Previous studies have shown both increased and decreased regional cerebral glucose metabolism-blood flow (rMRGlu-rCBF) values in diabetes. We sought to elucidate the influence of diabetes on rMRGlu-rCBF in 57 patients with pure cerebral microangiopathy. Sixteen of 57 patients had diabetes requiring therapy (11 NIDDM, 5 IDDM). Using a special head-holder for exact repositioning, rMRGlu (PET) and rCBF (SPET) were imaged and measured in slices, followed by MRI. White matter and cortex were defined within regions of interest taken topographically from MRI (overlay). Diabetic and non-diabetic microangiopathy patients were compared to 19 age-matched controls. The diabetic patients showed significantly lower rMRGlu-rCBF values in all regions than controls, whereas non-diabetic patients did not. There were no significant NIDDM-IDDM differences. rMRGlu-rCBF did not depend on venous blood glucose levels at the time of the PET examination. However, analysis of variance with the factors diabetes, atrophy and morphological severity of microangiopathy showed that lowered rMRGlu-rCBF in the diabetic group was due to concomitant atrophy only (P < 0.005), while neither diabetes nor microangiopathy had any influence on rMRGlu-rCBF (all P > 0.2). These results were confirmed by multivariate factor analysis. It can thus be concluded that a supposed decrease in rMRGlu-rCBF in diabetes mellitus is in fact only an artefact produced by the concomitant atrophy. All previous studies failed to correct for atrophy, and a critical reappraisal is required.
NPS (aphasia or neglect) are a regular concomitant symptom of cortical, and, occasionally, subcortical ischemic lesions. In 19 patients with subcortical lesions (eight with NPS, 11 without NPS), F/V-SPECT was employed to search for changes in rCPR in both, lesions and ipsilateral cortex. Results were correlated with NPS and MRI findings. Compared to the unaffected hemisphere, all subcortical lesions showed reduced regional cerebral blood flow (rCBF) (-16 to -23%), increased regional cerebral blood volume (rCBV) (+34 to +62%), and decreased or missing rCPR (-27 to -28%). Compared to MRI, there was no difference in lesion size in the thromboembolic lesions. Hemodynamic low-flow infarcts, however, were greater with SPECT than in MRI. In patients without NPS, the adjacent cortex was normal in SPECT and MRI. In addition, patients with NPS revealed reduced rCBF (-18%), increased rCBV (+19%), and decreased rCPR (-22%) in the adjacent cortex. MRI was normal in the same cortical area. These results indicate that NPS in subcortical lesions may be caused by a hemodynamic mechanism causing reduction of rCPR in the adjacent cortex.
Investigated was the significance of semiquantitative tests of the peripheral visual field in glaucoma. For that purpose 793 visual fields of 793 glaucoma patients or glaucoma suspects and 338 visual fields of 338 normal controls (normal central 26 degrees--area) were analysed. Perimetry was performed with an Octopus 201 with the help of program G1, which tests 14 peripheral test locations. In the majority of the 455 glaucoma patients (pathological findings in the central visual field) the periphery was also disturbed. Much to our surprise however, the 338 glaucoma suspects (having normal central visual fields) showed the same frequency of peripheral visual field disturbance as the normals. This holds true for the total peripheral visual field, as well as for the individual test locations. Therefore it makes sense to limit perimetry in glaucoma patients to the central area, provided that the central area is quantitatively measured with an adequate testgrid.
Sir,In childhood, the majority of cases of acquired isolated nervus abducens paresis are caused by neoplasm (39%), trauma (20 %), and inflammation (17%) [6]. In contrast, acquired isolated benign VIth cranial nerve palsy is a rare condition (3 to 5%) in a pediatric setting [6,8]. In several case series of unilateral benign paresis the symptomatology was believed to be due to neuritis after viral infection. Bilateral benign abducens nerve palsy has been reported only in single cases [8].In adults, VIth nerve palsy can occur in Miller-Fisher syndrome (MFS), where it is characterized by acute onset of external ophthalmoplegia, cerebral ataxia, and very frequently a loss of tendon reflexes, which is regarded as a cranial nerve variant of Guillain-BarrØ syndrome (GBS). As in GBS and Bickerstaff brainstem encephalitis, MFS is believed to be of autoimmune pathogenesis. The fact that over 90% of MFS show anti-ganglioside IgG-antibodies for the GQ1 b epitope [5], which is present predominantly in the extramedullary part of IIIrd, IVth, and VIth nerves [2, 3], speaks for this.
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