Despite the amount of studies on the etiopathogenesis
of Parkinson's disease, to date there are no univocal interpretation or
scientific models that allow us to identify a cause or a univocal mechanism,
but apart from the genetic variants’ description, the cases commonly
encountered in clinical practice as idiopathic are universally accepted as
probably of multifactorial origin. Various pathogenic models have been
speculated to explain neurodegeneration, calling into question the
histopathological findings of anomalous molecular structures (TAU proteins,
alpha synuclein, neurofibrils, Lewy bodies, etc.) in nervous tissue of affected
patients [2-6]. Recently Braak's theory has highlighted a possible primary role
of the peripheral visceral component as the starting mechanism for the central
neurodegenerative process, leading to the hypothesis of the "ascending
track" in the development of Parkinson's disease. In the scenario of
neurovegetative symptoms, the loss of smell has raised the attention of many
researchers, as it can precede the onset of the extrapyramidal symptoms by many
years, bringing them to consider it as a predictor of PD. Indeed, it has also
been taken into consideration as a possible biomarker of the disease [7,8]. In
more recent times, studies have been conducted on the possible role of
cerebrovascular damage in PD [9-12]. In particular, a significant incidence of
CVD has been observed in patients affected by the common, non-genetic form of
PD, through statistical analysis on cohort’ patients or descriptions of single
clinical cases [11,12]. The ‘central’ oxidative mechanism due to vascular
impairment is therefore listed as a possible contributing factor to
pathogenesis of PD, through a direct or indirect mechanism of the dopamine
receptor network damage. This configuration is commonly clearly distinguished
from the so-called vascular Parkinsonism, in which a poor response to
dopaminergic therapy suggests in clinical practice a probable structural
disruption of the extrapyramidal system, although with clinical phenomena
superimposable to idiopathic PD. However, this clear distinction has recently
been questioned with articles by several authors who report a good response to
dopaminergic therapy in patients classified as having vascular parkinsonism, in
which the clinical features did not allow a redefinition as PD (for example in
patients with abrupt onset of the syndrome after a stroke, but with good
response to dopaminergic therapy) [11, 13-15]. The aim of this retrospective
study was to investigate the statistical relationship between the two
parameters CVD and anosmia by means of the data extracted from the patients’
population in charge in the clinic for Parkinson’s disease and Movement
Disorders. This in order to speculate whether there is any link or if there are
possible independent or concurrent pathogenic mechanisms for idiopathic PD
genesis. Although an initial look draws attention to the relevance of the
numbers (patients with CVD and anosmia 39, patients with CVD without the
symptom 59, patients with the symptom without CVD 11), which highlight a
consistent coexistence of the two parameters, albeit with a prevalence of CVD
alone (59 patients), the cross-statistical study did not give a positive result
to confirm any significantl linkage (see table3, p=.20985). Again in this study
the numbers show an absolute prevalence of the CVD in the observed population
(98 out of 118, equal to 83%), if compared with the incidence of the anosmia
symptom (50 out of 118, equal to 42.4%), while anosmic patients affected also
by CVD resulted 39 on total subpopulation with anosmia (50), i.e. 78%. In
other words, especially in light of the statistical verification, in this study
CVD and anosmia seem to be independent parameters and therefore, they can be
said not correlated or linked, although a concurrence in PD pathogenesis cannot
be excluded, consistently with the multifactorial explanation. Ultimately, this
finding can be considered a further confirmation of the non-exclusiveness of
Braak's 'ascending' theory, being able to orient oneself towards the 'central'
origin of the disease in a predominant part of the cases and assuming that CVD
is indeed a critical factor in PD pathogenesis. Finally, it is well known to
clinicians that olfactory disorder is not a constant but has a relatively low
incidence in “sporadic” PD, which undermines its use as an absolute biomarker.
Acknowledgments
The Author wish to thank the coordinator of District H2,
Dr. Rita Bartolomei, the nurse coordinator Francesco Pepe, Mrs Marina Taddei
and the nurse staff of the 2nd District of ASL RM6.