eMedicine Specialties > Psychiatry > Psychosomatic
Postconcussive Syndrome: Treatment & Medication
Updated: Oct 1, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
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.
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
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
Documented hypersensitivity; MAOIs
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.
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
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
Documented hypersensitivity, concurrent MAOI therapy
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.
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
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
Documented hypersensitivity; concurrent MAOI or use within 14 d of MAOI; do not use during acute recovery phase of MI
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.
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
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
Documented hypersensitivity, MAOI within 14 d of initiating treatment; concurrent administration with pimozide
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.
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
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
Documented hypersensitivity
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.
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
Additive toxicity may increase with ergot alkaloids, amitriptyline, butyrophenones, imipramine, methyldopa, phenothiazines, and reserpine; antipsychotics may decrease effect; sympathomimetics and erythromycin may increase effect
Documented hypersensitivity, severe ischemic heart disease, severe peripheral vascular disorders
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.
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
Coadministration with MAOIs may precipitate hypertensive crisis; coadministration with anesthetics may precipitate arrhythmias; may increase toxicity of phenobarbital, propoxyphene, meperidine, TCAs, phenytoin, and norepinephrine
Documented hypersensitivity, hypertension, MAOIs used within 14 d, advanced arteriosclerosis, hyperthyroidism, glaucoma, diabetes mellitus, hyperthyroidism
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.
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
Carbamazepine may decrease serum levels; clozapine may increase serum levels; may antagonize levodopa effects
Documented hypersensitivity
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.
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
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
Documented hypersensitivity
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.
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
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
Documented hypersensitivity
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.
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
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)
Documented hypersensitivity, history of bone marrow depression, administration of MAOIs within last 14 d
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.
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
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
Documented hypersensitivity, hepatic disease
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.
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
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
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
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.
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
Toxicity of benzodiazepines increases when used concurrently with MAOIs, alcohol, phenothiazines, and barbiturates
Documented hypersensitivity, preexisting CNS depression, hypotension, narrow-angle glaucoma
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.
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
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
Documented hypersensitivity, uncompensated congestive heart failure, bradycardia, cardiogenic shock, AV conduction abnormalities, Raynaud syndrome, severe reactive airway conditions (eg, asthma, emphysema)
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
More on Postconcussive Syndrome |
| Overview: Postconcussive Syndrome |
| Differential Diagnoses & Workup: Postconcussive Syndrome |
 Treatment & Medication: Postconcussive Syndrome |
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Further Reading
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
