Positron emission tomography (PET) can be used to map brain regions that are active when a visual object (for example, a hand) is discriminated from its mirror form. Chronometric studies suggest that viewers 'solve' this visual shape task by mentally modelling it as a reaching task, implicitly moving their left hand into the orientation of any left-hand stimulus (and conversely for a right-hand stimulus). Here we describe an experiment in which visual and somatic processing are dissociated by presenting right hands to the left visual field and vice versa. Frontal (motor), parietal (somatosensory) and cerebellar (sensorimotor) regions similar to those activated by actual and imagined movement are strongly activated, whereas primary somatosensory and motor cortices are not. We conclude that mental imagery is realized at intermediate-to-high order, modality-specific cortical systems, but does not require primary cortex and is not constrained to the perceptual systems of the presented stimuli.

The cause of stuttering is unknown. Failure to develop left-hemispheric dominance for speech is a long-standing theory although others implicated the motor system more broadly, often postulating hyperactivity of the right (language nondominant) cerebral hemisphere. As knowledge of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postulating hyperactivity of premotor cortex, either directly or through connectivity with the thalamus and basal ganglia. Alternative theories target the auditory and speech production systems. By contrasting stuttering with fluent speech using positron emission tomography combined with chorus reading to induce fluency, we found support for each of these hypotheses. Stuttering induced widespread overactivations of the motor system in both cerebrum and cerebellum, with right cerebral dominance. Stuttered reading lacked left-lateralized activations of the auditory system, which are thought to support the self-monitoring of speech, and selectively deactivated a frontal-temporal system implicated in speech production. Induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed the auditory-system underactivations and the deactivation of the speech production system. Thus stuttering is a disorder affecting the multiple neural systems used for speaking.

Non-invasive imaging of human inter-regional neural connectivity by positron emission tomography (PET) during transcranial magnetic stimulation (TMS) was performed. The hand area of primary motor cortex (M1) in the left cerebral hemisphere was stimulated with TMS while local and remote effects were recorded with PET. At the stimulated site, TMS increased blood flow (12-20%) in a highly focal manner, without an inhibitory surround. Remote covariances, an index of connectivity with M1, were also focal. Connectivity patterns established in non-human species were generally confirmed. Excitatory connectivity (positive covariance) was observed in ipsilateral primary and secondary somatosensory areas (S1 and S2), in ipsilateral ventral, lateral premotor cortex (M2) and in contralateral supplementary motor area (SMA). Inhibitory connectivity (negative covariance) was observed in contralateral M1.

The relationship between pretreatment regional cerebral glucose metabolism and eventual antidepressant drug response was measured using positron emission tomography (PET) in hospitalized patients with unipolar depression. Rostral anterior cingulate metabolism uniquely differentiated eventual treatment responders from non-responders. Hypometabolism characterized non-responders when compared with controls, in contrast to responders who were hypermetabolic. Metabolism in no other region discriminated the two groups, nor did associated demographic, clinical or behavioral measures, including motor speed, cognitive performance, depression severity or illness chronicity. Cingulate hypermetabolism may represent an important adaptive response to depression and failure of this response may underlie poor outcome. A critical role for rostral cingulate area 24a/b in the limbic-cortical network involved in abnormal mood states is proposed.

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Cerebral blood flow PET scans and high-density event-related potentials (ERPs) were recorded (separate sessions) while subjects viewed rapidly-presented, lower-visual-field, bilateral stimuli. Active attention to a designated side of the stimuli (relative to passive-viewing conditions) resulted in an enhanced ERP positivity (P1 effect) from 80-150 msec over occipital scalp areas contralateral to the direction of attention. In PET scans, active attention vs. passive showed strong activation in the contralateral dorsal occipital cortex, thus following the retinotopic organization of the early extrastriate visual sensory areas, with some weaker activation in the contralateral fusiform. Dipole modeling seeded by the dorsal occipital PET foci yielded an excellent fit for the P1 attention effect. In contrast, dipoles constrained to the fusiform foci fit the P1 effect poorly, and, when the location constraints were released, moved upward to the dorsal occipital locations during iterative dipole fitting. These results argue that the early ERP P1 attention effects for lower-visual-field stimuli arise mainly from these dorsal occipital areas and thus also follow the retinotopic organization of the visual sensory input pathways. These combined PET/ERP data therefore provide strong evidence that sustained visual spatial attention results in a preset, top-down biasing of the early sensory input channels in a retinotopically organized way.

Whole body hyperthermia may produce vasodialation, nausea, and altered cognitive function. Animal research has identified brain regions that have important roles in thermoregulation. However, differences in both the cognitive and sweating abilities of humans and animals implicate the need for human research. Positron emission tomography (PET) was used to identify brain regions with altered activity during systemic hyperthermia. Human subjects were studied under cool (control) conditions and during steady-state hyperthermia induced by means of a liquid-conditioned suit perfused with hot water. PET images were obtained by injecting [(18)F]fluorodeoxyglucose, waiting 20 min for brain uptake, and then scanning for 10 min. Heating was associated with a 23% increase in resting metabolic rate. Significant increases in cerebral metabolic rate occurred in the hypothalamus, thalamus, corpus callosum, cingulate gyrus, and cerebellum. In contrast, significant decreases occurred in the caudate, putamen, insula, and posterior cingulum. These results are important for understanding the mechanisms responsible for altered cognitive and systemic responses during hyperthermia. Novel regions (e.g., lateral cerebellum) with possible thermoregulatory roles were identified.

In this work, a compartmental model to predict the concentration of hyperpolarized xenon (Xe) in the brain is developed based on the well established kinetics of Xe and estimated T1 values for the compartments. For the gaseous compartments, T1 was set to 12 seconds. For the tissue compartments, T1 was set to 6 seconds. Three gas delivery techniques were modeled: hyperventilation followed by breath-hold, continual breathing, and hyperventilation followed by continual breathing. Based on Xe CT, it is estimated that the maximum concentration of Xe that could be breathed is 80%. Based on this value and the estimated maximum polarization of 50%, the peak gray matter concentration of hyperpolarized Xe is calculated to be .036 mM. This leads to an estimated signal-to-noise ratio (SNR), at 2 T, for hyperpolarized Xe that is a factor of 50 lower than the SNR for proton MRI. The peak concentration of hyperpolarized Xe was also calculated over a wide range of gas and tissue T1 values. This model also predicts that the arterial blood will have a concentration of hyperpolarized Xe that is 10 times greater than the concentration in gray matter. An interactive version of the model can be found on the World Wide Web at http:(/)/ric.uthscsa.edu/staff /charlesmartinphd.html.