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The radial fibers in the globus pallidus.

In our Golgi collection of adult monkey brains the striatal efferents, i.e., the radial fibers in the globus pallidus and the "comb" bundle fibers in the internal capsule and in the cerebral peduncle, are well impregnated in the horizontally sectioned brain and in a sagittal sectioned brain. Since collaterals emerging from radial fibers are seen only in the horizontal series and not in the saggittal series, the interpretation is that they proceed anteriorly and posteriorly only, following the curvature of the pallidal segments, and do not run superiorly or inferiorly as they emerge. Although radial fibers emitting collaterals in the lateral segment and in the medial segment of the globus pallidus have been observed, it has not been possible to observe the same radial fiber emitting collaterals in both pallidal segments and the prospects of ever doing so are not good. The radial fibers converging in the globus pallidus pursue many radii and there is little coincidence between the plane of section and the planes in which they travel. At most only severed radial fiber segments 100-150 microns in length can be found in the horizontal sections needed to observe the collaterals. Moreover, sagittal sections trodorsally, as they pass through the internal medullary lamina to enter the medial segment of the globus pallidus. The radial fibers in the medial segment of the globus pallidus are continuous with the "comb" bundle fibers and appear to be thinner than the radial fibers in the lateral segment of the globus pallidus. It is not proved; nonetheless, the view expressed here is that the radial fibers are thinner in the medial segment of the globus pallidus because they may be the same fibers that gave off collaterals in the lateral segment of the globus pallidus. This is discussed in the light of the electrophysiological disclosure of Yoshida et al. ('71, '72) that caudatopallidal fibers are collaterals off caudatonigral fibers. The afferent plexuses of fine, "bouton en passage" fibers, which completely ensheath the long radiating dendrites in the globus pallidus (Fox et al., '66) are well impregnated in the horizontal series. Obviously, they are formed by a number of ultimate branches converging from the collateral brances of a number of different radial fibers. The divergence, too, in this system must be considerable; however, its true extent can only be surmised from the several radial fibers and radial fiber collaterals seen in the incompletely impregnanted Golgi section. Continued.

Animals↗

Two cases of anterior choroidal artery territory infarction.

Occlusion of the anterior choroidal artery (AChA) can cause infarction in the posterior limb of the internal capsule. Infarction is less frequently observed in the thalamus, midbrain, temporal lobe, and lateral geniculate body (LGB) territories of the AChA. The most common clinical finding is hemiparesis. Hemianesthesia may be severe at onset but is usually transient. Homonymous hemianopia, upper-quadrant anopia, or upper- and lower-quadrant sector anopia can be present. Occasionally these patients are reported to have transient abnormalities of higher cortical function. The most common stroke mechanism is known to be small-vessel occlusive disease, predominantly found in hypertensive and diabetic patients. Vasospasm due to ruptured aneurysm or intraoperative mechanical manipulation, and cardiac origin the AChA territory. The infarct lesion is usually recognized and diagnosed by computed tomography. The best treatment is still unknown.

Aged↗

[Infarction in the territory of the anterior choroidal artery due to embolic occlusion of the internal carotid artery--report of two cases].

A case with infarction in the territory of the anterior choroidal artery (AChA) due to embolic occlusion of the internal carotid artery (ICA) is rare. We described two cases and investigated the mechanism of the territory of the AChA. Case 1 was a 69-year-old man. Case 2 was a 71-year-old woman. The neurological examination in both cases showed left homonymous hemianopsia, left facial palsy, left hemiparesis and left hemisensory disturbance. CT scan in these cases showed infarctions of the right uncus, amygdaloid nucleus, genu and posterior limb of the internal capsule, globus pallidus, lateral geniculate body and tail of the caudate nucleus. The right common carotid angiogram showed a complete occlusion of the ICA at its cervical segment in case 1 and at its carotid siphon in case 2. In both cases, the left carotid injection visualized the right anterior cerebral artery and right middle cerebral artery via the anterior communicating artery well, but the right AChA was not visualized. In case 1, the collateral pathways from the right external carotid artery (ECA) and the right posterior communicating artery (PCoA) to the right ICA were not supplied and the precommunicating segment of the right posterior cerebral artery was hypoplastic. In case 2, the collateral pathway from the right ECA to the right ICA was not supplied.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Termination areas of corticobulbar and corticospinal fibres in the rat.

Solution of the cobaltic lysine complex compound injected into the bulbar pyramid was taken up by pyramidal tract (PT) fibres and intraaxonally transported as far rostral as the internal capsule, and as far caudal as segment C4 of the spinal cord. With sulfide-precipitation of the cobalt and silver-intensification of the CoS, terminal branches of corticobulbar and corticospinal fibres could be shown in the following structures: In the pons the medial, ventral and the medial part of the lateral pontine nuclei are supplied with collaterals of PT fibres. The medial pontine nucleus receives contralateral PT fibres as well. The nucleus raphe magnus receives PT fibre collaterals from both sides. In the reticular formation contralateral fibres terminate in n. reticularis pontis caudalis, n. gigantocellularis, n. paramedianus, n. reticularis ventralis and dorsalis. Ipsilateral fibers terminate in the n. gigantocellularis and n. reticularis ventralis. The inferior olive receives both ipsilateral and contralateral PT fibres. All parts of the central gray substance are supplied by ipsi-and contralateral fibres which emerge from the PT at the level of the pyramidal decussation. The caudal nucleus of the spinal nucleus of the trigeminus receives a strong bundle of crossing PT fibres which terminate in the subnucleus magnocellularis. The dorsal column nuclei are virtually outlined by the numerous terminals of PT fibres. An oval area at ventrolateral aspect of the cuneate nucleus is innervated by PT fibres. The neurones of this area send their axons to the dorsal white column. In the spinal cord PT fibre terminals delineate four areas of termination. The first is the internal basilar nucleus which is the most richly supplied. The second lies lateral and ventral to this nucleus including segments of laminae V, VI, and VII. The third area extends into the ventral horn including a small zone of the ventral part of lamina VII. Thin PT fibre collaterals may establish here direct contacts with motoneurone dendrites. The fourth area includes laminae III and IV and receives individual terminal formations of thicker PT fibres. Findings which corroborate and which extend previous results are discussed. A few notes are made on the functional significance of some of these fibre connections.

Animals↗

Sensorimotor stroke due to thalamocapsular ischemia.

A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 X 2 X 4-mm lacune in the ventral posterior nucleus of the left thalamus, with a zone of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct.

Cerebrovascular Disorders↗

Capsular infarcts: the underlying vascular lesions.

In ten patients, 11 infarcts involving mainly the internal capsule have been examined pathologically. Serial sections of the involved basal ganglia were studied in ten infarcts and only a gross dissection was made in the other. The implicated penetrating arteries were traced throughout their length and obstructive vascular lesions were found in nine instances. In two of the nine there was an atheromatous plaque with a superimposed thrombus, in four an atheromatous plaque had caused severe stenosis, in one a destructive arterial process lipohyalinosis had occurred, in one case the nature of the obstruction remained "uncertained," and in one the penetrating arteries were obstructed at their orifices by an atheroma in the superior division of the middle cerebral artery. In two cases the vessels were patent, suggesting embolism. The atheromas consisted almost exclusively of a conglomerate of fat-filled macrophages. The clinical correlate was a pure motor hemiplegia or hemiparesis involving the face, arm, and leg without sensory deficit, homonymous hemianopia, receptive aphasia, or apractognosia. Confusion was prominent in one patient.

Aged↗

The resolving stroke and aphasia. A case study with computerized tomography.

A 39-year-old man suffered an intracerebral hemorrhage in the region of the left internal capsule deep to Wernicke's area. The location of the lesion was confirmed by computerized tomography (CT) performed two days postictally. Two weeks after admission, the Boston Diagnostic Aphasia Examination (BDAE) diclosed Wernicke's aphasia. We hypothesize that the hematoma exerted pressure on Wernicke's cortical area, thus causing the resulting Wernicke's aphasia at that time. A CT scan three months later showed absorption of the hematoma, with a residual low-density lesion deep to Wernicke's area, in the region of the arcuate fasciculus. At that time, BDAE testing disclosed a mild conduction aphasia. Serial CT scanning combined with discriminating clinical evaluation of aphasia provides a valuable opportunity for study of the processes underlying stroke resolution and aphasia.

Adult↗

Subarachnoid spinal hemorrhage in a case of systemic lupus erythematosus.

A 50-year-old woman with an 18-year history of systemic lupus erythematosus (SLE) died after an exacerbation of the illness, characterized by deteriorating mentation and right hemiplegia. Necropsy revealed massive spinal subarachnoid hemorrhage resulting from aneurysmal dilation and rupture of the posterior spinal artery, which was involved by vasculitis. The left parietal lobe and internal capsule contained recent infarcts. To our knowledge, this is the first reported case of SLE with spinal subarachnoid hemorrhage revealed by necropsy.

Aneurysm↗

Ataxic hemiparesis from lesions of the corona radiata.

Ipsilateral cerebellar and pyramidal signs suddenly developed in three patients. Computed tomography revealed small infarcts of the corona radiata in two patients and a small infarct in the posterior limb of the internal capsule in the third. Ataxic hemiparesis can result from lesions of the corona radiata as well as many other points along the corticopontine pathways.

Aged↗

Mutism after closed head injury.

Prospective study of patients admitted to a hospital for closed head injury showed that nine patients (nearly 3%) became mute for varying periods despite recovery of consciousness and communication through a nonspeech channel. Computed tomography (CT) showed subcortical lesions situated primarily in the putamen and internal capsule of four patients, whereas four of the five patients without subcortical lesions had left-hemisphere cortical injury. The patients without subcortical injury visualized by CT exhibited a longer duration of impaired consciousness consistent with severe diffuse brain injury and they showed more long-term linguistic deficits. We related our findings to recent studies of atypical aphasia after occlusive vascular lesions of the basal ganglia.

Adolescent↗

Unilateral palatal paralysis caused by lesion in the corticobulbar tract.

A patient with a cerebral infarct affecting the anterior limit of the superior segment of the corona radiata had unilateral paralysis of the palatal muscles without notable weakness of the extremities. The site of the lesion corresponded to the location of the corticofugal motor tract from the motor cortex to the genu of the internal capsule.

Aged↗

Ataxic hemiparesis from small capsular hemorrhage. Computed tomography and somatosensory evoked potentials.

We studied three cases that fit the clinical syndrome of ataxic hemiparesis. Computed tomography revealed small hemorrhages of the posterior limb of the internal capsule in all the cases, and somatosensory evoked potential studies predicted a disturbance of the lemniscal pathway from the thalamus to the parietal sensory cortex without demonstrable sensory loss. These results suggested that ataxia of the contralateral limbs following capsular lesion might result from a disruption of the thalamocortical sensory projection. The site of the lesion, the pathologic cause, and the underlying mechanism of ataxia are not necessarily homogeneous within the syndrome.

Aged↗

Anterior choroidal artery-territory infarction. Report of cases and review.

Occlusion of the anterior choroidal artery (AChA) can cause infarction in the posterior limb of the internal capsule. Infarction is less frequent in the thalamus, midbrain, temporal lobe, and lateral geniculate body territories of the AChA. The most common clinical sign is hemiparesis. Hemisensory loss is usually transient but may be severe at onset. Homonymous upper-quadrant anopia, hemianopia, or upper- and lower-quadrant sector anopsia can be present. A homonymous defect in the upper and lower visual fields sparing the horizontal meridian is probably diagnostic of a lesion in the lateral geniculate body in the territory of the AChA. The most common stroke mechanism is small-vessel occlusive disease, predominantly found in hypertensive and diabetic patients, but cardiac-origin embolism also can affect the AChA territory. Two of our patients had infarction after temporal lobe resection for epilepsy. Occasionally patients have associated disabilities of higher cortical function that are usually transient. The lesion should be recognizable by computed tomography.

Adult↗

Acalculia following a dominant-hemisphere subcortical infarct.

A 60-year-old, right-handed woman experienced persistent impairment of calculating ability following a subcortical infarct involving the head of the left caudate nucleus, the anterior superior putamen, and the anterior limb of the internal capsule extending superiorly into the periventricular white matter. Acalculia resulted from defects of numerical syntax, the loss of ability to manipulate mathematical concepts, and impaired working memory.

Aphasia↗

Sensory aprosodia with left hemiparesis from subcortical infarction. Right hemisphere analogue of sensory-type aphasia with right hemiparesis?

We report a case of sensory aprosodia with left hemiparesis following an ischemic infarction of the right thalamus and posterior limb of the internal capsule. Bedside evaluation, confirmed by special quantitative tests, demonstrated normal spontaneous affective prosody and gesturing with marked impairment of affective repetition and comprehension of affective prosody and gestures. A left hemiparesis with sensory loss was also present. This combination of deficits appears to represent the right-side analog to the unusual syndrome of Wernicke-type aphasia with right hemiparesis occasionally observed following left subcortical injury, thus providing further support for the hypothesis that the functional-anatomic organization of affective language in the right hemisphere mirrors that of propositional language in the left.

Auditory Perception↗

Basal forebrain infarction. A clinicopathologic correlation.

Following the repair of a ruptured anterior communicating artery aneurysm, a patient had a severe anterograde amnesia with sparing of other intellectual functions, apathy and loss of volition, altered arousal, and partial diabetes insipidus. Postmortem examination of the brain revealed bilateral destruction of the septal gray, nucleus accumbens, and nucleus of the diagonal band of Broca. Also involved in the lesion were inferior portions of the anterior limb of the internal capsule and globus pallidus. Discrete, microinfarcts were present in the paraventricular hypothalamic gray. Long-term therapy with desaminoarginine vasopressin nasal spray had no effect on the patient's neuropsychologic deficits.

Adult↗

Lateral thalamic infarcts.

A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.

Aged↗

Subcortical structures in aphasia. An analysis based on (F-18)-fluorodeoxyglucose, positron emission tomography, and computed tomography.

Subcortical structural damage that includes the anterior and posterior internal capsule, caudate, thalamus, lenticular nuclei, and insula has been shown to cause aphasias. A critical question that has not been resolved is whether the role of these structures on behavior is a direct one or whether it is indirect through the cortex. We have used pathway analysis to evaluate computed tomography, glucose metabolic, and language data from 47 aphasic patients to answer this question. For fluency (from the Western Aphasia Battery), subcortical structural damage had direct and indirect (through frontal lobe) effects on the behavior. For a comprehension task (sequential commands), subcortical damage had no direct effect and only a slight indirect effect through the temporal lobe. Thus, both direct and indirect effects of subcortical damage can be demonstrated for specific behavioral measures.

Adult↗