The woman who lost her mind: Aphantasia presenting as Cotard's syndrome
Abstract
Aphantasia is defined as the absence or marked reduction of conscious, wakeful imagery. It has beenreported in 1% of the population. Most of them live normal lives with intact attention, memory, andintelligence.1 We are presenting a case of acquired aphantasia presenting as Cotard’s syndrome.
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1 The woman who lost her mind: Aphantasia presenting as Cotard’s syndrome Rajith K Ravindren MD a, b, *, Prasad Thotton Veedu MD C a Department of Psychiatry, Institute of Mental Health and Neurosciences (IMHANS), Kozhikode, Kerala, 673008, India b Neuroscience Research Laboratory, Center for Interdisciplinary Brain Sciences, Institute of Mental Health and Neurosciences (IMHANS), Kozhikode, Kerala, 673008, India c Radiology and Imaging Sciences, Sreechand Speciality Hospital, Kannur, Kerala, 670001, India Keywords: Aphantasia; Cotard’s syndrome Funding/Support: None Potential conflicts of interest: None 1 Corresponding author Rajith K Ravindren Department of Psychiatry & Neuroscience Research Laboratory, Center for Interdisciplinary Brain Sciences, Institute of Mental Health and Neurosciences (IMHANS), Kozhikode, Kerala, 673008, India [email protected].in
2 Introduction Aphantasia is defined as the absence or marked reduction of conscious, wakeful imagery. It has been reported in 1% of the population. Most of them live normal lives with intact attention, memory, and intelligence.1 We are presenting a case of acquired aphantasia presenting as Cotard’s syndrome. A 53-year-old woman presented with the complaint that she had lost her mind at the age of 29. She accused her mother of doing religious rituals, which caused her mind to disappear. She was unmarried and was staying with her mother and sister. There was no history of mental illness in her family. She was the first among 5 children of her parents. Her birth and early development were normal. She had completed her school education. When she was 13 years old, she started having progressive hearing loss in her left ear. By her 30th birthday, her right ear also started deteriorating. Around this time, her mental health problems began surfacing. She was adamant in her belief that she had lost her mind, and her mother was responsible for this. Her sleep, appetite, self-care, and interactions with others were normal during this period. Most of her time was spent watching television. She consulted multiple psychiatrists and was on antipsychotics for 20 years. She had tried risperidone 8mg, haloperidol 10 mg, and trifluoperazine 10 mg during this period, but there was no improvement in her complaints. She started using hearing aids, which helped her in day-to-day activities. The improvement in hearing had no impact on her delusion. She was evaluated multiple times over 3 years. Her conversation always revolved around her lost mind. When we asked her how she knew that she didn’t have a mind, she would remain silent. She did not have any other delusions, hallucinations, or first-rank symptoms. Her mood, intelligence, and attention were normal. On MMSE, she scored 29, indicating normal memory. She could read and write English and Malayalam. Her numerical skills were normal. Clinical evaluation of the lobe functions was normal except for poor abstraction. She had visual dreams, approximately once a month. She dreamt about the dead body of her relative, an event that occurred when she was 10 years old. She could identify herself in the mirror. Face recognition was normal in the familiar face recognition test. On the Vividness of Visual Imagery Questionnaire (VVIQ)2-a test for aphantasia-she scored the lowest possible score of 16. On the Plymouth Sensory Imagery Questionnaire 3, she could not voluntarily imagine sight, sound, smell, taste, body sensations, touch, or feeling. She could not mentally reverse the small case letter b to d or reverse the upper-case letter F to 7. We evaluated her theory of mind skills using the Sally Anne test 4, which she failed. MRI brain showed subcortical and deep cerebral white matter lesions in bilateral frontal and parietal lobes (Figure 1). Discussion This patient presented with a nihilistic delusion of the absence of mind. She did not have any features of schizophrenia or depression. Cotard’s syndrome is characterized by the appearance of such nihilistic delusions concerning one’s own body.5 This patient raises the question of how a person subjectively knows that he or she has a mind. And how the clinician can understand whether a person is having a subjective experience of mind, the philosophical problem of the other mind. The patient was able to recognize herself in the mirror, showing that her sense of self was intact.6 The frequent use of “I” in conversation further confirms this. We hypothesized that this patient might be having problems with generating internal images or internal talk. Or she might be having problems in monitoring her images and internal talk. To test these, we used the Vividness of Visual Imagery Questionnaire (VVIQ), which showed that she failed to intentionally generate visual images.2 The Plymouth Sensory Imagery questionnaire showed that she was having problems in generating images in all sensory modalities.3 These two tests showed that she cannot voluntarily generate /monitor images. Her ability to dream showed that involuntary image generation was happening without any hindrance. Voluntary imagery is generated in the frontal regions with contribution from the parietal lobes in attention and spatial aspects of the image (saliency).1 Lesions in the frontal and parietal lobes may explain the lack of voluntary images in this patient.
3 Her aphantasia may explain her complaint of a lost mind. But that will not explain her accusation against her mother. How does a person with no ability to voluntarily generate images/thoughts accuse another person of harming her? To explore this, we tested the patient using the Sally-Anne task. In this test, two cartoon characters are shown to the patient. One of them, Sally, places a marble in the basket and goes out. The other one, Anne, takes the marble and places it in her box. Sally returns after some time. The experimenter asked where Sally must look for her marble. Our patient could not give the correct response. This test requires knowing the perspective of Sally rather than one's own.4 This test thus measures a person's ability to model other minds. This ability is impaired in patients who have an injury to the granular prefrontal cortex.7 Bilateral white matter lesions in the frontal lobe may explain the theory of mind defect in this patient. Cotard’s syndrome is explained using a two-stage process. The first stage is characterised by abnormal perception, due to dysfunctions in particular brain areas, and the second stage is essentially based on one’s own typical attributional error.8 In this case, injury to the frontal and parietal regions resulted in impaired generation and monitoring of voluntary images. The frontal lobe lesion, which causes difficulty in modeling one's mind, also results in impaired modeling of the other mind.7 This two-step process may explain the symptoms in this patient. Her poor abstraction skills are a further pointer to her poor modeling abilities.7 Are there other conditions in which the subjective knowledge of one's own mind diminishes would be a fruitful line of enquiry. In Eastern meditation traditions, it is mentioned that the mind is responsible for all suffering, and quieting or ‘annihilation’ of the mind results in Moksha /nirvana/enlightenment. Ironically, we have a patient who claims that she has lost her mind and is upset about that, rather than feeling peace. She still attends the clinic in the hope of getting her mind back. Reference 1. Zeman A. Aphantasia and hyperphantasia: exploring imagery vividness extremes. Trends in Cognitive Sciences. 2024 Mar 9. 2. Marks DF. Vividness of visual imagery questionnaire. Journal of Mental Imagery. 1973. 3. Andrade J, May J, Deeprose C, Baugh SJ, Ganis G. Assessing vividness of mental imagery: The Plymouth sensory imagery questionnaire. British Journal of Psychology. 2014 Nov;105(4):547-63. 4. Baron-Cohen S, Leslie AM, Frith U. Does the autistic child have a “theory of mind”?. Cognition. 1985 Oct 1;21(1):3746. 5. Debruyne H, Portzky M, Van den Eynde F, Audenaert K. Cotard’s syndrome: a review. Current psychiatry reports. 2009 Jun;11(3):197-202. 6. Solms M. The hidden spring: A journey to the source of consciousness. Profile books; 2021 Jan 28. 7. Bennett MS. Five breakthroughs: a first approximation of brain evolution from early bilaterians to humans. Frontiers in Neuroanatomy. 2021 Aug 17;15:693346. 8. Tomasetti C, Valchera A, Fornaro M, Vellante F, Orsolini L, Carano A, Ventriglio A, Di Giannantonio M, De Berardis D. The ‘dead man walking’disorder: an update on Cotard’s syndrome. International Review of Psychiatry. 2020 Aug 17;32(5-6):500-9.
4 Figure 1: MRI images showing subcortical and deep cerebral white matter lesions in bilateral frontal and parietal lobes