**4. Paroxysmal disorders in the long-term period of pediatric TBI**

The vulnerability of structures of the immature brain associated with TBI can be also manifested in paroxysmal disorders: post-traumatic headache, post-traumatic epilepsy, subclinical epileptiform activity on the EEG. It is noteworthy, cognitive and behavioral disorders in children and adolescents in the long-term period of TBI significantly increase in the presence of paroxysmal disorders.

**Post-traumatic headache (PTH)**. Headache following traumatic brain injury (TBI) of any severity has been the most common physical symptom described and is a focus of research and clinical attention [39–41].

It is easy to establish the relationship between a headache and TBI when the headache develops immediately or in the first days after trauma has occurred. On the other hand it is very difficult when a headache develops weeks or even months after trauma, especially when the majority of these headaches have the pattern of tension-type headache and the prevalence of this type of headache in the population is very high. Frequently, headache that results from head trauma is accompanied by other symptoms such as dizziness, difficulty in concentration, fatigue, anxiety and insomnia. This constellation of symptoms is known as the post-traumatic or postconcussion syndrome; among them, headache is usually the most prominent [42].

In the International Classification of Headache Disorders (3rd edition) [43], PTH is considered a secondary headache defined by the onset of headache "within 7 days following trauma or injury, or within 7 days after recovering consciousness and/or within 7 days after recovering the ability to sense and report pain" [43]. PTH is further subdivided into "acute headache attributed to traumatic injury to the head" and "persistent headache attributed to traumatic injury to the head." If the headache resolves within 3 months of onset, it is characterized as acute PTH, whereas headaches that occur beyond 3 months are defined as persistent PTH.

The most common headache phenotypes in PTH are tension-type-like headache and migraine-like headache. In our cohort of patients suffered closed TBI of moderate and severe degrees persistent PTH were observed in 268 of 283 patients (95% of cases) recurring from one episode in a week to daily attacks [18, 19]. Headaches usually affected the lifestyle of the children, resulted significantly on their mood, behavior, intellectual and physical endurance, school learning. Headaches causation was established by their onset in temporal relation to TBI and persistence for more than 3 months after head trauma. The most commonly seen pattern, resembling tensiontype headache, occurred in 72.4% of patients. Headache associated with the increase of intracranial pressure due to long-lasting disorders of cerebrospinal fluid circulation was confirmed in 12.3% of cases. Migraine-like headaches were diagnosed in 11.9% and neuralgic pains in the frontal or occipital regions in 3.4%. Thus, our data evidence for the involvement of different causative mechanisms in PTH in children.

PTH pathophysiology remains largely unclear, but several possible mechanisms have been proposed, including impaired descending modulation, neurometabolic changes and activation of the trigeminal sensory system [39]. When indicating severe brain damage due to TBI and persistent PTH, it is necessary to exclude the epileptic origin of paroxysms. The combination of PTH and epilepsy, as well as epileptiform activity on the EEG in patients with PTH was firstly reported in 1963 by D.W. Cooper and D.C. Cavicke based on two cases [44]. Formisano et al. [45] revealed a high incidence of paroxysmal abnormalities on the EEG with the presence of sharp waves in 84.6% of patients with chronic PTH, which was also associated with the presence of fractures or damages to the skull and dura mater, either due to TBI or as a result of craniotomy.

Not only routine EEG, but also video-EEG monitoring with the recordings in different functional states (especially all phases of sleep) should be used in the examination of patients with chronic PTH. Studies on the use of multichannel EEG monitoring in combination with evoked brain potentials to assess the disruptions and delay of activation of neuronal networks in PTH, especially in posttraumatic migraines, is promising [46].

**Post-traumatic epilepsy** is one of the most threatening consequences of TBI. High risk of post-traumatic epilepsy is characteristic for patients with penetrating head injuries—as much as 50% of them develop seizures. Patients with focal neurological deficit and large cerebral lesions immediately after injury have the greatest risk for post-traumatic epilepsy. It is believed that post-traumatic epilepsy is much less common with closed head injuries.

We have determined the incidence of post-traumatic epilepsy in our cohort of children suffered moderate or severe closed TBI. A total of 18 cases of epilepsy were revealed in a total of 283 patients. A total of 16 patients (10 boys and 6 girls) or 5.7% developed secondarily generalized seizures, all in the period from 4 to 12 months post-injury; the severity of head injury was moderate in 12 and severe in 4 of them. In 2 of 18 patients head injury precipitated idiopathic generalized epilepsies: childhood absence epilepsy in a boy of 7 years of age and idiopathic epilepsy with grand mal seizures on awakening in a boy of 10 years of age. Although symptomatic posttraumatic epilepsy developed in 5.7% (16 of 283) of children suffered closed TBI of

**195**

*Neurobehavioral, Cognitive, and Paroxysmal Disorders in the Long-Term Period of Pediatric…*

moderate or severe degree, this incidence appears to be rather high. The findings are indicative of long-term follow-up in cases of moderate or severe TBI with the

cortex leads to formation the substrate of post-traumatic epileptogenesis.

The complexity and polymorphism of clinical manifestations of post-traumatic epilepsy are determined by the variety of injuries in TBI, which include both focal and diffuse components, blunt closed head injuries with or without a skull fracture, contusions, hematomas, and penetrating injuries to the brain [48]. Mostly focal injuries are accompanied by contusion of the hemispheric surface structures and the involvement of various epileptogenic zones of the brain. The subcortical structures are affected by strong mechanical impact; the superficial focal injuries often damage the frontal and temporal lobes, which have high epileptogenic potential. Therefore, the epileptic syndromes that occur with these lesions will correspond to frontal or temporal lobe epilepsy. During the course of post-traumatic epilepsy seizures remain focal in about one quarter of patients, in half they become secondary generalized with a focal onset, and in another quarter they are manifested by generalized convulsions only (after a closed TBI with diffuse damage to

Meanwhile, in recent years, the use of long-term video EEG monitoring allows to identify subclinical forms of seizures, as well as epileptic status in some patients

**5. Treatment of neurobehavioral consequences of pediatric traumatic** 

The long-term consequences of TBI are often more obvious in children because their longer life span and need for schooling make such deficits all the more apparent. The overall disability in children is often less than that in adults suffered TBI. However, in the majority of head-injured children neuropsychological studies have shown deficits in cognitive functions and learning skills ranging from subtle to obvious. Special supportive measures, including educational intervention, behavioral modification and medical treatment, are therefore important issues. Thus, the treatment of TBI cogni-

The study of cognitive functioning and recovery 10 years after TBI in young children by Anderson et al. [51] confirmed the high risk of persisting functional deficits associated with severe early brain insult but demonstrated an "injury threshold" beneath which children may escape serious sequelae. In contrast to the "severity"-specific recovery observed in acute and subacute periods, findings

tive and behavioral sequelae must be planned as multimodal.

One of the most well-known population studies on post-traumatic epilepsy risk factors conducted to date [47] included 4541 patients who were divided into four age groups: from birth to 4 years (n = 542), from 5 to 14 years (n = 1184), from 15 to 64 years (n = 2546), 65 years and older (n = 269). The total 5-year probability of developing epileptic seizures was 0.5% among patients with mild TBI (loss of consciousness or amnesia lasting less than 30 minutes and no skull fractures), 1.2% for those with moderate TBI (loss of consciousness for 30 minutes to 24 hours or a skull fracture), and 10% among patients with severe TBI (loss of consciousness or amnesia for more than 24 hours, brain contusion or subdural hematoma). Thirty years post-injury, the corresponding figures were 2.1% for mild TBI, 4.2% for moderate TBI, and 16.7% for severe TBI. Thus, the increased risk of seizures after TBI varies greatly according to the severity of the injury and the time since the injury. The probability of developing epilepsy after a mild TBI does not exceed the average population risk, but severe or moderate TBI with focal damage to the cerebral

*DOI: http://dx.doi.org/10.5772/intechopen.93733*

necessity of repetitive EEG recordings.

the deep brain structures) [49].

with post-traumatic epilepsy [50].

**brain injury**

#### *Neurobehavioral, Cognitive, and Paroxysmal Disorders in the Long-Term Period of Pediatric… DOI: http://dx.doi.org/10.5772/intechopen.93733*

moderate or severe degree, this incidence appears to be rather high. The findings are indicative of long-term follow-up in cases of moderate or severe TBI with the necessity of repetitive EEG recordings.

One of the most well-known population studies on post-traumatic epilepsy risk factors conducted to date [47] included 4541 patients who were divided into four age groups: from birth to 4 years (n = 542), from 5 to 14 years (n = 1184), from 15 to 64 years (n = 2546), 65 years and older (n = 269). The total 5-year probability of developing epileptic seizures was 0.5% among patients with mild TBI (loss of consciousness or amnesia lasting less than 30 minutes and no skull fractures), 1.2% for those with moderate TBI (loss of consciousness for 30 minutes to 24 hours or a skull fracture), and 10% among patients with severe TBI (loss of consciousness or amnesia for more than 24 hours, brain contusion or subdural hematoma). Thirty years post-injury, the corresponding figures were 2.1% for mild TBI, 4.2% for moderate TBI, and 16.7% for severe TBI. Thus, the increased risk of seizures after TBI varies greatly according to the severity of the injury and the time since the injury. The probability of developing epilepsy after a mild TBI does not exceed the average population risk, but severe or moderate TBI with focal damage to the cerebral cortex leads to formation the substrate of post-traumatic epileptogenesis.

The complexity and polymorphism of clinical manifestations of post-traumatic epilepsy are determined by the variety of injuries in TBI, which include both focal and diffuse components, blunt closed head injuries with or without a skull fracture, contusions, hematomas, and penetrating injuries to the brain [48]. Mostly focal injuries are accompanied by contusion of the hemispheric surface structures and the involvement of various epileptogenic zones of the brain. The subcortical structures are affected by strong mechanical impact; the superficial focal injuries often damage the frontal and temporal lobes, which have high epileptogenic potential. Therefore, the epileptic syndromes that occur with these lesions will correspond to frontal or temporal lobe epilepsy. During the course of post-traumatic epilepsy seizures remain focal in about one quarter of patients, in half they become secondary generalized with a focal onset, and in another quarter they are manifested by generalized convulsions only (after a closed TBI with diffuse damage to the deep brain structures) [49].

Meanwhile, in recent years, the use of long-term video EEG monitoring allows to identify subclinical forms of seizures, as well as epileptic status in some patients with post-traumatic epilepsy [50].
