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Traumatic Brain Injury

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K Tam

on 30 August 2013

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Transcript of Traumatic Brain Injury

The role of anti-epileptics in TBI patients
Traumatic Brain Injury
Introduction
Impacts of TBI
Literature review on prophylactic anti-epileptic use

Phenytoin
Mechanism: stabilizes threshold against neuronal hyperexcitability via promotion of sodium efflux
FDA approved for prevention and treatment of seizures occurring during or after neurosurgery
Requires close therapeutic monitoring
Severe head injury patients on phenytoin performed worse on most neuropsychological measures at 1 month (p < 0.05)
Levetiracetam
Mechanism: inhibits burst firing of neurons without affecting normal neuronal excitability
may selectively prevent the proliferation of seizures
Carbamazepine
Only one study on cabamazepine and PTS.
Glotzner et al. (1983) found that carbamazepine:
reduced the rate of early PTS by 61% compared to placebo (p<0.05)
reduced the rate of late PTS by 20%
n = 139
Patients with severe TBI
Valproate
Mechanism: unknown, believed to increase cerebral concentration of GABA
Clinical Vignette: a TBI patient
definition: an insult to the brain stemming from an external physical force and resulting in either temporary or permanent impairment, functional disability, or psychosocial maladjustment
http://www.mdconsult.com/books/linkTo?type=bookPage&isbn=978-1-4160-4007-1&eid=4-u1.0-B978-1-4160-4007-1..50155-3
Image: http://www.mi4nd.com/whowehelp/
Epidemiology and Etiology
Cuccurullo (2009)
http://emedicine.medscape.com/article/326510-overview#aw2aab6b3
1.74 million people sustain mild TBI yearly
About 200,000 cases of TBI per year require hospitalization
2.5 - 6.5 million Americans live with TBI related disabilities
Mortality rates
Outside hospital: 17 per 100,000
Hospitalized patients: 6 per 100,000
Financial cost: $4 billion per year
loss of potential income
patient
relatives (2/2 caretaker duties)
cost of acute care
cost of other medical expenses
continuous ambulatory care
continuous rehabilitation care
What is the impact of TBI?
Neurologic impact of TBI
Damage occurs over hours to days
Primary insult
direct disruption to brain parenchyma from shear forces of impact
immediate
not amenable to medical intervention
contusions, diffuse axonal injury, impact depolarization
Secondary insult
damage to neurons caused by physiologic response to initial injury
includes post-traumatic seizure
Torbic et al. (2013)
Image: http://www.wisegeek.com/what-is-traumatic-brain-injury-rehab.htm
Image: http://blog.mcleishorlando.com/blog/personal-injury-law/concussion/
http://emedicine.medscape.com/article/326510-overview#aw2aab6b3
Image: http://housingpanic.blogspot.com/2008/07/housingpanic-urgent-warning-to.html
Anterior temporal lobe
Inferior frontal lobe
Post-traumatic seizures (PTS)
Risk Factors
5-7% of the 275,000 TBI cases each year with PTS
Can occur early (within 7 days) or late (after 7+ days)
Mechanism:
early - changes neurotransmitter receptor and ion channel proteins
late - axonal sprouting, dendritic modifications
Risk factors for PTS after TBI
Early PTS
Late PTS
Risk Factors for Early PTS
Glasgow Coma Scale
score of 10 or less
Immediate seizures
Cortical contusion
Linear fracture
No or brief unconsciousness
Penetrating head injury


Risk Factors for Late PTS
Early PTS
Acute intracerebral hematoma
Cortical contusion
Increased severity of injury
Post-traumatic amnesia lasting longer than 24 hours
Loss of consciousness
Age 65+
Depressed skull fracture
Age 65+
Increased severity of injury
Chronic alcoholism
PTA lasting longer than 30 min
Subdural, epidural, or
intracerebral hematoma
Guidelines: PTS prophylaxis is recommended only during first 7 days.
No evidence to support PTS prophylaxis >7 days, even with + risk factors
Torbic et al. (2013)
Young et al. (1983)
No significant difference in the rate of occurrence of early PTS between the phenytoin and placebo groups
McQueen et al. (1983)
No patients experienced early PTS; however at 24 months 8 patients (phenytoin) and 7 patients (placebo) reported to have had clinical seizure
Temkin et al. (1990)
Patients in the phenytoin group had a lower rate of early PTS vs placebo group
p = 0.75; n = 244
randomized, double-blind, placebo controlled trial
Intervention: IV loading 11mg/kg; IM maintenance 13 mg/kg x 1 week
n = 164
Randomized, double-blind, placebo controlled trial
Intervention: PO Phenytoin 300mg QDay x 1 year
p < 0.001; n = 404
Participants: mod - severe TBI
No significant difference in frequency of seizure between groups at 12 and 24 months
p > 0.2
(Dilantin)
(Keppra)
Jones et al. (2008)
No significant difference in seizure activity between patients treated with levetiracetam vs phenytoin (p=0.556) in preventing early PTS
Szaflarski et al. (2010)
Levetiracetam had similar efficacy to phenytoin for early PTS prophylaxis after TBI and
may be more tolerable
Levetiracetam was associated with an increase in seizure tendency (p=0.007)
n = 73
Retrospective cohort study
More patients in the phenytoin group had worse
neurologic status (p=0.024)
GI upset (p=0.043)
anemia (p=0.076)
Phenobarbital
Mechanism: exhibits GABA-like effects similar to benzodiazepines, reversibly depresses activity of excitable tissue
cannot be recommended for PTS prophylaxis after TBI
Rish and Caveness (1973)
No difference in the occurrence of PTS in the patients who received prophylaxis compared to those who did not
Manaka (1992)
No effect on the occurrence of late PTS after TBI compared with placebo
n=1614
4% of patients prophylaxed with phenobarbital
most received phenytoin
results cannot be attributed to phenobarbital alone
n = 126
severe TBI patients
randomized, placebo-controlled trial
(Tegretol)
(Depacon)
Temkin et al. (1999)
Rates of early PTS were similar between the phenytoin and valproate groups (p = 0.14)
Dikmen et al. (2000)
No difference was found in neuropsychological or cognitive measures at any time point between phenytoin or valproate groups
No significant difference between groups in the occurrence of late PTS (0.19)
Greater mortality in patients assigned to valproate group (p=0.07)
n= 379
moderate or severe TBI
randomized, double-blind, parallel-group trial
n = 279
moderate or severe TBI
randomized, double-blind, parallel-group study
Mr. W is a 62 year old man with a past medical history significant for hypertension, hyperlipidemia who presented with intraventricular hemorrhage after being struck by a motor vehicle while walking on the street. Arrived at rehabilitation with mandibular and pelvic fracture. Medication included Keppra with no reports of seizures.
Question: Why was he on Keppra? What is the role of an anti-epileptic drug in TBI patients?
Torbic H. Use of antiepileptics for seizure prophylaxis after traumatic brain injury. American journal of health-system pharmacy. 2013-05-01;70:759-766.
Thank you for your attention
Torbic H. Use of antiepileptics for seizure prophylaxis after traumatic brain injury. American journal of health-system pharmacy. 2013-05-01;70:759-766.
Cuccurullo, Sara. Physical medicine and rehabilitation board review. New York: Demos, 2004. Print.
http://www.mdconsult.com/books/linkTo?type=bookPage&isbn=978-1-4160-4007-1&eid=4-u1.0-B978-1-4160-4007-1..50155-3
http://emedicine.medscape.com/article/326510-overview#aw2aab6b3
Image: http://www.mi4nd.com/whowehelp/
Image: http://housingpanic.blogspot.com/2008/07/housingpanic-urgent-warning-to.html
Image: http://www.wisegeek.com/what-is-traumatic-brain-injury-rehab.htm
Image: http://blog.mcleishorlando.com/blog/personal-injury-law/concussion/
References
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