Introduction:
Tinnitus is hearing sounds of different frequencies and qualities in the
ear without any external stimulus [1]. Tinnitus is evaluated in two
main groups as objective and subjective. Objective tinnitus is mostly
caused by temporomandibular joint disorder, arteriovenous malformations,
and spasm of the tensor timpani muscle, and in this form, the person
performing the test hears the sound together with the patient [2].
In subjective tinnitus, the sound is only heard by the patient, not the
person conducting the test. Subjective tinnitus may develop for many
reasons, such as hearing impairment, insomnia, medication use,
depression, chronic diseases, anxiety, and difficulty concentrating, and
it has a negative impact on the quality of life of patients [3].
Tinnitus can have various frequencies and qualities, as well as various
intensities. It can reach disturbing levels that seriously affect the
daily life and social performance of the sufferer.
Despite the abundance of studies on the etiology and treatment of
tinnitus, most do not present definitive conclusions. However, it is a
known fact that although the majority of tinnitus sounds heard are
considered to originate from the cochlea, tinnitus continues even after
the auditory nerve has been completely resected [4]. This situation
shows that tinnitus can originate not only from the cochlea but also
from all auditory pathways, and can be seen after the formation of some
inappropriate neural plasticities in the central nervous system.
Although these changes in the central nervous system are both structural
and functional, they can be seen in different parts of the brain, as
well as the auditory pathways [5, 6]. Among all these factors,
vascular and hematological abnormalities can be defined as an important
etiology when tinnitus cases are evaluated, and there may even be
underlying many structural and functional problems. In sudden hearing
loss and facial paralysis, the vascular and hematological dimensions of
tinnitus have been the subject of many studies, but a clear result has
not yet been determined. Among these possible hematological causes, the
neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio
(PLR) have been associated with the inflammatory process and some
thrombotic events [7]. The effect of these parameters on tinnitus
has been investigated in many publications, and results have been
reported based on different levels of evidence. However, considering
that the main function in thrombosis risk is related to thrombocytes,
they should be examined more carefully. In these thrombotic events, the
platelet mass index (PMI), which is considered to be very effective at
the microvascular level, comes to the fore. This is especially important
in organs with endarteria, such as the ear cochlea. Any microvascular
thrombotic event caused by platelets in these endarteria causes serious
problems in organ functions. This situation cannot always be revealed by
angiographic methods and it is vital to consider the possibility of
transient ischemic attacks, and thus tissue damage. In addition, in the
literature, it has been emphasized that the increase in the mean
platelet volume (MPV) is effective in inflammatory processes and that
increased MPV values are directly related to the activation of platelets
[8]. Although MPV is a parameter that has been previously
investigated, its evaluation alone may not be sufficiently reliable
since the number of platelets is at least as important as their volume.
Therefore, in this study, we aimed to explore whether there was a
correlation between PMI and tinnitus. To our knowledge, this is the
first study investigating the effect of platelet mass on tinnitus.
Material and method:
After obtaining the approval of the ethics committee of Harran
University, dated June 29, 2020 and numbered HRU/20.12.09, the detailed
medical records (examination notes, drug use, radiological evaluations,
audiological evaluations, and previous surgical procedures) of 1,079
tinnitus patients presenting to our clinic between January 2019 and May
2020 were examined, and the hemogram data of 177 cases meeting the
inclusion criteria were analyzed. Following a detailed evaluation of
medical records, patients with chronic tinnitus (continuing for at least
three months) in the 18-60 age group were included in the study. In line
with the medical records, cancer patients, patients with chronic
disease, those with a history of cardiac or vascular surgery in the head
and neck region, and those with platelet dysfunction were excluded from
the study to determine the independent effect of platelet mass. Further
excluded were patients with acute inflammation or infection, diabetes
mellitus, systemic hypertension, hyperlipidemia, coronary artery
disease, chronic liver disease, acute or chronic renal failure, chronic
obstructive pulmonary disease, connective tissue disease, inflammatory
bowel disease or a history of acoustic trauma, current smokers, patients
with a personal or family history of hearing loss due to noise, those
with a hearing loss above 20 dB caused by any otological disease, such
as chronic otitis media, otosclerosis and Meniere’s disease, and those
with chronic diseases. For the patients included in the study, age,
gender, hemoglobin, neutrophil, lymphocyte, platelet, and MPV were
examined. This was followed by the assessment of the distribution of
age, gender and hemoglobin level, NLR, PLR, and PMI (calculated as
platelet number x MPV/1000). The values of the tinnitus group were
compared with the data of 192 patients without a history of temporary
(lasting less than two weeks) or permanent tinnitus. The control group
consisted of patients daily presenting to the outpatient clinic for any
reason other than otologic complaints. Cancer patients with chronic
diseases, those with a history of cardiac or vascular surgery in the
head and neck region, and those with platelet dysfunction were not
included in this group. The medical history of this group were evaluated
at the same sensitivity as the tinnitus group in terms of chronic
diseases.