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PubMed2002

Sequential proton MRS study of brain metabolite changes monitored during a complete pathological cycle of demyelination and remyelination in a lysophosphatidyl choline (LPC)-induced experimental demyelinating lesion model.

Metabolite changes in rat brain internal capsule (ic) area were monitored using volume localized in vivo proton MR spectroscopy (MRS) in a lysophosphatidyl choline (LPC)-induced experimental demyelinating lesion model of multiple sclerosis (MS), during the early phase (pre-acute) as well as during the complete pathological cycle of de- and re-myelination processes. The N-acetyl aspartate (NAA) peak showed reduction during the early phase of the lesion progression (demyelination) until day 10 and increased thereafter during remyelination. However, choline (Cho) and lipid resonances showed increased signal intensity during the early phase and decreased during remyelination. A progressive reduction of the NAA/Cr metabolite ratio in lesioned rats was observed during demyelination (up to day 10) compared with before lesion (control), and the value increased thereafter during remyelination (from day 15). During this period, however, the Cho/Cr ratio was a higher until day 10 and subsequently declined and was close to that calculated before lesion creation. The changes in NAA/Cr and Cho/Cr metabolite ratios correspond to changes in the individual metabolite peaks such as NAA and Cho. The increase in the intensity of the choline resonance during the early phase is indicative of the onset of an inflammatory demyelination process, and its rapid decrease thereafter is due to reduction in the inflammatory process associated with remyelination. Similarly, the increase in the intensity of lipids during the pre-acute stage of the lesion is attributed to active demyelination, which significantly decreased during remyelination. These MR results correlate well with the histology data obtained.

Animals↗
PubMed2003

Three-dimensional MRI of cerebral projections in rat brain in vivo after intracortical injection of MnCl2.

In this study we investigated the potential of in vivo MRI detection of axonal Mn2+ transport for tracing neuronal projections originating in the sensorimotor cortex in healthy and lesioned rat brains. Special attention was given to the potential of visualizing neuronal sprouting of central nervous system across the midline. After injecting unchelated MnCl2 into the forelimb area of sensorimotor cortex of 18 healthy and 10 lesioned rats corticofugal projections could be traced through the internal capsule to the cerebral peduncle and the pyramidal decussation. Although the neuronal tract was visible as early as 6 h after MnCl2 injection, best contrast was achieved after 24-48 h. Beside the cortico-spinal tract, the cortico-thalamic fibres were also visualized by anterograde Mn2+ transport. Cortico-striatal fibres were partially masked by the very high signal near the MnCl2 injection site but could be discerned as well. Slight, diffuse signal enhancement of cortical tissue contralateral to the MnCl2 injection site in healthy rat brains suggests interhemispheric connections or passive diffusion of Mn2+. However, enhanced fibre tract contrast connecting both hemispheres was visible 16 weeks after onset of focal photothrombotic cortical injury. In conclusion our study has shown that we were able to visualize reproducibly the main descending corticofugal projections and interhemispheric connections by non-invasive MRI after localized injection of MnCl2. The appearance of interhemispheric Mn2+-enhanced fibres after photothrombotic focal injury indicates that the method may bear potential to follow non-invasively gross plastic changes of connectivity in the brain after injury.

Animals↗
PubMed1976

Electrophysiological study of corticocaudate projections in cats.

The potential waves evoked in the caudate nucleus (CN) of cats by stimulation of the cerebral neocortex were sterotactically recorded. The head and the body of the caudate nucleus were systematically explored. Stimulation of the ipsilateral sigmoid gyrus and the orbitofrontal cortex evoked waves with the largest amplitude in the CN. Smaller potentials were evoked from the ipsilateral ectosylvian and suprasylvian gyri and from the sigmoid gyrus on the contralateral side. Antidromic conduction from the caudate nucleus to the cortex demonstrated the directness of the corticocaudate pathway. By stimulating the white matter and by amking lesions, the corticocaudate pathway was shown to pass, in part, through the subcallosal fasciculus and, in part, through the internal capsule. Corticocaudate connections were shown to be separate from the fibers of the corticospinal tract. A staggered and extensively overlapping topographic progression of the corticocaudate projections was demonstrable along the antero-posterior axis, but was less evident in the medio-lateral direction. It was concluded that the intranuclear distribution of functional synaptic connections must be more profusely branched than was suspected from anatomical data.

Animals↗
PubMed2001

Comparison of paired-pulse facilitation of AMPA and NMDA synaptic currents in the lateral amygdala.

Stimulating thalamic fibers exiting from the internal capsule evokes a glutamatergic excitatory postsynaptic current (EPSC) recorded in vitro with patch electrodes in neurons of the rat lateral amygdala (LA). The purpose of this study is to compare paired-pulse facilitation (PPF), a form of short-term synaptic plasticity, of AMPA and NMDA receptor-mediated EPSCs. Analysis of PPF at this synapse is important since, in fear-conditioned animals, PPF reflects an enhanced transmitter release but the amplitude of only AMPA EPSCs is facilitated. PPF magnitude of the composite EPSC is a result of both AMPA and NMDA receptor activation; however, the characteristics of AMPA and NMDA PPF are dissimilar. Specifically, the NMDA EPSC shows greater PPF (NMDA PPF) than does the AMPA EPSC whether measuring the NMDA PPF magnitude in an AMPA antagonist/Mg(2+)-free solution or by subtracting the AMPA EPSC from the composite EPSC in normal Mg(2+). Presynaptic NMDA receptors neither influence AMPA PPF nor account for the difference between the NMDA and AMPA PPF. Another difference was that removal of inhibitory tone enhanced AMPA PPF, while it had mixed effects on NMDA PPF. Furthermore, AMPA PPF was independent of stimulus intensity and postsynaptic voltage, unlike the NMDA PPF. Another dissimilarity was that the amplitudes of pairs of AMPA EPSCs were not correlated, suggesting presynaptic mechanisms. In contrast, NMDA PPF was dependent on stimulus intensity and postsynaptic voltage and the amplitudes of paired NMDA EPSCs had a positive correlation, suggesting a postsynaptic influence. Both AMPA and NMDA PPF were influenced by GABA inhibition and this could be a factor in the magnitude disparity. These data show that AMPA and NMDA PPF have different characteristics and contribute to the composite PPF in the thalamic to lateral amygdala pathway.

Amygdala↗
PubMed2006

Connexin-36 gap junctions mediate electrical coupling between ventral tegmental area GABA neurons.

Communication between neurons in the mammalian brain is primarily through chemical synapses; however, evidence is accumulating in support of electrical synaptic transmission between some neuronal types in the mature nervous system. The authors have recently demonstrated that the gap junction (GJ) blocker quinidine suppresses stimulus-induced and dopamine-evoked coupling of gamma amino butyric acid (GABA) neurons in the ventral tegmental area (VTA) of mature rats (Stobbs et al., 2004). The aim of this study was to evaluate the role of connexin-36 (Cx36) GJs in mediating electrical coupling between VTA GABA neurons in P50-80 rats in vivo and P25-50 rats in vitro. Single stimulation of the internal capsule (IC) evoked VTA GABA neuron spike couplets in mature rats when activated antidromically, and multiple poststimulus spike discharges (PSDs) when activated with brief high-frequency stimulation of the IC (ICPSDs). The Cx36 GJ blocker mefloquine (30 mg/kg) suppressed VTA GABA neuron ICPSDs in mature freely behaving rats. VTA GABA neurons recorded via whole-cell patch clamp in the midbrain slice preparation of P25-50 rats showed robust expression of Cx36 transcripts when tested with single-cell quantitative reverse transcription polymerase chain reaction. In P50-80 rats, Cx36 protein immunoreactivity was evident in the VTA and surrounding structures. Dye-coupling between VTA neurons was observed following Neurobiotin labeling of VTA GABA neurons, as well as with the fluorochrome Alexa Fluor 488 using real-time video fluorescent microscopy. Thus, mature VTA GABA neurons appear to be connected by electrical synapses via Cx36 GJs, whose coupling is enhanced by corticotegmental input and by dopamine.

Animals↗
PubMed1997

Category-specific naming deficit for medical terms after dominant thalamic/capsular hemorrhage.

Postmortem, retrograde degeneration, and electrical stimulation studies have implicated the anterior pulvinar in language processing. We examined a patient who, after a hemorrhage affecting the dominant pulvinar and internal capsule, exhibited a circumscribed anomia for medical items and conditions. No other language disturbance was noted. Five category-specific word lists, matched for word frequency, were administered in a naming-to-definition format. Results indicated that the patient exhibited a significant category-specific naming deficit for medical items and conditions compared to matched control subjects. Although medical item lists were found to differ from nonmedical item lists in imageability and abstractness, B.C.'s category-specific deficit did not seem to be caused by word frequency, concept familiarity, imageability, or abstractness. Nor could the patient's performance be explained on the basis of deficits in broader semantic classifications (i.e., animate vs inanimate or man-made vs natural). The patient was unable to retrieve medical items even when given phonemic cues for those he could not name. Findings indicate that subtotal damage in the dominant pulvinar may create category-specific deficits.

Aphasia↗
PubMed2001

Subcortical anarthria: a case report.

A 56-year-old right-handed male with a history of hypertension and diabetes presented two episodes of stroke: The first affected territory was the left anterior coroidal artery (capsular and paracapsular infarcts at the level of the genu and posterior arm of the internal capsule) and the second was the right thalamus, due to a hematoma. Following the first stroke, the patient developed severe dysarthria and after the second stroke remained anarthric. The pathophysiology of the disorder is discussed, and the role of the left and right thalamus as far as speech is concerned is reviewed.

Cerebral Infarction↗
PubMed1994

Cytoarchitectonic development, axon-glia relationships, and long distance axon growth of porcine striatal xenografts in rats.

Porcine fetal lateral ganglionic eminence cells were transplanted into the quinolinic-acid-lesioned corpus striatum of immunosuppressed adult rats. The resulting grafts were analyzed for graft development with respect to donor age, donor cell dosage, and survival time from 5 to 22 weeks postimplantation. Graft development is prolonged by a factor of 3-4 times in porcine xenografts as compared to rat allografts. As grafts matured, neuronal somata developed in clusters that expressed acetylcholinesterase (AChE), tyrosine hydroxylase, and dopamine- and cAMP-associated phosphoprotein. These clusters were interspersed with AChE-poor graft regions consisting of small densely packed cells that stained for glial fibrillary acidic protein and porcine cluster of differentiation factor 44 (a species-specific glial marker). Graft axons could be selectively stained for 70-kDa neurofilament and were preferentially associated with AChE-poor, glial-rich regions in younger grafts (8 weeks), but AChE-rich neuronal regions in older grafts (22 weeks). Both graft axons and graft glial fibers projected for long distances into the host internal capsule, external capsule, corpus callosum, and anterior commissure. Donor axons also innervated host target structures including the globus pallidus and substantia nigra. This demonstrates a prolonged development of striatal cells that is appropriate to the donor species and which produces long-distance target-specific axonal growth within the adult host brain.

Animals↗
PubMed1997

3-Nitropropionic acid neurotoxicity: visualization by silver staining and implications for use as an animal model of Huntington's disease.

The neuronal damage produced by the mitochondrial toxin 3-nitropropionic acid (3NPA) has been suggested to replicate much of the neuropathology seen in Huntington's disease (HD) and therefore might be used in an animal model. We investigated the susceptibility to this toxin of different neuronal populations in addition to the commonly studied caudate putamen by injecting 3NPA into seven different brain regions as well as systemically. After different survival times, rats were intracardially perfused, brain sections were processed with the Gallyas silver technique, and impregnated neurons were mapped with a computerized microscope. Intracerebral administration of 3NPA resulted in a lesion, the center of which was devoid of tissue while the area was surrounded by a halo of Golgi-like impregnated neurons. In addition to local damage, rats receiving microinjections into the frontal cortex, caudate putamen, basal forebrain, and amygdala displayed argyrophilic neurons in the thalamus corresponding to the topography of thalamofugal neurons projecting to the individual injection sites. On the other hand, negligible secondary damage was seen after injections into the internal capsule, thalamus, or substantia nigra, implicating that thalamofugal axons are especially vulnerable to the local effect of this toxin. Two and a half days after systemic administration of 3NPA, a diffuse argyrophilic neuronal reaction was seen in the dorsolateral part of the caudate putamen, together with a more regionally selective staining of neurons in different cortical areas and the hippocampus. These morphopathological changes were also accompanied by motor deficits. The affected neurons in the cortical regions were primarily in those layers (V and VI) and areas (medial prefrontal, caudal insular/periphinal, and ventral temporal) that do not project toward the lesioned striatal area; therefore, the cortical pathology may represent another primary site of action of the toxin. Among the affected neurons in the hippocampal complex were pyramidal neurons in the CA1 region as well as various neurons in the CA3 region and dentate hilar area. These studies suggest that a combination of 3NPA administration and a sensitive silver-impregnation method may unravel the potential site of primary neuronal damage in this animal model. Furthermore, these findings may contribute to the understanding of how the disease progresses in HD from the originally affected neuronal population(s) by the recruitment of closely related systems and pathways.

Animals↗
PubMed2000

Long-term, EGF-stimulated cultures of attached GFAP-positive cells derived from the embryonic mouse lateral ganglionic eminence: in vitro and transplantation studies.

Long-term attached cultures, prepared from mouse embryonic days 15-17 lateral ganglionic eminence, were grown in a medium including epidermal growth factor and serum, and the survival, differentiation, and migration of cells from either early or late passages were analyzed following transplantation. The cultured cells had the morphology of type I astroglial cells, with the vast majority of the cells immunoreactive for glial fibrillary acidic protein (around 90%), the intermediate filament marker nestin, and also the mouse-specific neural markers M2 and M6. The cultures were kept over 25 passages (7 months). During the first 8 passages, the growth rate gradually declined, but it increased again after passage 9 and thereafter stabilized at values similar to those observed during the initial culture period. After passages 4-6 and 18, cell suspensions were implanted cross-species into the intact or lesioned striatum of adult (passages 4-5 only) or intact striatum of neonatal rats (passages 4-6 or 18). Both early and late passage cells formed M2 (and M6)-positive transplants. In the neonatal recipients, widespread migration was seen from the needle tract throughout most of the striatum, along the internal capsule, and into the globus pallidus. In the adult striatum, the cells remained mostly around the injection tract, or within 0.4-0.6 mm from the graft core. These long-term attached cultures are interesting to compare to nonattached neurosphere cultures, and might also offer a means of propagating relatively pure populations of astroglia-like cells for basic transplantation studies or for use in experimental trials with ex vivo gene transfer.

Animals↗
PubMed2000

Cyto- and chemoarchitecture of basal forebrain cholinergic neurons in the common marmoset (Callithrix jacchus).

The cyto- and chemoarchitecture of basal forebrain cholinergic neurons (BFCN) was investigated in the lower primate, the common marmoset (Callithrix jacchus). A large population of magnocellular, hyperchromic, and choline acetyltransferase (ChAT)-positive neurons was detected in the marmoset basal forebrain. The distribution of these neurons was similar to those in higher primates. Thus, ChAT-positive neurons were observed in the medial septum (Ch2), the vertical (Ch2) and horizontal (Ch3) limbs of the diagonal band of Broca, and the nucleus basalis of Meynert (Ch4). The Ch4 complex was relatively well differentiated and displayed distinct sectors. We detected anterior (Ch4a, with a medial and a lateral subdivision), intermediate (Ch4i, with a dorsal and a ventral subdivision), and posterior (Ch4p) sectors in the marmoset Ch4. The Ch4i was relatively small while the Ch4p was large. Similar to the rodent, the marmoset Ch1 extended quite a distance posteriorly, and the Ch4p displayed a major interstitial component distributed within the globus pallidus, its medullary laminae, and the internal capsule. Virtually all of the marmoset BFCN displayed acetylcholinesterase activity, and low affinity (p75(NTR)) and high affinity (Trk) neurotrophin receptor immunoreactivity. A majority contained immunoreactivity for calbindin-D(28K) and calretinin. Many of the Ch4 neurons also displayed tyrosine hydroxylase immunoreactivity. The BFCN lacked galanin immunoreactivity, but were innervated by galanin-positive fibers. None of the marmoset BFCN were NADPH-d-positive. Thus, the BFCN display major anatomical and biochemical differences in the marmoset when compared with higher primates. The marmoset BFCN also display many characteristics common to other primates. This fact, combined with the relatively short life span of the marmoset, indicates that this species may be ideal for studies of age-related changes in the BFCN.

Acetylcholinesterase↗
PubMed2002

Transplantation of human neural progenitor cells into the neonatal rat brain: extensive migration and differentiation with long-distance axonal projections.

Here we examined the ability of human neural progenitors from the embryonic forebrain, expanded for up to a year in culture in the presence of growth factors, to respond to environmental signals provided by the developing rat brain. After survival times of up to more than a year after transplantation into the striatum, the hippocampus, and the subventricular zone, the cells were analyzed using human-specific antisera and the reporter gene green fluorescent protein (GFP). From grafts implanted in the striatum, the cells migrated extensively, especially within white matter structures. Neuronal differentiation was most pronounced at the striatal graft core, with axonal projections extending caudally along the internal capsule into mesencephalon. In the hippocampus, cells migrated throughout the entire hippocampal formation and into adjacent white matter tracts, with differentiation into neurons both in the dentate gyrus and in the CA1-3 regions. Directed migration along the rostral migratory stream to the olfactory bulb and differentiation into granule cells were observed after implantation into the subventricular zone. Glial differentiation occurred at all three graft sites, predominantly at the injection sites, but also among the migrating cells. A lentiviral vector was used to transduce the cells with the GFP gene prior to grafting. The reporter gene was expressed for at least 15 weeks and the distribution of the gene product throughout the entire cytoplasmic compartment of the expressing cells allowed for a detailed morphological analysis of a portion of the grafted cells. The extensive integration and differentiation of in vitro-expanded human neural progenitor cells indicate that multipotent progenitors are capable of responding in a regionally specific manner to cues present in the developing rat brain.

Animals↗
PubMed1997

A general approach to error estimation and optimized experiment design, applied to multislice imaging of T1 in human brain at 4.1 T.

In this report, a procedure to optimize inversion-recovery times, in order to minimize the uncertainty in the measured T1 from 2-point multislice images of the human brain at 4.1 T, is discussed. The 2-point, 40-slice measurement employed inversion-recovery delays chosen based on the minimization of noise-based uncertainties. For comparison of the measured T1 values and uncertainties, 10-point, 3-slice measurements were also acquired. The measured T1 values using the 2-point method were 814, 1361, and 3386 ms for white matter, gray matter, and cerebral spinal fluid, respectively, in agreement with the respective T1 values of 817, 1329, and 3320 ms obtained using the 10-point measurement. The 2-point, 40-slice method was used to determine the T1 in the cortical gray matter, cerebellar gray matter, caudate nucleus, cerebral peduncle, globus pallidus, colliculus, lenticular nucleus, base of the pons, substantia nigra, thalamus, white matter, corpus callosum, and internal capsule.

Artifacts↗
PubMed2000

Regulation of the L1 cell adhesion molecule by thyroid hormone in the developing brain.

Thyroid hormone is essential for brain maturation, regulating neuronal differentiation and migration, myelination, and synaptogenesis. Mutations in the cell adhesion molecule L1 cause severe neurological abnormalities in humans. We studied the effect of thyroid hormone deprivation and administration on L1 expression. Northern and in situ hybridization studies showed that hypothyroidism induces a marked increase in L1 mRNA levels in the caudate putamen, cerebral cortex, amygdala, and some thalamic nuclei. L1 protein was overexpressed in embryonic and newborn hypothyroid rats in the caudate putamen, internal capsule, habenula, and neocortex. Later in development, an abnormally high L1 expression was found in the cortical and cerebellar white matter, corpus callosum, anterior commissure, thalamocortical projections, and striatal fiber tracts of hypothyroid animals. Thyroid hormone administration reversed the upregulation of L1 expression in vivo and in cultured cells. Thus, alterations of L1 expression may contribute to the profound abnormalities caused by hypothyroidism in the developing brain.

Animals↗
PubMed1997

Expression of the adrenoleukodystrophy protein in the human and mouse central nervous system.

The gene mutated in X-linked adrenoleukodystrophy (ALD), a progressive demyelinating disease, codes for a protein (ALDP) involved in very-long-chain fatty acid (VLCFA) transport. The expression of ALDP and of two peroxisomal enzymes involved in beta-oxidation of VLCFA, acyl-CoA oxidase, and catalase was studied in human and mouse brain. The pattern of expression was similar in both species. While acyl-CoA oxidase and catalase are found in all types of CNS cells, including neurons and oligodendrocytes, ALDP expression is restricted mostly to the white matter and endothelial cells. ALDP is highly expressed in astrocytes and microglial cells in vivo and in regenerating oligodendrocytes in vitro. In contrast, in vivo, ALDP is detected in much fewer oligodendrocytes and quantitative Western blot analysis confirmed the lower abundance of ALDP in these cells than in astrocytes. Only oligodendrocytes localized in corpus callosum, internal capsules, and anterior commissure express ALDP at levels comparable to those seen in astrocytes. In ALD, demyelination is first detected in these white matter regions, suggesting that the ALD gene mutation selectively affects those oligodendrocytes strongly expressing ALDP. Because of their failure to express ALDP, microglia and astrocytes may also contribute to demyelination in ALD patients.

ATP Binding Cassette Transporter, Subfamily D, Mem↗
PubMed2001

Water diffusion changes in Wallerian degeneration and their dependence on white matter architecture.

This study investigates water diffusion changes in Wallerian degeneration. We measured indices derived from the diffusion tensor (DT) and T2-weighted signal intensities in the descending motor pathways of patients with small chronic lacunar infarcts of the posterior limb of the internal capsule on one side. We compared these measurements in the healthy and lesioned sides at different levels in the brainstem caudal to the primary lesion. We found that secondary white matter degeneration is revealed by a large reduction in diffusion anisotropy only in regions where fibers are arranged in isolated bundles of parallel fibers, such as in the cerebral peduncle. In regions where the degenerated pathway crosses other tracts, such as in the rostral pons, paradoxically there is almost no change in diffusion anisotropy, but a significant change in the measured orientation of fibers. The trace of the diffusion tensor is moderately increased in all affected regions. This allows one to differentiate secondary and primary fiber loss where the increase in trace is considerably higher. We show that DT-MRI is more sensitive than T2-weighted MRI in detecting Wallerian degeneration. Significant diffusion abnormalities are observed over the entire trajectory of the affected pathway in each patient. This finding suggests that mapping degenerated pathways noninvasively with DT-MRI is feasible. However, the interpretation of water diffusion data is complex and requires a priori information about anatomy and architecture of the pathway under investigation. In particular, our study shows that in regions where fibers cross, existing DT-MRI-based fiber tractography algorithms may lead to erroneous conclusion about brain connectivity.

Aged↗
PubMed2002

Virtual in vivo interactive dissection of white matter fasciculi in the human brain.

This work reports the use of diffusion tensor magnetic resonance tractography to visualize the three-dimensional (3D) structure of the major white matter fasciculi within living human brain. Specifically, we applied this technique to visualize in vivo (i) the superior longitudinal (arcuate) fasciculus, (ii) the inferior longitudinal fasciculus, (iii) the superior fronto-occipital (subcallosal) fasciculus, (iv) the inferior frontooccipital fasciculus, (v) the uncinate fasciculus, (vi) the cingulum, (vii) the anterior commissure, (viii) the corpus callosum, (ix) the internal capsule, and (x) the fornix. These fasciculi were first isolated and were then interactively displayed as a 3D-rendered object. The virtual tract maps obtained in vivo using this approach were faithful to the classical descriptions of white matter anatomy that have previously been documented in postmortem studies. Since we have been able to interactively delineate and visualize white matter fasciculi over their entire length in vivo, in a manner that has only previously been possible by histological means, "virtual in vivo interactive dissection" (VIVID) adds a new dimension to anatomical descriptions of the living human brain.

Adult↗
PubMed2002

Magnetization transfer measurements of brain structures in patients with multiple system atrophy.

To determine whether magnetization transfer imaging (MTI) demonstrates abnormalities in the brain structures of patients with multiple system atrophy (MSA), we examined 12 patients with clinically probable MSA and 11 control subjects. We calculated magnetization transfer ratios (MTRs) using region of interest analysis from MTI and assessed abnormal signal changes on T2-weighted images. MTRs of the base of the pons, middle cerebellar peduncle, putamen, and white matter of the precentral gyrus were significantly lower in the MSA patients than in the controls. Abnormal signal changes on T2-weighted images were observed in the base of the pons (n = 6), middle cerebellar peduncle (n = 7), and putamen (n = 7). MTRs of regions with abnormal signals were significantly lower than those of regions without abnormal signals and those in the controls. Even the MTRs of the regions without abnormal signals were lower than those in the controls. MTRs of the pyramidal tract, including white matter of the precentral gyrus, posterior limb of the internal capsule, cerebral peduncle, and base of the pons, were significantly lower in patients with pyramidal tract sign (n = 7) than in the controls. Patients with asymmetrical parkinsonism (n = 5) showed significantly lower MTRs in the putamen contralateral to the predominant side of parkinsonian symptoms than the ipsilateral side, although asymmetry of abnormal signal changes on T2-weighted images was not evident in more than half of those patients. This study showed that MTI demonstrates abnormalities in the brains of patients with MSA that seem to reflect underlying pathological changes and that the pathological changes detected by MTI seem to give rise to clinical symptoms. This study also showed that the abnormalities are detected more sensitively and over a larger area by MTI than by conventional magnetic resonance imaging.

Aged↗