Source:Annales de Dermatologie et de Vénéréologie
Author(s): V. Descamps
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Over the years there have been numerous anecdotal reports of nasal tip enlargement and loss of tip definition post rhinoplasty. Subsequent revisionary procedures not only failed to reduce the tip size but aggravated the problem causing an even larger and less defined nasal tip. The final result was often worse than the preop condition and uncorrectable.
Six patients who demonstrated an aggravation of the postop result with subsequent revisionary or secondary surgeries were evaluated to find common causes or circumstances. All patients had 1) worsening of nasal tip result with subsequent procedures, e. g., nasal tip enlargement and/or loss of tip definition with subsequent procedures 2) exhibited substantial postop edema at one or more surgeries and 3) extensive subcutaneous fibrous tissue noted at revisionary procedures.
The nasal scenario described is referred to as postrhinoplasty fibrotic syndrome. It is recommended that if revision surgery is necessary by a surgeon, the scale of the surgery should be smaller than that of the primary operation. If yet another revision is necessary that surgery should be of an even smaller scale than the prior surgery. Augmentation rather than reduction rhinoplasty is clearly a better approach. With the surgical philosophy of smaller and/or less surgery with each revision (should it be necessary) the irreversible condition of postrhinoplasty fibrotic syndrome should be avoidable.
Deafferentation caused by cochlear pathology (which can be hidden from the audiogram) activates forms of neural plasticity in auditory pathways, generating tinnitus and its associated conditions including hyperacusis. This article discusses tinnitus mechanisms and suggests how these mechanisms may relate to those involved in normal auditory information processing.
Research findings from animal models of tinnitus and from electromagnetic imaging of tinnitus patients are reviewed which pertain to the role of deafferentation and neural plasticity in tinnitus and hyperacusis.
Auditory neurons compensate for deafferentation by increasing their input/output functions (gain) at multiple levels of the auditory system. Forms of homeostatic plasticity are believed to be responsible for this neural change, which increases the spontaneous and driven activity of neurons in central auditory structures in animals expressing behavioral evidence of tinnitus. Another tinnitus correlate, increased neural synchrony among the affected neurons, is forged by spike-timing-dependent neural plasticity in auditory pathways. Slow oscillations generated by bursting thalamic neurons verified in tinnitus animals appear to modulate neural plasticity in the cortex, integrating tinnitus neural activity with information in brain regions supporting memory, emotion, and consciousness which exhibit increased metabolic activity in tinnitus patients.
The latter process may be induced by transient auditory events in normal processing but it persists in tinnitus, driven by phantom signals from the auditory pathway. Several tinnitus therapies attempt to suppress tinnitus through plasticity, but repeated sessions will likely be needed to prevent tinnitus activity from returning owing to deafferentation as its initiating condition.