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Moderate to severe traumatic brain injuries commonly present with a wide range of long term emotional and behavioural problems which are often classed as organic neuropsychiatric conditions. These range from mood disorders such as depression, emotional lability, apathy, anxiety disorders such as panic disorder, specific phobia or Post-traumatic stress disorder (PTSD) or long term personality change. These neuropsychiatric co-morbidities influence quality of life and outcomes and cause significant distress to the patient. Hence, accurate and early recognition and appropriate management of these problems is important. Development of post-traumatic epilepsy can further influence neuropsychiatric presentations following moderate to severe brain injury. A range of neuropsychiatric presentations following moderate to severe traumatic brain injury are described and an approach to management is discussed.
The incidence of traumatic brain injury (TBI) in children is estimated to be high, being an important cause of mortality and morbidity. Post traumatic seizures (PTS), post-traumatic epilepsy (PTE), and neuropsychiatric sequelae after TBI contribute to the medical health burden in children. PTE has been recognized as one of the most common forms of acquired epilepsies in young people, and it is associated with poor functional and psychosocial outcome. In this chapter, clinical presentation, diagnosis and management of PTE, and the role of antiepileptic drugs in children are discussed. In addition, the poorly understood pathophysiology of PTE is discussed with reference to genetic and neurophysiologic biomarkers and potential risk factors that increase the risk of developing PTE.
Traumatic brain injury (TBI) is a major risk factor for the development of epilepsy, accounting for around 5% of all epilepsy cases. The risk is greatest within the first year of injury but persists for many years afterwards. Severity of injury is the biggest predictor of future risk of epilepsy, with evidence of intracerebral and sub-dural haemorrhage being important clinical indicators. Individual characteristics including medical co-morbidities and genetic predisposition also influence this risk.
TBI-related seizures are separated into those arising within the first week of injury (early post-traumatic seizures) and those happening later (late post-traumatic seizures). This distinction is useful because early post-traumatic seizures do not appear to be an independent risk factor for the future development of epilepsy. However, the risk of further seizures after a single late post-traumatic seizure is as high as 80%. Therefore, one late post-traumatic seizure signals an increased predisposition to generate future epileptic seizures. This fulfils the criteria for diagnosing epilepsy and the individual should be counselled and treated accordingly.
In this chapter, we discuss the classification of epilepsy and TBI severity before summarising the largest epidemiological studies that have attempted to ascertain the incidence and prevalence of post-traumatic epilepsy and the major risk factors.
Individuals with TBI are vulnerable to a range of cognitive impairments that can interact with psychological comorbidities to lead to chronic challenges with social and occupational functioning in the community. Epilepsy is similarly associated with cognitive difficulties that can be further undermined by the medical, psychological, and psychosocial sequelae of the illness. Although there are limited empirical studies specifically examining cognition in PTE to date, emerging evidence suggests that the development of seizures after TBI may result in a “double hit” to cognitive functioning. This chapter outlines the cognitive sequelae of TBI and epilepsy, and presents a model of cognitive impairment in PTE. It reviews the scant literature on the cognitive consequences of PTE, highlighting current gaps in the literature. Finally, it describes an approach to cognitive rehabilitation in PTE, based on the well-established principles in TBI adapted to accommodate the unique challenges of PTE.
The use of antiepileptic drugs (AEDs) is effective in reducing the risk of developing early (acute symptomatic) post-traumatic seizures compared to placebo or usual care in patients with severe TBI (low-quality evidence). With regards to the choice of the AED, the available evidence supports the use of phenytoin, starting with an intravenous loading dose initiated as soon as possible after severe TBI]. Despite the lack of evidence from comparative clinical trials, levetiracetam is increasingly used in primary prevention of early post-traumatic seizures due to its ease of use, favorable safety profile and lack of pharmacokinetic interactions. So far, there is no evidence to support the use of other neuroprotective agents for the primary prevention of early post-traumatic seizures. Patients with early post-traumatic seizures do not generally require long-term AED treatment since their risk to develop post-traumatic epilepsy is low. High-quality and adequately powered trials conducted in a selected population at high risk of developing late post-traumatic seizures are required to draw definite conclusions on the effectiveness of long-term prophylactic treatment. Further studies to explore the antiepileptogenic and neuroprotective effects of anti-inflammatory and immune-modulatory therapies are also warranted.
The frequency of epilepsy in certain conditions is well known, for example, de novo epilepsy after operative treatment of intracranial abscess is around 70% but this would probably occur independent of the surgical technique used. It seems that craniotomy probably increases the liability of de novo epilepsy by 5-10%. The complexity of the procedure also increases the incidence. Studies of post-traumatic epilepsy with modern imaging techniques have shown the relationship between cortical damage, in particular cortical contusions and post-traumatic epilepsy. The literature on cerebral tumors suggests that late postoperative seizures are more likely to be partial seizures and may be more difficult to control. Antiepileptic drugs (AEDs) are known to be metabolized along established pathways that they may share with other AEDs and also with non-anticonvulsant drugs. Other treatments such as further surgery and adjuvant therapy for intracranial tumors may be useful in treating difficult de novo seizures.
Open head injuries (OHI) may be classified according to the dynamics of trauma into perforating and penetrating: perforating injuries occur when an object enters and exits the skull, while penetrating injuries occur when the object does not exit the cranial vault. Two types of mechanism for brain damages are described in OHIs: primary and secondary. The diagnosis of post-traumatic epilepsy requires at least two seizures after head injury. Post-traumatic seizures are usually partial at onset even if secondary generalization may be rapid enough to simulate generalized seizures from onset. About 25% of seizures are focal, 50% focal with secondary generalization, while 25% are generalized. The number of damaged brain lobes may be a predictive factor to evaluate the volume of brain loss. Antiepileptic drugs (AEDs) should be administered to all patients with OHI, in both early and late post-injury phases, especially if a significant loss of brain tissue has occurred.
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