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. 2019 Oct 31;142(12):3672–3693. doi: 10.1093/brain/awz286

Table 1.

Neuropathology described as ‘characteristic’ of CTE in the literature

Gross pathological features
Cavum septum pelluciduma
Lateral or third ventricle enlargementa
Frontal atrophy
Temporal atrophy
Diencephalon atrophy
Basal ganglia atrophy
Brainstem atrophy
Cerebellar atrophy
Thinning of the hypothalamic floor
Shrinkage of the mammillary bodiesa
Pallor of the substantia nigra
Hippocampal sclerosis
Reduced brain weight
Microscopic neuropathology
Amyloid-β deposition (variable)
Multifocal axonal varicosities
        Frontal and temporal cortex
        Subcortical white matter
        Deep white matter tracts
Diffuse axonal loss
        Subcortical white matter
        White matter tracts
Neuronal loss
        Hippocampus
        Entorhinal cortex
        Amygdala
        Locus coeruleus
        Substantia nigra
        Medial thalamus
TDP-43
        Frontal cortex
        Medial temporal cortexa
        Hippocampusa
        Amygdalaa
        Insular cortices
        Basal ganglia
        Thalamus
        Hypothalamus
        Brainstem
Hyperphosphorylated tau
        Perivascular in the neocortex
        Depths of sulcib
        Superficial layers of cerebral cortexa

Supportive criteriaa and pathognomonic criterionb for CTE based on the preliminary consensus criteria (McKee et al., 2016). Prior to 2015, diverse and widespread non-specific neuropathology was described as ‘characteristic’ of CTE in some articles. Most of the neuropathology described in past articles is also present in association with ageing and in other neurological, neuropsychiatric, and neurodegenerative disorders—and is not unique to CTE. As of 2015, a small number of these are now considered preliminary asupportive criteria for the neuropathology of CTE, and a single finding, bp-tau in depths of sulci (neuronal and astrocytic), particularly in a perivascular distribution, is considered the sole necessary and sufficient pathognomonic criterion of CTE (McKee et al., 2016).