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title, docid, authors, breadcrumbs, category, cmeTopicId, documentVersionId, imageCount, lastUpdated, pageDescription, pageKeywords, pageTitle, enhancedTitle, type, references, breadcrumbs
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| Multiinfarct Dementia | 3823c4d4-5e98-46da-a717-892fef54b382 |
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Nuclear Medicine | 29e9ca9b-f22e-44aa-94a4-19393851339d | 2906e1eb-a93a-4cdb-8e7f-261c406e626c | 24 | 07/21/25 | Multiinfarct Dementia | Nuclear Medicine, Central Nervous System, Neurodegeneration, Multiinfarct Dementia | Multiinfarct Dementia | STATdx | Multiinfarct Dementia | DX | true |
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title: "Multiinfarct Dementia" docid: "3823c4d4-5e98-46da-a717-892fef54b382" authors:
- key: "9d40c5b1-57d2-442c-9daf-8d8d9d53e24b" value: "Akiva Mintz, MD, PhD, MHA, CFA"
- key: "bbc899b6-2885-44bb-a5b0-24eec7314d33" value: "Bryan J. Neth, BS"
- key: "1f262abe-db83-4f18-99af-00bd3045cd4d" value: "Marc Benayoun, MD, PhD" breadcrumbs:
- name: "Nuclear Medicine" slug: "nuclear-medicine" treeNodeId: "2406533f-6523-4211-841e-b92d6f8cf34e"
- name: "Central Nervous System" slug: "central-nervous-system" treeNodeId: "bd6b5c36-69df-4f18-af9c-96cc24b52d8f"
- name: "Neurodegeneration" slug: "neurodegeneration" treeNodeId: "f2b87cc7-926d-4915-8ec5-ca61a82e8bc9"
- name: "Multiinfarct Dementia" slug: "multiinfarct-dementia" treeNodeId: null category: "Nuclear Medicine" cmeTopicId: "29e9ca9b-f22e-44aa-94a4-19393851339d" documentVersionId: "2906e1eb-a93a-4cdb-8e7f-261c406e626c" imageCount: 24 lastUpdated: "07/21/25" pageDescription: "Multiinfarct Dementia" pageKeywords: "Nuclear Medicine, Central Nervous System, Neurodegeneration, Multiinfarct Dementia" pageTitle: "Multiinfarct Dementia | STATdx" enhancedTitle: "Multiinfarct Dementia" type: "DX" references: true breadcrumbs:
- "Nuclear Medicine"
- "Central Nervous System"
- "Neurodegeneration"
- "Multiinfarct Dementia"
KEY FACTS
-
Terminology
- Impairments in cognition and behavior affecting functional status due to pathologic changes resulting from various vascular insults throughout brain
-
Imaging
- F-18 FDG PET may be used in differential diagnosis between vascular dementia and Alzheimer disease
- Glucose hypometabolism in multifocal (scattered) pattern of cortical with subcortical regions is indicative of vascular dementia - Multifocal or unifocal hypometabolism involving cortical gray matter, subcortical white matter, and other structures - Generally involves cerebral hemispheres, thalamus, basal ganglia, hippocampi
- Amyloid PET imaging does not demonstrate gray matter amyloid deposition in vascular dementia
- SPECT with Tc-99m HMPAO or Tc-99m ECD shows similar asymmetrically decreased perfusion
-
Pathology
- Vascular-related lesions leading to loss of brain function
- Chronic small vessel insults > large vessel infarcts
-
Clinical Issues
- Significant heterogeneity in clinical presentation depending on location, type, and size of vascular lesion
- Overt disease: Cognitive impairment due to clinically evident vascular event (i.e., stroke)
- Covert disease: Insidious process of vascular insults (clinically silent strokes)
- 2nd most common cause of dementia after Alzheimer disease
TERMINOLOGY
-
Definitions
- Impairments in cognition and behavior affecting functional status due to pathologic changes resulting from various vascular insults throughout brain
- 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
IMAGING
-
General Features
-
Best diagnostic clue
- Multifocal or unifocal infarcts involving cortical gray matter, subcortical white matter, and other structures - Especially when correlates with other clinical findings - Generally involve cerebral hemispheres, thalamus, basal ganglia, hippocampi - Generally significant white matter involvement - Bilateral > unilateral - Size: Decreased due to atrophy - Morphology: Multiple small &/or large vessel with lacunar infarcts
-
-
Nuclear Medicine Findings
- F-18 FDG PET/CT - Glucose hypometabolism in multifocal (scattered) pattern of cortical with subcortical regions - Altered pattern depending on subtype (i.e., multifocal small vessel infarcts vs. large territory infarcts) - Hypometabolism often in clinically affected areas: Correlates with other clinical findings - May be used in differential diagnosis between VaD and Alzheimer disease (AD) - AD pattern: Hypometabolism in bilateral parietotemporal with posterior cingulate cortices: Extension to frontal/occipital - VaD may have hypometabolism in subcortical areas, which are spared in AD
- Amyloid PET without gray matter amyloid deposition - May be used in differential diagnosis between VaD and AD
- SPECT with Tc-99m HMPAO or Tc-99m ECD shows similar asymmetric decreased perfusion
-
Imaging Recommendations
-
Best imaging tool
- F-18 FDG PET may aid in differential diagnosis - MR to see vascular insults and look for potential reversible causes of dementia -
Protocol advice
- F-18 FDG PET - Patient preparation - Patient should fast, stop IV fluids containing dextrose, stop parenteral feeding for 4-6 hours - Blood sugar should be < 150-200 mg/dL - Patient should be placed in quiet, dimly lit room prior to and after injection for 30 min - Radiopharmaceutical: 5-15 mCi F-18 FDG - Dosimetry: Urinary bladder receives largest dose - Image acquisition: 30-60 min after injection
-
DIFFERENTIAL DIAGNOSIS
-
- Early F-18 FDG hypometabolism in parietotemporal and posterior cingulate cortices - Later changes include frontal lobe
- Positive amyloid PET
- Atrophy of medial temporal lobe structures on MR/CT
-
Dementia With Lewy Bodies
- Commonly presents with hallucinations, sleep disturbances, and parkinsonian motor features
- F-18 FDG PET hypometabolism in occipital cortex or striatal loss of dopamine transport
-
- Dilated ventricles on CT or MR
- Metabolic or perfusion reductions in lateral cortex (frontal and parietal), separation of caudate heads
- Reduced activity in periventricular WM and ventricular regions > expected for age
-
Mixed Dementia
- Characteristic features of > 1 type of dementia
- Commonly includes AD and another pathology (such as VaD)
-
Frontotemporal Dementia
- Commonly presents with personality and behavioral changes
- Atroph of frontal and anterior temporal lobes
- F-18 FDG PET hypometabolism primarily in frontal and anterior temporal lobes
-
- Major reduction in basal ganglia metabolism and perfusion (worse in caudate)
- Cortical reductions (late)
-
Posttraumatic Dementia
- Pattern of abnormality on functional imaging variable: Depends on severity, directional forces at injury
- Chronic subdural may cause significant asymmetry
- Deceleration injury may cause anterior frontal and temporal tip reductions
- Atrophic pattern may occur; worse with increasing severity of injury
- Focal reduction correlates with encephalomalacia and other cortical abnormalities on CT or MR
- Basal ganglia, thalamic abnormalities may be present
-
Drug-Related Dementia
- Cocaine and amphetamine abuse: Random small focal defects throughout brain - Swiss cheese pattern on FDG PET and SPECT
- Alcohol abuse: May demonstrate frontal lobe decrease
-
Autoimmune Dementia
- Vasculitis pattern in systemic lupus; frontal watershed abnormalities
- Small cortical defects mainly frontal lobe
-
- Rapidly fatal, prion-related disease with impairments in cognition and behavioral changes
- Diffusion-weighted imaging hyperintensity in striatum, cingulum, and neocortex
-
Causes of Reversible Dementia
- Normal-pressure hydrocephalus, vitamin B12 deficiency, hypothyroidism, depression, mass lesions, infections (neurosyphilis, HIV), trauma (chronic subdurals)
PATHOLOGY
-
General Features
- Vascular-related lesions leading to loss of brain function
- Chronic small vessel insults > large vessel infarcts
- Areas of infarction (focal or multifocal) with associated atrophy
-
Risk Factors
- History of myocardial infarction/coronary artery disease, stroke/transient ischemic attack (TIA)
- Atherosclerosis, hypertension, hyperlipidemia, atrial fibrillation
- Diabetes, obesity, smoking, advanced age
CLINICAL ISSUES
-
Presentation
- Significant heterogeneity in clinical presentation depending on location, type, and size of vascular lesion
- Impairment in at least 1 cognitive domain leading to decline in functional status - Executive function and attention more commonly initially affected than in AD - Slow motor/information processing - Language difficulties - Changes in behavior and personality - Depression and anxiety
- Other: Seizures, bladder incontinence, gait disturbance, and additional focal abnormalities
- Overt disease: Cognitive impairment due to clinically evident vascular event [large territory infarct(s)] - > 60% of stroke patients (dementia in ~ 30% of cases)
- Covert disease: Insidious process of vascular insults (clinically silent with extensive lacunar infarcts)
-
Demographics
- 2nd most common cause of dementia after AD - > 10% of dementia cases
- Age: Incidence increases with age
- Sex: M > F
DIAGNOSTIC CHECKLIST
-
Image Interpretation Pearls
- Heterogeneous F-18 FDG activity without any specific pattern suggests VaD
- Lesions can include basal ganglia and other areas typically spared in other diseases
- MR correlation helpful
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References
Selected References
- Minoshima S et al: FDG PET imaging evaluation of neurodegenerative dementias. In Cross DJ et al: Molecular Imaging of Neurodegenerative Disorders. Springer. 57-72, 2023
- Chang Wong E et al: Vascular cognitive impairment and dementia. Continuum (Minneap Minn). 28(3):750-80, 2022
- Minoshima S et al: (18)F-FDG PET imaging in neurodegenerative dementing disorders: insights into subtype classification, emerging disease categories, and mixed dementia with copathologies. J Nucl Med. 63(Suppl 1):2S-12S, 2022
- Nestor PJ et al: Clinical utility of FDG-PET for the differential diagnosis among the main forms of dementia. Eur J Nucl Med Mol Imaging. 45(9):1509-25, 2018
- Sawyer DM et al: Top-down systematic approach to interpretation of FDG-PET for dementia. Clin Nucl Med. 43(6):e212-4, 2018
- Heiss WD et al: PET imaging in the differential diagnosis of vascular dementia. J Neurol Sci. 322(1-2):268-73, 2012
- Román G et al: Contribution of neuroimaging to the diagnosis of Alzheimer's disease and vascular dementia. Arch Med Res. 43(8):671-6, 2012
Images
Selected Images
Axial graphic shows multifocal infarcts involving the cortical gray matter and subcortical white matter bilaterally.
Axial graphic shows multifocal infarcts involving the cortical gray matter and subcortical white matter bilaterally.
Axial graphic shows multifocal infarcts involving the cortical gray matter and subcortical white matter bilaterally.
Coronal FLAIR MR of a 72-year-old woman demonstrates FLAIR signal abnormality in the periventricular and subcortical white matter (leukoaraiosis). This finding is consistent with a small vessel ischemic etiology.
Surface mapping of an FDG PET scan performed in a 96-year-old man demonstrates multiple areas of significant cortical abnormality in glucose metabolism, including the left frontal lobe
, the right occipital lobe
and the cingulate gyrus
, consistent with multiinfarct dementia.
Axial F-18 FDG PET in a patient presenting with dementia shows more unilateral areas of hypometabolism
and globally decreased F-18 FDG uptake, also consistent with vascular dementia (VaD).
Additional Images
Alzheimer dementia is shown. Note the parietal and posterior temporal reductions
and sparing of occipital and frontal lobes.
Frontotemporal dementia (FTD) is shown. Note the frontal and anterior temporal reductions
and sparing of parietal, posterior temporal, and occipital regions.
Axial FDG PET in a patient with Lewy body disease shows parietal and posterior temporal reduction similar to Alzheimer disease (AD)
, but occipital cortex
is also involved.
Surface-rendered Tc-99m ECD SPECT in the same patient demonstrates severe reductions of parietal, temporal
, and occipital cortex
.
Axial FDG PET in a case of autopsy-proven Creutzfeldt-Jakob disease (CJD) shows multiple cortical defects
.
Surface-rendered Tc-99m ECD SPECT shows a pattern similar to AD
; however, clinical course was that of a rapid progressive dementia ending in death within 12 months of onset.
Axial Tc-99m ECD SPECT in a patient with clinical progressive supranuclear palsy (PSP) presentation shows severe frontal lobe decrease
and mild reduction in caudate heads
.
Surface-rendered Tc-99m ECD SPECT demonstrates severe frontal decrease relative to parietal and occipital cortex
.
Axial Tc-99m ECD SPECT (baseline) in a patient with early FTD shows frontal atrophy and mild reduction in perfusion
.
Axial Tc-99m ECD SPECT in the same patient (18 months post baseline) demonstrates significant decrease of frontal lobe activity from baseline study
, consistent with worsening dementia.
Surface-rendered Tc-99m ECD SPECT of the same patient (baseline) demonstrates mild frontal lobe findings
.
Surface-rendered Tc-99m ECD SPECT 18 months post baseline demonstrates worsening
.
Axial FDG PET in a patient with Huntington disease and mild dementia shows severe reduction in basal ganglia
.
Surface-rendered Tc-99m ECD SPECT in the same patient shows mild frontal
and parietal reductions
.
Surface-rendered Tc-99m ECD SPECT in a patient with normal pressure hydrocephalus (NPH) shows severe frontal and parietal defects
with preservation of vertex
.
In-111 DTPA cisternogram (24 hours) in the same patient shows abnormal ventricular activity
.
Axial Tc-99m ECD SPECT in a patient with multiinfarct dementia shows multiple infarcts of the frontal and parietal cortex
.
Surface-rendered Tc-99m ECD SPECT in the same patient shows asymmetric cortical findings
.
Surface-rendered Tc-99m ECD SPECT in a patient with history of cocaine abuse and early dementia shows diffuse cortical findings.
Surface-rendered Tc-99m ECD SPECT in a patient with history of methamphetamine abuse and early dementia is shown.