Postconcussive Syndrome Psychiatric Care

Updated: Jul 25, 2019
  • Author: Roy H Lubit, MD, PhD; Chief Editor: David Bienenfeld, MD  more...
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Practice Essentials

People with postconcussive symdrome have suffered a traumatic brain injury (TBI). Mild TBI is a silent epidemic. Medical personnel often fail to ask if accident victims have problems with concentration, memory, and irritability unless there was a substantial period of unconsciousness. Any alteration of consciousness after a blow to the head should lead to a diagnosis of a concussion. Shaking of the head, as in whiplash, is sufficient to cause a TBI. 

The symptoms of PTSD and TBI overlap and sometimes it is difficult to assess which is causing which symptoms. Frequently, after accidents, or in the military after blast exposure, people suffer from both TBI and PTSD. [1, 2, 3]

The initial injury is causd by rapid acceleration or deceleration of the head leading to stretching of and damage to white matter tracts and breaking of blood vessels. Further damage can occur as a result of impairment of cerebral blood flow, failure of cellular ion pumps, calcium and sodium overload in cells, excessive release of excitatory amino acids, free radical formation, proteolysis, and lipid peroxidation. Inflammatory responses may also have a role in causng apoptosis. 

Mild TBI is defined as loss of consciousness for less than 30 minutes and posttraumatic amnesia for less than 24 hours. Moderate TBI refers to loss of consciousness for 30 minutes to 24 hours and posttraumatic amnesia for 24 hours to 7 days. Severe TBI refers to loss of consciousness for more than 24 hours or posttraumatic amnesia for more than 7 days. 

After a concussion the individual should cease contact sports until all symptoms have resolved.  Total rest for several days is recommended, especially for children. [4]   

Research indicates that N-acetyl cysteine and phenserine, given shortly after the injury, may significantly lessen the secondary loss of neurons from the biochemical cascade that can occur. [5]  Research is also being done using hyperbaric oxygen. [6, 7]  Omega 3 supplementation is common.

Treatment is symptom focused. Magnesium oxide and boswellia are helpful with headaches.  Antidepressants are appropriate if mood is impaired. 



Closed head injuries frequently occur in car accidents, contact sports, structural collapse, and assaults. Any alteration of consciousness is sufficient to diagnose a concussion. Although most people fully recover from a mild TBI, some have serious disability. Traumatic brain injury can lead to deficits in multiple 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, (7) persistent headaches, and (8) 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. [8]

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. [9] 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. Twenty percent of athletes in football, soccer, and lacrosse suffer concussions each year. Detection, treatment, and prevention should be across all sports.

Separating neurologically based symptoms from psychologically based symptoms such as posttraumatic stress disorder (PTSD) can be difficult since both affect concentration, sleep, and irritability, and either can occur in accidents. Patients can also suffer from both PTSD and TBI.  

DSM-5 criteria

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: [10]

  1. The criteria are met for major or mild neurocognitive disorder (decline in cognitive ability: memory, concentration, processing speed).

  2. 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).

  3. 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.

Posttraumatic amnesia

Posttraumatic amnesia (PTA) refers to both retrograde amnesia (inability to recall what happened for a few minutes before the accident) and anterograde amnesia (not being able to form memories and being confused after the accident). 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. 

Second injury syndrome

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 a second head trauma. 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 contact sports who do not adequately rest after a concussion before participating in the sport.. The mechanism may be failed cerebral autoregulation with subsequent engorgement of the brain vasculature.

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. [11]  Diffusion tensor imaging frequently will show evidence of white matter damage when there are no observable problems on a standard MRI.

For example, Govindaraju et al examined volumetric proton spectroscopic imaging of the whole brain in mild TBI (mTBI) patients 1 month postinjury. [12] 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 [13] and that one can have a significant brain injury, yet have normal conventional structural imaging. This has also been shown by Gaetz et al. [14]

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 to 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 30 minutes of unconsciousness (GCS >13) or less than 24 hours of PTA in the absence of skull fracture. 

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. [15] 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. [16, 17]



Prognosis is variable. The Glasgow Coma Scale, period of unsconsciousness, and length of posttraumatic amnesia all provide 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. Of people who suffer a mild TBI, 85% recover in a few months.


Patient Education

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. Patients who do not recover in the first weeks can generally improve for 18 months.  

Online resources

The following websites may be helpful to patients: