Infarction posterior

FIGURE 4.5 A 72-year-old man with medical history remarkable for hypertension and dyslipidemia presented with posterior circulation infarct (a). CTA and posterior circulation angiography (left vertebral artery injection) performed demonstrated severe mid-basilar artery stenosis (b and c). Left vertebral artery injection demonstrated near-complete reversal of the stenosis after a drug-eluting balloon expandable stent (Cypher, Cordis Johnson Johnson) was deployed (d). 

Cardioembolism Cardioembolism accounts for approximately 30% of all stroke and 25-30% of strokes in the young (age <45 years)." AF accounts for a large proportion of these strokes (15-25%). Symptoms may be suggestive, but they are not diagnostic. Repetitive, stereotyped, transient ischemic attacks (TIAs) are unusual in embolic stroke. The classic presentation for cardioembolism is the sudden onset of maximal symptoms. The size of the embolic material determines, in part, the course of the embolic material. Small emboli can cause retinal ischemic or lacunar symptoms. Posterior cerebral artery territory infarcts, in particular, are often due to cardiac embolism. This predilection is not completely consistent across the various cardiac structural abnormalities that predispose to stroke, and may be due to patterns of blood flow associated with specific cardiac pathologies. 

If immediately available, primary PCI should be performed in patients with STEMI (including true posterior MI) or MI with new or presumably new LBBB who can undergo PCI of the infarct artery within 12 h of symptom onset, if performed in a timely fashion (balloon inflation within 90 min of presentation) by persons skilled in the procedure (individuals who perform more than 75 PCI procedures per year). The procedure should be supported by experienced personnel in an appropriate laboratory environment (a laboratory that performs more than 200 PCI procedures per year, of which at least 36 are primary PCI for STEMI, and has cardiac surgery capability). (Level of Evidence A)... 

A 48-year-old woman developed avascular necrosis 9 months after she had completed a 3-month course of hydrocortisone 100 mg retention enemas once or twice daily for ulcerative proctitis (470). An MRI scan showed multiple bony infarcts in her distal femora, proximal tibiae, and posterior proximal right fibular head, extending from the diaphysis to the epiphysis, consistent with avascular necrosis. 

A 71-year-old woman who had undergone total thyroidectomy with subsequent irradiation because of follicular carcinoma 3 years before (22). Since then, she had taken oral levothyroxine 0.15 mg and 0.2 mg on alternate days. When latent hypothyroidism became evident despite replacement therapy, the dose of levothyroxine was increased to 0.3 mg/day. Three weeks later, she had formed an acute posterior myocardial infarction, although she had no previous history of coronary artery disease. Subsequent coronary arteriograms revealed no evidence of disease of the major vessels. Myocardial scintigraphy 3 weeks after infarction still showed a persistent perfusion defect. 

Historically, the French neurologist Charles Foix in 1923 first described the syndrome of infarction in the PCA territory as a thalamocapsular deficit (Foix and Masson 1923). The PCAs arise from the BA, but about 30% of patients have a hypo- or aplastic PI segment with the PCA nourished by the ICA through the posterior communicating artery (Margolis et al. 1971). 

Amarenco P, Hauw JJ (1990) Cerebellar infarction in the territory of the anterior and inferior cerebellar artery. A clinico-pathological study of 20 cases. Brain 113 139-155 Baquis GD, Pessin MS, Scott RM (1985) Limb shaking - a carotid TIA. Stroke 16 444-448 Barth A, Bogousslavsky J, Regli F (1994) Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery. J Neurol Neurosurg Psychiatry 57 1073-1076 Baumgartner RW, Sidler C, Mosso M et al (2003) Ischemic lacunar stroke in patients with and without potential mechanism other than small-artery disease. Stroke 34 653-659... 

Brandt T, Steinke W, Thie A et al (2000) Posterior cerebral artery territory infarcts clinical features, infarct topography, causes and outcome 1. Cerebrovasc Dis 10 170-182 Braun M, Chech V, Boscheri A et al (2004) Transcatheter closure of patent foramen ovale (PFO) in patients with paradoxical embolism. Periprocedural safety and mid-term follow-up results of three different device occluder systems. Eur Heart J 25 424-430... 

Using only a few neurological findings the Oxfordshire Community Stroke Project (OCSP) classification allocates strokes to four subgroups, locating them either in the territory of the anterior (total anterior circulation infarct, TACI partial anterior circulation infarct, PACI lacunar infarct, LACI) and the posterior circulation, (posterior circulation infarct, POCI) (Bamford et al. 1991). The OCSP is a clinical syndromic classification, which... 

There are three parietal MCA branches anterior, angular and posterior. Anterior parietal or postcentral sulcus artery infarct causes a contralateral sensory loss, with upper limb predominance (pseudo-thalamic syndrome) with involvement of the touch, pain, temperature and vibration senses. Pain and hyperpathia and parietal ataxia can also be present. Conduction aphasia, which is a fluent form of aphasia with disproportionate impairment of repetition, anomia, agraphia and apraxia are present in left hemispheric infarcts while neglect follows in right hemispheric ones. 

There are usually five temporal branches of the MCA. Temporal MCA infarcts are often combined with lower posterior parietal infarcts. They cause upper quadrantanopia. Vertigo has occasionally been reported in association with superior temporal or insular infarcts. On the left side, the clinical picture is dominated by Wernicke s aphasia. On the right, limited infarcts can be pauci-symptomatic. Extended infarcts cause amusia, neglect, acute agitation and confusion and sometimes delusions and manic symptoms. 

These include infarcts in the territory of (1) the deep perforators of the MCA, anterior cerebral artery (ACA) and posterior cerebral artery (PCA), posterior communicating artery (PcomA), the lenticulo-striate arteries and the anterior choroidal artery (2) the superficial perforators (white matter medullary branches) of the superficial pial arteries (3) border-zone or junctional infarcts between 1 and 2 (4) combined infarcts. Small (< 1.5 mm infarcts - lacunes) are usually caused by single perforator disease while larger infarcts have a more diverse pathophysiology including embolism and MCA stenosis (Bang et al. 2002). 

Fig. 14.2. Complete right posterior cerebral artery (PCA) territorial infarct.Notice the anterolateral mesencephalic and the inferolateral thalamic infarcts. Old left striatocapsular infarct...

Bogousslavsky et al. 1988). Posterior choroidal artery infarcts result in visual field defects, variable sensory loss, hemiparesis, dystonia, hand tremor and occasionally amnesia and aphasia. Visual field defects, commonly quadrantanopia or hemianopia, are found if the lateral posterior choroidal arteries branches are involved in isolation. Unusual field defects such as homonymous horizontal sec-toranopia or wedge shaped homonymous hemianopia, may also be found and may be explained by the dual blood supply to the lateral geniculate body by... 

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