![]() Unfortunately, neuropathologists failed to provide a pathology-dependent hypothesis or mechanism for hysteria. The choice of the term “experimental” was primarily driven by the hope that the investigation of PP’s neuropathological underpinnings could shed light on the neurobiology of hysteria. PP was, therefore, named “Experimental disease/Maladie experiméntale” by the enthralled neuropsychiatrists. The appearance of PP offered, for the first time, evidence that hysteria could be a symptom of a specific neurological condition promoted by a defined underlining pathology. These clinical features were acknowledged as hysteria, a condition that just a few decades before was the focus and conceptual driver of the seminal psychodynamic theories put forward by Sigmund Freud. PP symptoms included dementia, psychoses with delusions and complex hallucinations, disinhibition, impulsivity (including hypersexuality, kleptomania, gambling), and a variety of behavioral disorders ranging from distractible neurological symptoms (i.e., “ histrionic” interpretations of motor disorders) to mannerisms and catatonia. Renowned neuropsychiatrists of those days (Neurology and Psychiatry were still a unified discipline) described the disease’s behavioral, emotional, and cognitive aspects in detail. Following the acute phase of Von Economo-Cruchet Encephalitis (also known as Von Economo Disease), a significant percentage of surviving patients developed a neurological syndrome named Post-encephalitic Parkinsonism (PP). The pandemic was due to an H1N1 influenza A virus inaccurately named “Spanish Flu”. In 1919, after the end of World War I, a pandemic caused millions of deaths in the following five years. Understanding the pathophysiological background of these conditions provides a conceptual bridge between neurology and psychiatry, thereby helping to generate a promising and converging area of investigation and therapeutic efforts. In support of this hypothesis, mind-altering psychedelic drugs also modulate thalamic-cortical pathways. These phenomena alter the brain metastability, creating dreamlike, dissociative, or altered states of consciousness. The process produces an input overload to the cortex, thereby exacerbating DMN decoupling from task-positive networks. TCD moves in parallel with altered thalamic filtering of external and internal information. TCD generates the loss of finely tuned cortico-cortical modulations promoted by the thalamus and unleashes the aberrant activity of the Default Mode Network (DMN). We propose that these mechanisms find a crucial driver and trigger in the dysregulated activity of high-order thalamic nuclei set in motion by ThalamoCortical Dysrhythmia (TCD). ![]() Mechanisms at the root of these symptoms also share similarities with processes promoting altered states of consciousness found in Rapid Eye Movement sleep, psychiatric disorders, or the intake of psychedelic compounds. These disorders exhibit similar presentation patterns and progression. ![]() The PD-DLB psychosis complex found in Parkinson’s disease (PD) and Dementia with Lewy Bodies (DLB) includes hallucinations, Somatic Symptom/Functional Disorders, and delusions.
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