Anatomy of Sensory Findings in Patients With Posterior Cerebral Artery Territory Infarction

Georgiadis, Alexandros; Yamamoto, Yasumasa; Kwan, Eddie; Pessin, Michael S.; Caplan, Louis R.

doi:10.1001/archneur.56.7.835

Cited by 38 publications

(18 citation statements)

References 11 publications

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“…In line with published data [26,32,33], in the present study most of the upper paramedian mesencephalic and thalamic infarcts (68%) were due to embolism, i.e., cardiac sources (42%) [34], intraarterial embolism (16%), and embolism of unknown origin (10%). Intraarterial embolism occurred with arteriosclerosis of the VA and proximal BA as well as with VA dissection [9,22,23,27,32]. In addition, paramedian infarcts have also been reported as a complication during angiographic exploration of the posterior circulation [22,25].…”

Section: Discussionmentioning

confidence: 99%

Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis

et al. 2004

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Considering the highly variable vascular supply of the thalamic nuclei, MRI and clinical syndromes can be heterogeneous in ischemic diseases. We attempt to determine MRI pattern and to analyse neurological features and prognosis of paramedian infarcts. In a prospective case series within 5 years from 1999 to 2003, MRI, MRA and clinical symptoms of 38 consecutive patients were analysed. The inferomedial (posterior thalamoperforating artery) territory was affected in 89%, and lesions in the anterolateral (tuberothalamic artery) territory occurred in 42%. However, definite attribution to anterolateral or inferomedial territories was not possible in 13%. Neurological manifestations were somnolence (87%), hemisyndromes (79%), cognitive deficits (58%), oculomotor nerve palsies (53%) and vertical gaze palsies (39%). The most common aetiologies were cardiac embolism (42%), intraarterial embolism (16%), small vessel disease (13%) and large artery arteriosclerosis (13%). Pathological MRA findings were encountered in 55%, and in 18%, lesions were only visible on diffusion-weighted imaging. Correlation of MRI pattern and neurological symptoms points out anterolateral thalamic lesions as the cause of amnestic deficits. Intracranial MRA allows a non-invasive prediction of basilar tip occlusion. Our results underline the necessity of additional diffusion-weighted imaging in detecting small thalamic and midbrain lesions.

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Section: Discussionmentioning

confidence: 99%

Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis

et al. 2004

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“…Patients with hemisensory symptoms had thalamic ischemia in relation to proximal occlusions of the PCA before the thalamogeniculate branches. 98 Hemiplegia occurred rarely.…”

Section: Vascular Occlusive Lesionsmentioning

confidence: 99%

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Caplan

2000

Stroke

168

101

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know and appreciate where we are now and where we are going in the future, it is essential to know where we have been. We cannot afford to relive and repeat the history of stroke every several decades. Posterior circulation stroke represents a microcosm of stroke in general. In this presentation I first review the development of ideas regarding brain and posterior circulation ischemia and its recognition and treatment. I then share some recent data from a large prospective registry of patients with posterior circulation ischemia. Finally, I look ahead to reflect on what I believe should be the future directions for research and for the care of patients with posterior circulation disease.Patients who present to physicians and hospitals with symptoms that suggest posterior circulation ischemia are handled differently from patients who have symptoms that suggest anterior circulation disease in the great majority of medical facilities in the United States and in the world. A patient who has an attack of dizziness with diplopia and ataxic gait usually has a brain image but seldom has vascular or cardiac investigations. A diagnosis of "vertebrobasilar insufficiency" (VBI) is often made, and physicians then debate whether or not to treat with warfarin-type anticoagulants, and, if so, for how long and at what intensity. In contrast, a patient who has right-hand weakness and aphasia is usually evaluated and treated quite differently at the very same facilities. Brain imaging, cardiac investigations, noninvasive vascular tests of the carotid and intracranial anterior circulation with the use of extracranial and transcranial ultrasound and/or MR angiography (MRA) and CT angiography, and catheter angiography are often pursued, depending on the local technological capabilities and experience of the treating physicians. An effort is made to identify the etiology and mechanism of the ischemia. Treatment is then chosen among a variety of possibilities (including carotid artery surgery, angioplasty, anticoagulants, and antiplatelet aggregants) depending on the nature, location, and severity of the occlusive disease and the mechanism of ischemia.Why should anterior and posterior circulation ischemia be handled so differently? Does this schizophrenic approach make sense? After all, the internal carotid artery and its branches and the vertebral (VA) and basilar arteries (BA) and their branches are just a few inches apart; they are made of the same coats and look the same under the microscope except for size. These vessels carry the same blood under the same blood pressure. The diseases that affect the blood vessels in the 2 circulations are the same. Do stroke mechanisms really differ between the 2 circulations? How did this differing approach originate, and does it continue to make sense today? These are some questions that I will attempt to answer as I review the development of ideas about posterior circulation ischemia and as I report recent data. Development of IdeasHerein I review how knowledge about the posterior circulation ...

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“…Patients that display cortical and deep infarcts (thalamic and/or mesencephalic involvement) also develop sensory (ventrolateral thalamic ischemia), and neuropsychological deficits including memory deficits, aphasia, neglect and anosognosia. Moreover, there was an increased risk of stroke recurrence and poor outcome in those patients with concurrent basilar artery disease (which gives rise to the PCA in most people) [16,[26][27][28]. Some cortical lesions may be more devastating in older persons, and other lesions may surprisingly have little effect on cognitive and behavioral function [29].…”

Section: Cognitive Deficits Following Strokementioning

confidence: 99%

Visualizing Recovery of Cognitive Function in Stroke

Hebb¹,

Brandman²,

Shankar³

et al. 2013

JBBS

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Hippocrates (460-377 BC) first described stroke over 2400 years ago. Stroke is the 4 th leading cause of death in Canada (3 rd in the USA) and the primary cause of permanent motor and cognitive disability. The majority of strokes are ischemic. The extent of cerebral dysfunction and thus the severity of stroke are based on the location, severity and duration of ischemia. Stroke management and prognosis encompass early recognition of the onset of stroke and post-stroke determination of the extent of brain injury aided by clinical stroke scores and diffusion-weighted imaging. Cognitive domains most likely to be affected following stroke are memory, orientation, language, attention and executive function. While the vast majority of functional recovery occurs within the first 3 months post-stroke, the neural mechanisms promoting recovery are not well understood. Investigations into the neural plasticity of brain areas after a lesion demonstrate that the adult brain can be shaped by environmental inputs, such as rehabilitation techniques. Many rehabilitation techniques are actively being pursued, including brain-computer interfaces providing sophisticated methods for detecting rehabilitation-associated changes in cerebral physiology. The success of such strategies visualized with functional magnetic resonance imaging and positron emission tomography may provide an objective complement to clinical evaluations.

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Anatomy of Sensory Findings in Patients With Posterior Cerebral Artery Territory Infarction

Abstract: 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.

Cited by 38 publications

References 11 publications

Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis

Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Visualizing Recovery of Cognitive Function in Stroke

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