CONTROL 601and his ability to perform in biofeedback. The more psychopathic the person is the more likely the tin nitus will fail to improve with biofeedback. The "healthy neurotics" do well with biofeedback. They are able to reduce their tinnitus and become more aware of some of the dynamics involved with it.A small group of our patients have benefitted from the use of the tinnitus masker and are grateful for the relief the masker provides. Certainly it is not a panacea, but it does offer some relief and should be offered as a possible treatment to these patients.The best results of treatment of tinnitus occur af ter complete evaluation, examination, and thorough explanation to the patient. 2. Fowler EP. Head noises in normal and disordered ears. Arch Otolaryngol 1944; 39:498-503. 3. House JW, Miller L, House PR. Severe tinnitus: treatment with biofeedback training (results in 41 cases). Trans Am Acad Ophthalmol Otolaryngol 1976; 84:697-703. 4. House PR. Personality of the tinnitus patient. GIBS Sym posium 1981; 85 (in press). 5. Dandy WE. Surgical treatment of Meniere's disease. Surg Gynecol Obstet 1941; 72:421-5. 6. Ward PH, Babin R, Calcaterra TC, Konrad HR. Opera tive treatment of surgical lesions with objective tinnitus. Ann Otol Rhinol Laryngol 1975; 84:473-81. 7. Classgold A, Altmann F. The effects of stapes surgery on tinnitus. Laryngoscope 1966; 76:1524-31. 8. House WF, Luetje CM, eds. A history of acoustic tumor surgery: 1800-1900, early history. Vol. 1. Baltimore: University Park Press, 1979. 9. House JW. Treatment of severe tinnitus with biofeedback training. Laryngoscope 1978; 78:406-12. 10. House JW, Johnson EW. Tinnitus: tinnitus masker and bi ofeedback training. Trans Pac Coast Otoophthalmol Soc Annu Meet 1979; 60:115-20. 11. Vernon J. Attempts to relieve tinnitus. J Am Audiol Soc 1977; 2:124-31. 12. Vernon J, Schleoning A. Tinnitus: a new management. Laryngoscope 1978; 88:413-9. 13. Saltzman M, Ersner MJ. A hearing aid for the relief of tin nitus aurium. Laryngoscope 1947; 51:358-66.Medical treatment is presented as the best hope of the various treatment methods available for the management of tinnitus. A test dose of 100 mg lidocaine given rapidly intravenously will give good or partial temporary relief to approximately 80% of patients with tinnitus. More permanent relief can then be achieved by the oral anticonvulsants carbamazepine or primidone but the side effects of these drugs are occasionally too severe to justify their use. Three preliminary clinical studies of the oral amide of lidocaine, tocainide hydrochloride, were conducted and results with 600 mg four times daily are very promising. Further long-term clinical trials with tocainide will be started soon. It would appear that local anesthetics when given intravenously block the multisynaptic slow pathways in tinnitus as well as in chronic pain, with which there are many other similarities. The delay in wave V in the BSER and the sudden sleep induced in patients with a good response to intravenous lidocaine further confirm the site of ...
The level of an endogenous opioid (peak B endorphin) was measured in chromatographically fractionated cerebrospinal fluid (CSF) sampled from two groups of chronic pain patients before and after intrathecal saline (placebo) injection. As assessed by a verbal rating scale, one group reported no change in their level of pain (non-responders, NR; n = 6) while the other group reported complete or greater than 50% pain relief (placebo responders, PR; n = 14). We find, as has been reported previously, that initial peak B levels were lower (by 50%) in these chronic pain patients' CSF than in CSF from pain-free (PF) normal controls (P less than 0.001, t-test). Peak B levels measured from CSF of the NR group undergoing this procedure did not change (P greater than 0.4, paired t-test). In contrast, a significant 2.3-fold increase was measured in the CSF peak B level of the PR group (P less than 0.05, paired t-test). This is the first direct evidence that a CSF opioid is correlated with placebo pain relief in chronic pain patients. Peak B is a potent analgesic substance when administered by the intracerebroventricular route in mice and its level is related to the patients' pain status in a presumably causal manner.
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