Biomedical subjects
Publications and source records attributed to R Nyberg-Hansen.
Botulinum toxin A was administered to 19 patients with spasmodic torticollis. A significant decrease of abnormal head and neck movements was recorded, and all the patients who suffered pain reported relief. Side effects were minor and transient. The results of this study indicate that botulinum toxin is an effective means of treating torticollis.
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We describe two patients with autoimmune optic neuritis. The initial symptom was severe loss of vision without clinical signs or symptoms of systemic autoimmune disease. The patients had recurrent attacks of optic neuritis in both eyes, causing permanent visual impairment despite conventional doses of corticosteroid. The only laboratory sign of autoimmune disease was a positive antinuclear antibody (ANA). These patients must be differentiated from cases with idiopathic optic neuritis or multiple sclerosis. Early diagnosis and high-dose corticosteroid therapy may be necessary, and may be successful in restoring visual function. Continued therapy with cytotoxic agents may be required.
Blood flow velocities were measured in both middle cerebral arteries (MCAs) of 36 healthy subjects using transcranial Doppler ultrasound. Measurements were first made using a hand-held probe. Velocities were then studied bilaterally with fixed probes under resting conditions and during simultaneous regional CBF (rCBF) measurements. A significant (p < 0.05) positive correlation was found between MCA flow velocities and rCBF in the estimated perfusion territory of this artery. The correlation coefficient was highest when the measurements were performed simultaneously (p < 0.001) or when velocities recorded with a hand-held probe were adjusted to take into account the significant velocity increase induced by the CBF study situation. The increased velocities during CBF measurements cannot be fully explained by the moderate but significant PCO2 increase. Other possible mechanisms are increased blood flow due to mental activation or MCA vasoconstriction secondary to stimulation of the sympathetic nervous system. The effect of mental activation and PCO2 differences should therefore be considered when comparing the results of repeated velocity and CBF measurements.
Sixteen former rayon viscose workers were investigated four years after the exposure to carbon disulfide was discontinued. Median age was 58 years (range 43-65 years), median exposure time was 17 years (range 10-35 years). Encephalopathy was diagnosed in altogether 14 workers. To further explore pathophysiological mechanisms, cerebrovascular investigations were employed. Doppler ultrasound examination of the precerebral vessels in 15 workers showed a slight stenosis of the left internal carotid artery in one. Regional cerebral blood flow investigation (rCBF) with single photon emission computerized tomography (SPECT) with Xenon-133 gas was performed in 14. There was no significant difference from a control group. Regional side-to-side asymmetries beyond reference limits were demonstrated in eight workers. The abnormalities were modest, but may indicate a tendency toward focal blood flow disturbances in workers with long-term exposure to carbon disulfide.
Three adult patients with moyamoya disease are described. They presented with intracerebral hematoma, cerebral infarction and subarachnoid hemorrhage, respectively. Subarachnoid hemorrhage is rare in moyamoya and is usually the result of aneurysm rupture. No aneurysm was found in our patient. Regional cerebral blood flow (rCBF) and the cerebral perfusion reserve assessed by the acetazolamide test, were significantly reduced in all three patients. The areas with most reduced baseline rCBF and most impaired vasoreactivity did not always correspond to the site of the vascular accident, indicating that these CBF changes were at least in part due to the moyamoya disease and/or its underlying causes, and not solely to the vascular accidents.
BACKGROUND AND PURPOSE: The aim of this study was to determine the ability of transcranial Doppler ultrasonography when used to assess cerebral vasoreactivity. The results of this method were compared with regional cerebral blood flow measurements. METHODS: Forty-three patients with symptoms suggesting cerebrovascular disease took part. Transcranial Doppler findings in the middle cerebral arteries were compared with regional cerebral blood flow in the corresponding perfusion territories before and after acetazolamide administration. RESULTS: There was a significant positive correlation between the absolute increase in cerebral blood flow in milliliters per 100 g per minute and the percent increase in velocity (r = 0.63). The right-left, side-to-side difference of the acetazolamide response obtained by the two methods also showed a positive correlation (r = 0.80). Control limits obtained from healthy subjects were used for both the blood flow increase (absolute values and asymmetry in absolute values) and the velocity increase (percent increase and asymmetry in percent increase). The two methods then agreed in their evaluation of vasoreactivity in 74 (86%) of the 86 middle cerebral artery perfusion territories; 20 (23%) were assessed by both methods as having a reduced vasodilatory reserve. Eleven hemispheres with a slightly reduced regional cerebral blood flow response to acetazolamide were not detected by transcranial Doppler, whereas all territories with a marked reduction were identified by Doppler. Only one hemisphere with a normal cerebral blood flow increase after acetazolamide administration was assessed by Doppler as having reduced vasoreactivity. CONCLUSIONS: Transcranial Doppler and the acetazolamide test may be used in clinical situations to assess cerebral vasoreactivity.
Focal dystonia and hemifacial spasms are difficult to treat. Medication and surgery may suppress the dystonic movements but the improvement is not satisfactory. The present article reviews use of Botulinum toxin in cases of focal dystonia. Injections of very small doses of Botulinum A toxin into the affected muscles is a new and efficient therapy for patients with focal dystonia. The toxin acts by inhibiting the release of acetylcholine from the nerve terminal, leading to a localized paralysis of the treated muscle. The effect is temporary and gradually diminishes, but the treatment can be repeated. The use of Botulinum toxin must be applied on the basis of a thorough knowledge of its effect and possible side effects.
Spontaneous dissection of the internal carotid artery is supposed to be a rare condition, but seems to be increasingly diagnosed. The symptoms are protean from unilateral headache, Horners syndrome, tinnitus, to cerebral ischemia and hemipareses. The condition is of unknown incidence and usually affects previously healthy persons. It is nearly always unilateral. The diagnosis is ascertained by characteristic angiographical findings. The prognosis depends on the exhibited symptoms. Three patients seen during the last year at the Department of Neurology at the National Hospital (Rikshospitalet) are presented, together with a brief survey of symptomatology, diagnosis, prognosis and treatment.
We describe two cases of chiasmal optic neuritis. The presenting symptoms were reduced visual acuity and bitemporal visual field defects. The enlargement of the optic chiasm in the acute stage and normalization after recovery is demonstrated by magnetic resonance imaging (MRI).
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In Norway's only viscose rayon plant, carbon disulfide (CS2) concentrations in ambient air usually were between 30 and 50 mg/m3 during the first 23 years of production. From 1970/1971 until the factory was closed in 1982, corresponding values were 10-25 mg/m3. Through all of these years, high peak exposures of CS2 and H2S occurred. In 1986, 16 of the 24 men still at work in 1982 and with at least 10 years' experience in the spinning room agreed to participate in this study. Clinical neurological examination demonstrated abnormalities in 15; neuropsychological tests showed impairments of probable organic origin in 14. Thirteen had cerebral atrophy demonstrated by cerebral computed tomography (CT). Electromyography (EMG) was abnormal in six, neurography in 11. Regional cerebral blood flow measurements indicated flow asymmetries in eight, whereas Doppler investigation of the extracranial carotid and vertebral arteries, electroencephalography (EEG), and evoked response investigations were mostly normal. Based on these results and the exposure data, a diagnosis of CS2-induced encephalopathy was reached in eight workers; another six had an encephalopathy in which CS2 exposure was regarded as a partial cause. Correspondingly, seven had a neuropathy probably caused by CS2 exposure alone; in three others, CS2 was found to be the partial cause of a neuropathy. This indicates that long-term, relatively moderate exposure to CS2 in association with high peak exposures to CS2 and H2S involves a substantial risk of developing neurotoxic disease.
Transcranial Doppler and rCBF examinations were carried out in 25 cluster headache patients. Spontaneous and glyceryl trinitrate (nitroglycerin) provoked attacks were accompanied by a bilateral decrease in middle cerebral artery blood flow velocities. This decrease was more pronounced on the symptomatic side but the difference did not reach statistical significance. Mean hemispheric blood flow and rCBF were within normal limits during provoked attacks and similar to those found when patients were attack-free. During cluster periods middle cerebral artery velocities were significantly higher on the symptomatic side. Glyceryl trinitrate caused a bilateral middle cerebral artery velocity decrease which was significantly greater on the symptomatic side. Attacks provoked by glyceryl trinitrate appeared to begin when the vasodilatory effect of this substance was receding.
A follow-up of 55 patients 2 years after a total of 60 carotid endarterectomies. Fifty-two patients who had a total of 57 endarterectomies survived the first 2 post-operative years and were re-examined using pulsed Doppler spectral analysis and intravenous digital subtraction angiography (IVDSA). One patient had died following a stroke and 2 after a cardiac infarction. The Doppler and IVDSA examinations revealed a non-symptomatic restenosis of the relevant internal carotid artery in 2 patients. There were no relevant occlusions and no symptomatic re-stenoses were detected. Spectral spreading of the Doppler signal at the site of the endarterectomy was found in 18% of the internal carotid arteries, whereas wall irregularities (diameter reduction less than 10%) were demonstrated in 25% by IVDSA. A stenosis or occlusion was found in 14 (25%) of the 57 ipsilateral external carotid arteries.
We studied the effect of acetazolamide on cerebellar blood flow in 11 stroke patients with large, unilateral cerebral hemispheric infarcts and no evidence of cerebellar infarction, but with cerebrocerebellar diaschisis of cerebral blood flow. Blood flow was determined with xenon-133 inhalation and dynamic single-photon emission computed tomography at rest and 20 minutes after the intravenous injection of 1.0 g acetazolamide. After acetazolamide, the mean +/- SD increases in blood flow in the affected and contralateral cerebellar hemispheres were 11.1 +/- 3.7 and 12.0 +/- 5.3 ml/100 g/min, respectively; the difference between hemispheres was not significant. The absolute increase in cerebellar flow in these 11 patients was of the same magnitude as that in 12 healthy controls. We conclude that cerebellar vasoreactivity is intact in stroke patients with crossed cerebrocerebellar diaschisis of cerebral blood flow. Our results lend further support to the concept that reduced cerebellar blood flow is secondary to functional deactivation. Our patients were studied 2 weeks to 5 years after their stroke, indicating that this phenomenon may be persistent.
We measured regional cerebral blood flow and cerebral vasoreactivity before and 3 months after carotid endarterectomy using xenon-133 inhalation with single-photon emission computed tomography and the acetazolamide test in 14 selected patients who had suffered cerebral transient ischemic attacks due to an ipsilateral internal carotid artery stenosis. The patients had neither clinical nor cerebral computed tomographic evidence of infarction. Baseline regional cerebral blood flow was symmetrical before and unchanged after endarterectomy. Before endarterectomy, vasoreactivity in the middle and anterior cerebral artery territories of the symptomatic side was significantly reduced (p less than 0.05); however, vasoreactivity was normalized 3 months after surgery. Our findings strongly suggest that the stenoses caused a reduction in perfusion reserve that was improved by carotid endarterectomy.
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Cerebral artery blood velocity and regional blood flow (rCBF) were investigated in 17 normal subjects. Blood velocity was measured with 2 MHz pulsed Doppler ultrasound in the proximal segments of the middle, anterior and posterior cerebral artery (MCA, ACA, and PCA) and in the distal extracranial internal carotid artery (ICA). The rCBF in the regions of interest tentatively corresponding to the perfusion territories of these vessels was estimated using 133Xe inhalation and a rapidly rotating single photon emission computer tomograph. Concomitant capnograph recordings showed that the end-expiratory pCO2 was higher during the rCBF than during the blood velocity examinations. This differences was highly significant. While there was no significant correlation between blood velocity and rCBF when these clear differences in pCO2 were disregarded, we did find significant positive correlations when the data were normalized to a standard pCO2 (5.3 kPa) using accepted formulas. The best correlation was found for the MCA (r = 0.630, p less than 0.001) and the PCA (r = 0.73, p less than 0.001), with a lower correlation in the ACA (r = 0.49, p less than 0.01) and the ICA (r = 0.41, p less than 0.05). The estimated blood velocity (V) given rCBF = 0 was not significantly different from 0. The results support the validity of expressing the relationship between blood velocity (V) and rCBF in defined cerebral artery systems as: V = 1/60 (rCBF) T (A)-1, where A represents the area of the lumen of the vessel segment where the velocity is being measured, and T denotes the size of the brain region being perfused from this artery.