Brain : a journal of neurology
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Brain atrophy as determined by quantitative MRI can be used to characterize disease progression in multiple sclerosis. Many studies have addressed white matter (WM) alterations leading to atrophy, while changes of the cerebral cortex have been studied to a lesser extent. In vivo, the cerebral cortex has been difficult to study due to its complex structure and regional variability. ⋯ Patients with longstanding disease or severe disability, however, presented additionally with focal thinning of the motor cortex area [2.35 mm (SD 0.19) versus 2.74 mm (SD 0.15)]. We conclude that in vivo measurement of cortical thickness is feasible in patients suffering from multiple sclerosis. The data provide new insight into the cortical pathology in multiple sclerosis patients, revealing focal cortical thinning beside an overall reduction of the cortical thickness with disease progression.
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Sensory abnormalities have been reported in Parkinson's disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of approximately 20 ms, and long latency afferent inhibition (LAI) at an ISI of approximately 200 ms. ⋯ This pathway is unaffected by Parkinson's disease but is altered by dopaminergic medication in Parkinson's disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non-dopaminergic manifestation of Parkinson's disease.
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The somatic marker hypothesis posits that deficits in emotional signalling (somatic states) lead to poor judgment in decision-making, especially in the personal and social realms. Similar to this hypothesis is the concept of emotional intelligence, which has been defined as an array of emotional and social abilities, competencies and skills that enable individuals to cope with daily demands and be more effective in their personal and social life. Patients with lesions to the ventromedial (VM) prefrontal cortex have defective somatic markers and tend to exercise poor judgment in decision-making, which is especially manifested in the disadvantageous choices they typically make in their personal lives and in the ways in which they relate with others. ⋯ Only patients with lesions in the somatic marker circuitry revealed significantly low emotional intelligence and poor judgment in decision-making as well as disturbances in social functioning, in spite of normal levels of cognitive intelligence (IQ) and the absence of psychopathology based on DSM-IV criteria. The findings provide preliminary evidence suggesting that emotional and social intelligence is different from cognitive intelligence. We suggest, moreover, that the neural systems supporting somatic state activation and personal judgment in decision-making may overlap with critical components of a neural circuitry subserving emotional and social intelligence, independent of the neural system supporting cognitive intelligence.
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To elucidate cortical correlates of vestibulo-ocular reflex (VOR) modulation, we observed cortical activation during fixation suppression and habituation of caloric vestibular nystagmus in 12 normal subjects, using PET. Significant positive correlation between regional cerebral blood flow (rCBF) and slow phase eye velocity of caloric nystagmus was observed in the middle and posterior insula, inferior parietal lobule, temporal pole, right fusiform gyrus, lingual gyrus, and cerebellar vermis and hemisphere. The rCBF increase in the insular region and the inferior parietal lobule was lateralized depending on the direction of the nystagmus. ⋯ Deactivation of vestibular cortices during visual fixation supports the concept of inhibitory visual-vestibular interaction in the cortex. Significant activation of the cingulate, superior parietal and visual cortices, and cerebellar vermis accompanying reduction of caloric response with repeated stimuli suggests possible involvement of these regions in vestibular habituation. Common activation of the cuneus in visual cortex and deactivation of vestibular and visuo-spatial association cortices by both visual suppression and habituation of VOR suggests that these two mechanisms are not completely independent but may share some cortical and subcortical regions.
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Tissue plasminogen activator (tPA), a neuronal as well as the key fibrinolytic enzyme, is found concentrated on demyelinated axons in multiple sclerosis lesions together with fibrin(ogen) deposits. The decreased tPA activity in normal-appearing white and grey matter and lesions of multiple sclerosis is reflected in diminished fibrinolysis as measured by a clot lysis assay. Nonetheless, peptide products of fibrin, including D-dimer, accumulate on demyelinated axons-the result of fibrinogen entry through a compromised blood-brain barrier (BBB). ⋯ As total tPA protein remains unchanged in acute lesions and the concentration of PAI-1 rises several fold, complex formation is a probable cause of the impaired fibrinolysis. Although the tPA-plasmin cascade promotes neurodegeneration in excitotoxin-induced neuronal death, in inflammatory conditions with BBB disruption it has been demonstrated to have a protective role in removing fibrin, which exacerbates axonal injury. The impaired fibrinolytic capacity resulting from increased PAI-1 synthesis and complex formation with tPA, which is detectable prior to lesion formation, therefore has the potential to contribute to axonal damage in multiple sclerosis.