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Abdelhaliem et al. Vessel Plus 2020;4:31 I http://dx.doi.org/10.20517/2574-1209.2020.13 Page 5 of 9

These studies were able to intrinsically shed light on patient characteristics and the severity of the tinnitus.
However, this was not uniformly applicable to both carotid artery disease, and independent predictors were
unable to be constructed.

Another hypothesized scope outside of vascular surgery practice discussed the abnormal presence of
neural activity inside the auditory system or tonotopic reorganization of the auditory cortex due to chronic
[21]
deafferentation .
In relation to vascular medicine and surgery terms, this was transcribed to the etiological factors that
may contribute to vascular hypoxia/ischemia, which have been considered as possible factors in the
pathophysiology of tinnitus. However, this inconclusive hypothesis has not revealed any meaning to the
cellular significance of vascular-related tinnitus and as such is irrelevant to pinpoint carotid system disease
as a culpable factor to the occurrence of tinnitus. Brain-related peptide elements and circulation are far
from being understood to conclude as an aforementioned hypothesis for this phenomenon.

Without scientifically led and clinically driven evidence, it is difficult to see how such a hypothesis can
determine a correlation between carotid artery disease and tinnitus based on this particular evidence and
much further study and exploration is needed to accept or negate this.

OTO-NEUROSURGICAL EVIDENCE: A PROMISING & INNOVATIVE APPROACH
Recent advances in neuroimaging techniques, including positron emission tomography,
magnetoencephalography, electroencephalography and functional magnetic resonance imaging, highlight
[22]
the involvement of the central nervous system in the pathophysiological mechanism for tinnitus . These
neuroimaging investigations have shown that brain regions that are considered to be unconnected to the
auditory system, including the anterior cingulate gyrus, amygdala, hippocampus, and parahippocampal
regions are strongly indicated in the pathogenesis of subjective tinnitus. Utilizing resting-state functional
magnetic resonance imaging (fMRI) in non-auditory brain regions, such as the rectus gyrus, thalamus,
cingulate gyrus, inferior temporal gyrus, hippocampus, cerebellar hemisphere, caudate and medial superior
frontal gyrus, demonstrated an association with tinnitus-related symptoms including depression, anxiety
[23]
and loudness .

However, studies surging on this front line were limited not only due to low numbers of control cases but
[24]
also to a lack of quantification and vague anatomical correlation and orientation. Laureano et al. , utilizing
single-photon emission computerised tomography study with a sufficient number of control cases (n = 17,
sound methods of statistics and particularly precise anatomical orientation) were able to demonstrate that
the cerebral blood flow in the left parahippocampus was significantly increased in tinnitus with normal
hearing. This particular study intended to reconfirm the previous results of other resting-state fMRI studies
using a different modality and method with intended benefit to identify ideal therapeutic targets for
repetitive transcranial magnetic stimulation .
[24]

Furthermore, attempts have been made to identify a different target for tinnitus and its correlation to
carotid artery disease. Lesion size or location of carotid artery disease and the ability to combine these
factors with arterial stiffness (using methods such as the carotid-femoral pulse wave velocity) and
comparisons of local stiffness measurements (performed via Doppler ultrasonography) achieved conceptual
[12]
accuracy in describing a meaningful mechanism with accurate values for tinnitus occurrence . However,
it is important to remain critical of emerging evidence, and as such, most of those studies had a small
number of recruits and were unwarranted in determining the significant difference between the patient and
control groups.