Parkinson’s disease (PD) is the most common neurodegenerative cause of parkinsonism
Parkinson’s disease (PD) is the most common neurodegenerative cause of parkinsonism (approximately 80% of cases of parkinsonism)
As a rule, PD begins between the ages of 40 and 70 years, with peak age onset in the seventh decade.
The prevalence of PD is approximately 160 cases per 100,000 population, and the incidence is about 20 cases per 100,000 population.
The pathological changes of PD may appear as early as three decades before the appearance of clinical signs.
The cause of PD is probably multifactorial, with contributions from hereditary predisposition (genetics), environmental toxins, and aging.
Several studies have indicated that PD is more common among relatives of index cases. When all studies are analysed, first degree relatives of probands are 2 to 3 times more likely to develop PD.
The treatment of PD can be divided into three major conceptual categories: symptomatic, protective and restorative.
Although the goal of therapy is to reverse the functional disability, abolition of all symptoms and signs is not currently possible even with high doses of medication.
The introduction of levodopa has been considered one of the success stories of modern medicine. It remains the most efficacious drug available for the relief of symptoms in PD since its first introduction in the 1960s.
The drug has produced dramatic results even in severely affected patients. However, complications of long term therapy and disease progression do eventually occur. Superimposed upon the disease-related problems are the additional burden of motor fluctuations (the “on-off” reaction), dyskinesias, and visual hallucinations.
Other different pharmacologic advances during the last 3 decades have resulted in additional drug therapies being available including: dopamine agonists, inhibitors of catechol-0-menthyltransferase (COMT) and monoamine oxidase type B (MAO-B) inhibitors.
Surgical interventions including deep brain stimulation (DBS) may be appropriate in selected individuals.
None of the current symptomatic therapeutic options (including surgery) have been shown in large successfully replicated studies to be neuroprotective.
Non-motor problems in PD
Dementia associated with PD has been estimated to affect at least 20% of patients, with prevalence higher among older patients, less common among those with young-onset disease.
An estimated 40% to 60% of PD patients suffer from depression, which appears to be related to duration of disease. Psychiatric adverse effects are much more likely to occur in patients with predisposing characteristics such as: dementia, advanced age, premorbid psychiatric illness and exposure to high daily doses of levodopa.
Other non-motor symptoms include sleep problems, bladder and bowel disturbance, pain, balance difficulties, feeling faint and problems with sweating.
Stem Cell Therapy for PD?
Many people ask about potential therapies that might help prevent the progression of disease in PD and other degenerative disorders and stem cell therapies are offered at some centres. I would recommend caution before committing to something that is expensive and has little evidence to support its effectiveness.
A summary of the literature on stem cell therapy in PD can be found by clicking here.
Other Movement Disorders
Tremor is an unintentional, rhythmic, oscillation of a body part in a fixed plane.
Tremor results from contractions of agonist and antagonist muscles entrained by a signal pattern originating from an oscillator in the CNS.
Resting tremor occurs in a body part that is not activated and completely supported against gravity.
Action tremor refers to tremor occurring with voluntary muscle contraction and is subdivided into postural tremor, isometric tremor and kinetic tremor. The latter is further subdivided into simple kinetic, intention tremor, and task specific tremor, such as writing tremor.
The aetiology of tremor is diverse, and includes hereditary, degenerative, and idiopathic disorders such as Wilson’s disease (very rare), Parkinson’s disease, and Essential Tremor.
Tremor can be secondary to metabolic diseases (such as thyroid-, parathyroid-, liver disease and hypoglycemia); peripheral nerve damage (associated with diabetes mellitus); toxins (nicotine, mercury, lead, CO, Manganese, arsenic, toluene); drug-induced (narcoleptics, tricyclics, lithium, cocaine, alcohol, adrenaline, bronchodilators, theophylline, caffeine, steroids, valproate, amiodarone, thyroid hormones, vincristine); and psychogenic disorders.
Clinically, tremor can be classified into: Physiologic tremor, Enhanced physiologic tremor, Essential Tremor Syndromes (including Classical ET, Primary orthostatic tremor Task- and position-specific tremor), Dystonic tremor, Parkinsonian tremor, Cerebellar tremor (often associated with multiple sclerosis), Holmes’ tremor (a.k.a. rubral tremor), Palatal tremor, Neuropathic tremor, Toxic or drug-induced tremor, and Psychogenic tremor.