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Mild cognitive impairment Mild cognitive impairment of the vascular type |
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(modified by Petersen et al. Arch Neurol.1999;56:303-308) |
| 1. Memory disturbance referred at least by one of following: - by patient - by family members - by personal physicians |
| 2. Presence of all of this characteristics: - normal activities of daily living - normal general cognitive functions (within 0.5 standard deviations of age- and education-matched control subjects) - abnormal memory for age (1.5 standard deviations below age- and education-matched control subjects) - absence of dementia |
| 3. Diagnosis is made by consensus committee involving neurologist, geriatrician, neuropsychologist, nurse and other study personnel who had evaluated the patient usig the following diagnostic tool: - clinical assessment Clinical history (with both patient and families) Objective neurological examination Short Test of Mental Status Geriatric Depression Scale di Yesavage Hachinski Ischemic Score Record of Indipendent Living |
| - neuropsychological assessment Wechsler Adult Intelligence Scale-Revised Wechsler Memory Scale-Revised Auditory Verbal Learning Test Wide-Range Achievement Test-III |
| - laboratory assessment: haemachrome sedimentation rate vitamin B12 and folic acid thyroid function syphilis serologic testing |
| - instrumental assessment Brain computer tomography or magnetic resonance If clinically indicated: lumbar puncture, EEG, SPECT |
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Mild cognitive impairment Mild cognitive impairment of the vascular type |
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I. The criteria for the clinical diagnosis of mild cognitive impairment of the vascular type include all of the following: A. COGNITIVE SYNDROME including both A1. DYSEXECUTIVE SYNDROME: Impairment in goal formulation, initiation, planning, organizing, sequencing, executing, set-shifting and -maintenace, abstracting A2. MEMORY DEFICIT (may be mild): Impaired recall, relative intact recognition, less severe forgetting, benefit from cues. A3. ROGRESSION: deterioration of A1 and A2 from a previous higher level of functioning, that are not per se interfering with complex (executive) occupational and social activities. B. CEREBROVASCULAR DISEASE including both B1 and B2 B1. EVIDENCE OF RELEVANT CEREBROVASCULAR DISEASE BY BRAIN IMAGING B2. PRESENCE OR A HISTORY OF NEUROLOGIC SIGNS as evidence for cerebrovascular disease such as hemiparesis, lower facial weakness, Babinski sign, sensory deficit, dysarthria, gait disorder, extrapyramidal signs consistent with subcortical brain lesion (s). II. Clinical features supporting the diagnosis of mild cognitive impairment of the vascular type include the following: a. Episodes of mild upper motor neuron involvement such as drift, reflex asymmetry, incordination. b. Early presence of a gait disturbance (small-step gait or marche a petits-pa magnetic, apraxic-ataxic or Parkinsonian gait). c. History of unsteadiness and frequent, unprovoked falls. d. Early urinary frequency, urgency, and other urinary symptoms not explained by urologic disease. e. Dysarthria, dysphagia, extrapyramidal signs (hypokinesia, rigidity). d. Behavioral and psychological symptoms such as depression, personality change, emotional incontinence, psychomotor retardation. III. Features that make the diagnosis of mild cognitive impairment of the vascular type uncertain or unlikely include: a. Early onset of memory deficit and progressive worsening of memory and other cognitive functions such as language (transcortical sensory aphasia), motor skills (apraxia), and perception (agnosia), in the absence of corresponding focal lesions on brain imaging. b. Absence of relevant cerebrovascular disease lesions on brain CT or MRI |
| BRAIN MAGING CRITERIA FOR MILD COGNITIVE IMPAIRMENT OF THE VASCULAR TYPE COMPUTED TOMOGRAPHY extensive periventricular and deep white matter lesions: patchy areas of low attenuation (intermediate density between that of normal white matter and that of intraventricular cerebro-spinal fluid) or diffuse symmetrical areas of low attenuation with ill defined margins extending to the centrum semiovale plus at least one lacunar infarct AND absence of cortical and/or cortico-subcortical non-lacunar territorial infarcts and watershed infarcts, haemorrhages indicating large vessel disease, signs of normal pressure hydrocephalus, and specific causes of white matter lesions (e.g. multiple sclerosis, sarcoidosis, brain irradiation). MAGNETIC RESONANCE CRITERIA FOR MILD COGNITIVE IMPAIRMENT OF THE VASCULAR TYPE HAVE NOT YET BEEN DEVELOPED. |
| ETIOLOGY AND BRAIN CHANGES OF MILD COGNITIVE IMPAIRMENT OF THE VASCULAR TYPE ETIOLOGY PRIMARY VASCULAR MECHANISMS SMALL VESSEL DISEASE: Obliteration and occlusion, increased resistance, decreased autoregulation, cerebral blood flow fluctuation, endothelia changes, -blood-brain-barrier and -carrier changes, perivascular changes PRIMARY RISK FACTORS AGE, ARTERIAL HYPERTENSION SECONDARY VASCULAR MECHANISMS HEMODYNAMIC CHANGES OF SYSTEMIC VASCULAR, CARDIAC AND CAROTID ORIGIN SECONDARY RISK FACTORS ARTERIAL HYPOTENSION, HYPOXIC-ISCHEMIC EVENTS, BLOOD PRESSURE FLUCTUATIONS, HYPERLIPIDEMIA, LOW EDUCATION BRAIN CHANGES PRIMARY TYPE ISCHEMIC WHITE MATTER LESIONS (WMLs): -Araiosis, état crible, demyelination, axonal loss, changes in oligodendrocytes and glial cells, incomplete infarcs. LACUNAR INFARCTS INCOMPLETE ISCHEMIC INJURY: -Laminar necrosis, focal gliosis, granular atrophy, incomplete white matter infarcts. PRIMARY LOCATION WMLs: Extending periventricular and deep WMLs affecting especially the genu or anterior limb of the internal capsule, anterior corona radiata and anterior centrum semiovale. LACUNES: Lacunes in the caudate, globus pallidus, thalamus, internal capsule, corona radiata, frontal white matter. CLINICAL SYNDROME COGNITIVE SYNDROME DYSEXECUTIVE SYNDROME: Impairment in goal formulation, initiation, planning, organizing, sequencing, executing, set-sifting and -maintenance, abstracting. MEMORY DEFICIT (may be mild): Impaired recall, relative intact recognition, less severe forgetting, benefit from cues. WHICH INDICATE DETERIORATION FROM A PREVIOUS HIGHER LEVEL OF FUNCTIONING THAT IS NOT PER SE INTERFERING WITH COMPLEX (EXECUTIVE) OCCUPATIONAL AND SOCIAL ACTIVITIES BEHAVIORAL AND PSYCHOLOGICAL SYMPTOMS DEPRESSION, PERSONALITY CHANGE, EMOTIONAL INCONTINENCE, PSYCHOMOTOR RETARDATION |