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    En Pubmed

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    ANALYSIS AND COMMENTARY Frontotemporal Dementia: A Window to Alexithymia Mario F. Mendez, M.D. Ph.D. Alexithymia is pervasive among psychiatric patients, but its ‘neurobiological mechanism is unclear. Patients with alex- 'thymia cannot “read emotions.” a process involving inter ‘oception, or the perception of the body's internal state, primarily in the insulae. The frontotemporal dementias are also associated with inability to correctly read emotions; hence, these dementias can provide a window into the ‘mechanism of alexithymia. Patients with behavioral variant frontotemporal dementia (byFTD) have a weak emotional signal with impaired emotional recognition, hypoemotion= ality, and decreased physiological arousal. bvFTD affects the insulae, and the weak emotional signal facilitates im- paired interoceptive accuracy, resulting in an overreliance Alexithymia, or the inability to identify and describe one’s, feelings, is a condition present in a broad range of psychiatric disorders. Although originally introduced to deseribe Feature of patients with psychosomatic disorders (I, 2), investigators have implicated alexithymia as part of the symptomatology of anxiety and obsessive-compulsive disorders, disturbances in eating and addiction, schizophrenia and other psychot conditions, psychopathy, autism, and a range of other disor- ders (3). Early theories for alexithymia stressed psychological traumas and high levels of psychological distress with overuse of defensive mechanisms, resulting in somatic symptoms and affect avoidance (4, 5). A further analysis of the neurobio- logical rather than psychodynamic mechanism of alexithymia could lead to a better understanding and management of this condition, ‘The term “alexithymia” means “lack of words, or inability to read emotions” (1). Indeed, patients with alexithymia are deficient in the cognitive processing of emotions. For ex- ample, alexithymia impairs emotion recognition from faces and voices (6,7), and itcan result in atypical emotional facial expressions (7, 8). Unraveling the nature of alexithymia re- quires a grounding in the neurobiology of emotion. ‘THE NEUROBIOLOGY OF EMOTION Emotion is a process that involves the insulae and a number of frontotemporal structures. Emotional processing in the brain begins with the identification of salient or emotional stimuli mediated by the amygdala, This results in physio: logical arousal and interoception, the perception of inter- nal body or somatie sensations. Interoceptive sensitivity is Neuropsychiatry Cin Neurose! 35:2, Spring 2024 Con cognitive appraisal rather than on internal sensations. In Contrast, patients with semantic dementia, another fronto temporal dementia syndrome, can have intact inter- ‘oception, but they have disturbed cognitive appraisal of the ‘meaning of their bodily sensations. This alexisomia" in se- ‘mantic dementia can lead to misinterpreted somatic symp- toms. Together, the findings in alexithymic patients and frontotemporal dementia syndromes support the model of impaired interoceptive accuracy as the mechanism of alex ithymia, possibly from dysfunction in the insula. INeuropsychiaty Cin Nourosc! 2021; 35:157-160; 60%: 10.176/appineuropsych 20100252 strongly correlated with the strength of the physiological arousal in the posterior insulae (9). The anterior insulae, particularly on the right, merge these internal sensations with comitive evaluation, resulting in the awareness of feel- ings (10). ‘This process involves reciprocal interactions be- tween the anterior insulze and the anterior cingulate cortex (ACO), which mediate emotional responding and the e: pression of affective arousal. ‘The anterior insulae and ACC are core regions of the salience network, which activates in response to emotionally salient cues in the environment (1). In addition to interoception, the cognitive appraisal of one’s internal and external environment also contributes to emo- tional experience (12). Cognitive appraisal involves frontal regions such as the orbitofrontal cortex for emotional control, the ventromedial prefrontal cortex for affective meaning, and the ventrolateral prefrontal cortex for emotional integration and regulation, Finally, other temporal lobe structures such as the inferior temporal and fusiform gyrus are important for affective signal detection and integration, and the anterior temporal poles specifically link interoceptive stimuli with their conceptual meaning (13). ALEXITHYMIA AND INTEROCEPTION ‘The mechanism for alexithymia may be a disassociation be- ween internal physiological arousal and externally-based cognitive appraisal (14). In alexithymia, investigators de- scribe difficulty “elevating emotions from a sensorimotor level of experience” to a representational level, where they can be used as signaling interoception (15). On the cogni- tive appraisal side, others propose relative dysfunction of euro psychiattyoniineorg 187, neocortical areas for symbolically and linguistically repre~ senting emotion (16). Indeed, reports of patients who un- derwent a commissurotomy, or surgical inci callosal commissure, indicate increased al preserved interoceptive feelings in the right hemisphere could no longer access left hemisphere language and s bolization (14). Still other information links alexithymia to a failure of, interoception (17, 18). Persons with higher levels of alex- ithymia appear to have poor knowledge of their internal states and decreased interoceptive accuracy (9); alexithymia interoception of cardiac and respiratory output, e sensitivity (17). Poor cardiae sen- y levels of alexithymia (19), and higher self-reported interoceptive confusion occurs among alexithymic individuals (18, 20). In autism, alexithymia is associated with decreased interoceptive sensitivity even in the presence of an intact interoceptive signal (21, 22), Much research also associates damage to the anterior insulae with both interoceptive difficulties and alexithymia (23, 24). F nally, poor recognition of facial negative emotions is linked to both high levels of alexithymia and low levels of inter- ception (25), EVIDENCE FROM THE FRONTOTEMPORAL DEMENTIAS An important degenerative disorder that alters emotion is ‘behavioral variant frontotemporal dementia (bvFTD). This, disorder is the second most common neurodegenerative dementia among patients <65 years, after early-onset Alz- heimer’s disease (26). Patients with bvFTD have behavioral changes such as impaired emotionality and empathy, apathy or abulia, disinhibition or impulsivity, dietary changes, and dysexecutive cognition from disease affecting the frontal and anterior lobes (26). The early focus of neuropathology in this disorder is in the anterior insulae, ACC, and the salience network In addition to bvF TD, the frontotemporal dement clude semantic dementia, also known as semantic variant primary progressive aphasia in its early stages. Semantic dementia results in a loss of semantics, or the meaning of, words and objects, from atrophy in the anterior temporal lobes (27). The earliest changes in semantic dementia affect the meaning of words, manifesting as a semantic anomia, but as the disease progresses, there is a multimodal impairment in knowledge for objects, faces, sounds, smells, and other perceptions, regardless of modality, including confusion over the nature of somatic or bodily sensations (27). ‘Most patients with bvPTD have emotional blunting with impaired recognition of emotions and decreased psycho- physiological arousal to emotional stimuli (28-33). Studi have shown that these patients are impaired in the recog- nition of emotions in pictures or videos (34, 35). Multiple 158. neuroppsychiatyontine org studies document lower baseline tonic levels and decreased or insufficient phasic reactivity in both sympathetic and parasympathetic activity in bvFTD (11, 28, 30, 32, 36, 37). Patients with PTD have shown reduced sensitivity to different types of emotional stimuli, such as pain (29) fear conditioning, to, loud noise (38), and aversive odors (39); when exposed to an unpleasant stimulus, patients with beFTD had attenuation of the expected initial heart rate deceleration characteristic of an orienting response (33). Hypoemotionality also contributes to the lack of insight for their disease, which is best charac- terized as an “anosodiaphoria,” or lack of emotional caring, rather than a true anosognosia, or lack of cognitive awareness (40). The emotional blunting and decreased physiological arousal in byFTD may correspond with atrophy or hypo- ‘metabolism involving the anterior insulae and pregenual and middle cingulate cortex (37) Beyond their impaired recognition of emotions and de- creased physiological arousal, patients with byFTD cannot accurately read their own interoceptive signals and do not reliably report their degree of emotional arousal (32). Pa- tients with byPTD have impaired explicit awareness of their own heartbeat (4, and they are unable to assess internal sensations for “gut level” cues (42). Investigators document. mismatch between intrinsic physiological arousal (implicitly feeling emotions) and reports of emotion or ratings of valence from the patients (explicit approval) (32). In general, those with bvFTD experience emotional stimuli as decreased in intensity, and they cannot estimate itexcept for differentiation of extremes of arousal (32). However, rather than underestimating, emotional stimuli, patients with bvFTD may exagrerate their interoceptive sensations from an overreliance on cognitive ap- praisal using external contextual information, established rules, or environmental cues to explain their feelings (32, 43,44) Alexisomia in Semantic Dementia Semantic dementia isa unique frontotemporal degeneration syndrome that affects the temporal poles, which are con- vergence zones for multimodal representations of knowledge, including interoceptive signals (45). In semantic dementia, dysfunetion of anterior temporal regions can impair semantic ‘meaning of interoceptive information, This results in im- paired interoceptive accuracy from a disassociation of somatic sensations from semantic knowledge (46, 47). “Alexisomia,” or difficulty in reading somatic symptoms, isthe alexithymia- related phenomenon in which somatic sensations are misread by patients with semantic dementia, Because of their alexisomia, patients with semantic de- mentia may be prone to somatic symptom disorder from inability to identify the meaning of bodily sensations (48). ‘Ten percent of autopsy-confirmed semantic dementia pa- tients have presented with somatization, especially those with prominent right temporal lobe atrophy (49). They may become excessively concerned and “somaticize” over thei normal bodily sensations because of confusion over their ‘meaning, origin, and identity, and may even conclude that their unknown somatic sensations or symptoms mean that INeuropsychiaty Clin Neurose! 33:2 Spring 2021 they are deteriorating or dying (Cotard’s syndrome) (50). Although pain and temperature awareness may be increased in patients with semantic dementia (29), this inereased sen- sory awareness does not seem to refleet genuine hypersensi tivity but rather an overattribution of salience in semantic dementia (29) (ie., because they do not know what th sations mean, they are primed to overreact to them [49)) CONCLUSIONS ‘Alexithymia is an important but poorly understood symptom, that is present among a wide range of psychiatric disorders. Early descriptions of the mechanism of alexithymia sug- «gested a primary disorder from a dissociation of “limbic” or interoceptive physiological signals from cortical represen tations or interpretations (15, 16). Investigators suggested that psychological trauma with overactive defense mecha- nisms blocked this “limbic-cortical” association; however more recent studies point to disturbed interoceptive pro- cessing itself as central to alexithymia. Similar difficulties among two frontotemporal dementia syndromes, bvFTD and semantic dementia, shed light on the neurobiological mecha- nism of this symptom, Alexithymia in byFTD results from a ‘weak emotional and physiological signal with impaired in- teroceptive accuracy and a consequent overreliance on external context and rules for explaining the experience. Alexisomia is semantic dementia results from inability to correctly read intact interoception due to an impairment in the ability to derive the meaning of bodily sensations. These findings in brain syndromes known to affect the emotional centers of the brain, particularly insulae where interoception is centered, support a deficit in in- teroceptive accuracy as central to alexithymia from a blunted emotional physiological signal, from impaired cognitive ap- praisal, or from disturbance in interoceptive processing in the insulae. Clearly, more research can offer further insights into the neurobiological basis of alexithymia based on this model. AUTHOR AND ARTICLE INFORMATION, Departments of Neurology and Behavioral Sciences, David Getfen School of Medicine, University of California, Los Angeles: and Neu rology Service, Neurabehavior Unit, VA Greater Los Angeles Health care System. Send correspondence to Dr. Mendez (mmendez@UCLA edu) ‘Supported by the National Insitute on Aging (grant IRFIAGOS0367) Dr. Mendez repors no financial relationships wth commecia interests, Received October 7, 2020: accepted October 21. 2020; published online Feb. 4, 2021, REFERENCES 1. Sifncos PE, ApfelSavitz R, Frankel FH: The phenomenon of alex ithymis: observations in neurotic and psychosomatic pationts, Psy- chother Psychosom 1977; 2847-57 2. Lépez-Muttoz F, Prez-Fernindez F:A history ofthe alexithymia concept and its explanatory models an epistemological perspec- tive. Front Psyehiatry 2020; 103026 4. Serafini G, De BeranlisD, Valchera A, etal: Alxithymia as a po sible specifier of adverse outcomes: clinica correlates in euthymie Unipolar individuals J Affect Disord 2020, 263-128-436 Neuropsychiatry Cin Neurose! 35:2, Spring 2024 M4. v. a. 22 m4, 2s, 22 Gags SB, Cornell AS, Bird G: MeDougall J: Alexthymia: a psychoanalytic viewpoint. Psychother Psychosom 1982; 3881-90 ‘Taylor GJ, Bagby RM, Parker JD: The alexithymia construct: a potential paradigm for psychosomatic medicine. Psychosomatics 1W0L 3283-164 Grynerg D, Chang B, Comeille 0, et al: Alexithymia and the processing of emotional facial expressions (EFES) systematic re- view, unanswered questions and further perspectives. PLoS One 2012; 7042429 Heaton P, Reichenbacher L, Sauter D, et al Measuring the effects ‘of slexthymia on perception of emotional vocalizations in stistie spectrum disorder and typical development. Psychol Med 2012; 42: 2453-2459 ‘Trevisan DA, Bowering M, Birmingham E: Alexithymia, but not autism spectrum disorder, may be related to the production of ‘emotional facial expressions. Mol Autism 2016; 7:46 Murphy J, Brewer R, Catmur C, et al: Interoception and psyeho- pathology: a developmental neuroscience perspective. Dev Cogn Neurosci 2017; 23:45-56 CCraig AD: How do you feel~now? The anterior insl awareness. Nat Rev Neurosci 2009: 1:59-70 Sturm VE, Brown JA, Hus AY, ef al: Network architecture un- derlying basal autonomic outflow: evidence from frontotemporal ‘dementia, 1 Neurosci 2014; 38:8943-8955 ‘Seth AK: Interoceptive inference, emotion, andthe embodied self. ‘Trends Coy Sci 2013; 1765-573, (Olson 1, Plotzker A, Ezzyat ¥: The enigmatic temporal pole: a review of findings on socal and emotional processing Brain 2007; oavis-a7ab ‘TenHouten WD, Hoppe KD, Bogen JE, et al: Alexithymia an ex- perimental study of cerebral commiscurotomy patients and normal control subjects. Am J Psychiatry 1986; 143:312-316 Meza-Concha N, Arancibia M, Salas F, et al: Towards a neurobi- ‘logical understanding of alexithymia. Medwave 2017; 17:e6960 MacLean PD: Psychosomatic disease andthe vseeral brain; recent

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