This is a longitudinal investigation of the psychophysiological mechanism for the development of delirium in coronary care units (CCUs). Ten patients satisfying DSM-III-R diagnostic criteria for delirium (group D) and 10 controls (group C) were drawn from patients admitted to CCU. Electroencephalogram (EEG) and eye movement recordings were observed over the days that patients were admitted to CCU and on a control day of admission and compared for each group and between each day. In the D group, slowing of background EEG activity, particularly on day 2, and many R (rapid) group eye movements and RS type (rapid superimposed on slow) eye movements, particularly on day 3, were observed. That is, from days 2 to 3, EEG findings showed an improvement in consciousness, and eye movement recordings manifested signs of anxiety and tension. These psychophysiological findings can be used to explain the transition from prodromal delirium to obvious delirium, and are supported by clinical features.
"A small study of postoperative patients in ICU using polysomnography found that sleep disturbances preceded the emergence of delirium . Matsushima et al. (1997) prospectively found prodromal changes of background slowing on EEG (theta/alpha ratio) and sleep disturbance associated with changing consciousness in CCU patients developing delirium . Moreover, sleep enhancement strategies and avoidance of hypnotics can reduce delirium risk  . "
[Show abstract][Hide abstract] ABSTRACT: Delirium is a serious neuropsychiatric syndrome of acute onset that occurs in approximately one in five general hospital patients and is associated with serious adverse outcomes that include loss of adaptive function, persistent cognitive problems and increased mortality. Recent studies indicate a three-domain model for delirium that includes generalised cognitive impairment, disturbed executive cognition, and disruption of behaviours that are under circadian control such as sleep-wake cycle and motor activity levels. As a consequence, attention has focused upon the possible role of the circadian timing system (CTS) in the pathophysiology of delirium. We explored this possibility by reviewing evidence that (1) many symptoms that occur in delirium are influenced by circadian rhythms, (2) many features of recognised circadian rhythm disorders are similar to characteristic features of delirium, (3) common risk factors for delirium are known to disrupt circadian systems, (4) physiological disturbances of circadian systems have been noted in delirious patients, and (5) positive effects in the treatment of delirium have been demonstrated for melatonin and related agents that influence the circadian timing system. A programme of future studies that can help to clarify the relevance of circadian integrity to delirium is described. Such work can provide a better understanding of the pathophysiology of delirium while also identifying opportunities for more targeted therapeutic efforts.
Medical Hypotheses 07/2013; 81(4). DOI:10.1016/j.mehy.2013.06.032 · 1.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The phenomenology of delirium has received little standardized longitudinal study but offers the prospect of valuable insights regarding clinical subtypes, differentiation from other neuropsychiatric disorders, identification of underlying pathophysiologies, management, and course. This review examines current approaches to the investigation of delirium phenomenology and how the findings to date illuminate our understanding of delirium. It concludes with recommendations for future investigations.
Journal of Geriatric Psychiatry and Neurology 02/1998; 11(3):150-6; discussion 157-8. DOI:10.1177/089198879801100306 · 2.24 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of the present study was to clarify the neurophysiological changes associated with analgesic and behavioral effects of low-dose ketamine HCl in patients suffering from chronic neuropathic pain. Ten in-patients with neuropathic pain participated in this single-blind, placebo-controlled study after giving written informed consent. Following intravenous injections of a saline solution (placebo), three bolus injections of 5 mg ketamine HCl were administered at 5 min intervals. Changes in pain perception were assessed using a numerical rating scale for pain. Behavioral changes, including psychotomimetic effects, were assessed using the Brief Psychiatric Rating Scale (BPRS). Electroencephalograms (EEG) and electrooculograms (EOG) were recorded continuously throughout the testing period. One minute EEG and closed-eye eye movements were quantified. The effects of ketamine were evaluated by comparing the neurophysiological and behavioral parameters obtained from the placebo and ketamine trials. Pain reduction was significantly correlated with ketamine-induced changes in hallucinatory behavior and excitement as measured by the BPRS. Ketamine injections caused a significant decrease in the EEGalpha amplitude without an accompanying reduction in EEG frequency. The EEGalpha amplitude reduction at the right central electrode was significantly related to subjective pain relief. Subanesthetic doses of ketamine significantly decreased rapid eye movements, but did not initiate slow eye movements. In conclusion, the present EEG-EOG/behavioral results indicate that ketamine-induced failure of neural integration between cortical-subcortical regions induces psychotic symptoms and alters pain perception on neuropathic pain.
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