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Objective: To investigate the clinical and anatomic correlates of a previously unreported form of chronic supernumerary phantom limb, which developed only in association with motor intent directed at a hemiplegic–anesthetic upper limb. Methods: We explored the phenomenology of the phantom illusion in the light of motor control models. Hemodynamic correlates of supernumerary phantom limb were studied with an fMRI sensorimotor paradigm consisting of finger–thumb opposition movements. Results: The kinesthetic–proprioceptive illusion of a third arm was triggered by any attempt to move the paretic limb, by bimanual actions, and by motor imagery involving the nonfunctional limb. The responsible lesion destroyed the posterior part of the posterior limb of the internal capsule on the opposite side, damaging corticospinal and thalamocortical tracts. Comparison between fMRI signals performed during virtual movement of the phantom hand vs imaginary movement of the paretic hand showed increased activation in thalamus and caudate nucleus in the first condition. Conclusions: A preserved sense of agency provided by intact premotor processes translating intention into action may lead to the vivid feeling of movement in a paralyzed limb, similar to kinesthetic illusions in amputees. The interruption of thalamic afferences may explain the persistence and stability of the phantom by preventing any correction of the mismatch between expected and effective movement. The increased blood oxygen level–dependent (BOLD) signal in the basal ganglia–thalamus–cortex pathway during movement of the supernumerary hand may reflect an abnormal closed-loop functioning of the thalamocortical system underlying the phantom phenomenon.

Auditory recognition and auditory spatial functions were studied in four patients with circumscribed left hemispheric lesions. Patient FD was severely deficient in recognition of environmental sounds but normal in auditory localisation and auditory motion perception. The lesion included the left superior, middle and inferior temporal gyri and lateral auditory areas (as identified in previous anatomical studies), but spared Heschl's gyrus, the acoustic radiation and the thalamus. Patient SD had the same profile as FD, with deficient recognition of environmental sounds but normal auditory localisation and motion perception. The lesion comprised the postero-inferior part of the frontal convexity and the anterior third of the temporal lobe; data from non-human primates indicate that the latter are interconnected with lateral auditory areas. Patient MA was deficient in recognition of environmental sounds, auditory localisation and auditory motion perception, confirming that auditory spatial functions can be disturbed by left unilateral damage; the lesion involved the supratemporal region as well as the temporal, postero-inferior frontal and antero-inferior parietal convexities. Patient CZ was severely deficient in auditory motion perception and partially deficient in auditory localisation, but normal in recognition of environmental sounds; the lesion involved large parts of the parieto-frontal convexity and the supratemporal region. We propose that auditory information is processed in the human auditory cortex along two distinct pathways, one lateral devoted to auditory recognition and one medial and posterior devoted to auditory spatial functions.

Two patients with severe and lasting prosopagnosia were studied for visuo-cognitive functions and anatomo-clinical correlations. Both patients were deficient in recognizing familiar faces and items of previously well known categories (plants and fish for patient 1, mountains for patient 2). Patient 2, but not patient 1, was also deficient for matching of unknown faces. Patient 1, but not patient 2, was achromatopsic. Both patients had bilateral symmetrical lesions. Patient 1 had a lesion of the inferior occipitotemporal cortex, including inferior parts of early stage visual areas. Patient 2 had a lesion of the inferior temporal and fusiform gyri anterior to the early stage visual areas. When compared in Talairach space, the lesions of both patients had minimal overlap. Thus, severe and lasting prosopagnosia was associated with two almost exclusive lesion sites in the postero-inferior part of the hemispheres. Comparison between activation studies of face processing (by others) and our lesion study uncovered several paradoxes. Lesions of regions involved in a given task in normal subjects do not produce a deficit in this task, as shown here for gender discrimination and partially for face matching. Conversely, lesions of a region not specifically involved in a given task in normal subjects can produce a deficit in the task, as shown here for face identification.

Three different aptitudes involved in sound object recognition were tested in 60 normal subjects and 20 brain-damaged patients: (i) capacity to segregate sound objects on different cues (intensity steps, coherent temporal modulations or signal onset synchrony); (ii) asemantic recognition of sounds of real objects by judging whether two different sound samples belonged to the same object; and (iii) semantic identification of sounds of real objects as judged by means of a multiple choice response test. In 12 patients, different aptitudes involved in auditory recognition were disrupted separately and in a way which speaks in favour of parallel rather than hierarchical processing. There was no strong association between deficits in non-verbal auditory recognition and aphasia or the side of lesion.

Article abstract-We describe a patient who had sequential strokes in both hemispheres with a severe unilateral spatial neglect after a first right-sided parietal infarct and abrupt disappearance of the neglect after a second left-sided frontal infarct. The first lesion involved the caudalmost right angular gyrus (area 39), whereas the second lesion involved the left frontal eye field (area 8) and surrounding cortex. Those two cortical areas are assumed to have a pivotal role in modulating both shifts of attention within extrapersonal space and saccadic eye movements through their connections with subcortical structures, in particular, superior colliculi and thalamic nuclei. Our case supports the existence of a distributed anatomic-functional network in subserving directed spatial attention.NEUROLOGY 19;: 184-189

We report a patient with complete callosal disconnection syndrome after severe closed head injury. MRI showed a complete destruction of the corpus callosum throughout its length. Although traumatic callosal lesions are a frequent finding in autopsy studies, as well as in some recent MRI studies, clinical signs of callosal disconnection are rarely observed after head injuries and a complete disconnection syndrome has not been reported yet. This case study and the review of other reported cases suggest that posttraumatic callosal disconnection is probably often overlooked. Our patient had also a severe memory disorder that might be partly related to the bilateral involvement of the fornix, as this structure is closely adjacent to the posterior corpus callosum, and was also shown by MRI to be very probably damaged.

A 70-year-old right-handed woman developed a complete Klüver-Bucy syndrome including psychic blindness, aberrant sexual behavior, hypermetamorphosis, aphasia and visual agnosia following left anterior temporal lobectomy for an anaplasic oligodendroglioma. MRI showed no argument for a contralateral ischemic infarct, tumoral growth or white matter damage. Thus the possibility that a unilateral anterior temporal lesion can cause the whole picture of Klüver-Bucy syndrome must therefore be considered.

Gottlieb Burckhardt, a Swiss psychiatrist who practiced in the late 19th century, was the founder of modern psychosurgery. In 1891 he reported the results of cortical extirpations on six patients who evidently suffered from intractable psychiatric disease; two of these cases are discussed here to illustrate how Burckhardt employed contemporary brain models of language and cognition as the basis for removing specific areas of the cerebral cortex with the intention of ameliorating his patients' disturbed behavior.

In March 1841, the year before he died of acute stroke, Stendhal, one of the most famous French novelists of the 19th century, developed a series of short-lived speech impairments which he precisely r

Two patients with bilateral thalamo-mesencephalic infarct in the paramedian territory developed vertical gaze dysfunction and marked behavioural changes, in the absence of significant motor inability and formal neuropsychological impairment. While they were physically and emotionally active before stroke, they became apathetic, aspontaneous, indifferent, and seemed to have lost motor and affectic drive, as well as the need itself for any psychic activity. However, this mental and motor inertia was reversible when the patients were repeatedly stimulated by another person. This need for constant external programming, together with a lack of emotional reactivity, made the patients resemble robots. CT and MRI suggested involvement of the dorsomedial and midline nuclei of the thalamus, and SPECT showed remote frontomesial hypoperfusion. A disturbance of the striatal-ventral pallidal-thalamic-frontomesial limbic loop is suggested by previous reports of a similar "loss of psychic self-activation", "pure psychic akinesia", or "athymhormia" with bipallidal, bistriatal, or subcortical bifrontal lesions.

The acclaimed Italian directors Luchino Visconti and Federico Fellini had very different life trajectories that led them to become major figures in the history of cinema. Similarities, however, can be found in their debuts with the neorealist genre, their personalities, creative styles and politicocultural involvement, and ultimately in the neurological disease that struck them at the end of their careers. Both suffered a right-hemispheric stroke that left them hemiplegic on the left side. We review their life and career to put that event into perspective, and then discuss its aftermath for both artists in the light of our current knowledge of right-hemispheric functions. Visconti showed a tremendous resilience following the accident and managed to direct several films and plays as an infirm, whereas Fellini had to put an end to his career but still was able to display his talents to the neuropsychologists that treated him. A speculative account is given of the links between right-hemispheric symptomatology and the premorbid personality of these highly prolific patients.

What about artistic creativity following a cerebral lesion? We studied the case of a prominent right-handed Swedish painter and sculptor who suffered a cerebral hemorrhage at the age of 55 years. Th

Patients' opinions about the aetiology of their disease and the implications for compliance have not been well documented at this time.To investigate prospectively aetiological beliefs of a cohort of neurological inpatients.Within two days of admission, patients orally answered a short questionnaire regarding their beliefs about the aetiology of their disease and the possible influence of psychological factors, stress, fatigue, excessive work or other activities, poor lifestyle, conflict with another person, a tragic event, chance, and destiny.Of the 342 patients who participated in the study, 49% spontaneously said that they had no idea of what could have caused their disease, 15% gave a congruent medical explanation, 11% mentioned stress and fatigue as a precipitating factor, and 6% evoked a non-congruent medical explanation. Thirty six per cent thought that psychological factors had triggered their disease; such factors being blamed by a higher proportion of young patients and patients with chronic central nervous system diseases. The triggering factors most often blamed were stress (48%, especially by patients with headache), fatigue (51%), chance (54%), and destiny (43%).Patients' aetiological beliefs only partially concur with medical opinion and this may influence compliance with treatment. This statement should be explored and confirmed by further studies-for example, in cerebrovascular risk factor follow up.

True prosopagnosy preserves the perception of human faces. However, the latter faces cannot be identified even by patients who have kept an intact implicit recognition. After a thorough examination of the visual recognition disorder, other kinds of information may be involved like, on one hand, those of places, landscapes and building constructions or, on the other hand, those of animals. We observed that a transitorily prosopagnosic farmer was definitively unable to recognize his cows. Arguments for a right hemisphere dominance are discussed.

Interhemispheric transfer of visual information was investigated behaviourally and with functional magnetic resonance imaging (fMRI) 6 months after a lesion of the posterior two-thirds of the corpus callosum. On tachistoscopical left hemifield presentation, the patient was severely impaired in reading letters, words and geographical names and moderately impaired in naming pictures and colours. In contrast, interhemispheric transfer of visual motion information, tested by verbal report of the direction of short sequences of coherent dot motion presented within the left hemifield, was preserved. The pattern of cerebral activation elicited by apparent motion stimuli was studied with fMRI and compared to that of normal subjects. In normal subjects, apparent motion stimuli, as compared to darkness, activated strongly striate and extrastriate cortex. When presented to one hemifield only, the contralateral calcarine region was activated while regions on the occipital convexity, including putative area V5, were activated bilaterally. A similar activation pattern was found in the patient with a posterior callosal lesion; unilateral left or right hemifield stimulation was accompanied by activation in the contralateral and ipsilateral occipital convexity. Ipsilateral hemifield representation in the extrastriate visual cortex is believed to depend on callosal input. Our observation suggests that this is not the case for visual motion representation and that other, probably parallel, pathways may mediate visual motion transfer after posterior callosotomy.

We report the behavioral symptoms presented by a 57-year-old man as the first sign of a Marchiafava-Bignami syndrome and by a 44-year-old woman with centro and extrapontine myelinolysis. These observations define a clinical entity, that we named callosal dementia characterized by: 5) fronto-limbic signs with coarse interjections, repetitive and antisocial behavior, alternation of lack of incitation and agitation; 6) elements of a Balint syndrome (suggestive of a posterior callosal involvement), with a pseudo-hallucinated look and a gaze apraxia; 7) signs of callosal dysconnection and; signs of adjacent white matter involvement, with paucity of vocal and facial expression modulation. Early recognition of these features of callosal dementia may be very helpful for diagnosis of suspected myelinolysis, leading to a more careful research of clinical signs of callosal dysconnection and prompting neuroimaging with MRI. A rapid confirmation of the diagnosis may prevent progression to centro or extrapontine myelinolysis, that may sometimes still be lethal, by adequate supportive measures (slow correction of electrolytes imbalance, correction of deficiencies, total alcohol withdrawal).

Short-term memory for colour was studied in five patients with circumscribed posterior hemispheric lesions. It was impaired independently of colour discrimination in one and more than colour discrimination in two patients. Two patients were normal in colour short-term memory, one with normal and one with deficient colour discrimination performance. Deficient performance in colour short-term memory was associated with bilateral lesions of the inferior occipitotemporal junction including the lateral part of the fusiform gyrus or with a unilateral lesion of the left parieto-occipital convexity. An additional colour constancy deficit was found in the former but not the latter condition. Thus, colour short-term memory can be affected independently of colour discrimination or colour constancy, and may depend on at least two distinct neural circuits.

Colour matching and colour constancy were studied in seven patients and 46 control subjects. Subjects were required to match Munsell Colour Chips presented under either identical or different illumination. Three of the patients had deficits in colour constancy, i.e. failure to compensate for the change in the wavelength composition of the illumination. Two of the patients with defective constancy had suffered bilateral cortical damage to the posterior lingual and fusiform gyri, and one patient had a lesion restricted to the same regions of the right hemisphere. Our observations indicate that these cortical areas, which include part of putative human area V4, play an important role in colour constancy.

The neuropsychological records of 56 patients operated for clipping were studied. Almost every patient remained autonomous and without invalidating motor defect. The present study was aimed at specifying the type and frequency of neuropsychological sequelae and, to a lesser extent, the role of various pathophysiological factors. A main concern was to examine to what extent and at what post-operative interval the neuropsychological assessment can predict the intellectual and socioprofessional outcome of each individual patient. The neuropsychological assessment performed beyond the acute phase showed evidence of intellectual sequelae in about two thirds of the patients. Only one case of permanent anterograde amnesia was observed, probably due to unavoidable inclusion of a hypothalamic artery in the clip during surgery. Transient anterograde amnesia and confabulations were occasionally observed, generally for less than three weeks. A common finding was impaired performance on memory and/or executive tests. In a minority of patients, language disorders, visuoperceptive and visuoconstructive disabilities were found, probably in relation with hemodynamic changes at distance from the aneurysm. Global impairment of intellectual function was not uncommon in the acute post-operative phase but it evolved in most cases towards a more selective impairment, for instance restricted to executive and memory functions, in the chronic phase. The neuropsychological investigation carried out 4 to 15 weeks post-operatively provided satisfactory information about possible long-lasting intellectual disturbances and professional resumption. In particular, persistent global intellectual impairment, persistent amnesia and confabulations 4-15 weeks post-operative were associated with cessation of professional activity; executive and memory impairment, behavioral disturbances such as those encountered in patients with frontal lobe damage were associated with a decreased probability of full-time employment. Pre- and post-operative angiography were not good predictors of long-term cognitive outcome: normal angiography was not necessarily followed by normal neuropsychological outcome, conversely abnormal angiography could be found together with normal neuropsychological outcome. By contrast, there was a relationship between left-lateralised abnormalities on post-operative angiography and occurrence of language disorders; similarly, there was a relationship between side of craniotomy and type of deficits, that is language disorders versus visuoperceptive-visuoconstructive impairments.

We report a 65-year-old man with a post-anoxic encephalopathy who showed compulsive sniffing at available objects. This stereotyped environment-driven behaviour has not been previously described. Other compulsive environment-driven responses, such as manipulation and utilization of tools and hyperlexia, were also present. The disorder shared several features with the Kluver-Bucy syndrome where mouthing of objects, rather than smelling them, is common. The patient had a severe dementia, with amnesia, anomia, apraxia, and visual agnosia. Whereas he could not recognize very familiar objects on sight, he could in contrast correctly identify several familiar odours. Although sniffing was a compulsive and purposeless environment-driven behaviour, the question may be asked whether a relatively preserved olfactory recognition, in the presence of a severe disorder of visual recognition and knowledge, could have favoured a stereotyped exploration of objects by smelling.

We report a 38 year-old patient who had temporoparietal epilepsy and unusual ictal "out of body" experiences that remained undiagnosed for more than ten years, until her admission for a motor seizure of the left hemibody. Out of body episodes were experienced as intense and ecstatic astral journeys. EEG showed a bilateral extension of epileptiform abnormalities to the parietal regions, predominantly on the right side. We discuss the various forms of heautoscopy and their putative mechanisms. We suggest that a disturbance in representing space in independent extrapersonal and personal coordinates might be as crucial as the elusive hypothesis of a body schema disorder. Combined involvement of the parietal neocortex and temporolimbic structures might allow those experiences to gain a subjective vividness which appears to be indissociable from normal conscious experiences.

A patient in whom mandibular and maxillary parts of right trigeminal ganglion were removed experienced referred sensations after stimulation of the right hand and right forehead. She described them either as parallel to the perception at the actual stimulation site or as coming uniquely from a (non-existent) stimulation of denervated territory. The latter occurred in 6-19% of stimulations performed on the right forehead and on digits 1, 3 and 4 of the right hand. Thumb stimulations were localized on the right side of the face, stimulations of right forehead, middle and ring fingers more precisely on right cheek. Referred sensations were present on postoperative day 7 and had a more real-like quality than 5 days later.

Three patients developed a striking visual and motor behaviour in the acute phase of a stroke involving the territory of the right anterior parietal artery (postcentral gyrus, parts or upper and middle temporal gyri, anterior part of inferior parietal gyrus, and supramarginal gyrus). The patients concentrated on the left side of their bodies, looking at it for long periods and relentlessly rubbing, touching, pinching, pressing, lifting, and manipulating parts of the left arm, trunk, and leg with their right hand or foot. They all had severe loss of elementary sensation on the left (touch, pain, temperature, vibration, position). The behaviour was not associated with overinterest in the left hemispace apart from their own bodies. It lasted no more than a few days, disappearing when left sided sensation improved. The findings suggest an association between sensory dysfunction and this "acute hemiconcern". None of 13 patients with a mirror infarct in the left hemisphere and none of 38 patients with acute hemisensory loss due to thalamic capsular or brainstem stroke showed hemiconcern behaviour. This behaviour may result from a feeling of strangeness critically associated with hemisensory loss without hemispatial neglect, due to involvement of the right anterior parietotemporal region.

A 54-year-old patient who had an isolated small polar thalamic infarct and acute global amnesia with slight frontal type dysfunction but without other neurological dysfunction was studied. Memory improved partially within 8 months. At all stages the impairment was more severe for verbal than non-verbal memory. Autobiographic recollections and newly acquired information tended to be disorganised with respect to temporal order. Procedural memory was unaffected. Both emotional involvement and pleasure in reading were lost. On MRI, the infarct was limited to the left anterior thalamic nuclei and the adjacent mamillothalamic tract. The regional cerebral metabolic rate of glucose (measured with PET) was decreased on the left in the thalamus, amygdala, and posterior cingulate cortex 2 weeks after the infarct, and in the thalamus and posterior cingulate cortex 9 months later. These findings stress the specific role of the left anterior thalamic region in memory and confirm that longlasting amnesia from a thalamic lesion can occur without significant structural damage to the dorsomedial nucleus. Furthermore, they suggest that the anterior thalamic nuclei and possibly their connections with the posterior cingulate cortex play a role in emotional involvement linked to ipsilateral hemispheric functions.

35 patients with subcortical ischemic or hemorrhagic stroke included in the Lausanne Stroke Registry underwent cerebral blood flow measurement using I-123-IMP and 99mTc-HMPAO single photon emission tomography (SPECT). Our findings suggest that neuropsychological disturbances are not systematically correlated to cortical hypoperfusion secondary to the deep lesion (diaschisis). The role of cortical diaschisis was especially prominent in patients with aphasia and left subcortical lesion.

We report the case of a 59-year old right-handed woman presenting with progressive aphasia without any other neurological deficit and characterized by anomia, agramatism and auditory comprehension difficulties. CT scan showed no abnormalities. Four years later, aphasia was complete but neurological examination was normal. CT scan disclosed a mild cortico-subcortical cerebral atrophy with slight widening of both sylvian fissures. The results obtained with the Wisconsin Card Sorting Test and the Raven's Matrices showed only minor deficits. The IQ (WAIS) was 90. During the following 6 years the patient remained fully self-sufficient and carried out her homework normally. At that time MRI showed progression of cerebral atrophy more pronounced on the left side. Besides a rapid deterioration, twelve months later she developed severe dementia and died 13 years after the onset of the illness. Brain examination disclosed a severe atrophy (brain weight: 880 g) prominent in both frontal lobes and in the anterior perisylvian structures, more pronounced on the left side. There were no vascular lesions. Microscopy revealed widespread neuronal loss and astrocytic fibrillary gliosis confined to cortical areas and vacuolation in the superficial layers. Neurofibrillary tangles and neuritic plaques were found in the most atrophic areas but not in sufficient number to fulfill the histological criteria for Alzheimer's disease. There were no neuropathological changes of Pick's disease or subcortical degeneration. Previous microscopical studies of primary progressive aphasia showed non specific, mostly lobar atrophy similar to that observed in our case, although Alzheimer, Pick and Creutzfeldt-Jakob diseases have been reported. This neuropathological heterogeneity confirms that progressive aphasia is a non-specific language disorder mostly observed in lobar forms of brain degeneration.

We report a of gelastic epilepsy. MRI showed a probable hamartoma in the diencephalic region.

Mental disorders after closed-head injury are reviewed. Post-concussive syndrome and post-contusional disability are described with particular emphasis on consciousness disorders, amnesia, frontal disturbance and long-term outcome.

Detailed study of the communication of one of the patients followed-up by Deonna et al. (1989) who has been suffering since age seven of an atypical acquired aphasia-epilepsia syndrome. Seizures as well as peculiar verbal productions persist at adult age. After a thirty year follow-up, only a small lexicon has been acquired, mostly made of onomatopeia and idiosyncrasies. We describe this lexicon and discuss the quality of the communication in a real-life ecological situation. We then compare it to the jargon and the aphasic productions of the standard neuropsychological examination.

This paper reviews the literature on clinical signs such as imitation behavior, grasp reaction, manipulation of tools, utilization behavior, environmental dependency, hyperlexia, hypergraphia and echolalia. Some aspects of this semiology are of special interest because they refer to essential notions such as free-will and autonomy.

We report here with a case of religious delusion in a 39 years old woman. She had suffered a head injury with right temporal concussion 13 years before but had no earlier history of psychiatric disorder. In view of the fact that this acute psychiatric state lasted for a short duration of time and that personality and affects were preserved, this incident is compared to the schizophreniform disorder of the type DSM-III-R. The hypothesis of an acquired predisposition due to head injury has been put forward as an explanation.

Two patients with bilateral thalamo-mesencephalic infarct in the paramedian territory developed vertical gaze dysfunction and marked behavioural changes, in the absence of significant motor inability and formal neuropsychological impairment. While they were physically and emotionally active before stroke, they became apathetic, aspontaneous, indifferent, and seemed to have lost motor and affectic drive, as well as the need itself for any psychic activity. However, this mental and motor inertia was reversible when the patients were repeatedly stimulated by another person. This need for constant external programming, together with a lack of emotional reactivity, made the patients resemble robots. CT and MRI suggested involvement of the dorsomedial and midline nuclei of the thalamus, and SPECT showed remote frontomesial hypoperfusion. A disturbance of the striatal-ventral pallidal-thalamic-frontomesial limbic loop is suggested by previous reports of a similar "loss of psychic self-activation", "pure psychic akinesia", or "athymhormia" with bipallidal, bistriatal, or subcortical bifrontal lesions.

We report a case of delusion characterized by a time disorientation with a constant three days advance. Five years previously, the patient had suffered a left hemisphere stroke with aphasia. The delusional belief appeared at the same time as a cortical deafness following a second right hemisphere infarction. There was severe behaviour disturbances which lasted seven months, then cleared without any other change in the clinical picture. The lesions involved the left parietal lobe as well as the temporal and insular regions of both hemispheres.

Case report. A 50-year-old, right-handed, French-speaking, Spanish worker was admitted 3 weeks after an acute right hemiparesis with"hyperproductive" global aphasia. He produced meaningless nonphonemic sounds("brr," "prck," "pfft"), accompanied by an emotional display of unmotivated laughing, crying, childish behavior, and transient anger, lasting for hours, in a pseudo-hebephrenic manner. He also hummed "Gregorian chants." He could not follow simple commands, imitate gestures, read, or write. He showed utilization behavior, manipulation of objects, and an inappropriate tendency to attempt to undress the examiner, but no grasping or cephalic frontal reflexes. On neurologic examination, severe right sensorimotor flaccid hemiparesis was found, with corticobulbar signs and left Horner's sign. On MRI, a subacute infarct was found in the deep territory of the left middle cerebral artery (MCA) and bilateral anterior cerebral arteries (ACAs)(figure), with hypoplasia of the A1 segment on the right. Doppler ultrasound of precerebral vessels was normal. On transthoracic echocardiography, atrial septal aneurysm was …

Four of 1,200 consecutive patients with their first stroke showed acute transcortical mixed aphasia (TMA) characterized by nonfluent speech with impaired naming, semantic paraphasias, echolalia, impaired comprehension, good repetition, reading, and writing on dictation. All 4 had left internal carotid artery (ICA) occlusion with ipsilateral anterior pial territory infarction (precentral-central sulcus artery territory) and watershed infarction between the middle and posterior cerebral artery territories, which spared and 'isolated' the perisylvian speech areas. Although rare, acute TMA is highly suggestive of infarction due to ICA occlusion, in that it is probably related to simultaneous embolism (anterior pial infarction) and haemodynamic insufficiency (posterior watershed infarction).