Anterior Cerebral Artery Territory Infarction in the Lausanne Stroke Registry Clinical and Etiologic Patterns Julien Bogousslavsky, MD, Franco Regli, MD
\s=b\ We studied 27 patients with acute stroke and a corresponding infarct in the anterior cerebral artery territory, as disclosed using computed tomography. Patients were selected from 1490 patients (1.8%) admitted consecutively to a community-based primary care center who underwent standard investigations. An embolic phenomenon from the internal carotid artery or from the heart explained the infarct in 17 patients (63%). Anterior cerebral artery occlusion without a potential source of embolism was found only in one Vietnamese patient. Neurologic features correlated well with the topography and size of infarct, including hemiparesis, hemihypesthesia, mutism at onset, transcortical motor aphasia, conflictual tasks impairment, mood disturbances,
and,
more
uncommonly, incontinence,
grasp reflex, hemineglect, acute confusional state, and unilateral left apraxia. These findings suggest that the etiologic spectrum of anterior cerebral artery infarcts is the same as that of middle cerebral artery infarcts. (Arch Neurol. 1990;47:144-150)
T^he topography and distribution of the anterior cerebral artery (ACA)
have been studied in detail,1 " but the etiologic and neurologic spectrum of ACA infarcts is not well known, prob¬ ably because of the rarity of these in¬ farcts in comparison with middle ce¬ rebral artery (MCA) infarcts. A series of computed tomographic (CT) scans of stroke patients suggests that ACA infarcts correspond to 0.6% to 3% of acute ischemie strokes.12·13 Using a standard protocol of investigations, we studied the potential causes of infarct Accepted for publication January 19, 1989. From the Service de Neurologie, Centre Hospi-
talier Universitaire Vaudois, Lausanne, Switzerland. Reprint requests to Service de Neurologie, CHUV, 1011 Lausanne, Switzerland (Dr Bogous-
slavsky).
and the clinical features of consecutive patients with acute stroke due to a CT-proved ACA infarct. PATIENTS AND METHODS
We studied 27 patients with a first stroke due to an ACA territory infarct as disclosed on CT scanning."1 Patients with infarcts as¬ sociated with an anterior communicating aneurysm and subarachnoid hemorrhage were excluded from the study. The patients studied were selected consecutively from 1490 patients admitted to our primary care center for a first stroke over 7 years who were coded into the prospective Lausanne (Switzerland) Stroke Registry. This regis¬ try has been presented in detail elsewhere15; all patients undergo a standard protocol of investigations, including CT scanning (one to five examinations), Doppler ultrasounds, electrocardiography, standard biologic tests, and, in selected cases, angiography (Seldinger technique) and further cardiac investigations (bidimensional echocardiography and 24-hour electrocardiographic monitoring). Presumed causes of infarct and risk factors have been diagnosed ac¬ cording to criteria defined previously." For
clinical-topographical
correlations,
we
have reconstructed the CT data in the sag¬ ittal plane using a method previously reported16"; this reconstruction allowed us to assess the involvement of the internal hemispheric cortex, including the supple¬ mentary motor area and underlying white matter. All patients were assessed neuro¬ logically by at least one staff neurologist. Neuropsychological examination included tests from a standard battery performed in our institution.18 RESULTS
Our study included 15
women, with
a mean
men and 12 age of 62 years.
All patients were right-handed. The topography of the infarct in the sagit¬ tal plane is schematized in Figs 1 through 3; 16 patients had a left-sided infarct, 9 had a right-sided infarct, and the infarct was bilateral in 2 patients (predominating on the left); 6 patients (1, 2, 17, 20, 26, and 27) had an exten¬ sive infarct; in 21 patients, the infarct
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partial, being anterior to the cen¬ tral sulcus in 13 patients (3-5,12-16,19, and 21-24), posterior to the central sulcus in 2 patients (9 and 10), and in¬ termediate in 6 patients (6-8, 11, 18, and 25); one patient (21) had an infarct limited to the deep territory of the ACA (Heubner's artery territory"19·20), but all the other patients had corticalsubcortical infarcts. was
Risk Factors and Heart Disease
Ten patients had hypertension, 8 had diabetes mellitus, and 9 were cig¬ arette smokers. Two patients had vas¬ cular claudication in the lower limbs. One patient had angina pectoris, and 1 patient had an acute myocardial in¬ farct 2 days before the stroke; in 4 other patients, ischemie changes were present on an electrocardiograph in the absence of cardiac symptoms. One patient had congestive heart failure. One patient had intermittent (parox¬ ysmal) atrial fibrillation, 2 patients had chronic atrial fibrillation (for 3 months in one patient and for 4 years in one patient), and atrial fibrillation was discovered on admission in a fourth patient. Two-dimensional echocardiography was done in 18 pa¬ tients and gave normal results or showed nonsignificant changes in 15 patients; significant changes included mitral valve prolapse in 2 patients with a typical click and a left ventric¬ ular thrombus in the patient with an acute myocardial infarct; no thrombus was seen in all 3 patients with atrial fibrillation who had undergone echo¬
cardiography.
Arterial Disease
Ultrasound scans of the carotid showed internal carotid artery (ICA) occlusion ipsilateral to the infarct in 4 patients (including 1 patient with ca¬ rotid dissection on angiography) and 50% or greater ICA stenosis in 6 pa-
Fig 1.—Case 16. Topography of left anterior cerebral artery infarcts. Sagittal reconstruction.
tients (50% stenosis in 1 patient, 75% stenosis in 4 patients, and 90% steno¬ sis in 1 patient). Nonstenosing plaques and less than 50% ICA stenosis were
present in 11 patients. Eight patients
showed less than 50% stenosis on the contralateral ICA. Angiography (Sel-
dinger technique) was performed on 12 patients, and showed an isolated oc¬ clusion of the ACA trunk (A2) in 1 Vietnamese patient (2) and ACA branch occlusions in 5 patients (4 pa¬ tients [10,13,18, and 23] had a cardiac or an arterial source of embolism, and 1 patient [12] had paraneoplastic Trousseau's syndrome with chronic disseminated intravascular coagula¬ tion). Angiography also provided an explanation why the infarct was bilat¬ eral in two instances. In the patient
with ICA dissection, there was an in¬ tracranial extension of the dissection up to the distal part of the carotid si¬ phon with embolie occlusion of the op¬ posite ACA, and both ACAs originated from a stenosed ICA in 1 patient.
Fig 2.—Case 16. Topography of right anterior cerebral artery infarcts. Sagittal reconstruction.
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the upper limb. One patient (11) with a cortical infarct had a syndrome of crural paresis with ipsilateral ataxia, which has previously been considered to be a lacunar syndrome.21 The tone in the paretic limbs became spastic within less than 10 days, and all pa¬ tients with leg weakness had a Babinski sign. Four patients (1,2,17, and 20) had hypertonia (Gegenhalten) in the contralateral nonparetic limbs, which correlated well with the size of the in¬ farct (Figs 1 through 3).
Sensory Dysfunction.—Hemihypeswas present in 14 patients, never without hemiparesis; in all of these patients, the sensory deficit pre¬ dominated in the lower limb, including 9 cases with faciobrachial sparing (Table 2). Tactile, pain, and position sense were usually involved together. Sensory dysfunction correlated with infarcts involving the postcentral cor¬ tex or underlying white matter (Figs 1 through 3). Gaze Disturbances.—No patient had gaze deviation, but the three patients with hemineglect had contralateral gaze preference. Incontinence.—Both patients with bilateral infarcts had persisting uri¬ nary incontinence, one also had fecal incontinence. Five (20%) of the 25 pa¬ thesia
Fig 3.—Case 16. Topography of bilateral anterior cerebral artery infarcts. Sagittal reconstruction. A indicates right; B, left.
Presumed Causes of the Infarct
Onset
The presumed causes of infarction detailed in Table 1. Carotid ath¬ erosclerosis seemed to be responsible in nine patients (all had a stenosis of 50% or greater or occlusion of the ICA, and half of the patients who had angiograms showed distal embolism). Cardioembolism was likely in seven patients (two patients had mitral valve prolapse and distal occlusions shown on angiograms, one patient had an acute myocardial infarct and left ventricular thrombus, and four pa¬ tients had atrial fibrillation, with dis¬ tal occlusions found in one of the two patients who had undergone angiogra¬ phy). Another cause was suspected in five patients (in situ occlusion of the ACA trunk in a Vietnamese patient without a carotid or cardiac source of embolism; paraneoplastic Trousseau's syndrome with chronic disseminated intravascular claudication due to an ovarian adenocarcinoma, in the ab¬ sence of endocarditis, in one patient; spontaneous ICA dissection in one pa¬ tient; acute alcohol intoxication in one patient; and lacunar infarction due to hypertension in an elderly woman with an isolated small, deep infarct in Heubner's artery territory). No obvi¬ ous cause was found in six patients who had no cardiac source of embo¬ lisms and no (plaque) changes or non¬ significant changes on the ipsilateral ICA; however, atherosclerosis was the most likely cause, as all six patients were older than 50 years, four had known risk factors, such as hyperten¬
previous transient ischemie at¬ (TIA) was reported by 4 patients (Table 2), with transient hemiparesis involving the leg (patients 8, 17, and 22) or speech disturbances with hemi¬ paresis (patient 13). The interval be¬
are
cigarette smoking, changes shown electrocardiogram.
sion, diabetes, and
one
on an
or
had ischemie
A tack
tween TIA and stroke
was 2 weeks to 6 months. Stroke was complete immedi¬ ately or within a few minutes in 20 pa¬ tients (74% ) and progressed smoothly in 7 patients, over a few hours to 3 weeks. Headaches at onset of the TIA were
reported by
5
patients, being
frontal in 4 patients (bilateral in 2 pa¬ tients) and occipital in 1 patient. Neurologic Disturbances Motor Weakness.—Neurologic dis¬ turbances were present in all but 1 pa¬ tient (14). In 18 patients, the hemipare¬ sis predominated in the lower limb, including pure monoparesis in 3 cases; 11 of these 18 patients had facial spar¬ ing. In 7 patients, the hemiparesis was faciobrachiocrural, with predomi¬ nance in the upper limb in 2 cases. In 1 patient, the hemiparesis was brachiofacial, with sparing of the lower limb. In these 8 patients, the faciobra¬ chiocrural or faciobrachial topogra¬ phy of motor weakness correlated with involvement of the anterior part of the ACA territory, usually with a deep ex¬ tension toward the internal capsule but without involvement of the precentral gyrus and underlying white matter.
Leg weakness, however, corre¬
lated with more posterior infarcts in¬ volving the precentrai gyrus (Pigs 1 through 3). The hemiparesis was usu¬ ally proximal and distal in the lower limb but predominated proximally in
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 05/31/2015
tients with a unilateral infarct had transient (
\s=b\ We studied 27 patients with acute stroke and a corresponding infarct in the anterior cerebral artery territory, as disclosed using computed tomography. Patients were selected from 1490 patients (1.8%) admitted consecutively to a community-based primary care center who underwent standard investigations. An embolic phenomenon from the internal carotid artery or from the heart explained the infarct in 17 patients (63%). Anterior cerebral artery occlusion without a potential source of embolism was found only in one Vietnamese patient. Neurologic features correlated well with the topography and size of infarct, including hemiparesis, hemihypesthesia, mutism at onset, transcortical motor aphasia, conflictual tasks impairment, mood disturbances,
and,
more
uncommonly, incontinence,
grasp reflex, hemineglect, acute confusional state, and unilateral left apraxia. These findings suggest that the etiologic spectrum of anterior cerebral artery infarcts is the same as that of middle cerebral artery infarcts. (Arch Neurol. 1990;47:144-150)
T^he topography and distribution of the anterior cerebral artery (ACA)
have been studied in detail,1 " but the etiologic and neurologic spectrum of ACA infarcts is not well known, prob¬ ably because of the rarity of these in¬ farcts in comparison with middle ce¬ rebral artery (MCA) infarcts. A series of computed tomographic (CT) scans of stroke patients suggests that ACA infarcts correspond to 0.6% to 3% of acute ischemie strokes.12·13 Using a standard protocol of investigations, we studied the potential causes of infarct Accepted for publication January 19, 1989. From the Service de Neurologie, Centre Hospi-
talier Universitaire Vaudois, Lausanne, Switzerland. Reprint requests to Service de Neurologie, CHUV, 1011 Lausanne, Switzerland (Dr Bogous-
slavsky).
and the clinical features of consecutive patients with acute stroke due to a CT-proved ACA infarct. PATIENTS AND METHODS
We studied 27 patients with a first stroke due to an ACA territory infarct as disclosed on CT scanning."1 Patients with infarcts as¬ sociated with an anterior communicating aneurysm and subarachnoid hemorrhage were excluded from the study. The patients studied were selected consecutively from 1490 patients admitted to our primary care center for a first stroke over 7 years who were coded into the prospective Lausanne (Switzerland) Stroke Registry. This regis¬ try has been presented in detail elsewhere15; all patients undergo a standard protocol of investigations, including CT scanning (one to five examinations), Doppler ultrasounds, electrocardiography, standard biologic tests, and, in selected cases, angiography (Seldinger technique) and further cardiac investigations (bidimensional echocardiography and 24-hour electrocardiographic monitoring). Presumed causes of infarct and risk factors have been diagnosed ac¬ cording to criteria defined previously." For
clinical-topographical
correlations,
we
have reconstructed the CT data in the sag¬ ittal plane using a method previously reported16"; this reconstruction allowed us to assess the involvement of the internal hemispheric cortex, including the supple¬ mentary motor area and underlying white matter. All patients were assessed neuro¬ logically by at least one staff neurologist. Neuropsychological examination included tests from a standard battery performed in our institution.18 RESULTS
Our study included 15
women, with
a mean
men and 12 age of 62 years.
All patients were right-handed. The topography of the infarct in the sagit¬ tal plane is schematized in Figs 1 through 3; 16 patients had a left-sided infarct, 9 had a right-sided infarct, and the infarct was bilateral in 2 patients (predominating on the left); 6 patients (1, 2, 17, 20, 26, and 27) had an exten¬ sive infarct; in 21 patients, the infarct
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 05/31/2015
partial, being anterior to the cen¬ tral sulcus in 13 patients (3-5,12-16,19, and 21-24), posterior to the central sulcus in 2 patients (9 and 10), and in¬ termediate in 6 patients (6-8, 11, 18, and 25); one patient (21) had an infarct limited to the deep territory of the ACA (Heubner's artery territory"19·20), but all the other patients had corticalsubcortical infarcts. was
Risk Factors and Heart Disease
Ten patients had hypertension, 8 had diabetes mellitus, and 9 were cig¬ arette smokers. Two patients had vas¬ cular claudication in the lower limbs. One patient had angina pectoris, and 1 patient had an acute myocardial in¬ farct 2 days before the stroke; in 4 other patients, ischemie changes were present on an electrocardiograph in the absence of cardiac symptoms. One patient had congestive heart failure. One patient had intermittent (parox¬ ysmal) atrial fibrillation, 2 patients had chronic atrial fibrillation (for 3 months in one patient and for 4 years in one patient), and atrial fibrillation was discovered on admission in a fourth patient. Two-dimensional echocardiography was done in 18 pa¬ tients and gave normal results or showed nonsignificant changes in 15 patients; significant changes included mitral valve prolapse in 2 patients with a typical click and a left ventric¬ ular thrombus in the patient with an acute myocardial infarct; no thrombus was seen in all 3 patients with atrial fibrillation who had undergone echo¬
cardiography.
Arterial Disease
Ultrasound scans of the carotid showed internal carotid artery (ICA) occlusion ipsilateral to the infarct in 4 patients (including 1 patient with ca¬ rotid dissection on angiography) and 50% or greater ICA stenosis in 6 pa-
Fig 1.—Case 16. Topography of left anterior cerebral artery infarcts. Sagittal reconstruction.
tients (50% stenosis in 1 patient, 75% stenosis in 4 patients, and 90% steno¬ sis in 1 patient). Nonstenosing plaques and less than 50% ICA stenosis were
present in 11 patients. Eight patients
showed less than 50% stenosis on the contralateral ICA. Angiography (Sel-
dinger technique) was performed on 12 patients, and showed an isolated oc¬ clusion of the ACA trunk (A2) in 1 Vietnamese patient (2) and ACA branch occlusions in 5 patients (4 pa¬ tients [10,13,18, and 23] had a cardiac or an arterial source of embolism, and 1 patient [12] had paraneoplastic Trousseau's syndrome with chronic disseminated intravascular coagula¬ tion). Angiography also provided an explanation why the infarct was bilat¬ eral in two instances. In the patient
with ICA dissection, there was an in¬ tracranial extension of the dissection up to the distal part of the carotid si¬ phon with embolie occlusion of the op¬ posite ACA, and both ACAs originated from a stenosed ICA in 1 patient.
Fig 2.—Case 16. Topography of right anterior cerebral artery infarcts. Sagittal reconstruction.
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 05/31/2015
the upper limb. One patient (11) with a cortical infarct had a syndrome of crural paresis with ipsilateral ataxia, which has previously been considered to be a lacunar syndrome.21 The tone in the paretic limbs became spastic within less than 10 days, and all pa¬ tients with leg weakness had a Babinski sign. Four patients (1,2,17, and 20) had hypertonia (Gegenhalten) in the contralateral nonparetic limbs, which correlated well with the size of the in¬ farct (Figs 1 through 3).
Sensory Dysfunction.—Hemihypeswas present in 14 patients, never without hemiparesis; in all of these patients, the sensory deficit pre¬ dominated in the lower limb, including 9 cases with faciobrachial sparing (Table 2). Tactile, pain, and position sense were usually involved together. Sensory dysfunction correlated with infarcts involving the postcentral cor¬ tex or underlying white matter (Figs 1 through 3). Gaze Disturbances.—No patient had gaze deviation, but the three patients with hemineglect had contralateral gaze preference. Incontinence.—Both patients with bilateral infarcts had persisting uri¬ nary incontinence, one also had fecal incontinence. Five (20%) of the 25 pa¬ thesia
Fig 3.—Case 16. Topography of bilateral anterior cerebral artery infarcts. Sagittal reconstruction. A indicates right; B, left.
Presumed Causes of the Infarct
Onset
The presumed causes of infarction detailed in Table 1. Carotid ath¬ erosclerosis seemed to be responsible in nine patients (all had a stenosis of 50% or greater or occlusion of the ICA, and half of the patients who had angiograms showed distal embolism). Cardioembolism was likely in seven patients (two patients had mitral valve prolapse and distal occlusions shown on angiograms, one patient had an acute myocardial infarct and left ventricular thrombus, and four pa¬ tients had atrial fibrillation, with dis¬ tal occlusions found in one of the two patients who had undergone angiogra¬ phy). Another cause was suspected in five patients (in situ occlusion of the ACA trunk in a Vietnamese patient without a carotid or cardiac source of embolism; paraneoplastic Trousseau's syndrome with chronic disseminated intravascular claudication due to an ovarian adenocarcinoma, in the ab¬ sence of endocarditis, in one patient; spontaneous ICA dissection in one pa¬ tient; acute alcohol intoxication in one patient; and lacunar infarction due to hypertension in an elderly woman with an isolated small, deep infarct in Heubner's artery territory). No obvi¬ ous cause was found in six patients who had no cardiac source of embo¬ lisms and no (plaque) changes or non¬ significant changes on the ipsilateral ICA; however, atherosclerosis was the most likely cause, as all six patients were older than 50 years, four had known risk factors, such as hyperten¬
previous transient ischemie at¬ (TIA) was reported by 4 patients (Table 2), with transient hemiparesis involving the leg (patients 8, 17, and 22) or speech disturbances with hemi¬ paresis (patient 13). The interval be¬
are
cigarette smoking, changes shown electrocardiogram.
sion, diabetes, and
one
on an
or
had ischemie
A tack
tween TIA and stroke
was 2 weeks to 6 months. Stroke was complete immedi¬ ately or within a few minutes in 20 pa¬ tients (74% ) and progressed smoothly in 7 patients, over a few hours to 3 weeks. Headaches at onset of the TIA were
reported by
5
patients, being
frontal in 4 patients (bilateral in 2 pa¬ tients) and occipital in 1 patient. Neurologic Disturbances Motor Weakness.—Neurologic dis¬ turbances were present in all but 1 pa¬ tient (14). In 18 patients, the hemipare¬ sis predominated in the lower limb, including pure monoparesis in 3 cases; 11 of these 18 patients had facial spar¬ ing. In 7 patients, the hemiparesis was faciobrachiocrural, with predomi¬ nance in the upper limb in 2 cases. In 1 patient, the hemiparesis was brachiofacial, with sparing of the lower limb. In these 8 patients, the faciobra¬ chiocrural or faciobrachial topogra¬ phy of motor weakness correlated with involvement of the anterior part of the ACA territory, usually with a deep ex¬ tension toward the internal capsule but without involvement of the precentral gyrus and underlying white matter.
Leg weakness, however, corre¬
lated with more posterior infarcts in¬ volving the precentrai gyrus (Pigs 1 through 3). The hemiparesis was usu¬ ally proximal and distal in the lower limb but predominated proximally in
Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 05/31/2015
tients with a unilateral infarct had transient (
