Addressing Evidence Linking Secondary Alexithymia to Aberrant Humor Processing

Abstract

In this review, we explore current literature and assess evidence linking secondary (acquired) alexithymia to aberrant humor processing, in terms of their neurobiological underpinnings. In addition, we suggest a possible common neuropathological substrate between secondary alexithymia and deficits in humor appreciation, by drawing on neurophysiologic and neuroradiological evidence, as well as on a recent and unique single-case study showing the cooccurrence of secondary alexithymia and deficit in humor appreciation. In summary, what emerges from the literature is that the cortical midline structures, in particular the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the insular cortex, seem to play a crucial role in the expression of both alexithymia and defective humor processing, while though to a lesser extent, a right hemisphere and bilateral frontoparietal contribution becomes evident. Neurobiological evidence of secondary alexithymia and aberrant humor processing points to the putative role of ACC/mPFC and the insular cortex in representing crucial processing nodes whose damage may produce both the above clinical conditions. We believe that the association of secondary alexithymia and aberrant humor processing, especially humor appreciation deficit, and their correlation with specific brain regions, mainly ACG/mPFC, as emerged from the literature, may be of some heuristic importance. Increased awareness on this topic may be of aid for neurosurgeons when accessing emotion-relevant structures, as well as for neuropsychologists to intensify their efforts to plan evidence-based neurorehabilitative interventions to alleviate the deleterious effects of such interpersonal communication deficits.

The Utility of Assessing Alexithymia, in Addition to Coping, in the Context of Posttraumatic Stress

“…In addition, some research has suggested the development of primary alexithymia may be attributable to early-life trauma (see Messina et al, 2014 for a review). Secondary alexithymia may develop as a consequence of illness (Wise et al, 1990), brain injury (Patrikelis et al, 2019), or exposure to other traumatic life events (Krystal, 1968). Again, due to the cross-sectional nature of the present study, we cannot make definitive claims regarding the primary or secondary development of alexithymia in this sample.…”

Alexithymia, Burnout, and Hopelessness in a Large Sample of Healthcare Workers during the Third Wave of COVID-19 in Italy

“…This often occurs following traumatic conditions experienced during critical periods of childhood development or due to strong emotions experienced in adulthood. In addition, secondary alexithymia has recently been related to certain diseases, such as myocardial infarction, hypertension, and rheumatoid arthritis, which suggests that it may also be a coping mechanism [73]. Moreover, acute secondary alexithymia is a temporary state-dependent condition due to distress (in the present study, the third wave of the COVID-19 pandemic in Italy), often decreasing when an acute or subacute stressful situation has finished [74].…”

Post-stroke alexithymia – a review

“…Alexithymia is a common clinical problem among stroke survivors [ 23 , 35 , 36 , 38 , 39 , 41 ]. Its occurrence among this population of patients is associated with elevated levels of interleukin-18 [ 36 ] and damage to brain structures which lie in the right hemisphere, mainly the anterior cingulate cortex (ACC), anterior insula (AI) and prefrontal cortex (PFC) [ 23 , 26 , 27 ], though insults to left hemisphere can also play an important, yet still not fully understood role [ 41 , 42 ]. Alexithymia has a positive correlation with the severity of post-stroke PTSD [ 34 ] and is a predictive factor for depression in stroke survivors [ 35 ].…”

“…In their work on neurobiological underpinnings of alexithymia, Meza-Concha et al [26] reviewed multiple papers concerning alexithymia and its neurobiological coordinates, mentioning damage to such structures as the amygdala, anterior cingulate cortex (ACC), anterior insula (AI), prefrontal cortex (PFC), cerebellum, and processes of abused interhemispheric connections being responsible for the occurrence of the trait. Patrikelis et al [27], who also reviewed multiple papers regarding alexithymia's neurobiological coordinates, conclude that insulting the anterior cortical midline structures like the aforementioned ACC, AI and medial prefrontal cortex (mPFC) can possibly play key roles in secondary alexithymia, as these structures take part in regulating various processes of our emotional life. Through regulating the interoceptive processing (receiving and transforming bodily states into feelings), AI regulates the conscious self-awareness of emotions [28]; ACC regulates the process of interoceptive awareness and mediates the appearance of emotional arousal, and along with mPFC regulates the limbic structures involved in generating emotions [27].…”

“…Patrikelis et al [27], who also reviewed multiple papers regarding alexithymia's neurobiological coordinates, conclude that insulting the anterior cortical midline structures like the aforementioned ACC, AI and medial prefrontal cortex (mPFC) can possibly play key roles in secondary alexithymia, as these structures take part in regulating various processes of our emotional life. Through regulating the interoceptive processing (receiving and transforming bodily states into feelings), AI regulates the conscious self-awareness of emotions [28]; ACC regulates the process of interoceptive awareness and mediates the appearance of emotional arousal, and along with mPFC regulates the limbic structures involved in generating emotions [27]. Papers reviewed in abovementioned studies on finding the damage to exact brain regions responsible for alexithymic traits were mostly based on careful examination of neuroimaging, including MRI, fMRI, PET and others.…”