The impact of prophylactic treatment on post-traumatic epilepsy after severe traumatic brain injury

Formisano, Rita; Barba, Carmen; Buzzi, Maria Gabriella; Newcomb-Fernandez, Jennifer; Menniti‐Ippolito, Francesca; Zafonte, Ross; Vinicola, V.; Spanedda, F.

doi:10.1080/02699050701310994

Cited by 23 publications

(9 citation statements)

References 41 publications

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“…Formisano et al evaluated patients with severe TBI. In their study, patients who did not receive prophylactic therapy did not develop PTE in the 2-year follow-up period [35]. In another clinical trial, 5 days of continuous infusion of magnesium – a glutamate antagonist – at the NMDA receptor, given within 8 h after moderate or severe TBI, was demonstrated not to be neuroprotective and might, in fact, have a negative effect in the treatment of significant head injury [36].…”

Section: Treatment Of Pts and Ptementioning

confidence: 99%

Post-traumatic epilepsy: an overview

Verellen

Cavazos

2010

Therapy

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Post-traumatic seizures (PTS) and post-traumatic epilepsy (PTE) are complications from traumatic brain injury (TBI). PTE refers to recurrent and unprovoked PTS that occur at least 1 week after TBI. Seizures during the first week after TBI are considered provoked, an acute complication from head injury, while seizures occurring 1 week after TBI are considered a manifestation of PTE and if only a single seizure occurs it is known as late PTS. EEG and neuroimaging help in the diagnosis of PTE. Predictors for PTE include TBI severity, presence of intracranial bleeding and early PTS. Several clinical trials have demonstrated that antiepileptic drugs are effective in reducing the frequency of acute PTS, but do not appear to alter the natural history of late PTS or PTE.

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Section: Treatment Of Pts and Ptementioning

confidence: 99%

Post-traumatic epilepsy: an overview

Verellen

Cavazos

2010

Therapy

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“…In fact, these patients receive antiepileptic therapy to treat behavioural disturbances and post-traumatic seizures [15] or beta-blockers, namely propranolol, which is the only effective drug in psychomotor agitation, according to Cochrane Analysis [16], which is also used for post-traumatic dysautonomic syndrome, all drugs that may affect pain perception. Anticonvulsants or GABAergic drugs such as gabapentin, pregabalin or clonazepam, which are given to reduce central or peripheral pain or indomethacin to prevent para-articular ossification [17], may well be responsible for attenuation of head pain, if present.…”

Section: Post-traumatic Headache After Moderate/severe and Very Severmentioning

confidence: 99%

“…PTH classification should therefore be revised in term of pathophysiological mechanisms and studied through neurophysiological and functional neuroimaging techniques along with neuropsychological assessment, rather than in term of temporal pattern. Furthermore, the occurrence of post-traumatic epilepsy [15] in TBI patients complaining of headache and pain, needs to be investigated in order to find common mechanisms that may drive to therapeutic approaches with neuromodulators of neuronal excitability that may show efficacy in post-traumatic syndromes in which pain and epilepsy may be associated.…”

Section: A Glimpse To the Futurementioning

confidence: 99%

Post-traumatic headache: facts and doubts

et al. 2009

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The International Classification of Headache Disorders does not separate the moderate from severe/very severe traumatic brain injury (TBI), since they are all defined by Glasgow coma scale (GCS) < 13. The distinction between the severe and very severe TBI (GCS < 8) should be made upon coma duration that in the latter may be longer than 15 days up to months in the case of vegetative state. Post-traumatic amnesia duration may double the coma duration itself. Therefore, the 3-month parameter proposed to define the occurrence or resolution of post-traumatic headache (PTH) appears inadequate. Following TBI, neuropathic pain, central pain, thalamic pain, combined pain are all possible and they call for proper pharmacological approaches. One more reason for having difficulties in obtaining information about headache in the early phase after regaining consciousness is the presence of concomitant medications that may affect pain perception. Post-traumatic stress disorder (PTSD) develops days or weeks after stress and tends to improve or disappear within 3 months after exposure; interestingly, this spontaneous timing resembles that of PTH. In our experience the number of TBI patients with PTH at 1-year follow-up is lower in those with longer coma duration and more severe TBI. Cognitive functioning evaluated after at least 12 months from TBI, showed mild or no impairment in these patients with severe TBI and PTH, whereas they have psychopathological changes, namely anxiety and depression. The majority of patients with PTH after severe/very severe TBI had skull fractures or dural lacerations and paroxystic EEG abnormalities. The combination of psychological changes (depression and anxiety) and organic features (skull fractures, dural lacerations, epileptic EEG abnormalities) in PTH may be inversely correlated with the severity of TBI, with prevalence of psychological disturbances in mild TBI and of organic lesions in severe TBI. On the other hand, only in severe TBI patients with good cognitive recovery the influence of the psychopathological disorders may play a role. In fact, the affective pain perception is probably related to the integrity of cognitive functions as in mild TBI and in severe TBI with good cognitive outcome.

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“…Those with PTE also are at a significant disadvantage regarding physical, cognitive, and psychosocial issues that adversely affect outcome . Despite evidence against effective PTE prevention treatments, people with traumatic brain injury (TBI) frequently receive long‐term anticonvulsant therapy, often resulting in unwanted side effects and regular monitoring. Thus identifying reliable biomarkers for epileptogenesis and PTE risk prognostication could have broad clinical implications for TBI treatment and recovery.…”

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confidence: 99%

IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

et al. 2015

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SUMMARYObjective: Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI-induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin-1beta (IL-1b) gene, Il-1b levels in cerebral spinal fluid (CSF) and serum, and CSF/serum IL-1b ratios would predict PTE development post-TBI. Methods: We investigated PTE development in 256 Caucasian adults with moderateto-severe TBI. IL-1b tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL-1b levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL-1b gene variants, and also PTE. Temporally matched CSF/serum IL-1b ratios were also generated to reflect the relative contribution of serum IL-1b to CSF IL-1b. Results: Multivariate analysis showed that higher CSF/serum IL-1b ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL-1b levels (p = 0.014) and higher IL-1b CSF/serum ratios (p = 0.093). Significance: This is the first report implicating IL-1b gene variability in PTE risk and linking (1) IL-1b gene variation with serum IL-1b levels observed after TBI and (2) IL-1b ratios with PTE risk. Given these findings, we propose that genetic and IL-1b ratio associations with PTE may be attributable to biologic variability with blood-brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL-1b production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL-1b CSF/serum associations with PTE, and (3) evaluating targeted IL-1b therapies that reduce PTE.

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The impact of prophylactic treatment on post-traumatic epilepsy after severe traumatic brain injury

Abstract: Due to the negative cognitive effects of anti-epileptic drugs, the preliminary results are of considerable interest for the rehabilitation of patients with very severe TBI.

Cited by 23 publications

References 41 publications

Post-traumatic epilepsy: an overview

Post-traumatic epilepsy: an overview

Post-traumatic headache: facts and doubts

IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

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