Dissociable systems of working memory for rhythm and melody.

Specialized neural systems are engaged by the rhythmic and melodic components of music. Here, we used PET to measure regional cerebral blood flow (rCBF) in a working memory task for sequences of rhythms and melodies, which were presented in separate blocks. Healthy subjects, without musical training, judged whether a target rhythm or melody was identical to a series of subsequently presented rhythms or melodies. When contrasted with passive listening to rhythms, working memory for rhythm activated the cerebellar hemispheres and vermis, right anterior insular cortex, and left anterior cingulate gyrus. These areas were not activated in a contrast between passive listening to rhythms and a non-auditory control, indicating their role in the temporal processing that was specific to working memory for rhythm. The contrast between working memory for melody and passive listening to melodies activated mainly a right-hemisphere network of frontal, parietal, and temporal cortices: areas involved in pitch processing and auditory working memory. Overall, these results demonstrate that rhythm and melody have unique neural signatures not only in the early stages of auditory processing, but also at the higher cognitive level of working memory.

Autobiographical memories of anger in violent and non-violent individuals: a script-driven imagery study.

Numerous studies have implicated frontal lobe dysfunction in anger-related impulsive violent behavior; however, few studies have looked at frontal activity during angry states in violent individuals. Using PET and a script-driven imagery paradigm, we report on autobiographical memories of angry vs. neutral memories in violent patients and psychiatric matched controls. Relative to recall of neutral memories, recall of anger-laden memories was associated with an activation of frontal regions among control subjects but not violent subjects. Violent subjects demonstrated relatively greater activations in the left amygdala, pontine, and cerebellar regions compared to control subjects.

Chronic vagus nerve stimulation for treatment-resistant depression decreases resting ventromedial prefrontal glucose metabolism.

Vagus nerve stimulation (VNS) is used as an adjunctive therapy for treatment-resistant depression (TRD). Its mechanism of action is not fully understood. Longitudinal measurement of changes in brain metabolism associated with VNS can provide insights into this new treatment modality. Eight severely depressed outpatients who were highly treatment-resistant underwent electrical stimulation of the left vagus nerve for approximately one year. The main outcome measures were resting regional brain glucose uptake measured with positron emission tomography (PET) and the 24-item Hamilton Depression Scale. The most significant and extensive change over one year of chronic VNS localized to the ventromedial prefrontal cortex extending from the subgenual cingulate to the frontal pole. This region continued to decline in metabolism even toward the end of the study. Clinically, this cohort showed a trend for improvement. No correlations surfaced between change in glucose uptake and depression scores. However, the sample size was small; none remitted; and the range of depression scores was limited. Chronic VNS as adjunctive therapy in patients with severe TRD produces protracted and robust declines in resting brain activity within the ventromedial prefrontal cortex, a network with dense connectivity to the amygdala and structures monitoring the internal milieu.

The neural correlates of aversive auditory stimulation.

Previous neuroimaging studies indicate that the human amygdala activates during exposure to aversive visual, olfactory and gustatory stimuli. To examine amygdala responses to aversive auditory stimuli, we exposed healthy human subjects to unpleasant sounds while regional cerebral blood flow (rCBF) was assayed with O-15 PET. Eight subjects, all of whom described themselves as reactive to aversive sounds, participated in the study. Relative to white noise, the aversive sounds produced significant rCBF increases in the lateral amygdala/claustrum region. Significant activations also localized to the dorsal brainstem, medial temporal pole, basal forebrain (nucleus accumbens), insula, right auditory association cortices, putamen, thalamus and cerebellum. These data indicate that the amygdala responds to aversive auditory stimuli in a manner similar to its response to unpleasant stimuli in other sensory modalities. The data further highlight a widely distributed network of cortical and subcortical areas activated during exposure to aversive sounds.