The prevalence of poststroke dementia (PSD) varies largely according to the composition of cohorts, setting, and delay after stroke. The cognitive syndrome of vascular dementia (VaD) is characterized by: memory deficit, dysexecutive syndrome, slowed information processing, and mood and personality changes. Cortical VaD relates to large vessel disease, cardiac emboli, and hypoperfusion. It prominently shows cortical and corticosubcortical arterial territorial and distal field infarcts. The occurrence of dementia depends on two factors: the total volume of brain loss because of infarcts and hemorrhages, and the location of these lesions. Many instances of dementia occurring in stroke patients are probably the consequence of the cumulative effect of the cerebrovascular lesions, Alzheimer pathology, and white matter changes. Patients with dementia after stroke are significantly less often treated with aspirin or warfarin than nondemented patients. Trials of secondary prevention of stroke usually exclude patients with obvious dementia.

Open head injuries (OHI) may be classified according to the dynamics of trauma into perforating and penetrating: perforating injuries occur when an object enters and exits the skull, while penetrating injuries occur when the object does not exit the cranial vault. Two types of mechanism for brain damages are described in OHIs: primary and secondary. The diagnosis of post-traumatic epilepsy requires at least two seizures after head injury. Post-traumatic seizures are usually partial at onset even if secondary generalization may be rapid enough to simulate generalized seizures from onset. About 25% of seizures are focal, 50% focal with secondary generalization, while 25% are generalized. The number of damaged brain lobes may be a predictive factor to evaluate the volume of brain loss. Antiepileptic drugs (AEDs) should be administered to all patients with OHI, in both early and late post-injury phases, especially if a significant loss of brain tissue has occurred.