Ipsilateral neglect in a patient following a unilateral frontal lesion.

Using a crossed-response task, it has been demonstrated that as a patient with unilateral frontal lesion recovers from visual inattention, he or she may inappropriately saccade to contralateral stimuli (visual grasp). We report a patient with a right frontal lesion who showed a similar phenomenon on sequential line bisection tasks. On day 1, he showed left-sided neglect on line bisections that enhanced with sequential trials. On day 5, he exhibited right-sided neglect (ipsilateral neglect) on line bisection tasks that also enhanced with repeated trials.     

Neglect: the phenomena of unilateral neglect following brain damage

The term "neglect" designates various kinds of failure to orient or respond to or to report stimuli appearing at the side contralateral to a cerebral lesion. This failure cannot be explained by primary sensory or motor disorders. Essentially the following symptoms of neglect have been reported: inattention to visual (or) acoustical stimuli in one hemifield under unilateral and simultaneous bilateral presentation reduction in orienting responses (eye and head movements) to the neglected hemispace and deviation of head and gaze axes towards the intact hemispace omission or incomplete reproduction of one side of a figure of a text when copying or drawing from memory omission of one half of a well-known scene or picture when reporting from memory deviation of the egocentre as tested by visual, acoustic and somatesthetic stimuli towards the intact hemispace reduction of motor activities, especially for the extremities of one half of the body, which cannot be attributed to a sensory motor deficit inattention to somatesthetic stimuli presented on one side of the body displacement of somatesthetic stimuli, presented on the affected body side, to the intact body side lack of "awareness" of the existence of one half of the body, resulting in, e.g., ignoring this body half when washing or dressing "reference" of the neglected body half to another person unawareness or denial of severe sensorimotor deficits (e.g. hemiparesis) in the affected body half. The syndrome of neglect should be carefully differentiated from inattention phenomena resulting from primary sensory (e.g. hemianopia, restriction of field of search) and motor deficits (hemiparesis, hemiakinesis). In some cases this differentiation is rather difficult, because both types of inattention may be combined. Thus, detailed testing of sensory and motor disorders is needed in order to avoid any precipitate diagnosis of "neglect". The neuropathology of the neglect syndrome is not yet known precisely. Damage to the parietal lobe (presumably of the nondominant hemisphere) is the most common cause for neglect. Lesions at the bank of the sulcus intraparietalis seem especially crucial. Lesions in the dorsolateral frontal lobe causing neglect are mainly situated in Brodmann's premotor areas 8, 9 and 46. Furthermore, lesions of the anterior cingular cortex (area 24), of the thalamus (intralaminar nuclei, nucleus ventralis lateralis, pulvinar) and of the basal ganglia seem to induce neglect.     

Visual hemispatial inattention: stimulus parameters and exploratory strategies.

Patients with unilateral hemispheric lesions were given visual target cancellation tasks. As expected, marked contralateral and less severe ipsilateral visual inattention were observed in patients with right-sided cerebral lesions whereas those with left-sided lesions showed only mild contralateral neglect. Stimulus material (shapes vs letters) and array (random vs structured) interacted in a complex manner to influence target detection only in patients with right-sided lesions. Furthermore, the search strategy of these patients tended to be erratic, particularly when the stimuli were in an unstructured array. A structured array prompted a more systematic and efficient search. It appears, therefore, that stimulus content and spatial array affect neglect behaviour in patients with right-sided lesions and that a lack of systematic visual exploration within the extrapersonal space is one factor that contributes to visual hemispatial inattention.     

Effects of right-hemisphere cortical infarction and muscarinic acetylcholine receptor blockade on spatial visual attention performance in rats

The syndrome of hemispatial neglect is defined as an inability to report, respond or orient to stimuli contralateral to a cerebral lesion despite intact elementary sensory or motor function. This syndrome is typically observed after lesions of the right cerebral cortex, and has been associated with impairment of attention. We studied whether visual attention performance is impaired after right-hemisphere infarction in rats. Using a behavioural paradigm measuring spatial visual attention, we tested the effects of photothrombotic infarction to either the frontal cortex or the parietal cortex on attention performance. Since the cholinergic system is known to modulate attention performance, we additionally evaluated the role of cholinergic receptor blockade with scopolamine in our task paradigm. Our results show a transient response bias immediately after cortical infarction, with a decrease in contralesional responses and an increase in contralesional omissions after frontal infarction. Parietal infarction and systemic administration of scopolamine also resulted in a decrease in correct responses and an increase in omissions, but without a difference in side responding. In conclusion, right frontal infarction induces a transient impairment in contralesional spatial visual attention that we explain as left-sided neglect. Right parietal infarction and cholinergic blockade shows non-lateralized deficits in spatial visual attention, suggestive of global attentional impairment. We postulate that both effects of cortical infarction on attention performance may be related to cholinergic dysfunction. Our study confirms the role of frontal and parietal cortices in attention performance in rats, and corroborates the theory that attention performance is impaired in hemispatial neglect in human stroke patients.     

The effect of lateralized dynamic stimuli on unilateral spatial neglect following right hemisphere lesions

Patients with unilateral (left-sided) spatial neglect following right-hemisphere stroke were tested for the effects of visual stimulation on performance of a line-bisection task. As predicted from research on brain mechanisms of spatial orientation and attention, dynamic visual stimuli presented on the left side substantially reduced neglect in the task. In contrast, left sided static stimuli reduced neglect significantly less and dynamic stimuli presented in the center had no effect on neglect. Neglect patients with hemianopia did not show significantly less benefit of left-sided dynamic stimuli compared to neglect patients without hemianopia, suggesting that the effect of these stimuli was unconscious and automatic. The potential advantages of lateralized dynamic stimuli in the rehabilitation of neglect are discussed.     

Persistent denial of handicap after infarction of the right basal ganglia: a case study.

A case is reported of persistent denial of handicap following stroke. Hemiplegia was due to infarction involving only sub-cortical structures, and there was no associated visual or sensory neglect or inattention, and no evidence of dementia.     

Sensory inattention produced by 6-hydroxydopamine-induced degeneration of ascending dopamine neurons in the brain

Unilateral 6-hydroxydopamine-induced degeneration of ascending dopamine neurons caused a pronounced deficiency in the ability of rats to orient toward sensory stimuli presented on the contralateral side of the body. The behavior of the animals went through three phases: The first 2 days after the operation the animals showed great individual variations with hypo- as well as hyperreactivity on the contralateral side. This phase coincided with the degeneration of the dopamine neurons. The second phase lasted from the third to the fifth day and was characterized by contralateral inattention to olfactory, tactile, auditory, and visual stimuli. The third phase started on Day 6 and was characterized by gradual recovery in the reaction to sensory stimuli. The fact that an animal was able to respond to olfactory, auditory, and visual stimuli at a time when it was not able to orient toward a tactile stimulus shows that the deficiency was not due to a motor impairment. The animals never regained their ability to orient toward tactile stimuli. The findings provide strong evidence that the syndrome of sensory inattention was due to a degeneration of ascending dopamine neurons, most probably the nigrostriatal pathway. The syndrome is interpreted as a disruption of sensory motor integration.     

Contralesional directional hypermetria associated with line bisection-specific ipsilesional neglect

Patients with contralesional neglect from right hemisphere injuries often fail to be aware of or respond to visual stimuli in the left hemispace. In contrast, other patients with right hemisphere damage rarely demonstrate behavior consistent with task-specific ipsilesional neglect (IN). We performed a series of experiments in a patient with IN on a line bisection task after a right frontal infarct. When asked to perform horizontal limb movements without visual feedback, the patient showed a leftward directional hypermetria. Similar performance was also observed during a representational production of a given distance without sensory input. These results suggest that IN is induced by a directional hypermetria resulting from disruption of the motor-intentional system.     

Clinical aspects and mechanisms of visual-spatial neglect

Several interpretations have been advanced to explain the nature of unilateral spatial neglect. According to some authors, unilateral neglect could be due to a sensory deficit or to an oculomotor disorder hampering the patient from completely exploring the half space contralateral to the damaged hemisphere. According to other authors, the unilateral neglect syndrome could result either from a mutilation of the inner representation of the outside space or from a lack of attention for stimuli falling in the half space opposite to the hemispheric locus of lesion. We have wondered whether the relationships between unilateral neglect and hemispheric lateralization could not help to understand the nature of the neglect phenomena. A retrospective analysis of data gathered in neuropsychological literature, and results of an experimental study in which we had contrasted results obtained on an "overlapping figures" task and on a visual search task and a qualitative analysis of neglect phenomena observed in right brain-damaged patients, have led to the following conclusions: a) unilateral neglect is specifically linked to right hemisphere lesions in tasks requiring extraction of information from the central part of the visual field, whereas no difference between right-sided and left-sided lesions is observed on tasks requiring a full exploration of extra-personal space; b) tasks selectively affected in right brain-damaged patients require an automatic orienting of attention toward the more peripheral parts of the stimuli, which could be partly impaired owing to an early orientation of attention toward the right side of the pattern and a subsequent difficulty to detach attention from this early focus to orient it toward parts fo the stimulus lying in the left half space.     

Impaired spatial working memory: one component of the visual neglect syndrome?

Both impaired spatial working memory (SWM) and unilateral neglect may follow damage to the right parietal lobe. We propose that impaired SWM can exacerbate visual neglect, due to failures in remembering locations that have already been searched. When combined with an attentional bias to the ipsilesional right side, such a SWM impairment should induce recursive search of ipsilesional locations. Here we studied a left neglect patient with a right temporoparietal haemorrhage. On a nonlateralised, purely vertical SWM task, he was impaired in retaining spatial locations.

In a visual search task, his eye position was monitored while his spatial memory was probed. He recursively searched through right stimuli, re-fixating previously inspected items, and critically treated them as if they were new discoveries, consistent with the SWM deficit. When his recovery was tracked over several months, his SWM deficit and left neglect showed concurrent improvements. We argue that impaired SWM may be one important component of the visual neglect syndrome.     

Upper visual space neglect and motor deficits after section of the midbrain commissures in the cat

The neurological deficits following section of the midbrain commissures were studied in the cat. After a lesion of the commissures between the superior and inferior colliculi, with or without involvement of the posterior commissure, the animals showed a long lasting inattention for stimuli in the upper visual space, lack of exploratory head movements towards the neglected space, head ventroflexion and vertical paralysis of gaze. After a lesion of the commissure between the superior colliculi or of its rostral part only, the same symptomatology appeared, but it was short lasting. After a lesion of the posterior commissure, the head was kept dorsiflexed, the exploratory head movements towards the lower visual space were reduced and the stimuli presented in this space were often neglected. There was a paralysis of vertical eye movements. The findings are discussed in the frame of a premotor theory of neglect.     

Lateralised cortical activity due to preparation of saccades and finger movements: a comparative study

The topography and time course of event-related asymmetries of the EEG associated with horizontal saccadic eye movements and finger movements was compared in a 4-choice response task, where the subjects had to respond to the imperative stimulus (S2) by moving the right or left index finger or by making a saccade to the right or the left. The cue stimulus (S1) contained full, partial, or no information about the direction and the effector. In case of finger movements 3 distinct lateralisations were found: (1) increased negativity over the motor cortex contralateral to the future movement direction, (2) increased contralateral negativity at temporoparietal sites beginning 200 ms after delivery of the directional information, and (3) increased ipsilateral negativity at temporo-parietal sites beginning 350–500 ms after delivered direction and effector information. The early temporo-parietal lateralisation was also visible in case of saccadic eye movements and in case of effector-unspecific directional information. Before saccadic eye movements no other distinct lateralisation could be observed at any recording site. In sum, lateralised cortical activities due to preparation processes for finger movements and due to effector-unspecific processing of directional information for motor preparation by the posterior parietal cortex could be demonstrated, whereas no distinct lateralisation due to preparation for saccadic eye movements was visible.     

Loss of left-sided volitional movements caused by a combined lesion of the corpus callosum and right hemisphere:'initiation pseudohemiakinesia'

We report a right-handed patient who showed a marked loss of unilateral volitional movements of the left limbs after the onset of a cerebral infarction in the combined territories of the right anterior and middle cerebral arteries. The same limbs retained their mobility in acts requiring bilateral sides of the body. This left-sided abnormal behavior resembled motor neglect resulting from lateralized brain damage. Behavioral and neuroradiological findings presented by this patient, however, suggested that callosal disconnection was definitely involved in this symptomatology. We postulate that in this patient, the diseased right hemisphere could no longer initiate movements of the left limbs despite its potential ability to realize them, and that the injured callosum prevented the intact left hemisphere from initiating unilateral voluntary movements of the left limbs. We suggest that this so far undescribed symptomatology be called 'initiation pseudohemiakinesia' in order to be distinguished from other rare forms of unilateral voluntary movements like motor neglect, extinction or directional hypokinesia.     

Non-dominant hemisphere syndrome as a result of a right thalamic infarct: an anatomoclinical case

A 71 year old man had a massive left sensory deficit and hemiplegia, with left heminanopia, visual neglect and constructional apraxia. Moreover he experienced an extra-left arm and illusions of movements. 3 weeks later he suffered "thalamic" pain on left side; he died suddenly 6 weeks after the stroke. Post-mortem examination revealed: a) a right inner temporal and occipital infarction; b) a right thalamic infarction in the thalamogeniculate and paramedian territories; c) an infarction in the adjacent right internal capsule. Considering this case and pertinent literature on clinicopathological studies of right thalamic infarction, the authors suggest that a simultaneous ischaemia of thalamogeniculate and paramedian territories should be necessary to induce somatognosic and visuospatial disturbances.     

Pineal lesion produces bilateral visual and auditory inattention in the rat

Unilateral lesions in such brain regions as medial frontal cortex and superior colliculus produce polysensory neglect contralateral to the lesion. Since the pineal gland is an unpaired brain structure, both electrophysiologically and hormonally responsive to visual and auditory stimulation, it may modulate bilateral sensory attention mechanisms. Long-Evans male rats were given pineal or sham lesions and were tested behaviourally. Sensory assessment revealed that in comparison to sham animals rats with pineal lesion exhibited unilateral visual and auditory neglect to stimuli presented on either side of the body. Animals with pineal lesions were more likely than sham-lesioned animals to demonstrate visual allesthesis and, compared to sham-lesioned rats, showed extinction on the left side to bilateral simultaneous visual stimulation. This is the first report that midline neuroendocrine damage can produce bilateral sensory inattention.     

"Bottom-up" and "top-down" effects on reading saccades: a case study

OBJECTIVE: To investigate the role right foveal/parafoveal sparing plays in reading single words, word arrays, and eye movement patterns in a single case with an incongruous hemianopia. METHODS: The patient, a 48-year-old right handed male with a macular sparing hemianopia in his left eye and a macular splitting hemianopia in his right eye, performed various reading tasks. Single word reading speeds were monitored using a "voice-trigger" system. Eye movements were recorded while reading three passages of text, and PET data were gathered while the subject performed a variety of reading tasks in the camera. RESULTS: The patient was faster at reading single words and text with his left eye compared with his right. A small word length effect was present in his right eye but not his left. His eye movement patterns were more orderly when reading text with his left eye, making fewer saccades. The PET data provided evidence of "top-down" processes involved in reading. Binocular single word reading produced activity in the representation of foveal V1 bilaterally; however, text reading with the left eye only was associated with activation in left but not right parafoveal V1, despite there being visual stimuli in both visual fields. CONCLUSIONS: The presence of a word length effect (typically associated with pure alexia) can be caused by a macular splitting hemianopia. Right parafoveal vision is not critically involved in single word identification, but is when planning left to right reading saccades. The influence of top-down attentional processes during text reading can be visualised in parafoveal V1 using PET.     

Spatial neglect

Unilateral spatial (hemi-)neglect or (hemi-)inattention are clinical terms used to describe a number of different clinical symptoms which have in common the patient's failure to attend to, respond adequately to, or orient voluntarily to people or objects in the contralesional space. Unilateral spatial neglect is most often observed following brain lesions affecting the right hemisphere, and in particular the right inferior parietal cortex (angular and supramarginal gyrus) and right temporoparietal junction. Importantly, the term hemineglect cannot be meaningfully used if the target behavior is explained by primary sensory or motor deficits only. Typically the patient's deficit is supramodal: patients with hemineglect fail to respond to novel or meaningful stimuli irrespective of whether they are presented in the visual, auditory, and somesthetic (somatosensory) domain. As adequate perception and spatial representation of both the body and the outside world are mandatory for almost all activities of daily living, hemineglect is known to limit the degree of active participation in rehabilitation programs and is thus commonly associated with poor functional recovery and less successful social reintegration. A number of new promising behavioral and pharmacological treatments may help to ameliorate neglect in the future.     

Visual hemineglect and hemihallucinations in a patient with a subcortical infarction

An alcoholic patient with a mainly right subcortical infarction developed contralateral left-sided neglect and then, in the context of alcohol withdrawal, unilateral hallucinations in the non-neglected right hemispace. It is hypothesized that an interruption of the striatocortical pathways could prevent the right hemisphere from representing appropriately internally produced stimuli.     

The contribution of the 'second' visual system to directed visual attention in man

The visual functions of a patient suffering from a brain lesion incorporating the left n. pulvinar was examined in order to assess the contribution of this structure to human vision. With the exception of the following abnormalities visual functions were normal. First, there was a decrease in the critical flicker frequency in the periphery (but not in the parafoveal region) of the right visual hemifield, that is, that contralateral to the pulvinar lesion. However, the second and most striking characteristic was--as shown by presenting visual stimuli bilaterally and simultaneously-a 'neglect' for the periphery of this contralateral visual half-field. This 'neglect' was a function of (a) position in the visual field (eccentricity), (b) stimulus properties (size and luminance), (c) temporal properties (length of presentation and interstimulus interval). In addition to this reduced capacity to detect stimuli appearing in the periphery of the right visual hemifield, there was also prolonged latency of visually evoked saccadic eye movements and a paucity of spontaneous eye movements directed towards the right visual hemifield. These results are interpreted in terms of a contribution of the n. pulvinar to the detection of light stimuli presented in the periphery of the visual field, and support the view that the tectopulvinar extrastriate visual pathway plays an important role in the control of visual attention.     

Directional hypokinesia: prolonged reaction times for leftward movements in patients with right hemisphere lesions and neglect

Patients with hemispatial neglect perform activities poorly in the hemispace contralateral to the lesion. We postulate that hemispatial neglect induced by right hemisphere lesions may be associated with a directional hypokinesia: initiation of movements toward the hemispace contralateral to the lesion is affected more than movements toward the lesion. We tested 6 patients with hemispatial neglect caused by right hemisphere damage, 7 with left hemisphere damage and no neglect, and 12 controls. Patients with left hemispatial neglect initiated responses to left hemispace more slowly than toward right hemispace.