Posttraumatic seizures (PTS), generalized or partial, are a common complication of head trauma. Seizures are more common with moderate to severe TBIs (brain contusions, hematomas, or penetrating head injuries) than mild TBIs.
Seizures can be early (occurring in <7 days of injury) or late (occurring after seven days of injury). The risk factors for early PTS include:
- GCS score of ≤10
- Immediate seizures
- Posttraumatic amnesia lasting longer than 30 min
- Linear or depressed skull fracture
- Penetrating head injury
- Subdural, epidural, or intracerebral hematoma
- Cortical contusion
- Chronic alcoholism (Younus et al., 2018)
Those with early seizures are at higher risk of developing posttraumatic epilepsy (PTE). PTE is defined as recurrent seizures >7 days following an injury. Reducing PTS should be a clinical goal to avoid PTE and decrease the associated morbidity and mortality rate. In patients with severe TBI, the rate of clinical PTS may be as high as 12%, whereas that of subclinical seizures detected on electroencephalography may be as high as 20% to 25% (Younus et al., 2018).
The Brain Trauma Foundation recommended using anticonvulsants such as phenytoin and valproate to prevent early but not late seizures because of the side effects associated with the chronic use of these medications. Phenobarbital and carbamazepine are avoided because of adverse effects (Younus et al., 2018).
The incidence of abnormal EEGs and seizure activity is the same for levetiracetam and phenytoin for the initial seven days posttrauma. However, the incidence of seizures is lower for patients who use levetiracetam on follow-up. So, levetiracetam is a better option for PTS prophylaxis. Levetiracetam is well tolerated and has fewer side effects (Younus et al., 2018).
Patients using selective serotonin reuptake inhibitors (SSRI) at TBI have a higher risk of epilepsy after TBI. The association may be causal but may also be due to other confounding factors. Underlying disease (depression or anxiety) can be the cause. Behaviors associated with depression, like poor adherence to anti-seizure medications, increased alcohol use, and poorer sleep/self-care may also be causal (Taiwo et al., 2019).
Brain injuries can lead to coagulopathy (a disorder of blood coagulation) as they lead to a systemic release of tissue factors and brain phospholipids into the circulation leading to abnormal intravascular coagulation and consumptive coagulopathy (Epstein et al., 2014). Those with coagulopathy after a TBI have a worse prognosis.
The ventricles can dilate when CSF builds up in the brain leading to hydrocephalus and an increased ICP. It often occurs soon after an injury but can occur after an extended time. Increased ICP may lead to cerebral edema, ischemia, hypoxia, and brain herniation.
Skull fractures are another complication. When the matter between the dura and the arachnoid membrane tears, CSF can leak out in a condition called subdural hygroma. Fluid can leak out of the nose, ears, and mouth. Any tear in the brain's protective matter increases the risk that bacteria can enter these spaces leading to meningitis.
Hemorrhagic stroke can result from an arterial bleed in the brain. Ischemic stroke can occur when a clot forms in the brain's vessels. Blood clots can occur in the sinuses next to the brain. These clots usually occur within a few days of the injury. They present with seizures, headache, emesis, hemiparesis, and a creased level of consciousness.
The cranial nerves can also be injured when there is a TBI. However, it is more common when there is a fracture and it is near the base of the skull. The most commonly injured cranial nerve is the facial nerve (CN VII), resulting in paralysis of the face. Cranial nerve injury may lead to an impaired sense of smell or taste. If the patients lose their sense of smell, it will likely be permanent if it lasts one year after the injury (Xydakis et al., 2015). Double vision may occur, and cranial nerve IV has likely been affected if it is to occur. Damage to the trigeminal nerve (CN V) leads to facial pain.
The post-concussion syndrome can occur days or even months after a TBI and can occur with any degree of head injury from mild to severe. A post-concussion syndrome is characterized by dizziness, vertigo, headache, reduced concentration, apathy, depression, sleep disturbance, confusion, irritability, and anxiety.
Amnesia can also occur after a head injury. Anterograde amnesia is impaired memory of events after the injury, whereas retrograde amnesia is memory deficits of events before the injury.
Brain dysfunction can take many forms after a TBI. The following are problems that may present after a TBI:
- Impaired concentration and attention
- Impaired executive function
- Reduced hand-eye coordination
- Sensory deficits: vision, smelling, touching, hearing
- Aphasia (inability or reduced ability to communicate, which can include impairments in expression or understanding of written or verbal language)
- Dysarthria (cannot speak the proper words due to dysfunction of the muscles used to speak)
- Reduced ability to carry out complex tasks
- Behavior changes or onset of mental illness (depression/anxiety)
- Social inappropriateness or aggression
Most of the recovery from a TBI occurs in the first six months and can be more gradual after six months.
Some problems may occur years after the head injury (CDC, 2017). Alzheimer's disease is the most common type of dementia and is linked to a prior history of head injury. Parkinson's disease can occur when there is a remote history of damage to the basal ganglia. As mentioned above, dementia pugilistica occurs in patients with a history of head trauma. Posttraumatic dementia is dementia that occurs after a single TBI that results in a coma.
Agitation is commonly seen after a head injury. Other causes of agitation seen after a head injury may include pain, depression, infection, side effects of medications, sleep deprivation, or electrolyte imbalance.
A myriad of other problems may occur after a TBI, including:
- Deep vein thrombosis
- Gastrointestinal and genitourinary problems
- Organ failure
- Chronic Traumatic Encephalopathy
Athletes who have experienced head injuries over the years may experience chronic traumatic encephalopathy (CTE), a neurodegenerative disease likely caused by repetitive brain trauma. It may result in memory problems, executive dysfunction, poor impulse control, depression, apathy, suicide, aggression, violence, substance abuse, and an increase in high-risk behaviors (e. g., increased food intake, risky sexual behavior, and gambling). Motor disturbances, such as rigidity with a slow shuffling gait may present in CTE. It may eventually lead to dementia.
CTE is thought to be secondary to hyperphosphorylated tau and TDP-43 in the brain. Once thought to be only a problem in boxers, it is now prevalent in football players.
CTE is likely caused by repetitive trauma to the brain (both concussions and subconcussive trauma). CTE is difficult to diagnose because it overlaps with multiple other syndromes. CTE may start during the post-concussive syndrome. As the disease progresses, it presents similarly to other dementing illnesses such as frontotemporal dementia and Alzheimer's.