Joseph P. Cousins

Cutaneous-evoked tinnitus. I. Phenomenology, psychophysics and functional imaging.

Complete and acute unilateral deafferentation of the auditory periphery (auditory and vestibular afferents) can induce changes in the central nervous system that may result in unique forms of tinnitus. These tinnitus perceptions can be controlled (turned on and off) or modulated (changed in pitch or loudness) by performing certain overt behaviors in other sensory/motor systems. Clinical reports from our laboratory and several other independent sources indicate that static change in eye gaze, from a neutral head-referenced position, is one such behavior that can evoke, modulate and/or suppress these phantom auditory events. This report deals with a new clinical entity and a form of tinnitus that can be evoked directly by cutaneous stimulation of the upper hand and fingertip regions. In 2 adults, cutaneous-evoked tinnitus was reported following neurosurgery for space-occupying lesions at the base of the skull and posterior craniofossa, where hearing and vestibular functions were lost completely and acutely in one ear (unilateral deafferentation) and facial nerve paralysis (unilateral deefferentation) was present either immediately following neurosurgery or had occurred as a delayed-onset event. Herein, we focus on the phenomenology of this discovery, provide perceptual correlates using contemporary psychophysical methods and document in one individual cutaneous-evoked tinnitus-related neural activity using functional magnetic resonance imaging. In a companion paper, neuroanatomical and physiological interactions between auditory and somatosensory systems, possible mechanistic accounts and relevant functional neuroimaging studies are reviewed.

Cutaneous-evoked tinnitus. II. Review of neuroanatomical, physiological and functional imaging studies

Cutaneous-evoked tinnitus is a clinical entity that has not been reported previously in the neurootological literature. Herein, a neuroscience framework that encompasses several distinct areas of research is used to conceptualize and help understand this phenomenon. We review normal neuroanatomical and physiological interactions between auditory and somatosensory systems in mammals. Also considered are mechanistic accounts of lesion-induced changes in the CNS following deafferentation/deefferentation of peripheral sensory or motor structures that may have a relationship to this phenomenon, as well as the role of functional imaging modalities in studying various phantom perceptions.

Neurobiochemical changes from Taxol/Neupogen chemotherapy for metastatic breast carcinoma corresponds with suicidal depression

A patient under Taxol and granulocyte colony stimulating factor (G-CSF, Neupogen) treatment for metastatic breast carcinoma of the liver experienced repeated suicidal depression on days 10 and 11 of therapy. MRI and MRS were performed during the fifth and sixth cycles of chemotherapy on days 1 and 10. The MRI was normal in all four examinations. The MRS showed normal levels of metabolites on days 1 of therapy, with remarkable reproducible declines in neurobiochemicals myo-inositol (23-27%), choline (20-24%), creatine (10-14%) and glutamate/glutamine (22-39%) on day 10 of therapy. The neurobiochemical declines coincided with the patients experience of suicidal depression. Patients reporting depression during standard cancer therapy may be experiencing previously undocumented chemotherapeutic neurobiochemical imbalances or neurotoxicity.

Longitudinal analysis of olfactory deficits in HIV infection

The presence and degree of odor identification deficits in 55 HIV-infected (30 asymptomatic, 25 symptomatic) and 29 HIV-negative at-risk control volunteers were examined longitudinally using the University of Pennsylvania Smell Identification Test (UPSIT). Factors other than HIV infection that could account for olfactory loss (i.e., sinusitis or upper respiratory infection) were also considered by obtaining MRI scans of the nasal passages and information from an olfaction questionnaire. No differences were found among groups at the first administration of the UPSIT, with significant differences among groups emerging at the 1-year and 2-year follow-ups. The symptomatic group showed a significant decline in odor identification scores across time, while means for the asymptomatic and control groups remained stable. The presence of sinusitis or an upper respiratory infection appeared to have no effect on odor identification. The implications for these findings in relationship to cognitive decline in neurodegenerative diseases are discussed.