Progress in brain research
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Before energy metabolism can take place, brain cells must be supplied with oxygen and glucose. Only then, in combination with normal mitochondrial function, sufficient energy (adenosine tri-phosphate (ATP)) can be produced. Glucose is virtually the sole fuel for the human brain. ⋯ This review focuses on three main issues: (1) Cerebral oxygen transport (CBF, and oxygen partial pressure (PO2) and delivery to the brain); (2) Energy metabolism (glycolysis, mitochondrial function: citric acid cycle and oxidative phosphorylation); and (3) The role of the above in the pathophysiology of severe head injury. Basic understanding of these issues in the normal as well as in the traumatized brain is essential in developing new treatment strategies. These issues also play a key role in interpreting data collected from monitoring techniques such as cerebral tissue PO2, jugular bulb oxygen saturation (SjvO2), near infra red spectroscopy (NIRS), microdialysis, intracranial pressure monitoring (ICP), laser Doppler flowmetry, and transcranial Doppler flowmetry--both in the experimental and in the clinical setting.
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Minor traumatic brain injury (mTBI) is caused by inertial effects, which induce sudden rotation and acceleration forces to and within the brain. At less severe levels of injury, for example in mTBI, there is probably only transient disturbance of ionic homeostasis with short-term, temporary disturbance of brain function. With increased levels of severity, however, studies in animal models of TBI and in humans have demonstrated focal intra-axonal alterations within the subaxolemmal, neurofilament and microtubular cytoskeletal network together with impairment of axoplasmic transport. ⋯ In ice hockey, current return-to-play guidelines do not take into account these new findings appropriately, for example allow returning to play in the same game. It has recently been hypothesized that the processes summarized above may predispose brain cells to assume a vulnerable state for an unknown period after mild injury (mTBI). Therefore, we recommend that any confused player with or without amnesia should be taken off the ice and not be permitted to play again for at least 72h.
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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.
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In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a decrease in the latency of mu rhythm event-related desynchronisation (ERD) compared with control subjects, suggesting hypo activation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in amplitude of beta rhythm ERS was observed over the same region and thought to be related to impairment in cortical deactivation. By monitoring ERD/ERS, we aimed (i) to extend to advanced PD the observations made in less-advanced parkinsonism and (ii) to test the effect of acute L-Dopa, internal pallidal or subthalamic stimulation on these abnormalities. ⋯ Mu rhythm ERD latency and the beta ERS amplitude further decreased in advanced PD compared with early stages, suggesting greater impairment of cortical activation/deactivation as the disease progresses and a partial restoration in relation to clinical improvement under treatments. Consequently, it appears that L-Dopa and deep brain stimulation partially restored the normal patterns of cortical oscillatory activity in PD, possibly by decreasing the low frequency hyper synchronisation at rest. This mechanism could be involved at the basal ganglia level in the sensorimotor integration implicated in the movement control.