Anosognosia
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Author: Dr. Anna Berti, Psychology Department & Neuroscience Institute of Turin (NIT)
Author: Dr. Lorenzo Pia, Psychology Department & Neuroscience Institute of Turin (NIT)
Neurological patients can be entirely unaware of their disease despite several unambiguous evidence. Such a phenomenon has been termed anosognosia (Babinski, 1914) and has been described in different sensorymotor (e.g. cortical blindness, cortical deafness, hemianopia and hemiplegia), and cognitive (e.g. language and memory deficits) domains as well as in schizophrenia and Alzheimer’s disease (for a review see (Prigatano and Schacter, 1991).
One of the most striking instance of this phenomenon can be found in right-brain-damaged patients, affected by left-sided hemiplegia, who may deny that there is anything wrong with their contralesional limbs (see (Orfei, Robinson et al., 2007; Pia, Neppi-Mòdona et al., 2004) for reviews).
From a clinical point of view, anosognosia for hemiplegia is one of the worst prognostic factors for the functional recovery of motor functions (Gialanella and Mattioli, 1992). From a theoretical point view the detailed study of patients’ report may provide us with many important hints for the understanding of motor monitoring operations, and, disclosing domain specific disorder of awareness, , for shedding light on the neural structures underlying conscious mental processes (Berti, Làdavas et al., 1998).
Contents |
Famous Cases and Media
Although no diagnosis has been accounted for the death of the novelist Charles Dickens, his varied symptoms has recently suggested a right parietal-temporal disorder including anosognosia of a whole range of bodily symptoms (McManus, 2001). On September 3, 1867, he wrote to a friend: “I never was better in my life – doubt if any body ever was or can be better – and have not had anything the matter with me but that squeezed foot, which was an affair of a few days [sic]”. During the 1997 trials, Prof Amador supplied the court with mounting evidence that Theodor Kaczynski, otherwise known as the unabomber, suffered from anosognosia for his schizophrenic sympthomatology (Amador and Paul-Odouard, 2000). In the fourth episode of the medical drama 3 lbs as well as in the fifth episode of Grey's anatomy, are shown two patients suffering from disorders of unawareness of left limb.
Symptoms
Anosognosic patients, if inquired about their potential capability to perform actions (either with the right or with the left hand, or even bimanual actions), can claim that they could perform any kind of movement without any sort of difficulties (see figure 1 for fragments of a typical conversation with an anosognosic patient). Such a false belief of being still able to move can remain unchanged even when patients are requested to actually perform actions. In these cases, they can be convinced they have done the given action. Interestingly, sensory and visual feedbacks from the affected motionless side that should suggest that no movement has been performed are not sufficient to modify the belief. For instance, it has been reported an anosognosic patient who was asked to clap the hands. The patient lifted the right hand in the correct position and shape, perfectly aligned with the trunk midline. Then, the patient moved the right hand it as if it was clapped against the left hand. She appeared satisfied with the performance without mentioning that left arm did not participate in the action (despite the patient could see that the left hand remained still). Additionally, when the examiner pointed out that, in clapping hands, one should make noise, the patient claimed that she never make noise (Berti, Làdavas et al., 1998).
The symptomatology of anosognosia for hemiplegia can vary between and within patients. Sometimes when explicitly questioned about the condition of their limbs, they may show different degrees of denial ranging from emotional indifference (anosodiaphoria), in which the motor problems may be admitted but without any concerns, to resolute and intractable unawareness of the disease. Additionally, productive symptoms, as verbal confabulations about the limbs, and delusional beliefs may coexist. In this latter case, patients may claim that the limbs are far from the body or belong to someone else, e.g. to another patient or to the doctor (somatoparaphrenia). The content of the confabulation can be very bizarre and patients may even claim that somebody else is lying on their beds or may show violent attitude against those ‘alien’ limbs (misoplegia).
Clinical Evaluation
Although anosognosia can be evident in patients’ everyday behavior (they may for instance, try to get off the bed in order to walk), structured interviews are used for a clinical diagnosis. Usually patients are first questioned about the reason why they are in the hospital and, if not openly acknowledging the motor deficit, more stringent questions about the affected limbs are asked (Bisiach, Perani et al., 1986). Scores range from zero (the patient readily acknowledges the left-side hemiplegia) to three (the patient resolutely denies any motor problem even when after the request of making an explicit motor act, no movement is actually executed).
It is worth noting that for an unambiguous diagnosis of anosognosia for hemiplegia the patient must be completely plegic on the affected side. If not, i.e. if the affected limb has some degrees of weakness but can still move, then the patient’s claim of still being able to move cannot be considered absolutely wrong and a score of 3 would not, in this case, relate to a condition of real unawareness.
Interpretations
Several interpretations of anosognosia for hemiplegia, although theoretically distant, have in common the fact of not considering the disturbance as a selective and specific cognitive disorder.
Psychodynamic mechanism
In the last century, anosognosia for hemiplegia has been mainly interpreted in terms of a generalized defensive mechanism or psychological denial that would protect the patients from the disease (Weinstein and Kahn, 1955). These theories had their ancient roots in Charcot’s demonstration of unawareness in patients without organic lesions (Charcot, 1892) and presumed that premorbid components of personality, rather than a direct effect of the brain damage, were causally related to illness onset. However, in a seminal paper, Bisiach and Geminiani (Bisiach and Geminiani, 1991) pointed out that some data falsify this hypothesis. First, anosognosia for hemiplegia is more frequent after right-brain damage and during the acute and post acute phases of the illness (Bisiach and Geminiani, 1991; Pia, Neppi-Mòdona et al., 2004); a general defensive mechanism view would predict anosognosia for both right and left motor disturbances as well as an increase with time (a goal-directed mechanism would take time to consolidate). Second, anosognosia can be transitorily ameliorated by vestibular stimulation (Cappa, Sterzi et al., 1987) whereas a psychodynamic reaction should not be influenced by physiological manipulation.
Secondary to neglect
Once motivational explanations had been rejected, anosognosia for hemiplegia was then considered a disorder directly related to the presence of a focal brain damage. However, most theories explained away anosognosia as due to the presence of other concomitant neurological and/or neuropsychological disorders.
Bisiach & Berti (Bisiach and Berti, 1987), for instance conceived anosognosia as part of a complex disorder of space representation (named dyschiria), associated with the manifestation of unilateral spatial neglect. However, anosognosia for hemiplegia has been found to be double dissociated from neglect phenomena (Berti, Bottini et al., 2005; Berti, Làdavas et al., 1996; Bisiach, Perani et al., 1986; Dauriac-Le Masson, Mailhan et al., 2002).
Therefore, although it is not possible to deny that there seem to be spatial constraints on the way in which anosognosia manifests itself, the unawareness of contralesional motor impairment cannot simply depend on patients ignoring the left part of either extrapersonal or personal space. Indeed, in dissociated cases, patients do not acknowledge their motor problems despite the fact that they are still able to direct attention to the left side of the body and that they are fully aware that the left side of the body belongs to them.
Secondary to cognitive and/or sensory disorders
Other authors pointed to the role of somatosensory disorders associated with intellectual deficits in determining the denial behavior. According to Levine and colleagues (Levine, Calvanio et al., 1991), the coexistence of these disorders would preclude patients discovering their impairment. In addition, the possibility of memory problems, which may prevent the acquisition and fixation of new information, including those related to the disease, has been considered a possible cause of anosognosia for hemiplegia (Berti, Làdavas et al., 1996).
However, it has been found that although most patients with anosognosia are also affected by left-side anesthesia, it is possible to observe anosognosic patients without sensory (tactile or proprioceptive) disorders, as tested at bedside examination. On the other hand, there are patients with severe somatosensory problems without denial of hemiplegia (Berti, Làdavas et al., 1996; Bisiach, Perani et al., 1986; Marcel, Tegnèr et al., 2004; Small and Ellis, 1996). In addition, the possibility of ascribing anosognosia to a general intellectual impairment or to memory problems has been ruled out by the observation of double dissociations between these disorders (Berti, Làdavas et al., 1996).
These findings showed that, although anosognosia is often associated with other neurological/neuropsychological disorders, which may shape or even aggravate the manifestations of the denial behavior, cognitive and sensorimotor impairments seem to be neither necessary nor sufficient to cause anosognosia for hemiplegia. Therefore, denial of hemiplegia in right-brain-damaged patients cannot be explained away by referring to other concomitant symptoms, but rather it has to be considered a specific neuropsychological disorder that calls for a proper explanation (Berti, 2000).
Generalized disorder of self-monitoring
The impairment in detecting contralesional hemiplegia may depend on a disorder of self-monitoring. The damage to a general multipurpose control mechanism, responsible for the inspection of subjects’ physical and cognitive capabilities, would cause a generalized impairment in detecting all possible concomitant disorders affecting, after the stroke, either personal or extrapersonal aspects of patients’ behavior. On the contrary, a disorder of a selective self-monitoring mechanism would predict the possibility that normal awareness for some of the deficits would be observed together with an impaired monitoring capacity for other coexisting deficits.
Indeed, anosognosia for hemiplegia has been described limited to one disorder (either the motor or the spatial and vice-versa; (Berti, Làdavas et al., 1996), to one limb (either the upper or the lower and vice-versa; (Berti, Làdavas et al., 1996; Berti, Làdavas et al., 1998), to some kind of movements Marcel, Tegnèr et al., 2004) and to specific kind of response (either a personal report or a self-evaluation task and vice-versa; (Berti, Làdavas et al., 1996; Berti, Làdavas et al., 1998; House and Hodges, 1988; Marcel, Tegnèr et al., 2004).
Domain specific disorder of motor monitoring
Overall, the aforementioned data suggest that anosognosia for hemiplegia could be a selective (rather than generalized), disorder that affects motor awareness. Therefore, it could not be explained as a disturbance of awareness related, for instance, to massive damage to prefrontal areas. In fact, this would imply a lack of monitoring for all concomitant deficits, both in the somatosensory domain (unawareness for upper and lower limb paresis) and in the cognitive domain (unawareness for hemiplegia and all concomitant neglect and related disorders). On the contrary, the selectivity of the disorder strongly suggests that awareness can have a complex structure, revealing even at the level of thought processes the modular organization of the cognitive system (Bisiach and Berti, 1995). Consequently, this would predict different neural basis for different form of awareness and not a unique cerebral localization for monitoring processes (such as pre-frontal areas). In a recent review of the literature on the neural basis of anosognosia for hemiplegia, it has benne shown that its occurrence is related to frontal and parietal lobes damages (Pia, Neppi-Mòdona et al., 2004). The authors suggested that anosognosia could be conceived as a disorder of motor awareness implemented in a fronto-parietal circuit related to space and motor representation where the parietal component may be responsible for the spatial computation necessary to act in space. However, an important limit of this study was the lack of anatomical details because most of the studies cited in the review did not report lesional maps of the damaged brains. This prevented to draw conclusions about the specific Brodmann areas involved in this putative fronto-parietal circuit.
A subsequent study, however (Berti, Bottini et al., 2005), showed that denial is related to lesions mainly involving regions devoted to motor control (See figure 3). These areas are well known to be closely linked to motor programming both in monkeys and humans (Rizzolatti, Luppino et al., 1998; Tanji, 1996), motor imagery (Jeannerod, 1994; Roth, Decety et al., 1996) and even interpretation of others’ actions (Jackson and Decety, 2004; Rizzolatti and Craighero, 2004). Less frequently, other regions such as the insula (a brain area involved in sensory motor control; Karnath, Baier et al., 2005) are affected.
Anosognosia as a disturbance of the comparator system of the feed-forward model of action generation
Awareness of movement
As we discussed above, somatosensory information seems to be neither sufficient nor necessary in order to have a coherent view of motor behavior. In patients with anosognosia for hemiplegia, even strong visual feedbacks, as, for instance, the view of the motionless limb may not modulate the false belief of being able to move. On the other hand, hemiplegic patients without anosognosia are fully aware of their motor impairment even when the plegic limb is out of sight. Therefore, this evidence suggests that although vision and proprioception are crucial aspects of our ability to evaluate the course, and the consequences, of a motor event, its full appreciation is somehow independent from their operations.
The aforementioned neuropsychological data are consistent with several results obtained with healthy participants. Normal subjects, for instance, can build their motor awareness without the sensations associated with the actual execution of movements (Fourneret and Jeannerod, 1998). Interestingly, the subjective judgment of the moment in which one become aware of an intended movement (the so-called ‘M’ judgment), precedes the actual initiation of the movement of 50–80 ms (Libet, Gleason et al., 1983)
Overall, these data demonstrate that motor awareness is not simply constructed on sensory feedbacks coming from the moving muscles, but instead emerges before the afference of any sensory proprioceptive input. Blakemore and Frith (Blakemore and Frith, 2003) proposed that motor awareness is related to some signal that precedes the movement and that is formed prior to the processing of sensory feedbacks. Based on the classical forward model of the motor system (Wolpert, Ghahramani et al., 1995), they suggested that once the appropriate motor commands are selected and sent to muscles for the execution of the desired movement, a prediction of the sensory consequences is built and compared with the feedback associated with the action. These predictions, based on the efference copy of the programmed motor act, are the signals on which motor awareness is constructed (Blakemore, Wolpert et al., 2002) and are responsible for Libet’s ‘M’ judgment (see Figure 2).
A crucial consequence of such a model is that whenever the motor system makes sensory predictions about the programmed movement, we might construct the belief that this movement is actually performed (Berti and Pia, 2006). Then, the comparator would match the congruency between the belief of the intended movement and the representation of the actual status of the system. When the motor act corresponds to the representation of the intended movement, motor awareness is veridically constructed. On the contrary, when the peripheral event does not correspond to the prediction, the comparator should detect the discrepancy.
Starting from this proposal, we proposed that in hemiplegic patients without anosognosia the comparator, still able to detect the mismatch between the prediction and the actual condition, allows a normal veridical motor awareness. Consequently, when hemiplegic patients without anosognosia are required to move their affected limb, they acknowledge the failure (Berti and Pia, 2006). On the contrary, hemiplegic–anosognosic patients may have damage to the comparator component of the forward model. Because of this, the comparator cannot detect the mismatch between the predictions and the feedback and the patients are not able to distinguish between a purely intended action and the real movement. This leads to the construction of a nonveridical motor awareness and therefore to the false beliefs of being able to move.
Motor intention
In the Libet and colleagues’ study (Libet, Gleason et al., 1983) subjects were required to indicate not only when they became aware of the movement (the ‘M’ judgment), but also when they first felt the emergence of their intention to move (the ‘W’ judgment). Such a conscious judgment about one’s motor intention preceded the movement execution of about 200 ms. Much more interestingly, the ‘W’ judgment followed, instead of preceded, the electrophysiological preparatory activity related to movement registered over the supplementary motor area (‘readiness potential) of hundreds of milliseconds. These findings have been confirmed with neuroimaging techniques. In an fMRI study with the same paradigm, Lau and colleagues (Lau, Rogers et al., 2004) showed that a similar area (pre-SMA) is specifically activated in the W judgment condition. In a subsequent study, Haggard and Magno (Haggard and Magno, 1999) reported that the conscious intention was more specifically associated to a brain potential considered an index of action selection (called ‘lateralized readiness potential’). In other words, the authors argued that lateralized readiness potentials are responsible for the specification of the characteristics of the movement as the arm used to act. This potential is subsequent to the very earliest neural preparation of action that may represent the initial decision to move (prior intention in Figure 2). Because of this evidence, we suggest that if the activity of the areas involved in the construction of conscious intention of action would be accessible to anosognosic patients, their verbal delusions would reflect their movement experience, which arises from the normal or quasi-normal functioning of the intentional system and of the prediction/awareness component of the model. Consequently, the intended movement would be actually experienced (however see Gold, Adair et al., 1994, for an alternative view). According to this explanation, the brain lesion should spare the activity of the areas involved in motor intention, such as the SMA and pre-SMA, whereas the area involved in the comparator activity should be affected.
From a pure anatomical point of view, Berti and colleagues (Berti, Bottini et al., 2005) showed that SMA and pre-SMA are significantly spared in anosognosic patients. This supports the idea of an experience of intentionality in anosognosic patients. In a recent single case study, Berti and colleagues (Berti, Spinazzola et al., 2007), tried to examine more in depth the presence of motor intentions. The authors showed that the patient affected by left side hemiplegia and anosognosia still activates the proximal muscles of the affected side because of the attempt to execute a purposeful movement with the plegic limb. These observations further demonstrate intact intentionality and programming of the spared brain regions (note that proximal muscles are bilaterally innervated, so can be still recruited in hemiplegic patients when the distal parts are completely paralyzed).
Therefore, we proposed that motor control areas constitute the neural bases of the comparator operations of the forward model of action generation, which is damaged in anosognosic patients (see Figure 3). The involvement of pre-motor areas in self-monitoring of body movements implies that, at least for motor functions, monitoring is neither the prerogative of some kind of central executive system, hierarchically superimposed to sensory-motor and cognitive functions, nor a function that is physiologically and anatomically separated from the primary process that has to be monitored. Instead, the anatomical correlates of anosognosia show that monitoring can be implemented in the same neural network responsible for the process that has to be controlled and not in a central-superimposed and anatomically separated system.
This hypothesis is consistent with data showing transient amelioration of anosognosia during vestibular stimulation (Cappa, Sterzi et al., 1987; Rode, Charles et al., 1992) when the injection of cold water into the patient’s left ear may cause a short-lasting awareness of contralesional hemiplegia. As shown by Bottini and colleagues (Bottini, Paulesu et al., 1995), vestibular signals project to the supramarginal gyrus, putamen, somatosensory areas, premotor cortex and insula. Therefore, considering that the insula and the premotor cortex are part of the proposed circuit for motor awareness, it is reasonable to assume that when, in an anosognosic patient, a subset of these areas is not completely destroyed by the lesion, and the vestibular stimulation may maximally activate the spared nodes of the comparator network, momentarily restoring the motor monitoring capacity. Interestingly, Rode and coworkers (Rode, Charles et al., 1992) described a patient who, during the effect of vestibular stimulation, was even able to report what happened when he had first had the stroke. The activation of some sort of implicit memory during the effect of caloric stimulation is more puzzling and might be due to spreading of activation outside the areas described by Bottini and colleagues (Bottini, Paulesu et al., 1995).
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