Postconcussive Syndrome Psychiatric Care

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

Frequency

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.

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 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.

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:

• 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

• CDC, What is Traumatic Brain Injury?

• MayoClinic.com, Traumatic Brain Injury

• WebMD, Dementia in Head Injury

• For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. Also, see eMedicineHealth's patient education articles Dementia in Head Injury, Dementia Overview, Dementia Medication Overview, and Concussion.

Rapid improvement of head injury typically occurs within the first 6 months and often continues for 18 months. Problems continuing after 18 months usually continue indefinitely. Headache, dizziness, memory impairment, and fatigue are present in 30–50% of people during the first month after a mild head injury. In a prospective study of mild CHI conducted in Belfast, these symptoms disappeared within 6 months in 52% of cases and persisted in 16%. Of survivors, 32% reported a worsening of symptoms between 6 weeks and 6 months.

Significant functional impairment, marked by unemployment and marital dysfunction, typically accompanies postconcussive syndrome. In research populations, involvement in litigation plays a relatively small role in either the genesis or the resolution of patients' complaints.

Symptoms

Physical

Physical symptoms include:

• Headache

• Dizziness

• Fatigue

• Trouble sleeping

• Vision problems

• Discomfort with noise and light

• Seizures

• Assaultive behavior

• Sleep apnea

• Tinnitus

Cognitive

Cognitive or mental symptoms include:

• Memory problems

• Concentration/focusing problems

• Impulsivity

• Slowed processing of information

• Trouble putting thoughts into words

Emotional

Emotional symptoms include:

• Depression

• Anger outbursts and quick to anger

• Anxiety (fear, worry, or feeling nervous)

• Personality changes

• Apathy

Rating scales can help assess and track symptoms, including the following:

• Beck Depression Index or PHQ-9

• Apathy Evaluation Scale (AES) and Apathy sub-scale of the Frontal Systems Behavior Scale (FrSBe-A) 

• Global Assessment of Migraine Severity (GAMS) and Migraine Disability Scale (MIDAS)

Obtain information from patients, ambulanc hospital records about the injury, the immediate sequelae including unconsciousness and seizures, and the medical treatment received.[17, 18]

Rates of apathy have been assessed to be occur in 23–71% of patients; it results from disruption of frontal-subcortical pathways. 

Neuropsychological testing is the most sensitive means of characterizing the cognitive deficits of survivors of head injury.

Neurologic examination should include special attention to the following:

• Cranial nerves: Anosmia stems from damage to the olfactory tracts, confirming injury to the limbic system. Visual-field mapping may identify damage to the optic nerves. Nystagmus may reflect subtle labyrinth injury.

• Weakness: Hemiparesis may reflect diffuse axonal injury (DAI).

• Cerebellar signs include dysmetria and nystagmus.

• Signs of parkinsonism, including tremor, cogwheeling, and abnormal gait, confirm damage to the basal ganglia.

• Mental status examinations should be conducted repeatedly, with the date and time carefully noted, to follow changes over time.

• Mental status:

  • Orientation: Patients with postconcussive syndrome may or may not be oriented to time and place. Disorientation is a very serious sign.

  • Appearance: Grooming and hygiene are usually intact, but in severe cases self-care declines.

  • Affect and mood: Depression, anxiety, labile mood, irritability or apathy may be present.

  • Speech: Fluidity may be impaired.

  • Concentration: Concentration is often significantly impaired.

  • Memory: Short-term memory and ability to learn new things is often impaired. Remote memory is intact.

  • Psychomotor activity: Patients are often slowed up but could be agitated from lack of control and stress.

  • Energy: Patients are easily fatigued.

  • Sleep: Patients are often disordered.

  • Headache: Headache is often present.

  • Dizziness or vertigo: Dizziness or vertigo is often present.[19]

  • Suicidal ideation: Suicidal ideation is a significant consideration in severe cases.

  • Homicidal ideation: Homicidal ideation is not typically associated with patients with postconcussive syndrome.

  • Delusions and hallucinations: Delusions and hallucinations are not part of the syndrome.

  • Comprehension: Comprehension may be impaired in severe cases.

  • Insight: Insight is variable.

  • Judgment: Patients with postconcussive syndrome may have impaired judgment from impaired cognitive abilities.

Causes of head injury in civilian populations include the following:

• Car accidents (50%)

• Falls (21%)

• Assault (12%)

• Recreational activity (10%)

Roughly 50% of these injuries are associated with alcohol use.

In children, bicycle accidents are a significant cause of head injury. Lacrosse, football, and soccer are the most dangerous sports. Simply repeatedly heading balls in soccer practice is harmful.

Among infants, most injuries reflect child abuse.

Elderly patients are especially vulnerable to falls.

Increased survival following severe injury contributes to the increasing overall number of people in need of treatment for late sequelae.

Complications of postconcussive syndrome include the following:

• Memory problems

• Concentration problems

• Irritability

• Sleep problems

• Impaired cognition

• Impaired multitasking

• PTSD

• Anxiety

• Depression

• Suicide attempts

• Subdural and epidural hematomas

• Seizures

• Early-onset dementia

• Personality changes

• Impulsivity

• Aggression

• Exacerbations of preexisting psychiatric disorders, including preexisting dementia

CT scan may show a fracture across the middle meningeal artery, or shifts in the brain from bleeds.

MRI scans are more sensitive than CT scans.

Diffusion tensor imaging is far better at showing white matter damage that can result from head trauma.[20]

Quantitative EEG may be helpful.[21]

Neuropsychological testing can help in the assessment of impairment after a head injury. 

Head trauma, rapid acceleration and deceleration of the brain can damage axons. A cascade of damage can occur.

Glasgow Scale

The Glasgow Scale is frequently used to assess the severity of the initial injury. It consists of measurements of eye, verbal, and motor responses. The total score is found by summing the numbers for the three tests. GCS ≥ 13 is defined as minor, GCS 9–12 is defined as moderate, and GCS ≤ 8 is considered severe (coma). 

Eyes

1. No eye opening
2. Eye opening in response to pain
3. Eye opening to speech
4. Eyes opening spontaneously

Verbal response

1. No verbal response
2. Incomprehensible sounds
3. Inappropriate words (no conversational exchange)
4. Confused (the patient responds to questions coherently but there is some disorientation and confusion)
5. Oriented

Motor response

1. No motor response
2. Extension to pain
3. Abnormal flexion to pain
4. Flexion/Withdrawal to pain
5. Localizes to pain (purposeful movements towards painful stimuli)
6. Obeys commands (the patient does simple things as asked) 

The individual should rest for several days. The degree of rest is debated, but standard recommendation is minimal stimulation.[22]  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 with hyperbaric oxygen both immediately after the injury and later on.[6, 7]

Indications for hospitalization include (1) severe or fluctuating neurologic symptoms that could indicate epidural or subdural hematoma, (2) patients who do not have someone to help and observe them, should they deteriorate in the first day after trauma, and (3) for suicidal/homicidal ideation. Some studies suggested a lower incidence of postconcussive syndrome in those who were hospitalized, possibly because of greater rest after the injury or because of more intensive explanation of symptoms leading to less anxiety and stress.

Patients benefit from psychological support and, when indicated, behavioral modification, cognitive rehabilitation, psychotropic medication for specific syndromes or symptoms, family or network intervention, social services, and medical support in legal proceedings.

Therapy involves helping patients and their families be realistic about their losses and impairments, while encouraging hope and continued effort in rehabilitation. Helping patients and caregivers to interpret subtle and disruptive changes in personality in light of organic damage is particularly important to relieve guilt and blame.

Psychological support

Damage to the brain impairs a person's ability to cope at a time when the need to adapt is greatest. Demoralization, depression, anger, anxiety, and irritability are likely.

The meaning of any injury varies in part based on the patient's prior concerns and personality. For example, narcissistic patients feel narcissistically wounded by even minor losses of function. Prior emotional lability or capacity for aggression in a patient who is borderline may worsen following a head injury.

Injury when a person is in transition or moving towards an important goal, such as marriage, school completion, or job performance, has a different meaning than injury occurring when someone feels stable, stagnant, or deteriorating. Injuries that occur on a job a person already dislikes or injuries that result from negligence may evoke resentment and feelings of entitlement that are absent in similar injuries in other circumstances.

Understanding the person's preinjury personality, stresses, and the circumstances of the injury help establish realistic goals and minimize stress during rehabilitation and reentry into life. Interpreting the person's reactions to injury in light of his or her previous state builds trust, reflecting the degree to which the patient feels understood and accepted.

Avoid interpreting changes in personality or behavior in light of developmental issues or conflicts without considering the impact of the injury itself. Such interpretations may produce confusion, guilt, unnecessary resentment, and fatalism. A present-oriented, problem-focussed therapy generally is best for patients after head injury, even those whose impairment appears to be driven by exaggerated emotional responses to the experience.

Different stages of recovery require different types of psychological support. In the first months after injury, validating symptoms, helping patients relinquish responsibilities, mourning losses of function or hopes, and counseling patience with the pace of improvement are critical. Later, patients may need encouragement to push themselves to regain self-confidence and reassume their previous roles and responsibilities.

Behavior modification

Behavioral techniques may be used to discourage impulsivity, aggression, and socially inappropriate behavior. They may also encourage patients to be less apathetic or withdrawn.

Teaching sleep hygiene is important.

Cognitive rehabilitation

The underlying principles are encouraging recovery in functions that are capable of improvement, compensation for areas of fixed deficit, and teaching substitute means of achieving particular ends. For example, gradually increasing time spent reading helps a patient both regain concentration and develop confidence in his or her ability to concentrate. Keeping lists allows a patient to compensate for decreased memory. Someone who has become dysarthric or aphasic may learn sign language as a substitute means of communication.

In general, cognitive rehabilitation is based on neuropsychological testing that clarifies deficits and suggests areas of preserved functioning in patients with dementia. Patients with postconcussive syndrome also have cognitive complaints, usually decreased attention and concentration. These symptoms may reflect slowly or partially reversible damage to white matter from DAI. Decreased attention and concentration seriously worsen anxiety and otherwise compromise patients' efforts to recover. When impaired concentration and attention are prominent in a patient with PCS, cognitive rehabilitation may be quite helpful.

Family or network intervention

The changes in personality, especially apathy, irritability, and aggression, in patients with head injury are especially burdensome to caregivers, family, or professional care providers. Head injuries cause more family distress than bodily injuries of equivalent severity. Counseling for caregivers is essential. When the patient is demented, interpreting impairments as organic and insisting on the legitimacy of the sick role are needed to relieve blame and guilt.

Even when the caregiver understands the person's behavior is not within his or her control, the patient's slowness, inappropriateness, and erratic responsiveness can be exasperating or even frightening. Family members become isolated from usual support, especially when the person's impairments are severe, protracted, or fixed. Direct communication between the caregiver and the physician allows caregivers to vent their feelings and voice their concerns. Problem-solving interventions and referral to support groups for family members improve morale and enhance patient outcome. Regular staff or team meetings sustain morale in professional caregivers.

Social services

Case management for patients with dementia sometimes is necessary to help patients apply for disability, locate specialized rehabilitation programs, attend to medical problems, and participate consistently in treatment.

When people have prominent severe problems of information procession or frontal lobe deficits manifested by impulsivity and poor judgment, they may be incompetent to make medical decisions or handle their own affairs. These 2 functions may differ. Guardianship, conservatorship, or some other protective legal arrangement may be needed. Physician evaluation typically is required, unless the person is competent enough to sign a power of attorney or designate a substitute payee.

Medical support in legal proceedings

Head injuries often occur in the context of car or workplace accidents, leading to legal proceedings for damages and compensation. The prognosis of mild or moderate dementia and postconcussive syndrome remain difficult to provide with certainty. Some patients recover fully from severe injuries with prolonged coma, others remain disabled for long periods after much milder insults. Moreover, involvement in legal proceedings seems to complicate recovery. Having to repeat the story of an injury to questioners, not knowing what expenses will be incurred and which will be covered by insurance, and proving the reality of impairment without visible scars increase patients' stress and anxiety. Stress seems to slow or impede recovery by both psychological and physiological mechanisms. Malingering also may occur.

Consultations with neuropsychologists and physical and occupational therapists are helpful in designing long-term treatment plans for patients with head injury.

Neurologic consultation is essential to diagnose and treat seizures, subdural or epidural hematomas, or hydrocephalus. Neurologists also may help with the management of headaches, dizziness, or fatigue.

Consult primary care physicians to ensure that concurrent medical conditions are not neglected.

Omega 3 supplementation is often recommended.

Antioxidents, Mg, Zinc, Vitamin D, B12, and all B vitamins are being studied.[23]

Expectations for school and work may need to be adjusted until, if and when, the person adequately recovers. Poor concentration and memory make school difficult and may not only impair work performance but may make it dangerous. Extra care needs to be taken in all activities that present a risk of injury since the person's functioning (and possibly judgment) are likely impaired increasing the risk beyond pre-injury levels. Victims may not fully appreciate their limitations and may need outside support to make good judgments.

Finally, patients who play contact sports should not be allowed to return to play until their concussive symptoms have resolved completely.[24] Failure to observe this restriction exposes these patients to the risk of sudden death from second impace syndrome (SIS).

It is generally recommended that the patient have a few days of complete rest followed by gradual increase in activities.[4]

Primary prevention of head injury involves the use of protective gear in contact sports, seat belts, bicycle and motorcycle helmets, and hard hats in appropriate jobs. For soccer, players should avoiding heading the ball.

For elderly patients, altering the environment to minimize the risk of falls is important.

Early detection of child abuse may prevent a head injury.

Avoiding risk factors such as reckless behavior, drinking/using drugs and driving, and dangerous sports aids prevention.

Some patients with head injury are parasuicidal. They may benefit from treatment of depression, character disorders, and other conditions associated with suicide.

Delaying return to sports for athletes with a head injury helps prevent sudden injury syndrome and death.

Hypothermia during the period of coma may mitigate tissue damage. 

Patients should be evaluated for co-morbid PTSD.  

Patients may need support and concrete help with work, school, and significant others so that they can understand the patients current limitations and prognosis.

Early-onset dementia should be periodically assessed.

N-acetylcysteine given in the hours after a TBI may decrease oxydative damage and speed healing.[25]

Patients with head injury may require treatment with psychotropic medication for the specific symptoms of which the patient is suffering. These symptoms include irritability, headaches, insomnia, apathy, and, in rare cases, psychosis.

Brain damage renders patients more sensitive to adverse anticholinergic effects, seizures, and drug-induced parkinsonism. Slower than normal titration may be needed.

Dopamine-blocking agents (eg, haloperidol) and adrenergic-blocking agents (eg, clonidine, prazosin) compromise brain tissue repair in animal laboratory models. Dopamine-potentiating agents (eg, dextroamphetamine) enhance recovery in animal models. These effects have not been documented in humans with head injury, although alpha-blockers, haloperidol, and benzodiazepines may adversely affect functional outcome after strokes.

According to an FDA advisory, atypical antipsychotic drugs of various classes (including aripiprazole, risperidone, quetiapine, olanzapine) increase mortality when given for behavioral disorders in patients who are elderly and have dementia. The implication of these findings for the treatment of dementia or behavioral disorders after head injury are unknown. In the studies cited by the FDA, the excess mortality reflected deaths from infections and heart disease, conditions more common in the elderly population than in the younger population of patients with head injury.

Practitioners should be aware, at minimum, that the use of antipsychotic drugs for conditions other than schizophrenia and mania is off-label and should be carefully monitored.