Phys. Ther. Rev.

1998; 3: 195-212

A modern interpretation of
the Rood Approach

The Rood Approach for the treatment of central nervous system

disorders was developed by Margaret Rood in the 1950s.Rood's
technique can be categorized as one of facilitation and inhibition
of movement. It is one of several of the neurophysiological
1 Physiotherapy Department, University of
Approaches which developed at that time and is centered upon
Hertfordshire, Hatfield Campus, College
four basic concepts to consider during treatment: duality, the
Lane, Hatfield, Herts AL10 9AB, U.K. and
ontogenetic sequence, manipulation of the autonomic nervous
2 Department of Health Science, University
system and the level of excitability of the anterior horn cell.
of East London, Stratford Campus,
As with the other neurophysiological Approaches (notably
Romford Road, Stratford,
Bobath, PNF and Brunnstrom), Rood's rationale for treatment
London E15 4LZ, U.K.
has been criticized for the naivete of its physiological rationale.
Although this criticism is justified, it does not mean that the
techniques are without value. This paper includes a brief
explanation of Rood's rationale for treatment and a review of the
literature which highlights the benefits and limitations of many
aspects of this approach. It can be seen that several of the
basic concepts are valid and viable within current neuroscientific
thinking. The conclusion is that the Rood Approach is a modular
model, and as such is capable of adapting to advancing
knowledge.

Key words: neurofacilitation; Rood; neurophysiology; treatment rationale; sensory stimulation;

physiotherapy; stroke rehabilitation

Introduction representations (or models) confined to essential

Ideally, therapeutic actions would be derived from a
full understanding of the events involved in a clinical
situation. In practice, however, the quantity of data
is overwhelmingly large and knowledge of processes
too sparse, so the therapist has to resort to partial
* Please address all correspondence to: Alison Baily Metcalfe,
Physiotherapy Department, University of Hertfordshire, Hatfield
Campus, College Lane, Hatfield, Herts ALIO 9AB.
components of the situation. Such models of a system
can be used to generate, and to justify, actions within
the system. Practice can develop empirically and a
post hoc model be attempted later.
Broadly, there are two styles of model: monolithic
models, in which every part is interdependent and
the entire model stands or falls as a single entity;
and modular models, in which components can stand
or fall independently without destroying the total
structure. Monolithic models tend to be deduced
from theory, whereas modular models tend to be

1083-3196/98/040195+ 18 $12.00/0 © 1998 W.E. Saunders Company Limited

196 A. Baily Metcalfe and N. Lawes
inferred from data. Monolithic models are often 'pur-
ist' and require a commitment to a single school of
thought; whereas modular models may be eclectic,
gathering their modules from whatever source con-
tributes. In a sense, monolithic models consist of
a single macro-model, while modular models are
collections of independent micro-models. Monolithic
models will tend to be intrinsically static because they
can develop only by wholesale revolution; whereas
modular models can be dynamic, evolving by gradual
reform of mistaken components. The recent rapid
development of new ideas in the Bobath Approach
is a good example of the latter.
Finally, construction of a model is not the final
step: wherever feasible, every assertion should be
tested empirically before it can be considered sci-
entific. Too often, a plausible model is left untested,
and by simple repetition comes to be seen as 'sci-
entifically proven'. Physiotherapy, like medicine in
general, has abounded with such untested models.
In its early life an untested model is a hypothesis,
stimulating exploration; in time though, when its
tenets have become enshrined in tradition, such mod-
els become dogmas, hindering development by clos-
ing practitioners' minds to the possibility of
alternative explanations. Explanations for the mode
of action of transcutaneous electrical nerve stimu-
lation (TENS) illustrate such a time course: a third
of a century ago, the underlying theory was a pro-
foundly stimulating influence, but now the same
theory delays exploration of newer, more molecular
explanations.
This paper examines one modet the Rood Ap-
proach. Is it monolithic, standing or falling in its
entirety, or is it modular, with components that can
be rescued despite fatal flaws elsewhere in the theory?
Can the original theories be replaced without aban-
doning the associated practices? Can more recent
formulations stand the test of scientific scrutiny, or
are they still speculative hypotheses awaiting con-
firmation?
What is Rood's Approach?
According to Stockmeyer,l Rood's philosophy of
treatment 'is concerned with the interaction of so-
matic, autonomic and psychic factors and their role
in the regulation of motor behavior'. This holism
is very much reflected in the organization of her
approach, and approach is an excellent word as Rood
described more of a philosophy of treatment than
anything absolute. Rood was an extensive reader and
based the techniques she proposed on the knowledge
of neurophysiology at the time combined with the
observations from her clinical practice.2
Rood's technique can be categorized as one of
facilitation and inhibition of movement. It was foun-
ded upon a Reflex/Hierarchical Model of the central
nervous system (CNS),therefore, it can be somewhat
focused upon basic circuitry and it relied heavily
upon the developmental sequence for its inspiration.
Although we now recognize these as flawed, there
are many aspects of Rood's Approach which still
deserve further consideration. This section will
briefly review the basic premises of Rood's model.
The basic points of Rood's Approach are:
Duality
The concept of duality is the basis of the entire
approach. Rood felt that the entire organism had
developed to respond in two ways. These are pro-
tection (mobility performed by light work muscles)
and growth of the individual through adaptation and
contact with the environment (stability performed
by heavy work muscles). Both muscles and receptors
are grouped to favor one of these functions more
than the other (although never exclusively). The de-
termining characteristics of muscles which favored
mobility or stability are listed in Table 1.
Ontogenetic sequence
Rood distinguished four bases for movement (in-
creasing in complexity):
These are roughly defined by Stockmeyer1 as follows:
Mobility - flexibility, both functionally and struc-
turally.
Stability - adequate fixation to allow weight-bearing,
it does not contain all the elements necessary for the
range of stabilizing which the body must manage.
Another term might be co-contraction.
 A modern interpretation
Table 1. Qualities of mobility and stability muscles in Rood's Approach.3
Characteristics of mobility
(light work) muscles
Phasic (fast glycolytic fibre type)
Superficial
Usually multiarthrodial
Fusiform or strap muscles
Small area of attachment
High metabolic cost/rapid fatigue
Tend to be flexors and adductors
+30mV
OmV
-50 mV ---------.- -.-----------------------.--
-70 mV JL-- .-!lAA-
t ttt ttt
Figure 1. Spatial and temporal summation of an AHC.
The arrows represent the strength and timing of the stimuli,
- 50 mV approximates threshold for the depolarization of
the cell.
Mobility superimposed on stability - a step beyond
the static maintenance of position, the distal end of
the extremity is fixed while the proximal end moves
over it. Rotation is a frequent result.
Distal mobility with proximal stability - the hand,
foot and tongue can move in discrete and finely
coordinated patterns.1
Effects upon the anterior horn cell
(AHC)
The theory works on the premise that the initial stages
of relearning movement can be enhanced through
facilitation, activation or inhibition of movement util-
izing afferent input to affect the AHC. These are
all based on the phenomena of summation - both
temporal and spatial (see Fig. 1).
Rood recognized that certain sensations seemed to
have different effects upon the AHC and that these
could be predicted based upon receptors and the size
of the Rood Approach 197
Characteristics of stability
(heavy work) muscles
Tonic (slow oxidative fibre type)
Deep
One-joint muscles
Pennate
Large area of attachment
Low metabolic cost/slow fatigue
Tend to be extensors and abductors
and qualities of the sensory fibres running from them.
She recognized four different types of receptors:
The basis of neurofacilitation techniques is the effect
of sensory stimulation upon the AHC through cir-
cuitry working at a variety of levels.4 Stimulation has
------------ an effect at the local spinal cord level and higher
centers through both short and long latency reflex
loops. The classifications of stimuli are provided for
quick reference in Tables 2 and 3.
To put the entire picture together, treatment is
based upon a number of considerations including:
Effects upon the autonomic nervous
system (ANS)
Rood's interest in the ANS was a continuation of her
idea that body systems had developed to aid in
the functions of mobility/protection and stability /
maintenance.s She recognized that motivation was
crucial to successfully regaining movement and that
there were several factors which aided motivation.
The patient must see the activity as meaningful and
as such, he must participate as much as he can in
all therapeutic activities. His participation may be
hindered by a high anxiety level, exaggerated emo-
tional responses, increased blood pressure, heart rate
or respiration, and hypertonicity-all responses af-
fected by the ANS. Rood's theory is that dominance
198 A. Baily Metcalfe and N. Lawes

Table 2. Rood's classification of the effects of proprioceptive stimuli.3

Facilitatory Inhibitory

Quick stretch Prolonged stretch

Resistance Inhibitory tendon pressure
Vibration (100-200Hz)
Traction
Tapping
Approximation

Table 3. Rood's classification of the effects of exteroceptive stimuli.3

Facilitatory Inhibitory

Light touch Prolonged ice

Quick icing Neutral warmth
Fast brushing Slow stroking

Table 4. Rood's classification of modalities useful for parasympathetic and

sympathetic system stimulation.6

Parasympathetic system responsive to: Sympathetic system responsive to:

Slow, rhythmical, repetitive rocking Icing

Rolling Unpleasant smells or tastes
Shaking Sharp, short vocal commands
Stroking the skin over the Bright flashing lights
paravertebral muscles Fast tempo, arrhythmical music
Soft, low voice
Neutral warmth
Contact on palms of hands, soles of feet,
upper lip or abdomen
Decreased light
Soft music
Pleasant odours

of parasympathetic or sympathetic activity affects What are the issues?

how the individual will interpret particular sensory
stimuli6 and therefore, manipulation of these stimuli
can be used in treatment. She suggested that the
intensity and frequency of the applied stimuli would
determine which system responded. Low intensity
and frequency of stimulation activates the para-
sympathetic system, the same stimuli at a high fre-
quency and intensity often excites the sympathetic
system.
Through appreciation of the effects sensory stimuli
have on a patient's unbalanced ANS, treatment can
be targeted specifically to redress the imbalance.
Table 4 categorizes stimuli as parasympathetic-
stirl1ulatingor sympathetic-stimulating according to
Rood's classification.
There are a number of issues concerning the building
blocks of Rood's model. This section will explore
these areas.
How you use Rood's techniques is dependent
upon the model of motor control to which you
subscribe
As Horak7 notes, 'each therapeutic rehab model in-
fluences how the therapist perceives the motor con-
trol problems in patients'. These are summarized in
Table 5. The Systems model maintains that normal
movements occur through the interaction of many
 A modern interpretation
Table 5. The views of the Central ervous System function based upon the different
models of motor controF
Model of motor control Goal of the central nervous system
Reflex To control individual and group muscle activation
Hierarchical To control initiation of movement in pattern
Systems To control motor performance in context of motor task
structures in response to the various demands upon
the nervous system. The dilemma is then in finding
a justified and valid argument for using any of the
neurofacilitation approaches, as their entire premise
is on production of parts of the whole in order to
regain normal movement. Several authorsS-lO suggest
that there is insufficient literature to argue that neuro-
facilitation techniques are without merit. Many of its
background explanations are incomplete, and many
techniques may be effective but not for the reasons
upon which they were first developed. As yet, no
model of treatment works universally. The argument
returns to one between monolithic and modular mod-
els.
At this point in time, emerging knowledge in the
field of Motor Learning suggests that a task-oriented
model of treatment should be most effective. But it
relies heavily upon the cognitive abilities of the
patient. If this is impaired, then the regaining of
movement might be facilitated more successfully
using a neurofacilitative method.
Can muscles be divided into the roles of
stability and mobility?
Although it is artificial to divide all the body's actions
into purely stability- or mobility-oriented, the concept
does have a certain degree of validity. Many muscles'
primary roles do tend to differentiate into postural
or powerful movements. Examples of postural and
powerful muscles are the soleus and the gastro-
cnemius, which fit Rood's classification of stability
and mobility muscles. This can easily be seen in their
fibre-type make-up, a property which had not been
discovered in Rood's time. Burke et a]l1,12 categorized
muscle fibre types into three classes, slow fatigue
resistant (tonic and postural), fast fatigable (phasic
and powerful) and fast fatigue resistant (phasic).
These correspond to Rood's stability and mobility
muscles, although it is recognized that this is an
oversimplification of muscle histochemistry, and that
no muscle is made of purely one type of fibre.13
Further defining characteristics of this division of
muscles are seen following CNS lesions. BurkeI4
of the Rood Approach 199
noted a difference in the reaction to stretch. While
slow stretch of spastic quadriceps resulted in in-
hibition and lengthening, the same stretch applied
to spastic hamstrings caused a build-up of over-
activity.14 Morphological changes in the fibre make-
up of muscles, secondary to the rearrangement of
motor units, have been found following a variety of
CNS pathologies, most notably spinal cord injury. IS-I?
stroke/8,19 and Parkinson's disease.2o,21Therefore, it
would seem both valid and practical to consider a
muscle's role and fibre-type during relearning of
movement.
How valid is the concept of the ontogenetic
sequence?
Developmental studies suggest that adult patterns of
behaviour emerge from a sequence of interactions
between inherited tendencies and experience-
dependent learning.22 These interactions begin with
simple tendencies relatively independent of post-
natal experience, often mediated by subcortical cir-
cuits (such as a tendency to look towards face-like
objects). These tendencies create selective experiences
(face-like images) which mould the development of
more sophisticated cortical circuits (capable of re-
cognizing specific faces, for example). The evidence
is not in favour of an exclusively innate unfolding
of predetermined movement, nor of the acquisition
of learned skills entirely dependent upon experience.
Consequently, the neurodevelopmental model
upon which Rood developed her ideas into the on-
togenetic sequence are generally accepted as out-
dated. Relearning of movement neither occurs from
proximal to distal, nor does it return in adults in a
style corresponding to development in children.
More contemporary models of treatment, especially
those of motor control and motor learning focus
treatment on the analysis of component parts of a
movement, finally combined into a task. This does
not seem incompatible with working on relearning
a movement through the progression of activities
which Rood suggested in the ontogenetic sequence.
One important concession Rood's model must make
200 A. Baily Metcalfe and N. Lawes
is that the sequence she suggests can no longer be
considered obligatory. It is entirely feasible that a
therapist might work with a patient to enable skilled
hand movements before concentrating upon shoulder
co-contraction.
How effective is stimulation of the AHC?
A number of issues arise in consideration of the
effects of sensory input on the AHC, both in the
normal and especially in the damaged CNS. Some
involve the rearrangement of CNS structures while
others centre on the relearning of movement.
eNS plasticity
Considerable reorganization takes place in the spinal
cord following damage to the central nervous system.
Reductions in presYnaptic, reciprocal (Ia), non-
reciprocal (Ib) and Renshaw cell inhibition occur.
Growth of new sYnapses, reconstruction of dendritic
trees, upregulation and downregulation of receptors,
transmitters and related enzymes have also been
observed or suggested. With so many changes oc-
curring simultaneously, it is unlikely that anyone of
them picked at random will correlate well with any
specified clinical phenomenon. It is far more likely
that many processes will have to be studied together
to determine their relation to several disparate clinical
phenomena, and dismissive reports that fail to con-
nect an identified process with a target phenomenon
are incomplete and premature. Maintained al-
terations in posture and in spinal reflexes have been
demonstrated, the changes being mediated by spinal
mechanisms additional to supraspinal learning. The
distal part of the cat transected spinal cord is able to
learn differentially to stand or to walk, for example.
The clear implication is that sensorimotor learning
is possible without the intervention of more complex
cognitive mechanisms such as attention and volition,
although obviously these greatly increase the ef-
ficiencyof learning. There is no reason to suppose that
sensory input is unable to effect long-term changes in
motor output without the participation of cognition:
it is barely conceivable that the distal end of the
transected spinal cord has any cognition, although,
despite this, it is capable of learning. Phylogenetically,
a capacity for learning preceded the evolution of
the cerebral cortex and human cognition by several
millennia. Any consistent pattern of sensory input,
such as therapeutic intervention, is likely to lead to
a sustained alteration of motor output, regardless of
more complex behavioural participation. Obviously,
if supraspinal mechanisms can be recruited, they will
greatly enhance acquisition and subsequent de-
ployment of new sensorimotor patterns, but they can
hardly be essential.
The discussion thus far has concentrated upon
the effects of stimulation at the spinal cord level.
However, it has been suggested that the architecture
of the sensory-motor cortex is such that sensory
stimulation can excite areas of the cortex.23 This is
based on the evidence that the sensory-motor cortex
is formed into cortical efferent zones which receive
information from both the muscle group and skin
for which that area is responsible. It is proposed that
sensory input can be provided therapeutically to
'wake up' motor responses from the cortex, which
have not been active secondary to the lesion. This
mayor may not be effective depending upon the
exact site of the lesion and the extent of its damage.
Dannenbaum and Dykes24 cite from a personal
communication with Merzenich that, in the sensori-
motor cortex, some neurons must remain intact in a
certain cytoarchitectonic area for the function of that
area to be regained. Jenkins et a[25 found that monkeys
trained to reach for food with only their middle
fingers developed an expanded cortical rep-
resentation of that finger, demonstrating that sensory
stimulation can have a direct effect upon cortical
cytoarchitecture. This reorganization of neural struc-
tures is not restricted to the cortex; dorsal column
nuclei have been shown to reorganize following peri-
pheral nerve lesions.26 The therapeutic significance,
especially with regard to Rood, is that there must be
some intact neurons in a particular cutaneous zone
and their stimulation might lead to enhanced re-
covery of movement. What percentage must remain
intact for this to occur is still unknown.
Sensory input diverges into several streams which
impinge on neurons at spinal, brainstem, cerebellar,
diencephalic, striatal and cortical levels. These mul-
tiple parallel streams interact throughout the neur-
axis, so that it is unlikely that the majority of sensory
inputs affect only one or two hierarchically distinct
levels. Singling out two areas of the CNS for dis-
cussion is recognized as somewhat artificial, but un-
surprising, as the spinal cord and sensory-motor
cortex are the most accessible and most studied.
The role of sensation in the recovery of
movement
The value of kinesthetic stimulation, first suggested
by Rood/7 has been advocated by some Motor Learn-
ing theorists for many years, working from the as-
sumption that a discrepancy between the kinesthetic
feedback and the motor programme allows necessary
adjustments to be made.28-3o This has been questioned
 A modern interpretation
by several authors who found that kinesthesia is
important, but not vital to acquisition and retention
of a skil1.31,32
In a randomized clinical trial of normals,
J arus and Loiter33investigated the effect of kinesthetic
stimulation on the acquisition of a lower extremity
skill and found that both performance and learning
were significantly enhanced in the kinesthetic group.
As kinesthesia involves both proprioceptors and ex-
teroceptors it was impossible to differentiate their
relative importance. The authors also suggested that
the increased attention to the joint studied might
have been a contributory factor, and it is likely that
it is the .combination of all elements which lead to
the enhanced learning.
The issue seems to be an argument of the relative
importance to movement of the open loop system, in
which sequences ofmovement are centrally stored and
accessed to cause movement patterns, and the closed
loop system which is dependent upon afferent feed-
back to elicit movement.28,34,35 Gandevia et al's31 find-
ings, that human subjects could successfully carry out
graded movements of the hand despite complete
absence of muscle afferent feedback, are frequently
cited as evidence to minimize the importance of the
closed loop system. Both systems are necessary in nor-
mal movements. The disagreements arise in de-
termining which system should be stimulated during
the relearning of movement in therapy. Contemporary
theorists highlight the importance of the open loop
system, but their arguments have been interpreted as
though this is to the exclusion of additional facilitation
via the closed loop system. As normal function in-
cludes the use of both systems, why shouldn't the
relearning of function utilize the same?
Carr and Shepherd36argue that sensory stimulation
to facilitate functional movement is ineffective, based
on the suggestion thatthe brain only attends to sensory
input which is relevant to the task. This is a con-
troversial issue. Researchers in the area of visuomotor
control are divided on the importance of attention in
successful functional movement. From his review of
the literature, Stein37concludes that, 'redirecting at-
tention ... allows us to consciously localize objectswith
respect to ourselves and thus plan voluntary move-
ments toward them'. However, Goodale et ap8 have
demonstrated that human subjects can make accurate
eye and hand movements to targets that move during
primary saccades so that the subjects cannot perceive
their movement. Furthermore, Lee et ap9 found that
their subjects, exposed to a moveable room, made pos-
tural adjustments despite being unaware of both the
tilting room or their own movements.
Finally, it has been found that the enhanced muscle
activity may not last beyond the stimulus ap-
plication.40 Studies of the phenomenon are limited
of the Rood Approach 201
and there has been no research to examine the ability
of sensory stimulation to enhance functional move-
ment over a long period of time.
Support for the positive role of sensation in re-
covery is the suggestion by Okuma and Lee/1 based
on their findings in humans of adaptive and mal-
adaptive reorganization of reciprocal inhibition fol-
lowing stroke, that early intervention, in the form of
stimulation, aids in the process of adaptive remolding
of the CNS and the diminution of spasticity.
All arguments provided thus far are not sufficiently
substantial to negate the value of sensory stimulation.
They do strongly suggest that the patient should be
involved as much as possible in the process and
closely attending to the stimulus as part of the final
response. It is also clear that when assessing a task,
the therapist must consider how best to promote
both the open and closed loop aspects of that task.
And in fact, Carr and Shepherd36 citing evidence
from Proteau42and Abrams and Pratt,43concede that,
'as a result of practice with relevant inputs and
feedback, individuals may be better able to use the
information available'.36
The relationship between sensory stimulation
and spasticity
Normalization of muscle tone, particularly the re-
duction of spasticity, is a primary goal of treatment in
many neurophysiotherapy approaches, most notably
the Bobath Approach. Surveys carried out in
Sweden44 and Australia45 found that normalizing
tonus was a major determinant for the most popular
choice of treatment (weight bearing) in Sweden, and
an important factor for those using the Bobath Ap-
proach in the Australian study. The common as-
sumption that sensory overactivity will further
stimulate increased spasticity has been refuted by
Burke14 who reports that disruption of the reflex
arc by posterior root section does not abolish the
spasticity which is already present. This supports
the argument that spasticity is not purely nervous
system-mediated. It also suggests that while sensory
stimulation may cause a response to a degree dif-
ferent to that desired, it should not increase spasticity.
Spasticity is a complicated phenomenon so that it
is impossible, at our current level of knowledge, to
make a blanket statement regarding the effect of
sensory stimulation on spasticity. The issue can be
simplified somewhat by dividing spasticity into its
component parts. Katz and Rymer46concluded from
a review of the literature that the upper motor neuron
syndrome consists of both negative and positive
symptoms. However, as noted by Bethune,8'although
clinicians often attribute inability to move to spas-
202 A. Baily Metcalfe and N. Lawes
ticity, spasticity is the result, not the cause, of the
loss of spontaneous movement'. To reinforce this
point, Landau47 proposed that there is no evidence
that inhibition of abnormal tone promotes motor
function or enhances recovery.
It is important not to confuse the concept of in-
hibition of spasticity (to which Landau refers) with
that of physiological inhibition, a well recognized
central nervous system phenomena. It is this physio-
logical inhibition to which Rood refers, with the
intention that its application will facilitate pre-
synaptic inhibition thereby improving the chance of
more normal movement.
Facilitated movements are not learned
Critics of the Neurofacilitation approaches argue that
if patients' movements are not self-initiated then they
are not learned. The counter argument is that patients
often cannot initiate a movement, either because the
necessary muscles cannot generate enough force or
because their antagonists prevent their movement.
By bombarding the AHC, thereby causing sum-
mation, you increase the probability that contractions
will be initiated. Once this occurs, active movement
can then be encouraged so that the functional move-
ments can be learned. As the Systems Model does
not deny the existence of reflexes, and they can be
used to initiate a movement, then it would seem
sensible to utilize sensory-stimulated movements
thereby adding to the repertoire of treatments at
therapists' disposal.
Duality
Using more contemporary terminology, Rood's light
work and heavy work muscles could correspond to
muscles with a predominance of phasic (fast glyco-
lytic) and tonic (slow oxidative) motor units, re-
spectively. Slow oxidative motor units have lower
current threshold,48,49so that they reach the voltage
threshold necessary for action potentials at lower
currents than do fast glycolytic units. This places a
higher metabolic demand upon slow muscle fibres,
leading to the metabolic changes characteristic of
these units.50 Possibly as a result of functional plas-
ticity during and after development, the slow ox-
idative units have a preferential input from Ia
afferents,51whereas fast glycolytic units have a dif-
ferential input from rubrospinal axons.52 In con-
sequence, slow oxidative units will contribute mainly
the low forces needed to counteract gravity in pos-
ture, whereas fast glycolytic units will provide the
high forces necessary to accelerate a body segment
into movement. These extremes of the motor unit
spectrum correspond to Rood's concept of stability
and mobility muscles.
The validity of treatment utilizing the ANS
Since the days of Cannon and others, it has been
evident that emotional states are accompanied by
visceral changes. James53 took the extreme view that
emotional states are determined by peripheral auto-
nomic events, but this has proved to be an over-
statement. Peripheral autonomic changes amplify
emotions but tend not to cause them in the absence
of plausible external circumstances. A more credible
model is that central circuits involved in emotion
and in motivation are strongly connected to auto-
nomic and neuroendocrine systems, so that emotional
states are accompanied by, and reflected in, auto-
nomic and endocrine changes which, in turn, feed
back to modulate the emotional state. These central
circuits, principally residing in the orbitofrontal cor-
tex, limbic cortex, amygdala, hypothalamus and
brainstem, influence somatic sensory and motor func-
tion as well. A prime example is the alteration in the
cutaneous receptive field eliciting the bite reflex in
carnivores: when hungry, the cutaneous field ex-
pands, shrinking again on satiation. The reticular
formation, informed by the cerebellum, has con-
siderable influence on the influx of sensory in-
formation at a spinal level, re-routing, permitting
and attenuating input to fit current circumstances.
Actions of the amygdala and periaqueductal grey
matter controlling noxious input in different states
of arousal and stress are additional examples of
emotional states controlling and filtering sensory
input. Thus, although autonomic accounts of emotion
have an antiquated flavour to them, related circuits
governing emotional state have a powerful influence
on what information may enter the CNS, and thereby
on what motor patterns will emerge in response. It
is hardly necessary to point out that any nervous
student entering a practical exam can confirm the
effect of emotion on attention and motor per-
formance.
It has been evident for some decades that the
assumed opposition between sympathetic and para-
sympathetic systems was a distortion: more often
they work interactively. Furthermore, alleged ant-
agonisms attributed to these systems have sometimes
turned out to be mediated by the same cells. For
example, low frequency stimulation of a neuron tends
to release conventional excitatory amino acid trans-
mitters from small clear vesicles, whereas high fre-
quency stimulation of the same neuron releases
 A modern interpretation
peptides from large, dense-cored vesicles. Therefore,
the link between types of stimulation and com-
ponents of the ANS is at best unnecessary and at
worst spurious.
Conclusion
In her review of the Bobath concept, Lennon9 ac-
knowledged the many factors which must be con-
sidered when planning a treatment programme,
'Clues from the environment will shape movement,
and emotion, arousal and cognitive states will in-
fluence the patient's ability to move. Varying com-
bination of afferent inputs will improve motor
performance in different patients according to which-
ever systems are intact or impaired following stroke.
The difficulty lies in deciding which systems to access
in therapy to promote recovery'. The CNS is a com-
plex system so that methods of accessing it following
damage, and aiding advantageous plastic recovery
must be individualized for each patient. Although
Rood's Approach was based on a Reflex/Hierarchical
view of the nervous system, as a modular model, it
has components which can be justified in light of
current scientific evidence. The previous section has
demonstrated that aspects of Rood's Approach are
valid and viable.
Putting the theory into practice
Having explored both Rood's philosophies and the
literature which supports and refutes them, it would
appear that of the four concepts, only that of duality
and anterior horn cell stimulation have survived in
a form recognizable from the original. Attention to
the ANS in treatment may still be a useful con-
sideration, but the understanding of the workings of
the ANS has advanced significantly so that Rood's
treatment suggestions are too simplistic. As has been
shown in research carried out since Rood's time, there
are more accurate explanations of the mechanisms by
which some of her ideas work and hence a more
accurate picture of how best to use her techniques.
The following sections will cover these suggestions
with an explanation of the physiological processes
which could be involved.
Duality
Knowledge of a muscle's predominant fibre-type will
enable the therapist to choose a modality of stimu-
lation which is most likely to gain the desired re-
of the Rood Approach 203
sponse. Garnett and Stephens54 observed from
Burke's55work that, 'cutaneous afferent input is not
distributed in qualitatively the same way to all motor-
neurons; for some its effects are excitatory while for
others its effects are inhibitory. Indeed, considering
only excitatory effects,the pattern for cutaneous input
is roughly the reverse of that found for Ia input
whose excitatory effect is most marked for type S
cells (tonic), and least effective for type FF (phasic)
cells.' The clinical significance of this information is
that cutaneous or exteroceptive stimulation would
appear to be largely inhibitory for tonic muscle fibres
and excitatory for phasic fibres. If the facilitation of
a tonic muscle is desired then Ia (proprioceptive)
fibres should be stimulated. If a predominantly phasic
muscle's response is desired, then cutaneous (ex-
teroceptive) stimuli should be utilized. This concept
will be revisited during consideration of the effects
of the modality of light touch.
Effects upon the AHC
Kidd et a1.56 state that the spinal cord is capable of
producing all basic patterns of movement auto-
nomously and that it contains the circuitry necessary
for all the more sophisticated movements and pos-
tural adjustments. The motorsensory cortex and
brainstem direct the spinal cord to produce these
movements. They can be initiated from the frontal
cortex and through sensory input to other areas of
the cerebral cortex. This suggests that in a damaged
CNS, the spinal cord may be a prime site from which
to stimulate movement. While they also go on to
suggest that peripheral inputs may raise the level of
excitation of some specificneuronal pools and inhibit
activity in others, how this occurs, and the specific
stimuli that should be used on which receptors is
still open to speculation. Rossignol and Gautier57
suggested that flexors and extensors have specific
pathways from receptors, but it seems most likely
that the pathways are not direct or straightforward.
Kidd et a1.56 suggest that modulation of transmission
in spinal reflex pathways is governed by a vast
network of pre- and post-synaptic inhibition. The
challenge is to determine the receptors which are
most potent in influencing abnormal movements.
Rood suggested that appropriate stimuli are chosen
based on several factors, whether facilitation or in-
hibition is desired, and which type of movement
is required, mobility or stability. Specific receptors,
proprioceptors and exteroceptors are targeted based
upon their ability to influence the excitability of
reflexes and motorneuron pools, in the spinal cord,
brainstem, and the cerebral cortex. From these bases,
204 A. Baily Metcalfe and N. Lawes

Table 6. Classification of afferent nerve fibres.58

Nerve fibre type Sensory organs from which they originate

Group Ia Muscle spindle

Ib Golgi tendon organ
Group II Touch & pressure receptors from skin joint receptors
Muscle spindle secondary ending
Group III Pressure receptors
Thermoreceptors
Nociceptors
Group IV Nociceptors
Some thermoreceptors

Rood used four principles to guide her choice of

sensory stimulation:

Unfortunately these rules are not quite so straight-

forward. While the stimuli in Tables 2 and 3 appear
to be equal in their effectiveness, there are several
characteristics of the receptors which make some
more effective than others. The important char-
acteristics are the type of afferent fibre and the point
at which it affects the alpha motor neuron.
The receptors listed in Table 6 are grouped in
descending order of afferent fibre size and hence
speed of transmission. Therefore, the influence of
group II afferents is less effective than that of group
I as a result of group II's smaller size and because
they make polysynaptic connections to the motor Figure 2. Post- (A) and pre- (B) synaptic cell influences
neuron pool as compared to the group 1's monosyn- upon an anterior horn cell.
aptic connection. 58 For example, if the aim was to
facilitate a contraction, a quick stretch would be most
effective. If the aim was to allow the muscle to
lengthen, a slow stretch would be appropriate as it stimulus as it only modulates one of the many in-
would be least conducive to a contraction. fluences on the cell body's excitability, whereas im-
As proposed, a major factor influencing effectiveness posing directly upon it exerts a much greater effect
of stimulation is whether the receptor facilitates or in- (see Fig. 2). However, pre-synaptic inhibition is more
hibits at the AHC directly or presynaptically. Which effective if the objective is to selectively tum on certain
mechanism is most effective is dependent upon the ac- cells and tum off others, for example, if the patient
tivity the therapist wants to facilitate. If the goal is to needs to increase activation of the dorsiflexors and in-
excite cells for a specific purpose, for instance, to tum hibit the plantarflexors. While this is potentially useful
on the anti-gravity muscles to enable someone to stand, information for practice, there is insufficient evidence at
then a direct stimulus is more effective. Presynaptic present to determine the mechanism of each modality.
inhibition (and facilitation) is not as 'potent' as a direct Our ability to predict the effects of specific stimuli is
 A modern interpretation
still rudimentary. For example, while there is a great
deal of evidence to suggest that receptor stimulation
leads to heightened excitation of the AHC through
stimulation of reflexes6D-62 and through summation59
this cannot be applied as an equal rule throughout the
body. For example, textbooks state that stimulation of
Group II, III, and IV afferents from the skin produces
excitation of flexor motor neurons and inhibition of
ipsilateral extensor motor neurons regardless of the site
of stimulation.59However, the pattern of response is not
always this consistent. Davey et al.63 found in pre-
liminary studies of normals, using transcranial mag-
netic stimulation of the motor cortex, that cutaneous
stimulation around the thumb varied in its ability to
facilitate from points located very close together. This
may have been due to the effectsupon the different fibre
types. Garnett and Stephens54found through electrical
stimulation of the digital nerves in normals that cu-
taneous stimulation has an inhibitory effect on slow
twitch, low threshold motor units and an excitatory
effect on high threshold fast twitch units. They spec-
ulated that the functional significance of this phe-
nomenon was that, especially in the hand where a
powerful pinch and grip are frequently required, a fa-
cilitatory effect of cutaneous stimulation would result
in less need of descending drive to produce the desired
force. This idea fits in with the results of Chen and
Ashby64who also used stimulation of the digital nerves
to investigate cutaneous reflexes in normals. They
found that cutaneous reflexes were more prominent
in the small muscles of the hand than in the forearm
muscles and that the proximal musculature (biceps/
triceps) had a special reciprocal relationship not seen
in any distal muscles.
The effects of stimulation may become even less pre-
dictable with the addition of disruption of the central
nervous system. Several authors have suggested that
the spinal cord excitability changes following upper
motor neuron lesions.65,66 Okuma and Lee41proposed
that, as a result of reduced descending motor drive to
flexor Ia interneurons, certain motor neurons com-
pensated by increasing their excitability,and this man-
ifested itself in significant functional changes. They
found increased Ia inhibition from anterior tibialis
flexor afferents to soleus (extensor) motor neurons cor-
related with good recovery of strength and minimal
spasticity, whereas Ia inhibition to the tibialis anterior
motor neurons was greater in the poor recovery
patients with marked spasticity. Although not spe-
cifically tested, the authors suggested the mechanism
for improving Ia inhibition from flexors to extensors
was to aid this synaptic modification through intensive
physiotherapy, specifically repeated attempts to pro-
duce ankle dorsiflexion. This is a direct example of how
a movement, facilitated through afferent stimulation,
of the Rood Approach 205
can aid plastic changes which will enable the patient to
activate complete motor programmes.
The conclusions which can be drawn from the
physiological literature at this point are limited. Cu-
taneous stimulation does have the ability to alter the
threshold (indirectly) of the AHC. The direction of the
change in threshold appears to be dependent upon the
location of the receptors and the type of muscle fibre
involved. The effects in damaged nervous systems are
still largely unknown.
Having examined the mechanisms by which the
AHC can be influenced, the following section will re-
view the forms of stimulation for which there is evi-
dence of efficacy.It is important to note that none of the
studies cited have been large-scale randomized clinical
trials. Rarely have there been resources to enable this
kind of study, but it highlights the difficulty in making
definitive claims about the effectiveness of physio-
therapy treatment modalities. As a consequence, the
results presented must be interpreted cautiously. Sev-
eral texts provide an excellent interpretation of Rood's
techniques should the reader require a more in-depth
description of application.3,lo,67--j)9
Proprioceptor-stimulating modalities
Proprioceptive techniques are based on facilitation
of muscle spindles, golgi tendon organs and joint
receptors. As a result of the types of receptors stim-
ulated there is very little recruitment, so that the
motor response lasts only as long as the stimulus is
applied.lOClinical use often involves the combination
of several techniques, exteroceptive and proprio-
ceptive, in order to maximize the effects through
summation.
Quick stretch
Rood suggested that quick stretch was most effective
on the phasic muscles because the response is phasic
in nature. However, as it works via stimulation of
the primary muscle spindle endings and the Ia alpha
motor neuron monosynaptic reflex,59,7o it ought to be
more effective in tonic muscles where there is a
greater proportion of receptors.71 It can be used to
facilitate a contraction or to accentuate an already
occurring contraction through autogenic facilitation.
The effect is immediate and short-lived so that any
reaction must be further stimulated, for instance
through resistance, to maintain the contraction. Quick
stretch is also used in other neurofacilitation tech-
niques, particularly proprioceptive neuromuscular
facilitation (PNF).72As Rood's techniques are often
206 A. Baily Metcalfe and N. Lawes
applied to the face, it is worth noting that because
the muscles of facial expression, as well as the di-
gastric do not contain muscle spindles, their ac-
tivation will be best through exteroceptive
stimulation and not stretch.58
Tapping
Tapping of the muscle belly is another form of quick
stretch, designed to stimulate muscle spindles and
cause a brief phasic contraction. Toincrease the effect,
O'Sullivan3 recommends that tapping follow po-
sitioning the muscle on stretch and against gravity,
while the patient attempts an active contraction, to
cause summation. Because tapping works on the
same physiological principles as quick stretch, if the
muscle is responsive to stretch then tapping ought
to augment the desired contraction.
Resistance
Rood advocated the use of resistance in a variety of
ways to stimulate both tonic and phasic muscles. 1As
resistance stretches the sensory part of the muscle
spindle thereby increasing the drive to the extrafusal
fibres, greater resistance produces a greater response,
up to a point. It was suggested that resistance to
muscles in their shortened range, or isometrically,
facilitated spindles in the deep postural muscles, and
that resistance in a more lengthened position, or
throughout the range of movement, stimulated the
mobilizing muscles. These principles are supported
by work carried out in a number of areas.73,74
Vibration
Vibration is one of the most studied of the prop-
rioceptive techniques. Extensive work has been car-
ried out by Eklund and Hagbarth75-77and the
physiology and clinical application reviewed by
Bishop.78-80 Vibration at high frequencies (100-300 Hz)
is facilitatory through stimulation of the tonic vi-
bratory reflex (TVR) via muscle spindles and Ia af-
ferent fibres. Bishop78 found that four factors
strengthened the TVR:
The effect is similar to a series of quick stretches
so that it causes a sustained contraction through
stimulation of the TVR and reciprocal inhibition of
the antagonist muscle.
Using the effects of vibration on the TVR 'in re-
verse', Lovgreen et al81 applied a vibrator to the ant-
agonist muscle of patients with cerebellar dysmetria.
They found that the amplitude of the hypermetric
movements decreased significantly, but that the ap-
plication of the vibrator was difficult due to the
nature of the disorder.81
Another less-studied use of the vibrator is to de-
sensitize hypersensitive skin through low frequency
vibration.6,lo Stimulation at frequencies between
50-60 Hz is thought to stimulate pacinian corpuscles
thereby suppressing the impulses along A delta and
C fibres.78-80
Traction and approximation
Most therapists will be familiar with these techniques
through their use in PNF. What research has been
done has mainly targeted the effects of ap-
proximation/joint compression. Rood's theory was
similar to that of Voss et aF2 who advocated the
use of traction to facilitate the mobilizing muscles
through stretch, and joint compression of greater
than body weight to facilitate stabilizing muscles.
Goff69explains the mechanism by which this was
thought to work as one in which compression inhibits
spasticity as well as promotes the activation of sta-
bility muscles. This idea was based largely on the
work and recommendations for practice by Wyke82
in which he proposed that Type I and IIjoint receptors
work to inhibit protective muscle spasm and elicit
proximal joint stability if stimulated correctly. Some
texts refer to approximation as 'jamming',68 which
sounds more forceful than approximation. The ap-
plication of jamming seems to be limited to use in
the lower extremity where the goal is to inhibit
plantarflexion and facilitate co-contraction around
the ankle. It is a combination of stimulation of joint
receptors within the ankle and osteopressure on the
heel. Evidence of efficacy is largely anecdotal for
both forms of approximation so that further work is
required before a verdict can be reached.
Prolonged stretch
Rood's27 recommendation of prolonged stretching
was based on the idea that it would cause the muscle
spindle to 'reset' in a longer, less easily excited state,
thereby causing inhibition. The concepts that muscles
 A modern interpretation
held in a shortened (or lengthened) position re-
structured their sarcomeres,83,84 and that golgi tendon
organs have a variety of roles85had not been re-
cognized at that time. This is one of many examples
where the practice was effective even though the
underlying mechanisms were unknown.
Despite the wealth of research which has been
published on the effects of stretch, both in normals
and in those with spasticity, there remains con-
troversy about the amount of time and degree of
stretch required to overcome spasticity. This is no
doubt a result of the fact that spasticity is an amalgam
of abnormalities,86each of which responds to stretch
differently. For instance, while Williams87found that
daily stretch of immobilized mouse muscle for 30 min
prevented the loss of sarcomeres and changes in
connective tissue, often cited as contributing factors
to 'spasticity'. Tardieu et al's88 study of CP children
found that 6 h per day were needed to prevent con-
tracture. Hale et aZ89 looked at the effects of stretching,
specifically on spasticity, which was measured by a
variety of subjective and objective methods-
analogue scale, Ashworth scale, speed of active flex-
ion and extension, and pendular test with an
isokinetic dynamometer. They found that a 10-min
stretch was more effective than 2 or 30min in re-
ducing spasticity. The discomfort of holding the
stretched position for 30 min, thereby increasing the
tone, was the suggestion given for its reduced ef-
ficacy.
Splinting and serial casting have both been found
effective as methods of reducing spasticity and pre-
venting or reducing contracture.91-95 The addition of
maintained contact may also have an exteroceptively-
mediated inhibitory effect, while the tendon pressure
applied during casting may have added a prop-
rioceptively-mediated inhibitory effect. However,
Goldspink and Williams90 advocate intermittent
stretching, rather than permanent, to avoid the
atrophy of the antagonist muscle.
Inhibitory tendon pressure
Rood27advocated the use of pressure from a hard
surface on the tendinous insertion of a muscle or
across the long tendons to produce inhibition of the
attached muscles. McCormacklOproposes that this
stimulates pacinian corpuscles and possibly golgi
tendon organs to cause autoinhibition. It is possible
that in some instances, inhibitory tendon pressure
is effective through the stimulation of acupressure
points.
Leone and Kukulka96 investigated the effect of
intermittent and continuous pressure at 5 and 10kg,
of the Rood Approach 207
on the Achilles tendon of subjects who had sustained
a CVA. Measurement of the soleus' H-reflex was
used to determine the excitability of the motorneuron.
Intermittent pressure was defined as one application/
second. While both intensities of intermittent pres-
sure and 5 kg of continuous pressure were found to
have a significant effect, these results lasted only as
long as the stimulus was applied. Muscle tone itself
was not measured, this was inferred from the changes
in motorneuron excitability. These findings were con-
sistent with those of Burke et aZ97 who examined
the effects of tendon pressure on spastic muscle in
subjects with spinal cord injury.
Exteroceptor-stimulating modalities
Rood's theory was that exteroceptive modalities tend
to cause rapid limb movements and increased arousal
whereas the slow, rhythmical ones induce calmness
and release, or stability if maintained instead of
rhythmica1.6,98,99
This idea is relatively sound given
the previously covered findings of Burke,l1,12,97
Kanda,?l
and Garnett and Stephens.55
Quick icing
Quick icing was advocated by Rood as a method of
facilitating muscle activity by stimulating A delta
fibres.1Knuttson et aZIOO reported that it has a localized
facilitatory effect on the tonic vibratory reflex. Al-
though its use is advocated in a number of skills-
oriented books,69,lOl,103others caution that it may pro-
duce unpredictable results.68The concerns are mainly
the effect upon arousal and the stimulation of a reflex
withdrawal response. The facilitation of the reflex
is also a subject of controversy, as Selbach104has
suggested that following the reflex a rebound occurs
such that the facilitated muscle is inhibited and the
antagonist is facilitated, so that a second stimulus
might produce exactly the opposite to the desired
response. These effects do not occur in all people,
probably as a result of individual differences in de-
gree and site of CNS damage. They also may not
necessarily be detrimental, but should be carefully
monitored.
Fast brushing
Fast brushing is one of the most controversial of
Rood's suggested modalities. It was recommended
that the brushing be applied to the derma tomes of
the same segment that supplies the muscles to be
208 A. Baily Metcalfe and N. Lawes
facilitated, approximately 30 min before the desired
effect. Rood suggested that brushing worked through
stimulation of C fibres and therefore the reticular
activating system.4 However, there is no evidence
that C fibres are involved, and arousal is not as
straightforward as Rood presented. It is likely that
any arousal involves cortical components related to
the novelty of the stimulus. Umphred and McCor-
mack68 warn that brushing works on the same prin-
ciple as quick icing so that caution should be used
if it is chosen for application and its effectiveness
closely monitored.
Spicer and Matyas105 in their comparison of icing
and fast brushing found the latter to be more effective,
and that both were most effective during the time of
stimulus application. Garland and Hayes106 found a
significant increase in EMG activity of hemiplegic
dorsiflexors during stimulation and at 30 min after-
ward. It appears that on the basis of a limited number
of studies, brushing is capable of producing a re-
sponse over a short time period, but the most effective
method of application is still undetermined.
Light touch
Rood2 advocated the use of light touch or stroking
of the skin to activate the phasic muscles. Light touch
activates low threshold mechanoreceptors which
send stimuli along A beta and A alpha fibres to
increase mobility. It can be applied to a specific area,
especially the fingertips and soles of the feet for a
mass movement, or applied over the derma tomes of
the muscles from which a more controlled movement
is required. Any movement elicited can be im-
mediately followed with resistance to enhance the
response.
Research in cats71 and humans55 has shown that
the normal order of recruitment of muscle fibres,
tonic followed by phasic, can be reversed following
electrical stimulation of low threshold mechano-
receptors. It is suggested that this occurs because
the weighting of synaptic input to different motor
neurons varies according to the motor command.85
The functional significance is that by recruiting phasic
fibres first, the animal can make very fast movements
(in cats, a rapid paw shake) with which tonic fibres
could not keep up and would therefore hinder if
firing. With regard to treatment, this research gives
credence to the hypothesis that stimulation of low
threshold mechanoreceptors, such as through light
touch, does preferentially fire phasic fibres. The
challenge for the physiotherapist then is to select
muscles with high phasic fibre proportions so that
the modality is used to greatest effect.
Prolonged icing
Rood suggested the use of prolonged icing to reduce
the activity of the AHC. Its underlying physiology
is not totally understood, but it is thought that despite
facilitating the alpha motor neuron, ice depresses
the muscle spindle excitability, thereby reducing the
phasic stretch reflex.24 There is also an overall re-
duction in metabolic rate of the tissues being cooled,
which leads to decreased activity,68 as well as a
slowing of conduction in the muscle, motor nerves,
and particularly the gamma efferents which are more
susceptible to cooling than alpha efferents.107
Several studies have shown that icing significantly
reduces spasticity. Miglietta108 found that after cold
application for 30 min, clonus was significantly re-
duced in 35 out of 40 patients, if the muscles them-
selves were sufficiently cooled. Price et al109 had more
variable results. The subjects consisted of people who
had had a stroke, closed head injury, or spinal cord
lesion. Two-thirds of them experienced a significant
decrease in elastic and viscous stiffness (the definition
of spasticity for this study). However, the other one-
third of the subjects experienced an increase in stiff-
ness, only two of whom to a significant level. Price
et al suggest that these subjects had the lowest levels
of spasticity and thus had least to change. Never-
theless, this highlights the paradoxical effect of tissue
cooling often referred to in the literature and em-
phasizes the need for close observation of effect.
Neutral warmth
The effects of neutral warmth are one of the least
studied of Rood's techniques. It is an inhibitory tech-
nique which can be applied as a tepid bath or through
extremity or body wrapping.3 JohnstonellO proposes
that the effectiveness of air splints in inhibiting spas-
ticity is partially due to the maintained pressure and
warmth which they provide, although she offers no
direct evidence to support her ideas. Twist111 studied
the effects of wrapping, using gloves and elastic
bandages, on the spastic upper extremities of four
patients recovering from stroke. All patients dem-
onstrated a significant increase in range of motion
(attributed to decreased spasticity) and decreased
pain, following 12 wrapping sessions. But as this
study had so few subjects and no control group the
results must be interpreted cautiously.
Dannenbaum and Dykes24 suggest that warmth
does not affect muscle tone directly, but works in-
directly through the autonomic control of muscle
tone during thermoregulation. However, as neutral
warmth is defined as 35-37°C, it is unlikely that
 A modern interpretation
thermal changes so close to body temperature will
cause stimulation of thermoreceptors. It is more likely
that the inhibition seen is due to inhibition of tonic
muscles via stimulation of the low threshold me-
chanoreceptors through light pressure.
Slow stroking
Goff69 writes that the inhibitory technique of slow
stroking was thought to 'reduce the central excitatory
state of neuronal sets of lower motor neurones in the
brainstem and spinal cord'. This view is echoed in
broader terms by Umphred and McCormack68 who
state that it is not the technique but the type of
movement (slow) employed. Brouwer and Sousa de
Andrade1l2 found slow stroking over the dermatomes
of the posterior primary rami of patients with MS,
was effective in reducing AHC excitability as meas-
ured by a reduction in H wave amplitude. There is
clearly insufficient evidence to support or refute the
use of slow stroking at present.
Caveats
Not all patients will respond in the same way to a
particular technique. A lack of response, especially
an immediate one, does not mean there has been no
effect. There may have been facilitation of the AHC
but not sufficient to cause activation. However, it
should make activation more likely next time, so close
monitoring for contractions is essential to determine
effectiveness of the technique
Sometimes there may be a paradoxical effect,where
the stimulus causes an effect opposite to the one
expected. Rood suggested that this was most likely
due to an imbalance in the ANS. However, there is
an alternative explanation. It has been suggested that
spasticity following complete spinal cord injury may
be due to afferent fibres covering the synapses left
vacant by the degenerated descending fibres. These
new connections give the afferent information an
enhanced role which may include making certain
reflexes more powerfuU9 Therefore, stimuli have the
potential to cause responses very different from those
expected.
The loss of descending inhibitory inputs to the
lower motor neurons can cause loss of both pre-
and post-synaptic inhibition. This may affect specific
muscle groups to different degrees.59 The un-
predictability of these changes gives further reason
to observe treatment effects closely.
of the Rood Approach 209
Conclusion
This review has attempted to show that Rood's Ap-
proach can be treated as a modular model and that
its practice can be dissociated from its theory. Parts
of the approach, such as the reliance on ontogenetic
sequence, are not sustainable. Other parts, such as
the influence of the autonomic nervous system, could
benefit from reformulation within a more a modern
framework of neural systems. But parts of the ap-
proach remain compatible with current neuroscient-
ific thinking, at least at the level of constructing
plausible explanatory hypotheses. The main chal-
lenge remaining, as for most schools of thought
in physiotherapy, is to devise a means of testing
explanatory hypotheses by empirical research. As
evidence becomes available, it is likely that the dif-
ferent schools of thought will converge, at least to
the extent that they are modular and data-driven
models. Monolithic and theory-based models, on the
other hand, are unlikely to be capable of adapting to
advancing knowledge and will, no doubt, pay the
evolutionary penalty for such inflexibility.
References
1 Stockmeyer S. An interpretation of the approach of
Rood to the treatment of neuromuscular dysfunction,
NUSTEP proceedings. Am J Phys Med 1967;46: 900-61
2 Duesterhaus Minor MA, ed. Proprioceptive
Neuromuscular Facilitation and the Approach of Rood.
Alexandria, VA: American Physical Therapy
Association, 1991. (Lister MJ, ed. Contemporary
management of motor control problems. Proceedings
of the II Step Conference.)
3 O'Sullivan SB.Strategies to improve motor control. In:
O'Sullivan SB, Schmitz T, eds. Physical Rehabilitation
Assessment and Treatment. Philadelphia: EA. Davis
Company 1988.
4 McDonough SM. The neurophysiological basis of
reciprocal inhibition in man. Phys Ther Rev 1997; 2:
19-28
5 Rood MS. Neurophysiological mechanisms utilized in
the treatment of neuromuscular dysfunction. Am J
Occup Ther 1956; 10(4):220-4
6 Heiniger MC, Randolph SL.Neurophysiological Concepts
in Human Behavior. St. Louis: c.v. Mosby Company
1981
7 Horak P, ed. Assumptions Underlying Motor Control
for Neurologic Rehabilitation. Alexandria, VA:American
Physical Therapy Association, 1991. (Lister MJ, ed.
Contemporary management of motor control
problems. Proceedings of the II Step Conference.)
8 Bethune D. Another look at neurological rehabilitation.
Aust Physio 1994;40(4): 255-61
9 Lennon S. The Bobath concept: a critical review of
the theoretical assumptions that guide physiotherapy
practice in stroke rehabilitation. Phys Ther Rev 1996;1:
35-45
210 A. Baily Metcalfe and N. Lawes
10 McCormack G. The Rood Approach to treatment of
neuromuscular dysfunction. In: Pedretti LW, ed.
Occupational Therapy: Practice Skills for Physical
Dysfunction. 4th ed. St. Louis: Mosby 1996:377-99
11 Burke RE, Levine DN, Zajac FE, Tsairis P, Engel WK.
Mammalian motor units: physiological-histochemical
correlation in three types in cat gastrocnemius. Science
1971a; 174: 709-12
12 Burke RE, Levine DN, Tsairis P, Zajac FEI.
Physiological types and histochemical profiles in
motor units of the cat gastrocnemius. J Physiol (Lon d)
1973; 234: 723-48
13 Pette D, Vrbova G. Invited review: neural control of
phenotypic expression in mammalian muscle fibres.
Muscle Nerve 1985; 8: 676-89
14 Burke D. Spasticity as an Adaptation of Pyramidal Tract
Injury. New York: Raven Press 1988. (Waxman SG, ed.
Functional Recovery in Neurological Disease,
Advances in Neurology; vol 47).
15 Gordon T, Mao J. Muscle atrophy and procedures for
training after spinal injury. Phys Ther 1994; 74: 50-60
16 Martin TP,Stein RB,Hoeppner PH, Reid De. Influence
of electrical stimulation on the morphological and
metabolic properties of paralyzed muscle. J Appl
Physiol 1992; 72: 1401-6
17 Graham SC, Roy RR, Navarro e. Enzyme and size
profiles in chronically inactive cat soleus muscle fibres.
Muscle Nerve 1992; 15: 27-36
18 Dattola R, Girlanda P, Vita G, et al. Muscle
rearrangement in patients with hemiparesis after
stroke: an electrophysiological and morphological
study. Eur Neural 1993; 33: 109-14
19 Cruz-Martinez A, Del Campo F, Mingo P, Ferrer M,
Perez Conde Me. Altered motor unit architecture in
hemiparetic patients. A single fibre EMG study. J
Neural Neurasurg Psychiatry 1982; 45(8): 756-7
20 Ahlqvist G, Landis S, Wroblewski R. Ultrastructure of
skeletal muscle in patients with Parkinson's disease
and upper motor lesions. Lab Invest 1975;32(5): 673-9
21 Edstrom L. Selective changes in the red and white
muscl fibres in upper motor lesions and parkinsonism.
J Neural Sci 1970; 11: 537-48
22 Johnson MH. Developmental Cognitive Neuroscience.
Cambridge: Blackwell Publishers Ltd. 1997
23 Lemon R. Cortical control of skilled movements. In:
Cody FWI, ed. Neural Control of Skilled Movement. 1995
24 Dannenbaum RM, Dykes RW.Sensory loss in the hand
after sensory stroke: therapeutic rationale. Arch Phys
Med Rehabill988; 69: 833-9
25 Jenkins WM, Merzenich MM, Och MT, Allard T, Guic-
Robles E. Functional reorganization of primary
somatosensory cortex in adult owl monkeys after
behaviorally controlled tactile stimulation.
Neurophysioll990; 63: 82-104
26 Wall PD, Egger MD. Receptive fields in the body-
surface map in adult cortex defined by temporally
correlated inputs. Nature 1988; 332: 444-5
27 Rood MS, ed. The Use of Sensory Receptors to Activate,
Facilitate, and Inhibit Motor Response, Autonomic and
Somatic, in Developmental Sequence. Dubuque: William
e. Brown 1962. (Sattely C, ed. Approaches to the
treatment of patients with neuromuscular
dysfunction).
28 Adams JA. A closed loop theory of motor learning. J
Mot Behav 1971; 3: 111-50
29 Schmidt RA. A schema theory of discrete motor skill
learning. Psychol Rev 1975; 82: 225-60
30 Bairstow PI, Lazlo JI.Kinaesthetic sensitivity to passive
movements and its relationship to motor development
and motor control. Dev Med Child Neural 1981; 23:
606-16
31 Gandevia SC, Macefield G, Burke D, McKenzie DK.
Voluntary activation of human motor axons in the
absence of muscle afferent feedback. Brain 1990; 113:
1563-81
32 Swartz L. Role of kinaesthesia in arousal and learning
behavior. Percept Mot Skills 1978; 47: 1219-25
33 Jarus T, Loiter Y.The effect of kinesthetic stimulation
on acquisition and retention of a gross motor skill.
Can J Occup Ther 1995; 62(1): 23-9
34 Mulder T,Hulstyn W.Special review: sensory feedback
therapy and theoretical knowledge of motor control
and learning. Am J Phys Med 1984; 63(5): 226-44
35 Keshner E. Reevaluting the theoretical model
underlying the neurodevelopmental theory. Phys Ther
1981; 61(7): 1035-40
36 Carr J, Shepherd R. Neurological Rehabilitation
Optimizing Motor Performance. Oxford: Butterworth
Heinemann 1998
37 Stein JE The representation of egocentric space in the
posterior parietal cortex. In: Cordo P, Hamad S,
eds. Movement Contral. Cambridge: Cambridge
University Press 1994: 89-98
38 Goodale MA, Pelisson D, Prablance e. Large
adjustments in visually guided reaching do not depend
on vision of the hand or perception of target
displacement. Nature 1986; 320: 748-50
39 Lee DN, Thomson JA. Vision in action: the control of
locomotion. In: Ingle DJ, Goodale MA, Mansfield RJW,
eds. Analysis of Visual Behavior. Boston: MIT Press 1982
40 Matyas TA, Galea MP, Spicer SD. Facilitation of
maximum voluntary contraction in hemiplegia by
concomitant cutaneous stimulation. Am J Phys Med
1986; 65: 125-34
41 Okuma Y,Lee RG. Reciprocal inhibition in hemiplegia:
correlation with clinical features and recovery. Can J
Neurol Sci 1996; 23: 15-23
42 Proteau L. On the specificity of learning and the role
of visual information for movement control. In:
Proteau L, Elliott D, eds. Vision and Motor Control.
New York: Elsevier Science 1992: 67-103
43 Abrams RA, Pratt J. Rapid aimed limb movements:
differential effects of practice on component
submovements. J Mot Behav 1993; 25(4): 288-98
44 Nilsson LM, Nordholm LA. Physical therapy in stroke
rehabilitation: bases for Swedish physiotherapists'
choice of treatment. Physio Theory Pract 1992; 8: 49-55
J 45 Carr JH, Mungovan SF, Shepherd RB, Dean CM,
Nordholm LA. Physiotherapy in stroke rehabilitation:
Bases for Australian physiotherapists' choice of
treatment. Physio Theory Pract 1994; 10: 201-9
46 Katz RT,Rymer WZ. Spastic hypertonia: mechanisms
and measurement. Arch Phys Med Rehabil 1989; 70:
144-55
47 Landau W. Spasticity: What is it? What is it not? In:
Feldman RG, Young RR, Koella WP, eds. Spasticity:
Disordered Motor Control. 2nd ed. Chicago: Year Book
Medical Publishers 1980
48 Fleshman JW, Munson JB, Sypert GW, Friedman WA.
Rheobase, input resistance and motor-unit type in
 A modern interpretation
medial gastrocnemius motoneurons in the cat. J
Neurophysiol1981; 60: 1326-38
49 Zengel JE,Reid SA, Sypert GW,Munson JB.Membrane
electrical properties and prediction of motor-unit type
of medial gastrocnemius motoneurons in the cat. J
Neurophysiol1985; 53: 1323-44
50 Pette D. Skeletal muscle adaptation in response to
chronic stimulation. In: Nix WA, Vrbova G, eds.
Electrical Stimulation and Neuromuscular Disorders.
Berlin: Springer-Verlag 1986
51 Heckman CJ,Binder MD. Analysis of effective synaptic
currents generated by homonymous la afferent fibres
in motoneurons of the cat. J Neurophysiol 1988; 60:
1946-66
52 Powers RK, Robinson FR, Konodi MA, Binder MD.
Distribution of rubrospinal synaptic input to cat triceps
surae motoneurons. J Neurophysiol1993; 70: 1460-68
53 James W. Principles of Psychology. New York: Dover
1950
54 Garnett R, Stephens JA. Changes in the recruitment
threshold of motor units produced by cutaneous
stimulation in man. J Physiol1981; 311:463-73
55 Burke RE. Motor units: physiological histochemical
profiles, neural connectivity and functional
specialisations. Am 20011978; 18: 127-34
56 Kidd G, Lawes N, Musa I. Understanding Neuromuscular
Plasticity. London: Edward Arnold 1992
57 Rossignol S, Gautier L. Reversal of contralateral limb
reflexes. Proc Int Union Physiol Sci 1980; 13: 639-41
58 Mitz AR, Winstein C. The motor system I: lower
centers. In: Cohen H, ed. Neuroscience for Rehabilitation.
Philadelphia: J.B. Lippincott Company 1993
59 Bovell D, Nimmo M, Wood L. Principles of Physiology:
A Scientific Foundation of Physiotherapy. London: W.B.
Saunders 1996
60 Hagbarth KE. Excitatory and inhibitory skin areas for
flexor and extensor motorneurones. Acta Physiol Scand
1952;26(Suppl. 94): 1-58
61 Pierrot-Deseilligny E, Bergego C, Katz R. Cutaneous
depression of Ib reflex pathways to motorneurones in
man. Exp Brain Res 1981;42: 351-61
62 Forget R, Hultborn H, Meunier S, Pantieri R, Pierrot-
Deseilligny E. Facilitation of quadriceps
motorneurones by group I afferents from pretibial
flexors in man. Exp Brain Res 1989; 78: 21-7
63 Davey NJ, Ellaway PH, Maskill DW. Facilitation by
mechanical cutaneous stimulation of muscle responses
to trans cranial magnetic stimulation in man. J Physiol
1991;438: 7P
64 Chen R, Ashby P. Reflex responses in upper limb
muscles to cutaneous stimuli. Can J Neurol Sci 1993;
20: 271-8
65 Lee RG, Murphy JT,Tatton WG. Long latency myotatic
relfexes in man: mechanisms, functional significance
and changes in patients with Parkinson's disease or
hemiplegia. In: Desmedt JE, ed. Advances in Neurology.
New York: Raven Press 1983
66 Yanigasawa N, Tanaka R, Ito Z. Reciprocal Ia inhibition
in spastic hemiplegia of man. Brain 1976;99: 555-74
67 Jackson J. Specific treatment techniques. In: Stokes M,
ed. Neurological Physiotherapy. London: Mosby 1998:
299-312
68 Umphred DA, McCormack GL. Classification of
common facilitatory and inhibitory treatment
techniques. In: Umphred DA, ed. Neurological
of the Rood Approach 211
Rehabilitation. 2nd ed. St. Louis: c.v. Mosby Company
1990: 111-62
69 Goff B. A neuro-physiological approach. In: Banks
MA, ed. International Perspectives in Physical Therapy 2
Stroke. Edinburgh: Churchill-Livingstone 1986:99-128
70 Ellaway PH. Applied neuroanatomy and
neurophysiology. In: Stokes M, ed. Neurological
Physiotherapy. London: Mosby 1998:3-22
71 Kanda K, Burke RE, Walmsley B. Differential control
of fast and slow twitch motor units in the decerebrate
cat. Exp Brain Res 1977;19: 57-74
72 Voss D, Ionta M, Meyers B. Proprioceptive
neuromuscular facilitation: patterns and techniques.
New York: Harper and Row 1985
73 Richardson CA, Jull GA. Muscle control-pain control.
What exercises would you prescribe? Manual Ther
1995;1(1): 2-10
74 Andersson GBJ.Role of muscle in postural tasks: spinal
loading and postural stability. In: Winters JM, Woo S-
Y, eds. Multiple Muscle Systems. New York:
Springer-Verlag 1990:375-95
75 Eklund G, Hagbarth KE. Motor effects of vibratory
muscle stimuli in man. Electroencephalogr Clin
Neurophysiol1966a; 19: 619-25
76 Eklund G, Hagbarth KE. Normal variability of tonic
vibration reflexes in man. Exp Neuro11966b; 16: 80-92
77 Hagbarth KE. The muscle vibrator-a useful tool in
neurological therapeutic work. Scand J Rehabil Med
1969;1: 26-34
78 Bishop B. Part I. Neurophysiology of motor responses
evoked by vibratory stimulation. Phys Ther 1974;
54(12):1273-81
79 Bishop B. Part II. Vibratory stimulation as an
evaluation tool. Phys Ther 1975a; 55(1):28-34
80 Bishop B. Part III. Possible application of vibration in
treatment of motor dysfunctions. Phys Ther 1975b;
55(2): 139-43
81 Lovgreen B, Cody FWJ, Schady W. Muscle vibration
alters the trajectories of voluntary movements in
cerebellar disorders-a method of counteracting
impaired movement accuracy? Clin Rehab 1993; 7:
327-36
82 Wyke BD.Articular neurology. A review. Physiotherapy
1972; 53(3):94-9
83 Williams PE, Goldspink G. Connective tissue changes
in immobilized muscle. J Anat 1984; 138: 343-50
84 Williams PE, Catanese T, Lucey EG. The importance
of stretch and contractile activity in the prevention of
connective tissue accumulation in muscle. J Anat 1988;
158: 109-14
85 Rothwell J. Control of Human Voluntary Movement. 2nd
ed. London: Chapman & Hall 1994
86 O'Dwyer NJ, Neilson PD. Spasticity and muscle
contracture following stroke. Brain 1996;119: 1737-49
87 Williams PE. Use of intermittent stretch in the
prevention of serial sarcomere loss in immobilized
muscle. Ann Rheum Dis 1990;49: 316-7
88 Tardieu C, Lespargot A, Tabary C, Bret MD. For how
long must the soleus muscle be stretched each day to
prevent contracture? Dev Med Child Neurol 1988; 30:
3-10
89 Hale LA, Fritz VU, Goodman M. Prolonged static
muscle stretch reduces spasticity-but for how long
should it be held? S Aft J Physiotherapy 1995; 51: 3-6
90 Goldspink G, Williams P. Muscle fibre and connective
tissue changes associated with use and disuse. In: Ada
212 A. Baily Metcalfe and N. Lawes
L, Canning C, eds. Key Issues in Physiotherapy. Oxford:
Butterworth Heinemann 1990; 197-217
91 Wallen M, Mackay S. An evaluation of the soft splint
in the acute management of elbow hypertonicity. Occup
Ther J Res 1995; 15(1): 3-16
92 Wallen M, O'Flaherty S. The use of the soft splint in
the management of spasticity of the upper limb. Aust
Occup Ther J 1991; 38: 227-31
93 Conine T, Sullivan T, Mackie T, Goodman M. Effect of
serial casting for the prevention of equinus in patients
with acute head injury. Arch Phys Med Rehabil 1990;
71: 310-2
94 Zachazewski JE, Eberle ED, Jefferies M. Effect of
tone-inhibiting casts and orthoses on gait: a case
report. Phys Ther 1982; 62(4): 453-5
95 Ada L, Scott D. Use of inhibitory weight-bearing
plasters to increase movement in the presence of
spasticity. Aust J Physio 1980; 26(2): 257
96 Leone JA, Kukulka CG. Effects of tendon pressure on
alpha motoneuron excitability in patients with stroke.
Phys Ther 1988; 68(4): 475-80
97 Burke D, Andrews C, Ashby P. Autogenic effects of
static muscle stretch in spastic man. Arch Neurol1971b;
25: 367-72
98 Ayres J. The Development of Sensory Integrative Theory
and Practice. Dubuque, IA: Kendall-Hunt Publishers
1974
99 Buchwald J. Exteroceptive reflexes and movement. Am
J Phys Med 1967; 46: 121
100 Knuttson E, Odeen I, Franzen H. Effects of therapeutic
exercise under local hypothermia in patients with
spastic pareses. Proceedings on treatment of spastic
pareses. Sjukgymnasten 1969;27: 26-8
101 Davies PM. Steps to Follow. Berlin: Springer-Verlag 1985
102 Low J, Reed A. Electrotherapy Explained: Principles and
Practice. London: Butterworth-Heinemann 1990
103 Simmons NN. Disorders in oral, speech, and language
functions. In: Umphred DA, ed. Neurological
Rehabilitation. 2nd ed. St. Louis: Mosby 1990: 683-703
104 Selbach H. The principle of relaxation oscillation as a
special instance of the law of initial value in cybernetic
functions. Ann NY Acad Sci 1962; 98: 1221-8
105 Spicer STAM. Facilitation of the tonic vibration reflex
(TVR)by cutaneous stimulation. Am J Phys Med 1980;
59: 223
106 Garland SJ, Hayes KC. Effects of brushing on
electromyographic activity and ankle dorsiflexion in
hemiplegic subjects with foot drop. Physiotherapy Can
1987; 39: 239-47
107 Johnson L, Kitchen S. Heat and cold: conduction
methods. In: Kitchen S, Bazin S, eds. Clayton's
Electrotherapy. 10th ed. London: WB Saunders
Company Ltd 1996; 127-40
108 Miglietta O. Action of cold on spasticity. Am J Phys
Med 1973; 52: 198-205
109 Price R, Lehmann JF, Boswell-Bessette S, Burleigh S,
deLateur B. Influence of cryotherapy on spasticity at
the human ankle. Arch Phys Med Rehab 1993;74: 300-4
110 Johnstone M. Restoration of Normal Movement After
Stroke. Edinburgh: Churchill Livingstone 1995
111 Twist D. Effects of a wrapping technique on passive
range of motion in a spastic upper extremity. Phys
Ther 1985; 65(3): 299-304
112 Brouwer B, Sousa de Andrade. The effects of slow
stroking on spasticity in patients with multiple
sclerosis: a pilot study. Physio Theory Pract 1995; 11:
13-21