Early Parkinson's signs that appear years before the tremor

Parkinson's disease is diagnosed on movement — bradykinesia, plus rest tremor or rigidity. By the time those appear, a substantial proportion of dopaminergic neurons in the substantia nigra have already been lost, commonly estimated at 50 to 70 per cent.

That means the disease process has been running for years, probably a decade or more, before the diagnosis is possible on current criteria. And it has been producing symptoms during that time — just not the ones anyone was looking for.

The prodromal features

Hyposmia. Reduced sense of smell affects the large majority of people with Parkinson's and often precedes motor symptoms by several years. It is common in the general population too, particularly with age and after viral infection, so on its own it means little — but combined with other features it becomes informative.

REM sleep behaviour disorder. This is the strongest single predictor known. Normally the body is paralysed during REM sleep; in RBD that paralysis fails, and people physically act out their dreams — shouting, punching, kicking, sometimes falling out of bed. Bed partners usually report it before the patient is aware.

Longitudinal studies of people with polysomnography-confirmed RBD find that a large majority — often quoted above 70 per cent at twelve years, and higher with longer follow-up — go on to develop Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. That is a remarkably high conversion rate for any prodromal marker in neurology.

Constipation. Often present many years before diagnosis, and consistent with the hypothesis that the disease process may begin in the enteric nervous system in at least some patients.

Depression and anxiety, which frequently precede motor symptoms rather than arising as a reaction to diagnosis.

Reduced arm swing on one side while walking, and smaller handwriting (micrographia), which family members often notice retrospectively.

The motor diagnosis

The core requirement is bradykinesia — slowness of movement with progressive reduction in amplitude on repetition. Ask someone to tap finger and thumb rapidly; in Parkinson's the movement gets smaller and slower as it goes.

Plus at least one of rest tremor, classically four to six hertz, present at rest and suppressed by voluntary movement, or rigidity, an increased resistance to passive movement often with a ratchet-like quality.

Asymmetry is characteristic and important. Parkinson's begins on one side and remains asymmetric for years. Symmetrical presentation should raise the question of an alternative diagnosis.

What it is not

Essential tremor is the commonest misdiagnosis in both directions. It is an action tremor — worse when reaching for a cup, absent at rest — usually bilateral, often affects the head and voice, frequently has a family history, and characteristically improves with alcohol. Parkinson's tremor is at rest, asymmetric, and does not affect the head.

Drug-induced parkinsonism is common, under-recognised and reversible. Antipsychotics are the obvious culprits, but metoclopramide and prochlorperazine — prescribed for nausea and dizziness — cause it frequently in older adults. It tends to be symmetrical and to develop over weeks to months after starting the drug.

Vascular parkinsonism from small vessel disease produces a lower-body predominant picture — gait problems out of proportion to arm involvement.

Atypical parkinsonian syndromes — progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration — progress faster, respond poorly to levodopa, and have distinguishing features such as early falls, early autonomic failure or eye movement abnormalities.

Treatment, briefly

Levodopa remains the most effective symptomatic treatment and has been since the 1960s. The old advice to delay starting it as long as possible, on the theory that it caused long-term complications, has largely been abandoned — the motor fluctuations and dyskinesias that develop appear to relate to disease duration and severity rather than to cumulative levodopa exposure. Delaying it costs years of function for no clear benefit.

Dopamine agonists are used, particularly in younger patients, and carry a specific and under-discussed risk: impulse control disorders — pathological gambling, compulsive shopping, hypersexuality, binge eating — affecting a significant minority. Patients and families should be warned explicitly, because the behaviour is otherwise deeply confusing and often concealed.

Exercise deserves emphasis. It is the only intervention with any suggestion of disease-modifying effect, and high-intensity aerobic exercise showed promise in the SPARX trials. Specific programmes for gait, balance and speech — LSVT among others — have good evidence for function.

The non-motor burden

Patients consistently rate non-motor symptoms as more disabling than the movement problems: constipation, urinary urgency, postural hypotension, sleep disturbance, pain, fatigue, depression, and cognitive impairment, which eventually affects a majority.

These are treatable, or at least manageable, and they are frequently not asked about in an appointment that focuses on tremor and gait. Raising them is worth doing deliberately.