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Seizures
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Genetics play a role in epilepsy, but it can sometimes be an acquired disorder. That is, if the brain changes in particular ways, someone who has never had a seizure before may begin having seizures. This process where the brain becomes capable of generating seizures is called epileptogenesis (Thijs et al., 2019). One common event that can lead to epileptogenesis is traumatic brain injury (Ding et al., 2016). This is referred to as post-traumatic epilepsy and, curiously, it often has a “silent period” of months or years between the injury and the onset of the seizures—perhaps up to 20 years in extreme cases (Piccenna et al., 2017, p. 123). More work is needed to understand it, but post-traumatic epilepsy seems to be a relatively common type of epilepsy (Semple et al., 2019). Other types of acquired epilepsy may come from tumors, strokes, parasites, and infections (Thijs et al., 2019). Epilepsy is not just a neurological disorder in which people have seizures however, as it is also affiliated with other less visible changes that may put a person at risk for heart disease, hypertension, migraine, and more (Yuen et al., 2018). But putting those complexities aside, let's focus on the major symptom which is not coincidentally the title of this chapter: seizures.
Sudden unexpected death in epilepsy
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
Christopher Milroy, Daniel du Plessis
When attributing epilepsy to a previous head injury, it may be prudent to obtain the opinion of a neurologist/epileptologist aided by a thorough review of the clinical/historical background. Risk factors for the development of post-traumatic epilepsy should also be borne in mind. These include old age, penetrating brain injuries, a Glasgow Coma Score of less than 10, biparietal or multiple contusions, intracranial haemorrhage, frontal or temporal location of lesional pathology, greater than 5 mm midline shift, duration of coma in excess of 24 hours, loss of consciousness for more than 24 hours, prolonged post-traumatic amnesia, multiple intracranial neurosurgical procedures and the occurrence of early post-traumatic seizures (Pitkänen and Tamuna 2012). Some studies have not associated diffuse traumatic axonal injury (as an isolated diagnosis) with an increased risk of post-traumatic epilepsy (Scheid and von Cramon 2010).
Medical Issues, Pharmacology and Nutrient Interaction
Published in Elizabeth Broad, Sports Nutrition for Paralympic Athletes, 2019
Yetsa Tuakli-Wosornu, Nida Naushad, Amos Laar, Christine Townsend, Emerald Lin
Another CNS-related issue in patients with chronic traumatic brain injury is post-traumatic epilepsy. The primary energy source in the brain is glucose, and in the absence of glucose, ketones are used. Low-carbohydrate diets such as the ketogenic or modified Atkins diets have been established as an alternative form of treatment in patients with epilepsy refractory to medications. Paediatric studies and more recently adult studies have shown trends towards decreasing the frequency of seizures in about 50% of patients refractory to medication (Cervenka et al. 2017; Nei et al. 2014). One drawback of these diets is difficulty with compliance in the adult population. Adverse effects must also be considered, as studies have shown increased blood lipid levels; unintentional weight loss; amenorrhea in women and gastrointestinal side effects such as nausea, vomiting, diarrhoea or constipation (Pasca et al. 2016). Furthermore, a ketogenic diet may not be compatible with the fuelling requirements of the athlete. The health and safety of the athlete must always be a sports nutrition practitioner's primary focus; therefore, working with the athlete and neurologist to find a compromise that minimises seizures whilst still supporting training and competition needs is paramount. It is important to note, these studies have only looked at post-traumatic epilepsy and therefore may not be fully applicable to the traumatic brain injury population.
In vivo KPT-350 treatment decreases cortical hyperexcitability following traumatic brain injury
Published in Brain Injury, 2020
David Cantu, Danielle Croker, Sharon Shacham, Sharon Tamir, Chris Dulla
To better understand if the novel small molecule KPT-350 played a protective role against cortical hyperexcitability following TBI, we used fEPSP recordings to measure network-level changes in neuronal connectivity. Electrophysiological markers of cortical network dysfunction such as epileptiform discharges, high-frequency activity of fEPSPs, and uncontrolled responses to scaled stimuli were all decreased by an oral 3-week treatment of KPT-350 (Figure 2, 3). An effective dosing regimen of KPT-350 consisted of starting drug treatment 1 h after brain injury and continuing for 3 weeks. This time window of drug administration supports that KPT-350 can prevent cortical network reorganization during the latent period between an initial injury and onset of the first unprovoked seizure. Preventing cortical network reorganization and hyperexcitability may have the potential to prevent the development of post-traumatic epilepsy.
Craniocerebral nail gun injuries: a definitive review of the literature
Published in Brain Injury, 2021
There was considerable variation in the severity of residual deficits; from persistent vegetative states and hemiplegia at one end of the spectrum, to minor unilateral visual deficits on the other. Some of these deficits are associated with significant compromise to activities of daily living and quality of life. Individuals with global aphasia or paralysis of ≥3 limbs secondary to their penetrating brain injury experienced difficulties returning to work even 15 years post-injury (59). The disabilities most commonly associated with the inability to work include post-traumatic epilepsy, paresis, visual field deficits, memory impairment, psychiatric conditions, and violent behaviors (59).
Protective effect of compound Danshen (Salvia miltiorrhiza) dripping pills alone and in combination with carbamazepine on kainic acid-induced temporal lobe epilepsy and cognitive impairment in rats
Published in Pharmaceutical Biology, 2018
Chen Jia, Shanshan Han, Liming Wei, Xiangji Dang, Qianqian Niu, Mengyu Chen, Boqun Cao, Yuting Liu, Haisheng Jiao
Traditional Chinese medicine (TCM) is primarily used as a complementary and alternative medical approach in the treatment of epilepsy. A combination of TCM and Western medicine may increase the curative effect and decrease the recurrence rate and adverse reactions to Western medicine. These combination therapies may offer a new way to treat TLE. Compound Danshen dripping pills (CDDP), consisting of Salvia miltiorrhiza Bunge (Labiatae) (known as “danshen” in Chinese), Panax notoginseng (Burk.) F.H. Chen (Araliaceae) (known as “sanqi” in Chinese) and borneol are a modern Chinese medicine preparation based on TCM theory and modern preparation technologies. With its multiple targets, components and effects, CDDP is now used extensively in China to prevent and treat diseases including angina pectoris, hyperlipidemia, and coronary heart disease (Chu et al. 2011; Yao et al. 2015). The compound preparation is the first traditional Chinese medicine to complete Phase III clinical trials by the US Food and Drug Administration (FDA). In recent years, some studies have demonstrated several beneficial effects of CDDP. The main component, Salvia miltiorrhiza, was found to exert an anticonvulsant effect in a rat model of penicillin-induced epilepsy (Bahadir et al. 2015). Another main component, Panax notoginseng, has been shown to have neuroprotective effects against cerebral ischemia/reperfusion injury (Zeng et al. 2014). Clinical studies of patients with epilepsy have shown that combined therapy using CDDP and AEDs is an effective treatment for posttraumatic epilepsy (Jiang et al. 2013). Moreover, compound Danshen tablets, which contain the same ingredients as CDDP, greatly improved cognition impairment in rats with Alzheimer’s disease (Qin et al. 2012; Teng et al. 2014). To date, however, no relevant studies have been published on the protective effects of CDDP in a TLE rat model or the mechanism behind the effects.