(Stroke. 1996;27:30-36.)
© 1996 American Heart Association, Inc.
Articles |
Comparison of Different Diagnostic Criteria for Vascular Dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN)
From the Department of Psychiatry and the Institute of Radiology (K.-J.B), University School of Medicine, Lübeck, FRG.
Correspondence to Dr T. Wetterling, Department of Psychiatry, University Medical School of Lübeck, 23538 Lübeck, FRG.
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Abstract |
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 Top Abstract IntroductionSubjects and Methods Results Discussion References |
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Background and Purpose Vascular dementia (VD) has been an ill-defined term thus far. Recently detailed criteria for the diagnosis of VD have been proposed (Alzheimer's Disease Diagnostic and Treatment Centers [ADDTC], 1992; Diagnostic and Statistical Manual of Mental Disorders, 4th edition [DSM-IV], 1994; International Classification of Diseases, 10th revision [ICD-10], 1992, 1993; and National Institute of Neurological Disorders and Stroke–Association Internationale pour la Recherche et l'Enseignement en Neurosciences [NINDS-AIREN], 1993). Until now the clinical feasibility of these diagnostic guidelines has not been evaluated.
Methods This study aimed to compare these criteria in an unselected sample of 167 elderly patients (mean age, 72.0±9.9 years) admitted with probable dementia.
Results The number of cases that could be classified as VD differed widely between the various diagnostic guidelines. According to DSM-IV criteria, 45 cases were diagnosed as VD. Twenty-one cases fulfilled the ICD-10 research criteria, but only 12 met the NINDS-AIREN criteria for VD. Twenty-three cases were classified as ischemic VD as defined by the ADDTC criteria. The concordance was very poor since only 5 cases met the criteria for VD of all diagnostic guidelines.
Conclusions Our results show that the classification according to different diagnostic guidelines yields rather distinct groups of patients. The reasons responsible for these findings are as follows: (1) different criteria for dementia, (2) limitation to ischemic VD in the ADDTC criteria, (3) no further differentiation of VD into subtypes according to CT or MRI findings (DSM-IV), and (4) the multifactorial etiopathology of VD. Major diagnostic difficulties ensue from the very frequent cases with white matter lesions, since their etiology and classification remain widely unknown.
Key Words: cerebrovascular disorders • dementia • diagnosis
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Introduction |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Although cerebrovascular diseases, after Alzheimer's disease, are the most common cause of dementia,1 VD has remained a vague term. Only a few attempts have been made to define VD clinically.2 3 The main problems in the definition of VD arise from determining criteria for both the terms "vascular" and "dementia." Recently, detailed criteria for the diagnosis of VD have been proposed by several groups or institutions.4 5 6 7 8 However, the criteria are developed for different purposes. Those published by a workshop of the neuroepidemiology branch of the NINDS and AIREN6 mainly aim to define VD for research studies, while those criteria proposed by the state of California ADDTC,5 and particularly the diagnostic guidelines given in DSM-IV4 and ICD-10,7 are for clinical use. Moreover, the World Health Organization published more precise criteria in the DCR-108 (for details, see Reference 9). The objective of this study was to compare the clinical feasibility of these new criteria for VD in an unselected sample of elderly patients admitted for evaluation of probable dementia.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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The sample consisted of 167 consecutive patients referred to the psychiatric or neurological department of the University School of Medicine in Lübeck for the evaluation of possible dementia. All 114 women (mean age, 72.3±9.2 years) and 53 men (mean age, 71.4±11.2 years) were white and had at least 8 years of education. All but 22 subjects were retired or housewives. Eighteen subjects lived in a residential home. Each patient underwent an extended medical, neurological, psychopathologic, and functional examination. The clinical data were abstracted on a standardized form. The calculations were made by specific algorithms according to the various diagnostic guidelines.4 5 6 8
According to the NINDS-AIREN6 and ICD-108
criteria, hemiparesis, lower facial weakness, unilateral weakness of
the limbs, Babinski's sign, sensory deficit, hemianopia, and bulbar
palsy were considered focal neurological signs. The CT scans were
evaluated according to the NINDS-AIREN proposals6 by a
radiologist (K.-J.B.) without any information on the clinical findings
(Table 1
). For diagnosis of dementia, the guidelines
given in the DSM-IV,4 DCR-10,8 and by the
NINDS-AIREN6 were applied. An impairment of ADL, an
essential criterion in the DSM-IV4 and
ICD-10,7 8 was assessed by the BFAS.10
The
impairment was considered mild at BFAS scores 
15, moderate at BFAS
scores 10, and severe at BFAS scores 5.
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The ADDTC criteria emphasize functional impairment in the intellectual
components of ADL but do not include operational criteria for
dementia.5 However, the ADDTC criteria5 were
established to ensure compatibility with those for Alzheimer's
disease established by the NINCDS and the ADRDA.11
Therefore, similar to the NINCDS-ADRDA criteria,11 the
IMCT10 (slightly modified for use in Germany; maximum
score, 38) and the MMSE12 were applied to assess the
severity of dementia in this study. An IMCT score <30, an MMSE score
<24, and/or a BFAS score 15 were considered to establish a diagnosis
of dementia.
Mental status was assessed by SIDAM (structured interview for the diagnosis of dementia of the Alzheimer type, multi-infarct dementia, and dementias of other etiology according to ICD-10 and DSM-III-R).13 This interview also includes a short testing of the following domains: orientation, attention, short-term memory, long-term memory, abstract thinking, judgment, higher cortical functions (eg, constructional and visuospatial abilities, calculation), aphasia, and apraxia. The maximum score of each cognitive function was set at 100%. An unequal distribution of cognitive deficits as required in the ICD-107 was assumed if in one individual distinct functions differed more than 25%.14 An impairment was considered if the score was lower than 70%.14 The course of the illness underlying dementia (eg, gradual deterioration of cognitive impairment, acute onset) as well as a history of stroke or transient ischemic attack was obtained from a semistandardized interview of the patients and if possible also from a caregiver (spouse, children). Stroke was defined as sudden onset of focal neurological symptoms.
Statistical Analysis
All statistical calculations were
performed by the
SPSS program for personal computer, version 3.1. A stepwise
discriminant analysis (according to the method of Mahalanobis)
was used to determine which factors maximally differentiate between the
groups classified by the applied diagnostic guidelines.
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Results |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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The diagnosis of VD was based on two criteria: (1) evidence of dementia and (2) evidence of a cerebrovascular process severe enough to cause dementia.
Diagnosis of Dementia
Although the number of cases diagnosed
as demented by the various
guidelines was very similar (85 or 86) (Tables 2 through
5), the
evaluation yielded rather distinct groups, probably as a result of the
different criteria for dementia. In total, 109 of the 167 investigated
cases (65.3%) met at least one of the definitions for
dementia, but only 58 (53.2%) of these cases complied with all the
criteria for dementia. To determine factors that
differentiated between the groups, we performed a discriminant
analysis including the following variables: age,
duration of education and illness, impairment of ADL (BFAS
score10 ), and intellectual impairment (MMSE12
or IMCT10 ). The calculations only revealed factors that
significantly discriminate between the ICD-10 and the
NINDS-AIREN groups. In order of entry, the significant
variables were duration of illness and intellectual impairment.
However, a correct classification could be achieved in only 59%.
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Diagnosis of Cerebrovascular Process
In the diagnostic
guidelines,4 5 6 8 rather
different criteria for a cerebrovascular process are proposed (Tables 2
through 5
). In
most guidelines evidence of vascular lesions is judged
to be an essential criterion of VD. CT scans showed vascular lesions in
59 (54.1%) of the 109 subjects classified as demented (Table
1).
Forty-four (74.6%) of them had bilateral vascular lesions, and
pure white matter lesions were present in 42.2%. Cortical areas
were involved in 12.8% and the thalamus and the basal ganglia in
4.6%. Small-vessel disease manifest as white matter lesions
(leukoaraiosis and lacunar infarcts) was the most frequent type of
lesion seen on CT (48.6%). Large-vessel infarcts were the second
most common vascular lesion (11.9%); they were most often located in
the supply area of the arteria cerebri media. The CT of 6 subjects
(5.5%) revealed a combination of large- and small-vessel
lesions.
Classification According to Different Diagnostic
Guidelines
Sixty-five subjects fulfilled all DSM-IV
criteria4 for VD (Table 2). However, in only 45
subjects
(52.3% of all patients classified as demented by DSM-IV criteria A and
B) did CT scan reveal a cerebral vascular lesion. The general ICD-10
research criteria8 for VD were met by 28 subjects (32.9%
of those classified as demented by the ICD-10) (Table 3), but 7
of
these subjects showed no vascular lesion on CT. The ADDTC
criteria5 (Table 4) were restricted to the
diagnosis of
ischemic VD. Nevertheless, 23 patients (27.1% of those
classified as demented) fulfilled the criteria for ischemic VD.
Although the NINDS-AIREN criteria6 for the diagnosis of
probable VD encompass all types, only 12 cases (14.1%) were classified
as VD (Table 5). Thus, the various criteria for VD showed quite
different selectivity. In sum, the applied criteria for VD resulted in
rather different groups of subjects categorized as VD (Table
6), ie, 22 subjects met the VD criteria of only one
diagnostic guideline (primarily the DSM-IV). The
concordance (percentage of overlapping cases) between the groups was
poor (<50%) (Table 7). The discriminant
analysis that used the variables number of strokes,
large-vessel infarcts, lacunes, cognitive deficits, and focal
neurological signs as well as the degree of leukoaraiosis (categorized
according to Reference 15) revealed some factors that significantly
differentiated between some groups (Table 7).
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Traditionally, VD or, more precisely, MID is diagnosed by means of
ischemic scales.16 17 18 Clinically 32
cases were
diagnosed as MID and 14 as probable MID, with an ischemic
score16 
7 or 5, respectively, and MMSE score <24. The
ADDTC classification is closest to this clinical diagnosis
(
2=25.3, df=1, P<.001).
The ischemic scores of the cases classified as VD by the
diagnostic guidelines are presented in Table 8. The DSM-IV and
ICD-10 groups scored significantly
lower than the ADDTC and NINDS-AIREN groups (P<.01). To
evaluate the sensitivity of the various diagnostic
guidelines, the cases classified as demented by any of the applied
criteria and showing vascular lesions on CT scan were set at 100%
(n=59). The sensitivity of the different criteria for VD was calculated
as follows: ADDTC, 38.9%; DSM-IV, 76.3%; ICD-10, 35.6%; and
NINDS-AIREN, 20.3%. In total, 51 subjects were diagnosed with VD.
Thus, 86.4% of all demented subjects with vascular lesions met the
criteria for VD of at least one diagnostic guideline.
Nevertheless, only 5 patients (8.5% of all demented subjects showing
vascular lesions on CT) fulfilled the criteria of all guidelines for VD
(Table 6). These subjects are characterized by (1) large-vessel
infarcts involving cortical areas, (2) three or more focal neurological
signs, and (3) stepwise deterioration. Nevertheless, 16 of the 51 VD
subjects (31.4%) also fulfilled either the ICD-10 (14 cases) or DSM-IV
(8 cases) criteria for Alzheimer's dementia, but none met
those of the NINCDS-ADRDA.11 The percentage of cases that
received two diagnoses varied between the groups: ADDTC, 21.7%;
DSM-IV, 31.1%; ICD-10, 23.8%; and NINDS-AIREN, 16.6%.
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Discussion |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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As Hachinski19 pointed out, problems in the definition of VD arise from finding criteria for both the terms "vascular" and "dementia." The ADDTC criteria5 are limited to ischemic brain injury. In the DSM-IV,4 no specification of an underlying vascular process is given. The ICD-106 distinguishes some subtypes of VD14 without respect of etiopathology (acute VD, MID, and subcortical VD), while the NINDS-AIREN criteria6 compile a description of many possible etiopathological causes of VD. Thus, the concepts underlying the definitions of "vascular" are rather heterogeneous.
The diagnosis of dementia is not clearly defined by the ADDTC criteria.6 The definitions of dementia in the DSM-IV,4 ICD-10,8 and NINDS-AIREN criteria6 are rather similar, mainly focusing on an impairment of memory and higher cognitive functions. Whether general criteria for dementia such as that in the ICD-10, mainly elaborated for Alzheimer's disease, can be transferred to VD without modification is controversial.19 However, this investigation reveals rather different groups of cases classified as demented by the applied criteria. Only 58 cases fulfilled all criteria for dementia. The variance in categorization can likely be attributed to the following factors: (1) duration of symptomatology and (2) severity of dementia. For a definite diagnosis of dementia according to ICD-10 criteria, cognitive impairment must be present for more than 6 months, while the other guidelines do not specify any time criterion. Cases fulfilling the criteria of only one or two diagnostic guidelines have high IMCT and MMS scores, indicating a (very) mild degree of dementia. These "borderline" cases are mostly responsible for the poor agreement on dementia diagnosis.
Since the criteria of VD differ, the number of cases classified as VD by the diagnostic guidelines varies widely. As shown in discriminant analysis, the following factors may have an impact on these results:
1. Different definitions of cognitive deficits considered typical
of VD. In the ICD-10, VD is characterized by an unequal
distribution of cognitive deficits (ie, involving some functions while
sparing others), but how to assess this factor is an open question. The
different number of cognitive deficits required for the diagnosis of VD
in the DSM-IV (1) and the NINDS-AIREN (2) criteria yields rather
distinct groups. The high number of cases classified as
ischemic VD is likely attributed to the relatively broad
definition of dementia used for ADDTC in this study (see "Subjects
and Methods").
2. Evidence of two or more strokes. In the ADDTC criteria, evidence of two or more ischemic strokes or a history of multiple transient ischemic attacks is judged essential for ischemic VD, while in the other criteria a history of stroke or transient ischemic attack is not strictly required. Only approximately 25% of the cases showed evidence of two or more strokes.
3. Neurological symptoms. In all diagnostic guidelines, focal neurological signs are considered to be characteristic of VD. Only the NINDS-AIREN criteria also include certain other neurological symptoms that are consistent with the diagnosis of VD. In our sample, the small percentage of cases that could be classified as VD mainly depends on the small number of subjects showing focal neurological signs. Focal neurological signs are frequently lacking in subjects with white matter lesions.
4. Neuroimaging. In contrast to the ADDTC and NINDS-AIREN criteria, which contain evidence of vascular lesions on neuroimaging techniques such as CT or MRI as an essential criterion, the DSM-IV and ICD-10 do not explicitly contain a CT/MRI criterion. However, there are no pathognomonic brain CT or MRI images of VD, because only a portion of the subjects affected with a certain vascular lesion become demented. However, brain imaging often allows etiopathological clues. In addition, the absence of cerebrovascular lesions on CT or MRI provides strong evidence against a vascular etiology of dementia.20 However, the evaluation of CT or MRI scans is hampered by some bias, ie, in lacunar strokes often no lesion responsible for the symptoms can be detected on CT or MRI,21 22 and conversely, lacunae are often asymptomatic.22 Furthermore, the diagnostic value of small high-signal intensities in the white matter on MRI remains doubtful (other possibilities include increased water content in the Virchow-Robin space, gliosis, or microinfarct).
Former clinical and neuropathological studies20 23 24 25 stressed the importance of bilateral vascular lesions for dementia. In this study the majority of VD cases revealed bilateral vascular lesions on CT scan. Otherwise, territory infarcts primarily occur unilaterally. This fact is probably responsible for the small portion of VD cases in this sample caused by thromboembolism. Nevertheless, in stroke survivors VD is often associated with unilateral territory infarcts.26 In this study CT scan frequently showed bilateral subcortical lesions (often leukoaraiosis), and in only a very few cases were cortical areas involved. These findings agree with the results of some other studies.20 23 24 25 27 However, the etiology of leukoaraiosis and its association with dementia are still a matter of controversy.28 29 30 31 32 33 34
The factors yielding a high selectivity can be extracted from data
compiled in Tables 2 through
5. Findings
occurring in less than one
third of the cases include (1) evidence of two or more strokes, (2)
evidence of two or more infarcts on CT scan, (3) a history of multiple
transient ischemic attacks, and (4) focal neurological
symptoms. These factors are very similar to the well-known items of
the ischemic scale16 or its
modifications.17 18 However, the various groups of
cases
scored rather differently on the ischemic scales. The
ischemic scores correlated negatively with the sensitivity of
the applied diagnostic criteria. Criteria developed for
clinical routine, particularly those of the DSM-IV, show a high
sensitivity; however, the specificity is rather low, since CT scan
reveals no vascular lesions in a great portion of cases (30.8%)
classified as VD by DSM-IV. Furthermore, a high percentage of the
DSM-IV cases also fulfilled the criteria for Alzheimer's
dementia (31.1%).
Recent reviews of VD stress the need to distinguish between the various causes of VD,27 35 36 particularly the development of more specific therapeutic strategies. Detailed diagnostic guidelines for various vascular disorders underlying VD are only proposed in the NINDS-AIREN criteria. The ICD-10 criteria for VD subtypes are not based on etiologically defined types of vascular lesions but rather on miscellaneous criteria (ie, onset [acute VD], course [MID], location [MID and subcortical VD], and hypertension [subcortical VD]). Moreover, the ICD-10 criteria for subcortical VD are rather conflicting,14 because on the one hand such cases should show focal neurological symptoms and an unequal distribution of cognitive functions (general criteria for VD), and on the other hand evidence of bilateral subcortical brain damage is required (criteria for subcortical VD).
Although in approximately 20% of demented people autopsy reveals both vascular and degenerative changes, no agreement on neuropathological criteria to discriminate vascular from Alzheimer's dementia could be obtained thus far.37 38 39 40 41 How VD can clinically be diagnosed correctly is also a matter of discussion. All applied diagnostic guidelines provide only rather imprecise criteria for mixed vascular/Alzheimer's dementia, although 31.4% of the 51 VD cases also meet the ICD-108 or DSM-IV4 criteria for Alzheimer's dementia. However, evidence of a vascular disease does not establish the etiology of dementia as purely vascular, but in view of different treatment strategies available for VD, the recognition of an underlying vascular process is urgent, since degenerative dementia still remains untreatable. Moreover, the vascular disease may become the pacemaker of the demential decline. A further problem is the interrater reliability of the diagnostic classification. Until now only data for the NINDS-AIREN criteria, using both clinical information and MRIs, have been available, showing a moderate interrater agreement, probably attributable to patient-, clinician-, or criteria-centered sources of variance.42
Conclusions
Our results show that classification according to
different
diagnostic clinical guidelines yields rather distinct
groups of patients. The reasons responsible for these findings are (1)
the different criteria for dementia; (2) the limitation of some
diagnostic guidelines to special types of VD (eg, ADDTC);
(3) no further differentiation of VD into subtypes according to the CT
or MRI findings, as proposed in a recent study42 ; and (4)
the multifactorial etiopathology of dementia.36 43 As
in
some other studies, our results demonstrate that the major
diagnostic difficulties ensue from the very frequent cases
involving subjects with white matter lesions and a general slowing of
cognitive functions and not from those showing severe focal
neurological symptoms at the beginning of the demential decline. The
etiology of white matter lesions remains widely unknown. By the applied
criteria, only a small portion of the cases with leukoaraiosis could be
classified correctly.
However, the guidelines have been developed for different purposes. The DSM-IV and the ICD-10 provide diagnostic guidelines for daily routine with a high sensitivity but a rather low specificity (approximately 25% to 30% of the cases show no vascular lesion on CT). The NINDS-AIREN criteria proposed for research studies have a high specificity, as required for research studies, but the evaluated sensitivity is low (approximately 20%). The ADDTC criteria for ischemic VD yield results rather similar to those obtained by the traditional manner of diagnosing VD.
Finally, the question arises as to whether it is practicable to define general criteria for all types of VD or whether it would be more promising to establish neuropathologically verified criteria for each VD subtype, such as those for Binswanger's dementia.44 Another approach to VD that allows differentiation into etiologically defined subtypes can be achieved by hierarchically determined criteria. Furthermore, all proposed clinical criteria need a neuropathological verification, which is still lacking for the ADDTC, ICD-10, and NINDS-AIREN criteria.
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Selected Abbreviations and Acronyms |
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Received June 26, 1995; revision received August 11, 1995; accepted October 9, 1995.
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