Chapter 1
Introduction
The purpose of this book is to improve the treatment of stroke by increasing the attention paid to its mental aspects. It is meant to help all those who have to deal with the behavioral and emotional disturbances that arise in stroke. I have made an assumption of knowledge at a professional level, but tried to write so that specialists in one field can understand contributions made to the subject from other fields. My own experience has mostly been as a psychiatrist working with stroke survivors; however, stroke does not respect specialty boundaries.
The aim is therefore to produce a book that can be widely understood. Some stroke survivors and their families may find it useful. Many excellent works directed at the general public are available, including some written by stroke survivors, but some nonmedical caregivers want more technical knowledge. To make it more widely understandable the technical terms are defined in a glossary and an appendix has been added explaining the relevant basic neuroanatomy in simple terms.
Several developments have led to the work being offered at this time. These include the advent of new imaging techniques, greater precision in psychiatric diagnosis, new psychiatric treatment methods, more recognition of the psychiatric needs of nursing home patients, increased psychiatric interest in dementia, and the development of a specialized field of geriatric psychiatry. There is increased medical interest in the chronic patient with multiple medical and mental disabilities, and in the active treatment of long-term illness. This has brought a realization that the limits to therapy and rehabilitation are largely set by mental impairment, and that this mental impairment may be treatable, and must be evaluated.
In the acute treatment of the fresh stroke, technology has outpaced but not eliminated psychology. Decisions about whether to seek treatment, and whether to treat, have become more critical but not less emotional.
Writings about this subject often emphasize either neuropsychiatry or social psychiatry. Neuropsychiatrists and neuropsychologists are concerned with the physical foundations of particular syndromes. These are important, because much of our knowledge of the relationship between the brain and the mind comes from the study of stroke, but are different from clinical psychiatry. Social psychiatry is concerned with the social and economic consequences of stroke. These are also important, but to alter them demands changes in the health delivery system that are mostly outside the scope of the individual practitioner. Thus a gap needs to be filled. I have tried to fill this gap and to bring neuropsychiatry and social psychiatry together.
In deciding what to include I have envisaged someone who is treating a stroke patient, encounters a psychiatric problem, and needs information about it. The advent of computerized literature searches has probably outdated some of the need for a comprehensive literature review. This has become even truer since the last edition. I have taken advantage of this to omit some detail, and have even been able to shorten the text. The original literature is discussed in the case of classical papers, such as those that have given rise to eponyms. In some areas of controversy, fairness demands that the literature review should be in detail that may be tedious to those seeking a general overview of the subject. Such detailed reviews are preceded by more elementary outlines and can be skipped easily.
The book has been organized approximately into three main sections. The first section concerns mainly the background, the causative factors, and basic science. The second concerns the specific syndromes produced by stroke. The third concerns the outcome and psychosocial consequences. The first section trespasses on neurology and the last section on sociology.
Terminology dichotomizing the physical from the mental is used loosely. In many cases the terms âpsychiatricâ or âpsychologicalâ are used as an antithesis to âorganicâ or âneurological.â Such loose terminology, or the existence of such a dichotomy, could be disputed, but the context should make clear what is meant. In avoiding sexist terminology, pronouns are used that reflect the sex incidence of the conditions discussed, rather than resorting to the subterfuges of the passive voice and the plural number.
The wide aim at readership must produce inconsistencies in voice and sophistication, and errors in style. I hope that these errors are in the direction of oversimplification rather than obscurity. Neurologists and internists may find this fault of oversimplification in the first part and psychiatrists in the second part. Simplification may sound like dogmatism to some readers, and their indulgence is requested. This especially applies to material that has been highly condensed and put in tabular form. In spite of scientific advances, psychiatry continues to be a subject where opinions differ.
Part 1:
Background and Causation
Chapter 2
Diagnosis of Storke
Defining Stroke
Someone who suffers a sudden attack of unconsciousness, then becomes paralyzed on one side, and loses the power of speech has probably suffered a stroke, but it is not always easy to say exactly what the word âstrokeâ means. Families often ask whether a patientâs mental symptoms are due to a stroke. They may ask this because of the presence of physical symptoms at the onset of the illness, the suddenness of onset, the presence of stroke risk factors, or the finding of abnormalities on the Computer axial tomography (CAT) scan or Magnetic resonance imaging (MRI). The answer to the question, âWas it a stroke?â may be needed in order to decide on therapy. In this case the question will probably be about what is going on in the patientâs brain: Is there an infarct? Is there an artery obstruction? Is there an embolism? Is there bleeding?
Official Definitions
Official definitions (see Table 2.1) mostly ignore mental symptoms. The World Health Organization (WHO) defines stroke as a vascular lesion of the brain, resulting in a neurological deficit persisting for more than twenty-four hours or resulting in death (Hatono, 1976). The major classifications in the United States are those of the Stroke Data Bank (Mohr et al., 1978; Kunitz et al., 1984; Gross et al., 1986) and of NINDS, the National Institute for Communicative Disorders and Stroke (1990). Separate criteria for neonatal stroke have not been formalized.
Table 2.1. Definitions of stroke
Source | Definition |
World Health Organization | A vascular lesion of the brain, resulting in a neurologic deficit persisting for more than twenty-four hours or resulting in death. |
Stroke Data Bank | Seven entities: brain infarction due to atherosclerosis and distal insufficiency, infarction of unproved etiology, infarction due to embolism, lacunar stroke, parenchymal hemorrhage, subarachnoid hemorrhage, and transient ischemic attack (TIA). |
National Institute of Neurological Disorders and Stroke | Classifies cerebrovascular disease into four categories: asymptomatic, focal brain dysfunction, vascular dementia, and hypertensive encephalopathy. Focal brain dysfunction is divided into: transient ischemic attacks (TIAs) and stroke. |
Community survey instruments | Questionnaire (Gurland et al., 1978). |
| Recorded medical diagnosis (Bamford, 1992). |
Community Survey Instruments
The official definitions are largely neuropathological. They assume the ability to do a full physical examination and the availability of special investigations or autopsy follow-up. This limits their usefulness in situations where these resources are not available. Research surveys of entire populations outside of a hospital setting must therefore use different diagnostic criteria (Gurland et al., 1977; Bamford, 1992). A survey instrument that depends on subjectively self-reported symptoms, rather than objectively observed signs, can lead to overestimation of the association of stroke with depression and anxiety, since the depressed and anxious may be more likely to say they have suffered stroke-like symptoms.
Rating Scales
Several scales of stroke severity such as the National Institutes of Health Stroke Scale (NIHSS) are available and are useful in tracking progress and response to treatment. They can be downloaded from www.strokecenter.org/trials/scales/nihss.
âSilentâ Strokes
Some people with cavities in their brains produced by vascular disease (old infarcts) have no symptoms. They have been referred to as having âsilent strokes.â It is not always certain how silent these silent strokes really are. A stroke may produce neurological signs other than obvious hemi-plegia. Some of these may be quite subtle but can be revealed by a full and careful examination by a skilled clinician, especially if the patient is alert and cooperative. Further uncertainty is added by the fact that published studies of this phenomenon often ignore mental symptoms. Although no difference in terminology has been formalized, the term âsilentâ is more commonly used for those without any nonpsychiatric clinical signs, and ânonobviousâ for those where such signs might have been found on full examination, but this was not carried out. Blass and Ratan (2003) think âunrecognizedâ stroke is the best term. They are not strokes as officially defined by NINDS, the Stroke Data Bank, and WHO.
About a fifth of older people have such infarcts. They tend to get additional infarcts and to become demented (Vermeer et al., 2003).
Transient Ischemic Attacks (TIAs)
In TIAs it is assumed that no brain tissue dies, and the CAT scan is normal. (The reversible ischemic neurological defect or RIND is a TIA which is not quite as transient.) Agreement between observers on the diagnosis of TIA is not very good (Landi, 1992).
There is disagreement about the use of the terms âminor strokeâ and âlittle stroke.â These are sometimes used for TIAs, sometimes for RINDs, and sometimes for stroke due to small infarcts that give rise to strokes with limited symptoms.
Infarction versus Hemorrhage
Infarction means the death of a part of the body due to cutting off of its blood supply (ischemia). Brain infarcts due to ischemia become softened and eventually liquefy.
It was thought that parenchymal brain hemorrhage, bleeding into the substance of the brain, was an invariably fatal event leaving no residuum of impaired survivors. With the advent of the new imaging methods, small areas of hemorrhage have been recognized more frequently, and they often cannot be distinguished clinically from infarcts (Steinke et al., 1992). Subarach-noid hemorrhage differs considerably from infarcts when it first presents, although survivors have much in common with other stroke victims and commonly have mental impairment (Suarez, 2007).
A third pathological entity affecting blood vessels in the brain is venous thrombosis, which usually presents as headache without clinical features of a typical stroke.
Brain Imaging Techniques
The introduction of new imaging techniques has added to our knowledge but posed new questions. Infarcts may be found in psychiatric patients with no focal neurological signs or symptoms. Decisions have to be made about which psychiatric patients to subject to these techniques; techniques that can be frightening and may need patient cooperation and informed consent.
The two major imaging methods in clinical use are the CAT scan and magnetic resonance imaging (MRI) scan. These work by showing up parts of the brain that have become softened or liquefied. Methods now in research use are gradually moving into clinical use. These include positron emitting tomography (PET), functional magnetic resonance imaging (fMRI), regional cerebral blood flow (rCBF), and the kind of rCBF called single photon emitting computerized tomography (SPECT). These research methods can show up localizations of disordered brain function that were not apparent from studies of brain injury and cerebral infarction. For example, decreased metabolism has been found in frontal areas with schizophrenia, and in parietal brain areas with dementia. The decreased activity with vascular dementia may be in the parietal areas even if the parietal areas do not contain an infarct (see Chapter 16).
CAT Scan
An old infarct, that has liquefied, shows up clearly on the CAT scan of the brain as a dark area. Before softening occurs the picture is less clear, and immediately after the stroke the CAT scan is normal in 50 percent of cases (Bamford, 1992). Compared with newer techniques, CAT scans are cheaper, quicker, and demand less patient cooperation. Their rapidity is a particular advantage in determining the absence of hemorrhage in patients with very recent strokes who might be helped by clot-busting or blood-thinning drugs. CAT remains the most widely used neuroimaging technique for the evaluation of acute stroke.
Magnetic Resonance Imaging
MRI does not depend on how radio-opaque objects are, but on how much hydrogen ions or protons (in effect how much water) they contain. As nerve cell bodies contain more water than the nerve fibers, the gray and white matter can be seen separately (fMRI works differently). There are two main kinds of MRI picture. One kind is longitudinal (spin-lattice) relaxation time, also designated T2. The other kind is called transverse (spin-spin) relaxation time, also designated T1.
Although MRI is very sensitive, cases have been described with all the signs and symptoms of a stroke, including hemiplegia and aphasia, in which the MRI was negative (Alberts, Faulstisch, and Gray, 1992; Besson et al., 1993).
MRI sometimes shows areas of ârarefactionâ that are not visible on CAT scan. They are in the white matter, typically around the ventricles. These areas show up as high intensity signals. (It can be confusing to hear the terms âhigh intensityâ or âhyperintensityâ used for an area that is, histologically speaking, an area of rarefaction. Such areas look bright and white on the T2 MRI because they are more watery.)
Several refinements of the MRI are in regular clinical use. FLAIR (fluid-attenuated-inversion-recovery) eliminates the hyperdensity due to cerebro-spinal fluid, thus producing a clearer picture. Diffusion-weighted MRI shows parts that have become edematous, which is an early stage in brain damage (see Chapter 17). Perfusion-weighted MRI (which involves injecting a contrast agent) reveals parts that have only partially had their blood supply reduced (the ischemic penumbra). Using combinations of these kinds of MRI is useful in distinguishing conditions such as MELAS (mitochondrial encephalomyopathy, ...