O.K., so the title is not very original. Akin to "you can tune a piano, but you can't tuna fish". Don't get me started; there's plenty of one-liners in my repetoire.
I enjoy a play on words; their meaning can differ by context. For neuropsychologists, "denial" has multiple meanings. Denial is a psychological defense mechanism used (consciously or unconsciously) to minimize or ward off conflicted feelings, urges or responsibility for behavior. In the hierarchy of psychological defenses (e.g., repression, projection, rationalization) it is arguably the most primitive and fragile. In early stages of recovery, alcoholics are said to be in denial of their illness. Stages of grief are said to begin with denial. When denial is breached, a flood of emotion will invariably emerge. At this point the psychological integrity of the individual depends on support from family, friends and professionals as well as an ability to marshal healthier defenses and a willingness to face the conflict.
Neurologically, "denial" is associated with brain damage, particularly to the right frontal-parietal regions. This is different from psychological denial. I observed a classic form of neurological denial during my first year of internship at Mt. Sinai Hospital's Department of Neurosurgery service. A patient was admitted for surgical removal of a brain tumor located on the right frontal-parietal brain region. The tumor was compressing the motor and sensory portion of the brain that caused the patient to experience no sensation and paresis of the (opposite side) left upper extremity. On morning rounds, the patient was alarmed that someone had played a cruel joke on him by placing someone else's left arm in his bed! To demonstrate his concern, he routinely raised the limp left arm, as if it was not his own. I was amazed that I was witnessing the classic "anosognosia" described by the French neurologist Babinski many years ago. A less severe form of neurologic denial is termed "neglect," wherein a person will neglect the left side of space. We had a patient with spatial neglect who would not eat from the left side of his plate or shave the left side of his face. Though vision (optic nerve) is functional, damage to right parietal regions can cause a neglect or inability to integrate visual information on the left side of each eye (not blindness). Not surprisingly, patients with slow growing tumors to right parietal brain regions may have a tendency to bump into objects on their left side. This can be of great concern when multiple car accidents result from left-sided inattention. Sometimes, a history of multiple car accidents to one side may alert an astute clinician to rule out neurological neglect of space. When patients are confronted with these facts (i.e., hemiparetic left arm, bumping into objects, motor vehicle accidents on the left side of the car), neurologic"denial" is the typical response (not their arm, someone else caused the car accidents). This condition should be differentiated from a recent syndrome (SMS-Soccer Mom Syndrome) caused by mini-vans rapidly backing out of the garage (clipping the side view mirror or knocking over the mailbox) to get a child to soccer practice. Denial in this case is often attributed to the garage opening being too narrow or the mailbox "getting in the way".
I became very interested in the role of parietal lobe dysfunction and denial when I evaluated more cases at the hospital. Critchley's 1950's book on the "Parietal Lobes" helped me understand neurologic denial. Critchley posited that body image perception was one function of the parietal lobe, particularly on the right side of the brain. Therefore, damage or dysfunction to this region could lead to altered body perception. So, denial of deficits could be the result of body misperception. I concluded this is likely on a continuum, as some patients were aware of their deficits but exhibited "la belle indifference". By contrast, patients with left parietal lobe damage may often exhibit a catastrophic reaction to their deficits. For example, neuropsychological testing can include immediate performance feedback (to the patient) measuring their learning curve on a new task. Left parietal lobe patients often cry, or become angry with their mistakes. The right parietal lobe patient may seem indifferent to their errors.
Right parietal lobe dysfunction, affecting body image perception, led me to think about anorexia. Some studies on anorexics had demonstrated their tendency to over-estimate body size. I hypothesized that perhaps anorexics had some parietal lobe dysfunction that could be measured on neuropsychological tests. I was very excited about pursuing this line of research. However, I already started a major study on frontal lobe dysfunction for my doctoral thesis. To this day, I believe the anorexic study would be a very fascinating topic (if not already done) for a budding graduate student.
Neurologic denial is not limited to hemiparetic arms or not shaving the left side of one's face. Its complexity is seen particularly with individuals who make a good recovery in a patient's adjustment to his permanent deficits. A few examples of this challenge are: denial of memory deficits, inability to safely operate a motor vehicle, and difficulty accepting vocational/educational limitations. The neuropsychologist, often called upon to conduct objective testing of a patient's abilities (and limitations), can become a target of patient frustration when a "reality check" is rendered. Patients who sustain right parietal lobe damage, can "neglect" the left side of space. Neuropsychological testing can assess a patient's reaction time, visual scanning speed and ability to make rapid visual judgments. Through the course of my career, I have had the unpleasant duty (on numerous occasions) of advising that an individual's driver's license be suspended. Though family members of the patient are relieved and grateful for this news, the patient usually feels otherwise. I always offer a patient the option of a second opinion. Some patients, upon hearing the same recommendation from colleagues, will seek out a 3rd, 4th and 5th opinion. Sadly, even when referred for counseling, neurologic denial can be life-long and intransient. Other patients begin to undertstand their limitations over time, but vehemently insist that, with additional physical or occupational therapy, they will drive again...get their old job back...or even regain full use of a hemiparetic limb.
I have compassion for these patients, even if I'm unpopular with them for taking their license away. When an individual's freedom and independence are limited, it is difficult to accept. This is true with the elderly as well, who must relinquish their freedoms when physical or mental demands exceed their abilities. This "hit home" for me a few years ago, when I received a frantic call from my oldest daughter who was watching the younger children while my wife and I were attending a jazz concert. She said, "Dad, grandma just drove through the garage door with her car." After hearing the children (and my mother) were unharmed, I advised my daughter to contact the fire department to inspect the integrity of the house. The damage was significant, but reparable. My mother's reaction was that a child on a tricycle could have caused the same damage. This is when I knew it was time to take the keys away. She, in her late 80s, simply did not have the coordination and reaction time to drive any longer. I knew she was in denial. Not neurologic denial, but I am your mother-tough-as-nails-who changed-your-diapers-smarty-pants-doctor denial. So, I left the decision to her. I would either take away the keys, or refer the issue to her primary care physician. Reluctantly, she conceded with grace, knowing it was the right thing to do.
So, denial is an overcrowded river with many people. Some have psychological issues, some neurologically based, and others, a mixture of both. Wading through the river, while keeping afloat, is part of our challenge. This week I saw a classic case of neurological denial for evaluation. It was also a week of remembrance for me; one of my mother's recent passing. Undeniably, she is missed by many.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
Diplomate, American Board of Professional Neuropsychology
Thursday, October 1, 2009
Sunday, September 27, 2009
Attention: Please!
I evaluate children, adolescents and adults referred for the question of ADHD diagnosis. One of my favorite questions for adults is: "Have you read the book Driven To Distraction?"(Halowell, 1994). A typical response: "I started reading it Doc, but got distracted and never finished it!" Does this cap a diagnosis of ADHD? No, but it's amusing. The real challenges are: defining ADHD, understanding the subtypes, differential diagnosis, intervention strategies and further research.
The acronym "ADD" no longer exists in DSM-IV (Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition) or most diagnostic manuals and textbooks. Attention Deficit Hyperactivity Disorder (ADHD) now applies to both the hyperactive and non-hyperactive types. DSM-IV lists four subtypes of ADHD: Inattentive, Hyperactive-Impulsive, Combined and Not Otherwise Specified. Years ago, it was believed that a child must be hyperactive to have "ADD". Boys outnumbered girls 4:1, as they tended to display greater hyperactivity. The ratio is now closer to 2:1 with the advent of the non-hyperactive variety attributed more girls with ADHD. Recent estimates suggest that 5% of the general population may have ADHD. This implies that many individuals, particularly adults, were never diagnosed, but manifested symptoms as children that have persisted to adulthood. When news of adult ADHD hit the media, a large influx of individuals contacted our office for evaluation and treatment.
PET scan studies have identified three neurotransmitters (dopamine, serotonin, and norepinephrine) that are depleted in individuals with ADHD. Dopamine plays a critical role in attention and concentration, with serotonin and norepinephrine affecting mood. One theory about ADHD is that diminished dopamine leads to chronic"under-stimulation". The hyperactive-impulsive subtype will seek out stimulation (many times to their detriment) to compensate for under-stimulation. This may account for living on the edge, risky behaviors, and impulsive actions designed to stimulate an otherwise sluggish attentional system. To the extreme, impulsive behaviors serve to create conflict and trauma for the individual. They achieve a high level of stimulation, but at the expense of self-sabotage. Statistics note that hyperactive-impulsive boys have, on average, two misdemeanors by age 14. Their female counterparts, on average, have four times the national average of pregnancy by age 16. One-third of hyperactive-impulsive individuals are substance abusers (typically marijuana and cocaine) to self-medicate dopaminergic stimulation. Many do not complete high school, with even fewer completing a college education. The pattern of instability persists in adulthood. Frequent job changes (e.g., 20 jobs in 5 years), living at home with their parents (in their 30's), multiple divorces, bankruptcy, projects started and left undone, and chronic substance abuse are some of the sobering trends. In my opinion, the hyperactive-impulsive subtype has the poorest long-term prognosis of all four subtypes. Some of these individuals are charged with criminal activity resulting from impulsive acts (which may also correlate with a high incidence of co-morbid Oppositional Defiant Disorder).
In the past few years, some defense attorneys have requested my "expert" assessment that their clients' ADHD behavior "caused" them to commit various crimes (petit larceny, breaking and entering, burglary). The "Twinkie Defense" comes to mind (e.g., suing McDonalds because their food caused a person to become obese). I was asked to consult on a case where an ADHD young adult broke into a pizza establishment at 1:00 a.m. because he was hungry for chicken wings. Amazingly, despite the security alarm alerting the police, the ADHD perpetrator did not run away, as the wings were not fully cooked. He was arrested, wings (medium hot sauce) and all. This is a great example of impulsivity and very poor judgement for good measure. Though I will evaluate and promote appropriate treatment for ADHD individuals, I also believe taking personal responsibility for one's actions is an important developmental life skill.
The Inattentive ADHD individual is quite different from the Hyperactive-Impulsive subtype. They are often described as: "daydreamers," disorganized, visually inattentive and/or forgetful (e.g., misplacing keys, wallet), slow to initiate and complete tasks, and as having difficulty with time management. Literature reviews and case studies (e.g., Wasserstein, 2001; Halperin et al., 2008) have suggested possible right hemispheric dysfunction in Inattentive subtypes paralleling similar attributes with Non-Verbal Learning Disabilities (NVLD). Recent articles have coined the term "sluggish cognitive tempo" to describe the Inattentive Type. Generally, Inattentive children and adults do not exhibit hyperactivity (likely resembling the old ADD type) or highly impulsive behaviors. I observe some co-morbid anxiety, obsessive-compulsive behaviors, and mood disorders in this group who may improve with psycho-stimulants and/or SSRIs (e.g. Fluoxetine). The perception of time seems "off" with these individuals (e.g., what ten minutes "feels" like). Using specific time frames for an activity (while the child or adult refers to a digital watch) may improve initiation and perception of time with task completion.
Treating the Combined Type of ADHD is quite challenging. Patients exhibit both Hyperactive-Impulsive behaviors and Inattentive features. They are risk-takers living on the edge who are not always vigilant of their surroundings. Thoughts of George of The Jungle come to mind ("watch out for that tree!"). Many accidental traumatic brain injury children I evaluated over the years had a pre-morbid history of ADHD. This may relate to the statistic that ADHD children have a four-fold greater chance of sustaining a serious brain injury due to accidents (e.g., not looking both ways when crossing the street) compared to non-ADHD children.
The Not Otherwise Specified subtype of ADHD is likely not utilized by clinicians very often. This subtype is basically anyone who does not fulfill criteria for the other three. This subtype may in fact be one of the other three, but in a milder form. ADHD subtypes seem to be on a continuum. Often the rule of thumb is, to what extent is the condition disabling or limiting the individuals' social, educational and vocational potential? It is important to ask this question when interviewing a patient (and family members) as the patient may be compensating quite well for their ADHD challenges. I suspect that well before ADHD became a chic diagnosis, some individuals developed their own home grown methods to compensate for their difficulties (and strict teachers who, according to some patients, used inappropriate methods to gain a student's attention, such as striking their knuckles with a ruler).
In my opinion, misdiagnosis (and overdiagnosis) of ADHD certainly exists. In some clinics, an individual can report a laundry list of ADHD symptoms (often derived from the Internet) and walk out with a controlled substance prescription 15 minutes later. Another scenario is the double-blind method of diagnosis. Two packets, A and B, are given to a parent. One packet contains medication (e.g. Ritalin), the other, a placebo. For week 1 packet A is administered, week 2 packet B. Parents and teachers are "blind" to which packet contains medication. The child's performance is rated in class. If the child is more attentive when the medication packet was administered (with no behavioral change during the placebo trial), lo and behold they must have ADHD! Science is a wonderful thing! The problem is, most people (who are not ADHD) would experience improved attention and concentration with a psycho-stimulant; it is a matter of degree. This may be one reason ADHD is over-diagnosed and over-medicated. So how can we improve the accuracy of ADHD diagnosis?
We do not (yet) have a blood test for ADHD. PET scan studies are highly expensive and used mostly as a research tool. Most neuropsychologists would agree that one systematic, objective test does not yet exist to reliably diagnose ADHD. The research on ADHD neuropsychological testing protocols is promising as some trends are evolving (e.g., potential right hemispheric dysfunction in Inattentive subtypes). It is also important to distinguish ADHD (familial?) from acquired forms, arising from TBI or perhaps toxins. Some research has suggested a possible link of mothers smoking during pregnancy and having a ADHD child (incidentally, ADHD mothers may have a higher incidence of smoking cigarettes thus the child's ADHD may be familial).
Many physicians require their patients undergo testing to confirm an ADHD diagnosis. In my practice, neuropsychological ADHD testing includes: clinical interview of the patient and family members, review of school/work/medical records, and measures of: intelligence, working memory, short-term memory, visual-motor development, perceptual organization, tests of vigilance (both auditory and visual of increasing complexity), achievement, central auditory processing, executive functions, simple and divided attention, personality assessment, and behavioral assessment scales. This in-depth examination objectively measures various components of information processing and attention/concentration compared to the individual's overall abilities. Statistically significant differences between ability and measures of ADHD attributes (while ruling out other potential causes for diminished attention) aids the objective diagnosis. I am analyzing neuropsychological test data collected on my ADHD patients over the past ten years. If specific tests cluster and have predictive power or loading on ADHD behaviors, a systematic testing battery may emerge.
When a diagnosis of ADHD (and subtype) is rendered, the findings and recommendations are shared with the patient, family (when appropriate and consented), and primary care physician. Medication options, if advised, are discussed. In school-aged children, various accommodations are integrated with a 504 Plan or Individualized Education Plan. For adults, job modifications or the services of a job coach may be needed. The suggestion of individual and couples therapy may also emerge to help educate and navigate the ADHD behaviors. Balancing these recommendations can be challenging, depending on the subtype, and if co-morbid psychological issues (e.g. anxiety, OCD behaviors, mood dysfunction) are part of the equation.
Our knowledge of ADHD is expanding. As with any clinical condition, keen observation, rigorous research and education is important. I am in the process of completing my first book on various clinical conditions through the stories of my patients. One of the chapters is dedicated to pediatric and adult ADHD. I am grateful to these patients for allowing me to share their stories.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
Diplomate, American Board of Professional Neuropsychology
The acronym "ADD" no longer exists in DSM-IV (Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition) or most diagnostic manuals and textbooks. Attention Deficit Hyperactivity Disorder (ADHD) now applies to both the hyperactive and non-hyperactive types. DSM-IV lists four subtypes of ADHD: Inattentive, Hyperactive-Impulsive, Combined and Not Otherwise Specified. Years ago, it was believed that a child must be hyperactive to have "ADD". Boys outnumbered girls 4:1, as they tended to display greater hyperactivity. The ratio is now closer to 2:1 with the advent of the non-hyperactive variety attributed more girls with ADHD. Recent estimates suggest that 5% of the general population may have ADHD. This implies that many individuals, particularly adults, were never diagnosed, but manifested symptoms as children that have persisted to adulthood. When news of adult ADHD hit the media, a large influx of individuals contacted our office for evaluation and treatment.
PET scan studies have identified three neurotransmitters (dopamine, serotonin, and norepinephrine) that are depleted in individuals with ADHD. Dopamine plays a critical role in attention and concentration, with serotonin and norepinephrine affecting mood. One theory about ADHD is that diminished dopamine leads to chronic"under-stimulation". The hyperactive-impulsive subtype will seek out stimulation (many times to their detriment) to compensate for under-stimulation. This may account for living on the edge, risky behaviors, and impulsive actions designed to stimulate an otherwise sluggish attentional system. To the extreme, impulsive behaviors serve to create conflict and trauma for the individual. They achieve a high level of stimulation, but at the expense of self-sabotage. Statistics note that hyperactive-impulsive boys have, on average, two misdemeanors by age 14. Their female counterparts, on average, have four times the national average of pregnancy by age 16. One-third of hyperactive-impulsive individuals are substance abusers (typically marijuana and cocaine) to self-medicate dopaminergic stimulation. Many do not complete high school, with even fewer completing a college education. The pattern of instability persists in adulthood. Frequent job changes (e.g., 20 jobs in 5 years), living at home with their parents (in their 30's), multiple divorces, bankruptcy, projects started and left undone, and chronic substance abuse are some of the sobering trends. In my opinion, the hyperactive-impulsive subtype has the poorest long-term prognosis of all four subtypes. Some of these individuals are charged with criminal activity resulting from impulsive acts (which may also correlate with a high incidence of co-morbid Oppositional Defiant Disorder).
In the past few years, some defense attorneys have requested my "expert" assessment that their clients' ADHD behavior "caused" them to commit various crimes (petit larceny, breaking and entering, burglary). The "Twinkie Defense" comes to mind (e.g., suing McDonalds because their food caused a person to become obese). I was asked to consult on a case where an ADHD young adult broke into a pizza establishment at 1:00 a.m. because he was hungry for chicken wings. Amazingly, despite the security alarm alerting the police, the ADHD perpetrator did not run away, as the wings were not fully cooked. He was arrested, wings (medium hot sauce) and all. This is a great example of impulsivity and very poor judgement for good measure. Though I will evaluate and promote appropriate treatment for ADHD individuals, I also believe taking personal responsibility for one's actions is an important developmental life skill.
The Inattentive ADHD individual is quite different from the Hyperactive-Impulsive subtype. They are often described as: "daydreamers," disorganized, visually inattentive and/or forgetful (e.g., misplacing keys, wallet), slow to initiate and complete tasks, and as having difficulty with time management. Literature reviews and case studies (e.g., Wasserstein, 2001; Halperin et al., 2008) have suggested possible right hemispheric dysfunction in Inattentive subtypes paralleling similar attributes with Non-Verbal Learning Disabilities (NVLD). Recent articles have coined the term "sluggish cognitive tempo" to describe the Inattentive Type. Generally, Inattentive children and adults do not exhibit hyperactivity (likely resembling the old ADD type) or highly impulsive behaviors. I observe some co-morbid anxiety, obsessive-compulsive behaviors, and mood disorders in this group who may improve with psycho-stimulants and/or SSRIs (e.g. Fluoxetine). The perception of time seems "off" with these individuals (e.g., what ten minutes "feels" like). Using specific time frames for an activity (while the child or adult refers to a digital watch) may improve initiation and perception of time with task completion.
Treating the Combined Type of ADHD is quite challenging. Patients exhibit both Hyperactive-Impulsive behaviors and Inattentive features. They are risk-takers living on the edge who are not always vigilant of their surroundings. Thoughts of George of The Jungle come to mind ("watch out for that tree!"). Many accidental traumatic brain injury children I evaluated over the years had a pre-morbid history of ADHD. This may relate to the statistic that ADHD children have a four-fold greater chance of sustaining a serious brain injury due to accidents (e.g., not looking both ways when crossing the street) compared to non-ADHD children.
The Not Otherwise Specified subtype of ADHD is likely not utilized by clinicians very often. This subtype is basically anyone who does not fulfill criteria for the other three. This subtype may in fact be one of the other three, but in a milder form. ADHD subtypes seem to be on a continuum. Often the rule of thumb is, to what extent is the condition disabling or limiting the individuals' social, educational and vocational potential? It is important to ask this question when interviewing a patient (and family members) as the patient may be compensating quite well for their ADHD challenges. I suspect that well before ADHD became a chic diagnosis, some individuals developed their own home grown methods to compensate for their difficulties (and strict teachers who, according to some patients, used inappropriate methods to gain a student's attention, such as striking their knuckles with a ruler).
In my opinion, misdiagnosis (and overdiagnosis) of ADHD certainly exists. In some clinics, an individual can report a laundry list of ADHD symptoms (often derived from the Internet) and walk out with a controlled substance prescription 15 minutes later. Another scenario is the double-blind method of diagnosis. Two packets, A and B, are given to a parent. One packet contains medication (e.g. Ritalin), the other, a placebo. For week 1 packet A is administered, week 2 packet B. Parents and teachers are "blind" to which packet contains medication. The child's performance is rated in class. If the child is more attentive when the medication packet was administered (with no behavioral change during the placebo trial), lo and behold they must have ADHD! Science is a wonderful thing! The problem is, most people (who are not ADHD) would experience improved attention and concentration with a psycho-stimulant; it is a matter of degree. This may be one reason ADHD is over-diagnosed and over-medicated. So how can we improve the accuracy of ADHD diagnosis?
We do not (yet) have a blood test for ADHD. PET scan studies are highly expensive and used mostly as a research tool. Most neuropsychologists would agree that one systematic, objective test does not yet exist to reliably diagnose ADHD. The research on ADHD neuropsychological testing protocols is promising as some trends are evolving (e.g., potential right hemispheric dysfunction in Inattentive subtypes). It is also important to distinguish ADHD (familial?) from acquired forms, arising from TBI or perhaps toxins. Some research has suggested a possible link of mothers smoking during pregnancy and having a ADHD child (incidentally, ADHD mothers may have a higher incidence of smoking cigarettes thus the child's ADHD may be familial).
Many physicians require their patients undergo testing to confirm an ADHD diagnosis. In my practice, neuropsychological ADHD testing includes: clinical interview of the patient and family members, review of school/work/medical records, and measures of: intelligence, working memory, short-term memory, visual-motor development, perceptual organization, tests of vigilance (both auditory and visual of increasing complexity), achievement, central auditory processing, executive functions, simple and divided attention, personality assessment, and behavioral assessment scales. This in-depth examination objectively measures various components of information processing and attention/concentration compared to the individual's overall abilities. Statistically significant differences between ability and measures of ADHD attributes (while ruling out other potential causes for diminished attention) aids the objective diagnosis. I am analyzing neuropsychological test data collected on my ADHD patients over the past ten years. If specific tests cluster and have predictive power or loading on ADHD behaviors, a systematic testing battery may emerge.
When a diagnosis of ADHD (and subtype) is rendered, the findings and recommendations are shared with the patient, family (when appropriate and consented), and primary care physician. Medication options, if advised, are discussed. In school-aged children, various accommodations are integrated with a 504 Plan or Individualized Education Plan. For adults, job modifications or the services of a job coach may be needed. The suggestion of individual and couples therapy may also emerge to help educate and navigate the ADHD behaviors. Balancing these recommendations can be challenging, depending on the subtype, and if co-morbid psychological issues (e.g. anxiety, OCD behaviors, mood dysfunction) are part of the equation.
Our knowledge of ADHD is expanding. As with any clinical condition, keen observation, rigorous research and education is important. I am in the process of completing my first book on various clinical conditions through the stories of my patients. One of the chapters is dedicated to pediatric and adult ADHD. I am grateful to these patients for allowing me to share their stories.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
Diplomate, American Board of Professional Neuropsychology
Monday, September 21, 2009
Shaken Baby Syndrome: Contra-Coo
Although infants and young children do sustain accidental head injuries, in most cases, minor and mild head trauma symptoms are transient. An accidental head injury usually has an outward sign such as a bump, goose-egg, bruising or swelling, which is caused by the head striking an object or surface. Non-accidental head injuries- perhaps the euphemistic term for child abuse- are often not outwardly visible. They are usually caused by the violent shaking of an infant or very young child, which can result in brain damage or death. There has been recent renewed interest in Shaken Baby Syndrome (SBS), as ihas been reported that many cases may be undetected or under-acknowledged (Sydney Morning Herald, 9/18/09).
Studies suggest that approximately 1500 cases of SBS occur in the United States each year. The majority of children are under one year of age, though cases have been reported in the 2-5 year age group as well. An infant's brain is vulnerable to shaking due to the immature protective coating of brain cells and the sheath surrounding it. The classic "contre-coup" brain injury is exemplified in SBS. The primary impact of the brain hitting the skull is followed by a second force of the brain rocketing to the opposite side. The secondary point of impact (contre-coup) delivers a more severe blow. With multiple rounds of forceful shaking, the brain hits the skull repeatedly. There is also a rotational force of the brain causing a shearing of brain cells (both at higher and lower centers of the brain). As the network of blood vessels are still immature under the dura (brain sheath covering), they easily rupture and cause subdural hematomas. These hematomas are readily seen on CT scan or MRI. Neurological examination commonly reveals hemorrhaging blood vessels in the eye (retina). When external injuries (e.g. limb injuries) are absent, the presence of retinal hemorrhages may raise the red flag of SBS, but does not conclusively prove it. Retinal hemorrhages can arise from accidental trauma, arterio-venous malformations, and spontaneous subarachnoid bleeds. History, and a bit of detective work, are often needed to confirm the diagnosis.
A few years ago, an assistant district attorney requested my input on a case of suspected SBS. A three-year old (not your typical SBS aged child) sustained a brain injury documented on CT scan to both the back and front part of the brain (occipital and frontal subarachnoid hemorrhages). The parents signed sworn depositions that the injury occurred when the child, riding a tricycle, slammed her head into the bumper of the family's large 4x4 truck. There were no broken limbs. Retinal examination revealed some small "old" hemorrhages, that did not coincide with the time frame of the reported injury, yet perhaps significant evidence. I offered a narrative opinion after reviewing numerous records and CT scans . If the child actually hit her head on the large metal bumper, it would have required more significant force. Though she did have a bump on her forehead after the injury, it appeared too small to have resulted from a full frontal impact. The hemorrhages on CT scan were unequal. The larger hemorrhage was in the frontal region. If contre-coup physics are correct, and the child struck the frontal region on the metal bumper first, the smaller hemorrhage should have been in the frontal area and the larger one in the occipital region. On the contrary, a forceful shaking of the head backwards would likely produce a smaller occipital hemorrhage and larger frontal hemorrhage (as the brain rockets forward on secondary impact).
I concluded that the child's injuries were likely not due to hitting the bumper, but more consistent with a contre-coup SBS. My report was read aloud in the court though I was not present during the proceedings. The assistant DA called me with interesting news. When my report was concluded, the child's mother began to cry and yelled at her husband that she knew they would "get caught". I wish I could say I shared the assistant DA's enthusiasm for the confession and conviction. Yes, the child would now be remanded to foster care, and hopefully, placed in a stable and safe environment. Yet, she had sustained permanent brain damage at the hands of her own parents and would have to live with this knowledge. I wondered how many of these children go undetected or simply never reported.
Recently, I have read stories of young, single mothers whose babies died or were permanently brain injured by angry boyfriends. This is consistent with the statistics. Typically, males (husbands or boyfriends) are the perpetrators who become easily frustrated and angry with a baby's only form of communication, crying, and shake the children in an attempt to quiet them. Some mothers are also guilty of this behavior, but to a lesser degree.
Some intiative actions aimed at reducing this problem are raising public awareness of SBS and offering young parents child rearing and anger management classes.
Though this is speculative, some children with learning disabilities, neurodevelopmental delays and perhaps a subset of those with ADHD, may have sustained unreported SBS. In the future, a greater understanding of this public health issue may be gained through research and more accurate reporting of SBS.
So what about Uncle Harry who visits the new baby and loves to play "toss the kid" in the air? Most authorities agree that knee bouncing or lifting the baby gently in the air is fine. Common sense is the rule of thumb. I have to wonder, however, about the grey area between the gentle lifting and SBS, particularly during the first 18 months of life. If there is mounting concern internationally that many cases of SBS are under-detected (due to the fact that symptoms of lethargy and seizures can mirror other clinical conditions), vigilance (not hysteria) is appropriate and warranted. We should encourage gentle knee bouncing and discourage any behavior that is contra-coo.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
American Board of Professional Neuropsychology
Studies suggest that approximately 1500 cases of SBS occur in the United States each year. The majority of children are under one year of age, though cases have been reported in the 2-5 year age group as well. An infant's brain is vulnerable to shaking due to the immature protective coating of brain cells and the sheath surrounding it. The classic "contre-coup" brain injury is exemplified in SBS. The primary impact of the brain hitting the skull is followed by a second force of the brain rocketing to the opposite side. The secondary point of impact (contre-coup) delivers a more severe blow. With multiple rounds of forceful shaking, the brain hits the skull repeatedly. There is also a rotational force of the brain causing a shearing of brain cells (both at higher and lower centers of the brain). As the network of blood vessels are still immature under the dura (brain sheath covering), they easily rupture and cause subdural hematomas. These hematomas are readily seen on CT scan or MRI. Neurological examination commonly reveals hemorrhaging blood vessels in the eye (retina). When external injuries (e.g. limb injuries) are absent, the presence of retinal hemorrhages may raise the red flag of SBS, but does not conclusively prove it. Retinal hemorrhages can arise from accidental trauma, arterio-venous malformations, and spontaneous subarachnoid bleeds. History, and a bit of detective work, are often needed to confirm the diagnosis.
A few years ago, an assistant district attorney requested my input on a case of suspected SBS. A three-year old (not your typical SBS aged child) sustained a brain injury documented on CT scan to both the back and front part of the brain (occipital and frontal subarachnoid hemorrhages). The parents signed sworn depositions that the injury occurred when the child, riding a tricycle, slammed her head into the bumper of the family's large 4x4 truck. There were no broken limbs. Retinal examination revealed some small "old" hemorrhages, that did not coincide with the time frame of the reported injury, yet perhaps significant evidence. I offered a narrative opinion after reviewing numerous records and CT scans . If the child actually hit her head on the large metal bumper, it would have required more significant force. Though she did have a bump on her forehead after the injury, it appeared too small to have resulted from a full frontal impact. The hemorrhages on CT scan were unequal. The larger hemorrhage was in the frontal region. If contre-coup physics are correct, and the child struck the frontal region on the metal bumper first, the smaller hemorrhage should have been in the frontal area and the larger one in the occipital region. On the contrary, a forceful shaking of the head backwards would likely produce a smaller occipital hemorrhage and larger frontal hemorrhage (as the brain rockets forward on secondary impact).
I concluded that the child's injuries were likely not due to hitting the bumper, but more consistent with a contre-coup SBS. My report was read aloud in the court though I was not present during the proceedings. The assistant DA called me with interesting news. When my report was concluded, the child's mother began to cry and yelled at her husband that she knew they would "get caught". I wish I could say I shared the assistant DA's enthusiasm for the confession and conviction. Yes, the child would now be remanded to foster care, and hopefully, placed in a stable and safe environment. Yet, she had sustained permanent brain damage at the hands of her own parents and would have to live with this knowledge. I wondered how many of these children go undetected or simply never reported.
Recently, I have read stories of young, single mothers whose babies died or were permanently brain injured by angry boyfriends. This is consistent with the statistics. Typically, males (husbands or boyfriends) are the perpetrators who become easily frustrated and angry with a baby's only form of communication, crying, and shake the children in an attempt to quiet them. Some mothers are also guilty of this behavior, but to a lesser degree.
Some intiative actions aimed at reducing this problem are raising public awareness of SBS and offering young parents child rearing and anger management classes.
Though this is speculative, some children with learning disabilities, neurodevelopmental delays and perhaps a subset of those with ADHD, may have sustained unreported SBS. In the future, a greater understanding of this public health issue may be gained through research and more accurate reporting of SBS.
So what about Uncle Harry who visits the new baby and loves to play "toss the kid" in the air? Most authorities agree that knee bouncing or lifting the baby gently in the air is fine. Common sense is the rule of thumb. I have to wonder, however, about the grey area between the gentle lifting and SBS, particularly during the first 18 months of life. If there is mounting concern internationally that many cases of SBS are under-detected (due to the fact that symptoms of lethargy and seizures can mirror other clinical conditions), vigilance (not hysteria) is appropriate and warranted. We should encourage gentle knee bouncing and discourage any behavior that is contra-coo.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
American Board of Professional Neuropsychology
Thursday, September 17, 2009
Post Concussion Syndrome: Facts, Myth, and Enigma
Multiple blows to the head are not good. Circa 1997, I received a call from a colleague in Buffalo, New York asking if I would evaluate the Buffalo Sabres Hockey Team. One of their key players sustained two "concussions" within 12 hours. Their trainers wanted to know if he should play the next game. The battery of tests on all players were to be used as baseline data. Should a injury arise, I was to return within 24 hours and re-test the player to help determine their "fitness for duty". I was not a big hockey fan in those days, but my son really wanted an autographed hockey stick from the guys. Besides, the era of having professional evaluations of sports concussions was on the rise. A colleague who trained with me at Mt. Sinai Hospital in New York City's Department of Neurosurgey, was about to evaluate the New York Jets with a similar set of neuropsychological tests. The data accumulated from many professional contact sports teams evolved into screening instruments used widely today for professional sports and school football/hockey and even soccer teams.
My staff and I shuffled off to Buffalo in the dreary cold of February to arrive at the relatively new HSBC arena. After two days of testing the team members who were very cooperative we fowarded our findings to the team physician and key researcher in Pittsburgh.
The team was very careful to avoid concussional injuries from that point onward. They probably couldn't tolerate another Dr. Sorman evaluation. Unfortunately, the player who sustained the two concussions in 12 hours never returned to regular play, and became a footnote in the annals of hockey.
I learned from this experience, and through many sports related injuries sustained by my private patients over the years, that concussions are not additive; they are logarithmic. One plus one concussion does not equal two. The compounding effects of multiple concussions, over a short period of time, is problematic and potentially permenant. This is where the story of concussions, and the Post-Concussive Syndrome, becomes muddled.
A "concussion" is derived from the Latin "concussuss" meaning shake or shock. As noted in my earlier paper ("What's So Mild About Mild Traumatic Brain Injury"), operational definitions differ in MTBI. Similar differences are found in the literature on concussions and the so-called, Post-Concussion Syndrome.
According to the American Academy of Neurology, a concussion is a "trauma-induced alteration in mental status that may or may not involve a loss of consciousness. Confusion and amnesia are the hallmarks of concussion". Confusion and amnesia typically occur immediately after a blow to the head or several minutes later. Guidelines for the Management of Sports Concussions include the following symptoms:
1. A vacant stare
2. Slower to answer questions
3. Easily distracted
4. Slurred speech
5. Stumbling, inability to walk a straight line
6. Exterme emotions
7. Memory problems
8. Any period of loss of consciousness
A grading scale, developed by AAN, is often assigned to patients seen in the emrgency room:
Grade 1: Confusion and/or mental status changes with no loss of consciousness that resolves in less than 15 minutes.
Grade 2: Same as Grade 1, but symptoms last more than 15 minutes
Grade 3: Any loss of consciousness.
Typical concussion symptoms include: headache, confusion, nausea or vomiting, diminished attention/concentration, short-term memory problems, fatigue, irritability, hypersensivity to noise or bright lights, ringing in the ears, sleep difficulties, anxiety and/or depressed mood.
Symptoms that resolve within 7-10 days are considered a "simple concussion" and those symptoms that persist, a "complex concussion" that may involve multiple concussions within a short period of time (Prague Statement, 2004).
A Post-Concussion Syndrome (PCS), commonly cited by medical and legal practitioners, involves the challenge of evaluating criteria different from Mild Traumatic Brain Injury. In MTBI, the condition can occur with or without a loss of consciousness. In PCS, the ICD-10 and DSM-IV Research Criteria both require a loss of consciousness. Therefore, 90% of individuals sustaining a MTBI, would be precluded from a PCS diagnosis. In addition, the DSM-IV criteria requires that neuropsychological data substantiates difficulties with attention and memory. This would also require that a patient is evaluated for symptom validity, to determine the presence or absence of potential malingering. Remember that patients with MTBI symptoms will typically resolve within weeks or a few months post-trauma. Long standing symptoms are often a psychological reaction to the trauma, or the unleashing of old, unresolved traumas from prior experiences.
The Post-Concussion Syndrome is more elusive. This label has been assigned to patients who complain of physical, cognitive and emotional symptoms years after a trauma, that often times never involved a loss of consciousness. In fact, when reviewing many patient files, one notes mutiple Worker's Compensation Claims, history of previously unreported psychiatric issues and claims of cognitive alterations (i.e., memory probelms) years after the trauma in question.
Is PCS a real phenomenon? I believe it may be, depending on the individual's case history. The Buffalo Sabre Hockey player who sustained 2 serious (grade 2 and 3) concussions within 12 hours, had a Post-Concussion Syndrome lasting quite some time. Boxers, who accrue numerous concussions over the course of their careers, can sustain serious and life altering brain damage (e.g. Muhammed Ali) with "dementia pugilistica". Snowboarders who receive multiple (unhelmeted) head injuries within 6-9 months can have permanent brain damage affecting short-term memory. High school football and hockey players can sustain permanent brain damage from repeated concussions within a season.
How do we begin to determine true PCS from fabrication or psychological (psychogenic) origins? My work in Independent Medical Examinations has taught me that history, corroborated by hard medical facts, is a starting point. Neuropsychological screening devices for professional and school-age athletes are another objective measure to evaluate pre and post injury mental status. The consensus from recent research data on PCS is that unresolved subjective complaints of physical or cognitive impairments must be evaluated carefully and objectively. The PCS diagnosis is often times used as a convenient label for a simple concussion. Medical and legal pratitioners should be aware of these differences when rendering a diagnosis or making a legal claim.
I would like to add that my review of MTBI and PCS does not necessarily apply to concussional traumas sustained by individuals in combat by explosions or rapid ballistic injuries. I believe this domain deserves and requires a separate set of research criteria and evaluation. The physical force of such trauma, would, at the very least, likely produce potential dysfunction to inner ear systems regulating balance and proprioception. The psychological impact of such trauma I defer to my colleagues who specialize in this domain. There is also the question of acceleration trauma bearing on potential intracranial injury, where frontal and temporal regions of the brain are most vulnerable due to the boney protuberances in the skull.
The bottom line is we are only beginning to understand the complexity of concussional traumas and their potential for long term dysfunction. A thorough analysis of a patient's history, medical records, assessment of symptom validity and rigorous neuropsychological testing is a starting point to untangle this elusive diagnostic puzzle.
Peter B. Sorman, PhD, ABN
Diplomate, American Board of Professional Neuropsychology
Board Certified Clinical Neuropsychologist
My staff and I shuffled off to Buffalo in the dreary cold of February to arrive at the relatively new HSBC arena. After two days of testing the team members who were very cooperative we fowarded our findings to the team physician and key researcher in Pittsburgh.
The team was very careful to avoid concussional injuries from that point onward. They probably couldn't tolerate another Dr. Sorman evaluation. Unfortunately, the player who sustained the two concussions in 12 hours never returned to regular play, and became a footnote in the annals of hockey.
I learned from this experience, and through many sports related injuries sustained by my private patients over the years, that concussions are not additive; they are logarithmic. One plus one concussion does not equal two. The compounding effects of multiple concussions, over a short period of time, is problematic and potentially permenant. This is where the story of concussions, and the Post-Concussive Syndrome, becomes muddled.
A "concussion" is derived from the Latin "concussuss" meaning shake or shock. As noted in my earlier paper ("What's So Mild About Mild Traumatic Brain Injury"), operational definitions differ in MTBI. Similar differences are found in the literature on concussions and the so-called, Post-Concussion Syndrome.
According to the American Academy of Neurology, a concussion is a "trauma-induced alteration in mental status that may or may not involve a loss of consciousness. Confusion and amnesia are the hallmarks of concussion". Confusion and amnesia typically occur immediately after a blow to the head or several minutes later. Guidelines for the Management of Sports Concussions include the following symptoms:
1. A vacant stare
2. Slower to answer questions
3. Easily distracted
4. Slurred speech
5. Stumbling, inability to walk a straight line
6. Exterme emotions
7. Memory problems
8. Any period of loss of consciousness
A grading scale, developed by AAN, is often assigned to patients seen in the emrgency room:
Grade 1: Confusion and/or mental status changes with no loss of consciousness that resolves in less than 15 minutes.
Grade 2: Same as Grade 1, but symptoms last more than 15 minutes
Grade 3: Any loss of consciousness.
Typical concussion symptoms include: headache, confusion, nausea or vomiting, diminished attention/concentration, short-term memory problems, fatigue, irritability, hypersensivity to noise or bright lights, ringing in the ears, sleep difficulties, anxiety and/or depressed mood.
Symptoms that resolve within 7-10 days are considered a "simple concussion" and those symptoms that persist, a "complex concussion" that may involve multiple concussions within a short period of time (Prague Statement, 2004).
A Post-Concussion Syndrome (PCS), commonly cited by medical and legal practitioners, involves the challenge of evaluating criteria different from Mild Traumatic Brain Injury. In MTBI, the condition can occur with or without a loss of consciousness. In PCS, the ICD-10 and DSM-IV Research Criteria both require a loss of consciousness. Therefore, 90% of individuals sustaining a MTBI, would be precluded from a PCS diagnosis. In addition, the DSM-IV criteria requires that neuropsychological data substantiates difficulties with attention and memory. This would also require that a patient is evaluated for symptom validity, to determine the presence or absence of potential malingering. Remember that patients with MTBI symptoms will typically resolve within weeks or a few months post-trauma. Long standing symptoms are often a psychological reaction to the trauma, or the unleashing of old, unresolved traumas from prior experiences.
The Post-Concussion Syndrome is more elusive. This label has been assigned to patients who complain of physical, cognitive and emotional symptoms years after a trauma, that often times never involved a loss of consciousness. In fact, when reviewing many patient files, one notes mutiple Worker's Compensation Claims, history of previously unreported psychiatric issues and claims of cognitive alterations (i.e., memory probelms) years after the trauma in question.
Is PCS a real phenomenon? I believe it may be, depending on the individual's case history. The Buffalo Sabre Hockey player who sustained 2 serious (grade 2 and 3) concussions within 12 hours, had a Post-Concussion Syndrome lasting quite some time. Boxers, who accrue numerous concussions over the course of their careers, can sustain serious and life altering brain damage (e.g. Muhammed Ali) with "dementia pugilistica". Snowboarders who receive multiple (unhelmeted) head injuries within 6-9 months can have permanent brain damage affecting short-term memory. High school football and hockey players can sustain permanent brain damage from repeated concussions within a season.
How do we begin to determine true PCS from fabrication or psychological (psychogenic) origins? My work in Independent Medical Examinations has taught me that history, corroborated by hard medical facts, is a starting point. Neuropsychological screening devices for professional and school-age athletes are another objective measure to evaluate pre and post injury mental status. The consensus from recent research data on PCS is that unresolved subjective complaints of physical or cognitive impairments must be evaluated carefully and objectively. The PCS diagnosis is often times used as a convenient label for a simple concussion. Medical and legal pratitioners should be aware of these differences when rendering a diagnosis or making a legal claim.
I would like to add that my review of MTBI and PCS does not necessarily apply to concussional traumas sustained by individuals in combat by explosions or rapid ballistic injuries. I believe this domain deserves and requires a separate set of research criteria and evaluation. The physical force of such trauma, would, at the very least, likely produce potential dysfunction to inner ear systems regulating balance and proprioception. The psychological impact of such trauma I defer to my colleagues who specialize in this domain. There is also the question of acceleration trauma bearing on potential intracranial injury, where frontal and temporal regions of the brain are most vulnerable due to the boney protuberances in the skull.
The bottom line is we are only beginning to understand the complexity of concussional traumas and their potential for long term dysfunction. A thorough analysis of a patient's history, medical records, assessment of symptom validity and rigorous neuropsychological testing is a starting point to untangle this elusive diagnostic puzzle.
Peter B. Sorman, PhD, ABN
Diplomate, American Board of Professional Neuropsychology
Board Certified Clinical Neuropsychologist
Sunday, September 13, 2009
What's So Mild About Mild Traumatic Brain Injury?
Bumps to the head are common; children attain many a goose-egg through falls and collisions while playing. Adult antics seen on America's Funniest Home Videos likely results in bruises and minor head bumps. So when does a bump to the head become a problem? Welcome to the world of Mild Traumatic Brain Injury (MTBI): often misunderstood, hotly debated in professional circles, and the subject of new research data.
Defining MTBI depends on the authoritative source. Most sources (e.g., Center For Disease Control, 2003; American Congress of Rehabilitation Medicine, 1993, American Academy of Neurology, 1997) agree that: a person with MTBI has a acute brain injury resulting from blunt trauma, acceleration or deceleration forces, physiologic disruption of brain function that may (loss of consciousness less than 30 minutes) or may not result in loss of consciousness. This definition differs (presently) from the Post-Concussion Syndrome which does require loss of consciousness in it's description.
Additional initial symptoms of MTBI can include: confusion or disorientation, amnesia around the time of injury (not to exceed 24 hours), seizures following the head injury, lethargy, irritability,vomiting (typically in infants and young children), headaches, and dizziness.
The incidence rate of MTBI is 500/100,000 individuals in the general population. Typically, the highest rates of these incidence are attributed to the very young and very old, males, individuals with the hyperactive variety of ADHD, substance abusers and individuals from lower socioeconomic groups. In children, falls (sometimes when falling backward on a swing) are most common. In adults, motor vehicle accidents (with or without striking the head depending on physical forces of the vehicle in motion or at rest), work-related injuries, blunt trauma, and falls (particularly in the elderly) are most common.
Often times, MTBI individuals are brought to the emergency room of a local hospital. Ambulance and medical staff use coding systems to grade the severity of the injury. In some cases, patients are seen for a neurological examination, have x-rays, and often CT scans of the head are observed. Most commonly, patients are released with a "Head Injury Precaution" sheet and instructions to follow-up with their primary care physician.
Patients, however, are not always told what to expect from their MTBI. The most common set of symptoms, usually evident within minutes of the injury are physical and cognitive. Delayed onset of symptoms is rare. Immediate symptoms can include: headache, nausea, dizziness, fatigue, light and noise sensitivity, feeling mentally "foggy" or slowed down, and difficulty with concentration and short-term memory. There is usually a significant improvement in symptoms within hours of the trauma. Symptom recovery, in 80-90 percent of cases, occur over a 7-10 day period post-trauma. Children and adults usually show the same rate of recovery. Headaches may linger the longest, representing what many practitioners term the Post-Traumatic Headache. If an individual has sustained a more severe form of head trauma, the above symptoms can last longer, and the period of recovery slower. MTBI symptoms that persist well beyond expected time of recovery (i.e., months) can often be attributable to psychological factors, or even external incentives (e.g., litigation).
Review of recent research (McCrea, 2008) has documented the changes in brain functioning after MTBI called the "neurometabolic cascade". For many years, it was believed that MTBI caused damage to brain cells. In fact, brain cells are not damaged but "dysfunctional". That is, a change in the brain's metabolism and connections with other brain cells and normal communication (neurotransmission) is altered. The return or reversal to "normal" functioning occurs in days or weeks after the MTBI.
The news of rapid recovery after MTBI has many implications. First, it could help practitioners educate their patients about what to expect after injury. It also mandates a paradigm shift within the professional community. For years it was believed that MTBI can result in long-lasting symptoms and problems as a result of damage to brain cells and their connections. Though still relevant on a case-by-case basis, the majority of individuals with MTBI will get better within weeks to months.
As a neuropsychologist who conducts Independent Medical Examinations (as part of my practice), I am often faced with the question of MTBI permanent deficits by attorneys (plaintiff and defense), courts, and employers/insurance carriers. Evidence for rapid recovery following MTBI aids in the analysis of a claimant's subjective symptoms and potential alternative explanations for their complaints. It also affords practitioners a more detailed procedure when conducting neuropsychological testing.
There is nothing "mild" about Mild Traumatic Brain Injury. Appropriate medical intervention should always be the first step after sustaining a head injury. Follow-up care with your treating physician and specialists (neurologist, neuropsychologist) is an important part in the recovery process. The brain has an amazing (and not yet fully understood) capacity for re-compensation of function.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
Respond via Twitter to: DrPeterSorman
Defining MTBI depends on the authoritative source. Most sources (e.g., Center For Disease Control, 2003; American Congress of Rehabilitation Medicine, 1993, American Academy of Neurology, 1997) agree that: a person with MTBI has a acute brain injury resulting from blunt trauma, acceleration or deceleration forces, physiologic disruption of brain function that may (loss of consciousness less than 30 minutes) or may not result in loss of consciousness. This definition differs (presently) from the Post-Concussion Syndrome which does require loss of consciousness in it's description.
Additional initial symptoms of MTBI can include: confusion or disorientation, amnesia around the time of injury (not to exceed 24 hours), seizures following the head injury, lethargy, irritability,vomiting (typically in infants and young children), headaches, and dizziness.
The incidence rate of MTBI is 500/100,000 individuals in the general population. Typically, the highest rates of these incidence are attributed to the very young and very old, males, individuals with the hyperactive variety of ADHD, substance abusers and individuals from lower socioeconomic groups. In children, falls (sometimes when falling backward on a swing) are most common. In adults, motor vehicle accidents (with or without striking the head depending on physical forces of the vehicle in motion or at rest), work-related injuries, blunt trauma, and falls (particularly in the elderly) are most common.
Often times, MTBI individuals are brought to the emergency room of a local hospital. Ambulance and medical staff use coding systems to grade the severity of the injury. In some cases, patients are seen for a neurological examination, have x-rays, and often CT scans of the head are observed. Most commonly, patients are released with a "Head Injury Precaution" sheet and instructions to follow-up with their primary care physician.
Patients, however, are not always told what to expect from their MTBI. The most common set of symptoms, usually evident within minutes of the injury are physical and cognitive. Delayed onset of symptoms is rare. Immediate symptoms can include: headache, nausea, dizziness, fatigue, light and noise sensitivity, feeling mentally "foggy" or slowed down, and difficulty with concentration and short-term memory. There is usually a significant improvement in symptoms within hours of the trauma. Symptom recovery, in 80-90 percent of cases, occur over a 7-10 day period post-trauma. Children and adults usually show the same rate of recovery. Headaches may linger the longest, representing what many practitioners term the Post-Traumatic Headache. If an individual has sustained a more severe form of head trauma, the above symptoms can last longer, and the period of recovery slower. MTBI symptoms that persist well beyond expected time of recovery (i.e., months) can often be attributable to psychological factors, or even external incentives (e.g., litigation).
Review of recent research (McCrea, 2008) has documented the changes in brain functioning after MTBI called the "neurometabolic cascade". For many years, it was believed that MTBI caused damage to brain cells. In fact, brain cells are not damaged but "dysfunctional". That is, a change in the brain's metabolism and connections with other brain cells and normal communication (neurotransmission) is altered. The return or reversal to "normal" functioning occurs in days or weeks after the MTBI.
The news of rapid recovery after MTBI has many implications. First, it could help practitioners educate their patients about what to expect after injury. It also mandates a paradigm shift within the professional community. For years it was believed that MTBI can result in long-lasting symptoms and problems as a result of damage to brain cells and their connections. Though still relevant on a case-by-case basis, the majority of individuals with MTBI will get better within weeks to months.
As a neuropsychologist who conducts Independent Medical Examinations (as part of my practice), I am often faced with the question of MTBI permanent deficits by attorneys (plaintiff and defense), courts, and employers/insurance carriers. Evidence for rapid recovery following MTBI aids in the analysis of a claimant's subjective symptoms and potential alternative explanations for their complaints. It also affords practitioners a more detailed procedure when conducting neuropsychological testing.
There is nothing "mild" about Mild Traumatic Brain Injury. Appropriate medical intervention should always be the first step after sustaining a head injury. Follow-up care with your treating physician and specialists (neurologist, neuropsychologist) is an important part in the recovery process. The brain has an amazing (and not yet fully understood) capacity for re-compensation of function.
Peter B. Sorman, PhD, ABN
Board Certified Clinical Neuropsychologist
Respond via Twitter to: DrPeterSorman
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