Silica glass plates (Corning 7940 excimer grade) were implanted sequentially with N+ at 52 keV to different doses, ranging from 0 to 1.2 × 1017 ions cm−2, and then with Fe+ at 160 keV to 6 × 1016 ions cm−2 at room temperature and 4 µA cm−2. The intensity of ferromagnetic magnetic resonance (FMR) absorption and the magnetization calculated by the angular dependence of the FMR field reach maxima at an N/Fe atomic ratio ∼0.2. Two peaks due to Fe 2p3/2 electron are observed at 707.2 ± 0.2 and 710.9 ± 0.2 eV in the x-ray photoelectron spectra. The intensity of the former relative to the latter decreases with increasing the N dose. The conversion electron Mössbauer spectrum reveals the formation of superparamagnetic iron nitride as well as the existence of Fe2+ and Fe3+ in silica when implanting N+ to 7.5 × 1015 ions cm−2 and then Fe+ to 6 × 1016 ions cm−2 at N/Fe = 0.125. These results suggest that sequential ion-implantation of N+ and Fe+ produces iron nitride in silica glasses.

Magnetic susceptibilities of samples of Libyan desert glass have been measured by the Faraday technique. The samples were cut from specimens in which neither striae, nor spherulites, nor bubbles could be observed with the unaided eye. They were transparent with a pale yellow-green colour. The temperature dependent susceptibility can be explained as primarily due to a 'Brillouin' system of 'non-interacting' paramagnetic centres in a diamagnetic matrix. Assuming that Fe3+ ions are the source of the para- and ferromagnetic susceptibilities, an analysis of the data shows that a fraction, about 0.4, of the Fe ions are single ions isolated in the matrix and the remainder are in pairs, with the exception of aggregates. The concentration of Fe atoms, determined by the susceptibility data, indicates that in the samples a fraction of the iron ions are anti-ferromagnetic coupled. Less than 2% of the Fe ions are in aggregates that are ferromagnetic at room temperature. Based on our analysis of the data we suggest that, in the samples, the distribution of iron ions is approximately random, with the ions with the smallest separations having ferromagnetic or anti-ferromagnetic interaction at temperatures <300 K. (C) 2003 Elsevier B.V. All rights reserved.

We describe a 68‐year‐old woman who presented with falls, mild limb bradykinesia, axial rigidity, and a severe supranuclear gaze palsy, which failed to benefit from levodopa. She subsequently developed severe apraxia, progressive dysarthria, dysphagia, and a frontal cognitive impairment. Pyramidal weakness with fasciculations and widespread chronic partial denervation appeared shortly before her death from bronchopneumonia, 6 months after disease onset. A severe cerebral amyloid angiopathy diffusely involving the cerebral hemispheres and cerebellum was present at autopsy as well as a second pathological condition indicative of motor neurone disease. Cerebral amyloid angiopathy may rarely present with a progressive supranuclear palsy–like phenotype.

We sought to determine how the pattern of cerebral activation, and in particular in frontal motor areas, during the performance of conditional motor tasks is dependent upon the modality of instruction (visual, auditory, or somatosensory). Regional cerebral blood flow (rCBF) changes with externally instructed movements were also compared with internally generated, self-paced, movements. We used positron emission tomography (PET) with the tracer H2(15O) to measure rCBF in 22 healthy volunteers. External stimuli consisted of the randomized presentation of single or double impulses using a single modality for each condition. In the movement scans, the subjects used the index and middle fingers of their right hands to press a left button for a single and a right button for a double impulse, respectively. In the control scans, subjects were required to covertly distinguish a single from a double stimulus without a motor response. Data were analyzed using conventional subtraction techniques with a statistical threshold of Z > 2.33 with corrections for multiple comparisons. When the activation differences between the three externally instructed movement conditions were statistically compared, nonsignificant trends toward increased rCBF in the sensory cortex of the modality of the cue were observed but no differential activity in cortical motor areas. Internally generated movements, when compared to externally triggered movements, were associated with enhanced activation in bilateral medial and lateral premotor, dorsolateral prefrontal and superior parietal regions, largely confirming previous reports. The data indicate that, on a regional level, modality-specific processing in a conditional motor task does not occur in frontal motor areas and is probably confined to sensory areas.

We have used positron emission tomography (PET) to measure regional cerebral blood flow (rCBF) in sighted and congenitally blind subjects performing auditory localization tasks. During scanning, the spectral and binaural cues of localized sound were reproduced by a sound system and delivered via headphones. During tasks that required auditory localization both the sighted and blind subjects strongly activated posterior parietal areas. In addition, the blind subjects activated association areas in the right occipital cortex, the foci of which were similar to areas previously identified in visual location and motion detection experiments in sighted subjects. The blind subjects, therefore, demonstrated visual to auditory cross-modal plasticity with auditory localization activating occipital association areas originally intended for dorsal-stream visual processing. To determine the functional connectivity of pre-selected brain regions in primary and non-primary auditory and posterior parietal cortex in the two cohorts, we performed an inter-regional correlation analysis on the rCBF data set. During auditory localization in the blind subjects, rCBF activity in the right posterior parietal cortex was positively correlated with that in the right occipital region, whereas in sighted subjects correlations were generally negative. There were no significant positive occipital correlations in either cohort when reference regions in temporal or left parietal cortex were chosen. This indicates that in congenitally blind subjects the right occipital cortex participates in a functional network for auditory localization and that occipital activity is more likely to arise from connections with posterior parietal cortex.

It is with great pleasure that I accept the George W. Morey Award for 1998 honoring as it does the research of my collaborators and me over the past 45 yrs and the many other activities related to glass science in which I have been engaged. Here I review some of my research on the glassy state of matter. When my adventures in an amorphous landscape began in 1952 my concept of glassy materials was something through which one looked or from which one drank. (C) Elsevier Science B.V. All rights reserved.

Using serial [(11)C]SCH 23390- and [11C]raclopride-PET, we have measured the rate of loss of striatal dopamine D1 and D2 receptor binding over a mean of 40 months in nine asymptomatic adult Huntington's disease mutation carriers, four patients with symptomatic disease, seven mutation-negative controls and three subjects at risk for the disease. Eight of the nine asymptomatic Huntington's disease mutation carriers had serial [11C]raclopride-PET and showed a mean annual loss of striatal D2 binding of 4.0%. Only five of these eight, however, showed active progression, and they had a mean annual loss of D2 binding of 6.5%. All nine asymptomatic mutation carriers had serial [11C]SCH 23390-PET and showed a mean annual loss of striatal D1 binding of 2. 0%. Four of these subjects demonstrated active progression and they had a mean annual loss of 4.5%. Our four symptomatic Huntington's disease patients showed a mean annual loss of D2 binding of 3.0% and of D1 binding of 5.0%. Loss of striatal D1 and D2 binding was significantly greater in the known mutation carriers than in the combined at-risk and gene-negative groups (P < 0.05). At follow-up PET all subjects were clinically assessed using the Unified Huntington's Disease Rating Scale. Scores for motor function and total functional capacity correlated with PET measures of striatal dopamine receptor binding both in the asymptomatic mutation carriers (D1, P < 0.01) and across the combined asymptomatic and clinically affected Huntington's disease mutation carrier group (D1 and D2, P < 0.001). We conclude that PET measures of striatal D1 and D2 dopamine binding can be used to identify asymptomatic Huntington's disease mutation carriers who are actively progressing and who would thus be suitable for putative neuroprotective therapies. Measures of disease progression rates in Huntington's disease patients and asymptomatic mutation carriers will be of critical importance in future trials of experimental restorative treatments.

To learn more about human auditory spatial processing, we used positron emission tomography (PET) to measure regional cerebral blood flow in human volunteers engaged in sound localization tasks. Spectral and binaural cues of localized sound were reproduced by a sound system and delivered via headphones. During localization tasks, subjects activated inferior parietal lobules (IPL) bilaterally. In a second experiment, matched in design to the first, subjects made non-spatial auditory discriminations based on frequency, activating the IPL bilaterally with left hemispheric predominance. A between-study comparison revealed that the right IPL was significantly more activated during the sound localization task compared with the feature discrimination task, suggesting a preferential role for the right IPL in auditory spatial processing.

Cross-modal plasticity in blind subjects contributes to sensory compensation when vision is lost early in life, but it is not known if it does so when visual loss occurs at an older age. We used H 2 15 O positron emission tomography to identify cerebral regions activated in association with Braille reading, and repetitive transcranial magnetic stimulation to induce focal transient disruption of function during Braille reading, in 8 subjects who became blind after age 14 years (late-onset blind), after a lengthy period of normal vision. Results were compared with those previously reported obtained from congenitally and early-onset blind subjects. As shown by H 2 15 O positron emission tomographic scanning, the occipital cortex was strongly activated in the congenitally blind and early-onset blind groups but not in the late-onset blind group. Occipital repetitive transcranial magnetic stimulation disrupted the Braille reading task in congenitally blind and early-onset blind subjects but not in late-onset blind subjects. These results indicate that the susceptible period for this form of functionally relevant cross-modal plasticity does not extend beyond 14 years. Ann Neurol 1999;45:451–460

A 63 year old man presented to his general practioner complaining of a stinging sensation on the left side of his abdomen without evidence of a skin rash. Six months later he developed …

Although the importance of the posterior parietal and prefrontal regions in spatial localization of visual stimuli is well established, their role in auditory space perception is less clear. Using positron emission tomography (PET) during auditory and visual spatial localization in the same subjects, modality-specific areas were identified in the superior parietal lobule, middle temporal and lateral prefrontal cortices. These findings suggest that, similar to the visual system, the hierarchical organization of the auditory system extends beyond the temporal lobe to include areas in the posterior parietal and prefrontal regions specialized in auditory spatial processing. Our results may explain the dissociation of visual and auditory spatial localization deficits following lesions involving these regions.

Although patients with sensory neuropathies and normal muscle power are rare, they have been extensively studied because they are a model for dissociating the sensory and motor components of movement. We have examined these patients to determine the cerebral functional anatomy of movement in the absence of proprioceptive input. In addition, the disabling symptoms of these patients can be substantially improved by visually monitoring their movements. We hypothesized that, during visually guided movements, these patients would show overactivity of regions specialized for visuomotor control with the possible additional involvement of areas that normally process somatosensory information. We used positron emission tomography (PET) and the tracer H 2 15 O to determine the functional anatomy of visually and non-visually guided finger movements in three patients with long-standing pan-sensory neuropathies and normal muscle power and six healthy controls. Five conditions were performed with the right hand: a sequential finger movement task under visual guidance, the same motor task without observation of the hand, monitoring a video of the same sequential finger movement, a passive visual task observing a reversing checkerboard, and an unconstrained rest condition. Data were analyzed using conventional subtraction techniques with a statistical threshold of z >2.33 with corrections for multiple comparisons. When compared with the control group, activation was not deficient in any brain areas of the patient cohort in any of the contrasts tested. In particular, in the non-visually guided movement task, in which meaningful visual and proprioceptive input was absent, the patient group activated primary motor, premotor, and cerebellar regions. This suggests that these areas are involved in motor processing independent of sensory input. In all conditions involving visual observation of hand movements, there was highly significant overactivity of the left parietal operculum (SII) and right parieto-occipital cortex (PO) in the patient group. Recent non-human primate studies have suggested that the PO region contains a visual representation of hand movements. Overactivity of this area and the activation of SII by visual input appear to indicate that compensatory overactivity of visual areas and cross-modal plasticity of somatosensory areas occur in deafferented patients. These processes may underlie their ability to compensate for their proprioceptive deficits.

Movement-related cerebellar activation may be due to sensory or motor processing. Ordinarily, sensory and motor processing are obligatorily linked, but in patients who have severe pansensory neuropathies with normal muscle strength, motor activity occurs in isolation. In the present study, positron emission tomography and functional magnetic resonance imaging in such patients showed no cerebellar activation with passive movement, whereas there was prominent movement-related cerebellar activation despite absence of proprioceptive or visual input. The results indicate that motor processing occurs within the cerebellum and do not support the recently advanced view that the cerebellum is primarily a sensory organ.

Seventeen individuals at risk for Huntington's disease and five symptomatic patients, who had previously undergone [11C]SCH23390 and [11C]raclopride PET to assess in vivo levels of striatal dopamine D1 and D2 receptor binding, had neuropsychological assessment on a series of tests known to be sensitive to symptomatic Huntington's disease, including tests of verbal fluency, memory, attention and planning. Compared with age- and IQ-matched healthy volunteers, clinically symptomatic carriers of the Huntington's disease mutation were found to be impaired on tests of verbal fluency, spatial span, planning and sequence generation, as were clinically asymptomatic Huntington's disease mutation carriers. In asymptomatic individuals, both striatal dopamine receptor levels and cognitive performance were lower in subjects approaching their estimated age of onset. In addition, performance on these tasks was found to correlate with PET measures of striatal D1 and D2 receptor binding levels, especially D2 binding. These results are consistent with a role for the striatum, as part of the complex corticobasal ganglia-thalamocortical circuitry, in the optimal scheduling and sequencing of responses, and suggest that cognitive manifestations of striatal dysfunction can be evidenced in carriers of the Huntington's disease mutation prior to the onset of overt clinical movement disorder.