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title: "Multiinfarct Dementia"
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docid: "3823c4d4-5e98-46da-a717-892fef54b382"
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breadcrumbs:
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- "Nuclear Medicine"
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- "Central Nervous System"
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- "Neurodegeneration"
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- "Multiinfarct Dementia"
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---
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# KEY FACTS
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- ## Terminology
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- Impairments in cognition and behavior affecting functional status due to pathologic changes resulting from various vascular insults throughout brain
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- ## Imaging
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- F-18 FDG PET may be used in differential diagnosis between vascular dementia and Alzheimer disease
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- Glucose hypometabolism in multifocal (scattered) pattern of cortical with subcortical regions is indicative of vascular dementia
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- Multifocal or unifocal hypometabolism involving cortical gray matter, subcortical white matter, and other structures
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- Generally involves cerebral hemispheres, thalamus, basal ganglia, hippocampi
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- Amyloid PET imaging does not demonstrate gray matter amyloid deposition in vascular dementia
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- SPECT with Tc-99m HMPAO or Tc-99m ECD shows similar asymmetrically decreased perfusion
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- ## Pathology
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- Vascular-related lesions leading to loss of brain function
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- Chronic small vessel insults > large vessel infarcts
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- ## Clinical Issues
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- Significant heterogeneity in clinical presentation depending on location, type, and size of vascular lesion
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- Overt disease: Cognitive impairment due to clinically evident vascular event (i.e., stroke)
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- Covert disease: Insidious process of vascular insults (clinically silent strokes)
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- 2nd most common cause of dementia after Alzheimer disease
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# TERMINOLOGY
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- ## Definitions
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- Impairments in cognition and behavior affecting functional status due to pathologic changes resulting from various vascular insults throughout brain
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- Vascular cognitive impairment (VCI) is more comprehensive term incorporating vascular dementia (VaD) as well as other vascular-related cognitive impairment, including mild cognitive impairment due to vascular disease
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- Multifocal or unifocal infarcts involving cortical gray matter, subcortical white matter, and other structures
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- Especially when correlates with other clinical findings
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- Generally involve cerebral hemispheres, thalamus, basal ganglia, hippocampi
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- Generally significant white matter involvement
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- Bilateral > unilateral
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- Size: Decreased due to atrophy
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- Morphology: Multiple small &/or large vessel with lacunar infarcts
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- ## Nuclear Medicine Findings
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- F-18 FDG PET/CT
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- Glucose hypometabolism in multifocal (scattered) pattern of cortical with subcortical regions
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- Altered pattern depending on subtype (i.e., multifocal small vessel infarcts vs. large territory infarcts)
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- Hypometabolism often in clinically affected areas: Correlates with other clinical findings
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- May be used in differential diagnosis between VaD and Alzheimer disease (AD)
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- AD pattern: Hypometabolism in bilateral parietotemporal with posterior cingulate cortices: Extension to frontal/occipital
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- VaD may have hypometabolism in subcortical areas, which are spared in AD
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- Amyloid PET without gray matter amyloid deposition
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- May be used in differential diagnosis between VaD and AD
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- SPECT with Tc-99m HMPAO or Tc-99m ECD shows similar asymmetric decreased perfusion
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- ## Imaging Recommendations
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- ### Best imaging tool
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- F-18 FDG PET may aid in differential diagnosis
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- MR to see vascular insults and look for potential reversible causes of dementia
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- ### Protocol advice
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- F-18 FDG PET
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- Patient preparation
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- Patient should fast, stop IV fluids containing dextrose, stop parenteral feeding for 4-6 hours
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- Blood sugar should be < 150-200 mg/dL
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- Patient should be placed in quiet, dimly lit room prior to and after injection for 30 min
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- Radiopharmaceutical: 5-15 mCi F-18 FDG
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- Dosimetry: Urinary bladder receives largest dose
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- Image acquisition: 30-60 min after injection
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# DIFFERENTIAL DIAGNOSIS
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- [Alzheimer Disease](/document/alzheimer-disease/2aad3ac4-44fd-43e5-8e50-a86987483af3)
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- Early F-18 FDG hypometabolism in parietotemporal and posterior cingulate cortices
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- Later changes include frontal lobe
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- Positive amyloid PET
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- Atrophy of medial temporal lobe structures on MR/CT
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- ## Dementia With Lewy Bodies
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- Commonly presents with hallucinations, sleep disturbances, and parkinsonian motor features
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- F-18 FDG PET hypometabolism in occipital cortex or striatal loss of dopamine transport
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- [Normal-Pressure Hydrocephalus](/document/normal-pressure-hydrocephalus/834ccc3e-2116-4295-8408-0ac9a06bd2ff)
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- Dilated ventricles on CT or MR
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- Metabolic or perfusion reductions in lateral cortex (frontal and parietal), separation of caudate heads
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- Reduced activity in periventricular WM and ventricular regions > expected for age
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- ## Mixed Dementia
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- Characteristic features of > 1 type of dementia
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- Commonly includes AD and another pathology (such as VaD)
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- ## Frontotemporal Dementia
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- Commonly presents with personality and behavioral changes
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- Atroph of frontal and anterior temporal lobes
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- F-18 FDG PET hypometabolism primarily in frontal and anterior temporal lobes
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- [Huntington Disease](/document/huntington-disease/4abd9bb7-7d47-4308-a71f-9985fdb23c2c)
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- Major reduction in basal ganglia metabolism and perfusion (worse in caudate)
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- Cortical reductions (late)
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- ## Posttraumatic Dementia
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- Pattern of abnormality on functional imaging variable: Depends on severity, directional forces at injury
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- Chronic subdural may cause significant asymmetry
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- Deceleration injury may cause anterior frontal and temporal tip reductions
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- Atrophic pattern may occur; worse with increasing severity of injury
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- Focal reduction correlates with encephalomalacia and other cortical abnormalities on CT or MR
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- Basal ganglia, thalamic abnormalities may be present
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- ## Drug-Related Dementia
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- Cocaine and amphetamine abuse: Random small focal defects throughout brain
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- Swiss cheese pattern on FDG PET and SPECT
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- Alcohol abuse: May demonstrate frontal lobe decrease
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- ## Autoimmune Dementia
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- Vasculitis pattern in systemic lupus; frontal watershed abnormalities
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- Small cortical defects mainly frontal lobe
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- [Creutzfeldt-Jakob Disease](/document/creutzfeldt-jakob-disease-cjd/e1b27954-6591-4bb0-a659-b13790492620)
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- Rapidly fatal, prion-related disease with impairments in cognition and behavioral changes
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- Diffusion-weighted imaging hyperintensity in striatum, cingulum, and neocortex
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- ## Causes of Reversible Dementia
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- Normal-pressure hydrocephalus, vitamin B12 deficiency, hypothyroidism, depression, mass lesions, infections (neurosyphilis, HIV), trauma (chronic subdurals)
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# PATHOLOGY
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- ## General Features
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- Vascular-related lesions leading to loss of brain function
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- Chronic small vessel insults > large vessel infarcts
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- Areas of infarction (focal or multifocal) with associated atrophy
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- ## Risk Factors
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- History of myocardial infarction/coronary artery disease, stroke/transient ischemic attack (TIA)
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- Atherosclerosis, hypertension, hyperlipidemia, atrial fibrillation
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- Diabetes, obesity, smoking, advanced age
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# CLINICAL ISSUES
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- ## Presentation
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- Significant heterogeneity in clinical presentation depending on location, type, and size of vascular lesion
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- Impairment in at least 1 cognitive domain leading to decline in functional status
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- Executive function and attention more commonly initially affected than in AD
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- Slow motor/information processing
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- Language difficulties
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- Changes in behavior and personality
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- Depression and anxiety
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- Other: Seizures, bladder incontinence, gait disturbance, and additional focal abnormalities
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- Overt disease: Cognitive impairment due to clinically evident vascular event [large territory infarct(s)]
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- > 60% of stroke patients (dementia in ~ 30% of cases)
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- Covert disease: Insidious process of vascular insults (clinically silent with extensive lacunar infarcts)
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- ## Demographics
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- 2nd most common cause of dementia after AD
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- > 10% of dementia cases
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- Age: Incidence increases with age
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- Sex: M > F
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# DIAGNOSTIC CHECKLIST
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- ## Image Interpretation Pearls
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- Heterogeneous F-18 FDG activity without any specific pattern suggests VaD
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- Lesions can include basal ganglia and other areas typically spared in other diseases
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- MR correlation helpful
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