Brain : a journal of neurology
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Multicenter Study
Dissociation of phantom limb phenomena from stump tactile spatial acuity and sensory thresholds.
Most amputees experience phantom limb sensations and/or phantom limb pain as well as residual limb (stump) pain that are resistant to treatment. Phantom phenomena are not homogeneous; each patient presents with a unique combination of spontaneous or evoked sensations, pain, and/or awareness. In an effort to understand the underlying mechanisms, postamputation pain has been subclassified based on the perceived sensory qualities reported by the individual. ⋯ Thus, despite a common injury, the sensory abnormalities varied within this cohort of subjects. In addition, psychophysical threshold measures of sensory function did not reflect, in any simple way, subjective phantom phenomena. Therefore, classification of phantom phenomena based on peripheral sensory function may be a misleading step in the search for specific mechanisms underlying postamputation sensory phenomena.
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Autism is a disorder of neurodevelopment resulting in pervasive abnormalities in social interaction and communication, repetitive behaviours and restricted interests. There is evidence for functional abnormalities and metabolic dysconnectivity in 'social brain' circuitry in this condition, but its structural basis has proved difficult to establish reliably. Explanations for this include replication difficulties inherent in 'region of interest' approaches usually adopted, and variable inclusion criteria for subjects across the autism spectrum. ⋯ Correlation analysis revealed significantly more numerous and more positive grey matter volumetric correlations in controls compared with children with autism. Thus, using similar diagnostic criteria and image analysis methods in otherwise healthy populations with an autistic spectrum disorder from different countries, cultures and age groups, we report a number of consistent findings. Taken together, our data suggest abnormalities in the anatomy and connectivity of limbic-striatal 'social' brain systems which may contribute to the brain metabolic differences and behavioural phenotype in autism.
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Case Reports
Illusory persistence of touch after right parietal damage: neural correlates of tactile awareness.
We studied a patient who experienced 'palinaesthesia', an illusion of persistent touch following tactile stimulation on the left hand, subsequent to a right parietal meningioma affecting primary somatosensory regions in the postcentral gyrus (SI) and superior parietal gyrus (Brodmann area 7), but preserving the secondary somatosensory cortex (SII) in the upper lateral sulcus. This subjective sensation was accompanied by transient increases in objective measures of tactile threshold. The patient had mild deficits in superficial tactile perception, but showed severe left-sided extinction for offsets of tactile stimuli during bilateral stimulation, but not for onsets of stimuli. ⋯ By contrast, any tactile events on either hand modulated activity in contralateral SII regions, even undetected left-sided offsets. These data demonstrate that illusory persistence of touch following stimulation on the hand may result from sustained neural activity in a restricted region of the SI cortex outlasting the offset of the actual tactile stimuli. These findings also provide direct evidence for a critical role of SI in mediating conscious somatosensory experience on contralateral parts of the body.
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Axonal dystrophy is the hallmark of axon pathology in many neurodegenerative disorders of the CNS, including Alzheimer's disease, Parkinson's disease and stroke. Axons can also form larger swellings, or spheroids, as in multiple sclerosis and traumatic brain injury. Some spheroids are terminal endbulbs of axon stumps, but swellings may also occur on unbroken axons and their role in axon loss remains uncertain. ⋯ Motor nerve terminals at neuromuscular junctions continued to degenerate in gad/Wld(S) mice, consistent with previous observations that Wld(S) has a weaker effect on synapses than on axons, and probably contributing to the fact that Wld(S) did not alleviate gad symptoms. Wld(S) acts downstream of the initial pathogenic events to block gad pathology, suggesting that its effect on axonal swelling need not be specific to this disease. We conclude that axon degeneration mechanisms are more closely related than previously thought and that a link exists in gad between spheroid pathology and Wallerian degeneration that could hold for other disorders.
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Writer's cramp, or focal hand dystonia, is characterized by involuntary coactivation of antagonist or unnecessary muscles while writing or performing other tasks. Although the mechanism underlying this muscle overactivation is unknown, recent studies of changes in cerebral blood flow during writing have demonstrated a reduction in the activation of the primary motor cortex (MC) and hyperactivity of parts of the frontal non-primary motor areas. Therefore, any measures that decrease the activities of non-primary motor areas such as the premotor cortex (PMC) and the supplementary motor area (SMA) might improve dystonic symptoms. ⋯ Stimulation of the PMC but not the MC significantly improved the rating of handwriting (mean tracking error from the target, P = 0.004; pen pressure, P = 0.01) and prolonged the silent period (P = 0.02) in the patient group. rTMS over the other sites or using a sham coil in the patient group or trials in the control group revealed no physiological or clinical changes. This increased susceptibility of the PMC in dystonia suggests that the lack of inhibition in the MC is secondary to the hyperactivity of PMC neurons. Inhibition of the PMC using rTMS could provide a therapeutic measure of writer's cramp.