SPREAD V Ed.

Post-stroke cognitive impairment
and mood disorders

 
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Collaborations
Authors
Introduction
Methodology
Epidemiology
Diagnostic work-up
Risk factors
Primary prevention
Acute stroke: pre-hospital
Acute stroke: diagnosis
Acute stroke: treatment
Acute stroke: steady-state
Secondary prevention
Surgical treatment
Organising rehabilitation
Rehabilitation
Post-stroke sequels
Juvenile-uncommon causes

Post-stroke cognitive impairment
and mood disorders

R 16.1
Grade C		 The use of benzodiazepines and neuroleptics is not recommended, except in selected cases, for the treatment of post-stroke psychiatric disorders, since they may affect recovery.
S 16-1 The onset of a depressive episode is frequent within 6-12 months of stroke. About 30% of stroke victims are reported to have mood disorders, even if there is a wide variability between studies due to diagnostic and methodological differences.
S 16-2 The presence of a possible post-stroke depression should be carefully investigated since confounding somatic symptoms and variability of diagnostic approaches may lead to an under- or overestimation.
S 16-3 Aphasia, anosognosia, hemineglect and cognitive impairment, may affect the diagnosis of post-stroke depression.
R 16.2
Grade C		 A multidimensional clinical approach (conversation with patients, relatives, non-medical health workers and use of specific tests and scales), in combination with the DSM-IV-TR criteria, is recommended for the diagnosis of post-stroke depression.
S 16-4 The scales commonly used for psychiatric diagnosis of depression appear to be equally reliable in detecting post-stroke depression, even if the use of lower cut-off values is suggested.
R 16.3
Grade C		 The use of psychiatric scales is recommended for quantification and monitoring of post-stroke depression.
S 16-5 At present the Post-Stroke Depression Rating Scale (PSDRS) is the only scale specifically designed to assess post-stroke depression.
R 16.4
Grade D		 The assessment of post-stroke depression is recommended also in aphasic patients by means of the clinical evaluation and non-verbal tests.
R 16.5
*GPP		 Searching for a possible post-stroke depression is recommended in the acute as well as in later phases, to reduce patient's disability, caregiver's burden and costs.
S 16-6 Patients with post-stroke depression exhibit less melancholy but more somatic complaints (fatigue, sleep and concentration disorders, reduced appetite, etc.) than patients with functional depression. Patients with stroke and depression report more somatic symptoms than stroke patients without depression.
S 16-7 The distinction between major and minor depression is not widely accepted when applied to post-stroke depression.
S 16-8 Post-stroke depression has probably a multifactorial aetiopathogenesis. Previous psychiatric and/or cerebrovascular disorders, higher education, severe disability, social or family problems and female gender increase the risk of depression. The probability to develop depression increases exponentially with the number of risk factors.
S 16-9 Based on recent metanalyses, still affected by the extreme heterogeneity of the studies, the risk of post-stroke depression is not associated with brain lesion site. Inclusion or exclusion of aphasic patients in several studies contributed to yield contrasting results.
S 16-10 The onset of depressive symptoms after stroke does not significantly differ from that observed after myocardial infarction.
S 16-11 Post-stroke depression increases the short- and long-term mortality risk after stroke.
S 16-12 Post-stroke depression is a short- and long-term unfavourable predictor of functional recovery.
S 16-13 In patients with post-stroke depression, antidepressant therapy may be beneficial to functional recovery but it cannot abolish the detrimental effect of depression on functional outcome. The patients with post-stroke depression who do not receive antidepressant therapy exhibit a more unfavourable rehabilitative prognosis, in comparison with those who are treated.
S 16-14 Post-stroke depression increases the risk of fall and it is detrimental to quality of life.
S 16-15 Post-stroke depression is still under-treated, despite evidence in favour of effectiveness of antidepressant drugs also in patients with organic diseases.
R 16.6
Grade C		 Early antidepressant therapy for post-stroke depression is recommended to reduce its detrimental effect on rehabilitation.
R 16.7
Grade C		 Selective serotonin re-uptake inhibitors are the recommended pharmacotherapy of post-stroke depression for their favourable tolerability profile.

*GPP

 The pharmacological therapy of post-stroke depression should be continued for at least 4-6 months.
S 16-16 The use of SSRI is not associated to an increased risk of cerebral haemorrhage.
R 16.8
Grade A		 To date, pharmacotherapy or psychotherapy to prevent the onset of post-stroke depression are not recommended.
S 16-17 “Vascular depression” indicates the depressive disorders seen in elderly patients with signs of vascular cerebral damage.
S 16-18 Patients with vascular dementia exhibit depressive symptoms more frequently than patients with Alzheimer’s disease.
S 16-19 Anxious disorders are frequently seen post-stroke, with an average prevalence of 20%~28%.
S 16-20 An anxious disorder may aggravate the course of depression and impair the functional condition.
S 16-21 Cerebrovascular diseases are associated with an increased risk of cognitive impairment.
S 16-22 Vascular dementia is the second cause of chronic cognitive deterioration. Cerebrovascular diseases are responsible for 20%-25% of total dementia cases.
S 16-23 In Italy, prevalent cases of vascular dementia are estimated to be about 150,000.
S 16-24 In Italy, about 40,000 new cases of vascular dementia are estimated to occur every year.
S 16-25 Vascular dementia is an unfavourable prognostic factor, because it is associated with increased mortality compared with both the general population and patients affected by degenerative dementias.
S 16-26 Primary risk factors for vascular dementia are:
1. arterial hypertension;
2. age;
3. atrial fibrillation;
4. diabetes mellitus;
5. myocardial infarction;
6. cigarette smoking and alcohol abuse.
S 16-27 Secondary risk factors for vascular dementia are:
1. low educational level
2. e4 allele of the ApoE gene polymorphism
S 16-28 Neuroimaging predictors of vascular dementia are:
bulletbilateral, multiple infarctions in the dominant hemisphere and in frontal and mesolimbic areas;
bulletperiventricular and deep white matter lesions.
S 16-29 According to current diagnostic criteria, the presence of vascular dementia is characterised by cognitive impairment (memory, executive functions, mental flexibility) associated with clinical and neuroimaging signs or symptoms of cerebrovascular disease, possibly temporally related to the onset of dementia.
R 16.9
Grade C		 Assessment of executive functions is recommended in patients with suspected vascular dementia because memory impairment is not the main feature in this dementia type.
S 16-30 Vascular dementia encompasses the following clinical-pathological subtypes:
1. multiple large complete infarcts;
2. strategic single infarcts;
3. small vessels disease;
4. hypoperfusion;
5. haemorrhage;
6. of genetic origin.
S 16-31 Sub-cortical vascular dementia is defined by the presence of a cognitive syndrome, characterised by executive functions disorder and memory deficit, and by a cerebrovascular disease detected at neuroimaging and characterized by the relevant neurological signs and signs of pre-existent disease (including gait disorders).
S 16-32 CADASIL is a genetic disorder that may evolve into a form of subcortical vascular dementia.
R 16.10
Grade A		 The search for a mutation of the NOTCH 3 gene is recommended for the diagnosis of CADASIL.
S 16-33 Different frequencies of mutation on the various CADASIL exons have been reported in several Italian regions. In Italy, those affecting exons 11, 3, 4, 8, 6 and 19 appear the most frequent.
In all other Countries, the prevailing mutations affect the exons 4, 3 and 11, with different frequency.
R 16.11
Grade A		 The ultrastructural morphologic study of the skin biopsy is recommended in patients with symptoms of CADASIL, (specificity 100%; sensibility less than 50%), when the genetic test cannot be performed.
R 16.12
*GPP		 The NINDS-AIREN criteria are recommended to evaluate the vascular cognitive impairment.
S 16-34 The different sets of criteria for the diagnosis of vascular dementia are not interchangeable. The highest frequency of diagnosis is achieved with the DSM-IV-TR criteria that are the most inclusive; the lowest with the National Institute of Neurological Disorders and Stroke - Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria, which are the most restrictive.
S 16-35 The Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC) criteria together with the Hachinski Ischemic Score (HIS) appear to be the most sensitive criteria for diagnosis of vascular dementia. The National Institute of Neurological Disorders and Stroke - Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria in combination with the Hachinski Ischemic Score (HIS) are the most specific.
S 16-36 According to the Hachinski Ischemic Score the characteristic features of vascular dementia are: fluctuating course, stepwise progression, history of hypertension and stroke, and focal neurological signs.
R 16.13
*GPP		 The Hachinski Ischemic Score is not recommended to be used as exclusive instrument to diagnose vascular dementia.
S 16-37 The term mixed dementia indicates those patients who present an overlapping of criteria for vascular dementia and Alzheimer's disease. According to the NINDS-AIREN criteria, the term mixed dementia should be replaced with that of "Alzheimer's disease with cerebrovascular disease", referring to subjects with a diagnosis of possible Alzheimer's disease associated to clinical and instrumental signs of cerebrovascular disease.
S 16-38 The concept of Vascular Cognitive Impairment (VCI) has been proposed to include subjects who are affected by a cognitive impairment resulting from cerebrovascular disease but do not completely satisfy the criteria for the diagnosis of vascular dementia.
S 16-39 More than 45% of patients with VCI without dementia exhibit after 5 years a definite progression towards evident cognitive impairment. This confirms that the early detection of their condition might facilitate the prevention of dementia.
R 16.14
Grade D		 A standard neuro-psychological screening is recommended in presence of a cerebrovascular accident.
R 16.15
*GPP		 In the acute phase of stroke, the neuro-psychological work-up should be performed with tests that are quick and easy to perform (at the bedside). The tests should be calibrated or controlled and specific.
R 16.16
*GPP		 The administration of at least the Mini Mental State Examination (MMSE) is recommended because it supplies a global index of cognitive performance.
R 16.17
*GPP		 A detailed neuropsychological assessment is recommended if the clinical features indicate the presence of several cognitive deficits. The possibility of extended work-up depends, however, from the patient's co-operation.
R 16.18
*GPP		 Duplex US examination of supra-aortic vessels is recommended to assess the risk factors and the aetiology of vascular dementia.
R 16.19
*GPP		 The Transcranial Doppler is recommended only as a complementary examination.
R 16.20
*GPP		 Use of SPECT or PET, or electrophysiological examinations or cerebrospinal fluid analysis are not recommended for the diagnosis of vascular dementia, unless for scientific researches or for selecting patients in clinical trials.
R 16.21
*GPP		 Serum chemistry assays are recommended in vascular dementia to identify the profile of vascular risk factors.
S 16-40 Neuroimaging techniques may be particularly helpful for the diagnosis of vascular dementia because they allow to:
1. exclude other causes of cognitive impairment (tumours, severe cortical atrophy, hydrocephalus, etc.);
2. detect cerebrovascular lesions;
3. classify vascular dementia subtypes:
4. provide information for inclusion of patients in controlled clinical trials.
S 16-41 There is no evidence that the presence of cortical or subcortical territorial or border zone infarcts, lacunar strategic infarcts or diffuse white matter changes, found in some cases of dementia, can surely be considered responsible for the cognitive deterioration. In fact neurodegenerative processes, possibly undetectable by neuroimaging, could coexist in these cases.
R 16.22
Grade A		 At least cranial CT without contrast or, whenever possible, T1- and T2-weighted and FLAIR MRI are recommended for the diagnosis of vascular dementia. Usually the administration of contrast agents is not necessary.
R 16.23
Grade C		 The lack of cerebrovascular lesions on cranial CT or MRI is significant evidence against the diagnosis of a possible vascular dementia.
S 16-42 Therapeutic interventions for vascular dementia may be differentiated into:
1. primary prevention in subjects with vascular risk factors but no cognitive impairment;
2. secondary prevention in subjects with initial cognitive impairment but not yet demented;
3. secondary prevention and therapy in demented patients;
4. tertiary prevention of complications in patients with severe dementia.
R 16.24
Grade C		 The treatment of hypertension is recommended in all subjects with elevated blood pressure to prevent the occurrence of cognitive impairment. At present there are no comparative data suggesting that a class of antihypertensive drugs is superior to others in preventing dementia.
R 16.25
*GPP		 Oral anticoagulants in patients with large lesions of the white substance should carefully be evaluated in terms of risk-to-benefit ratio. The target INR should anyway be kept in the lower range (1.8-2.5).
S 16-43 Data derived from pharmacological clinical trials suggest that:
1. administration of nimodipine improves cognitive functions and the clinical global impression;
2. administration of acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) is effective in heterogeneous groups of patients affected by vascular dementia either pure or associated with Alzheimer's disease;
3. none of these drugs significantly improves the independence in the activities of daily living.
R 16.26
*GPP		 Carotid endarterectomy or extracranial-intracranial by-pass are not recommended for the treatment of cognitive impairment due to vascular dementia.

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