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Behavioral state is known to influence interactions between thalamus and cortex, which are important for sensation, action, and cognition.
Recent works suggest that an abnormal rhythmic activity between thalamus and cortex, namely thalamocortical dysrhythmia, may be the pathophysiological mechanism subtending abnormal information processing in migraine.
An abnormal rhythmic activity between thalamus and cortex, namely thalamocortical dysrhythmia, may be the pathophysiological mechanism subtending abnormal information processing in migraine.
The lack of habituation may be explained by a possible "thalamo-cortical dysrhythmia", an altered rhythmic stream between thalamus and cortex, or by an abnormal glutamatergic neurotransmission [40, 41].
3) Analysis of the high frequency somatosensory evoked potentials showed early response sensitization and late habituation, most probably due an increased coupling between thalamus and cortex in chronic migraine [55].
The thalamocortical network for generation of gamma oscillations is well documented and consists in principle of two recurrent loops between thalamus and cortex [28], [33], [34].
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In this book, two pioneers in research on the thalamus examine the close two-way relationships between thalamus and cerebral cortex and look at the distinctive functions of the links between the thalamus and the rest of the brain.
In grapheme color synesthetes, low white matter densities in pulvinar, medial and lateral ventral posterior nuclei, and low fractional anisotropy in medial dorsal and ventral anterior nuclei suggest a constitutional disconnection and hypoconnection between thalamus and cerebral cortex [ 64▪▪].
Loss of fezf2 results in various forebrain defects, including loss of monoaminergic neurons (Jeong et al., 2006; Levkowitz et al., 2003), disruption of diencephalon subdivisions (Levkowitz et al., 2003), and defects in reciprocal projections between thalamus and cerebral cortex (Komuta et al., 2007).
The HFO analysis suggests that this sensory sensitization may be explained by an increase in the strength of the connections between the thalamus and cortex compared to episodic migraine between attacks.
Moreover, from the analysis of high-frequency oscillations, it clearly emerges that this sensory sensitization may be explained by the fact that in both groups, the connections between the thalamus and cortex intensify compared to episodic migraine between attacks.
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