E. Lee Murray, MD
CHAPTER CONTENTS
OVERVIEW
Hospital neurologists play a varied role in evaluation and management of patients with traumatic brain injury (TBI). Facilities with well-developed trauma programs or good neurosurgical coverage often involve neurology only at times of specific need, such as seizures or secondary infarction. Here, we discuss some of the conditions that neurologists may be asked to address.
The terms concussion and contusion have become matters of some debate, but since they are useful in practice and still in widespread use, they will be used here.
CONCUSSION
Concussion is identified as head injury with transient loss of consciousness followed by confusion. This is the most common diagnosis for patients with head injury reaching medical attention. This is classified as mild TBI (MTBI).
PRESENTATION to the ED is usually after the phase of initial recovery. Patients usually have headache, dizziness, and mild confusion. Exam immediately after the injury, during a phase of unconsciousness, shows no focal signs and good brainstem reflexes. Prolonged unconsciousness or focal signs suggests that the injury is beyond concussion.
DIAGNOSIS is clinical. Computed tomography (CT) of the brain is usually done but may be able to be avoided if the patient is beyond childhood, not elderly, had rapid return of function, is neurologically normal, and is on no anticoagulants. CT should not show findings of acute intracranial injury.
MANAGEMENT is conservative. Symptoms improve over hours. Hospital admission is often not needed. Post-concussive syndrome may follow (discussed later). However, observation and return-to-ED instructions should be given since approximately 1% of patients with MTBI ultimately need neurosurgery.1
CONTUSION
Contusion is often categorized with intracerebral hemorrhage, but in this context refers to injury to the brain more severe than that of concussion, with microhemorrhages and development of edema.
PRESENTATION is with headache, confusion, and dizziness, as with concussion, but additionally there may be prolonged unconsciousness, seizures, and focal neurologic signs. Extensive contusions with edema can cause critical increase in intracranial pressure (ICP).
DIAGNOSIS is clinical and supported by brain imaging. There is a continuum between contusion with petechial hemorrhage and large intraparenchymal hemorrhage, discussed later.
MANAGEMENT depends on the size and extent of the injuries. Edema with increased ICP is managed with osmotherapy and sedation. Surgical decompression is tried for critical increase in ICP refractory to medical measures. Hypothermia has not been proved to improve outcome for most patients. Seizure treatment is discussed below.
INTRACEREBRAL HEMORRHAGE
Intracerebral hemorrhage (ICH) is indicative of more severe TBI. ICH is more likely in the elderly and in patients on anticoagulants and other antithrombotics. Location of the bleeding can be subarachnoid, subdural, epidural, or intraparenchymal. ICH is discussed also in Chapter 16. Neurosurgery should be consulted for these disorders.
Intraparenchymal Hemorrhage
Intraparenchymal hemorrhage may have direct effects on neuronal function but also increase ICP and produce global symptoms.
PRESENTATION is with persistent cognitive change and headache after an injury. Consciousness may not have been restored. Seizures and focal signs may be seen.
DIAGNOSIS is suspected by prolonged unconsciousness, focal signs, or seizures after a severe head injury, or after a milder head injury in a patient with coagulopathy. CT brain shows the hemorrhage. Magnetic resonance imaging (MRI) may also show the blood.
MANAGEMENT is supportive with ICU observation. Coagulation studies are checked and corrected if abnormal. Increased ICP is generally treated as discussed in Chapter 13. Corticosteroids are of no benefit. Seizures are treated as discussed later. Surgery for intraparenchymal hemorrhage does not generally have a good outcome, but some patients may benefit from craniectomy or drainage.
Subdural Hematoma
Subdural hematoma (SDH) is blood accumulated between the inner layer of the dura and the arachnoid membrane. In general, SDH is indicative of a severe head injury, but it can develop with more mild head injuries, especially if the patient is on anticoagulants or other antithrombotics or is elderly. In these latter cases, the onset may be more insidious.
PRESENTATION can span a spectrum. Some presentations can be: