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A 61 year-old man with severe hypertension present with a crural paresis and ipsilateral ataxia. CT scan showed a low density area suggestive of a lacuna in the posterior limb of the internal capsule.
Efferent pathways of the LD nucleus of the thalamus were studied in 6 Papio-papio baboons with the retrograde transport technique utilizing HRP. Injections were made in cingular and parietal cortex and hippocampal formation. Large projection from the LD to the cingular and subicular cortex were visualized as reciprocal connections. No pathway to parietal area 7 was found. The course of the fibers is via the fornix, the cingular bundle and the retro-lenticular portion of the internal capsule. The result of this study make it necessary to reconsider neuropathological hypotheses on memory.
A 84-year-old diabetic man had a complete right-sided hemiplegia with ipsilateral hypoesthesia and vertical diplopia, but no aphasia or hemianopia. The CT scan showed a low-density area in the posterior limb of the left internal capsule, in the territory of the anterior choroidal artery. The mechanism of diplopia is discussed and is attributed to the involvement of the mesencephalic territory of the anterior choroidal artery.
Forty-two dynamic CT studies were performed on 27 patients with cerebral infarction (11 to 75 years of age), and perfusion patterns of low density areas on plain CT were evaluated. The initial studies were performed 1.5 hours to 60 days after acute onset. In 14 patients, repeat studies were carried out to know how the perfusion pattern changes with time. All scannings were done on the level which includes anterior horns and trigones of lateral ventricle, thalamus, and internal capsules. CT scanners used were SIEMENS SOMATOM 2 and GE CT/T 8800. Procedures were as follows: 65% amidotrizomeglumin (1 ml/kg) was injected over 5 seconds through 18G needle placed in a antecubital vein. Injection of the contrast media was started with initiation of the second scanning. Totally 8 and 10 serial scans were performed, in SOMATOM 2 and CT/T 8800 respectively. Perfusion pattern is evaluated by comparing two time-density curves obtained from low density area on plain CT and the same region of contralateral side. The following results were obtained. The perfusion pattern in the low density area on plain CT varies among patients at any periods after onset, ranging from absent perfusion pattern to hyperfusion pattern. No consistent perfusion pattern was obtained at any given time after onset. Repeat dynamic CT revealed that the perfusion pattern in the low density area changed with time variously. The perfusion pattern or change of perfusion pattern did not correlate with outcome of the patient.(ABSTRACT TRUNCATED AT 250 WORDS)
A patient with chronic hypertension presented clinically with the dysarthria--clumsy hand syndrome. A CT scan demonstrated putaminal hemorrhage sparing the internal capsule. This case provides additional evidence that lacunar syndromes may not be due to lacunar infarction. The localization of dysarthria--clumsy hand appears similar to that of ataxic hemiparesis.
Although the therapeutic effect of spinal cord stimulation (SCS) for spastic movement disorders is still controversial, its effect for multiple sclerosis has been supported by several authors. Among various clinical beneficial effects, reduction of the spasticity may be attractive for physical therapy of post-apoplectic patients. Two patients suffered from post-apoplectic spastic hemiplegia were selected for SCS. Electrodes of Medtronic's SCS system were placed at lower cervical or upper thoracic spinal cord extradura. Stimulation of 30-75 Hz in frequency and 0.3-0.5 in voltage continued for 12-14 hours during daytime every days. U.S., a 74-year-old man, suffered from cerebral infarction in the right internal capsule was treated by SCS at one year after the stroke . At the fourth day after SCS spasticity of the lower extremity reduced and his gait improved remarkably. Upper extremity also showed reduction of spasticity at the seventh day after SCS. H/M ratio before SCS was 0.85 and reduced to 0.77 at 68 th day after SCS. Recovery curve of H-wave also improved after SCS. Y.K., a 47-year-old man, suffered from pontine hemorrhage showed right spastic hemiplegia. He was treated by SCS at 13th month after the hemorrhage. Spasticity of the upper extremity reduced slightly and his gait improved obviously. H/M ratio which was 1.05 before SCS, reduced to 0.75 at 122 nd day after SCS. Recovery curve of H-wave improved remarkably after the treatment. It was obvious that the spasticity reduced after SCS and function of the extremities recovered to some extent in above patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The author choroidal artery syndrome is a rare disorder associating, in its complete form, a hemiplegia, a hemianesthesia, and a homonymous lateral hemianopia. Four cases are reported in which the diagnosis was confirmed by a CT scan, which demonstrated a low density area in the posterior part of the posterior limb of the internal capsule, sparing the thalamus medially, and extending laterally to the apex of the pallidum thus corresponding to the area supplied by the anterior choroidal artery. The incomplete forms of this syndrome and clinicopathological correlations are discussed.
The projections from the visual cortex to thalamic nuclei in the opossum were investigated by degeneration and radioautographic methods. Efferent axons from the striate cortex course from the internal capsule to the thalamus in two bundles, one of which innervates the reticular and dorsal lateral geniculate nuclei, while the other bundle innervates the external layer of the ventral lateral geniculate nucleus. Both bundles course along and through terminal fields found in the lateral posterior nucleus. The visuotopic organization inferred from the corticofugal pathway shows that projection lines in the dorsal lateral geniculate nucleus (DLGN) run along medio-lateral strips including both the beta and alpha segments, across the quasi-laminae of retino-geniculate projection, and that naso-temporal axes in the visual field run in a dorso-ventral direction through the DLGN. The external layer of the ventral lateral geniculate nucleus receives a projection from the striate cortex and bilateral projections from the retina, and naso-temporal axes in the visual field are represented along a dorso-ventral direction in this layer. The striate cortical projections cover approximately the lateral two-thirds of the lateral posterior nucleus, overlapping a small retinal terminal field, and naso-temporal axes in the visual field are represented onto the cortico-recipient zone in a mirror-symmetric direction to that of the adjoining DLGN. In all these three cortico-recipient zones, dorso-ventral axes in the visual field are represented in a rostro-caudal direction.
We reported three cases of an aphasic syndrome caused by unusual lesion distribution. Our patients, language disorders could be summarized as transcortical sensory aphasia and showed following symptoms; (1) fluent paraphasic verbal output, (2) anomia which was not facilitated by cueing, (3) impaired comprehension of spoken language, (4) preserved capacity of repetition, (5) preserved ability of reading aloud with impaired comprehension of the written material and (6) agraphia. In addition, all had no associated physical neurological signs such as hemiparesis or hemianopsia. All were right handed. All three cases showed the similar lesion distribution by computed tomographic scanning of the brain. All had low density areas in the anterior portion of the left basal ganglia including the head of the caudate nucleus, the anterior portion of the putamen, the anterior portion of the anterior limb of the internal capsule and the nearby white matter. Case 2 also had the small right hemisphere lesion in the white matter near the anterior portion of the lateral ventricle. Transcortical sensory aphasia with this lesion distribution has not been reported. We attributed the causative damage to lesions of the white matter and not to lesions of the basal ganglia per se. It was also speculated that fluent aphasia can be produced by the anteriorly situated white matter lesion if issuing fibers from the Broca's area were spared. Finally a possible anatomoclinical correlation for "transcortical alexia" (preserved oral reading and impaired reading comprehension) was attempted. The symptom is probably a reflection of the fact that the posterior speech area including the angular gyrus was left intact.
Local cerebral glucose utilisation (LCGU) was measured with the [14C] deoxyglucose ([14C] DG) method in the awake, free moving Mouse. Values vary from 112 mumoles. 100 g-1. min.-1 in the superior colliculus, the most active structure, to 22 mumoles. 100 g-1. min.-1 in the internal capsule. Glucose consumption is high in fasciculus retroflexus, a result peculiar to the Mouse when compared to the other Mammals were studied so far with this method. The modifications in plasma sampling proposed in this paper should facilitate the use of the [14C] DG method in free moving animals as small as the Mouse, and allow for study of the effects of behavior on local cerebral energy consumption.
Parameters of motor asymmetry and the process of learning were studied in cats during elaboration of an active defensive reflex, following unilateral coagulation of various subcortical formations, predominantly of the extrapyramidal system. The changes of these parameters developed after the coagulation independently of each other. Lesion of the globus pallidus was attended, as a rule, with non-reversible changes of motor asymmetry and slight changes of the learning parameter. Destruction of the putamen and claustrum produced temporary disturbances of lateralization and learning processes. At early stages of the instrumental habit elaboration, the destruction of pathways passing in the internal capsule from different cortical structures to formations of the extrapyramidal system, brings about changes in the parameters of motor asymmetry and the learning process; at final stages--a similar lesion does not affect either parameter.
Unilateral hemichorea-hemiballismus developed suddenly in a 60-year-old man. Computed tomography revealed a small area of low density in the region of the left anterior limb of the internal capsule and the head of the caudate nucleus which was consistent with a lacunar infarction. Haloperidol gradually abolished the symptoms within 7 days of their onset. No further choreoballistic movements were experienced. This report reveals that ballistic movements may occasionally be caused by lesions lying some distance from the subthalamic nucleus of Luys.
The fibre systems of the developing mouse forebrain were examined by a combination of scanning and transmission electron microscopy. No clear pattern of ependymoglial fibre distribution emerged, due to the numerous intersecting fibre pathways. Scanning electron microscopy did show the presence of numerous fine fibres, particularly in regions rich in ependymoglial processes, such as the caudopallial angle; but definite identification of processes as ependymoglial or neuronal was not possible. Transmission electron microscopy confirmed the presence of numerous intersecting fibre bundles, particularly in the intermediate layer. In the neostriatum, scattered fibre bundles of the internal capsule frequently contained ependymoglial fibres which may act as a skeleton for guiding developing axons to their appropriate destinations. The difference in depth of the ventricular layer at different parts of the ventricle was clearly shown in the scanning electron microscope and, at the stages examined, a subventricular layer was apparent in the region of the ventricular elevations.
Two weeks after epidemic parotitis a 10-year old boy developed an acute extrapyramidal syndrome together with pyramidal tract signs but without impairment of consciousness. The CSF showed mild pleocytosis. The CT of the brain exhibited a well defined circumscribed and symmetrical swelling and hypodensity of the basal ganglia and of the internal capsule. Only slight and transient dysrhythmia was to be found in the EEG. Therapy with Prednisolone, Biperidene and Tiapride resulted in regression of symptoms. But one year later rigor and pyramidal tract signs remained evident in spite of intensive physiotherapy and logopaedic measures. Residual symmetric atrophia of the basal ganglia became evident in the CT by dilatation of the anterior horns of the lateral ventricles caused by lacking of the vault of the caudate nuclei heads.
The radiation effects of 192Ir permanent implants into the cat brain were studied with respect to morphological changes, blood flow, brain water and electrolytes. 192Ir wires (10 animals) and non-radioactive silver wires (5 control animals) were placed stereotactically into the left internal capsule. Activity of 192Ir was 0.31 mCi, and accumulated dose at 5 mm distance was 3060 rad after 21 days and 4680 rad after 35 days, respectively. None of the animals presented a neurological deficit, and the EEG recording was without significant changes. Histological damage which could be attributed to the radiation was not observed. Serum proteins, however, were detected immunohistochemically in reactive astrocytes (3x), in macrophages (2x) and as diffuse perivascular accumulation. Brain water in the white matter near the implantation site increased from 68.6 to 73.2%, corresponding to a volume increase of about 17%. There was no change in the grey matter or the opposite hemisphere. Cerebral blood flow decreased slightly but there was no relationship with the development of edema. The findings suggest that low dose rate topical irradiation of the brain produces primarily membrane dependent changes, resulting in local brain edema.
Degree of motor impairment, some sensory qualities and self-care ADL were registered in 53 patients with hemisyndrome due to stroke in whom the brain lesion could be visualized by computerized tomography or by cerebral angiography. Central brain damage (internal capsule, basal ganglia, thalamus) resulted in significantly higher degree of motor impairment than neo-cortical damage, while the size of the damage apparently did not influence the motor-function. Self-care ADL was significantly associated with level of motor impairment. Moreover, significantly less final recovery of exteroception and kinesthesia was observed for lesions in the non-dominant than the dominant hemisphere. It is suggested that in patients found suited for admittance to rehabilitation wards visualization of the brain damage may be a useful adjunct when stating the goals for the rehabilitation process.
Much can be learned about the brain's function in pain processing through electrical stimulation. The spinothalamic tract which is conceived to be the chief pathway for nociceptive pain and whose interruption induces dissociated sensory loss can be recognized from the anterolateral columns of the spinal cord to the posterior thalamus by the induction of feelings of chiefly contralateral, somatotopographically organized, warm, cool, or cold sensations, less often burning and rarely pain. The spinoreticulothalamic tract, whose function in normal pain processing is controversial and whose interruption produces no clinically detectable sensory loss, is normally silent to stimulation. However, in patients with deafferentation pain, it appears to become sensitive to electrical stimulation, both in the anterolateral columns and in midbrain and medial thalamus, giving rise to chiefly contralateral, non-somatotopographically organized, burning or painful sensations which often reproduce fairly accurately the patient's pain. This phenomenon, which does not appear to occur in patients with nociceptive pain, may reflect denervation neuronal hypersensitivity which is a possible pathophysiological mechanism explaining deafferentation pain. The dorsal column/lemniscal system can be recognized by electrical stimulation from the spinal cord to the somatosensory cortex by the induction of paraesthesiae. Its chronic stimulation at the level of the dorsal column, the ventrocaudal nucleus or the internal capsule appears capable of suppressing deafferentation pain. The arc of neuronal tissue extending from the septal area through hypothalamus and periventricular grey to the periaqueductal grey, which acts as a receptor area for opiates and endorphins, thereby exerting an inhibitory effect on access to the spinothalamic tract, can also be exploited through chronic stimulation for the control of pain. Stimulation of the periventricular area gives rise to feelings of warmth, comfort and relaxation, of the hypothalamus, horror and autonomic effects while that of the periaqueductal grey induces discomfort, distress, anxiety and weeping, and of the septal area flushing, paraesthesiae, nausea, nystagmus and a feeling of warmth. Thus four brain systems involved in pain signalling can be recognized by electrical stimulation, one which conveys nociceptive pain to consciousness, another that suppresses it, one that may undergo denervation neuronal hypersensitivity and bring deafferentation pain into consciousness, possibly by establishing novel connectivity and one that is presumably capable of suppressing that hyperactivity.
Unilateral or bilateral removal of kitten sensorimotor (SM) cortex prior to the fourth postnatal week was followed by recovery of contact placing (CP) to stimulation of any of the four forepaw cutaneous fields. However, immediately after a removal under ethyl chloride, CP was depressed contralaterally, especially to lateral stimulation (lateral CP). When the operated kitten aged to 5--9 weeks, the likelihood of CP secondarily declined contralateral to the SM cortical extirpation, but was restored by administration of d-amphetamine. An initial extirpation after the fifth postnatal week was followed by a severe deficit in CP. 2. Cooling the SM cortex, internal capsule or bulbar pyramid during the 2nd and 3rd week was followed by reversible, contralateral loss of lateral CP, extension of the forelimb and, later, by reduced movements. Lateral CPs were often hypermetric prior to loss. By contrast, cooling SM cortex in the first week was usually ineffective. Thus, during the 2nd week, lateral CP developed a dependence on SM cortex, and in particular on PT neurons. 3. After a delay usually of 1 or more min, cooling the SM cortex reduced the resting discharge of individual neurons in buried motor cortex; the antidromic conduction time in PT neurons was significantly increased and the spike height was reduced.