Parkinson’s disease was first described by James Parkinson in 1817, who named it the ‘shaking palsy’. It is the most common of all the a kinetic–rigid syndromes with a prevalence of 170 per 100000 of population in the UK. It is more common in men than in women, and the average age at disease onset is 60 years. It is a slowly progressive, degenerative disease involving the basal ganglia as well as other brain areas. It causes an a kinetic–rigid syndrome, commonly associated with a rest tremor, that is later accompanied by a flexed posture, shuffling gait and impaired balance. The disease also manifests with a variety of non-motor symptoms, cognitive and psychiatric complications. The cause of Parkinson’s disease is unknown.
Clinical features of Parkinson’s disease comprise the classical triad of rest tremor, limb rigidity and not only bradykinesia but also akinesia, with progressive fatiguing of movements, in association with changes in posture and gait and a host of non-motor symptoms and cognitive decline. An important and characteristic feature of Parkinson’s disease is the striking asymmetry of the clinical signs. If a patient presents with symmetrical parkinsonian clinical signs, they are unlikely to have idiopathic Parkinson’s disease.
Tremor is the initial presenting symptoms in about 60% of patients with Parkinson’s disease. This is a characteristic coarse resting tremor (4–7 Hz) of the hands and can affect any part of the body, including the chin, tongue and the legs. It can be exacerbated by emotion and distraction, e.g. walking or using the contralateral limbs. The rest tremor disappears in sleep. It is often ‘pill-rolling’ in nature on account of the thumb moving rhythmically backwards and forwards on the palmar surface of the fingers. The rest tremor may lessen or disappear during voluntary movement (e.g. when raising arms in front of body), but then reappears after a delay, in the new position (‘re-emergent tremor’).
There is stiffness of the limbs, which can be felt as resistance throughout passive movement of the arms and, equally, in the flexors and extensors. This is termed ‘lead-pipe’ rigidity. When combined with the tremor which can be subclinical, there is a jerky element (‘cog-wheel’ rigidity). The increase in tone can be felt most easily when the wrist is rotated in both clockwise and anticlockwise directions and can be made more apparent when the patient is asked to voluntarily move the opposite limb (synkinesis). The rigidity is usually asymmetrical in the limbs.
Bradykinesia, hypokinesia and akinesia
Akinesia is often the most disabling feature of Parkinson’s disease. It is a grouping of symptoms that includes bradykinesia (slowness of movement with additional fatiguing and decrement of repetitive alternating movements) and hypokinesia (reduced amplitude of movements). Bradykinesia and hypokinesia affect not only the limbs but also the muscles of facial expression to give mask-like facies known as hypomimia and reduced blinking. The muscles of mastication, speech and voluntary swallowing, and some of the axial muscles, can also be involved. There is particular difficulty in initiating and terminating movements.
Speech is altered, producing a monotonous, hypophonic dysarthria, due to a combination of bradykinesia, rigidity and tremor. Power is usually preserved, although in advanced disease the slowness (bradykinesia) and rigidity make testing power difficult. Sensory examination is also normal, although patients can often describe discomfort and sensory abnormalities in the legs. Handwriting reduces in size and becomes spidery (micrographia).
The posture is characteristically stooped, with a shuffling, flexed, festinant (steps that become increasingly fast) gait with poor asymmetrical arm swing. Falls are common later in the disease process, as the normal righting reflexes are affected. There may be difficulty initiating gait (‘start hesitation’), and when the patient tries to turn either when walking or lying (e.g. in bed), there are great difficulties (‘freezing’) and the patient is said to move ‘en bloc’.
Parkinson’s disease is a clinical diagnosis, and an MRI brain in uncomplicated disease is typically normal. A dopamine transporter (DaT) single-photon emission computed tomography (SPECT) scan typically shows decreased dopamine transporter binding in the basal ganglia. DaT scans should not be routinely used to confirm a diagnosis of Parkinson’s disease, nor can they distinguish between Parkinson’s disease, multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). However a normal scan can be used to exclude Parkinson’s disease. NICE therefore recommends its use where it is difficult to differentiate essential tremor from parkinsonism.
The main aim of treatment is to restore the dopamine levels within the striatum. NICE guidelines highlight that it is not possible to pick a universal first-choice drug therapy for patients with early or late Parkinson’s disease. Instead, a patient’s clinical and lifestyle characteristics, together with their preference once fully informed about medication options, should be taken into consideration.