Parkinson's Disease

Parkinson's disease is a progressive neurological condition that affects movement and many other body functions. It usually develops gradually, often begins on one side and is diagnosed mainly from the clinical pattern. Treatment can improve symptoms, but careful medicine timing and multidisciplinary support remain essential throughout the condition.

What Parkinson's disease is Parkinson's disease is a progressive neurodegenerative condition. Particular nerve cells and connected brain networks gradually lose function over time. The best known change is loss of dopamine producing neurons in a region called the substantia nigra. These neurons normally supply dopamine to movement circuits within the basal ganglia. Dopamine helps the brain select, start and scale purposeful movement. When dopamine signalling falls, movement may become slower, smaller, stiffer and less automatic. Parkinson's disease is not only a dopamine deficiency and not only a movement disorder. Changes occur in wider brain and nervous system networks, which helps explain the many non motor symptoms. What happens in the brain The dopamine producing cells most closely linked with the motor syndrome lie in the substantia nigra pars compacta. Their projections reach the striatum, an important part of the basal ganglia. The basal ganglia do not directly move a limb like a muscle. They help competing movement plans, learned habits and automatic actions to be selected and adjusted. As dopamine input falls, these networks become less efficient. A person may need more conscious effort to begin walking, turn, write or perform a sequence of small movements. Many affected nerve cells contain abnormal aggregates of a protein called alpha synuclein. Lewy bodies are microscopic inclusions containing alpha synuclein, but they cannot be seen on a routine living person scan. The presence of Lewy pathology does not mean that every symptom has one simple mechanism. Cholinergic, noradrenergic, serotonergic and autonomic networks may also be involved. This wider involvement helps explain why sleep, mood, smell, blood pressure, bowel function and cognition can change before or alongside movement. A progressive condition with a variable course Progressive means that the underlying condition changes over time. It does not mean that every symptom worsens steadily each day. Symptoms can fluctuate during the day, particularly once treatment timing becomes important. Infection, constipation, dehydration, poor sleep, stress and missed medication can temporarily worsen function. The rate of progression varies greatly between people. Age, other illnesses, treatment response, cognition, mobility and support needs all influence the practical effect of the condition. Treatment can improve symptoms and daily function, sometimes substantially. Current routine treatments do not cure Parkinson's disease or reliably stop the neurodegenerative process. A diagnosis should therefore lead to continuing review rather than a one off label. The clinical pattern, treatment response and new features may strengthen or challenge the original diagnosis. The classic motor triad The three best known motor features are bradykinesia, rigidity and resting tremor. They are often described as the classic motor triad. A person does not need all three features. Tremor may be absent, and some people first notice slowness, stiffness or reduced dexterity. Bradykinesia is the required core feature when clinicians identify motor parkinsonism. It must occur with resting tremor, rigidity or both. This definition matters because a tremor alone is not parkinsonism. It also prevents ordinary age related slowness or joint stiffness from being labelled Parkinson's disease without the correct movement pattern. Bradykinesia: more than moving slowly Bradykinesia means slowness of voluntary movement with progressive reduction in speed, range or amplitude during repeated action. The second part is important. During examination, a clinician may ask the person to tap finger and thumb, open and close the hand, turn the forearm or tap a foot. Movements may become slower, smaller or interrupted. In daily life, bradykinesia can appear as difficulty starting a task, taking longer to dress, reduced arm swing, smaller handwriting or less spontaneous gesture. Facial expression may become reduced, which is called hypomimia. Speech may become quieter and less varied, although voice change has several possible causes. Automatic actions can be particularly affected. A person may walk reasonably when concentrating but lose arm swing, blink less or struggle when attention is divided. Bradykinesia is not the same as weakness. Muscles may still generate force, but movement is difficult to initiate and scale efficiently. Rigidity and the feeling of stiffness Rigidity is increased resistance when an examiner moves a relaxed joint through its range. It may feel smooth or have a ratcheting quality called cogwheeling. The person may describe stiffness, aching or shoulder discomfort before recognising a movement problem. These symptoms are non specific and may initially resemble a musculoskeletal condition. Rigidity can affect the neck, trunk and limbs. When it is asymmetric, one shoulder may sit differently or one arm may swing less. Stiffness reported by a person does not itself establish rigidity. Pain, arthritis, muscle guarding and spasticity from other neurological conditions can also resist movement. Clinical examination helps distinguish these patterns, but the finding still needs interpretation alongside bradykinesia and the wider symptoms and background. Resting tremor and other tremors A typical Parkinson's tremor is most visible when the affected limb is relaxed and supported. It often begins in one hand and may have a slow pill rolling appearance. The tremor may reduce during purposeful movement and reappear after the person holds a posture. Anxiety, tiredness or mental effort can make it more noticeable. Not everyone with Parkinson's disease develops tremor. A marked action tremor may point towards essential tremor, although both conditions can coexist. Essential tremor usually becomes most evident when holding a posture or performing an action. It may affect both hands and can involve the head or voice. No single tremor pattern is perfectly specific. Diagnosis depends on bradykinesia, rigidity, asymmetry, progression, associated features and specialist examination. Asymmetric onset is a useful clue Typical Parkinson's disease often begins on one side. One hand may tremble, one arm may swing less or one foot may drag before the other side becomes involved. The difference can remain noticeable for years, even after both sides are affected. This persistent asymmetry is a supportive clue rather than a compulsory rule. A symmetric presentation from the beginning is less typical. It can occur with drug induced parkinsonism, vascular parkinsonism or some atypical syndromes. However, symmetry is not a diagnosis. Drug induced parkinsonism can be asymmetric, and Parkinson's disease can occasionally appear fairly even. Clinicians use asymmetry as one part of a pattern. They do not use it alone to confirm or exclude Parkinson's disease. Posture, gait and turning Walking can become slower with shorter steps, reduced heel strike and less arm swing. The trunk may become more flexed, and turning may require several small steps. Festination describes steps becoming progressively shorter and quicker, as though the upper body moves ahead of the feet. It can increase the risk of losing balance. Freezing is a brief inability to step despite intending to move. The feet may feel glued to the floor when starting, turning, approaching a doorway or entering a crowded space. External cues can sometimes help. A physiotherapist may teach rhythmic counting, visual stepping targets or deliberate weight shifting. These strategies are individual. They do not replace assessment of falls, blood pressure, vision, footwear, environment and other contributors to walking difficulty. Postural instability usually becomes important later Postural instability means impaired balance and reduced ability to recover after being displaced. It can lead to backward or sideways falls. In typical Parkinson's disease, prominent postural instability and repeated falls usually develop later than bradykinesia, rigidity or resting tremor. Repeated falls very early in the illness are therefore atypical. They may suggest progressive supranuclear palsy, another neurological disorder or an additional cause of imbalance. Falls in established Parkinson's disease are often multifactorial. Freezing, low blood pressure, medication effects, poor vision, muscle weakness and unsafe surroundings may all contribute. A fall should not automatically be attributed to Parkinson's disease. Injury, infection, cardiovascular causes and other acute problems may need assessment. Non motor symptoms are central, not optional extras Parkinson's disease can affect sleep, mood, thinking, pain, bowel function, bladder control, blood pressure and sexual function. These problems may be as disabling as the movement disorder. Some non motor symptoms appear before motor parkinsonism. This earlier phase is sometimes called the prodromal phase. Reduced smell, REM sleep behaviour disorder, constipation and depression are recognised prodromal features. They can precede motor symptoms by years. These symptoms are common in the general population and have many causes. Most people with constipation, depression or reduced smell do not develop Parkinson's disease. They therefore provide context rather than a home screening test. Their significance rises when they occur in a compatible neurological pattern assessed by a clinician. Reduced smell Hyposmia means a reduced sense of smell, while anosmia means complete loss. Smell may decline gradually and go unnoticed until someone comments on food tasting different. Reduced smell can occur years before the motor syndrome. It reflects involvement beyond the main movement circuits. However, nasal disease, viral infection, head injury, ageing and several other conditions can reduce smell. A recent change should not be assumed to indicate Parkinson's disease. NICE does not recommend objective smell testing as a routine diagnostic test for parkinsonian syndromes outside research. The symptom is supportive, not confirmatory. REM sleep behaviour disorder During normal rapid eye movement sleep, most skeletal muscles are temporarily relaxed. This helps prevent the body from acting out dreams. In REM sleep behaviour disorder, this muscle relaxation is reduced. A person may shout, punch, kick or make complex movements during vivid dreams. The behaviour can injure the person or a bed partner. It deserves clinical assessment and practical attention to bedroom safety. REM sleep behaviour disorder is associated with Parkinson's disease and related synuclein disorders. It can begin many years before motor symptoms. Dream enactment is not always REM sleep behaviour disorder. Sleep apnoea, medicines, trauma related sleep disturbance and other parasomnias can resemble it, so specialist sleep assessment may be needed. Constipation, mood and other early changes Constipation can precede movement symptoms, partly because Parkinson's can affect autonomic and enteric nervous system function. Reduced activity, diet, medicines and fluid intake may add to it. Depression and anxiety may also occur before or after diagnosis. They can reflect brain changes, psychological adjustment, other illnesses or a combination. Fatigue, pain and apathy are also common. Apathy means reduced motivation and is not identical to depression, although both can coexist. These symptoms deserve assessment in their own right. They should not be dismissed as an inevitable emotional response to a neurological diagnosis. Parkinson's disease and parkinsonism are different terms Parkinsonism describes a motor syndrome. It is defined by bradykinesia together with resting tremor, rigidity or both. Parkinson's disease is one cause of parkinsonism and is the most common degenerative cause. The two terms should not be used as exact synonyms. Other causes include medicines that block dopamine, cerebrovascular disease and atypical neurodegenerative syndromes. Structural, metabolic and toxic causes are less common. The distinction matters because prognosis, treatment response and associated complications differ. A person can have parkinsonism without having Parkinson's disease. Drug induced parkinsonism Some medicines reduce dopamine signalling or block dopamine receptors. Examples include certain antipsychotics and some anti sickness medicines. Drug induced parkinsonism may produce bradykinesia and rigidity, sometimes with tremor. It often affects both sides more evenly than Parkinson's disease. The pattern is not always symmetric. A dopamine blocking medicine can also reveal previously subtle Parkinson's disease. Symptoms may improve after the responsible medicine is reduced or stopped, but recovery can take time. Changes must be supervised because abrupt withdrawal may be unsafe for the condition being treated. A medicine review should include prescribed, over the counter and recently stopped drugs. The aim is not to blame a medicine automatically but to identify a potentially reversible contributor. Vascular parkinsonism Vascular parkinsonism is associated with cerebrovascular disease affecting movement networks. It is a clinical concept rather than one single scan appearance. Walking and lower body problems may be prominent. Steps can be short, balance may be impaired and the arms may be less affected. The onset may be stepwise or linked with other vascular neurological features, but some cases progress gradually. Tremor may be less typical. Brain imaging can support the assessment of cerebrovascular disease, yet age related vascular changes are common. A scan abnormality does not prove that it causes the movement pattern. Management includes reviewing the diagnosis, treating vascular risk appropriately and addressing mobility. Levodopa response is often limited, but some people may benefit. Atypical parkinsonian syndromes Atypical parkinsonian syndromes are progressive neurological conditions that can resemble Parkinson's disease but have additional early features. Progressive supranuclear palsy, or PSP, can cause early falls, neck or trunk rigidity, slowed vertical eye movements, swallowing difficulty and changes in thinking or behaviour. Multiple system atrophy, or MSA, can cause parkinsonism with severe autonomic failure, including marked postural hypotension, urinary retention or incontinence, and sometimes cerebellar features. Corticobasal syndrome can cause striking asymmetry, limb apraxia, cortical sensory problems or a limb that feels difficult to control. It is not necessary to recognise this syndrome from a lay description. Dementia with Lewy bodies can include cognitive fluctuations, visual hallucinations and parkinsonism. When dementia is very early or precedes the motor syndrome, clinicians consider this broader diagnostic relationship. These conditions overlap clinically, especially early. The purpose of the distinctions is to explain why follow up matters, not to encourage self classification. Features that make typical Parkinson's disease less likely No single atypical feature automatically excludes Parkinson's disease. Clinicians consider the number, severity and timing of features. Repeated falls within the early years are concerning because balance failure is usually later in typical Parkinson's disease. A poor response to an adequate levodopa trial raises doubt, especially when adherence, timing, dose and absorption have been addressed. Severe autonomic failure early in the course can suggest MSA or another cause. Examples include marked postural hypotension, urinary retention or severe urinary dysfunction. Early dementia, early recurrent visual hallucinations without a medicine or illness trigger, vertical eye movement abnormalities and rapid progression also warrant review. A strongly symmetric onset is another clue. These features support reconsideration rather than a definitive alternative diagnosis by themselves. How diagnosis is made Parkinson's disease is diagnosed primarily from the symptoms and background and neurological examination. There is no routine blood test, MRI scan or biomarker that confirms it. The clinician first establishes whether true motor parkinsonism is present. Bradykinesia must be demonstrated with resting tremor, rigidity or both. They then look for supportive features. These include asymmetric onset, rest tremor, a clear sustained levodopa response and levodopa induced dyskinesia. They also look for exclusionary or atypical features. The balance between supportive and concerning findings determines diagnostic confidence. NICE recommends prompt referral, preferably before starting treatment, to a specialist experienced in the differential diagnosis of Parkinson's disease. The diagnosis should be reviewed regularly. New information can justify changing it, particularly if the course differs from what was expected. What the neurological examination looks for The examiner observes the person before formal testing. Facial expression, blinking, voice, posture, spontaneous movement and arm swing can provide clues. Repeated finger tapping, hand opening, forearm rotation and foot tapping help assess bradykinesia. The examiner looks for slowness and progressive reduction in movement size. Passive movement of the wrists, elbows, neck or legs helps identify rigidity. Tremor is observed at rest, during posture and during action. Standing, walking, turning and recovery from a gentle backward pull may be assessed when safe. Eye movements, coordination, reflexes, strength and sensation help identify other disorders. Cognition, mood and autonomic symptoms may also be assessed. Parkinson's disease is not adequately evaluated by watching a hand tremor alone. What a DaTscan can and cannot show DaTscan is a common name for dopamine transporter SPECT imaging using a radiotracer. It assesses presynaptic dopaminergic nerve terminal activity in the striatum. An abnormal scan supports a degenerative loss of nigrostriatal dopamine terminals. A normal scan can make degenerative parkinsonism less likely in the appropriate context. NICE recommends considering this scan when essential tremor cannot be clinically distinguished from parkinsonism. It is not a routine test for every suspected case. DaTscan does not reliably distinguish Parkinson's disease from PSP, MSA or other degenerative parkinsonian syndromes. These conditions can all produce reduced uptake. It also does not measure symptom severity, predict an individual's course or replace specialist examination. The scan answers a narrow question rather than naming the whole diagnosis. Levodopa: the most effective motor treatment Levodopa is a precursor that crosses into the brain and is converted into dopamine. It is usually combined with carbidopa or benserazide. These companion medicines reduce levodopa breakdown outside the brain. This improves delivery and reduces peripheral adverse effects such as nausea. Levodopa is the most effective symptomatic treatment for bradykinesia and rigidity. Tremor often improves, although response varies. NICE recommends offering levodopa when early motor symptoms affect quality of life. The choice still depends on shared decision making and individual circumstances. A good response supports the diagnosis but does not prove it. Some atypical syndromes respond partially, while poor absorption or inadequate dosing can falsely suggest non response. Levodopa does not replace therapy for balance, speech, swallowing, mood, cognition or autonomic symptoms. Parkinson's care cannot be reduced to dopamine replacement alone. Wearing off and motor fluctuations Early in treatment, each levodopa dose may give a relatively smooth benefit. As the disease progresses, the therapeutic window can become narrower. Wearing off means symptoms return before the next dose is due. Slowness, stiffness, tremor, pain, anxiety or other non motor symptoms may reappear. An 'off' period is a time when medication benefit is reduced and Parkinson's symptoms are more prominent. An 'on' period is when medication is working better. Delayed on means a dose takes longer than expected to work. Dose failure means the expected benefit does not arrive. Constipation, slow stomach emptying, protein intake and medication timing can influence absorption. These factors should be assessed before assuming the drug has stopped working. Specialists may adjust dose size, dose frequency, formulation or add another medicine. Changes require individual review because reducing off time can increase dyskinesia or adverse effects. Dyskinesia Dyskinesia describes involuntary extra movements associated with dopaminergic treatment. They may look like writhing, twisting, fidgeting or irregular flowing movement. Dyskinesia is different from tremor. Tremor is rhythmic, while dyskinesia is usually less regular and often occurs when levodopa levels are higher. Mild dyskinesia may be less disabling than severe off time. The importance depends on pain, falls, embarrassment, exhaustion and interference with tasks. Treatment may involve redistributing levodopa, changing adjunctive medicines or considering advanced therapies. Simply stopping levodopa abruptly is unsafe. The balance is individual. The goal is useful function with the least troublesome off time, dyskinesia and treatment burden. Dopamine agonists Dopamine agonists stimulate dopamine receptors directly. Examples include pramipexole, ropinirole and rotigotine. They generally improve motor symptoms less than levodopa. They may be used alone in selected early disease or added when levodopa control becomes uneven. Important adverse effects include nausea, low blood pressure, ankle swelling, hallucinations, daytime sleepiness and sudden sleep episodes. Impulse control disorders can cause compulsive gambling, shopping, eating, sexual behaviour or repetitive purposeless activities. The person may not recognise the change. Risk is greater with dopamine agonists but can occur with other dopaminergic treatment. Patients and families should receive clear information and know how to report behavioural change. Dopamine agonists should not be stopped suddenly without specialist advice. Withdrawal can cause anxiety, depression, pain, fatigue and autonomic symptoms. MAO B inhibitors and other adjuncts Monoamine oxidase B, or MAO B, inhibitors reduce dopamine breakdown in the brain. Selegiline, rasagiline and safinamide are examples used in Parkinson's care. Their motor effect is generally smaller than levodopa. They may be considered in early disease or added to levodopa for fluctuations. Other adjunct classes include COMT inhibitors, which prolong levodopa effect, and amantadine, which can help selected people with dyskinesia. Anticholinergic drugs now have a limited role because confusion, blurred vision, urinary retention and other adverse effects can be important, particularly in older adults. Medicine combinations can create interactions and complex schedules. The purpose of this overview is to explain the classes, not to guide self adjustment. All changes should be made with a clinician who understands the person's motor pattern, cognition, blood pressure, sleep and other medicines. The critical rule: never stop dopaminergic medication abruptly Antiparkinsonian medicines should not be withdrawn abruptly or allowed to fail suddenly. This includes failure caused by vomiting, severe constipation, poor absorption or inability to swallow. Sudden interruption can cause acute akinesia, profound rigidity, fever, reduced consciousness and autonomic instability. This emergency resembles neuroleptic malignant syndrome and is often called parkinsonism hyperpyrexia syndrome. Infection, dehydration and other illness may trigger or worsen it. The response is urgent medical assessment, restoration of dopaminergic treatment by an appropriate route and treatment of complications under specialist guidance. A planned medicine reduction is different from abrupt interruption. Even planned withdrawal should be gradual and clinically supervised. Hospital admissions and time critical medicines Parkinson's medication timing is individual. A standard hospital round may not match the person's prescribed schedule. Even short delays can cause painful stiffness, loss of mobility, swallowing difficulty, anxiety, falls or inability to communicate. On admission, staff should record the exact medicine, formulation, dose and usual time. 'Three times daily' is not precise enough when the person's timings are specific. NICE advises that medicines are given at the appropriate times and adjusted only by, or after discussion with, a Parkinson's specialist. If swallowing is unsafe, the answer is not simply to omit doses. Urgent pharmacy, specialist and speech and language advice may be needed to establish a safe alternative. Some anti sickness and antipsychotic medicines block dopamine and can worsen parkinsonism. Clinicians should choose compatible alternatives where possible. Patients and families can help by carrying an up to date medication list, but responsibility for safe prescribing and administration remains with the healthcare team. Falls and mobility complications Falls become more common as balance, freezing and postural responses worsen. They may lead to injury, fear and reduced activity. A falls assessment should consider blood pressure, vision, feet, footwear, bone health, cognition, environment and medicines as well as Parkinson's. Physiotherapy can teach cueing, turning strategies, strength work and safer transfers. Occupational therapy can assess home hazards and equipment. Walking aids require individual instruction. An unsuitable aid can worsen freezing or posture rather than improve safety. Sudden new falls, marked weakness or inability to walk may signal acute illness, injury or a medication problem. They should not automatically be labelled progression. Speech, saliva and swallowing Speech may become quieter, faster, less distinct or more monotonous. Communication can also be affected by facial expression, thinking speed and fatigue. Speech and language therapy can teach strategies to increase effort, clarity and communication participation. Alternative communication tools may be considered later. Drooling often reflects reduced automatic swallowing rather than excessive saliva production. Posture and mouth closure can contribute. Swallowing difficulty can affect liquids, food, tablets or saliva. Signs include coughing during meals, a wet voice, prolonged eating, weight loss or recurrent chest infections. Silent aspiration can occur without obvious coughing. New swallowing difficulty requires assessment because aspiration, dehydration and missed medication can follow. Diet texture should not be changed casually. Speech and language therapists and dietitians help balance swallowing safety, nutrition, hydration and quality of life. Autonomic dysfunction The autonomic nervous system controls functions that usually operate without conscious effort. Parkinson's can disrupt several of these functions. Orthostatic hypotension means blood pressure falls on standing. It can cause dizziness, blurred vision, weakness, falls or fainting. Dopaminergic medicines, antihypertensives, dehydration and other illnesses can worsen this problem. Lying and standing blood pressure helps define the pattern. Urinary urgency, frequency, nocturia, incontinence or incomplete emptying may occur. Infection, prostate disease, pelvic floor problems and medicines must still be considered. Constipation may become severe and can interfere with comfort, nutrition and medicine absorption. Treatment may involve fluid, fibre, activity and laxatives tailored to the person. Sweating changes and sexual dysfunction also occur. These symptoms should be discussed openly because effective support may be available. Hallucinations, delusions and sudden confusion Visual hallucinations are common later in Parkinson's disease and can be promoted by dopaminergic treatment. A person may see people, animals or shapes that are not present. Delusions are fixed false beliefs, such as believing someone is stealing. They can be distressing and increase safeguarding risk. New hallucinations or confusion require a general medical assessment. Infection, dehydration, pain, constipation, sleep loss and recently changed medicines can trigger delirium. Medication review may be needed, but Parkinson's drugs should not be reduced casually. Specialist advice helps balance psychosis against severe motor deterioration and withdrawal risk. Many antipsychotics worsen parkinsonism because they block dopamine. Treatment choices and doses therefore require Parkinson's expertise. Sudden fluctuating confusion is not simply 'Parkinson's dementia'. It should be treated as a possible acute medical problem. Cognition and Parkinson's disease dementia Some people develop mild cognitive changes involving attention, planning, visual processing or retrieval of information. Others remain cognitively independent for many years. Parkinson's disease dementia describes cognitive decline severe enough to interfere with daily function in someone with established Parkinson's disease. Risk increases with age, disease duration, hallucinations and more advanced motor disease, but dementia is not inevitable. Very early dementia, especially when it precedes or appears around the same time as parkinsonism, changes the diagnostic discussion and may suggest dementia with Lewy bodies. Assessment considers delirium, depression, sleep, medicines, hearing, vision and other neurological disease. A brief memory score alone does not define the cause. Support may include cognitive treatment, communication adaptation, carer support, capacity assessment and future care planning. Mood, apathy, fatigue and sleepiness Depression and anxiety are common and treatable. They can affect quality of life, medication adherence and perception of motor disability. Apathy causes reduced initiation and motivation. It may occur with or without sadness, guilt or hopelessness. Fatigue can feel like overwhelming physical or mental exhaustion. Sleep disturbance, depression, medication, pain and other medical conditions may contribute. Daytime sleepiness can result from poor night time sleep or dopaminergic treatment. Dopamine agonists can occasionally cause sudden sleep episodes. People with daytime sleepiness or sudden sleep onset should not drive and need prompt medication review with specialist advice. Treatment may include addressing sleep disorders, adjusting medicines, psychological therapy, antidepressant treatment, activity planning and social support. Multidisciplinary management Parkinson's disease is best managed through coordinated medical, therapy, nursing and social support. Needs change over time and should be reviewed. A neurologist or specialist geriatrician confirms and reviews the diagnosis, adjusts treatment and considers advanced options. A Parkinson's disease nurse specialist can provide continuity, education, monitoring and a route back into specialist care. Physiotherapists address movement, balance, posture, strength, cueing, transfers and physical activity. Occupational therapists address daily activities, fatigue management, work, equipment, home adaptations and participation. Speech and language therapists assess communication, saliva and swallowing. Dietitians support nutrition, weight, constipation and complex levodopa food interactions. Mental health professionals, continence teams, pharmacists, social care staff and palliative care teams may contribute according to need. The person with Parkinson's and those close to them remain central to decisions. Care should reflect goals, risks, culture, work and home circumstances.

Parkinson's disease is one cause of parkinsonism. Motor parkinsonism requires bradykinesia with resting tremor or rigidity, while the diagnosis of Parkinson's disease depends on the wider pattern, response to treatment and continued specialist review.