Chapter 14 Physical management of altered tone and movement
Introduction
The term muscle tone describes the normal resistance felt when moving a limb passively through range (Burke, 1988). Muscle tone is an integral part of movement and posture but following neurological insult may present in a variety of altered states (Table 14.1). The importance of tone alterations remains the subject of debate, at both a physiological level and within the wider discussion of its relevance to physiotherapists treating neurological patients (Boyd & Ada, 2008). Furthermore, secondary changes within the peripheral tissues are known to contribute to and complicate the clincial picture (O’Dwyer & Ada, 1996). Irrespective of the underlying cause, physiotherapists manage the effects of tone alterations using their skills of clinical reasoning to judge whether tone changes enable or inhibit an individual’s function. For example, patients may use extensor spasticity to stand and transfer; conversely, muscle spasms may be so disabling that they hinder comfortable seating (Thompson et al., 2005). Movement disorders that include dysfunction of muscle tone are complex and challenge the interpretation and identification of which component primarily contributes to the movement dysfunction. Currently within clinical practice there is inconsistent use of terminology to describe tonal alterations and peripheral adaptations, which hinders effective decision-making and communication between health-care professionals. Drawing upon recent literature, this chapter defines the most commonly used terms (Tables 14.1–14.4) and places the physical management of these manifestations within the International Classification of Functioning, Disability and Health (ICF) (World Health Organization (WHO), 2001).
| Normal muscle tone | ‘The resistance of the limb to passive stretch determined by the physical inertia of the limb as well as the passive mechanical properties of the soft tissues because in a normal, relaxed muscle, there is no neural response to the stretch’ (Burke, 1988). |
| Hypertonia | ‘An increase in stiffness with resistance to stretch in one direction’ (Ada & Canning, 2009, p. 81). There may be neural (e.g. spastic dystonia) and non-neural (e.g. contracture) contributory impairments. The term hypertonia should not be used interchangeably with spasticity because it is inaccurate and confusing (Ada & Canning, 2009). |
| Hypotonia | ‘Less than normal resistance to passive movement’ (Ada & Canning, 2009). |
Table 14.2 Features of upper motor neurone syndrome (Sheean, 2002, 2008)
| Positive features | Afferent drive: in response to peripheral stimulation | |
| (additional or exaggerated phenomena: muscle overactivity) | Proprioceptive stretch reflexes: | |
| Spasticity Clonus Tendon hyperreflexia with irradiation Positive support reaction |
||
| Nociceptive reflexes: | ||
| Flexor spasms | ||
| Cutaneous reflexes: | ||
| Extensor spasms | ||
| Extensor plantar response (positive Babinski) | ||
| Efferent drive: supraspinal activity, observed during movement | ||
| Spastic dystonia | ||
| Associated reactions | ||
| Disordered control of voluntary movement: | ||
| Reduced reciprocal inhibition leading to pathological (spastic) co-contraction | ||
| Excessive reciprocal inhibition leading to apparent weakness | ||
| Negative features | ||
| (loss or reduction of phenomena) | Weakness | |
| Fatiguability | ||
| Loss of dexterity | ||
| Acute hypotonia | ||
| Adaptive features | ||
| (soft tissue) | Non-neural contributions (biomechanical component) | Stiffness and shortening of peripheral soft tissue structures |
| Neural contributions (overactive muscle contraction) | ||
| Spasticity | ||
| Spastic dystonia | ||
| Hyperreflexia | ||
Table 14.3 Definitions of the positive features of upper motor neurone syndrome
| Positive features | |
| Spasticity | ‘A motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex as one component of the upper motor neurone syndrome’ (Lance, 1980, 485). |
| Clasp knife phenomenon | The response of a muscle with spasticity to passive stretch – a rapid stretch to the muscle elicits a velocity dependent tonic stretch reflex. The resistance produced by the reflex contraction of the muscle slows the movement thereby reducing the stimulus eliciting the stretch reflex to below threshold and the resistance to the passive movement melts away. As the stretch continues, a second mechanism comes into play which suggests that as the muscle continues to lengthen the sensitivity to stretch reduces, indicating that the tonic stretch reflex is length – as well as velocity – dependent (Burke, 1988; Sheean, 2008). |
| Clonus | A rhythmical contraction of a muscle in response to a brisk stretch, maintained. Often seen in the gastrocnemius/soleus as the heel hangs off the footplate of a wheelchair and stretches the back of the calf. The stretch of the calf elicits a stretch reflex causing gastrocnemius/soleus to contract, plantarflexing the ankle and eliminating the stretch. If the relaxation is rapid and the stretch is maintained, another stretch reflex will be elicited and the ankle will plantarflex, again setting up the cycle for a sustained rhythmic contraction. This will continue as long as the stretch is maintained (Burke, 1988; Sheean, 2008). |
| Hyperreflexia | A greater than normal reflex response (e.g. the presence of reflex responses when a relaxed muscle is stretched at the speed of normal movement (Boyd & Ada, 2008, p. 80). |
| Positive support reaction | A response of the lower limb, evoked by the foot coming into contact with the ground and eliciting a proprioceptive stretch of the intrinsic foot muscles and an exteroceptive stimulus, caused by pressure on the sole of the foot during attempted weight bearing. It produces plantar flexion and inversion of the ankle, and sometimes knee extension (Bobath, 1990). |
| Flexor spasms
Extensor spasms |
Usually lower limb spasms that are probably distorted flexor withdrawal reflexes. Caused by nociceptive (e.g. pressure sores), cutaneous (e.g. bed sheets moving across the legs) or visceral (e.g. distended bladder or bowel) stimuli (Sheean, 2008). Extension of the lower limb usually evoked by cutaneous stimulation of the groin, buttock, or back of the leg or following a sudden stretch to the iliopsoas and thus evoking the extensor component of the crossed extensor reflex (Burke, 1988; Sheean, 2008). |
| Extensor plantar response (Babinski sign) | Upward movement (dorsiflexion/extension) of the great toe with ankle dorsiflexion in response to a non-painful cutaneous stimulation on the plantar aspect of the foot moving from a lateral to medial direction; a disinhibited flexor withdrawal reflex. A normal Babinski test would produce flexion of the great toe and plantar flexion of the ankle (Burke, 1988; Sheean, 2008). |
| Spastic dystonia | ‘Continuous muscle contractions that occur in the apparent absence of voluntary contraction and of any sensory feedback from the periphery (proprioceptive, cutaneous or nociceptive)’ (Sheean, 2002, p. 7). Thought to be due to tonic supraspinal drive to the alpha motor neurones, e.g. the hemiplegic posture (Sheean, 2008). Spastic dystonia can be altered by changes in posture (Denny-Brown (1966) cited in Sheean, 2008) and through stretch modulation via proprioceptive or vestibular mechanisms (Burke, 1988). |
| Associated reactions | An involuntary activation of muscles remote from those normally engaged in the task, e.g. upper limb flexion during sit to stand. The amount of activation and movement is usually in proportion to the effort expended in executing the task. Thought to be due to tonic efferent drive of alpha motor neurones and may be due to a failure to inhibit spread of motor activity through propriospinal pathways in addition to soft tissue adaptation (Sheean, 2002, 2008). |
| Reciprocal innervation (coordination): Task dependent control of agonists and antagonists minimising the number of commands sent to individual muscles mediated by the Ia inhibitory interneurone (Gordon, 1991). Reciprocal inhibition: Inhibition of antagonists which would otherwise inhibit voluntary movement; enhances speed and efficiency of movement by making sure that prime movers are not opposed by antagonists (Gordon, 1991). Co-contraction: The simultaneous contraction of agonist and agonist, e.g. around the wrist during a gripping activity (Gordon, 1991). |
|
| Disordered reciprocal inhibition | Disruption to the descending excitatory and inhibitory signals from the major descending pathways converging on the Ia inhibitory interneurone, causing difficulty with reciprocal co-ordination and shifting between co-contraction and reciprocal inhibition and impairing reciprocal innervation and the task-dependent coordination of agonists and antagonists. The clinical picture may be complicated by soft tissue adaptation and remains a topic of debate in the literature (Sheean, 2008). |
| Reduced reciprocal inhibition | Pathological (spastic) co-contraction, e.g. elbow flexors are not inhibited as the elbow extends due to simultaneous activation of the flexors and extensors (Sheean, 2008). |
| Excessive reciprocal inhibition | Sustained activation of one muscle group causing inability to activate the antagonist when required, e.g. activation of soleus during the gait cycle which is sustained during swing phase and results in inhibition of tibialis anterior; often attributed to weakness in tibialis anterior (Sheean, 2008). |
Table 14.4 Definitions of the negative features of upper motor neurone syndrome
| Negative features | |
| Weakness | An inability to generate, sustain and synchronize the necessary voluntary force for effective motor behaviour (Landau, 1988) causing disorganization of motor behaviour inappropriate to the task and context (Carr & Shepherd, 2003). Mechanisms involve: (a) disrupted descending input onto the motor neurone pool; (b) decreased number of motor units activated; (c) decreased motor unit discharge rate; and (d) disrupted motor unit recruitment (Gemperline, et al., 1995; Rosenfalck & Andreassen, 1980). |
| Fatiguability | Combined influence of disuse and deconditioning, as well as an increase in the proportion of functionally slow motor units which result in poor endurance for sustained voluntary force output (Carr & Shepherd, 1998). |
| Loss of dexterity | An inability or difficulty in performing actions quickly and skilfully using independent movements of any part of the body (particularly loss of fractionation – independent movement of individual fingers, e.g. typing or manipulating objects), spatial and/or temporal inaccuracies due to slow production of force and an inability to rapidly alter the degree of contraction in specific muscles or muscle groups during task performance, resulting in a loss of flexibility of motor control with respect to the changing environment or task demands (Ada & Canning, 2009). |
| Acute hypotonia (neural shock) |
Suppression of spinal reflexes for a variable amount of time (depending on the site of the lesion), the return of spinal reflex behaviour suggests that mechanisms of neuronal plasticity may be involved (Sheean, 2002). |
Overview of upper motor neurone syndrome
The upper motor neurone syndrome (UMNS) occurs following a lesion affecting part or all of the long descending tracts that control tone and movement, and which have a direct or indirect influence on the excitability of the motor neurone pool (Barnes, 2008). The clinical picture following an upper motor neurone (UMN) lesion depends on the site and size of the lesion and how much neural adaptation has taken place since the lesion occurred (Sheean, 2002).
Impairments arising from nervous system lesions were originally classified into two groups described as either ‘positive’ or ‘negative’ (Jackson, 1958). This classification is still used, particularly with reference to UMNS (see Table 14.2). This system has good clinical utility and provides a helpful structure for the assessment of the underlying causes of activity limitations and their relative contribution to the overall clinical picture (Ada & Canning, 2009; Carr & Shepherd, 2003).
Positive features
Positive features describe exaggerations of normally occurring motor activity, e.g. hyperreflexia. These impairments are further classified into two groups (Sheean, 2008):
Negative features
Negative features refer to a loss or reduction in normal activity, e.g. weakness. The functional significance of the negative features in terms of their contribution to disability cannot be underestimated (Ada & Canning, 2009; Barnes, 2008; Canning et al, 2004; Landau, 1980). For example, most of the rehabilitation effort for recovery of functional movement for people with cerebral lesions (e.g. stroke) is usually directed towards the negative features because of their proportionally greater contribution to the prevailing activity limitations and participation restrictions (Carr & Shepherd, 2003). This is not to say that the positive features do not have functional consequences, but that simply reducing impairment like spasticity will not necessarily improve function unless the negative and adaptive features are also addressed (Boyd & Ada, 2008).
Adaptive features
Adaptive features are secondary impairments that develop as adaptations to the primary impairments (the positive and negative features); their combined effects have a profound influence on functional performance (e.g. the effect of shortening of gastrocnemius/soleus on walking and sit to stand) such that the adaptive features are usually considered alongside the positive and negative features as part of the clinical assessment (Carr & Shepherd, 2003). Adaptive changes result in an increased resistance to passive movement termed hypertonia. In UMNS, hypertonia should be understood simply as an increased resistance to passive movement. Further assessment should help determine whether the resistance is principally due to neural influences, e.g. hyperreflexia, or non-neural influences (local or peripheral adaptation of soft tissue structures) or a combination of the two. This is an important distinction because stiffness and contracture may exist in the absence of neural influences (O’Dwyer et al., 1996) or may be primarily due to neural activity or a combination of both (O’Dwyer & Ada, 1996). As the treatment for the neural component differs from that of the non-neural component, further clinical investigation will be required to identify the most appropriate intervention (O’Dwyer & Ada, 1996).
The characteristic features of UNMS are outlined in Table 14.2. Tables 14.3 and 14.4 provide definitions for each of the impairments.
The primary impairments of UMNS result from disruption of the supraspinal control of descending pathways that normally control excitatory and inhibitory influences on proprioceptive, cutaneous and nociceptive spinal reflexes (Sheean, 2008). These reflexes become hyperactive and account for the majority of the positive features of UMNS (Sheean, 2008). It is likely that the positive features emerge due to a combination of diminished descending cortical control in addition to plastic reorganization at spinal cord and cortical level (Sheean, 2008).
The inhibitory system
Corticoreticular fibres, which travel with, but are separate from, the corticospinal tract, facilitate an inhibitory area in the medulla called the ventromedial reticular formation. This area gives rise to the dorsal reticulospinal tract which is located in the dorsolateral funiculus (a column of fibres in the spinal cord). The main influence of the dorsal reticulospinal tract, which acts weakly with the corticospinal tract, is inhibitory to stretch reflexes and flexor reflexes (Sheean, 2008) (see Figure 14.1A).
The excitatory system
This system is slightly more diffusely organized in the brain stem and is not under tight cortical control; the bulbopontine tegmentum is the most important area because it gives rise to the medial reticulospinal tract. This tract, acting weakly with the vestibulospinal tract, is excitatory to stretch reflexes and extensor reflexes but, like the inhibitory system, is also inhibitory to flexor reflexes (Sheean, 2008) (see Figure 14.1A).
It is already possible to see from the above how disruption to one or all of the descending pathways will disrupt the balance of the excitatory and inhibitory inputs to the spinal motor neurones. The critical features of the descending system are therefore identified by Sheean (2008) as:
Figure 14.1 A–E explains the origin of the clinical presentations resulting from lesions to different anatomical locations of the descending tracts, after Sheean (1998, 2008). Figure 14.1E refers to flexor reflex afferent (FRA) reflexes, which are described in more detail in Box 14.1.
Box 14.1 What are flexor reflex afferent (FRA) reflexes?
FRA reflexes are multi-connected spinal reflex pathways that are normally tightly controlled by supraspinal activity in both the excitatory and inhibitory systems (Sheean, 2008). FRA reflexes carry information from the skin, fascia, muscle, bone, capsule, bursa and gastrointestinal tract. Their activity can result in either facilitation of flexor activity, flexor inhibition or excitation of extensor activity (Sheean, 2008). It is thought that under normal conditions supraspinal control determines which pathways are activated according to the functional task (Burke, 1988). In UMNS with extensive spinal lesions (e.g. multiple sclerosis) the activity of the FRAs is no longer controlled by descending input. Therefore, constipation or pressures sores for example, may increase the input from flexor reflex afferents to the spinal cord and tip the reflex activity towards flexor dominance reflected clinically as flexor spasms or paraplegia in flexion (Sheean, 2008).
Physical management of positive, negative and adaptive features
Limitations in activities and restrictions in participation from loss of movement can arise from the combined effect of positive (i.e. spasticity), negative (i.e. weakness) and adaptive features (i.e. contractures) (Ada et al., 2006b). Interventions include manual (hands on), specific adjuncts to treatment and education.
Use of movement
Manual techniques are amongst the principle means available to the physiotherapists in the treatment and management of the altered tone seen post neurological insult. The importance of afferent inputs and their effects on muscle tone and postural/biomechanical alignment have been well documented in the literature (Rothwell, 1994; Shumway-Cook & Woollacott, 2007). Changes in cortical representations have been shown to accompany functional gains after rehabilitation (Johansson, 2000; Richards et al., 2008). Such studies help to provide direct evidence that altering passive or active sensory input can drive motor output; therapeutic movement and handling is a means of altering afferent input to the patient. An understanding of the basic principles that affect neural plasticity is key to enhancing motor recovery after neurological insult (Kleim & Jones, 2008).
The main aims of physical interventions are:
Maintenance of soft tissue length
The need for prevention of soft tissue changes in people with neurological impairments as a prerequisite to the prevention of contractures is widely acknowledged (Bovend’Eerdt et al., 2008; Katalinic et al., 2008). Without full range of motion, peripheral changes cause muscle imbalance and can compound any central motor dysfunction (Fitzgerald & Stokes, 2004). The physiotherapist must be able to make an in-depth analysis of posture and movement patterns as a basis for clinical reasoning and deciding upon primary problems and secondary compensations (Meadows & Williams, 2009). Stretching is widely used as an intervention to prevent or minimize contracture formation.
Stretching, assisted and passive movements
When handling a patient, the therapist must be ready to adapt to any changes in the response of the muscle to the afferent input from the movement. The aim of stretch interventions is to maintain or increase range of movement in soft tissues and can be carried out by the therapist or by the patient. Stretching can have immediate and lasting effects; the former being related to changes in the viscous properties whereas the mechanism behind longer lasting effects is still not fully understood but thought to be connected to changes in sarcomeres; Katalinic et al. (2008) and Bovend’Eerdt et al. (2008) provide detailed overviews. Changes in the muscle itself include thixotrophy (Vattanaslip et al., 2000) and even where there is no neurological damage, the normal resistance to movement is the result of such things as muscle, tendon and connective tissue inherent stiffness.
The length of time required to prevent contracture formation also remains an area of debate; the literature suggests intervals from 30 minutes to 6 hours (Tardieu et al, 1988; Williams, 1990). Discussion continues in clinical practice as to the effectiveness of applying stretch and remains an active area of research (Katalinic et al., 2008).
Changes in the motor and sensory systems can be expected even when movement is passive (Lotze et al., 2003) or, indeed, if physical movements are cognitively rehearsed (mental practice; Page et al., 2009). The importance of carrying out active/assisted or passive movements through their full range is paramount and attention should be paid to muscles that cross two or more joints. Movements should be performed with care, confidence and variety, and the patient should be taken out of his or her preferred posture. Movement should not be vigorous, and never forced, as this could be a causative factor in heterotopic ossification (HO), although the underlying mechanism remains poorly understood (Chua & Kong, 2003). However, movement can prevent the development of HO and should be carefully encouraged even when HO is present (Knight et al., 2003).
Modulation of muscle tone
Therapeutic movement and alteration in alignment of body parts are thought to be able to influence muscle tone in other areas indirectly. The trunk, head and shoulder and pelvic girdles have been proposed to be particularly influential in altering muscle tone (Meadows et al., 2009). Schmit et al. (2000) found that repeated joint movements had beneficial, albeit short-term, effects on spastic hypertonia at the elbow. This alteration of muscle tone may be augmented by presynaptic inhibition from the periphery, leading to neuroplastic adaptation (Rothwell, 1994). Additional preliminary findings around therapeutic touch, such as slow stroking on hypertonic muscles in multiple sclerosis, has indicated a reduction in alpha-motor neuron excitability (Brouwer & de Andrade, 1995). The use of rotation is also thought to be important in modulating tone (Proske et al., 2000) and the additional components of traction and compression can likewise be used (Rosche et al., 1996). Mayston (2002) also suggests that therapists alter tone at a non-neural level by affecting muscle length and range, which gives an improved alignment as a prerequisite for better movement.
Re-education of movement
As movement dysfunction arises from a combination of positive, negative and adaptive impairments, the clinical reasoning process and interventions subsequently selected should reflect this balance. Many therapists believe that a higher quality of movement translates directly to greater functional ability (Davidson & Waters, 2000) but this relationship has yet to be proven empirically. Reduction of tone should be only part of a treatment so as not to affect function inadvertently for those who rely upon positive features for the achievement of motor goals, e.g. transfers. Other factors such as practice, specificity of training, transfer of training and feedback need to be considered as part of the overall framework of therapeutic practice (Lennon & Bassile, 2009). Treatment can be based on one or more of the various models of motor control and some of these treatment approaches are discussed in Chapter 12, as well as in the chapters on specific conditons (Chs 2–10).
Weight-bearing
Therapeutic standing is a way of maintaining length in the soft tissues, modulating tone and encouraging extensor activity. To be most effective it should be dynamic to promote tonal changes (Massion, 1994), activating the extensor muscles whilst reciprocally inhibiting the flexors via the vestibuar system (Markham, 1987; Brown, 1994). Standing can be effective in modulating tone and reducing the frequency of spasms, whilst maintaining joint range (Bohannon, 1993). A pilot study looking at the efficacy and feasibility of a therapeutic standing programme for people with multiple sclerosis showed increased range of movement in wheelchair-dependent subjects and a downward trend in spasticity and spasms was noted (Baker et al., 2007). A decrease in motor neuron excitability in patients with spastic hemiparesis was also noted after a single session of standing on a tilt table for 30 minutes (Tsai et al., 2001). Tilt tables can be used to stand medically stable patients in the early stages of rehabilitation, even if they are still unconscious; wedges under the feet can be used as required to increase the stretch on the calf musculature. Alternatively, in the more awake patient, backslabs (Carter & Edwards, 2002) or electrical standing frames may be used (Figure 14.2). With the current emphasis on risk management it is recommended that, where possible and practicable, equipment should be used to minimize the manual handling risk (Chartered Society of Physiotherapy (CSP), 2008). The use of standing hoists can allow patients to weight-bear regularly in a normal functional task and so should be encouraged (Figure 14.3).
Weight-bearing with specific alignment can also be achieved through the upper limbs to maintain length and influence tone, but must be performed with extreme care. Normal biomechanical alignment is maintained by external rotation at the shoulder and the wrist joint should not be overstretched (Champion & Barber, 2009).
Adjuncts to physical management
Positioning and seating
Therapeutic positioning and seating is underpinned by the premise of providing sufficient external support to enable a person to cope better with the effects of gravity, and to maintain postural alignment without using undue muscular activity; the reader is referred to Pope (2007) for a detailed review of posture and seating.
The relationship between positioning and outcome is still the subject of debate, with research evidence, whilst not conclusive, showing limited effectiveness (de Jong et al., 2006; Fox et al., 2000; Gustafsson & McKenna, 2006). However, there remains a consensus view in the literature advocating the importance of positioning and the need for multidisciplinary team involvement (Pope, 2007; Intercollegiate Stroke Working Party (ISWP), 2008). Where possible, positioning should be integrated into functional activities in a normal daily routine (Figure 14.4) and appropriate manual handling equipment and techniques always considered (CSP, 2008). Standard positioning charts are useful to promote consistency across the team and can be personalized, for example drawing on additional pillows to illustrate adjustment for specific postural needs; alternatively, photographs obtained with informed consent can be used.
Positioning in bed
Optimal positioning of a patient in supine can present a variety of challenges for the therapist. For example, patients with predominantly negative impairments may all too readily accept the supportive surface and be at risk of loss of range, whereas those with positive or indeed adaptive impairments may not be able to adapt their posture to the base provided. The use of pillows, wedges and T-rolls can assist in altering limb and body postures and help provide appropriate support (Figure 14.5). Profiling electrical beds can also be utilized to help maintain different postural alignment, likewise side-lying can be used for introducing change and breaking up any predominant tonal patterns or preferred postures. Positioning a patient in prone can be beneficial for some but its use must be considered carefully, for instance those with tracheotomies or severe contractures may be unable to achieve this position. As the head, shoulders, thighs and knees are the main load-bearing areas in prone, the introduction of a wedge can facilitate function by moving the fulcrum of movement to the pelvis (Pope,2007) or a commercially produced beanbag can also be tried to encourage head extension and shoulder protraction (Figure 14.6).
Mattresses
All patients should have a mattress that matches his or her pressure and positoning needs; a recent Cochrane Review by McInnes et al. (2008) provides comprehensive evaluation of the different support surfaces for pressure ulcer prevention. Physiotherapists should collaborate with nursing staff to facilitate optimal prescription for function. For example, the use of overlays on a standard mattress may be sufficient for pressure care yet affect transfers, as it increases the overall bed height so only a standing hoist can be used with taller patients. A replacement mattress that is the same height as a standard mattress but has higher pressure relieving properties may be preferable in terms of rehabilitation, although it is more costly. Overhead hoists may have to be used for air-filled mattresses. Findings from the PRESSURE Trial Group (Nixon et al., 2006) indicated that more than one-third of patients reported difficulties associated with movement in bed, and getting in and out of bed with overlays.
For acute head injuries where intracranial pressure (ICP) is a concern, electronic pressure beds can offer an effective way to achieve weight transference and positive effects on respiratory function. For patients with uncontrolled movements (e.g. Huntington’s disease, see Ch. 7), reduced sensation, or cognitive or perceptual deficits, the use of cot sides, or placing the mattress on the floor, should be considered to reduce the risk of injury to the patient from falling out of bed.
Sitting
Being able to sit well not only is central to an effective posture management system, but it can also help with respiration, eating and communication whilst promoting social interaction. The position of the pelvis is the keystone for building a framework of postural support, whereas hips, knees and feet should be at 90°, and consideration given to the provision of head and arm support (Pope, 2007
