Home Explore Handbook of Practical Medicine Stroke

Handbook of Practical Medicine Stroke

Published by andiny.clock, 2014-07-25 10:34:00

Description: We don’t care much for abbreviations. They are not literate (Oliver Twist was not abbreviated to OT each time
Dickens mentioned his name!), they don’t look good on
the printed page, and they make things more difficult to
read and understand, particularly for non-experts. But
they do save space and so we have to use them a bit.
However, we will avoid them as far as we can in tables,
figures and the practice points. We will try to define any
abbreviations the first time they are used in each chapter, or even in each section if they are not very familiar.
But, if we fail to be comprehensible, then here is a rather
long list to refer to.

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9781405127660_4_011.qxd 10/13/07 10:55 AM Page 614 614 Chapter 11 What are this patient’s problems? Table 11.53 Problems with food preparation and solutions. predict how the patient and carer will cope in the longer term. The layout of the home is obviously important. Cannot open cans with one functional hand Are there steps up to the front door which make access Solution: Wall-mounted (electric) tin opener difﬁcult? Are the toilet and bathroom upstairs? Is the Cannot open bottles with one functional hand house cluttered with furniture? Are the carpets deep Solution: A bottle or jar stabilizer to ﬁx the bottles to work pile which may cause difﬁculty for a patient with a foot surface drop? Some stroke units have predischarge apartments Cannot cut up or peel ingredients with one functional hand in the hospital which allow the team and the patient to Solution: A plate or board with spikes on which to impale the item to be cut assess under supervision how well the patient copes. This may not be the same as discharge into the community, however. When to do an accommodation assessment is difﬁcult can prepare meals. Often, relatives and social services to predict because it often takes a considerable time to provide these services. ﬁnd alternative accommodation, or to make major struc- tural changes to the patient’s current home. Thus, if one is going to avoid unnecessary delays in hospital, one has to make a decision before the patient has achieved their optimal functional status. Considerable judgement is 11.33 Social difficulties required to ‘best guess’ the patient’s ﬁnal functional level and to identify their accommodation needs well in advance of hospital discharge. We have already discussed how stroke-related impair- After a thorough assessment, the patient and their ments result in disability or dependency in activities of family, with help from the team, need to decide where daily living (ADL). However, there is more to life than they wish to live, taking into account all the practical just ADL. Environmental factors become extremely issues – including any ﬁnancial constraints. After all, important in determining the effect of the stroke on a given unlimited funds, it is almost always possible to person’s role in society and their handicap. This section maintain even the most severely disabled patient at will address some of the social factors which are often of home. The ﬁnal decision is often a result of negotia- greatest concern to patients and their carers. tion between the patient, carer and team members. For instance, patients with visuospatial or cognitive problems may not appreciate the likely problems which 11.33.1 Accommodation will face their carers after discharge. For these sorts of About 50% of the patients who survive a stroke are reasons it is not always possible to fulﬁl the wishes of dependent in ADL (Table 11.45). Some patients with both patient and carer. complex or worsening disability may not, if admitted to Options for alternative accommodation, and the hospital, be able to return to their own home. A patient’s availability of support in the community, vary from ability to return home depends on the answers to the place to place, country to country, and from time to following questions, among others: time. However, in general, one needs a range of accom- • Is the disability likely to improve or worsen with time? modation offering a variety of levels of support and • Will aids and adaptations reduce dependency? supervision to meet the needs of individual patients. • What is the patient’s accommodation like? • What level of informal support is available, e.g. family? 11.33.2 Employment • What level of community support is available, e.g. community nursing, home helps? About one-third of patients who have a stroke are of Any assessment has to identify the needs of the patient employment age. Estmates of the proportion who return to determine whether those needs can be practically pro- to work have varied widely due mainly to method- vided in the patient’s current accommodation, or ological factors. 419 Obviously, the nature of previous whether alternative or modiﬁed accommodation will be employment, residual impairments and disabilities, the needed. This may involve one or more visits home with patient’s own wishes, the attitudes and policies of the patient and any carer to establish exactly what the employers, health and safety legislation and insurance practical problems are. If a short visit is not enough, then issues will determine whether return to employment is home visits (with the potential for ‘round the clock’ feasible. 420 It is also likely that the local arrangements for supervision) for a few days and nights can be useful to paying sickness beneﬁt will inﬂuence whether patients .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 615 11.33 Social difficulties 615 return to work, and the timing of their return. Of course, Counselling the patient and their carers about the many patients who are approaching retirement age may value of maintaining leisure activities and social con- not want to return to work anyway. tacts is useful, and can have dramatic consequences Assessment of the patient’s ability to return to work is (Fig. 11.37), along with practical help in achieving them. often left to the patient and family, but involvement of Therapy speciﬁcally directed at improving participation members of the team (i.e. occupational therapist, speech in leisure activities, or using leisure goals to improve and language therapist, physiotherapist and social activities of daily living function, was not effective in a worker) can be very useful to help explore the possible large multicentre trial. 425 work options. Some employers have occupational health departments which can provide further specialist advice 11.33.4 Air travel on their own speciﬁc regulations covering return to work, and on any alterations to the working environ- We are frequently asked whether a patient can travel on ment or the job itself which would facilitate this. a commercial ﬂight after a stroke. We are not aware of It is important that patients and their families are coun- any research into the safety, or otherwise, of doing so. selled about the patient’s limitations. They are often Prolonged immobility on longhaul ﬂights with the attend- under the misconception that patients should rest after a ant risk of venous thromboembolism, and the effect of stroke and that physical activity will bring on another altitude (most commercial aeroplanes are pressurized stroke. 421 This misconception may have made them rule to a level equivalent to an altitude of about 7000 feet) out, inappropriately, the possibility of return to work. on the brain, are two issues which need to be considered. In all patients, but especially those who have had an Many patients and their carers are under the ischaemic stroke associated with a patent foramen ovale, misconception that exercise, hard work or stress will it may be wise to emphasize simple measures to reduce bring on another stroke. They should be counselled to the risk of venous thromboembolism such as adequate dispel these myths. hydration and avoiding prolonged immobility. 426 In giving advice one also needs to take into account: Patients may require speciﬁc occupational therapy to • the importance of the ﬂight (e.g. is it to get home or improve the physical skills required for particular jobs, simply part of a holiday?); and/or retraining to change employment. Patients often • the interval from the stroke which will in part deter- complain of marked fatigue (section 11.31.4) so that a mine the risk of recurrent stroke; return to part-time work, at least initially, is often more • the ability of the patient to manage everyday activities, successful than struggling to cope with full-time work. such as toileting and feeding, on an aeroplane; And they may ﬁnd that although they can perform the • the availability of an accompanying carer; physical aspects of their work, their concentration may be • the attitude of the airline and the patient’s travel insurer. impaired. In many countries, special schemes are avail- Many patients who have a stroke while on holiday are able to provide employment for disabled people. repatriated by air within a week or two without apparent ill effects. 11.33.3 Leisure 11.33.5 Sex Two-thirds of stroke patients are retired from employ- ment. For them, resumption of a leisure activity is more Although many stroke patients are elderly, they were relevant than work. Restriction in leisure activities may often sexually active before their stroke. But after stroke, be the result of physical or cognitive impairments but libido, coital frequency and satisfaction are reduced may also be caused by psychological factors and even among both patients and their partners. 427 This reduc- fear that an activity may bring on a further stroke. Many tion in activity is due to both physical and psychosocial disabled stroke patients are unable to continue with factors, the latter probably being of greater importance their normal leisure activities and do not take up new (Table 11.54). Reduced sexual activity may contribute to ones which are within their abilities. 422 Reduction in a worsening emotional relationship with their partner. leisure activities will exacerbate social isolation, lower A patient and their partner may believe that reduced mood and adversely affect relationships with carers. The satisfaction with their sexual relationship is an in- level of social activities, including leisure, can be meas- evitable consequence of stroke. Although we often feel ured using the Frenchay activities index; however, the embarrassed about talking to people about these aspects Nottingham leisure questionnaire has been developed of their lives, it is important that sexual problems are speciﬁcally for this purpose. 423,424 discussed. Physical difﬁculties due to the patient’s .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 616 616 Chapter 11 What are this patient’s problems? (a) Fig. 11.37 Leisure activities for patients with mobility problems after stroke: (a) abseiling in a wheelchair; (b) preparing to go canoeing; (c) horse riding. (Photographs by Renzo Mazzolini for the Chest Heart and Stroke Association, (b) (c) Scotland.) impairments can often be overcome with a little com- We encourage patients to resume sexual activity as monsense and a realization that intercourse, with soon as they wish after a stroke. One exception might be vaginal penetration, is not an absolute requirement. The a patient with a recent rupture of an aneurysm which has psychological problems contributing to sexual dysfunc- not for some reason been coiled or clipped. One might tion are often the most difﬁcult to sort out. Sometimes imagine that the increase in blood pressure associated patients and their partners simply need to be reassured with orgasm could cause a rebleed. that sexual activity, like any other physical activity, Unfortunately, strokes can put tremendous strains will not precipitate another stroke. Verbal information on a relationship which are more difﬁcult to manage. may usefully be supplemented by leaﬂets, supplied by Where sexual dysfunction is due to medication (Table charities and patient organizations, which include 11.54), withdrawal and substitution with an alternative advice for patients and carers. drug may be effective. In men with impotence, sildenaﬁl .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 617 11.34 Carers 617 Table 11.54 Causes of reduced sexual activity and satisfaction and other sources (e.g. superannuation schemes, insur- after stroke. ance policies, etc.). Psychosocial factors Loss of interest Fear of impotence Fear of bringing on another stroke 11.34 Carer problems Emotional changes may adversely affect the relationship Inability to discuss problems Physical factors Physical disability may make sexual intercourse difﬁcult or Looking after a patient with disability places consider- impossible, e.g. indwelling catheter, contractures able physical and emotional strains on the carer. Carers Impotence and reduced libido due to: worry about the patient’s needs and their ability to fulﬁl Drugs (e.g. thiazide diuretics, beta-blockers, tricyclic them. Caring may well limit the carer’s employment and antidepressants) leisure activities and lead to social isolation and loneli- Comorbidity (e.g. diabetes, peripheral vascular disease) ness. Carers of disabled stroke patients are often anxious and depressed and have poor physical health. 429 The extent of these difﬁculties appears to be related to the patient’s level of dependency, mood, behaviour and cog- (Viagra) may be useful although experience of its use nitive function. However, the magnitude of the burden after stroke is limited and the manufacturers recommend of caregiving, as perceived by the carer, may relate to caution in this situation. Many patients with stroke will their own physical and emotional state as much as that be taking nitrates for ischaemic heart disease which of the patient. The impact that a stroke has on the family precludes the concurrent use of sildenaﬁl. Referral to a changes over time. Periods which are likely to cause sexual dysfunction clinic, or for marital guidance, may carers particular stress and when extra support may be be useful if problems persist after attending to the simple needed are: and obvious. • immediately after the stroke when the carer has to come to terms with what is potentially a life-threatening event and one which may have a major effect on the 11.33.6 Finance patient’s and potential carer’s future life together; Stroke may place a considerable ﬁnancial burden on • during a prolonged period of in-patient care; visiting patients and their families. Employment, and therefore may be difﬁcult because of travelling and also because income, may be affected. 428 Disability, and the aids and the patient’s behaviour may put emotional pressure adaptations needed to overcome it, may also be costly. on the carer; Even when the patient is still in hospital, carers may have • around the period of hospital discharge; suddenly the difﬁculty meeting the costs of transport to visit the pa- patient who has been looked after by a team of skilled tient and, if driving, parking when they get there. This professionals appears, at least to the carer, to be only is important because the patient’s morale may suffer if the carer’s sole responsibility; and regular visiting is not possible and this may adversely • during the weeks and months following hospital affect outcome. Of course, in some unenlightened health discharge when professional support dwindles systems, the patient or family may have to pay directly (sometimes inappropriately and abruptly), friends stop for their healthcare and ﬁnancial constraints may even calling, and the carer becomes physically and emo- prevent patients from receiving the necessary treatment. tionally exhausted. The professionals involved must be alert to any ﬁnan- Several stages of adjustment which families typically cial problems which affect patients and be ready to offer go through have been identiﬁed (Table 11.55). These do help as required. In the UK, and other countries, where not apply to all carers, but it is useful to be aware of them the level of government support for home care depends in managing patients and their families. on the patient’s personal ﬁnances, a ﬁnancial assessment Although the physical aspects of caring for a person may be necessary for planning care. In the UK, social with a disabling stroke are hard, it is often the patient’s workers are responsible for these assessments although psychological and resulting behavioural problems which other agencies may become involved. cause most distress to carers. Carers may note a change in Depending on assessment of their needs, and some- personality, the patient may become short-tempered times a ﬁnancial assessment, patients or carers may be and irritable, depressed or apathetic. Such changes may eligible for ﬁnancial beneﬁts from government, charitable lead to a deterioration in their relationship which may .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 618 618 Chapter 11 What are this patient’s problems? Table 11.55 Stages of adjustment Stage 1: Crisis Shock amongst families of patients with Confusion stroke. 428 High anxiety Stage 2: Treatment stage High expectation of recovery Denial that disability is permanent Periods of grieving Fears for the future Job Mobility Lifestyle About coping Stage 3: Realization of disability Anger Feelings of rejection Despair Frustration Depression Stage 4: Adjustment be compounded by a cessation or disturbance of their therapy sessions. This gives the carer an indication of sexual relationship (section 11.33.5). what caring may involve, it can help the carer and team Carers often have feelings of guilt which add to their members identify and hopefully resolve problems before distress. They worry that they contributed to the stroke, discharge, and it provides a valuable opportunity to perhaps by giving the patient the wrong diet or because ‘train’ the carer. Pre-discharge visits home for a day of some petty incident which the carer feels should have or weekend fulﬁl similar functions. Carers may need been avoided. They feel guilty about not visiting enough physical or simply psychological support. A wide range or for not having the patient home soon enough. After of assessment tools have been developed to measure hospital discharge they feel guilty about wanting to carry the amount of caregiving provided and the subjective on with their own lives. They often worry that the burden this places on the caregiver (e.g. caregiver strain patient will fall, have another stroke or even die unless index). 430 they are in constant attendance. These fears, apart from adding to the distress of carers, may also cause the carers Prevention and treatment to become overprotective towards the patient, which may prejudice the patient’s outcome. Physical support is usually limited while the patient is in hospital, although some carers may need help with ﬁn- ances (section 11.33.6) and visiting. However, physical Assessment support is likely to become more important after the It is important that all those involved in managing a patient is discharged home. Examples include: stroke patient are aware of the burden that caring for a • providing help with housework to give the carer more disabled patient places on the family and other carers. time for providing personal care; The carer should be invited to discuss their problems. • providing a care assistant or district nurse to help with This is usually best done when the patient is absent since the patient’s personal care; carers often feel uncomfortable or guilty when talking • providing training in practical aspects of caring e.g. about their own problems if the patient is present. transfers, dressing; 431 Indeed, carers often need a lot of encouragement to dis- • providing a laundry service if the patient has persisting cuss their problems at all. However, they should be urinary or faecal incontinence; encouraged to do so not only for their own sake, but also • arranging for the patient to attend a day hospital or for the patient’s. If they are not coping this will adversely day centre, or arranging ‘patient sitting’ services to affect the patient. allow the carer to go shopping, have their hair done, It is important to assess the carer’s physical and mental or attend some social function; and ability to go on providing the necessary care. If the • arranging regular respite admissions to a hospital or patient is in hospital, it is often useful to get the carer to nursing home to allow the carer to go on holiday, or help with the patient’s nursing care and attend their simply to have a well-earned rest. .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 619 References 619 Table 11.56 Common questions asked by carers. Giving information (section 17.10.1): Carers may know little about stroke, its causes and consequences and have Acutely often received misleading information from families What is a stroke? 421 and friends. Carers, like patients, vary in the amount, Will they die? type and format of information they want about stroke. Will they be disabled? Information-giving therefore needs to be tailored to the Why did this happen? individual. Leaﬂets, audio or video tapes may usefully Was it my fault? reinforce verbal transfer of information but more formal Will it happen again? After hospital discharge evaluation of their relative effectiveness is required. How long will they keep improving for? Education programmes appear to increase carers’ knowl- Will their speech get better? edge and satisfaction with information received but not Why are they not the person I knew before? necessarily their emotional outcome. 432 It is important Can I leave them alone to go out? that patients and carers are given consistent information Can they exercise, will it bring on another stroke? and advice to avoid confusion. Good communication Will I always feel so tired? between potential providers of information is therefore Where can I get help with money? vital. Where can I get help with bathing? Can I have a rest or holiday, i.e. respite? Such services may be expensive but they probably pre- vent or delay the need for long-term institutional care References which is even more expensive. Psychological support: Carers often need help coming to terms with the changes in the person who has had a 1 Houston JG, Morris AD, Grosset DG, Lees KR, McMillan N, Bone I. Ultrasonic evaluation of movement stroke. They have many questions and sources of con- of the diaphragm after acute cerebral infarction. J Neurol cern (Table 11.56). Support is needed while the patient is Neurosurg Psychiatry 1995; 58(6):738–41. in hospital and thereafter. It may take a variety of forms: 2 Turkington PM, Bamford J, Wanklyn P, Elliott MW. • an informal talk with the consultant, nurse, therapist Prevalence and predictors of upper airway obstruction in or social worker; these are valuable opportunities for the ﬁrst 24 hours after acute stroke. Stroke 2002; carers to ask questions; 33(8):2037–42. • a carers’ group where they can ask team members ques- 3 Rowat AM, Dennis MS, Wardlaw JM. Hypoxaemia in acute tions, share experiences and provide mutual support; stroke is frequent and worsens outcome. Cerebrovascular • formal sessions with a counsellor which may help Diseases 2006; 21(3):166–72. them come to terms with their problems. 432 4 Tyson SF, Nightingale P. The effects of position on oxygen The setting in which support is given needs to be tai- saturation in acute stroke: a systematic review. Clin Rehabil 2004; 18(8):863–71. lored to the individual since, for example, not everybody 5 North JB, Jennett S. Abnormal breathing patterns wants to attend a group. The need for these sorts of ser- associated with acute brain damage. Arch Neurol 1974; vices may not be apparent while patients are in hospital, 31(5):338–44. or when they attend an outpatient department. Also, for 6 Turkington PM, Bamford J, Wanklyn P, Elliott MW. Effect patients who are not admitted after their stroke, or who of upper airway obstruction on blood pressure variability remain in hospital for just a few days, the opportunities after stroke. Clin Sci (Lond) 2004; 107(1):75–9. for the patient and their carer to ask questions and 7 Bassetti CL, Milanova M, Gugger M. Sleep-disordered obtain advice are often limited. One approach is to pro- breathing and acute ischemic stroke: diagnosis, risk vide a dedicated stroke family support worker who can factors, treatment, evolution, and long-term clinical identify the physical and emotional needs of patients outcome. Stroke 2006; 37(4):967–72. and their families and try to meet them using all avail- 8 Rowat AM, Dennis MS, Wardlaw JM. Central periodic breathing observed on hospital admission is associated able resources. In many places this role is already, at least with an adverse prognosis in conscious acute stroke partially, carried out by social workers and other mem- patients. Cerebrovasc Dis 2006; 21(5–6):340–7. bers of the team, but there are often difﬁculties in bridg- 9 Naughton MT. Pathophysiology and treatment of ing the gap between hospital and community care. Cheyne-Stokes respiration. Thorax 1998; 53(6):514–18. Although such support is valued by its recipients, its 10 Cherniack NS, Longobardo G, Evangelista CJ. Causes impact on patient and carer outcomes is unclear (section of Cheyne-Stokes respiration. Neurocrit Care 2005; 17.8.2). 3(3):271–9. .. ..

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Stroke 2004; 352 Greener J, Enderby P, Whurr R. Speech and language 35(3):794–802. therapy for aphasia following stroke. Cochrane Database 369 Singh A, Herrmann N, Black SE. The importance of lesion Syst Rev 2006; (3). location in poststroke depression: a critical review. Can J 353 Roby RR. A meta-analysis of clinical outcomes in the Psychiatry 1998; 43(9):921–7. treatment of aphasia. J Speech Hearing Res 1998; 370 Carson AJ, MacHale S, Allen K, Lawrie SM, Dennis M, 41:172–87. House A, Sharpe M. Depression after stroke and lesion 354 Bakheit AM. Drug treatment of poststroke aphasia. Exp Rev location: a systematic review. Lancet 2000; Neurotherapeutics 2004; 4(2):211–17. 356(9224):122–6. 355 Greener J, Enderby P, Whurr R. Pharmacological treatment 371 Morrison V, Pollard B, Johnston M, MacWalter R. Anxiety for aphasia following stroke. Cochrane Database Syst Rev and depression 3 years following stroke: demographic, 2006; (3). clinical, and psychological predictors. J Psychosom Res 356 Sellars C, Hughes T, Langhorne P. Speech and language 2005; 59(4):209–13. therapy for dysarthria due to non-progressive brain 372 Bruggimann L, Annoni JM, Staub F, von Steinbuchel N, damage. Cochrane Database Syst Rev 2006; (3). Van der Linden M, Bogousslavsky J. Chronic posttraumatic 357 Beekman AT, Penninx BW, Deeg DJ, Ormel J, Smit JH, stress symptoms after nonsevere stroke. Neurology 2006; Braam AW, van Tilburg W. Depression in survivor of 66(4):513–16. stroke: a community-based study of prevalence, risk factors 373 Ramasubbu R, Patten SB. Effect of depression on stroke and consequences. Soc Psychiatry Psychiatr Epidemiol 1998; morbidity and mortality. Can J Psychiatry 2003; 33(10):463–70. 48(4):250–7. .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 631 References 631 374 Spalletta G, Ripa A, Caltagirone C. Symptom proﬁle of 391 Lincoln NB, Willis D, Philips SA, Juby LC, Berman P. DSM-IV major and minor depressive disorders in ﬁrst-ever Comparison of rehabilitation practice on hospital wards stroke patients. Am J Geriatr Psychiatry 2005; 13(2):108–15. for stroke patients. Stroke 1996; 27(1):18–23. 375 Watkins C, Daniels L, Jack C, Dickinson H, van Den BM. 392 Choi-Kwon S, Han SW, Kwon SU, Kim JS. Poststroke Accuracy of a single question in screening for depression in fatigue: characteristics and related factors. Cerebrovasc Dis a cohort of patients after stroke: comparative study. Br Med 2005; 19(2):84–90. J 2001; 323(7322):1159. 393 De Groot MH, Phillips SJ, Eskes GA. Fatigue associated with 376 Aben I, Verhey F, Lousberg R, Lodder J, Honig A. stroke and other neurologic conditions: Implications for Validity of the Beck depression inventory, hospital stroke rehabilitation. Arch Phys Med Rehabil 2003; anxiety and depression scale, SCL-90, and Hamilton 84(11):1714–20. depression rating scale as screening instruments for 394 Glader EL, Stegmayr B, Asplund K. Poststroke fatigue: depression in stroke patients. Psychosomatics 2002; a 2-year follow-up study of stroke patients in Sweden. 43(5):386–93. Stroke 2002; 33(5):1327–33. 377 Benaim C, Cailly B, Perennou D, Pelissier J. Validation of 395 Outpatient Service Trialists. Therapy-based rehabilitation the aphasic depression rating scale. Stroke 2004; services for stroke patients at home. Cochrane Database Syst 35(7):1692–6. Rev 2003; 1. 378 Leeds L, Meara RJ, Hobson JP. The utility of the Stroke 396 Logan PA, Gladman JR, Drummond AE, Radford KA. Aphasia Depression Questionnaire (SADQ) in a stroke A study of interventions and related outcomes in a rehabilitation unit. Clin Rehabil 2004; 18(2):228–31. randomized controlled trial of occupational therapy and 379 Forster A, Smith J, Young J, Knapp P, House A, Wright J. leisure therapy for community stroke patients. Clin Rehabil Information provision for stroke patients and their 2003; 17(3):249–55. caregivers. Cochrane Database Syst Rev 2006; (3). 397 Collen FM, Wade DT. Residual mobility problems after 380 Anderson CS, Hackett ML, House AO. Interventions for stroke. Int Disabil Stud 1991; 13(1):12–5. preventing depression after stroke. Cochrane Database Syst 398 Collen FM, Wade DT, Robb GF, Bradshaw CM. The Rev 2006; (3). Rivermead Mobility Index: a further development of the 381 Hackett ML, Anderson CS, House AO. Management Rivermead Motor Assessment. Int Disabil Stud 1991; of depression after stroke: a systematic review of 13(2):50–4. pharmacological therapies. Stroke 2005; 399 Wade DT, Wood VA, Heller A, Maggs J, Langton HR. 36(5):1098–103. Walking after stroke. Measurement and recovery 382 Mottram P, Wilson K, Strobl J. Antidepressants for over the ﬁrst 3 months. Scand J Rehabil Med 1987; depressed elderly. Cochrane Database Syst Rev 2006; 19(1):25–30. (1):CD003491. 400 Green J, Young J, Forster A, Collen F, Wade D. Combined 383 Cipriani A, Brambilla P, Furukawa T, Geddes J, Gregis M, analysis of two randomized trials of community Hotopf M et al. Fluoxetine versus other types of physiotherapy for patients more than one year post stroke. pharmacotherapy for depression. Cochrane Database Clin Rehabil 2004; 18(3):249–52. Syst Rev 2005; (4):CD004185. 401 Saunders DH, Greig CA, Young A, Mead GE. Physical 384 Hackett ML, Anderson CS, House AO. Interventions for ﬁtness training for stroke patients. Cochrane Database treating depression after stroke. Cochrane Database Syst Rev Syst Rev 2006; (3). 2006; (3). 402 Gladman J, Forster A, Young J. Hospital- and home-based 385 Cole MG, Elie LM, McCusker J, Bellavance F, Mansour A. rehabilitation after discharge from hospital for stroke Feasibility and effectiveness of treatments for post-stroke patients: analysis of two trials. Age Ageing 1995; depression in elderly inpatients: systematic review. J 24(1):49–53. Geriatr Psychiatry Neurol 2001; 14(1):37–41. 403 Legh-Smith J, Wade DT, Hewer RL. Driving after a stroke. 386 Murray GB, Shea V, Conn DK. Electroconvulsive therapy J R Soc Med 1986; 79(4):200–3. for poststroke depression. J Clin Psychiatry 1986; 404 Fisk GD, Owsley C, Pulley LV. Driving after stroke: driving 47(5):258–60. exposure, advice, and evaluations. Arch Phys Med Rehabil 387 House AO, Hackett ML, Anderson CS, Horrocks JA. 1997; 78(12):1338–45. Pharmaceutical interventions for emotionalism after 405 Gommans J, Sye D, MacDonald A. Guideline stroke. Cochrane Database Syst Rev 2006; (3). recommendations for the management of patients 388 Calvert T, Knapp P, House A. Psychological associations admitted with acute stroke: implications of a local audit. with emotionalism after stroke. J Neurol Neurosurg N Z Med J 2005; 118(1214):U1435. Psychiatry 1998; 65(6):928–9. 406 Samuelsson SM. Physicians’ control of driving after 389 Lincoln NB, Gamlen R, Thomason H. Behavioural stroke attacks. Tidsskr Den Norske Laegef 2005; mapping of patients on a stroke unit. Int Disabil Stud 1989; 125(19):2610–12. 11(4):149–54. 407 Haselkorn JK, Mueller BA, Rivara FA. Characteristics of 390 Bernhardt J, Dewey H, Thrift A, Donnan G. Inactive and drivers and driving record after traumatic and alone: physical activity within the ﬁrst 14 days of acute nontraumatic brain injury. Arch Phys Med Rehabil 1998; stroke unit care. Stroke 2004; 35(4):1005–9. 79(7):738–42. .. ..

9781405127660_4_011.qxd 10/13/07 10:55 AM Page 632 632 Chapter 11 What are this patient’s problems? 408 Akinwuntan AE, Feys H, De Weerdt W, Baten G, Arno P, controlled trial of leisure therapy and conventional Kiekens C. Prediction of driving after stroke: A prospective occupational therapy after stroke. TOTAL Study Group. study. Neurorehabilitation & Neural Repair 2006; Trial of Occupational Therapy and Leisure. Clin Rehabil 20(3):417–23. 2001; 15(1):42–52. 409 Mazer BL, Korner-Bitensky NA, Sofer S. Predicting ability to 426 Kakkos SK, Geroulakos G. Economy class stroke syndrome: drive after stroke. Arch Phys Med Rehabil 1998; case report and review of the literature. Eur J Vasc Endovasc 79(7):743–50. Surg 2004; 27(3):239–43. 410 Radford KA, Lincoln NB. Concurrent validity of the stroke 427 Cheung RT. Sexual functioning in Chinese stroke patients drivers screening assessment. Arch Phys Med Rehabil 2004; with mild or no disability. Cerebrovasc Dis 2002; 85(2):324–8. 14(2):122–8. 411 Fox GK, Bowden SC, Smith DS. On-road assessment of 428 Holbrook M. Stroke: social and emotional outcome. J R Coll driving competence after brain impairment: review of Physicians Lond 1982; 16(2):100–4. current practice and recommendations for a standardized 429 Van Exel NJ, Koopmanschap MA, van den BB, Brouwer examination. Arch Phys Med Rehabil 1998; 79(10):1288–96. WB, van den Bos GA. Burden of informal caregiving for 412 Akinwuntan AE, DeWeerdt W, Feys H, Baten G, Arno P, stroke patients. Identiﬁcation of caregivers at risk of Kiekens C. Reliability of a Road Test after Stroke. Arch Phys adverse health effects. Cerebrovasc Dis 2005; 19(1):11–17. Med Rehabil 2003; 84(12):1792–6. 430 Visser-Meily JM, Post MW, Riphagen II, Lindeman E. 413 Akinwuntan AE, De Weerdt W, Feys H, Baten G, Arno P, Measures used to assess burden among caregivers of stroke Kiekens C. The validity of a road test after stroke. Arch Phys patients: a review. Clin Rehabil 2004; 18(6):601–23. Med Rehabil 2005; 86(3):421–6. 431 Kalra L, Evans A, Perez I, Melbourn A, Patel A, Knapp M, 414 Akinwuntan AE, De Weerdt W, Feys H, Pauwels J, Baten G, Donaldson N. Training carers of stroke patients: Arno P, Kiekens C. Effect of simulator training on driving randomised controlled trial. Br Med J 2004; after stroke: A randomized controlled trial. Neurology 2005; 328(7448):1099. 65(6):843–50. 432 Visser-Meily A, van Heugten C, Post M, Schepers V, 415 Chiu CWY, Man DWK. The effect of training older adults Lindeman E. Intervention studies for caregivers of stroke with stroke to use home-based assistive devices. OTJR: survivors: a critical review. Patient Educ Couns 2005; Occupation, Participation, & Health 2006; 24(3):113–20. 56(3):257–67. 416 Walker CM, Sunderland A, Sharma J, Walker MF. The 433 Hodkinson HM. Evaluation of a mental test score for impact of cognitive impairment on upper body dressing assessment of mental impairment in the elderly. Age Ageing difﬁculties after stroke: a video analysis of patterns of 1972; 1(4):233–8. recovery. J Neurol Neurosurg Psychiatry 2004; 75(1):43–8. 434 Belﬁeld PW. Urinary catheters. In: GP Mulley, ed. Everyday 417 Huck J, Bonhotal BH. Fastener systems on apparel for Aids and Appliances. London: BMJ Publishers, 1989, hemiplegic stroke victims. Appl Ergon 1997; 28(4):277–82. pp. 55–9. 418 Perry L, McLaren S. An exploration of nutrition and eating 435 Smith N. Aids for urinary incontinence. In: GP Mulley, ed. disabilities in relation to quality of life at 6 months post- Everyday Aids and Appliances. London: BMJ Publishers, stroke. Health Soc Care Community 2004; 12(4):288–97. 1989, pp. 50–4. 419 Wozniak MA, Kittner SJ. Return to work after ischemic 436 Kidd D, Lawson J, Nesbitt R, MacMahon J. Aspiration in stroke: a methodological review. Neuroepidemiology 2002; acute stroke: a clinical study with videoﬂuoroscopy. Q J 21(4):159–66. Med 1993; 86(12):825–9. 420 Vestling M, Tufvesson B, Iwarsson S. Indicators for return 437 Scottish Intercollegiate Guidelines Network. Management to work after stroke and the importance of work for of Patients with Stroke: Identiﬁcation and Management of subjective well-being and life satisfaction. J Rehabil Med Dysphagia. Edinburgh: Scottish Intercollegiate Guidelines 2003; 35(3):127–31. Network, 2004. 421 Wellwood I, Dennis MS, Warlow CP. Perceptions and 438 Ashworth B. Preliminary trial of carisoprodol in multiple knowledge of stroke among surviving patients with stroke sclerosis. Practitioner 1964; 192:540–2. and their carers. Age Ageing 1994; 23(4):293–8. 439 Wade DT. Measurement in neurological rehabilitation. 422 Drummond A. Leisure activity after stroke. Int Disabil Stud Curr Opin Neurol Neurosurg 1992; 5(5):682–6. 1990; 12(4):157–60. 440 Martin J, Meltzer H, Elliot D. The Prevalence of Disability 423 Green J, Forster A, Young J. 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9781405127660_4_011.qxd 10/13/07 10:55 AM Page 633 References 633 444 Folstein MF, Folstein SE, McHugh PR. ‘Mini-mental state’: 453 Lu CL, Yu B, Basford JR, Johnson ME, An KN. Inﬂuences of a practical method for grading the cognitive state of cane length on the stability of stroke patients. J Rehabil Res patients for the clinician. J Psychiatr Res 1975; Dev 1997; 34(1):91–100. 12(3):189–98. 454 Tyson SF. The support taken through walking aids during 445 O’Rourke S, MacHale S, Signorini D, Dennis M. Detecting hemiplegic gait. Clin Rehabil 1998; 12(5):395–401. psychiatric morbidity after stroke: comparison of the GHQ 455 Tyson S, Thornton H, Downes A. The effect of a hinged and the HAD Scale. Stroke 1998; 29(5):980–5. ankle-foot orthosis on hemiplegic gait: four single case 446 Johnson G, Burvill PW, Anderson CS, Jamrozik K, Stewart- studies. Physiother Theory Pract 1998; 14:75–85. Wynne EG, Chakera TM. Screening instruments for 456 Beckerman H, Becher J, Lankhorst GJ, Verbeek AL. Walking depression and anxiety following stroke: experience in the ability of stroke patients: efﬁcacy of tibial nerve blocking Perth community stroke study. Acta Psychiatr Scand 1995; and a polypropylene ankle-foot orthosis. Arch Phys Med 91(4):252–7. Rehabil 1996; 77(11):1144–51. 447 House A, Dennis M, Hawton K, Warlow C. Methods of 457 Roberts K, Porter K. How do you size a nasopharyngeal identifying mood disorders in stroke patients: experience airway. Resuscitation 2003; 56(1):19–23. in the Oxfordshire Community Stroke Project. Age Ageing 458 Roberts K, Whalley H, Bleetman A. The nasopharyngeal 1989; 18(6):371–9. airway: dispelling myths and establishing the facts. Emerg 448 Shinar D, Gross CR, Price TR, Banko M, Bolduc PL, Med J 2005; 22(6):394–6. Robinson RG. Screening for depression in stroke patients: 459 St Clair M. Survey of the uses of the Pegasus Airwave the reliability and validity of the Center for Epidemiologic System in the United Kingdom. J Tiss Viabil 1992; 2:9–16. Studies Depression Scale. Stroke 1986; 17(2):241–5. 460 Levine JA, Morris JC. The use of a football helmet to secure 449 Agrell B, Dehlin O. Comparison of six depression rating a nasogastric tube. Nutrition 1995; 11(3):285. scales in geriatric stroke patients. Stroke 1989; 461 Marson AG, Al-Kharusi AM, Alwaidh M, Appleton R, 20(9):1190–4. Baker GA, Chadwick DW, et al. The SANAD study of 450 Williams LS, Brizendine EJ, Plue L, Bakas T, Tu W, Hendrie effectiveness of carbamazepine, gabapentin, lamotrigine, H, Kroenke K. Performance of the PHQ-9 as a screening oxcarbazepine, or topiramate for treatment of partial tool for depression after stroke. Stroke 2005; 36(3):635–8. epilepsy: an unblinded randomised controlled trial. 451 Mulley G. Walking frames. In: G Mulley, ed. More Everyday Lancet 2007; 369:1000–15. Aids and Appliances. London: BMJ Publishing, 1991, 462 Marson AG, Al-Kharusi AM, Alwaidh M, Appleton R, pp. 174–81. Baker GA, Chadwick DW, et al. The SANAD study of 452 Tyson SF, Ashburn A. The inﬂuence of walking aids effectiveness of valproate, lamotrigine or topiramate for on hemiplegic gait. Physiother Theory Pract 1994; generalised and unclassiﬁable epilepsy: an unblinded 10:77–86. randomised controlled trial. Lancet 2007; 369:1016–26. .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 635 12 Specific treatments for acute ischaemic stroke 12.1 Pathophysiology of acute ischaemic stroke 635 12.2 General treatment considerations 654 12.3 Routine use: aspirin 660 12.4 Selective use: anticoagulants 665 12.5 Selective use: reperfusion with thrombolytic drugs and other methods 675 12.6 Unproven value: other reperfusion strategies 687 12.7 Unproven value: treatment of cerebral oedema and raised intracranial pressure 689 12.8 Unproven value: other interventions 691 Focal cerebral ischaemia, caused by acute occlusion of a clinical risk and beneﬁt associated with its use. In view cerebral blood vessel or sometimes just by low blood of this, the section on each of the speciﬁc treatments ﬂow, initiates a series of events which can lead to irre- will assess the strength of evidence available and, where versible neuronal damage and cell death (i.e. infarction) possible, base any recommendations on the results of a in the part of the brain supplied or drained by that vessel. systematic review (and meta-analysis) of all the relevant Several pathophysiological cascades run in sequence randomized trials of that particular treatment. (and in parallel). 1,2 In the vascular system, rapid changes in platelet and coagulation factors, the vessel wall (par- ticularly the endothelium) and in the thrombus itself interact to produce a very dynamic state, not only at the site of vessel occlusion, but also more remotely, in both 12.1 Pathophysiology of acute ischaemic the macro- and microcirculation. stroke In brain tissue, changes occur in neurones, glial cells and other structural components in differing degrees and at different times after the onset of ischaemia, The pathophysiology of acute ischaemic stroke encom- which means that cerebral infarction is a dynamic and passes two sequential processes: the vascular, haemato- highly unstable process, not a discrete ‘one-off’ event. In logical or cardiac events that cause the initial reduction other words, infarction is not an ‘all-or-nothing’ episode in local cerebral blood ﬂow (Chapters 6 and 7) and then which is instantaneous in onset, maximal in severity the alterations of cellular chemistry that are caused by at the moment of onset and irreversibly complete within ischaemia and which lead to necrosis of neurones, glia 6h. 3 and other brain cells. This section will discuss cerebral This chapter begins with a review of pathophysiology, metabolism, regulation of cerebral blood ﬂow, molecular particularly aspects which relate to the speciﬁc treat- consequences of cerebral ischaemia and how under- ments that are described later in the chapter. As far as standing these processes leads to the development of possible, we base the decision whether or not to use a various treatments for acute ischaemic stroke. particular treatment, not merely on its putative physio- logical effects, but on the evidence from randomized 12.1.1 Cerebral metabolism trials in patients which demonstrate the balance of Energy demand and cerebral blood flow Stroke: practical management, 3rd edition. C. Warlow, J. van Gijn, The human brain has a high metabolic demand for M. Dennis, J. Wardlaw, J. Bamford, G. Hankey, P. Sandercock, G. Rinkel, P. Langhorne, C. Sudlow and P. Rothwell. Published energy and, unlike other organs, uses glucose (about 2008 Blackwell Publishing. ISBN 978-1-4051-2766-0. 75–100 mg/min, or 125 g/day) as its main substrate for 635 ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 636 636 Chapter 12 Specific treatments for acute ischaemic stroke Glucose ATP ADP Glucose-6-phosphate Fructose-6-phosphate ATP ADP Fructose-1,6-phosphate 2NAD + Glyceraldehyde-3-phosphate (2) Glycolysis +2P i Glucose + 2P i + 2ADP 2ADP 3-phosphoglyceroyl phosphate (2) 2lactate + 2ATP + 2ATP 2H 2 O for glycolysis 3-phosphoglycerate (2) 2-phosphoglycerate (2) Phosphoenolpyruvate (2) 2ADP 2ATP Pyruvate (2) NAD + 2NADH NADH CoA 2NAD + CO 2 Acetyl-CoA Lactate (2) Oxaloacetate The tricarboxylic Citrate acid cycle Malate 2Pyruvate + 5O 2 + Isocitrate 30ADP + 30P i Fumarate CO 2 6CO 2 + 30ATP + 34H 2 O -ketoglutarate Succinate Succinyl-CoA CO 2 2H 2H 2H 2H NAD + Flavoprotein ADP + P i Coenzyme Q ATP Cytochrome b Electron transport ADP + P i and oxidative phosphorylation Cytochrome c ATP Cytochrome a 3 ADP + P i ATP + 1 2H + / 2 O 2 H 2 O Fig. 12.1 Biochemical pathway of the aerobic Overall: glucose + 6O 2 + 36P i + 36ADP 6CO 2 + 36ATP + 42H 2 O metabolism of glucose. energy metabolism. Glucose is metabolized in the brain nicotinamide – adenine dinucleotide (NAD+) – is reduced entirely via the glycolytic sequence and the tricarboxylic (to NADH) and 2 m each of adenosine diphosphate acid cycle (Fig. 12.1). (ADP) and intracellular phosphorus are converted to Each molecule of glucose is broken down in a series of 2 m of adenosine triphosphate (ATP). In the presence enzymatic steps (glycolysis) into two molecules (2 m) of oxygen, pyruvate is metabolized, ﬁrst by pyruvate of pyruvate. During these reactions, the oxidized form of dehydrogenase and then by a series of mitochondrial .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 637 12.1 Pathophysiology of acute ischaemic stroke 637 reactions, to carbon dioxide (CO ) and water (H O) with 2 2 The resting brain consumes energy at the same rate as the formation of 36 m of ATP. This is the maximum a 20-watt light bulb. ATP yield. In the absence of oxygen, this sequence of events is blocked or retarded at the stage of pyruvate Global cerebral blood ﬂow (CBF), reﬂecting both grey oxidation, leading to the reduction of pyruvate to lactate and white matter compartments, per unit of brain in a by NADH and lactic dehydrogenase. Anaerobic glycolysis healthy young adult, is about 50–55 mL/100 g of brain therefore still leads to the formation of ATP, as well as per minute, with signiﬁcantly higher values in those lactate, but the energy yield is relatively small (2 m rather below 20 years of age and lower values in those over than 36 m of ATP from 1 m of glucose). In addition, lactic 60 years. 10 For a brain of average weight (1300–1400 g acid accumulates within and outside cells (hence, the in a 60–65 kg adult), which is only 2% of total adult cell is acidiﬁed) and mitochondria lose their ability to body weight, the total CBF at rest is disproportionately sequester calcium, so any calcium entering or released large at about 800 mL/min, which is 15–20% of the total within the cell will raise the intracellular calcium cardiac output. At this level of blood ﬂow, whole brain level. 4–6 oxygen consumption, usually measured as the cerebral Although classical neuroenergetics states that glucose metabolic rate of oxygen (CMRo ), is about 3.3–3.5 mL/ 2 is the exclusive energy substrate of brain cells, and its 100 g of brain per minute, or 45 mL of oxygen per minute, full oxidation provides all the necessary energy to sup- which is 20% of the total oxygen consumption of the port brain function, recent data have revealed a more body at rest. intricate picture in which astrocytes play a central role in metabolic coupling and supplying lactate as an additional 12.1.2 Cerebral blood flow regulation energy substrate in register with glutamatergic activity. 7 The basic mechanism involves glutamate-stimulated The fraction of oxygen extracted from the blood, the aerobic glycolysis; the sodium-coupled reuptake of gluta- oxygen extraction fraction (OEF), is fairly constant mate by astrocytes and the ensuing activation of the throughout the brain because CBF, cerebral blood Na-K-ATPase triggers glucose uptake and processing volume (CBV) and CMRo as well as the cerebral meta- 2 via glycolysis, resulting in the release of lactate from bolic rate of glucose (CMRglu) are all coupled. 10 In the astrocytes. Lactate can then contribute to the activity- normal resting brain, measurements of CBF are therefore dependent fuelling of the neuronal energy demands a reliable reﬂection of cerebral metabolism (CMRo ). 2 associated with synaptic transmission. An operational If CBF falls, however (down to 20–25 mL/100 g brain model, the ‘astrocyte-neurone lactate shuttle’, is sup- per minute), the OEF increases to maintain the CMRo 2 ported experimentally by a large body of evidence, (see below). which provides a molecular and cellular basis for inter- Over the past 60 years, the methods for measuring CBF preting data obtained from functional brain imaging have become more accurate and reliable, and have had 8 studies. When neurones are in the presence of both a major impact on our understanding of the regulation glucose and lactate, they preferentially use lactate as of CBF and the pathogenesis of cerebral ischaemia. 3,11–17 their main oxidative substrate. 9 Positron emission tomography (PET) now enables CBF, CMRo , OEF and CMRglu all to be measured in various 2 The brain uses glucose as its main source of energy. regions of interest in the brain, both in normal people During aerobic metabolism each molecule of glucose and after stroke. 11,14,18 produces 36 molecules of adenosine triphosphate (ATP), but during anaerobic metabolism only Cerebral perfusion pressure (CPP) two molecules of ATP are produced along with lactic acid. Under normal conditions, blood ﬂow through the brain is determined by the CPP and by the cerebrovascular ATP is the universal currency for energy. Neurones in resistance (CVR) imposed by blood viscosity and the size the brain require a constant supply of ATP to maintain of the intracranial vessels (i.e. ﬂow = pressure/resistance). their integrity and to keep the major intracellular cation, The CPP represents the difference between arterial + potassium ions (K ), within the cell, and the major extra- pressure forcing blood into the cerebral circulation and ++ + cellular cations, sodium (Na ) and calcium ions (Ca ), the venous pressure. The mean CPP is the mean sys- outside the cell. Because the brain is unable to store temic arterial pressure at the base of the brain in the energy, it requires a constant supply of oxygenated recumbent position, which approximates to the diastolic blood containing an adequate glucose concentration to blood pressure (about 80 mmHg), plus one-third of the maintain its function and structural integrity. pulse pressure (one-third of about 40 mmHg) minus the .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 638 638 Chapter 12 Specific treatments for acute ischaemic stroke intracranial venous pressure (about 10 mmHg), i.e. fairly stable under steady state conditions. For example, 80–85 mmHg. during voluntary hand movements, the metabolic activity of the contralateral motor cortex increases over a few seconds and is accompanied by rapid vasodilatation of Cerebrovascular resistance the local cerebral resistance vessels, leading to an increase Under normal conditions, when resting CPP is constant, in CBF and CBV, rather than any increase in the OEF or any change in CBF must be caused by a change in CVR, glucose extraction fraction. Conversely, low regional meta- usually as a result of alteration in the diameter of small bolic activity (as may occur in a cerebral infarct) is asso- intracranial arteries or arterioles. Under these circum- ciated with reduced metabolic demand and so low CBF. stances, there is a direct correlation between CBF and the Therefore, low ﬂow does not necessarily mean vessel occlu- intravascular CBV. CBF and CBV will both increase as sion but, as in this case, it can mean non-functioning vessels dilate and both decrease as vessels constrict. The brain. Although this coupling of ﬂow with metabolism CBV : CBF ratio remains relatively constant over a wide and function has been suspected for over a century, the range of CBF at normal CPP. mechanism is unknown; it may be that the metabolically When an artery narrows causing CVR to increase, or active areas of brain produce vasodilatory metabolites, when CBF increases, the blood ﬂow velocity in that or the resistance vessels may be under neural regulation, segment of artery increases. Although it may seem para- or a combination of both. This is the principle under- doxical that a reduction in luminal diameter causes an pinning functional magnetic resonance imaging (fMRI). 19 increase in blood ﬂow velocity, think of using a hose: putting one’s ﬁnger over the nozzle generates a high- In normal brain, blood ﬂow is closely coupled with pressure jet of water. The narrower the lumen at the metabolic demand. However, if the brain is damaged, nozzle, the greater the pressure (and velocity of ﬂow) in blood ﬂow and metabolism become uncoupled and the stream of water until the lumen is nearly occluded, so normal ﬂow no longer necessarily implies normal at which point velocity becomes substantially reduced metabolism and function. and the water dribbles out of the hose. This is one of the principles governing the interpretation of blood Arterial carbon dioxide tension ﬂow velocities in the major basal arteries by transcranial Doppler ultrasound (section 6.8.9). Mean blood ﬂow Arterial carbon dioxide tension (PaCO ) has a potent 2 20 velocities within the intracranial arteries vary from 40 effect on CBF; a 1 mmHg rise in PaCO within the range 2 to 70 cm/s. As blood ﬂow velocity is proportional to the of 20–60 mmHg (2.7–8.0 kPa) in normal individuals second power of the vessel radius, it cannot be equated causes an immediate 3–5% increase in CBF due to dilata- linearly with volume blood ﬂow (mL/s), which is propor- tion of cerebral resistance vessels. In chronic respiratory tional to the fourth power of the vessel radius. If vessel failure however, causing CO retention, CBF is normal. 2 calibre were constant, some assumptions could be made Changes in arterial oxygen tension (PaO ) have a modest 2 about volume ﬂow from velocity measures, but the inverse effect on CBF, unless the PaO falls below about 2 calibre of large cerebral arteries varies with changes in 50 mmHg (6.7 kPa), when the resultant decline in the blood pressure, partial pressure of arterial carbon dioxide oxygen saturation of the blood leads to a fall in CVR and (PaCO ), intracranial pressure and age. an increase in CBF. Increasing the PaO above the normal 2 2 level has little effect on CBF. Metabolic rate of cerebral tissue Whole-blood viscosity In the resting brain with normal CPP, CBF is closely matched to the metabolic demands of the tissue. There- Normally, CBF is inversely related to whole-blood visco- fore, grey matter (which has a high metabolic rate) has sity. As the main determinant of whole-blood viscosity higher regional CBF than white matter, which has a (at normal shear rates) is the haematocrit, it follows that relatively low metabolic rate. The ratio between CBF and CBF and haematocrit are inversely related. However, this metabolism is fairly uniform in all areas of the brain relationship is not because the high haematocrit raises and, consequently, the OEF and functional extraction of viscosity and thereby slows ﬂow (at least not in normal glucose from the blood are much the same in different vessels); rather, the higher oxygen content of high hae- areas. Normally, regional OEF is about one-third and matocrit blood allows CBF to be lower and yet to maintain the regional glucose extraction fraction is about 10%. normal oxygen delivery to the tissues in accordance with Similarly, local ﬂow varies directly with local brain func- metabolic demands. A practical example is encountered tion by 10–20%, even though global CBF tends to be in patients with leukaemia or paraproteinaemia who .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 639 12.1 Pathophysiology of acute ischaemic stroke 639 have very high blood viscosity but normal CBF (or even Autoregulation is achieved primarily by varying pre- high CBF if anaemia coexists), because CBF depends more capillary resistance; compensatory vasodilatation of pial on the oxygen content of the blood (which is normal or and intracerebral arterioles occurs when the blood pres- low) than the viscosity (which is high). However, at very sure falls, and compensatory vasoconstriction when the low shear rates, which might be found in ischaemic brain, blood pressure rises. Whether myogenic, metabolic or for example, because of local vasodilatation, whole-blood neurogenic processes are responsible for this response is viscosity depends more on plasma ﬁbrinogen than hae- unknown. matocrit. In addition, other local factors such as red cell If mean arterial pressure falls below about 40–50 aggregation, platelet aggregation and perhaps increasing mmHg, compensatory vasodilatation and therefore cere- red cell fragility as a result of anoxia, all of which increase bral perfusion reserve is exhausted, and CBF parallels blood viscosity, may come into play to reduce ﬂow. the blood pressure (section 6.7.5). Because oxygen delivery to the brain normally far exceeds demand, metabolic activity can still be maintained at a mean Autoregulation blood pressure of around 40–50 mmHg by increasing Under normal conditions (i.e. mean systemic arterial the oxygen extraction from the blood (Fig. 12.3). This blood pressure within 60–160 mmHg), CBF is main- state of increased OEF has been termed ‘misery perfu- tained at a relatively constant level despite changes in sion’. 14 However, when the OEF is maximal, a state of the cerebral perfusion pressure (Fig. 12.2). This capacity ‘ischaemia’ exists; ﬂow is inadequate (<20 mL/100 g to maintain a constant CBF is due to the phenomenon of brain per minute) to meet metabolic demands, cellular autoregulation. 21–23 metabolism is impaired, and so CMRo begins to fall (see 2 below). 24 As neuronal activity ceases, the patient usually Autoregulation is the ability of cerebral blood ﬂow develops symptoms of neurological dysfunction (if the to remain constant in the face of changes in mean whole brain is ischaemic, non-focal symptoms such as arterial pressure and cerebral perfusion pressure. faintness, and if only part of the brain is ischaemic, focal symptoms such as hemiparesis). If the mean arterial pressure rises above the autoregu- 100 latory range where compensatory vasoconstriction is maximal (i.e. above about 160 mmHg in normal people), then hyperaemia occurs followed by vasogenic oedema, Cerebral blood flow (mL/100 g brain per minute) 50 raised intracranial pressure and the clinical syndrome of 75 hypertensive encephalopathy (section 3.4.5). Dynamic cerebral autoregulation is not affected by 25 but the autoregulatory curve is ‘set’ normal ageing, higher in patients with long-standing hypertension. 25 against increasing blood pressure and develop symptoms 0 Consequently, hypertensive patients are ‘protected’ of ischaemia at higher blood pressure (e.g. mean below 20 60 100 140 180 about 70 mmHg) than in non-hypertensive patients (e.g. Mean systemic arterial pressure (mmHg) mean below 50 mmHg) (Fig. 12.2). Autoregulation is impaired in a variety of disease states Normal brain tissue such as head trauma, diffuse cerebral hypoxia, ischaemic Normal brain tissue, chronic hypertension Mildly ischaemic brain tissue stroke, delayed ischaemia secondary to subarachnoid Moderately ischaemic brain tissue haemorrhage and in some patients with carotid stenosis Severely ischaemic brain tissue or occlusion. 21–23 Autoregulation is also impaired if the PaCO is high, presumably because further vasodilatation 2 Fig. 12.2 Autoregulation: relationship between mean systemic 26 cannot occur and so the perfusion reserve is exhausted. arterial blood pressure and cerebral blood ﬂow (CBF) in normal In some patients who have had transient ischaemic brain tissue and in brain ischaemia. Under normal conditions, attacks or a mild ischaemic stroke, with subsequently CBF is maintained at a relatively constant level, independent normal angiograms, autoregulation and the cerebro- of the systemic arterial blood pressure, as long as the mean vascular response to PaCO may be deranged for several pressure remains between about 60 and 160 mmHg. This 2 capacity to maintain a constant CBF is due to the phenomenon weeks. In all of these situations of impaired autoregula- of autoregulation. In chronic hypertension the curve is shifted tion, CBF varies directly with blood pressure, becoming to the right. ‘pressure passive’, and so predisposing to an increased .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 640 640 Chapter 12 Specific treatments for acute ischaemic stroke Cerebral perfusion pressure (CPP) Cerebral blood volume (CBV) Cerebral blood flow (CBF) Fig. 12.3 Schematic representation of the protective responses to a progressive fall in cerebral perfusion pressure (CPP). With falling CPP, intracranial arteries dilate to maintain the cerebral blood ﬂow (CBF) – Oxygen extraction autoregulation. This results in an increase in cerebral fraction (OEF) blood volume (CBV). When vasodilatation is maximal, further falls in CPP result in a fall in CBF Cerebral metabolic and therefore a fall in the CBF : CBV ratio, and an rate of oxygen (CMRO 2 ) increase in the oxygen extraction fraction (OEF) to maintain tissue oxygenation. This represents a state of impaired cerebral perfusion reserve. When the OEF is maximal, further falls in CPP lead to reduction in Autoregulation; Impaired perfusion Ischaemia; the cerebral metabolic rate of oxygen (CMRo ) and 2 no symptoms reserve; no symptoms symptoms the symptoms of cerebral ischaemia. stroke risk, particularly following exposure to hypo- blood pressure by a servo-controlled plethysmograph. 27 tensive agents, as occurs perioperatively. The temporal pattern of the change in blood pressure Traditionally, cerebral autoregulation has been meas- is correlated with the change in the middle cerebral ured in animals, and in response to static changes in artery (MCA) CBF velocity as measured by TCD. 26 There arterial blood pressure. CBF, or an estimate of CBF such is close agreement between these two methods, and as cerebral blood ﬂow velocity, is measured during a between the thigh method and the classic assessment of large change in blood pressure, usually induced phar- static autoregulation, despite the fact that TCD measure- macologically. 27 However, such techniques are not suit- ment of MCA CBF velocity is only a suitable technique if able for patients with stroke, or who are at risk of stroke, there is no change in MCA diameter during the change because the blood pressure change induced could cause in blood pressure. or increase brain ischaemia. Subsequent attempts to safely and non-invasively monitor autoregulation of CBF, or Cerebral perfusion reserve at least the lower limit of autoregulation, have used indirect and dynamic measures such as CBF velocity, as The ratio of CBF : CBV (see above) is a measure of cere- determined by transcranial Doppler (TCD) ultrasound, bral perfusion reserve; a ratio below about 6.0 indicates in response to vasodilatory stimuli such as hypercapnoea maximal vasodilatation and CBV, and exhausted reserve, (rather than changes in blood pressure). 22 Although even if the CBF is still normal. If available, PET scanning these indirect measures generally correlate with direct will show a rising OEF at this stage, to maintain CMRo 2 measures of cerebral autoregulation, they do measure a (Fig. 12.4). 10,15,28,29 If PET is unavailable, the mean cere- slightly different physiological response. Other methods bral transit time (MCTT), which is the reciprocal of of measuring dynamic autoregulation which are non- CBF : CBV, can be used instead. 30 Other techniques for invasive, and suitable for use in patients at risk of stroke, measuring CBF at rest and after exposure to vasodilatory aim to evaluate the response of CBF or CBF velocity to stimuli (e.g. inhalation of CO , intravenous administra- 2 small physiological changes in arterial blood pressure. tion of acetazolamide, or breath holding), and thus These include changes in blood pressure induced by the cerebrovascular reserve capacity, include: use of bilateral leg cuffs which are inﬂated suprasystolic- • xenon-133 ( 133 Xe) inhalation; 133 Xe is a lipophilic ally and then suddenly deﬂated to cause a transient fall radioactive tracer that can be inhaled or injected and in blood pressure, and spontaneous variability in arterial easily diffuses through the blood–brain barrier. Probes .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 641 12.1 Pathophysiology of acute ischaemic stroke 641 1.0 In clinical practice, cerebral perfusion reserve is generally assessed indirectly by measuring the relative 0.9 difference between CBF at baseline and then in response Oxygen extraction fraction 0.7 administration), which increase CBF unless the capacity 0.8 to a vasomotor stimulus such as CO (by inhalation 2 or breath holding) or acetazolamide (by intravenous 0.6 for cerebral dilatation is exhausted. For example, intra- venous injection of 1 g of the vasodilating agent acetazo- 0.5 lamide (Diamox) produces an increase in CBF of 5–100% 0.4 0.3 indicates a loss of autoregulation and inadequate cere- 36,42 brovascular reserve. 0.2 within 20–30 min. The lack of such ﬂow augmentation The completely non-invasive evaluation of cere- 0 0 3 456 7 8 9101112 13 brovascular reserve capacity with TCD CO testing is 2 the most widely applied method in clinical practice. CBF/CBV Drawbacks of TCD CO testing are an insufﬁcient tem- 2 Normal poral bone ultrasound window in 10–20% of patients Patent Unilateral and relatively low diagnostic accuracy. 32 Indeed, all of Occluded Occluded bilateral the indirect methods of measuring perfusion reserve (e.g. SPECT, TCD, MCTT) are inaccurate when the normal Fig. 12.4 Relationship between oxygen extraction fraction relationships between CBF, CBV, OEF and vascular react- (OEF) and cerebral blood ﬂow (CBF) : cerebral blood volume ivity are distorted, as occurs in ischaemic and infarcted ratio (CBF : CBV) in each of 82 middle cerebral artery regions brain. 28 from 32 patients with varying degrees of carotid artery stenosis A common clinical scenario of potentially impaired and occlusion and nine normal subjects (with permission from reserve is a patient with stenosis or occlusion of one or 15 Gibbs et al. (1984) ). CBF : CBV is a measure of cerebral both internal carotid arteries, severe enough (at least perfusion reserve. A CBF : CBV ratio below about 6.0 indicates 50% diameter stenosis) to produce a fall in CPP distally. maximal vasodilatation and CBV, and exhausted reserve, even If the ophthalmic and leptomeningeal collateral CBF is if the CBF is still normal. If cerebral blood ﬂow continues to fall inadequate, and the oxygen extraction fraction increases, at this stage, OEF rises to maintain CMRo . 2 a state of ‘misery perfusion’ exists. 16,43 Under these circumstances, the brain is vulnerable to any further placed over the scalp can measure perfusion to the fall in CPP, as may occur when the patient stands up cerebral cortex; 19,31 quickly, when undergoing anaesthesia (e.g. for coronary • stable (‘cold’) xenon-enhanced computed tomography artery bypass surgery) or starts or increases antihyper- (CT); 32 tensive medication or vasodilators. In patients with • single-photon emission computed tomography (SPECT) symptomatic ICA occlusion, misery perfusion (or severely with 133 Xe-, iodine-123 ( 123 I)-labelled isopropyliodo- impaired cerebral vasomotor reactivity as a surrogate) 99 amphetamine, or technetium-99m ( Tc)-labelled increases the risk of future ipsilateral ischaemic stroke by hexamethylpropyleneamine oxime (HMPAO); 19,33 as much as seven- to eightfold. 15,44,45 • perfusion-weighted MRI; 13,16,17,19 Perfusion imaging with a challenge test (e.g. PET-OEF, • CT perfusion. 34–37 Xe/CT perfusion with acetazolamide) may be able to Cerebrovascular reactivity can also be evaluated by: identify patients with enough reduction in cerebral per- • three-dimensional time-of-ﬂight magnetic resonance fusion reserve to beneﬁt from an extracranial to intracra- angiography; a severely saturated ﬂow signal indicates nial (EC-IC) bypass to augment the CBF. 28,42,46 However, a higher probability of impaired cerebrovascular react- correlation of the different methods of measuring auto- ivity, but is neither sensitive nor speciﬁc; 19 regulatory vasodilatation, secondary to reduced perfusion • blood oxygen level-dependent (BOLD) contrast MRI pressure, is sufﬁciently variable to have limited the valid- coupled with administration of CO ; 38–40 ity of studies associating haemodynamic impairment 2 • transcranial Doppler ultrasound (TCD), which meas- with stroke risk. 28 An ongoing clinical trial using the OEF ures velocity ﬂow in the MCA as a surrogate for CBF, as measured with PET scanning will attempt to deﬁne coupled with administration of CO with or without the patient population with occlusive vascular disease at 2 colour duplex M-mode ultrasound (to estimate extra- high enough risk for stroke that the risk of EC-IC bypass cranial carotid ﬂow volume). 19,32,41 is worth taking for the potential long-term beneﬁt. 46,47 .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 642 642 Chapter 12 Specific treatments for acute ischaemic stroke 3 anterior and posterior cerebral arteries. The lentiform 12.1.3 Pathophysiology of cerebral ischaemia nucleus and some of the white matter, which have far 3 fewer anastamoses, are the most severely affected. PET Thrombosis studies show that in early proximal MCA occlusion, the Acute cerebral ischaemia usually begins with the occlu- core typically involves the striatocapsular area, whereas sion of a cerebral blood vessel, more often on the arterial the penumbra (see below) typically involves the cortical than venous side of the circulation, usually by thrombus mantle. 19 However, occasionally the core extends widely or embolus (Chapter 6). It is rarely due to low ﬂow into cortical areas as early as 4 h after onset, 19 probably alone. due to inadequate pial collaterals or a carotid occlusion. When a major artery is suddenly occluded, arterial The volume of core is associated with both admission blood pressure and blood ﬂow fall distal to the occlusion, clinical scores, and ﬁnal infarct volume. and the region of brain supplied by that vessel is acutely deprived of its blood supply and is rendered ischaemic. Availability of collateral blood flow Presumably the pathophysiology of venous infarction is similar, but less has been published about it. Occlusion of a cerebral artery reduces but seldom abo- Activated platelets play a critical role in arterial throm- lishes the delivery of oxygen and glucose to the relevant bosis (section 6.3.3) and also in mediating an inﬂamma- region of the brain because collateral channels partly tory response in the brain (see Inﬂammation below). maintain blood ﬂow in the ischaemic territory. This Activated platelets degranulate and adhere to leucocytes, incomplete ischaemia is responsible for the spatial and thus forming platelet–leucocyte coaggregates. They do temporal dynamics of cerebral infarction. 24 Some other this by expressing P-selectin on their surface which binds areas of the brain, including infarcted tissue, may show to the leucocyte counter-receptor P-selecting GP ligand- relative or absolute hyperaemia (called ‘luxury perfu- 1. This induces leucocyte activation and the release of sion’) due to good collateral blood supply, recanalization inﬂammatory cytokines. 48 of the occluded artery, or inﬂammation or vasodilata- The metabolic and clinical consequences of cerebral tion in response to hypercapnia, i.e. ﬂow is in excess ischaemia depend not only on the cascade of events of the metabolic demands and so the oxygen extraction induced by thrombus formation (i.e. biosynthesis of fraction is reduced. thrombogenic and neurotoxic eicosanoids, inﬂamma- tion, breakdown of the blood–brain barrier, diffusion Severity of ischaemia: critical flow thresholds of these products into surrounding brain and reduced microvascular ﬂow in the ischaemic penumbra around The transition from normal CBF through to cerebral the initial focus), but also on the site, severity and dura- oligaemia, the ischaemic penumbra and frank tissue tion of cerebral ischaemia, the availability of collateral infarction (see below) occurs, operationally, in phases, blood ﬂow, other systemic and tissue factors, and the depending on the severity and duration of brain effect of any reperfusion therapies. 49 ischaemia (Fig. 12.5). The key pathophysiological concept is the division Site of cerebral ischaemia of hypoperfused tissue into three operational Neurones are the brain cells most vulnerable to ischaemia, compartments: tissue that will in principle survive followed by oligodendroglia, astrocytes and endothelial (oligaemia), tissue that may either die or survive (the cells. However, even within the population of neurones, ischaemic penumbra), and tissue that will inevitably there are many different types that also vary in their die (core). sensitivity to ischaemia, and in some cases the vulner- ability varies with the location of the cells. The most Experimental models of focal cerebral ischaemia have vulnerable neurones to mild ischaemia are the pyramidal identiﬁed critical ﬂow thresholds for certain cell func- neurones in the CA1 and CA4 zones of the hippocam- tions (Fig. 12.5), notably a threshold for tissue at risk, pus, followed by neurones in the cerebellum, striatum electrical failure (loss of neuronal electrical activity) and and neocortex. membrane failure (loss of cellular ion homeostasis). 4,5,21 Acute occlusion of the proximal middle cerebral artery Initially, small declines in perfusion pressure and CBF (MCA) reduces distal cerebral perfusion pressure. Cerebral (<50 mL/100 g/min) are compensated for by regional perfusion pressure reductions in the cortical MCA territ- vasodilatation to maintain CBF (autoregulation), resulting ory are most severe in its centre (perisylvian) region and in a regional increase in CBV (section 12.1.2) (Fig. 12.3). least in the border zone areas between the MCA and With continued reductions in perfusion pressure (<45 mL/ .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 643 12.1 Pathophysiology of acute ischaemic stroke 643 100 50 Physiological 40 80 Cerebral blood flow (%) 60 Acidosis 30 Cerebral blood flow (mL/100 g brain per min) compensation Oedema + 2+ K /Ca transients Protein synthesis 40 20 inhibited Dissipative ion 20 fluxes Death 10 (time dependent) 0 0 Tissue at risk Electrical Membrane Fig. 12.5 Cerebral blood ﬂow (CBF) failure failure thresholds for cell dysfunction and death. 100 g/min), and the dilatation of all vessels to capacity, Loss of neuronal electrical activity and function the oxygen extraction fraction (OEF) and glucose extrac- tion fraction (GEF) are increased to maintain a normal The threshold for loss of neuronal electrical activity cerebral metabolic rate of oxygen (CMRo ) and glucose (i.e. electrical failure) is reached when the CBF falls 2 (CMRglu). 29 Protein synthesis also becomes inhibited. below about 20–25 mL/100 g of brain per minute. 4,5 At This is a state of ‘misery perfusion’ which is characterized this point, the OEF is maximal, the CMRo begins to fall 2 by reduced CBF, increased OEF (ranging from the normal (Fig. 12.3), normal neuronal function of the cerebral value of about 30–40% up to the theoretical maximum cortex is affected, neurotransmitters are released, evoked of 100%) and relatively preserved or even normal oxy- cerebral responses from the area of focal ischaemia 3 gen consumption (CMRo ). The tissue is at risk. decrease in amplitude and electrical activity in cortical 2 cells begins to fail. 50 With further falls in ﬂow, evoked potentials are lost, the EEG ﬂattens and then becomes Oligaemia isoelectric. With further cerebral ischaemia (<35 mL/100 g/min), lack of oxygen inhibits mitochondrial metabolism Reduction of cerebral blood from its mean of around and activates the inefﬁcient anaerobic metabolism of 50 mL/100 g per min to less than 20 mL/100 g per min glucose, causing a local rise in lactate production and results in impaired neural function, but preserves so a fall in pH, leading to intra- and extracellular acidosis tissue integrity; this deﬁnes the penumbra. (Fig. 12.5). The energy-dependent functions of cell mem- branes to maintain ion homeostasis become progres- Loss of cellular ion homeostasis + sively impaired; K leaks out of cells into the extracellular + space, Na and water enter cells (cytotoxic oedema), and The threshold for loss of cellular ion homeostasis (i.e. Ca ++ also moves into cells (where it causes mitochondrial membrane failure) and anoxic depolarization is reached failure and compromises the ability of intracellular when blood ﬂow falls to about 15 mL/100 g of brain per membranes to control subsequent ion ﬂuxes, leading minute. 4,5 The water and electrolyte content of ischaemic to cytotoxicity). 2,6 tissue changes due to cell pump failure (see below). The Several compensatory mechanisms come into play critical threshold for the beginning of irreversible cell which sacriﬁce electrophysiological activity to maintain damage is a CBF of about 10 mL/100 g of brain per minute. near-normal ATP concentrations and membrane ion For a short period, the neurones may remain viable and gradients and preserve cell viability, at least temporarily. recover function if perfusion is restored. Otherwise, + Hence, the suppression of neuronal electrical activity as rapid efﬂux of K and inﬂux of Ca ++ ensue due to failure seen on the electroencephalogram (EEG) in order to of the plasma membrane, and there is swelling of the cell reduce energy use. If moderate ischaemia persists, how- and internal organelles, protein degradation and DNA ever (i.e. for several hours), the tissue at risk dies. breakup. .. ..

9781405127660_4_012.qxd 10/16/07 10:47 AM Page 644 644 Chapter 12 Specific treatments for acute ischaemic stroke possible to predict just how long the time window is to Normal flow, normal neuronal function allow successful therapeutic intervention in any one 3 individual. Indeed, there is unlikely to be a rigid and 50 universal time window for all patients because there is so much heterogeneity among individuals in the pattern of Low flow, raised oxygen extraction, arterial occlusion and collateral ﬂow, the duration of normal neuronal function Cerebral blood flow (ml/100 g brain per minute) 20 Reversible reduced Irreversible reduced ischaemia, the size of the ischaemic area, where it is and which cells are involved, and perhaps even the genetic 3 make-up of the patient. The therapeutic time window may also vary for different sites of arterial occlusion function, i.e. and brain ischaemia, and for different interventions. ischaemia function, i.e. infarction For example, the therapeutic time window for throm- bolytics may be shorter than for neuroprotective agents, 0 than for antithrombotic agents; we do not know yet. Time passing Fig. 12.6 Combined effects of residual cerebral blood ﬂow In humans it is not clear how long ischaemic brain (CBF) and duration of ischaemia on reversibility of neuronal can survive and still be salvaged by reperfusion dysfunction during focal cerebral ischaemia. The solid line or measures to protect neurones from dying. delineates the limits of severity and duration of ischaemia Consequently, the duration of the ‘time window’ that allow survival of any neurones. 50 for effective therapeutic intervention is unknown. Duration of ischaemia Other systemic and tissue factors Tissue outcome depends on two factors – the severity of Tissue with small reductions in cerebral blood ﬂow – ﬂow reduction (see above) and its duration (Fig. 12.6). 50 20–50 ml/100 g per min, deﬁned as oligaemia, probably The CBF threshold that deﬁnes the core increases with maintains its function for a long time and is unlikely to time until it reaches the penumbra threshold, at which proceed to infarction. However, oligaemia may become point all the penumbra has been recruited. Thus, within penumbral – and hence potentially the core – because of the penumbra, the lower the CBF, the higher the risk of secondary events that reduce cerebral perfusion pressure, early infarction. PET studies indicate that substantial such as vasogenic oedema and systemic hypotension, or penumbra is present in up to 90% of patients within by factors that aggravate the ﬂow–metabolism mismatch 6 h of onset; this falls to about 50% within 9 h but is still such as hyperglycaemia and pyrexia. 11 This may explain 3 intact in about 30% of patients 18 h after onset. Up to the possible beneﬁts from avoiding physiological com- 52% of the ultimate infarct still shows penumbra 16 h plications and maintaining blood pressure early after after onset. 51 ischaemic stroke. Two trials suggesting effectiveness of the thrombolytic drug desmoteplase when given 3–9 h afer onset of Concept of an ischaemic penumbra ischaemic stroke (in patients with a DWI-PWI mismatch > 20%), coupled with imaging studies showing a pro- The ﬁnding of two separate thresholds, one for cessation longed persistence of substantial volumes of ‘at risk’, but of electrical signals and the other for loss of ion homeo- potentially viable, brain tissue for up to 16–18 h after stasis, which are separated by an intermediate zone ischaemic stroke in some patients, suggest that the time characterized by cessation of cellular electrical activity window for effective therapeutic intervention may be but with preservation of their membrane potential, longer in humans than predicted from animal stud- led to the concept of an ischaemic penumbra of brain ies. 3,51–53 Indeed, we have learnt from randomized trials tissue. 19 The ischaemic penumbra can be deﬁned as an in acute myocardial infarction (MI) that thrombolysis is area of severely ischaemic, functionally impaired, but still effective in reducing case fatality even when given surviving brain tissue which is at risk of infarction but up to 24 h after the onset of chest pain, despite the can be saved, and recover, if it is reperfused before it widely held belief prior to these studies, mainly based on is irreversibly damaged (hence the concept of ‘time is animal models, that thrombolysis could not possibly be brain’). 3,11,13,55,56 Otherwise, it will be progressively re- effective if given more than a few hours after acute MI. 54 cruited into the core of the infarct until maximum infarct Cerebral ischaemia is a dynamic process of ﬂuctuat- extension is reached. The ischaemic penumbra is not ing severity over the ﬁrst few hours and it may not be just a topographic locus, but a dynamic (time × space) .. ..

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