Tuesday, June 4, 2019
Cognitiveââ¬behavioural Syndromes of Neglect and Anosognosia
Cognitivebehavioural Syndromes of Neglect and AnosognosiaConsidering the neuropsychological diseases discussed during the course, critically comp be and discuss hypothetic interpretations of at least 2 syndromes instinct is one of the most interesting phenomena of the human mind. Consciousness refers to the integration of the cognitive experiences about ego and the external environment (Orfei et al., 2007). However, when this psychological function is rail atd, it may pass along to disfunctions in the aid and cognizance of personal identity. The focus of the following essay is to come through incursion into why the cognitivebehavioural syndromes of degenerate and anosognosia for hemiplegia that occur following the right wayfield hemisphere separatrix develop, and to evaluate to what expiration this is true, taking into consideration their a priori interpretations.Anosognosia has been defined by Babinsky (1914) as an impairment leading to unawareness of neurological a nd cognitive deficits following a adept injury. Individuals who suffer from anosognosia present with locomote impairments which lead to gait and self-care deficits and are unaware of their impairments in functioning (Kortte Hillis, 2010). The syndrome of anosognosia often co-occurs with visuo-spacial neglect (Prigatano et al., 2011). Heilman, Watson and Valenstein (1994) defined neglect as a deterioration in precaution towards or in response to a stimuli, which is not attribut equal to(p) to a push back or sensory impairment. Neglect is presented as a spectrum, with a variety of forms ground on the regions of the lesion, the mode of outputs, reference frame and the sensory modality (Hillis Caramazza, 1995).Alongside their co-occurrence, anosognosia and neglect also overlap in terms of lesion sites, to be more unique(predicate), the right temporo-parietal junction, the superior and middle temporal gyri and the right insula (Beschin, Cocchini, Allen Della Sala, 2012). The lesi on in the right temporo-parietal junction is extremely important in mechanisms of selective attention. More recent neuroimaging studies have recommended that split of the parietal and temporal lens cortex are creating a supramodal structure that interposes goal-directed attention in multiple sensory modalities (Chambers, Stokes Mattingley, 2004). Furthermore, neuroimaging studies show that the insula is very important in self-awareness and in ones convictions about the functioning of their body separate (Karnath, Baier Nagele, 2005).Taking these in consideration, a lesion in these areas will lead to a dysfunction in directional attention towards a specific stimulus and about their beliefs of body parts functioning, therefore affecting the motor system.The two theoretical interpretations that deliver a link mingled with anosognosia and neglect, taking in consideration the dysfunctions presented earlier, are the attentional interpretation simulation for neglect and the feed-f orward illustration for anosognosia.The attentional interpretation model is a model proposed by Heilman et al. (1993) which states that each hemisphere is provided with its own attentional neurological system, with the attentional system in the right hemisphere directing attention towards both sides of the visual field, whereas the attentional system in the remaining hemisphere directing attention merely towards the right visual field. Therefore, if there is a damage to the go away hemisphere, there wont be a severe right neglect, whereas if there is a lesion to the right hemisphere, the diligent will be ineffective to direct his/hers attention to the left visual field (Bisiach et al., 1998).Corbetta et al. (1993) conducted a PET study on 24 healthy volunteers in order to identify what are the neural systems involved in changing spatial attention towards a visual stimulus in the right or left visual field. Results showed that the right parietal cortex was activated when the pa rticipant was required to shift their attention in each visual field, whereas the left parietal lobe was active only when the participants had to diverseness their attention to the right visual field. These finding suggest that the parietal and frontal regions control different aspects of special selection and also support the model proposed by Heilman et al. (1993).However, the attentional interpretation model cannot rate for the dysfunctions in the motor system on its own. Therefore, we have to also take in consideration the attentional-arousal hypothesis and the guiding hypokenisia. The attentional-arousal hypothesis suggests that neglect is predominantly a form of inattention emerging from the failure of triggering arousal that is needed to activate the neuronal systems necessary for spatial attention (Heilman Valenstien, 1972 Watson et al., 1973, 1974). Furthermore, the attentional hypothesis appears to be in close connection with the motor intention, since when one is direc ting his/hers attention towards a specific location, one is also plant to perform an action in that direction (Heilman Valenstien, 2003).Directional hypokenisia suggests that patients who suffer from neglect are reluctant in initiating movements towards the contralesional side. Moreover, even when patients are directing attention towards the omit side and have imposed on them a strategy, their performance not only remained abnormal, but it doesnt improve (Heilman Valenstien, 1979).In a study conducted by Heilman and Valenties (1979), six patients with neglect were asked to identify a letter that was presented either to the left or right at the end of a line, before bisecting it. The task include lines that were placed at either the left of the body midline, the right, or the centre. Results showed that participants performed significantly better when the line was placed to the right side of the body rather than the left side. These results suggest that the neglect syndrome is a defect in the orienting response. Heilman and Valenstien (1979) suggested that this response appears in anticipation of an action, using the increased arousal to lower the sensory threshold. Therefore, lesions induce neglect are affecting the arousal (as previously mentioned via the attentional-arousal hypothesis), leading to the inability of the hemisphere to prepare for the action.Based on the same dysfunction of the computational model of motor control is the feed-forward model for anosognosia. More recent theories established on the recent computational models of motor control proposed by Frith et al. (2000), suggest that anosognosia results from an abnormality in motor planning. This theory suggests that, under normal circumstances, in order to develop the intention to move, forward models are being used in order to arrest accurate indicators about the approaching sensory feedback. However, if an intended movement is not executed as planned, than a comparator will detect a di screpancy between what it was predicted and the absence of sensory feedback. Therefore, this error can be used to inform the motor system of a malfunction. Furthermore, Heilman and colleagues (1998) proposed that anosognosia is a motor intentional deficit which appears from a failure to form motor intentions. Therefore, if the development of an intention to move is deficient, then the comparator doesnt receive any instructions about the outline of the movement and the patient considers that the movement has been executed, although no movement has taken place (Gold et. al, 1994).Fotopoulou et al. (2008) conducted a study in which they investigated the role of motor intention in anosognosic patients compared to non-anosognosic patients by detecting whether the anosognosic patients were able to identify the presence or absence of movement focusing only in the visual evidence. False visual feedback of movement in the left paralysed offshoot was used on four hemiplegic with and four wit hout anosognosic patients. This false visual feedback was delivered using a prosthetic rubber hand. Results showed that patients with anosognosia were more likely than patients without anosognosia to ignore the visual feedback and regard that they moved they hand if there was an intention to move the hand (in the self-generated condition) than when the experimenter moved the rubber hand or when there was no movement. These results support that anosognosia reflects a dominance of motor intention prior to action over the sensory information received by and by the movement was made (Fotopoulou et al., 2008).Although the studies presented above do provide a lot of insight in the computational model of awareness and provide an explanation of why these disorders have symptoms such as dysfunctions in directing attention towards a specific stimulus and also about their beliefs of body parts functioning, there are a few limitations to whether these theoretical interpretations can account b y their one for the two syndromes.Firstly, although they may co-occur, anosognosia and neglect have also been observed separately. Cocchini, et al. (2009) investigated whether anosognosic patients present with unawareness in a group of 42 left hemisphere damaged patients, using a structured interview and the optical-Analogue Test for Anosognosia for Motor Impairment (Della Sala, Cocchini, Beschin Cameron, in press). Their results showed that eight anosognosic patients and another twelve patients who were aware of their motor impairments didnt showed signs of neglect. These results confirm that anosognosia couldnt be thought of always co-occurring with neglect. Secondly, these results also suggest that there is a pronged dissociation between anosognosia and neglect (Bisiach et al., 1986).Dauriac-Le Masson et al. (2002) investigated this double dissociation by looking at two patients with a subacute right hemisphere stroke. Their investigation revealed that one of the patients suffe red from a severe left hemiplegia which was associated with unilateral neglect and he showed signs of being aware of his motor impairment, whereas the second patient showed a severe anosognosia for hemiplegia, therefore with unawareness towards his motor impairment. These results suggest that although these two syndromes co-occur, they may rely on independent mechanisms because of their double dissociation.And lastly, both anosognosia and neglect are multifaceted processes (Marcel et al., 2004) and only the dysfunction in the computational model of motor control cannot account for all the symptoms of these two syndromes. To be more specific, even when patients who suffer from neglect and anosognosia are aware of their deficits, they excuse deny them.House and Hodges (1988) lucubrate the case of an 89-year-old woman who suffered left-side paralysis aft(prenominal) a right-hemisphere stroke. Although the experimenters demonstrated that her left arm was completely paralysed and her leg nearly paralysed, she failed to understand the severity of her condition and believed that she could still look after herself and walk, although she was in a wheelchair. Furthermore, Marcel et al. (2004) also described the case of several patients who although they were aware of their paralysed limbs, they still overestimated their abilities and believed they can perform bi-manual activities such as clapping their hands or tying a knot. These patients provide examples of another theory of anosognosia, the motivational theory which the patient denies his/hers deficit in order to state unharmed his/hers psychological balance (Weinstein Kahn, 1955 Weinstein, 1991).In conclusion, the focus of the essay was to provide insight into why the cognitivebehavioural syndromes of neglect and anosognosia for hemiplegia occur, and to evaluate to what extent this was true, by paying attention to their theoretical interpretations. As stated before, due to the lesions to the tempo-parietal regi on, the gyrus and insula there are dysfunctions in attention and beliefs about body parts functionality. The attentional intention model for neglect (together with the attentional-arousal hypothesis and the directional hypokenisia) and the feed-forward model for anosognosia provide a satisfactory explanation for these deficits by suggesting that there is a dysfunction in the motor system. For the neglect patients the lesions affect the arousal which leads to the inability to prepare them for action. For the anosognosic patients the lesions lead to a failure to form motor intentions, to be more specific if the intention to move is impaired , then the comparator doesnt receive instructions about the planned action and the patient considers that the movement has been executed, even if that didnt happen.However, these theoretical interpretations of dysfunctions in motor control cannot account on their own for all the symptoms of neglect and anosognosia. Previous literature suggests that although the incidence of co-occurrence is high, there are cases where anosognosia and neglect appear independently and present double dissociations. Furthermore, as proposed by Marcel et al. (2004) both syndromes are multifaceted syndromes and it cant be possible that only one theoretical interpretation can account for these.In conclusion, both anosognosia and neglect are very interesting phenomena which have captured the attention of many researches, provided fundamental issues of theoretical interpretations have not still been answered.ReferencesBabinski J. (1914) Contribution a letude de troubles mentaux dans lhemiplegie organique cerebrale. Revue Neurologique 27, 845847.Beschin, N., Cocchini, G., Allen, R., Della Sala, S. (2012). disassociation between anosognosia and neglect demonstrated by mean of a treatment response bias. Neuropsychological Rehabilitation, 22(4), 550-562.Bisiach,E.,Vallar,G.,Perani,D.,Papagno,C.,Berti,A (1986).Unawareness of disease following lesions of t he right hemisphere anosognosia for hemiplegia and anosognosia for hemianopia.Neuropsychologia, 24, 471-482.Bisiach, E., Ricci, R., Modona, M.N. (1998). Visual Awareness and Anisometry of Space Representation in Unilateral Neglect A Panoramic Investigation by Means of a Line Extension Task. Consciousness and Cognition, 7(3), 327-355.Chambers, C.D., Stokes, M.G., Mattingley, J.B. (2004). Modality specific control of strategic spatial attention in parietal cortex. Neuron, 44(6), 925-930.Cocchini, G., Beschin, N., Cameron, A., Fotopoulou A. Della Sala, S. (2009). Anosognosia for motor impairment following left-brain damage. Neuropsychology, 23, 223-230.Corbetta, M., Miezin, F.M., Shulman, G.L., Petersen, S.E. (1993). A PET study of visuospatial attention. daybook of Neuroscience, 12, 12021226.Dauriac- Le Masson, V., Mailhan, L., Louis- Dreyfus, A., De Montety, G., Denys, P., Bussel, B., Azouvi, P. (2002). Double dissociation between unilateral neglect and anosognosia. Revue neurologi que, 158(4), 427-430.Della Sala S., Cocchini G., Beschin N., Cameron A. (in press).VATAm Visual-analogue test for anosognosia for motor impairment A new test to assess awareness for motor impairment. The clinical NeuropsychologistFotopoulou, A., Tsakiris, M., Haggard, P., Vagopoulou, A., Rudd, A., Kopelman, M. (2008). The role of motor intention in motor awareness An experimental study on anosognosia for hemiplegia. Brain, 131, 3432-3442.Frith,C.D.,Blakemore,S.J.,Wolpert,D.M. (2000).Abnormalities in the awareness and control of action.Philosophical proceedings of the Royal Society B Biological Sciences, 355, 1771-8.Gold,M.,Adair,J.C.,Daniel,H.J.,Heilman,K.M. (1994).Anosognosia for hemiplegia an electrophysiologic investigation of the feed-forward hypothesis,Neurology, 44, 1804.Heilman, K. M. and Valenstien, E. (1972) Frontal lobe neglect in man. Neurology, 22, 660-664.Heilman, K.M, Valenstein E. (1979) Mechanisms underlying hemispatial neglect. Annals of Neurology 5, 166- 170.Heil man, K.M., Watson, R.T., Valenstein, E. (1993).Neglect and related disorders. In Heilman, K.M. and Valenstein, E. (Eds.), Clinical Neuropsychology. New York Oxford University Press, Ch. 10, 279-336.Heilman, K.M, Watson, R., Valenstein E. (1994). Localization of lesions in neglect and related disorders. In Kertez, A.,editor, Localization and Neuroimaging in Neuropsychology. San Diego Academic Peers, 495-524.Heilman,K.M.,Barret,A.M.,Adair,J.C. (1998). Possible mechanisms of anosognosia a defect in self awareness.Philosophical proceeding of the Royal Society B Biological Sciences, 355, 1903-1909.Heilman K.M, Valenstein, E. (2003) Clinical Neuropsychology, Fourth Edition. Oxford University Press, Oxford, UKHillis, A., Caramazza, A.(1995). A framework for interpreting distinct pattern of hemispatial neglect. Neurocase, 1, 189-207.House, A. and Hodges, J. (1988). Persistent denial of handicap after infarction of the right basal ganglia A case study. Journal of Neurology, Neurosurgery, and Psychiatry, 51, 112-115.Karnath, H.O., Baier, B., Nagele, T. (2005), Awareness of the functioning of ones own limbs mediated by the insular cortex?. Journal of neuroscience, 25(31), 7134-7138.Kortte, K., Hillis A.E.( 2010). Recent Advances in the Understanding of Neglect and Anosognosia Following Right Hemisphere Stroke. Current Neurology and Neuroscience Reports, 9(6), 459465.Marcel,A.J.,Tegner,R.,Nimmo-Smith,I. (2004). Anosognosia for plegia specificity, extension, partiality and disunity of bodily awareness.Cortex, 40, 19-40.Orfei, M.D., Robinson, R.G., Prigatano, G.P., Starkstein, S., Rusch, N., Bria, P., Caltagirone, C., Spalletta, G. (2007). Anosognosia for hemiplegia after stroke is a multifaceted phenomenon a systematic review of the literature. Brain, 130, 3075-3090.Prigatano, G.P., Matthes, J., Hill, S., Wolf, T.R. Heiserman, J.E. (2011). Anosognosia for hemiplegia with preserved awareness of complete cortical blindness following intracranial haemorrhage. Cortex, 47(10), 1219-1227.Watson, R.T., Heilman,K.M., Cauthen, J.C., King, F.A (1973). Neglect after cingulectomy. Neurology, 23(9), 1003-1007.Watson, R. T., Heilman, K. M., Millar, B. D. and King, F. A. (1974). Neglect after mesencephalic reticular formation lesions. Neurology, 24, 294-298.Weinstein, E.A. and Kahn, R.L. (1955). Denial of illness Symbolic and physiological aspects, Springfield, IL Thomas.Weinstein E. A. (1991).Anosognosia and denial of illness. In Prigatano G. P. Schacter D. L. (Eds.), Awareness of deficit after brain injury, 240257.
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