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PubMed1982

Capsular ataxic hemiparesis.

Left hemiparesis and left-sided ataxia developed in a 67-year-old man. Computed tomography (CT) showed an area of decreased attenuation in the anterior part of the rostral posterior limb of the right internal capsule that enhanced with contrast. As the patient's condition improved, the contrast enhancement resolved. The clinical course combined with the changes in CT scans indicates that the responsible lesion was an infarct. This report suggests that ataxic hemiparesis can result from an infarct of the posterior limb of the internal capsule.

Aged↗
PubMed1999

Cree leukoencephalopathy: neuroimaging findings.

PURPOSE: To describe the computed tomographic (CT) and magnetic resonance (MR) imaging findings in Cree leukoencephalopathy. MATERIALS AND METHODS: The authors retrospectively reviewed the medical records and neuroimaging studies in 12 infants with Cree leukoencephalopathy (CT in 12 infants, MR in six). The diagnosis was established clinically in six patients and at autopsy in the other six. RESULTS: At CT, extensive, diffuse, and symmetric hypoattenuation was seen in the cerebral and cerebellar white matter in all 12 patients. Hypoattenuation was also seen in the corpus callosum in 11 (92%), internal capsule in 10 (83%), globus pallidus in nine (75%), brainstem in nine (75%), and thalamus in four (33%). The caudate nucleus and putamen were spared. On T2-weighted MR images in six patients, the cerebral and cerebellar white matter, including the subcortical arcuate fibers, was hyperintense as were the internal capsule, corpus callosum, corticospinal tracts, and globus pallidus. The thalamus was affected in four (67%) patients, pons in five (83%), and medulla in four (33%). The caudate nucleus and putamen were not affected. CONCLUSION: Cree leukoencephalopathy causes striking symmetric and diffuse involvement of the cerebral and cerebellar white matter and brainstem with sparing of the caudate nucleus and putamen.

Encephalitis↗
PubMed1997

[Bilateral caudate head infarcts].

We reported a 67-year-old woman with bilateral caudate head infarcts. She developed sudden mutism followed by abulia. She was admitted to our hospital 2 months after ictus for further examination. She showed prominent abulia and was inactive, slow and apathetic. Spontaneous activity and speech, immediate response to queries, spontaneous word recall and attention and persistence to complex programs were disturbed. Apparent motor disturbance, gait disturbance, motor aphasia, apraxia and remote memory disturbance were not identified. She seemed to be depressed but not sad. Brain CT and MRI revealed bilateral caudate head hemorrhagic infarcts including bilateral anterior internal capsules, in which the left lesion was more extensive than right one and involved the part of the left putamen. These infarct locations were thought to be supplied by the area around the medial striate artery including Heubner's arteries and the A1 perforator. Digital subtraction angiography showed asymptomatic right internal carotid artery occlusion. She bad had hypertension, diabetes mellitus and atrial fibrillation and also had a left atrium with a large diameter. The infarcts were thought to be caused by cardioembolic occlusion to the distal portion of the left internal carotid artery. Although some variations of vasculature at the anterior communicating artery might contribute to bilateral medial striate artery infarcts, we could not demonstrate such abnormalities by angiography. Bilateral caudate head infarcts involving the anterior internal capsule may cause prominent abulia. The patient did not improve by drug and rehabilitation therapy and died suddenly a year after discharge.

Aged↗
PubMed1992

Bursting and tonic discharges in two classes of reticular thalamic neurons.

1. Two types of cat reticular (RE) thalamic cells were disclosed by means of intracellular recordings under urethan anesthesia. The RE neurons were identified by their typical depolarizing spindle oscillations in response to synchronous stimulation of the internal capsule. 2. In type I neurons (n = 41), depolarizing current pulses induced tonic firing at the resting or slightly depolarized membrane potential (Vm) and triggered high-frequency spike bursts at a Vm more negative than -75 mV. As well, these cells discharged rebound bursts at the break of a hyperpolarizing current pulse. Internal capsule stimulation elicited spindle sequences made off by depolarizing waves giving rise to spike bursts. 3. Type II cells (n = 9) did not discharge spike bursts to large depolarizing current pulses even when the Vm reached -100 mV, nor did they fire rebound bursts after long-lasting hyperpolarizing current pulses or spike bursts riding on the rhythmic depolarizing components of spindle sequences. 4. Compared with type I cells, type II cells showed less frequency accommodation during tonic firing. The latter neuronal class discharged at high frequencies (40 Hz) with slight DC depolarization, approximately 8-10 Hz at the resting Vm, and no underlying synaptic or subthreshold oscillatory events could be detected when the firing was blocked by DC hyperpolarization. 5. The presence of two cell classes in the RE nucleus challenges the common view that this nucleus consists of a single neuronal class. We suggest that a different set of conductances is present in type II RE neurons, thus preventing the low-threshold Ca2+ current from dominating the behavior of these cells.

Animals↗
PubMed1979

Development of the diencephalon in the rat. VI. Re-evaluation of the embryonic development of the thalamus on the basis of thymidine-radiographic datings.

The development of the thalamus was examined in normal and X-irradiated embryos from day 13 (E13) to the day before birth (E22). The differentiating, radioresistant neurons of the lateral habenular nucleus, derived from a portion of the superior neuroepithelial lobule (SL1), were settling by day E15 and by this time the habenulopeduncular tract was forming. The neurons of the reticular nucleus, derived from the middle neuroepithelial lobe, began to settle on day E15 but a massive migration was still evident on day E16. Adjacent to the reticular nucleus the internal capsule appeared on day E16; this fiber bundle seemed to be continuous with fibers embedded in the first transitory zone of cells issuing from the dorsal neuroepithelial lobe. Because of the immaturity of the neocortex at this time, it was postulated that thalamocortical fibers of the dorsal thalamus are the earliest components of the internal capsule. By day E17 all the sensory relay nuclei of the thalamus were recognizable and it was assumed that the second transitory zone issuing from the receding dorsal neuroepithelial lobe contained the neurons of the later forming intralaminar nuclei. Suggestive evidence was obtained that the late arising neurons of the medial thalamus (the anterior nuclei, the mediodorsal nucleus, and some or all of the midline nuclei) originate in a portion of the superior neuroepithelial lobule designated as SL2. Our present and previous studies showed that the major divisions of the hypothalamus and thalamus are derived embryonically from distinguishable parts of the third ventricle neuroepithelium. This implies the te third ventricle neuroepithelium has a "mosaic" organization and suggests that the fate of hypothalamic and thalamic neurons may be determined to some extent while their precursors are still proliferating.

Animals↗
PubMed1990

Effects of capsular or thalamic stroke on metabolism in the cortex and cerebellum: a positron tomography study.

We used positron emission tomography to study the cortical and cerebellar metabolic rates in 21 strictly selected patients with pure internal capsular infarct (n = 8), thalamocapsular hemorrhage (n = 6), or pure thalamic stroke (n = 7). Significant diffuse ipsilateral cortical hypometabolism relative to 62 controls free of cerebrovascular risk factors was frequently, although not consistently, found in the 13 patients with thalamocapsular or thalamic lesions and neuropsychological impairment but was absent from the eight patients with pure internal capsule infarct and free of neuropsychological deficit. These data suggest that damage to the thalamus or the thalamocortical projections is important in the development of ipsilateral cortical hypometabolism and that the latter may underlie the associated neuropsychological impairment. Significant contralateral cerebellar hypometabolism relative to 49 controls was found in three of six patients with pure internal capsule infarct, suggesting a pathogenetic role for the corticopontocerebellar system. However, the occurrence of hypometabolism in two of six patients with thalamic lesions indicates that this phenomenon may also result either from damage to the ascending cerebellothalamocortical system or indirectly from hypofunction of the cerebral cortex. No systematic association was observed between crossed cerebellar hypometabolism and ipsilateral ataxia.

Analysis of Variance↗
PubMed2002

Axonal damage and demyelination in the white matter after chronic cerebral hypoperfusion in the rat.

Cerebral white matter (WM) lesions are observed frequently in human ischemic cerebrovascular disease and have been thought to contribute to cognitive impairment. This type of lesion can be experimentally induced in rat brains under chronic cerebral hypoperfusion by the permanent occlusion of both common carotid arteries. However, it remains uncertain whether chronic ischemia can damage both the gray and white matter, and whether it can induce demyelination with or without axonal damage. Therefore, we examined axonal damage using immunohistochemistry for the amyloid beta/A4 precursor protein (APP), chromogranin A (CgA) and demyelination using immunohistochemistry for the encephalitogenic peptide (EP) in this model. Severe WM lesions such as vacuolation and the loss of nerve fibers appeared in the optic nerve and optic tract after 3 days of ligation, and less intense changes were observed in the corpus callosum, internal capsule, and fiber bundles of the caudoputamen after 7 days with Klüver-Barrera and Bielschowsky staining. These WM lesions persisted even after 30 days. The APP, CgA, and EP-immunopositive fibers increased in number from 1 to 30 days after the ligation in the following WM regions: the optic nerve, optic tract, corpus callosum, internal capsule, and fiber bundles of the caudoputamen. In contrast, only a few APP, CgA, or EP-immunopositive fibers were detected in the gray matter regions, including the cerebral cortex and hippocampus. These results indicate that the WM is more susceptible to chronic cerebral hypoperfusion than the gray matter, with an involvement of both axonal and myelin components. Furthermore, immunohistochemistry for APP, CgA, and EP is far superior to routine histological staining in sensitivity and may become a useful tool to investigate WM lesions caused by various pathoetiologies.

Amyloid beta-Protein Precursor↗
PubMed1999

A new model of white matter injury in neonatal rats with bilateral carotid artery occlusion.

Periventricular leukomalacia is an important cause of cerebral palsy and characterized by cysts and coagulation necrosis in the periventricular white matter. Since no model of periventricular leukomalacia has been established in small animals, it is expected to establish a new model of white matter injury in immature rodents. Bilateral carotid arteries were occluded in neonatal rats at 5 days of age, and the brain neuropathologically examined at 7 days of age. Among 22 brains histologically examined, 20 (90.9%) had white matter changes including coagulation necrosis and cystic lesions in and around the internal capsule, while only two had small cerebral infarction and five showed some ischemic neurons in the cerebral cortex. Cerebral blood flow (CBF) decreased to about 25% of controls in the subcortical white matter in the animals with bilateral carotid artery occlusion (BCAO). Amyloid precursor protein (APP) immunohistochemistry demonstrated various APP-immunoreactive axonal profiles in the internal capsule and the subcortical white matter, and stronger expression of APP in pyramidal neurons in the cerebral cortex of BCAO brains. These results indicated that the white matter is more vulnerable than the cerebral cortex in 5-day-old rats when CBF decreases to about 25% and suggested that this model is useful for investigating the white matter changes induced by cerebral hypoperfusion in the neonatal brain, since previous models of hypoxic-ischemic brain injury in neonatal mice and rats revealed preferential susceptibility of the gray matter. It was also indicated that APP is a sensitive marker for mild axonal disruption in the white matter of the immature brain.

Amyloid beta-Protein Precursor↗
PubMed2003

Specific functions of the motor cortex in reorganizing coordinations during motor training in animals and humans.

The involvement of the motor cortex in learning movements has recently attracted much attention. One aspect of motor learning is the inhibition of innate synergies which interfere with performance of the acquired movement. Various models of operant responses in dogs have demonstrated the critical role of the motor cortex in the reorganization and inhibition of interfering synergies during learning. The role of the motor cortex and corticospinal influences in the formation of new coordinations in humans was studied here in patients with organic lesions of the cerebral circulation involving the internal capsule, using postural coordination and movements in a bimanual unloading response as an example. Formation of the forearm stabilization response was deeply lesioned on the afflicted side. Some degree of impairment was also seen on the ipsilateral side, but it was no different from the level of learning impairment in patients with lesions not involving the internal capsule or in patients with parkinsonism. The existence of specific contralateral influences of the motor cortex and non-specific descending influences on the process of motor learning is proposed.

Aged↗
PubMed1998

Mechanisms underlying the early establishment of thalamocortical connections in the rat.

We labeled axonal projections using carbocyanine dyes in the developing rat brain to study cellular interactions that might underlie the establishment of thalamocortical connectivity. By embryonic day 14 (E14), groups of neurons in the ventral diencephalon and the primitive internal capsule have established projections to the dorsal thalamus, and thalamic fibers pass in topographic order among them. Simultaneously, axons from the early-born cells in both subplate and marginal zone (i.e., the original cortical preplate) establish an ordered array that fills the intermediate zone. Thalamic axons and preplate fibers meet in the lateral part of the internal capsule (at E15 for occipital cortex and dorsolateral thalamus). Subsequently, selective labeling of corresponding thalamic and early corticofugal projections reveals thalamic fibers growing in association with early corticofugal axons, right up to the cortical subplate. A small carbocyanine crystal implanted at any point in the cortex shortly after the arrival of thalamic axons (E16 for the occipital cortex) labels a single, tight bundle containing both descending and ascending fibers, rather than two separate tracts, providing further evidence for intimate topographic association of the two axon systems. Crystals placed in a row, parasagittally or coronally along the hemisphere, reveal separate, topographically distributed, discrete fiber bundles throughout the pathway, leading to spatially ordered groups of back-labeled thalamic cells. These results indicate that the topography of thalamic axons is maintained throughout the pathway and that they reach the cortex by associating with the projections of a number of preexisting cells, including the preplate scaffold.

Animals↗
PubMed2004

[Clinical study of 23 patients with ataxic hemiparesis].

BACKGROUND AND OBJECTIVE: To characterize the clinical features, etiology and prognosis in ataxic hemiparesis syndrome. PATIENTS AND METHOD: Descriptive study of 23 patients with ataxic hemiparesis included in the Sagrat Cor Hospital of Barcelona Stroke Registry over a 12 year period. RESULTS: Ataxic hemiparesis was caused by a lacunar infarct in 87% of patients, by atherothrombotic infarcts in 8.7% and by cardioembolic infarct in 4.3%. Ataxic hemiparesis accounted for 0.9% of all acute strokes (n = 2,500), 1.25% of all cerebral infarcts (n = 1,840), and 4.1% of all lacunar infarcts (n = 484). Internal capsule (22%), pons (13%), and corona radiata involvement (9%) were the most frequent cerebral topographies. Absence of in hospital mortality and absence of neurological deficit at discharge from the hospital were present in 39% of the patients. CONCLUSIONS: Lacune hypothesis is present in ataxic hemiparesis syndrome. Ataxic hemiparesis is caused by a lacunar infarct in 87% of patients. The internal capsule topography is the most frequent and the prognosis in ataxic hemiparesis is good.

Aged↗
PubMed1983

The noradrenergic system of the amygdala and aversive information processing.

Water-deprived rats were trained to drink in a passive avoidance apparatus. After reaching a predetermined latency criterion, rats were given a single 3-sec, 3-mA footshock. Immediately or 12 hr after the footshock, rats were given intracranial injections of vehicular saline, norepinephrine (NE), propranolol, or dopamine (DA) into the amygdala, internal capsule, lateral ventricles, or caudate-putamen. Subjects were tested for passive avoidance at 30 min or 24 hr following footshock. No memory deficits were seen as a consequence of short-term retention or because of proactive or toxicity effects. Retention deficits were seen in the 24 hr test only in rats injected with NE in the amygdala, internal capsule, or lateral ventricles. However, qualitative differences in stress-indicative behaviors were noted in the NE groups and in the DA-amygdala animals. The results specifically suggest that the noradrenergic system of the amygdala is involved in the long-term processing of the emotional attributes of aversive information.

Adrenergic Fibers↗
PubMed2000

Tropism of AAV-2 vectors for neurons of the globus pallidus.

A recombinant AAV-2 vector encoding the green fluorescent protein (gfp) under the control of the cytomegalovirus (CMV) promoter was injected into the striatum at varying antero-posterior coordinates. When the virus was delivered to the anterior part of the striatum, transduction efficiency was low and limited to the vicinity of the needle tract. In contrast, after injection into the posterior part of the striatum, in addition to a localized transduced area in the striatum, efficient and widespread transduction was observed at distance from the injection site, in the globus pallidus. In the latter case, labelled cells were also detected in the internal capsule and in the stria terminalis. The number of transduced cells in the striatum increased up to I month and then decreased whereas in the globus pallidus, transduction was maximal as early as 2 weeks post-injection. In the striatum and in the globus pallidus, the labelled cells had a neuron-like morphology. In contrast, in the internal capsule, labelled cells had a glial-like morphology.

Animals↗
PubMed1990

Capsular genu syndrome.

We report 5 patients with unilateral infarct and 1 with hemorrhage limited to the genu of the internal capsule. The most prominent finding was contralateral facial and lingual hemiparesis with dysarthria. Three patients also showed unilateral mastication-palatal-pharyngeal weakness, and 1 had unilateral vocal cord paresis. Mild limb involvement was limited to hand weakness in 4 patients. Our findings suggest that the majority of motor corticopontine and corticocobulbar fibers are located in the genu of the internal capsule. The faciolingual syndrome and its variants are highly suggestive of capsular genu stroke.

Aged↗
PubMed1985

Quantification of lesion-induced dopaminergic supersensitivity using the rotational model in the mouse.

A dual lesion technique was used to determine the degree of supersensitivity resulting from nigrostriatal lesions in C57BL/6J mice. Internal capsule lesions encroaching on globus pallidus resulted in reliable ipsilateral rotation both to apomorphine and amphetamine. Dose-response curves to apomorphine were determined before and 21 days after 6-hydroxydopamine lesion of the contralateral nigrostriatal pathway. A 31.5-fold shift to the left was observed following the nigrostriatal lesion, with no change in slope. The extent and placement of the internal capsule lesion, as well as the magnitude of supersensitization correspond closely to those previously reported in the rat.

Animals↗
PubMedDate not supplied

Serial MRI and CT findings in infantile Krabbe disease.

Krabbe disease (globoid cell leukodystrophy) is an autosomal recessive childhood disorder characterized by severe motor and mental deterioration. The disease has been divided into 3 main types and further subdivided into several subtypes based on age of onset and symptoms. Initial clinical findings and magnetic resonance imaging (MRI) with several follow-up scans are presented to identify the order and extent of white matter involvement and developing brain atrophy in a child with the floppy infant variant of Krabbe disease. When the patient's clinical condition proceeded to stage 2, MRI disclosed severe involvement of the deep white matter around the atria and posterior limbs of the internal capsules. At the same time there was progression of normal myelination around the frontal horns. At age 32 months, the patient's clinical condition proceeded to stage 3; she did not interact with her environment. MRI revealed a significant decrease of white matter volume, generalized atrophy, and abnormal high signal in all white matter areas except the anterior limbs of the internal capsules. At the same time the volume of the central gray nuclei was decreased and also demonstrated abnormal high signal. Despite its sensitivity, MRI could not differentiate the findings of this variant of Krabbe disease from the classic form; therefore, subclassifications of Krabbe disease should be made on clinical grounds because they cannot be distinguished by biochemical or radiologic (MRI) criteria.

Brain↗
PubMed1991

Measurement of regional cerebral blood flow in the dog using ultrafast computed tomography. Experimental validation.

The applicability, feasibility, reproducibility, and accuracy of the method of measuring regional cerebral blood flow using ultrafast computed tomography were evaluated in 25 dogs under varying physiological and pathophysiological conditions. Regional cerebral blood flow values were 75.6 +/- 29.4 ml/100 g/min (mean +/- standard deviation) for the hemisphere, 68.4 +/- 28.2 ml/100 g/min for the basal ganglia, 41.2 +/- 15.0 ml/100 g/min for the internal capsule, and 80.8 +/- 37.2 ml/100 g/min for the neocortex. Measurements made 10 minutes apart were significantly (p less than 0.05) correlated. Simultaneous measurements of regional cerebral blood flow by the microsphere and ultrafast computed tomography methods showed a significant (p less than 0.05) correlation for the hemisphere (r = 0.95), basal ganglia (r = 0.95), and neocortex (r = 0.94) but not for the internal capsule (r = 0.51). Microsphere and ultrafast computed tomography regional cerebral blood flow values were also in agreement in radiation-damaged brain with appreciable blood-brain barrier breakdown, and the two methods demonstrated similar responsiveness of regional cerebral blood flow to alterations in arterial carbon dioxide tension. The accuracy and sensitivity of the ultrafast computed tomography technique suggests that it affords a useful new tool for studying normal and abnormal regional cerebral blood flow.

Animals↗
PubMedDate not supplied

Origin of frontal N15 component of somatosensory evoked potential in man.

Origin of the frontal somatosensory evoked potential (SEP) by median nerve stimulation was investigated in normal volunteers and in patients with localized cerebrovascular diseases, and the following results were obtained. (1) In normal subjects, SEPs recorded at F3 (or F4) contralateral to the stimulating median nerve were composed of P12, N15, P18.5 and N26. Similar components were recognized in SEP recorded at Fz. (2) In patients in whom putaminal or thalamic hemorrhages had destroyed the posterior limbs of the internal capsules, frontal N15 and parietal N18 (N20) disappeared. These components were also absent in patients with cortical (parietal) infarctions. Among these patients, the thalamus was not affected in cases with putaminal hemorrhages and cortical infarctions. These facts indicate that the generator of the frontal N15 does not exist in the thalamus but that it originates from the neural structure central to the internal capsule, which suggests a similarity to the generator of the parietal N18. Because N15 was recorded in the midline of the frontal region with shorter latency than parietal N18, the frontal N15 might represent a response to the sensory input of the frontal lobe via the non-specific sensory system.

Brain Mapping↗