Concurrent radionecrosis within the spinal cord and the bone marrow at the same thoracic level was observed 8 years after localized therapeutic irradiation in a patient who had undergone repeated cycles of radiotherapy, glucocorticoid treatment, and chemotherapy for a non-Hodgkin's lymphoma. Mechanisms combining radiotoxic potentialization by glucocorticoids/alkylating agents and delayed radiation-induced vasculitis involving the common arterial pathways to the spinal cord and to the vertebrae were speculated to have acted in a synergistic way.
trying t o decorticalize auditory hallucinations," we began with the test of the null hypothesis that there would be no blood flowneural activity differences between loud and soft tinnitus states.' Detection of significant differences confined to the cortex opposite the ear in which tinnitus occurred led to rejection of the null hypothesis. Neural activation tests using real, unilaterally presented sounds were also performed in our patients and controls. We again rejected the null hypothesis when the analysis revealed bilateral cortical responses. When we sought to explain these data, we saw no clear alternative to our statement that "Our data suggest that the tinnitus experienced by our patients (emphasis added) arises in the central auditory system and not the cochlea." As we indicated in our paper, more studies are needed before generalization of our conclusions to all tinnitus patients is warranted. Although our patients had the ability to exert transient control over the loudness of their tinnitus, in every other way they were typical of most patients with the disorder. Thus, we believe that a central origin is probable for tinnitus patients with sensorineural hearing loss who are likely to have plastic changes in their auditory system due to partial deafferentation. There are many patients with tinnitus that is clearly of central origin. There can be no other explanation for tinnitus in patients with complete ablation of the cochlea, transection of the auditory nerve: or ictal tinnitus.7In the review of the theoretical basis for tinnitus cited by Dr. Gordon, Wilson concludes, "Although abnormalities in the electrical condition of the cochlea would seem t o be a likely cause for tinnitus, there is so far little evidence for this . . ."l The cochlea is clearly capable of producing real sounds, such as otoacoustic emissions (excluded in our patients) and distortion products (present only during cochlear stimulation). Contraction of various muscles in and around the ear may be audible: these are typically low frequency sounds and not in the 3-4 kHz range found in our subjects. Muscle contraction may alter existing ear-produced sounds. These sounds did not exist in our subjects. For each of these situations, we would expect a cochlear or bilateral pattern of neural activation similar to that found during 2-kHz stimulation of one ear. Because similar patterns of temporal lobe activation are produced by much less intense stimuli (e.g., 30 dB HL at 0.5 and 4 kHz, presented at the annual meeting of the American Academy of Neurology, April 28, 1998) and because of the construction of the insert earphones, we are confident that our stimuli are restricted to just one cochlea. We would welcome any data (as opposed to conjecture) that would clearly demonstrate a cochlear origin for tinnitus in the absence of sounds detectable by microphones positioned in the external auditory meatus.We discourage the use of the term "hallucinations" to refer to the sounds perceived by tinnitus patients. Although this term may be strictly...
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