What is the difference between ptsd and tbi

If you were knocked out for more than 30 minutes but less than six hours, your TBI was most likely moderate. Few people will have all of the symptoms, but even one or two of the symptoms can be unpleasant. PCS makes it hard to work, get along at home, or relax. In the days, weeks, and months following a TBI the most common symptoms are:. These symptoms are part of the normal process of getting better.

They are not signs of lasting brain damage. These symptoms are to be expected and are not a cause for concern or worry. More serious symptoms include severe forms of those listed above, decreased response to standard treatments, and seizures. Because TBI is caused by trauma and there is symptom overlap, it can be hard to tell what the underlying problem is. It means that you should be assessed further.

Diagnosing a TBI is hard because there may not be any physical signs of injury. Details of the trauma may be hard to pin down. Sometimes right after the injury the effects are so brief that they are not noticed.

You may go to the doctor some time later when details of the injury are not as clear. TBI can occur in confused times of crisis, such as combat. In the heat of events the injury may be ignored. For these reasons, the best way to diagnose a TBI is an interview by a skilled clinician. Many people recover from TBI without any formal treatment. Problems that linger may clear up in a few weeks. You may notice some problems more as you return to your normal routine. For example, you may not realize that you get tired more quickly until you return to your regular chores, work, or school.

Even so, people usually get better after a head injury, not worse. Professional treatment for the symptoms that follow TBI usually involves rehabilitation to improve functioning. The best way to deal with symptoms following TBI is to go back slowly to your normal routine, a little at a time.

How much time you spend at work, with family, with others, or exercising depends on what feels comfortable. Pace yourself, and be sure to get all the rest you need. Avoiding alcohol and not taking any unnecessary medications is a good idea, to help allow the brain to heal.

If your symptoms get worse, or if you notice new PCS symptoms, this is a sign that you are pushing yourself too hard. Ignoring your symptoms and trying to "tough it out" often make the symptoms worse. Symptoms are your body's way of giving you information. A broken bone or a torn muscle hurts so that you won't use it and it has time to heal.

Often those suffering with either of these conditions can feel alone, isolated and that they have no one to turn to. Even if friends, family and professionals are there to offer support, communicating how they are feeling inside their heads can be a challenging task.

As both conditions are a result of a traumatic event, physical symptoms may be likely to occur. This could include loss of mobility, weakness, paralysis, ataxia or spasticity. With PTSD, memories are intrusive and relived repeatedly.

The person may be unable to stop thinking about the traumatic event, and this can lead to nightmares or panic attacks. For this reason, the person is usually unwilling to discuss the memories of the event as it is too traumatic and painful. With regard to a TBI, the person suffers more with memory loss. In the short term, they may not remember the event that led to the injury. In the long term, it may affect day to day life if they are unable to form new memories.

This depends on the severity of the brain injury. A common symptom of PTSD is a reluctance to talk about the traumatic event or experience.

This can make it difficult to enrol the person in counselling or therapy. This can differ to someone with a TBI who may openly talk about the traumatic event and continuously repeat the topic, which is known as perseveration. Although they may share similar emotional symptoms, the way they are shared and expressed can be very different.

Someone with PTSD is likely to supress these emotions and feel unable to share them with anyone in their support network. In someone with a TBI the emotional affects are likely to be more visible and a personality change is more evident to those close to them.

For example, an ex-serviceman may have suffered a limb injury that lead to amputation. With a TBI, the physical symptoms can be harder to detect. Sensory loss, fatigue and speech difficulty are common physical symptoms of this type of injury. At AJCM we have a strong belief in the importance of setting goals. If you or a loved one is struggling with a brain injury, we urge you to find the right support, so you can gain control of your life again.

It is overwhelming for anyone to cope with this on their own, and there is so much help available to get you on the road to recovery. A case manager takes away the stress of organising treatment, seeking out professionals and creating rehabilitation plans. Our team of passionate case managers have the experience, values and knowledge to guide you through the best plan for your circumstances.

Get in touch today for free, impartial and professional advice. Se ofrecen algunas explicaciones para este incremento del riesgo. The intersection between traumatic brain injury TBI and post-traumatic stress disorder PTSD has become a major focus of attention in recent years.

Stimulated largely by injuries sustained in the Iraq and Afghanistan wars, this issue has been debated widely because these conditions, both independently and additively, are regarded as being responsible for much impairment following deployments. This review will commence with defining these conditions, explain potential overlaps between them, and discuss the differential diagnosis challenges of determining the extent to which presenting symptoms can be attributed to organic or psychological factors.

Finally, the implications for managing the effects of TBI and PTSD are discussed in terms of recent developments in how each condition can affect the other. TBI involves damage to the brain from an external force. Brain injuries can involve contusion, brain laceration, intracranial hematoma, contrecoup injury, shearing of nerve fibers, intracranial hypertension, hypoxia, anemia, metabolic anomalies, hydrocephalus, and subarachnoid hemorrhage.

Severe TBI involves more extended loss of consciousness and post-traumatic amnesia, which typically results in more severe cognitive impairment.

It is important to distinguish between immediate and longer-term PTSD reactions. Most diagnostic systems have distinguished between these two types of trauma response because acute stress reactions are frequent, but often transient, and they need to be distinguished from the less common persistent PTSD responses. Second, one must report a re-experiencing symptom, which may include intrusive memories, nightmares, a sense of reliving the trauma, or psychological or physiological distress when reminded of the trauma.

Third, there need to be at least three avoidance symptoms, which can include active avoidance of thoughts, feelings, or reminders of the trauma, inability to recall some aspect of the trauma, withdrawal from others, or emotional numbing.

Fourth, one must suffer marked arousal, which can include insomnia, irritability, difficulty concentrating, hypervigilence, or heightened startle response. These symptoms must cause marked impairment to one's functioning, and can only be diagnosed when they are present at least 1 month after the trauma. As PTSD is only diagnosed 1 month after trauma, it was decided that there was a need to fill the nosological gap between the traumatic event and PTSD, in part to facilitate diagnosis and access to health care.

A second major goal of the ASD diagnosis was to describe acute stress responses that precede longer-term PTSD, and therefore could be used to identify people who were at high risk for subsequent disorder and could benefit from early intervention.

Specifically, ASD requires the individual to experience at least three of the following: emotional numbing, reduced awareness of one's surroundings, derealization, depersonalization, and dissociative amnesia. These symptoms may occur either at the time of the trauma or during the subsequent month. The dissociative symptoms were included in ASD on the premise that dissociative responses following trauma are predictive of subsequent PTSD, presumably because they limit emotional processing of the traumatic experience.

A key issue in this discussion is the overlap between symptoms accompanying each condition. In terms of the dissociative symptoms often observed in PTSD, and especially in the acute phase in ASD, there is much evidence that TBI can result in emotional numbing, derealization, reduced awareness of surroundings, depersonalization, and amnesia.

This is important for patients with because many patients, especially those with more severe TBI, do not initially respond with a sense of fear or helplessness because of their impaired consciousness. This is relevant because numbing and withdrawal can often be observed in more severe TBI; by separating these passive responses into a separate requisite cluster, it raises the possibility of differential diagnosis problems for more severe TBI patients, many of whom will display these symptoms.

This cluster also includes alterations in mood and cognition, and comprises a range of symptoms that may include a range of emotional responses beyond fear and anxiety. These latter symptoms can be observed in the context of reduced inhibition in more severe TBI patients, thereby raising further differential diagnosis problems in distinguishing between symptoms of severe TBI and PTSD.

In contrast to ASD, the International Classification of Diseases 26 conceptualizes acute stress reaction as a transient reaction that can be evident immediately after the traumatic event and usually resolves within 2 to 3 days after trauma exposure. The ICD description of acute stress reaction includes dissociative daze, stupor, amnesia , anxiety tachycardia, sweating, flushing , anger, or depressive reactions, which may have more utility for clinicians than the more focused ASD criteria.

For example, depression is highly prevalent with both conditions. Numerous studies have suggested that TBI increases the risk for developing depression, 29 , 30 eg, refs 31,32, Some of the core symptoms noted across TBI and PTSD are also seen in depression, especially the more severe forms of TBI, including concentration problems, memory problems, irritability, reduced motivation, and fatigue. Complicating the issue of comorbidity is compounded by the fact that TBI, PTSD, and depression commonly occur in the context of chronic pain, which also results in symptoms that overlap with each of these conditions.

Epidemiological studies indicate that most people in the community have been exposed to traumatic stressors, 42 , 43 although anly a minority develop PTSD. In terms of TBI, there are between 1. Some earlier commentators argued that PTSD could not develop following TBI because the impaired consciousness at the time of trauma precluded encoding of the traumatic experience, and this prevented trauma memories that are necessary for PTSD development.

In many of the latter cases, these individuals suffer very significant periods of retrograde and anterograde amnesia, such that they do not recall any episodes of the traumatic experience.

Fear conditioning models posit that the fear elicited during a traumatic event results in conditioning in which subsequent reminders of the trauma elicit anxiety in response to trauma reminders conditioned stimuli.

This proposal is consistent with animal studies that indicate that epinephrine administration after an aversivc experience enhances fear conditioning. Indirect support for this hypothesis comes from multiple longitudinal studies that indicate that elevated heart rate in the acute post-trauma phase is associated with subsequent development of PTSD 72 ; elevated heart rate in the initial days after trauma may reflect stronger conditioning, which can then translate into longer-term PTSD.

Although conditioning occurs optimally when one is aware of the contingency between the unconditioned and conditioned stimuli, 73 conditioning may occur with varying levels of awareness of the contingency between the trauma and the consequences, which may allow for some fear conditioning following TBI.

Consistent with this proposal, there is evidence that people can develop PTSD following severe TBI, even though these patients do not recall the trauma and do not suffer intrusive memories of the event. An alternate mechanism is that TBI patients reconstruct trauma memories in ways that result in a traumatic representation of what occurred during impaired consciousness.

When this man was directed to resume driving he developed distressing and intrusive images of his accident that were based on a newspaper photograph of his wrecked car. Although he was densely amnesic of the accident, he developed a series of images that were founded on his memory of the photograph. Interestingly, these images changed with time. For example, when he became concerned that his children may be harmed when he was driving, his intrusive images changed to include his children lying dead in the car.

All participants were asked to listen to an audio tape of a car crash sound effect, and were then interviewed about their cognitive and emotional responses. When these responses were independently rated on a range of constructs, it was found that those PTSD participants with and without TBI reported comparable levels of vivid imagery, emotional response, in voluntariness, and sense of reality.

The only difference was that those with a TBI tended to report stationary images rather than moving sequential imagery. A third possible mechanism is that many people who sustain a TBI, and frequently those with MTBI, suffer traumatic experiences following resolution of their posttraumatic amnesia. One may be knocked unconscious in a motor vehicle accident victim but be fully aware of the experience of being cut out of the car by paramedics, experiencing severe pain, being treated in an emergency room, and fearing for their safety.

Many MTBI patients will report distressing memories of their experience, despite islands of amnesia in which they cannot recall the point of impact in which they sustained their MTBI.

For example, Fann and colleagues reported from a large-scale study of health plan members that patients with a history of mild TBI were 2. This observation may have several possible explanations. The prevailing neurobiological model posits that PTSD involves exaggerated amygdala response associated with impaired regulation by the medial prefrontal cortex. Alternately, the management of post-traumatic stress, as well as problems caused by ongoing stressors in one's environment, requires adequate working memory and cognitive resources 83 ; it is possible that TBI depletes these resources to some extent, and this may contribute to increased PTSD risk.

There is much evidence that PTSD is influenced by the compounding effects of stressors that occur following the precipitating trauma. There is evidence of an inverse relationship between extent of one's memory of the traumatic experience and the occurrence of re-experiencing memories.

One study of motor vehicle accident survivors indexed the extent to which patients with MUM recalled details of the traumatic accident, 87 and found that the less patients recalled of their traumatic event, the less likely they were to develop PTSD. This finding suggests that although duration of amnesia appears protective of development of intrusive traumatic memories, MTBI nonetheless confers risk for developing PTSD.

Post-traumatic stress symptoms typically occur in the initial days and weeks after trauma exposure, and then gradually abate in most people; a minority of trauma survivors can suffer persistent PTSD. Most studies indicate that delayed-onset PTSD is rare. Although uncommon following civilian trauma, it has been reported to occur more frequently in troops returning home from deployment. It is possible that following MTBI sustained in combat, one feels the need to fill the gap of knowledge of the events that affected them.

Consistent with reports of TBI patients confabulating events in order to make sense of what occurred to them during the loss of consciousness, 61 it is possible that one explanation of delayed-onset PTSD, especially in the military, is the pattern of subsequently reconstructing the traumatic events in the wake of impaired consciousness. The possibility that trauma memory reconstruction in the post-deployment period contributes to PTSD needs to be studied in military populations, and points to the potential importance of ensuring that adaptive, rather than maladaptive, reconstructions of events occur in the months after injury.

Many millions of dollars arc being devoted to rehabilitation procedures to minimize the potential adverse effects of MTBI on soldiers affected by it.

Recent studies are indicating, however, that MTBI itself is responsible for minimal impairment. One large-scale survey of US troops reported that health impairment was markedly higher in deployed personnel who sustained a MTBI, including reported poor general health, days off work, and medical visits. The issue of postconcussive syndrome is a vexed one, both in terms of its definition and its purported causes.

It is also an issue that intersects with symptoms of PTSD. PCS is generally defined as a syndrome that involves headache, dizziness, fatigue, sensitivity to light or sound, sleep disturbance, and concentration difficulties.

For example, the International Classification of Diseases ICD 26 stipulates that PCS is defined by headaches, dizziness, general malaise, fatigue, noise intolerance, irritability, emotional lability, depression, or anxiety, concentration or memory difficulty, sleep disturbance, reduced tolerance to alcohol, and a preoccupation with these symptoms and fear of permanent brain damage.

The Appendix of the DSM. These descriptions clearly overlap with common symptoms of post-traumatic stress, and represent differential diagnosis problems insofar as how one attributes these symptoms to PCS or PTSD. Recent evidence is highlighting that symptoms described as PCS are common in many populations, and actually reflect a diffuse collection of frequently experienced sensations.

In healthy individuals, headaches, sleep difficulty, irritability, and memory failures are relatively common in daily life.

There has been much debate over the extent to which persistent PCS develops as a result of neurological damage, psychological distress, or a combination of both. Military agencies have implemented programs for troops in Iraq and Afghanistan targeted towards treating the effects of MTBI. Given the evidence that so-called postconcussion-like symptoms and general health problems are largely related to psychological factors, there are likely risks in suggesting to troops that the problems experienced following MTBI should be attributed to neurological damage.

Communicating to personnel who sustained a MTBI that a range of nonspecific symptoms are caused by brain damage communicates a cause with a poor prognosis. This expectation that common sensations are signs of permanent dysfunction can result in hypervigilance to every sensation, followed by catastrophic attributions about the adverse consequences of the sensations. This pattern has been well-documented across a range of disorders, including panic disorder, health anxiety, and hypochondriasis.

For example, the patient with panic disorder may believe that an alteration in his or her respiration is a sign of imminent choking or that a slight pain in the chest is indicative of an approaching cardiac arrest. Similarly, someone with health anxiety may constantly search their body for any alterations in appearance of function to determine if there arc signs of malignancy. Once the sensation or sign is detected, the person can catastrophize the sign in an extremely negative manner, such that the slightest somatic cue is perceived as indicative of dire outcomes.

This is a common pattern in people with PTSD. Fear network models of PTSD propose that these individuals preferentially allocate attention to stimuli of concern because of their fear of threat. This response may exacerbate the PTSD reaction, as well as promote continued hypervigilence to sensations and subsecpent maladaptive appraisals that these reactions arc indicative of permanent brain injury. This pattern was reflected in the aftermath of the Gulf War, when there were widespread concern of chemical weapons, which apparently contributed to medically unexplained symptoms that were linked to concerns about somatic sensations purportedly linked to chemical agents.

There are potential similarities between Gulf War Syndrome and the manner in which MTBI is currently being understood; both comprise general sensations that are commonly reported in stress responses, and both mistakenly attributed to common stress reactions. This can be problematic because it can reduce people's optimism or expectancy for recovery.

This review has several implications for how symptoms following TBI are addressed in treatment. In terms of treating the symptoms of PCS, current evidence suggests that simple neuropsychological education is modestly useful in reducing symptoms of PCS. That is, by reducing the arousal-inducing symptoms of PTSD, it is possible that many of the symptoms associated with PCS will be alleviated. Similarly, by minimizing catastrophic appraisals that exaggerate the severity or adversity of PCS sensations it is probable that anxiety about these reactions would be eased.

For example, patients who are overly concerned about the adverse outcomes of dizziness or sensitivity to light can be taught to normalize these reactions in ways that minimize distress about these sensations. Cognitively reframing the perception of these reactions is akin to established treatments for panic disorder or health anxiety, in which patients are taught to tolerate somatic experiences in ways that discourage inferences involving an adverse outcome.

Although this approach has been proven to be very effective in treating panic disorder and health anxiety, it has yet to be tested with PCS. In terms of treating symptoms of PTSD, prevailing cognitive models posit that recovery from a traumatic experience involves integrating the trauma memory into one's autobiographical memory base in a way that allows a coherent narrative of the experience in which the person can contextualize the experience and consequently currently feel safe.

Fragmented memories of the traumatic experience can also occur in the context of TBI because of the impaired consciousness secondary to the injury. As noted above, TBI patients can reconstruct aspects of the traumatic experience that were not adequately encoded during the period of impaired consciousness. This scenario raises the possibility that treating PTSD after TBI will require adaptive reconstruction of this narrative in a way that facilitates adaptation rather than retraumatization.

For example, a patient who reconstructs their memory of a car accident in which they were excessively responsible for someone's death will have marked depressive responses relative to a patient who reconstructs the memory in a way that accepts a more reasonable level of responsibility.

Alternately, a patient can be encouraged to tolerate a level of uncertainty insofar as there is permanent amnesia of some aspect of the event; inability to tolerate uncertainty is linked to enhanced anxiety and worry.

The extent to which a person with TBI needs to reconstruct the trauma narrative to recover from PTSD has yet to be empirically determined. In the context of therapy, presenting memories or reminders of the trauma to the patient in the safety of therapy typically leads to symptom reduction. Exposure can either be imaginai, which involves focusing on one's memories of the traumatic event, or in vivo, in which approaches and remains with reminders that usually trigger anxiety about the event.

On the premise that fear conditioning and extinction still occurs in the context of TBI, it would seem that that exposure-based therapy is the indicated intervention for PTSD following TBI.

Imaginal exposure with people following TBI will usually be dependent on the amount of memory that the patient is reporting. It may not be as useful to patients with more severe TBI because they are largely amnesic of their trauma. As noted above, some severe TBI patients can have nightmares or intrusive memories on the basis of reconstructions of their trauma; in these cases, imaginable exposure to those mental representations that are causing anxiety.

A survivor of a motor vehicle accident who sustained a severe TBI may experience marked fear when watching film footage of traffic; in such a case, the patient could complete exposure by repeatedly watching traffic footage. Through these techniques it would be hoped that extinction learning can be achieved, even though the patient may never retrieve direct memories of the traumatic event.

Increasing evidence indicates that many previously termed PCS responses are a function of psychological responses, and it hampers a patient's recovery if they mistakenly perceive these reactions as indicators of a brain injury that may be permanent. The likelihood that the presumed secpelae of MTBI are actually attributed to psychological responses to the traumatic experience is becoming more apparent. Accurate identification of the true nature and cause of the symptoms experienced after TBI is important because if stress-related disturbances are mistakenly attributed to neurological factors, patients may be deprived of effective treatments that can, in most cases, alleviate the symptoms.

As we learn more about the interaction of TBI and PTSD, it seems that we will be discovering much about how the brain responds to traumatic experiences, both in cases when there has and has not been a TBI. Understanding this interaction between neurological insult and psychological response has the potential to shed light on the key mechanisms underpinning trauma response generally, and how it is impacted by different levels of brain injury.

National Center for Biotechnology Information , U. Journal List Dialogues Clin Neurosci v. Dialogues Clin Neurosci. Author information Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Abstract Post-traumatic stress disorder PTSD and traumatic brain injury TBI often coexist because brain injuries are often sustained in traumatic experiences. Keywords: post-traumatic stress disorder , traumatic brain injury , trauma , postconcussive syndrome.

Overview The intersection between traumatic brain injury TBI and post-traumatic stress disorder PTSD has become a major focus of attention in recent years.

Differential diagnosis A key issue in this discussion is the overlap between symptoms accompanying each condition. Memory reconstruction An alternate mechanism is that TBI patients reconstruct trauma memories in ways that result in a traumatic representation of what occurred during impaired consciousness. Postamnesia resolution A third possible mechanism is that many people who sustain a TBI, and frequently those with MTBI, suffer traumatic experiences following resolution of their posttraumatic amnesia.

Delayed-onset PTSD Post-traumatic stress symptoms typically occur in the initial days and weeks after trauma exposure, and then gradually abate in most people; a minority of trauma survivors can suffer persistent PTSD.

Postconcussive syndrome and PTSD The issue of postconcussive syndrome is a vexed one, both in terms of its definition and its purported causes. Implications for treatment This review has several implications for how symptoms following TBI are addressed in treatment. American Congress of Rehabilitation Medicine.