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Diagnosis and Treatment of Subcortical Ischemic …

4 The Canadian Review of Alzheimer s Disease and Other DementiasVascular DementiaApoplectic dementia was theterm utilized in the past whenpatients presented with suddencerebral bleeding, softening ortumors that resulted in an abruptchange in cognition, which couldbe progressive and incurable. Inthe early 1900s, it was widelyaccepted that atherosclerosiscaused gradual stenosis of thebrain vessels, causing paren chy-mal lesions that lead to , the differentiation bet -ween other dementias and VADwere not clear, and the associationbetween clinical strokes and cogni-tive changes were not firmly estab-lished. Har dening of the arterieswas a term applied to a number ofdifferent dementia syndromes, in -cluding at times, and erroneously,Alzheimer s disease (AD).

6 † The Canadian Review of Alzheimer’s Disease and Other Dementias Vascular Dementia palsy, and gait disturbances. The neurobehavioral symptoms inclu -

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1 4 The Canadian Review of Alzheimer s Disease and Other DementiasVascular DementiaApoplectic dementia was theterm utilized in the past whenpatients presented with suddencerebral bleeding, softening ortumors that resulted in an abruptchange in cognition, which couldbe progressive and incurable. Inthe early 1900s, it was widelyaccepted that atherosclerosiscaused gradual stenosis of thebrain vessels, causing paren chy-mal lesions that lead to , the differentiation bet -ween other dementias and VADwere not clear, and the associationbetween clinical strokes and cogni-tive changes were not firmly estab-lished. Har dening of the arterieswas a term applied to a number ofdifferent dementia syndromes, in -cluding at times, and erroneously,Alzheimer s disease (AD).

2 Vascular DementiaModern concepts of VAD began toevolve in the 1970s when studiesfrom Newcastle revealed that sub-jects with dementia and little, if any,AD pathology demonstrated a rela-tionship between lost tissue volumefrom infarctions and the degree ofglobal cognitive decline. Hachin -ski1subsequently introduced theterm multi-infarct dementia (MID)in 1974, which includes a history ofclinical strokes with focal neurolog-ic signs and symptoms, and step-wise cognitive medical community hasperhaps over-focused on thismodel of VAD, neglecting the size-able contribution from small-ves-sel disease to the overall cere-brovascular path ologic , this article pertains to thesmall-vessel variant of ischemicvascular disease: SIVD.

3 Subcortical Ischemic VascularDementia The greatest challenge in diagnos-ing SIVD lies in establishing acausal relationship between themagnetic resonance imaging (MRI)changes and the cognitive deficit(s)from the viewpoint of a primary-carephysician. One can argue thatcausality is irrelevant, but if apatient has SIVD, management ofthe vascular risk factors should beoptimized, regardless of their exactrole in causing the dementia syn-drome. What is clear is that the eti-ology of SIVD involves hyperten-sion and diabetes mellitus (DM),particularly if poorly and Treatment ofSubcortical Ischemic VascularDementiaThe small-vessel variant of Ischemic vascular disease appears to have been neglected in thevascular dementia (VAD) model and the overall cerebrovascular pathologic Ischemic vascular dementia (SIVD) is quite difficult to identify and diagnosedue to the difficulty of establishing a causal relationship between the changes and cognitivedeficits seen by a primary-care physician, as well as identified through various brain-mapping Peter N.

4 McCracken, MD, FRCPCP eter N. McCracken, MD, FRCPCP rofessor Emeritus of Medicine, Division of Geriatric Medicine,University of Alberta Edmonton, AlbertaThe Canadian Review of Alzheimer s Disease and Other Dementias 5 Although there are minor differ-ences in wording, most dementia def-initions share the following elements: 1) acquired intellectual decline despite a clear sensorium;2) effects on multiple cognitivedomains which usually includememory; and3) sufficient severity to interfere withcustomary everyday the past five years,emphasis has been placed on iden-tifying early stages of vascular cog-nitive impairment in order toadminister treatments earlier in thedisease.

5 Three historic syndromesfall under the current rubric ofSIVD:31) lacunar state, first described byMarie4and Perraud;52) thalamic or strategic infarctiondementia; and 3) Subcortical arteriosclerotic ence -phalopathy, or Binswanger syndromes are associatedwith frontal-type behavioral symp-toms. A unifying hypothesis basedon disruption of cortical and subcor-tical circuits has been such circuits are relevant tonon-motor behavior: 1) a dorsomedial prefrontal circuitrelated to executive function; 2) a medial prefrontal circuit relat-ed to initiation and drive; and3) an orbital prefrontal circuit relat-ed to social behavior.

6 An alternate hypothesis is thatdeep white-matter lesions disruptthe white-matter tracts necessaryfor cognition and emotion. Theseinclude association and commissur-al, striatal and Subcortical fibresthat interconnect with distributedneural circuits. Widespread lesionsof the white matter have majoreffects on initiation and frontalexecutive function because of pref-erential disruption of long associa-tion fibres. However, it should beremembered that such changes attimes remain clinically silent, grad-ually exhausting the clinical reserveof affected SIVD features includesudden hemiparesis, dementia, dy -sarthria, pseudobulbar palsy, andchanges in affect including inap-propriate laughing or crying,small-stepped gait, and urinaryincontinence.

7 Aphasia and hemi-anopsia are usually absent. The dis-tribution of lacunes in the subcorti-cal gray matter and diffuse softeningof the white matter, particularly ofthe frontal lobes, have been ral symptoms include lackof volition and akinetic mutism,which were thought to be character-istic of prefrontal lobe infarct dementia ( ,thalamic dementia) typically invo -lves distribution of the paramedianthalamic artery. This usually inclu -des the dorsomedial nuclei, closelyconnected with the prefrontal associated with suchstrategic syndromes are featured bymarked apathy, impaired attentionand mental control, with anterogradeand retrograde amnesia, as well asstriking executive s syndrome was firstdescribed by Otto eight cases of slowly pro-gressive mental deterioration andpronounced white-matter changeswith secondary dilatation of theventricles.

8 Alzheimer subsequentlyreported the microscopic features,including severe gliosis of the whitematter and hyalination, intimalfibrosis, and onion-skinning of thelong medullary arteries. Chronichypoperfusion of the periventricularand deep white-matter zones is pos-tulated as the mechanism of clinical features of Bins -wanger s include an insidiouslyprogressive dementia, persistenthypertension or systemic vasculardisease, lengthy clinical coursewith long plateaus, and the accu-mulation of focal neurologic signsincluding asymmetric weakness,pyramidal signs, pseudobulbarSubcortical Ischemic Vascular Dementia The greatest challenge in diagnosing SIVD lies inestablishing a causal relationship between the magneticresonance imaging (MRI) changes and the cognitivedeficit(s) from the viewpoint of a primary-care physician.

9 Clinical SIVD features include sudden hemiparesis,dementia, dysarthria, pseudobulbar palsy, and changes inaffect including inappropriate laughing or crying, small-stepped gait, and urinary The Canadian Review of Alzheimer s Disease and Other DementiasVascular Dementiapalsy, and gait disturbances. Theneurobehavioral symptoms inclu -de apathy, lack of drive, depres-sion, and alterations of mood. Ofcourse, the periods of slowly pro-gressive deterioration can mimicAD. Sensitivity for detecting vas-cular brain injury widened signifi-cantly with the advent of modernimaging: computed tomography(CT) in the 1970s, and MRI in the1980s and 1990s.

10 The previousthreshold occurred at the level ofsymptomatic stroke. More recent-ly, neuroimaging has revealed evi-dence of silent brain injury with-out a history of a correspondingclinical event. However, we should be clearthat evidence-based standards thataddress sensitivity and specificityof clinical criteria against a refer-ence standard are limited. In con-trast to AD, there is no gold stan-dard agreed upon for the diagnosisof VAD. Several findings in theclinical history and examinationincrease the likelihood of SIVD(Table 1).3 The versatility andpower of MRI do offer excitingclinical and research MRI at three or moretesla offer unprecedented anatomicresolution; functional MRI andperfusion MRI give excellent tem-poral resolution; and diffusion ten-sor imaging provides informationabout architectural AD, cerebrovascular diseaseis the second most common type ofdementia.


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