1. Department of Neurosurgery, Newcastle General Hospital, Newcastle upon Tyne
  2. Dept of Medicine, Ogun State University Teaching Hospital; Sagamu Ogun State. Nigeria
  3. School of Population & Health Sciences, The Medical School, Newcastle upon Tyne, United Kingdom
  4. Department of Medicine, North Tyneside General Hospital, North Shields, Tyne and Wear, United Kingdom

E-Mail Contact - OGUNGBO Biodun : biodun-ogungbo@supanet.com


Stroke is a significant economic, social and medical problem all over the world.
This article discusses recent developments in stroke management worldwide. We reviewed and highlighted published clinical guidelines from several countries. The current thoughts on stroke care are discussed and summarized in concise and unambiguous terms. Limitation to optimal management in developing countries as well as areas requiring development and research are highlighted. It should be possible to utilize this in stimulating the development of management strategies for stroke, customized to the unique health structure in Nigeria.

The management of stroke in Nigeria is suboptimal as there are significant deficiencies in the provision of diagnostic, treatment, rehabilitation and support services. The limited resources, manpower shortage, lack of organized stroke unit, neuro-imaging facilities, ambulance services, education of patients and general practitioners as well as impracticable use of thrombolytics are contributory. Training of stroke experts in collaboration with experts in the developed world with provision of neuro-imaging facilities would improve the outlook of stroke management in Nigeria.

The focus in Nigeria must be on preventive strategies and ways to harness local resources in the acute treatment of stroke patients. Health education of the community with emphasis on control of the predisposing factors would reduce the burden of stroke in the country. Risk factor management should begin in childhood, with emphasis on exercise, nutrition, weight and blood sugar control, avoidance of tobacco and excessive alcohol, as well as effective treatment of hypertension and hyperlipidaemia.

Keywords : Africa, Accident vasculaire cérébral, Stroke, Nigeria


Stroke is the acute and dramatic onset of focal or global neurological deficit, which is most often caused by interruption of the blood supply to the brain or indeed hemorrhage into brain tissue lasting more than one hour or leading to death 86,95 . The incidence of stroke is increasing worldwide, in part mostly due to the increasing aging population 95,96,50. Stroke is now the third leading cause of death in most industrialized countries, among adults aged 65 years or more11. The estimated incidence is about 150-200 cases per 100,000 of the population 53, 72, 77, 78, 89, 93. though there is a wide range of variation between areas; Japan and Finland experience the highest age-adjusted rates.16, 42, 47. The age-adjusted incidence rate of 145.6/100,000 population in Kuwait is very low due to the young average age of the Kuwaiti population1.
Stroke causes significant disability and death in many countries and places a huge financial burden on health services. This is estimated at £2.318 billion costs to the National Health Service in the United Kingdom for 1995-6 alone 11. In America, approximately 500,000 strokes occur each year. The direct cost of providing care for stroke victims in 1993 was estimated to be USD17 billion, with an additional USD13 billion in indirect costs attributable to lost earnings due to stroke-related mortality and morbidity 88.
In Nigeria, the impact on the local economy and the financial burden of stroke in Nigeria has not been estimated. The size of the problem appears to be underestimated by the government as no actual publications or statements exist acknowledging the impact of stroke on the health of the nation. A more up to date and current information on the magnitude of the stroke problem in Nigeria is needed 66, 91. Majority of the stroke costs are borne by individual families. There is the need to evaluate the percentage of patients dependent on carers and the yearly expenditure on hospital stay, home rehabilitation as well as information on the loss of income for the patient and carers. The information required for more rational predictions of the burden of stroke in the community are as follows: 1) Number of new stroke cases per year (incidence), 2) Total number of existing stroke patients (prevalence), 3) Number of recurrent stroke, 4) Morbidity and mortality data.


The actual incidence and prevalence of stroke have not been established in Nigeria. Previous reports detailed an increasing incidence but as these were hospital-based studies, they could be inaccurate and probably represent the tip of the iceberg (35, 51, 66, 69). The frequencies in hospital populations varied from 0.9% to 4.0% and stroke accounted for 0.5% to 45% of neurological admissions 69. At the Lagos University teaching Hospital, Stroke was the second commonest cause of neurological admissions and constituted 3.7% of all medical emergencies. At the Ogun State University Teaching Hospital (OSUTH), Sagamu, it accounted for 8.7% of medical admissions and was the third commonest cause of medical admissions. At the University College Hospital, Ibadan, and OSUTH, sagamu, stroke accounted for 4.6% and 17% of medical deaths respectively compared to 7.7% of all deaths at LUTH emergency(64). This therefore appears to be a huge problem in African Nigerians.
The population of Nigeria exceeds 126 million people. If we assume an average stroke incidence of 116 per 100,000 of the population in Nigeria, then 147,000 people suffer a stroke in Nigeria yearly. Using figures from Sagamu, Nigeria, it can be estimated that roughly 34% (n = 49,980) will die within a month and 60% (n=56,700) within six months(65).


There are 3 main types and over 100 underlying causes of stroke.

– Ischemic stroke or cerebral infarction (CI):
In CI, there is interruption of the flow of blood to part of the brain (17). This could be thrombotic, embolic or due to vasospasm, and the mechanical obstruction leads to ischemia of the affected area of brain tissue. Emboli can originate from the heart or the arteries in the neck. Thrombosis of intracranial or extracranial vessels is a major cause of cerebral infarction. Modifiable risk factors are hypertension, diabetes mellitus and cardiac diseases.

– Subarachnoid haemorrhage (SAH)
SAH is a type of stroke in which bleeding occurs in the Subarachnoid space alone or in conjunction with bleeding elsewhere in the central nervous system. Primary SAH is often due to the rupture of an intracranial aneurysm while secondary SAH is most commonly due to trauma. The major risk factors for SAH are increasing age, female gender and smoking (27, 39, 43, 45, 57, 92).

– Intracerebral haemorrhage (ICH)
ICH is a type of stroke in which the rupture of an intracranial blood vessel leads to the loss of blood into the brain tissue. It can be caused by a variety of conditions such as hypertension, arteriovenous malformation, intracranial aneurysms, blood dyscrasias, anticoagulation, chronic alcoholism, vasculitis and possibly tumors 80. The main cause of ICH is hypertension with frequency as high as 72-81% (31, 62).

Cerebral ischemia comprises over 80% of all strokes, with strokes caused by ICH occurring in 10-15% and SAH making up the rest (5-10%).(10, 16, 22, 49, 52, 58, 82). The percentages are highly variable in different communities and changing patterns have been reported in several communities including Nigeria (12,16). According to a clinical report from Ibadan, Nigeria, cerebral ischaemia (CI) occurred in 48% of patients, Intracerebral haemorrhage (ICH) in 15.7% and Subarachnoid haemorrhage (SAH) in 11.3%. The stroke type was undiagnosed in 24.2% (70). Clinical diagnosis is fraught with danger and a high degree of misdiagnosis has been previously highlighted (5, 51, 64, 66). There was confusion of stroke with surgically treatable conditions such as brain abscess, glioma and subdural haematoma in 8.6-13.5% of cases (35, 51, 66, 69).


Stroke is no longer an untreatable condition (24). The real challenge of stroke therapy at the outset of this millennium is how to translate basic pathophysiologic evidence of ischemic neuronal injury into novel neuroprotective therapies either independently or combined with thrombolysis (60). The management of stroke is changing rapidly as new ideas appear for acute treatment, rehabilitation and secondary prevention (24). Stroke care has therefore become a specialized field, requiring input from physicians interested in stroke, as well as a multidisciplinary rehabilitation team (3).
The care of patients in Nigeria must focus on preventive strategies and ways to harness local resources in the acute treatment of stroke patients. Rational treatment requires individual causes of stroke to be identified early and treatment targeted at the mechanism (33).
What follows now is an analysis of stroke guidelines from several different countries.(3, 4, 7, 8, 13-15, 28, 30, 32, 34, 38, 40, 41, 63, 71, 84, 85, 87). This has been organized into 4 main targets areas; 1) Population strategy in stroke care, 2) The role of the physician in preventive care, 3) Managing the acute stroke patient and 4) The place of rehabilitation and prevention of recurrence. We also evaluate strategies to enlist the support of politicians and the general public in stroke awareness (3, 11, 25, 63, 67, 73).

(1): Population strategy

Public awareness programs are important
Previously, a patient cannot be considered to have had a stroke until at least 24 hours have elapsed. This leads to patient apathy and physician inactivity for such a long time! It is important to emphasize that defining stroke in terms of time (24 hours) is no longer satisfactory (33). ‘Brain’ attack’ is a term used to describe the acute presentation of stroke which emphasizes the need for urgent action (33).
Stroke evaluation must be performed within hours as delays lead to loss of brain tissue. Studies have shown that delays in presentation are caused mostly by lack of awareness of stroke (84). All patients within the age range and with a high stroke risk should know the symptoms of stroke. The need to present early for evaluation, treatment and prevention of further attacks must be discussed at various levels. Information about stroke should be made widely available to the public (67). The local press, celebrities and television personalities should be educated on the risks of stroke and the importance of wide public awareness. Stroke issues should be introduced in schools, churches, mosques, plays on television, in the theater and brought to national attention. Health talks as well as the use of posters and radio jingles would assist in re-education of relatives of stroke patients and the community at large.

Life style modification is a key move
High blood pressure and high blood cholesterol are closely related to excessive consumption of fatty, sugary and salty foods. They become an even more lethal combination when combined with tobacco and excessive alcohol consumption. Cigarette smoking should be avoided by all and especially by patients following a stroke or TIA (14, 15). Excessive alcohol should also be eliminated. Eating fruits and vegetables can help prevent cardiovascular diseases. Physical inactivity causes about 15% of diabetes and heart disease. The American Heart Association recommends 30-60 minutes of exercise 3-4 times per week 7.
Reduction of salt in food and drink
Reduction of salt intake is an important message for the population at risk of a stroke. Salt reduction leads to reduction in high blood pressure and risk of stroke (37, 59, 74).

(2): Doctors’ strategy for managing risk factors

Stroke study groups and development of local guidelines
We need to organize into stroke study groups and produce guidelines to assist physicians at different health care levels in stroke care. The purpose of stroke study groups is to increase the capacity for all hospitals to treat stroke patients according to standards of care, recognizing that levels of involvement will vary according to the resources of hospitals and systems (3). The major aim of clinical guidelines is to assist clinicians in producing local protocols for the prevention, diagnosis and management of stroke (3). This leads to improved management of risk factors and improved training of junior doctors. Further, guidelines assist in developing methods for implementation and audit of practice.

Physicians must identify patients at risk
The key must be to evaluate patients from the 4th decade for their stroke risk. This risk assessment include taking a good history of risk factors, a thorough clinical examination and simple tests such as measurement of BP, pulse (ECG if concerned), and cholesterol level, level of C-reactive protein (CRP) and calculate the body mass index. Currently, research suggests that CRP levels in apparently normal individuals may prove to be a better indicator of stroke and heart attack risk than the level of cholesterol 29. Body mass index should be between 18.5-24.9 in healthy individuals. An individual patients’ percentage risk of stroke can be calculated online via the website of the American Heart Association (http://www.americanheart.org/presenter.jhtml?identifier=3003500).
Identifying patients with hypertension and diabetes.
Age, gender and heredity are non-modifiable risks of stroke, and they should serve as risk markers to alert the clinician as to patients at risk (7). Undiagnosed hypertension and diabetes remain significant problems in many communities (66, 90). This is partly because of ignorance and lack of funds to afford the cost of medical screening. Hypertension is the single most important cause of stroke and the one, which is eminently reducible by treatment (90, 97). It has been estimated that between 52-70% of stroke patients have hypertension (35, 69, 68). Up to 60% of patients have undiagnosed high blood pressure (BP) prior to presentation (6, 90). Reduction in both systolic and diastolic pressures substantially reduces stroke risk (7, 14, 15, 37, 63, 74). The recent British Hypertension Society guidelines recommend a target blood pressure of 140/85 mmHg 75. Rodgers et al. deduced that each 5mmHg reduction in diastolic pressure reduced stroke risk by 34%, and each 10mmHg reduction of systolic pressure reduced stroke risk by 28%. It is the duty of every clinician or nurse to at least check the BP of all adults they are reviewing for any health problem (66).

Management of hypertension
Treating hypertension with drugs is the most cost-effective way to reduce this important risk factor for cardiovascular disease and stroke (87). Population attributable risks (or fractions) indicated that up to 22% of premature all-cause, and 45% of stroke mortality could be reduced by appropriate detection and treatment. It is, however, important to determine absolute risk, and thereby estimate indication for drug treatment, in order to maintain a cost-effective drug treatment. The elderly patient (most especially) should be treated starting in most cases with a simple Thiazide diuretic (87).
One crucial problem is the lack of control of BP for many patients despite medications. In Nigeria, unavailability of essential drugs, cost and sometimes fake medications are also huge problems that require concerted efforts from the government.

Diabetes is a modifiable risk factor for stroke
In view of the high prevalence of undiagnosed diabetes among stroke patients and the increased morbidity and mortality associated with diabetes mellitus, screening for diabetes is recommended especially in those with ischaemic stroke (58, 56). Diabetics should avoid refined simple sugars and excessive weight gain. Care of the feet and prompt treatment of infections should also be emphasised

Management of atrial fibrillation
The detection of atrial fibrillation and its proper treatment are essential in prevention of embolic strokes (40, 46, 71, 94). Patients suitable for anticoagulation should be treated (14, 15, 63). Cardiac medications for the control of abnormal rates may also be of value.

Treatment of hyperlipidaemia with statins is essential.
Risk factor management should be part of general health care and should begin in childhood, with emphasis on nutrition, exercise, weight control, and avoidance of tobacco. Health screening and early treatment of hypercholesterolemia has decreased the incidence of stroke and heart disease (44). Clinical trials in the 1990s using HMG-CoA reductase inhibitors (statins) showed that cholesterol-lowering treatment significantly reduces cardiovascular events including strokes in the primary and secondary prevention of myocardial infarction (MI) (9). After these observations, it is now generally accepted that lipid-lowering treatment should be considered in all stroke patients with a history of CHD/MI (9). The anti-inflammatory effect of statins and the stabilization of atherosclerotic plaque are additional benefits

Treatment of transient ischemic attacks
It is important to recognize and diagnose a patient with TIA. Confusion, blurring of vision, speech impairment, difficulty walking and weakness of an arm or a leg are possible pointers to impending major stroke. TIA could be caused by cardioemboli or from stenosis of the carotid arteries in the neck. In areas without access to Doppler Ultrasound, MR or CT, as applicable to most medical centers in Nigeria, some clinical parameters may indicate possible carotid stenosis. In one study, stepwise logistic regression showed that there were significant positive associations between severe carotid stenosis and an ipsilateral bruit, diabetes mellitus, and previous TIA 61. The strategy with the highest sensitivity (99%) was to use one or more of the four features, but specificity was only 22%.61. When access to carotid imaging is severely limited as the case in many areas in Nigeria, simple clinical features may be of some use, but access to carotid imaging should be improved.

Carotid endarterectomy is a safe preventive procedure
Severe narrowing (or stenosis) of the carotid artery in the neck is an important cause of ischemic stroke. Carotid endarterectomy (CEA) is the gold standard for the management of carotid artery disease (CAD) and the appropriateness of CEA for symptomatic and asymptomatic patients has emerged from 7 randomized trials (2, 23). Carotid endarterectomy is a safe and effective way of reducing the risk of stroke in patients with TIA (33). It is also helpful in patients with amaurosis fugax, and may benefit selected patients with acute stroke or those with asymptomatic but hemodynamically. significant stenosis (83).

(3): Treatment of first ever stroke needs to be expedient

Acute stroke treatment aims to preserve the ischaemic penumbra, protect neurons against further ischaemia and enhance brain plasticity to maximise recovery. There is a strong evidence base supporting the routine use of aspirin, but not heparin, in acute ischaemic stroke. There is also convincing evidence supporting intravenous thrombolysis using recombinant tissue plasminogen activator in selected patients within 3 hours of stroke onset.(4, 7, 8, 14, 30, 63, 71, 79, 84, 81). Although, its use in Nigeria is not feasible because of late presentation and lack of neuro-imaging facilities. Neuroprotective drugs have proved disappointing and active neuroprotection in acute stroke should include control of blood pressure within certain limits, antipyretic therapy, maintenance of blood glucose, early feeding and fluid replacement 33.

Admission to a dedicated ‘stroke unit’ is important
To enable patients to benefit from the early active approach outlined in the article, the following are needed: the development of acute stroke units; affordable imaging facilities; and education of patients, general practitioners and the ambulance services. There is good evidence that the best way to enhance recovery from stroke is to admit the patient to a stroke unit (33, 36, 38, 73). Treatment in a stroke unit raises the proportion of stroke patients who are able to live at home, improves functional outcome, reduces the need for institutional care, and brings down mortality 18, 36.
Clinical assessment should be thorough

A full medical assessment should be undertaken to define the nature of the stroke event. Is it a stroke or a TIA? Is it ischemic or haemorrhagic ? What part of the brain is affected ? What specific problems do the patients have ? What other medical problems coexist and need to be managed ? And finally, what facilities are available for the care of the patient. The use of the WHO criteria is thought to be better than the Siriraj stroke tool in clinical classification of stroke subtypes 65.
Cranial imaging is essential

Investigations that are important should be agreed locally. Many accept that a CT scan is mandatory within 48 hours of a stroke event. A cranial CT scan is important to accurately diagnose CI, ICH or SAH. The differentiation of an ICH from a SAH is not always possible on clinical grounds alone and indeed they often coexist on CT scan. Clinical evaluation without CT scan is practiced in many areas in Nigeria. This is due to shortage of imaging facilities and cost. However, increase in referral for CT scans may bring down the costs for each individual patient and may stimulate the establishment of more facilities in the private sector. The need for such critical investigations must be stressed to local community leaders, councilors and local business entrepreneurs.
Immediate management can save lives
There is not enough evidence reliably to evaluate the effect of altering BP on outcome after acute stroke. However, high BP should not normally be lowered in the acute phase as the stroke may worsen. Stroke-in-progression occurs in about 30% of patients with acute stroke and negatively affects the prognosis and mortality. The underlying causes are thought to be clot propagation, cerebral haemorrhage, oedema or decrease in BP.
Many advocate withholding antihypertensive therapy during the acute phase of focal cerebral ischaemia. The main idea is that, to assure sufficient collateral flow to the damaged part of the brain, a high perfusion pressure must be maintained. Routine use of drugs such as steroids, plasma volume expanders and streptokinase are of unproven benefit and should be discouraged.
Management of raised intracranial pressure
First, maintenance of respiration and an adequate airway are of prime concern. Adequate oxygenation of the brain will prevent or ameliorate secondary ischemic insults. Sedation with ventilation, if necessary, mannitol and diuretics are useful in controlling raised intracranial pressure (20). Surgical hemicraniectomy should be considered in patients with malignant cerebral oedema (19, 20, 33, 54). Hemicraniectomy appears most promising as a method of avoiding death from brain compression, but the optimum timing and manner of patient selection vital (54, 60). Urgent neurosurgical care must be made available to selected patients such as those with large cerebellar infarcts, severe brain oedema and patients with SAH or ICH. In this regard, there should be close communication and early discussions with the neurosurgeon in patients with depressed level of consciousness. There is an important role for the neurosurgeon in acute stroke management in patients with CI, SAH or ICH. However, in Nigeria, the role of neurosurgeons in the management of stroke is minimal. This is partly because majority of our patients with stroke have involvement of the deep penetrating end arteries consequent of lipohyalinosis and development of Charcot-Bouchard aneurysms in long standing hypertensive .

Managing dysphagia
Swallowing assessment should be undertaken as part of the initial evaluation of stroke patients. Dysphagia leads to aspiration pneumonia and complicates recovery. It is however unclear how dysphagic patients should be fed and treated after acute stroke. Further research is required to assess how and when patients are fed, and the effect of swallowing or drug therapy on dysphagia (26). Percutaneous Endoscopic Gastroscopic feeding may improve outcome and nutrition as compared with Naso Gastric Tube feeding (26).

Thrombolysis may be a problem in Nigeria
The use of thrombolytic therapy represents one of many recent developments in the management of acute ischemic stroke. The development of stroke teams and protocols has been driven by these new demands for an urgent response to ischemic stroke. The short time window of 3 hours for therapy with intravenous recombinant tissue plasminogen activator requires efficient evaluation and treatment of stroke patients and also necessitates a rigorous approach to blood pressure management, electrolytes, fluids, and temperature. At the present time, thrombolysis appears to be impractical in Nigeria because of time delay and scarcity of neuro-imaging facilities.
Patients on anticoagulant therapy demand urgent correction of the coagulation defects. Aspirin should be discontinued in patients with haemorrhagic stroke.

(4): Prevention of stroke recurrence is crucial

Transient ischemic attacks are associated with a 30 to 35 percent risk of stroke within five years of the initial episode. Every patient who has experienced a noncardioembolic stroke or TIA should be started on an antiplatelet agent. Aspirin is also the recognized treatment for acute ischaemic stroke (ICH having been excluded), and can be continued for secondary prevention (24, 33). It should be started as soon as possible and within 48 hours (40, 71, 46, 94). Aspirin dose as low as 25mg per day is effective in stroke prevention. The combination of Aspirin and extended release Dipyridamole 200mg is more effective than Aspirin alone.
Long-term oral anticoagulation should be prescribed for patients with atrial fibrillation who have suffered a recent stroke. Biological follow-up is based on control of the international normalized ratio (INR) 55. The target INR should be 2.5. Clinical and biological follow-up is necessary for patients on anticoagulants; minor bleeding complications may be the prelude to major haemorrhage 55. Control of hypertension, hyperlipidaemia and cessation of smoking are paramount and should be encouraged following the acute event.
Rehabilitation is a key step in management
This is of value in returning the patient to as close as possible to the pre-morbid level. It should be started early and be patient centred. Relatives need to be involved and taught to carry out certain procedures as necessary. We also need to assist in lifting the phobias and stigma surrounding the disabled stroke patient.

Overall, the management of stroke patients in Nigeria is sub-optimal. Stroke units are not yet developed. Neuro-imaging centers are very few and assess limited by cost and distance. Lack of facilities to monitor coagulation profiles limits the use of anti-coagulants in cardioembolic stroke in most centers in the rural areas. Most patients settle for intravenous infusion of hypertonic / isotonic infusion, medical decompression with steroid or mannitol, use of free radical scavengers, folate supplement, statins, anti-platelets and antihypertensives when indicated.
A significant proportion is seen by non-Neurologist and general practitioners who inadvertently bring down the blood pressure and compromise cerebral perfusion with its attendant poorer prognosis. There are very few neurologists, and fewer neurosurgeons, in Nigeria (membership register of the Nigerian Society of neurological Sciences) with a projected population ratio of 1:10 million population. Furthermore, multidisciplinary rehabilitation team management is difficult because of dearth of paramedical staff, physiotherapists, occupational therapists and stroke nurses.
What do our patients deserve?
Our patients deserve timely access to quality services appropriate to their needs. There are significant deficiencies in the provision of services such as diagnostic, treatment, rehabilitation and support services. Patients and their care givers want to be looked after by knowledgeable staffs that understand the full range of their needs. The diagnosis and treatment should be explained to patients and relatives by competent staff. There should be provision for regular communication and sharing of information should be encouraged between staff and patients and their relatives through constant health talks, radio jingles and use of flyers. Patients need to be closely involved in development of local services and lobbying of government officials for assistance.
No one person can claim to understand the full requirements of the patient and multidisciplinary care is of importance. Medical personnel should seek information and advice from colleagues and other staff without prejudice.


Knowledge of stroke and stroke risk factors is generally low in many communities (76). The level of awareness of the Nigerian public need to be evaluated and more tests applied for continuing learning. Enduring stroke registers need to be established in defined populations in the country. This will provide a firm basis for future statistical analysis and help to define the heterogeneity of stroke. The value of such a register has been highlighted previously (22, 48, 66, 86, 97). Critical information on all aspects of stroke care is also lacking and needs to be updated. Collaboration with experts from resource-rich nations with experts in Nigeria will be of tremendous benefit in generating much needed data on the extent of cardiovascular and cerebrovascular diseases in the country. This is particularly important when attempting to validate any developed guidelines (97).


The most important strategy for stroke treatment is modification of risk factors. Effective treatment of hypertension, control of blood sugar, treatment of hyperlipidaemia, and exercise are undoubtedly effective but underused (36).
The existing evidence strongly implies that good care of patients with stroke starts with organization of the entire stroke chain; from the prehospital scene, through the emergency room, to the stroke unit. Most patients need immediate evaluation and the seriousness of the condition recognized (3). Without structured stroke services no pharmacological or intervening therapy is likely to improve the outcome of the patient with a stroke (60).
Thrombolysis apart, our patients deserve better care from the moment they have their first TIA. Patients with mild stroke should be managed in a specialist stroke/TIA clinic. Those needing admission should be managed on an acute stroke unit for stabilization, CT scanning and other investigation, and diagnosis, and then referred, if possible, to a specialist stroke rehabilitation unit. Attention should be paid to risk factors to prevent recurrence. This is the ideal that requires modification for the situation in Nigeria.


  1. ABDUL-GHAFFAR NU, EL-SONBATY MR, EL-DIN ABDUL-BAKY MS, MARAFIE AA, AL-SAID AM. Stroke in Kuwait: a three-year prospective study. Neuroepidemiology 1997;16(1):40-7.
  2. ABURAHMA AF, HANNAY RS. A study of 510 carotid endarterectomies and a review of the recent carotid endarterectomy trials. West Virginia Medical Journal 2001;97(4):197-200.
  3. ADAMS R, ACKER J, ALBERTS M, ANDREWS L, ATKINSON R, FENELON K, et al. Recommendations for improving the quality of care through stroke centers and systems: an examination of stroke center identification options: multidisciplinary consensus recommendations from the Advisory Working Group on Stroke Center Identification Options of the American Stroke Association. [Review] [23 refs]. Stroke 2002;33(1):e1-7.
  4. ADAMS HPJ, BROTT TG, FURLAN AJ. A. Guidelines for Thrombolytic Therapy for Acute Stroke: a Supplement to the Guidelines for the Management of Patients with Acute Ischemic Stroke. A statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Stroke 1996;27:1711-1718.
  5. AIYESIMOJU AB, OSUNTOKUN BO, ADEUJA AO, OLUMIDE A, OGUNSEYINDE AO. Misdiagnosis of stroke. African Journal of Medicine & Medical Sciences 1983;12(2):107-12.
  6. AKINKUGBE OO. Epidemiology of hypertension and stroke in Africa. [Monograph Citation] 1976;29:28-42..
  7. ALBERS GW, HART RG, LUTSEP HLEA. AH. A Scientific Statement. Supplement to the guidelines for the management of transient ischemic attacks: A statement from the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks, Stroke Council, American Heart Association. Stroke 1999;30:2502-2511.
  8. ALBERTS MJ, GOLDSTEIN LB, SMITH T. Guidelines on the use of thrombolytic agents in stroke. Jama 1995;274:218.
  9. AMARENCO P. Hypercholesterolemia, lipid-lowering agents, and the risk for brain infarction. [Review] [108 refs]. Neurology 2001;57(5 Suppl 2):S35-44.
  10. ANDERSON CS, JAMROZIK KD, BURVILL PW, CHAKERA TM, JOHNSON GA, STEWART-WYNNE EG. Determining the incidence of different subtypes of stroke: results from the Perth Community Stroke Study, 1989-1990. Medical Journal of Australia 1993;158(2):85-9.
  11. Anonymous. Stroke care: reducing the burden of disease. London: The Stroke Association, 1998.
  12. Anonymous. Epidemiology of cerebrovascular disease in Korea–a Collaborative Study, 1989-1990. Korean Neurological Association. Journal of Korean Medical Science 1993;8(4):281-9.
  13. Anonymous. Recommendations of the Cerebrovascular Disease Study Group of the Sociedade Portuguesa de Neurologia. Acta Medica Portuguesa 1997;10(8-9):607-11.
  14. Anonymous. Guidelines for medical treatment for stroke prevention. American College of Physicians. Annals of Internal Medicine. 1994;121:54-55.
  15. Anonymous. Guidelines for the management of hypertension at primary health care level. Hypertension Society of Southern Africa, endorsed by the Medical Association of South Africa and the Medical Research Council. South African Medical Journal. 1995;85:1321-1325.
  16. APPELROS P, NYDEVIK I, SEIGER A, TERENT A. High incidence rates of stroke in Orebro, Sweden: Further support for regional incidence differences within Scandinavia. Cerebrovascular Diseases 2002;14(3-4):161-8.
  17. ASPLUND K. Update of Cochrane Database Syst Rev. 2000;(2):CD000103; PMID: 1079629 . Cochrane Database of Systematic Reviews 2002(4):CD000103.
  18. ATKINSON RP, DELEMOS C. Acute ischemic stroke management. Thrombosis Research 2000;98(3):97-111.
  19. AUER RN. Hemicraniectomy for ischemic stroke: temerity or death cure? [Canadian Journal of Neurological Sciences 2000;27(4):269.
  20. AYATA C, ROPPER AH. Ischaemic brain oedema. Journal of Clinical Neuroscience 2002;9(2):113-24.
  21. BAMFORD J, DENNIS M, SANDERCOCK P, BURN J, WARLOW C. The frequency, causes and timing of death within 30 days of a first stroke: the Oxfordshire Community Stroke Project. Journal of Neurology, Neurosurgery & Psychiatry 1990;53(10):824-9.
  22. BAMFORD J, SANDERCOCK P, DENNIS M, BURN J, WARLOW C. A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project–1981-86. 2. Incidence, case fatality rates and overall outcome at one year of cerebral infarction, primary intracerebral and subarachnoid haemorrhage. Journal of Neurology, Neurosurgery & Psychiatry 1990;53(1):16-22.
  23. BARNETT HJ, MELDRUM HE, ELIASZIW M. North American Symptomatic Carotid Endarterectomy Trial c. The appropriate use of carotid endarterectomy. [Review] [66 refs]. CMAJ (Canadian Medical Association Journal) 2002;166(9):1169-79.
  24. BATH PM. The medical management of stroke. International Journal of Clinical Practice 1997;51(8):504-10.
  25. BATH P, BUTTERWORTH RJ, SOO J, KERR JE. The King’s College Hospital Acute Stroke Unit. [see comments.]. Comment in: J R Coll Physicians Lond. 1996 May-Jun;30(3):269-70 ; 8811609. Journal of the Royal College of Physicians of London 1996;30(1):13-7.
  26. BATH PMW, BATH FJ, SMITHARD DG. Interventions for dysphagia in acute stroke. Cochrane Database of Systematic Reviews. Issue 2002;3.
  27. BELL BA, SYMON L. Smoking and subarachnoid haemorrhage. British Medical Journal 1979;1(6163):577-8.
  28. BILLER J, FEINBERG WM, CASTALDO JE. A. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1998;29:554-562.
  29. BLAKE GJ, RIDKER PM, KUNTZ KM. Projected life-expectancy gains with statin therapy for individuals with elevated C-reactive protein levels. Journal of the American College of Cardiology 2002;40(1):49-55.
  30. BROCKINGTON CD, LYDEN PD. Criteria for selection of older patients for thrombolytic therapy. Clinics in Geriatric Medicine 1999;15(4):721-39.
  31. BRODERICK J, BROTT T, TOMSICK T, LEACH A. Lobar Haemorrhage in the Elderly. The Undiminishing Importance of Hypertension. Stroke 1993;24:49-51.
  32. BRODERICK JP, ADAMS HP JR, BARSAN W. A Guidelines for the management of spontaneous intracerebral hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1999;30:905-915.
  33. BROWN MM. Brain attack: a new approach to stroke. [Review] [20 refs]. Clinical Medicine 2002;2(1):60-5.
  34. BUTCHER K, LAIDLAW J. Current intracerebral haemorrhage management. Journal of Clinical Neuroscience 2003;10(2):158-67.
  35. BWALA SA. Stroke in a subsaharan Nigerian hospital–a retrospective study. Tropical Doctor 1989;19(1):11-4.
  36. CAPLAN LR. Treatment of patients with stroke. Archives of Neurology 2002;59:703-707.
  37. CAPPUCCIO FP, PLANGE-RHULE J, PHILLIPS RO, EASTWOOD JB. Prevention of hypertension and stroke in Africa. Lancet 2000;356(9230):677-8.
  38. DESFONTAINES P, VANHOOREN G, PEETERS A, LALOUX P. Proposal of guidelines for stroke units. Acta Neurologica Belgica 2002;102:49-52.
  39. ELLAMUSHI HE, GRIEVE JP, JAGER HR, KITCHEN ND. Risk factors for the formation of multiple intracranial aneurysms. Journal of Neurosurgery 2001;94(5):728-32.
  40. FEINBERG WM, ALBERS GW, BARNETT HJ. A Guidelines for the management of transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks of the Stroke Council of the American Heart Association. Circulation. 1994;89:2950-2965.
  41. FINDLAY JM, TUCKER WS, FERGUSON G. A Guidelines for the use of carotid endarterectomy: current recommendations from the Canadian Neurosurgical Society. Canadian Medical Association Journal 1997;157:653-659.
  42. FOGELHOLM R, NUUTILA M, VUORELA AL. Primary intracerebral haemorrhage in the Jyvaskyla region, central Finland, 1985-89: incidence, case fatality rate, and functional outcome. Journal of Neurology, Neurosurgery & Psychiatry 1992;55(7):546-52.
  43. FOGELHOLM R, MURROS K. Cigarette smoking and subarachnoid haemorrhage: a population-based case-control study. Journal of Neurology, Neurosurgery & Psychiatry 1987;50(1):78-80.
  44. FUTRELL N, MILLIKAN CH. Stroke is an emergency. Disease-A-Month 1996;42(4):199-264.
  45. GAIST D, VAETH M, TSIROPOULOS I, CHRISTENSEN K, CORDER E, OLSEN J, et al. Risk of subarachnoid haemorrhage in first degree relatives of patients with subarachnoid haemorrhage: follow up study based on national registries in Denmark. [see comments.]. Comment in: BMJ. 2000 May 6;320(7244):1277 ; 10797055. British Medical Journal 2000;320(7228):141-5.
  46. GORDON MTS. Developing clinical guidelines for the management of patients with stroke. Scottish Intercollegiate Guidelines Network (SIGN). International Journal of Language & Communication Disorders. 1998;33(Suppl):S152-157.
  47. HABERMAN S, CAPILDEO R, ROSE FC. Sex differences in the incidence of cerebrovascular disease. Journal of Epidemiology & Community Health 1981;35(1):45-50.
  48. HATANO S. Experience from a multicentre stroke register: a preliminary report. Bulletin of the World Health Organization 1976;54(5):541-53
  49. HEMPHILL JC. New treatments for stroke. [Review] [22 refs]. Progress in Cardiovascular Nursing 1998;13(1):4-15.
  50. HERMAN B, LEYTEN AC, VAN LUIJK JH, FRENKEN CW, SCHULTE BP. Epidemiology of stroke in Tilburg, the Netherlands. The population-based stroke incidence register: 2. Incidence, initial clinical picture and medical care, and three-week case fatality. Stroke 1982;13(5):629-34.
  51. IKEH VO, NWOSU CM, NWABUEZE AC. The epidemiology of stroke in Nigerians: a study of 328 cases. Tropical Cardiology 1988;14:63.
  52. JAYA F, WIN MN, ABDULLAH MR, ABDULLAH JM. Stroke patterns in Northeast Malaysia: a hospital-based prospective study. Neuroepidemiology 2002;21(1):28-35.
  53. KOLOMINSKY-RABAS PL, SARTI C, HEUSCHMANN PU, GRAF C, SIEMONSEN S, NEUNDOERFER B, et al. A prospective community-based study of stroke in Germany–the Erlangen Stroke Project (ESPro): incidence and case fatality at 1, 3, and 12 months. Stroke 1998;29(12):2501-6.
  54. KRISTENSEN BO, LINDSTEN H, MALM J, SHAMSGOVARA P, RIDDERHEIM PA, A’ROCH R, et al. Hemicraniectomy in malignant mid-cerebral infarction. Further trials needed before its acceptance in clinical practice. Lakartidningen 1998;95(11):1145-8.
  55. LACROIX P, PORTEFAIX O, BOUCHER M, RAMIANDRISOA H, DUMAS M, RAVON R, et al. [The causes of intracranial hemorrhagic complications induced by antivitamins K]. [Review] [22 refs] [French]. Archives des Maladies du Coeur et des Vaisseaux 1994;87(12):1715-9.
  56. LAM KS, MA JT, WOO E, LAM C, YU YL. High prevalence of undiagnosed diabetes among Chinese patients with ischaemic stroke. Diabetes Research & Clinical Practice 1991;14(2):133-7.
  57. LANZINO G, KASSELL NL, GERMASSON TP, KONGABLE GL, TRUSKOWSKI LL, TORNER JC, et al. Age and outcome after aneurysmal subarachnoid haemorrhage: why do older patients fare worse? Journal of Neurosurgery 1996;85:410-418.
  58. LEFKOVITS J, DAVIS SM, ROSSITER SC, KILPATRICK CJ, HOPPER JL, GREEN R, et al. Acute stroke outcome: effects of stroke type and risk factors. Australian & New Zealand Journal of Medicine 1992;22(1):30-5.
  59. LINDLEY RI, WARLOW CP. Clinical trials in cerebrovascular disease. [Review] [33 refs]. Current Opinion in Neurology & Neurosurgery 1992;5(1):58-62.
  60. LINDSBERG PJ, ROINE RO, TATLISUMAK T, SAIRANEN T, KASTE M. The future of stroke treatment. Neurologic Clinics 2000;18(2):495-510.
  61. Mead GE, Wardlaw JM, Lewis SC, McDowall M, Dennis MS. Can simple clinical features be used to identify patients with severe carotid stenosis on Doppler ultrasound? [see comments.]. Comment in: J Neurol Neurosurg Psychiatry. 1999 Jan;66(1):4 ; 9886442. Journal of Neurology, Neurosurgery & Psychiatry 1999;66(1):16-9.
  62. MENDELOW AD. Spontaneous intracerebral haemorrhage [editorial] [see comments]. [Review] [52 refs] Comment in: J Neurol Neurosurg Psychiatry 1992 Jan;55(1):84. Journal of Neurology, Neurosurgery & Psychiatry 1991;54(3):193-5.
  63. National clinical guidelines for stroke: a concise update. Clinical Medicine 2002;2:231-233.
  64. OGUN SA, OLUWOLE O, OGUNSEYINDE AO, FATADE B, ODUSOTE KA. Misdiagnosis of stroke–a computerised tomography scan study. West African Journal of Medicine 2000;19(1):19-22.
  65. OGUN SA, OLUWOLE O, FATADE B, OGUNSEYINDE AO, OJINI FI, ODUSOTE KA. Comparison of the Siriraj stroke score and the WHO criteria in the classical classification of stroke subtypes. African Journal of Medicine and Medical Sciences 2002;31:13-16.
  66. OGUNGBO BI, GREGSON B, MENDELOW AD, WALKER R. Cerebrovascular diseases in Nigeria: what do we know and what do we need to know?. Tropical Doctor 2003;33(1):25-30.
  67. OGUNGBO B. Stoke website and the World stroke mailing list: Project report. Tropical Doctor 2003;33:122-124.
  68. OGUNNIYI A, TALABI O. Cerebrovascular complications of hypertension. Nigerian Journal of Medicine: Journal of the National Association of Resident Doctors of Nigeria 2001;10(4):158-61.
  69. OSUNTOKUN BO. Stroke in the Africans. African Journal of Medicine & Medical Sciences 1977;6(2):39-53.
  70. OSUNTOKUN BO, BADEMOSI O, AKINKUGBE OO, OYEDIRAN AB, CARLISLE R. Incidence of stroke in an African City: results from the Stroke Registry at Ibadan, Nigeria, 1973-1975. Stroke 1979;10(2):205-7.
  71. PEETERS A, CRAS P, BLECIC S. Proposal of guidelines for acute stroke treatment and management. Acta Neurologica Belgica. 2002;102:46-48.
  72. PENMAN AD. The epidemiology of stroke in Mississippi and the United States. Journal of the Mississippi State Medical Association 1999;40(8):270-2.
  73. PHILLIPS SJ, ESKES GA, GUBITZ GJ, Queen Elizabeth IIHSCAST. Description and evaluation of an acute stroke unit. CMAJ: Canadian Medical Association Journal 2002;167(6):655-60.
  74. PLANGE-RHULE J, PHILLIPS R, ACHEAMPONG JW, SAGGAR-MALIK AK, CAPPUCCIO FP, EASTWOOD JB. Hypertension and renal failure in Kumasi, Ghana. Journal of Human Hypertension 1999;13:37-40.
  75. RAMSAY L, WILLIAMS B, JOHNSTON G, MACGREGOR G, POSTON L, POTTER J, et al. Guidelines for management of hypertension: report of the third working party of the British Hypertension Society. Journal of Human Hypertension 1999;13(9):569-92.
  76. REEVES MJ, HOGAN JG, RAFFERTY AP. Knowledge of stroke rik factors and warning signs among Michigan adults. Neurology 2002;59:1547-1552.
  77. REITSMA JB, LIMBURG M, KLEIJNEN J, BONSEL GJ, TIJSSEN JG. Epidemiology of stroke in The Netherlands from 1972 to 1994: the end of the decline in stroke mortality. Neuroepidemiology 1998;17(3):121-31.
  78. SAEZ T, SUAREZ C, BLANCO F, GABRIEL R. Epidemiology of cardiovascular diseases in the Spanish elderly population. Revista Espanola de Cardiologia 1998;51(11):864-73.
  79. SAREEN D. Current concepts in the management of acute ischemic stroke. [Review] [47 refs]. Journal of the Association of Physicians of India 2002;50:407-14.
  80. SCHISANO G, FRANCO A. The treatment of intracerebral haemorrhage. Acta Neurologica 1979;1(1):23-32.
  81. SEGATORE M. Thrombolysis after stroke hope for the future. [Review] [69 refs]. Axone 1995;16(3):71-8.
  82. SHAH S, COOPER B. The epidemiology of stroke and transient ischaemia in Brisbane, Australia. Italian Journal of Neurological Sciences 1995;16(9):603-12.
  83. SHENG FC, BUSUTTIL RW. Carotid surgery in stroke prevention. [Review] [58 refs]. American Family Physician 1986;33(4):109-24.
  84. SLYTER H. Guidelines for the management of patients with acute ischemic stroke. Stroke 1995;26(137-138).
  85. Stroke TIWPf. National Clinical Guidelines for Stroke. London: Clinical Effectiveness & Evaluation Unit. Royal College of Physicians of London, 2000.
  86. SUDLOW CLM, WARLOW CP. Comparing stroke incidence worldwide: What makes studies comparable? Stroke 1996;27:550-558.
  87. SWALES JD. Current status of hypertensive disease treatment: results from the Evaluation and Interventions for Systolic Blood pressure Elevation: Regional and Global (EISBERG) project. [Review] [11 refs]. Journal of Hypertension – Supplement 1999;17(2):S15-9.
  88. TAYLOR TN. The medical economics of stroke. [Review] [13 refs]. Drugs 1997;3:51-7.
  89. VIRIYAVEJAKUL A, SENANARONG V, PRAYOONWIWAT N, PRADITSUWAN R, CHAISEVIKUL R, POUNGVARIN N. Epidemiology of stroke in the elderly in Thailand. Journal of the Medical Association of Thailand 1998;81(7):497-505.
  90. WALKER RW, MCLARTY DG, KITANGE HM, WHITING D, MASUKI G, MTASIWA DM, et al. Stroke mortality in urban and rural Tanzania. Adult Morbidity and Mortality Project. Lancet 2000;355(9216):1684-7.
  91. WALKER R, OGUNGBO B. The profile of stroke in Nigeria’s Federal Capital Territory, Imam and Olorunfemi. Tropical Doctor 2003;33:122-124.
  92. WARDLAW JM, WHITE PM. The detection and management of unruptured intracranial aneurysms. [Review] [102 refs]. Brain 2000;123(Pt 2):205-21.
  93. WARLOW CP. Epidemiology of stroke. [Review] [21 refs]. Lancet 1998;352 Suppl 3:SIII1-4.
  94. WHITE RH, MCBURNIE MA, MANOLIO T. Oral anticoagulation in patients with atrial fibrillation: adherence with guidelines in an elderly cohort. American Journal of Medicine. 1999;106:165-171.
  95. WOLF PA, KANNEL WB, DAWBER TR. Prospective investigations: the Framingham study and the epidemiology of stroke. Advances in Neurology 1978;19:107-20.
  96. WOLF PA, DAWBER TR, THOMAS HE, COLTON T, KANNEL WB. Epidemiology of stroke. Advances in Neurology 1977;16:5-19.
  97. YIKONA J. Prevention of hypertension and stroke in Africa. Lancet 2000;356(9230):678-9.

© 2002-2018 African Journal of Neurological Sciences.
All rights reserved. Terms of use.
Tous droits réservés. Termes d'Utilisation.
ISSN: 1992-2647