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| British Journal of Psychiatry | Psychiatric Bulletin | All RCPsych Journals |
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John O'Brien is a Senior Lecturer in Old Age Psychiatry at the Institute for the Health of the Elderly (Wolfson Research Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, Tel: 0191 256 3323; fax: 0191 219 5051; e-mail: j.t.O\|[apos ]\|Brien{at}ncl.ac.uk). Bob Barber is a consultant psychiatrist and Honorary Lecturer in Old Age Psychiatry at the Centre for the Health of the Elderly at Newcastle General Hospital.
Neuroimaging is traditionally divided into structural and functional imaging. Structural imaging looks at brain structure or anatomy and includes computed tomography (CT) and magnetic resonance imaging (MRI). Functional techniques seek to examine the physiological functioning of the brain, either at rest or during activation, and include single photon emission computed tomography (SPECT), positron emission tomography (PET), MRI spectroscopy, functional MRI (fMRI) and encephalographic brain mapping. Although fMRI, MRI spectroscopy and brain mapping are likely to have clinical applications in the near future, the main imaging modalities of current clinical relevance to psychiatrists are CT, MRI and SPECT, which will be the focus of this article.
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Computed tomography |
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 Top Computed tomography Magnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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Magnetic resonance imaging |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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. Good anatomical resolution is provided by heavily T1-weighted images, whereas proton density- and T2-weighted images are sensitive to changes in water content and provide good visualisation of white matter lesions and smaller infarcts. The cerebrospinal fluid spaces appear dark on proton density- and T1-weighted images (as on CT) and bright on T2-weighted images. In practice, a combination of sequences is often used to provide optimum anatomical and pathological differentiation. | Box 1. Main types of MRI sequences T1-weighted Provides good definition of anatomy T2-weighted Provides high contrast and definition of soft tissue pathology Proton density-weighted Provides good brain/cerebrospinal fluid contrast
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The different advantages and disadvantages of MRI and CT are summarised in Box 2. Magnetic resonance imaging provides a sensitive method to study brain morphology, white matter and vascular pathology and abnormalities associated with epilepsy, such as medial temporal sclerosis. The improved resolution and superior soft tissue contrast of MRI may offer greater potential for early diagnosis. Moreover, MRI can examine the structure of the whole brain in any plane and generate three-dimensional images suitable for detailed volumetric quantification. As MRI does not use ionising radiation it is more suited for serial monitoring and the study of normal controls. The noise and confinement of the scanner is poorly tolerated in approximately 1 in 20 subjects. The main contraindication of MRI is the presence of ferromagnetic materials such as cardiac pacemakers and intracranial aneurysm clips. Orthopaedic implants are not contraindicated although may introduce local artefacts.
| Box 2. Comparison between MRI and CT MRI CT Higher spatial and anatomical resolution Shorter scan times Superior soft tissue definition and contrast Widely available Image in multiple planes; therefore Lower cost superior views of middle and posterior Better tolerated fossa, pituitary, brain stem and spinal cord Limited to axial plane Uses non-ionising radiation Good for bone abnormalities Wide application for quantitative analysis Better for lesions with little or no water Greater sensitivity to detect white mattercontent (e.g. meningiomas) and detection pathology and lesions causing epilepsy of acute intracerebral haemorrhage
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SPECT scanning |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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Disadvantages of SPECT include the fact that, unlike PET, imaging is not performed in real time. Resolution is poor (10–15 mm) and, like CT, there is a need for exposure to radiation. Scanning takes 10–40 minutes, limiting its utility for restless or uncooperative patients. Because of the poor resolution and the similar appearances of some lesions, despite different pathologies (i.e. severe hypoperfusion on SPECT may be due to either infarction or degenerative change), accurate interpretation of a SPECT image almost invariably requires availability of a contemporary CT scan. Other applications of SPECT are hampered by the lack of suitable radioligands, although one for the dopaminergic D2-receptor (IBZM) and one for the dopamine transporter (FP–CIT) may become available in clinical practice this year.
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Uses of neuroimaging in psychiatry |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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Typical neuroimaging changes in the different subtypes of dementia are summarised in Table 1.
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). It has been suggested that a measurement of the minimal width of the medial temporal lobe on CT (between the anterior and posterior margins of the brain stem) is a sensitive and specific marker for Alzheimer's disease (Jobst et al, 1998). A cut-off of around 11 mm was found to differentiate those with Alzheimer's disease from normal controls. However, although this may be useful in separating those with dementia from normal controls and non-organic causes of cognitive impairment (e.g. depression), its usefulness in separating Alzheimer's disease from other types of dementia such as vascular dementia and dementia with Lewy bodies remains to be shown (O'Brien et al, 1999). Cross-sectional measures are invariably limited by the huge variability between individuals that often masks important differences between disease states. Several studies suggest that longitudinal changes between successive scans (e.g. an increase in atrophy) are useful in identifying those with Alzheimer's disease (Jobst et al, 1994; Fox et al, 1996).
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. Patients with Alzheimer's disease have significantly smaller hippocampi (10–50% reduction), amygdalae (up to 40% reduction) and parahippocampi (up to 40%) than age-matched controls.
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However, although medial temporal lobe atrophy provides good discrimination between patients with Alzheimer's disease and controls, as with CT it is not specific to Alzheimer's disease and has been described in a number of other conditions including other dementias, Parkinson's disease (Laakso et al, 1996), temporal lobe epilepsy and schizophrenia. However, the volume reductions are less extensive than with Alzheimer's disease.
SPECT scanning
Characteristic SPECT changes associated with Alzheimer's disease include temporo-parietal hypoperfusion (O'Brien et al, 1992; Jobst et al, 1998). Such change can separate those with Alzheimer's disease from normal controls and those with other causes of cognitive impairment in 60–90% of cases (O'Brien et al, 1992; Read et al, 1995; Jobst et al, 1998).
The relative place of structural and functional imaging in the diagnosis of Alzheimer's disease remains to be determined. In practice, structural imaging is usually performed first and may be helpful in supporting the diagnosis of Alzheimer's disease if temporal lobe atrophy is seen (especially on MRI). However, SPECT may be helpful in supporting the diagnosis of Alzheimer's disease either in cases where structural imaging is normal or equivocal or when MRI is not available.
Vascular dementia
CT and MRI
Several studies have compared structural imaging changes between patients with vascular dementia and Alzheimer's disease. Degree of cortical atrophy or ventricular enlargement does not seem to separate the groups, although vascular dementia is invariably associated with an increased prevalence of infarcts and more extensive white matter change. Evidence from studies of patients with established vascular dementia suggests that vascular disease is associated with cortical and central atrophy and that both the volume and location of lesions are important. In particular, bilateral, left-sided lesions, diffuse white matter change and small infarcts in strategic areas may all be important in causing cognitive impairment.
SPECT scanning
In vascular dementia, a variable pattern of perfusion on SPECT is seen. Classically, a ‘patchy’ multi-focal pattern is seen, corresponding to perfusion deficits, but that depends on the actual site of vascular lesions (Read et al, 1995). Large cortical infarcts are represented by areas of absent blood flow. Greater diffuse white matter change can be associated with greater generalised cortical reduction in blood flow, with some regional variations that depend both on the site of lesion and projection pathways. For example, infarcts in the basal ganglia can result in reduced cortical blood flow to frontal lobes, consistent with deafferentation of the main projection pathways. At present, it is probably sensible to reserve the use of SPECT as an investigation when information from clinical assessment and structural imaging is not definitive enough to confirm or refute a diagnosis of vascular dementia.
Imaging changes needed for diagnosis
With vascular dementia, even more so than with Alzheimer's disease, the extent of imaging that may be considered necessary in individual patients very much depends on which set of diagnostic criteria is being applied. Imaging requirements for the application of several current sets of diagnostic criteria for vascular dementia are summarised in Box 3. The NINDS/AIREN criteria (National Institute of Neurological Disorders and Stroke and the Association Internationale pour la Recherche et l’Enseignement Neurosciences; Roman et al, 1993) are perhaps the most rigorous with regard to the need for neuroimaging confirmation. The criteria for probable vascular dementia include multiple infarcts or strategic single infarcts as well as multiple subcortical or white matter lesions. The criteria specifically state that the absence of cerebrovascular lesions on brain CT or MRI makes the diagnosis of vascular dementia uncertain (Box 4).
| Box 3. Neuroimaging requirements for application of current diagnostic systems Diagnostic system Vascular brain changes required on structural imaging criteria Hachinski Ischaemic Scale (Hachinski et al, 1975) No requirement for brain imaging. ICD–10 (World Health Organization, 1992) In some cases, confirmation can be provided only by computerised axial tomography or, ultimately, neuropathological examination. In addition, the ICD–10 research diagnostic criteria require evidence from the history, examination, or tests of significant cerebrovascular disease that may be reasonably be judged to be aetiologically related to the dementia (e.g. a history of stroke or evidence of cerebral infarction). DSM–IV (American Psychiatric Association, 1994) There must be evidence of cerebrovascular disease (i.e. focal neurological signs and symptoms or laboratory evidence) that is judged to be aetiologically related to the dementia. CT of the head and MRI usually demonstrate multiple vascular lesions of the cerebral cortex and subcortical structures. The extent of central nervous system lesions detected by CT and MRI in vascular dementia typically exceeds the extent of changes detected in the brains of healthy elderly persons (e.g. periventricular and white matter hyperintensities noted on MRI scans). Lesions often appear in both white matter and grey matter structures, including subcortical regions and nuclei. Evidence of old infarctions (e.g. focal atrophy) as well as of more recent disease may be detected. California Criteria (Chui et al, 1992) The criteria for the clinical diagnosis of probable ischaemic vascular dementia (IVD) include evidence of two or more ischaemic strokes by history, neurological signs and/or neuroimaging studies (CT or T1-weighted MRI) and evidence of at least one infarct outside the cerebellum on CT or T1-weighted MRI. The diagnosis of probable IVD is supported by evidence of multiple infarcts in brain regions known to affect cognition. Features that are thought to be associated with IVD, but await further research, include periventricular and deep white matter changes on T2-weighted MRI that are excessive for age. A clinical diagnosis of possible IVD may be made when there is dementia and Binswanger's syndrome (without multiple strokes) that includes extensive white matter changes on neuroimaging. NINDS/AIREN Criteria (Roman et al, 1993) The criteria for the clinical diagnosis of probable vascular dementia require the presence of cerebrovascular disease (CVD), defined by the presence of focal signs on neurological examination and evidence of relevant CVD by brain imaging (CT or MRI) including multiple large-vessel infarcts (angular gyrus, thalamus, basal forebrain, or posterior or anterior cerebral artery territories), as well as multiple basal ganglia and white matter lesions, or combinations thereof. Features that make the diagnosis of vascular dementia uncertain or unlikely include absence of cerebrovascular lesions on brain CT or MRI.
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| Box 4. Brain imaging lesions associated with vascular dementia (NINDS/AIREN Criteria) Topography Radiological lesions associated with dementia include any of the following or combinations thereof: Large-vessel strokes in the following territories: Bilateral anterior cerebral artery Posterior cerebral artery, including paramedian thalamic infarctions, inferior medial temporal lobe lesions Association areas: parietotemporal, temporo-occipital territories (including angular gyrus) Watershed carotid territories: superior frontal and parietal regions Small-vessel disease: Basal ganglia and frontal white matter lacunes Extensive periventricular white matter lesions Bilateral thalamic lesions Severity In addition to the above, relevant radiological lesions associated with dementia include: Large-vessel lesions of the dominant hemisphere Bilateral large-vessel hemispheric strokes Leukoencephalopathy involving at least one-quarter of the total white matter Although volume of lesion is weakly related to dementia, an additive effect may be present. White matter changes observed only on T2- but not on T1-weighted MRI, or CT, may not be significant Absence of vascular lesions on brain CT/MRI rules out probable vascular dementia
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Perhaps one of the more difficult areas is the role of white matter change alone. Although white matter changes seen on imaging can be caused by vascular disease, they are in fact pathologically heterogeneous. The NINDS/AIREN criteria deal with this by stating that white matter lesions on CT or MRI may be considered as evidence for cerebrovascular disease, but for this to be the case they must be diffuse and extensive, extending to deep white matter. The differences between infarcts and white matter changes on MRI are summarised in Box 5 and Fig. 3. Changes observed only on T2-weighted MRI are felt to be of doubtful significance. Importantly, the criteria suggest that the changes should involve at least a one-quarter of the total of white matter, based on previous studies (Erkinjuntti et al, 1987). The discussion emphasises the need to correlate radiological images with clinical and neuropsychological changes combined with neuropathology in patients with vascular dementia, and prospective validation of the NINDS/AIREN and other criteria is certainly needed.
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| Box 5. Differences between cerebral infarcts and deep white matter hyperintensities on MRI Infarcts Deep white matter hyperintensities Hypointense on T1 and proton density-Hyperintense on T2- and proton density- weighted imagesweighted images Hyperintense on T2-weighted images No change/invisible on T1-weighted images Well-defined; wedge shape if peripheral Range from punctuate to diffuse confluent lesions Often single or low numbers Often multiple Often evidence of cortical extension Restricted to white matter with no cortical extension May be associated with focal enlargement of ventricles and sulci Ventricles and sulci unchanged
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Dementia with Lewy bodies
CT and MRI
So far, MRI studies have shown dementia with Lewy bodies to be associated with relative preservation of temporal lobe structures compared with Alzheimer's disease (Hashimoto et al, 1998; Barber et al, 1999a; Harvey et al, 1999). Initial reports of frontal atrophy in subjects with Lewy body pathology were not confirmed by a recent study (Harvey et al, 1999). Dementia with Lewy bodies does not seem to differ from Alzheimer's disease in terms of white matter changes on MRI (Barber et al, 1999b).
In summary, the limited evidence available suggests that structural imaging in dementia with Lewy bodies reveals similar generalised atrophic changes to Alzheimer's disease in most cases, although approximately 40% of subjects show preservation of medial temporal lobe structures.
Functional imaging changes in dementia with Lewy bodies
In Parkinson's disease, decreased blood flow in basal ganglia occurs and, when associated with dementia, biparietal changes similar to those seen in Alzheimer's disease are reported. Similarly, in the few SPECT studies of dementia with Lewy bodies, similar patterns of blood flow changes to Alzheimer's disease have been found – although Donnemiller et al (1997) also found a subtle difference in perfusion patterns with a greater degree of occipital hypoperfusion in dementia with Lewy bodies compared with Alzheimer's disease.
The more powerful, although still research-based, use of SPECT involves specific ligands for different neurochemical systems. Ligands have been developed for pre- and post-synaptic dopaminergic and cholinergic systems. Donnemiller et al (1997) found significant differences between dementia with Lewy bodies and Alzheimer's disease in beta-CIT binding (a ligand for the dopamine transporter) – differences that would be predicted from known neurochemical differences between Alzheimer's disease and dementia with Lewy bodies. Reduced D2-receptor density in basal ganglia using IBZM has also been reported in dementia with Lewy bodies (Walker et al, 1997). Using a marker of the choline transporter, significant differences between Alzheimer's disease subjects and controls as well as between Parkinson's disease subjects with and without dementia have been found (Kuhl et al, 1996). In summary, current evidence suggests that blood flow SPECT shows similar appearances in dementia with Lewy bodies to those seen in Alzheimer's disease although, as with Alzheimer's disease, SPECT may still be useful in distinguishing dementia with Lewy bodies from frontal lobe dementia or vascular dementia. However, new chemical imaging techniques, although not yet available in practice, show great promise in differentiating dementia with Lewy bodies from other disorders and are an exciting area of current research.
Specific lobar atrophies
Focal atrophy of the frontal or frontotemporal lobes on CT or MRI may be helpful in the diagnosis of frontotemporal dementia and has recently been incorporated into consensus diagnostic criteria (Neary et al, 1998). However, in general, although such lobar atrophy is a fairly specific finding (i.e. when it occurs it lends strong support to the diagnosis), it is not particularly sensitive and may be lacking in up to 50% of cases that have the diagnosis. Similarly, anterior, rather than posterior, perfusion deficits are characteristic of frontotemporal dementia and are thought to be a more sensitive marker of the disorder than structural changes and similarly form part of recently proposed diagnostic criteria (Neary et al, 1998).
Depression
Studies in the early 1980s demonstrated that depression in late life is associated with structural changes, including ventricular enlargement on CT. These findings have generally been confirmed and similar changes are also known to occur in younger patients with unipolar and bipolar disorder (Videbech, 1997). These abnormalities are non-specific and recent interest has focused on other changes, such as the presence of volume reductions in the caudate (Krishnan et al, 1992) and frontal lobe (Coffey et al, 1993; Drevets et al, 1997). However, the most consistent abnormality described in depression, in particular late-life depression, comes from the many studies that have repeatedly shown an increase in the number and/or severity of signal hyperintensities in the white matter in both unipolar and bipolar disorder (Rabins et al, 1991; O'Brien et al, 1996). White matter lesions are found scattered in the deep white matter, the periventricular white matter, the basal ganglia and the pons. They may be divided on the basis of scan appearance and neuropathological substrate into those adjacent to the ventricular system (periventricular lesions; see Fig. 3
) and those distinct from the ventricles and located in deep white matter (deep white matter lesions; see Fig. 3). Rabins et al (1991) showed a particular increase in deep white matter lesions in elderly patients with unipolar disorder, with the predominance of lesions in the frontal lobes and basal ganglia. The location of these lesions fits with functional imaging changes suggesting frontal and caudate abnormalities in depression and supports the notion of ‘frontostriatal dysfunction’ in depression. The increase in white matter lesions in those with depression may be most marked for those presenting with their first ever depression in late life (O'Brien et al, 1996). Such findings add credence to the long-held view that subtle organic changes may be one important reason why elderly patients develop their first ever depression in late life. However, the clinical relevance of such deep white matter lesions remains to be fully determined. They may be associated with poor initial treatment response (Simpson et al, 1998) and poor long-term outcome. In a three-year study, O'Brien et al (1998) found that every single elderly patient with depression who had severe (confluent) deep white matter change relapsed. Similar findings with regard to an association between white matter lesions and poor treatment response have been reported for younger patients with bipolar disorder. This emphasises the need for careful clinical assessment and follow-up of cases with lesions and indicates that the presence of lesions may be one consideration when deciding upon long-term prophylactic therapy.
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Improving access to neuroimaging |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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Another problem is in scan interpretation, with which psychiatrists are involved far too rarely. Many imaging changes of particular interest to psychiatrists, such as relatively subtle degrees of atrophy or white matter change, may not be particularly commented on in a standardised way, with traditional reporting methods being more concerned with the presence of gross structural pathology. Dialogue between the main disciplines involved (psychiatry, neuroradiology, medical physics, neurology, and others) is important and, from our own experience, joint meetings to discuss cases and view scans are invaluable in terms of clarifying areas of uncertainty and providing a focus for education, audit and research.
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Conclusions |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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One sensible way forward may not be to ask "When should I do a scan?" since there can never be a comprehensive list of all indications for any investigation. The question may be more appropriately phrased: "If I need to make a diagnosis using a certain set of diagnostic criteria, what sort of imaging do I need to perform?".
Computed tomography will, for cost and practical reasons, invariably be the imaging modality of first choice, although an MRI, if accessible, is almost always the superior imaging modality. Outside of research settings, it is more difficult to be clear when functional imaging such as SPECT scanning should be performed. SPECT changes can add support to a diagnosis of Alzheimer's disease, vascular dementia or frontotemporal dementia and may be very helpful in excluding these diagnoses in those presenting with a functional psychiatric disorder and cognitive impairment. SPECT may also be helpful in difficult cases where there is diagnostic doubt, for example in a patient with a seemingly clear history of a stroke with cognitive impairment in whom a CT is normal.
Increasingly, as further therapeutic options become available and imaging techniques become more able to provide useful diagnostic and prognostic information, structural and functional neuroimaging will become an important part of the clinical work-up in psychiatry.
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Multiple choice questions |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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References |
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TopComputed tomographyMagnetic resonance imagingSPECT scanningUses of neuroimaging in...Improving access to neuroimagingConclusionsMultiple choice questionsReferences |
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| British Journal of Psychiatry | Psychiatric Bulletin | All RCPsych Journals |
