Anosognosia (pron.: //, //) (uh no sog NOH zee uh) is viewed as a deficit of self-awareness, a condition in which a person who suffers certain disability seems unaware of the existence of his or her disability. The word comes from the Greek words nosos, "disease", and gnosis, "knowledge", with an- or a- as a negative prefix. It was first named by the neurologist, Joseph Babinski, in 1914. Unlike denial, which is a psychological defence mechanism, anosognosia results from physiological damage on brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere.
Relatively little has been discovered about the cause of the condition since its initial identification. Recent studies from the empirical data are prone to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems. Anosognosia is relatively common following different etiologies of brain injury, such as stroke and traumatic brain injury (e.g. 10%–18% in the case of anosognosia for hemiparesis with onset of acute stroke), but can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left kinds. However, it is not related to global mental confusion, cognitive flexibility, other major intellectual disturbance, or mere sensory/perceptual deficits. Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. For example, anosognosia for hemiplegia may occur with intact awareness of visuo-spatial unilateral neglect, or vice versa. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function.
The condition does not seem to be directly related to sensory loss and is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which sufferers seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left). There are also studies showing that the maneuver of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association to spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and their neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.
Those diagnosed with dementia of the Alzheimer's type often display this lack of awareness and insist that nothing is wrong with them.
Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetic errors and shows "anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him." This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.
Clinically, anosognosia is often assessed by giving patients an asnosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon nor the responses obtained via offline questionnaire are capable of revealing the discrepancy of awareness observed from their online task performance. The discrepancy is noticed when patients showed no awareness of their deficits from the offline responses to the questionnaire but demonstrated reluctance or verbal circumlocution when asked to perform an online task. For example, patients with anosognosia for hemiplegia may find excuses not to perform a bimanual task even though they do not admit it is because of their paralyzed arms. Similar situation can happen on patients with anosognosia for cognitive deficits after traumatic brain injury when monitoring their errors during the tasks regarding their memory and attention (online emergent awareness) and when predicting their performance right before the same tasks (online anticipatory awareness. It can also occur among patients with dementia and anosognosia for memory deficit when prompted with dementia-related words, showing possible pre-attentive processing and implicit knowledge of their memory problems. More interestingly, patients with anosognosia may overestimate their performance when asked in first-person formed questions but not from a third-person perspective when the questions referring to others.
When assessing the causes of anosognosia within stroke patients, CT scans have been used to assess where the greatest amount of damage is found within the various areas of the brain. Stroke patients with mild and severe levels of anosognosia (determined by response to an anosognosia questionnaire) have been linked to lesions within the temporoparietal and thalamic regions, when compared to those who experience moderate anosognosia, or none at all. In contrast, after suffering a stroke, people who have moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.
Although largely used to describe unawareness of impairment after brain injury or stroke, the term 'anosognosia' is occasionally used to describe the lack of insight shown by some people who suffer from a mental illness such as bipolar disorder or psychosis. They do not have the insight to recognize that they suffer from a mental illness. There is evidence that schizophrenic anosognosia may be the result of frontal lobe damage.
In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train the patient to adjust for their inoperable limbs (though it is believed that these patients still are not "aware" of their disability). Another commonly used method is the use of feedback – comparing clients' self-predicted performance with their actual performance on a task in an attempt to improve insight.
Neurorehabilitation is difficult because, as anosognosia impairs the patient's desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.
In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalization. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia.
One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognize their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.
Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.
See also 
- Prigatano, George P.; Schacter, Daniel L (1991). Awareness of deficit after brain injury: clinical and theoretical issues. Oxford [Oxfordshire]: Oxford University Press. pp. 53–55. ISBN 0-19-505941-7.
- Moro, Valentina; Pernigo, S., Zapparoli, P., Cordioli, Z., & Aglioti, S. M. (2011). "Phenomenology and neural correlates of implicit and emergent motor awareness in patients with anosognosia for hemiplegia". International Journal of Geriatric Psychiatry 225 (1): 259–269. doi:10.1016/j.bbr.2011.07.010.
- Vallar, Giuseppe; Ronchi, R. (2006). "Anosognosia for motor and sensory deficits after unilateral brain damage: A review". Restorative Neurology and Neuroscience 24 (4–6): 247–257. PMID 17119302.
- Vuilleumier, Patrik (2004). "Anosognosia: The neurology of beliefs and uncertaint". Cortex 40 (1): 9–17. doi:10.1016/S0010-9452(08)70918-3. PMID 15070000.
- B Baier and H Karnath (2005 March). "Incidence and diagnosis of anosognosia for hemiparesis revisited". J Neurol Neurosurg Psychiatry 76 (3): 358–361. doi:10.1136/jnnp.2004.036731. PMC 1739568. PMID 15716526.
- Orfei, M.D.; Caltagirone, C., & Spalletta, G. (2009). "The evaluation of anosognosia in stroke patients". Cerebrovascular diseases 27 (3): 280–289. doi:10.1159/000199466. PMID 19202333.
- Hirstein, William (2005). Brain fiction: self-deception and the riddle of confabulation. MIT Press. p. 148. ISBN 0-262-08338-8.
- Spinazzola, Lucia; Pia, L., Folegatti, A., Marchetti, C., & Berti, A. (2008). "Modular structure of awareness for sensorimotor disorders: evidence from anosognosia for hemiplegia and anosognosia for hemianaesthesia". Neuropsychologia 46 (3): 915–926. doi:10.1016/j.neuropsychologia.2007.12.015. PMID 18281065.
- Breier J, Adair J C, Gold M, Fennell E, Gilmore R, Heilman K (April 20, 1995). "Dissociation of anosognosia for hemiplegia and aphasia during left-hemisphere anesthesia". Neurology 45 (1): 65–7. doi:10.1212/WNL.45.1.65. PMID 7824138.
- K M Heilman, A M Barrett, and J C Adair (1998-11-29). "Possible mechanisms of anosognosia: a defect in self-awareness". Philosophical Transactions of the Royal Society B: Biological Sciences 353 (1377): 1903–1909. doi:10.1098/rstb.1998.0342. PMC 1692420. PMID 9854262.
- Ellis, Andrew W.; Miller, Diane; Sin, Gillian (1983). "Wernicke's aphasia and normal language processing: A case study in cognitive neuropsychology". Cognition 15 (1–3): 111–144. doi:10.1016/0010-0277(83)90036-7. PMID 6686505.
- Marcel, Anthony; Tegner, R., & Nimmo-Smith, I. (2004). "Anosognosia for plegia: specificity, extension, partiality and disunity of bodily unawareness". Cortex 40 (1): 19–40. doi:10.1016/s0010-9452(08)70919-5. PMID 15070001.
- O'Keeffe, Fiadhnait; Dockree, P., Moloney, P, Carton, S., & Robertson, I. H. (2007). "Awareness of deficits in traumatic brain injury: A multidimensional approach to assessing metacognitive knowledge and online-awareness". Journal of the International Neuropsychological Society 13 (1): 38–49. doi:10.1017/S1355617707070075. PMID 17166302.
- Martyr, Anthony; Clare, L., Nelis, S. M., Roberts, J. L., Robinson, J. U., Roth, I., Markova, I. S., Woods, R. T., Whitaker, C. J., & Morris, R. G. (2011). "Dissociation between implicit and explicit manifestations of awareness in early stage dementia: evidence from the emotional Stroop effect for dementia-related words". International Journal of Geriatric Psychiatry 26 (1): 92–99. doi:10.1002/gps.2495. PMID 21157854.
- Starkstein, S., Fedoroff, J., Price, T., Leigurda, R., & Robinson, R. Anosognosia in patients with cerebrovascular lesions. A study of causative factors. doi:10.1161/01.STR.28.10.1446.
- Pia L, Tamietto M (2006). "Unawareness in schizophrenia: neuropsychological and neuroanatomical findings". Psychiatry Clin. Neurosci. 60 (5): 531–7. doi:10.1111/j.1440-1819.2006.01576.x. PMID 16958934.
- Prigatano, G.P. (1991). Awareness of deficit after brain injury: clinical and theoretical issues. New York, New York: Oxford University Press.
- Prigatano, G.P. (2005). "Disturbances of self-awareness and rehabilitation of patients with traumatic brain injury: A 20-year perspective". The Journal of head trauma rehabilitation 20 (1): 19–29. PMID 15668568.
- McEvoy J (1998). "The Relationship Between Insight in Psychosis and Compliance With Medications". In Xavier F. Amador & Anthony S. David eds. Insight and Psychosis. Oxford University Press US. p. 299. ISBN 978-0-19-508497-9.
- David, Anthony S.; Amador, Xavier Francisco (2004). Insight and psychosis: awareness of illness in schizophrenia and related disorders. Oxford [Oxfordshire]: Oxford University Press. p. 293. ISBN 0-19-852568-0.
- McEvoy JP, Applebaum PS, Apperson LJ, Geller JL, Freter S (1989). "Why must some schizophrenic patients be involuntarily committed? The role of insight". Compr Psychiatry 30 (1): 13–7. doi:10.1016/0010-440X(89)90113-2. PMID 2564330.
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Further reading 
- Amador, Xavier Francisco (2000). I am not sick, I don't need help! Helping the seriously mentally ill accept treatment. A practical guide for families and therapists. Vida Press. ISBN 0-9677189-0-2.
- Berti A, Bottini G, Gandola M et al. (2005). "Shared cortical anatomy for motor awareness and motor control". Science 309 (5733): 488–91. doi:10.1126/science.1110625. PMID 16020740.
- Clare L, Halligan P (2006). "Neuropsychological Rehabilitation.". Pathologies of Awareness: Bridging the Gap between Theory and Practice. Taylor & Francis(Psychology Press). ISBN 978-1-84169-810-6.
- Lysaker P, Bell M, Milstein R, Bryson G, Beam-Goulet J (1994). "Insight and psychosocial treatment compliance in schizophrenia". Psychiatry 57 (4): 307–15. PMID 7899525.
- McGlynn S, Schacter DL (1997). "The Neuropsychology of Insight: Impaired Awareness of Deficits in a Psychiatric Context". Psychiatric Annals 27: 806.
- Pia L, Neppi-Modona M, Ricci R, Berti A (2004). "The anatomy of anosognosia for hemiplegia: a meta-analysis". Cortex 40 (2): 367–77. doi:10.1016/S0010-9452(08)70131-X. PMID 15156794.
- Ramachandran, V. S.; Blakeslee, Sandra (1999). Phantoms in the brain: probing the mysteries of the human mind. New York: Quill. ISBN 0-688-17217-2.
- Torrey, E. Fuller (2012). The Insanity Offense. New York: W.W. Norton & Company. pp. 111–122. ISBN 978-0-393-34137-9.
- Vuilleumier P (2004). "Anosognosia: the neurology of beliefs and uncertainties" (PDF). Cortex 40 (1): 9–17. doi:10.1016/S0010-9452(08)70918-3. PMID 15070000.