eMedicine Specialties > Psychiatry > Psychosomatic
Postconcussive Syndrome
Updated: Oct 1, 2008
Introduction
Background
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.
Separating neurologically based symptoms from psychologically based symptoms such as posttraumatic stress disorder (PTSD) or adjustment disorder can be difficult.
DSM-IV-TR 1 criteria outline for postconcussional disorder
- 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 easily2. Disordered sleep
- 3. Headache4. Vertigo or dizziness5. Irritability or aggression on little or no provocation6. Anxiety, depression, or affective lability7. Changes in personality (eg, social or sexual inappropriateness)8. Apathy or lack of spontaneity
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.
Pathophysiology
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.2
For example, Govindaraju et al examined volumetric proton spectroscopic imaging of the whole brain in mild TBI (mTBI) patients 1 month postinjury.3 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 injury4 and that one can have a significant brain injury, yet have normal conventional structural imaging. This has also been shown by Gaetz et al.5
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. In 1968, a study by Lishman of 670 patients with either closed or penetrating head injuries yielded the following relationships between PTA and psychiatric disability or cognitive impairment.
Relationship Between Posttraumatic Amnesia and Psychiatric Disability or Cognitive Impairment| Impairment | PTA <1 h, % patients | PTA <7 d, % patients | PTA > 7 d, % patients |
|---|---|---|---|
| No psychiatric disability | 67 | 18 | 15 |
| Mild disability | 52 | 19 | 29 |
| Severe disability | 28 | 22 | 50 |
| No cognitive impairment | 65 | 18 | 17 |
| Mild cognitive impairment | 45 | 21 | 34 |
| Severe cognitive impairment | 16 | 12 | 72 |
The numbers may have changed somewhat since 1968 due to improved survival and better means of assessment. Nevertheless, these data describe relationships that remain valid. 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 PCS.
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.
Clinical
History
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 PCS. In research populations, involvement in litigation plays a relatively small role in either the genesis or the resolution of patients' complaints.
- Patients treated for sequelae of head injury should be screened for the development or recurrence of any major psychiatric syndrome, with specific screening for the following:
- Depression (See Medscape's Depression Resource Center.)
- Anxiety
- Mania
- Psychosis
- Obsessive-compulsive symptoms
- Impulsivity
- Suicide risk
- Homicide risk: Because of their impulsivity and impatience, persons with head trauma can be combative to others, including family members and caregivers.
- Standard rating scales, especially the Hamilton Depression Rating Scale and the Positive and Negative Symptom Scales, are sometimes useful.
- Also inquire about subsyndromal complaints and nonspecific somatic distress, especially fatigue and headache. These, along with irritability, anxiety, apathy, and dysphoria, are cardinal features of PCS. Seizure phenomena, especially partial-complex seizures, should be explored specifically.
- The nature and severity of head trauma affect the nature and severity of sequelae. Obtain information from patients and usually from their hospital records about the injury, the immediate sequelae including unconsciousness and seizures, and the medical treatment received.
- Neuropsychological testing is the most sensitive means of characterizing the cognitive deficits of survivors of head injury.
Physical
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. Remove 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.
- 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
- 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, a clear indication for the need to wear a helmet when riding a bicycle.
- 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.
Differential Diagnoses
Other Problems to Be Considered
Differential or comorbid diagnoses of postconcussional syndrome
Posttraumatic stress disorder (PTSD)
Depression
Adjustment disorders
Attention deficit hyperactivity disorder (ADHD)
Conversion disorder
Malingering
Subdural hematoma
Many head injuries occur in situations that may lead to litigation and compensation, a source of motivation for secondary gain. Dissatisfaction with a work or family situation also may prompt a person to magnify or create symptoms after a head injury.
Workup
Imaging Studies
- Other than collecting hospital records and neuropsychological testing, specialized workup may require the following:
- Serial sleep-deprived electroencephalograms can be used to diagnose seizures, and a quantitative EEG may show abnormalities in postconcussive syndrome.
- CT scan performed 1-3 months after injury may detect cerebral contusions not visible immediately.
- MRI scans are more sensitive than CT scans in demonstrating DAI and frontal and temporal lesions.
- Single-photon emission computed tomography (SPECT) scan is a relatively accessible form of functional imaging that, in the future, may prove the most sensitive measure of white matter lesions. Further research is needed to correlate such lesions with their clinical effects.
Other Tests
Neuropsychological testing is the most reliable way to document and quantify cognitive impairments following head injury.
Histologic Findings
The pathophysiology of CHI results from contusions and DAI. DAI occurs in high-velocity trauma, especially trauma with an element of twisting or rotation. The shearing forces of impact cause axons to stretch and break. Disruption of axons triggers a cascade of further insults, including calcium influx, excitotoxin release, phospholipase activation, and lipid peroxidation (see Pathophysiology).
Staging
Head injury severity is rated based on the GCS and the GOAT results. Severity of sequelae may be rated on the Ranchos Los Amigos Cognitive Scale or the Neurobehavioral Rating Scale.
Treatment
Medical Care
Indications for hospitalization include (1) severe or fluctuating neurologic symptoms that could indicate epidural or subdural hematoma, (2) if a patient does 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. Patient with PCS 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 PCS 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 subtle 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
- Consultations with neuropsychologists and physical and occupational therapists are helpful in designing or altering the long-term treatment plan of a patient 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.
Diet
- Patients with impairment in their ability to prepare food or feed themselves must have their diets monitored to be sure that they do not become malnourished or vitamin deficient.
- Otherwise, no special dietary prescriptions or restrictions apply.
Activity
- In the early phases of rehabilitation, simple, graduated physical exercises and games may improve endurance and self-confidence. Head injuries may lead to ataxia, parkinsonism, hemiparesis, or paraparesis, requiring mobility aids and monitoring. In elderly patients, altering the environment to prevent falls is important to prevent repeat injuries.
- Recommending that patients resume normal activities or responsibilities is not always simple. Patients who work night-shift jobs, work with heavy machinery, work off the ground, or who are in overstimulating environments may not be able to return to their previous positions. Returning to work when cognitive impairments are in flux may lead to failure and regression in recovery. However, patients also may be unduly reluctant to return to previous activities for fear of further injury, embarrassment about their disabilities, and underestimation of their competence. Encouraging gradual return to work or requesting temporary accommodations that allow patients to relearn or reacclimate to their jobs often is helpful, although not always possible.
- Finally, patients who play contact sports should not be allowed to return to play until their concussive symptoms have resolved completely. Failure to observe this restriction exposes these patients to the risk of sudden death from SIS.
Medication
Patients with head injury may require treatment with psychotropic medication for depression, mania, psychosis, aggression, irritability, emotional lability, insomnia, apathy, or impaired concentration. Headaches also may respond to psychopharmacologic treatment.
Brain damage renders patients more sensitive to adverse anticholinergic effects, seizures, and drug-induced parkinsonism. Doses in the usual therapeutic range may be needed to relieve target symptoms, especially for depression and mania; however, initiate at lower doses and titrate upward more slowly than in other patients under psychiatric care.
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 a recent 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.
Drug treatments for patients with brain injury are extrapolated from studies of patients after stroke or other types of brain damage. These patients may not be comparable to patients with head injuries, especially those with diffuse axonal injury (DAI). Clinical trials in patients with head injury are typically small. No broad consensus or established guidelines exist regarding psychotropic drug treatment after head injury.
Specific target symptoms and appropriate medications include the following:
- Depression - Selective serotonin reuptake inhibitors (SSRIs), nefazodone, bupropion, nortriptyline
- Insomnia - Trazodone, mirtazapine
- Mania - Valproic acid, carbamazepine, lithium
- Emotional lability (eg, pathological laughing, crying) - Bromocriptine, nortriptyline, fluoxetine
- Psychosis - Olanzapine, quetiapine, aripiprazole, ziprasidone, risperidone, haloperidol
- Hypoarousal - Dextroamphetamine, methylphenidate
- Poor concentration (eg, apathy, fatigue) - Methylphenidate, bromocriptine, amantadine, levodopa and carbidopa (improvement may not be sustained)
- Chronic aggression and irritability - Antiepileptic drugs, SSRIs, olanzapine
- Headaches - Amitriptyline, nonsteroidal anti-inflammatory drugs (NSAIDs), antimigraine drugs
- Anxiety - Buspirone
Acute agitation or aggression may be treated with benzodiazepines; however, first-line treatment of chronic symptoms includes drugs having less sedative effects or impact on cognition. Avoid phenobarbital for treating seizures due to sedation. Over-the-counter anticholinergic hypnotics are not to be used for patients with head injury.
Antidepressants
Treatment of depressive syndromes due to traumatic brain injury. Indications include signs and symptoms of major depression with or without psychosis, dysthymia, or adjustment disorder.
SSRIs are the antidepressants of choice due to minimal anticholinergic effects. All are equally efficacious. The choice depends on adverse effects and drug interactions. SSRIs also are used to treat behavioral disturbances resulting from head trauma.
Tricyclic antidepressants (TCAs) are used when unable to use SSRIs. Their unfavorable adverse effect profile prompted development of newer antidepressants. Advantages include ability to obtain blood levels, thus ensuring therapeutic response and avoiding toxicity. Prior to initiating, obtain ECG and blood pressure.
Newer antidepressants useful for sleep disturbances include trazodone and mirtazapine. They are structurally unrelated to TCAs, tetracyclics, or MAOIs. Cardiac conduction effects of trazodone are qualitatively dissimilar and quantitatively less pronounced than TCAs and therefore are less toxic in overdose.
Fluoxetine (Prozac)
Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in the reuptake of norepinephrine or dopamine.
Dosing
Adult
10 mg/d PO every am; increase after several wk to 20 mg/d; may increase further as tolerated; not to exceed 80 mg/d
Pediatric
<18 years: Not established
>18 years: Administer as in adults
Interactions
Inhibits CYP3A4; thus, increases toxicity of isoenzyme substrates (eg, diazepam, trazodone, TCAs) by decreasing clearance; increases toxicity of MAOIs, wait at least 10 d after discontinuing MAOIs to initiate fluoxetine, wait at least 5 wk after discontinuing fluoxetine to initiate MAOIs; may displace highly protein-bound drugs (eg, warfarin); serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) may occur when coadministered with full doses of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); however, cautious use of small doses of agents such as trazodone for sleep or buspirone for anxiety may be effective; close monitoring for emergence of serotonergic adverse effects is warranted
Contraindications
Documented hypersensitivity; MAOIs
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hepatic impairment (adjust dose) and history of seizures; common adverse effects include headache, somnolence, nervousness, dizziness, nausea, diarrhea, xerostomia, general weakness, and sexual dysfunction; symptoms of weakness, lethargy, headache, anorexia, weight gain, confusion, or constipation may indicate hyponatremia
Citalopram (Celexa)
Enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane. No head-to-head comparisons of SSRIs exist, although, based on metabolism and adverse effects, citalopram is considered SSRI of choice for patients with head injury.
Dosing
Adult
20-60 mg PO qd; 10 mg/d initially, titrate by 10 mg/wk
Pediatric
Not established; child psychiatrists treating patients with head injury recommend starting with half the usual adult dose when using drugs for which pediatric dosages have not been established
Interactions
Serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan), discontinue other serotonergic agents at least 2 wk prior to SSRIs; low doses of SSRIs and buspirone or trazodone may be combined if carefully monitored; may be potentiated by azole antifungals, omeprazole, and macrolides
Contraindications
Documented hypersensitivity, concurrent MAOI therapy
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cirrhosis (adjust dose), suicidal tendencies, SIADH, DM, seizure disorders, orthostasis, and breastfeeding; common adverse effects include fatigue, GI toxicity, and sexual dysfunction
Amitriptyline (Elavil)
Tricyclic tertiary amine. Inhibits neuronal reuptake of serotonin and/or norepinephrine at presynaptic neuronal membrane, which increases concentration in the CNS. Highly anticholinergic, although considered one of the best-studied antidepressants. Use for chronic pain, including headache. Doses for chronic pain are one-half to one-third of those for depression.
Dosing
Adult
10-25 mg PO hs initially; may increase gradually to desired effect; not to exceed blood level >150 ng/mL
Pediatric
Children: 0.05 mg/kg PO hs initially, gradually increase over 2-3 wk to 0.25-1 mg/kg PO hs
Adolescents: 3-5 mg/kg PO hs initially, gradually increase to 10 mg PO tid
Interactions
Phenobarbital may decrease effects; coadministration with CYP2D6, CYP3A4, or CYP2C9 inhibitors may increase amitriptyline levels; additive effect with drugs prolonging QT interval (eg, sotalol, amiodarone, gatifloxacin); inhibits hypotensive effects of guanethidine; increases toxicity of alcohol, disulfiram, and warfarin
Contraindications
Documented hypersensitivity; concurrent MAOI or use within 14 d of MAOI; do not use during acute recovery phase of MI
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Use nortriptyline (amitriptyline active metabolite) if anticholinergic effects intolerable; cautious use in seizures, suicidal ideation, arrhythmias, orthostasis, angle-closure glaucoma, urinary retention, hepatic dysfunction (adjust dose), or hyperthyroidism
Nefazodone (Serzone)
5-HT2–receptor antagonist and inhibits the reuptake of 5-HT. Negligible affinity for cholinergic and histaminergic receptors. Does not suppress REM activity, unlike other antidepressants. Decreases light-stage sleep and frequency of awakenings.
Dosing
Adult
50 mg PO bid initially, gradually increase at weekly intervals to 200-500 mg/d PO divided bid; not to exceed 600 mg/d
Pediatric
Not established
Interactions
Inhibits CYP3A4, thus increasing serum levels of substrates (eg, carbamazepine, cyclosporine, triazolam); increased risk of serotonin syndrome with other serotonergic drugs (eg, SSRIs, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); decreases effect of anticoagulants, oral hypoglycemics, diuretics, clonidine, and methyldopa; increased toxic effects of digoxin and MAOIs; increased risk of myopathy and rhabdomyolysis with HMG Co-A inhibitors (eg, pravastatin, simvastatin); may enhance response to alcohol, barbiturates, and other CNS depressants
Contraindications
Documented hypersensitivity, MAOI within 14 d of initiating treatment; concurrent administration with pimozide
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in preexisting cardiac disease, hepatic dysfunction (adjust dose), initial recovery phase of MI, and priapism; common adverse effects include hypotension (including orthostatic hypotension and syncope), drowsiness, dizziness, or blurred vision; caution patient regarding tasks requiring alertness, coordination, or dexterity
Trazodone (Desyrel)
5-HT2–receptor antagonist that inhibits reuptake of 5-HT. Negligible affinity for cholinergic, adrenergic, dopaminergic, or histaminic receptors. Good hypnotic properties. Effective in reducing agitation in patients with head trauma or dementia.
Dosing
Adult
25-50 mg PO hs initially, gradually increase by 50 mg/d q3-7d to sedating effect; not to exceed 400 mg/d
Pediatric
Not established
Interactions
May enhance response to alcohol, barbiturates, and other CNS depressants; may increase digoxin and phenytoin serum levels; may decrease hypoprothrombinemic effects of Coumadin; increased risk of serotonin syndrome with other serotonergic drugs (eg, SSRIs, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); may increase hypotensive effects of antipsychotics; drugs inhibiting CYP2D6 (eg, fluoxetine) may decrease trazodone metabolism
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in preexisting cardiac disease, initial recovery phase of MI, and priapism; common adverse effects include hypotension (including orthostatic hypotension and syncope), drowsiness, dizziness, or blurred vision; caution patient regarding tasks requiring alertness, coordination, or dexterity
Dopaminergic agents
Enhancing dopamine function may improve concentration, attention, and interest in patients after head injury. Dopaminergic drugs include bromocriptine, amantadine, and levodopa/carbidopa. Animal studies demonstrate that dopamine function enhancement may have neuroprotective effects. Bromocriptine combined with antidepressants has been used for pathological emotional lability. The most potent dopaminergic drug is levodopa; therefore, it also produces the highest toxicity (see Parkinson Disease Dementia). Other drugs should be tried first. Stimulants (eg, dextroamphetamine, methylphenidate) also enhance dopamine function. Stimulants and direct or indirect dopamine agonists affect dopamine pathways differently, despite similar mechanisms of action.
Bromocriptine (Parlodel)
Semisynthetic ergot alkaloid derivative. Strong dopamine D2-receptor agonist. Partial dopamine D1-receptor agonist.
Dosing
Adult
1.25 mg (one-half of 2.5-mg tab) PO pc bid, increase by 2.5 mg/d q2-4wk prn; usual dosing range is 10-40 mg/d; not to exceed 100 mg/d
Pediatric
Not established
Interactions
Additive toxicity may increase with ergot alkaloids, amitriptyline, butyrophenones, imipramine, methyldopa, phenothiazines, and reserpine; antipsychotics may decrease effect; sympathomimetics and erythromycin may increase effect
Contraindications
Documented hypersensitivity, severe ischemic heart disease, severe peripheral vascular disorders
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hypotension, CNS toxicity, GI toxicity, or leg cramps; caution in hepatic disease (adjust dose) and breastfeeding
Dextroamphetamine (Dexedrine)
Increases circulating dopamine and norepinephrine in cerebral cortex by blocking reuptake of norepinephrine or dopamine from synapse.
Dosing
Adult
5-30 mg/d PO 30-60 min ac in divided doses
Pediatric
<3 years: Not established
3-5 years: 2.5 mg PO every am initially, increase by 2.5 mg/d qwk to response
>5 years: 5 mg qd or bid, increase by 5 mg/d qwk to response; not to exceed 40 mg/d
Interactions
Coadministration with MAOIs may precipitate hypertensive crisis; coadministration with anesthetics may precipitate arrhythmias; may increase toxicity of phenobarbital, propoxyphene, meperidine, TCAs, phenytoin, and norepinephrine
Contraindications
Documented hypersensitivity, hypertension, MAOIs used within 14 d, advanced arteriosclerosis, hyperthyroidism, glaucoma, diabetes mellitus, hyperthyroidism
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in angina, glaucoma, cardiovascular disease, and psychopathic personalities; may worsen Tourette syndrome or other disorders with motor tics
Antipsychotic agents
Treatment of hallucinations, ideas of reference, delusional preoccupation, and agitation. Older antipsychotics with strong anticholinergic adverse effects (eg, chlorpromazine, thioridazine) may worsen cognitive function. Potent conventional antipsychotics (eg, haloperidol) have been used in patients with dementia with psychotic symptoms. While these drugs are effective, patients with brain damage are more susceptible to drug-induced parkinsonism. Haloperidol produces high levels of parkinsonian symptoms and risk of irreversible syndrome of tardive dyskinesia.
New antipsychotic drugs (eg, risperidone, olanzapine) may have particular efficacy in treating agitation and psychosis in patients with Alzheimer disease and for cognitive symptoms in schizophrenia. However, these drugs, along with atypical antipsychotic drugs of other classes (eg, aripiprazole, quetiapine) may also increase mortality from infection and heart attacks in older patients with dementia. Taken together, these findings suggest that patients with head injuries may benefit from these drugs, but they should be used with caution and carefully monitored. The adverse effects of somnolence, dizziness, and unsteady gait are of particular concern in patients with head injury. The known potential of many antipsychotic drugs to cause hyperglycemia, weight gain, and type 2 diabetes mellitus is of concern in every patient group.
The atypical antipsychotic drugs olanzapine and ziprasidone are available to be administered parenterally, as may occasionally be needed in an emergency to control agitation or when patients have met local legal standards for the involuntary use of psychotropic medication. Behavioral interventions, such as controlling stimulation or engaging the patient verbally, may allow for the voluntary use of oral medication, which is preferable in all but the most imminently dangerous situations.
Risperidone (Risperdal)
Binds to dopamine D2-receptor with 20 times lower affinity than for 5-HT2-receptor. Improves negative symptoms of psychoses and lowers incidence of extrapyramidal adverse effects.
Dosing
Adult
0.5 mg PO qd initially, gradually increase to optimum range of 4-8 mg/d; not to exceed 10 mg/d
Pediatric
Not established
Interactions
Carbamazepine may decrease serum levels; clozapine may increase serum levels; may antagonize levodopa effects
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause extrapyramidal reactions (especially > 6 mg/d); hypotension/orthostasis, tachycardia, arrhythmias, amenorrhea, galactorrhea, sexual dysfunction, GI toxicity, cholestatic jaundice
Quetiapine (Seroquel)
May act by antagonizing dopamine and serotonin effects.
Dosing
Adult
25 mg bid/tid initially, gradually increase (patients with head injury require a slower upward titration than usually is recommended) to 300-400 mg/d divided bid/tid; not to exceed 750 mg/d
Pediatric
Not established
Interactions
May antagonize levodopa and dopamine agonists; CYP3A4 inducers (eg, phenytoin, thioridazine) may reduce levels; CYP3A4 inhibitors (eg, itraconazole, erythromycin) may increase levels; may decrease warfarin clearance, monitor aPTT
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May induce orthostatic hypotension associated with dizziness, tachycardia, and syncope; neuroleptic malignant syndrome has been reported; caution with seizures, cerebrovascular disease, and hepatic dysfunction (adjust dose); common adverse effects include somnolence, agitation, headache, and dizziness
Olanzapine (Zyprexa)
May inhibit serotonin, muscarinic, and dopamine effects.
Dosing
Adult
5 mg PO initially, increase as tolerated, not to exceed 10 mg
Higher doses, while sometimes needed for the treatment of psychosis, have not been more effective than placebo in dementia patients with Alzheimer disease
Pediatric
Not established
Interactions
Fluvoxamine may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease effects
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration
Antiepileptic drugs
Behavioral disturbances (eg, chronic aggression, agitation) are severe complications of head injury. Pharmacological agents used to treat these behaviors include antiepileptic drugs, SSRIs, and beta-blockers.
Carbamazepine (Tegretol)
Originally indicated for the treatment of epilepsy involving the temporal lobes. Became known as a mood stabilizer in 1970s when Japanese researchers found it to be helpful in patients with bipolar disease who were refractory to lithium.
Used for reducing frequency and severity of manic and depressive components of bipolar disorder. Not considered first-line treatment. Used to stabilize episodic aggressive behavior.
Double-blind studies have demonstrated moderate effect in decreasing aggressive behavior in patients with dementia and those with impulse control disorders.
Case studies describe effect in patients with seizures or previous head injury. Serum levels of 8-12 mcg/mL may lessen impulsivity, irritability, and hostility in patients with cognitive disorders.
Dosing
Adult
IR: 50-100 mg PO tid initially, gradually titrate to response by 200 mg/d qwk to 300 mg PO qid; not to exceed blood level >12 mcg/mL
ER: Total daily dose divided bid
Pediatric
50 mg PO bid (suspension: 25 mg PO qid) initially; gradually increase qwk by 50 mg/d until desired effect; not to exceed blood levels >12 mcg/mL
Interactions
Induces its own metabolism; therefore, half-life declines over 1 mo from 36 h to 10-20 h, adjust dose accordingly; serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister within 14 d of MAOIs; cimetidine may increase toxicity, especially within first 4 wk of therapy; may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)
Contraindications
Documented hypersensitivity, history of bone marrow depression, administration of MAOIs within last 14 d
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Cross-sensitivity with TCAs; obtain CBCs, LFTs, and serum iron prior to treatment, during the first 2 mo, and yearly thereafter; monitor low-normal or below normal WBC counts and neutrophil counts q2wk for the first 3 mo; thereafter, individualize monitoring based on previous results, discontinue if WBC <3000/mm3 or neutrophils <1000/mm3; recommend target blood levels of 4-8 mcg/mL in patients with head injury; caution with increased intraocular pressure; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; other adverse effects include Stevens-Johnson syndrome, hepatitis, nausea, ataxia, and pancreatitis
Valproic acid (Depacon, Depakene, Depakote)
Mechanism of action is not established, although activity may be related to increased brain levels of gamma-aminobutyric acid (GABA) or enhanced GABA action. May potentiate postsynaptic GABA responses, affect potassium channel, or have a direct membrane-stabilizing effect. Anticonvulsant used for mood stabilization in patients with head injury. Used in treatment of bipolar disorder. Effective in management of agitation and aggression in patients with dementia. Specific therapeutic range has not been defined for management of aggression. Available in capsules, tablets, syrup, and sprinkles.
Dosing
Adult
125 mg PO tid initially; not to exceed blood level >100 mcg/mL; lower doses required compared to treatment of mania or seizures
Pediatric
5-10 mg/kg/d initially, gradually titrate to response; not to exceed blood level >100 mcg/mL
Interactions
Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations; valproate may increase diazepam and ethosuximide toxicity (monitor closely); may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; may displace warfarin from protein-binding sites (monitor coagulation tests); may increase zidovudine levels in patients who are HIV seropositive
Contraindications
Documented hypersensitivity, hepatic disease
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Thrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations >110 mcg/mL in females and >135 mcg/mL in males; at periodic intervals and prior to surgery, determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or a hemostasis/coagulation disorder occurs; hyperammonemia may occur, resulting in hepatotoxicity
Use in patients receiving multiple drugs increases risk of hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness; caution in renal disease, Addison disease, blood dyscrasias, and organic brain disease; monitor LFTs and serum level; children may be more vulnerable to hepatotoxicity; divalproex sodium form of valproic acid (Depakote) may improve GI tolerability; fatal pancreatitis has been reported, check amylase/lipase and discontinue medication if patient develops symptoms of pancreatitis
Mood stabilizers
The mood stabilizer that is not an anticonvulsant is lithium. Studies have demonstrated potential benefit of lithium for explosive and violent behavior in patients with organic disorders. Double-blind placebo-controlled trials conducted over 16 wk on violent adult prisoners, patients with mental retardation, and patients with brain injury demonstrated decreased impulsivity and aggressive behavior. Lithium levels during the trials were maintained at 0.7-1.0 mEq/L.
Lithium (Eskalith, Lithane, Lithobid, Lithotabs)
Primarily used for acute manic episodes and depression of bipolar disorder and unipolar depression. Also used to treat agitation and violence. Alters sodium transport in nerve and muscle cells, resulting in intraneuronal metabolism of catecholamines; however, specific mechanism of action is unknown.
Dosing
Adult
IR: 150 mg PO tid initially, titrate to maintain serum level of 0.5-1 mEq/L
ER: Total daily dose divided bid
Pediatric
<6 years: Not established
6-12 years: 7.5-30 mg/kg/d PO divided tid/qid; not to exceed usual adult dose; adjust dose according to serum levels
>12 years: Administer as in adults
Interactions
Medications that increase levels include thiazide diuretics, NSAIDs, erythromycin, metronidazole, spironolactone, triamterene, enalapril, and tetracycline; medications that decrease levels include acetazolamide and aminophylline; medications that have increased toxicity when administered concurrently with lithium include haloperidol, succinylcholine, digoxin, alpha-methyldopa, and calcium channel blockers
Contraindications
Documented hypersensitivity; renal impairment; patients with severe cardiovascular disease should be placed on alternate mood stabilizer because lithium may worsen arrhythmias in patients with sinus node dysfunction
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in sodium depletion, thyroid insufficiency, dehydration, diabetes, and infection; reduce dose in elderly patients or in cases of renal dysfunction; monitor lithium levels and renal function; common adverse effects include tremor, polyuria, and polydipsia; signs and symptoms of toxicity may occur at lower serum levels among patients with head injury; toxicity includes mental confusion, nausea/vomiting, diarrhea, tremor, goiter, polyuria, and flattened or inverted T waves on ECG; may cause reversible real or subclinical hypothyroidism or hyperparathyroidism, monitor TSH and calcium levels
Benzodiazepines
Used for rapid control of agitation in dementia. They potentially worsen cognition; thus, their use in correcting sleep-wake cycle disturbances or treating anxiety in this population is discouraged. Used primarily to produce rapid calming needed for patients who are violent or agitated.
Lorazepam (Ativan)
DOC for acute agitation in dementia. Short duration and less accumulation with repeated doses.
Dosing
Adult
1-2 mg/dose PO/IM initially; may repeat q1h prn; alternatively, 1-2 mg/dose IV; not to exceed administration rate of 2 mg/min; may repeat q30min prn
Pediatric
Not established
Interactions
Toxicity of benzodiazepines increases when used concurrently with MAOIs, alcohol, phenothiazines, and barbiturates
Contraindications
Documented hypersensitivity, preexisting CNS depression, hypotension, narrow-angle glaucoma
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in hepatic or renal impairment (adjust dose), dehydration, myasthenia gravis, organic brain disease, and Parkinson disease
Beta-blockers
Effective for treating aggression resulting from head injury. They also are used for reducing restlessness and disinhibition. Treatment for persistent agitation and aggression in organic brain syndromes.
Propranolol (Inderal)
Nonselective beta-adrenergic receptor antagonist. Widely studied for its therapeutic effects on agitation due to organic brain syndrome. Therapeutic effect may be observed within 2-4 wk, improvement within 8 wk.
Dosing
Adult
20 mg PO tid initially; if hypotensive or bradycardic, initiate at 20 mg PO qd; gradually increase by 60 mg/d q3d as tolerated until symptoms controlled
Pediatric
0.5 mg/kg/d PO divided q12h, gradually titrate as tolerated to 1-2 mg/kg/d divided q12h
Interactions
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines (eg, thioridazine) may increase
Contraindications
Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, cardiogenic shock, AV conduction abnormalities, Raynaud syndrome, severe reactive airway conditions (eg, asthma, emphysema)
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may mask signs of acute hypoglycemia and hyperthyroidism; may exacerbate asthma/COPD; caution in angina, CHF, or asthma; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor BP and pulse during dose titration; drug requires gradual discontinuation
Follow-up
Deterrence/Prevention
- 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 elderly patients, altering the environment to minimize the risk of falls is important.
- Protecting children from child abuse helps prevent head injuries.
- Patients who have had one head injury are at risk for others.
- Identification and treatment of substance abuse makes subsequent injury less likely.
- Some patients with head injury are parasuicidal. They may benefit from treatment of depression, character disorders, and other conditions associated with suicide.
- Restricting return to play for athletes prevents SIS.
- Prevention of sequelae in patients once they have been injured is an active area of research. Recent reviews of the subject suggest hypothermia during the period of coma may mitigate tissue damage. Prophylactic use of anticonvulsants is not recommended.
Complications
- Reactions to anticholinergic, analeptic, and parkinsonian adverse effects of medication
- Subdural and epidural hematomas
- Hydrocephalus
- Partial complex or grand mal seizures
- Exacerbations of preexisting psychiatric disorders, including preexisting dementia
- Conversion symptoms
- Conversion symptoms typically occur when a person feels trapped in a threatening situation, especially if he or she is unable to openly talk about the dilemma with others who are trusted.
- Patients with head injury often face such dilemmas, being forced to return to work when they feel unable, being expected to perform normal family roles despite significant problems of cognition or mood, and being subject to hostile legal scrutiny. Moreover, the head is a symbolically significant part of the body. For all of these reasons, some of the nonspecific distress of patients with head injury and, more rarely, some of their focal complaints may be understood as conversion symptoms or somatization.
Prognosis
The prognosis of mild or moderate dementia and PCS remains 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.
Patient Education
Patients with dementia
- These patients need simple explanations of their impairments. While they may be aware of cognitive dysfunction, they may lack insight into impairments in judgment, changes in personality, elevated mood, or paranoid symptoms. Education should include the expected course of improvement, with the greatest improvement expected in the first 6 months but delayed improvement possible as long as 5 years after injury.
- Caretakers of patients with dementia need a great deal of ongoing education and support. Importantly, the patient's environment must be neither tedious nor overstimulating. Maintaining consistent routines of light and dark, eating, sleeping or lying in bed, performing bathroom activities, and participating in therapeutic or recreational activities help patients remain emotionally balanced and minimize caregiver burden.
- Keeping the environment safe by eliminating area rugs to reduce falls, providing tub bars, and putting child locks on cabinets or stove knobs also is important in the care of patients with dementia. If the patient is capable of going out alone, the caregiver should ensure that he or she knows the routes well, carries identification, wears a medic alert bracelet, and knows how to use phones (especially cell phones) and busses.
- Caregivers for patients with mild dementia need to decide whether the person should continue to have access to checking accounts or credit cards. If the person is willing and competent, the caretaker should consider getting power of attorney, in order to monitor the person's use of financial resources. If the patient has markedly poor judgment or seems seriously incompetent, the caregiver should seek formal conservatorship, to have legal authority to manage the person's resources.
- Caregivers should be included in the patient's relationship with health care professionals. They should be specifically told to seek help if the patient has very disrupted sleep; does not eat a balanced diet; or is incontinent, aggressive, or sexually inappropriate. Any marked change in behavior should prompt a call to the clinician. Because patients with dementia do not always show typical symptoms when acutely ill, taking the patient's temperature and looking for signs of infection is a particularly important step if the patient shows a change.
- Clinicians, in turn, must be accessible to caregivers. Meeting with more than one family member to stress the importance of having family members and friends share the burdens of providing care often is an overlooked step. Although one particular friend or relative may know the most about a patient and assume most of the responsibility, sharing this with others reduces the likelihood of the caregiver becoming isolated or depressed, an otherwise common outcome of providing long-term family care.
Patients with postconcussional syndrome
- Patients with PCS need to know that headaches, dizziness, fatigue, irritability, poor concentration, and decreased memory are common in the first 3-6 months after injury. These symptoms fully resolve in most patients after mild injury. However, persistent impairment is possible. Patients should know that anxiety, depression, decreased concentration, and other persistent symptoms may improve with rehabilitation, psychological support, and medication.
- Caregivers need to adopt a posture of encouragement and expectation that the patient will try to be as independent and productive as possible. At the same time, caregivers need to be patient and tolerant. They should accept that the patient may have real limitations and that these will likely worsen if the person is tired, ill, or acutely stressed. Emphasizing what the person can still do, rather than what seems to be lost, is generally helpful.
Online resources
- The traumatic brain injury page of the National Institutes of Health contains links to other organizations providing education and support (see National Institute of Neurological Disorders and Stroke).
- CDC, What is Traumatic Brain Injury?
- MayoClinic.com, Traumatic Brain Injury
- WebMD, Dementia in Head Injury
- For excellent patient education resources, visit eMedicine's Dementia Center and Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education articles Dementia in Head Injury, Dementia Overview, Dementia Medication Overview, and Concussion.
Miscellaneous
Medicolegal Pitfalls
- In treating patients with head injuries, the physician needs to know if the patient is involved in litigation related to the injury.
- Anticipate having to testify in depositions or court proceedings.
- Document impairment and objective findings clearly, quantifying symptoms and progress in recovery whenever possible.
- When called to testify, be aware of personal attitudes towards patients who are dependent, not improving quickly, not functioning to their ability, or expressing undesirable attitudes of resentment or entitlement. None of these factors should blind the physician to the reality of patients' distress and impairment. Testifying for either the defendant or the plaintiff in a head injury case requires honesty, humility, and awareness of the uncertainty surrounding the causes and the outcomes of the symptoms that patients develop.
- Involvement in litigation does not reliably predict the severity or extent of symptoms after head injury. Settlement of pending lawsuits also does not cause resolution of symptoms.
- 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. 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.
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Keywords
concussion, post concussive syndrome, PCS, concussion syndrome, traumatic brain injury, TBI, closed head injury, memory impairment, second injury syndrome, SIS, posttraumatic amnesia, PTA, posttraumatic thalamic syndrome
Contributor Information and Disclosures
Author
Roy H Lubit, MD, PhD, Assistant Clinical Professor, Mount Sinai School of Medicine; Clinical Faculty, Department of Child Psychiatry, New York University School of Medicine; Private Practice
Disclosure: Nothing to disclose.
Medical Editor
Jennifer S Morse, MD, Assistant Clinical Professor, Department of Psychiatry, University of California at San Diego
Jennifer S Morse, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, Aerospace Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.
CME Editor
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; BMS Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Other; Northstar Grant/research funds Other; Novartis Other; Pfizer Honoraria Speaking and teaching
Chief Editor
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.