Management of vascular dementia


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Management of vascular dementia

  1. 1. Management of vascular dementiaVascular dementia (VaD) is the loss of cognitive function resulting frominadequate blood and oxygen flow to the brain or bleeding into the brain due tocerebrovascular and cardiovascular disease. Intervention such as controllingblood pressure may bring reduction in the incidence of VaD and in this article, DrIain McIntosh discusses diagnosis and management.Improvements in x-ray screening and neuro-imaging have brought betterunderstanding of the underlying pathological vascular processes in dementia.Vascular dementia (VaD) has historically been considered to be a number ofdisorders with different underlying mechanisms, all probably sharing a vascularcause. Mixed dementias, however, include VaD and Alzheimers disease (AD),which can complicate diagnosis.VaD may yet prove more common than AD in those aged over 85 years1. Riskfactors are well recognized, with many of them avoidable and their effectsreversible. Intervention may bring reduction in the incidence of VaD and newdrug treatments may slow, or halt the cognitive decline associated with thecondition. General practitioners (GPs) and supporting staff have a crucial role inmanagement through health promotion, case recognition, assessment andtherapy.Vascular dementiaVaD is the loss of cognitive function resulting from inadequate blood and oxygenflow to the brain or bleeding into the brain due to cerebrovascular andcardiovascular disease (CVD). It is associated with decline in cognitive, motorand functional abilities and occurs after: • Single strokes affecting strategic parts of the brain • Multiple strokes • Chronic poor blood and oxygen perfusion through the brain • Rare genetic forms of the condition can also occur.PrevalenceVaD is the second most common cause of dementia in the elderly. Prevalenceincreases with age ranging from 1.2 per cent to 4.2 per cent of people over 65years, with the rate doubling every five years. Control of risk factors with bloodpressure agents and statins in primary and secondary prevention of stroke andcardiovascular disease can reduce its prevalence2.ClassificationClinical classifications of VaD are confusing. Practically, diagnosis requiresclinical or radiological evidence of a primary cause (cerebrovascular disease)with, secondary distinguishable dementia syndrome. Traditional diagnostic
  2. 2. systems subdivide dementia into mutually exclusive categories and may havelimited usefulness in assessing the role of disease processes that affect both.Vascular risk factors may be important in the aetiology not only of dementia ingeneral but also in AD. However VaD is classified, it is a largely preventable formof dementia meriting identification, investigation and treatment. The diagnosticseparation of dementias to permit and institute appropriate therapeutic responseis therefore important.CausationVaD is often caused by: • Partial or complete blocking of a blood vessel leading to the brain • Detached emboli from the heart, blocking small brain blood vessels (infarction) • Cerebral haemorrhage.The result is lack of blood perfusion through the brain and ultimately neuronaldeath in surrounding areas. Dementia will follow sufficient brain damage.Cerebrovascular lesions are usually the only cause of dementia in strategicinfarcts and lacunar states. Computerized tomography (CT) scanning and brainimaging have improved knowledge of pathological processes involved but itremains uncertain how often VaD is the sole cause of dementia in the absence ofunderlying vulnerability or comorbid disease.PathologyIn Multi-Infarct Dementia (MID), infarcts occur in the cerebral cortex, subcorticalareas or both. Size and bilaterality of the lesion, the coexistence of hypertensionand central nervous system pathology, such as AD, determines presentation inthe individual. These ischaemic changes can be detected on CT scan andmagnetic resonance imaging (MRI) in 75 per cent of people with MID based onclinical grounds3.Multiple lacunar infarcts involve small vessels and are associated with whitematter ischaemia and dementia. A single infarct, occurring in a strategicallyimportant part of brain, can result in dementia. Brain white matter ischaemia withinadequate blood and oxygen flow to the brain commonly produces VaD.Binswanger’s disease, one of the causes of MID, involves vascular damage tothe nerve cell fibres of the deep white matter of the brain by demyelination of thesheath. These white matter lesions are associated with high blood pressure,diabetes and heart disease and appear to cause dementia by disconnecting thepathways between the cortical and subcortical brain areas.Risk factors such as hypertension, diabetes, smoking, atrial fibrillation, highcholesterol, increased coagulation and blood viscosity are associated with
  3. 3. increased risk of cognitive decline in both vascular and AD sub-types. The riskfactors for cerebrovascular disease are also risk factors for dementia4.Particularly high rates of dementia occur after stroke with a nine fold increase inrisk over the first year and a two fold raised annual risk persisting for at least 25years post-stroke. High mid-life blood pressure is a strong and independentpredictor of later life cognitive impairment with increased risk of dementia 15–20years later5. Raised blood pressure levels contribute to cognitive impairment insusceptible people, particularly those with concomitant conditions, whichpredispose them to cerebral ischaemia.DiagnosisAlthough AD can be diagnosed with some accuracy, the distinction betweenisolated AD, VaD and mixed dementia (MD) – where both pathologies coexist,remains controversial and a diagnostic challenge6. Nevertheless, accuratediagnosis is important for preventive and therapeutic reasons.MIDMID describes VaD at the clear end of the spectrum with a related history anddistinct cortical infarcts on neuroimaging. There is progressive dementiaassociated with cerebral ischaemic events and evidence of infarction mainlyassociated with the larger arteries. It is caused by mini-strokes and large vesselarteriosclerosis. Patients are likely to have other problems such as heart disease,diabetes and high blood pressure but tend to have better insight into theircondition and personality may remain intact for longer than in AD. Symptoms caninclude: • Mild weakness in arm or leg • Trouble remembering especially for recent events • Difficulty following a conversation and communicating • Depression with emotional swings • Confusion and hallucinations • Epileptic fits • Incontinence.Multiple lacunar dementiaIn multiple lacunar dementia there is often hemiparesis, small stepping gait,difficulty in speech and/or swallowing and impairment of thinking. Usuallypatients also have high blood pressure.Binswanger’s diseaseIn Binswanger’s disease there is arteriosclerosis and high blood pressure but nostrokes, with slowly progressive intellectual impairment and recurrent stroke-likeevents. There is also slowness and lethargy in thinking and actions, difficultywalking and feet wide apart gait, emotional ups and downs in behaviour andearly loss of bladder control. In addition, there is an association with
  4. 4. microvascular disease caused by diabetes, hypertension and periventricularhypoperfusion disorders such as cardiac failure, arrhythmias and systemichypotension. Diagnosis requires evidence of: • Cognitive loss • Vascular brain lesions shown by brain imaging • Exclusion of other causes of dementia such as AD.VaD is excluded if brain imaging shows no evidence of vascular lesions.Clinically, VaD typically presents with sudden onset and a stepwise course ofcognitive decline, history of strokes, transient ischaemic attacks (TIA) or both. Asource of thromboembolism, such as carotid disease, atrial fibrillation or valveheart disease is also common. There could also be focal neurological deficit suchas hemiparesis and sensory loss, associated decline in cognitive, motor andfunctional abilities. In addition to the following: • Patchy cognitive impairment • Subcortical features • Parietal dysfunction • Dysphasia • Visual hallucinations.Confusion and convulsions may also be associated. Patients often displayimpaired basic and instrumental activities of daily living including self careprocesses of feeding, grooming, toileting and difficulties in house keeping,financial and medication management7. Retained insight, relative preservation ofpersonality and short term memory recall with depressive symptoms andemotional lability support the diagnosis. There will be evidence ofcerebrovascular disease on CT.However, mixed AD and VaD can be difficult to diagnose because the vascularelement can follow a progressive course in half of the patients.AssessmentA detailed history is required from patient and carer. A physical exam should alsoseek the following; high blood pressure, diabetes, atrial fibrillation, carotidstenosis and dysarthria as well as psychological assessment checks fordepression. The Hachinsky ischaemic scale8 aids diagnosis, with dementiadiagnosed if the score is seven or higher. It is a useful diagnostic aid, excludingVaD at a low score. However, a high score however fails to differentiate betweenVaD and the coexistence of vascular and degenerative dementia.
  5. 5. InvestigationsInvestigations for VaD include tests for: • Hypothyroidism • Vitamin B12 deficiency • Antiphospholipid antibodies • Normal pressure hydrocephalus • Frontal lobe tumours.Echocardiography and ultrasonography may be also be indicated. CT or MRI ofthe brain should exclude treatable causes and confirm the extent of thecerebrovascular disease. With CT the extent of vascular lesions reflects theseverity of associated neuropsychological effects. MRI is more sensitive indetecting ischaemic areas than CT.PreventionRaised blood pressure and hypercholesterolaemia in mid life are strong riskfactors for dementia with an effect at an early stage in cognitive decline. Theirprevention or modification reduces subsequent risk of dementia. Atherosclerosisis responsible for much cognitive impairment and reduction of its effects is ofbenefit. Treatment of hypertension in over 65 years olds with diastolichypertension can bring a 40 per cent reduction in non fatal strokes and in 60 yearolds with isolated hypertension it can bring a one third reduction and benefitsrelating to cognitive decline and dementia9.A very large study of cognition and prognosis in mild hypertension in the elderlyusing an angiotensin II receptor antagonist showed it reduced the risk of non fatalstroke by 28 per cent and cognitive function was maintained in those ontreatment, with no adverse effects on mental function10. Worries about loweredblood pressure worsening cognitive decline have not been substantiated.Treating moderate hypertension in older people may not benefit cognition but itwill not affect it adversely. Older people with hypertension should be treatedwhether or not they are cognitively impaired11. Reduction in risk occurs quickly,with average time from treatment start to a significant impact on major vascularevents in about two and a half years12. Many patients currently do not receivetreatment or are inadequately treated13.Government guidelines recommend that after heart attack or stroke antiplatelettherapy (aspirin) should be prescribed but this is poorly implemented14.TreatmentEven in the absence of dementia, vascular factors such as hypertension,diabetes and high cholesterol blood concentrations can themselves causecognitive impairment. Controlling vascular risk factors such as diabetes and high
  6. 6. blood pressure and use of antiplatelet drugs can improve cognitive functioning12.If physicians and nurses recognise the importance of the early detection ofvascular disease and treat the risk factors there is an opportunity to prevent orslow cognitive decline and the onset of dementia. Limited evidence suggests thatinterventions to halt or slow progression of generalized vascular disease mayprevent further cognitive decline if not improve cognitive function15. Patients withmulti-infarct dementia show improved cognitive scores and improved cerebralblood flow over the first two years of treatment with aspirin16 and men at risk ofcardiovascular disease seemed to show better cognition on aspirin daily thanthose on placebo after five years17. Treatment with aspirin or with a hypotensiveagent in a patient with dementia may not only prevent stroke but may preventdecline in cognitive function.Cholinesterase inhibitors currently licensed for use in AD are also beingprescribed for VaD. Results of preliminary trials indicate treatment is feasible andpossibly a benefit in slowing cognitive decline18.ConclusionIntervention may bring reduction in the incidence of VaD and new drugtreatments may slow or halt the cognitive decline associated with the condition.There should be early intervention to control even mild high blood pressure inelderly people and good management of all elderly hypertensives should be withdrugs that have minimal side effects. There should also be statin prescriptions forhypercholestrolaemia irrespective of advanced age, aniticoagulation with warfarinfor those with atrial fibrillation and antiplatelet medication with aspirin whereappropriate.Dr Iain B McIntosh is a General Practitioner from St Ninians, Stirling and aFormer Hospital Practitioner at the Geriatrics and Trustee Dementia ServicesDevelopment Centre, Stirling UniversityLinksReturn to ArchiveReferences 1. Breteler M, Claus J. Cardiovascular disease and distribution of cognitive function in elderly people. BMJ 1994: 304; 1604–8 2. Passmore P. Vascular dementia: diagnosis and treatment. Geriatric Medicine 2003; 33: 77–80 3. Roman G. Vascular dementia. Diagnostic criteria for research studies. Neurology 1993; 43: 250–60
  7. 7. 4. Stewart R. Cardiovascular factors in Alzheimers disease. J. Neurology, Neurosurgery Psychiatry 1998; 65: 143–75. Stewart R. Cardiovascular factors in Alzheimers disease. J Neurology, Neurosurgery, Psychiatry 1998; 65: 1436. Skoog I, Lernfelt B, Landstrom A, et al. 15 year longitudinal study of blood pressure and dementia. Lancet 1996; 347: 1141–57. Amer K, Wilcock G. Vascular dementia. BMJ 1996; 312: 277–318. Hachinski VC. Multi infarct dementia, a cause of mental deterioration in the elderly. Lancet 1974; 2: 207–109. SHEP Coop research. Prevention of stroke by hypotensive drug treatment in older persons. JAMA 1991; 254: 3255–6410. Hansson L, Lithell H, Hope I, et al. Study on cognition and prognosis in the elderly (SCOPE). Blood Pressure 1999; 8: 177–8311. Starr JM, Whalley JJ. Hypertension 1992; 10 (2): 531–4212. McIntosh I. Sign guidelines for hypertension in the elderly. Update 2002; 9: 194–7013. Jackson RT, Sackett DL. Guidelines for managing raised blood pressure. BMJ 1999; 313: 64–514. Campbell NC. Secondary prevention in coronary heart disease. BMJ 1998; 316: 1430–3415. Bloom J. Alzheimers disease and vascular dementia. International J of Clin Practice 2003; 57: 219–2316. Meyer JS, Rogers Rl, Knowle A et al. Randomized clinical trial of daily aspirin therapy in multi-infarct -dementia. J Amer Ger Soc 1989; 37: 549–5517. Richards M, Meade T, Peart S, et al. Is there any evidence for protective effect of antithrombotic medication on cognitive function in men at risk from cardiovascular disease. J. Neurology, Neurosurgery and Psychiatry 1997; 62: 269–7218. Yangsheng L. Feasibility of VaD treatment with cholinesterase inhibitors. Intern J Ger Psychiatry 2002; 50(8): 1431–8