This morning it appears i shouted at a co worker and client, for a really insignificant reason, i can't even recall. My co worker took me aside and asked me how i felt after my concussion, she was great, listening to me tell her about my fear and the way i had spoken to meredith. she told me about a number of people she knew had undergone severe personality changes, profound changes, mild people suddenly becoming agggressive, and we looked up some stuff on the net about post concussion syndrome. the descriptions matched my behaviour.
i went to the drs. and was told i had brain damage, that my personality had transformed and that i will need pychiatric help. fucking great hey, i guess all those previous blows to the head must have caused some damage and this recent one been the one that sent me over the edge.
I printed some info out to send to meredith, and then went to see a dr. apparently the dr. says i have brain damage and will need to see a psychiatrist and that it may take up to 6 months for my old personality to make an appearence, so understandably i am somewhat bewildered.
part of me wnats to have a bit of fun with captain mission V2 but to be honest i was quite happy with V1


Traumatic Brain Injury:
A brief overview of traumatic injuries and the neurobehavioral deficits that can occur

What is a neurobehavioral deficit?

Neurobehavioral deficits or disorders include impairments of cognition, mood and/or behavior. Cognition includes intellectual functions of the brain such as memory, attention, and problem solving.

What is the scope of the problem in TBI?

Traumatic brain injury (TBI) is a widespread and very significant source of disability, often due to neurobehavioral deficits. But there are no clear guidelines on how to manage these deficits. There is a critical need for research in this area.

TBI is an insult to the brain caused by an external physical force that may produce a diminished or altered state of consciousness. According to the CDC, an estimated 5.3 million Americans (just over 2% of the population) currently live with disabilities resulting from TBI. Yearly, 80,000 Americans experience the onset of long-term disability following TBI. Vehicle crashes are the leading cause of TBI. Falls are second, and the leading cause of brain injury in the elderly. Risk of TBI is highest among adolescents, young adults and those older than 75 years of age. The cost of traumatic brain injury in the US is estimated to be $48.3 billion annually. The number of TBI patients seeking services has increased, as survival rates have improved due to improved care.

The purpose of this information is to provide the reader with a basic knowledge of the mechanics of TBI, and the resulting neurobehavioral deficits. General information regarding evaluation and treatment will be covered. It is important to identify problems as early as possible so that appropriate evaluations and treatment can be established.

How does TBI cause changes in mental functions?

The way in which TBI affects the brain, which is referred to as the neuropathology of TBI, may be especially pertinent to the risk for neurobehavioral problems. There are several important components that can contribute to neurobehavioral (intellect, mood, behavior) outcome:

What was the person’s level of function and medical condition before the injury?
What is the location and severity of the brain injury?
How diffusely is the brain injured?
Has the person had previous injuries or diseases of the brain?
Has the person used, or still use, certain street drugs or alcohol?

The direct effects of trauma may be skull fractures, contusions (sort of a brain "bruise"), and/or bleeding into or around the brain. Injury to the brain can occur at several different levels, and depends upon the nature of the trauma. Penetrating injuries can be fairly well circumscribed, such as from a knife or bullet. In injuries such as from motor vehicle accidents or blunt trauma, common sites of contusions are the front part of the brain (frontal lobes) and the temporal lobes. This is because these parts of the brain sit next to bony prominences within the skull (see figure 1).



Figure 1: Picture of the brain with major areas identified. The frontal and temporal lobes are commonly damaged in trauma such as from motor vehicle accidents.

The majority of trauma, however, seems to result in diffuse or more widespread damage, and hence diffuse deficits and symptoms. The more diffuse injury to the brain is called diffuse axonal injury (DAI). It is characterized by stretching and shearing of individual axons, which are parts of the nerve cells. The brain normally floats in fluid within the skull. In accidents where there is an abrupt change in acceleration or deceleration, such as in a motor vehicle accident, the brain can be thrust forward and backward against the inside of the skull. This can cause a contusion to the part of the brain that directly strikes the skull, but it also results in the more diffuse injury to other nerve cells in the brain. This diffuse injury may underlie a broad range of symptomatology, such as deficits in arousal, attention, mood disturbance, and behavioral changes, even in "mild" head injury.

Severity of TBI: In assessing severity of the original injury, several factors are involved. Duration of loss of consciousness (LOC), initial score on the GCS (Glascow Coma Scale - a 15-point scale that determines depth of coma), and length of PTA (posttraumatic amnesia) are generally the measures used. Definitions can vary, especially in the area of so called "mild" injury, and can include brain-imaging criteria. In cases of mild injury, the initial GCS is usually 13-15; moderate 9-15; and for severe, 8 or less. In terms of LOC, there are also general guidelines. A mild injury usually results in LOC of less than 30 minutes; moderate injuries up to 24 hours; and severe injuries may have LOC greater than 24 hours. A mild injury generally results in PTA less than 1 hour. Within the spectrum of mild injury, attempts have been made to more accurately classify but there is no real consensus as of yet. Moderate injuries are associated with PTA of 1 - 24 hours. Moderate-severe injuries have PTA's of 1-7 days, and severe injuries usually result in PTA of over 7 days.

Post traumatic amnesia (PTA): PTA is the period of time after a patient emerges from coma that he has no continuous memory for day to day events. In other words, there is impaired memory for new information. Staff has to continually orient them to time and events. The end of PTA is defined as the return of continuous memory.

Seizure disorders: If seizures develop, they may have a role in certain symptoms. The incidence of seizure disorder or epilepsy developing within five years of closed head injury (CHI) is about 2 - 5%. The incidence following penetrating injuries is much higher. Since the type of seizure can often be complex partial (a type of seizure that may have motor and behavior changes associated with it), this contributes to the risk of developing mood and/or behavior symptoms.

Secondary mechanisms of injury: There are also secondary mechanisms of injury, besides the direct effects. Secondary mechanisms include delayed damage to the brain due to the release in the brain of substances that may aggravate the injury (excitatory neurotransmitters), or derangements in neurotransmitter function. Neurotransmitters are substances that naturally occur in the brain and allow cells to communicate and function. Examples include dopamine, norepinephrine, and serotonin. Although the status of neurotransmitters in more chronic TBI is not fully understood, disturbances in the function of these substances may underlie certain problems that follow TBI, such as mood, behavior or intellect problems. Medications may be used to try and normalize function, and consequently improve symptoms.

Chronic pain: Not infrequently, patients will develop acute or chronic pain after the TBI, such as headaches, which can be quite debilitating and aggravate mood, thinking, and behavior. Or the pain may be from other injuries that were sustained. This needs to be fully assessed and adequately treated.

What are the Neurobehavioral Deficits that can result?

TBI can result in variable constellations of cognitive or intellectual deficits, mood disturbances, personality changes, or behavioral problems (Table 1). The nature and severity of these changes depend upon a number of factors as mentioned, such as location and size of lesion, duration of coma and posttraumatic amnesia (PTA). Premorbid level of function, history of any substance abuse, as well as psychosocial factors also interact with the actual injury to affect outcome. Other factors also play a role, such as age and medical health, and history of previous brain injury. Different problems may arise at different stages of recovery.

Certain types of symptoms or deficits can be explained by the areas that are commonly damaged in TBI, such as the frontal lobes or temporal lobes. Injury to these parts of the brain can result in a range of behavioral, mood, and cognitive problems. But the more diffuse injury that can occur also contributes to the outcome. In general, there are certain loosely defined syndromes that can be referred to, such as post-concussion syndrome, or frontal lobe syndrome. But the qualification and quantification of symptoms that comprise these syndromes has not been standardized. Certain of these will be reviewed below.

Table 1: COMMON NEUROBEHAVIORAL DISORDERS OF TBI

Post concussion syndrome
Frontal lobe syndromes
Behavioral/personality changes
Cognitive (intellectual) deficits
Mood disorders
Sleep disorders
Post traumatic epilepsy or seizures
Chronic Pain, such as headaches

Postconcussion syndrome (PCS): The postconcussion syndrome (PCS) has been poorly defined and controversial for many years. It has come to refer to a rather broad range of symptoms and signs that can follow a brain injury (table 2). The term PCS is generally used to describe the cluster of symptoms that often follow mild brain injury and persist for a variable period of time, although the symptoms themselves can be seen after any severity of injury. Estimates of how often this syndrome can develop may not be entirely accurate, as many people do not seek medical attention for milder cases, but reports of 50% or so is not unusual. Although the majority of patients who develop these symptoms seem to show recovery over time, there appears to be a significant minority with persistent difficulties. Hence, even milder injuries can result in disabling symptoms in some cases.

In general, the symptoms can occur directly following an injury, or after a period of time. The role of other variables, such as psychological factors in delayed PCS is debated. Symptoms fall into several categories including somatic (physical symptoms), mood, behavior, and cognitive difficulties. They include headaches, dizziness, sensitivity to noise and light, irritability, anxiety, depression, fatigue, sleep and appetite disturbances, as well as problems with information processing, attention, concentration and memory. The symptoms can be variable and diverse, and very distressing to the patient and family members. The patient may worry that they sound like a hypochondriac, or that people will think they are "crazy." But these symptoms can be explained by the nature of the injury to the brain. Hence, they are truly neurological symptoms, and not primary psychiatric symptoms.

Loss of consciousness is not necessary for brain injury or for the development of PCS. In general, a mild injury is usually diagnosed when loss of consciousness is 30 minutes or less, and the patient does not show evidence of specific abnormalities on neurologic exam. Brain injury or dysfunction can be present even if the neurologic exam and tests such as a CT or MRI are normal. These tests may not be sensitive to the more subtle or diffuse effects of trauma on the brain (e.g., DAI). Cognitive impairments include deficits in information processing, attention, and concentration, which can persist in some cases.

Table 2: POSTCONCUSSION SYNDROME

Drowsiness
Blurred vision
Nausea/vomiting
Headache
Fatigue
Dizziness/light headedness
Memory problems
Concentration/attention problems
Depression
Anxiety/irritability
Insomnia
Sensitivity to noise and light
Somatic complaints
ETOH intolerance

Headaches: Headaches are fairly common following even mild brain injury. They can resolve over time, even up to a year out from the injury. In some cases, they persist, and can be disabling. They can be migrainous, tension type or mixed in nature. There is very little research on posttraumatic headaches, and their treatment is often that of other chronic headaches. This approach can be effective, but not always.

Frontal Lobe Syndromes: Trauma commonly effects the frontal regions, either directly or indirectly. Dysfunction of the prefrontal regions can result in a variety of neurobehavioral symptoms. Generally referred to as "frontal lobe" syndrome, the profile includes symptoms of behavioral dyscontrol such as impulsivity and aggression, amotivation, apathy, disorganization, attentional and memory deficits, and mood dysregulation (e.g., moodiness, irritability, "mood swings"). Neuropsychological testing (see below) and reports from family and caretakers who know the patient are essential to the assessment.

Essentially, treatment consists of several components. These include pharmacologic treatment, behavioral strategies, and education and support of the family. The frontal lobe patient often losses his ability to control or monitor his own behavior, but will respond well when consistent external structure is set up. Treatment can focus on particular aspects, such as dyscontrol, aggression, or mood disturbances using certain medications.

Mood Disorders: Mood disturbances following brain injury can present in a variety of ways. It is not unusual for the mood symptoms to be subtle, but for behavioral manifestations to predominate, such as irritability, uncooperativeness, apathy, poor progression or effort in rehabilitation. The mood disturbances may not necessarily meet traditional psychiatric criteria, but may present more as a mood lability or dyscontrol. Often, it is more accurate to refer to a dysregulation of mood, as brain injured patients can show features of several mood disorders, rather than fit neatly into any one diagnostic category currently used. The traumatic brain injured population is at increased risk for developing depressive disorders, with estimates of major depression occurring at about 25% or higher.

In general, a depressive disorder should be suspected when the patient's degree of disability is greater than would be expected given the severity of injury, or when the patient fails to meet rehabilitation goals, or cooperate with treatment. It is not unusual for some mood disturbed patients to deny a depressed mood upon questioning. Since mood disturbances can often be missed in this population, and can have deleterious effects on outcome, it is wise to have a high level of suspicion.

For depression, the treatment is often similar to that of non-neurologically impaired depressed patients. Choice of treatment often depends on the patient’s individual response and side effect profiles of these drugs. Another disturbance of mood, mania or hypomania, can result, but is not as common. Mania refers to the presence of pressured speech, inability to stay on topic or on track, hyperactivity, a feeling of racing thoughts, and sometimes unusual ideas. The person may seem "wired" and edgy. It is important not to equate symptoms with diagnosis in this population. A patient who shows features of mania does not necessarily have a true bipolar disorder, and this may be over-diagnosed. Damage to the frontal lobes can produce a similar picture, and may respond to certain treatments.

Behavioral / Personality Changes: Depending on the location and severity of the injury, different types of behavioral disturbances can occur. These include irritability, lability, impulsivity, disinhibition, aggression, poor motivation, poor self-regulation of behavior, poor judgement and insight, risk taking, or sexual disturbances. Certain of these symptoms are separated out for purposes of discussing assessment and treatment, but clinically, they often occur together, as in a more generalized frontal lobe syndrome. Aggression can occur following brain injury, particularly in the more acute stages, and cause significant disruption of rehabilitation efforts. It can range from mild verbal abusiveness to physical assaultiveness. It is important to characterize the aggressive behavior. Is the patient labile? Is the patient impulsive and unable to self regulate? Is there a mood change associated with the behavior? What are the triggers? Is the aggression against self, others, or objects? A thorough evaluation of the behavior is needed. Only then can an appropriate behavioral strategy and possibly pharmacologic intervention be instituted. Behavioral strategies are beyond the scope of this review, but can be very helpful.

Aggression is a symptom that can have a variety of underlying causes. For example, if it is part of a frontal lobe syndrome, then the treatment may be different than for aggression resulting from psychosis, mood disturbance, or seizure disorder. This is often not obvious, and treatment may be trial and error. Polypharmacy (the use of more than one medication) may be unavoidable in the complex patient, and it is best to obtain a consultation.

Personality Changes can be viewed as existing on a spectrum with other behavioral problems. The patient may not seem like his or her "old self." On the milder end, you can see an exaggeration of the patient's premorbid negative personality traits. For example, an impulsive, irritable person may become more so. In more serious cases, it is common for families to complain that the patient has become a "different person." Children can appear hyperactive or develop symptoms consistent with attention deficit disorder, or conduct disorder.

Personality and behavioral changes can be seen as a result of two factors. First, damage to structures directly responsible for behavior and emotion. Second, cognitive (intellectual) deficits can alter and impair the patient’s interpretation of the environment or a situation, which in turn effects the patient's response.

It is important to educate the families concerning these possible changes, as they will tend to interpret the patient as purposefully aggravating them or being mean or difficult. Pharmacologic treatment is usually aimed at a syndrome, such as PCS or frontal dysfunction, or could target predominant symptoms such as depression or irritability.

Cognitive Deficits: These can be a significant cause of disability and distress for the patient and family. In general, the common nonspecific symptoms are disturbances in arousal, attention and concentration. Memory impairments can occur, either due to direct effects on memory function, or secondary to poor attention and concentration. Disturbances of higher level or executive functions (frontal lobe functions) are fairly common, due to the high percentage with frontal lobe involvement. These include poor planning, sequencing, and judgment. The patient may make errors due to impulsivity, and have trouble shifting between tasks. Specific deficits in cognition will depend upon location and severity of injury, as well as some of the factors already mentioned, such as level of education. These deficits may not be apparent while the patient is recovering at home, if no real intellectual challenges are present. Not uncommonly, the patient will realize these problems when they try and return to work, and they find they can’t do the quality or amount of work they used to do.

Pharmacotherapy has expanded and has great potential in the area of cognition. Cognitive Rehabilitation is gaining increased acceptance as an important component in the rehabilitation of brain injured patients. It may be particularly critical in the acute stage of recovery (up to 6 months post-injury), and could complement pharmacotherapy. It often involves techniques to retrain the patient in specific domains such as memory and attention. Different theoretical frameworks have been proposed to guide remediation strategies, and recent assessments support their effectiveness.

Sleep disturbance: This can be a significant problem following brain injury. It can be overlooked, but can significantly impede the patient's rehabilitation. Lack of sleep can worsen cognition, behavior and mood, and undermine treatment attempts. Disturbed sleep is very common in the first few months following traumatic brain injury, and may or may not resolve. Daytime sleepiness can also be a problem. There is often a reversal of the sleep-wake cycle, which seems to be part of a general dysregulation that can also be seen in other functions such as appetite. Treatment consists of medication and behavioral management. Behaviorally, standard sleep hygiene should be used. The patient should keep regular hours, avoid caffeine, alcohol and tobacco, and activities that are too stimulating before bedtime. If a sleep disorder is persistent and treatment refractory, a sleep study is warranted. In our clinic there have been at cases of sleep apnea identified after an injury, although there is no clear data on the incidence of this disorder following trauma.

How should someone with these difficulties be evaluated?

It is important to see someone with expertise in the assessment of TBI, as it is a specialized area. This is a multidisciplinary area, so there are neurologists, rehabilitation doctors, neuropsychiatrists, neuropsychologists, and other specialists who can provide components of the assessment.

Physician Exam: Part of the evaluation often consists of an examination by a physician with expertise in TBI. This may include obtaining a thorough history, as well as a neurological examination.

Neuropsychological testing: Another important part of the assessment is a battery of tests referred to as the neuropsychological assessment. This will give a clear picture of the quantity and type of intellectual deficits, as well as assess emotional and behavior problems. This evaluation may take several hours or longer, depending on the length of the battery. The results provide an excellent "map" of the actual brain functions that can serve as a guide to direct treatment.

Brain Imaging: With the advances in neuroimaging, or brain scanning techniques, it is rapidly becoming an excellent tool to help assess brain injury. Usually it is most helpful in conjunction with the other parts of the evaluation. In resting imaging, such as with CT or MRI, we can take a snapshot of the brain to look for structural changes. Brain injury, particularly the more diffuse kind, is not always visible on routine brain imaging, such as CT or routine MRI. There are now more specialized ways to image this type of injury, such as advanced techniques with MRI.

Functional imaging such as with MRI (magnetic resonance imaging), PET (positron emission tomography) or SPECT (single photon emission computed tomography) may be more likely to show areas of injury or dysfunction in the brain, but are not usually routine in a clinical setting. In functional imaging, the patient is asked to perform certain tasks such as finger tapping, remembering a list of words, or choosing a response while in the scanner. This allows us a window to look at how the brain actually works during a task. Details of types of brain imaging will be covered in another review. Brain imaging also has allowed us to advance the type of research we can do. It provides a way to assess how certain drugs or other interventions may work in TBI.

What are Options for Treatment?

Neuropharmacology: This is a complicated and evolving area that shows considerable promise for improving outcome and quality of life for brain injured patients. Treatment is driven by several considerations: alleviation of specific syndromes/symptoms (such as depression or apathy), the underlying neuropathology (nature of the injury) , improving cognition, and potential effects on recovery. Choice of a medication that can cover more than one area is always preferable. Specific medications will be covered in separate reviews.

General guidelines to pharmacologic treatment can be followed:

Use neuropharmacology based on underlying disturbances related to TBI- such as knowledge about which neurotransmitters or brain chemicals are affected.
In addition, certain target symptoms, such as insomnia, fatigue, depression or attentional problems can be addressed
Associated problems such as chronic pain or seizures must be addressed and adequately treated.
All efforts to be made to avid drugs for any condition that could worsen mental status or possibly interfere with recovery
Conclusion:

As technology improves, more people who suffer brain injury can survive. And even the less life threatening forms of TBI can result in significant problems that may persist, or even arise down the road from the injury. These individuals are often young, and otherwise healthy. Persistent cognitive, behavioral, or mood disturbances significantly affect short and long term outcomes. They are commonly referred to as the "walking wounded." They may appear physically recovered, but problems reintegrating into family, work, or school can quickly become apparent. They become labeled as difficult, lazy, somatic, or histrionic. They may be diagnosed and treated incorrectly, resulting in a worsening of the situation.

Education and appropriate referrals /interventions must be initiated as early as possible. Too often, these patients receive excellent acute care and initial rehabilitation, then are lost to follow-up. The loop of care must be closed. A significant number of these patients can achieve good function, but will require continuous and possibly life long access to various components of an interdisciplinary team. This ensures maximized quality of life, and is the most efficient, cost-effective route in the long term. This process should start at the initial contact with the patient and family. It should involve close collaboration between the family, patient, neurosurgeons, neuropsychiatrists, rehabilitation medicine, neurologists, other therapists, rehabilitation facilities, the workplace if applicable, and community groups.

Our emphasis on the neurologic basis for the outcome of TBI in no way negates the important role of other factors and non-medication treatments. TBI patients suffer significant losses, and these should be addressed. In general, supportive therapy and education of the patient as well as family are important components of treatment. Also, behavioral strategies are an essential component in the management of these patients. Cognitive rehabilitation is a promising and expanding area, that may either by itself or in conjunction with medication result in improved outcomes and function. Medication alone is rarely adequate.