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Three cases of unilateral dystonia of vascular origin are presented and compared with those in the literature. Damage in the region of the lenticulostriate arteries accounted for ischaemic lesions of the putamino-capsulo-caudate region, the external pallidum probably also being involved. This syndrome appears if the ischaemic accident took place during childhood. The functions of each of these structures and the possible role of the anterior limb of the internal capsule are discussed.

The authors report the results of a Positron Emission Tomographic (PET) study of local cerebral blood flow and oxygen consumption in one patient with a right capsulo-thalamic ischemic lesion. That lesion is well demonstrated using X-ray CT Scan. PET study demonstrates a decreased perfusion and metabolism at three levels: first in right thalamus region, second in whole right hemisphere, more marked at orbitofrontal area and third at the level of the left cerebellar hemisphere. The authors point out the usefulness of PET studies which allow a better understanding of clinical signs by demonstrating functional consequences of damage in deeply located structures such as thalamus and internal capsule on cerebral and cerebellar cortices.

Vascular changes occurring after stereotaxic injection of the excitatory neurotoxin kainic acid (KA) into the rat striatum were studied at various time intervals after the lesion using laminin immunohistochemistry. Laminin immunohistochemistry revealed marked vascular changes, including presumed neovascularization, in the lesioned striatum. Vessels with increased laminin immunoreactivity were demonstrated from 2 days up to at least 5 months following the injection. The majority was capillary vasculature, which was distributed throughout the lesioned striatum, sometimes being arranged densely along the needle tract. Fine spike-like sprouts called streamers were also loaded with laminin immunoreactivity. In contrast, laminin immunoreactivity in vessels in the control striatum was negligible. Vascular changes detected by laminin immunohistochemistry preceded but then almost paralleled gliosis demonstrated by glial fibrillary acidic protein immunohistochemistry. These results indicate that striatal injection of KA causes marked vascular changes including neovascularizations which are demonstrable by laminin immunohistochemistry.

A new angiographical classification of primary intracerebral hemorrhage is presented. We have clarified the predilection sites of intracerebral hemorrhage and the advancing direction of the hematoma by studying autopsy cases. Furthermore, we tried to detect the presence or absence of destruction of the internal capsule and ventricular rupture by means of angiography. Our classification, introducing the idea of dynamic changes of hematoma advancement from localized to advanced type, can be applied to clinical practice. This classification, along with the patient's level of consciousness, it felt to be the most important indication for operation.

The permeability of microvasculature in the cerebral cortex, neostriatum, and spinal cord to i.v. injected horseradish peroxidase (HRP) has been investigated in rats following experimental compression to 6.1 bars (abs.) air for 90 min, and subsequent decompression to the ambient pressure in 1 min. For comparison, 1 ml of 2.0 M urea was injected into the right common carotid artery of rats during 15 s. After exposure to compression-decompression, under the light microscope focal leaky areas were found in all the regions examined. The leakage was most prominent in the grey matter of the spinal cord, and the cerebral cortex. In decompressed rats, arterioles were most often the site of peroxidase extravasation, whereas extravasation of HRP was less frequently displayed by capillaries and venules. In urea-treated rats, capillaries and venules frequently displayed extravasation of HRP as well. Parenchymal cells accumulated the trace adjacent to the leaky areas. Under the electron microscope, the extravasation of HRP was associated with peroxidase-containing pleomorphic vesicular structures in the endothelium, both in decompressed and urea-injected rats. Moreover, in contrast to decompressed rats, the junctions between endothelial cells were penetrated by the trace in urea-treated rats. Accordingly, the results indicate that during decompression sickness the pathway for the extravasation of proteins is through vesicular transfer, whereas the injection of hyperosmolar urea induces extravasation, both through vesicular transfer and junctions between the endothelial cells.

A 6-year-old male with bilateral lenticulostriate arteriovenous malformations (AVMs) had suffered an intraventricular hemorrhage at the age of 10 days. Transfemoral cerebral angiography performed 6 years later revealed bilateral AVMs at the basal ganglia accompanied by vascular anomalies. Both AVMs appeared inoperable, and were treated conservatively. Bilateral, symmetrical cerebral AVMs are extremely rare, only three such cases having been reported.

A 58 year old hypertensive man suffered an acute right-sided hemiataxia associated with painful hypoesthesia. CT showed an infarct in the territory of the left anterior choroidal artery. The sensory defect involved all the elementary modes, but predominated on pain sensation. The ataxia suggested a cerebellar type of dysfunction, with hypermetria, intentional tremor, dysdiadochokinesia and a positive rebound phenomenon. There was no hemiparesis, no hemianopia, no neuropsychological dysfunction and no oculomotor abnormality. Hemiataxia with hemisensory defect has not been reported in stroke, and it constitutes a new clinical form of lacunar syndrome. The hemiataxia may be related to the finding on single-photon emission computed tomography (SPECT) using 123 I-amphetamine of a crossed cerebellar diaschisis, which may suggest a transneuronal deactivation. This metabolic depression may have been due to involvement of the temporo-parieto-pontine bundle of Türck in the retro and sub-lenticular portion of the internal capsule. The finding of a normal cortical blood flow may explain why no neuropsychological impairment was present, because of the absence of functional deactivation of the cortex by the underlying deep infarct.

A 72-year-old diabetic woman developed paroxysmal hemichoreoathetosis during an episode of nonketotic hyperglycemia. The movement disorder abated as the blood glucose normalized. A computed tomographic scan revealed a vascular malformation involving the lenticular nucleus on the side contralateral to the dyskinesia. Hyperglycemia has rarely been reported to cause episodic dyskinesias, but there have been no prior reports of patients with striatal vascular abnormalities in whom hyperglycemia seemingly caused a transient movement disorder.

To determine the possible role of age in motor rehabilitation, the authors compared the degree of restoration of impaired motor functions in patients of different age groups with infarction foci in the large hemispheres of the brain. Localization and size of post-ischemic changes in the cerebral substance were assessed by computer-aided tomography. By the end of the late rehabilitative period. (12 months after the development of infarction), there were no statistically significant differences between the degree of recovery of impaired motor possibilities. Most important for recovery seems to be an intactness of functionally significant structures, especially of the posterior femur of the internal capsule.

Severe displacement of the thalamostriate and internal cerebral veins from the midline results in an unfamiliar distortion of these vessels arteriographically. Depending on the side of the mass effect, the thalamostriate-internal cerebral vein complex will have either an infinity (infinity) or a W configuration. Because these configurations appear frequently, recognition and understanding of them aid in the interpretation of cerebral arteriograms.

We have previously reported that periventricular structures are hypoperfused in attention deficit and hyperactivity disorder (ADHD). This study has expanded the number of patients, who were divided into two groups: six patients with pure ADHD, and 13 patients with ADHD in combination with other neurologic symptoms. By using xenon 133 inhalation and emission tomography, the regional cerebral blood flow distribution was determined and compared with a control group. Striatal regions were found to be hypoperfused and, by inference, hypofunctional in both groups. This hypoperfusion was statistically significant in the right striatum in ADHD, and in both striatal regions in ADHD with other neuropsychologic and neurologic symptoms. The primary sensory and sensorimotor cortical regions were highly perfused. Methylphenidate increased flow to striatal and posterior periventricular regions, and tended to decrease flow to primary sensory regions. Low striatal activity, partially reversible with methylphenidate, appears to be a cardinal feature in ADHD.

The effects of neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) on local cerebral blood flow (LCBF) were studied in vivo in rat striatum. Administration of 1 and 5 nmol NPY as a bolus into the internal carotid artery caused a dose-dependent decrease in the ipsilateral striatal LCBF. This decrease developed slowly and persisted for at least 2 h, without affecting mean blood pressure. In contrast, CGRP, at a concentration of 10 pmol, increased striatal LCBF by about 30%, and the duration of the increase was about 1 h. However, at higher doses of CGRP no increase in LCBF was observed. These results suggest that NPY and CGRP released from nerve fibers innervating blood vessels can function as long-acting modulators of CBF.

Regional and mean cerebral blood flow (rCBF, CBF) were measured by tomography of inhaled 133Xe in 18 hemiparkinsonian patients before and after levodopa (L-dopa). Baseline mean CBF was 55 ml/ (100 g X min) after an L-dopa-free interval of at least 10 h (range 10-13) and remained unchanged at 56.1 ml/ (100 g X min) after optimal clinical improvement was achieved by L-dopa. However, L-dopa reduced rCBF significantly (P less than 0.05) in the striatum contralateral to the symptomatic limbs. In patients with adverse reactions such as hyperkinesias and on/off symptoms, flow tended to increase bilaterally in striatum and often markedly in midline structures anatomically related to globus pallidus and thalamus. Compared with a normal population, the subcortical rCBF distribution was asymmetrical with a reduced flow (-18%) in the striatum contralateral to the symptomatic limbs and in midline structures anatomically related to globus pallidus and thalamus (-12%). Cortical CBF was inverse related to the duration of Parkinson's disease (P less than 0.05), probably reflecting an increasing mental deterioration with time.