Anterior Cerebral Artery Infarction Research Articles

Bilateral Anterior Cerebral Artery Infarction Leading to Paraplegia and Abulia

Bilateral Anterior Cerebral Artery Infarction Leading to Paraplegia and Abulia

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.

Anterior Cerebral Infarction by Fronto-Basal Meningioma

The association between stroke and meningioma is rarely reported in the data. In most etiology classification, there is no compressive cause. The association between meningioma and stroke is increasingly reported. We report a case of 52-year-old woman, previously healthy, presented with sudden right hemiplegia with some transient mood disorders. The CT-scan revealed acute left anterior cerebral artery infarction associated with fronto-basale meningioma infiltrating both anterior cerebral arteries. She was treated by corticosteroid and rehabilitation, with partial recovery. No stroke prevention was used before surgical treatment.

Acute Loss of Bladder Control in a Stroke of the Frontal Cortex

Lesions of the medial frontal micturition center can result in the activation of the pontine and spinal micturition centers when the bladder is full, causing urinary incontinence. Recognition of acute bladder incontinence as part of a cortical hemispheric stroke syndrome may reduce the likelihood of false localization to the spinal cord in patients with acute ischemic stroke eligible for acute reperfusion therapy. We describe a case of urinary incontinence due to anterior cerebral artery infarction and discuss the cortical localization of voluntary bladder control to the anterior cingulate gyrus, inferior frontal gyrus, middle frontal gyrus, and superior frontal gyrus.

Prevalence, timing, risk factors, and mechanisms of anterior cerebral artery infarctions following subarachnoid hemorrhage

Anterior cerebral artery (ACA) ischemia may be underdiagnosed following subarachnoid hemorrhage (SAH). The purpose of this study is to characterize the prevalence, timing, and risk factors for ACA infarction, following primary spontaneous SAH. This was a retrospective study of consecutive SAH patients. Final admission CT scans were reviewed for the presence of ACA infarction, and prior scans serially reviewed to determine timing of infarct. Infarctions were categorized as any, early (days 0-3), late (days 4-15), or perioperative (2 days after aneurysm treatment). Demographic and clinical variables were statistically interrogated to identify predictors of infarct types. Of the 474 study patients, ACA infarctions occurred in 8 % of patients, with 42 % occurring during the early period. Multivariate logistic regression identified H/H grade 4/5 (p < 0.001), ACA/ACom aneurysm location (p < 0.001), and surgical clipping (p = 0.011) as independent predictors of any ACA infarct. In Cox hazards analysis, H/H grade 4/5 (p < 0.001), CT score 3/4 (p = 0.042), ACA/ACom aneurysm location (p < 0.001), and surgical clipping (p = 0.012) independently predicted any ACA infarct. Bivariate logistic regression identified non-Caucasian race (p = 0.032), H/H grade 3/4 (p < 0.001), CT score 3/4 (p = 0.006), IVH (p = 0.027), and ACA/ACom aneurysm (p = 0.001) as predictors of early infarct (EI). Late infarct (LI) was predicted by H/H grade 4/5 (p = 0.040), ACA/ACom aneurysm (p < 0.001), and vasospasm (p = 0.027), while postoperative infarct (PI) was predicted by surgical clipping (p = 0.044). Log-rank analyses confirmed non-Caucasian race (p = 0.024), H/H grade 3/4 (p < 0.001), CT score 3/4 (p = 0.003), IVH (p = 0.010), and ACA/ACom aneurysm (p < 0.001) as predictors of EI. LI was predicted by ACA/ACom aneurysm (p < 0.001) while surgical clipping (p = 0.046) again predicted PI. Clinical severity/grade and ACA/ACom aneurysm location are the most consistent predictors of ACA infarctions. Vasospastic and non-vasospastic processes may concurrently contribute to ACA infarcts.

Facial Numbness: An Early Clinical Sign in Cerebral Mucormycosis (P01.254)

Objective: To describe a case of isolated facial numbness as the first symptom of cerebral mucormycosis. Background Rhino-orbital-cerebral mucormycosis is a relatively rare entity. It is classically seen in diabetics with ketoacidosis, as the fungi have a reductase that allows growth in high glucose and acidic conditions. The syndrome typically has a prodrome consisting of purulent nasal discharge, perinasal or periorbital cellulitis, and vision changes. A rare and late complication of the disease is invasion of the intracranial vessels (typically by local invasion of the cavernous sinus), which can lead to cerebral infarcts. The disease has a very high mortality and early recognition is imperative to prevent serious complications and death. Design/Methods: Case report. Results: The patient was a 64 year old male with uncontrolled diabetes and HIV who was admitted to a community hospital with complaints of severe lethargy and unilateral facial numbness. He was treated for diabetic ketoacidosis and urinary tract infection. Several days later he developed hemiparesis and was found to have acute anterior cerebral artery infarct. Following clinical deterioration and transfer to a tertiary stroke center, he was found to have multiple additional vascular territory infarcts. Post-mortem studies revealed extensive mucormycosis involving intracranial vessels. Conclusions: Unless recognized and treated early, cerebral mucormycosis is invariably fatal. The early clues to diagnosis in this case were presence of diabetic ketoacidosis, facial numbness, and sinusitis present on imaging. In this setting, ENT consultation for exploration of sinuses should be considered. Disclosure: Dr. Miller has nothing to disclose. Dr. Kittner has nothing to disclose.

Erectile Dysfunction (ED) after Ischemic Stroke - Association between Prevalence and Localization of Lesion (P07.025)

Objective: To assess ED prevalence before and after ischemic stroke and associate ED with stroke location. Background Stroke may cause or worsen erectile dysfunction (ED). ED prevalence and association with the location of stroke lesions is not well established. Design/Methods: In 56 men, aged 64.39±10.64 years, who had ischemic stroke within 24 months before evaluation, we determined ED prevalence before and after stroke using the five item International Index of Erectile Function (IIEF-5) ranging from 1 (poorest score) to 25 (optimal score). We compared pre- and post-stroke IIEF-5-scores (Wilcoxon test; significance assumed for p Results: 46/56 (82.14%) patients reported ED after stroke vs. 27/56 (48.21%) patients before stroke. IIEF-5-values decreased from 22.5 (median; inter-quartile range (IQR) 19-24) before stroke to 14.5 (median; IQR 4-20) after stroke (p=0.0001). 32/56 (57.14%) patients had middle cerebral artery (MCA) stroke, 5/56 (8.93%) had posterior cerebral artery (PCA) stroke, 1/56 (1.79%) had anterior cerebral artery (ACA) stroke, 7/56 (12.5%) had brainstem infarction and 4/56 (7.14%) had ischemic lesions in more than 1 territory. ED was associated with MCA-infarction in 26/32 (81.25%) patients, PCA-infarction in 4/5 (80%) patients, ACA-infarction in 1/1 (100%) patient, brainstem-infarction in 7/7 (100%) patients, lesions in more than 1 region in 3/4 (75%) patients. Conclusions: Already before stroke, our patients had a high ED prevalence suggesting possible associations between ED and stroke risk factors. Stroke increases ED prevalence and severity as shown by deteriorating IIEF-5-values. MCA stroke was most common (32/56 patients) and thus most frequently associated with ED (26/32 patients). However, the relative risk of developing ED after stroke seems highest after brainstem infarction (7/7 patients), while the number of ACA infarctions was too low to determine the risk of ED development. Disclosure: Dr. Hilz has received personal compensation for activities with Genzyme Corporation and International Brain Research Foundation, Inc. as a speaker and/or consultant.Dr. Hilz has received research support from Genzyme Corporation and International Brain Research Foundation, Inc. Dr. Schramm has nothing to disclose. Dr. Cordel has nothing to disclose. Dr. Staykov has nothing to disclose. Dr. Pauli has nothing to disclose. Dr. Kolominsky-Rabas has nothing to disclose. Dr. Schwab has nothing to disclose. Dr. Wagner has nothing to disclose.

Alien Hand Syndrome in Stroke - Case Report &amp; Neurophysiologic Study -

Alien Hand Syndrome is defined as unwilled, uncontrollable, but seemingly purposeful movements of an upper limb. Two major criteria for the diagnosis are complaint of a foreign limb and complex, autonomous, involuntary motor activity that is not part of an identifiable movement disorder. After a cerebrovascular accident in the corpus callosum, the parietal, or frontal regions, various abnormal involuntary motor behaviors may follow. Although different subtypes of Alien Hand Syndrome have been distinguished, this classification clearly does not cover the wide clinical variety of abnormal motor behaviors of the upper extremity. And there are few known studies about the neurophysiology of this syndrome using transcranial magnetic stimulation (TMS). We recently experienced 2 rare cases of Alien Hand Syndrome which occurred after anterior cerebral artery (ACA) infarction. A 72 year-old male with right hemiplegia following a left ACA infarct had difficulty with voluntarily releasing an object from his grasp. A 47 year-old female with left hemiplegia following a right ACA infarct had a problem termed 'intermanual conflict' in which the two hands appear to be directed at opposing purposes. Both of them had neurophysiologic studies done, and showed reduced amplitude by single pulse MEP and a lack of intracortical inhibition (ICI) by paired pulse TMS. No abnormalities were found in SSEP.

A Case Of Utilization Behavior and Hyperorality Following Bilateral Anterior Cerebral Artery Infarct Partially Responsive to Carbamazepine: Can Both Behaviors Be Attributed To Lesions In Different Frontal Lobe Circuits?

Lhermitte (1983) coined the term “utilization behavior” (UB) to define a neurobehavioral syndrome in which the visuo-tactile presentation of objects compels patients to grasp and use them, despite the fact that they have not been instructed to do so. The author suggested that UB was the consequence of frontal lobe damage. There are various interpretations as to the pathophysiology that brings about UB. Authors have described UB as an executive function deficit, intimating impairment in dorsolateral frontal-subcortical circuits. Yet, others have proposed disconnection between frontal and parietal lobe circuits or intra-frontal lobe pathology. Hyperorality and “bulimic type eating” (BTE) are symptoms of Kluver-Bucy Syndrome (KBS). While typically occurring after bilateral amygdala lesions/removal, others have suggested that symptoms of KBS may develop due to selective neurotoxicity in the basolateral amygdala and its cortical connections. Furthermore, the circuit between amygdala and cortex are reciprocal. Thus, disruption of a frontal-amygdalar circuit, with the latter projecting to the hypothalamus, may result in the production of Kluver-Bucy symptoms. We present a case of a woman with a bifrontal craniotomy and subsequent anterior cerebral artery cerebrovascular accident who developed manifestations of UB and Kluver-Bucy symptoms of hyperorality and BTE. We treated this patient with carbamazepine (CBZ), with the latter symptoms significantly improving, but the former essentially unchanged. We suggest that it is possible that this result may have occurred because while UB may not improve with CBZ, both bulimic type eating and symptoms of KBS have been reported to respond to treatment with CBZ.

Infarctions in the vascular territory of the posterior cerebral artery: clinical features in 232 patients

BackgroundIschemic stroke caused by infarction in the territory of the posterior cerebral artery (PCA) has not been studied as extensively as infarctions in other vascular territories. This single centre, retrospective clinical study was conducted a) to describe salient characteristics of stroke patients with PCA infarction, b) to compare data of these patients with those with ischaemic stroke due to middle cerebral artery (MCA) and anterior cerebral artery (ACA) infarctions, and c) to identify predictors of PCA stroke.FindingsA total of 232 patients with PCA stroke were included in the "Sagrat Cor Hospital of Barcelona Stroke Registry" during a period of 19 years (1986-2004). Data from stroke patients are entered in the stroke registry following a standardized protocol with 161 items regarding demographics, risk factors, clinical features, laboratory and neuroimaging data, complications and outcome. The characteristics of these 232 patients with PCA stroke were compared with those of the 1355 patients with MCA infarctions and 51 patients with ACA infarctions included in the registry.Infarctions of the PCA accounted for 6.8% of all cases of stroke (n = 3808) and 9.6% of cerebral infarctions (n = 2704). Lacunar infarction was the most frequent stroke subtype (34.5%) followed by atherothrombotic infarction (29.3%) and cardioembolic infarction (21.6%). In-hospital mortality was 3.9% (n = 9). Forty-five patients (19.4%) were symptom-free at hospital discharge. Hemianopia (odds ratio [OR] = 6.43), lacunar stroke subtype (OR = 2.18), symptom-free at discharge (OR = 1.92), limb weakness (OR = 0.10), speech disorders (OR = 0.33) and cardioembolism (OR = 0.65) were independent variables of PCA stroke in comparison with MCA infarction, whereas sensory deficit (OR = 2.36), limb weakness (OR = 0.11) and cardioembolism as stroke mechanism (OR = 0.43) were independent variables associated with PCA stroke in comparison with ACA infarction.ConclusionsLacunar stroke is the main subtype of infarction occurring in the PCA territory. Several clinical features are more frequent in stroke patients with PCA infarction than in patients with ischaemic stroke due to infarction in the MCA and ACA territories. In-hospital mortality in patients with PCA territory is low.

Improving safety for the neurologic patient: Evaluating medications, literacy, and abuse

# {#article-title-2} To the Editor: I read with interest the recent article on improving safety for the neurologic patient.1 The article highlighted issues of medications, literacy, and abuse. Another aspect of patient safety for the neurologist is preventing patients from undergoing unnecessary procedures. A 79-year-old woman with a history of coronary artery disease had a carotid ultrasound in a cardiology office. She had moderate carotid stenosis and was advised to have an angiogram, which showed 40% stenosis bilaterally. Four hours after this procedure, she developed sudden onset of right-sided hemiparesis and aphasia. The patient was treated with thrombolysis but still suffered a large anterior cerebral artery infarct. She required intensive care for …

Spontaneous intra-cranial arterial dissection frequently causes anterior cerebral artery infarction

Background and purpose Spontaneous intra-cranial arterial dissection (SICAD) without history of head and neck injury is now recognized as an important cause of stroke. However, the frequency of SICAD involving the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA) territories remains unclear. This study therefore investigated the distribution of SICAD. Methods Subjects comprised 194 patients (126 men, 68 women; median age, 68.0 years) with infarct isolated to the ACA, MCA or PCA territories who underwent conventional angiography. Diagnosis of SICAD was based on clinical and neuroradiological findings. Frequency of SICAD was compared among ACA, MCA, and PCA infarcts. All patients were divided into SICAD and non-SICAD groups, and clinical characteristics were compared between groups. Results Infarcts involved the ACA in 14 cases (7.2%), MCA in 165 cases (85.1%), and PCA in 15 cases (7.7%). SICAD was diagnosed in 17 of 194 cases (8.8%), with cerebral angiography showing main findings of the string sign in 11 patients (64.7%), the pearl and string sign in 6 patients (35.3%), and pseudoaneurysm formation in 2 patients (11.7%). SICAD most frequently involved the ACA (ACA, 64.3%; MCA, 4.2%; PCA, 6.7%; P < 0.001). Conclusion SICAD was seen in 64.3% of patients with ACA infarct. The mechanisms of ACA infarction may thus differ from those of MCA and PCA infarction.

Crossed Transcortical Motor Aphasia, Left Spatial Neglect, and Limb and Magnetic Apraxia Due to Right Anterior Cerebral Artery Infarction

Crossed aphasia refers to language disturbance due to right-hemisphere lesions in right-handed individuals, while magnetic apraxia is described as 'forced grasping and groping' caused by lesions in the contralateral frontal lobe. This is a case report of a 70-year-old right handed woman who suffered from crossed transcortical motor aphasia and left hand magnetic apraxia due to right anterior cerebral artery infarction. The definite mechanism of this disorder is not yet understood, but neurophysiological observations suggest that affected supplementary motor areas may be responsible for this phenomenon.

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.

Dopamine Deficiency May Lead to Capgras Syndrome in Parkinson's Disease With Dementia

Back to table of contents Previous article Next article LETTERFull AccessDopamine Deficiency May Lead to Capgras Syndrome in Parkinson’s Disease With DementiaHiromi Shiotsuki M.D.Yumiko Motoi M.D., Ph.D.,Shin-Ichiro Nakamura M.D., Ph.D.,Yoshikuni Mizuno M.D., Ph.D.Nobutaka Hattori M.D., Ph.D.,Hiromi Shiotsuki M.D.Search for more papers by this authorYumiko Motoi M.D., Ph.D.Search for more papers by this author,Shin-Ichiro Nakamura M.D., Ph.D.Search for more papers by this author,Yoshikuni Mizuno M.D., Ph.D.Search for more papers by this authorNobutaka Hattori M.D., Ph.D.Search for more papers by this author,Published Online:1 Jul 2010https://doi.org/10.1176/jnp.2010.22.3.352.e14AboutSectionsView articlePDFView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View articleTo the Editor: Capgras syndrome has been described in neurodegenerative diseases such as dementia with Lewy bodies as well as in psychiatric diseases. 1 Thus far, the atypical antipsychotics and decreased dosage of l -dopa have been utilized to treat Capgras syndrome in patients with Parkinson’s disease, and the outcomes have not been satisfactory. 2 , 3 Here we report a patient with Parkinson’s disease who showed Capgras delusions only during the “off” state. Increased doses of l -dopa resolved wearing-off and at the same time alleviated Capgras syndrome. Case Report Our patient was a 64-year-old housewife. At the age of 58, she developed a tremor in her left upper extremity that responded to a combination of l -dopa/carbidopa, 300 mg/day. At the age of 61, she showed difficulty in walking. Dopamine agonists pramipexole and pergolide relieved her symptoms. At the age of 63, she developed apathy, recent memory disturbance, and wearing off phenomenon. At the age of 64, she developed Capgras syndrome, and then she was admitted to our hospital. She showed an hour off state before each time she took l -dopa/carbidopa three times per day. In the off state, she was severely disabled (Hoehn and Yahr stage IV) and expressed anxiety such as restlessness, tension and hypersweating. She also developed the firm belief that an imposter replaced her husband. When the doctor asked her “Is this man your husband?” she answered “No, he is not my husband. He looks like my husband. My husband is walking outside. This man is posing as my husband and trying to steal my money.” In the “on” state, she was able to walk (Hoehn and Yahr stage III). Her conviction disappeared. She scored 20/30 on the Mini-Mental State Examination and 11/18 on the Frontal Assessment Battery. Verbal fluency was disturbed. Parkinsonism was typical for Parkinson’s disease such as asymmetric, predominantly resting tremor; limb rigidity; bradykinesia; and postural instability. She did not show frontal release signs, and other neurological examinations produced normal findings. A brain MRI revealed slight frontotemporal cortical atrophy, and SPECT imaging showed hypoperfusion in the posterior cingulated cortex, precuneus, and prefrontal cortex. Treatment with 5 mg donepezil did not improve her Capgras syndrome. Two weeks later, an increase in the l -dopa/carbidopa dosage to 500 mg/day was prescribed, and the wearing off phenomenon resolved. At the same time, the patient’s Capgras syndrome completely disappeared. Comment In our patient, symptoms of Capgras syndrome developed while she showed motor symptoms associated with dopamine deficiency. We increased the dosage of l -dopa and succeeded in alleviating the Capgras syndrome. Thus, we postulate that Capgras syndrome in our patient is not likely dopaminergic psychosis. It has been reported that loss of dopamine and subsequent dopamine replacement therapy lead to imbalances in many nondopaminergic transmitter systems. 4 Furthermore, Spiegel et al. 5 reported successful treatment with an antidepressant, a serotonin 2A receptor antagonist, to treat Capgras syndrome after a right anterior cerebral artery infarction. Taken together, the mechanism underlying Capgras syndrome might be associated with the balance of various neurotransmitter systems. Department of Neurology, Juntendo University School of Medicine, Tokyo, JapanDepartment of Neurology, Juntendo Tokyo Koto Geriatric Medical CenterDepartment of Neurology, Juntendo University School of Medicine

Dopamine Deficiency May Lead to Capgras Syndrome in Parkinson’s Disease With Dementia

Back to table of contents Previous article Next article LETTERFull AccessDopamine Deficiency May Lead to Capgras Syndrome in Parkinson’s Disease With DementiaHiromi Shiotsuki M.D.Yumiko Motoi M.D., Ph.D.,Shin-Ichiro Nakamura M.D., Ph.D.,Yoshikuni Mizuno M.D., Ph.D.Nobutaka Hattori M.D., Ph.D.,Hiromi Shiotsuki M.D.Search for more papers by this authorYumiko Motoi M.D., Ph.D.Search for more papers by this author,Shin-Ichiro Nakamura M.D., Ph.D.Search for more papers by this author,Yoshikuni Mizuno M.D., Ph.D.Search for more papers by this authorNobutaka Hattori M.D., Ph.D.Search for more papers by this author,Published Online:1 Jul 2010https://doi.org/10.1176/jnp.2010.22.3.352.e14AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Capgras syndrome has been described in neurodegenerative diseases such as dementia with Lewy bodies as well as in psychiatric diseases. 1 Thus far, the atypical antipsychotics and decreased dosage of l -dopa have been utilized to treat Capgras syndrome in patients with Parkinson’s disease, and the outcomes have not been satisfactory. 2 , 3 Here we report a patient with Parkinson’s disease who showed Capgras delusions only during the “off” state. Increased doses of l -dopa resolved wearing-off and at the same time alleviated Capgras syndrome. Case Report Our patient was a 64-year-old housewife. At the age of 58, she developed a tremor in her left upper extremity that responded to a combination of l -dopa/carbidopa, 300 mg/day. At the age of 61, she showed difficulty in walking. Dopamine agonists pramipexole and pergolide relieved her symptoms. At the age of 63, she developed apathy, recent memory disturbance, and wearing off phenomenon. At the age of 64, she developed Capgras syndrome, and then she was admitted to our hospital. She showed an hour off state before each time she took l -dopa/carbidopa three times per day. In the off state, she was severely disabled (Hoehn and Yahr stage IV) and expressed anxiety such as restlessness, tension and hypersweating. She also developed the firm belief that an imposter replaced her husband. When the doctor asked her “Is this man your husband?” she answered “No, he is not my husband. He looks like my husband. My husband is walking outside. This man is posing as my husband and trying to steal my money.” In the “on” state, she was able to walk (Hoehn and Yahr stage III). Her conviction disappeared. She scored 20/30 on the Mini-Mental State Examination and 11/18 on the Frontal Assessment Battery. Verbal fluency was disturbed. Parkinsonism was typical for Parkinson’s disease such as asymmetric, predominantly resting tremor; limb rigidity; bradykinesia; and postural instability. She did not show frontal release signs, and other neurological examinations produced normal findings. A brain MRI revealed slight frontotemporal cortical atrophy, and SPECT imaging showed hypoperfusion in the posterior cingulated cortex, precuneus, and prefrontal cortex. Treatment with 5 mg donepezil did not improve her Capgras syndrome. Two weeks later, an increase in the l -dopa/carbidopa dosage to 500 mg/day was prescribed, and the wearing off phenomenon resolved. At the same time, the patient’s Capgras syndrome completely disappeared. Comment In our patient, symptoms of Capgras syndrome developed while she showed motor symptoms associated with dopamine deficiency. We increased the dosage of l -dopa and succeeded in alleviating the Capgras syndrome. Thus, we postulate that Capgras syndrome in our patient is not likely dopaminergic psychosis. It has been reported that loss of dopamine and subsequent dopamine replacement therapy lead to imbalances in many nondopaminergic transmitter systems. 4 Furthermore, Spiegel et al. 5 reported successful treatment with an antidepressant, a serotonin 2A receptor antagonist, to treat Capgras syndrome after a right anterior cerebral artery infarction. Taken together, the mechanism underlying Capgras syndrome might be associated with the balance of various neurotransmitter systems. Department of Neurology, Juntendo University School of Medicine, Tokyo, JapanDepartment of Neurology, Juntendo Tokyo Koto Geriatric Medical CenterDepartment of Neurology, Juntendo University School of Medicine

E-029 Symptomatic cerebral vasospasm after trans-sphenoidal resection of pituitary macroadenomas

IntroductionDelayed ischemic events are recognized complications following aneurysmal subarachnoid hemorrhage (SAH). Delayed cerebral vasospasm may also occur following traumatic SAH or craniotomy for skull base tumors. The occurrence of a...

Deviation of the subjective visual vertical (SVV) in anterior cerebral artery infarction

Healthy humans can determine what is „upright“ within a mean error of less than±2.5 degrees of the earth vertical1. Errors in verticality perception, reflected in a deviation of subjective visual vertical (SVV), frequently occur in labyrinthine and peripheral vestibular nerve lesions2, as well as in brainstem and thalamic lesions involving central vestibular pathways1–4. So far, SVV deviation in supratentorial cortical lesions has only been reported in patients with middle cerebral artery infarctions affecting vestibular cortical areas5,6. Here, we present two cases of SVV deviation in anterior cerebral artery (ACA) infarction.

Fatal Bilateral ACA Territory Infarcts after Pituitary Apoplexy: A Case Report and Literature Review

Apoplexy of pituitary tumors is a common occurrence. In addition to commonly known presentations, cerebral infarcts and consequent focal neurologic deficits are a rare presentation. A rare case of pituitary apoplexy with associated subarachnoid bleed and bilateral anterior cerebral artery infarcts is described. Vasospasm leading to cerebral infarcts and consequent focal neurologic deficits as a presentation of pituitary apoplexy needs to be better appreciated.

Embolus Trajectory Through a Physical Replica of the Major Cerebral Arteries

The observed distribution of cerebral infarcts varies markedly from expectations based on blood-flow volume or Doppler embolus detection. In this study, we used an in vitro model of the cerebral arteries to test whether embolus microspheres encountering the circle of Willis are carried proportionally to volume flow or express a preferred trajectory related to arterial morphology or embolus size. Our model consisted of a patient-specific silicone replica of the cerebral macrocirculation featuring physiologically realistic pulsatile flow of a blood-mimicking fluid at approximately 1000 mL/min and an input pressure of approximately 150/70 mm Hg. Particles of 200, 500, and 1000 microm diameter with equivalent density to thrombus were introduced to the carotid arteries and counted on exiting the model outlets. The middle cerebral arteries (MCAs) of the replica attracted a disproportionate number of emboli compared with the anterior cerebral arteries; 98%+/-3% of 1000 microm and 93%+/-2% of 500 microm emboli entered the MCA compared with 82%+/-5% of the flow. The observed distribution of large emboli was consistent with the ratio of MCA:anterior cerebral artery infarcts, approximately 95% of which occur in territories supplied by the MCA. With decreasing embolus size, the distribution of emboli approaches that of the flow (approximately 89% of 200 microm emboli took the MCA). Embolus trajectory through the cerebral arteries is dependent on embolus size and strongly favors the MCA for large emboli. The 70:30 ratio of MCA:anterior cerebral artery emboli observed by Doppler ultrasound is consistent with the trajectories of small emboli that tend to be asymptomatic.