Tremor

The typical Parkinson’s rest tremor occurs at 4–6 Hz. It begins unilaterally, described in the hand as a ‘pill rolling tremor’ (resembling a pill being rolled between the thumb and fingertips) and can occur in the feet, jaw, chin and lips. It is distinct from ‘essential tremor’ and varies during the course of the condition and within the Parkinson’s population.

Rigidity

A form of hyper-tonicity causing stiffness or inflexibility of the muscles from loss of normal reciprocal inhibition – is thought to be a result of excessive excitation of alpha motor neurones that are normally inhibited by the basal ganglia. You may observe rigidity as reduced arm swing during walking or reduced heel strike owing to rigidity in the calf. Rigidity can cause pain and cramping, impoverished movement and added internal resistance when undertaking exercise. It is described as:

Akinesias

There are several forms of akinesias:

These forms of akinesia cause reduction in movement range and velocity, making automatic and repetitive movements difficult.

Postural instability

Postural instability equates to the loss of postural reflexes essential for normal movement and alongside freezing of gait, is a major cause of falls and hip fractures in those with Parkinson’s; it usually manifests in the later stages of the condition. The ‘pull test’ of the Unified Parkinson’s Disease Rating Scale (UPDRS) or ‘retropulsion test’ is used to assess this clinical feature by pulling the person being tested backwards or forwards by their shoulders (or hips), and noting their response to displacement. An abnormal response (positive postural instability) is identified if no postural correction is observed or more than two steps backwards are taken.

Combinations of TRAP (tremor, rigidity, akinesia, postural instability) can lead to secondary motor symptoms. A classic one is the ‘Simian’ posture where the spinal curvature results in a flattened lumbar lordosis, rounded shoulders and a poking chin (hyperextended cervical spine). The consequent forward flexed upper body results in the ‘ape-like’ posture. Examples of secondary motor and common non-motor symptoms are tabulated above (Table 24.3).

Diagnosis

Currently, no reliable test exists for Parkinson’s so diagnosis is determined through the history and clinical signs of at least two of the four cardinal motor symptoms described earlier using the UK Brain Bank Criteria and investigations (scans) (NICE 2006).

Parkinson’s is the most common presentation within a collection of motor system disorders known as ‘Parkinsonism’ (Table 24.4). The various disorders can be identified using positron emission tomography (PET) and structural magnetic resonance imaging (MRI) scanning. They are also referred to as ‘Parkinson’s Plus’ as they involve a wider area of the nervous system than idiopathic Parkinson’s (SIGN 2010: 11–13).

Medication is less effective or may have to be withdrawn for people with Parkinson’s Plus syndromes, and the course and presentation differs from those with ‘idiopathic’ Parkinson’s described in this chapter.

Aetiology and epidemiology

There are approximately 120,000 people with Parkinson’s in the UK and an estimated 6.3 million worldwide. The average age of onset is 60–65 years. The term ‘idiopathic’ is used when there is no known cause of the Parkinson’s, as no known single, universal causative factor has yet been identified. Several theories exist – the most common of which proposes Parkinson’s to result from a variety of pathological processes in addition to influencing factors, such as the environment, the ageing process and genetics.

Neuropathology

The ‘ascending hypothesis’ of idiopathic Parkinson’s conceptualises a pathological progression from the lower brainstem (pre-clinical stage) to the midbrain (substantia nigra clinical stage) and cortex (end-stage) (Braak et al. 2003; Yanagisawa 2006). Extra-pyramidal system dysfunction leads to the loss of the internal ‘go’ setting, essential for movement initiation that becomes evident after the pre-clinical stage.

Pathologically, Parkinson’s is characterised by a reduction of neuromelanin cells in the brainstem, primarily dopamine neurones in the substantia nigra, but also in the corpus striatum (caudate nucleus and putamen). People with Parkinson’s will have lost over 70% of dopamine-producing cells before motor signs (TRAP) are visible. This is thought to cause an inability to direct and control movements (rigidity and loss of inhibition of tremor), while increasing inhibition to the thalamus (bradykinesia). A lack of inhibition mainly of the reticulospinal and vestibulospinal pathways results in excessive contraction of postural muscles. The imbalance of inhibition and excitation result in the classical clinical features of Parkinson’s.

Classification

Parkinson’s is classed in various ways. The most common method is by severity according to the (modified) Hoehn and Yahr scale (1967), categorising people along a continuum from asymmetry at Stage 1 to Stage 5 palliation. Physiotherapy referrals usually occur when signs of poor balance develop and possibly a fall from Stage 3 onwards.

MacMahon and Thomas (1998) have provided a clinical staging classification, allowing for periods of deterioration during illness, but regaining the ability on recovery. Details of both these can be read in the Parkinson’s Professional Guide (PDS 2007).

In light of evolving information regarding the pre-clinical development of Parkinson’s, Stern et al. (2012) have proposed the following phases to reflect the progress of the condition (Table 24.5).

A cluster analysis of presentation at diagnosis has provided detail according to a person’s age, cognitive state (presence of dementia or not) and symptom dominance (van Rooden et al. 2010). The four subtypes of Parkinson’s are identified below.

The importance of such classifications for physiotherapists is evident when decision-making about progression and intervention have to be considered, and equipment and support networks put into place.

The International Classification of Functioning, Disability and Health

The International Classification of Functioning, Disability and Health (ICF) (WHO 2001) offers a model for consideration of multiple impairments, relating them to domains that guide assessment, goal-setting and treatment-planning (Figure 24.1).

Impairments often impact on activities of daily living and how the person can participate in societal roles in later life (Izaks and Westendorp 2003), and the ICF framework considers issues in context. For example, environmental (physical and attitudinal) and personal (medication, support) factors which can act as barriers or facilitators in the analysis and subsequent planning of appropriate intervention. Consideration of the target level (whether an impairment, activity or participation issue) ensures that therapeutic management meets the current status and needs of the individual. An appreciation of how people live with ongoing (a set of) conditions using such a bio-psychosocial and partnership approach to practice is key to achieving person-centred management.