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At least 19 recordsLinked to original sources
PubMed2004

Spectrum of superficial posterior cerebral artery territory infarcts.

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.

Adult↗
PubMed2003

Agitated delirium with posterior cerebral artery infarction.

Infarction of the posterior cerebral artery may present only with signs of agitated delirium and an acute confusional state. In the absence of other prominent neurological deficits, this can be easily mistaken for toxic-metabolic encephalopathy, head trauma, post-ictal confusion, or a psychiatric disorder. Appropriate head imaging studies are important to detect an illness that might otherwise be missed and left untreated.

Cerebral Infarction↗
PubMed2005

Posterior cerebral artery infarction from middle cerebral artery infarction.

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.

Aged↗
PubMed1988

Confusional states following posterior cerebral artery infarction.

Four patients with left-sided posterior cerebral artery infarction developed acute confusional states. Fifteen additional patients with confusion following unilateral posterior cerebral artery infarction were identified from a review of the literature; in 14 the lesion was left sided. Destruction or disconnection of dominant hemisphere neocortex from limbic structures, resulting in impairment of focal attention, loss of linguistically organized memory, and/or disruption of temporal sequencing may be responsible for this syndrome.

Acute Disease↗
PubMed2003

Zonal frequency analysis of infarct extent. Part II: anterior and posterior cerebral artery infarctions.

The object of the study was to test the hypotheses that analysis of the anatomic zones affected by single anterior (A), posterior (P), and middle (M) cerebral artery (CA) infarcts, and by dual- and triple-vessel infarcts, will disclose (i) sites most frequently involved by each infarct type (peak sites), (ii) sites most frequently injured by multiple different infarct types (vulnerable zones), and (iii) anatomically overlapping sites in which the relative infarct frequency becomes equal for two or more different infarct types and/or in which infarct frequency shifts greatly between single and multivessel infarcts (potential border zones). Precise definitions of each vascular territory were adopted. CT and MRI studies from 20 ACA, 20 PCA, three dual ACA-PCA, and four triple ACA-PCA-MCA infarcts were mapped onto a standard template (Part I). Relative infarct frequencies in each zone were analyzed within and across infarct types to identify the centers and peripheries of each infarct type, the zones most frequently affected by multiple different infarct types, the zones where relative infarct frequency was equal for different infarcts, and the zones where infarct frequency shifted markedly from single- to multiple-vessel infarcts. Zonal frequency analysis provided quantitative data on the relative infarct frequency in each anatomic zone for each infarct type. It displayed zones of peak infarct frequency for each infarct, zones more vulnerable to diverse types of infarct, peripheral "overlap" zones of equal infarct frequency, and zones where infarct frequency shifted markedly between single- and multiple-vessel infarcts. It is concluded that the hypotheses are correct.

Adolescent↗
PubMed2006

Deafferentation-disconnection neglect induced by posterior cerebral artery infarction.

OBJECTIVE: To investigate patients with posterior cerebral artery (PCA) infarctions to learn whether hemispatial neglect is more frequent and severe after right than left PCA infarction; whether visual field defects (VFDs) influence the presence or severity of hemispatial neglect; and the anatomic loci of lesions that are associated with hemispatial neglect. METHODS: The authors recruited 45 patients with PCA infarction that involved only the occipital lobe or the occipital lobe plus other areas served by the PCA. All subjects received seven neglect tests within 2 months after onset. RESULTS: Overall, the frequency of hemispatial neglect was 42.2%. The frequency did not significantly differ between the right (48.0%) and left (35.0%) PCA groups, but the severity of hemispatial neglect was significantly greater in the right group. VFD alone did not influence the frequency or severity of neglect after controlling other variables. Isolated occipital lesions were rarely associated with hemispatial neglect, and it was only the occipital plus splenial lesion that significantly influenced the frequency and severity of neglect. CONCLUSIONS: This study suggests that after excluding such confounding factors as aphasia or hemiplegia, neglect frequency does not differ between the right and left posterior cerebral artery (PCA) groups, but the severity of neglect is greater after right PCA infarctions; even in the acute stage of PCA infarction; visual field defect from an isolated occipital lesion does not cause hemispatial neglect; and the injury to both the occipital lobe and the splenium of the corpus callosum is important for producing hemispatial neglect with PCA infarction.

Adult↗
PubMed1991

[Clinical features and imaging findings of posterior cerebral artery infarction].

The clinical features and imaging findings of posterior cerebral artery infarction (PCAI) in 18 cases verified by CT scan and/or MRI, DSA, SPECT were reported, and their interrelation were analyzed. It was found that the main clinical feature of PCAI was visual defect with amnesia syndrome, the lesion was predominant in the right hemisphere. In examining the structure and function of brain and vessels, each of CT, MRI, ECT and DSA had its own advantage and might complement the others, CT and MRI were better in displaying the structure of cerebral parenchyma than ECT and DSA, whereas, MRI was superior in distinguishing the lesions in deep white matter and subtentorial region. DSA was better than MRI and CT in displaying vascular structure, but was inferior in disclosing the occlusion of deep perforating branches or cortical arterioles. ECT, besides its ability to show the morphological changes of brain, was mainly used to disclose the functional changes of cerebral parenchyma, being a method to make early diagnosis for CVD. However, ECT was inferior than MRI and CT, in displaying lacunar infarction and lesions of brain-stem.

Adult↗
PubMed1987

The pattern of neuropsychological impairment associated with left posterior cerebral artery infarcts.

We investigated the neuropsychological correlates of left posterior cerebral artery (LPCA) infarcts with a quantitative systematic approach and found a pattern of impairment extending well beyond the classical syndrome of alexia without agraphia. Sixteen consecutive patients with CT scan evidence of an infarct confined to the territory of LPCA were given a battery of tests assessing the following abilities. (1) Reading and writing; (2) naming and pointing to colours; (3) naming the same 30 objects on visual (objects and coloured photographs), tactile and verbal presentation; and (4) verbal memory. These tests were administered to large control samples and the performance of LPCA patients was considered pathological if it fell below the score of the last or second to last control patient. Seventy five per cent of PCA patients had alexia without agraphia. Although a lesion of the CT scan slice where the pineal is represented appeared to be crucially associated with alexia, the severity of the disorder increased when contiguous upper or lower slices were also involved. Not only colour anomia, but also object and especially photograph anomia could almost always be shown in alexics and were highly correlated with the degree of the reading impairment. The naming deficit was also present when items were presented in the tactile and verbal modality, in spite of the integrity of the oral language areas. Every right-handed patient, alexic as well as nonalexic, was impaired on at least two of the three verbal memory tests and most on all of them. The findings are discussed in terms of the anatomofunctional mechanisms subserving verbal memory and the transmission of visual information to the speech areas.

Cerebral Arteries↗
PubMed1992

Late onset unilateral asterixis secondary to posterior cerebral artery infarction.

Unilateral asterixis developed in a 56 year old man, 5 months after an infarct in the posterior cerebral artery territory, involving the posterolateral nuclear complex of the thalamus, documented by CT-scan and MRI. Unilateral asterixis in rarely reported in association with thalamic lesions and usually develops as an immediate postictal phenomenon. We discuss possible physiopathological mechanisms explaining the occurrence and the delayed onset of these involuntary movements.

Brain↗
PubMedDate not supplied

[Hemiplegia in posterior cerebral artery infarctions: analysis of various responsible mechanisms].

When cerebral infarction determines hemiplegia or hemiparesia which accompany a hemilateral sensitive deficit and hemianopsia and even neuropsychologic symptoms (aphasic alterations in the case of injury to the left hemisphere, heminegligence and anosognosy in the case of injury to the right hemisphere) the involvement of a sylvian artery syndrome is usually considered. Nonetheless, recent contributions have reported that such symptoms may appear in infarctions of the territory of the posterior cerebral artery. Two clinical-radiologic observations in this line are presented. Nuclear magnetic resonance demonstrated injury to the posterior arm of the internal capsule in one case and in the other the lesion developed over three times, in the latter of which injury to the cerebral peduncle was produced causing hemiparesia. The authors emphasize that hemiplegia or hemiparesia in some infarctions of the posterior cerebral artery may be due to 1) mesencephalic infarction in the posterior plane of the retromamillar Foix and Hillemand pediculum (or G. Lazorthes interpedunculum), 2) infarction or "ischemic penumbra" in the internal capsule by involvement of any of the perforating branches of the posterior cerebrum irrigating the thalamus, except for the medial posterior choroid artery or even of the Foix and Hillemand thalamus-tuberian pediculum (or Lazorthes inferior and anterior) which principally initiates at the posterior communicating branch with a fragment of the posterior branch of the internal capsule perhaps not always being under its control. In this case, the thrombus occupying the posterior cerebrum may extend to the cited communicating branch or a hemodynamic deficit may be produced in the territory of the same.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1999

Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.

Cerebral Arterial Diseases↗
PubMed2006

Visual neglect after right posterior cerebral artery infarction.

OBJECTIVES: To investigate the characteristics and neuroanatomical correlates of visual neglect after right-sided posterior cerebral artery (PCA) infarction. METHODS: 15 patients with acute PCA strokes were screened for the presence of neglect on a comprehensive battery of cognitive tests. Extra tests of visual perception were also carried out on six patients. To establish which areas were critically associated with neglect, the lesions of patients with and without neglect were compared. RESULTS: Neglect of varying severity was documented in 8 patients. In addition, higher-order visual perception was impaired in 5 of the 6 patients. Neglect was critically associated with damage to an area of white matter in the occipital lobe corresponding to a white matter tract connecting the parahippocampal gyrus with the angular gyrus of the parietal lobe. Lesions of the thalamus or splenium of the corpus callosum did not appear necessary or sufficient to cause neglect, but may mediate its severity in these patients. CONCLUSIONS: PCA stroke can result in visual neglect. Interruption of the white matter fibres connecting the parahippocampal gyrus to the angular gyrus may be important in determining whether a patient will manifest neglect.

Aged↗
PubMed1981

Three types of abnormal scan patterns in posterior cerebral artery infarction.

It has been reported that the tentorial confluence sign and/or hockey stick pattern on static imaging are useful in evaluating posterior cerebral artery (PCA) infarctions. In 16 cases with PCA infarction, the tentorial confluence sign was found in all cases, but a hockey stick pattern was seen in only half of these patients. The abnormal accumulations may be classified into three types. These three types seem to be consistent with the territory of the blood supply from the cortical, temporal, and/or occipital branches of the posterior cerebral artery. Emission computed tomography images may also demonstrate this consistency.

Adolescent↗
PubMed2006

Preserved cognition and functional independence after a large right posterior cerebral artery infarct: longitudinal clinical and neuropathological findings.

BVR was 77 years old when he sustained a large posterior cerebral artery territory infarct. Medical, cognitive and functional data collected on four occasions over 10 years initially revealed circumscribed neurological signs, no functional or cognitive deficits. BVR became significantly impaired only after two other strokes, 3 years before death. On brain MRI, the lesions involved large portions of the right occipital and temporal cortices, the right thalamus, and the left cerebellum, as well as thinning of the corpus callosum. Postmortem investigations revealed additional recent vascular lesions in the occipital region. This case study underscores the importance of comprehensive assessment methods combining neurological, neuroimaging and cognitive tools.

Aged, 80 and over↗
PubMed1997

Carotid artery dissections presenting as isolated posterior cerebral artery infarctions.

A spontaneous dissection of the carotid artery is a well-known cause of cerebral infarction, mostly due to an embolus from the affected vessel segment. For haemodynamic and anatomical reasons the territories of the middle and anterior cerebral arteries are usually involved. We report two cases of carotid artery dissections resulting in infarctions exclusively in the territory of the posterior cerebral artery. The underlying anatomical conditions were a fetal origin of the posterior cerebral artery and an embolic supra-ophthalmic occlusion of the internal carotid artery. To our knowledge similar cases have not previously been documented.

Aortic Dissection↗