Post-traumatic seizures (PTS) are a common and debilitating complication of traumatic brain injury (TBI) and could have a harmful impact on the progress of patient rehabilitation. To assess the effect of PTS and relative therapy on outcome in the initial phase after TBI, during the rehabilitation process when neuroplasticity is at its highest, we retrospectively examined the clinical data of 341 adult patients undergoing rehabilitation for at least 6 months post-TBI in our neurorehabilitation unit between 2008 and 2019. We correlated through logistic regression the occurrence of seizures and use of anti-seizure medication (ASM) with neurological and functional outcomes, respectively assessed with the Glasgow Coma Scale (GCS) and the Functional Independence Measure (FIM). PTS were documented in 19.4% of patients: early PTS (EPTS) in 7.0%; late PTS (LPTS) in 9.4%; both types in 3.0%. Patients who developed EPTS had an increased risk of developing LPTS (OR = 3.90, CI 95% 1.58–9.63, p = 0.003). Patients with LPTS had a significantly higher risk of worse neurological (p < 0.0001) and rehabilitation (p < 0.05) outcome. Overall, 38.7% of patients underwent therapy with ASM; prophylactic therapy was prescribed in 24.0% of patients, of whom 14.6% subsequently developed seizures. Mortality was associated with a lower FIM and GCS score on admission but not significantly with PTS. The use of ASM was associated with a worse rehabilitation outcome, independently of the onset of epilepsy during treatment. LPTS appear to exert a negative impact on rehabilitation outcome and their occurrence is not reduced by prophylactic therapy, whereas EPTS do not influence outcome. Our findings caution against the generic use of prophylactic therapy to prevent post-traumatic epilepsy in patients with TBI.
In patients with poststroke dysphagia, treatment with dual tDCS in the early phase of rehabilitation does not significantly increase the probability of recovery compared with sham stimulation.
The incidence of traumatic brain injury (TBI) has increased over the last years with an important impact on public health. Many preclinical and clinical studies identified multiple and heterogeneous TBI-related pathophysiological mechanisms that are responsible for functional, cognitive, and behavioral alterations. Recent evidence has suggested that post-TBI neuroinflammation is responsible for several long-term clinical consequences, including hypopituitarism. This review aims to summarize current evidence on TBI-induced neuroinflammation and its potential role in determining hypothalamic-pituitary dysfunctions.
(1) Background: Sustained axonal degeneration may play a critical role in prolonged disorder of consciousness (DOCs) pathophysiology. We evaluated levels of neurofilament light chain (NFL), an axonal injury marker, in patients with unresponsive wakefulness syndrome (UWS) and in the minimally conscious state (MCS) after traumatic brain injury (TBI) and hypoxic-ischemic brain injury (HIBI). (2) Methods: This prospective multicenter blinded study involved 70 patients with prolonged DOC and 70 sex-/age-matched healthy controls. Serum NFL levels were evaluated at 1–3 and 6 months post-injury and compared with those of controls. NFL levels were compared by DOC severity (UWS vs. MCS) and etiology (TBI vs. HIBI). (3) Results: Patients’ serum NFL levels were significantly higher than those of controls at 1–3 and 6 months post-injury (medians, 1729 and 426 vs. 90 pg/mL; both p < 0.0001). NFL levels were higher in patients with UWS than in those in MCS at 1–3 months post-injury (p = 0.008) and in patients with HIBI than in those with TBI at 6 months post-injury (p = 0.037). (4) Conclusions: Patients with prolonged DOC present sustained axonal degeneration that is affected differently over time by brain injury severity and etiology.
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