Incidence and predictors of posttraumatic epilepsy and cognitive impairment in patients with traumatic brain injury: A retrospective cohort study in Malaysia.

OBJECTIVE: Posttraumatic epilepsy (PTE) significantly impacts morbidity and mortality, yet local PTE data remain scarce. In addition, there is a lack of evidence on cognitive comorbidity in individuals with PTE in the literature. We sought to identify potential PTE predictors and evaluate cognitive comorbidity in patients with PTE. METHODS: A 2-year retrospective cohort study was employed, in which adults with a history of admission for traumatic brain injury (TBI) in 2019 and 2020 were contacted. Three hundred one individuals agreed to participate, with a median follow-up time of 30.75 months. The development of epilepsy was ascertained using a validated tool and confirmed by our neurologists during visits. Clinical psychologists assessed the patients' cognitive performance. RESULTS: The 2-year cumulative incidence of PTE was 9.3% (95% confidence interval [CI] 5.9-12.7). The significant predictors of PTE were identified as a previous history of brain injury [hazard ratio [HR] 4.025, p = .021], and intraparenchymal hemorrhage (HR: 2.291, p = .036), after adjusting for other confounders. TBI patients with PTE performed significantly worse on the total ACE-III cognitive test (73.5 vs 87.0, p = .018), CTMT (27.5 vs 33.0, p = .044), and PSI (74.0 vs 86.0, p = .006) than TBI patients without PTE. A significantly higher percentage of individuals in the PTE group had cognitive impairment, compared to the non-PTE group based on ACE-III (53.6% vs 46.4%, p = .001) and PSI (70% vs 31.7%, p = .005) scores at 2 years post-TBI follow-up. SIGNIFICANCE: This study emphasizes the link between TBI and PTE and the chance of developing cognitive impairment in the future. Clinicians can target interventions to prevent PTE by identifying specific predictors, which helps them make care decisions and develop therapies to improve patients' quality of life.

Patient Outcomes following Immediate Tracheostomy and Emergency Decompressive Craniectomy in the Same Setting.

Early tracheostomy is recommended for patients with severe traumatic brain injury or stroke. Tracheostomy in the same setting as emergency decompressive craniectomy, on the other hand, has never been investigated. Our goal was to compare the outcomes related to the duration of mechanical ventilation in patients who had immediate (IT) vs. early (ET) tracheostomy following an emergency decompressive craniectomy in a Neurosurgical centre in Sabah, Malaysia. We reviewed 135 patients who underwent emergency decompressive craniectomy for traumatic brain injury (TBI) and stroke patients between January 2013 and January 2018 in this retrospective cohort study. The cohort included 49 patients who received immediate tracheostomy (IT), while the control group included 86 patients who received a tracheostomy within 7 days of decompressive surgery (ET). The duration of mechanical ventilation, length of stay (LOS) in the critical-care unit, and intravenous sedation were significantly shorter in the IT group compared to the ET group, according to the study. There was no significant difference between the two groups in the incidence of ventilator-associated pneumonia (VAP), tracheostomy-related complications, or 30-day mortality rate. In conclusion, compared to early tracheostomy, immediate tracheostomy in the same setting as emergency decompressive craniectomy is associated with a shorter duration of mechanical ventilation and LOS in critical-care units with acceptable morbidity and mortality rates. This practise could be used in busy centres with limited resources, such as those where mechanical ventilators, critical-care unit beds, or OT wait times are an issue.

Value of Repeat CT Brain in Mild Traumatic Brain Injury Patients with High Risk of Intracerebral Hemorrhage Progression.

Patients with mild traumatic brain injury (MTBI) with intracerebral hemorrhage (ICH), particularly those at higher risk of having ICH progression, are typically prescribed a second head Computer Tomography (CT) scan to monitor the disease development. This study aimed to evaluate the role of a repeat head CT in MTBI patients at a higher risk of ICH progression by comparing the intervention rate between patients with and without ICH progression. METHODS: 192 patients with MTBI and ICH were treated between November 2019 to December 2020 at a single level II trauma center. The Glasgow Coma Scale (GCS) was used to classify MTBI, and initial head CT was performed according to the Canadian CT head rule. Patients with a higher risk of ICH progression, including the elderly (≥65 years old), patients on antiplatelets or anticoagulants, or patients with an initial head CT that revealed EDH, contusional bleeding, or SDH > 5 mm, and multiple ICH underwent a repeat head CT within 12 to 24 h later. Data regarding types of intervention, length of stay in the hospital, and outcome were collected. The risk of further neurological deterioration and readmission rates were compared between these two groups. All patients were followed up in the clinic after one month or contacted via phone if they did not return. RESULTS: 189 patients underwent scheduled repeated head CT, 18% had radiological intracranial bleed progression, and 82% had no changes. There were no statistically significant differences in terms of intervention rate, risk of neurological deterioration in the future, or readmission between them. CONCLUSION: Repeat head CT in mild TBI patients with no neurological deterioration is not recommended, even in patients with a higher risk of ICH progression.

Somatic mitochondrial DNA mutations in different grades of glioma.

Aim: Mitochondrial DNA (mtDNA) alterations play an important role in the multistep processes of cancer development. Gliomas are among the most diagnosed brain cancer. The relationship between mtDNA alterations and different grades of gliomas are still elusive. This study aimed to elucidate the profile of somatic mtDNA mutations in different grades of gliomas and correlate it with clinical phenotype. Materials & methods: Forty histopathologically confirmed glioma tissue samples and their matched blood were collected and subjected for mtDNA sequencing. Results & conclusion: About 75% of the gliomas harbored at least one somatic mutation in the mtDNA gene, and 45% of these mutations were pathogenic. Mutations were scattered across the mtDNA genome, and the commonest nonsynonymous mutations were located at complex I and IV of the mitochondrial respiratory chain. These findings may have implication for future research to determine the mitochondrial energetics and its downstream metabolomics on gliomas.

Now You See, Now You Don't: A Case Of Spontaneous Regression of Pituitary Tumour.

Spontaneous regression of pituitary tumours are rare and can be due to tumour ischaemia, pituitary apoplexy, or lymphocytic hypophysitis. We report a case of a 32-year-old female, who presented with symptoms and signs of extrasellar pituitary enlargement and hypothyroidism. MRI revealed a pituitary mass that spontaneously regressed after a month, with complete resolution of symptoms. Not all pituitary tumours require surgical intervention especially in the case of autoimmune lymphocytic hypophysitis.

Safety and Use of MLC601/MLC901 (NeuroAiDTM) in Primary Intracerebral Hemorrhage: A Cohort Study from the NeuroAiD Safe Treatment Registry.

BACKGROUND: MLC601/MLC901 (NeuroAiD™) is a combination of natural products shown to be safe and to aid neurological recovery after brain injuries, especially ischemic stroke. Few studies have investigated NeuroAiD in primary intracerebral hemorrhage (ICH). The NeuroAiD Safe Treatment (NeST) Registry explores NeuroAiD use in the real-world setting. This cohort study aimed to assess its use and safety in ICH. METHODS: The online NeST Registry of subjects with ICH given NeuroAiD prospectively collected clinical data at baseline and monthly visits (V) 1 to 3. Outcome measures included compliance, side effects, Glasgow Coma Scale (GCS), National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), and Short Orientation-Memory-Concentration Test (SOMCT). RESULTS: Sixty-six subjects were included. NeuroAiD was well-tolerated with fair compliance over three months. Two non-serious side effects were reported. Mean scores significantly improved on all outcome scales. The proportion of subjects with favorable outcomes significantly improved from baseline to V3: NIHSS 0-4, from 12% to 59% (p < 0.0001); GCS 13-15, from 64% to 88% (p = 0.007); mRS 0-1, from 9% to 37% (p = 0.004); and SOMCT score 0-8, from 44% to 68% (p = 0.029). CONCLUSIONS: NeuroAiD in the real-world setting was safe and showed potential for a sustained positive effect on neurological recovery after ICH.

An Unusual Case of the Successful Treatment of Carbapenem-resistant Ventriculitis with Intravenous Colistin.

Ventriculitis is a well-documented complication of ventriculostomy, which is difficult to treat and is associated with high rates of mortality. There is a growing trend of resistance among many organisms, such as Acinetobacter baumannii, in particular, to most antibiotics with the exception of colistin. It is thought that colistin has poor blood-brain barrier penetration; therefore, in cases of ventriculitis, it is preferentially administered via the intrathecal or intraventricular route. These routes, in turn, risk introducing infections, which may perpetuate the problem. We report a case of multidrug-resistant Acinetobacter baumannii ventriculitis, which was treated successfully with intravenous colistin monotherapy.

Mitochondrial DNA Mutations in Grade II and III Glioma Cell Lines Are Associated with Significant Mitochondrial Dysfunction and Higher Oxidative Stress.

The role of mitochondria in tumorigenesis has regained much attention as it could dysregulate cellular energetics, oxidative stress and apoptosis. However, the role of mitochondria in different grade gliomasis still unknown. This study aimed to identify mitochondrial DNA (mtDNA) sequence variations that could possibly affect the mitochondrial functions and also the oxidative stress status. Three different grades of human glioma cell lines and a normal human astrocyte cell line were cultured in-vitro and tested for oxidative stress biomarkers. Relative oxidative stress level, mitochondria activity, and mitochondrial mass were determined by live cell imaging with confocal laser scanning microscope using CM-H2DCFDA, MitoTracker Green, and MitoTracker Orange stains. The entire mitochondrial genome was sequenced using the AffymetrixGeneChip Human Mitochondrial Resequencing Array 2.0. The mitochondrial sequence variations were subjected to phylogenetic haplogroup assessment and pathogenicity of the mutations were predicted using pMUT and PolyPhen2. The Grade II astrocytoma cells showed increased oxidative stress wherea high level of 8-OHdG and oxidative stress indicator were observed. Simultaneously, Grade II and III glioma cells showed relatively poor mitochondria functions and increased number of mutations in the coding region of the mtDNA which could be due to high levels of oxidative stress in these cells. These non-synonymous mtDNA sequence variations were predicted to be pathogenic and could possibly lead to protein dysfunction, leading to oxidative phosphorylation (OXPHOS) impairment, mitochondria dysfunction and could create a vicious cycle of oxidative stress. The Grade IV cells had no missense mutation but preserved intact mitochondria and excellent antioxidant defense mechanisms thus ensuring better survival. In conclusion, Grade II and III glioma cells demonstrated coding region mtDNA mutations, leading to mitochondrial dysfunction and higher oxidative stress.