Anterior Cerebral Artery Infarction Research Articles

Transtentorial Herniation After Unilateral Infarction of the Anterior Cerebral Artery

Fatal cerebral herniation is a common complication of large ("malignant") middle cerebral artery infarcts but has not been reported in unilateral anterior cerebral artery (ACA) infarction. We report a 47-year-old woman who developed an acute left hemiparesis during an attack of migraine. Cranial CT (CCT) was normal but demonstrated narrow external cerebrospinal fluid compartments. Transcranial Doppler sonography was compatible with occlusion of the right ACA. Systemic thrombolytic therapy with tissue plasminogen activator was initiated 105 minutes after symptom onset. Follow-up CCT 24 hours after treatment revealed subtotal ACA infarction with hemorrhagic conversion. Two days later, the patient suddenly deteriorated with clinical signs of cerebral herniation, as confirmed by CCT. An extended right hemicraniectomy was immediately performed. Within 6 months, the patient regained her ability to walk but remained moderately disabled. This is the first reported case of unilateral ACA infarct leading to almost fatal cerebral herniation. Narrow external cerebrospinal fluid compartments in combination with early reperfusion, hemorrhagic transformation, and additional dysfunction of the blood-brain barrier promoted by tissue plasminogen activator and migraine may have contributed to this unusual course.

Ischemic stroke and depression

P219 Objective: To investigate the frequency and clinical determinants of depression after ischemic stroke. Methods: We administered the Structured Interview Guide for the Hamilton Depression Rating Scale (SIGH-D) and neurological, neuropsychological, and functional assessments to 421 patients (age = 71.5 ± 8.0 years) three months after ischemic stroke and 249 stroke-free control subjects. We required a SIGH-D total score > 11 for the identification of clinically significant depression. Results: We identified clinically significant depression in 47 of the 421 patients (11.2%) and 13 of the 249 control subjects (5.2%), yielding an unadjusted odds ratio (OR) of 2.3 (95% confidence interval, 1.2 to 4.3) for depression associated with stroke. Logistic regression suggested that depression was independently associated with dementia (OR, 3.2), a major hemispheral stroke syndrome (OR, 1.7), infarcts in the anterior and posterior cerebral artery territories vs. infarcts in other vascular territories (OR, 1.6), and female sex (OR, 1.7). When present, depression tended to be mild and typically remitted in follow-up examinations. Somatic SIGH-D items but not depressed mood best distinguished stroke patients from control subjects and demented from nondemented stroke patients. Conclusions: Depression was less frequent, less severe, and less persistent in our stroke cohort than previously reported, possibly due to the underrepresentation of patients with a premorbid history of affective illness. It was associated with more severe stroke, particularly in vascular territories that supply limbic structures, and it was more frequent among patients with dementia and women. Somatic symptoms but not depressed mood best distinguished stroke patients from control subjects and demented from nondemented stroke patients, however, suggesting that stroke is more likely to be associated with a “pseudo-depression of dementia” than a “pseudo-dementia of depression.”

Early abnormalities related to postinfarction Wallerian degeneration: evaluation with MR diffusion-weighted imaging.

Wallerian degeneration (WD) is most commonly seen after cerebral infarctions and results in persistent neurological deficits. MRI may detect changes related to WD as early as 4 weeks after the insult. We sought to determine if MR diffusion-weighted imaging (DWI) detects changes of WD during the acute period that follows a cerebral infarction. Eleven patients with cerebral infarctions underwent DWI within 72 h of the onset of symptoms. DWI was performed using a high diffusion gradient strength (B = 1,000) in a single axis and trace imaging. We reviewed all images with special attention to the signal intensity in the location of the corticospinal tracts. Ten patients harbored 11 middle cerebral artery (MCA) infarcts, and one patient had an anterior cerebral artery (ACA) infarction. Only one patient with an MCA infarct showed a subtle abnormality in the ipsilateral corticospinal tract. The patient with the ACA infarct showed an abnormality in the region of the corticopontine tract. As used in this study, DWI depicted presumed early WD in only 20% of instances.

Clinical effects of anterior cerebral artery infarction

Anterior cerebral artery infarction is uncommon. We studied the topographical distribution of the lesions and the resulting clinical effects for a better understanding of their relationship and the functional outcome. There were 17 patients; the mean age of the cohort was 71 years. There were 10 men and 7 women. Two clinical syndromes were identified in accordance to the two anatomic areas of distribution. The paracentral lobule syndrome (group 1) was characterized by contralateral motor weakness, the leg more than the arm. The second group involved mainly the motor and supplementary motor areas. Beside contralateral weakness, they had a clinical picture of extrapyramidal symptomatology, which was designated as pseudoparkinsonian syndrome (group 2). Sixty percent of the patients in group 2 had bilateral occlusive carotid artery disease compared with 14% in the group 1, and it is likely that the mechanism was artery-to-artery embolism or cardioembolism in this group. In group 1, the lesions were smaller but superficial and it is possible that small emboli from the heart or parent large artery caused the obstruction. The location of the occlusion may be indicative of the stroke mechanism. The pseudoparkinsonian group with extrapyramidal features attributable to involvement of the supplementary motor area had an unfavorable outcome. There was poor correlation between size of the infarct and functional outcome (P=.12) in both groups.

Motor behavior in stroke patients with isolated medial frontal ischemic infarction.

Current interpretation of hemiparesis in anterior cerebral artery infarction holds that whereas leg weakness correlates with destruction of the corticospinal tract at the paracentral lobe, faciobrachial symptoms indicate extension of the infarct to the upper lateral convexity or to subcortical structures, where the corticospinal tract subserving the arm would be interrupted. We analyzed the motor behavior in eight patients with purely medial hemispheric infarctions who had face, arm, and leg involvement. In addition to careful clinical testing, we performed neuroimaging or pathological studies to exclude the involvement of the primary motor cortex or subcortical structures. Motor function was further tested in three patients by studying the reaction time to an auditory stimulus and by stimulating the motor cortex and the cervical and lumbar spine with a magnetic stimulator. All patients had signs of motor neglect, such as lack of spontaneous movement in the upper limb, unilateral reaction to pain stimuli, clumsy voluntary movements, or motor impairment on bimanual tasks. Electrophysiologically, we found absent or poor voluntary activity in both upper and lower limbs contralateral to the infarction. However, whereas cortical stimulation showed absent responses in the lower limb, it disclosed normal latencies in the upper limb, indicating that the corticospinal tract to paretic muscles of the upper limb was intact. Our findings suggest that faciobrachial symptoms in purely medial hemispheric infarctions in the anterior cerebral artery territory reflect motor neglect caused not by involvement of primary motor pathways but by damage to medial premotor areas.

Alien Hand Syndrome: Influence of Neglect on the Clinical Presentation of Frontal and Callosal Variants

Three patients with mesial frontal and extensive callosal lesions due to anterior cerebral artery infarction manifested an alien hand syndrome (AHS) with varied features. Patient 1 with left hemispheric lesion showed right hand's impulsive reaching and grasping and left hand's antagonistic movements to the right (intermanual conflict; IMC). Patients 2 and 3 with right hemispheric lesion manifested a left hemihypokinesia which was thought to have suppressed the frequency and amplitude or even the occurrence of left hand's reaching and grasping. IMC and other left hand's non-antagonistic, irrelevant movements to the right remained. Because the term “IMC” is often misused and not strictly defined, its association with right hand's reaching and grasping is quite uncommon, its significance as a sign of callosal disconnection is not well validated, and because left hand's reaching and grasping tend to be suppressed by motor neglect, a trend may then develop for the right hand to be the sole focus of pathological behaviour in patients with the so-called frontal AHS (Feinberg, Schindler, Flanagan et al., 1992)

Hyperkinetic motor behaviors contralateral to hemiplegia in acute stroke.

Motor behaviors on the 'good side' of the body, i.e. ipsilateral to the hemispheric lesion, have not been studied systematically. We assessed motor behaviors in 20 consecutive patients during the acute phase (first 1-2 weeks) of a hemispheric stroke with hemiparesis. The behaviors were essentially rotations of the head, neck, eyes and trunk, orofaciopharyngeal or limb stereotypes, compulsive manipulation of the surroundings, or passive mobilization of the paralyzed arm or leg. These behaviors were found only with large infarcts in the territory of the internal carotid artery, middle cerebral artery and/or the anterior cerebral artery (ACA). All but two ACA infarcts involved the internal capsule and basal ganglia. The severity of the motor deficit and the presence of aphasia, neglect, or sensory loss were significantly correlated with the motor behaviors. Although the understanding of these behaviors remains unclear, we suggest that they may represent the clinical expression of early plastic changes of brain maps and circuits after an acute lesion; this is probably an active process induced by disinhibition, in order to establish new compensatory pathways.

Left Unilateral Ideomotor Apraxia in Ischemic Stroke within the Territory of the Anterior Cerebral Artery

To clarify the regions most contributory to the manifestation of left unilateral ideomotor apraxia (LUIMA), clinical studies were performed in 12 consecutive patients with cerebral infarction confined to the unilateral anterior cerebral artery (ACA) territory. LUIMA was observed in 3 patients, all of whom had left ACA infarction involving the anterior four-fifths of the corpus callosum. LUIMA was absent in 5 other patients with left ACA infarction invading only the anterior half of the corpus callosum. The posterior trunk of the corpus callosum may thus be most crucial for the manifestation of LUIMA.

Bilateral anterior cerebral artery infarction resulting from explosion-type injury to the head and neck.

A 43-year-old woman suffered a blast-type injury to the head and neck. She subsequently developed bilateral internal carotid artery occlusion and bilateral anterior cerebral artery infarction not demonstrated by magnetic resonance imaging scan 24 hours after the explosion, but confirmed by a second scan 8 days after the explosion. In patients with blast-type injury to the head and neck who develop coma with a nonfocal neurological exam, the possibility of bilateral carotid artery occlusion and bilateral ischemic infarction should be considered.

Anterior Cerebral Artery Territory Infarction in the Lausanne Stroke Registry

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.

Ataxic Hemiparesis Associated with Transcortical Motor Aphasia

Two patients, ages 51 and 76 years, suddenly developed transcortical motor aphasia combined with pyramidal signs and ataxia of the right extremities that affected the leg more severely than the arm. Computed tomography revealed nonenhancing lucencies in the distribution territory of the left anterior cerebral artery involving the genu of the corpus callosum, white matter ventral to the left frontal horn, medial primary motor area, supplementary motor area, and superior part of the premotor area. It is postulated that aphasia, ataxia, and weakness resulted from involvement of the supplementary motor area and deep white matter, premotor, and primary motor areas, respectively. Anterior cerebral artery infarctions of the dominant hemisphere may result in transcortical motor aphasia associated with contralateral ataxic hemiparesis.

Radiology of anterior cerebral artery infarction

Twenty patients with anterior cerebral artery infarction are reviewed. Usual and unusual clinical presentation and radiographic findings (angiography and computed tomography) are correlated.