STUDY - Technical - New Dacian's Medicine
Aphasia
and other Focal Disorders (4)
Translation Draft
Let me now switch to the parietofrontal network for spatial orientation presenting some elements about neglect and related states. Several clinical syndromes are recognized after deficits in this function. These syndromes are hemispatial neglect, Balint syndrome, simultanagnosia, dressing apraxia and constructive apraxia.
I'll start with the hemispatial neglect. Adaptive orientation to significant events in extra-personal space is served by a large neural network containing three major cortical components.
The cingulate cortex provides access to the limbic-motivational representation of extrapersonal space, the posterior pariental cortex, sensory representation and frontal visual fields in the frontal lobe, motor-exploratory representation. The subcortical components of this network include the striated and pulvinary talcus of the thalamus.
Contralezional hemispatial neglect is the result of damage to any subcortical or cortical component of this network. The traditional conception that hemispatial neglect always reflects a pariental lobe lesion is incorrect.
Corresponding to this anatomical organization, the clinical picture of neglect has three behavioural manifestations: 1. sensory events (or their mental representation) in neglected hemispace have a lower impact on the state of consciousness in general 2. acts of exploration and orientation towards neglected hemispace are rare and 3. the patient behaves as if the neglected hemispace is devalued motivationally.
The neural organization of spatial orientation shows a dominance of the right hemisphere. The right hemisphere directs attention to the entire extrapersonal space, while the left hemisphere directs attention only to hemispace as a contralateral. Unilateral damage to the left hemisphere does not cause contralezional neglect, since the ipsiversive attentional mechanisms of the right hemisphere may compensate for the loss of the functions of the left hemisphere of counterlateral attention direction.
However, unilateral damage to the right hemisphere causes severe left contralezional hemispatial neglect, since the unaffected left hemisphere does not contain ipsiversive attentional mechanisms. Consequently, contralezional neglect is much more frequent, severe and lasting after damage to the right hemisphere than after damage to the left hemisphere.
Severe neglect for right hemispace is rare, even in lefties with lesions in the left hemisphere. Patients with severe neglect may be unable to dress, shave or care for the left side of their body, cannot eat what is placed on the left side of the plate, and cannot read the left half of the sentences.
When the examiner draws a large circle (about 15 cm in diameter) and asks the patient to place numbers from 1 to 12, as if the circle were the dial of a clock, there is a tendency to squeeze the numbers into the right half, leaving the left half empty. Asked to copy a simple drawing, the patient does not copy the details on the left, and when asked to write, there is a tendency to leave an unusually wide edge on the left.
Simultaneous bilateral stimulation and elimination of visual targets are two tests that can be performed at the patient's bedside, useful in assessing neglect. In the first test, the examiner stimulates either unilaterally or bilaterally simultaneously the visual, auditory and tactile pathways.
After damage to the right hemisphere, the patient, who has no difficulty detecting unilateral stimuli on either side, receives bilateral stimulation as coming only from the right. This phenomenon is called extinction and is a manifestation of alteration of sensory representation from hemispatial neglect.
In the target detection test, targets (e.g. letter A) are mixed with other graphics (e.g. other letters of the alphabet) on a sheet of Type A4 paper and the patient is asked to circle them. The inability to detect targets on the left is the manifestation of exploratory deficiency in hemispatial neglect.
Hemianopsia itself does not interfere with the fulfilment of this requirement, since the patient can rotate his head and eyes to the left. The normal trend in this test is to start from the left upper quadrant and move systematically horizontally and vertically. Some patients tend to start right and continue at random.
This is a subtle manifestation of left neglect, even if the patient eventually manages to find all the necessary targets. Some neglected patients may also deny the existence of hemiparesis or hemihypoesthesia or even the fact that the paralyzed limb belongs to them, a manifestation called anosognosia.
Clinical manifestations of neglect are not the same in all patients. In general, lesions that are located around the frontal component of the spatial orientation network mainly cause a neglect syndrome with more advanced motor-exploratory deficits, while lesions around the parietal component more frequently cause a neglect syndrome with the dominance of sensory representation deficits.
The most common causes of hemispatial neglect are cerebrovascular lesions or neoplasms in the right hemisphere. Depending on the location of the lesion, neglecting patients may also experience hemiparesis, hemihypoesthesia and hemianopsia on the left, but these symptoms do not appear constantly.
To move now to Balint syndrome, simultanagnosia, dressaxia and constructive apraxia. Bilateral network damage for spatial orientation, especially its parietal components, leads to a state of severe spatial disorientation, known as Balint syndrome.
Balint syndrome involves alterations in the systematic visual exploration of the surrounding space (oculomotor apraxia) and of the achievement of a visual target by hand (optical ataxia). The third and most serious manifestation of Balint syndrome is simultanagnosia which designates the inability to integrate visual information from the center of the eye with that of the periphery.
Patients notice the details that enter the eye focus without trying to explore the surrounding space for further information. Patients with simultagnosia "don't see the forest because of the trees". Complex visual scenes cannot be viewed in their entirety, which leads to a severe limitation in the ability to identify objects and scenes.
For example, a patient who is shown a table lamp and asked to name the object can only observe its circular base, naming it an ashtray. Some patients with simultanagnosia report that the objects they are looking at suddenly disappear, which probably reflects the inability to return to the initial point of view after a short jerky shift.
Movement and distracting stimuli greatly exacerbate the difficulties of visual perception. Simultagnosia can sometimes occur unaccompanied by the other two manifestations of Balint syndrome. A modified form of the letter-removal test described above can be used to diagnose simultagnosis.
In this test, several targets (A letters) are drawn much larger than the others (approximately 10 cm in height compared to an average size of 2 to 3 cm) and all targets are mixed among the other graphics. The patient with simultanagmousity presents a counter-intuitive but characteristic tendency not to notice the large targets.
This is because the information needed to identify large targets cannot be compressed to a smaller field of view, obtaining it requiring the integration of visual information along a wider field of view.
Also, the greater difficulty of detecting larger targets shows that it is not the decrease in acuity that is responsible for altering visual function and that the problem is rather central and not peripheral. Balint syndrome is caused by bilateral dorsal parietal lesions (these are usually caused by the infarction of the vascular crossing area, located between the territories of the cerebral and posterior arteries, hypoglycaemia, sagittal sinus thrombosis or degenerative diseases such as Alzheimer's disease).
In patients with Balint syndrome due to a stroke, alterations in the bilateral field of vision (usually anopsia of the lower quadrant) frequently occur. Another manifestation of bilateral dorsal parietal lobe damage (or only on the right) is the apraxia of dressing. The patient with this disorder cannot align the axis of the head with that of the coat he wants to wear and can be seen making efforts while holding the coat at the bottom or stretching his arm in a fold of it rather than up his sleeve.
Injuries that comprise the posterior parietal cortex in the right hemisphere also cause severe difficulties in copying simple drawings. This manifestation is called constructive apraxia. In some patients the difficulties of drawing are limited to the left side of the figure and represent a manifestation of the neglect of hemispace (in others there is a more general deficiency in the reproduction of contours and graphics in a three-dimensional perspective). Clothing and constructive apraxia are specific manifestations within a more general alteration of spatial orientation.
I will complete this post with some presentations related to the occipitotemporal network of object recognition (prosopagnosia and agnosia for objects). Perceived information related to physiosomes and objects is initially encoded in the primary visual cortex (striated) and the visual areas of side-by-side peristriate association (upstream).
Next, the information is transmitted first to the occipitotemporal visual areas of downstream association and then to other heteromodal and paralimbic cortical areas. Bilateral lesions in the fusiform and lingual gyrus in the occipitotemporal cortex interrupt this flow and interfere with the correctly perceived ability of information to activate the distributive multimodal associations leading to the recognition of figures and objects.
The resulting alterations of the recognition of physiognomies and objects are known as prosopagnosia and agnosia for objects. Patients with prosopagnosia cannot recognize familiar figures, sometimes even reflecting their own mirror image. This is not a lack of perception, since patients with prosopagnosia can easily tell whether two figures are identical or not.
Moreover, prosopagnosic patients who cannot recognize a close person only by physiognomy, can recognize it using auditory cues if they are allowed to listen to their voice. Thus, the prosopagnosia deficiency is specific and reflects the existence of a lesion that prevents the activation of intact multimodal schemes by relevant visual stimuli.
The deficit in prosopagnosia is not limited to the recognition of physiognomies, but also extends to the recognition of individual components of a broad generic group of objects. For example, prosopagnozic patients typically have no difficulty in identifying a figure as a figure or a car as a car, but cannot recognize the identity of a particular figure or car.
This reflects the deficit of visual recognition of traits that individualize the components of an object class. When recognition problems generalize, extending to the generic identification of common objects, the manifestation is called visual agnosia for objects. Unlike prosopagnosic patients, those with object agnosia cannot recognize a figure as a figure or a car as a car.
It is important that the agnosia for objects is distinguished from the anomie. Patients with anomie cannot name the object, but they can describe its use. On the contrary, the patient with visual agnosia is unable either to name a visually presented object or to describe its use.
Characteristic lesions in prosopagnosia and agnosia for objects are bilateral infarctions in the territory of the posterior cerebral artery and comprise lingual and fusiform gyrus. Associated deficits may be alterations in the field of vision (especially anopsia in the upper quadrant) or lack of color perception of central origin called acromatopsia.
Rarely, the responsible injury is one-sided. In such cases, prosopagnosia is associated with lesions in the right hemisphere, and agnosia for objects with lesions in the left hemisphere. As we have shown previously, patients with Balint syndrome also exhibit severe difficulties in visual recognition, based on abnormalities of the integration of visual perceptions.
The lack of recognition of physiosomes and objects in Balint syndrome is known as aperceptive visual agnosia, while prosopagnosia and visual agnosia for objects are associative agnosias because they are determined by the inability of a normal perception to evoke relevant multimodal associations.
Let me now switch to the parietofrontal network for spatial orientation presenting some elements about neglect and related states. Several clinical syndromes are recognized after deficits in this function. These syndromes are hemispatial neglect, Balint syndrome, simultanagnosia, dressing apraxia and constructive apraxia.
I'll start with the hemispatial neglect. Adaptive orientation to significant events in extra-personal space is served by a large neural network containing three major cortical components.
The cingulate cortex provides access to the limbic-motivational representation of extrapersonal space, the posterior pariental cortex, sensory representation and frontal visual fields in the frontal lobe, motor-exploratory representation. The subcortical components of this network include the striated and pulvinary talcus of the thalamus.
Contralezional hemispatial neglect is the result of damage to any subcortical or cortical component of this network. The traditional conception that hemispatial neglect always reflects a pariental lobe lesion is incorrect.
Corresponding to this anatomical organization, the clinical picture of neglect has three behavioural manifestations: 1. sensory events (or their mental representation) in neglected hemispace have a lower impact on the state of consciousness in general 2. acts of exploration and orientation towards neglected hemispace are rare and 3. the patient behaves as if the neglected hemispace is devalued motivationally.
The neural organization of spatial orientation shows a dominance of the right hemisphere. The right hemisphere directs attention to the entire extrapersonal space, while the left hemisphere directs attention only to hemispace as a contralateral. Unilateral damage to the left hemisphere does not cause contralezional neglect, since the ipsiversive attentional mechanisms of the right hemisphere may compensate for the loss of the functions of the left hemisphere of counterlateral attention direction.
However, unilateral damage to the right hemisphere causes severe left contralezional hemispatial neglect, since the unaffected left hemisphere does not contain ipsiversive attentional mechanisms. Consequently, contralezional neglect is much more frequent, severe and lasting after damage to the right hemisphere than after damage to the left hemisphere.
Severe neglect for right hemispace is rare, even in lefties with lesions in the left hemisphere. Patients with severe neglect may be unable to dress, shave or care for the left side of their body, cannot eat what is placed on the left side of the plate, and cannot read the left half of the sentences.
When the examiner draws a large circle (about 15 cm in diameter) and asks the patient to place numbers from 1 to 12, as if the circle were the dial of a clock, there is a tendency to squeeze the numbers into the right half, leaving the left half empty. Asked to copy a simple drawing, the patient does not copy the details on the left, and when asked to write, there is a tendency to leave an unusually wide edge on the left.
Simultaneous bilateral stimulation and elimination of visual targets are two tests that can be performed at the patient's bedside, useful in assessing neglect. In the first test, the examiner stimulates either unilaterally or bilaterally simultaneously the visual, auditory and tactile pathways.
After damage to the right hemisphere, the patient, who has no difficulty detecting unilateral stimuli on either side, receives bilateral stimulation as coming only from the right. This phenomenon is called extinction and is a manifestation of alteration of sensory representation from hemispatial neglect.
In the target detection test, targets (e.g. letter A) are mixed with other graphics (e.g. other letters of the alphabet) on a sheet of Type A4 paper and the patient is asked to circle them. The inability to detect targets on the left is the manifestation of exploratory deficiency in hemispatial neglect.
Hemianopsia itself does not interfere with the fulfilment of this requirement, since the patient can rotate his head and eyes to the left. The normal trend in this test is to start from the left upper quadrant and move systematically horizontally and vertically. Some patients tend to start right and continue at random.
This is a subtle manifestation of left neglect, even if the patient eventually manages to find all the necessary targets. Some neglected patients may also deny the existence of hemiparesis or hemihypoesthesia or even the fact that the paralyzed limb belongs to them, a manifestation called anosognosia.
Clinical manifestations of neglect are not the same in all patients. In general, lesions that are located around the frontal component of the spatial orientation network mainly cause a neglect syndrome with more advanced motor-exploratory deficits, while lesions around the parietal component more frequently cause a neglect syndrome with the dominance of sensory representation deficits.
The most common causes of hemispatial neglect are cerebrovascular lesions or neoplasms in the right hemisphere. Depending on the location of the lesion, neglecting patients may also experience hemiparesis, hemihypoesthesia and hemianopsia on the left, but these symptoms do not appear constantly.
To move now to Balint syndrome, simultanagnosia, dressaxia and constructive apraxia. Bilateral network damage for spatial orientation, especially its parietal components, leads to a state of severe spatial disorientation, known as Balint syndrome.
Balint syndrome involves alterations in the systematic visual exploration of the surrounding space (oculomotor apraxia) and of the achievement of a visual target by hand (optical ataxia). The third and most serious manifestation of Balint syndrome is simultanagnosia which designates the inability to integrate visual information from the center of the eye with that of the periphery.
Patients notice the details that enter the eye focus without trying to explore the surrounding space for further information. Patients with simultagnosia "don't see the forest because of the trees". Complex visual scenes cannot be viewed in their entirety, which leads to a severe limitation in the ability to identify objects and scenes.
For example, a patient who is shown a table lamp and asked to name the object can only observe its circular base, naming it an ashtray. Some patients with simultanagnosia report that the objects they are looking at suddenly disappear, which probably reflects the inability to return to the initial point of view after a short jerky shift.
Movement and distracting stimuli greatly exacerbate the difficulties of visual perception. Simultagnosia can sometimes occur unaccompanied by the other two manifestations of Balint syndrome. A modified form of the letter-removal test described above can be used to diagnose simultagnosis.
In this test, several targets (A letters) are drawn much larger than the others (approximately 10 cm in height compared to an average size of 2 to 3 cm) and all targets are mixed among the other graphics. The patient with simultanagmousity presents a counter-intuitive but characteristic tendency not to notice the large targets.
This is because the information needed to identify large targets cannot be compressed to a smaller field of view, obtaining it requiring the integration of visual information along a wider field of view.
Also, the greater difficulty of detecting larger targets shows that it is not the decrease in acuity that is responsible for altering visual function and that the problem is rather central and not peripheral. Balint syndrome is caused by bilateral dorsal parietal lesions (these are usually caused by the infarction of the vascular crossing area, located between the territories of the cerebral and posterior arteries, hypoglycaemia, sagittal sinus thrombosis or degenerative diseases such as Alzheimer's disease).
In patients with Balint syndrome due to a stroke, alterations in the bilateral field of vision (usually anopsia of the lower quadrant) frequently occur. Another manifestation of bilateral dorsal parietal lobe damage (or only on the right) is the apraxia of dressing. The patient with this disorder cannot align the axis of the head with that of the coat he wants to wear and can be seen making efforts while holding the coat at the bottom or stretching his arm in a fold of it rather than up his sleeve.
Injuries that comprise the posterior parietal cortex in the right hemisphere also cause severe difficulties in copying simple drawings. This manifestation is called constructive apraxia. In some patients the difficulties of drawing are limited to the left side of the figure and represent a manifestation of the neglect of hemispace (in others there is a more general deficiency in the reproduction of contours and graphics in a three-dimensional perspective). Clothing and constructive apraxia are specific manifestations within a more general alteration of spatial orientation.
I will complete this post with some presentations related to the occipitotemporal network of object recognition (prosopagnosia and agnosia for objects). Perceived information related to physiosomes and objects is initially encoded in the primary visual cortex (striated) and the visual areas of side-by-side peristriate association (upstream).
Next, the information is transmitted first to the occipitotemporal visual areas of downstream association and then to other heteromodal and paralimbic cortical areas. Bilateral lesions in the fusiform and lingual gyrus in the occipitotemporal cortex interrupt this flow and interfere with the correctly perceived ability of information to activate the distributive multimodal associations leading to the recognition of figures and objects.
The resulting alterations of the recognition of physiognomies and objects are known as prosopagnosia and agnosia for objects. Patients with prosopagnosia cannot recognize familiar figures, sometimes even reflecting their own mirror image. This is not a lack of perception, since patients with prosopagnosia can easily tell whether two figures are identical or not.
Moreover, prosopagnosic patients who cannot recognize a close person only by physiognomy, can recognize it using auditory cues if they are allowed to listen to their voice. Thus, the prosopagnosia deficiency is specific and reflects the existence of a lesion that prevents the activation of intact multimodal schemes by relevant visual stimuli.
The deficit in prosopagnosia is not limited to the recognition of physiognomies, but also extends to the recognition of individual components of a broad generic group of objects. For example, prosopagnozic patients typically have no difficulty in identifying a figure as a figure or a car as a car, but cannot recognize the identity of a particular figure or car.
This reflects the deficit of visual recognition of traits that individualize the components of an object class. When recognition problems generalize, extending to the generic identification of common objects, the manifestation is called visual agnosia for objects. Unlike prosopagnosic patients, those with object agnosia cannot recognize a figure as a figure or a car as a car.
It is important that the agnosia for objects is distinguished from the anomie. Patients with anomie cannot name the object, but they can describe its use. On the contrary, the patient with visual agnosia is unable either to name a visually presented object or to describe its use.
Characteristic lesions in prosopagnosia and agnosia for objects are bilateral infarctions in the territory of the posterior cerebral artery and comprise lingual and fusiform gyrus. Associated deficits may be alterations in the field of vision (especially anopsia in the upper quadrant) or lack of color perception of central origin called acromatopsia.
Rarely, the responsible injury is one-sided. In such cases, prosopagnosia is associated with lesions in the right hemisphere, and agnosia for objects with lesions in the left hemisphere. As we have shown previously, patients with Balint syndrome also exhibit severe difficulties in visual recognition, based on abnormalities of the integration of visual perceptions.
The lack of recognition of physiosomes and objects in Balint syndrome is known as aperceptive visual agnosia, while prosopagnosia and visual agnosia for objects are associative agnosias because they are determined by the inability of a normal perception to evoke relevant multimodal associations.
Soothing and restful
Sunday!!
Dorin, Merticaru