Anterior Cerebral Artery Territory Infarction Research Articles

Bilateral Anterior Cerebral Artery Territory Infarction Due to Subarachnoid Hemorrhage: Two Case Reports

Bilateral Anterior Cerebral Artery Territory Infarction Due to Subarachnoid Hemorrhage: Two Case Reports

Beyond Kluver–/INS;Bucy syndrome: Colorful clinical picture of bilateral anterior cerebral artery infarction

Introduction: Kluver–/INS;Bucy syndrome, which is mostly caused by bilateral anterior temporal lobe lesions, is characterized by typical triad of hypersexuality, hyperorality and hyperphagia. Bilateral anterior cerebral artery (ACA) territory infarction is very rare and it has been reported even more rarely to cause Kluver–/INS;Bucy syndrome.

Akinetic Mutism Case Following Stroke

Ischemic strokes less common in the area of the anterior cerebral artery infarcts and bilateral occurrence is extremely rare. 86-year-old female patient, admitted to our emergency department with complaints of sudden loss of strength in both arms and legs and inability to speak. Case diagnosed as akinetic mutism due to bilateral anterior cerebral artery territory infarction presented because it is rare.

Clinical symptoms of bilateral anterior cerebral artery territory infarction

Bilateral anterior cerebral artery (ACA) territory infarction is rare and its associated symptoms are still not well understood. We evaluated the clinical symptoms of four patients with bilateral ACA infarction. The common clinical features were various primitive reflexes and parkinsonian symptoms including akinesia, rigidity and hypophonia. Frontal release signs were present in all patients with ACA infarction even without direct involvement of the prefrontal cortex. Enhanced glabellar tap response, previously not reported in patients with ACA infarction, was the most consistent finding, and electrophysiological studies confirmed hyperexcitability of the late component of the blink reflex. The bilateral lesions in the deep white matter may be associated with the observed symptoms, reflecting functional disconnection of the medial prefrontal–subcortical circuitry.

Isolated Anterior Cerebral Artery Territory Infarction: Dissection as an Etiological Mechanism

Background: Intracranial arterial lesions are important causes of ischemic stroke, particularly in the Asian population. Of the intracranial lesions, the etiology of isolated anterior cerebral artery (ACA) territory infarction is not fully elucidated. The purpose of this study was to determine the etiological and clinical characteristics of patients with isolated ACA territory infarction, especially those with ACA dissection. Methods: Of 3,115 consecutive patients with acute ischemic stroke, 42 patients (1.3%, 30 men, 38–88 years old) having an isolated ACA territory infarction were studied. Infarcts were principally verified by diffusion-weighted MRI, and vascular lesions were identified by MRA, CTA, or digital subtraction angiography. Three-dimensional rotational angiography was performed if needed. Results: Eighteen patients (43%) were diagnosed as having ACA dissection. The stroke subtypes of the other 24 patients included cardioembolism for 6 patients and large-artery atherosclerosis for 8. Patients with dissection were younger (p < 0.001) and heavier (p = 0.026), less commonly had heart disease (p = 0.002) and previous stroke (p = 0.002), and had lower initial systolic blood pressure (p = 0.029) and lower levels of D-dimer (p = 0.041) than patients without dissection. Stroke onset more commonly followed physical exertion (p = 0.013) and headache (p = 0.041) in patients with dissection than in patients without dissection. At hospital discharge, the modified Rankin scale score was lower in patients with dissection than in patients without dissection (p = 0.005). Conclusions: Arterial dissection was the most common vascular lesion underlying an isolated ACA territory infarction in our Japanese cohort. Patients with ACA dissection had unique baseline characteristics and unique conditions at stroke onset.

DELAYED SYMPTOMATIC COIL MIGRATION AFTER INITIALLY SUCCESSFUL BALLOON-ASSISTED ANEURYSM COILING

To describe delayed migration of a coil loop after adjunctive balloon remodeling of an anterior communicating artery aneurysm. A 56-year-old man with a subarachnoid hemorrhage from a small anterior communicating artery aneurysm underwent successful coil embolization with adjunctive balloon remodeling. Eight days after the procedure, the patient returned with the acute onset of right lower extremity paralysis. Magnetic resonance imaging demonstrated an acute left anterior cerebral artery territory infarction. Angiography demonstrated that this infarct was secondary to the delayed migration of a coil loop out of the aneurysm and into the left A1 to A2 junction. Delayed migration of a coil loop after adjunctive balloon remodeling represents a rare but potentially severe complication of this technique.

Anterior cerebral artery infarction

Stroke mechanisms and clinical features of anterior cerebral artery (ACA) territory infarction have rarely been investigated using MRI. To verify stroke mechanisms and to make clinical imaging correlation. Clinical, MRI, and angiographic findings of 100 consecutive patients with ACA infarction were studied. Motor dysfunction (n = 91) was the most common symptom, and severe motor dysfunction was related to supplementary motor area/paracentral lobule involvement (p = 0.016). Hypobulia/apathy (n = 43) was related to involvement of frontal pole (p = 0.002), corpus callosum/cingulate gyrus (p = 0.003), and superior frontal gyrus (p < 0.001), and occurred more frequently in patients with bilateral lesions followed by left lesions. Urinary incontinence (n = 30) was not related to any specific lesion locations. Grasp reflex (n = 25) was related to corpus callosum involvement (p = 0.035). Angiographic (mostly MR angiography) results showed that 68 patients had local ACA atherosclerosis, most often at A2 segment. The stroke mechanisms included cardiogenic embolism in 10, internal carotid artery-ACA embolism in 6, and ACA atherosclerosis in 61 patients. In the latter group, detailed stroke mechanisms included local branch occlusion (n = 20), in situ thrombotic occlusion (n = 20), artery-to-artery embolism (n = 12), and a combination (n = 9). Patients with intrinsic ACA disease more often had hypobulia (p = 0.077) and corpus callosal involvement (p = 0.016) than those with embolism either from the internal carotid artery or the heart. Anterior cerebral artery (ACA) atherosclerosis is the most important stroke etiology in our population, causing infarction with various mechanisms. Topographic lesion patterns and consequent clinical features of ACA infarction are determined by diverse pathogenic mechanisms and the status of collateral circulation.

Acute bilateral anterior circulation stroke due to anomalous cerebral vasculature: a case report.

IntroductionSimultaneous bilateral cerebrovascular infarction is relatively rare and its initial presentation as a space-occupying lesion is extremely uncommon. However, bilateral infarction can result from unilateral occlusion of anomalous cerebral vasculature.Case presentationWe report the case of a man presenting with lower limb weakness and aphasia of acute onset with initial computerised tomography suggesting bifrontal neoplasm. However, further investigation confirmed bilateral anterior cerebral artery territory infarction with a hypoplastic left anterior cerebral artery with the right anterior cerebral artery supplying both frontal lobes (an anatomical variant). We present the clinical and diagnostic features of this presentation and attempt to ascertain, by reviewing existent medical literature, the frequency and patterns of structural variations in cerebral vasculature.ConclusionSimultaneous bilateral cerebral infarction can be the result of a unilateral cerebral artery occlusion and this can potentially mimic a space-occupying lesion. Anomalies of cerebral vasculature are not as rare as is usually believed and this should be borne in mind when investigating unusual presentations of cerebrovascular infarction.

Anterior Cerebral Artery Territory Infarction

In 100 Korean patients with anterior cerebral artery (ACA) territory infarction, these investigators analyzed the distribution of infarcts within the brain, underlying vascular lesions, stroke mechanisms, and clinical findings. Most patients (61%) had intrinsic atherosclerotic lesions within the ACA; 10% had cardiac-origin embolism to the ACA, and 13% had internal carotid artery stenotic or occlusive lesions. In 15% of patients …

Nicotine replacement therapy and ischaemic stroke

A52-year-old right-handed businessman developed sudden onset of non-fluent dysphasia, weakness and sensory disturbance on the right side of his body 3 weeks after starting Nicorette patches (21 mg). He continued to smoke 3–5 cigars a day while on these patches. The patient had a history of depression and excessive alcohol intake. Examination confirmed an expressive dysphasia with verbal fluency limited to five words beginning with ‘C’ or ‘S’ but with no problems in comprehension, naming or praxis. Rapid alternating movements were impaired on the right and reflexes were brisker on the right side, although both planters were flexor. Cardiovascular and general examination was unremarkable. Magnetic resonance imaging (MRI) brain scan confirmed a left anterior cerebral artery territory infarct. The following blood tests were normal or unhelpful: erythrocyte sedimentation rate (ESR), C-reactive protein, protein culture and sensitivity, antithrombin, antiphospholipid coagulant, treponemal serology, thyroid screen and autoantibody screen. The patient was found to have mildly raised triglyceride (2.42 mmol/l) and low density lipoprotein (LDL) cholesterol (4.61 mmo/l). Electrocardiogram (ECG), echocardiography and carotid Dopplers were all normal. Two previous cases of stroke following nicotine patches have been reported by Jackson (1993) and Pierce (1994). In addition, the Medicines and Healthcare products Regulatory Agency (MHRA) have received 12 further cases of cerebrovascular disorders following nicotine replacement (Table 1).

Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings.

To evaluate and review the clinical spectrum of anterior cerebral artery (ACA) territory infarction, we studied 48 consecutive patients who admitted to our stroke unit over a 6-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) in all patients, and diffusion magnetic resonance imaging (DWI) in 21. In our stroke registry, patients with ACA infarction represented 1.3% of 3705 patients with ischemic stroke. The main risk factors of ACA infarcts was hypertension in 58% of patients, diabetes mellitus in 29%, hypercholesterolemia in 25%, cigarette smoking in 19%, atrial fibrillation in 19%, and myocardial infarct in 6%. Presumed causes of ACA infarct were large-artery disease and cardioembolism in 13 patients each, small-artery disease (SAD) in the territory of Heubner's artery in two and atherosclerosis of large-arteries (<50% stenosis) in 16. On clinico-radiologic analysis there were three main clinical patterns depending on lesion side; left-side infarction (30 patients) consisting of mutism, transcortical motor aphasia, and hemiparesis with lower limb predominance; right side infarction (16 patients) accompanied by acute confusional state, motor hemineglect and hemiparesis; bilateral infarction (two patients) presented with akinetic mutism, severe sphincter dysfunction, and dependent functional outcome. Our findings suggest that clinical and etiologic spectrum of ACA infarction may present similar features as that of middle cerebral artery infarction, but frontal dysfunctions and callosal syndromes can help to make a clinical differential diagnosis. Moreover, at the early phase of stroke, DWI is useful imaging method to locate and delineate the boundary of lesion in the territory of ACA.

BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction

Introduction: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. Case report: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24 h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. Discussion: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction.

Angiographic evaluation of brain infarction limited to the anterior cerebral artery territory.

Brain infarction localized in the anterior cerebral artery territory is rather uncommon, and its etiology has not yet been fully elucidated. Based on computed tomographic findings, 17 patients with solitary anterior cerebral artery territory infarction were selected from among 3,619 patients admitted consecutively to our institute. Patients without angiographic examinations were excluded. The angiographic findings and clinical category of stroke were analyzed in each patient. Angiographic abnormalities were revealed in all patients. These consisted of occlusive changes (n = 10) or reversible segmental dilatation (n = 3) of the anterior cerebral artery, A1 hypoplasia (n = 5), and occlusive changes of the carotid artery (n = 3). In one patient with anterior cerebral artery occlusion, the occluded artery was reopened and subsequently became reoccluded. The clinical category of stroke was classified as atherothrombotic in 10 patients, cardioembolic in three, and undetermined in the remaining four. In eight of the 10 patients with atherothrombotic infarction, the anterior cerebral artery was narrowed or occluded. In all patients with cardioembolic infarction, the A1 segment contralateral to the infarction was hypoplastic. In our series, solitary anterior cerebral artery territory infarction was attributable most commonly to local atherothrombosis and occasionally to cardiogenic embolism. A hypoplastic A1 segment may facilitate the occurrence of embolism in the anterior cerebral artery. Reversible dilatatory and occlusive changes of this artery may be another important cause of infarction.

Reversible Segmental Dilatation of the Anterior Cerebral Artery

We report 3 patients with anterior cerebral artery (ACA) territory infarction, angiograms of whom demonstrated segmental dilatation of the homolateral A2 portion with no other abnormality at the acute phase. The dilatatory changes were found to have disappeared, when angiography was repeated 1–6 years after infarction. A reversible segmental dilatation of the ACA may be an important cause of ACA territory infarction.