Anosognosia is a common, fascinating, and ill-understood disorder following brain damage, where patients who suffer severe deficits such as hemiplegia may remain unaware of and deny their handicap. Many studies including recent work published in this journal have attempted to determine the neurological, cognitive, and motivational bases of anosognosia. These studies have typically focused on descriptive correlations between anosognosia and various clinical factors, but did not identify a consistent pattern of brain lesion or dysfunction. Rather, the results have emphasized the complex and multifacet nature of anosognosia.


Anosognosia is a perplexing condition. It can affect patients with various neurological impairments who appear unable to notice and acknowledge the existence of their deficits, often despite blatant evidence for their handicap. Typical examples are hemiplegic patients who may assert that their paralyzed limbs are still functioning normally. Other patients with bilateral cortical blindness may claim that their vision is intact, or amnesics may contend that their memory is excellent. In fact, patients may be anosognosic for virtually any neurological deficit following brain injury, including aphasia, prosopagnosia , or apraxia.

Anosognosia for hemiplegia (AHP) is thought to be relatively common, encountered in at least 20- 30% of hemiplegics after an acute stroke.

However, we still have a very poor understanding of anosognosia. This is perhaps not too surprising given the heterogeneity of this phenomenon. But more surprisingly, only few systematic studies have been carried out in these patients with the aim of better characterizing the crucial clinical features and their possible underlying cognitive mechanisms. Most existing studies have been descriptive (e.g., examining the correlation with different lesion types, severity of neurological impairment, etc.), whereas experimental investigations have been rare or performed only in a few single cases.

Confabulation and anosognosia


Anosognosia is a condition in which a person who suffers disability seems unaware of or denies the existence of his or her disability.  It can occur after brain injury or other neurological impairment.  Anosognosia  occurs in over half of right hemisphere stroke patients (J. Cutting put the figure at 58% in  a study described in 1978), while it hardly ever occurs in left hemisphere stroke victims.

The right hemisphere of our brain is the part which directly perceives the complexity of reality.  The left brain relies on conceptualisations which can only ever be an approximation to reality. The left brain relies on new information updates from the right brain to refresh its views on what is happening.  Without this input it stays stuck in the same beliefs and story lines which become increasingly divorced from on-going reality.

Confabulation is the formation of false memories, perceptions, or beliefs… as a result of neurological dysfunction (wikipedia).  It leads to a situation where people lie without realising they are lying. Clearly this can happen as a result of anosognosia.

Modern humans are all dominated by the left brain, particularly in terms of thought and speech, and the right hemisphere has to take a back seat, its impressions becoming sub-conscious. Therefore we do not consciously perceive full reality.  And, as part of this very scenario, we are not habitually aware of this limitation.  We could all be said to be suffering from partial anosognosia.  This is why we all confabulate to some degree.

 In a new investigation, Aikaterini Fotopoulou and her colleagues have shown that some patients fitting this description have a residual, subconscious awareness of their disability.

The researchers recruited 14 brain-damaged patients with a completely paralysed left arm, half of whom denied their paralysis (ie they had anosognosia). Next, all the patients were presented with a series of sentences for which they had to provide the final word. The twist to the task is that the word had to be completely unrelated in meaning to its adjoining sentence.

Some of the sentences were emotionally neutral (about cars), some were negatively emotional (about violence), and finally some pertained to stroke and physical disabilities. The patients with anosognosia performed no differently from the paralysed controls on the neutral and negative sentences, but they took longer to complete the sentences about stroke and disabilities. This was taken as a sign of competition between subconscious self-threatening information about disability and the task requirement to find an unrelated word. It suggests the anosognosic patients had a subconscious awareness of their own disability. 

The patients were also asked to rate the same set of sentences for their self-relevance – this was an explicit test of their awareness. Again, the anosognosic patients differed from controls on precisely the sentences that pertained to stroke and disability. This time, as you might expect, they tended to say such sentences were less relevant to them than did the controls.

A final component of the study involved scanning the brains of all fourteen of the patients. This showed that the patients with anosognosia had damage in brain regions involved in motor control (including the basal ganglia) and body representation (including the anterior insula) that were unaffected in patients without anosognosia.

Fotopoulou’s theory is that patients with anosognosia have a subconscious awareness of their deficits but that the brain circuits responsible for creating an up-to-date representation of self are compromised. Consistent with this, inprevious research, patients with anosnognosia have shown greater insight when describing their impairments from a third-person perspective and also after viewing themselves on video. A related theory is that patients with anosognosia have intact motor planning brain circuits but that their feedback circuits are damaged. So, when asked to move, they feel that they’ve sent a successful motor command to their limb but are left unaware that the command wasn’t enacted.

One reason anosognosia is so intriguing is that it has both neurobiological and psychological components. Some experts have interpreted it as a form of Freudian defence against the emotional trauma of paralysis. Consistent with this, when insight into their paralysis has been achieved, previously anosognosic patients have subsequently suffered from an increase indepressive symptoms.

‘The combination of our behavioural and neural findings suggest that an explicit, affectively personalised sensorimotor awareness requires the re-representation of sensorimotor information in the insular cortex, with possible involvement of limbic areas and basal ganglia circuits,’ the researchers said. ‘The delusional features of anosognosia for hemiplegia can be explained as a failure of this re-representation.’


As in

Patrick Haggard, Department of Psychology, UCL:


Patrik Vuilleumier, (Laboratory for Behavioural Neurology and Imaging of Cognition, Departments of Clinical Neurosciences and Physiology, University Medical Center, Geneva):

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