Postconcussive Syndrome 

Closed head injuries frequently occur in car accidents, contact sports, and other accidents. Dizziness or loss of consciousness indicates a concussion has occurred. Although most people fully recover, some have serious disability. Traumatic brain injury can lead to deficits in 5 general areas: (1) short-term memory impairment, (2) slowed processing speed, (3) impaired executive function, (4) disrupted abilities of attention and concentration (which likely contributes to the deficits noted in the first 3 categories), and (5) emotional dysregulation.

Research of high school football players has shown that even without clinically observed symptoms of concussion, blows to the head can lead to demonstrated measurable neurocognitive (primarily visual working memory) and neurophysiologic (altered activation in dorsolateral prefrontal cortex) impairments.^[1]

In a prospective 11-year study by Lincoln et al that aimed to understand the risks of sports-related concussion among 12 scholastic sports, football and boys’ lacrosse had the highest number of concussions while football had the highest concussion rate.^[2] Concussions occurred in all other sports and was observed in girls’ sports at rates similar to or higher than those of boys’ sports. The high-participation collision sports warrant continued vigilance, but the findings suggest that focus on concussion detection, treatment, and prevention should be across all sports and not just the sports with the highest rates.

Separating neurologically based symptoms from psychologically based symptoms such as posttraumatic stress disorder (PTSD) or adjustment disorder can be difficult.

Case study

John was a very active young man. He played sports, got together with friends, worked hard in school, and generally enjoyed life. One day he was riding in a friend's car when a truck ran into their vehicle. He banged his head against the side of the vehicle in the accident.

He didn't remember the actual accident. He recalled riding and then he recalled being in pain in the car, which wasn't moving. The next thing he recalled was being in an ambulance. He was brought to the emergency department where the doctors found no significant injuries other than a concussion. The CAT scan was unremarkable; no subdurals, no epidurals, and no sign of contusion were apparent.

John seemed different after the accident. He had headaches a few times a week that lasted a few hours. He had headaches, before but never as bad or as frequent. He also had dizzy spells a few times a week. For reasons he could not understand, he now began waking up 2 or 3 times a night and had difficulty falling asleep. His energy was gone. However, it was more than his energy being gone. He no longer seemed to care. He would sit and stare and have little interest in doing things. At the same time, if someone or something was irritating him, he would flare up. He would also make inappropriate hurtful comments, things he would never have said in the past. He seemed to be a different person.

John's memory also suffered. Learning new things was much harder. He could not focus attention in class and could not maintain his concentration when reading. His grades declined significantly. He would readily forget what he was doing if something else came up. If he stepped away from the stove or left a pot to boil and the phone rang or he went to look at the TV, he would forget he was cooking. He would take his wallet when he walked out the door but forget his keys.

Over the next 18 months he improved considerably. He became less irritable, the headaches and dizziness markedly improved, he became more engaged in life, and his concentration and memory were better; however, they never returned to his baseline.

DSM-IV-TR criteria outline for postconcussional disorder

The DSM-IV-TR criteria for postconcussional disorder are as follows:^[3]

A. A history of head trauma that has caused significant cerebral concussion.

B. Evidence from neuropsychological testing or quantified cognitive assessment of difficulty in attention (concentrating, shifting focus of attention, performing simultaneous cognitive tasks), or memory (learning or recalling information).

C. Three (or more) of the following occur shortly after the trauma and last at least 3 months:

1. Becoming fatigued easily
2. Disordered sleep
3. Headache
4. Vertigo or dizziness
5. Irritability or aggression with little or no provocation
6. Anxiety, depression, or affective lability
7. Changes in personality (eg, social or sexual inappropriateness)
8. Apathy or lack of spontaneity

D. The symptoms in criteria B and C have their onset following head trauma or else represent a substantial worsening of preexisting symptoms.

E. The disturbance causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning. In school-aged children, the impairment may be manifested by a significant worsening in school or academic performance dating from the trauma.

F. The symptoms do not meet criteria for dementia due to head trauma and are not better accounted for by another mental disorder (eg, amnestic disorder due to head trauma, personality change due to head trauma).

Second injury syndrome

The second injury syndrome (SIS), although rare, is important as a cause of preventable sudden death. SIS occurs when someone not yet fully recovered from a head injury experiences another head or upper body injury, even seemingly trivial injury. After a brief delay, the person suddenly loses consciousness. Signs of brainstem compression follow, leading to death or permanent coma. The syndrome typically affects young men who participate in rough sports. The mechanism may be failed cerebral autoregulation with subsequent engorgement of the brain vasculature.

Posttraumatic amnesia

Posttraumatic amnesia (PTA) describes the mental state of patients immediately following closed head injury (CHI) or after awakening from coma. PTA may persist for hours to weeks or, occasionally, months. Patients with PTA are alert and capable of complex behavior. However, they experience severe memory problems, feelings of confusion, inability to learn new information, and poor concentration. PTA sometimes involves peculiar alterations of consciousness and self-awareness. As a measure of injury severity, the duration of PTA has prognostic significance.

Posttraumatic thalamic syndrome

Injury to the thalamus following CHI produces posttraumatic thalamic syndrome. In this condition, the person progresses from generalized numbness to episodes of spontaneous pain or pain in response to nonnoxious stimuli. Patients also experience constant or episodic unpleasant sensations (burning, freezing, crushing, formication), paresthesias, outbursts of fear or anger, aphasia, abusive behavior, and signs of frontal lobe dysfunction.

The pathophysiology of postconcussive syndrome (PCS) results from contusions and diffuse axonal injury (DAI). Disruption of axons triggers a cascade of further insults, including calcium influx, excitotoxin release, phospholipase activation, and lipid peroxidation.

Postmortem studies of traumatic brain injury (TBI) have demonstrated pathological changes that cannot be detected by conventional neuroimaging studies. In fact, much of the pathology of TBI is under the threshold of detection in conventional MRI, which in humans is approved only to be done at 3 Tesla or less. Even when standard structural neuroimaging of the brain reveals no visible abnormality, underlying structural, biochemical, or electrophysiological abnormalities may be present.^[4]

For example, Govindaraju et al examined volumetric proton spectroscopic imaging of the whole brain in mild TBI (mTBI) patients 1 month postinjury.^[5] This method provides a mechanism for detecting biochemical perturbations of the brain brought on by injury that would not necessarily show-up in standard imaging. The authors found “widespread metabolic changes following mTBI in regions that appear normal...” on conventional MRI. This supports the notion of nonspecific damaging effects from mTBI that occur at a subtle, microscopic level of injury^[6] and that one can have a significant brain injury, yet have normal conventional structural imaging. This has also been shown by Gaetz et al.^[7]

Regarding pathophysiology, specifically of dementia after head injury, the pattern of symptoms reflects the nature of the injury and the location of tissue damage. Symptoms related to particular brain areas include the following:

• Prefrontal cortex - Disinhibition, apathy, personality change (coarsening, flattening), decreased fluency of speech, obsessions, hypochondria, delusions
• Basal ganglia - Depression, mania, tremor, cogwheeling, bradykinesia, obsessions, compulsions
• Thalamus - Apathy, irritability, pathological crying, paresthesias, pain, hypersomnia
• White matter - Apathy, lability, loss of spontaneity, transient hemiparesis or hemiplegia, bradykinesia, bradyphrenia
• Cerebellum/pons - Mild avolition, disinhibition, cerebellar signs, loss of ability to execute motor routines automatically

Frequency

United States

Persistent neuropsychiatric impairment following head injury is a significant public health problem. Military populations are especially prone to penetrating injuries, with relatively more closed head injuries occurring in civilian populations. From 400,000-500,000 people are hospitalized in the United States every year for head injury; many more people are injured and do not require admission. Head injury is the third most likely cause of dementia, after infection and alcoholism, in people younger than 50 years. The overall incidence of traumatic brain injury is roughly 200 cases per 100,000 population.

International

No information is available.

Mortality/Morbidity

Morbidity from closed head injury is variable and difficult to predict. Most estimates of morbidity stratify populations into those with mild, moderate, or severe injury, based on their scores on the Glasgow Coma Scale (GCS) and the duration of posttraumatic amnesia (PTA). By definition, mild injury entails less than 15 minutes of unconsciousness (GCS >13) or less than 1 hour of PTA in the absence of skull fracture. PTA of less than 1 hour predicts full recovery, while PTA of greater than 24 hours in adults predicts neuropsychiatric disability. Between these benchmarks, the prognosis of an injury varies from complete recovery to persistent symptoms and disability.

Although severity of head injury as measured by depth of coma and length of PTA correlates with long-term sequelae, mild injuries sometimes lead to severe impairment and disability.^[8] Conversely, not all severe injuries have severe consequences. Other factors that predict morbidity include patient age, history of prior injury, history of alcohol use (especially at time of injury), history of psychiatric disorder prior to injury, location and extent of focal brain damage, degree of diffuse axonal injury (DAI), evidence of brain stem dysfunction at the time of injury, and psychosocial adversity before or following injury.

The factors related to injury severity correlate most strongly with problems of memory, cognitive slowing, and impaired information processing. They contribute to mood, personality, and behavioral sequelae to an immeasurable degree. Psychosocial adversity and stress also contribute to the morbidity of post–head injury dementia and of postconcussive syndrome.

Race

No relevant information is available.

Sex

Men experience head injuries more frequently than do women.

Age

Head injuries and their sequelae are most frequent in males aged 14-24 years. However, patients who are middle-aged or older are likely to have sequelae that are more persistent. Very young children with head injuries also have worse outcomes.^[9]