Parkinson's disease and tremor

What Parkinson's disease is

In Parkinson's disease the neurons that produce dopamine in a deep area of the brain called the substantia nigra gradually degenerate. Dopamine is the transmitter that helps the brain start and regulate purposeful movement; when it is lacking, movements become slow, stiff and smaller in amplitude. Deposits of the protein alpha-synuclein (Lewy bodies) accumulate in the surviving neurons. The exact cause of this process is not fully known: genetic and environmental factors are thought to combine. The disease usually appears after age 50–60 and is slightly more common in men; early forms (before 50) are rarer and often have a genetic component.

The disease progresses slowly, at a different pace from one patient to another. With appropriate treatment, most patients keep a good quality of life for many years and life expectancy is close to normal.

What the signs of Parkinson's are

The diagnosis requires the presence of bradykinesia (slowing and decreasing amplitude of repetitive movements, for example fingers tapping slowly, handwriting that becomes smaller and smaller), plus at least one of these:

• muscle rigidity (high resistance to passive movement, often with a “cogwheel” feel);
• rest tremor (4–6 cycles per second, often “pill-rolling” with the fingers and hand, which lessens during movement);
• in later stages, postural instability, short steps, “freezing” while walking and a tendency to fall.

The disease is also accompanied by non-motor symptoms, which often precede the movement problems by years: reduced sense of smell (hyposmia), constipation, sleep disturbances (including acting out dreams during REM sleep), depression and anxiety, fatigue, a fall in blood pressure on standing, urinary disturbances and, in late stages, cognitive changes. Symptoms and the pace of progression differ between patients.

What else can cause tremor

Tremor is not a synonym for Parkinson's. For the differential diagnosis it matters whether it occurs at rest, while holding a position or during action:

• essential tremor: the most common form, bilateral, in the hands when holding a posture or acting (eating, writing), often familial and eased by a little alcohol; there is no bradykinesia;
• physiological tremor increased by stress, caffeine, lack of sleep and thyroid disorders (hyperthyroidism);
• drugs that cause it: antipsychotics, metoclopramide, valproate, lithium, bronchodilators, corticosteroids;
• secondary or atypical parkinsonism (from drugs, from cerebrovascular disease, or from other neurodegenerative syndromes).

Do not stop prescribed drugs just because you suspect they cause tremor; talk to your doctor.

How the diagnosis is made

The diagnosis of Parkinson's is clinical: it rests mainly on the history and the neurological examination, in which the doctor assesses movement, muscle tone, tremor and gait, as well as the response to dopamine. There is no blood test that confirms the disease. Tests or specialized examinations (MRI, sometimes functional imaging of the dopamine transporter) may be recommended at another center to exclude other causes or when the picture is atypical; a single CT or MRI does not establish the diagnosis.

How it is treated

There is still no drug that halts the disease, but symptoms can be controlled well for many years. Treatment is individualized and includes:

• Levodopa (combined with a decarboxylase inhibitor, carbidopa or benserazide) is the most effective drug: it is converted into dopamine in the brain. It is used when symptoms limit function.
• Dopamine agonists (pramipexole, ropinirole, rotigotine) and MAO-B inhibitors (rasagiline, selegiline, safinamide) are used in the early phase or as add-ons; COMT inhibitors (entacapone) prolong the effect of levodopa.
• After years, the effect of each dose may shorten and fluctuations appear (“on” and “off” periods) or involuntary movements (dyskinesia); the timing and mix of drugs are then adjusted. In selected patients with fluctuations that cannot be controlled, advanced treatments (deep brain stimulation, levodopa pumps) are recommended at a specialized center.
• Rehabilitation: physiotherapy, balance and gait exercises, speech and swallowing therapy, occupational therapy. Regular exercise is part of treatment, not just advice.

The timing of drugs matters: take them at fixed times and, where possible, away from protein-rich meals, which compete with levodopa for absorption. Do not change doses and do not stop treatment suddenly (abrupt withdrawal can cause a severe condition). Report difficulty swallowing, falls, hallucinations, sudden sleepiness or new behaviors (shopping, gambling, compulsive eating) after starting a drug. Some drugs (for example metoclopramide, haloperidol) should be avoided in patients with Parkinson's.

Follow-up in daily life

Regular check-ups, every 6 months to a year or sooner when the doctor considers it reasonable, assess movement and non-motor symptoms (sleep, mood, constipation, blood pressure on standing, memory). Suitable exercise, walking, and adapting the home (removing obstacles, grab rails in the bathroom, lighting) increase safety. Involving family members is helpful when support is needed.

Care at Tirana Polyclinic: we offer neurology consultation, follow-up and coordination with physiotherapy as needed, and interpretation of examinations performed outside the clinic.