Module 2 The integration of postural control and selective movement for functional activities (Part A) (Formerly Part A management of the acute and sub-acute patient ) Training on a motor task results in performance improvements that are accompanied by increases in motor cortex excitability. Moreover, periods of afferent stimulation result in increased motor cortex excitability. There is increasing evidence to suggest that raised motor cortical excitability may facilitate movement and learning (Mc Donnell 2006). This module will focus on the development of handling skills using postural transitions between sitting and supine as well as therapeutic handling of the upper limb The aims of the module are: 1. To discuss the assessment and treatment of the acute / sub-acute patient 2. To explore and enhance skills of observation and analysis in neurologically intact subjects 3. To link theory and clinical practice 4. To promote clinical effectiveness The acute / sub-acute patient Neuronal changes following CNS lesions result in an ishaemic cascade, diaschsis and associated transneuronal changes. For example following a stroke a clot / haemorrhage interrupts the blood supply to an area of the brain, and neurons starved of oxygen for more than a few minutes die. Following this focal ischaemic insult a penumbral region exists around a densely irreversibly damaged tissue (Markus 2004). Cell function in the penumbra can decline unless adequate blood supply can be restored The cascade of events that can lead to further cell death includes reduced oxygen delivery, generation of lactic acid, disruption of ions, cell depolarisation, excessive release of glutamate, and calcium influx. High concentrations of extra cellular glutamate activate receptors on neighbouring cells recruiting them into the infarct. High calcium concentration also has devastating consequences for cell function, resulting in destruction of cell structure, synthesis of nitric oxide and production of oxygen radicals. Consequently, internal structures may fail and cells die. Immediate management to improve survival of cell function and thus minimise disability includes the early recognition of stroke, using a tool such as FAST (Face Arms Speech Test) and early admission and assessment in hospital (NICE guideline 68 Stroke.) In the acute stages many patients present with a flaccid / hypontonic state BBTA 2016 1
The flaccid state is strongly associated with cerebral oedema and is not experienced by all patients. Once oedema has resolved the true neurological deficit may be apparent. Flaccidity therefore may be: A brief / transitory phase Not representative of damage A response to shock Is not seen in all patients In the presence of flaccidity it is difficult to elicit a response from the neuromuscular system to either maintain a posture or follow a movement. Hypotonia is where: A stimulus can elicit a response but might need guidance of various parameters of sensory and proprioceptive controls (gravity / bos / alignment) More potential to recruit tone although may only be temporary Likewise functional deficits after spinal cord injury originate not only from direct physical damage itself but from secondary biochemical and pathological changes (Ditunno et al 2004). Neurons can be damaged at the site of the injury and the consequences of synaptic loss from these neurons produce a cascading degeneration along neuronal pathways, increasing the extent of neuronal disruption with time (Shumway-Cook and Woollacott 2011). Hypotonia and weakness are negative features of the upper motor syndrome, and reflect a deviation in reciprocal innervation, resulting in a loss of dexterity and strength. Compared to flaccidity, in the presence of hypotonia, there is potential to recruit tone and activity. However this may be temporary, and as such, requires manipulation of various parameters of sensory and proprioceptive controls such as gravity, alignment, and base of support. The patient with a predominance of hypotonia and weakness demonstrates a loss of influence of descending pathways from the cortex, and brainstem, on spinal inter neurons and motor neurons. This predominantly involves the medial and lateral descending pathways. The system involved in the production of antigravity activity is the reticular system which, when damaged, creates a loss of drive to the muscle spindle. Subcorticalcortical loops including the cortex-basal ganglia-thalamus-cortex loop may also be disrupted (Takakusaki 2004). These circuits are suggested to be more widely and more severely affected in patients with prolonged flaccidity. Recovery that continues beyond four weeks has been attributed to plasticity, a reorganisation of the brain in which functions previously performed by the ischaemic area are assumed by other ipsilateral or contralateral brain areas (Green-Joseph, 2003). There is now overwhelming evidence to indicate that the brain continuously remodels its neural circuitry in order to encode new experiences and enable behavioural change. Research shows that neurons, including brain cells, have the remarkable ability to alter their structure and function in response to a variety of internal and external pressures including behavioural training (Kleim & Jones 2008). BBTA 2016 2
This seems obvious during development but the adult brain must also possess at least some plasticity to learn new skills, establish new memories, and to respond to injury throughout life (Purves et al 2011). Recovery versus compensation Recovery at the Activity level requires that the task is performed using the same end effectors and joints in the same movement patterns typically used by non-disabled individuals. Compensation at this level often takes the form of substitution and would be noted if the patient were able to accomplish the task using alternate joints or end effectors, for example, opening a package of food using one hand and the mouth instead of two hands. On some scales that measure functional ability, this patient would get a perfect score for accomplishing the task, other scales allow for a partial score to be given if the task is partially completed or done too slowly or with difficulty (Levin 2009). Therefore without attention to the quality of the task performance it is not possible to distinguish between recovery and compensation at the level of the basic motor pattern. Although compensatory movements may help patients in the short term, the presence of compensation may be associated with long term problems such as decreased joint range of motion and pain The use of motor compensation could lead to a pattern of learned non use limiting the capacity for subsequent gain in motor function in the paretic arm and leg. (Levin 2009). As stated cortical [and spinal injury] injury can trigger both adaptive and maladaptive processes (Nudo 2006). Factors affecting functional organisation include: Postures the patient is exposed to The environment Handling Transfers Postural support, both perceptual and physical Self movement It is important however To allow the patient to move To adapt the environment to make movement easier To take care with the choice of functional goal (must be meaningful to the patient) To work at an appropriate level for the individual patient It is vital that the patient is helped to explore the environment to his / her level of control and it may therefore be necessary to modify the environment accordingly. Consideration should be given to positioning, handling, seating and transfers. BBTA 2016 3
The importance of somatosensory information Somato-sensation is thought to play an important role in skilled motor learning & formation of internal models for learned movements. It has been shown that disruption of somatosensation during task practice impairs the magnitude of change associated with motor learning probably through development of an inaccurate internal model and that even mild sensory impairment impacts on motor learning. (Marigold et al, 2004) This highlights the importance of developing novel rehabilitation approaches to enhance recovery of sensory loss. (Vidoni et al, 2010) and the importance of re-weighting of sensory information & limiting misleading sensory cues. It has been noted that impaired sensory integration may have a more significant effect on postural instability than on strength. (Marigold et al 2004) The hand has huge cortical representation thus, increasing sensory information to the hand is a potent source of increasing the postural body schema, light hand contact is good for enhancing body orientation (Baccini et al 2007).Therefore working towards achieving hand contact during functional activities is an important goal. This will improve the contactual hand orientating response (CHOR), which is the ability to maintain a frictional contact with a surface either by volitional extension or the facilitation of an extensor response. (Kandel et al 2000). This contactual response activates the hand in such a way that it can oppose flexor activity in the upper limb. Handling: Treatment aims to: Create tone through achievement of a postural alignment from which movement can take place Re-access core stability Facilitate appropriate antigravity activity Restore balance mechanisms Facilitate awareness of midline through movement Maintain mobility and viability of key points Minimise unnecessary compensation Maintain muscle viability, length and potential force Handling should be consistent in order to: Minimise compensation Prevent trauma Prevent fear Prevent the establishment of the hypotonic state and the development of hypertonia Activate the patient so that they can participate as appropriate Treatment In treatment it is important to consider the use of sensory and proprioceptive modalities, for example: Gravity Base of support BBTA 2016 4
Selective movement Stability / mobility Muscle length through rotation Compression Alignment Speed and timing of facilitation / movement It is vital that the patient develops postural stability and therefore movement up against gravity in order to develop efficient postural control and balance. Exploration of movement and postures that investigate selective extension, through linear acceleration, are therefore important. Positioning Positioning is an important part of practice and is individual to each patient (Scottish Intercollegiate Guidelines, 2010). There is however a danger in the acute/subacute patient of waiting for recovery of movement and relying totally on positioning to promote optimal recovery. Seating Appropriate seating can: Reinforce correct alignment of the trunk and limbs Support postural activity Provide external scaffolding to support low tone selectively; maintain alignment of body parts; minimise fixation and facilitate activity Allow for movement in the chair and away from the chair It is also important however to consider how long a patient can sit out. The presence of hypotonia or weakness automatically gears the nervous system and musculoskeletal systems to compensate for a lack of postural stability, which can lead to fixation and an inability to move selectively. An appropriate level of tone and reciprocal innervation are produced through selective movement. Static fixation reduces the ability to access selective movement. Transfers The choice of hoist versus active participation in the transfer will be dictated by: Risk assessment Adaptability of postural tone Alignment of body parts in sitting Ability to access feed forward anticipatory postural control mechanisms The seating The skill of the handler The environment Patient compliance BBTA 2016 5
Early facilitation of walking is an important factor in the development of balance Patients need early experience of walking Limb loading and unloading are crucial in the production of muscular activity, and in particular in walking, to access central pattern generators. Following a stroke, unequal limb loading exists correlating with an inability to generate forward momentum in the initiation of gait (Patchay 2003). Summary Treatment works through the application of an appropriate modality of sensory and proprioceptive information relevant to function. Therapists manipulate afferent information from the periphery to influence movement control. Facilitation is an active sensorimotor learning process that is goal orientated to updating the body schema. It is important not to wait for recovery but to facilitate the patient to access their potential. Treatment guides appropriate plastic adaptation and maximises efficiency of functional movement. References Baccini et al (2007) Effectiveness of fingertip light contact in reducing postural sway in older people. Age and Ageing 36:30-35. Department of Health National Stroke Strategy (2007). London. Department of Health. Ditunno JF, Little JW, Tessler A, Burns AS (2004) Spinal shock revisited: a four-phase model. Spinal Cord 42:383-95. Greenberg E, Treger I, Ring H. (2006) Rehabilitation outcomes in patients with brain tumours and acute stroke: comparative study of inpatient rehabilitation. American Journal of Physical Medicine and Rehabilitation 85(7):568-73. Green-Joseph B. (2003) Brain reorganisation after stroke. Topics in Stroke Rehabilitation 10(3):1-20. Kleim JA, Jones TA. (2008) Principles of experience dependant neural plasticity: implications for rehabilitation after brain damage. Journal of Speech Language and Hearing Research 51:S225-239. Levin MF, Kleim JA, Wolf SL (2009) What do motor recovery and compenation mean in patients following stroke? Neurorehabilitation and Neural Repair. 23:313-319. Levin MF, Panturin E (2011) Sensorimotor integration for functional recovery and teh Boabth approach. Motor Control 15:285-301. Marigold DS, Eng JJ, Tokuna CD, Donnelly CA. (2004) Contribution of muscle strength and integration of afferent input to postural stability in persons with stroke. Neurorehabilitation and Neural Repair 18(4):222-229. Markus HS. (2004) Cerebral perfusion and stroke. Journal of Neurology Neurosurgery and Psychiatry 75:353-61. McDonnell MN, Ridding MC. (2006) Afferent stimulation facilitates performance on a novel motor task. Experimental Brain Research 170:109-115. BBTA 2016 6
NICE Guideline 68 Stroke. Diagnosis and initial management of acute stroke and transient ischaemic attack (www.nice.org.uk). Nudo RJ (2006) Mechanisms for recovery of motor function following cortical damage. Current Opinion in Neurobiology 16:638-644. Patchay S, Gahery Y. (2003) The effect of limb loading on early postural adjustments associated with gait initiation in healthy adults. Gait and Posture 18:85-94. Scottish Intercollegiate Guidelines. SIGN - Therapeutic Handling (2010). www.sign.ac.uk Shumway-Cook A, Woollacott M. (2011). Motor Control: Theory and Practical Applications. Fourth Edition. Williams and Wilkins, USA. Takakusaki K, Saitoh K, Harada H, Kashiwayanagi M. (2004) Role of the basal ganglia in the control of motor behaviours. Neuroscience Research 50:137-151. Vidoni ED, Acerra NE, Dao E, Meehan SK, Boyd LA. (2010) Role of the primary somatosensory cortex in motor learning: An rtms study. Neurobiology, Learning and Memory 93(4):532-539. Winstein C, Wing A, Whitall J. (2003) Motor control and learning principles for rehabilitation of upper limb movements after brain injury in Handbook of Neuropsychology, Second Edition. Vol 9:77-137. BBTA 2016 7