Leukoaraiosis and Cause of Death: a Five Year J Neurol Neurosurg Psychiatry: First Published As 10.1136/Jnnp.58.5.586 on 1 May 1995
Total Page:16
File Type:pdf, Size:1020Kb
58656ournal ofNeurology, Neurosurgery, and Psychiatry 1995;58:586-589 Leukoaraiosis and cause of death: a five year J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.5.586 on 1 May 1995. Downloaded from follow up S Tarvonen-Schr6der, T Kurki, I Riiha, L Sourander Abstract researchers disagree.' 17 Hypoperfusion associ- The causes of death of 127 patients, who ated with IA in a number of perfusion stud- had undergone CT examination of the ies" 18 may be not only causal, but may also be brain in 1989, were investigated. The CT a consequence of it." As well as the common was re-evaluated. Twenty five patients neuropathological finding of hyaline vascular were excluded because of pathological stenosis in association with LA,"78 amyloid findings on CT other than leukoaraiosis angiopathy has been considered a possible (LA), infarction, or their combination or, pathogenetic basis for it14 18 19-but not unani- because of a specific known aetiology for mOUsly.3 7 8 LA. Ofthe remaining 102 patients, 25 had To test further the significance of pure LA, 18 had pure infarction, 37 had leukoaraiosis on CT, we investigated its asso- LA combined with infarction (cLA), and ciation with the cause of death, especially 22 had a normal CT. The mean time from vascular disease. between the CT and death was 1-8 (SD 1.5) years. A vascular cause of death was clearly associated with LA and with the Patients and methods severity ofLA. Patients with pure LA had PATIENTS a vascular cause ofdeath as often as those In the geriatric department of Turku City with pure infarction and those with LA Hospital, CT examination of the brain for combined with infarction. These groups various reasons was performed in 253 patients differed significantly from each other from January to December 1989. It was stan- when comparing the occurrence of cere- dard practice in the department that a neurol- brovascular, cardiovascular and other ogist examined patients with neurological or vascular causes of death. The results sug- mental problems and decided whether CT gest that LA on CT is more likely to be examination of the brain was necessary. It was associated with a cardiovascular cause of possible to obtain sufficient data on 208 death, and pure infarction is more often patients, of whom 25 were excluded because associated with a cerebrovascular death. of a specific known aetiology for LA or pathology on CT other than LA, or infarction, (T Neurol Neurosurg Psychiatry 1995;58:586-589) or their combination. At the time of this http://jnnp.bmj.com/ investigation (May 1994) 102 patients had died. Of these 62 had LA; 25 as the sole Keywords: cause of death; computed tomography; pathological finding on CT-that is, pure LA leukoaraiosis; vascular death and 37 with LA combined with infarction- that is, combined LA. Of the 40 patients who Leukoaraiosis (LA) is a non-specific radiologi- did not have LA lesions, 18 had infarction as cal in the cerebral white matter shown by the sole pathological finding on CT, (pure sign on September 25, 2021 by guest. Protected copyright. CT or MRI.' The clinical relevance and infarction) and 22 had a normal CT finding. aetiopathogenesis of these white matter The mean time between the CT and death lesions are far from clear. They may be was 1-8 (SD 1.5) years. heterogeneous in origin, an end stage due to Department of or a of a CLINICAL INFORMATION Geriatrics, University various mechanisms,2 manifestation of Turku, Turku, vascular process,2 4but most likely not an end The hospital records including the detailed Finland point of it.3-5 LA can be found in normal medical history of the patients, death certifi- S Tarvonen-Schroder and in those with no evidence cates, and necropsy reports were interpreted I Riiiha elderly subjects2 L Sourander of vascular disease6 as well as in pathological by the same neurologist (ST-S) without Department of conditions. In some studies LA has been asso- knowing whether LA was present, but know- Radiology, Turku ciated with various cerebrovascular risk fac- ing other findings on CT. Necropsies were University Hospital, tors2 including both hypertension2 5 and done on 47 (46%) of the 102 patients. The Turku, Finland T Kurki hypotension7-9; LA itself has been found to be diagnosis of dementia was based on DMS-III- a risk factor for future for develop- R.20 The patients were divided into four Correspondence to: strokes,'10-2 Dr S Tarvonen-Schroder, ment of clinically relevant cerebrovascular dis- groups: (a) no dementia; (b) Alzheimer's dis- Department of Geriatrics, ease in accordance with the University of Turku, ease,'1'3 and for poor overall prognosis.'214 diagnosed Kunnallissairaalantie 20, Causes that have been suggested for LA NINCDS-ADRDA criteria for probable Fin-20700 Turku, Finland. include Wallerian degeneration secondary to Alzheimer's disease21; (c) vascular dementia Received 12 August 1994 with the NINDS- and in revised form neuronal death in association with diagnosed in accordance 24 November 1994. Alzheimer's disease'5 and also in association AIREN criteria22 for "probable VAD" and the Accepted 31 January 1995 with cortical infarction,'6 but other ischaemic score of Hachinski23; (d) other Leukoaraiosis and cause ofdeath: afive yearfollow up 587 Table I Demographic data on patients with pure LA (pLA), pure infarction (pIn]), atrophies with a distribution corresponding to J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.5.586 on 1 May 1995. Downloaded from combined LA and infarction (cLA), and a normal CTfinding (nCT) major brain arteries were considered postin- pLA pInf cLA nCT P value farction lesions. To simplify matters, the dif- (n = 25) (n = 18) (n = 37) (n = 22) ferent types of infarctions (for example, Mean age (y (SD)) 85-9 (1-3) 75-2 (2-1) 82-5 (1-0) 73-1 (1-6) 0-0000 lacunes and large cortical infarcts) were not Sex (women) 20 (80) 8 (44) 26 (70) 17 (77) NS Cognitive status: differentiated even though they may have No dementia 6 (24) 8 (44) 6 (16) 8 (36) NS been consequences of different pathophysio- AD 2 (8) 0 (0) 2 (5) 4 (18) NS VAD 14 (56) 10 (56) 29 (78) 5 (23) 0-0006 logical processes. Other dementia 3 (12) 0 (0) 0 (0) 5 (23) 0-0073 Except for age, values are numbers of patients (%). STATISTICAL ANALYSIS AD = probable Alzheimer's disease; VAD = probable vascular dementia or combined vascular The Mann-Whitney test was used for com- and degenerative dementia. parison of means of severity (extent) of LA between the groups with pure LA and com- dementia (aetiology other than Alzheimer's bined LA. The Kruskall-Wallis test was used disease or vasicular dementia-for instance, for multiple comparisons of means of the alcoholism, previous trauma, or schizophre- Hachinski score among the four study groups. nia). The diagnosis of the primary cause of A one way analysis of variance (ANOVA) test death was based on the International was used for multiple comparisons of mean Statistical Classification of Diseases, Injuries, ages at death among the four groups, and a t and Causes of Death (ICD-9).24 test with Bonferroni correction for paired comparisons. Associations between categorial COMPUTED TOMOGRAPHY variables were analysed with Pearson's X2 test. Findings from CT were interpreted by the When the counts in the cells were less than 5, same neuroradiologist (TK), who was not Fisher's two tailed exact test was used. aware of the clinical data. A Toshiba 80A Associations between categorical (causes of scanner had been used in all examinations. death) and continuous (age at death) variables The CT had been obtained from the base to were analysed by dichotomous and multino- the vertex ofthe brain. The slice thickness was mial logistic regression analysis. The limit of 10 mm with the exception of the base of the significance used was P < 0 05. brain where it was 5 mm. The evaluation was done from hard copy x ray films. Bilateral symmetric confluent areas with Results reduced CT attenuation contiguous with the Table 1 shows demographic data on the margins of the lateral ventricles were desig- patients in the four different study groups; LA nated as LA lesions. Areas with decreased (both pure LA and combined LA as com- attenuation of the white matter could be pared with normal CT) was strongly associ- located at the margins of the frontal and ated with age, but pure infarction was not. occipital horns of the lateral ventricles or they The cause of death, however, vascular or non- may have extended towards the centrum vascular on the one hand and the type of vas- semiovale. Lesions could be irregular or cular death (cerebrovascular, cardiovascular, patchy but mostly they tended to be uniform and other vascular) on the other were not and diffuse. associated with age or with sex. Thus adjust- http://jnnp.bmj.com/ The distribution of LA was divided into ment for age or sex among the different three areas: frontal, central, and occipital. groups was not needed. The extent of LA in these areas was graded on Table 2 shows that a vascular cause of visual impression as follows: 0, no LA; 1, death was clearly associated with pure LA and under 1/4 of the area; 2, 1/4-1/2 of the area, the severity of pure LA. Patients with severe and 3, over 1/2 of the area. The severity of LA pure LA had a vascular cause of death as often was graded from 1 to 9 on the basis of the as those with pure infarction.