It has been known for over 30 years that olfactory function is disordered i
n idiopathic Parkinson's disease (IPD). The severity and partial specificit
y of anosmia was not realized until recently, with the advent of more detai
led analysis and sophisticated measurement. The olfactory vector hypothesis
suggests that the causative agent for IPD enters the brain via the nasal r
oute, but the reason for olfactory dysfunction may be more subtle. Evidence
for olfactory disturbance is reviewed from pathological, psychological, ne
urophysiological and genetic standpoints. It is proposed that the initial c
ausative event in IPD may start in the rhinencephalon (olfactory brain) pri
or to damage in the basal ganglia.