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At least 793 records · Page 44Linked to original sources
PubMed1994

MR imaging and angiography in tuberculous meningitis.

MRI was performed on 26 patients with tuberculous meningitis, with particular reference to document the cranial nerve abnormalities. MR angiography (MRA) was performed in 20 of the patients. Meningeal enhancement in the basal cisterns or over the convexity of brain was seen in all patients; two show ependymal enhancement. Tuberculomas, single (3), multiple (12) or miliary (2) were detected in 17 patients. Of the 9 patients with cranial nerve palsies, 7 showed contrast enhancement with or without thickening of the involved nerve. Abnormality signal intensity of the involved nerve was seen on proton density and T2-weighted images in one of these patients. MRA revealed focal arterial narrowing in 10 patients, the vessels commonly affected being the terminal segment of the internal carotid artery and the proximal segments of the middle and anterior cerebral arteries. One patient also had a small aneurysm of the proximal middle cerebral artery. Infarcts, haemorrhagic (8) or bland (6), were detected in 14 patients; most were the basal ganglia and internal capsules, large middle or anterior cerebral arterial territory infarcts being seen in only two cases.

Adolescent↗
PubMed1992

Cerebral sparganosis: analysis of 34 cases with emphasis on CT features.

Cerebral sparganosis is a rare parasitic CNS disease, producing chronic active granulomatous inflammation. We retrospectively reviewed the clinical data, CT scans and histopathologic specimens in 34 patients with cerebral sparganosis. The majority of the patients (89%) were rural inhabitants; 75% had a history of ingestion of frogs and/or snakes. The major presenting symptoms were seizure (84%), hemiparesis (59%) and headache (56%) of chronic course. On CT scans, the disease most frequently involved the cerebral hemispheres, particularly frontoparietal lobes, with occasional extension to the external and internal capsules and basal ganglia. The cerebellum was rarely involved. Bilateral involvement was seen in 26%. The main CT findings consisted of white matter hypodensity with adjacent ventricular dilatation (88%), irregular or nodular enhancing lesion (88%), and small punctate calcifications (76%). In combination, the CT triad above appears to be specific for this disease, and was noted in 62% of cases. Of 16 follow-up CT scans, 5 (38%) showed a change in the location of the enhancing nodule. With a single CT scan, it does not appear to be possible to determine whether the worm is alive or dead, information important for deciding whether to intervene surgically. Change in the location of the enhancing nodule and/or worsening of the other CT findings on sequential CT scans would suggest that the worm is alive and that the patient is a candidate for surgery.

Adult↗
PubMed1991

MR imaging of adrenoleukodystrophy.

We performed MRI in 7 cases with adrenoleukodystrophy (ALD), including 3 cases with childhood ALD, 3 cases with adrenomyeloneuropathy (AMN) and one symptomatic heterozygote. The symptomatic heterozygote was the mother of the patient with AMN. High-field-strength (2.0T) MRI was used in two cases with childhood ALD. In all 3 cases of childhood ALD, MR showed widespread lesions in both cerebral hemispheres. Areas of low intensity in the diencephalon or striatum on heavily T2-weighted images at 2.0T were seen in 2 cases with childhood ALD. Cerebral lesions confined to the internal capsule, cerebral peduncle and optic radiation in the adult onset ALD including AMN and symptomatic heterozygote, have not been reported and this confinement may indicate an early stage of the disease.

Adrenoleukodystrophy↗
PubMed1991

The MR spectrum of peroxisomal disorders.

In the last decade an increasing number of peroxisomal disorders has been recognized. Almost all peroxisomal disorders affect the central nervous system. Many of them lead to demyelination, some of them lead to migrational disturbances. The MR pattern of X-linked adrenoleukodystrophy is well known, but the pattern of the other peroxisomal disorders is less well known. We evaluated the gray and white matter abnormalities of 20 patients on 32 occasions. We compared the results with histological data and in this way came to the description of a number of characteristic MR patterns occurring in peroxisomal disorders: (1) Neuronal migrational disturbances in combination with hypomyelination, dysmyelination or demyelination. (2) Symmetrical demyelination of posterior limb of the internal capsule, cerebellar white matter and brain stem tracts with a variable affection of cerebral hemispheres. (3) Symmetrical demyelination, exhibiting two zones, starting in the occipital area and spreading outwards and forwards; affection of brain stem tracts. (4) Less characteristic patterns of demyelination. The patterns are illustrated and differentiation from other disorders is discussed.

Adolescent↗
PubMed1993

Gadolinium-enhanced MRI in central nervous system Behçet's disease.

Two cases of central nervous system Behçet's disease, studied by gadolinium-enhanced MRI, are presented. In one patient, whose clinical picture was dominated by a brain syndrome, the gadolinium enhancement resolved with clinical improvement, although the hyperintense areas in the mesencephalon on T2-weighted images persisted. In the second, who had a pseudobulbar palsy and a mild right hemiparesis, there were many abnormal areas, but an enhancing focus in the posterior limb of the left internal capsule was probably the lesion responsible for the hemiparesis.

Adult↗
PubMed1992

Radiological study of the brain at various stages of human immunodeficiency virus infection: early development of brain atrophy.

One hundred and one persons infected with human immunodeficiency virus (HIV-1), in whom other central nervous system infections or diseases were excluded, underwent brain CT and/or MRI at various stages of HIV-1 infection: 29 were asymptomatic (ASX), 35 had lymphadenopathy syndrome (LAS), 17 had AIDS-related complex (ARC), and 20 had AIDS. A control group of 32 HIV-1-seronegative healthy persons underwent brain MRI. The most common finding was brain atrophy, found in 9% of controls, and 31% of ASX cases, 29% of LAS, 59% of ARC and 70% of AIDS. Even the difference between the ASX or LAS groups and controls was significant. The changes were bilateral and symmetrical, and they were more severe at later stages of infection. Infratentorial atrophy was seen in the early stages; supratentorial atrophy became more pronounced at ARC, and generalized atrophy was typical of AIDS. Non-specific small hyperintense foci were found on MRI in 13% of controls and 6-15% of the infected groups. Larger, diffuse, bilateral white matter infiltrates were detected in 4 demented patients with AIDS. Four patients with AIDS and 1 with LAS had focal hyperintense lesions in the internal capsules, lentiform nuclei or thalamus, often bilateral on MRI. One patient with AIDS, examined with CT only, had low density in the lentiform nucleus. Loss of brain parenchyma can occur at an early stage of HIV-1 infection, and the atrophic process becomes more intense at later stages (ARC and AIDS). Parenchymal infiltration, seen as hyperintense areas on MRI, is most often associated with severe clinical symptoms, in the later stages of the disease.

Acquired Immunodeficiency Syndrome↗
PubMed1992

MRI and SPECT findings in amyotrophic lateral sclerosis. Demonstration of upper motor neurone involvement by clinical neuroimaging.

MRI was performed in 21 patients and single photon emission computed tomography (SPECT) with N-isopropyl-p-123I iodoamphetamine in 16 patients, to visualize upper motor neurone lesions in amyotrophic lateral sclerosis. T2-weighted MRI revealed high signal along the course of the pyramidal tract in the internal capsule and cerebral peduncle in 4 of 21 patients. SPECT images were normal in 4 patients, but uptake was reduced in the cerebral cortex that includes the motor area in 11.

Adult↗
PubMed1996

MR signal intensity of the perirolandic cortex in the neonate and infant.

Our purpose was the study the magnetic resonance (MR) signal intensity of the perirolandic gyri perinatally and to correlate it with the histological findings in formalin-fixed brains, focusing on myelination. MRI of 20 neurologically normal neonates and infants, of 37-64 weeks postconception (PCA), were studied retrospectively. We reviewed four formalin-fixed brains of infants 37-46 weeks PCA microscopically. The posterior cortex of the precentral gyrus (P-PRE) and the anterior cortex of the postcentral gyrus (A-PST) had different signal intensity from the adjacent surrounding cortex. On T1-weighted images P-PRE and A-PST gave higher signal 41-44 weeks PCA; on T2-weighted images, they gave lower signal 37-51 weeks PCA. Histological examination revealed very little myelination of the nerve fibres within both the P-PRE and the A-PST, while considerable myelination was present in the internal capsule and central corona radiata. The changes in signal intensity in the perirolandic gyri may reflect not only the degree of myelination but also the more advanced development of the nerve cells, associated with rapid proliferation and formation of oligodendroglial cells, synapses and dendrites. They could be another important landmark for brain maturation.

Age Factors↗
PubMed1982

Brain lesions in a case of cystinosis.

Cystinosis usually spares the brain or causes only deposition of cystine crystals without destructive lesions in choroid plexus or, rarely, in brain parenchyma. A case of cystinosis is presented with unusually long survival and with bilateral necrosis, numerous concretions, and extensive demyelination of internal capsule and brachium pontis. No cystine crystals could be demonstrated in these lesions although they were present in the choroid plexus. The symmetry and unique distribution of the lesions as well as their histopathology suggested a progressive process caused by the metabolic dysfunction of cystinosis. The validity of this hypothesis will be determined by future experience as renal transplants enable more patients to survive into adult life.

Adult↗
PubMed1984

Neuropathologic study on chronic neurotoxicity of 5-fluorouracil and its masked compounds in dogs.

5-Fluorouracil (FU) and its masked compounds tegafur (FT) and carmofur (HCFU) were administered orally to Beagle dogs daily for 6 months, and their chronic neurotoxic effects were examined morphologically. In ten dogs that survived the 6-month treatment large vacuoles produced by splitting of the intraperiod line of myelin were observed in the fornix in the wall of the third ventricle. In severely affected dogs large vacuoles developed in the medial preoptic area, medial portion of the internal capsule, the area around the subthalamic nucleus and the mammillo-thalamic tract. Axons of myelinated fibers affected by vacuolation were generally well maintained, and destruction of myelin was not detected. Though proliferation of glia cells or abnormality of oligodendroglia was not detected, a lipid deposit covered by a single layer membrane was observed in the cell bodies and processes of astrocytes. No abnormality was detected by electron microscopy in the cerebrum, inferior colliculus, cerebellum, or pons. Of eight dogs that died during the treatment period, large vacuoles were observed in the fornix in the wall of the third ventricle of four dogs treated for more than 1 month, and large vacuoles were present in the inferior colliculus in two dogs of the FT group in the above four dogs. In the HCFU group, the interruption of treatment for 6 months resulted in alleviation or disappearance of the vacuolar lesions. The above findings suggest that the neurotoxicity of FU and its masked compounds FT and HCFU in long-term treatment produces changes morphologically identical with one another in respect to the site of their manifestation and nature of lesion, that their common degraded product alpha-fluoro-beta-alanine (FBAL) plays a crucial role in their neurotoxic actions, and that vacuolar lesions, to which myelin was more vulnerable than neurons, can develop where the toxic substance readily deposits and accumulates.

Animals↗
PubMed1984

Effect of dexamethasone on glial fibrillary acidic protein in peritumorous edema of cats: a morphometric study.

In 54 cats experimental brain tumors were produced by xenotransplantation of the blastomatous glial cell clone RG2 into the internal capsule of the left hemisphere. Fifteen of these animals were treated with dexamethasone for 1 week and four animals for 2 h. The occurrence of glial fibrillary acidic (GFA) protein in tumor and peritumoral edema was studied by immunocytochemistry at intervals ranging between 3 and 35 days after implantation. High concentrations of GFA protein were present in giant and many of the larger tumor cells but not in small tumor cells. In peritumorous white matter it appeared in reactive astrocytes, where it reached its maximum 2 weeks after implantation. At this time, morphometric evaluation of GFA protein-positive areas revealed an increase from 0.095 +/- 0.035% to 5.17 +/- 1.42%. Application of dexamethasone for 1 week reduced this area to 1.67 +/- 0.57% (P less than 0.001). The results obtained demonstrate that the development of peritumorous edema is associated with considerable stimulation of GFA protein production which is inhibited by dexamethasone. Production of GFA protein by reactive astrocytes, in consequence, does not seem to be involved in the resolution process of peritumoral edema under dexamethasone therapy.

Animals↗
PubMed1986

Early and late effects on the normal dog brain of permanent interstitial iridium-192 irradiation.

To investigate the effects of a permanent interstitial source of gamma-irradiation on normal brain tissue, single iridium-192 (Ir-192) wires (1.05 mCi) were stereotactically implanted into the left centrum semiovale of adult dogs (survival times, 25, 46, 74, 230 and 362 days). Within 25 days, a coagulation necrosis developed in the immediate vicinity of the radioactive source. In later stages, the necrosis increased in size and became progressively mineralized. Staining for extravascular immunoreactive serum proteins revealed the presence of a chronic perifocal vasogenic edema, which extended into the white matter of the entire ipsilateral hemisphere. This edema persisted through all stages and showed a significant decrease only in the animal with a 1-year survival. A reactive gliosis with formation of a dense network of glial fibrillary acidic protein-positive astrocytes developed around the central necrosis in the adjacent white matter and, at later stages, in the contralateral hemisphere. Demyelination was restricted to the ipsilateral centrum semiovale without affecting the internal capsule or the contralateral hemisphere. It was present as early as 25 days and showed no tendency to increase at later stages. Analysis of the sequential morphological changes following Ir-192 implantation suggests that the central coagulation necrosis represents a direct radiation effect, the sharp focal delineation of which can be explained by the physical characteristics of the radiation source, i.e., rapid fall-off of the dose at short distances. Due to the continuous emission of radiation energy, there is a perifocal zone with overlapping of progressive radiation damage and tissue organization. This focus becomes the source of a chronic vasogenic edema, which in turn is most likely to be responsible for the partial demyelination of the adjacent centrum semiovale. The widespread reactive gliosis observed at all stages may also, in part, be a consequence of chronic vasogenic edema, but its distribution suggests that direct radiation effects may also be involved.

Animals↗
PubMed1983

The effect of dexamethasone on serum protein extravasation and edema development in experimental brain tumors of cat.

Experimental brain tumors were produced in 20 cats by stereotaxic xenotransplantation of a blastomatous glial cell clone into the internal capsule of the left hemisphere. Ten of these animals were treated after 2 weeks with a single injection of 10 mg dexamethasone in crystalline suspension. Three weeks after xenotransplantation vascular permeability was studied by electron microscopy with horseradish peroxidase as the barrier tracer (four animals), and extravasation of serum proteins was visualized by immunohistochemistry, using an image processing system (16 animals). In animals used for immunohistochemistry, the water content of peritumoral brain tissue was also determined. In both treated and untreated animals, spherical tumors with a diameter of about 10 mm were present at the implantation site. Extravasation of horseradish peroxidase was detected only in the tumor, but there was accumulation of serum proteins both in the tumor and the peritumoral white matter. Edema, in consequence, originated mainly in the tumor from where it spread into the surrounding brain tissue. Corticosteroid therapy reduced the water content of peritumoral brain tissue but did not affect increased barrier permeability of tumor vessels, and only slightly improved peritumoral accumulation of serum proteins. It is concluded that amelioration of tumor edema by corticosteroids cannot result solely from tightening of the blood-brain barrier to circulating macromolecules but must be due to an active restoration of cerebral water homeostasis despite persisting serum protein extravasation.

Animals↗
PubMed1981

Gliomatosis cerebri diffusa. A case report.

The clinico-pathologic findings in an additional case of gliomatosis cerebri are reported: a 60-year-old woman died 8 months after the onset of a progressive deterioration of both the neurologic and mental conditions. Neuropathologic examination disclosed wide demyelination of both hemispheres, communicating through the corpus callosum, extending downward along the internal capsule to the brainstem structures. Cellular stains showed the presence of elongated astrocytes, multinucleated cells, mitotic and anaplastic figures, involving the demyelinated areas and the neighboring regions, and allowed the diagnosis of gliomatosis cerebri diffusa. The nosologic and pathogenetic aspects of this rare entity are discussed.

Autopsy↗
PubMed1987

Proton relaxation time of immature brain. II. In vivo measurement of proton relaxation time (T1 and T2) in pediatric brain by MRI.

T1 and T2 of brain tissue were measured in vivo in children by means of an NMR imaging system (resistive magnet 0.15 T). The subjects were 47 children aged from 2 weeks to 15 years. The sites measured were the basal ganglia (thalamus, caudate nucleus and putamen), internal capsule, cerebral cortex and white matter. T1 and T2 in the infant cases were prolonged significantly compared with those in the older children. The prolongation in the white matter was particularly remarkable. In infants approximately 1 year of age, T1 of cerebral cortex already showed no significant changes as compared with T1 in cases aged 15 years. On the other hand, T2 was prolonged significantly up to 3 years of age.

Adolescent↗
PubMed1988

An immunohistochemical and electron microscopic study of extra-renal basement membranes in dogs with Samoyed hereditary glomerulopathy.

Samoyed hereditary glomerulopathy (SHG) in dogs has been employed as a model for human hereditary nephritis (HN), since affected dogs and patients show splitting of glomerular capillary basement membranes by electron microscopy (EM) and absent staining of glomerular capillaries for Goodpasture antigen (GPA) by immunofluorescence (IF). EM and IF were used to examine basement membranes (BM) in skin, lung, choroid plexus, lens, retina, and inner ear in SHG. By EM, BM in these tissues appeared similar in affected male, carrier female, and unaffected dogs. By IF, GPA could be detected only in lens capsule, internal limiting membrane of retina and basilar membrane of inner ear of unaffected and carrier female dogs, but not in affected male dogs. However, eye abnormalities and hearing loss were not present in any dogs, in contrast to their frequent occurrence in human HN. Our findings on extra-renal BM in SHG suggest that GPA is not required to maintain normal vision or hearing in affected male dogs and permit a greater understanding of the pathogenesis of human HN.

Animals↗
PubMed1993

Dysarthria in bilateral thalamic infarction. A case study.

A patient suffering from bilateral thalamic infarction in the region supplied by the paramedian arteries sparing the internal capsules underwent acoustic analysis of sentence utterances. The results were compared with the findings obtained in parkinsonian subjects, in patients with upper motor neuron lesions, and in normal subjects. Acoustic measurements revealed increased pitch, monotonous speech, rough voice quality, and normal speech tempo concomitant with articulatory impreciseness in terms of incomplete closure productions. This constellation resembled parkinsonian dysarthria. Damage to the thalamic projection area of the pallidal efferents, therefore, seems to be the most probable cause of the patient's speech disorders. In parkinsonian subjects stereotactical lesions of this structure ameliorate rigor, but not akinesia. Thus, our patient's speech deficits, and by analogy the corresponding parkinsonian dysarthric disturbances, may be considered akinetic signs.

Adult↗
PubMed1992

Thalamic ataxia.

Seventeen patients with hemiataxia as a manifestation of thalamic infarction were studied. Hemiataxia had the main clinical characteristics of a "cerebellar type" of ataxia, though it never occurred in isolation, being associated with ipsilateral sensory disturbance (hemiataxia-hypaesthesia) in 7 patients, with ipsilateral sensory disturbance and hemiparesis (hypaesthetic ataxic hemiparesis) in 8 patients, and with hemiparesis (ataxic hemiparesis) in 2 patients. Recovery was good, and in all patients the sensory and motor disturbances improved or cleared before the hemiataxia. All patients had an infarct involving the lateral part of the thalamus (thalamogeniculate territory in 16, tuberothalamic territory in 1), also affecting the posterior limb of the internal capsule (PLIC) in 7 patients. Hemiataxia seemed linked to involvement of the caudal part of the ventral lateral nucleus of the thalamus or the immediately adjacent medial part of the PLIC. These structures are near the corticospinal pathways and the ventral posterior nucleus of the thalamus, explaining why hemiataxia is associated with hemiparesis or hypaesthesia in this type of infarct.

Adult↗