What is Anosognosia?

Introduction

Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical or psychological (e.g. PTSD, Stockholm syndrome, schizophrenia, bipolar disorder, dementia) condition.

Anosognosia can result from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, it was first named by the neurologist Joseph Babinski in 1914. Phenomenologically, anosognosia has similarities to denial, which is a psychological defence mechanism; attempts have been made at a unified explanation. Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of body parts such as their limbs. The term is from Ancient Greek ἀ- a-, ‘without’, νόσος nosos, ‘disease’ and γνῶσις gnōsis, ‘knowledge’. It is also considered a disorder that makes the treatment of the patient more difficult, since it may affect negatively the therapeutic relationship.

Causes

Relatively little has been discovered about the cause of the condition since its initial identification. Recent empirical studies tend 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 causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it 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. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but 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 people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

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. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the manoeuvre 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 with 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 that 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.

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 phonetics 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.

Psychiatry

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 with anorexia nervosa. They do not seem to recognise that they have a mental illness. There is evidence that anosognosia related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

Diagnosis

Clinically, anosognosia is often assessed by giving patients an anosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither of the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon; nor are the responses obtained via offline questionnaire 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 paralysed arms.

A similar situation can happen to 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. Patients with anosognosia may also 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 a stroke, people with moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.

Treatment

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 patients 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-hospitalisation. 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. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.

One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognise 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.

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What is Alogia?

Introduction

In psychology, alogia (from Greek ἀ-, “without”, and λόγος, “speech” + New Latin -ia) is poor thinking inferred from speech and language usage.

There may be a general lack of additional, unprompted content seen in normal speech, so replies to questions may be brief and concrete, with less spontaneous speech. This is termed poverty of speech or laconic speech. The amount of speech may be normal but conveys little information because it is vague, empty, stereotyped, overconcrete, overabstract, or repetitive. This is termed poverty of content or poverty of content of speech. Under Scale for the Assessment of Negative Symptoms (SANS) used in clinical research, thought blocking is considered a part of alogia, and so is increased latency in response.

This condition is associated with schizophrenia, dementia, severe depression, and autism. As a symptom, it is commonly seen in patients suffering from schizophrenia and schizotypal personality disorder, and is traditionally considered a negative symptom. It can complicate psychotherapy severely because of the considerable difficulty in holding a fluent conversation.

The alternative meaning of alogia is inability to speak because of dysfunction in the central nervous system, found in mental deficiency and dementia. In this sense, the word is synonymous with aphasia, and in less severe form, it is sometimes called dyslogia.

Characteristics

Alogia may be on a continuum with normal behaviours. People without mental illness may have it occasionally including when fatigued or disinhibited, when writers use language creatively, when people in certain disciplines – such as politicians, administrators, philosophers, ministers, and scientists – use language pedantically, or in people with intelligence or little education. Hence, deciding if an individual has alogia depends on contextual clues. Is the person in control? Can the person moderate the effect if asked to be specific or concise? Is it better with another topic? Are there other significant symptoms?

Alogia is characterised by a lack of speech, often caused by a disruption in the thought process. Usually, an injury to the left side of the brain may cause alogia to appear in an individual. While in conversation, alogic patients will reply very sparsely and their answers to questions will lack spontaneous content; sometimes, they will even fail to answer at all. Their responses will be brief, generally only appearing as a response to a question or prompt.

Apart from the lack of content in a reply, the manner in which the person delivers the reply is affected as well. Patients affected by alogia will often slur their responses, and not pronounce the consonants as clearly as usual. The few words spoken usually trail off into a whisper, or are just ended by the second syllable. Studies have shown a correlation between alogic ratings in individuals and the amount and duration of pauses in their speech when responding to a series of questions posed by the researcher. The inability to speak stems from a deeper mental inability that causes alogic patients to have difficulty grasping the right words mentally, as well as formulating their thoughts. A study investigating alogiacs and their results on the category fluency task showed that people with schizophrenia who exhibit alogia display a more disorganised semantic memory than controls. While both groups produced the same number of words, the words produced by people with schizophrenia were much more disorderly and the results of cluster analysis revealed bizarre coherence in the alogiac group.

If the condition is assessed using a language other than the individual’s primary language, the medical professional needs to make sure that the problem is not from language barriers.

This condition is associated with schizophrenia, dementia, and severe depression.

Example

The following table shows an example of “poverty of speech” which shows replies to questions that are brief and concrete, with a reduction in spontaneous speech:

Poverty of SpeechNormal Speech
Q: Do you have any children?
A: Yes.
Q: Do you have any children?
A: Yes, a boy and a girl.
Q: How many?
A: Two.
Q: How old are they?
A: Edmond is sixteen and Alice is six.
Q: How old are they?
A: Six and sixteen.
Q: Are they boys or girls?
A: One of each.
Q: Who is the sixteen-year-old?
A: The boy.
Q: What is his name?
A: Edmond.
Q: And the girl’s?
A: Alice.

The following example of “poverty of content of speech” is a response from a patient when asked why he was in a hospital. Speech is vague, conveys little information, but is not grossly incoherent and the amount of speech is not reduced. “I often contemplate—it is a general stance of the world—it is a tendency which varies from time to time—it defines things more than others—it is in the nature of habit—this is what I would like to say to explain everything.”

Causes

Alogia can be brought on by frontostriatal dysfunction which causes degradation of the semantic store, the centre located in the temporal lobe that processes meaning in language. A subgroup of chronic schizophrenia patients in a word generation experiment generated fewer words than the unaffected subjects and had limited lexicons, evidence of the weakening of the semantic store. Another study found that when given the task of naming items in a category, schizophrenia patients displayed a great struggle but improved significantly when experimenters employed a second stimulus to guide behaviour unconsciously. This conclusion was similar to results produced from patients with Huntington’s and Parkinson’s disease, ailments which also involve frontostriatal dysfunction.

Treatment

Medical studies conclude that certain adjunctive drugs effectively palliate the negative symptoms of schizophrenia, mainly alogia. In one study, Maprotiline produced the greatest reduction in alogia symptoms with severity reduction in 50% of patients (out of 10). Of the negative symptoms of schizophrenia, alogia had the second best responsiveness to the drugs, surpassed only by attention deficiency. D-amphetamine is another drug that has been tested on people with schizophrenia and found success in alleviating negative symptoms. This treatment, however, has not been developed greatly as it seems to have adverse effects on other aspects of schizophrenia such as increasing the severity of positive symptoms.

Relation to Schizophrenia

Although alogia is found as a symptom in a variety of health disorders, it is most commonly found as a negative symptom of schizophrenia.

Previous studies and analyses conclude that at least three factors are needed to cover both the positive and negative symptoms of schizophrenia; the three are: psychotic, disorganization, and negative symptom factors. Studies suggest that an inappropriate affect is strongly associated with bizarre behaviour and positive formal thought disorder on a disorganisation factor; attention impairment correlates significantly with psychotic, disorganization, and negative symptom factors. Alogia contains both positive and negative symptoms, with the poverty of content of speech as the disorganization factor, and poverty of speech, response latency, and thought blocking as the negative symptom factors.

Alogia is a major diagnostic sign of schizophrenia, when organic mental disorders have been excluded.

In schizophrenia, negative symptoms including flattening of affect, avolition, and alogia are responsible for the considerable morbidity of the disease compared with other psychotic disorders. Negative symptoms are common in the prodromal and residual phases of the disease and can be severe. During the first year, negative symptoms can progress, especially alogia, which may start off from a relatively low rate. Within 2 years, up to 25% of patients will have significant negative symptoms. Psychotic symptoms tend to diminish as the individuals age, but negative symptoms tend to persist. Prominent negative symptoms at disease onset, including alogia, are good predictors of worse outcomes.

Negative symptoms can arise in the presence of other psychiatric symptoms. Positive symptoms are a common cause of apathy, social withdrawal, and alogia. Secondary causes of negative symptoms, such as depression and demoralisation, often remit within a year, which helps distinguishing them from primary negative symptoms. Symptoms that don’t diminish over a year with medications should be reconsidered as possible primary negative symptoms.

Pre-Clinical Dementia & Depression

Research Paper Title

A cross-national study of depression in preclinical dementia: A COSMIC collaboration study.

Background

Depression commonly accompanies Alzheimer’s disease, but the nature of this association remains uncertain.

Methods

Longitudinal data from the COSMIC consortium were harmonized for eight population-based cohorts from four continents.

Incident dementia was diagnosed in 646 participants, with a median follow-up time of 5.6 years to diagnosis.

The association between years to dementia diagnosis and successive depressive states was assessed using a mixed effect logistic regression model.

A generic inverse variance method was used to group study results, construct forest plots, and generate heterogeneity statistics.

Results

A common trajectory was observed showing an increase in the incidence of depression as the time to dementia diagnosis decreased despite cross-national variability in depression rates.

Conclusions

The results support the hypothesis that depression occurring in the preclinical phases of dementia is more likely to be attributable to dementia-related brain changes than environment or reverse causality.

Reference

Carles, S., Carriere, I., Reppermund, S., Davin, A., Guaita, A. et al. (2020) A cross-national study of depression in preclinical dementia: A COSMIC collaboration study. Alzheimer’s & Dementia. doi: 10.1002/alz.12149. Online ahead of print.

Book: Dementia: Support for Family and Friends

Book Title:

Dementia: Support for Family and Friends

Author(s): Dave Pulsford and Rachel Thompson.

Year: 2019.

Edition: Second (2nd).

Publisher: Jessica Kingsley Publishers.

Type(s): Paperback and Kindle.

Synopsis:

A comprehensive and practical guide to dementia, this book is essential reading for anyone who has a friend or relative with the condition.

This updated edition reflects new guidance on approaches to supporting people with dementia, focussing especially on the UK, and includes quotes from people with dementia as well as from family carers.

The book explores each stage of the journey people with dementia face and explains how it affects the person, as well as those around them both at home and in residential settings.

It shows how best to offer support and where to get professional and informal assistance.

Focussing on the progressive nature of dementia and the issues that can arise as a result, it gives practical advice that can help to ensure the best possible quality of life both for the person with dementia and the people around them.