Psychogenic Tetraparesis and Bilateral Upper Limb Dystonia, Regressive Under Short Propofol-Induced Sedation and During Hepatic Encephalopathy

Abstract

Psychogenic neurologic disorders are common in clinical practice, but their underlying mechanisms are largely unknown. These disorders represent “functional” neurologic deficits, such as amnesia, paralysis, or somatosensory losses that are not explained by organic lesions in the nervous system but arise in the context of “psychogenic” stress or emotional conflicts. Therefore, even though the pathophysiology of the spectrum of these disorders is unclear, the patients fall in different psychiatric categories with possible psychological and psychodynamic etiologies. Recently, this topic has received increasing attention. Indeed, several studies have used functional brain imaging techniques in an attempt to identify specific neurologic hallmarks associated with conversion disorder and its multiple clinical manifestations. 1–3 For psychogenic dystonia, the clinical distinction between an organic and psychogenic origin is even more difficult because they frequently overlap. 4 Published studies remain inconclusive so far, but promising theories have been proposed. These theories are based on active inhibition of motor areas by limbic brain areas, 5–7 and on the concept of impaired movement conceptualization, 8 such as in psychogenic paralysis. Interestingly, hypnosis-induced paresis—a model of “functional” paresis— of the left leg showed enhanced cerebral blood flow in the right orbitofrontal and right anterior cingulate cortices (limbic system). This is accompanied by decreased activation of the right primary motor cortex in a positron emission tomography (PET) study. Both observations support the concept of modulation of sensorimotor representations by affective and stressful events via increased limbic input. 9 Following up on this concept, we present a clinical long-term follow up of Mrs. B, a 47 year-old female, who progressively developed psychogenic tetraparesis and bilateral upper limb dystonia. Both completely returned to normal under two specific conditions: initially under a short propofol-induced sedation, and later at an advanced stage of hepatic encephalopathy. We hypothesize that these two conditions interfered with the abnormal limbic input, allowing for the alleviation of the symptoms.