Traumatic brain injury: Pathology review

At the emergency department, 65-year-old Christian came in complaining of headaches, vision problems, and memory loss. These symptoms have gradually progressed over the past couple of weeks. On examination, there’s slurred speech, and his gait is unsteady. He has a history of chronic alcohol abuse. Head CT shows a “crescent-shaped” hyperdense mass that crosses the suture lines. Later that day, 33-year-old Max is brought in after a fight. They reported being knocked unconscious, but regained consciousness after an unknown period of time. Head CT is ordered and shows a “lens-shaped” hyperdense mass that doesn’t cross the suture lines. Max was very agitated and said they felt fine. They then left the hospital against medical advice. Later that day, Max lost consciousness again and died at home.

Okay, so Christian and Max had some form of traumatic brain injury. When an external force damages the head resulting in temporary or permanent brain dysfunction, we call it a traumatic brain injury, or TBI. Now, as a direct result of the external force, TBIs can cause extra-axial and intra-axial injuries. Extra-axial injuries are within the skull but don’t involve the brain parenchyma. The most high yield ones are epidural and subdural hematomas, as well as a subarachnoid hemorrhage. Intra-axial injuries - on the other hand - do involve the brain parenchyma, and the most high yield one for your exams is diffuse axonal injury. Now, the initial brain injury can impair the normal functioning of the cerebral metabolism and result in complications, such as tissue hypoxia, cognitive impairment, and seizures. Additionally, if the brain injury is associated with intracranial bleeding or severe inflammation followed by edema, the pressure within the skull may rise and result in severe complications. For your exams, it’s important to note that the most important complication of increased intracranial pressure is brain herniation. Trauma initiates a series of molecular events along with the primary brain injury, which can persist for hours, or even days. These are referred to as “secondary brain injury”, and eventually can result in increased intracranial pressure, which in turn, has numerous consequences, and for the exams, the most important is brain herniation.

Okay, now let’s take a closer look at these different types of traumatic brain injury, starting with the extra-axial injuries.

Epidural hematomas οccur when blood collects in the space between the dura mater (which is the outer layer of the meninges) and the inner aspect of the skull periosteum. This happens when a linear fracture occurs at the region where the frontal, parietal, temporal, and sphenoid bones join together. This region is called pterion, and it’s the thinnest part of the lateral wall of the skull. For the test, remember that a fracture at the pterion can tear open the middle meningeal artery (a branch of the maxillary artery) causing profuse bleeding. The most important concept to keep in mind is that individuals with epidural hematoma classically have a period of loss of consciousness and then a lucid interval. During this time the individual regains consciousness and feels fine, but a lucid interval isn’t always seen. Symptoms are due to the build of blood trapped between the dura mater and skull, which increases intracranial pressure. Now, what makes epidural hematomas so dangerous is that the dura mater is attached tightly to the sutures of the skull, so the blood can’t cross these sutures and is trapped with nowhere to go. This means the intracranial pressure can increase rapidly. The individual can develop headaches, nausea, vomiting, and focal neurological symptoms like weakness, numbness, vision and auditory problems. As the hematoma grows rapidly, it can cause a life-threatening brain herniation resulting in the loss of consciousness, coma, and death.

A brain CT is diagnostic, and classically shows a convex, “lens-shaped” hyperdense collection of blood that does not cross the suture lines of the skull. There can also be evidence of scalp hematoma due to the head trauma. In addition to the bleeding, there can be surrounding cerebral edema, and if the edema is significant, it can cause a shift of the midline to the contralateral side. This signifies an impending brain herniation, most commonly a transtentorial herniation. Epidural hematomas are an emergency, and neurosurgical intervention is often necessary.

All right, moving onto subdural hematomas. For your exams, it’s important to know that a subdural hematoma occurs when blood collects between the dura mater (the outer layer of the meninges) and arachnoid mater, which is the middle layer of the meninges. Another high yield fact you have to know is that, unlike epidural hematomas, the bleeding source is usually the bridging veins that connect the cerebral venous sinuses to the superficial veins of the skull. Now, the bridging veins are very vulnerable to rapid acceleration or deceleration, so they are easily damaged in car crashes. It’s also high yield to remember that when there’s brain atrophy and shrinkage - like in chronic alcohol users or the elderly - the bridging veins get stretched out. So even minor head trauma, like walking into a door, can lead to a subdural hematoma in these individuals. Oftentimes, individuals don’t even remember the traumatic event, so it’s important to always consider a subdural hematoma especially in elderly individuals with neurological symptoms. If a subdural hematoma is detected in an infant or young child, it could be due to non-accidental trauma, or child abuse. Infants and children have large heads with relatively small brains, so vigorously shaking a young child can cause a subdural hematoma, as well as other signs of non-accidental trauma like retinal hemorrhages on fundoscopy. Okay, because the source of the bleeding is venous, the hematoma usually grows slower than epidural hematomas caused by arterial bleeding. Also, since the blood isn’t restricted by sutures, it can be distributed over a larger area, so pressure doesn’t build up as quickly, unless the hemorrhage is very large. Because of these factors, subdural hematomas tend to be more insidious. Now, as the blood accumulates, intracranial pressure increases causing symptoms like worsening headaches, nausea or vomiting, visual problems, slurred speech, dizziness, unsteady gait, confusion, cognitive impairment, seizures, and hemiparesis that can be ipsilateral or contralateral. A subdural hematoma is considered acute if symptoms develop within 2 days of a head trauma, subacute if they develop between 2 days and 2 weeks of a head trauma, and chronic if they develop 2 weeks or more after a head trauma. Just like with epidural hematomas, if a subdural hematoma grows large enough, it can lead to brain herniation and coma or death.

Now, a brain CT is usually diagnostic, and classically shows a concave, “crescent-shaped” density that crosses the suture lines, and that’s extremely high yield! And the density on the brain CT helps determine the age of the hematoma. Acute subdural hematomas are hyperdense, while chronic subdural hematomas are hypodense. Subacute subdural hematomas appear isodense, meaning they blend in with the adjacent brain parenchyma, making them easy to miss. Also, a midline shift can be seen on CT. The morbidity and mortality of subdural hematomas are high because they can develop more insidiously and are therefore harder to detect in the early stages.

Similar to epidural hematomas, the mainstay of treatment is prompt surgical hematoma evacuation. Sometimes, stable individuals with acute small hematomas can be managed nonoperatively, as the hematoma is reabsorbed naturally.

Next, there’s a subarachnoid hemorrhage, which is bleeding between the arachnoid mater and pia mater: the innermost layer of the meninges. In general, the most common cause of subarachnoid hemorrhage is head trauma, while the most common cause of spontaneous subarachnoid hemorrhage is the rupture of an aneurysm. Aneurysms can burst open when there’s an increase in intracranial pressure. The most common aneurysms in the brain are saccular cerebral aneurysms, also called berry aneurysms. They typically arise in the anterior half of the circle of Willis at bifurcations. Bifurcations are junctions between arteries, and the most common junction where saccular aneurysms take place is between the anterior communicating artery, or ACoA for short, and the anterior cerebral artery, or ACA. Some genetic disorders like autosomal dominant polycystic kidney disease, Marfan syndrome, and Ehlers-Danlos syndrome can predispose even young individuals to saccular aneurysms, and that’s a fact that gets frequently tested on the exams! And a less frequent cause of spontaneous subarachnoid hemorrhage is an arteriovenous malformation, which is formed by abnormal tangled blood vessels that aren’t used to high arterial pressures and can rupture easily.

In most cases, subarachnoid hemorrhage progresses rapidly due to arterial bleeding, and individuals complain of an excruciating headache also known as thunderclap headaches that are described as "the worst headache of my life". There can also be nuchal rigidity, seizures, and symptoms of increased intracranial pressure like vomiting, vision changes, and confusion.

The diagnosis of a subarachnoid hemorrhage is usually made with brain imaging; in most cases, this is done with a CT scan. Brain imaging shows blood in the ventricular cisterns, interhemispheric fissures, and within the sulci. The more blood that’s seen, the worse the outcome. Now, in cases of a spontaneous subarachnoid hemorrhage, if the brain imaging is negative, then the diagnosis can be made with a lumbar puncture and cerebrospinal fluid analysis. When there is spontaneous subarachnoid hemorrhage, the test will show red blood cells or xanthochromia; which is a result of red blood cell breakdown. In the case of a traumatic subarachnoid hemorrhage, a lumbar puncture is contraindicated due to the high intracranial pressure and the risk of brain herniation.

Initial management of a subarachnoid hemorrhage is supportive. But rebleeding is very frequent, so the only effective treatment is prompt surgery like aneurysm repair. A complication that can occur about 2 days to 2 weeks after a subarachnoid hemorrhage is post-traumatic vasospasm of the subarachnoid vessels, which can cause cerebral ischemia. Therefore, individuals are given a calcium channel blocker called nimodipine, which relaxes the cerebral vascular smooth muscle, preventing vasospasm. Another potential complication is hydrocephalus, which can lead to increased intracranial pressure. This can present with progressive deterioration in the level of consciousness, and ventricular dilation can be seen on CT scan. Some individuals with a subarachnoid hemorrhage develop electrolyte imbalances like hyponatremia due to water retention. This can result from one of three things: the syndrome of inappropriate secretion of antidiuretic hormone or SIADH, cerebral salt wasting caused by excessive secretion of natriuretic peptides, or diminished central sympathetic activity. Other common complications of a subarachnoid hemorrhage are fever of infectious and noninfectious origin and seizures.