Progress in brain research
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Tinnitus has many similarities with the symptoms of neurological disorders such as paresthesia and central neuropathic pain. There is considerable evidence that the symptoms and signs of some forms of tinnitus and central neuropathic pain are caused by functional changes in specific parts of the central nervous system and that these changes are caused by expression of neural plasticity. ⋯ In this chapter we will discuss specific similarities between tinnitus and pain, and compare tinnitus with other phantom disorders. Since much more is known about pain than about tinnitus, it is valuable to take advantage of the knowledge about pain in efforts to understand the pathophysiology of tinnitus and find treatments for tinnitus.
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Acute spinal cord injury (SCI) is a devastating neurological disorder that can affect any individual at a given instance. Current treatment options for SCI include the use of high dose methylprednisolone sodium succinate, a corticosteroid, surgical interventions to stabilize and decompress the spinal cord, intensive multisystem medical management, and rehabilitative care. ⋯ These include the Surgical Treatment for Acute Spinal Cord Injury Study (STASCIS) Trial to evaluate the role and timing of surgical decompression for acute SCI, neuroprotection with the semisynthetic second generation tetracycline derivative, minocycline; aiding axonal conduction with the potassium channel blockers, neuroregenerative/neuroprotective approaches with the Rho antagonist, Cethrin; the use of anti-NOGO monoclonal antibodies to augment plasticity and regeneration; as well as cell-mediated repair with stem cells, bone marrow stromal cells, and olfactory ensheathing cells. This review overviews the pathobiology of SCI and current treatment choices before focusing the rest of the discussion on the variety of promising neuroprotective and cell-based approaches that have recently moved, or are very close, to clinical testing.
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Traumatic brain injury (TBI) and traumatic spinal cord injury (SCI) are acquired when an external physical insult causes damage to the central nervous system (CNS). Functional disabilities resulting from CNS trauma are dependent upon the mode, severity, and anatomical location of the mechanical impact as well as the mechanical properties of the tissue. Although the biomechanical insult is the initiating factor in the pathophysiology of CNS trauma, the anatomical loading distribution and the resulting cellular responses are currently not well understood. ⋯ Correlation of insult parameters with cellular changes and subsequent deficits may lead to refined tolerance criteria and facilitate the development of improved protective gear. In addition, advancements in the understanding of injury biomechanics are essential for the development and interpretation of experimental studies at both the in vitro and in vivo levels and may lead to the development of new treatment approaches by determining injury mechanisms across the temporal spectrum of the injury response. Here we discuss basic concepts relevant to the biomechanics of CNS trauma, injury models used to experimentally simulate TBI and SCI, and novel multilevel approaches for improving the current understanding of primary damage mechanisms.
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This chapter is focused on drug-induced hyperthermia with special regard to use of antipsychotics and antidepressants for the treatment of schizophrenia and major depression, respectively. Neuroleptic malignant syndrome (NMS) develops during the use of neuroleptics, whereas serotonin syndrome is caused mainly by serotoninergic antidepressants. Although both syndromes show various symptoms, hyperthermia is the main clinical manifestation. In this review we describe the historical background, clinical manifestations, diagnosis, and differential diagnosis of these two syndromes based on our observations on the experimental and clinical data.
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Case Reports Clinical Trial
Electrical stimulation of auditory and somatosensory cortices for treatment of tinnitus and pain.
The efficacy of electrical stimulation of the auditory cortex using extradural implanted electrodes for treatment of tinnitus was studied in 12 patients suffering tinnitus. The effect of similar stimulation of the somatosensory cortex for treatment of neuropathic pain was studied in five patients. ⋯ It is concluded that electrical stimulation of sensory cortices can be effective treatments of severe unilateral tinnitus and unilateral neuropathic pain in selected patients. The results suggest that similar pathophysiological mechanisms underlie some forms of these phantom sensations, and therefore, similar treatment such as electrical stimulation of the respective sensory cortices can suppress tinnitus and pain.