Psychic trauma causing grossly reduced brain metabolism and cognitive deterioration

doi:10.1016/S0028-3932(97)00093-6

Neuropsychologia

Volume 36, Issue 1, January 1998, Pages 77-82

https://doi.org/10.1016/S0028-3932(97)00093-6 Get rights and content

Abstract

While amnesia and other cognitive disturbances are usually caused by structural brain damage, there are a few instances in which environmental stress may induce neuronal death in memory-sensitive brain regions such as the hippocampus. Here we report on a patient who, after a single brief exposure to an event reminding him of a similar stressful event from his childhood, deteriorated immediately and persistently without manifesting structural, but manifesting functional, brain damage as measured by position emission tomography. This patient probably represents the first case in which a direct relation between a single psychic event and the occurrence of brain malfunctioning in cognition is documented by dynamic neuroimaging methods. Psychic shock may cause lasting reductions in brain metabolism with the consequence of severe intellectual malfunctioning.

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Autobiographical amnesia is found in patients with focal or diffuse brain damage (“organic amnesia”), but also without overt brain damage (at least when measured with conventional brain imaging methods). This last condition is usually named dissociative amnesia at present, and was originally described as hysteria. Classically and traditionally, dissociative amnesia is seen as a disorder that causes retrograde amnesia in the autobiographical domain in the aftermath of incidents of major psychological stress or trauma. In the present study one of the probably largest published collections of patients (28) with psychogenically caused autobiographical amnesia, who were assessed with comprehensive neuropsychological tests, will be described and documented in order to identify variables which are central for the occurrence of dissociative amnesia. The presented cases demonstrate that autobiographical amnesia without direct brain damage can have very mixed clinical presentations, causes and consequences. The described cases of psychogenic amnesia are clustered according to a number of manifestations and features, which include a reduced effort to perform cognitively at a normal level, a forensic background, anterograde (instead of retrograde) autobiographical amnesia, the fugue condition, concurrent somatic diseases, and their appearance in childhood and youth. It is concluded that autobiographical amnesia of a psychogenic origin may occur within a variety of symptom pictures. For all patients, it probably serves a protective function by offering them a mechanism to exit a life situation which appears to them unmanageable or adverse.
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Citation Excerpt :
Dissociative amnesia is characterized by retrieval blockade of episodic autobiographical memories arising in the context of psychological trauma (whether known or not), with no evidence of brain damage on structural imaging [1–4].
Dissociative amnesias have been reported in neurological episodes mild enough to not cause any visible lesions on morphological examination. Disproportionate retrograde amnesia with or without identity loss happens in the context of psychological trauma (known or not). In metabolic imaging studies, some authors have reported functional alterations, particularly in the bilateral hippocampus, right temporal regions and inferolateral prefrontal cortex, despite normal morphological imaging. To avoid the presumption of an organic, psychogenic or mixed origin for such changes, De Renzi et al. suggested the term ‘functional amnesia’ to describe the condition. Patients have sometimes recovered during events similar to those preceding the amnesia in either a spectacular fashion or never. Also, in some cases, distraction or sedation may trigger the start of recovery. During psychotherapy, one patient remembered seeing a car on fire when he was a boy, and his amnesia started when his house was on fire. This suggests control by the frontal cortex, with repression blocking amnesic traces in the new emotional and biological context.
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2017, Neuroscience and Biobehavioral Reviews
Electrical brain stimulations (EBS) sometimes induce reminiscences, but it is largely unknown what type of memories they can trigger. We reviewed 80 years of literature on reminiscences induced by EBS and added our own database. We classified them according to modern conceptions of memory.
We observed a surprisingly large variety of reminiscences covering all aspects of declarative memory. However, most were poorly detailed and only a few were episodic. This result does not support theories of a highly stable and detailed memory, as initially postulated, and still widely believed as true by the general public.
Moreover, memory networks could only be activated by some of their nodes: 94.1% of EBS were temporal, although the parietal and frontal lobes, also involved in memory networks, were stimulated. The qualitative nature of memories largely depended on the site of stimulation: EBS to rhinal cortex mostly induced personal semantic reminiscences, while only hippocampal EBS induced episodic memories. This result supports the view that EBS can activate memory in predictable ways in humans.
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In patients with dissociative (conversion) amnesia heart rate variability is lower than in healthy participants (Tramoni et al., 2009; van der Kruijs et al., 2014). Furthermore, patients with dissociative amnesia frequently show signs of depression and alexithymia (Markowitsch et al., 1998, 1999c, 2000b; Maldano and Spiegel, 2008; Moriguchi et al., 2009; Staniloiu et al., 2010). All this impairs theory of mind functions and foresight, and reduces the patient to an extended noetic present (Suddendorf et al., 2009) with resignation and lack of concern.
Retrograde amnesia is described as condition which can occur after direct brain damage, but which occurs more frequently as a result of a psychiatric illness. In order to understand the amnesic condition, content-based divisions of memory are defined. The measurement of retrograde memory is discussed and the dichotomy between “organic” and “psychogenic” retrograde amnesia is questioned. Briefly, brain damage-related etiologies of retrograde amnesia are mentioned. The major portion of the review is devoted to dissociative amnesia (also named psychogenic or functional amnesia) and to the discussion of an overlap between psychogenic and “brain organic” forms of amnesia. The “inability of access hypothesis” is proposed to account for most of both the organic and psychogenic (dissociative) patients with primarily retrograde amnesia. Questions such as why recovery from retrograde amnesia can occur in retrograde (dissociative) amnesia, and why long-term new learning of episodic-autobiographic episodes is possible, are addressed. It is concluded that research on retrograde amnesia research is still in its infancy, as the neural correlates of memory storage are still unknown. It is argued that the recollection of episodic-autobiographic episodes most likely involves frontotemporal regions of the right hemisphere, a region which appears to be hypometabolic in patients with dissociative amnesia.
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Conversion hysteria refers to neurological disorders at the borderline between neurology and psychiatry, characterized by impaired awareness of bodily or cognitive function (such as paralysis, anesthesia, blindness, or amnesia) in the absence of apparent organic lesion in the nervous system. Although it is assumed that conversion hysteria may result from a transformation of psychological trauma or emotional stress into physical symptoms, which can distort self-awareness for a particular neurological function in the patient, the exact mechanisms underlying this transformation remain largely unknown, in terms of both mental processes and neurocognitive substrates. Recent studies using functional neuroimaging techniques have pointed to altered patterns of activation in brain areas involved in emotional regulation, self-monitoring, and memory, including ventral and lateral prefrontal cortex, which might in turn influence activity in sensory or motor pathways responsible for specific functional impairments (e.g., paralysis or anesthesia). However, the exact mechanisms of these disorders and the triggering causes still remain largely unresolved.

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Psychic trauma causing grossly reduced brain metabolism and cognitive deterioration

Abstract

Journal of Psychosomatic Research

Neuropsychologia

Biological Psychiatry

Cortex

Biological Psychiatry

Brain Research Reviews

Cortex

Cognitive functioning and post-traumatic stress disorder

American Journal of Psychiatry

Functional neuroanatomical correlates of the effects of stress on memory

Journal of Traumatic Stress

MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder

American Journal of Psychiatry

Right temporofrontal cortex as critical locus for the ecphory of old episodic memories

Journal of Neurology, Neurosurgery and Psychiatry

Neuroimaging findings in anxiety disorders

Seminars in Clinical Neuropsychiatry

Structural brain changes in mood disorder: clinical correlates and significance

Seminars in Clinical Neuropsychiatry

Linking combat and physical health: the legacy of World War II in men's lives

American Journal of Psychiatry