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PubMed2007

Functional potential in chronic stroke patients depends on corticospinal tract integrity.

Determining whether a person with stroke has reached their full potential for recovery is difficult. While techniques such as transcranial magnetic stimulation (TMS) and MRI have some prognostic value, their role in rehabilitation is undefined. This study used TMS and MRI to determine which factors predict functional potential, defined as an individual's capacity for further functional improvement at least 6 months following stroke. We studied 21 chronic stroke patients with upper limb impairment. The functional integrity of the corticospinal tracts (CSTs) was assessed using TMS and functional MRI. The presence or absence of motor-evoked responses (MEPs) to TMS in the affected upper limb, and the lateralization of cortical activity during affected hand use were determined. The structural integrity of the CST was assessed using MRI, and diffusion tensor imaging was used to measure the asymmetry in fractional anisotropy (FA) of the internal capsules. A multiple linear regression analysis was performed, to predict both clinical score at inception and change in clinical score for 17 patients who completed a 30 day programme of motor practice with the affected upper limb. The main findings were that in patients with MEPs, meaningful gains were still possible 3 years after stroke, although the capacity for improvement declined with time. In patients without MEPs, functional potential declines with increasing CST disruption, with no meaningful gains possible if FA asymmetry exceeds a value of 0.25. This study is the first to demonstrate the complementary nature of TMS and MRI techniques in predicting functional potential in chronic stroke patients. An algorithm is proposed for the selection of individualized rehabilitation strategies, based on the prediction of functional potential. These strategies could include neuromodulation using a range of emerging techniques, to prime the motor system for a plastic response to rehabilitation.

Adult↗
PubMed2000

Connectivity of ectopic neurons in the molecular layer of the somatosensory cortex in autoimmune mice.

Approximately 50% of New Zealand Black mice (NZB/BINJ) and 80% of NXSM-D/EiJ mice prenatally develop neocortical layer I ectopias, mostly in somatosensory cortices. These cortical anomalies are similar to those seen in the brains of individuals with dyslexia. Neurofilament staining revealed a radial column of tightly packed fiber bundles in the layers underlying ectopias. This suggested that the connectivity of the ectopic neurons was aberrant. The present study used the tracers 1,1'-dioctadecyl- 3,3,3',3'-tetramethylindo- carbocyanine perchlorate (DiI) and biotinylated dextran amine (BDA) to more thoroughly explore the cortical and thalamic connectivity of the ectopias. DiI placement into ectopias again revealed a distinct bundle of fibers extending from the ectopic neurons to the deep cortical layers. This bundle split in the white matter with some fibers traveling to the corpus callosum and others to the internal capsule. Thalamic connections were concentrated in the ventrobasal com- plex (VB) and posterior thalamic nucleus group (Po). Injections of BDA into VB revealed reciprocal connections between VB and the ectopic cortical neurons. Ipsilateral corticocortical projections were seen between ectopias in primary somatosensory and motor and secondary somatosensory cortices, but no contralateral connections of the ectopic neurons were seen. These findings confirm the notion that layer I ectopias are anomalously connected by comparison to neurons in homologous cortex, which may underlie widespread dysfunction of brains containing ectopias.

Animals↗
PubMed2000

Cellular mosaics in the rat marginal zone define an early neocortical territorialization.

We describe a novel neuronal group of the neocortical primordium that is formed by the pioneer neurons, unlike the Cajal-Retzius cells and the subplate component of the preplate. These pioneer neurons of the preplate and the marginal zone send transient axonal projections into the nascent internal capsule, preceding the formation of the axonal projection from the subplate neurons. In wholemount preparations, the pioneer neurons of the preplate and the marginal zone cover the prospective neocortical territory from embryonic day (E) 12 to E17. Two subpopulations of pioneer neurons (defined by differential expression of calcium-binding proteins) group into well-defined cell clusters, separated by spaces containing a lower packing density of cells immunoreactive to the corresponding calcium-binding protein. In both cases, cell clustering was concomitant with fasciculation of their axons. Although both subpopulations cohabit in the same areas of the marginal zone, their clustering occurs in specific, well-delineated territories, giving a mosaic appearance to the surface of the neocortical primordium before the arrival of thalamocortical axons. We hypothesize that the fascicles of descending axons arising from defined territories of the marginal zone may intervene in the initial guidance of the subcortical projection from the subplate.

Animals↗
PubMedDate not supplied

Emergence of connectivity in the embryonic rat parietal cortex.

In order to understand how cortical circuitry is put together, we examined the emergence of corticofugal projection cells and the arrival of subcortical afferents in the presumptive parietal cortex of the embryonic rat cerebrum. Afferent and efferent projections were selectively labeled by applications of the lipophilic tracers DiI and DiA in aldehyde-fixed brains of 12-18-d-old rat embryos (E12-E18; gestation: 21 d). On E12 and E13, the neocortical anlage consists of a ventricular zone and a preplate, with no extracortical connections. By E14, just prior to the appearance of the cortical plate, polymorphic cells located in the ventrolateral preplate of the telencephalic vesicle send out the first group of corticofugal axons toward the ganglionic eminence. Shortly thereafter, the cortical plate emerges as a dense band of radially oriented cells that also contribute to the corticofugal projection. By E15, axons of the early cortical projection cells cascade through the striatal primordium, the future site of the internal capsule. At the time of cortical plate formation and initial corticofugal axon outgrowth, ascending corticopetal axon systems have not yet arrived in the neocortex. Double-labeling experiments in which one dye is placed in the neocortex and the other in the ipsilateral dorsal thalamus reveal that cortical efferents encounter the first ascending wave of thalamofugal axons at the level of the striatum. Collectively, these two axonal systems bridge the necortex and the diencephalon. Upon their arrival in the neocortex on E16, thalamic axons follow a ventrolateral to dorsomedial course within the intermediate zone. Thalamic axons are the first subcortical afferent system to arrive in the neocortex. Other ascending afferent systems arising from the midbrain tegmentum enter the neocortex after E17. Comparison of thalamocortical and tegmentocortical projections in two halves of the same brain and across various embryonic ages clearly reveals that the two projection systems differ in their trajectories as well as in their time of arrival. Present observations challenge the view that the precocious arrival of subcortical axons provides the impetus for cortical maturation, and suggest that cortical plate differentiation and the initial organization of corticofugal projection patterns occur independent of ascending pathways.

Afferent Pathways↗
PubMedDate not supplied

Postnatal maturation of the direct corticospinal projections in the macaque monkey.

Postnatal changes in the topography of the multiple corticospinal projections in the macaque monkey were followed using retrogradely transported fluorescent tracers, and related to the monkey's acquisition of manual dexterity; both behavioral and anatomical maturation were completed by about 8 postnatal months. Cortical origins of the corticospinal projections were examined by constructing planar projection maps of the distributions of labeled corticospinal neuron somas; these somas were found only in lamina V. At birth elaborate somatotopically organized corticospinal projections from primary motor cortex (area 4), the mesial supplementary motor area and cingulate areas 23 and 24, area 12, dorsolateral area 6a beta, the dorsolateral and ventral area 6a alpha (area F4), parietal areas 2/5, 7b and the peri-insular cortex (including area SII), were clearly defined, with axons extending to all spinal cord segments. While this pattern of regional projections broadly resembled that of the mature macaque, there were, however, substantial maturational changes during the 8 months after birth. These included (1) a halving of the area of cerebral cortex from which the contralateral corticospinal projection originated and (2) a threefold reduction in the number of labeled corticospinal neurons projecting to all segments of the cord. Collateral elimination rather than neuronal cell death was the likely mechanism for this reduction in the population and areal extent of corticospinal neurons in the maturing macaque. The surviving corticospinal axon terminals also developed substantially during the postnatal period. At birth some terminals had invaded the intermediate zone in each spinal segment, but few had penetrated the dorsal and ventral horns. By 6 postnatal months, however, many corticospinal neurons were retrogradely labeled following the injection of fluorescent labels into each of these spinal zones in cervical and lumbar spinal segments. These data demonstrate a considerable postnatal reduction in corticospinal neurons projecting to the contralateral spinal cord, and imply that many of the axons that are eliminated never synapse on spinal neurons. It is suggested that during the middle fetal period the axons of many of the cortical neurons in lamina V that in the mature monkey will terminate on particular neuron populations in the thalamus, brainstem, or spinal cord, traverse a common pathway down through the internal capsule into the spinal cord, passing close to these successive targets, and possibly forming collaterals at these levels. In the postnatal period each such neuron establishes a stable, effective synaptic input to only one or a few of these subcortical target populations, and the remaining collateral branches regress. The postnatal maturation of corticospinal neurons, examined in this study, is compatible with such a model.

Animals↗
PubMed2000

Enhanced CD9 expression in the mouse and human brains infected with transmissible spongiform encephalopathies.

A tetraspan protein CD9, normally expressed in the myelin sheath of the central and peripheral nervous system, was identified to be up-regulated in mouse brains infected with transmissible spongiform encephalopathy (TSE), by mRNA differential display screening. To elucidate its role in the neurodegeneration process observed in TSE, CD9 expression was examined in the murine disease model and in the human disease materials. Up-regulation of CD9 gene expression in the TSE-infected mouse brains was detected as early as a preclinical stage, when abnormal prion protein deposition and vacuolation were obviously manifested in the internal capsule and thalamus. In contrast, other myelin protein genes showed a reverse pattern of CD9 gene expression. Enhanced CD9 expression was immunohistochemically detected in the astrocytes of such pathological regions. In human specimens of TSE, enhanced CD9 immunoreactivity was observed in the astrocytes and some oligodendrocytes in the brains, but no relevant alteration in CD9 immunoreactivity was observed in the other organs or tissues. Positive CD9 immunoreactivity in astrocytes was also manifest in other neurological disorders in a less prominent manner. The findings indicate that up-regulated CD9 plays a role in glial cells in pathological conditions, especially in such a devastating condition as TSE.

Adult↗
PubMed2001

Cerebral infarction in chronic meningitis: a comparison of tuberculous meningitis and cryptococcal meningitis.

Twenty-eight patients with cerebral infarction secondary to chronic meningitis were retrospectively identified at our institution over a period of 5 years. They accounted for 47% (17/36) of tuberculous meningitis (TBM) and 32% (11/34) of cryptococcal meningitis cases. Single infarctions were found in 15 patients and multiple infarctions in 13. The distribution of single infarctions was: basal ganglia 7; internal capsule 3; thalamus 1; cerebellum 1; and cortical infarct 3. Therapeutic outcomes at 3 months were determined using a modified Barthel INDEX: At follow-up of 3 months or more, 10 had good outcomes while the other 18 had poor outcomes. The 18 with poor outcomes included six who died, and 12 who had severe neurological sequelae. TBM and cryptococcal meningitis shared similar clinical features, both being frequently associated with other neurological complications, including hydrocephalus, cranial nerve palsy, and seizures in our patients. However, extracranial involvement, such as spinal and pulmonary involvement, was more commonly found in TBM patients. Cerebral infarction can occur in both the acute stage and later stages of treatment. Mortality and morbidity are high, and early diagnosis and appropriate antimicrobial treatment are essential. If hydrocephalus is demonstrated, early ventricular decompression is needed to prevent further cerebral ischaemia.

Adolescent↗
PubMed1990

Oversized, auditory responsive units of rostral, mid, and posterolateral thalamus.

Activity was recorded from 343 units of rostral, mid, and posterolateral thalamus following a conditioned click stimulus (CS). Over 40% of units responded with increased discharge in cats conditioned to blink to the CS. Twenty-nine units with short latency (less than 40 ms) responses were injected intracellularly with phaseolus lectin and identified morphologically; 83% had long, thick primary dendrites with smaller secondary branches. Almost half (46%) had larger somata than the largest previously described thalamic neurons of this morphologic classification. The results suggest that a previously unidentified class of oversized cells is likely to contain many short latency, auditory responsive units. A substantial number of these cells (36%) projected extrathalamically into the internal capsule, and thus may constitute a new auditory pathway between thalamus and cortex.

Acoustic Stimulation↗
PubMed1996

High temporal resolution diffusion MRI of global cerebral ischemia and reperfusion.

Although brain ischemia has been extensively studied using diffusion-weighted magnetic resonance imaging, most studies performed so far have not had adequate time resolution to follow the temporal changes in the water apparent diffusion coefficient (ADC) in hyperacute ischemia. Using diffusion echo planar imaging, we obtained ADC maps (calculated from measurements made with 8 b-values) with a time resolution of 43 s in a feline model of global brain ischemia and reperfusion. Different protocols were performed: 10-min hypoperfusion, 10- and 22-min ischemia followed by reperfusion, and cardiac arrest. ADC values were obtained from white matter of the internal capsule and from the thalamus. Cortical gray matter measurements were not deemed reliable due to the close proximity of CSF in the cortical sulci. Following occlusion, the ADC declined in the thalamus to < 2 SD of its normal baseline value within 1.5-2.5 min. This decay was exponential with a time constant (tau +/- SD) of 6.0 +/- 2.6 min; no further decrease in the ADC was observed 10 min following ischemia. Following reperfusion, in animals that showed ADC recovery, the ADC began increasing immediately, returning to its preischemic value in approximately 15 min. No significant ADC changes were observed during hypoperfusion. Following cardiac arrest, the decay of ADC was more rapid in the thalamus (tau = 2.6 +/- 0.6 min) than in white matter (tau = 6.6 +/- 1.8 min). We observed that the ADC at 40 min after cardiac arrest was similar to the ADC at 10 min after ischemia. Given that all animals subjected to 10-min ischemic episodes showed ADC recovery with reperfusion, doubt is cast on whether it is possible to define a threshold value of the ADC below which brain tissue is irreversibly damaged. Finally, despite variability in the time constants of the ADC decay induced by ischemia, the ADC values at 10 min were very similar in all the animals. This suggests that when blood flow is diminished sufficiently to induce an ADC reduction, differences in perfusion affect the rapidity of the decrease but not the final asymptotic value reached.

Animals↗
PubMed1996

Relationships between high oxygen extraction fraction in the acute stage and final infarction in reversible middle cerebral artery occlusion: an investigation in anesthetized baboons with positron emission tomography.

Studies in humans suggest that regions that show maximal increases in brain oxygen extraction fraction (OEF) in the hours following an ischemic episode are those most vulnerable for infarction and are often, although not always, associated with the final site of infarction. To clarify this issue, we followed the hemodynamic and metabolic characteristics of regions with an initially maximally increased OEF and compared them with the ultimately infarcted region in an experimental stroke model. Positron emission tomography (PET) was used to obtain functional images of the brain prior to and following reversible unilateral middle cerebral artery occlusion (MCAO) in 11 anesthetized baboons. To model early reperfusion, the clips were removed 6 h after occlusion. Successive measurements of regional CBF (rCBF), regional CMRO2 (rCMRO2), regional cerebral blood volume, and regional OEF (rOEF) were performed during the acute (up to 2 days) and chronic (> 15 days) stage. Late magnetic resonance imaging (MRI) scans (co-registered with PET) were obtained to identify infarction. Reversible MCAO produced an MRI-measurable infarction in 6 of 11 baboons; the others had no evidence of ischemic damage. Histological analysis confirmed the results of the MRI investigation but failed to show any evidence of cortical ischemic damage. The lesion was restricted to the head of the caudate nucleus, internal capsule, and putamen. The infarct volume obtained was 0.58 +/- 0.31 cm3. The infarcts were situated in the deep MCA territory, while the area of initially maximally increased OEF was within the cortical mantle. The mean absolute rCBF value in the infarct region of interest (ROI) was not significantly lower than in the highest-OEF ROI until 1-2 days post-MCAO. Cerebral metabolism in the deep MCA territory was always significantly lower than that of the cortical mantle; decreases in CMRO2 in the former region were evident as early as 1 h post-MCAO. In the cortical mantle, the rOEF was initially significantly higher than in the infarct-to-be zone. Subsequently, the OEF declined in both regions. The differences in the time course of changes in CMRO2 and OEF between these two regions, with the eventually infarcted area showing earlier metabolic degradation and in turn decline in OEF, presumably underlie their different final outcomes. In conclusion, following MCAO, the region that shows an early maximal increase in the OEF is both topographically and physiologically distinct from the region with final consolidated infarction if reperfusion is allowed at 6 h. This high OEF, although indicative of a threatened condition, is not an indicator of inescapable consolidated infarction and is thus a situation in which therapy could be envisaged. Whether or not it is at risk of infarction and thus constitutes one target for therapy remains to be seen.

Animals↗
PubMed1997

The effect of nitric oxide synthase inhibition on acute platelet accumulation and hemodynamic depression in a rat model of thromboembolic stroke.

The relative importance of hemodynamic factors in the pathogenesis of thrombotic or embolic stroke is unclear. Of particular therapeutic interest are those substances that facilitate vasodilation and the clearance of platelet aggregates in the compromised microvasculature. A likely contributor to these functions is nitric oxide because it is known to inhibit platelet aggregability and promote vascular relaxation. To investigate the involvement of nitric oxide in the hemodynamic changes after experimental ischemia, photochemically induced nonocclusive common carotid artery thrombosis (CCAT) was studied. CCAT is a rat model of unilateral carotid artery stenosis and platelet embolization to the brain. This study characterized the acute hemodynamic consequences of CCAT and the resultant pattern of platelet deposits with and without nitric oxide synthase inhibition by nitro-L-arginine methyl ester (L-NAME). In addition, the subacute local cerebral blood flow changes were studied at 24 hours. Right CCAT was produced in 30 male Wistar rats injected with (111)In-labeled platelets. Between 5 and 15 minutes after thrombosis, rats were treated with either 15 mg/kg of L-NAME (intravenously) or saline vehicle. Hemodynamic changes were studied 30 to 45 minutes after thrombosis using [14C]iodoantipyrine autoradiography. Eight coronal levels were analyzed, and cortical and subcortical regions of interest were defined. Significant increases were observed in total platelets in the ipsilateral hemisphere after L-NAME treatment, and in the distribution of platelets in the anterior frontal and occipital cortices with nitric oxide synthase inhibition, encompassing the anterior and posterior border zone areas of the ipsilateral cortex. Otherwise, foci of labeled platelets were detected throughout the ipsilateral and contralateral hemispheres. Mean local cerebral blood flow images (n = 5) revealed a moderate bilateral global reduction in flow acutely, which normalized in the untreated thrombosed group by 24 hours. In contrast, the L-NAME-treated groups (sham and experimental) had lasting, widespread reductions in flow of approximately 25%. Pairwise comparisons between groups showed that CCAT/L-NAME was significantly different from shams in the corpus callosum and different from L-NAME shams in the internal capsule (P < 0.05) These hemodynamic and platelet accumulation changes may partially account for the aggravation of cognitive and sensorimotor deficits previously reported in this model of thromboembolic stroke.

Animals↗
PubMed1981

Case report. Atypical findings in adrenoleukodystrophy.

Computed tomography (CT) in a child with typical clinical and biochemical features of adrenoleukodystrophy (ALD) revealed striking pathologic enhancement in the centra semiovalia, posterior corpus callosum, and corticospinal tracts within the internal capsules, cerebral peduncles, and basis pontis. Central calcifications were detected within otherwise typical symmetrical low attenuation lesions in the periatrial white matter. These findings further expand the spectrum of CT abnormalities in ALD and may represent a link between the recently described Type 1 and Type 11 CT patterns.

Adrenal Glands↗
PubMedDate not supplied

MR imaging in adrenoleukomyeloneuropathy.

A 54-year-old patient with clinical and biochemical features of the adrenoleukomyeloneuropathy-complex is reported. Although CT was essentially normal, magnetic resonance (MR) showed areas of prolonged T1 and T2 values in the corpus callosum, around the trigones of the lateral ventricles, in the internal capsules, in the pons, and in the cervical spinal cord. This case report indicates that MR is better suited than CT to detect demyelination of the cerebral white matter and of descending tracts.

Adrenal Insufficiency↗
PubMedDate not supplied

MR imaging of cerebral hemiatrophy.

Computed tomography has been the procedure of choice in evaluation of cerebral hemiatrophy, particularly in those instances where plain radiographic studies of the skull are nondiagnostic. Our experience suggests that magnetic resonance (MR) can easily accomplish the same task. Furthermore, by virtue of its exquisite soft tissue detail, MR can afford additional clarity and information with respect to relative gray-white matter loss, subarachnoid space size, gyral deformity, as well as highlighting asymmetry of the cerebral peduncles, internal capsules and the thalami.

Adolescent↗
PubMedDate not supplied

Developmental stages of human brain: an MR study.

The differentiation of the telencephalon (TC) gyri and the myelination of TC and diencephalon were analyzed quantitatively in 50 children, 32-240 weeks' postconceptional age (PCA). For this purpose, a four-stage grading system was developed by correlating magnetic resonance images from age-matched postmortem brains with subsequently prepared myelin-stained macroslices. Gyration and myelination progressed in a occipito-rostral direction. Stages 3 and 4 myelination were recognized earlier on T1-weighted images [spin echo (SE) 500/30] than on T2-weighted images (SE 3,000/120). However, long repetition time/echo time sequences yielded better contrast and allowed finer differentiation between myelinated and nonmyelinated structures. At term, the posterior limb of the internal capsule was generally myelinated (stage 2), whereas in 50% of the children, myelin appeared in the TC between 55 and 65 weeks' PCA, e.g., between 3 and 6 months postnatally. The morphological differentiation of the brain surface preceded the biochemical maturation (myelination) by an average of 12 months. Applying such a grading system to a larger population will help establish normal standards for brain maturation and a "brain age" scale during the first 4 years of life.

Brain↗
PubMedDate not supplied

Dilated Virchow-Robin spaces in cryptococcal meningitis associated with AIDS: CT and MR findings.

We present two patients with AIDS complicated by cryptococcal meningitis who displayed focal hypodense nonenhancing lesions in CT in the basal ganglia with corresponding areas of increased T2 and decreased T1 signal on magnetic resonance (MR). These lesions corresponded precisely to the distribution of the perforating arteries. Review of pathological specimens showed these lesions to be small cystic collections of cryptococcal organisms in the perivascular spaces of the arteries with minimal or no inflammatory reaction. The cryptococcal organisms spread from the basal cisterns through the Virchow-Robin spaces, dilating these spaces, to ultimately propagate in the basal ganglia, internal capsule, thalamus, and brain stem. Such lesions have been described as characteristic for cryptococcosis in the pathology literature before the AIDS epidemic, but the radiological manifestations have not been reported previously. The changes appear characteristic for cryptococcosis, which generally incites no host response in the form of perifocal edema or enhancement. These findings in a young adult, with otherwise normal CT or MR scans, may be the first indication that the patient has AIDS. The T2-weighted image sequences are more sensitive in the detection of these lesions when compared to CT or T1-weighted MR images.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

High intensity areas on noncontrast T1-weighted MR images in cerebral infarction.

Among 46 noncontrast magnetic resonance studies on patients with cerebral infarction, 11 showed areas of high signal intensity of the involved brain on T1-weighted images. These areas were more frequent in cerebral or cerebellar cortical lesions. Lacunar infarcts in lenticular nuclei, internal capsules, corona radiata, or brain stem did not show any high signal intensity areas on T1-weighted images, whereas the thalamic infarcts did. Sequential studies revealed that these lesions displayed low signal intensity on T2-weighted images at first, and then a high signal intensity area appeared on T1-weighted images. We suggest that these high signal intensity areas on the T1-weighted images in cerebral infarction are caused by hemorrhagic changes at the periphery of the infarction, where blood flow is restored by recanalization or collateral supply.

Adult↗
PubMedDate not supplied

MR imaging of brain maturation in normal and developmentally handicapped children.

White matter myelination was assessed in the frontal, temporal, and occipital lobes and in the internal capsule in 91 neurodevelopmentally handicapped infants on T2-weighted images (spin echo 3,000/120 ms) and compared with myelination scores from 53 normal control subjects. Clinical diagnosis was birth asphyxia (34), seizures with delays of various causes (33), congenital infections (15), and intracerebral hemorrhages (9). Myelination in the total group of patients was generally delayed. However, we found distinct differences in myelin deposition between groups. Myelination of handicapped children with seizures or with intrauterine infections was retarded most severely at all ages. Children with intracerebral hemorrhages were almost never significantly different from normals in any part of the brain, whereas children with birth asphyxia had myelination scores in between. We conclude that magnetic resonance staging of developmental processes, such as myelination, in the infants' brain helps to recognize delays at an early age.

Asphyxia Neonatorum↗