Microcomputed tomography examination of the cortical and trabecular structures of the cranial cervical spine in dogs and cats.

Traumatic brain injury (TBI) remains one of the leading causes of acquired neurological disability among adults worldwide. Although improvements in intensive care have increased survival rates, a substantial proportion of patients develop chronic neurological deterioration that challenges long-term recovery. This spectrum encompasses entities ranging from diffuse axonal injury (DAI), a largely irreversible structural lesion, to post-traumatic hydrocephalus (PTH), a potentially reversible disorder. Within this spectrum, it is important to distinguish between chronic traumatic encephalopathy (CTE), a neuropathological diagnosis confirmed exclusively at autopsy by perivascular hyperphosphorylated tau aggregates associated with repetitive head impacts, and traumatic encephalopathy syndrome (TES), its proposed clinical counterpart in living patients, defined by progressive cognitive impairment and/or neurobehavioral dysregulation following repeated head trauma. We use the term chronic post-traumatic encephalopathy (CPTE) as a pragmatic umbrella to describe chronic neurological deterioration after TBI, encompassing both irreversible neurodegeneration (e.g., DAI) and potentially reversible processes such as PTH. This construct is distinct from CTE, a neuropathological diagnosis. The ability to distinguish between these entities is crucial, as it determines whether the patient might benefit from surgical treatment or if the deficit results from irreversible axonal damage. DAI arises from rotational or acceleration–deceleration forces that shear axons within the deep white matter, corpus callosum, and brainstem. This leads to widespread neuronal disconnection and progressive neurodegeneration. Advanced imaging techniques such as diffusion tensor imaging (DTI) have demonstrated persistent reductions in fractional anisotropy (FA) correlating with long-term cognitive and functional deficits. In contrast, PTH develops due to impaired cerebrospinal fluid (CSF) absorption following subarachnoid or intraventricular hemorrhage, leading to progressive ventriculomegaly and decreased intracranial compliance. Unlike DAI, neurological symptoms in PTH can improve significantly once CSF dynamics are restored through shunting. The challenge arises from the frequent coexistence of both processes. Many patients fall within an overlapping zone where the clinical presentation, magnetic gait, apathy, and urinary incontinence, can be attributed to either DAI or communicating hydrocephalus. This diagnostic ambiguity often results in under-recognition of treatable hydrocephalus or, conversely, unnecessary surgical procedures in patients without CSF dynamic disturbance. Because standardized diagnostic criteria are lacking, clinicians increasingly rely on complementary tools. Quantitative neuroimaging can reveal ventriculomegaly disproportionate to cortical atrophy, while intracranial pressure (ICP) monitoring and CSF dynamic tests, such as the tap test or extended lumbar drainage, help determine physiological reversibility. Moreover, emerging neuronal and glial biomarkers, including neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP), offer promise in quantifying axonal injury burden and predicting long-term neurodegeneration after TBI, potentially informing patient selection for rehabilitative and surgical strategies.