Rudi A.J.O. Dierckx, Andreas Otte, Erik F. J. de Vries, Aren van Waarde and Johan A. den Boer (eds.)PET and SPECT in Psychiatry201410.1007/978-3-642-40384-2_19
© Springer-Verlag Berlin Heidelberg 2014
19. Neuroimaging of Delirium
(1)
Department of Intensive Care Medicine, University Medical Center Utrecht, University of Utrecht, Heidelberglaan 100, Utrecht, 3584 CX, The Netherlands
(2)
Department of Radiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands
19.1 Introduction
19.2 Neuroimaging
19.2.1 Feasibility
19.2.2 CT
19.2.3 MRI: Structural Imaging
19.2.4 MRI: Functional Imaging
19.2.5 SPECT
19.4 Conclusion
Abstract
Delirium is an acute change of consciousness and cognition that is associated with poor outcome. The arsenal to treat delirium is limited due to the poor understanding of the pathophysiology of the underlying encephalopathy. Neuroimaging can be used to elucidate possible neural mechanisms. In delirium, however, neuroimaging is still in its infancy. Despite concerns about the feasibility of neuroimaging in delirious patients, several investigations have been performed. Most structural imaging studies suggest that delirium is associated with more brain atrophy and focal abnormalities, such as infarcts and white matter disruption. Functional imaging studies suggest perfusion abnormalities and altered functional connectivity. More advanced imaging techniques may provide new insight in the pathophysiology of delirium.
Abbreviations
ASL
Arterial Spin labelling
CBF
Cerebral Blood Flow
CT
Computed Tomography
DIR
Double Inversion Recovery
DSM-IV-R
Diagnostic and Statistical Manual of Mental disorders, fourth revised edition
DTI
Diffusion Tensor Imaging
fMRI
Functional Magnetic Resonance Imaging
MRI
Magnetic Resonance Imaging
MRS
Magnetic Resonance Spectroscopy
PET
Positron Emission Tomography
SPECT
Single Photon Emission Computed Tomography
19.1 Introduction
Delirium is a common condition in elderly patients, particularly in those with pre-existing cognitive impairment and in critically ill patients. It can be defined according to the Diagnostic and Statistical Manual of Mental Disorders (fourth revised edition, DSM-IV-R) (American Psychiatric Association 2000) as a disturbance of consciousness and a change in cognition that develops over a short period of time and tends to fluctuate during the day. Of all cognitive domains, attention is particularly affected in delirium (Blazer and van Nieuwenhuizen 2012). Other common features are sleep-wake cycle disturbances, memory problems, perceptual disturbances and hallucinations, language disturbances, thought process abnormalities and affective disorders (Inouye 2006; Blazer and van Nieuwenhuizen 2012). Delirium is present in hyperactive, hypoactive and mixed forms. However, patients may rapidly switch from one type to another (Inouye 2006; Blazer and van Nieuwenhuizen 2012).
Delirium is associated with an increased risk of death, institutionalization and dementia, independent of important confounders, such as age, co-morbidity, illness severity and pre-existing cognitive impairment (Witlox et al. 2010). In addition, delirium increases hospital length of stay and medical costs (Inouye 2006). Despite its frequency and consequences, delirium is ill recognized by general physicians (Van Eijk et al. 2009).
The development of delirium involves the complex interrelationship between predisposing factors, including advanced age and exposure to precipitating factors, such as an infectious disease or dehydration (Inouye 2006). Delirium is a manifestation of encephalopathy with altered function of neural networks. The pathophysiology of the underlying encephalopathy is incompletely known and may involve neurotransmitter alterations, especially acetylcholine and dopamine, inflammatory pathways and an aberrant stress response (Hughes et al. 2012).
A multicomponent, non-pharmacological approach may prevent delirium. Once delirium develops, symptomatic treatment with antipsychotics is usually started (Zaal and Slooter 2012). Atypical antipsychotics may have less side effects but seem not to be more effective than haloperidol. However, the effectiveness of antipsychotics in delirium has not been proven in a large-scale, placebo-controlled randomized clinical trial (Zaal and Slooter 2012). One reason for the limited therapeutic arsenal is the poor understanding of the pathophysiology. Neuroimaging may be used to elucidate possible neural mechanisms underlying delirium.
19.2 Neuroimaging
Neuroimaging techniques have provided numerous new insights in the pathogenesis of a variety of neuropsychiatric disorders, particularly dementia, schizophrenia and mood disorders. In delirium, however, neuroimaging is still in its infancy. Neuroimaging can be used to clarify structural or functional predictors, correlates or consequences of delirium. This includes the use of Computed Tomography (CT), Magnetic Resonance Imaging (MRI), Single Photon Emission Computed Tomography (SPECT) or Positron Emission Tomography (PET).
19.2.1 Feasibility
An important concern though is the feasibility of neuroimaging in delirious patients. Attention deficits, clouding of consciousness, restlessness and agitation may seriously hamper procedures that require the subject to lay still in a supine position for quite some time. This is particularly important in MRI where additional discomfort might be induced by the head coil, needed to obtain adequate signal. Motion artefacts can be prevented by sedating the patient. Although the use of sedatives will not affect structural imaging, it may seriously interfere with functional imaging. Functional MRI (fMRI) resting-state studies have shown that sedation reduces default mode network connectivity, the network that has been linked to self-related processes (Heine et al. 2012). Most previous neuroimaging studies in delirium, however, do not report on the proportion of dropout patients due to motion artefacts.
19.2.2 CT
Most previous CT studies showed that delirious patients had larger ventricles and wider sulci than non-delirious controls, suggesting more cortical and subcortical atrophy (Soiza et al. 2008). In addition, delirium was found to be associated with focal abnormalities, such as cerebral infarcts (Soiza et al. 2008).
In one study, xenon-enhanced CT was used to measure cerebral blood flow (CBF) in ten patients during and after delirium (Yokota et al. 2003). Delirium was found to be associated with bilateral reductions in global CBF, in particular the caudate head, thalamus and lenticular nuclei. With recovery from delirium, there was an increase of regional CBF to normal values for each of these regions. These findings suggest that cerebral hypoperfusion may contribute to the pathogenesis of delirium, although it cannot be excluded that hypoperfusion may be a consequence of microcirculatory alterations due to the underlying encephalopathy.
It should, however, be noted that the methodological quality of previous CT studies in delirium was low, with small and heterogeneous groups of patients, confounded by age and use of nonvalidated outcome measures. Yet, from these studies it may be concluded that structural brain abnormalities such as atrophy may predispose to delirium.
19.2.3 MRI: Structural Imaging
Structural imaging using MRI confirmed CT studies, in showing that delirium appears to be associated with cortical and subcortical atrophy as well as an increased proportion of structural lesions (Soiza et al. 2008). These studies showed in particular an increased frequency of periventricular and deep white matter hyperintensities, possibly with a predominance of the basal ganglia (Soiza et al. 2008). In a combined CT/MRI study in stroke patients, a higher proportion of cerebral hemisphere (as opposed to brainstem or cerebellum) stroke was found in delirious patients, as compared to non-delirious controls (Caeiro et al. 2004). Several case reports have been published on delirium in response to a variety of focal lesions (Alsop et al. 2006). However, in a large combined CT/MRI study (n = 235), abnormal brain scans were not predictive for delirium (Kishi et al. 1995). The relationship between cerebral lesions and the occurrence of delirium seems therefore not to be strong.
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