Current issues of ACP Journal Club are published in Annals of Internal Medicine


Clinical classification of cerebral infarction improved prediction of death, dependence, and recurrence

ACP J Club. 1991 Nov-Dec;115:89. doi:10.7326/ACPJC-1991-115-3-089

Source Citation

Bamford J, Sandercock P, Dennis M, Burn J, Warlow C. Classification and natural history of clinically identifiable subtypes of cerebral infarction. Lancet. 1991 Jun 22;337:1521-6.



To differentiate clinical subtypes of cerebral infarction and indicate the prognosis for each.


An inception cohort was classified according to type of cerebral infarction and followed for 1 year.


Community-based study in a population of about 105 000 during a 4-year period.


All 675 patients presenting with a clinically definite first stroke—rapidly developing clinical symptoms of focal or global loss of cerebral function that lasted > 24 hours or led to death—were investigated by a neurologist. 545 (81%) strokes were caused by cerebral infarction, confirmed by computed tomographic scan or autopsy in 439 (81%) and by the Guy's Hospital Stroke Diagnostic Scale score in the remaining 106 (19%). All patients were followed until death or for 1 year.

Assessment of prognostic factors

Infarctions were classified by patients' symptoms and signs during maximal deficit: lacunar infarcts (LACI)—pure motor or sensory stroke, sensorimotor stroke, or ataxic hemiparesis (n = 137, 25%); total anterior circulation infarcts (TACI)—a combination of new higher cerebral dysfunction (e.g., dysphasia), homonymous visual field defect, and ipsilateral motor or sensory deficit of at least 2 areas of face, arm, and leg (n = 92, 17%); partial anterior circulation infarcts (PACI)—only 2 of 3 components of TACI higher cerebral dysfunction alone or with motor/sensory deficit more restricted than for LACI (n = 185, 34%); posterior circulationinfarcts (POCI)—brain stem or cerebellar dysfunction (n = 129, 24%).

Main outcome measures

Death, dependence, recurrence of stroke.

Main results

Of 543 classifiable patients, the post-stroke case-fatality rate was 10% (n = 56) at 30 days, 18% (n = 99) at 6 months, and 23% (n = 124) at 1 year. At these times 39%, 29%, and 28% of patients were functionally dependent, respectively. 15 deaths were attributed to neurologic consequences of stroke; all occurred ≤ 7 days after the stroke, 9 among TACI patients and 6 among POCI patients. 65% of deaths ≤ 30 days after stroke were among TACI patients. 4% of TACI patients were functionally independent after 1 year, compared with 55% to 62% of patients in the other groups. 76 patients (14%) had a fatal or nonfatal recurrent stroke. The rates among the subgroups were POCI, 20% (26 of 129 patients), PACI, 17% (32 of 185 patients); LACI, 9% (12 of 137 patients); TACI, 6% (6 of 92 patients).


Classification of first cerebral infarcts into 4 subgroups allowed greater refinement in predicting death, dependence, and recurrence of stroke at 1 year.

Source of funding: Not stated.

Address for article reprint: Dr. J. Bamford, Department of Neurology, St. James's University Hospital, Beckett Street, Leeds LS9 7TF, England, UK.


Stroke is a heterogeneous disease that may be classified into definable subtypes based on pathophysiologic mechanism (1). Advances in imaging techniques and noninvasive cardiac diagnosis have led to classification of 5 basic subtypes: large artery atherothrombotic occlusive disease, cerebral embolism, small vessel arteriopathy (lacunae), infarction of undetermined cause, and nonatherosclerotic disorders. These classifications can lead to more effective therapeutic options, including carotid endarterectomy, anticoagulants for embolic stroke, aspirin for atherosclerotic disorders, and surgery for some nonatherosclerotic disorders. It is important for readers to bear in mind these mechanism-therapeutic connections (2) when interpreting the study by Bamford and colleagues.

Bamford's study set out to determine the value of a strictly clinical classification of stroke based on nature and extent of neurologic findings and the likely anatomic location of the cerebral infarction that caused them. Although the pathophysiologic classification leads to some treatment options, it can only be applied to those patients for whom the pathophysiology can be discerned. This approach can be applied to all patients and provides useful prognostic information, but does not allow delineation of the most appropriate therapy. Thus, the 2 approaches should be considered complementary. Further, new findings concerning the value of anticoagulation for atrial fibrillation (3) and endarterectomy for high-grade carotid stenosis (4) may mean better prognoses for some patients than were observed in Bamford's study.

Philip B. Gorelick, MD, MPH
Rush-Presbyterian-St.Luke's Medical CenterChicago, Illinois, USA


1. Caplan LR. Treatment of cerebral ischemia. Where are we headed? Stroke. 1984;15:571-4.

2. Caplan LR. TIAs: we need to return to the question, "What is wrong with Mr. Jones?" Neurology. 1988;38:791-3.

3. Stroke Prevention in Atrial Fibrillation Study Group Investigators. Preliminary report of the Stroke Prevention in Atrial Fibrillation Study. N Engl J Med. 1990;322:863-8.

4. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high grade stenosis. N Engl J Med.1991;325:445-53.