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PubMed1995

White matter lesions and disequilibrium in older people. I. Case-control comparison.

OBJECTIVE: To investigate the relationship between subcortical white matter lesions identified on magnetic resonance imaging and gait and balance problems in older people. DESIGN: Magnetic resonance imaging scans of the brain in 27 community-dwelling older patients (> 75 years of age) who had subjective and objective abnormalities of gait and balance of unknown cause were compared with those of 27 age- and sex-matched control subjects. The T2-weighted intense lesions of the subcortical white matter were graded on a scale of 0 to 2. SETTING: Outpatient clinic. RESULTS: The patient had significantly (P < .01, chi 2) more severe subcortical white matter hyperintensities on magnetic resonance imaging than did the control group. Patients fell more frequently than did the control subjects and had slower motor responses and prolonged reaction times compared with the control subjects. CONCLUSIONS: Subcortical white matter lesions identified on magnetic resonance imaging are associated with gait and balance dysfunction in ambulatory older people. These lesions probably interfere with central processing of sensorimotor signals leading to impaired postural responses.

Aged↗
PubMed1995

White matter lesions and disequilibrium in older people. II. Clinicopathologic correlation.

OBJECTIVE: To identify the cause of subcortical white matter lesions seen on magnetic resonance imaging in older patients with progressive deterioration of gait and balance. DESIGN: Postmortem examination of three patients with objective impairment of gait and balance thought to be due to subcortical white matter lesions identified on magnetic resonance imaging. Brain sections were stained with routine methods and for glial fibrillary acid protein using an immunoperoxidase technique. PATIENTS: Part of a prospective study of gait and balance problems in older people. None had a history of hypertension or discrete strokelike episodes. RESULTS: Other than a few small infarcts in the basal ganglia and internal capsule in the patient with the mildest gait disorder, there were no gross or microscopic features on routine examination post mortem to explain the white matter hyperintensities on magnetic resonance imaging or the progressive gait deterioration. By contrast, immunohistochemical staining with anti-glial fibrillary acid protein showed prominent astrocytosis T2-weighted high-intensity signal areas on magnetic resonance imaging. CONCLUSIONS: The astrocytes presumably swell as they take up extravasated protein at the site of a breakdown in the blood-brain barrier, and the increased water content per unit volume increases the magnetic resonance imaging proton signal. We hypothesized that the astrocytes may have been initially activated by small infarcts or subclinical ischemia, but the process then became self-perpetuating, ultimately involving most of the white matter and producing the severe gait disorder.

Aged↗
PubMed1996

White matter lesions and cognitive deterioration in presymptomatic carriers of the amyloid precursor protein gene codon 693 mutation.

OBJECTIVE: To determine early manifestations of hereditary cerebral hemorrhage with amyloidosis (Dutch). DESIGN: Survey. SETTING: Neurologic outpatient department of the University Hospital Leiden in the Netherlands. PARTICIPANTS: Ten presymptomatic carriers of the amyloid precursor protein gene codon 693 mutation. MAIN OUTCOME MEASUREMENTS: Extensive neuropsychological examination and cerebral magnetic resonance imaging. RESULTS: Six subjects older than 40 years showed white matter hyperintensities on magnetic resonance imaging. Three of these six individuals had signs of cognitive deterioration. The four younger subjects (age, < 31 years) showed no abnormalities on magnetic resonance imaging or on neuropsychological examination. CONCLUSIONS: We suggest that white matter hyperintensities in hereditary cerebral hemorrhage with amyloidosis (Dutch) are probably caused by chronic ischemia due to stenosis of the meningocortical arterioles, which becomes visible on magnetic resonance imaging scans in individuals who are between the ages of 30 and 40 years. The finding of cognitive deterioration in three of 10 presymptomatic mutation carriers supports the finding that in hereditary cerebral hemorrhage with amyloidosis (Dutch), deterioration can occur without stroke. A direct relation between cognitive deterioration and white matter hyperintensities is unlikely, because only half of the individuals with white matter hyperintensities showed signs of deterioration.

Adult↗
PubMed1997

Localized proton magnetic resonance spectroscopy in patients with adult adrenoleukodystrophy. Increase of choline compounds in normal appearing white matter.

OBJECTIVES: To describe the changes in the results of magnetic resonance imaging and spectroscopy occurring in the normal-appearing white matter of patients with adult adrenoleukodystrophy and to present evidence of a particular change that may serve as a marker for the follow-up of the disease. DESIGN: Neurologic, magnetic resonance imaging, and localized proton spectroscopic examinations were performed in 11 patients with adult adrenoleukodystrophy and compared with 11 sex- and age-matched controls. PATIENTS: Eleven patients with adult adrenoleukodystrophy participated in a trial of dietary therapy with glyceryl trioleate and glyceryl trierucate (Lorenzo's oil) in the Fédération de Neurologie and the Institut National de la Santé et de la Recherche Médicale, Unité 134, at the Hôpital de la Salpêtrière in Paris, France. RESULTS: The results of magnetic resonance imaging of the white matter were normal in 2 patients and showed areas of mild symmetrical hypersignals on T2-weighted images and fluid attenuated inversion recovery sequences, localized in the posterior white matter in 9 patients. The results of spectroscopy indicated that the peak of the area of choline-containing compounds was increased at long echo times in patients with adult adrenoleukodystrophy, which may reflect very long-chain fatty acid accumulation in this disease. The peak of the area of myo-inositol-containing compounds was increased at short echo times in patients with adult adrenoleukodystrophy, which may indicate a rise in this metabolite concentration. The N-acetylaspartate-creatine amplitude ratio was significantly decreased in patients with motor deficit. The significance of this finding remains to be established. CONCLUSIONS: The results of localized proton magnetic resonance spectroscopy show abnormalities in the cerebral white matter of patients with adult adrenoleukodystrophy, which may contribute to the understanding of the pathophysiologic characteristics of the disease. Although changes in the results of spectroscopy found in this disease are not specific, the increase of choline-containing compounds may reflect the accumulation of very long-chain fatty acids in the central nervous system. Localized proton magnetic resonance spectroscopy may prove a valuable technique, in addition to magnetic resonance imaging, for noninvasive investigation of patients with adult adrenoleukodystrophy undergoing future clinical trials.

Adrenoleukodystrophy↗
PubMed2002

Assessment of normal-appearing white and gray matter in patients with primary progressive multiple sclerosis: a diffusion-tensor magnetic resonance imaging study.

BACKGROUND: Diffusion-tensor magnetic resonance imaging is sensitive to the more destructive aspects of multiple sclerosis (MS) evolution occurring outside and within T2-visible lesions and, as a consequence, holds promise for providing a more complete picture of primary progressive (PP) MS-related tissue damage than conventional magnetic resonance imaging. OBJECTIVE: To improve our understanding of PPMS by assessing the extent of occult pathological features in the normal-appearing white and gray matter of the brain using diffusion-tensor magnetic resonance imaging. METHODS: Ninety-six patients with PPMS, 47 patients with secondary progressive (SP) MS, and 44 healthy control subjects were studied. T2-hyperintense and T1-hypointense lesion volumes were calculated, and the volume of the whole brain tissue was measured. Diffusion-tensor magnetic resonance imaging scans were postprocessed and analyzed to obtain the mean diffusivity and fractional anisotropy histograms from the brain and from the normal-appearing white and gray matter in isolation. RESULTS: The mean T2-hyperintense and T1-hypointense lesion volumes were lower in patients with PPMS than in patients with SPMS, while the mean absolute brain volumes were similar in the 2 groups. The average lesion diffusivity was significantly higher in patients with SPMS than in patients with PPMS (P<.001). Histogram-derived metrics of the brain tissue and normal-appearing white and gray matter were significantly different between patients with PPMS and healthy subjects (range, P =.004 to <.001). Average diffusivity values were significantly higher in patients with SPMS than in patients with PPMS for all the tissues studied (range, P =.001 to <.001). Fractional anisotropy histogram-derived quantities did not significantly differ between the 2 patient groups (range, P =.94 to.03). CONCLUSION: This study confirms that, in patients with PPMS, normal-appearing white and gray matter are not spared by disease-related pathological processes, although they are affected to a lesser degree than in patients with SPMS.

Adult↗
PubMed2003

White matter structural integrity in healthy aging adults and patients with Alzheimer disease: a magnetic resonance imaging study.

BACKGROUND: Imaging and postmortem studies suggest that frontal lobe white matter (FLWM) volume expands until about the age of 44.6 years and then declines. Postmortem evidence indicates that the structural integrity of myelin sheaths deteriorates during normal aging, especially in late myelinating regions such as the frontal lobes. OBJECTIVES: To assess the integrity of FLWM by magnetic resonance imaging and, thus, to provide an important index of brain aging and its relationship to Alzheimer disease (AD). DESIGN: Cross-sectional study. SETTING: Two metropolitan university hospitals and AD research centers. PARTICIPANTS: Two hundred fifty-two healthy adults (127 men and 125 women), aged 19 to 82 years, and 34 subjects with AD (16 men and 18 women), aged 59 to 85 years. MAIN OUTCOME MEASURE: Calculated transverse relaxation rate (R( 2)) of the FLWM (an indirect measure of the structural integrity of white matter). RESULTS: As expected from prior imaging data on FLWM volume, the quadratic function best represented the relationship between age and the FLWM R(2) (P<.001). In healthy individuals, the FLWM R(2) increased until the age of 38 years and then declined markedly with age. The R( 2) of subjects with AD was significantly lower than that of a group of healthy control subjects who were of similar age and sex (P<.001). CONCLUSIONS: The R(2) changes in white matter suggest that the healthy adult brain is in a constant state of change, roughly defined as periods of maturation continuing into middle age followed by progressive loss of myelin integrity. Clinically diagnosed AD is associated with more severe myelin breakdown. Noninvasive measures, such as the determination of the R(2), may have the potential to track prospectively the trajectory of deteriorating white matter integrity during normal aging and the development of AD and, thus, may be a useful marker for medication development aimed at the prevention of AD.

Adult↗
PubMed2005

Metabolite changes in normal-appearing gray and white matter are linked with disability in early primary progressive multiple sclerosis.

BACKGROUND: Abnormalities in normal-appearing brain tissues may contribute to disability in primary progressive multiple sclerosis (PPMS), where few lesions are seen on conventional imaging. OBJECTIVES: To evaluate the mechanisms underlying disease progression in the early phase of PPMS by measuring metabolite concentrations in normal-appearing white matter (NAWM) and cortical gray matter (CGM) and to assess their relationship with clinical outcomes. DESIGN: Case-control study. SETTING: Tertiary referral hospital. Patients Forty-three consecutive patients within 5 years of onset of PPMS and 44 healthy control subjects. MAIN OUTCOME MEASURES: Concentrations of choline-containing compounds, phosphocreatine, myo-inositol, total N-acetyl-aspartate (tNAA), and glutamate-glutamine were estimated using proton magnetic resonance spectroscopic imaging. Brain parenchymal, white matter and gray matter fractions and proton density and gadolinium-enhancing lesion loads were calculated. The Expanded Disability Status Scale and Multiple Sclerosis Functional Composite scores were recorded. RESULTS: In CGM, concentrations of the tNAA (P<.001) and glutamate-glutamine (P = .005) were lower in patients with PPMS than in controls. In NAWM, myo-inositol levels were higher (P = .002) and tNAA levels were lower (P = .005) in patients with PPMS than in controls. The Expanded Disability Status Scale score correlated with the tNAA concentration in CGM (r = -0.44; P = .03) and with myo-inositol (r = 0.41; P = .01) and glutamate-glutamine concentrations (r = 0.41; P = .01) in NAWM. Proton density lesion load correlated negatively with CGM tNAA concentration and positively with NAWM myo-inositol concentration. CONCLUSION: Metabolite changes, which differ in CGM and NAWM, occur in early PPMS and are linked with disability.

Adult↗
PubMed2005

Deep white matter pathologic features in watershed regions: a novel pattern of central nervous system involvement in MELAS.

BACKGROUND: Myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome typically manifests in adults younger than 40 years with encephalopathy, stroke-like episodes, and lactic acidosis. Magnetic resonance imaging (MRI) abnormalities typically involve the cortical gray and the adjacent subcortical white matter. OBJECTIVE: To describe a 58-year-old woman diagnosed with MELAS who was initially seen with acute myopathy, cardiac ischemia, psychosis, and MRI changes in a watershed distribution. RESULTS: Initial MRI of the brain showed the characteristic parieto-occipital gray matter lesions involving the adjacent white matter. Follow-up MRI revealed striking deep white matter involvement in a watershed distribution. A cerebral angiogram and thorough hypercoagulable workup results were normal. Electromyography showed acute denervation and myopathy. A muscle biopsy specimen revealed ragged red and cytochrome-c oxidase-negative fibers. Mitochondrial DNA analysis revealed an A3243G mutation. CONCLUSIONS: Myopathy, encephalopathy, lactic acidosis, and stroke-like episodes should be considered in older patients with myopathy, cardiomyopathy, encephalopathy, and unaccountable MRI findings. Watershed pathologic features are a rare pattern of cerebral involvement in MELAS.

Acute Disease↗
PubMed2005

Prediction of longitudinal brain atrophy in multiple sclerosis by gray matter magnetic resonance imaging T2 hypointensity.

BACKGROUND: Gray matter magnetic resonance imaging T2 hypointensity, a marker of iron deposition, is associated with clinical impairment and brain atrophy in cross-sectional studies of multiple sclerosis. Treatment with intramuscular interferon beta-1a limits brain atrophy in the second year of treatment. OBJECTIVE: To test whether T2 hypointensity predicts brain atrophy and whether interferon affects this relationship. DESIGN: Post hoc analysis. SETTING: A multicenter treatment trial conducted at tertiary care comprehensive multiple sclerosis centers. Patients Patients with multiple sclerosis who took part in a 2-year clinical trial in which they received intramuscular interferon beta-1a (30 mug/wk) or placebo. MAIN OUTCOME MEASURES: Deep gray matter T2 hypointensity, brain parenchymal fraction (BPF), and total T2, gadolinium-enhancing, and T1 lesion volumes. RESULTS: T2 hypointensity in various gray matter areas correlated with baseline BPF (r = 0.19-0.39; P = .001-.03). In placebo-treated patients (n = 68), baseline T2 hypointensity predicted the change in BPF in the first year and throughout 2 years (r = 0.26-0.42; P<.001-.03). T2 hypointensity was chosen in regression modeling as the best predictor of BPF change at the 1-year (R(2) = 0.23; P = .002) and 2-year (R(2) = 0.33; P<.001) time points after accounting for all magnetic resonance imaging variables. In the interferon group (n = 65), no relationship existed between baseline T2 hypointensity and BPF change. CONCLUSIONS: Gray matter T2 hypointensity predicts the progression of brain atrophy in placebo- but not interferon beta-1a-treated patients. This predictive effect is seen as early as the first year. We hypothesize that interferon beta may exert its effect on brain atrophy in part by reducing a cascade of events that involve iron deposition as a mediator of neurotoxicity or as a disease epiphenomenon.

Adult↗
PubMed1995

Magnetic resonance imaging and mood disorders. Localization of white matter and other subcortical abnormalities.

BACKGROUND: Recent reports in the literature document an association between focal white matter abnormalities in bipolar as well as unipolar mood disorder. The importance of this finding and other associated anatomic differences is uncertain. METHODS: We examined the volume of abnormal white matter and other brain volumes using quantitative magnetic resonance imaging analysis. We explored the relationship of these variables with diagnosis, cognitive function, and clinical variables in 36 patients with bipolar disorder, 30 patients with unipolar disorder, and 26 control subjects who were free from significant medical and neurologic illness. RESULTS: Younger patients with bipolar disorder (but not similarly aged patients with unipolar disorder or controls) have an increased volume of abnormal white matter. Data also indicate that the total volume of abnormal white matter may be associated with increased cognitive impairment, increased rate of psychiatric illness in the family, and onset after adolescence. CONCLUSION: Patients with bipolar disorder demonstrate a pattern of subcortical brain morphologic abnormalities and cognitive impairment.

Adult↗
PubMed1998

A controlled study of cortical gray matter and ventricular changes in alcoholic men over a 5-year interval.

BACKGROUND: We report on structural brain changes during a 5-year period in healthy control and alcoholic men. METHODS: Alcoholic patients (n = 16), from an initial group of 58 who underwent brain magnetic resonance imaging scanning while in treatment, were rescanned with the same acquisition sequence approximately 5 years later. Control subjects (n = 28) spanning the same age range also were scanned twice at a comparable interval. Changes in brain volume were corrected for error due to differences in head placement between scans and expressed as slopes (cubic centimeters per year), percentage of change over baseline for the control subjects, and standardized change for the alcoholic patients. The alcoholic patients varied considerably in the percentage of time that symptoms of alcohol dependence were present and in the amount of alcohol consumed during follow-up. RESULTS: The cortical gray matter diminished in volume over time in the control subjects, most prominently in the prefrontal cortex, while the lateral and third ventricles enlarged. The alcoholic patients showed similar age-related changes with a greater rate of gray matter volume loss than the control subjects in the anterior superior temporal lobe. The amount of alcohol consumed during follow-up predicted the rate of cortical gray matter volume loss, as well as sulcal expansion. The rate of ventricular enlargement in alcoholic patients who maintained virtual sobriety was comparable to that in the control subjects. CONCLUSIONS: During a 5-year period, brain volume shrinkage is exaggerated in the prefrontal cortex in normal aging with additional loss in the anterior superior temporal cortex in alcoholism. The association of cortical gray matter volume reduction with alcohol consumption over time suggests that continued alcohol abuse results in progressive brain tissue volume shrinkage.

Aging↗
PubMed2002

Ischemic basis for deep white matter hyperintensities in major depression: a neuropathological study.

BACKGROUND: White matter hyperintensities on magnetic resonance imaging are increased in major depression in the deep white matter, especially in frontal areas. These lesions have been hypothesized to be ischemic in origin, but there have been no previous neuropathological studies in depression. We investigated the neuropathological basis of these lesions in depression, hypothesizing that they would be more frequently ischemic in origin in depressed subjects. METHODS: We carried out in vitro magnetic resonance imaging on 3 slices of brain tissue (2 frontal, 1 occipital) from 20 elderly subjects who had a history of major depression and 20 elderly controls. The films were blindly rated, and sections were prepared for neuropathological analysis from the same slices and stained conventionally and by means of immunohistochemistry for microglia, macrophages, and astroglia. Lesions on the films were identified in the tissue, blindly described neuropathologically, and subsequently divided into ischemic and nonischemic lesions. RESULTS: All the deep white matter hyperintensities in the depressed group were found to be ischemic, compared with less than a third of those in the control group, a highly significant difference (P<.001). This difference was due to smaller punctate lesions (<3 mm), which were predominantly ischemic in depressed subjects but not in control subjects. Larger lesions were usually ischemic in both groups. Compared with control subjects, ischemic lesions were significantly more likely to be in the dorsolateral prefrontal cortex compared with the anterior cingulate cortex (P =.003) and the occipital cortex (P =.01) in the depressed subjects. CONCLUSIONS: Deep white matter hyperintensities are more frequently due to cerebral ischemia, and such ischemic lesions are more frequently located at the level of dorsolateral prefrontal cortex in depressed subjects. Our findings strongly support the "vascular depression" hypothesis of late-life depression.

Age Factors↗
PubMed2004

Pathways that make voices: white matter changes in auditory hallucinations.

BACKGROUND: The origin of auditory hallucinations, which are one of the core symptoms of schizophrenia, is still a matter of debate. It has been hypothesized that alterations in connectivity between frontal and parietotemporal speech-related areas might contribute to the pathogenesis of auditory hallucinations. These networks are assumed to become dysfunctional during the generation and monitoring of inner speech. Magnetic resonance diffusion tensor imaging is a relatively new in vivo method to investigate the directionality of cortical white matter tracts. OBJECTIVE: To investigate, using diffusion tensor imaging, whether previously described abnormal activation patterns observed during auditory hallucinations relate to changes in structural interconnections between the frontal and parietotemporal speech-related areas. METHODS: A 1.5 T magnetic resonance scanner was used to acquire twelve 5-mm slices covering the Sylvian fissure. Fractional anisotropy was assessed in 13 patients prone to auditory hallucinations, in 13 patients without auditory hallucinations, and in 13 healthy control subjects. Structural magnetic resonance imaging was conducted in the same session. Based on an analysis of variance, areas with significantly different fractional anisotropy values between groups were selected for a confirmatory region of interest analysis. Additionally, descriptive voxel-based t tests between the groups were computed. RESULTS: In patients with hallucinations, we found significantly higher white matter directionality in the lateral parts of the temporoparietal section of the arcuate fasciculus and in parts of the anterior corpus callosum compared with control subjects and patients without hallucinations. Comparing patients with hallucinations with patients without hallucinations, we found significant differences most pronounced in the left hemispheric fiber tracts, including the cingulate bundle. CONCLUSION: Our findings suggest that during inner speech, the alterations of white matter fiber tracts in patients with frequent hallucinations lead to abnormal coactivation in regions related to the acoustical processing of external stimuli. This abnormal activation may account for the patients' inability to distinguish self-generated thoughts from external stimulation.

Adult↗
PubMed1997

Glutamate-positive neurons and terminals in the cat periaqueductal gray matter (PAG): a light and electron microscopic immunocytochemical study.

The morphology, distribution, proportion, size, and synaptic organization of periaqueductal gray matter neurons labeled with immunocytochemical techniques by an anti-glutamate (Glu) polyclonal serum were investigated in six adult cats (PAG-GLU 1-6). At the light microscopic level, numerous Glu-positive neurons were found throughout each subdivision of the periaqueductal gray matter. Their proportion and size, calculated in semi-thin sections (1-microm-thick), varied slightly among the subdivisions of the periaqueductal gray matter. The morphology of Glu-positive neurons was similar to that of the multipolar, triangular, and fusiform cells described in previous Golgi studies. Numerous puncta, interpreted as dendrites, axons, and axon terminals were also present in all subdivisions without preferential distribution. At the electron microscopic level, all synaptic contacts made by Glu-positive axon terminals were of the asymmetric type, but not all presynaptic elements making asymmetric synapses were labeled. The vast majority of postsynaptic elements contacted by Glu-positive axon terminals were labeled and unlabeled dendrites. The present results describe for the first time the presence of both Glu-positive neurons and terminals in the feline periaqueductal gray matter and provide further evidence that Glu is the probable neurotransmitter of numerous excitatory neurons of this structure.

Animals↗
PubMed1997

Identification of transient microglial cell colonies in the forebrain white matter of developing rats.

Herein, we describe the existence of distinct colonies of transient microglial cells that reside in well-defined zones of the forebrain white matter. Rats, aged at postnatal day (P) 0, P2, P5, P7, P10, P15 or adult, were anaesthetised with halothane gas, and various neural centres were injected unilaterally with the tracer biotinylated Dextran. The neural centres injected were cingulate or sensorimotor cortices, ventral nuclei of the dorsal thalamus, and the pontine reticular formation of the brainstem. Rats were allowed to survive to various stages, from 4 hours to 21 days, after the injection. They were then anaesthetised with sodium pentobarbitone, and their brains were aldehyde-fixed and processed by using standard methods. The following is a description of what is seen after injections at P0, P2, P5, P7, P10; we saw no labelled cells (described below) in the rats injected at P15 or adult. From 2 to 21 days after an injection of dextran into the above-mentioned centres, labelled microglial cell colonies, identified by using double-labelling with anti-OX-6 or Griffonia simplicifolia (Bandeiraea; isolectin B4), were seen in small isolated zones in the forebrain white matter. These colonies were in the corpus callosum, the dorsal and ventral regions of the external capsule, and the internal capsule. A striking feature of these labelled microglial cell colonies was that they were seen on both sides of the brain. Thus, regardless of the location of the injection site in either the cortex, thalamus, or brainstem, the same microglial cell colonies were labelled with dextran in the forebrain white matter. After injections of different coloured fluorescent dextrans into the cortex and into the brainstem of the same animal, many double-labelled cells in each of the colonies were seen. From our short-term survival cases (4 hours to 1 day), a rather strict sequence or progression of labelling of the colonies across the white matter from the injection site was seen; in general, the microglial cell colonies closest to the injection site became labelled well before (about a day) those further away. These results lead us to suggest that the microglial cells in each colony become labelled after a slow diffusion of the tracer through the extracellular space from the injection site.

Aging↗
PubMed1997

Grid-mapped freeze-fracture analysis of gap junctions in gray and white matter of adult rat central nervous system, with evidence for a "panglial syncytium" that is not coupled to neurons.

In white matter regions of the brain and spinal cord of adult mammals, gap junctions previously were observed linking astrocytes to astrocytes, as well as to oligodendrocytes and ependymacytes. The resulting "functional syncytium" was proposed to modulate the ion fluxes that occur during electrical activity of the associated axons. Gap junctions also have been reported linking neurons with glia, and functional neuronal-glial coupling has been postulated. To investigate the glial syncytium and the neuron-to-glial coupling hypotheses, we used "grid-mapped freeze fracture," conventional thin-section electron microscopy, and light microscope immunocytochemistry to examine and characterize neurons and glia in gray and white matter of adult rat brain and spinal cord. We have obtained quantitative evidence for the abundance and widespread distribution of gap junctions interlinking the three primary types of macroglia throughout both gray and white matter of the mammalian central nervous system (CNS), thereby extending the concept to that of a functional panglial syncytium. In contrast to previous reports, we show that of more than 400 gap junctions in which both participating cells were identified, none were between neurons and glia. Thus, neuronal coupling and glial coupling involved separate and distinct pathways. Finally, putative water channels (i.e., "square arrays") were confirmed to be abundant and in close association with gap junctions in astrocytes and ependymacytes. Because the astrocyte "intermediaries" extend cytoplasmic conduits throughout gray and white matter of brain and spinal cord, from the ependymal layer to the pia-glial limitans, and from oligodendrocytes surrounding axons to astrocyte endfeet surrounding capillaries, the proposed panglial syncytium, with its abundance of water channels and intercellular ion channels, is optimally positioned and equipped to modulate water and ion fluxes across broad regions of the CNS.

Animals↗
PubMed2000

Development, neurochemical properties, and axonal projections of a population of last-order premotor interneurons in the white matter of the chick lumbosacral spinal cord.

There is general agreement that last-order premotor interneurons-a set of neurons that integrate activities generated by the spinal motor apparatus, sensory information and volleys arising from higher motor centres, and transmit the integrated signals to motoneurons through monosynaptic contacts-play crucial roles in the initiation and maintenance of spinal motor activities. Here, we demonstrate the development, neurochemical properties, and axonal projections of a unique group of last-order premotor interneurons within the ventrolateral aspect of the lateral funiculus of the chick lumbosacral spinal cord. Neurons expressing immunoreactivity for neuron-specific enolase were first detected in the ventrolateral white matter at embryonic day 9 (E9). The numbers of immunoreactive neurons were significantly increased at E10-E12, while most of them were gradually concentrated in small segmentally arranged nuclei (referred to as major nuclei of Hofmann) protruding from the white matter in a necklace like fashion dorsal to the ventral roots. The major nuclei of Hofmann became more prominent at E12-E16, but substantial numbers of cells were still located within the ventrolateral white matter (referred to as minor nucleus of Hofmann). The distribution of immunoreactive neurons achieved by E16 was maintained during later developmental stages and was also characteristic of adult animals. After injection of Phaseolus vulgaris-leucoagglutinin unilaterally into the minor nucleus of Hofmann, labeled fibres were detected in the ventrolateral white matter ipsilateral to the injection site. Ascending and descending fibres were revealed throughout the entire rostro-caudal length of the lumbosacral spinal cord. Axon terminals were predominantly found within the lateral motor column and the ventral regions of lamina VII ipsilateral to the injection site. Several axon varicosities made close appositions with somata and dendrites of motoneurons, which were identified as synaptic contacts in a consecutive electron microscopic study. With the postembedding immunogold method, 21 of 97 labeled terminals investigated were immunoreactive for glycine and 2 of them showed immunoreactivity for gamma-aminobutyric acid (GABA). The axon trajectories of neurons within the minor nucleus of Hofmann suggest that some of these cells might represent a population of last-order premotor interneurons. J. Exp. Zool. 286:157-172, 2000.

Animals↗
PubMed1996

Predilection of brain metastasis in gray and white matter junction and vascular border zones.

BACKGROUND: The purpose of this study was to asses the importance of the vascular border zone and the gray and white matter junction on the distribution of brain metastases. METHODS: We reviewed the medical records, computed tomography (CT) of magnetic resonance imaging (MRI) of 105 patients with secondary brain tumors. The metastatic lesions noted on CT scans of MRI ere matched with a predetermined standard sheet containing axial images with shading on the border zones. To be included in the border zones, the center on more than 50% of the lesion had to be situated within these zones. RESULTS: Among 100 evaluable patients, there were 302 metastatic brain lesions. Of the 302 lesions, 210 lesions were 2 cm or smaller in greatest dimension and located in the cerebral and cerebellar hemispheres. The major vascular border zones were the site of predilection for 103 lesions (62%) although the border zones constitute only 29% of the area. Gray and white matter junction was the preferred site for 135 lesions (64%). CONCLUSION: The results demonstrated that brain metastasis occurs in the vascular border zone regions and the gray and white matter junction more frequently than previously recognized, and also supported the notion that metastatic emboli tend to lodge in an area of sudden reduction of vascular caliber (gray/white matter junction) and in the area most distal vascular field (border zone).

Adult↗