Recognizing Manifestations of Posttraumatic Stress Disorder in Patients With Traumatic Brain Injury

Eric B. Larson

BACKGROUND

Definition

Posttraumatic stress disorder (PTSD) is a psychiatric syndrome characterized by persistent symptoms of anxiety after exposure to a traumatic event. In patients with traumatic brain injury (TBI), PTSD is sometimes confused with postconcussion disorder, adjustment disorder, personality change due to TBI, and with dementia due to TBI.

Diagnostic Criteria

Problems from each of the following five categories must be observed [1]: (a) history of exposure to trauma, (b) intrusion of trauma-related symptoms after the event, (c) avoidant behavior, (d) dysfunctional changes in cognition and mood associated with trauma, and (e) increased autonomic arousal. Duration of the previously noted symptoms is more than 1 month, and significant distress or functional impairment results from these symptoms.

Epidemiology

In the general population, lifetime prevalence of PTSD is 7.8%. In patients with mild TBI (MTBI), estimates of prevalence range from 10% to 27%. Prevalence of PTSD has been shown to be the same among MTBI patients as it is among patients with other traumatic injuries [2]. In patients with severe TBI, the best estimate of prevalence is 3%, although self-report of symptoms is much higher [3].

Etiology

A Behavioral Account

Most forms of anxiety are a result of appraisal of an impending (future) threat. PTSD involves processing a past trauma as a current threat, possibly because of activation of implicit memories of the traumatic events. Discrimination between current experience and past implicit memories may be more difficult because the latter are more vaguely defined than are explicit memories [4].

A Neurobiological Account

The implicit learning involved in PTSD may be mediated by neural circuits that are characterized by:

• Inadequate frontal inhibition (associated with inability to suppress attention to stimuli related to trauma)

• Excessive amygdala response (associated with conditioned fear and reactivity to potential threats)

• Compromised hippocampus function (associated with deficient ability to distinguish safe and unsafe environments) [5]

Pathophysiology

Inconsistent evidence of atrophy in the hippocampus and in the anterior cingulate cortex has been reported in structural imaging studies of PTSD patients. Some have proposed these are stress-induced changes, but twin studies suggest that reduced volume in these structures is a pretrauma vulnerability factor [6]. Similarly, comparisons of structural, perfusion, and diffusion MRI data in 17 veterans with PTSD and in 15 age-matched veterans without PTSD showed increased regional cerebral blood flow in the right parietal and superior temporal cortices, and reduced functional anisotropy in white matter regions near the anterior cingulate, prefrontal lobe, and the posterior angulus gyrus. As in previous imaging studies, it was concluded that these abnormalities may be the result of PTSD or may be risk factors that cause individuals to be predisposed to the disorder [18].

DIAGNOSIS

Risk Factors

Knowledge of characteristics that leave patients vulnerable to PTSD can help determine if that disorder is present in a TBI survivor with an ambiguous clinical presentation.

• Pretrauma risk factors—Sex and marital status are the strongest demographic predictors of PTSD. Women and previously married (e.g., divorced or widowed) individuals have the highest risk for PTSD [7].

• Trauma-related risk factors—For men, the highest risk for PTSD is for those who have been in combat and for those who have witnessed someone being killed or severely injured. For women, the highest risk is associated with rape or sexual molestation.

• Posttrauma risk factors—A lack of subsequent social support and experience of additional life stressors are both stronger predictors of PTSD than pretrauma risk factors [8].

• Poor cognitive function [9]—A pretrauma cognitive deficit may leave an individual less able to cope with stressors, which may make them more vulnerable to PTSD.

• TBI patients are at increased risk for PTSD at 6 months after injuries if they experienced acute stress disorder after their injuries, if they exhibited symptoms of depression and anxiety within 1 week of injuries, if they have previous histories of psychiatric disorders, or if they had memories for the traumatic events [10].

Clinical Presentation

In MTBI, PTSD patients often present symptoms of trauma-related emotional distress along with symptoms of postconcussion disorder. Symptoms observed in both disorders include noise sensitivity, fatigue, anxiety, insomnia, poor concentration, poor memory, and irritability. The presence of these symptoms alone is not diagnostic of either disorder because all have high base rates in the general population as well.

Symptoms

• Intrusion symptoms

Recurrent involuntary, intrusive distressing recollections of the traumatic event. Such memories are sudden, unwanted, and disruptive to one’s activities

Recurrent distressing dreams of the event (nightmares)

Dissociative behavior in which one acts or feels like the event is recurring (e.g., flashbacks). This involves perception that the trauma is happening in the present and differs from remembering the traumatic event as a past occurrence. Contact with present reality is diminished and in extreme cases may be entirely lost.

Intense psychological distress at exposure to trauma-related cues

Physiological reactivity on exposure to trauma-related cues

• Persistent avoidance

Efforts to avoid thoughts or feelings associated with the trauma

Efforts to avoid activities or situations that arouse recollections of trauma (e.g., appointment cancelations, failed appointments, and tardiness to treatment sessions)

• Maladaptive changes in mood and cognition

Inability to recall an important aspect of the trauma, only if determined not to be because of posttraumatic amnesia

Persistent and overgeneralized dysfunctional beliefs about oneself, other individuals, or the world

Persistent and distorted thoughts of blame

Markedly diminished interest in significant activities that are still available despite physical disability

Feeling of detachment or estrangement from others

Persistent inability to experience positive emotions

Reckless or self-destructive behavior

• Maladaptive changes in arousal and reactivity

Difficulty falling or staying asleep

Irritability or outbursts of anger

Difficulty concentrating

Hypervigilance—This does not necessarily exclude situations in which an individual’s perception of threat is justified by actual danger in his or her environment

Exaggerated startle response

Evaluation

• Symptom checklists—Questionnaires that rely on self-report like the PTSD Checklist [11] require little time to complete (5 minutes or less) and may be used as screening measures but should not be used for diagnosis given their poor specificity. Further, in TBI patients, self-report is notoriously inaccurate.

• Structured interviews—The “gold standard” for PTSD diagnosis, clinician interviews require extended time to complete (30–120 minutes). They also require formal training to assure inter-rater reliability. Measures include the Clinician-Administered PTSD Scale for DSM-IV [12] and the Structured Clinical Interview for DSM-5 Disorders—Clinician Version (SCID-5-CV) [13].

• Neuropsychological evaluation—Standardized psychological assessment provides a detailed description of the nature of cognitive impairment and emotional distress. However, in cases where it is unclear whether a patient has sustained an MTBI, identifying cognitive impairment does not assist with differential diagnosis, because such impairment can be seen in individuals with PTSD alone [14].

Controversies

It has been suggested that TBI does not produce PTSD because the disturbance of consciousness that must occur in the former interferes with formation of memories of trauma, which is presumably the cause of symptoms in the latter [15]. Although some evidence supports this conclusion, other studies show that PTSD exists in individuals who lost consciousness at the time of their injuries [10,16]. The formation of implicit memories (that may not require clear consciousness at the time of trauma and that may exist in the absence of explicit recall) has been offered as an explanation for this counterintuitive finding.

TREATMENT

Guiding Principles

Exposure and Avoidance

Treatment that increases exposure to trauma-related stimuli in a supportive, controlled environment is effective at reducing symptoms. Avoidance of stimuli that provoke distress results in increased anxiety when those triggers can no longer be escaped.

Medication and Cognition

Some pharmacological interventions are effective at short-term management of anxiety but can result in iatrogenic cognitive impairment, which makes them bad choices for TBI survivors.

Psychopharmacology

• Selective serotonin reputake inhibitors (SSRIs) are more effective than older antidepressants for most symptoms of PTSD.

• Trazodone can be helpful in reducing nightmares and daytime anxiety.

• Prazosin, a centrally acting noradrenergic alpha1-blocker, can also be used to reduce nightmares and daytime anxiety.

• Propranolol, a centrally acting noradrenergic beta-blocker, can reduce autonomic hyperarousal.

• Most antipsychotic medications are not used to treat PTSD, especially in patients with comorbid TBI because these agents can interfere with neurological recovery.

• Atypical antipsychotics (e.g., Zyprexa and Risperdal) may be helpful for control of psychotic symptoms of PTSD (e.g., hallucinations), possibly due to serotonergic effects.

• Sedative-hypnotics (e.g., benzodiazepines)

Provide only temporary relief of symptoms.

May interfere with recovery.

May cause rebound and dependence (they are not recommended).

Psychotherapy

• Cognitive-behavioral treatment that includes exposure therapy can be introduced early for patients with MTBI and later in the course of recovery for moderate-to-severe TBI patients. Memory deficits are a substantial obstacle to efficacy; in fact, such impairment may never resolve to the point that psychotherapy is possible.

• Referral to PTSD specialists can be particularly helpful. Centralized referral databases are now offered (listed under “Electronic References”).

Treatment Controversies

Eye Movement Desensitization and Reprocessing

An ongoing debate continues about the efficacy of eye movement desensitization and reprocessing (EMDR). Although outcome studies support the use of this technique, many clinicians argue that it is effective because it includes elements of exposure therapy, and that there are no advantages to EMDR over traditional exposure therapy [17].

Additional Considerations

Disability Evaluations

In veterans, a diagnosis of PTSD may be used to support claims of disability. Disabled veterans can receive disability income if they can substantiate these claims. Secondary monetary gains may result in many false disability claims.

Personal Injury Cases

Individuals who file personal injury lawsuits may argue that their injuries resulted in PTSD. Again, secondary gains may influence symptom reporting. Consider referral for evaluation by a PTSD specialist and/or neuropsychologist who can determine the extent to which this influence may result in symptom magnification or malingering.

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