An anatomical landmark for the supplementary eye fields in human revealed with functional magnetic resonance imaging.
(25/1471)
Together with the frontal and parietal eye fields, the supplementary eye field (SEF) is involved in the performance and control of voluntary and reflexive saccades and of ocular pursuit. This region was first described in non-human primates and is rather well localized on the dorsal surface of the medial frontal cortex. In humans the site of the SEF is still ill-defined. Functional imaging techniques have allowed investigation of the location and function of the SEF. However, there is great variability with regard to the published standardized coordinates of this area. We used here the spatial precision of functional magnetic resonance imaging (fMRI) in order to better localize the SEF in individuals. We identified as the SEF a region on the medial wall that was significantly activated when subjects executed self-paced horizontal saccades in darkness as compared to rest. This region appeared to be predominantly activated in the left hemisphere. We found that, despite a discrepancy of >2 cm found in the standardized Talairach coordinates, the location of this SEF-region could be precisely and reliably described by referring to a sulcal landmark found in each individual: the upper part of the paracentral sulcus. (+info)
Ocular dominance column formation in visual cortex depends on both the presence of subplate neurons and the endogenous expression of neurotrophins. Here we show that deletion of subplate neurons, which supply glutamatergic inputs to visual cortex, leads to a paradoxical increase in brain-derived neurotrophic factor mRNA in the same region of visual cortex in which ocular dominance columns are absent. Subplate neuron ablation also increases glutamic acid decarboxylase-67 levels, indicating an alteration in cortical inhibition. These observations imply a role for this special class of neurons in modulating activity-dependent competition by regulating levels of neurotrophins and excitability within a developing cortical circuit. (+info)
Specificity of color connectivity between primate V1 and V2.
(27/1471)
To examine the functional interactions between the color and form pathways in the primate visual cortex, we have examined the functional connectivity between pairs of color oriented and nonoriented V1 and V2 neurons in Macaque monkeys. Optical imaging maps for color selectivity, orientation preference, and ocular dominance were used to identify specific functional compartments within V1 and V2 (blobs and thin stripes). These sites then were targeted with multiple electrodes, single neurons isolated, and their receptive fields characterized for orientation selectivity and color selectivity. Functional interactions between pairs of V1 and V2 neurons were inferred by cross-correlation analysis of spike firing. Three types of color interactions were studied: nonoriented V1/nonoriented V2 cell pairs, nonoriented V1/oriented V2 cell pairs, and oriented V1/nonoriented V2 cell pairs. In general, interactions between V1 and V2 neurons are highly dependent on color matching. Different cell pairs exhibited differing dependencies on spatial overlap. Interactions between nonoriented color cells in V1 and V2 are dependent on color matching but not on receptive field overlap, suggesting a role for these interactions in coding of color surfaces. In contrast, interactions between nonoriented V1 and oriented V2 color cells exhibit a strong dependency on receptive field overlap, suggesting a separate pathway for processing of color contour information. Yet another pattern of connectivity was observed between oriented V1 and nonoriented V2 cells; these cells exhibited interactions only when receptive fields were far apart and failed to interact when spatially overlapped. Such interactions may underlie the induction of color and brightness percepts from border contrasts. Our findings thus suggest the presence of separate color pathways between V1 and V2, each with differing patterns of convergence and divergence and distinct roles in color and form vision. (+info)
Local mitochondrial function following traumatic brain injury in rats.
(28/1471)
The effect of lateral fluid percussion injury on mitochondrial function in the rat brain was investigated by quantitative imaging of changes in the regional activity of succinate dehydrogenase (SDH), a mitochondrial enzyme of the tricarboxylic acid cycle for adenosine triphosphate production. Regional SDH was measured in the frontal, parietal, temporal, and occipital cortices, CA1 and CA2-3 of the hippocampus, thalamus, corpus callosum, caudate/putamen, and cerebellum 1 hour and 72 hours after low, medium, and high pressure injury. No regional difference between the hemispheres in the activity of SDH was observed in the sham group. The hippocampus showed high SDH activity. The CA2-3 regions showed the highest activity among the regions examined. The corpus callosum, which is white matter, showed the lowest. One hour after low pressure fluid percussion injury, only the frontal lobe showed significantly lower SDH activity than the sham control in the ipsilateral hemisphere, whereas after 72 hours SDH activity was significantly lower in the frontal, parietal, and temporal lobes. SDH activity was significantly lower in the frontal, parietal, and temporal lobes in the medium and high pressure injury groups than in the sham control 1 hour after injury, and SDH activity in the CA1 and CA2-3 of the hippocampus was significantly decreased 72 hours after injury. No decrease in SDH activity was observed in any region of the contralateral hemisphere either 1 hour or 72 hours after injury. Mitochondrial dysfunction of the ipsilateral cortex and hippocampus following fluid percussion injury is correlated with the severity of injury and advances with time after injury. The results suggest that progression of mitochondrial dysfunction is associated with secondary bioenergetic deterioration. (+info)
Syndromes of bilateral symmetrical polymicrogyria.
(29/1471)
BACKGROUND AND PURPOSE: A number of anatomicoclinical syndromes have been described in which bilateral symmetrical polymicrogyria is the underlying morphologic abnormality. We retrospectively reviewed the clinical, epileptic, and morphologic manifestations of bilateral symmetrical polymicrogyria in 21 patients to determine whether certain areas are at particular risk for these syndromes. METHODS: Clinical records and brain MR studies of 21 patients with bilateral symmetrical polymicrogyria were reviewed to confirm the presence and determine the location of polymicrogyria and to qualitatively correlate location with developmental, neurologic, and epileptic histories. The locations we found were compared with published reports of bilateral symmetrical polymicrogyria to determine whether these locations were random or whether predilections exist for certain areas. RESULTS: Analysis revealed six patients with bilateral frontal polymicrogyria, nine with bilateral perisylvian polymicrogyria, one with bilateral parietal polymicrogyria, one with bilateral parasagittal parieto-occipital polymicrogyria, two with bilateral frontal polymicrogyria and bilateral perisylvian polymicrogyria, one with bilateral perisylvian and bilateral parasagittal parieto-occipital polymicrogyria, and one with bilateral perisylvian, bilateral parieto-occipital, and bilateral parasagittal parieto-occipital polymicrogyria. Symptom complexes were non-specific, but seemed additive according to the regions of brain involved. CONCLUSION: Bilateral symmetrical polymicrogyria has a propensity to develop in specific regions of the cerebral cortex. When the regions are extensive, the areas involved often appear to be simple topological additions of those regions. These locations and the identification of several familial cases raise the possibility that genetic mechanisms influence the development of these malformations in some patients. (+info)
Acute stroke evaluated by time-to-peak mapping during initial and early follow-up perfusion CT studies.
(30/1471)
BACKGROUND AND PURPOSE: Early diagnosis of perfusion deficits in patients with acute stroke could guide treatment decisions and improve prognosis. We investigated the sensitivity of perfusion CT studies using parametric time-to-peak maps to assess ischemic brain tissue with respect to early infarct signs on native CT scans. METHODS: First-pass, single-section perfusion CT was performed in 20 patients who presented with symptoms of acute stroke within 6 hours of onset. Initial CT perfusion studies were compared with follow-up studies within 30 hours in 10 patients. A manual, region of interest (ROI)-based, local evaluation procedure was performed to determine delayed time-to-peak values and diminished peak amplitudes. In addition, time-to-peak parameter maps were processed off-line from the dynamic CT data sets to identify areas of perfusion deficits, which were expressed as hemispheric lesion areas (HLAs). Evolution of the ischemic regions was assessed by comparing the HLA on the initial and follow-up studies as well as on the native CT scan of the follow-up studies. RESULTS: Diagnostic time-to-peak maps were generated in 19 of 20 initial and in nine of 10 follow-up perfusion CT studies. The initial time-to-peak map showed perfusion deficits in 14 of 20 patients. Hemispheric territorial infarcts were diagnosed with a sensitivity of 93%. Perfusion deficits in two patients with brain stem infarctions and three patients with lacunar strokes were missed. Follow-up time-to-peak maps showed the extent of reperfusion after various therapeutic strategies. CONCLUSION: Perfusion CT is potentially useful for detecting cerebral perfusion deficits in acute ischemic stroke before morphologic changes are observable on native CT scans. Compared with a locally restricted ROI-based evaluation, time-to-peak maps provide sensitive, global indications of malperfused brain areas, facilitate lesion localization, and allow assessment of the evolution of the infarction during follow-up. (+info)
Noninvasive direct stimulation of the cochlear nerve for functional MR imaging of the auditory cortex.
(31/1471)
We herein present our preliminary experience with functional MR imaging of the direct electrical stimulation of the cochlear nerve using an MR imaging-compatible electrode placed in the external auditory meatus of five patients with binaural sensorineural hearing loss. The stimulator was placed outside the imager's bore, and the electrode produced virtually no susceptibility artifacts. In three of five patients, it was possible to activate the superior temporal gyrus during functional MR imaging. No side effects were observed. (+info)
Serotonergic neurons transiently require a midline-derived FGF signal.
(32/1471)
In the grasshopper CNS, serotonergic growth cones cross the midline early in development and initiate expression of serotonin uptake activity, or SERT. To test if the midline contains an activity that induces SERT, cuts were made that separated serotonergic cell bodies from the midline. SERT activity is completely lost when the midline is separated but is then rescued by bath-applied FGF2 (fibroblast growth factor 2), which can activate the heartless FGF receptor. heartless is expressed specifically in serotonergic neurons. A candidate FGF-like molecule was identified that is expressed in a subset of midline glia. SERT-expressing severed growth cones continue to migrate to their correct targets, which indicates that by the time SERT is activated, the serotonergic growth cones are committed to target-directed growth. (+info)