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Posterior circulation

Acute ischemic stroke s3miptoms with onset or last known well, clearly defined. Treatment within 6 h of established, nonfluctuating deficits due to Anterior Circulation (carotid/MCA) stroke, between 6 and 8 h mechanical treatment (e.g.. Concentric Retriever) should be considered. The window of opportunity for treatment is less well defined in posterior circulation (vertebral/basilar) ischemia, and patients may have fluctuating, reversible ischemic symptoms over many hours or even days and stiU be appropriate candidates for therapy. [Pg.72]

FIGURE 4.2 Seventy-three-year-old female with sudden right hemiparesis, left facial weakness, dysarthria, nausea, and downheat nystagmus. Posterior circulation angioplasty demonstrated occlusion of the proximal hasilar artery (arrows— a and b). Note the retrograde opacification of the superior cerebellar arteries through postero-inferior cerebellar to superior cerebellar arteries collaterals (b). [Pg.80]

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). [Pg.88]

Endo S, Nishijima M, Nomura H, Takaku A, Okada E. A pathological study of intracranial posterior circulation dissecting aneurysms with subarachnoid hemorrhage report of three autopsied cases and review of the literature. Neurosurgery 1993 33 732-738. [Pg.160]

Patients with vertigo and double vision are likely to have posterior circulation involvement. [Pg.165]

Patients usually have multiple signs of neurologic dysfunction on physical examination. The specific deficits observed depend upon the area of the brain involved. Hemi- or monoparesis and hemisensory deficits are common. Patients with posterior circulation involvement may present with vertigo and diplopia. Anterior circulation strokes commonly result in aphasia. Patients may also experience dysarthria, visual field defects, and altered levels of consciousness. [Pg.170]

Large Vessel Occlusive Disease of the Posterior Circulation 6... [Pg.4]

VA obstruction causes hemodynamic problems in approximately one third of patients with posterior circulation ischemia (Caplan et al. 2004). Asymmetrical caliber of the two VAs is normal. In the neck multiple nuchal and muscular branches provide a network for potential collateral pathways, that can be activated in VA obstruction. [Pg.7]

Caplan LR, Wityk RJ, Glass TA et al (2004) New England Medical Center Posterior Circulation registry. Ann Neurol... [Pg.15]

Smooth dissections (Lucas et al. 2000) or less impressive vessel lesions, especially in elongated vessels of the posterior circulation, are diagnostically problematic. In these cases, a DSA is sometimes necessary. False positive findings arise if vascular steps in secondary reconstructions of MR angiographic data sets are mistaken as pathologic wall lesions, which predominantly occur with insufficient spatial resolution. [Pg.94]

As shown above, MRA techniques are susceptible to artificial effects. High resolution time consuming measurements such as TOF-MRA are usually not suitable for the agitated patient suffering from acute stroke. Very fast and robust measurements, on the other hand, might be less detailed. In acute stroke with suspected arterial occlusion, the question of localization in the anterior or posterior circulation is of particular significance. [Pg.96]

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... [Pg.209]

Different topographical patterns of AMBI are associated with different vascular pathologies. Hemorheologic abnormalities or vascular anatomic variations may be contributing factors of AMBI in both hemispheres or in both the anterior and the posterior circulation (Roh et al. 2000). A scattered lesion pattern on DWI in patients with an initial negative CT is indicative of an arterial or embolic source and associated with favorable clinical outcome (Koennecke et al. 2001). Occlusion of the... [Pg.219]

Simultaneous or sequential strokes in different arterial territories, multi-level posterior circulation infarcts, simultaneous infarcts in the three subterritories (superficial anterior, superficial posterior and deep) of the MCA, and hemorrhagic transformation of an ischemic infarct also point to a cardiac origin of the stroke (Arquizan et al. 1997 Ay et al. 1999 Ferro 2003a,b). Occlusion of the carotid artery by a mobile thrombus, early recanalization of an occluded vessel and the identification of microembolism in both MCAs are all highly indicative of a cardiac source of emboli. [Pg.220]

Kumral E, Afsar N, Kirbas D et al (2002a) Spectrum of medial medullary infarction clinical and magnetic resonance imaging findings. J Neurol 249 85-93 Kumral E, Bayulkem G, Akyol A et al (2002b) Mesencephalic and associated posterior circulation infarcts. Stroke 33 2224-2231... [Pg.222]

A 29-year-old woman had a sudden severe occipital headache and photophobia with nausea and vomiting. She had marked nuchal rigidity. Her head CT scan was normal, but the CSF was blood-stained with spectro-photometric evidence of xanthochromia. Cerebral angiography showed beading of vessels in the posterior circulation. However, MRI/MRA did not show any abnormality and the ESR was normal. The patient admitted to having used ecstasy for the first time. Cerebral angiography 2 months later showed that the abnormalities had completely resolved. [Pg.594]

Giant cell arteritis is the most common vascuUtic cause of stroke and is associated particularly with posterior circulation ischemia (Nesher 2000 Ronthal et al. 2003 Eberhardt and Dhadly 2007). Medium and large arteries are affected, especially branches of the external carotid artery, the ophthalmic artery and the vertebral artery. The patients are elderly, with the diagnosis being rare under age 60 years. Malaise, polymyalgia and other systemic symptoms are frequently present. The erythrocyte sedimentation rate is usually raised, often to over 100 mm/h in the first hour. [Pg.72]

Neurological involvement in Behcet s disease may be subclassified into two major forms a vascular-inflammatory process with focal or multifocal parenchymal involvement and a cerebral venous sinus thrombosis with intracranial hypertension. The vasculitis and meningitis may affect cerebral arteries, particularly in the posterior circulation, to cause ischemic stroke and possibly intracranial hemorrhage (Farah et al. 1998 Krespi et al 2001 Siva et al. 2004 Borhani Haghighi et al. 2005). [Pg.73]

Simultaneous bilateral transient motor or sensory loss is almost always caused by brainstem ischemia. Sudden simultaneous bilateral blindness in elderly patients usually indicates bilateral occipital ischemia. Vertigo, diplopia, dysphagia, unsteadiness, tinnitus, amnesia, drop attacks and dysarthria may be caused by posterior circulation or more global cerebral ischemia, or by non-vascular causes such as motor neuron disease or myesthenia in the case of dysarthria. If these symptoms occur in isolation, the diagnosis of TIA should only be considered after exclusion of other possibilities (Gomez et al. 1996 Bos et al. 2007). Global symptoms such as a reduced level of consciousness are almost never caused by a TIA. They can only be accepted as resulting from a TIA if there are additional focal symptoms that are unlikely to be epileptic or syncopal. [Pg.102]

If more than one body part is involved, the symptoms usually start simultaneously in all parts, persist for a while and then gradually wear off over a few minutes, particularly in the case of transient monocular blindness, or an hour or so. If a patient still has symptoms more than an hour after the onset, the chances are that complete recovery will take more than 24-hours. A mild headache accompanying the neurological symptoms is quite common, usually ipsilateral to the affected carotid territory, but most common in posterior circulation TIAs. If cerebral symptoms last less than a minute, particularly if they are sensory, the diagnosis of TIA is difficult to sustain. In contrast, symptoms of retinal ischemia may be very short lived. [Pg.102]


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