Table 1

Neuropathology findings

Neuropathologyn/Total (%)
Hypoxia41/41 (100) focal to global
Infarctsa18/41 (43.9)
Haemorrhage8/41 (19.5)
Lymphocytic infiltrates38/41 (92.6) mild
Microglial activation, focal or diffuse34/41 (80.5)
Microglial nodules/neuronophagia26/41 (63.4)
Acute thrombosis3/41 (7.3)
Athero- arteriolo-sclerosis36/41 (87.8) mild to severe
AD, CAA, PD, PSP, PART pathology18/41 (43.9)
Herpes encephalitis1/41 (2.4)
Neuropathologyn/Total (%)
Hypoxia41/41 (100) focal to global
Infarctsa18/41 (43.9)
Haemorrhage8/41 (19.5)
Lymphocytic infiltrates38/41 (92.6) mild
Microglial activation, focal or diffuse34/41 (80.5)
Microglial nodules/neuronophagia26/41 (63.4)
Acute thrombosis3/41 (7.3)
Athero- arteriolo-sclerosis36/41 (87.8) mild to severe
AD, CAA, PD, PSP, PART pathology18/41 (43.9)
Herpes encephalitis1/41 (2.4)

For the cases with Alzheimer’s and Lewy body pathology, the median and range of Braak neurofibrillary tangle score and the Lewy body disease type was assessed. Using the NIA ‘A, B, C’ Alzheimer’s disease pathology score,32 we observed the following: brains with Alzheimer’s disease pathologies ranged from A0–A5 with a mean of 43/19 = 2.26 and median of 2; B0–B6 with a mean of 64/19 = 3.34 and median of 3; C0 (10), C sparse (2), C moderate (4), C severe (1). Lewy body disease type: brainstem (3), cortical (2). AD = Alzheimer’s disease; CAA = cerebral amyloid angiopathy; PD = Parkinson’s disease; PSP-progressive supranuclear palsy; PART = primary age-related tauopathy.

aInfarcts: six brains with chronic infarcts, 12 with acute or subacute infarcts; seven with microscopic acute or subacute infarcts (not seen grossly); nine with multiple infarcts, one of them with chronic infarcts; locations: isocortex (n = 9), corpus callosum (n = 5), pons (n = 5), midbrain (n = 1), thalamus (n = 2), caudate (n = 1), putamen (n = 1), hippocampus (n = 2, both chronic) and pituitary (n = 2).

Table 1

Neuropathology findings

Neuropathologyn/Total (%)
Hypoxia41/41 (100) focal to global
Infarctsa18/41 (43.9)
Haemorrhage8/41 (19.5)
Lymphocytic infiltrates38/41 (92.6) mild
Microglial activation, focal or diffuse34/41 (80.5)
Microglial nodules/neuronophagia26/41 (63.4)
Acute thrombosis3/41 (7.3)
Athero- arteriolo-sclerosis36/41 (87.8) mild to severe
AD, CAA, PD, PSP, PART pathology18/41 (43.9)
Herpes encephalitis1/41 (2.4)
Neuropathologyn/Total (%)
Hypoxia41/41 (100) focal to global
Infarctsa18/41 (43.9)
Haemorrhage8/41 (19.5)
Lymphocytic infiltrates38/41 (92.6) mild
Microglial activation, focal or diffuse34/41 (80.5)
Microglial nodules/neuronophagia26/41 (63.4)
Acute thrombosis3/41 (7.3)
Athero- arteriolo-sclerosis36/41 (87.8) mild to severe
AD, CAA, PD, PSP, PART pathology18/41 (43.9)
Herpes encephalitis1/41 (2.4)

For the cases with Alzheimer’s and Lewy body pathology, the median and range of Braak neurofibrillary tangle score and the Lewy body disease type was assessed. Using the NIA ‘A, B, C’ Alzheimer’s disease pathology score,32 we observed the following: brains with Alzheimer’s disease pathologies ranged from A0–A5 with a mean of 43/19 = 2.26 and median of 2; B0–B6 with a mean of 64/19 = 3.34 and median of 3; C0 (10), C sparse (2), C moderate (4), C severe (1). Lewy body disease type: brainstem (3), cortical (2). AD = Alzheimer’s disease; CAA = cerebral amyloid angiopathy; PD = Parkinson’s disease; PSP-progressive supranuclear palsy; PART = primary age-related tauopathy.

aInfarcts: six brains with chronic infarcts, 12 with acute or subacute infarcts; seven with microscopic acute or subacute infarcts (not seen grossly); nine with multiple infarcts, one of them with chronic infarcts; locations: isocortex (n = 9), corpus callosum (n = 5), pons (n = 5), midbrain (n = 1), thalamus (n = 2), caudate (n = 1), putamen (n = 1), hippocampus (n = 2, both chronic) and pituitary (n = 2).

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