Loneliness and Brain Injury
In the early history of human evolution, the need to belong to others may have been protective as those who were on the periphery of social groups may have been less likely to survive. Group participation likely ensured more access to food, shelter, protection from external threat, and increased opportunity to mate (Hienrich and Gullone, ). It has been proposed that, through processes of natural selection, humans have evolved the need for social connectedness at both a biological and psychological level (Masi et al., ). Thus, the subjective feeling of loneliness has been proposed as an adaptive form of ‘social pain' which motivates humans to seek social connection (Eisenberger, ).
Although transient loneliness may be considered adaptive, studies have demonstrated that persistent loneliness can become maladaptive, resulting in various negative outcomes across both psychological and physical domains (Cacioppo and Patrick, ; Holt-Lunstad et al., ; Hakulinen et al., ). Several reports have established positive correlations between loneliness and increased morbidity. For example, the deleterious effects of loneliness have been shown to be comparable with other well-known clinical risk indicators such as smoking, and even greater to other factors such as obesity and high cholesterol (Pantell et al., ). Large meta-analytical studies have demonstrated that those who live alone, are socially isolated and subjectively feel lonely demonstrate an average 26–32% increased likelihood of mortality (Holt-Lunstad et al., ). The mechanisms that underpin the deleterious effects of loneliness, such as increased morbidity, are not yet fully established, but are likely to span a range of physiological systems (Friedler et al., ). A detailed review on recent neurophysiological models of loneliness is outlined in Quadt et al. (), and summarized by Gronewold and Engels (). Additionally, a large cohort study using the UK biobank data (Hakulinen et al., ), highlights the association between social isolation and mortality, which may be mediated by a reduction in access to support during illness.
The terms loneliness and social isolation have been often used interchangeably. However, they should be considered as two distinct concepts. Social isolation refers to a decreased quantity of social relations with other people (Zavaleta et al., 2014). Studies often conceptualize the quantity of social contact as the structural characteristics of a social network (size, composition, frequency and length of contact). In contrast, the quality of social contact has been defined as the individual's subjective assessment of how satisfied they are with their social relationships. Importantly, the qualitative interpretation that your social needs are not being met is the hallmark of loneliness. Moreover, several studies have shown that quantitative and qualitative components of social relationships are dissociable (Salas et al., ; Byrne et al., ). For example, a person may have a small social network but experience it as supportive, or have a large social network and feel lonely.
Despite evidence regarding the presence and heterogeneity of loneliness across the life span (Qualter et al., ), the current literature is dominated by research examining loneliness in older normotypical/non-neurological populations, or those with progressive neurological conditions such as dementia. It has been noted nevertheless that individuals and groups with different forms of disability may be particularly vulnerable to social isolation (Durcan and Bell, ). People with different forms of neurological illnesses are especially vulnerable to social isolation due to participation limitations imposed by motor, cognitive and socio-emotional impairments. Furthermore, loneliness and social isolation have also been shown to mediate the trajectory of recovery, stagnation, or indeed deterioration, of neurological conditions (Glass and Maddox, ).
There is a growing literature reporting higher levels of loneliness in adults with acquired brain injury. Recent research (Byrne et al., ) demonstrated that 30–44% of those with a history of stroke report experiencing loneliness. Furthermore, those with a history of stroke were found to be 70% more likely to report loneliness when compared to the healthy individuals. To put this into perspective, amongst those that live with brain injury, loneliness has similar, if not greater, prevalence rate than other psychological complaints, such as depression (31%) and anxiety (20%) (Schöttke and Giabbiconi, ). Importantly, it has been reported that loneliness, and not the size of the network, or level of perceived social support, is the best predictor of quality of life, emotional wellbeing and depression in people with acquired brain injury (ABI) who live in the community (Salas et al., ).
Despite this emerging evidence, there is a lack of information regarding why people with ABI may feel persistently lonely, exploring the potential contribution of cognitive/behavioral deficits and interpersonal factors. Therefore, the goal of this article is to contribute to this discussion by linking two lines of research: loneliness and executive functioning. To do so, we introduce a model of loneliness (The Reaffiliation Motive (RAM) model; Qualter et al., ) as a useful theoretical framework that can be used to map how cognitive impairments may contribute to persistent loneliness after brain injury. In the following, we present the RAM model, its components and theoretical background. We then introduce the model of executive functions proposed by Stuss (2011), which describes different profiles of executive impairment: energization, executive cognition, emotion/behavioral regulation and metacognition. Each of these profiles is discussed in relation to the RAM model, underscoring how diverse profiles of neurocognitive impairment could compromise different stages of the reaffiliation process.
In Search of a Model to Understand Loneliness After Brain Injury
There is currently a lack of models that aim to understand loneliness after brain injury. However, there are models developed to explain the experience of loneliness in normotypical individuals, which may be generalized to explore this problem in brain injury survivors. The Evolutionary Theory of Loneliness (ETL), proposed by Cacioppo and colleagues (Cacioppo and Cacioppo, ) suggests that the experience of loneliness, like physical pain, is ultimately an evolutionary protective mechanism - a type of social pain. Like pain, loneliness is an aversive experience, but with the primary purpose to motivate individuals to reintegrate and seek safety in the form of social connection. However, this model does not account for all individuals. For example, the Evolutionary Theory of Loneliness does not account for those who actively avoid social connection because of their anxiety or social phobia, or persons with personality structures driving them to avoid social contact.
The RAM model (Qualter et al., ) expands on the motivational aspect of Cacioppo's ETL. Like the ETL, the RAM model suggests that the experience of loneliness is an adaptive signal that motivates individuals to reconnect with other people. The RAM model describes specific components of the re-affiliation process, placing the perception of social isolation at the start (Figure 1). The perception of social isolation activates the motivation to reconnect (reaffiliation motive), which in turn results in a paradoxical behavioral response - withdrawal. The paradoxical withdrawal response refers to an increase in the motivation to connect with others but at the same time an increase in the implicit hypervigilance for social cues to monitor social interactions and social threats. This response allows individuals to appraise their own behavior and the social environment to analyze it for threats; thus, modifying cognitive-behavioral responses that may lead to either reaffiliation, ending the transient feeling of loneliness, or persistent loneliness. The direction of outcome is mediated by the cognitive-behavioral processes that take place. For example, prolonged loneliness is associated with maladaptive cognitive bias such as attentional bias, memory bias, attribution bias and external locus of control. These cognitive biases can compromise reaffiliation resulting in further behavioral withdrawal and subsequent negative affect.
Figure 1
The RAM model is a promising theoretical tool since it suggests that the process by which people reconnect to others when feeling lonely is complex and requires cognitive, behavioral and interpersonal resources. Consequently, it can be expected that individuals who present with cognitive, behavioral or interpersonal impairments after brain injury, will experience difficulties navigating through this process in order to reconnect. Acquired brain injury not only can generate loneliness, but more importantly, it can also compromise people's capacity to overcome loneliness by actively reconnecting with others, thus generating persistent loneliness. Because brain injured survivors can experience a wide and varied range of cognitive, behavioral and socio-emotional deficits, there are many ways in which reaffiliation can be compromised. In this article we use the case of executive impairment profiles as an example to show how specific neuropsychological deficits can compromise different components or tasks in the RAM model.
Reaffiliation Failure in People With Executive Impairment
Executive Dysfunction is a common problem after several forms of ABI (e.g., stroke, traumatic brain injury), often -but not exclusively- related to prefrontal lobe damage. It has been defined as an impairment in a wide set of skills required for effective problem solving, planning and organization, self-monitoring, initiation, error correction and behavioral regulation (Evans,
The Model of Frontal Lobe Functioning (Stuss, 2011) has been widely used in Neuropsychological Rehabilitation (Winson et al., 2017). It suggests that four executive components can be differentially compromised after brain injury: Energization, Executive Cognition, Emotional and Behavioral Self-Regulation and Metacognition. It can be argued that individuals with dysexecutive impairment can be clustered in four groups or profiles, each of them with a predominant deficit in one or more of these components. In this section we will describe the main clinical presentation of each profile and formulate hypotheses regarding how the RAM model and its components might be differentially compromised (Figure 2).
Figure 2

Executive components associated with the reaffiliation motive (RAM) model of loneliness. Components of the RAM model (Qualter et al.,
Energisation
Energization has been defined as the capacity to internally initiate, and sustain, a voluntary or non-reflexive response. Energisation problems are common after damage to superior medial prefrontal structures (BA 24,9 and 6, Stuss, 2011) and have been related to amotivational syndromes such as apathy and abulia (Moretti and Signori,
Energization problems can compromise several reaffiliation components. Perhaps the most important one is the perception of social isolation, or social pain, which can be altered due to impairment in emotional reactivity. Emotional reactivity has been defined as an emotional process related to the activation of emotional responses, its intensity and duration (Becerra and Campitelli,
Executive Cognition
Executive Cognition has been described as a process that involves both the capacity to develop and implement a plan when facing a novel task (task setting) and the ability to check that one remains on task over time adjusting behavior if needed (monitoring) (Henri-Bhargava et al.,
Individuals with problems in executive cognition might struggle moving along the different phases of the reaffiliation process. They might experience significant difficulties during the cognitive reaffiliation phase, where the formulation of a social assessment is required. Due to a tendency to consider only what is apparent and can be seen, people with executive cognition impairments may struggle reading subtle and complex social interactions and mental states. People with executive cognition impairments can also struggle “seeing the forest and not just the trees”, thus, becoming stuck in one or two aspects when reading a social situation (Winegardner, 2017).
There is also evidence showing that individuals that tend to perseverate can become fixated on negative elements of a social situation, easily falling into a negative emotional and interpersonal loop and struggling to downregulate negative feelings on their own (Salas C. E. et al.,
Emotional and Behavioral Regulation
Emotional and behavioral self-regulation is a capacity related to the integration of motivational, reward/risk, emotional and social aspects of behaviors (Stuss, 2011). Damage to the ventromedial prefrontal cortex (BA 32, 25, 24, 14, 13, 12, 11) often compromises this ability (Henri-Bhargava et al.,
Impairments in behavioral and emotional self-regulation would very likely compromise several components of the RAM. First, the behavioral reaffiliation component indicates that individuals initially withdraw from the immediate social environment once loneliness is perceived, in order to assess the level of social threat. Those with behavioral and emotion regulation difficulties may struggle inhibiting their behavior in order to withdraw, as a means to assess changes in a social situation. In other words, they may struggle stopping behavior in order to think about what is going on, thus tending to “act or speak without thinking”. For example, a survivor may become over familiar with people he/she just met, in order to manage feelings of isolation or exclusion during a social gathering.
Second, emotional dysregulation can compromise cognitive reaffiliation by strengthening perceptual, attentional and negative memory biases. Here, inhibitory failures are relevant to consider, since the inhibition of self-perspective is necessary to comprehend other people's emotions, desires and experiences, particularly those that differ from ours (Samson et al.,
Metacognition
Finally, metacognition has been defined as an integrative function that coordinates the other three executive components (Stuss, 2011). Metacognition can be compromised after damage to the frontal poles (BA 10s and 10i) and is often observed as a difficulty in observing one's own mental processes (self-awareness) and understanding other people's mental states, particularly when they differ (theory of mind) (Fleming et al.,
Higher-level metacognitive processes are likely required throughout the reaffiliation process. Therefore, when impaired, metacognitive difficulties can pose a barrier at several points of the model. The perception of loneliness may be compromised due to an inability to interpret and reflect on the social situation. Here, concrete patients are an illustrative example. Concreteness has been defined as a form of metacognitive impairment, characterized by a difficulty in detaching from immediate experience in order to observe and reflect upon emotions and mental states related to the self and others (Salas C. et al.,
Metacognitive processes are also likely to be important for the cognitive reaffiliation component of the RAM model. Individuals with metacognitive difficulties may be unable to reflect on their behavior and thoughts, thus perpetuating maladaptive cognitive and behavioral responses that led to social isolation. For example, individuals with egocentricity may be unable to see the perspective of others, or consider the contribution of their own behavior to the experience of others, leading to interpersonal conflicts.
Summary of Integration Between Models
The main corollary that stems from our attempt to integrate theory and clinical practice in this area, is that discrete cognitive and behavioral impairments are likely to alter specific components of the RAM model. In this paper we have only underscored the relevance of considering how different forms of executive dysfunction can compromise a survivor's ability to reconnect with others. It is hoped that highlighting how specific impairments of executive function may impact specific processes of reaffiliation will lead to testable predictions in clinical practice and in further empirical research. However, it is sensible to consider that impairment of other non-executive skills (e.g., language, communication, memory, attention) could also alter the reaffiliation process. It is our belief that the systematic study of reaffiliation difficulties experienced by people with diverse profiles of neurocognitive disorders could offer valuable information to understand the neuropsychological bases of this process and its components. A summary of this adapted model including the contribution of executive skills at the different stages of the process can be found in Figure 2.
Discussion
The main goal of this article was to advance our understanding of loneliness after brain injury by introducing the RAM model and theoretically exploring how different forms of executive impairment could alter the reconnection process generating persistent loneliness. This article proposes that diverse forms of cognitive impairment can alter different aspects of social interaction, such as social reconnection. Similar ideas have been proposed before, particularly by those interested in the relational impact of brain injury (Bowen et al.,
The emphasis on the relationship between neuropsychological impairments and difficulties in the reaffiliation process attempts to shed light on the many factors that can contribute to loneliness after brain injury. Even though we have focused on this variable here, other factors need to be considered as well. Negative bias during the cognitive reaffiliation phase may well be influenced by real experiences of social rejection and misunderstanding. It is well-known that brain injury, and its visible and non-visible sequelae, are poorly understood by people in the community (Code et al.,
If executive impairment can compromise a survivor's capacity to reconnect to others when feeling lonely, other types of cognitive impairment should also have an impact in the reaffiliation process. Difficulties in social interaction, and social isolation, have been described as key long-term problems in people with aphasia, impacting quality of life and emotional adjustment (Code and Herrmann,
Deep or profound amnesia is another interesting type of impairment to consider. Profound amnesia is often caused by diencephalic lesions, after different forms of encephalitis, strokes of the posterior cerebral artery, hypoxia or tumors. The socio-emotional consequences of profound amnesia are less well-known, despite the long-term observations of historical cases. It is known, however, that people with deep amnesia are able to develop new interpersonal relationships, despite not being able to remember who the new person is or where they met him/her (Tranel and Damasio, 1993; Turnbull et al., 2006; Moore et al.,
Clinical Implications
In principle, the RAM model could be generalized to any form of ABI. However, based on the type of ABI alone, it is difficult to infer functional outcome or cognitive sequelae with a high degree of confidence. Each ABI may result in a broad range of cognitive and emotional sequelae dependent on a multitude of pre and post morbid factors. The focus of the current paper related to executive functioning, which is common following many forms of ABI (e.g., traumatic injury, anoxia, cerebrovascular accidents and infection), which makes executive functions a good candidate for regulating loneliness across a range of brain injuries.
The primary clinical implication of this article highlights the need to consider how diverse types of cognitive impairments can impact social interaction, compromising reaffiliation and contributing to persistent loneliness. All clinicians involved in neurorehabilitation should routinely assess for markers of social isolation (e.g., number and frequency of social contacts, social support), paying particular attention to the survivor's subjective experience of loneliness. This could be completed using well-validated questionnaires such as the UCLA Loneliness scale. Loneliness has systematically emerged as a key variable predicting quality of life and depressive symptoms (Salas et al.,
In addition, clinicians may complement the clinical interview using self-report measures to screen and quantify loneliness (Valtorta et al., 2016), such as the De Jong Gierveld Loneliness Scale (De Jong Gierveld and Van Tilburg,
Another clinical implication is the need to study and develop interventions that specifically address loneliness after brain injury. There is some evidence that enlarging social networks of survivors can reduce loneliness (Rowlands,
Depending on the neuropsychological profile of the survivor, clinicians could design specific interventions using the RAM model as a theoretical framework, thus targeting specific components of the process that may be particularly compromised. For example, those with specific energisation difficulties may struggle more at early stages of the reaffiliation process (perception of social isolation and activation of reaffiliation), than those with executive cognition difficulties, who may require support later along the process (cognitive reaffiliation). Classic neuropsychological rehabilitation strategies could be adapted to promote reaffiliation at different stages, since evidence-based interventions developed to manage different forms of executive impairment have been widely reported in the literature. People with energization problems could benefit from developing and sustaining routines that include social interaction as a central activity (Jackson et al.,
Brain injured survivors with executive cognition problems may benefit from learning strategies that enhance thinking skills when appraising a social situation or when solving a problem that emerges during an interpersonal encounter, thus avoiding confusion and perseveration. Goal Management Training (Levine et al.,
Funding
This research was performed as part of an all-Wales Economic and Social Research Council (ESRC) Doctoral Training Centre Ph.D. Studentship (awarded to RR and RC, Ph.D. student: CB).
Publisher's Note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Statements
Author contributions
CB and CS conceived the presented idea linking existing models of executive function to a model of loneliness. CB, CS, RC, and RR further refined the presented ideas and contributed to the final manuscript. All authors contributed to the article and approved the submitted version.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
References
1
BecerraR.CampitelliG. (2013). Emotional reactivity: critical analysis and proposal of a new scale. Int. J. Appl. Psychol.3, 161–168. 10.5923/j.ijap.20130306.03
2
Bennett-LevyJ. E.ButlerG. E.FennellM. E.HackmanA. E.MuellerM. E.WestbrookD. E. (2004). Oxford Guide to Behavioural Experiments in Cognitive Therapy. Oxford: Oxford University Press.
3
Ben-YishayY.DillerL. (2011). Handbook of Holistic Neuropsychological Rehabilitation: Outpatient Rehabilitation of Traumatic Brain Injury. Oxford, NY: Oxford University Press.
4
Blom JohanssonM.CarlssonM.ÖstbergP.SonnanderK. (2012). Communication changes and SLP-services according to significant others of persons with aphasia. Aphasiology. 26, 1005–1028. 10.1080/02687038.2012.671927
5
BowenC.PalmerS.YeatesG. (2018). A Relational Approach to Rehabilitation: Thinking About Relationships After Brain Injury. New York, NY: Routledge.
6
ByrneC.SavilleC.CoetzerR.RamseyR. (2022). Stroke survivors experience elevated levels of loneliness: A multi-year analysis of the national survey for wales. Arch. Clin. Neuropsychol. 37, 390–407. 10.1093/arclin/acab046
7
CacioppoJ. T.CacioppoS. (2018). Loneliness in the modern age: an evolutionary theory of loneliness (ETL), in Advances in Experimental Social Psychology: Vol. 58. Advances in Experimental Social Psychology, ed OlsonJ. M. (Ontario: Elsevier Academic Press), 127–197.
8
CacioppoJ. T.PatrickW. (2008). Loneliness: Human nature and the Need for Social Connection. New York, NY: WW Norton and Company.
9
ChowT. W. (2000). Personality in frontal lobe disorders. Curr. Psychiatry Rep. 2, 446–451. 10.1007/s11920-000-0031-5
10
CodeC.HerrmannM. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychol. Rehabil.13, 109–132. 10.1080/09602010244000291
11
CodeC.PapathanasiouI.Rubio-BrunoS.de la Paz CabanaM.VillanuevaM. M.Haaland-JohansenL.et al. (2016). International patterns of the public awareness of aphasia. Int. J. Lang. Commun. Disord.51, 276–284. 10.1111/1460-6984.12204
12
CoetzerB. R. (2003). Grief following traumatic brain injury. Grief Matters. 6, 31–33. 10.3316/INFORMIT.81175048580112
13
CristoforiI.PalS.ZhongW.GordonB.KruegerF.GrafmanJ. (2019). The lonely brain: evidence from studying patients with penetrating brain injury. Soc. Neurosci.14, 663–675. 10.1080/17470919.2018.1553798
14
CritchleyH. D. (2004). The human cortex responds to an interoceptive challenge. Proc. Natl. Acad. Sci. U. S. A. 101, 6333–6334. 10.1073/pnas.0401510101
15
DalemansR. J. P.de WitteL.WadeD.van den HeuvelW. (2010). Social participation through the eyes of people with aphasia. Int. J. Lang. Commun. Disord.45, 537–550. 10.3109/13682820903223633
16
De Jong GierveldJ.Van TilburgT. (1999). Manual of the Loneliness Scale 1999. Amsterdam: Department of Social Research Methodology, Vrije Universiteit Amsterdam, (updated version 18.01.02).
17
DurcanD.BellR. (2015). Local Action on Health Inequalities: Reducing Social Isolation Across the Lifecourse. London: Public Health England and UCL Institute of Health Equity. Available online at: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/461120/3a_Social_isolation-Full-revised.pdf
18
EisenbergerN. I. (2012). The neural bases of social pain: evidence for shared representations with physical pain. Psychosomat. Med.74, 126–135. 10.1097/PSY.0b013e3182464dd1
19
EvansJ. J. (2005). Can executive impairments be effectively treated?, in The Effectiveness of Rehabilitation for Cognitive Deficits, eds HalliganP.WadeD. (Oxford: Oxford University Press).
20
FeinsteinJ. S.DuffM. C.TranelD. (2010). Sustained experience of emotion after loss of memory in patients with amnesia. Proc. Nat. Acad. Sci. U. S. A.107, 7674–7679. 10.1073/pnas.0914054107
21
FlemingS. M.RyuJ.GolfinosJ. G.BlackmonK. E. (2014). Domain-specific impairment in metacognitive accuracy following anterior prefrontal lesions. Brain137 (Pt 10), 2811–2822. 10.1093/brain/awu221
22
FriedlerB.CrasperJ.McCullough (2015). One is the deadliest number: the detrimental effects of social isolation on cerebrovascular disease and cognition. Acta Neuropathol.129, 493–509. 10.1007/s00401-014-1377-9
23
GlassT. A.MaddoxG. L. (1992). The quality and quantity of social support: stroke recovery as psycho-social transition. Soc. Sci. Med. 11, 1249–1261. 10.1016/0277-9536(92)90317-J
24
GronewoldJ.EngelsM. (2022). The lonely brain - associations between social isolation and (cerebro-) vascular disease from the perspective of social neuroscience. Front. Integr. Neurosci.16, 729621. 10.3389/fnint.2022.729621
25
HaggerB. F.RileyG. A. (2017). The social consequences of stigma-related self-concealment after acquired brain injury. Neuropsychol. Rehabil. 29, 1129–1148. 10.1080/09602011.2017.1375416
26
HakulinenC.Pulkki-RåbackL.VirtanenM.JokelaM.KivimäkiM.ElovainioM. (2018). Social isolation and loneliness as risk factors for myocardial infarction, stroke and mortality: UK Biobank cohort study of 479 054 men and women. Heart104, 1536–1542. 10.1136/heartjnl-2017-312663
27
Henri-BhargavaA.StussD. T.FreedmanM. (2018). Clinical assessment of prefrontal lobe functions. Continuum (Minneapolis, Minn.). 24, 704–726. 10.1212/CON.0000000000000609
28
HienrichL. M.GulloneE. (2006). The clinical significance of loneliness: a literature review. Clin. Psychol. Rev.26, 695–718. 10.1016/j.cpr.2006.04.002
29
Holt-LunstadJ.SmithT. B.BakerM.HarrisT.StephensonD. (2015). Loneliness and social isolation as risk factors for mortality: a meta-analytic review. Perspect. Psychol. Sci. 10, 227–237. 10.1177/1745691614568352
30
HydénL. C. (2017). Entangled Narratives: Collaborative Storytelling and the Re-imagining of Dementia. Oxford: Oxford University Press.
31
JacksonH. F.HagueG.DanielsL.Aguilar JrR.CarrD.KenyonW. (2014). Structure to self-structuring: Infrastructures and processes in neurobehavioural rehabilitation. NeuroRehabilitation34, 681–694. 10.3233/NRE-141082
32
JamiesonM.EvansJ. J. (2014). Assistive technology for executive functions, in Assistive Technology for Cognition: A Handbook for Clinicians and Developers, eds O'NeillB.GillespieA. (London: Psychology Press), 81–92.
33
JamiesonM.JackR.O'NeillB.CullenB.LennonM.BrewsterS.et al. (2020). Technology to encourage meaningful activities following brain injury. Disabil. Rehabil. Assist. Technol.15, 453–466. 10.1080/17483107.2019.1594402
34
KrpanK. M.LevineB.StussD. T.DawsonD. R. (2007). Executive function and coping at one-year post traumatic brain injury. J. Clin. Exp. Neuropsychol.29, 36–46. 10.1080/13803390500376816
35
LevineB.RobertsonI. H.ClareL.CarterG.HongJ.WilsonB. A.et al. (2000). Rehabilitation of executive functioning: an experimental-clinical validation of goal management training. J. Int. Neuropsychol. Soc. 6, 299–312. 10.1017/s1355617700633052
36
MasiC. M.ChenH.HawkleyL. C.CacioppoJ. T. (2011). A meta-analysis of interventions to reduce loneliness. Pers. Soc. Psychol. Rev. 15, 1–25. 10.1177/1088868310377394
37
McMillanT.WoodR. (2017). Neurobehavioral Disability and Social Handicap Following Traumatic Brain Injury. Routledge: Milton Park.
38
MooreP. A.SalasC. E.DockreeS.TurnbullO. H. (2017). Observations on working psychoanalytically with a profoundly amnesic patient. Front. Psychol.8, 1418. 10.3389/fpsyg.2017.01418
39
MorettiR.SignoriR. (2016). Neural correlates for apathy: frontal-prefrontal and parietal cortical-subcortical circuits. Front. Aging Neurosci.8, 289. 10.3389/fnagi.2016.00289
40
NorthcottS.HilariK. (2011). Why do people lose their friends after a stroke?. Int. J. Lang. Commun. Disord.46, 524–534. 10.1111/j.1460-6984.2011.00079.x
41
PantellM.RehkopfD.JutteD.SymeS. L.BalmesJ.AdlerN. (2013). Social isolation: a predictor of mortality comparable to traditional clinical risk factors. Am. J. Public Health103, 2056–2062. 10.2105/AJPH.2013.301261
42
PrigatanoG. P. (1999). Principles of Neuropsychological Rehabilitation. New York, NY: Oxford University Press.
43
QuadtL.EspositoG.CritchleyH. D.GarfinkelS. N. (2020). Brain-body interactions underlying the association of loneliness with mental and physical health. Neurosci. Biobehav. Rev.116, 283–300. 10.1016/j.neubiorev.2020.06.015
44
QualterP.VanhalstJ.HarrisR.Van RoekelE.LodderG.BangeeM.et al. (2015). Loneliness across the life span. Pers. Psychol. Sci. 10, 250–264. 10.1177/1745691615568999
45
RigonA.DuffM.BeadleJ. (2019). Lonely but not alone: Neuroticism mediates the relationship between social network size and loneliness in individuals with traumatic brain injury. J. Int. Neuropsychol. Soc. 25, 285–292. 10.1017/S1355617718001108
46
RowlandsA. (2002). Circles of support: Building social networks. Bri. J. Ther. Rehabil. 9, 56–65. 10.12968/bjtr.2002.9.2.13602
47
RussellD.PeplauL. A.FergusonM. L. (1978). Developing a measure of loneliness. J. Person. Assess.42, 290–294. 10.1207/s15327752jpa4203_11
48
SalasC.VaughanF.ShankerS.TurnbullO. (2013). Stuck in a moment: concreteness and psychotherapy after acquired brain injury. Neurodisabil. Psychother.1, 1–38.
49
SalasC. E.CasassusM.RowlandsL.PimmS.FlanaganD. A. (2018). “Relating through sameness”: a qualitative study of friendship and social isolation in chronic traumatic brain injury. Neuropsychol. Rehabil.28, 1161–1178. 10.1080/09602011.2016.1247730
50
SalasC. E.CoetzerR. (2015). Is concreteness the invisible link between altered emotional processing, impaired awareness and mourning difficulties after traumatic brain injury?. Neuropsychoanalysis17, 3–18. 10.1080/15294145.2015.1025819
51
SalasC. E.GrossJ. J.RafalR. D.Viñas-GuaschN.TurnbullO. H. (2013). Concrete behaviour and reappraisal deficits after a left frontal stroke: a case study. Neuropsychol. Rehabil.23, 467–500. 10.1080/09602011.2013.784709
52
SalasC. E.RadovicD.YuenK. S.YeatesG. N.CastroO.TurnbullO. H. (2014). “Opening an emotional dimension in me”: changes in emotional reactivity and emotion regulation in a case of executive impairment after left fronto-parietal damage. Bull. Menninger Clin.78, 301–334. 10.1521/bumc.2014.78.4.301
53
SalasC. E.Rojas-LíbanoD.CastroO.CrucesR.EvansJ.RadovicD.et al. (2021). Social isolation after acquired brain injury: exploring the relationship between network size, functional support, loneliness and mental health. Neuropsychol. Rehabil.17, 1–25. 10.1080/09602011.2021.1939062
54
SamsonD.ApperlyI. A.KathirgamanathanU.HumphreysG. W. (2005). Seeing it my way: a case of a selective deficit in inhibiting self-perspective. Brain. 128, 1102–1111. 10.1093/brain/awh464
55
SandsonJ.AlbertM. L. (1984). Varieties of perseveration. Neuropsychologia22, 715–732. 10.1016/0028-3932(84)90098-8
56
SchäferR.PoppK.JörgensS.LindenbergR.FranzM.SeitzR. J. (2007). Alexithymia-like disorder in right anterior cingulate infarction. Neurocase13, 201–208. 10.1080/13554790701494964
57
SchmidtJ.LanninN.FlemingJ.OwnsworthT. (2011). Feedback interventions for impaired self-awareness following brain injury: a systematic review. J. Rehabil. Med.43, 673–680. 10.2340/16501977-0846
58
SchöttkeH.GiabbiconiC. (2015). Post-stroke depression and post-stroke anxiety: prevalence and predictors. Int. Psychogeriatr.27, 1805–1812. 10.1017/S1041610215000988
59
SiegelJ. S.SnyderA. Z.MetcalfN. V.FucetolaR. P.HackerC. D.ShimonyJ. S.et al. (2014). The circuitry of abulia: insights from functional connectivity MRI. NeuroImage Clin.6, 320–326. 10.1016/j.nicl.2014.09.012
60
StussD. T. (2011). Functions of the frontal lobes: relation to executive functions. J. Int. Neuropsychol. Soc.17, 759. 10.1017/S1355617711000695
61
StussD. T.AlexanderM. P. (2007). Is there a dysexecutive syndrome?. Philos. Trans. Royal Soc. Lond. Ser. B. Biol. Sci. 362, 901–915. 10.1098/rstb.2007.2096
62
StussD. T.GallupG. G.Jr.AlexanderM. P. (2001). The frontal lobes are necessary for ‘theory of mind'. Brain124, 2, 279–286. 10.1093/brain/124.2.279
63
TateR. L. (2000). Emotional and social consequences of memory disorders, in The Handbook of Memory Disorders, 2nd Edn, eds BaddeleyA. D.KopelmanM. D.WilsonB. A. (Chichester: John Wiley), 786–805.
64
TranelD.DamasioA. R. (1993). The covert learning of affective valence does not require structures in hippocampal system or amygdala. J. Cogn. Neurosci.5, 79–88. 10.1162/jocn.1993.5.1.79
65
TurnbullO. H.ZoisE.Kaplan-SolmsK.SolmsM. (2006). The developing transference in amnesia: changes in interpersonal relationship, despite profound episodic-memory loss. Neuropsychoanalysis8, 199–204. 10.1080/15294145.2006.10773530
66
ValtortaN. K.KanaanM.GilbodyS.HanrattyB. (2016). Loneliness, social isolation and social relationships: what are we measuring? A novel framework for classifying and comparing tools. BMJ Open6:1–7. 10.1136/bmjopen-2015-010799
67
VickersC. P. (2010). Social networks after the onset of aphasia: the impact of aphasia group attendance. Aphasiology24, 902–913. 10.1080/02687030903438532
68
VillaD.CauserH.RileyG. A. (2021). Experiences that challenge self-identity following traumatic brain injury: a meta-synthesis of qualitative research. Disabil. Rehabil. 43, 3298–3314. 10.1080/09638288.2020.1743773
69
WinegardnerJ. (2017). Executive functions, in The Brain Injury Rehabilitation Workbook, eds WinsonR.WilsonB.BatemanA. (New York, NY: Guilford Publications), 106–122.
70
WinsonR.WilsonB. A.BatemanA. (eds.). (2017). The Brain Injury Rehabilitation Workbook.New York, NY: Guilford Publications.
71
XiaoX.ZhangY. Q. (2018). A new perspective on the anterior cingulate cortex and affective pain. Neurosci. Biobehav. Rev.90, 200–211. 10.1016/j.neubiorev.2018.03.022
72
YasminN.RileyG. A. (2021). Are spousal partner perceptions of continuity and discontinuity within the relationship linked to the symptoms of acquired brain injury?Disabil. Rehabil.18, 1–8. 10.1080/09638288.2021.1900410
73
YeatesG. (2013). Towards the neuropsychological foundations of couples therapy following acquired brain injury (ABI): a review of empirical evidence and relevant concepts. Neurodisabil. Psychother.1, 108–150.
74
ZavaletaD.SamuelK.MillsC. (2014). Social isolation: A conceptual and measurement proposal, working paper 67. Oxford: Oxford Poverty & Human Development Initiative (OPHI). Available online at: www.ophi.org.uk/social-isolation-a-conceptual-and-measurement-proposal
Summary
Keywords
acquired brain injury (ABI), executive impairments, loneliness, neuropsychological rehabilitation, social isolation
Citation
Byrne C, Salas CE, Coetzer R and Ramsey R (2022) Understanding Loneliness in Brain Injury: Linking the Reaffiliation Motive Model of Loneliness With a Model of Executive Impairment. Front. Integr. Neurosci. 16:883746. doi: 10.3389/fnint.2022.883746
Received
25 February 2022
Accepted
03 June 2022
Published
14 July 2022
Volume
16 - 2022
Edited by
Joseph F. X. DeSouza, York University, Canada
Reviewed by
Janine Gronewold, Essen University Hospital, Germany
Updates

Check for updates
Copyright
© 2022 Byrne, Salas, Coetzer and Ramsey.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Christopher Byrne christopher.byrne@thedtgroup.org
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.