Anosognosia is a neurological condition where the patient is unaware of his or her neurological deficit or psychiatric condition. The French neurologist, Joseph Babinski, first described anosognosia in 1914. It is associated with mental illness, dementia, and structural brain lesion, as in right hemisphere stroke patients. It can affect the patient’s conscious awareness of deficits involving judgment, emotions, memory, executive function, language skills, and motor ability.
Typically, anosognosia appears when there is a lesion in the right parietal lobe but can occur with temporoparietal, thalamic, or basal ganglia lesions. The exact cause of anosognosia is unknown but is likely due to a derangement of the anatomical or functional monitoring unit that mediates the conscious awareness of deficits. The most likely physiopathologic mechanism is that the brain lesion that causes anosognosia disrupts neurocognitive, secondary integration areas. Damage to these areas can lead to a lack of conscious awareness of the cognitive or sensorimotor function loss.
Anosognosia can occur after acute brain injuries such as stroke or traumatic brain injury but also can occur in other conditions that damage the brain. In stroke patients with hemiparesis, the incidence of anosognosia is 10% to 18%. The term anosognosia can also refer to the lack of awareness seen in psychiatric conditions when patients deny or minimize psychiatric symptoms. It is estimated that 50% of patients with schizophrenia and 40% of patients with bipolar disorder have anosognosia, or the so-called poor or lack of insight into their disease. In the setting of dementia, 60% of patients with mild cognitive impairment and 81% of patients with Alzheimer disease appear to have some form of anosognosia: patients suffering from these conditions deny or minimize their memory impairment.
Patients with anosognosia due to brain injury often exhibit a lack of awareness of hemiparesis, hemisensory deficits, neglect, memory deficits, and language deficits. Patients may be unaware of one deficit while recognizing others. Anosognosia can co-occur with somatosensory neglect (asomatognosia), which also localizes to the right parietal lobe. The latter consists of the patient's denial that part of their body belongs to them.
Although anosognosia usually accompanies a right parietal, temporoparietal, thalamic, or basal ganglia lesion, recent studies suggest that the deficit sometimes can relate to non-structural changes. These changes cause problems with the connectivity of different parts of the brain.
The fundamental neurophysiologic or psychopathologic problem in anosognosia relates probably to an inability of the patient to update their self-image. Because of a lesion in the brain or dysfunction due to illness, the patient cannot incorporate new information regarding their deficits into their self-image. Therefore, they deny their illness or deficit or downplay its significance.
Typically, the health professionals diagnose anosognosia at the bedside by assessing the patient’s knowledge of their deficits. In subtle cases, it takes time and a long conversation with the patient to note anosognosia when patients make excuses for not performing activities on the affected side or do not acknowledge the paralysis or other deficits. In the setting of dementia, patients do not acknowledge or minimize their memory deficits. In the setting of mental illness, patients rationalize aberrant behavior or psychiatric symptoms and often confabulate. This involves the creation of a false answer or response by combining real and imagined details.
When anosognosia is due to structural brain damage, neuroradiological findings typically show damage to the right parietal or right temporoparietal region. Less common are lesions in the thalamus, basal ganglia, or left parietal region. Neuroimaging in dementia typically shows more global brain atrophy. Neuroimaging in psychiatric disorders usually show non-specific findings.
There are publications on an anosognosia rating scale, which rates the level of unawareness of patients with dementia suffering from this condition:
There is no specific treatment for anosognosia, but vestibular stimulation seems to improve this condition temporarily. This maneuver probably influences awareness of the neglected side temporarily. Where anosognosia persists, cognitive therapy can help patients better understand and compensate for their deficit.
Anosognosia differs from denial, a psychological defense mechanism that involves avoiding or rejecting information that provokes stress or pain. With denial, the patient may acknowledge a deficit but minimize its consequences and avoid treatments geared to remedy the deficits. Anosognosia also differs from a more global derangement such as encephalopathy where there may be problems with wakefulness and attention. It differs from other deficits such as visual, sensory, and cognitive deficits which limits the ability of patients to realize their deficit.
When anosognosia is due to a focal structural lesion of the brain, it typically resolves over time, though it can persist over the long-term. When anosognosia is due to mental illness or dementing illness, it may persist and lead to poor compliance with medication regimens.
Anosognosia can impair rehabilitation and recovery because patients that lack awareness of a deficit may show less inclination to take part in rehabilitation therapy to tackle the neurological dysfunction. Patients with anosognosia also may suffer more frequent falls due to their lack of awareness of their deficits. Health providers may need to take safety precautions that they see fit in order to avoid injury.
Recently A.R. Egbert described an ethical framework to involve patients with anosognosia in their rehabilitation treatment. Rehabilitation specialists must always think of and consider this condition because it may affect the outcome of their treatment plan.
Education on how to deal with and help avoid problems related to anosognosia for patients and family members of the patients with this dysfunction is of utter importance, and lack of collaboration from the sufferer is typical due to the patient's failure to acknowledge or minimization of their condition. Issues such as driving, handling money, and walking without help may become areas of conflict. It is important to do a thorough safety evaluation to avoid injury to the patient suffering from anosognosia. Simplifying tasks, maintaining a positive approach, showing concern and empathy, and providing a structured environment are helpful to avoid negative outcomes.
It is very important for emergency medicine clinicians to know of anosognosia. For example, in the setting of acute stroke, the timing of symptom onset is crucial to the administration of thrombolytic therapy. If the patient is unaware of their deficit, they may not give accurate information on the exact time of stroke symptom onset. In this situation, collateral history from a family member is crucial to making an informed treatment decision.
The management of anosognosia is very difficult. Because there are many causes, the management is with an interprofessional team that includes a neurologist, psychiatrist, mental health nurse, primary care physician, and a psychotherapist. There is no specific treatment for anosognosia, but vestibular stimulation seems to improve this condition temporarily. This maneuver probably influences awareness of the neglected side temporarily. Where anosognosia persists, cognitive therapy can help patients better understand and compensate for their deficit. If the cause is a stroke, dementia, or a mass lesion, the prognosis in most cases is poor. If the cause is related to a mental health disorder, the condition leads to difficulty in medication compliance. The overall quality of life is poor.
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