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.

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.

Background. Poststroke dysphagia is associated with considerable morbidity and has high health care cost implications. Objective. To evaluate whether anodal transcranial direct current stimulation (tDCS) over the lesioned hemisphere and cathodal tDCS to the contralateral one during the early stage of rehabilitation can improve poststroke dysphagia. Methods. A total of 40 patients referred to our neurorehabilitation department were randomized to receive anodal tDCS over the damaged hemisphere plus cathodal stimulation over the contralateral one versus sham stimulation during swallowing maneuvers over the course of 10 sessions of treatment. Swallowing function was evaluated before and after stimulation using the Dysphagia Outcome and Severity Scale (DOSS). Results. The percentage of patients who reached various thresholds of improvement was higher in the tDCS group than in the sham group, but the differences were not significant (eg, DOSS score ≥ 20% increase from baseline: 55% in the tDCS group vs 40% in the sham group; P = .53). Among all variables recorded at baseline, only a subgroup of patients without nasogastric tube showed a significantly higher improvement with tDCS treatment versus sham (DOSS score ≥10% and ≥20% from baseline: 64.29% vs 0%, P = .01). Conclusions. 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.

(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.

Background: Some authors have hypothesized that cranioplasty after decompressive craniectomy (DC) could positively influence functional recovery through several mechanisms. However, only a few studies with small sample sizes have investigated the effects of cranioplasty on functional recovery. Our study aims at evaluating the role of post-DC cranioplasty in influencing the functional recovery in a large cohort of patients with different etiologies of acquired brain injury (ABI). Methods: This retrospective study consecutively enrolled 253 patients with ABI, consisting of 108 adults who underwent post-DC cranioplasty and 145 adults who did not. All the subjects underwent a 6-month individual rehabilitation program. Demographic data, etiology, classification and anatomical site of brain injury, neurological and functional assessment at baseline and on discharge, and number of deaths during hospitalization were recorded. Results: In our cohort, 145 patients (57.3%) and 108 patients (42.7%) had, respectively, a hemorrhagic stroke (HS) and a traumatic brain injury (TBI). Only in the patients with TBI cranioplasty emerged as an independent predictor of better functional outcome in terms of the Functional Independence Measure (FIM) total score at discharge (β = 0.217, p = 0.001) and of the FIM variation during rehabilitation (ΔFIM) (β = 0.315, p = 0.001). Conversely, in the case of HS, no associations were found between post-DC cranioplasty and functional recovery. Conclusions: Post-DC cranioplasty was associated with better functional recovery six months after TBI but not in the patients with HS. Although the pathophysiological mechanisms underlying HS are different from those of TBI and possibly play a role in the different outcomes between the two groups, further studies are needed to investigate the mechanisms underlying the observed differences.