98 research outputs found
Correlation of Clinical Neuromusculoskeletal and Central Somatosensory Performance: Variability in Controls and Patients With Severe and Mild Focal Hand Dystonia
Focal hand dystonia (FHd) is a recalcitrant,
disabling movement disorder, characterized by
involuntary co-contractions of agonists and
antagonists, that can develop in patients who
overuse or misuse their hands. The aim of this
study was to document clinical neuromusculoskeletal
performance and somatosensory
responses (magnetoencephalography) in healthy
controls and in FHd subjects with mild versus
severe hand dystonia. The performance of
healthy subjects (n = 17) was significantly better
than that of FHd subjects (n = 17) on all clinical
parameters. Those with mild dystonia (n = 10)
demonstrated better musculoskeletal skills,
task-specific motor performance, and sensory
discrimination, but the performance of sensory
and fine motor tasks was slower than that of
patients with severe dystonia. In terms of
somatosensory evoked field responses (SEFs),
FHd subjects demonstrated a significant
difference in the location of the hand
representation on the x and y axes, lower
amplitude of SEFs integrated across latency,
and a higher ratio of mean SEF amplitude to
latency than the controls. Bilaterally,. those with
FHd (mild and severe) lacked progressive
sequencing of the digits from inferior to
superior. On the affected digits, subjects with
severe dystonia had a significantly higher ratio
of SEF amplitude to latency and a significantly
smaller mean volume of the cortical hand
representation than those with mild dystonia.
Severity of dystonia positively correlated with
the ratio of SEF mean amplitude to latency
(0.9029 affected, 0.8477 unaffected; p<0.01).
The results of the present study strengthen the
evidence that patients with FHd demonstrate
signs of somatosensory degradation of the hand
that correlates with clinical sensorimotor
dysfunction, with characteristics of the dedifferentiation
varying by the severity of hand
dystonia. If these findings represent aberrant
learning, then effective rehabilitation must
incorporate the principles of neuroplasticity.
Training must be individualized to each patient
to rebalance the sensorimotor feedback loop
and to restore normal fine motor control
Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence
Long-term modification of cortical synapses improves sensory perception
Synapses and receptive fields of the cerebral cortex are plastic. However, changes to specific inputs must be coordinated within neural networks to ensure that excitability and feature selectivity are appropriately configured for perception of the sensory environment. Long-lasting enhancements and decrements to rat primary auditory cortical excitatory synaptic strength were induced by pairing acoustic stimuli with activation of the nucleus basalis neuromodulatory system. Here we report that these synaptic modifications were approximately balanced across individual receptive fields, conserving mean excitation while reducing overall response variability. Decreased response variability should increase detection and recognition of near-threshold or previously imperceptible stimuli, as we found in behaving animals. Thus, modification of cortical inputs leads to wide-scale synaptic changes, which are related to improved sensory perception and enhanced behavioral performance
Time-Warp–Invariant Neuronal Processing
A biophysical mechanism acting in auditory neurons allows the brain to process the high variability of speaking rates in natural speech in a time-warp-invariant manner
Perinatal Asphyxia Affects Rat Auditory Processing: Implications for Auditory Perceptual Impairments in Neurodevelopmental Disorders
Perinatal asphyxia, a naturally and commonly occurring risk factor in birthing, represents one of the major causes of neonatal encephalopathy with long term consequences for infants. Here, degraded spectral and temporal responses to sounds were recorded from neurons in the primary auditory cortex (A1) of adult rats exposed to asphyxia at birth. Response onset latencies and durations were increased. Response amplitudes were reduced. Tuning curves were broader. Degraded successive-stimulus masking inhibitory mechanisms were associated with a reduced capability of neurons to follow higher-rate repetitive stimuli. The architecture of peripheral inner ear sensory epithelium was preserved, suggesting that recorded abnormalities can be of central origin. Some implications of these findings for the genesis of language perception deficits or for impaired language expression recorded in developmental disorders, such as autism spectrum disorders, contributed to by perinatal asphyxia, are discussed
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