a reduction in

EMG can be measured. In manual therapy research the influence of a

treatment technique on muscle spasm has been measured with EMG (Thabe,

1986). In asymptomatic subjects, however, when the muscle being recorded

is completely relaxed with no spasm present, then a reduction in muscle

activity cannot be calculated and an inhibitory effect cannot be measured. If

an inhibition of motoneurons to the muscle being recorded occurs then it is

not possible to record ‘negative’ EMG. EMG, therefore, may not be a suitable

measure to detect subtle changes in muscle activity following neural tension

tests.

The Hoffmann-reflex (H-reflex), however, can measure inhibitory and

facilitatory effects on the α-motoneuron pool (Hugon, 1973). There have

been no studies investigating the effect of the slump test and the cervical

sensitising manoeuvre on the H-reflex recorded from the soleus muscle. In

the field of manual therapy the H-reflex has been used to assess excitability

changes in response to spinal manipulative therapy (Murphy, Dawson, &

Slack, 1995), manual traction (Bradnam, Rochester, & Vujnovich, 2000),

massage (Morelli, Chapman, & Sullivan, 1999; Morelli, Seaborne, & Sullivan,

1990; Morelli, Seaborne, & Sullivan, 1991; Morelli, Sullivan, & Chapman,

1998; Sulllivan, Williams, Seabourne, & Morelli, 1991) and muscle stretch

(Etnyre & Abraham, 1986; Misiaszek, Cheng, Brooke, & Staines, 1998;

Robinson, McComas, & Belanger, 1982; Vujnovich & Dawson, 1994).

Evidence of change in α-motoneuron excitability may be used to either

support or refute the proposal that reflex muscle activity is responsible for the

restriction of movement in neural tension testing.

5 1.5 H-Reflex Methodology

Hoffmann first described the delayed reflex response in the calf muscle

following stimulation of the tibial nerve in 1918. The reflex was subsequently

named the H-reflex by Magladery and McDougal in 1950 (Braddom &

Johnson, 1974). The H-reflex is used in both clinical and research settings.

In the clinical setting it is used as a diagnostic tool to detect neurological

abnormalities (Braddom & Johnson, 1974). As a research tool, the H-reflex,

used experimentally is a means of measuring the excitability of the α-

motoneuron pool (Hugon, 1973).

A 0.5-1.0 ms duration electrical pulse that preferentially stimulates Ia

afferents in the mixed tibial nerve at the popliteal fossa evokes the soleus H-

reflex. The Ia afferent volley produces excitation of homonymous α-

motoneurons and a reflex muscle contraction is recorded by EMG from the

soleus muscle (Hugon, 1973). The H-reflex is an essentially monosynaptic

reflex (Burke, Gandevia, & Mckeon, 1983; Burke, Gandevia, & McKeon, 1984)

that occurs at a latency of approximately 21-38ms in the lower limb soleus

reflex arc (Buschbacher, 1999; Fisher, 1992; Maryniak & Yaworski, 1987;

Sabbahi & Khalil, 1990a). The amplitude of the H-reflex gives an indication of

the number of motoneurons recruited from the α-motoneuron pool in

response to a given stimulus.

1.5.1 H-Reflex Modulation

The amplitude of the H-reflex reflects activation of a portion of a segmental

motoneuron pool and can be enhanced by manoeuvres that increase

motoneuron pool excitability and attenuated by factors that decrease

motoneuron pool excitability. The effect of manual therapy treatment

modalities on α-motoneuron excitability has been studied in an endeavour to

establish why these treatments are effective. Joint manipulation, mobilisation

and soft tissue massage in normal subjects has been shown to inhibit α-

motoneurons (Bradnam et al., 2000; Goldberg, Sullivan, & Seaborne, 1992;

Morelli et al., 1999; Morelli et al., 1990; Morelli et al., 1991; Morelli et al.,

1998; Murphy et al., 1995; Sulllivan et al., 1991). Inhibition of α-

motoneurons has also been demonstrated with stretch of homonymous

muscles (Burke et al., 1984; Etnyre & Abraham, 1986; Robinson et al., 1982;

Romano & Schieppati, 1987; Vujnovich & Dawson, 1994). Additionally,

stretch of muscles remote from the soleus produced an inhibition of α-

motoneurons when passive movement of the hip and/or the knee was

performed (Misiaszek et al., 1998). Muscle contraction facilitated the α-

motoneuron pool (Abbruzzese, Reni, Minatel, & Favale, 1998; McHugh,

Reeser, & Johnson, 1997; Miller, Newall, & Jackson, 1995) and passive

pedalling and stepping movements have been shown to inhibit the α-

motoneuron pool (Brooke, Cheng, Misiaszek, & Lafferty, 1995; Misiaszek,

Brooke, Lafferty, Cheng, & Staines, 1995). During gait, α-motoneurons of

various leg muscles were also inhibited (Brooke, Collins, Boucher, & McIlroy,

1991).

1.5.2 H-Reflex Parameter Used to Measure Changes

Measurement of the slope of the rising portion of the H-reflex recruitment

curve (Hslp) is a relatively new parameter used to assess H-reflex change.

Hslp has been shown to be a valuable indicator of the excitability of the α-

motoneuron pool (Bradnam et al., 2000; Funase, Higashi, Yoshimura,

Imanaka, & Nishihira, 1996; Funase, Imanaka, & Nishihira, 1994; Komiyama,

Kawai, & Fumoto, 1999). By analysing the central two-thirds of the rising

portion of the H-reflex recruitment curve, the variability in responses

associated with threshold level H-reflex responses (Crone et al., 1990) and

the possible extinction of H-reflexes at or near Hmax due to the collision effect

are avoided (Hugon, 1973).

It is argued that analysis of an H-reflex / M-wave (H/M) ratio or using the M-

wave as a covariate in analysis gives the change in H-reflex that is due to the

intervention and removes any variation due to the change in the M-wave (Bell

& Lehmann, 1987; Funase et al., 1994; Ruegg, Krauer, & Drews, 1990). The

analysis of the H/M ratio however, is flawed since changes in the numerator

(central H-reflex changes) or the denominator (peripheral M-wave changes)

can result in a changed ratio and the investigator is unable to distinguish to

what extent either value is responsible for the ratio change. Using the M-

wave as a covariate is also an unsound method for the same reasons.

The most satisfactory alternative to using a ratio or covariate analysis is to

ensure that accurate methods are used to establish M-wave stability. When

the M-wave is stable during testing, consistency in peripheral conditions is

assured and it is possible to analyse the H-reflex data alone without the

complicating factor of the M-wave included in a ratio or covariate analysis.

Bradnam et al (2000) have demonstrated that in subjects where the limb

being stimulated and recorded from was not moved, the Hslp parameter alone

was able to accurately measure changes in α-motoneuron excitability

(Bradnam et al., 2000).

1.5.3 M-Wave Stability Analysis

The M-wave is a short latency response that occurs as a result of direct

stimulation of the motor fibres of the tibial nerve during H-reflex recording

(Hugon, 1973). M-wave recruitment curve stability during recording of H-

reflex recruitment curves is an intrinsic means of controlling for possible

changes in the H-reflex due to factors affecting the peripheral stimulating and

recording environment. If a consistent number of motor fibres are recruited

in response to a given stimulus as determined by a stable M-wave, this will

result in a constant monosynaptic bombardment of the α-motoneuron pool by

Ia impulses (Taborikova, 1973). Similarly when identical M-wave recruitment

curves are recorded in separate experiments on the same subject, the

technical conditions for stimulation have been stable. In this manner changes

to the H-reflex can safely be attributed to a change in excitability of α-

motoneurons indicating excitatory or inhibitory influences on the motoneuron

pool (Hugon, 1973; Taborikova, 1973).

M-wave changes do occur using H-reflex experimentation in human subjects

(Allison & Abraham, 1994; Bell & Lehmann, 1987; Funase et al., 1994; Ruegg

et al., 1990). Change in the M-wave may indicate an alteration in the

stimulus intensity delivered to the nerve or a change in the population of

motor efferents stimulated. Thus a possible change in the population of Ia

afferents activated would confound the results of the experiment. M-wave

changes may also indicate a change in the conduction velocity of nerve fibres

(Bell & Lehmann, 1987) or a variation in the orientation of muscle fibres

under the recording electrode (Gerilovsky, Tsvetinov, & Trenkova, 1989;

Myklebust, Gottlieb, & Agarwal, 1984).

Factors producing a change in the M-wave may be responsible for changes in

the H-reflex amplitude. When this occurs it cannot be accepted that changes

in the H-reflex result from the intervention alone. The stability of the M-

wave, therefore, is an important component of experimental H-reflex

methodology. The correct analysis of M-wave stability is vital to establishing

the likelihood that H-reflex changes are attributable to central neural effects

of the intervention and do not result from an alteration in peripheral

stimulating and recording conditions.

1.5.4 Methods Used to Establish M-Wave Stability

Despite the importance of ensuring consistency in the M-wave amplitude

during H-reflex recording there is disagreement in the experimental literature

on the most valid method of M-wave stability analysis. Many experimenters

have not reported criteria used for monitoring M-wave stability or give

insufficient information about the criteria used (Abbruzzese et al., 1998;

Etnyre & Abraham, 1986; Gollhofer, Schopp, Rapp, & Stoinik, 1998; McHugh

et al., 1997; Robinson et al., 1982).

Stimulus Adjustment

In previous work authors have controlled for expected M-wave variation in

the M-wave by adjusting the stimulus intensity to the required percentage

(eg. 25% Mmax) of the previous Mmax recorded (Simonsen & Dyhre-Poulsen,

1999). This method is commonly used when analysing H-reflex changes

during gait (Brooke et al., 1995; Brooke et al., 1991; Capaday & Stein, 1987;

Simonsen & Dyhre-Poulsen, 1999).

Ratio or Covariate

Other studies have used the M-wave as a covariate with the H-reflex in

analysis in an attempt to remove the variability in the H-reflex that may be

due to variability in the M-wave (Bell & Lehmann, 1987). This method has a

fundamental flaw as has previously been discussed. The analysis of changes

to the H-reflex with the M-wave used as a covariate will indicate whether

changes seen are due to M-wave variability but the extent of those effects

cannot be established. By the same token, measuring the H-reflex as a ratio

of the M-response when there are visible changes in the M-wave (Ruegg et

al., 1990) gives no indication of whether the H-reflex or the M-wave or both

has changed and to what extent the change may have been.

Percent Deviation

Using a nominated percent deviation in the M-wave as a rejection criteria is

an accepted method for establishing the stability of the M-wave (Andersen &

Sinkjaer, 1999; Brooke et al., 1991; Misiaszek et al., 1995; Morelli et al.,

1999; Paquet & Hui-Chan, 1999). The M-wave should not deviate in any one

recording by more than 5-10% from the mean M-wave at the intensity level

chosen (Morelli et al., 1999; Paquet & Hui-Chan, 1999). Some authors have

used a variation of less than 2.5% (Brooke et al., 1995; Misiaszek et al.,

1998).

Statistical Analysis

Allison et al (1994) suggested that the method of percent change variation for

the M-wave was an inadequate rejection criterion when compared to using an

analysis of variance (ANOVA) criterion with the 95% probability (Allison &

Abraham, 1994). Testing for M-wave stability with ANOVA has been used by

many authors (Goldberg et al., 1992; Misiaszek et al., 1998; Morelli et al.,

1999; Morelli et al., 1991; Morelli et al., 1998; Sulllivan et al., 1991). A

contention with this method, however, is the inherent neurophysiological

variability in the population (Crayton & King, 1981; McIlroy & Brooke, 1987;

Williams, Sulllivan, Seabourne, & Morelli, 1992). Large inter-individual

variability in H-reflex and M-wave amplitudes makes the detection of a

significant difference within or between the group means extremely difficult

unless the difference is exceptional.

A specialised method of stability analysis for the M-wave recruitment curve is

lacking in the literature. Many of the above mentioned methods have been

demonstrated for use with constant stimulus intensity recordings (Andersen &

Sinkjaer, 1999; Brooke et al., 1991; Misiaszek et al., 1995; Morelli et al.,

1999; Paquet & Hui-Chan, 1999) or for use during gait (Brooke et al., 1995;

Brooke et al., 1991; Capaday & Stein, 1987; Simonsen & Dyhre-Poulsen,

1999) but it is questionable as to whether these methods are appropriate for

use with the M-wave recruitment curve methodology.

6 References

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