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1.
OBJECTIVES—There is controversy regarding theneed for invasive monitoring in the preoperative assessment of patientswith temporal lobe epilepsy. The use of a series of non-invasiveinvestigations in identifying the seizure focus is reported in 75 consecutive adults referred for epilepsy surgery.
METHODS—All had video-EEG monitoring using scalpelectrodes, high resolution MRI, and neuropsychology assessment. Otherinvestigations included volumetric MRI, PET, and ictal and interictalSPECT. The seizure focus was localised and surgery offered if MRIdisclosed unilateral hippocampal atrophy or a foreign tissue lesion and other investigations were either concordant or not discordant.
RESULTS—In 68 patients the seizure focus waslocalised and three patients were inoperable. Sixty five patients havebeen offered surgery and 50 have undergone temporal lobe surgery andhave a follow up of at least 12 months (mean 24 months). All hadpathology: hippocampal sclerosis 34, dysembryoblastic neuroepithelialtumour six, cavernoma four, dysplasia two, low grade glioma two,ganglioglioma two. Thirty nine patients (78%) are seizure freepostoperatively, 29/34 with hippocampal sclerosis and 10/16 with aforeign tissue lesion. Of the 11 patients with postoperative recurrentseizures, eight have a >90% reduction in seizure frequency and threehave <90% reduction in seizure frequency but a worthwhile improvement.
CONCLUSIONS—Non-invasive investigationssuccessfully select most patients for temporal lobe surgery.

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2.
OBJECTIVES—Firstly, to compare the findingsof interictal 18F-fluorodeoxyglucose (FDG) positronemission tomography (PET) and of single photon emission computedtomography (SPECT) using 99mTc-hexamethylpropylene-amine-oxime (HMPAO) and 123I-iomazenil inlocalising the epileptogenic cortex in patients who were candidates forepilepsy surgery, but in whom clinical findings, video EEG monitoring(V-EEG), MRI, and neuropsychological evaluations did not give anydefinite localisation of the seizure onset. Secondly, to assess theability of these functional methods to help in the decision about theepilepsy surgery.
METHODS—Eighteen epileptic patients were studiedwith FDG-PET and iomazenil-SPECT. HMPAO-SPECT was performed in 11 ofthese 18 patients. Two references for localisation was used—ictalsubdural EEG recordings (S-EEG) and the operated region.
RESULTS—Fifteen of 18 patients had localisingfindings in S-EEG. FDG-PET findings were in accordance with thereferences in 13 patients and iomazenil-SPECT in nine patients.HMPAO-SPECT visualised the focus less accurately than the two othermethods. In three patients S-EEG showed independent bitemporal seizureonset. In these patients FDG-PET showed no lateralisation. However,iomazenil-SPECT showed temporal lobe lateralisation in two of them.
CONCLUSION—FDG-PET seemed to localise theepileptogenic cortex more accurately than interictal iomazenil-SPECT inpatients with complicated focal epilepsy.

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3.
OBJECTIVES—Existing speculations regardingthe cognitive functions of the right hippocampus suggest a specialinvolvement in non-verbal memory functions. However, all supportingevidence in epileptic patients came from postoperative studies that didnot consider the preoperative functioning level. The present studyinvestigates in patients with right temporal lobe epilepsy (RTLE), bothpreoperatively and postoperatively, the role of the righthippocampus for visual memory, visuoconstruction, and spatial visualisation.
METHODS—Two groups of patients with RTLE with andwithout right hippocampal damage (HC+/n=15 vHC /n=13) were set up retrospectively thereby taking intoaccount the surgical treatment (selective amygdalohippocampectomyv temporal resections sparing the hippocampus), thepostoperative pathological findings (hippocampal sclerosis in theHC+ group) and the seizure outcome (all seizure free). Thetwo groups were compared with regard to their neuropsychologicalperformance preoperatively and 3 months after temporal lobe surgery.
RESULTS—The preoperative results indicatedimpaired visual memory performance only for the HC+patients, whereas the HC patients exhibited nodeficiencies in any of the assessed functions. Postoperatively,both groups exhibited partially improved performances. The type ofsurgical treatment had no different effects on the postoperativeperformance changes.
CONCLUSIONS—The results suggest that hippocampaldamage is the major cause of non-verbal memory deficiencies inpreoperative patients with right temporal lobe epilepsy. Hence theresults support and extend findings from previous postoperativestudies. Right hippocampal resections did not increase the preoperativevisual memory deficiencies, thus supporting the view that righttemporal lobe resection in general bears only small risks for cognitve deteriorations.

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4.
OBJECTIVE—To consider the relation betweenfunctional experiential hallucinosis and brain injury induced by radiotherapy.
METHODS—Single case report.
RESULTS—A female patient presented with a fouryear history of functional experiential hallucinosis after two coursesof radiotherapy for nasopharyngeal carcinoma. Brain MRI showedhyperintense changes over the left temporal lobe.
CONCLUSION— It is proposed that the hallucinosiswas causally related to temporal lobe injury, a documented latecomplication of radiotherapy for nasopharyngeal carcinoma.

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5.
OBJECTIVES—To assess patterns of postictalcerebral blood flow in the mesial temporal lobe by coregistration ofpostictal 99mTc-HMPAO SPECT with MRI in patients withconfirmed mesial temporal lobe epilepsy.
METHODS—Ten postictal and interictal99mTc-HMPAO SPECT scans were coregistered with MRI in 10 patients with confirmed mesial temporal lobe epilepsy. Volumetrictracings of the hippocampus and amygdala from the MRI were superimposedon the postictal and interictal SPECT. Asymmetries in hippocampal andamygdala SPECT signal were then calculated using the equation:
% Asymmetry =100 × (right − left) / (right + left)/2.
RESULTS—In the postictal studies, quantitativemeasurements of amygdala SPECT intensities were greatest on the side ofseizure onset in all cases, with an average % asymmetry of 11.1, range5.2-21.9.Hippocampal intensities were greatest on the side of seizureonset in six studies, with an average % asymmetry of 9.6, range4.7-12.0.In four scans the hippocampal intensities were less on theside of seizure onset, with an average % asymmetry of 10.2, range5.7-15.5.There was no localising quantitative pattern in interictal studies.
CONCLUSIONS—Postictal SPECT shows distinctiveperfusion patterns when coregistered with MRI, which assist inlateralisation of temporal lobe seizures. Hyperperfusion in the regionof the amygdala is more consistently lateralising than hyperperfusionin the region of the hippocampus in postictal studies.

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6.
BACKGROUND—Proton magnetic resonance spectroscopy(1H-MRS) is a potentially useful tool in the in vivoinvestigation of brain metabolites in intractable temporal lobeepilepsy (TLE). Focal N-acetylaspartatate (NAA) reductions have beencorrelated with mesial temporal sclerosis (MTS) in surgically resectedepileptogenic foci.
OBJECTIVE—To evaluate the abnormalities in themetabolites NAA, creatine+ phosphocreatine (Cr), and cholinecontaining compounds (Cho) in the temporal lobe of medically refractorypatients with temporal lobe epilepsy, seizure free patients withtemporal lobe epilepsy, and normal controls.
PATIENTS AND METHODS—Ten refractory patients, 12 seizure free patients with temporal lobe epilepsy, and 10 age matchednormal controls were studied by 1H-magnetic resonancespectroscopy. All patients had consistently unilateral temporal EEGabnormalities and a normal brain MRI. Proton MR spectra were obtainedfrom an 8 ml volume in the medial temporal lobes in patients withtemporal lobe epilepsy (ipsilateral to EEG foci) and the normalcontrols. The signals measured were expressed in terms of NAA/Cr,NAA/Cho, and Cho/Cr.
RESULTS—When compared with seizure free patientswith temporal lobe epilepsy and normal controls, the 10 refractorypatients with temporal lobe epilepsy had a lower mean (SEM) NAA/Crratio (1.65(0.53) v 2.62 (0.60), and 2.66 (0.73);p<0.002 and p<0.006) and a lower mean NAA/Cho ratio (1.59 (0.79)v 2.83 (1.33) and 2.58(0.67); p<0.02 andp<0.007).Furthermore, the two patients showing the lowest NAA/Cr ratios (1.47 and 1.73) in the seizure free group had had a past period of poorseizure control.
CONCLUSIONS—There were reduced temporal NAA/Cr andNAA/Cho ratios, suggesting neuronal loss or damage, associated withpast or present poor seizure control in the patients with temporal lobeepilepsy, but it does not exclude the possibility of a future completeseizure control (seizure free patients with temporal lobe epilepsy at the time of 1H-MRS). This study warrants further1H-MRS investigation with a larger series of patients withtemporal lobe epilepsy.

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7.
BACKGROUND—A retrospective study of patients withlow grade astrocytoma was carried out because the best management ofsuch patients remains controversial. Prognostic factors were identifiedby multivariate analysis. Special attention was paid to the effect ofextent and timing of surgery.
METHODS—Ninety patients with low grade astrocytomawere studied. Seventy two patients had resective surgery, 15 had adiagnostic biopsy only, and three patients had resective surgery afterinitial biopsy.
RESULTS—Significant prognostic factors forsurvival were age, preoperative neurological condition, epilepsy as thesingle sign, extent of surgery, and histology. The extent of surgerywas highly significant on univariate analysis (p=0.002); however, aftercorrection for age and preoperative symptoms this was considerablyreduced (p=0.04). A subgroup of 30 patients with epilepsy as theirsingle presenting symptom was identified. Thirteen of these patientswere treated immediately after diagnosis, whereas the other 17 patientswere initially followed up and treated only after clinical orradiological progression. Survival in both groups was identical (63%survival rate after five years) and much better than survival for thewhole group (27% survival rate after five years). Malignantdedifferentiation was observed in 25 (70%) of 36 patients who werereoperated, after a median period of 37 months. This period was 41 months for the subgroup of patients with epilepsy only and 28 monthsfor the remaining patients.
CONCLUSIONS—Due to the retrospective nature of thestudy only restricted conclusions can be drawn. Low grade glioma withepilepsy as the single symptom has a much better prognosis than ifaccompanied by other symptoms. This prognosis is not influenced by thetiming of surgery. It seems, therefore, safe to defer surgery untilclinical or radiological progression in low grade glioma with epilepsy only.

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8.
OBJECTIVES—Perfusion SPECT and MRI were used totest the hypothesis that late onset depression is associated with brain abnormalities.
METHODS—Forty depressed patients (DSM-III-R majordepressive episode, not demented at two year follow up) were recruitedwho were either drug free, or on a stable dose of antidepressants forat least three weeks, as well as 22 demented patients (DSM-IIIR and NINCDS/ADRDA criteria for probable Alzheimer's disease). Patients wereimaged at rest with a high resolution single slice 12 detector headscanner (SME-Neuro 900) and the cerebral perfusion marker 99mTc-exametazime (HM-PAO). Temporal lobe templates werefitted with brains pitched by 20°-30°. A subgroup of 41 patients(22 depressed) were also scanned using a Siemens Magnetron 1.0 Teslamagnetic resonance imager, using a FLAIR imaging sequence for theassessment of white matter hyperintensities, and a Turbo FLASH sequencefor the measurement of medial temporal lobe width.
RESULTS—Demented patients showed reducedperfusion, particularly in the left temporoparietal cortex. In theseregions of interest, patients with late onset depression tended to haveperfusion values intermediate between patients with early onsetdepression and demented patients. Differences in changes in whitematter between demented and early and late onset depressive patientsdid not reach conventional levels of significance. Temporal lobe width differed between demented and depressed patients, but not between earlyand late onset depressed patients. Perfusion and temporal lobe widthwere not associated, but reductions of perfusion were associated withperiventricular white matter changes. Mini mental state examinationscores were associated with temporal perfusion in demented patients andwith changes in deep white matter in depressed patients. Finally,severity of depressive symptoms was associated with decreased perfusionin frontotemporal and basal ganglia regions of interest.
CONCLUSION—A cumulative effect of duration ofillness on regional cerebral perfusion could not be confirmed. Lateonset depression may show more abnormalities of deep whitematter and of left temporoparietal perfusion than early onsetdepression, but the underlying pathology remains to be established.

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9.
OBJECTIVE—To test the hypothesis that depressionin patients being considered for cervical disc surgery is associatedwith severe organic pathology. Secondly, to test whether depression andabnormal illness attitudes recorded preoperatively would predict poorer recovery.
METHODS—Seventy four patients with pain anddisability from cervical arthrosis were examined during investigationsbefore potential cervical surgery. The prevalence of psychiatricdisorder was assessed using the SCAN, and attitude to illness using theillness attitude scale.
RESULTS—There was a rate of depressive disorderin the sample of 37%. The depressed patients did not have more severeorganic pathology, more neurological symptoms or signs, or moredisablement. They reported more pain and displayed more abnormalillness behaviour. Fifty patients went on to cervical surgery. Outcomefour to eight months postoperatively was not related to the presence ofpsychiatric disorder or illness attitude recorded preoperatively.
CONCLUSION—Depressive disorder is not secondaryto severe pathology; the outcome of surgery is predominantly determinedby physical factors.

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10.
OBJECTIVE—To confirmthat patients admitted to hospital with a head injury benefit from aroutinely offered early intervention service.
PATIENTS AND METHODS—Amixed rural and urban Health District of 560 000 people with twoaccident and emergency departments provided the setting. Existingroutine services for most patients with head injury are minimal. Allpatients aged 16-65 years admitted to hospital after a head injury ofany severity, with or without other injuries entered the trial.Prospective randomisation, with a block randomisation procedure wasused to allocate all eligible patients to either: a group offered anadditional service by a specialist team; or a group receiving existingstandard services. Patients were assessed at follow up six months afterinjury. The primary outcome measure was the Rivermead head injuryfollow up questionnaire, a validated and reliable measure of socialdisability. The Rivermead post-concussion symptoms questionnaire wasused to estimate severity of post-concussion symptoms. Each patient inthe trial group was contacted 7-10 days after injury, and offeredassessment and interventions as needed. These initially focused on theprovision of information, support, and advice. Forty six per cent ofpatients in the trial group also received further outpatientintervention or additional support by telephone.
RESULTS—314 patientswere registered: 184 were randomised into the trial group, 130 into thecontrol group. For prognostic data, the groups were comparable atrandomisation, and remained comparable when assessed at six months. 132 trial and 86 control patients were followed up at six months afterinjury. Patients' post-traumatic amnesia ranged from mild (n=79,40%), and moderate (n=62, 32%), to severe (n=38, 19%) and verysevere (n=17, 9%). The trial group patients had significantly lesssocial disability (p=0.01) and significantly less severepost-concussion symptoms (p=0.02) at follow up at six months afterinjury than the control group patients.
CONCLUSIONS—The earlyinterventions offered by a specialist service significantly reducedsocial morbidity and severity of post-concussion symptoms in trialgroup patients at six months after head injury. Recommendations abouthow specialist services should be targeted are made both in the lightof these results and those from a previous randomised controlled trial.

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11.
OBJECTIVE—The principal MRI features of hippocampal sclerosis are volume loss and increased T2 weighted signal intensity. Minor and localised abnormalities may be overlooked without careful quantitation. Hippocampal T2 relaxation time (HT2) can be quantified, but previously has only been measured on a few thick coronal slices with interslice gaps. In this study HT2 was measured along the entire length of the hippocampus on contiguous slices and used, with quantitative measures of hippocampal volume (HV) and distribution of atrophy, to better define the range of hippocampal sclerosis.
METHODS—Thirty patients with temporal lobe epilepsy, 10 patients with extratemporal localisation related epilepsy and extratemporal lesions, and 20 control subjects were studied using MRI T2 relaxometry and volumetry.
RESULTS—In controls and patients, HT2 was higher in the anterior than the posterior hippocampus. Using HV, morphometric, and HT2 data, patients with temporal lobe epilepsy were classified as unilateral diffuse hippocampal sclerosis (n=16), unilateral focal (n=6), bilaterally affected (n=6), and normal (n=2). In patients with unilateral hippocampal sclerosis, the anterior hippocampus was always affected. In three patients with normal HV, HT2 measurements disclosed unilateral focal abnormalities that corresponded to the EEG lateralisation of epileptic activity. Patients with bilateral hippocampal involvement had an earlier onset of epilepsy than patients with unilateral hippocampal sclerosis.
CONCLUSIONS—Measurement of regional abnormalities of HT2 along the length of the hippocampus provides further refinement to the MRI assessment of the hippocampi in patients with temporal lobe epilepsy and is complementary to volumetric and morphological data.

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12.
Quality of life after epilepsy surgery   总被引:14,自引:0,他引:14       下载免费PDF全文
OBJECTIVE—To assess the relation between seizurestatus and quality of life after surgery for drug resistant epilepsy,using a previously validated quality of life model developed for use in epilepsy.
METHODS—A retrospective postal survey was made on94 patients who underwent surgery for epilepsy between 1986 and 1994, and 36 patients who after investigation during the same period werefound to be unsuitable for surgery. A health related quality of lifemodel was used containing validated measures of anxiety, depression, self esteem, mastery, impact of epilepsy, affect balance, stigma, overall health status, and overall quality of life, to examine therelation between postoperative seizure status and quality of life.
RESULTS—Overall 47.9% of patients were seizurefree after surgery. On all measures seizure free patients scoredsignificantly better than either patients deemed unsuitable for surgeryor those having more than 10 seizures per year after surgery. Patientshaving less than 10 seizures per year obtained intermediate scores.There was no difference between the groups unsuitable for surgery or having more than 10 seizures per year postoperatively. Employment rateswere significantly different between groups, 80% of seizure free and53% of patients having less than 10 seizures per year in gainfulemployment postoperatively, compared with 28% and 27% of patientshaving greater than 10 seizures per year or those who were unsuitablefor surgery.
CONCLUSIONS—Within broad categories,postoperative quality of life is clearly related to seizure outcome,but the study emphasises the importance of long term follow up indefining the tangible psychosocial effects of freedom from seizures.

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13.
OBJECTIVES—Thephenomenon of interictal regional slow activity (IRSA) in temporal lobeepilepsy and its relation with cerebral glucose metabolism, clinicaldata, MRI, and histopathological findings was studied.
METHODS—Interictal18F-fluorodeoxyglucose positron emission tomography(FDG PET) was performed under continuous scalp EEG monitoring in 28 patients with temporal lobe epilepsy not associated with intracranialforeign tissue lesions, all of whom subsequently underwent resectivesurgery. Regions of interest (ROIs) were drawn according to a standardtemplate. IRSA was considered lateralised when showing a 4:1 or greaterratio of predominance on one side.
RESULTS—Sixteenpatients (57%) had lateralised IRSA which was always ipsilateral tothe resection and of maximal amplitude over the temporal areas. Itspresence was significantly related to the presence of hypometabolism inthe lateral temporal neocortex (p=0.0009). Logistic regression of theasymmetry indices for all measured cerebral regions confirmed a strongassociation between IRSA and decreased metabolism of the posteriorlateral temporal neocortex only (p=0.009). No significant relationcould be shown between slow activity and age at onset, duration of theepilepsy, seizure frequency, and MRI evidence for hippocampal atrophy.Furthermore, IRSA was not specifically related to mesial temporalsclerosis or any other pathology.
CONCLUSIONS—Interictalregional slowing in patients with temporal lobe epilepsy not associatedwith a mass lesion is topographically related to the epileptogenic areaand therefore has a reliable lateralising, and possibly localising,value. Its presence is irrelevant to the severity or chronicity of theepilepsy as well as to lateral deactivation secondary to neuronal lossin the mesial temporal structures. Although slow EEG activity isgenerally considered as a non-specific sign of functional disturbance,interictal regional slowing in temporal lobe epilepsy should beconceptualised as a distinct electrographic phenomenon which isdirectly related to the epileptogenic abnormality. The strongcorrelation between interictal regional slowing and lateral temporalhypometabolism suggests in turn that the second may delineate a fieldof reduced neuronal inhibition which can receive interictal and ictal propagation.

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14.
Poisoning by organophosphorus insecticides and sensory neuropathy   总被引:5,自引:0,他引:5       下载免费PDF全文
OBJECTIVES—Poisoning by organophosphateinsecticides causes cholinergic toxicity. Organophosphate induceddelayed polyneuropathy (OPIDP) is a sensory-motor distal axonopathywhich usually occurs after ingestion of large doses of certainorganophosphate insecticides and has so far only been reported inpatients with preceding cholinergic toxicity. Surprisingly, it wasrecently reported by other authors that an exclusively sensoryneuropathy developed in eight patients after repeated unquantifiedexposures to chlorpyrifos, which did not cause clear-cut cholinergictoxicity. The objective was to assess whether an exclusively sensoryneuropathy develops in patients severely poisoned by various OPs.
METHODS—Toxicological studies andelectrophysiological measurements were performed in peripheral motorand sensory nerves in 11 patients after acute organophosphate poisoningamong which two subjects were poisoned with chlorpyrifos.
RESULTS—Three patients developed OPIDP, includingone poisoned by chlorpyrifos. Exclusively sensory neuropathy was neverseen after either single or repeated acute organophosphate poisoning. Amild sensory component was associated with a severe motor component intwo of the three cases of OPIDP, the other was an exclusively motor polyneuropathy.
CONCLUSION—A sensory-motor polyneuropathy causedby organophosphate insecticides might occur after a severe poisoningand the sensory component, if present, is milder than the motor one.Bearing in mind the toxicological characteristics of theseorganophosphate insecticides, other causes should be sought for sensoryperipheral neuropathies in patients who did not display severecholinergic toxicity a few weeks before the onset of symptoms and signs.

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15.
BACKGROUND—Striatal necrosis has been related tovarious clinical syndromes, with acute or chronic progression, andjuvenile or late occurrence, but the most common type is Leigh's encephalopathy.
METHODS—Between 1967 and 1995, six out of sevenrelated patients with chronic familial dystonia were examined. MRIswere performed in four, between 1992-1994. The seven members, affectedover three generations, were the father, three daughters (onesurviving), and three surviving grandsons.
RESULTS—The leading symptoms were gaitdisorders and dystonia in all, dysarthria in six, verbal and motorstereotypies in two, and parkinsonian and cerebellar signs in three.Optic neuropathy was found in three. A frontal lobe syndrome withoutamnesia occurred in two. Symptoms occurred between the second and thefifth decade, with progressive deterioration. Magnetic resonanceimaging, performed in four, showed in the two patients with severeneurological signs diffuse striatopallidal abnormal hyposignal(comparable with CSF signal) in T1 weighted images, suggestingextensive necrosis of the striatum and pallidum, associated withthalamo-subthalamo-rubro-dentato-nigral and substantia innominatahypersignals in T2 weighted images suggesting gliosis in theserespective areas. The same images were described to a lesser extent ina third patient. Concentrations of lactate in CSF and serum were normalin three. Muscle biopsy, performed in four, was shown to be normal.Enzyme histochemistry showed complex I, III, and IV deficiency insurviving patients.
CONCLUSION—This familial dystonia of chronicprogression may be related to basal ganglia necrosis or gliosis,associated with alterations in the respiratory chain. These metabolicalterations probably play a part in the pathophysiology of theseunusual brain lesions.

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16.
OBJECTIVE—To investigate prospectively theproportion of patients actually operated on early in units that aim atsurgery in the acute phase of aneurysmal subarachnoid haemorrhage (SAH)and what is the main current determinant of poor outcome.
METHODS—A prospective analysis of all SAHpatients admitted during a one year period at three neurosurgical unitsthat aim at early surgery. The following clinical details wererecorded: age, sex, date of SAH, date of admission to the neurosurgicalcentre, whether a patient was referred by a regional hospital or ageneral practitioner, Glasgow coma scale and grade of SAH (WorldFederation of Neurological Surgeons (WFNS) score) on admission at theneurosurgical unit, results of CT and CSF examination, the presence ofan aneurysm on angiography, details of treatment with nimodipine orantifibrinolytic agents, and the date of surgery to clip the aneurysm.At follow up at three months, the patients' clinical outcome wasdetermined with the Glasgow outcome scale and in cases of poor outcomethe cause for this was recorded.
RESULTS—The proportion of patients that wasoperated on early—that is, within three days after SAH—was 55%.Thirty seven of all 102admitted patients had a poor outcome.Rebleeding and the initial bleeding were the main causes of this in35% and 32% respectively of all patients with poor outcome.
CONCLUSIONS—In neurosurgical units with what hasbeen termed "modern management" including early surgery, about halfof the patients are operated on early. Rebleeding is still the majorcause of poor outcome.

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17.
OBJECTIVES—Although long term outcome ofpatients with perimesencephalic haemorrhage, a benign subset ofsubarachnoid haemorrhage, is excellent, some patients report an episodeof amnesia for the first hours to days after the ictus. The relationbetween the occurrence of amnesia and the size of the ventricles on CT,including the temporal horns, were studied in patients withperimesencephalic haemorrhage.
METHODS—Twenty seven consecutive patientswith perimesencephalic haemorrhage were asked about the occurrence ofamnesia. Age adjusted bicaudate indices and third ventricle sizes werecalculated. Linear measurements of the temporal horn were taken inthree directions: anterior-posterior, medial-lateral, and oblique.Additionally, enlargement of the temporal horns was assessed with the"naked eye".
RESULTS—Ten of the 27 patients reported an episodeof transient amnesia; in these patients the mean sizes of the temporalhorns were larger than in patients without amnesia, ranging from afactor of 1.7 for the medial-lateral measurement to a factor of 2.3 for the anterior-posterior measurement. Most of the patients with amnesiahad relative bicaudate indices and relative third ventricle sizes> 1, and all had enlarged temporal horns at "naked eye" assessment.
CONCLUSION—About one third of patients withperimesencephalic haemorrhage have an episode of amnesia shortly afterthe bleed. The occurrence of amnesia is associated with enlargement ofthe temporal horns, and might be explained by temporary hippocampal dysfunction.

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18.
OBJECTIVE—To evaluate the efficacy of a computerbased retraining of specific impairments of four different attentionaldomains in patients with multiple sclerosis.
METHODS—Twenty two outpatients with multiplesclerosis received consecutively a specific training comprising 12 sessions in each of the two most impaired attention functions. Thebaseline of attentional deficits, the performance after each trainingperiod, and the course of performance in the next nine weeks wasassessed by a computerised attention test battery. Additionally, theimpact of the training on daily functioning was evaluated with a self rating inventory.
RESULTS—Subgroups of patients with multiplesclerosis showing different patterns of attentional impairment could beseparated. Significant improvements of performance could almostexclusively be achieved by the specific training programmes. Theincrease of performance remained stable for at least nine weeks. Forquality of life patients reported less attention related problems ineveryday situations.
CONCLUSIONS—In patients with multiple sclerosis itseems worthwhile to assess attentional functions in detail and to trainspecific attention impairments selectively.

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19.
OBJECTIVES—Among the classification criteria for the diagnosis of Creutzfeldt-Jakob disease, akinetic mutism is described as a symptom which helps to establish the diagnosis as possible or probable. Akinetic mutism has been anatomically divided into two forms—the mesencephalic form and the frontal form. The aim of this study was to delimit the symptom of akinetic mutism in patients with Creutzfeldt-Jakob disease from the complex of symptoms of an apallic syndrome and to assign it to the individual forms.
METHODS—Between April and December 1996, 25 akinetic and mute patients with Creutzfeldt-Jakob disease were consecutively examined. The patients were classified according to the definition of akinetic mutism by Cairns and secondly in accordance with the features constituting the complete picture of an appalic syndrome (defined by Gerstenbrand).
RESULTS—From 25 patients with definite Creutzfeldt-Jakob disease, 24 patients showed impoverishment of speech and, after a mean duration of four (range 1.1-11.2) months, almost complete absence of voluntary movements and speech. Seven patients were classified as being mute and akinetic and assigned to the mesencephalic form whereas 13 patients were classified as apallic. One patient was mute without being akinetic and four patients were comatose.
CONCLUSION—Diffuse brain damage underlies akinetic mutism in patients with Creutzfeldt-Jakob disease. The term can be used as a classification criterion for the diagnosis of Creutzfeldt-Jakob disease; however, it should be applied very carefully and delimited clearly from the apallic syndrome.

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20.
OBJECTIVES—The polyneuropathy associated with amonoclonal IgM directed to the myelin associated glycoprotein (MAG) isa specific entity with a putative causal link between the IgM and theneuropathy. The small benefit offered by alkylating agents or plasmaexchanges in these patients justifies the search for alternative treatments.
METHODS—A 12 month multicentre, prospective,randomised, open clinical trial was carried out comparing intravenousimmunoglobulin (IVIg; 2g/kg and then 1 g/kg every three weeks) andrecombinant interferon-α (IFN-α; 3 MU/m2 subcutaneouslythree times weekly). The main end point was a clinical neuropathydisability score (CNDS) after six months of treatment. Twenty patientswere enrolled; 10 were assigned to IVIg and 10 to IFN-α.
RESULTS—At six months, one out of 10 patientstreated with IVIg had a CNDS improvement of more than 20% whereaseight out of 10 patients treated with IFN-α had such an improvement(P=0.005). The mean CNDS worsened by 2.3 (SD 7.6) (8%) in the IVIggroup whereas it improved by 7.5 (SD 11.1) (31%) in the IFN-α group(P=0.02). This improvement persisted after 12 months and was mainlyrelated to an improvement of the sensory component (P=0.02) whereas themotor component was unchanged (P=0.39). Electrophysiological data did not show improvement of motor nerve conduction velocities whereas sensory nerve conduction velocities improved in the upper limbs. Adecrease in the level of the monoclonal IgM was seen in two patientstreated with IFN-α. At the end of the treatment, antibody activity toMAG was still detected in the serum of all patients.
CONCLUSION—IVIg, as used in this study, did notimprove patients with polyneuropathy and monoclonal IgM. By contrast,although its mechanism of action remains to be fully elucided, IFN-αwas effective in eight out of 10 patients at six months.

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