Long-term cognitive deficits in patients surgeryon ofthe ...Stenhouse,Knight,Longmore,Bishara more...

Journal of Neurology, Neurosurgery, and Psychiatry 199 1;54:909-914

Long-term cognitive deficits in patients aftersurgery on aneurysms of the anteriorcommunicating artery

Lynley M Stenhouse, Robert G Knight, Barry E Longmore, Samir N Bishara

AbstractThe long term recovery of a series of 27patients who had undergone rupture andrepair of an aneurysm of the anteriorcommunicating artery was assessedusing a number of neuropsychologicalmeasures. Testing took place 12 to 84months post surgery. On the basis of theresults from tests of intellect, memory,and conceptual learning, three sub-groups of patients were identified: thosewith persuasive cognitive defects, thosewith evidence of residual frontal lobedamage and those who showed noevidence of dysfunction. The occurrenceof cerebral vasospasm was the most con-sistent predictor of long term cognitivedeficit.

Departments ofPsychology,PsychologicalMedicine, andNeurosurgery,University of Otago,Dunedin, New ZealandL M StenhouseR G KnightB E LongmoreS N BisharaCorrespondence to:Dr Knight, Department ofPsychology, University ofOtago, Box 56, Dunedin,New Zealand.

Received 14 May 1990and in revised form30 January 1991.Accepted 19 February 1991

Patients surviving an aneurysmal subarach-noid haemorrhage (SAH) with no clinicalsigns of neurological impairment may,however, show evidence of cognitive dysfunc-tion on standardised neuropsychologicaltests.'" For example, Ljunggren et al6 foundneuropsychological deficits in 83% of patientstested an average of 3-5 years after an SAH,with memory loss being the most commondeficit. Although estimates of the incidence ofpersisting deficits in cognition are lower inother studies,27 it is apparent that detectablecognitive impairment is a common result ofSAH. The nature and severity of neuro-psychological deficit is dependent on the arteryaffected. Ruptures of aneurysms of the internalcarotid or middle cerebral artery frequentlycause pronounced aphasic, spatial, andmemory impairments.' Aneurysmal ruptureinvolving the anterior communicating arteryfrequently results in persistent memoryproblems and personality changes.5" In par-ticular, severe amnesic deficits have beenreported in patients who have had surgicalrepair of ruptured aneurysms arising from theanterior communicating artery (ACoA).'1-6As well as being a common site for the

development of aneurysms, the ACoA is nota-ble for the considerable number of anomalousvariations to normal anatomy that occur.7 18In addition, numerous small perforatingarteries arise from the ACoA. The preserva-tion of these presents the neurosurgeon with aconsiderable challenge, even though theapplication of microsurgical techniques andother advances in neurosurgical techniquesand in neuroanaesthesia, have substantially

reduced the incidence of mortality and mor-bidity."

Neurological damage following ACoAaneurysm rupture may be a consequence ofischaemia and infarction in the territories ofthe anterior cerebral artery or the ACoAperforating branches, or raised intracranialpressure from intracerebral bleeding, brainswelling, or hydrocephalus.'9 Ischaemia andinfarction are often a consequence of cerebralvasospasm, a common pre- or postoperativecomplication.20 It is not surprising thereforethat survivors of the rupture and consequentsurgery do not always return to their premor-bid level of functioning and may be left withprofound changes in their personality or cog-nition. The global amnesic syndrome, whichhas been reported in some patients survivingACoA aneurysm rupture, has been of par-ticular interest.'0 1-16 The principal reason forthis is that the amnesia appears to be a sequelof damage to structures in the basalforebrain,'3 an important segment of the dien-cephalic-limbic memory circuit proposed byMishkin et al.2 22 The pattern of amnesicdeficits is similar in quality to that shown byalcoholic Korsakoff patients. In particular,both alcoholic Korsakoff and ACoA aneurys-mal amnesics show a greater incidence ofconfabulation, and dysfunction on memory/learning tasks associated with frontal lobedamage (such as conceptual learning, recencydiscrimination, and temporal sequencing),than those with global amnesia with lesionsprimarily confined to limbic structures in thetemporal lobes.'014 15 It is apparent also thatpatients recovering from ACoA aneurysmrupture may show signs of intellectualdeterioration and deficits on tasks measuringputative frontal lobe functions, independentlyof, or in addition to their memory deficits.Although psychometric data on ACoA

aneurysm rupture patients are available,results tend to be presented for subjects whohave been selected because they have establi-shed cognitive deficits,'0 14 23 many of whom aretested in the first few weeks or months aftersurgery. An exception are two studies of theincidence and severity of persistent intellec-tual and memory deficits in patients survivinga rupture of an ACoA aneurysm.2425 Neitherstudy, however, incorporated an age matchedcontrol group, nor were tests likely to bespecifically sensitive to frontal damageincluded in the assessment battery. Our aimwas to report the incidence of cognitive deficitsin a series of 27 unselected patients tested

909

on July 10, 2021 by guest. Protected by copyright.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.54.10.909 on 1 October 1991. D

ownloaded from

http://jnnp.bmj.com/

Stenhouse, Knight, Longmore, Bishara

more than 12 months after surgical repair ofan ACoA aneurysm rupture and, where possi-ble, to relate such deficits to pre- and post-operative variables.

Patients and methodsThe files of all patients who had undergonerupture and surgical repair of an ACoAaneurysm at the neurosurgical unit of Dun-edin Hospital between August 1980 andAugust 1987, were reviewed. Of the total of 47patients who had had surgery, two had sub-sequently died (one postoperatively and theother of carcinoma of the colon 3 5 years afterthe operation). A further 15 patients wereexcluded from follow up for reasons whichincluded: premorbid history of psychiatricdisturbance or mental retardation, deafness,age more than 70 years at the time of followup, or were no longer able to be contacted.Letters were sent to the remaining 30 patients,inviting them to take part in the study. A totalof 27 patients aged between 33 and 70 yearsaqgreed to participate. The average (SD) age ofthe patients was 55 2 (10-7) years; 13 weremale, 14 were female. They had an average of1042 (1-25) years formal school education.The average length of time since surgery atfollow up was 54-2 months (range = 12 to 84months). All patients were graded at the timeof operation using the Hunt and Hess scale.26The preoperative grades were I for sevenpatients, II for 15, and III for five patients.Essentially, the same operation was performedfor all 27 subjects by the same neurosurgeon(SNB). The side of approach was on the rightfor 14 patients, and on the left for 13 patients.The neck of the aneurysm was satisfactorilyclipped in each case.A control group of 20 volunteers with no

history of neurological or psychiatric disorderwas recruited from among the spouses of thepatients and from local service groups. Thisgroup was matched for age [average 55-1(10-99) years], and years of school education[average 10-5 (1-09) years]. There were 10males and 10 females in the sample. Bothgroups were also matched for performance onthe National Adult Reading Test (NART).2"This is a measure comprising 50 words ofirregular pronunciation (for example, thyme,demesne), which the subject is requested toread aloud. The number of pronunciationerrors provides an index used to estimatepremorbid IQ level. The two groups did not

differ in their average NART estimated IQscores (table 1), t = 0-66, p = 0 3, implyingthat the matching for premorbid cognitive/educational factors was successful.During the testing session, all subjects com-

pleted the following measures: Four subtestsof the Wechsler Adult Intelligence Scale(WAIS; Picture Arrangement, Block Design,Vocabulary, and Arithmetic28), the WechslerMemory Scale29 (WMS), the NART, and theWisconsin Card Sorting Test30 (WCST). Foreach subject, a Full Scale IQ (FSIQ) based onthe 4-subtest short-form of the WAIS and aWMS Memory Quotient (MQ), were cal-culated.

ResultsMeans and standard deviations for neuropsy-chological tests are presented in table 1. Theseresults are based on data from 25 patients; twoof the 27 subjects were unable to complete thetests. One patient (case 26) was unwilling toattempt some tests. Time constraints preven-ted completion of testing of the second patient(case 9). The individual results of the 27aneurysm patients are discussed in more detailbelow. Of the 25 patients included in the groupdata, four patients (cases 18, 19, 20 and 27)were unable to attempt all the tests used. TheWAIS could not be administered to case 18because of severe visual impairment. Cases 19and 20 were unable to carry out the WCSTbecause the severity of their cognitive impair-ment was such that they could not understandthe test instructions. Case 27 was so severelyimpaired that she could attempt only theNART and the WMS.The WAIS IQ scores did not significantly

discriminate between the two. groups,t 153, p < 0-07, although the patientgroup's mean score was some five points lowerthan that of the comparison group. The dif-ference between the premorbid IQ estimateprovided by the NART and the current IQestimate obtained from the WAIS, was cal-culated for each subject for use as an index ofintellectual deterioration. The mean IQdeterioration scores (table 1) ofthe surgical andcontrol groups were significantly different,t = 2-56,p < 0*01. A deterioration score of 15(one SD ofthe IQ scale) is generally accepted assuggesting clinically significant deterioration.In this case, the mean deterioration score of thepatient group, which was 4-6 IQ points, lay wellabove the cut off score of 15. On average

Table 1 Means and standard deviations of the neuropsychological test scores

ACoA patients (n = 25) Controls (n = 20)M SD M SD

WAIS IQ 1070 11-4 1118 8-7NART IQ 111-8 6-0 110-6 6.7IQ Deterioration 4-6 8-7 1-6 7-7WMS MQ 107 8 15 9 1228 16-7

Logical Memory 8-3 3-1 10-9 2-8Associate Learning 12-0 4-6 15-4 3 1

WCST Categories 3-2 2-1 4-7 1 5WCST Perseverative Responses 36 4 34 0 17 9 12-3

Note: WAIS - Wechsler Adult Intelligence Scale; NART - National Adult Reading Test; WMS - Wechsler Memory Scale;WCST - Wisconsin Card Sorting Test.

910


http://jnnp.bmj.com

/J N

eurol Neurosurg P


ownloaded from


Long-term cognitive deficits in patients after surgery on aneurysms of the anterior communicating artery

therefore the surgical group did not showevidence of a clinically significant level ofdementia using this particular index.On the WMS, the between group MQ score

difference was significant, t = 3 06, p < 0-01,as were the differences on the two subtests oftheWMS measuring verbal memory: LogicalMemory, t = 2 93, p < 0-01, and AssociateLearning, t = 2-82, p < 0-01. On the WCST,the aneurysm patients made significantly fewersuccessful category shifts, t = 2-44, p < 0-01,and more perseverative responses, t = 2 34,p < 0-01.The group mean scores, however, disguise

important individual differences among theaneurysm patients. Results from individualcases were therefore examined in more detail.For each neuropsychological measure, criteriafor test performance strongly indicatingimpairment were formulated as follows:intellectual deterioration was defined as a dif-ference score between the NART IQ andWAIS IQ of 15 or more points (that is, greaterthan one standard deviation on the IQ scale). Atotal of five surgical patients, but no controlsubjects, met this criterion for intellectualdeterioration. Memory impairment was definedas either a difference between NART IQ andWMS IQ of 15 or more points or an absoluteMQ score lower than 85 (one standard devia-tion below the MQ mean of 100). Sevenaneurysm patients met one or both of thesestandards. One control subject had a NARTIQ-MQ difference of 16 points. Finally, apathological score on theWCST was defined aseither a failure to learn three or more categoriesor the commission of 30 or more perseverativeresponses. One control subject scored in thepathological range on both criteria (learningtwo categories and making 34 perseverativeresponses), and a further five learned at leastthree categories, but made more than 30 per-

severative errors. Eleven surgical patients per-formed below the cut offstandards, 10 failing onboth criteria. A further three patients wereunable to attempt the test, as mentionedpreviously, because of their degree of cognitiveimpairment.

In table 2, we present the individual testscores for the 27 surgical patients. Scoresdefined as pathological in terms of the criteriaabove are denoted by an asterisk. Results arepresented in detail to allow the possibleapplication of different criteria by otherresearchers. The case results have been rankedand grouped according to the range of deficitsthe patients showed. In table 2, UA indicatesthat a particular subject was unable to attempt aparticular test because oftheir level ofcognitivedeficit. For example, testing was abandoned forcases 19, 20, and 27 on the WCST when itbecame clear that they were unable to under-stand the nature of the test and were sortingcards at random. NC denotes a test not com-pleted for reasons not indicative of cognitiveimpairment. Two cases, 26 and 9, are groupedtogether and were labelled "unclassifiable"because of incomplete testing. Case 26 dis-played clear signs ofdysmnesia but was unwill-ing to complete testing on the WCST. Case 9had a history ofpoor social adjustment startingafter the operation, but showed no evidence ofintellectual or memory decline. She was,however, unable to undertake the WCST forreasons unrelated to any neuropsychologicalimpairment.The first six patients listed in table 2 were

classified as having test results suggesting"pervasive global impairment". All six eithercould not undertake or performed poorly ontheWCST. The first four cases showed markeddeficits on the WMS, having scores well belowtheir IQ estimates and more than one standarddeviation below the mean of the WMS. The

Table 2 Individual test resultsfor the ACoA patient group (n = 27)

NART WAIS IQ WMS WCSTCase IQ IQ Difference MQ Categories Persev. Resp.

(a) Pervasive Global Impairment27 98 UA UA* 59* UA* UA*20 99 81 18* 79* UA* UA*21 111 96 15* 76* 3 51*17 107 92 15* 83* 0* 32*25 120 107 13 103* 1* 36*19 114 97 17* 99* UA* UA*(b) Unclassified26 92 90 2 77* NC NC9 108 104 4 101 NC NC

(c) Focal Frontal deficits13 113 99 14 108 0* 124*14 118 123 0 143 2* 51*23 113 102 11 100 0* 125*

1 116 128 0 114 1* 34*7 109 99 10 96 2* 56*8 119 119 0 106 2* 2912 109 102 7 108 3 45*24 106 106 0 143 3 70*(d) Recovered2 115 119 0 122 3 173 117 112 5 122 4 84 121 113 8 116 6 145 108 115 0 106 6 106 110 95 15* 137 6 110 120 124 0 126 6 311 102 104 0 106 4 2115 108 112 0 118 6 316 115 112 3 105 6 1718 96 UA UA UA 3 2922 104 105 0 108 3 24

Note: *Denotes scores indicative of impairment. UA = Unable to attempt test; NC = Test not completed.

911


http://jnnp.bmj.com

/J N

eurol Neurosurg P


ownloaded from



NART IQ - WAIS IQ differences were alsosignificant in four of the cases, approachedsignificance for case 25, and were undeterminedfor the patient who presented clinically as themost severely impaired (case 27). A secondgroup of six patients (cases 13 to 8) showedevidence of deficit on the WCST. There isconsiderable evidence available to suggest thatpoor performance on this test is indicative offrontal lobe damage,303' therefore, this groupcomprised subjects who might be described as:"Impaired with signs of focal frontal lobedamage". Interestingly, three of these patientsreported significant memory problems duringthe period of their recovery. Case 7, for exam-ple, was unable to return to his job as a truckdriver because of his inability to rememberschedules of deliveries. Case 1 had considerabledifficulty learning to find his way about in newsurroundings. Two further patients (cases 12and 24) performed poorly on the WCST,making a large number of perseverative res-ponses but mastering at least three categorychanges. For both these patients, there werefamily or clinical reports of memory impair-ment during recovery, but no evidence ofmemory failure on the WMS. Of these eightpatients, six had CT-determined evidence ofinfarction in the frontal lobes at the time ofsurgery. In contrast only one of the 11 patientsdesignated below as recovered had similarevidence of frontal lobe infarction. Finally,there was a group of 11 patients for whom therewas no evidence of impairment on formaltesting or from informal clinical report; these

subjects were designated as "Recovered".Unlike the preceding group of patients, onlyone of the unimpaired subjects had evidence ofa frontal lobe infarction in the CT scan at thetime of surgery.There were no significant correlations bet-

ween level of deficit and either age or length oftime since surgery. The cognitive outcome datawere further examined to determine the effectsof other potential causes of neurologicaldamage. Tables 3 (a), (b), and (c) report ages,preoperative clinical grades, degrees ofpreoperative cerebral vasospasm, and post-operative complications for 24 of the patientswho completed the full test battery. Cases arearranged according to cognitive outcome asdefined above: Table 3 (a) Pervasive CognitiveImpairment; Table 3 (b) Presumed FocalFrontal Lobe Impairment; and Table 3 (c)Recovered.

It is clear from column 3 of the tables thatthere was no relationship between clinicalgrade immediately before surgery and cog-nitive outcome in our sample. However, whenoperation delay due to an unstable clinical statewas examined a clear relationship emerged. Infive of the six patients with pervasive globalimpairment, surgery had been delayed until thepatient's condition was stable, whereas this hadoccurred in only three of eight cases withconceptual learning impairment and in oneof ten unimpaired cases. These proportionsdiffered significantly, chi-square = 8-61,p < 0.025.Examination of column 4 of tables 3 (a), (b),

Table 3(a) Cases ofpervasive global cognitive impairment

Hunt and Hess Cerebral Vasospasm* Post-OperativeCase Age grade (severity and distribution) complications

17 58 2 mild, focal wound infection19 38 2 severe, diffuse nil20 40 2 severe, diffuse hydrocephalus21 50 3 severe, focal nil25 68 1 nil nil27 62 1 mild, focal hydrocephalus

*Vasospasm was recorded as severe only if the diameter of vessels was reduced by more than 50%.

Table 3(b) Cases of cognitive impairment suggestingfocalfrontal lobe lesions


1 47 2 mild, multi-focal extradural haematoma7 45 3 severe, diffuse hydrocephalus8 57 2 mild, diffuse nil12 62 1 nil nil13 58 1 nil nil14 64 1 nil nil23 64 2 mild, focal subdural haematoma24 70 2 nil nil

Table 3(c) Cases with no measured cognitive impairment


2 67 3 nil nil3 54 1 nil nil4 69 3 nil nil5 63 2 nil nil6 51 2 nil wound infection10 64 2 nil nil11 45 2 severe, multifocal nil15 33 1 nil nil16 66 3 nil nil18 51 2 severe, focal nil22 41 2 nil nil

912


http://jnnp.bmj.com

/J N

eurol Neurosurg P


ownloaded from


Long-term cognitive deficits in patients after surgery on aneurysms of the anterior communicating artery

and (c) suggests a strong relationship betweenthe presence of preoperative cerebral vaso-spasm, observed in angiography, and cognitiveoutcome. Angiographic studies were conduc-ted on average seven days (range 2-11 days)after the haemorrhage. Those patients whosecognitive outcome was poor were more likely tohave had cerebral vasospasm (five of six cases),than were those with conceptual learningimpairments (four of eight cases), or thosewithout deficits (one of ten cases). Theseproportionsdifferedsignificantly,chi-square =11-31, p < 0-005. The size of this sample wastoo small to determine the influence of severityand distribution of the vasospasm.

Postoperative complications were reportedin four of the twenty five cases and hydro-cephalus treated by ventriculo-peritonealshunting developed in three patients. Thesecomplications are noted in column five of tables3 (a), (b), and (c). The relationship betweencognitive outcome and such complications isnot clear in our sample. What is apparent,however, is that cerebral vasospasm, with orwithout other complications, is associated withcognitive impairment at long term follow up.To illustrate the range of neurological

damage and surgical complications amongstthe three identifiable groups (Pervasive Cog-nitive Impairment, Presumed Frontal LobeImpairment, and Recovered), three case his-tories are presented.

Case 20 (Pervasive cognitive impairment): This40 year old widow sustained a coma producingsubarachnoid haemorrhage. An unenhancedCT head scan performed the following dayrevealed a relatively thick layer of blood in allthe basal cisterns. On day 6 angiography wascarried out. This demonstrated a medium sizedmultilobular anterior communicating aneur-ysm projecting forwards. There was severe anddiffuse spasm. By day 15, communicatinghydrocephalus was revealed by the CT scan.The aneurysm was clipped without incidenton day 20 post haemorrhage and externalventricular drainage was established andcontinued postoperatively for five days. Sub-sequent angiography 18 days after the oper-ation showed satisfactory obliteration of theaneurysm and confirmed that the pre-existingvasospasm had resolved completely. A subtledecrease in her performance ability, less spon-taneity, and easy distractibility just beforedischarge caused some concern and a predis-charge CT scan showed the ventricular size tobe greater than at any time previously. On day47 a ventriculoperitoneal shunt was estab-lished. The patient recovered well from thisoperation and was discharged three weeks later.

Case 23 (Presumed frontal lobe impairment):This 64 year old retired man developed a comaproducing subarachnoid haemorrhage. TheCT scan on day 2 revealed a sausage-shaped5 x 2 x 15 'cm intracerebral haematoma inthe infero-medial part of the right frontal lobe,surrounded by a rim ofhypodensity. There wasalso a thick layer of subarachnoid blood.Angiography on day 9 revealed a medium sized

anterior communicating aneurysm. The onlysignificant spasm was in the right Al segment ofthe anterior cerebral artery. On day 10 post-haemorrhage the aneurysm was clipped with-out incident. The right frontal pole was excisedand the haematoma evacuated. Three days latera postoperative subdural haematoma wasevacuated. The patient improved over the nexttwo weeks and was discharged five weeks later.

Case 3 (Good recovery): This 54 year oldforeman was admitted to hospital after asubarachnoid haemorrhage that did not cause acoma. The CT scan on day 2 revealed a diffusebut thin layer of subarachnoid blood.Angiography on day 10 revealed an almostrounded medium-sized anterior communicat-ing aneurysm projecting forwards and down-wards. There was no spasm. The aneurysm wasclipped without incident on day 14 posthaemorrhage. The postoperative recovery wasuneventful.

DiscussionResults from the neuropsychological assess-ment of the present series, confirm that long-term cognitive deficits do occur in a significantproportion of patients who have surgical repairof ACoA aneurysm rupture. In our sample of27 patients, a total of 11 (41%) showed nodemonstrable evidence of impairment andcould be designated as having made anexcellent recovery. The patients' reports, clin-ical examination, and neuropsychological test-ing suggested that they had returned to theirpremorbid level of functioning, and had suf-fered no social, psychological, or cognitiveconsequences as a result of their subarachnoidhaemorrhage and its treatment. Indeed, all 11patients were able to resume their premorbidactivities. These results are consistent withprevious reports describing the range ofoutcome following ACoA aneurysmal rup-ture. 116 24 25On average, the ACoA ruptured aneurysm

patients showed a greater degree of intellectualand memory deterioration than the controlgroup and their performance was poorer on theWCST, a measure of conceptual learning. Inprevious research there has been considerablefocus on the presence of amnesia in cases.Three of our cases scored below 79 on theWMS, within the range usually indicative ofsevere memory impairment, and typical of thescores of alcoholic Korsakoff patients.323' Forexample, the average MQ score of a group ofnon-demented Korsakoffpatients tested as partof our research programme'2 was 76. However,it is clear that specific dense amnesia, uncom-plicated by other cognitive changes, is unusualin cases of ACoA aneurysm rupture. Severeamnesia more typically occurs in the presenceof concurrent and often severe intellectualdecline, as is apparent for the three impairedcases in our sample, and the samples of ACoAaneurysm amnesics reported by other researchworkers.'0 12 5 A mild to moderate degree ofmemory impairment, frequently complicatedby signs of frontal lobe damage (for example,

913


http://jnnp.bmj.com

/J N

eurol Neurosurg P


ownloaded from



poor WCST scores), is more typical ofaneurysmal cases. This conclusion is also cons-istent with data reported by Mishkin" demon-strating that monkeys with basal forebrainlesions show memory impairments, but thatthese are not as severe as for monkeys withspecific bilateral temporal lobe or diencephaliclesions.

Analysis of the individual results revealedtwo putative groups of impaired subjects. Thefirst group showed global impairment and theircase notes revealed a greater incidence ofvasospasm. The patients in this group did notmake a good recovery and most showed thesigns of poor social adjustment or cognitivedecline in their everyday lives. In three patientsthere was moderate or severe impairment ofsocial functioning; in four others, emotional orpersonality changes were reported includinglability, disinhibition, and inconsistent motiva-tion. The second group performed poorly onthe WCST. This well known test is a par-ticularly useful measure of perseveration andfailure to shift mental sets, deficits found to beparticularly characteristic of patients with dif-fuse or frontal lobe lesions. Patients in theaneurysmal sample were particularly deficienton this test. In all, 14 of the 25 surgical patientswho attempted this test were impaired.There are several potential causes of cerebral

damage after ACoA aneurysm rupture andrepair. These include: generalised vasospasmwith ischaemia or infarction, haemorrhagicinfarction of the frontal lobe following retrac-tion during surgical intervention, and hernia-tion of the mesial temporal lobes as a result ofpost operative brain swelling and hydro-cephalus.9"3 The most frequent mechanism ofcerebral damage in our sample was ischaemiapresumably resulting from vasospasm. Thedata reported here add to the accumulatingevidence that suggests that vasospasm alonecan produce long term cognitive impair-ment. 1633 Our sample was too small to commenton the effects of the other potential mechanismswith any certainty.

Ischaemia from vasospasm does not alwayscause the complete destruction of cortical andsubcortical matter typically observed afterarteri& occlusion,20 but will cause neuronaldamage by depressing metabolism."4 There-fore, neurological damage sufficient to causeglobal cognitive impairment may not always beseen on CT scan."5Our results suggest that after memory deficits

have resolved, substantial impairment of func-tion attributable to frontal lobe damage mayremain. This is much more likely when therehas been cerebral vasospasm in vessels supply-ing this part of the brain.

1 Vilkki J, Holst P, Ohman J, Servo A, Heiskanen 0.Cognitive deficits related to computed tomographicfindings after surgery for a ruptured intracranialaneurysm. Neurosurgery 1989;25:166-72.

2 Romner B, Sonesson B, Ljunggren B, Brandt L, SavelandK, Holtas S. Late magnetic resonance imaging related to

neurobehavioral functioning after aneurysmal subarach-noid hemorrhage. Neurosurgery 1989;25:390-7.

3 Levin HS, Goldstein FC, Ghostine SY, Weiner RL, Crof-ford MJ, Eisenberg HM. Hemispheric disconnectionsyndrome persisting after anterior cerebral arteryaneurysm rupture. Neurosurgery 1987;21:831-8.

4 Ljunggren B, Sonesson B, Saveland H, Brandt L. Cognitiveimpairment and adjustment in patients with neurologicaldeficits after aneurysmal SAH and early operation. JNeurosurg 1985;62:673-9.

5 Sonesson B, Ljunggren B, Saveland H, Brandt L. Cognitionand adjustment after late and early operation for rupturedaneurysm. Neurosurgery 1987;21:279-87.

6 Saveland H, Sonesson B, Ljunggren B, Brandt L, Uski T,Zygmunt S, Hindfelt B. Outcome evaluation followingsubarachnoid hemorrhage. J Neurosurg 1986;64:191-6.

7 Bornstein RA, Wer BKA, Petruk KC, Disney LB. Neuro-psychological function in patients after subarachnoidhemorrhage. Neurosurgery 1987;21:651-4.

8 Logue V, Durward M, Pratt RTC, Piercy M, Nixon WLB.The quantity of survival after rupture of an anteriorcerebral aneurysm. Brit J Psychiat 1968;1 14:137-60.

9 Hori S, Suzuki J. Early and late results of intracranial directsurgery of anterior communicating artery aneurysms. JNeurosurg 1979;50:433-40.

10 Damasio AR, Graff-Radford NR, Eslinger PJ, Damasio M,Kassell N. Amnesic following basal forebrain lesions.Arch Neurol 1985;42:263-71.

11 Lindquist G, Norlen G. Korsakoffs syndrome after opera-tion on the ruptured aneurysm of the anterior commun-icating artery. Acta Psychiat Scand 1966;42:234.

12 Alexander MP, Freedman M. Amnesia after anterior com-municating artery aneurysm rupture. Neurology 1984;34:752-7.

13 Gade A. Amnesia after operations on aneurysms of theanterior communicating artery. Surg Neurology 1982;18:46-9.

14 Parkin AJ, Leng NR, Stanhope N, Smith AP. Memoryimpairment following ruptured aneurysm of the anteriorcommunicating artery. Brain and Cog 1988;7:231-43.

15 Richardson JTE. Performance in free recall following rup-ture and repair of intracranial aneurysm. Brain and Cog1989;9:210-26.

16 Vilkki J. Amnesic syndromes after surgery of anteriorcommunicating artery aneurysms. Cortex 1985;21:431-44.

17 Perlmutter D, Rhoton AL, Microsurgical anatomy of theanterior cerebral-anterior communicating recurrentartery complex. J Neurosurg 1976;45:259-72.

18 Crowell RM, Morawetz RB. The anterior communicatingartery has significant branches. Stroke 1977;8:272-3.

19 Yasargil MG, Smith RD. Management of aneurysms ofanterior circulation by intracranial procedures. In:Youmans JR, ed. Neurological neurosurgery, vol 3.Philadelphia: WB Saunders, 1979.

20 Bouillin DJ, ed. Cerebral vasospasm. Chichester: Wiley,1980.

21 Mishkin M, Malamut B, Bechevalier J. Memories andhabits. Two neural systems. In: Lynch G, McGaugh JL,Weinberger NM, eds. The neurobiology of learning andmemory. New York. Guildford Press, 1984:65-77.

22 Markowitsch HJ, Pritzel M. The neuropathology ofamnesia. Progress in Neurobiology 1985;25:189-287.

23 Corkin S, Cohen NJ, Sullivan EV, Clegg RA, Rosen TJ,Ackerman RH. Analyses of global memory impairment ofdifferent etiologies. Annals of the N Y Acad of Sciences1985;444: 10-40.

24 Sengupta RP, Chiu JSP, Brierley H. Quality of survivalfollowing direct surgery for anterior communicatingartery aneurysms. J Neurosurg 1975;43:58-64.

25 du Cros JT, Lhermitte F. Neuropsychological analysis ofrupture saccular aneurysms of the anterior communicat-ing artery after radical therapy (32 cases). Surg Neurol1984;22:353-9.

26 Hunt WE, Hess RM. Surgical risk as related to the time ofintervention in the repair of intracranial aneurysms. JNeurosurg 1968;28:14-20.

27 Nelson H. Manual for the National Adult Reading Test.Windsor, UK: NFER-Nelson, 1982.

28 Wechsler D. Manual for the Wechsler Adult IntelligenceScale. NY: The Psychological Corporation, 1955.

29 Wechsler D. A standardized memory scale for clinical use. JPsychol 1945;19:87-95.

30 Heaton RK. A Manualfor the Wisconsin Card Sorting Test.Odessa, FL: Psychological Assessment Resources, 1981.

31 Lezak M. Neuropsychological assessment, 2nd ed. NY:Oxford University Press, 1983.

32 Longmore BE, Knight RG. The effect of intellectualdeterioration on retention deficits in amnesic alcoholics. JAbnorm Psychol 1988;97:448-54.

33 Squire LR. Comparisons between forms of amnesia: Somedeficits areunique to Korsakoff's syndrome. JExp Psychol:Learning, Memory and Cognition 1982;8:560-71.

34 Grubb RL, Raichle ME, Eichliy JO, Gado MH. Effects ofsubarachnoid haemorrhage on cerebral blood volume,blood flow, and oxygen utilization in humans. J Neurosurg1977;46:446-52.

35 Volpe BT, Hirst W. Amnesia following the rupture andrepair of an anterior communicating artery aneurysm. JNeurol Neurosurg Psychiatry 1983;46:704-9.

914


http://jnnp.bmj.com

/J N

eurol Neurosurg P


ownloaded from

Date post:	20-Feb-2021
Category:	Documents
Upload:	others
View:	1 times
Download:	0 times

Long-term cognitive deficits in patients surgeryon ofthe ...Stenhouse,Knight,Longmore,Bishara more...

Documents