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Increased complement biosynthesis by microglia and complement activation on neurons in Huntington's disease.

In this study complement activation and biosynthesis have been analysed in the brains of Huntington's disease (HD) (n = 9) and normal (n = 3) individuals. In HD striatum, neurons, myelin and astrocytes were strongly stained with antibodies to C1q, C4, C3, iC3b-neoepitope and C9-neoepitope. In contrast, no staining for complement components was found in the normal striatum. Marked astrogliosis and microgliosis were observed in all HD caudate and the internal capsule samples but not in normal brain. RT-PCR analysis and in-situ hybridisation were carried out to determine whether complement was synthesised locally by activated glial cells. By RT-PCR, we found that complement activators of the classical pathway C1q C chain, C1r, C4, C3, as well as the complement regulators, C1 inhibitor, clusterin, MCP, DAF, CD59, were all expressed constitutively and at much higher level in HD brains compared to normal brain. Complement anaphylatoxin receptor mRNAs (C5a receptor and C3a receptor) were strongly expressed in HD caudate. In general, we found that the level of complement mRNA in normal control brains was from 2 to 5 fold lower compared to HD striatum. Using in-situ hybridisation, we confirmed that C3 mRNA and C9 mRNA were expressed by reactive microglia in HD internal capsule. We propose that complement produced locally by reactive microglia is activated on the membranes of neurons, contributing to neuronal necrosis but also to proinflammatory activities. Complement opsonins (iC3b) and anaphylatoxins (C3a, C5a) may be involved in the recruitment and stimulation of glial cells and phagocytes bearing specific complement receptors.

Adult↗

Asymmetries of visual attention after circumscribed subcortical vascular lesions.

OBJECTIVE: To investigate the role of the basal ganglia and the thalamus for basic processes of visuospatial attention METHODS: Fifteen patients with acute circumscribed vascular lesions (10 with haemorrhage and five with infarction) were included in the study. The lesions were confined exclusively to subcortical structures, such as the basal ganglia, internal capsule, and thalamus, which was confirmed by initial CT on the day of referral and MRI taken 14-28 days after clinical onset. These patients were examined with two computerised attentional tasks (one detection and one search task) measuring spatial visual attention. RESULTS: There was a clear attentional asymmetry in patients with right hemispheric lesions (RHLs) in the visual search task. Seven out of eight patients with RHLs tended to be slower and/or missed significantly more target stimuli in the left sided part of a stimulus array consisting of 25 small squares than in right sided parts, although none of these patients showed signs of visual hemineglect in the visual detection task presenting visual information simultaneously to the right and left visual hemispace. All but one of these patients showed lesions in the posterior limb of the internal capsule and the putamen. On the other hand, patients with left hemispheric lesions were not impaired in the search task with only one patient showing more contralesional omissions of target stimuli than could be expected from the behaviour of normal controls. CONCLUSIONS: The results are in line with previous results showing a dominant role of right hemispheric neuronal structures for spatial attention. Furthermore, the data suggest that even with right hemispheric subcortical lesions without cortical involvement deficits in spatial orienting of attention to the left hemispace can be seen. These asymmetries of visual attention in the absence of neglect symptoms are supposed to be caused (1) by a disruption of the motor corticostriato-pallidothalamo-cortical neuronal circuit or (2) by a (partial) disconnection of relevant parts within the posterior attention network-namely, parietal and thalamic structures.

Adult↗

Improved functional outcome in patients with hemorrhagic stroke in putamen and thalamus compared with those with stroke restricted to the putamen or thalamus.

BACKGROUND AND PURPOSE: We analyzed the effect of late intensive inpatient rehabilitation on the functional outcome of patients with subcortical hemorrhagic stroke. METHODS: Patients who were nonambulatory with hemorrhagic stroke in the internal capsule and putamen (n=55), the thalamus (n=24), or all 3 regions (n=15) underwent intensive inpatient rehabilitation. Patients with surgical intervention or an episode of ventricular hemorrhage were excluded. Lesion location was evaluated by MRI 4 months after the ictus. RESULTS: Demographic data, initial disability, and impairment measures were comparable in the 3 groups. Functional outcome demonstrated significant differences in mobility subscores (P<0.05) of the Functional Independence Measure such that patients with injury in the 3 regions were more likely to ambulate independently than were patients in the other groups. Lesion location data demonstrated that the ventral anterior nucleus of the thalamus was always spared; the ventral posterior (lateral and medial) nucleus was always damaged, and the ventral lateral nucleus was frequently damaged. Putaminal damage always included the postcommissural area. In addition, the entire posterior half limb of the internal capsule was always damaged. CONCLUSIONS: Subcortical lesions to multiple structures in the basal ganglia-thalamocortical motor circuits permitted enhanced motor recovery. Lesion location predicted the level of independent ambulation and the rate of recovery in patients with stroke who were nonambulatory before neurorehabilitation therapy.

Aged↗

The early development of thalamocortical and corticothalamic projections in the mouse.

The initial ingrowth of corticothalamic and thalamocortical projections was examined in mice at embryonic and perinatal stages. Fibers, in fixed brains, were labeled with the carbocyanine dye 1, 1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocianine perchlorate (DiI). By E13, the corticofugal fibers had entered the lowest intermediate zone through which they ran, turned over the corpus striatum, and left the cortex. The fibers were arranged in scattered bundles throughout the corpus striatum. At E14 corticofugal axons reached the internal capsule and at E14.5-E15 they established contact within the thalamus. Meanwhile, the thalamocortical afferents reached the neocortex at E13. At this time fibers ran tangentially within the intermediate zone, immediately underneath the cortical plate. By E14, the fibers had started to invade the subplate and, by E15, thalamocortical fibers had begun their radial growth into the cortex. Such radial growth proceeded steadily, invading each cortical layer as it differentiated cytoarchitectonically from the dense cortical plate. The first retrogradely labeled cells were detected at the cortical plate at E15. By the day of birth (E20), thalamocortical fibers had formed a dense branching system within layers VI and V. Our observations indicate that, in mice, the thalamic axons reach the cortex before corticothalamic projections enter the thalamic nuclei. Moreover, the results suggest that the pathway followed by each fiber system is different. By DiI injections into the internal capsule we have also determined that subplate cells are the first to send axons to the thalamus.

Animals↗

Embryonic development of connections in turtle pallium.

We are interested in similarities and conserved mechanisms in early development of the reptilian and mammalian thalamocortical connections. We set out to analyse connectivity in embryonic turtle brains (Pseudemys scripta elegans, between stages 17 and 25), by using carbocyanine dye tracing. From the earliest stages studied, labelling from dorsal and ventral thalamus revealed backlabelled cells among developing thalamic fibres within the lateral forebrain bundle and striatum, which had similar morphology to backlabelled internal capsule cells in embryonic rat (Molnár and Cordery, 1999). However, thalamic crystal placements did not label cells in the dorsal ventricular ridge (DVR) at any stage examined. Crystal placements into both dorsal and lateral cortex labelled cells in the DVR and, reciprocally, DVR crystal placements labelled cells in the dorsal and lateral cortices. Retrograde labelling revealed that thalamic fibres arrive in the DVR and dorsal cortex by stage 19. The DVR received projections from the nucleus rotundus and the dorsal cortex exclusively from the perirotundal complex (including lateral geniculate nucleus). Thalamic fibres show this remarkable degree of specificity from the earliest stage we could examine with selective retrograde labelling (stage 19). Our study demonstrates that axons of similar cells are among the first to reach dorsal and ventral thalamus in mammals and reptiles. Our connectional analysis in turtle suggests that some cells of the mammalian primitive internal capsule are homologous to a cell group within the reptilian lateral forebrain bundle and striatum and that diverse vertebrate brains might use a highly conserved pattern of early thalamocortical development.

Animals↗

[A case of aortitis syndrome associated with hypertensive intracranial hemorrhage (author's transl)].

A case of aortitis syndrome associated with hypertensive intracranial hemorrhage is reported. A 38-year-old female was admitted in 1980 suffering from hypertension and blood pressure difference between the left and right arms which had existed for 10 years. Two weeks prior to admission, she noticed weakness and numbness of the right arm and leg. She was orientated and alert at the time of admission. Her right upper and lower extremities could not function with full strength against resistance. Also, right hemihypesthesia and hemiparesthesia were present. Left arm systolic blood pressure was 195 mmHg. Her pulse was palpable in both radial arteries. CT scans revealed a small high density area in the posterior crus of the internal capsule with a slight mass effect. There was no ventricular dilatation. She was given conservative treatment, such as with antihemorrhagic and antihypertensive drugs, and was discharged with good recovery after three months. Various studies were performed during her hospital stay. Based on angiographic findings, the most probable diagnosis was an extensive type of aortitis syndrome. Hypertension resulted from narrowing of the abdominal aorta and the right renal artery. Pulmonary scintiscanning using 99mTc-macroaggregated albumin revealed that her pulmonary arteries were also involved. Aortitis syndrome is not infrequent, but intracranial hemorrhage following after aortitis syndrome is rare. This may be because the carotid artery is involved in a high incidence of such cases, and therefore the intracranial blood flow is disturbed in most cases. Although the left common carotid artery was involved in the subject case, hypertensive intracranial hemorrhage occurred in the left posterior crus of the internal capsule. In a case of aortitis syndrome, therapy resulting in recirculation to the carotid artery involved is generally carried out in order to improve poor intracranial blood flow. However, it is suggested that control of blood pressure is necessary to prevent intracranial hemorrhage in aortitis syndrome.

Adult↗

Glial activation and white matter changes in the rat brain induced by chronic cerebral hypoperfusion: an immunohistochemical study.

Activation of glial cells and white matter changes (rarefaction of the white matter) induced in the rat brain by permanent bilateral occlusion of the common carotid arteries were immunohistochemically investigated up to 90 days. One day after ligation of the arteries, expression of the major histocompatibility complex (MHC) class I antigen in microglia increased in the white matter including the optic nerve, optic tract, corpus callosum, internal capsule, anterior commissure and traversing fiber bundles of the caudoputamen. After 3 days of occlusion, MHC class I antigen was still elevated and in addition MHC class II antigen and leukocyte common antigen were up-regulated in the microglia in these same regions. Astroglia, labeled with glial fibrillary acidic protein, increased in number in these regions after 7 days of occlusion. A few lymphocytes, labeled with CD4 or CD8 antibodies, were scattered in the neural parenchyma 1 h after occlusion. Activation of glial cells and infiltration of lymphocytes persisted after 90 days of occlusion in the white matter and the retinofugal pathway. However, cellular activation and infiltration in microinfarcts of the gray matter was less extensive and was substantially diminished 30 days after occlusion. The white matter changes were most intense in the optic nerve and optic tract, moderate in the medial part of the corpus callosum, internal capsule and anterior commissure, and slight in the fiber bundles of the caudoputamen. These results indicated that chronic cerebral hypoperfusion induced glial activation preferentially in the white matter. This activation seemed to be an early indicator of the subsequent changes in the white matter.

Animals↗

[beta-Endorphin and monoamine metabolite concentrations in patients with intractable pain--changes before and after deep brain or spinal dorsal column stimulation].

Baseline concentrations of beta-endorphin (beta-EP) and monoamine metabolites (MHPG: 3-methoxy-4-hydroxy-phenylglycol, HVA: homovanillic acid, 5-HIAA: 5-hydroxyindoleacetic acid) in lumbar CSF (LCSF) and ventricular CSF (VCSF) were measured in 18 patients with intractable pain; 10 with deafferented pain and 8 with peripheral pain. Control values were obtained from 37 individuals of various ages. Changes in the concentrations of these substances were determined before and after giving stimulations (2-5 V, 0.2-0.5 msec, 40-50 Hz, 20-sec duration) to 6 patients through electrodes implanted in deep brain structures (DBS; posterior limb of the internal capsule in 5 patients and rostral mesencephalic lemniscus medialis in one patient), and to 2 other patients through electrodes implanted in the spinal dorsal column (DCS). The control value of beta-EP in LCSF was 57.6 +/- 24.7 pg/ml, which was not significantly different from that of VCSF. Great variation in the individual control LCSF beta-EP concentrations was found, but it was not related to differences in age. The mean baseline LCSF beta-EP concentration was significantly higher (p less than 0.05) than the control in the patients with deaffernted pain before stimulation. One of the monoamine-metabolites, MHPG, showed higher level in the patients with peripheral pain (p less than 0.01). The LCSF beta-EP concentration was not affected by deep brain stimulation, but was increased by dorsal column stimulation. In one patient with excellent pain relief by stimulation of the posterior limb of the internal capsule, the LCSF HVA and 5-HIAA concentrations were conspicuously increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The insular lobe: physiopathological and surgical considerations.

OBJECTIVE: Surgery of the insula represents a technical challenge, because of the proximity of the internal capsule to the lenticulostriate arteries and the lack of certainty concerning its functionality. Using intraoperative direct cerebral stimulation, combined with neuronavigation, the authors operated on 12 insular gliomas. On the basis of this experience, the physiopathological and surgical implications are discussed. METHODS: A low-grade insular glioma, revealed by seizures, was diagnosed in 12 right-handed patients with a normal neurological status. Preoperative magnetic resonance imaging showed that, according to Yasargil's classification system, three patients harbored Type 3 lesions and nine patients had Type 5 lesions (10 tumors on the right side and 2 on the left dominant side). All patients underwent surgery using direct cerebral stimulation, under general anesthesia in nine patients (motor mapping) and under local anesthesia in three patients (sensorimotor and language mapping). Ultrasonography and/or neuronavigation was used in all cases. Preoperative angio-computed tomographic scanning showed the lenticulostriate arteries in two patients. RESULTS: The internal capsule was systematically detected, and the language areas were identified within the left insula in the awake patients. The lenticulostriate arteries were seen in two patients. Seven patients presented an immediate postoperative deficit; six of them recovered completely within 3 months. Four resections were total, six were subtotal, and two were partial (left insula). CONCLUSION: The use of intraoperative direct cerebral stimulation and neuronavigation allows surgery of the insula with minimization of the risk of sequelae, but its use is still limited with regard to the dominant hemisphere, owing to the essential role of this structure in language.

Adult↗

Patterns of antigenic expression in the thalamic reticular nucleus of developing rats.

The present study describes the development of the thalamic reticular nucleus in rats with the use of Nissl staining and antibodies to parvalbumin and pro-alpha-thyrotropin-releasing hormone (alpha TRH). Two major subdivisions of the reticular nucleus are apparent: 1) the main body, which is itself heterogeneous and lies for the most part between the fibres of the internal capsule and external medullary lamina, and 2) the perireticular nucleus, which lies lateral to the main body and medial to the globus pallidus. In the main body of the reticular nucleus of adults, most cells in all regions are immunoreactive to parvalbumin and alpha TRH. During development there are two waves of parvalbumin and alpha TRH expression. The first wave occurs between postnatal day (P) 0 and P10, and labelled cells are apparent in rostrolateral areas of the main body of the nucleus only. At P10, such cells are not apparent. From P7 to adult, there is a second wave of parvalbumin and alpha TRH expression: labelled cells emerge first in central, then in caudal, and finally in rostral areas of the nucleus. In adults, the perireticular nucleus is made up of a few small cells which are immunostained for parvalbumin and alpha TRH. These cells are more frequent in areas of the internal capsule adjacent to the ventral regions of the main body of the reticular nucleus, rostrodorsal to the entopeduncular nucleus. From E (embryonic day) 17 to about P10, the perireticular nucleus consists of a surprisingly large population of neurones, many of which are parvalbumin and alpha TRH immunoreactive. By about P10, as in adults, there are few perireticular cells.

Aging↗

Induction of NADPH-diaphorase activity in the forebrain in a model of intracerebral hemorrhage and its inhibition by the traditional Chinese medicine complex Nao Yi An.

Induction of NADPH-diaphorase (NDP) activity in the rat cerebral cortex was studied after autologous blood injection into the internal capsule as experimental model of intracerebral hemorrhage. The potential inhibitory effect on NDP induction by Nao Yi An (NYA), a complex derived from materials of animal and plant origin used in the treatment of intracerebral hemorrhage in traditional Chinese medicine, was also investigated. In animals without therapeutic treatment 2 and 4 days after injection of autologous blood, NDP activity was highly induced in pyramidal neurons in the neocortex, piriform, and entorhinal cortices, in astrocytes and in phagocytes in the hematoma and the area surrounding it, as well as in the subcortical white matter, and in endothelial cells in both the cortex and subcortical white matter bilaterally. Oral administration of NYA failed to inhibit NDP induction in endothelial cells but demonstrated a strong inhibitory effect on NDP activity induced in pyramidal neurons and astrocytes. NDP induction in phagocytes was also inhibited by the administration of NYA. Altogether the present results suggest that intracerebral hemorrhage in the internal capsule may induce nitric oxide synthase activity in different cell populations in the cortex and that administration of NYA can selectively inhibit such induction and, thus, potentially play a neuroprotective role.

Animals↗

Proton magnetic resonance spectroscopic changes of the primary motor cortex and supplementary motor area in hemiparetic patients with corticospinal tract injury due to deep intracerebral hematoma.

This study was conducted to investigate the metabolic changes in the motor and motor association cortices following axonal injury in the internal capsule that was caused by deep intracerebral hematoma. Using proton magnetic resonance spectroscopy (1H MRS), the authors studied the primary motor cortices (M-1) and supplementary motor areas (SMA) of 9 hemiparetic patients with documentable hemiparesis of varying severity, and we studied 10 normal volunteers as controls. To measure the M-1 and SMA biochemical changes, 4 separate single volumes of interest (VOIs) were located bilaterally in the affected and unaffected hemisphere (AH and UH). 1H MRS provided a neuronal and axonal viability index by measuring levels of N-acetylaspartate (NAA) and creatine/phosphocreatine (Cr). The M-1/SMA NAA/Cr ratios of the AH and UH in patients, and the AH and normal volunteers were compared. The NAA/Cr ratios of the M-1 and SMA in AH, and the SMA in UH were significantly lower than those of normal volunteers. These 1H MRS findings indicate that axonal injury in the descending motor pathway at the level of internal capsule could induce metabolic changes in the higher centers of the motor pathway.

Adult↗

[MR findings of the pyramidal tract in amyotrophic lateral sclerosis].

MR imaging using the conventional spin each technique along with diffusion weighted imaging and water-fat imaging was performed in 16 patients with amyotrophic lateral sclerosis (ALS), 20 normal subjects, and 113 controls with other neurological disorders. Diffusion weighted images in the patients with ALS and the controls disclosed a high signal band from the subcortical area to the medullary pyramids. The high signal band on the diffusion weighted images corresponded to the pyramidal tract in the anatomical atlas described by Talairach. The T1- and T2-relaxation times, proton density, diffusion coefficient and diffusion anisotropy were measured at the points where high signal bands appeared on the diffusion weighted images. The T2-weighted images revealed high signal areas on the posterior limbs of the internal capsules in all the patients with ALS, 60% of the normal subjects, and 73% of the disease controls. The T1-weighted images disclosed high signal areas on the posterior limbs in 62% of the patients with ALS, but not in any of the normal subjects and the disease controls. The proton weighted images disclosed high signal areas on the posterior limbs in all the patients with ALS and 5% of the disease controls, but not in any of the normal subjects. Analysis of diffusion weighted images revealed no significant difference between the patients with ALS and the normal subjects in diffusion coefficient and diffusion anisotropy on the posterior limbs. Measurement of MR parameters (T1- and T2-relaxation times and proton density) showed that the proton density at the posterior limbs increased in ALS. Water-fat images using the method of Dixon revealed abnormal signals in the water images. These signal abnormalities were more prominent in the internal capsule than in the medullary pyramids. Our findings confirm that there is an increase in water molecules that have normal diffusion coefficient and diffusion anisotropy values in patients with ALS.

Adult↗

Small primary intracerebral hemorrhage. Clinical presentation of 28 cases.

BACKGROUND: Although there have been sporadic reports of patients with small intracerebral hemorrhages presenting with discrete clinical features, the clinical and distributional characteristics of these hemorrhages have not been adequately investigated. CASE DESCRIPTIONS: We studied 28 patients who had primary intracerebral hemorrhage of a longest diameter < or = 1.5 cm as seen in computed tomographic scan and/or magnetic resonance imaging. Small primary intracerebral hemorrhages were found in the basal ganglia in 8 patients (2 with intraventricular hemorrhage), the posterior limb of the internal capsule in 8, the area of the fourth ventricle of the cerebellum in 7 (5 with intraventricular hemorrhage), the pontine tegmentum in 4, and the thalamomesencephalic area in 1. All patients except 3 were hypertensive, suggesting that most of the hemorrhages may have occurred because of rupture of small end arteries secondary to long-standing hypertension. Depending on their location, the hemorrhages clinically manifested as pure motor stroke in 7, pure sensory stroke in 6, vertigo/ataxia in 7, sensorimotor stroke in 4, and ataxic hemiparesis in 2 patients. One patient with thalamomesencephalic hemorrhage showed vertical gaze disturbance, and 1 with basal ganglionic hemorrhage presented with symptoms of acute hydrocephalus secondary to a relatively large amount of intraventricular hemorrhage. The prognosis of small intracerebral hemorrhage was generally excellent except for when patients were very old or when there was a significant amount of intraventricular bleeding. CONCLUSIONS: Small primary intracerebral hemorrhage has its predilection sites: basal ganglia, posterior limb of the internal capsule, area of the fourth ventricle of the cerebellum, and pontine tegmentum. Most of the hemorrhages are probably caused by rupturing of the small end arteries in the setting of chronic hypertension. They produce discrete clinical syndromes often mimicking classic lacunar syndrome, of which pure sensory stroke is relatively common.

Adult↗

In vivo MR study of brain maturation in normal fetuses.

PURPOSE: To illustrate normal maturation of the fetal brain, including the migrational layer, gray matter, early myelination of internal capsules, optic radiations, and corona radiata. METHODS: Seventy-seven fetal brains, ranging from 21 to 38 weeks of gestational age, were examined with MR in vivo; 33 were considered normal. MR examinations were performed as T1-weighted sequences in the axial, sagittal, and coronal planes. The neuropathologic examination (four cases) and clinical and/or neuroradiologic examinations confirmed the antenatal data. RESULTS: From 21 to 25 weeks, the cerebral ventricles are large, corresponding to the relative fetal hydrocephalus. A slight high signal intensity can be observed in the basal ganglia as early as 21 weeks. In the cerebral hemispheres, a multilayered pattern that can be observed from 23 to 28 weeks includes the cortical ribbon, the germinal matrix, and an intermediate layer corresponding to the migrating glial cells. These findings are probably related to areas of increased cellularity. A high signal intensity can be seen within the dorsal part of the brain stem as early as 23 weeks, within the posterior limb of the internal capsules at 31 weeks, and within the central area of the cerebral hemispheres at 35 weeks. Those patterns are probably caused by the evolving process of myelination. CONCLUSIONS: MR allows depiction of signal changes corresponding either to an increase in cellularity or to the evolving processes of myelination, depending on the stage of the pregnancy.

Brain↗

Brain MR: pathologic correlation with gross and histopathology. 1. Lacunar infarction and Virchow-Robin spaces.

MR imaging was performed on 36 formalin-fixed brain specimens. For three of these specimens, in vivo MR studies had also been performed before death. Changes that take place in the MR appearance of the brain after fixation are discussed. Gross and microscopic pathology revealed 14 lacunar infarctions in seven cases and enlarged Virchow-Robin spaces (état criblé) in four. Both types of lesion were seen in specimens from predominantly elderly, hypertensive patients. Eight lacunae were in the deep gray-matter nuclei (four in the putamen with variable involvement of the internal capsule and caudate nuclei, two in the thalami, and two in the dentate nuclei), five were in the supratentorial white matter, and one was in the brainstem. Enlarged Virchow-Robin spaces were identified in the basal ganglia. All lesions were detected on MR. CT failed to disclose the brainstem and dentate lacunae and the enlarged Virchow-Robin spaces. On MR, all lacunae were slitlike or ovoid, except one that was round. They were less than 1 cm in greatest diameter in all but two cases. The lacunae were hyperintense relative to brain parenchyma on both long TR sequences (short and long TEs) in all cases except that of a chronic infarct that underwent cystic change and was isointense relative to CSF on all pulse sequences. In contrast, dilated Virchow-Robin spaces were isointense relative to CSF in vivo or to fluid in the subarachnoid space in the postmortem state on all pulse sequences in all four cases. They were round or linear, and in general were smaller than the lacunae, although some overlap in size did occur. They were seen at the level immediately above the bifurcation of the internal carotid into the middle and anterior cerebral arteries and were seen on successive axial sections in the putamen (most prominent along its lateral margin) and in the internal capsule. MR studies of gross and microscopic pathology of lacunae and dilated Virchow-Robin spaces are useful in correlating MR and pathologic findings. However, changes resulting from the fixation process must be considered when postmortem and in vivo MR findings are correlated.

Adult↗

[MRI of white matter pathways].

CT scan shows some relatively large white matter pathways such as corpus callosum or internal capsule, while MRI provides more sophisticated display of cerebral white matter pathways, based partly on difference in the water content, which improves contrast resolution of structures that cannot be appreciated on CT scanning. The white matter shows slightly high signal intensity in T1WI as compared with the peripheral gray matter. In contrast, it is relatively low signal intensity in long TR sequence. The signal intensity is correlated with myelination, density of myelin fibers and possibly iron deposition. In this study, we collected data on 30 patient, aged from 3 to 60 years average 38 years of normal MRI study of the brain. We routinely obtained T1 Weighted image (T1WI, TR/TE 500-600/20 msec), dual echoes image of proton density image (PDI, TR/TE 2000-3000/20 msec), T2 weighted image (T2WI, TR/TE 2000-3000/80-120 msec), in axial and coronal sections. In some cases sagittal section was also imaged. We identified the white matter pathways based on the data from the axial and coronal sections of 2 autopsy specimens. We also consulted several textbooks and literature reviews of gross and MRI anatomy. The following white matter pathways could be clearly observed on MRI: 1. Projection fibers: corona radiata and internal capsule; 2. Commissural fibers: corpus callosum and anterior commissure; 3. Associated fibers: superior occipito-frontal fasciculus, superior longitudinal fasciculus, ucinate fasciculus, cingulum bundle, optic radiation fornix and mammillothalamic tract.

Adolescent↗

Axonal trajectories between mouse somatosensory thalamus and cortex.

An in vitro brain slice preparation has been used to label fibers connecting the somatosensory thalamus and cortex of the mouse. In 400-800-micron brain slices, the pathway between the ventrobasal complex and somatosensory cortex was labeled under direct vision with horseradish peroxidase crystals (HRP), HRP-Nonidet P-40 (NP40) detergent chips, or a solution of HRP/dimethylsulfoxide. Thalamocortical and corticofugal fibers are organized into a plexiform system of bundles that appears to be fairly constant from animal to animal. Bundles of fibers projecting from the ventrobasal complex course between regularly spaced groups of thalamic neurons. Thalamocortical axons do not invariably leave the thalamus via the fiber bundle closest to the perikarya. Thus, nearest-neighbor relationships are abolished before these axons have even left the thalamus. The axon bundles traverse the thalamic reticular nucleus lateral to the complex. The axons then rotate about one another, analogous to the coiling of strands in rope about a central axis. This accounts for the well known 180 degrees rotation in the mediolateral direction between thalamic and cortical maps. Laterally, fiber bundles converge and diverge within the internal capsule so that nearest-neighbor relationships are lost. Individual thalamocortical axons do not bifurcate proximal to the subcortical white matter. After single bundles of fibers reach a point just below the subcortical white matter, their individual fibers diverge widely. Within the subcortical white matter most afferent fibers make a small dorsally concave loop prior to taking one of two possible courses: some of the fibers ascend directly into the overlying cortex usually angled towards the dorsal surface of the brain; other fibers run in the subcortical white matter for variable distances prior to ascending into cortex. Within somatosensory cortex, smooth axons branch near their terminals in layers IV and VI. Axonal terminal and branching patterns of these axons within somatosensory cortex are similar to those found in in vivo preparations. Most axons are smooth, but other axons are beaded. Some beaded axons project to layer I. Corticofugal fibers are labeled. Fibers leaving somatosensory cortex have an angle of descent opposite to the angle of ascent for afferent fibers, and are often fasciculated in the cortex and subcortical white matter. Within the subcortical white matter efferent fibers often loop in a direction opposite to that of afferent fibers. Corticofugal fibers occasionally give off a collateral corticostriatal branch within the internal capsule.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗