Lesion topography of posterior cerebral artery infarcts.

This study analyzed the topography of acute ischemic stroke in the posterior cerebral artery (PCA) territory. We studied 84 patients with unilateral ischemic PCA stroke. Patients were classified according to lesion levels as cortico-subcortical (superficial), combined (cortical and mesodiencephalic) or isolated thalamic. To receive a lesion map, data from acute MR and CT imaging were normalized and labelled automatically by mapping to stereotaxic anatomical atlases. Cortical lesions accounted for 41.7%, combined for 36.9%, and isolated thalamic lesions for 21.4%. The maximum overlay of ischemia and, thus, highest occurrence of PCA ischemic stroke was found in the ventral and medial occipito-temporal cortex and adjacent white matter association tracts. Dorsal and peripheral segments of the occipito-temporo-parietal region were only rarely lesioned. This configuration was similar in both hemispheres. Consistent with this lesion pattern, visual field defects (VFD) were the most frequent signs, followed by sensorimotor signs, dizziness and sopor, cognitive and oculomotor deficits, and ataxia. The three vascular subgroups differed not only by their anatomical lesion profile and lesion load, but also by their clinical manifestation; although patients with combined and thalamic lesions were sigificantly younger, they were more disabled than participants with cortical lesions. VFD were only found in cortical and combined, and oculomotor deficits only in mesodiencephalic lesions. White matter lesions were common in the cortico-subcortical and the combined group. Basal occipito-temporal and calcarine regions, and neighbouring white matter tracts have the highest risk of ischemia in acute PCA stroke.

[Posterior cerebral artery infarctions with possible interaction between hypoperfusion and embolism]. / Infarctus cérébraux multiples : éléments en faveur de la coexistence de mécanismes emboliques et hémodynamiques dans le territoire postérieur.

Although embolism and hypoperfusion may well occur concurrently in a non-negligible proportion of cerebral infarction patients, there is currently lack of proof, especially in the posterior circulation. Here, we are reporting on a case of multiple cerebral infarctions in a patient with neurofibromatosis type 1, multiple vascular abnormalities of the posterior cerebral circulation and intracranial artery occlusion. We hypothesize that cerebral blood flow impairment may have affected the clearance and destination of embolic particles.

Bilateral paramedian thalamic infarction with hypothalamic dysfunction.

Unilateral thalamic lesions cause transient or permanent behavioral, sensory and oculomotor disturbances; bilateral lesions of thalamus result in more severe and longer lasting symptoms. We present an atypical case of bilateral paramedian thalamic infarct with concomitant hypothalamic dysfunction. The only risk factor of ischaemic stroke found in the patient was a short lasting episode of atrial fibrillation. Bilateral paramedian thalamic infarcts may result from occlusion of one paramedian thalamic artery, which arises from the posterior cerebral artery, either with separated or with a common trunk, thus supplying the thalamus bilaterally. Independently of anatomical variants of thalamus blood supply, the most probable cause of infarct in our patient was unilateral or bilateral occlusion of the posterior cerebral artery by cardioembolism, probably in the course of basilar artery occlusion. Hypothalamic dysfunction may accompany thalamic infarcts; thus hypothalamo-pituitary function should be routinely assessed in bithalamic infarcts.

Topographic patterns of thalamic infarcts in association with stroke syndromes and aetiologies.

OBJECTIVE: To characterise the topographic patterns of thalamic infarcts associated with various stroke syndromes and aetiologies. METHODS: In this study, 168 consecutive patients with acute infarcts involving the thalamus were investigated by use of diffusion weighted MR imaging. Involved thalamic territories were classified into four vascular territories: anterior (polar artery), posteromedial (thalamoperforating artery), ventrolateral (thalamogeniculate artery) and posterolateral (posterior choroidal artery) territory. The distribution of thalamic infarcts involving specific vascular territories in association with various stroke syndromes and aetiologies were analysed. RESULTS: There was a significant association between involvement of the ventrolateral thalamus and isolated thalamic infarcts (49 patients (73%), p<0.01) or posterior cerebral artery infarcts (29 patients (76%), p=0.02), and between involvement of the posteromedial thalamus and top of the basilar artery syndrome (17 patients (77%), p<0.001) or extended posterior circulation infarcts (29 patients (71%), p<0.001). The ventrolateral territory was most commonly affected in association with small vessel disease (43 patients (72%), p=0.03) and the posteromedial territory in association with large artery disease (19 patients (63%), p<0.01). In cardioembolic stroke, the ventrolateral, posteromedial and posterolateral territories were equally affected. CONCLUSIONS: The results of the present study indicate a specific association between the topographic patterns of thalamic infarcts and the stroke syndromes and aetiologies.

Alien hand syndrome in left posterior stroke.

Alien hand syndrome is a rare neurological disorder characterized by involuntary and uncontrollable motor behaviour, usually of an arm or hand. The patient perceives the affected limb as alien, and may personify it. The case of a 61-year-old right-handed woman who developed right posterior AHS after ischaemic stroke in the left posterior cerebral artery territory is reported. Neuroimaging studies disclosed no frontal or parietal involvement, while a posterior thalamic lesion was detected. A possible role of the thalamus in the genesis of AHS is discussed.

Complete bilateral ophthalmoplegia resistant to caloric stimulation in bilateral paramedian midbrain-thalamic infarction.

A 79-year-old woman who developed bilateral paramedian midbrain-thalamic infarction manifested complete bilateral ophthalmoplegia resistant to caloric stimulation, indicating impairment of the vestibulo-ocular reflex (VOR). Previous reports have mentioned this phenomenon but have not explicitly reported the results of caloric testing. Why a lesion apparently confined to the upper brainstem should produce impairment of the horizontal VOR remains unexplained.

Homonymous central quadrantanopia caused by an extrastriate (v2/v3) infarction: a case report.

A 66-year-old Taiwanese aboriginal male had complained of right-side blurred vision for 2 months, especially when reading. He had a 10-year history of hypertension and cardiovascular disease. His best-corrected visual acuity was 20/25 in each eye. Ophthalmoscopy revealed asymmetrical cupping, but a normal disc. Humphrey perimetry showed an upper homonymous paracentral quadrantanopic defect. Brain magnetic resonance imaging showed an infarction in the left lower calcarine area over the extrastriate (V2/V3) cortical area and a narrowing of the left middle and posterior cerebral arteries due to severe arteriosclerosis.

An investigation of attentional contributions to visual errors in right "neglect dyslexia".

One type of error that is sometimes produced by patients with acquired dyslexia is the substitution of an orthographically similar word with letters that overlap the target either in early or late letter positions. When such errors affect the left sides of words, they are usually produced by patients with focal right hemisphere lesions who typically show evidence of left neglect in non-reading tasks. This pattern has thus been termed "neglect dyslexia". When the right sides of words are affected, however, patients frequently fail to show any signs of neglect in tasks other than reading. This study presents results from a patient with left hemisphere damage, and a very clear pattern of right "neglect" errors in reading, on a series of tasks testing attentional and imagery processes. Given the magnitude and consistency of the patient's reading errors, there was little evidence that these errors resulted from inattention to the right side of space or to the right side of an internally generated visual image. It is argued that the positional errors result from an impairment to an abstract ordinal code with graded activation of letter positions from first to last, and that this code is specific to tasks involving orthographic representations.

Aggressive behavior and posterior cerebral artery stroke.

OBJECTIVE: To describe the mechanisms leading to aggressive behavior among patients with acute posterior cerebral artery stroke. DESIGN, SETTING, AND PATIENTS: We prospectively included all of the patients with posterior cerebral artery stroke and aggressive behavior admitted to our department from January 1, 2003, to December 31, 2004. Patients with history of stroke, cognitive impairment, or prior history of psychiatric disease were excluded. RESULTS: Aggressive behavior was found in 3 patients (7.3%) among 41 patients with posterior cerebral artery stroke. One patient had right occipitotemporal and ventrolateral thalamic stroke. The second patient had left occipitotemporal and lateral thalamic stroke. The third patient had right isolated occipital stroke. In addition to a contralateral homonymous hemianopsia, the patients, who were physically and emotionally balanced before the stroke, suddenly manifested an acute, unusual, aggressive behavior. The patients became agitated and aggressive when they were stimulated by the environment, and they responded to solicitation by their relatives or medical personnel by shouting obscenities and hitting and biting others. In all of the 3 cases, temporary physical restraint was required and neuroleptics were administered. This unusual behavioral pattern resolved within 2 weeks after stroke. CONCLUSIONS: Aggressive behavior is a rare presentation of acute posterior cerebral artery stroke, which may be difficult to diagnose in patients presenting with hemianopsia as the only concomitant neurological sign. The postulated mechanisms include dysfunction of the limbic or serotoninergic system.

Domain-specific impairment of source memory following a right posterior medial temporal lobe lesion.

This single case analysis of memory performance in a patient with an ischemic lesion affecting posterior but not anterior right medial temporal lobe (MTL) indicates that source memory can be disrupted in a domain-specific manner. The patient showed normal recognition memory for gray-scale photos of objects (visual condition) and spoken words (auditory condition). While memory for visual source (texture/color of the background against which pictures appeared) was within the normal range, auditory source memory (male/female speaker voice) was at chance level, a performance pattern significantly different from the control group. This dissociation is consistent with recent fMRI evidence of anterior/posterior MTL dissociations depending upon the nature of source information (visual texture/color vs. auditory speaker voice). The findings are in good agreement with the view of dissociable memory processing by the perirhinal cortex (anterior MTL) and parahippocampal cortex (posterior MTL), depending upon the neocortical input that these regions receive.

Double dissociation between representational personal and extrapersonal neglect.

BACKGROUND: Although perceptual and representational neglect are frequently associated, the demonstration of a double dissociation between both neglect forms suggests that both rely on different central mechanisms. In addition, perceptual neglect can be selectively observed within personal space or extrapersonal space. However, it is not known whether the latter dissociation also exists in representational neglect. METHODS: The authors investigated this question in two brain-damaged patients with anatomically different lesions sites, using neuropsychological tests specifically designed to assess perceptual and representational neglect in both personal and extrapersonal space. RESULTS: Patients presented a double dissociation with respect to personal and extrapersonal space in representational neglect. CONCLUSIONS: These data suggest that the cerebral networks that process mental space representation use similar principles of space compartmentalization as those used by cerebral networks processing perceived space.

[A case of alien hand syndrome after right posterior cerebral artery territory infarction].

We report a 63-year-old right-handed man who presented an alien hand syndrome (AHS). He complained of clumsiness of his left hand and admitted to our hospital. On the first examination, he presented left homonymous hemianopia, left spatial neglect and left limb ataxia, but neither paralysis nor sensory impairment. A few days after, he complained that his left hand was controlled by someone else, and we considered this phenomenon as AHS. At that time, he lost sensation of almost all modalities including deep sensation on his left upper and lower limb. Magnetic resonance image examination was performed, and it showed acute cerebral infarction at right posterior cerebral artery territory including right thalamus (ventral posterior lateral nucleus). Generally, AHS is caused by left mediofrontal and callosal lesion (frontal type AHS), or by callosal with bilateral frontal or without frontal lesion (callosal type AHS). However, some cases were reported that they presented AHS after damage of the basal ganglia, right thalamus, right occipital or inferior parietal lobe. Some authors described this phenomenon as "sensory" or "posterior" type AHS. In such cases, included our case, we speculate that sensory impairment causes AHS. Especially in our case, AHS might be caused by not only the sensory impairment but also by left homonymous hemianopia and left spatial neglect. So, because of these symptoms, our patient could not recognize the motion of the left hand, and presented AHS. We think that this "sensory" or "posterior" type AHS should be distinguished from frontal and callosal type AHS.

Face imagery and its relation to perception and covert recognition in prosopagnosia.

BACKGROUND: Face imagery can access facial memories without the use of perceptual stimuli. Current data on the relation of imagery to the perceptual function and neuroanatomy of prosopagnosic patients are mixed, and little is known about the type of facial information patients can access through imagery. OBJECTIVE: The authors wished to determine 1) which lesions abolished face imagery in prosopagnosia, 2) if deficits in perceiving facial structure were paralleled by similar deficits in imagery, and 3) if covert recognition of faces correlated with the degree of residual imagery for faces. METHODS: The authors tested nine prosopagnosic patients who had been tested previously for perception of facial configuration and covert recognition of famous faces. The authors constructed a battery of 37 questions that asked subjects to imagine the faces of two celebrities and to choose which one had a certain facial property. Half were questions about facial features and half were about overall facial shape. RESULTS: Imagery was abolished only by anterior temporal lesions. Imagery for facial shape but not features was degraded by lesions of the right hemisphere's fusiform face area, which severely impaired perception of facial configuration. Feature imagery was degraded only when there was associated left occipito-temporal damage. Covert recognition was found when either configural perception or imagery was severely damaged, but not when both were abnormal. In patients with impaired configural perception, covert recognition correlated with feature imagery, suggesting that feature-based processing may drive residual covert abilities in these patients. CONCLUSION: Although anterior temporal cortex may be the site of facial memory stores, these data also support hypotheses that perceptual areas like the fusiform face area have parallel contributions to mental imagery. The data on covert recognition are consistent with a view that it is the residue of a partially damaged face-recognition network. Covert recognition may reflect the degree of damage across components of a network rather than mark a specific form of prosopagnosia or a dissociated pathway.