Closed head injuries frequently occur in car accidents, contact sports, structural collapse, and assaults. 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 6 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), (5) emotional dysregulation, and (6) disrupted sleep, as well as persistent headaches and periodic dizziness.
Research on 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. 
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.  Concussions are not, however, limited to football and lacrosse. Practice sessions in soccer (e.g., heading the ball) can cause alterations in consciousness and hence concussions. Detection, treatment, and prevention should be across all sports.
Separating neurologically based symptoms from psychologically based symptoms such as posttraumatic stress disorder (PTSD) is important since both affect concentration and sleep, and either can occur in accidents.
According to the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), postconcussive syndrome is given a diagnosis of either major or mild neurocognitive disorder (NCD) due to traumatic brain injury TBI. The specific DSM-5 criteria for neurocognitive disorder (NCD) due to traumatic brain injury are as follows: 
- The criteria are met for major or mild neurocognitive disorder
There is evidence of a traumatic brain injury - that is, an impact to the head or other mechanisms of rapid movement or displacement of the brain within the skull, with one or more of the following:
- Loss of consciousness
- Posttraumatic amnesia
- Disorientation and confusion
- Neurological signs (e.g., neuroimaging demonstrating injury; a new onset of seizures; a morked worsening of a preexisting seizure disorder; visual field cuts; anosmia; hemiparesis).
- The neurocognitive disorder presents immediately after the occurrence of the traumatic brain injury or immediately after recovery of consciousness and persists past the acute post-injury period.
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 and delirium
Posttraumatic amnesia (PTA) and delirium describe the mental states of patients immediately following closed head injury or after awakening from coma. The amnesia or delirium 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. 
For example, Govindaraju et al examined volumetric proton spectroscopic imaging of the whole brain in mild TBI (mTBI) patients 1 month postinjury.  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  and that one can have a significant brain injury, yet have normal conventional structural imaging. This has also been shown by Gaetz et al. 
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
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.
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.  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.
Sex- and age-related demographics
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, 10]
Prognosis is variable. The Glasgow Coma Scale provides a way of measuring severity of a head injury, but people with mild injuries may have enduring loss of abilities while people with far more serious ones may fully recover.
Patients with PCS should be informed that headaches, dizziness, fatigue, irritability, poor concentration, and decreased memory are common in the first weeks to months after injury and that these symptoms fully resolve in most patients after mild injury. Improvement generally continues for 18 months.
The following websites may be helpful to patients:
Medscape Reference, Postconcussive Syndrome in Emergency Medicine
National Institute of Neurological Disorders and Stroke, Traumatic Brain Injury: Hope Through Research
MedlinePlus, Traumatic Brain Injury
National Institute of Neurological Disorders and Stroke, Traumatic Brain Injury Information Page
MayoClinic.com, Traumatic Brain Injury
WebMD, Dementia in Head Injury
What would you like to print?