mTBI

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Blood biomarkers in mTBI

Several studies have demonstrated that elevated levels of S100B, GFAP, UCH-L1, and NFL correlate with the presence and severity of mTBI. S100B, a marker of astrocytic damage, has been shown to have high sensitivity but moderate specificity for mTBI. GFAP, another astrocytic marker, exhibits higher specificity and is particularly useful in differentiating mTBI from other conditions. UCH-L1, a marker of neuronal cell body injury, and NFL, indicative of axonal damage, both show promise in reflecting the extent of neuronal injury and predicting recovery outcomes. Additionally, combinations of these biomarkers may enhance diagnostic accuracy and provide more comprehensive insights into the injury mechanisms and prognosis.
The use of blood biomarkers in mTBI offers several advantages, including non-invasiveness, rapid turnaround time, and the potential for point-of-care testing. However, challenges such as variability in biomarker levels due to individual differences, the influence of extracranial injuries, and the need for standardized protocols must be addressed. Further research is required to validate these biomarkers in larger, diverse populations and to establish clear clinical guidelines for their use.

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Foreign Accent Syndrome

Foreign Accent Syndrome (FAS) is an uncommon speech disorder where individuals develop a new, seemingly foreign accent in their native language. This review explores FAS within the contexts of functional neurological disorders (FND) and mild traumatic brain injuries (mTBIs).

In FNDs, FAS is often classified as a functional speech disorder, where no definitive structural brain lesions or neurological causes are identified. Cases suggest a psychogenic or functional origin, possibly triggered by psychological stress. Studies highlight that FAS in FNDs features inconsistencies and intermittency in speech patterns, which can occur even in the presence of structural brain damage.

In mTBIs, FAS can emerge without significant structural lesions visible on imaging. Reports indicate that even minor head injuries might lead to FAS, with functional or metabolic brain changes undetected by standard imaging techniques. For instance, abnormal functions in specific brain regions, such as the left dorsolateral inferior frontal gyrus and caudate nucleus, have been implicated.

Overall, the occurrence of FAS in both FNDs and post-mTBI contexts underscores the complexity of this speech disorder and the need for integrated diagnostic and therapeutic approaches. The studies reviewed suggest that functional and metabolic assessments, alongside behavioural interventions, are crucial for understanding and managing FAS effectively.

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Epidemiology of Post-Traumatic Epilepsy after Mild Traumatic Brain Injury

In exploring the epidemiological facets of mild traumatic brain injury (mTBI) and its subsequent risk of post-traumatic epilepsy (PTE), it becomes evident that while mTBI poses a lower risk for PTE compared to moderate or severe traumatic brain injuries, specific factors notably heighten this risk. These include the presence of intracranial hemorrhage, the occurrence of early post-traumatic seizures (EPTS) within the first week following the injury, and a history of alcohol misuse. The manifestations of seizures post-mTBI exhibit a broad spectrum, ranging from cases that progress to PTE to those with no lasting sequelae, underscoring the variability and complexity of post-traumatic seizure pathophysiology.

Annually, over 2% of the population in England and Wales seek emergency care for head injuries, with a significant proportion of these cases involving children. Approximately 20% of these incidents include a skull fracture or evidence of TBI, necessitating hospital admission for about 15% of the affected individuals. The nature of seizures following TBI can vary widely, from immediate concussive episodes to early seizures within the first week, and late epileptic seizures occurring more than a week after the injury. Notably, concussive seizures, which are distinct from tonic-clonic seizures and believed to include elements of primitive reflexes, typically do not lead to later epilepsy.

Studies reveal a nuanced picture of early seizures following head injuries, with findings from Oxford showing a 4.5% incidence rate often associated with skull fractures or intracranial hemorrhage. Further research, such as the study by Lee and Lui, indicates that even among initially classified mild head injury cases, significant hemorrhage uncovered upon subsequent imaging suggests more severe injuries. Additionally, investigations into subclinical seizures, detectable through EEG monitoring, have highlighted the significance of continuous EEG monitoring in patients with moderate to severe TBI, where seizures are suspected.

With TBI being a contributory factor in approximately 5% of new epilepsy cases and 20% of existing cases, the risk of developing epilepsy post-TBI is particularly pronounced in young adults and the elderly, especially following penetrating brain injuries. This risk assessment underscores the importance of a comprehensive understanding of TBI severity, its implications for the development of PTE, and the need for tailored monitoring and management strategies to mitigate the long-term consequences of TBI.

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Post-traumatic headache: Treatment Overview

In the management of post-traumatic headaches (PTH), a multifaceted approach is essential due to the complex nature of the condition and the variability in patient response to treatment. Pharmacological treatments, such as NSAIDs and paracetamol, offer initial relief for mild to moderate headaches, while antiepileptic drugs and tricyclic antidepressants have been shown to provide significant improvements over time. Notably, the effectiveness of prophylactic medications like topiramate and triptan-class medications underscores the tailored approach needed in treating chronic PTH, especially when considering the etiology of the headache, whether related to blast injuries or not.

Beyond pharmacology, non-invasive interventions such as repetitive transcranial magnetic stimulation (rTMS) have emerged as promising options for addressing both PTH and associated depressive symptoms, highlighting the interconnectedness of post-concussion symptomatology. Similarly, the application of neutralizing prismatic lenses for patients with vertical heterophoria (VH) has demonstrated significant reductions in headache, dizziness, and anxiety, offering a novel avenue for symptom management.

For cases resistant to conventional therapies, surgical interventions like peripheral nerve surgery present a viable option, with substantial evidence supporting its efficacy in reducing headache pain and improving patient outcomes. Furthermore, the use of botulinum toxin has been reported to effectively alleviate chronic tension-type PTHs, providing relief when other treatments have failed.

This diverse treatment landscape emphasizes the importance of a personalized and comprehensive approach in the management of PTH, incorporating both traditional pharmacological treatments and innovative therapeutic modalities to address the unique needs of each patient.

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