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We have explored two aspects of internal capsule development that have not been described previously, namely, the development of glia and of blood vessels. To these ends, we used antibodies to glial fibrillary acidic protein (GFAP) and to vimentin (to identify astrocytes and to radial glia) and Griffonia simplicifolia (lectin; to identify microglia and blood vessels). Further, we made intracardiac injections of Evans Blue to examine the permeability of this dye in the vessels of the internal capsule during neonatal development. Our results show that large numbers of radial glia, astrocytes and microglia are not labelled with these markers in the white matter of the internal capsule until about birth; very few are labelled earlier, during the critical stages of corticofugal and corticopetal axonal ingrowth (E15-E20). The large glial labelling in the internal capsule at birth is accompanied by a dense vascular innervation of the capsule; as with the glia, very few labelled patent vessels are seen earlier. After intracardiac injections of Evans Blue, we find that the blood vessels of the internal capsule are not particularly permeable to Evans Blue. At each age examined (P0, P5, P15), blood vessels are outlined very clearly and there is no diffuse haze of fluorescence within the extracellular space, which is indicative of a leaky vessel. There are three striking differences between the glial environment of the internal capsule and that of the adjacent thalamus. First, the internal capsule is never rich with radial glial fibres (vimentin- and GFAP-immunoreactive) during development (except at P0), whereas the thalamus has many radial fibres from very early development (E15-E17). Second, astrocytes (vimentin- and GFAP-immunoreactive) first become apparent in the internal capsule (E20-P0) well before they do in the thalamus (P15). Third, the internal capsule houses a large transient population of amoeboid microglia (P0-P22), whereas the thalamus does not; only ramified microglia are seen in the thalamus. In summary, our results indicate that all three types of glia in the internal capsule are associated closely with the vasculature, suggesting they may play a role in the development of the blood-brain barrier among the vessels in this white matter region of the forebrain.
Although many pathological changes in the internal capsule may lead to neurological deficits, we often encounter ill-defined focal low attenuation in the posterior limb of the internal capsule (PIC) on CT in patients with no neurological disturbance. Brain CT studies of 141 patients without neurological deficits were reviewed to investigate the position of the focal low attenuation by analysis of a profile density curve. Nine patients with lacunar infarcts only within the posterior internal capsule were also studied. The focal low attenuation areas were ill-defined and bilaterally symmetrical, without mass effect. They were seen consistently within the posterior limb of the posterior internal capsule. Correlation between the distribution of these foci and the position of lacunar infarcts in the posterior internal capsule in nine patients with neurological deficits suggests that they may be related to the corticospinal tract.
The effect of conditioning stimulation of the internal capsule on nociceptive neurones in the rat diencephalon was investigated. The animals were anaesthetised with N(2)O/O(2) (2:1) and 0.5% halothane, and immobilised with pancuronium bromide. Nociceptive neurones responding to noxious stimulation of the face and oral structures were recorded in the ventral posteromedial nucleus, posterior group and zona incerta. These neurones were classified into wide dynamic range and nociceptive-specific types. Functional segregation of these nociceptive neurones was not apparent within the nucleus or between nuclei. A test stimulus with a single rectangular pulse (5-70 V) was applied to the centre of the receptive field; the nociceptive neurones exhibited short- and/or long-latency responses. Both responses in about 45% of the nociceptive neurones were inhibited by conditioning stimuli to the contralateral internal capsule with trains of 33 pulses (300 microA) at 330 Hz. The percent inhibitory effects on the nociceptive neurones of each area were 68.0+/-14.8% (n = 6) in the ventral posteromedial nucleus, 72.8+/-12.4% (n = 4) in the posterior group and 61.5+/-7.5% (n = 4) in the zona incerta. Effective sites for conditioning stimulation were concentrated in the lateral side of the internal capsule, through which the corticofugal fibres from the somatosensory cortex pass. These findings suggest that the transmission of nociceptive information to the diencephalon is modulated by stimulation of the internal capsule at the level of the trigeminal sensory complex in the brainstem. They might provide a novel way to elucidate the neurophysiological basis for antinociception by stimulation of the internal capsule observed in clinical studies.
We treated a consecutive series of 309 patients with hypertensive thalamic hemorrhage from April 1981 to December 1987. In 99 cases of involvement of the internal capsule, the relationship between the extent of destruction of the internal capsule and motor disturbance was clinically investigated and discussed. First, these 99 cases were classified into three groups on the basis of the location of the hematoma in the internal capsule on the CT image. All the cases were confined to the anterior, middle and posterior portions of the posterior limb of the internal capsule. The correlation between hematoma extension and the severity of motor weakness, its improvement nd prognosis were discussed. The severity of motor weakness was found not to be related to hematoma extension. On the other hand, the prognosis was frequently poor when the hematoma was located at the posterior portion within the posterior limb of the internal capsule. In hypertensive thalamic hemorrhage, there seemed to be a narrow and significant area within the posterior limb of the internal capsule which determined morbidity. And, as a matter of course, the nearer the hematoma was located to the border between the middle and posterior portions, the worse the outcome was. Cases treated by aspiration surgery were evaluated to investigate the utility of aspiration surgery for thalamic hemorrhage. (Special attention was given to the ADL of those cases with severe motor weakness.) When the hematoma was located at the posterior portion of the posterior limb of the internal capsule, the percentage of patients with good outcome was significantly higher in the aspirated group than in the medical group (p less than 0.05).
Following unilateral damage to the internal capsule, rats failed to use the contralateral forelimb during tests of contact, chin, and visual placing reactions. Infusion of potassium chloride onto the sensorimotor cortex contralateral to the lesion reinstated placing in the impaired limb and abolished placing in the normal limb. As the drug dissipated, placing in the impaired limb gradually deteriorated, while placing in the normal limb returned. In contrast, potassium chloride applied to the ipsilateral cortex did not reinstate placing. These findings suggest that the loss of forelimb placing following lesions of the internal capsule is due, at least in part, to tonic inhibition from the cortex contralateral to the lesion.
The myelogenetic development of the corticospinal fibres in the internal capsule was studied using eight brains of the Yakovlev Collection and two brains of the collection in Hannover Medical School. The myelin sheaths of the corticospinal fibres stained by the Loyez method can best be seen in the third postnatal month. During their course through the internal capsule their relative position changes. In the superior portion of the internal capsule, at the level of the interventricular foramen, the pyramidal tract is located in the middle of the posterior limb and in the inferior portion, at the level of the subthalamic nucleus and metathalamus, in the posterior third of the posterior limb. The classical concept of the localisation of the pyramidal tract has, therefore, to be revised for the inferior portion of the internal capsule. The result of this study confirms those of stereotactic, neuropathological and macroscopic observations and underlines the importance of the Yakovlev Collection for the neurosciences.
Clinical and evoked-potential studies in internal capsule and corona radiata infarction are lacking. We report the results of a clinical and central motor conduction time (CMCT) study in 16 patients with internal capsule and 17 with computed tomography (CT)-proven corona radiata infarction. Patients's outcome was defined at the end of 3 months on the basis of the Barthel Index score. Four patients with type A capsular infarction (middle third of posterior limb of internal capsule) all had severe weakness, while 2 also had persistently unrecordable CMCT and poor outcome. Twelve patients with type B internal capsular infarction (genu, anterior limb, anterior or posterior third of posterior limb) had a milder degree of weakness, and CMCT was recordable in 9. At 3 months' follow-up, however, CMCT was recordable in all 12 patients. All of these patients had a partial (n = 4) or complete (n = 5) recovery. Thirteen patients with type A corona radiata infarction (middle third of corona radiata) had more pronounced weakness, and CMCT was unrecordable in all of these patients except 1 on initial examination. Follow-up after 3 months was possible in 8 patients, and CMCT became recordable in 3. One of these patients had complete, 3 partial, and 4 poor recovery. In type B corona radiata infarction (anterior or posterior third of corona radiata), the clinical signs and CMCT did not follow a regular pattern. Clinical and CMCT abnormalities in internal capsular infarction followed a more predictable pattern compared with those in corona radiata infarction. A less predictable pattern of weakness and CMCT change in corona radiata infarction may be attributed to a less definite organisation of motor pathways compared with the internal capsule.
A memory deficit model has been developed following bilateral internal capsule lesions in rats. During 12-49 days after internal capsule lesions, the rats showed a marked impairment of active avoidance acquisition in a step-through apparatus, while they exhibited no observable change in native behaviors, except a slight increase in exploratory activity. A passive avoidance task in the same apparatus was also impaired in internal capsule lesioned rats when examined after one-trial training, though the task was gradually acquired by repeated trainings. Moreover, the retention of both the active and passive avoidance responses in well-trained rats deteriorated after internal capsule lesions. On the other hand, internal capsule-lesioned rats did not perform any worse than sham-operated rats in a T-maze spontaneous alternation behavior and in a habituation response to a novel environment. In the frontal cortex and striatum of internal capsule-lesioned rats, there was a significant decrease of dopamine, serotonin and their metabolites, but no change of acetylcholine levels. The acquisition deficit of active avoidance in internal capsule-lesioned rats was improved by thyrotropin-releasing hormone (TRH, 10 mg/kg, i.p.) and L-6-ketopiperidine-2-carbonyl-L-leucyl-L-proline amide (RGH-2202, 10 mg/kg, i.p., 0.2 and 1 mg/kg i.v.), but not by physostigmine sulfate (0.2 mg/kg, i.p.). These results indicate that bilateral internal capsule lesions in rats induce long-term memory deficits which are paralleled with a decrease of the contents of monoamines and their metabolites and improved by TRH and RGH-2202.
The aim of our study is to understand the development of the earliest connections in the mammalian pallium by documenting the distribution of cells and fibres labelled from the dorsal and ventral thalamus, internal capsule, perirhinal, and dorsal cortex during the period between embryonic day (E) 14 and 17 by using carbocyanine dye tracing in fixed embryonic rat brains. Dye placed in the thalamus of E14 brains backlabels cells in the thalamic reticular nucleus and within the primitive internal capsule. Both anterograde and retrograde tracing confirmed that the first corticofugal projections reach the internal capsule by E14. At E15-E16, after the first cortical plate cells have migrated into the lateral cortex, some cells of the cortical plate and subplate and marginal zone, are backlabelled from the internal capsule, but still not from the dorsal thalamus, even with very long incubation periods. Crystal placement into the perirhinal cortex at E14-E15 labels numerous cells within the internal capsule, whereas no such cells are revealed from dorsal cerebral cortex until E17, suggesting that internal capsule cells establish early connections with the perirhinal and ventral but not dorsal cortex. We propose that the growth of axons from cortex to dorsal thalamus is delayed in two regions: first from E14-E15 at the lateral entrance of the internal capsule and then, from E16, closer to the thalamus, probably within the thalamic reticular nucleus. Subplate projections reach the proximity of the diencephalon at an early stage, but they might never enter the dorsal thalamus.
BACKGROUND: The anterior limb of the internal capsule (ALIC) contains the anterior thalamic peduncle connecting the medial and anterior thalamic nuclei with the prefrontal cortex and the cingulate gyrus. The purpose of this study was to detect the volumetric changes in the ALIC in view of the putative abnormal frontothalamic connectivity in schizophrenia. METHODS: High-resolution, three-dimensional magnetic resonance imaging was acquired from 53 schizophrenia patients and 48 age- and gender-matched control subjects. Volumetric analysis was performed using consecutive 1-mm-thick coronal slices rostral to the anterior commissure, on the ALIC, caudate nucleus, and lentiform nucleus. White matter concentration over the whole brain was compared using the voxel-based morphometry (VBM) with Statistical Parametric Mapping 99. RESULTS: The patients had significantly decreased volumes in the bilateral ALIC and showed significantly increased right-greater-than-left asymmetry of the ALIC; VBM revealed a reduction in white matter concentration of the bilateral internal capsule in patients. No volumetric difference was found in the rostral part of the caudate and lentiform nucleus between groups. CONCLUSIONS: Decreased volume found in the ALIC supports the hypothesis of abnormal frontothalamic connectivity in schizophrenia. Increased asymmetry of the internal capsule seems consistent with the notion of predominantly left-side pathology of schizophrenia.
The nervous fibers in the human internal capsule were mapped according to their three-dimensional orientation. Four human cadaver brains were cut into comparable and standardized sections parallel to the ACPC-plane, stained with DiI, and analyzed using a combination of confocal and polarized light microscopy at the same time. This combination provides information about the structure and orientation of the fibers in great detail with confocal microscopy, and information about the localization and orientation of long myelinated fiber tracts with polarization microscopy. The internal capsule was parcellated in the areas CI 1 to CI 4 containing fibers of distinct orientation and structure, which enriches the macroscopically definable parcellation in the anterior and posterior limb. Fibers of the anterior thalamic peduncle intermingle with frontopontine tract fibers. Single fibers connect the caudate and the lentiform nucleus. The pyramidal tract is located in the anterior half of the posterior limb intermingled with fibers of the superior thalamic peduncle. Parietooccipitopontine fibers are located in the posterior part of the posterior limb. The slopes of the different systems of fibers change continuously in the anterior posterior direction of the internal capsule. Using the 3D orientation of fibers as a criterion for parcellation, as well as the description of bundles as a collection of fibers belonging to particular tracts leads to a more function-related description of the anatomy of the internal capsule. The method can be used for interindividual, sex- or age-related comparisons of particular systems of fibers.
The topology of the motor pathways in the posterior peduncle of the internal capsule is discussed with regard to the literature and computer tomographic analysis of three patients with capsular lesions. Contradictory findings from morphologic, stereotactic, and computer tomographic investigations of the topology of the motor pathways in the posterior peduncle of the internal capsule have led to concepts which are mutually incompatible. It was first maintained that the motor pathways are located in the anterior third or two-thirds of the posterior peduncle and arranged somatotopically in the craniocaudal direction. A new interpretation which has received wide support from stereotactic investigations and studies of the pathologic anatomy of amyotrophic lateral sclerosis agrees on the somatotopic arrangement, but claims that the motor pathways are located rather in the posterior third of the posterior peduncle. By including ontogenetic factors and a critical relativistic consideration of the somatotopic arrangement of the posterior peduncle of the internal capsule in the analysis of the topology of the motor pathways in the posterior peduncle of the internal capsule, it can be demonstrated that the contradictions of published results and hypotheses are only apparent, thus making a uniform interpretation possible.
Background and Purpose--Magnetic resonance spectroscopy (MRS) in ischemic stroke has shown a correlation between N-acetylaspartate (NAA) loss from the infarcted region and disability. We tested the hypothesis that NAA loss in the descending motor pathways, measured at the level of the posterior limb of the internal capsule, would determine motor deficit after a cortical, subcortical, or striatocapsular stroke. Methods--Eighteen patients with first ischemic stroke causing a motor deficit were examined between 1 month and 5 years after stroke. T2-weighted imaging of the brain and localized proton (voxel, 1.5x2x2 cm3) MRS from the posterior limb of each internal capsule were performed and correlated to a motor deficit score. Results--Mean internal capsule NAA was significantly lower in the patient group as a whole compared with the control group (P<0.001). Reductions in internal capsule NAA on the side of the lesion were seen in cases of cortical stroke in which there was no extension of the stroke into the voxel as well as in cases of striatocapsular stroke involving the voxel region. There was a strong relationship between reduction in capsule NAA and contralateral motor deficit (log curve, r2=0.9, P<0.001). Conclusions--Axonal injury in the descending motor pathways at the level of the internal capsule correlated with motor deficit in patients after stroke. This was the case for strokes directly involving the internal capsule and for strokes in the motor cortex and subcortex in which there was presumed anterograde axonal injury.
We reported five patients having presented only with clumsy hand and dysarthria which resulted from motor paresis confined to one side of the fingers and the ipsilateral face and tongue. All of them were right-handed, and their manifestation was transient. They had no abnormalities of muscle tonus and sensation, and no ataxia. The features of these cases differed from those of the dysarthria-clumsy hand syndrome because of absence of ataxia, and could be distinguished from pure motor hemiplegia by a motor paresis with cheiro-oral topography. MRI examinations showed a localized lesion at the border between internal capsule and corona radiata (two cases), or in the corona radiata just over this region (three cases). In the former cases in which the internal capsule was involved, we confirmed the lesion in the genu and anterior half of the posterior limb of the internal capsule. The lesion was on the left side in all five patients. It has been known that the pyramidal tract consists of the large and small fibers. The large ones are localized in the posterior part of the posterior limb of the internal capsule, and the damage of them produces sustained and serious motor paralysis. The small ones are widely distributed in the genu and the posterior limb of the internal capsule. The findings of our study suggest that the small fibers have adjacent somatotopy for the hand and mouth in the region of the genu and the anterior part of the posterior limb of the internal capsule, and that the damage of them may lead to mild, transient motor paresis without spasticity.
BACKGROUND AND PURPOSE: Diffusion-weighted MR images have enabled measurement of directionality of diffusion (anisotropy) in white matter. To investigate differences in the anisotropy for various types of pathologic findings and the association between the anisotropy of tracts and neurologic dysfunction, we compared the anisotropy of the posterior limb of the internal capsule and the corona radiata between patients with stroke and those with tumors and between patients with and without hemiparesis. METHODS: Thirty-three patients consisting of 11 with tumors and 22 with ischemic disease (16 acute infarction, four old infarction, and two transient ischemic attack) and nine control patients were studied with a 1.5-T MR imager. Diffusion-weighted images were obtained with diffusion gradients applied in three orthogonal directions. The diffusion anisotropy measurements were obtained from regions of interests defined within the internal capsule and the corona radiata. RESULTS: The diffusion anisotropy was significantly reduced in all internal capsules and coronae radiata involved by infarcts, tumors, and peritumoral edema compared with that of the control patients (P <.0001). This reduction was most prominent in the tracts involved by tumors (P <.05). The anisotropy of the internal capsules and coronae radiata was significantly decreased in cases with moderate-to-severe hemiparesis as compared with those with no or mild hemiparesis (P <.0001). Diffusion anisotropy tended to be also reduced in normal-appearing internal capsules and coronae radiata that were remote from the involved segment of the corticospinal tract. CONCLUSION: The degree of impaired diffusion anisotropy may vary in different pathologic conditions and correlate with neurologic dysfunction. The measurement of diffusion anisotropy may provide additional information relating to neurologic function and transneuronal effects.
AIM: To prospectively assess the predictive value of asymmetrical myelination on MRI of the posterior limb of the internal capsule (PLIC) in newborn infants with an intraventricular haemorrhage (IVH) associated with unilateral haemorrhagic parenchymal involvement (PI), for subsequent development of a hemiplegia. METHODS: 12 preterm infants (GA 25-36 wks) and 4 full-term infants were studied. Using cranial ultrasound (US), the pre-term infants were diagnosed to have an IVH with unilateral PI. The term infants presented with a porencephalic cyst (PC) on the first postnatal US, following an antenatal IVH with PI. MRI was performed at 40 wks postmenstrual age in the pre-term infants and during the first 2 weeks of life in the full-term infants, using a 1.5T magnet. Using an inversion recovery sequence, the myelination of the internal capsule was recorded as normal, abnormal or equivocal. Neurological assessment > or = 12 months disclosed the presence of a hemiplegia or asymmetry in tone pattern. RESULTS: All 4 cases with a normal internal capsule had a normal outcome in spite of the development of a PC. All 9 cases with an abnormal PLIC developed a hemiplegia, while 1 of the 3 cases with an equivocal PLIC is normal on neurological assessment, one developed a mild asymmetry in tone and 1 a mild hemiplegia. CONCLUSION: While a symmetrical signal intensity within the internal capsule on MRI, performed at 40 weeks PMA, in infants with an IVH and unilateral PI appears to be strongly related to a normal outcome, an asymmetrical PLIC is an early predictor of future hemiplegia.
Electrical stimulation of the posterior limb of the internal capsule was performed in six patients with central pain due to vascular lesions of the thalamus. Three patients suffered from thalamic hemorrhage and the other three from ischemic insult. These patients developed dysesthesia, hyperpathia and spontaneous burning pain several months after cerebral vascular diseases. These severe pain were not relieved by any trials of anticonvulsants, psychopharmacological and analgesic drugs. Stimulating electrode system manufactured by Medtronic, Co. was implanted stereo-taxically in the posterior limb of the internal capsule which was 25 mm lateral to the posterior commissure. Ramped bipolar stimulation with a square pulse 2-3 V, 0.2 msec, 50 Hz elicited sensory response such as warm or comfortable sensation. Satisfactory relief of pain was obtained in most cases by 30-minutes-long stimulation twice or three times a day for various period of time ranging from 10 to 14 days. Long-term follow-up ranging from three months to two years showed that three patients had a good result (incomplete pain relief by stimulator with no medication required), two had a fair (incomplete pain relief by stimulator with decreased doses of medication) and another one had a poor result in which the pain had not been relieved with the stimulation in one month. No remarkable side effects were seen. These results indicate that the internal capsule stimulation is more effective and lasts longer than the various ablative methods to relieve central pain.(ABSTRACT TRUNCATED AT 250 WORDS)