A variety of cognitive dysfunctions occur after subcortical damage. Aphasia and unilateral spatial neglect often result from lesions of the putamen and thalamus. They are particularly frequent during the acute stage of cerebral hemorrhage, with approximately 80 % of patients presenting such symptoms. To understand the mechanism by which they appear, we must not only consider causes related to damage to the subcortical white matter fibers, but also secondary functional decline caused by direct damage to the cortex as well as by diaschisis. Infratentorial lesions are known to cause language deficits, visuospatial inattention, executive function disorders, personal change, and other symptoms. Many of these reports pertain to cerebellar lesions; however, there are not a few cases where cognitive dysfunction develops because of brainstem lesions. Impairment of the cortical pontocerebellar tract’s fiber connections and damage to the brainstem reticular regulatory system may be considered as the mechanism by which cognitive dysfunction appears. Because of this, detailed cognitive function assessments must also be performed for patients with infratentorial lesions.
Continuous wave functional near-infrared spectroscopy (CW-fNIRS) has potential advantages in the detection of cerebral functional activation, such as safety, portability, resistance to electromagnetic noise, time resolution higher than that of functional magnetic resonance imaging (fMRI), spatial resolution higher than that of electroencephalography (EEG), and the lack of need for subject restraint. However, for practical application of the fNIRS technique, a careful study design is required for experiments, practical measurements, and data analysis. Each step should be based on accurate knowledge of both the advantages and drawbacks of the fNIRS technique. This review will describe various signal components in the fNIRS measurement and their appropriate management through critical discussions on the measurement principle and the physiological origin of the signal.
Dyspnea is defined as “a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity”. In patients especially with pulmonary diseases, dyspnea reduces daily activity, which worsens the physical condition, and thereby further increases dyspnea, forming a vicious cycle. In clinical practice, reduction of dyspnea in patients with diseases is crucial. One of the goals in pulmonary rehabilitation is reduction of dyspnea to break the above-mentioned vicious cycle. However, the mechanism of dyspnea perception has not been fully elucidated because it is complex and is not explained by a single factor such as changes in blood gas. Not all patients with chronic respiratory failure with hypercapnia are dyspneic, or not all patients with COPD with severe hypoxemia perceive dyspnea. To date, sufficiently effective methods to relieve dyspnea have not been established. We integrated the theories which explain the mechanisms of dyspnea perception with our considerations from the viewpoint of respiratory neurophysiology, and propose a model of dyspnea perception mechanism. In our model, dyspnea results from disassociation or mismatch between the neural respiratory motor output from the respiratory neural network in the lower brainstem and the actually accomplished ventilation. The projection modality of neural information on dyspnea to the higher sensory center of the brain, and the brain regions for comparison of the intended respiratory neural output from the brainstem respiratory center and the monitored actual ventilatory output remain unknown. Further clarification of these issues will enlighten understanding of the pathophysiology of dyspnea and contribute to more effective practice of pulmonary rehabilitation.
The Trail Making Test (TMT) is widely used as a measure of attention impairment. The time needed to complete TMT (TMT score) is prolonged in association with attention impairment in patients with brain diseases. Thus far, however, there have been no reports of serial changes in the TMT score after minor ischemic stroke. We retrospectively investigated serial changes in the TMT score of 19 patients with minor ischemic stroke. We included patients in whom TMT could be performed both 4-11 days after onset (initial evaluation) and 14-47 days after onset (second evaluation). The mean value of the initial TMT-A scores was 58 seconds, and that of the initial TMT-B scores was 144 seconds. The mean value of the second TMT-A scores was 43 seconds, and that of the second TMT-B scores was 119 seconds. The TMT-A and TMT-B scores improved in 89 % and 74 % of patients, respectively. This study demonstrated that most minor ischemic stroke patients showed improvement in the TMT score 14 days or later after onset.