PMID- 12856295

OWN - NLM
STAT- MEDLINE
DA - 20030714
DCOM- 20030807
LR - 20051116
IS - 0030-6665 (Print)
IS - 0030-6665 (Linking)
VI - 36
IP - 2
DP - 2003 Apr
TI - Pathophysiology of tinnitus.
PG - 249-66, v-vi
AB - Tinnitus is not a single entity but a rather diverse group of disorders. D
espite
symptoms that indicate the ear is the site of the pathology, there is stro
ng
evidence that most forms of severe tinnitus are caused by functional chang
es in
the central nervous system. The changes are induced through expression of
neural
plasticity, some of which may have been caused initially by abnormalities
in the
ear or the auditory nerve. The involvement of the nonclassical ascending a
uditory
pathway with its subcortical connections to limbic structures (the amygdal
a) may
explain some of the symptoms of some forms of tinnitus including hyperacus
is and
affective disorders, such as phonophobia and depression, which often accom
pany
severe tinnitus.
FAU - Moller, Aage R
AU - Moller AR
AD - Callier Center for Communication Disorders, University of Texas at Dallas,
School
of Human Development, 1966 Inwood Road, Dallas, TX 75235, USA.
amoller@utdallas.edu
LA - eng
PT - Journal Article
PT - Review
PL - United States
TA - Otolaryngol Clin North Am
JT - Otolaryngologic clinics of North America
JID - 0144042
SB - IM
MH - Auditory Pathways/physiopathology
MH - Central Nervous System/physiopathology
MH - Humans
MH - Neuronal Plasticity
MH - Tinnitus/etiology/*physiopathology
RF - 104
EDAT- 2003/07/15 05:00
MHDA- 2003/08/09 05:00
CRDT- 2003/07/15 05:00
PST - ppublish
SO - Otolaryngol Clin North Am. 2003 Apr;36(2):249-66, v-vi.