“What do you mean, I can’t walk!” Two Theories on Anosognosia for Hemiplegia

bbaum's picture
Bailey Baumann
Web Paper #2
Professor Grobstein

“What do you mean, I can’t walk!” Two Theories on Anosognosia for Hemiplegia

“She raised one hand and flexed its fingers and wondered, as she had sometimes before, how this thing, this machine for gripping, this fleshy spider on the end of her arm, came to be hers, entirely at her command. Or did it have some little life of its own? She bent her finger and straightened it. The mystery was in the instant before it moved, the dividing moment between not moving and moving, when her intention took effect. It was like a wave breaking. If she could only find herself at the crest, she thought, she might find the secret of herself, that part of her that was really in charge.” –Atonement pp. 33

What if you were walking down the street and saw one of your good friends. You walk up to her and shake her hand, exchange a few words and walk away, nothing special. The majority of the population would have no problem dealing with this situation, but there are people, for whom this present major issues. Image shaking hands with your good friend and looking down to realize that you have no idea which hand belongs to you and which hand belongs to your friend. There are many types of rare disorders that deal with defects in body ownership. When an individual has a disorder of this kind, she is unable to distinguish herself and her body from the bodies of others. My interest in this topic began after discussion was raised concerning phantom limbs; a disorder where an individual feels what isn’t there, this made me wonder what would prompt an individual to deny what is obviously present.
Anosognosia for hemiplegia (AHP) is a specific type of anosognosia that is characterized by an individual’s denial and unawareness of their paralysis or motor impairment following damage to the brain. Most commonly, AHP is seen in stroke victims with damage to the right brain hemisphere, leading to hemiplegia in the left side of the body (1). The presentation of anosognosia is varied and ranges from patients who don’t acknowledge the severity of their impairment to individuals who no longer feel any connection with their limb and will actually deny limb ownership (2). At first, it may seem logical that the denial that is present in these individuals is a façade, a belief that they don’t truly hold. To test this notion, Dr. Ramachandran, one of the pioneers in the study of anosognosia tried to force patients to admit their limited mobility by creating tasks that required patients to perform a spontaneous motor activity that required two hands and by trying to award patients for their honesty (3). Both of these tests produced the same results; patients with AHP truly believe that they had complete range of movement, despite incentive to admit otherwise.
In spite of decades of research on AHP and other similar disorders, there is still no clear explanation of its origins (4). The lack of concrete answers has arisen, in part because of our inability to adequately and definitively define and categorize the disorder. At first glance, anosognosia seems to simply be a mental disorder, a Freudian defense mechanism concocted because of a horrific experience, but emerging evidence seems to point towards a more neurobiological explanation (5). One of the most convincing arguments for a neurobiological origin of anosognosia is that it is found mostly in patients that present with right hemisphere damage, but rarely seen in patients with damage in the left hemisphere. The discovery of the sidedness of the disorder has created a chance for neurobiologists to help explain the disorder using a more biological approach.  Although I don’t believe that the disorder is caused by one factor working alone, which is usually the case with such a complex disorder, I do believe that evidence demonstrates that AHP is clearly not simply a psychological disorder. I would like to look at two interconnected theories of the emergence of AHP, the first deals with deficits in reality monitoring and the second deals with Freudian defense mechanisms explained with a neurobiological twist.
It is best to investigate anosognosia by first looking at the production of self-awareness of movement in individuals not suffering from the disorder. Before one can understand how an individual lacks motor awareness, it is important to understand how the majority of humans develop this essential process.  In a normal individual, there is an intimate relationship between predicted actions and motor awareness, but less of a connection between actual movement and awareness (6). This would mean that an individual is less aware of what their finger is doing than what they predict or intend to do with their finger. This phenomenon has been demonstrated in several experiments including a study conducted by Fourneret et al (1998) (7). In one of these experiments, individuals were instructed to draw straight lines without being able to see the movements of their hands. The test required the participants to make large deviations from a straight trajectory, but even though the participants did not produce straight lines, the majority believed that the products were perfectly correct.
The deficit in motor awareness occurs because our understanding of what our body is actually doing is based mostly on what we think or predict that it will do, and not on what it actually does. The participants intended to draw straight lines, so despite the contradictory evidence from the motor neurons that control the hand and fingers, the participants still believed that they were drawing straight lines (6). This shows that before a signal is transported from the finger to the brain or the brain to the finger, there is another signal that begins within the nervous system that tells the body that a specific neuron is going to be fired. In normal individuals, the fact that perceived movement controls our motor awareness causes no practical issues because the vast majority of the time, the perceived movement and the actual movement are one in the same.
In patients suffering from AHP, there may be deficits in the patient’s ability to predict sensory consequences of movement. From the reports of suffers, patients with AHP have the ability to make predictions about motor behavior, but may not be aware of when these predictions differ from actual motor behavior. In other words, “…impaired reality monitoring might form a barrier to natural awareness of hemiplegia because of the breakdown in the ability to check what is real and assess the veracity of mental contents” (5).  When an AHP sufferer intends to move his leg, he believes that he has moved his leg because there is damage to the neural pathway that tells him what movement has actually occurred. So even though his leg has not moved, the patient will have no awareness of any problem, falsely believing that his leg has moved in the intended.
Eventually I believe that the nervous system, being so self-sufficient, will detect a problem with the lack of signals from motor neurons in a certain area and will send out pain signals, a phenomenon that occurs when an individual experiences phantom limb pain. But because the individual has acquired brain damage, and the motor neurons that connected the affected limb to the brain have been temporarily shut down or destroyed, the individual does not feel pain, and the false sense of normalcy can continue. Despite the heterogeneous presentation of anosognosia, it is essentially a disorder that involves deficits in reality monitoring, a disconnection between two stimuli that are typically so interconnected that normally we are not clued into their harmony.
In order to understand motor awareness, one needs to understand how the perceived and actual motor input are received in the brain. By investigating the pathway in a healthy patient, researchers may be better prepared to explain the deficits in an AHP patient. When researchers take images of an individual’s brain while being asked to both visualize a movement and actually execute a movement, essentially the same areas of the brain are being activated (4). One of the possible reasons that the time between visualizing a movement and the actual execution of the movement is so short is that the region that controls both actions is located in the same area of the nervous system, the parietal lobe (8).
The parietal lobe is thought to be especially important in the role of motor imagery, which is why it is common to see visualization problems in patients that have damage to this particular region. More importantly, the right inferior parietal cortex is intimately involved in motor awareness. This specific area of the brain may be heavily involved in our ability to classify movements as internal or external and our ability to represent imaged movements (6). AHP patients all seem to have lost some type of connection with their body, be it through denial of paralysis or through the actual denial that one’s body is their own. It makes sense that AHP patients have damage to the parietal lobe; they have the ability to perceive their limbs from within their brains but have lost the ability to connect this internal image to an external cue.
To look more closely at AHP, researchers are starting to draw connections between more heavily studies disorders and AHP to find similarities. One of the disorders that seems to share many of the same deficits as anosognosia is schizophrenia. It has been suggested that schizophrenia may be caused by a deficit in discriminating between self-generated and externally generated events (9). The similarities between AHP and schizophrenia suggest that individuals with AHP may show reality monitoring failure in other areas of behavior not related to motor movement.
One study by Jenkinson et al tried to determine if AHP patients could discriminate between memories of imagined and perceived images (10). In this experiment, AHP patients and a control group saw a noun on a computer screen and asked to say that word out loud. After 3 seconds, the word would disappear and a box would appear. This box contained either a drawing of the noun that the patient had just seen, or a blank circle. If a blank circle appeared, the patient was asked to mentally draw the object in the circle. After the experiment, patients were asked to indicate, on a list of nouns, which nouns they had been displayed and which objects they mentally drew. The results of this study show that AHP patients have a decreased ability to determine the source of visual data (10). The results of this study shows that damage to the parietal lobe, which impairs reality monitoring is not localized to motor impairment, but may create more generalized damage.
Despite evidence that supports the idea that AHP is caused by deficits in reality monitoring, there is also contradictory evidence that seems to point in another direction. According to the reality monitoring theory, a patient is unaware of their paralysis, despite evidence that suggests otherwise. This explanation seems to be very fitting until you realize that these patients actually look at their limbs and see the lack of movement, but still acknowledge no paralysis. If AHP is simply a disorder of unawareness, what is keeping these patients from seeing reason after several sources have confirmed their hemiplegia? 
In light of new evidence that pokes holes in the reality monitoring theory, Dr. Ramachandran has worked to find alternative theories concerning the development of anosognosia.  In his book “Phantoms in the Brain,” Dr. Ramachandran explains how outdated concepts such as denial may actually lead to the development of anosognosia.
Our world is constantly shifting and introducing novel concepts and ideas that go against our established worldview. The left hemisphere is responsible for keeping our brains from becoming completely chaotic and ineffective by integrating these small discrepancies or anomalies or by lying, a concept that is not unlike what the brain accomplishes in regards to our blind spot. The right side of the brain will usually sit back and be content with the left side controlling our image of the world, and will only react if an anomaly is too large for the left hemisphere to control. In individuals who have right hemisphere damage, the right side of the brain can no longer play “devil’s advocate” and the brain will continue to lie to itself about the motor impairments (11). 
When an individual has become paralyzed, the right side of the brain will be unable to tell the body that something has gone awry, and the right hemisphere will continue its lies. This theory is supported by evidence that show that when an individual has right hemisphere damage, they can show deficits in the right side of their body as well (11). Denial can travel from one side of the body to the next. In one case study, a woman with AHP places her right hand into a mirror box and is asked to move it in time with a metronome. Next, the tester puts a wall up so she can’t see her hand while an assistant puts his hand into the box. The patient is asked to move her hand again, but the assistant does not move his hand. When asked if she is moving her hand in time with the metronome, she answers very definitively, “yes.” Dr. Ramachandran has also proven that some AHP patient’s denial is not limited to their body. When two stroke patient’s that presented symptoms of anosognosia were asked if a man sitting a wheelchair, who the doctor had said was paralyzed, could walk, the patients said “yes.” The results of these investigations demonstrate that, in some cases, anosognosia is not contained in one part of the body, but can be generalized both throughout the body and beyond. This facet of anosognosia is consistent with deficits in the parietal lobe, while prevents individuals from determining what inputs are external and which are internal.
Although these two theories are somewhat contradictory, I believe that they both deal with very similar issues. Both theories acknowledge that the right side of the brain is responsible for awareness for motor disorders and that damages to the parietal lobe is partially responsible for anosognosia symptoms. In patients with AHP, there is a disconnection between the internal and the external environment; a disconnect that cannot be corrected by simple evidence. Researchers are still not clear what exactly causes the disconnection, but with the help of researchers such as Dr. Ramachandran, we are getting closer to a concrete answer.


























Works Cited

1. S.J. Ellis and M. Small, Denial of illness in stroke, Stroke 24 (1993), pp. 757–759.

2. M.D. Orfei, R.G. Robinson, G.P. Prigatano, S. Starkstein, N. Rüsch and P. Bria et al., Anosognosia for hemiplegia after stroke is a multifaceted phenomenon: A systematic review of the literature, Brain 130 (2007), pp. 3075–3090.

3. Ramachandran, V.S. Anosognosia in parietal lobe syndrome. Consciousness and Cognition 4 (1995). pp 22-51.

4. Jenkinson, P. M., Edelstyn, N. M. J., & Ellis, S. J. (in press). Imagining the impossible: Motor representations in anosognosia for hemiplegia. Neuropsychologia

5. A. Venneri and M.F. Shanks, Belief and awareness: Reflections on a case of persistent anosognosia, Neuropsychologia 42 (2004), pp. 230–238.

6. S.-J. Blakemore and C. Frith, Self-awareness and action, Current Opinion in Neurobiology 13 (2003), pp. 219–224

7. Fourneret, P., Jeannerod, M. Limited conscious monitoring of motor performance in normal subjects. Neuropsychologia 1998, 36: 1133-1140

8. L. Pia, M. Neppi-Modona, R. Ricci and A. Berti, The anatomy of anosognosia for hemiplegia: A meta-analysis, Cortex 40 (2004), pp. 367–377

9. Brébion, J.M. Gorman, X. Amador, D. Malaspina and Z. Sharif, Source monitoring impairments in schizophrenia: Characterisation and associations with positive and negative symptomatology, Psychiatry Research 112 (2002), pp. 27–39

10. Jenkinson, P.M., Edelstyn, N.M.J., Drakeford, J.L., Ellis, S.J. Reality monitoring in anosognosia for hemiplegia. Consciousness and Cognition (2008) Article in Press.

11. Ramachandran, V.S. (1998) Phantoms in the brain: Probing the mysteries of the human mind. New York: William Morrow and Company, Inc.


Further Readings

Cocchini, G., Cameron, A., Beschin, N., Fotopoulou, A., Della Sala, S. Anogognosia for motor impairment following left brain damage. Neuropsychology 23 (2009), pp. 223-230.

An alternative theory on why the majority of individuals with AHP have right hemisphere damage.

Carruthers, G. Types of body representation and the sense of embodiment. Consciousness and Cognition 17 (2008) pp. 1302-1316.

An more philosophical view of AHP, which explores our sense of embodiment.


Comments

Paul Grobstein's picture

anosognia: denial and defense

Very interesting exploration of ways in which "denial" of what seems obvious to an external observer might make sense in terms of nervous system organization.  What's the relation between that and "Freudian defense mechanisms"? 

Post new comment

The content of this field is kept private and will not be shown publicly.
randomness