Early and correct diagnosis and treatment of Parkinson's disease (PD) are c
rucial for the patient's well being. At the first visit, it is important to
deal with the patient's misconceptions of the disease and its course, to o
ffer sources of information and to suggest exercises. To make a correct ini
tial diagnosis of PD we need to assess the course of the initial levodopa r
esponsiveness. The most frequent challenges in diagnosing PD are the condit
ions of essential tremor and multiple system atrophy. PD has 3 stages of de
velopment: (i) early - from the onset of symptoms to the appearance of moto
r fluctuations; (ii) middle - from motor fluctuations to the appearance of
moderate-to-severe disability; and (iii) advanced - when moderate-to-severe
disability is present.
The medical treatment of early PD should be started when functional disabil
ity appears, which is a different threshold for each patient. For patients
below 65 years old, or above 65 years old but with presented mental functio
n and with no severe comorbidity, initial monotherapy with a dopamine agoni
st is advisable. This approach appears to delay the appearance and reduce t
he amount of late motor complications with subsequent levodopa treatment. A
ll dopamine agonists have similar efficacy, which is less than that of levo
dopa. It is important to consider the adverse effect profile when a choice
for initial or adjunctive therapy is made. When levodopa therapy is started
as an adjunct in younger patients or as initial monotherapy in older patie
nts, sustained-release levodopa preparations are preferred. They have a lon
ger half-life and possibly stimulate the dopamine receptors more continuous
ly.
Anticholinergic drugs are appropriate for younger patients with tremor-domi
nant PD. Amantadine is mainly used for dyskinesia control. Catechol-O-methy
l-transferase inhibitors and neurosurgery are not treatments of choice for
early PD but can be very effective for more advanced disease. The presence
of presymptomatic markers of PD, such as changes in odour detection, handwr
iting, speech, movement time of self-initiated motor acts, personality trai
ts, presence of antibodies against dopaminergic neurons, pattern of positro
n emission tomography results, appearance of mitochondrial DNA mutation pro
files, etc., appear to be very important in the light of the emerging neuro
protective therapies. Neuroprotection is aimed at slowing the rate of disea
se progression. Selegiline has been shown to cause a mild delay in the need
for levodopa, possibly suggesting some protection. However, this initial b
enefit was not sustained in long term studies. Currently, there is no neuro
protective drug for PD.