First clinical encounters

Three memorable encounters with disturbances in higher order consciousness stimulated my research interest in this field of study. The first occurred before establishing a neuropsychological rehabilitation program. Dr Richard Carpenter, a neurologist, allowed me to attend rounds with him at St Anthony’s Hospital in Oklahoma City, OK. I observed him evaluating a woman in her 70’s who recently suffered a stroke and was paralyzed on the left side of her body. Dr. Carpenter asked her what brought her into the hospital, and she could not answer him. He asked if she had difficulty moving her hands and arms. She reported “not that I know.” He then asked her to raise both hands, and she raised only the right hand. When asked about the left hand/arm, she appeared to ignore his question and showed no emotional reaction. It quickly became apparent she was not aware of her left hemiplegia. This was the first time I witnessed anosognosia for hemiplegia (AHP) with associated anosodiaphoria.

A second encounter occurred during the neuropsychological rehabilitation of a young man with a history of severe TBI. Neuroimaging revealed large bilateral frontal lobe contusions, but he performed amazingly well on many neuropsychological tests, including the Halstead Category Test. He was calm and congenial, showing none of the irritability or impulsiveness often seen in young men several months post severe TBI. He was cooperative with all rehabilitation activities but occasionally would ask why he was in this rehabilitation program. He felt he had completely recovered from his TBI. One afternoon I observed him trying to talk to a young female physical therapist. She acknowledged his comments but quickly turned her head away, attempting to discourage any further dialogue. He did not pick up the social cues, continuing to speak with her and making somewhat inane comments. Eventually she became openly irritated with him, but he seemed perplexed by her reaction. When later talking with him about the incident, he did not perceive that he had done anything to make the young woman socially uncomfortable. His response was “you psychologists look for problems everywhere.” He was clearly unaware of his socially inappropriate behavior, although he did not appear emotionally upset with my inquiry. This was the first time I witnessed impaired self-awareness (ISA) after severe TBI.

The third memorable encounter occurred during the neuropsychological rehabilitation of a 37-year-old woman who also suffered a severe TBI. She was densely amnestic. When asked about her memory difficulties, she smiled, saying she had no problems with her memory. Her only difficulty, from her perspective, was her inability to walk. When pressed about her memory impairments, she became anxious, angry, and insisted that “my memory is just fine!!!!!” Her response seemed to reflect something more than just ISA. I later referred to this phenomenon as denial of disability (DD).

Initial research efforts on ISA after severe TBI

Since ISA seemed to be prevalent in many of the patients with a history of moderate to severe TBI enrolled in the neuropsychological rehabilitation program, the first step was to collect “some data” on this problem. Using a question borrowed from Dr Yehuda Ben-Yishay, I asked the patient to rate on a scale from 0 (not aware at all) to 10 (totally aware): “How aware are you today of how your TBI has affected you? Patients who underwent intensive neuropsychological rehabilitation and were considered “treatment successes” stated they were not totally aware. The rehabilitation team who had worked with them for several months independently agreed with their ratings. In contrast, “treatment failures” insisted that they were “totally aware,” while the staff’s ratings considered them to demonstrate persistent and severe difficulties with self-awareness.

The correlates of ISA after TBI

The first research attempt to explore the possible neuropsychological correlates of ISA after moderate to severe TBI employed the Patient Competency Rating Scale (PCRS, Prigatano et al., Reference Prigatano, Fordyce, Zeiner, Roueche, Pepping and Wood1986). Prigatano and Altman (Reference Prigatano and Altman1990) classified 64 traumatically brain injured patients into three groups: Group 1 overestimated their behavioral competencies on the PCRS compared to relatives’ ratings of the patients’ functional abilities (on the PCRS-Relatives form). Group 2 patients’ PCRS ratings were at a level similar to the PCRS-R ratings. Group 3 underestimated their behavioral competencies compared to relative’s ratings of them. Group 1 was considered to represent the group who showed primarily ISA. Many neuropsychological tests were administered, and group comparisons made. Of the many neuropsychological tests administered, only the performance on the Halstead finger tapping test (HFTT) separated the groups, with those who showed primarily ISA demonstrating the worst tapping speeds in the left hand. The paper concluded that there was not a simple or straightforward relationship between ISA and neuropsychological test performance. Findings appeared compatible with the existing literature linking behavioral indicators of right cerebral hemisphere dysfunction with disturbances in self-awareness. It also suggested (for the first time) that ISA might reflect a disturbance in the integration of thinking and feeling. Standardized neuropsychological tests were not able to measure this complex interaction. Using Mesulam’s (Reference Mesulam1985) conceptualization of the brain regions associated with the integration of feeling and thinking, it was proposed that ISA may be related to disturbances in “heteromodal cortex.” Furthermore, evaluation of neuroradiographic findings among the groups noted that those who demonstrated primarily ISA showed many more lesions in their brain than did those who rated themselves similarly or worse compared to relatives’ ratings of them. This basic finding was later replicated by Sherer et al. (Reference Sherer, Hart, Nick, Whyte, Thompson and Yablon2003).

The finger tapping findings were not always replicated, and the issue of sampling bias has repeatedly occurred when attempting to do clinical research on ISA in patients with TBI using convenience samples (e.g., Prigatano & Leathern, Reference Prigatano and Leathern1993; Prigatano et al., Reference Prigatano, Ogano and Amakusa1997).The research by Dikmen et al. (Reference Dikmen, Machamer, Winn and Temkin1995), however, unequivocally demonstrated that speed of finger tapping using the HFTT strongly correlated with initial severity of TBI.

This led to repeated observations that the initial severity of TBI was related to the severity of ISA several months post TBI. In a cross-cultural study with Spanish speaking individuals, ISA as measured by the PCRS, correlated r=+ 0.41 with the period of post traumatic amnesia (Prigatano et al., Reference Prigatano, Bruna, Mataró, Munoz, Fernandez and Junque1998). Other investigators later also reported similar findings (Sandhaug et al, Reference Sandhaug, Andelic, Berntsen, Seiler and Mygland2012; Sherer et al, Reference Sherer, Hart, Nick, Whyte, Thompson and Yablon2003). It is important to note, however, that the severity of injury often accounts for less than 25% of the variance and has not been replicated in every study (Ciurli et al, Reference Ciurli, Formisano, Bivona, Cantagallo and Angelelli2011).

Functional imaging correlates of self-reflection and ISA after TBI

Johnson et al. (Reference Johnson, Baxter, Wilder, Pipe, Heiserman and Prigatano2002) explored the functional imaging correlates of self-reflection in adults without known neurological injury. “Individual analyses revealed consistent anterior medial prefrontal and posterior cingulate activation for all participants” (pg. 1808) when performing a self-reflection task. This was the first neuroimaging study to suggest that brain structures associated with self-reflection (i.e., self-awareness) involve brain circuitry associated with both cognitive and affective information processing and problem solving. Using the same research paradigm, Schmitz et al. (Reference Schmitz, Rowley, Kawahara and Johnson2006) later concluded that individuals with TBI and with ISA showed fMRI findings implicating disruption of the medial and right dorsal prefrontal cortex.

At the time of these studies, the concept of “functional neural networks” was starting to appear. Raichle et al. (Reference Raichle, MacLeod, Snyder, Powers, Gusnard and Shulman2001) described the “default mode network” (DMN). Carhart-Harris and Friston (Reference Carhart-Harris and Friston2010)’s later review of the DMN concluded that, when an individual is involved in self-reflection, there is high blood flow activity in “the medial prefrontal cortex, the posterior cingulate cortex, the inferior parietal lobe, the lateral inferior temporal cortex and the medial temporal lobes” (pg. 1286). A subsequent study from Ham et al. (Reference Ham, Bonnelle, Hellyer, Jilka, Robertson, Leech and Sharp2014) reported that ISA following TBI clearly was associated with reduced functional connectivity of the fronto-parietal network and related limbic structures. Collectively, these findings were compatible with the hypothesis that ISA associated with severe TBI reflects disruption of “heteromodal” cortex.

Impaired awareness in various brain disorders

As my direct clinical work in neuropsychological rehabilitation came to an end, I became more involved in the neuropsychological evaluation of a wide range of persons with various brain disorders. I observed unique patterns of impaired self-awareness in different patient groups (Prigatano, Reference Prigatano2014). I noted, for example, that patients with multiple sclerosis (Prigatano et al., Reference Prigatano, Hendin and Heiserman2014) and Parkinson’s disease (Prigatano et al., Reference Prigatano, Maier, Burns and Prigatano2010; Maier et al., Reference Maier, Prigatano, Kalbe, Barbe, Eggers, Lewis, Burns, Morrone‐Strupinsky, Moguel‐Cobos, Fink and Timmermann2012) demonstrated ISA for different features of their neurological/neuropsychological impairments. One dramatic case involved AHP in which there was preserved awareness of complete cortical blindness following intracranial hemorrhage (Prigatano et al., Reference Prigatano, Matthes, Hill, Wolf and Heiserman2011). It became increasingly clear that Anton’s (Reference Anton1898) original observations and those echoed and expanded upon by Bisiach et al. (Reference Bisiach, Vallar, Perani, Papagno and Berti1986) were extremely important. Namely, “…. unawareness of the failure of a particular function betrays a disorder at the highest levels of organization of that function.” (pg. 478).

The strong implication was that subjective awareness of different cognitive (and perhaps affective, motor, language, behavioral etc.) functions may be “modularly” organized. Namely one can be aware of one functional limitation and at the same time not aware of another functional limitation. Bisiach and Geminiani (Reference Bisiach, Geminiani, Prigatano and Schacter1991) emphasize that, when there is a disturbance of any brain-behavioral connection, there is some negative alteration of the conscious experience or self-awareness of that functional disconnection. This makes the entire study of impaired self-awareness and anosognosia extremely complex; my research has only touched on a very small portion of this important area of study.

Denial and impaired self awareness

Efforts at both neuropsychological rehabilitation and neuropsychological assessment brought me face to face with the phenomena of denial of both disability and ability. Is denial (as a psychological defense mechanism) truly different from unawareness (as a neuropsychological disturbance)? Can they be separated to aid clinical diagnosis and treatment? The early work of Weinstein and Kahn (Reference Weinstein and Kahn1955) provided many convincing clinical examples of apparent denial of neurological conditions. Denial is, of course, a hypothetical construct that attempts to explain behavioral phenomena repeatedly observed in the practice of medicine, including neurology and psychiatry. The patient shows overwhelming behavioral evidence of significant limitations or impairments in some domain of functioning and reports no such impairments exist. The easiest examples come from addictions. The person is an alcoholic but reports alcohol poses no specific threat to his life or health, even when confronted with evidence of cirrhosis of the liver and the fact he has lost three jobs in the last two years because he was intoxicated. We also see denial of ability. The person is functioning quite well in life and yet reports significant cognitive impairments when none can be found on neuropsychological examination (Denney & Prigatano, Reference Denney and Prigatano2019). When presented with psychometric evidence of normal cognitive functioning, the patient often doubts the findings and considers them inadequate measures of their impairments in everyday life (Prigatano, Reference Prigatano2012).

Early clinical impressions, working in neuropsychological rehabilitation, were that denial had a “defense” quality, while ISA did not. Prigatano and Klonoff (Reference Prigatano and Klonoff1998) attempted to operationalize behavioral features that were observed in patients with TBI who appeared to be denying their neuropsychological impairments versus those with ISA as a direct result of their brain injury. While one study provided empirical support for the proposed observations by Prigatano and Klonoff (Reference Prigatano and Klonoff1998) (e.g., Kortte et al., Reference Kortte, Wegener and Chwalisz2003), a more recent attempt could neither confirm nor disconfirm their suggestions (Terneusen et al., Reference Terneusen, Winkens, Smeets, Prigatano, Porcerelli, Kamoo, van Heugten and Ponds2022). Again, the problem of sample bias was encountered. Individuals with TBIs who tended to get upset when talking about their disabilities/impairments often declined participating in community-based research on ISA and denial. This is what Prigatano & Klonoff (Reference Prigatano and Klonoff1998) suggested would be common in persons with denial of disability (DD).

From a phenomenological perspective, the differences observed in impaired self-awareness as a direct effect of a brain disorder versus alterations of self-awareness as a direct effect of psychological distress (Prigatano, Reference Prigatano2019, pg. 159) are listed in Table 1.

Table 1. Clinical features of persons with impaired self-awareness due to a brain disorder versus psychological distress

One major difference is the patient’s emotional reactions to feedback regarding their clinical condition. In anosognosia, the patient shows “blunted” affect with little or no concern over the feedback received. In contrast, there are often signs of anxiety and/or anger when hearing the feedback in denial. The patient in denial often behaves in a manner that discourages the clinician from asking further questions about their clinical condition. In “organically mediated unawareness,” the patient does not avoid or discourage discussion of their situation. They are more indifferent than defensive. Another clinical cue comes from neuroimaging studies. When ISA is present, neuroimaging studies often show brain lesions in regions known to be important for the functional impairment the patient reports not experiencing. In contrast, if a brain lesion is present in someone with DD, it is not in a region associated with that function.

Since ISA frequently (but not always) involves frontal lobe neural networks, these patients may have difficulty following new instructions and picking up social cues. For example, they may not know when they have said or done something that upsets someone else. Prigatano et al. (Reference Prigatano, Russell and Meites2024) suggested that this latter characteristic should be considered when screening for denial in patients with neurodegenerative memory impairments who are thought to be anosognosic of their memory difficulties.

Cross-cultural considerations

An early cross-cultural study by Gainotti (Reference Gainotti1975) reported that Swiss patients with “lack of awareness” of the memory impairments secondary to Alzheimer’s disease had a higher incidence of denial than Italian patients. The prevailing idea that stimulated this study was that a person’s attitude toward their health influenced the self-reporting of any cognitive impairment that may reflect a “character weakness” or psychiatric disorder. I conducted my first cross-culture study on ISA in New Zealand with this idea in mind (Prigatano & Leathern, Reference Prigatano and Leathern1993). In Maori culture, emotional, and cognitive difficulties are not viewed as a sign of personal weakness or lack of moral character. Instead, they are viewed with the same attitude as any physical illness. We anticipated observing fewer “denial” or “unawareness” indicators in patients with TBI with Maori ancestry compared to New Zealanders with non-Maori (English) ancestry. Using a translated version of the PCRS, we observed that Non-Maori English ancestry persons with TBI reported greater competency than their relative’s ratings of them while Maori ancestry patients did not. Cultural factors did appear to influence the self-reporting of severity of cognitive and behavioral symptoms after TBI. A second cross-cultural study on ISA with Spanish patients with TBI (Prigatano et al., Reference Prigatano, Bruna, Mataró, Munoz, Fernandez and Junque1998), reported similar findings to a study of American patients with TBI (e.g., Prigatano & Altman, Reference Prigatano and Altman1990; Prigatano, Reference Prigatano1996).

A third study using the PCRS with Japanese patients with brain dysfunction revealed an important cultural finding (Prigatano et al., Reference Prigatano, Ogano and Amakusa1997). While the Japanese patients tended to overreport their behavioral competencies compared to therapists’ ratings (suggesting ISA), there was a greater tendency for the Japanese relatives of the patients to agree with the patients’ ratings. In that culture, individuals “rarely engage in an open discussion of a person’s emotional characteristics or social interactions” (pg. 140). Relatives, therefore, might view it as a sign of disrespect or socially inappropriate behavior on their part to say that the person is more impaired than what the person reports. This study highlighted the importance of taking into consideration cultural mores when constructing tests that attempt to indirectly measure ISA or DD.

Cultural differences in ISA of memory impairment in persons with dementia have also been noted in India, Latin America, and China (e.g., Mograbi et al., Reference Mograbi, Ferri, Sosa, Stewart, Laks, Brown and Morris2012). In addition to demonstrating that individuals from India appear to have less awareness of their memory impairments, the authors make the point that the educational level of the person is associated with the frequency of unawareness, which was highest in persons with higher education. They argue that unawareness should be considered a common neurobiological disturbance associated with dementia, but one that is influenced by social and cultural factors. Weinstein and Kahn (Reference Weinstein and Kahn1955) would most likely add that it is also influenced by the premorbid personality characteristics of the individual.

It is my opinion that in any given patient population who demonstrates probable ISA, measures of DD should be included to adequately characterize the study sample (Prigatano et al., Reference Prigatano, Russell and Meites2024).

The negative effects of ISA on caregivers including rehabilitation therapists

Patients who persistently report that their cognitive abilities are greater than what their therapists observe can eventually irritate rehabilitation therapists, which can negatively impact patient care. This topic is often not adequately discussed in the literature, although the quality of the therapeutic alliance correlates with neuropsychological rehabilitation outcome (e.g., Prigatano et al., Reference Prigatano, Klonoff, O’Brien, Altman, Amin, Chiapello and Mora1994). I have previously described a case of a young man with an amnestic disorder who would not use memory compensation techniques because he insisted his memory was better than what the therapists were telling him (Prigatano, Reference Prigatano1999, pg. 231–231). To teach the patient a lesson (with the secret hope of convincing him of his misperception of himself), the therapists participated in actions that caused the patient considerable anxiety. This fractured, not helped, the therapeutic alliance with the patient.

Equally importantly, patients with severe ISA often produce considerable emotional distress in family members. We reported that “the correlation between relatives’ level of distress and their ratings of the patients’ unawareness of their difficulties for persons with TBI was –0.52, p = .006” (Prigatano et al., Reference Prigatano, Borgaro, Baker and Wethe2005). Collectively these findings argue for the importance of training rehabilitation staff and family members to understand the problem of ISA (and DD). This has been recognized not only in neuropsychological rehabilitation of persons with acquired brain injuries (Prigatano, Reference Prigatano1999), but in the care of persons with dementia as well (Clare, Reference Clare2010).

A clinical classification model for distinguishing anosognosia, impaired self-awareness, and denial

As noted earlier, the work of Weinstein and Kahn (Reference Weinstein and Kahn1955) was the only scholarly and extensive study on anosognosia that was available in the 1970’s. Their methods included extensive and repeated interviews with patients (often however only in the acute phases of illness), psychometric testing, EEG recordings, and comparison of their findings of patients with anosognosia to patients with similar types of brain lesions without anosognosia. They make a distinction between explicit verbal denial versus implicit denial. They reviewed cases in which patients who denied their paralyzed limbs might ascribe ownership of their paralyzed limb to someone else (pg.4). Such patients may also refer to their affected paralyzed limb in pejorative terms (pg.4). This basic approach and identification of important comorbid features of persons with anosognosia were later studied using somewhat more contemporary terminology and more sophisticated technologies (see Prigatano, Reference Prigatano2010). Weinstein and Kahn’s (Reference Weinstein and Kahn1955) work anticipated many important issues involved in studying disturbances in higher order consciousness associated with brain disorders.

Based on their data and Weinstein’s training in psychiatry as well as in neurology, they concluded: “Our findings indicate that the various forms of anosognosia are not discrete entities that can be localized in different areas of the brain. Whether a lesion involves the frontal or parietal lobe determines the disability that may be denied, not the mechanism of denial.” (pg. 123). Later Weinstein recognized that this conclusion was misleading (personal communication, 1997). Denial is indeed a mechanism that may not be in or mediated by specific frontal or parietal lobe neurocircuits. However, the unawareness of a disability/impairment can be discrete (as many studies have subsequently shown, see Bisiach et al., Reference Bisiach, Vallar, Perani, Papagno and Berti1986; Prigatano et al., Reference Prigatano, Matthes, Hill, Wolf and Heiserman2011). He attempted to clarify this point and concurred that both neurologically mediated impaired self-awareness and psychologically mediated denial can exist in the same patient at the same time. Both phenomena are “real” and need to be better understood to advance the field of neuropsychological rehabilitation (Prigatano & Weinstein, Reference Prigatano and Weinstein1996).

Selected studies have subsequently appeared which attempted to investigate the neuroanatomical and functional imaging correlates of anosognosia for hemiplegia (AHP) (e.g., Berti et al., Reference Berti, Bottini, Gandola, Pia, Smania, Stracciari and Paulesu2005; Karnath et al., Reference Karnath, Baier and Nägele2005; Vocat and Vuilleumier, Reference Vocat, Vuilleumier and Prigatano2010) as well as denial in patients with “hysterical sensorimotor loss” (Vulleumier et al., Reference Vuilleumier, Chicherio, Assal, Schwartz, Slosman and Landis2001). Patients with classical AHP often show damage or disruption to frontal-parietal regions in addition to the insular cortex. In the few patients studied with hysterical sensorimotor loss (in which denial is thought to play an important role in their symptoms), alterations of blood flow in the thalamus and basal ganglia have been reported (Vulleumier et al., Reference Vuilleumier, Chicherio, Assal, Schwartz, Slosman and Landis2001).

While the technological advancements in neuroimaging allowed for a more detailed assessment of brain regions associated with AHP, there is no overall neurological model of human consciousness that allowed us to integrate these findings. Zeman (Reference Zeman2001), however, provided an innovative model that could be of potential help. Zeman noted that the term “consciousness” can be applied to three different types of human experience. He gave these examples. “After a lucid interval, the injured soldier lapsed into unconsciousness.” “I am conscious of a feeling of dread and overpowering smell of burning rubber.” “I am conscious that I am straining your patience.” In conjunction with Sterling Johnson, we proposed that Zeman’s (Reference Zeman2001) insights could be restated as “three vectors of consciousness” (Prigatano & Johnson, Reference Prigatano and Johnson2003). These three vectors of consciousness must: “(1) interact; (2) be subserved by overlapping neurocircuits in the brain and brain stem; (3) evolve to meet different needs of the organism that aid the never-ending processes geared towards survival.” (pg. 16). By using the term ‘vector,’ we were proposing that these three components of human consciousness have a “magnitude and a direction.” As such they appear to be “energy forces” that influence one another and yet are somehow “united,” the result being a preserved “sense of self” even when “islands” of self-unawareness exist. There are many behavioral examples which are compatible with this view that disturbances in human consciousness are associated with changes in the arousal/energy systems of the brain. For example, after a right hemisphere stroke, many patients with AHP appear hypoaroused with their heads bent forward. Many patients with severe TBI with ISA often appear tired (i.e., frequently yawning) and can sleep long hours each day, especially with the first few months of their brain injuries. Patients with depression (and possible denial of that depression) often speak of low interest and energy. While we certainly do not understand how consciousness emerges and reflects different overlapping energy systems of brain functions, Sperry’s (Reference Sperry1969) observations are insightful. He proposed that conscious awareness is “…. A dynamic emergent property of cerebral excitation” (pg. 533) that can have “….causal effects in brain function that control subset events in the flow pattern of neural excitation.” (pg. 533). It is an “emergent” (I would add energy) product or consequence of brain function that at same time influences brain function. Perhaps this is why we are so interested in consciously understanding consciousness.

Adapting Zeman’s model (2001), we suggested (Prigatano & Johnson, Reference Prigatano and Johnson2003) that “Vector 1” allows for the biological foundation of wakefulness. It involves the upper brainstem, the posterior hypothalamus, and the thalamus (Zeman, Reference Zeman2001). It is the “gatekeeper of the sleep-wakefulness continuum.” It allows us to awake from sleep and know “what is real.” It forms the foundational basis from which “Vector 2” can emerge. Vector 2 emerges as basic limbic system structures evolve, which includes primitive cortical structures (i.e., the anterior and posterior cingulate gyrus). Luria (Reference Luria1976) made the important evolutionary observation that the frontal lobes are an evolutionary extension (he referred to them as a “tertiary zone”) of both limbic and motor cortex. Thus, the frontal lobes are involved in the regulation of movement and the experience and expression of emotion. These two domains are often affected in both ISA and DD but in somewhat different manifestations as I have attempted to partially illustrate in Table 1. Another term for this “tertiary zone” is “heteromodal cortex.” In this model, Vector 2 provides the biological basis of the phenomenological state of “self-reflection” in the “here and now.” It provides the individual with their subjective experience of specific personal needs and motorically necessary responses to external threats/opportunities. It does not form the “I,” “me,” or “sense of self.” Rather it appears modularly organized, providing self-awareness of whether specific needs are experienced and or acted upon. Depending on which areas of the heteromodal cortex are rendered dysfunctional, different (specific) disorders of self-awareness (i.e., self-reflection) can be observed (see Prigatano, Reference Prigatano2010). Vectors 1 and 2 are anatomically connected as recent neuroimaging had demonstrated (Edlow et al., Reference Edlow, Olchanyi, Freeman, Li, Maffei, Snider, Zöllei, Iglesias, Augustinack, Bodien, Haynes, Greve, Diamond, Stevens, Giacino, Destrieux, van der Kouwe, Brown, Folkerth, Fischl and Kinney2024).

Vector 3 is viewed as a further evolutionary development of Vectors 1 & 2 that may be unique to mammals (Humphrey, Reference Humphrey2023). It allows the animal to sense what another is experiencing and to act accordingly. In humans, we often refer to this as “theory of mind” or “metacognitive judgments” about our own “mind” and the “mind of others.” As such, disturbances in self-awareness are often associated with disturbances of awareness of another’s emotional or mental state. This is exemplified in the second clinical state I noted. In that case the young man with bilateral frontal contusions secondary to severe TBI was not aware that he was making another person uncomfortable with his socially awkward statements.

The model proposed by Zeman (Reference Zeman2001) and modified by Prigatano and Johnson (Reference Prigatano and Johnson2003) has implications for understanding denial (of both disability and ability). Denial of hemiplegia several months or years post stroke is indeed rare (see Prigatano, Reference Prigatano2010). Yet House and Hodges (Reference House and Hodges1988) reported such a case in an individual with damage primarily to the basal ganglia. The study by Vuilleumier et al. (Reference Vuilleumier, Chicherio, Assal, Schwartz, Slosman and Landis2001) cited above noted that alterations of blood flow in thalamus and basal ganglia were observed in patients with hysterical sensorimotor loss. The implication is that psychological defense referred to as denial may reflect a disruption of the energy system emerging from Vector 1 which influences Vector 2. This, of course, is a conjecture, but conjectures are necessary when testing any model, especially a model that helps capture key aspects of human consciousness. Figure 2 illustrates my attempt to portray the relationships between anosognosia, from impaired self-awareness from denial (Prigatano, Reference Prigatano2014).

Figure 2. Disturbances of self-awareness in “awake” neurological and psychiatric patients: an integrated clinical model.

The model assumes that disturbances in self-awareness are different in their phenomenology if they are associated with a neurological disturbance versus a psychological adjustment problem. In the former, a lack of self-awareness is a direct result of underlying brain pathology. Analogous to aphasic syndromes, in which one can have “global aphasia” versus “fluent” versus “nonfluent” aphasia, one can have a complete loss of awareness of a specific function or partial loss of awareness of a specific function. In the former case, we have a “complete syndrome” or anosognosia, whereas in the latter case, we have an “incomplete syndrome” or ISA. When there is partial awareness of an impaired function, a person may use defensive or non-defensive methods of coping with their partial perceived functional change. This was a position that Weinstein eventually agreed with (personal communication, 1997). Note that in defensive methods of coping, denial may occur, but other psychological defenses might also come to play.

In one extreme scenario, the person believes they are substantially more capable than others, which can reach psychotic proportions in the form of delusions of grandeur. The opposite can also occur, in which the individual perceives themselves as unable to perform some functional skill that neurologically and neuropsychologically of which they appear capable. In this case, one might refer to “denial of ability,” which is seen in the traditional conversion disorders. If this diagnostic model is useful, it should help guide treatment strategies.

Treatment considerations in neuropsychological rehabilitation, psychological care, and psychotherapy

Treatment of disorders of higher levels of consciousness (i.e., those emanating from a disruption of Vectors 2 and 3) is a difficult task that requires hours of effort on the part of both the patient and therapist(s). When Vectors 2 and 3 are altered because of underlying brain dysfunction, the approach is different than when they are altered due to psychological conflicts or crises. Table 2 lists suggested approaches when dealing with ISA and DD after moderate to severe TBI (from Prigatano & Sherer, Reference Prigatano and Sherer2020). In the case of ISA, engaging the patient in meaningful rehabilitation activities that allow them to observe their behavior helps them to experience potential “strengths” or “weakness.” In some instances, this helps improve self-awareness, which may increase the likelihood of using compensatory strategies. As they benefit from such activity, there is often improvement in the therapeutic alliance, and the patient is more easily guided into activities that he or she can successfully perform. When DD is strongly suspected, a traditional psychotherapy approach is often more helpful. Understanding the patient’s life history and methods of dealing with anxiety or conflict can give clues as to how to talk to the patient in a manner that allows them to explore the source of the anxiety that stimulates denial.

Table 2. Different approaches to treating/managing clinically significant ISA verse clinically significant dd after moderate to severe TBI

TBI = traumatic brain injury, ISA = impaired self-awareness, DD = denial of disability.

Understanding disturbances in higher order consciousness can guide the psychological care of persons with various brain disorders. In Parkinson’s disease, for example, patients’ neuropsychological difficulties can include limited awareness of their motor impairments (Maier & Prigatano, Reference Maier and Prigatano2017). The patient may therefore repeatedly attempt to walk without a walker and have several falls. This can infuriate family members and produce considerable emotional conflict within the home. Explaining to a spouse that the person is not fully aware of these limitations and has underlying problems with working memory can ease the tension between a family member and patient (Prigatano, Reference Prigatano2019, pg.266; also, Prigatano & Salins, Reference Prigatano and Salins2022).

Understanding the difference between denial and ISA can also be useful in psychotherapy. A young man suffered a TBI after “falling” from a building. Medical recorders raised the question of whether this was an accidental fall or an attempt at suicide. In the context of working with him in psychodynamic psychotherapy (as described in Prigatano & Salas, Reference Prigatano, Salas, McMillian and Wood2017), it eventually came to light that he was experiencing considerable shame in his life prior to his injury. He began to recognize (i.e., experience) this after many hours of psychotherapy. That shame, while under the influence of various unprescribed drugs, led to a suicide attempt, to which he could now admit. He became able to talk about his feelings in more detail, and his use of drugs substantially reduced.

Theoretical implications for understanding human consciousness

There has been a resurgence of interest in the neuroscience community to understand the brain mechanisms that allow consciousness to emerge and change over time. The latter question has been referred to as the “hard problem” of consciousness (Chalmers, Reference Chalmers1995).

Using multimodal MRI of the brain, Edlow et al., Reference Edlow, Olchanyi, Freeman, Li, Maffei, Snider, Zöllei, Iglesias, Augustinack, Bodien, Haynes, Greve, Diamond, Stevens, Giacino, Destrieux, van der Kouwe, Brown, Folkerth, Fischl and Kinney2024) have recently described a default ascending arousal network (dAAN) that supports the functioning of the DMN. That network includes the brainstem, hypothalamus, thalamus, and basal forebrain. Further they highlight the potentially important role of the dopaminergic ventral tegmental area of the midbrain in the arousal component of awareness.

Solms (Reference Solms2021) has suggested that brainstem networks are the foundation for the sense of “I” or “self” and are not to be found in the cortex. This is an interesting proposition. The sense that “I am I” does not change in cases of anosognosia, ISA, or denial. The subjective experience is so robust that even when an arm is seen as not belonging to the person with AHP (i.e., the phenomenon of somatoparaphrenia), the person feels/believes that they are who they are. Their self-hood, if you wish, is preserved. But their awareness of specific functioning limitations is impaired. The dopaminergic ventral tegmental area in the midbrain is known to be an important brain region involved in early “reward processing, aversion, stress modulations…” (Cai & Tong, Reference Cai and Tong2022). As such it appears to be a primitive response system to reward and aversive stimuli. It might in fact play a key role in the development of the “sense of self” in which humans have an emerging subjective experience that “this is good for me” or “this is bad for me.” This may be the earliest experiences of “me.”

The recent work of Humphrey’s on the evolution of consciousness (Humphrey, Reference Humphrey2023) adds further intriguing insights into this proposition. While he does not indicate that “sense of self” evolves purely from a specific brain region, he does suggest that “sensations” are the rudimentary building blocks of consciousness awareness. He states: “sensations are ideas that represent what’s happening to your sense organs and how you feel about it. They do this by tracking motor responses that the stimuli evoke in your brain: covert-unrealized-forms of bodily expression. They have acquired phenomenal properties as a secondary overlay. These properties are not illusory. They are veridical properties of the feeling of ‘what it’s like.’” (pg. 105). Humphrey’s (Reference Humphrey2023) work is especially interesting since it attempts to provide an evolutionary explanation of consciousness and directly relates the emergence of human consciousness with sensations associated with feelings and movements.

Concluding comments

A major emphasis of my clinical work and research has been to highlight the importance of the patient’s subjective experience for neuropsychological rehabilitation, neuropsychological assessment, and in the psychological care of patients. A second major emphasis has been on the importance of integrating knowledge of neuropsychology (and other branches of the neurosciences) with nonbiological explanations of human behavior when attempting to understand disturbances of higher order consciousness. If clinical neuropsychologists do this, they often enrich their professional work; both they and the patients they serve benefit from this integrative approach. The ultimate “cost-benefit” analysis of clinical neuropsychology in the health care environment (Prigatano & Pliskin, Reference Prigatano and Pliskin2003) and in the scientific and academic communities is determined by how our integrated understanding of human beings aids patient care.