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Subcortical Dementia{{ the Evolution of the Concept

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Subcortical Dementia{{ the Evolution of the Concept BRITISH JOURNAL OF PSYCHIATRY #2002),#2002),180,148^151 180, 148^151 Subcortical dementia{{ The evolution of the concept In 1872, at a time when dementia was a MARK A. TURNER, NICHOLAS F. MORAN and MICHAEL D. KOPELMAN unitary concept, Huntington published `On Chorea', describing the cognitive impairments in the disease that bears his name. In 1874 Meynert, whose interests were both clinical and neuroanatomical, publishedpublished Psychiatry: A Clinical Treatise on Diseases of the Forebrain Based upon its Structure, Function and its Nutrition.. In this book he sought to relate brain struc- Background Drawing a distinction The concept of subcortical dementia devel- ture to function, and postulated that certain between cortical and subcortical oped out of clinical observations of de- psychiatric symptoms resulted from an mentia in the context of disease processes imbalance of blood flow between the sub- dementias seems both useful andjustified. preferentially affecting the subcortical cortical and cortical structures. Meynert Recent research has, however, castdoubt structures. The syndrome was claimed to may have been mistaken in making his on the clinical, neuropsychological, be distinct in its clinical manifestations emphasis on blood flow, but if he had neuroimaging and neuroanatomical basis and its anatomicopathological correlates. talked in neural terms instead, he would of the distinction. The dichotomy between cortical and sub- surely have pre-empted current thinking cortical dementias has now come under about the aetiology of subcortical demen- Aims Toarrive at a reasoned conclusion attack from both the neuropsychological tia. In 1894 Binswanger introduced a aboutaboutthe the relationship between the two and neuroanatomical perspectives. vascular perspective and characterised encephalitis subcorticalis chronica pro- types of dementia and the validity of gressivagressiva, subsequently renamed subcortical distinguishing between them. arteriosclerotic encephalopathy by Olszewski BACKGROUND in 1962.in1962. MethodMethod The historical and recent In 1912 Wilson related subcortical clinical and scientific literature on Dementia is a degenerative disorder invol- disease to a clinical picture distinct from subcortical dementia was reviewed. ving the compromise of multiple domains that seen in cortical dementia when he of cognition. This definition excludes acute described cognitive impairments in the ResultsResults The traditional claimthat confusion of any cause and also chronic absence of apraxia and agnosia in cases of subcortical dementia has distinctclinical focal brain syndromes, in particular the `progressive lenticular degeneration: a manifestations, neuroimaging findings and amnesic syndrome. The further classifica- familial nervous disease associated with tion of dementia, whether based on clinical cirrhosis of the liver', commonly known a neuropathological profile is not presentation or on aetiology, is, however, nowadays as Wilson's disease. Sub- altogether borne out by the literature. fraught with difficulties. Despite this, the sequently a number of other predominantly Some studies show thatfrontal executive emerging view since the mid-1970s has subcortical disease processes have been dysfunction and the profile of memory been that dementia can be separated into characterised and found to be associated cortical and subcortical types, a distinction with a pattern of cognitive impairment that deficits are not significantly different from that has found support from both the clini- supports the idea of distinction between those seenseenin in Alzheimer's disease. cal !Pilloncal!Pillon et aletal, 1993, for example) and cortical and subcortical dementias. Parkin- Neuropathological findings also overlap. aetiological perspectives !see Darvesh & son's disease was not formally incorporated Freedman, 1996, for a review). The differ- into the notion of subcortical dementia Conclusions The category of entiating features of subcortical dementia until 1978, following work by Albert, subcortical dementia may be clinically were said to be a profound slowing of cog- although debate about its aetiology and its usefulusefulin in highlighting the likelihood that an nition, memory disturbances, frontal execu- relationship with cognitive impairment individual with dementia is more likely to tive dysfunction, and changes in personality started as far back as 1932 when Von and affect in the absence of aphasias, Stockert introduced the term subcorticale suffer from bradyphrenia and motor apraxias and agnosias !Cummings, 1986). demenzdemenz to characterise the cognitive difficulties. As neuroscience advances a Other authors have highlighted the dif- impairment evident in a case of encephalitis preoccupation with the distinction may ficulties with the distinction by arguing that lethargica. Concerning more obscure hinder the assessment and treatment of the neuropsychological profiles of cortical causes, in 1938 Smyth and Stern had and subcortical cases are not sufficiently described cognitive impairment in the pre- individual cases. dissimilar !Brown & Marsden, 1988) or sence of thalamic disease. More recently, Declaration of interest None. that cortical abnormalities often occur in in 1974 Segarra and co-workers supported so-called subcortical disease !Hughes et aletal,, the contention that subcortical dementia 1993). With improvements in investigative can occur in the presence of isolated thala- techniques, notably neuroimaging, the mic disease, and in 1984 Katz also specu- ySee editorial, pp. 97^98, thisissue. debate about this matter is likely to continue. lated that the dementia associated with 148 Downloaded from https://www.cambridge.org/core. 30 Sep 2021 at 19:27:30, subject to the Cambridge Core terms of use. SUBCORTICAL DEMENTIA multi-system atrophy may be of thalamic dysfunction and impairment in memory there is a learning impairment which can origin.origin. characteristic of subcortical dementia may be partially corrected by providing richer Although McHugh apparently used the be present.bepresent. !more salient) cues to encourage learning term `subcortical dementia' to characterise The psychiatric manifestations of sub- and promote recognition !Pillon et aletal,, the deficits seen in Huntington's disease in cortical disease come primarily in the form 1993). In contrast, it was claimed that an unpublished communication in 1973, it of personality changes and affective dis- cortical dementias !such as Alzheimer's was Albert and colleagues in 1974 who order. Apathy and irritability are particu- dementia) are characterised by accelerated formally articulated the concept: in a dis- larly common !Aarsland et aletal, 1999), and forgetting !e.g. Cummings, 1986). cussion of the cognitive impairments associ- depression is said to be significantly more However, this distinction does not hold ated with progressive supranuclear palsy, common in subcortical disorders such as good on detailed neuropsychological AlbertAlbert et aletal !1974) specified the clinical Parkinson's disease than it is in Alzheimer's analysis of the patterns of learning and features of the syndrome for the first time. disease. Aarsland et aletal !1999) found that forgetting in, for example, Huntington's Subsequently, a similar clinical picture 38% of a series of patients with Parkinson's disease and Alzheimer's dementia was described in association with basal disease had depression, and Cummings !Kopelman, 1985), and Kuzis et aletal !1999)!1999) ganglionic calcification in hyperpara- !1995) gave a figure of 30% for Hunting- could not demonstrate a different profile thyroidism by Bachman & Albert !1984) ton's disease that is broadly in keeping with of memory deficits between patients with and in human immunodeficiency virus the figure of 41% reported by Dewhurst Alzheimer's dementia and those with dementia by Navia et aletal !1986). There are et aletal !1969) for their series of Huntington's dementia consequent upon Parkinson's a number of other neurological disorders, cases. Psychotic illness and mania are also disease. In remote memory, there are including normal pressure hydrocephalus, overrepresented, particularly in Hunting- variable patterns of impairment. In Alz- the `pugilistic encephalopathy' of repeated ton's disease: psychotic illness was present heimer's dementia a gentle `temporal head injury, multiple sclerosis and the in over 50% and mania in 21% of the gradient' !an extensive remote memory loss spinocerebellar degenerations, that can be Dewhurst series, and in the Parkinson's with some degree or relative sparing of postulated as subcortical dementias but disease series 27% had hallucinations early memories) is found in many studies are not mentioned again here. From the !Aarsland!Aarsland et aletal, 1999).,1999). !Kopelman, 1989), although there have psychiatric perspective, there are similari- In terms of cognition, some evidence been claims that this is specific for auto- ties between the clinical features of sub- suggests that cortical dementia evolves biographical memories as opposed to cortical dementia and those of depressive differently from subcortical dementia. Stern memories of famous events !Dorrego et aletal,, pseudodementia !Caine, 1981) and type II et aletal !1998) evaluated cognitive changes 1999), whereas in Huntington's disease schizophrenia !Pantelis et aletal, 1992).,1992). over 1±3 years prior to the time dementia there is a `flat', uniform loss of remote was diagnosed in 40matched pairs of memories across all earlier periods.
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