Neuro Landscape
A Brain Injury Blog by Centre for Neuro Skills
(Brain injury associated fatigue and altered cognition has been associated with a subset of individuals with mild traumatic brain injuries who develop posttraumatic hypopituitarism, including altered gut microbiome and amino acid utilization. In this article, Senior CNS Neuroscientist Dr. Stefanie Howell discusses BIAFAC and posttraumatic gut-brain axis dysfunction).
Brain injury associated fatigue and altered cognition (BIAFAC) is characterized by profound fatigue (not ameliorated by sleep), altered cognition (predominantly short-term memory loss and altered executive functioning capabilities), abnormal growth hormone (GH) stimulation test, and a positive response to GH replacement. This condition has been associated with a subset of individuals with mild traumatic brain injuries (TBI) who develop posttraumatic hypopituitarism (PTHP), a condition characterized by a decrease in function of the pituitary gland, and other metabolic abnormalities, including altered gut microbiome and amino acid utilization.1
Similar complaints are common to post-concussion syndrome; however, the symptoms of BIAFAC tend to be delayed, generally not appearing until at least 6 months post-injury. Improvements in fatigue and cognition have been seen following GH replacement, with fatigue improving at about 3 months and cognition improving in about 5 to 6 months. When GH replacement is stopped, symptoms return (fatigue returns in approximately 3 months and cognitive impairment at around 6 months).2 This article aims to provide an introduction to the role of amino acids and disruptions in the gut-brain axis in BIAFAC symptoms post-brain injury.
Role of Amino Acids and Neuroendocrine Dysfunction
Amino acids are the building blocks of our bodies and can be broken down into 2 categories, essential and nonessential amino acids. Essential amino acids are those which must be ingested through food, while nonessential amino acids are synthesized by our bodies. Though they are referred to as nonessential amino acids, this is a misnomer, as they are indeed essential to our bodily functions. In the body, amino acids are the building blocks of proteins. The types and patterns of the amino acids determine the function of each protein they synthesize. Thus, by being responsible for the production of proteins, amino acids help in breaking down food, growing and repairing bodily tissue, building muscle, boosting the immune system, providing energy, etc.
Another major role they play is producing hormones and neurotransmitters; therefore, hypoaminoacidemia (abnormally low levels of amino acids in the blood), such has been discovered in TBI, can produce profound physical, cognitive, and neurological dysfunction.3 As an example, glutamate, one of the most abundant amino acids, also functions as the primary excitatory neurotransmitter in the central nervous system. In addition, arginine, an essential amino acid, is a precursor for nitric oxide, while tryptophan, another essential amino acid, is a precursor to serotonin. Serotonin and nitric oxide are both tied to cognition and mood.4 Disruption of this delicate balance of amino acids, proteins and neurotransmitters can contribute to the symptoms of BIAFAC seen post-TBI.
Hypoaminoacidemia and Gut Microbiome Dysbiosis in TBI
Studies have shown that an altered gut microbiome may be responsible for amino acid abnormalities after TBI.5
The gut microbiome is unique to each individual and is originally introduced at birth via microbes present at the time of delivery and through formula or breast milk. Later, other microbes are introduced to the biome via our diet and through environmental exposure. The microbiome consists of both helpful and potentially harmful microbes. Bacteria in our gut decide what our body absorbs, what gets flushed out in the feces, and what gets absorbed by bacteria for their own growth. A consistent balance of gut microbiota is required for optimal health.
Literature supports the concept that the gut-brain axis is a functional organ system that includes amino acid signals and short chain fatty acids as part of a bidirectional relationship between the central nervous system and the gut microbiome. It appears that the vagus nerve and the autonomic nervous system in the spinal cord are the conduits for communication between the gut and the brain. Thus, as one might expect, gut dysbiosis has also been found in spinal cord injuries.6
A brain injury triggers countless cellular and molecular processes that may lead to rapid changes in the gut microbiome due to the bidirectional relationship that exists between the brain and the gut. Changes in the gut microbiome include alterations in the motility and permeability of the intestinal wall and activation of immune cells. Studies in both animals and humans have shown that TBI significantly impacts circulating amino acids the amount and diversity of gut bacteria.3,5
Addressing Gut Microbiome Dysbiosis
Studies investigating the post-injury disruption of hormones, amino acids, and the gut microbiome are helping to illustrate TBI as a chronic disease state. Understanding the underlying mechanisms may lead to better treatments and/or prevention of secondary consequences of TBI, including BIAFAC. Some promising interventions include the use of prebiotics, which foster the growth and activity of beneficial microorganisms, ie bacteria and fungi (acting as “food” or energy for the bacteria), probiotics, which are live microorganisms, ie, the bacteria itself, or even the potential of fecal transplants.
Dr Howell is a senior neuroscientist at the Centre for Neuro Skills. She is a specialist in brain injury rehabilitation, neurodegenerative disease, and clinical research.
References
1. Yuen KCJ, Masel BE, Reifschneider KL, et al. Alterations of the GH/IGF-I axis and gut microbiome after traumatic brain injury: a new clinical syndrome? J Clin Endocrinol Metab. 2020;105(9):3054-3064.
2. Urban RJ. A treatable syndrome in patients with traumatic brain injury. J Neurotrauma. 2020;37(8):1124-1125.
3. Durham WJ, Foreman JP, Randolph KM, et al. Hypoaminoacidemia characterizes chronic traumatic brain injury. J Neurotrauma.2017;34(2):385-390.
4. Armstrong PA, Venugopal N, Wright TJ, et al. Traumatic brain injury, abnormal growth hormone secretion, and gut dysbiosis. Best Pract Res Clin Endocrinol Metab. 2023;37(6):1018-1041.
5. Urban RJ, Pyles R, Stewart C, et al. Altered fecal microbiome years after traumatic brain injury. J Neurotrauma. 2020;37(8):1037-1051.
6. Jing Y, Bai F, Yu Y. Spinal cord injury and gut microbiota: a review. Life Sci. 2021;266:118865.
(Aphasia is an impairment of language that frequently occurs following a neurological injury, particularly a stroke. CNS Regional Director of Clinical Services Dr. Gary Seale discusses the various types of aphasia, treatment modalities, and the importance of family education and training that can empower clinicians in directing treatment).
An estimated 1.7 million traumatic brain injuries (TBI) occur each yearin the United States.1 Additionally, more than 795,000 individuals experience stroke annually.2 A common consequence of acquired brain injury is aphasia, an impairment of language that can affect speech, as well as reading or writing.3,4 While aphasia can be caused by any neurological insult, such as cerebral tumors, infection, or a degenerative process, stroke is a leading cause of aphasia.3,5 It is estimated that 20% to 40% of individuals diagnosed with stroke have aphasia; the incidence of aphasia following TBI is between 2% to 32%.6
Despite the frequency of aphasia following TBI, there is limited public awareness. Simmons-Mackie and colleagues conducted face-to-face surveys of individuals in England, the United States, and Australia to determine the number of individuals who had “heard of aphasia” and the number of people who had a “basic knowledge of aphasia.”7 Results of the survey demonstrated that 13.6% of the sample had “heard of aphasia,” but only 5.4% had a “basic knowledge of aphasia.” To increase awareness and understanding of aphasia, June is designated as National Aphasia Awareness Month.
Types of Aphasia
Aphasia can be classified by lesion location and observed language deficits. Several types of aphasia have been described, but 4 types are more frequently encountered: Broca aphasia, Wernicke aphasia, global aphasia, and anomic aphasia.8
Broca aphasia (first described by Pierre Paul Broca in 1861) is caused by damage to the lateral, inferior aspect of the frontal lobe, usually in the left hemisphere of the brain. Broca aphasia is also called nonfluent aphasia and is characterized by difficulty with expression, while comprehension of language is relatively preserved. Individuals with Broca aphasia demonstrate limited vocabulary, severely reduced speech that is limited to short utterances, awkward or uncoordinated formation of sounds, and difficulty writing. Broca aphasia can be very frustrating because the individual knows what they want to say, and they are aware that their attempts to communicate are inaccurate. Broca aphasia is diagnosed in about 12% to 18% of acute and subacute strokes.
Wernicke aphasia (first described by neurologist Carl Wernicke in 1874), is caused by damage to the posterior segment of the superior temporal lobe, usually in the left hemisphere of the brain. Wernicke aphasia, also called fluent aphasia, is characterized by impaired language comprehension, while speech may be relatively preserved. However, though word formation and rate, rhythm, and grammar may be correct, sentences may not make sense. Additionally, the individual may not be aware of the communication errors they are making, and they may become frustrated when the listener does not understand them. Wernicke aphasia is diagnosed in about 15% to 25% of acute and subacute strokes.
Global aphasia results from damage to both Broca and Wernicke areas of the brain, typically in the left hemisphere. Global aphasia is considered among the most severe forms of aphasia. Individuals diagnosed with global aphasia produce few recognizable words, comprehend very little (if any) spoken language, and can neither read nor write. Global aphasia may be diagnosed immediately after a brain injury, but can improve significantly if the brain lesion is not too extensive. Global aphasia is diagnosed in approximately 20% to 40% of acute and subacute strokes.
Anomic aphasia is a mild, fluent type of aphasia, and may involve multiple areas of the brain. Anomic aphasia is characterized by word retrieval failures. Individuals with anomic aphasia are not able to express the words they want to say (particularly nouns and verbs). They often describe objects in detail and may use gestures to demonstrate how an object is used, but cannot find the appropriate word to name the object. Speech fluency, repetition, comprehension, and grammar are relatively preserved. Anomic aphasia is diagnosed in approximately 10% to 25% of acute and subacute strokes.
Treatment
Just as there are different types of aphasia, each individual demonstrates a unique presentation of symptoms; therefore, an individualized treatment program, tailored to the observed language impairment(s), is indicated. Preferably, therapy is delivered by a speech/language pathologist in consultation with other disciplines (ie, neuropsychology, neurology or physiatry, counseling, etc).
Two broad treatment approaches exist for the treatment of aphasia: remedial or restorative therapies, and compensatory strategies. Restorative approaches address the underlying impairment and focus on restoring a lost function, for example, reading paired with spoken naming, or matching pictures with words to improve naming and word-finding impairments.9 Compensatory strategies, also called external strategies, compensate for a lost function. They can include, for example, gesturing or pointing to pictures or icons to compensate for naming or word-finding impairments. It is theorized that both restorative and compensatory approaches promote cortical reorganization after brain injury. Research also indicates that specific pharmacologic agents, such as stimulants, dopamine agonists, and cholinesterase inhibitors, may augment language therapy.10,11 Finally, transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS) has been used to enhance recovery from aphasia.11
Several treatment factors that promote recovery from aphasia have been identified. These factors include, timing (engaging the individual in treatment early, as soon as they are medically stable and able to participate in therapy), intensity (multiple days per week; individualized treatment versus group therapy), and structure, consistency, and repetition.12,13
Treatment for aphasia also involves training for family members or other care givers.14 Strategies that families and caregivers can deploy to improve expression and comprehension include:
-Keeping communication clear and simple (short phrases, simple vocabulary) and speaking slowly
-After making a statement or asking a question, give the individual time to formulate their thoughts and respond; do not “pepper” them with questions or overwhelm them with too much information
-Reduce background noise/distractions; face the individual so they can see your face
-Use all forms of communication to reinforce what you are saying—gestures, exaggerated facial expression, drawings or pictures, etc
-Ask questions that require only a “yes/no” response versus open ended questions
-Narrow the topic, “I am talking about shopping,” or “Are you talking about our summer vacation?”
Families can also consult the American Speech and Hearing Association website for information and tips for improving communication with a loved one that has aphasia.
Recovery
Aphasia is treatable. While most individuals with aphasia demonstrate some recovery, particularly early after injury, a large majority demonstrate substantial improvement.5 Perderson and colleagues found that while 61% of their sample still had aphasia 1 year after stroke, the aphasia has progressed to a milder form of aphasia and the change was from a nonfluent to a fluent form. They also found evidence of recovery for both comprehension and speech.8
Determinants of recovery from aphasia include initial severity of brain injury, level of intelligence and communication ability pre-injury, emotional and affective adjustment to injury, and the quality, intensity and duration of therapy (as mentioned in the previous section).3,5,8 Type of aphasia, age, and gender have not been shown to be reliable determinants of recovery from aphasia.8
Concluding Thoughts
Aphasia is an impairment of language that frequently occurs following neurological injury, particularly stroke. While aphasia is a common consequence of brain injury, few people have a basic understanding of aphasia. Understanding the various types of aphasia, treatment modalities, and the importance of family education and training can empower clinicians in directing care.
References
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States: national estimates of prevalence and incidence, 2002–2006. Injury Prevention. 2010;16(Suppl 1):A268-A268.
2. Williams GR. Incidence and characteristics of total stroke in the United States. BMC Neurol. 2001;1:2.
3. Damasio AR. Aphasia. N Engl J Med. 1992;326:531-539.
4. McNeil MR, Pratt SR. Defining aphasia: some theoretical and clinical implications from a formal definition. Aphasiology. 2001;15(10-11):901-911.
5. Hillis AE. Aphasia: progress in the last quarter of a century. Neurology. 2007;69(2):200-213.
6. Sarno MT. The nature of verbal impairment after closed head injury. J Nerv Ment Dis. 1980;168(11):685-692.
7. Simons-Mackie N, Code C, Armstrong E, et al. What is aphasia? Results of an international survey. Aphasiology. 2002;16(8):837-848.
8. Pedersen PM, Vinter K, Olsen TS. Aphasia after stroke: type, severity and prognosis. Cerebrovasc Dis. 2004;17(1):35-43.
9. Beeson PM, Egnor H. Combining treatment for written and spoken naming. J Int Neuropsychol Soc. 2006;12(6):816-827.
10. Walker-Batson D, Curtis S, Natarajan R, et al. A double-blind, placebo-controlled study of the use of amphetamine in the treatment of aphasia. Stroke. 2001;32(9):2093-2098.
11. Berube S, Hillis AE. Advances and innovations in aphasia treatment trials. Stroke. 2019;50(10):2977-2984.
12. Robey RR. The efficacy of treatment for aphasia persons: a meta-analysis. Brain Lang. 1994;47(4):585-608.
13. Bhogal SK, Teasell R, Speehley M. Intensity of aphasia therapy, impact on recovery. Stroke. 2003;34(4):987-993.
14. Simmons-Mackie N, Kearns K, Potechin G. Treatment of aphasia through family member training. Aphasiology. 2005;19(6):583-593.
(Note: In this guest blog from Dr. Gary Seale, CNS Director of Clinical Services, he explores the relationship between substance misuse and acquired brain injury).
The relationship between substance misuse and acquired brain injury (ABI) is well documented. Studies examining Traumatic Brain Injury (TBI) Model Systems data revealed that more than 50% of patients treated for a traumatic brain injury (TBI) were intoxicated at the time of injury1. Alcohol misuse is also a risk factor for stroke. Chronic alcohol misuse has been associated with heart arrhythmias, blood clotting disorders, hypertension, and diabetes, all of which are risk factors for stroke2. Opioids and illicit “street drugs”, have also been linked to ABI. Non-fatal opioid overdose is associated with anoxic and hypoxic brain injuries due to the depressive effect of opioids on the respiratory system3. Use of illicit stimulant drugs, i.e., cocaine, methamphetamine, etc., can elevate heart rate and blood pressure to dangerous levels, and have been associated with hemorrhagic stroke4,5. It is important for practitioners to understand the relationship between substance misuse and acquired brain injury, and to accurately diagnose and treat these co-occurring conditions as a substantial number of people with ABI return to risky levels of alcohol and/or drug consumption within the first few years after injury6. Individuals that continue to misuse substances following discharge from rehabilitation are at higher risk for reinjury, development of mood disorders, increased mortality, and decreased life satisfaction7.
ASSESSMENT
A thorough clinical interview can provide a subjective measure of both the extent and the impact of substance misuse. Evidence demonstrates that using Motivational Interviewing techniques, i.e., asking open-ended questions, reflective listening, and eliciting the patient’s thoughts about change can assist in obtaining information, building rapport, and begin the process of behavior change8. Gauging a patient’s readiness for change can also guide treatment planning and selection of appropriate interventions in order to meet the patient where he/she is in the change process9. Standardized assessments provide an objective measure of substance use/misuse. Instruments that have been used successfully with the ABI population include: the CAGE10 and the Alcohol Use Disorders Identification Test (AUDIT)11 for alcohol use, and the Alcohol, Smoking, and Substance-Use Involvement Screening Test (ASSIST)12 and the Substance Abuse Subtle Screening Inventory (SASSI)13 for both alcohol and drug use.
TREATMENT
A number of treatment interventions for co-occurring ABI and substance misuse have been proposed and evaluated. Brief treatment including screening, patient education, and brief interventions may slow the resumption of future alcohol use14. Other best practices for the treatment of substance use disorders in the ABI population include: patient and family education, incentives to encourage treatment attendance and retention, use of motivational interviewing techniques, and interventions to support adaptive coping and adjustment15-18. Patient and family education that includes information about the negative effects of continued substance misuse, particularly suppression of cognitive recovery, increased risk for seizures, potential interactive effects of alcohol and prescribed medications, and increased risk for sustaining a second TBI, have been shown to be beneficial in reducing resumption of substance use19. Some studies suggest that providing firm recommendations regarding abstinence, at least for the 1st full year following injury, can also impact substance misuse following rehabilitation. Corrigan20 has suggested tailoring substance misuse treatment and modifying any written materials to account for cognitive and linguistic deficits stemming from brain injury (i.e., attention, memory, information processing speed, etc.). Additionally, Corrigan21 has recommended a four quadrant model that describes the various settings where people with ABI can receive treatment, as well as the best treatment based on the severity of the brain injury and severity of substance misuse. Quadrant I (low severity of brain injury and substance misuse) includes acute medical and primary care settings and interventions that provide screening, and brief interventions. Quadrant II (low severity of substance misuse, and high severity of brain injury) includes brain injury rehabilitation settings and interventions that provide education, screening, brief interventions, and linkages to community supports and referral for ongoing substance use treatment. Quadrant III (high severity of substance misuse and low severity of brain injury) includes substance use treatment settings and interventions that provide screening, accommodations (for cognitive-linguistic deficits), and service linkage. Quadrant IV (high severity of substance misuse and brain injury) includes specialized brain injury and substance use services, including integrated programming. Community supports such as Alcoholics Anonymous (AA) and Narcotics Anonymous (NA) have also been suggested as helpful resources in providing education, social support, and promoting personal responsibility/accountability. Finally, pharmacological treatments of substance misuse in the ABI population have been recommended as an adjunct to traditional therapies, or when therapy alone has been unsuccessful22. Naltrexone, acamprosate, and disulfiram (Antabuse) are United States Food and Drug Administration (FDA) approved medications for the treatment of alcohol use disorder. Naltrexone and acamprosate act to reduce alcohol cravings, whereas disulfiram operates via aversive counterconditioning. It is recommended that these medications be initiated after a period of abstinence and may require liver function tests. Naltrexone, methadone, and buprenorphine are FDA approved to treat opioid dependence. These medications also reduce cravings by binding with opioid receptors.
Gary S. Seale, PhD is the Regional Director of Clinical Services at the Centre for Neuro Skills, which operates post-acute brain injury rehabilitation programs in California and Texas. He is licensed in Texas as a Chemical Dependency Counselor and Psychological Associate with Independent Practiced. He also holds a clinical appointment at the University of Texas Medical Branch (UTMB) in Galveston in the Department of Rehabilitation Sciences.
REFERENCES
1. Corrigan JD. (1995). Substance abuse as a mediating factor in outcome from traumatic brain Injury. Archives of Physical Medicine and Rehabilitation. 76: 302-309.
2. Gorelick PB. Alcohol and stroke (1987). Stroke. 18: 268-271.
3. Shirmer DM & Seale GS. (2018). Non-lethal opioid overdose and acquired brain injury. Vienna, VA: Brain Injury Association of America.
4. Sordo L, Indave BI, Barrio G, et al. (2014). Cocaine use and risk for stroke: A systematic review. Drug and Alcohol Dependence. 142: 1-13.
5. Lappin JM, Danke S & Farrell M. (2017). Stroke and methamphetamine use in young adults: A review. Journal of Neurology, Neurosurgery, and Psychiatry. 88: 1079-1091.
6. Ponsford J, Whelan-Goodinson R & Bahar-Fuchs A. (2007). Alcohol and drug use following traumatic brain injury: A prospective study. Brain Injury. 21: 1385-1392.
7. Zgaljardic DJ, Seale GS, Schaefer LA, et al. (2105). Psychiatric disease and post-acute traumatic brain injury. Journal of Neurotrauma. 32: 1911-1925.
8. Miller W R & Rollnick S. (2013). Motivational interviewing: Helping people change. New York, NY: Guilford Press.
9. DiClemente, CC. (2018). Addiction and change: How addictions develop and addicted people recover. New York, NY: Guilford Press.
10. Ewing JA. (1984). Detecting alcoholism, the CAGE questionnaire. JAMA. 252 (28): 1905-1907.
11. World Health Organization. (2001). Alcohol Use Disorders Identification Test: Guidelines for use in Primary Care, 2nd Edition. Geneva, Switzerland: WHO.
12. World Heath Organization. Alcohol, Smoking, and Substance-Use Involvement Screening Test (ASSIST). Available at: http://www.who.int/substance_abuse/activities/assist/en/indecx.html
13. Miller, G.A. (1985, 1999). The Substance Abuse Subtle Screening Inventory (SASSI) Manual, Second Edition. Springville, IN: The SASSI Institute.
14. Bogner J, Corrigan, J D, Peng J, et al. (2021). Comparative effectiveness of a brief intervention for alcohol misuse following traumatic brain injury: A randomized controlled trial. Rehabilitation Psychology. 66: 345–355.
15. Jones, G.A. (1992). Substance abuse treatment for persons with brain injuries: identifying models and modalities. Neurorehabilitation 2, 27–34.
16. Bombardier, C.H., and Rimmele C.T. (1999). Motivational interviewing to prevent alcohol abuse after traumatic brain injury: a case series. Rehabilitation Psychology 44, 52–67.
17. Corrigan, J.D., and Bogner, J. (2007). Interventions to promote retention in substance abuse treatment. Brain Injury 21, 343–356.
18. Vungkhanching, M., Heinemann, A.W., Langley, M.J., Ridgely, M., and Kramer, K.M. (2007). Feasibility of a skills–based substance abuse prevention program following traumatic brain injury. Journal of Head Trauma Rehabilitation 22, 167–176.
19. Seton, J.D., and David, C.O. (1990). Family role in substance abuse and traumatic brain injury rehabilitation. Journal of Head Trauma Rehabilitation 5, 41–46.
20. Corrigan JD. (2005). Substance Abuse. In High WM, Sander AM, Struchen MA, Hart KA, eds. Rehabilitation for Traumatic Brain Injury. New York, USA: Oxford University Press: 133-155.
21. Corrigan JD. (2007).The Treatment of Substance Abuse. In Zasler N, Datz D, Zafonte R, eds. Brain Injury Medicine: Principles and Practice. New York, USA: Demos Publications: 1105-1115.
22. Corrigan JD, Mysiw WJ. (2012). Substance abuse among persons with TBI. In: Zasler ND, Katz DI, Zafonte RD, Arciniegas DB, Bullock MR, Kreutzer JS, eds. Brain Injury Medicine: Principles and Practice, 2nds ed. New York, USA: Demos Medical Publishing: 1315-1328.
As Covid-19 and stroke remain in the forefront of health news this year, Centre for Neuro Skills’ clinical leadership showed their media savvy in TV, radio, and print venues. Chief Medical Officer Dr. Matt Ashley and Regional Director of Clinical Services Dr. Gary Seale spoke eloquently about long haul Covid, stroke in young people, and aphasia. These appearances showcase CNS’ expertise and its legacy of brain injury rehabilitation.
Dr. Ashley was featured in Psychiatric Times during Brain Injury Awareness Month in March, writing for the column Clinical Conversations. He addressed questions about causes of and treatment for TBI in his debut piece: Bringing Awareness to Brain Injury Awareness Month (psychiatrictimes.com). As a result of Dr. Ashley’s contribution, CNS is excited to announce that both he and Dr. Seale are new columnists in Psychiatric Times, each taking on brain injury subjects in the monthly online publication.
In April, trending news focused on actor Bruce Willis’ aphasia diagnosis, noting his long-standing struggle with speech and memory. Leveraging this breaking news, Landis Communications, Inc., CNS’ media agency, arranged an interview with Dr. Ashley, who discussed aphasia, raising awareness of its origins and symptoms as a potential aspect of brain injury: Speaking with specialists: Dr. Matt Ashley on aphasia symptoms, causes, & treatments | KBAK (bakersfieldnow.com)
Always eloquent, Dr. Seale was also in demand as an expert during Stroke Awareness Month in May. In two radio segments, he focused on prevention and the rising occurrence of stroke in young people: Dr. Gary Seale on Stroke Awareness Month (newschannel10.com) and Dr. Gary Seale Talks Stroke Risk and Prevention in Young Adults – News Talk Sports 710AM & 97.5FM (kgncnewsnow.com)
Also in May, CNS President and Chief Operating Officer David Harrington demonstrated his clinical knowledge and interview savvy on Bakersfield TV station KGET 17. Covid outbreaks continue despite fluctuating rates of infection. Long haul Covid has become a public health issue, as serious deficits may cause lifelong challenges. David showed us his trademark approachability in a piece that covered the realities of life post-Covid. Recovery is possible, he noted, with appropriate medical care: Rising to the challenge of Long COVID | KGET 17
In one of spring’s most powerful stories, Bakersfield Discharge Coordinator Olivia Kerchner and her husband John (a former CNS patient) were featured in a moving piece about their TBI journey as a couple: Tragedy turned inspiration: Local veteran surviving TBI, wife becomes community leader | KBAK (bakersfieldnow.com).
In each news story, our staff, leadership, and patients reflected the power of CNS’ approach to rehabilitation.
Humans are endowed with the ability to communicate using language skills that develop in a spoken form, a listening form, a written form, and a gestural form. In most instances, people communicate with each other using a combination of these forms. Many people learn to use more than one language, while some learn several languages.
When a person experiences a stroke or an injury to the brain, the areas of the brain that enable us to speak, listen and understand, repeat words, phrases or sentences, and write and/or read can be damaged. Though related to one another, each of these skills is generally located in different areas of the brain. As a result, when the brain is injured, the effect on the ability to communicate is most likely to be largely restricted to one ability. For example, a common form of aphasia affects the ability to speak, that is, to use expressive language skills. Another type often seen affects the ability to understand what is said to a person, to use receptive language skills.
Eight types of aphasia have been identified. Of these, Broca’s (expressive) and Wernicke’s (receptive) aphasias are more commonly diagnosed. Several of the other types of aphasia share some similarities with these two, though they differ slightly, enabling finer discrimination. A person who has learned more than one language may have better skills in one language than another after the onset of aphasia, and their recovery may follow a similar pattern.
Primary progressive aphasia is the most difficult and persistent aphasia related to other underlying disease processes in the brain. This type of aphasia is most often permanent and worsens progressively over time in concert with the progression of underlying disease.
Diagnosis of aphasia is often made by a physician or by a speech-language pathologist. These two professionals work closely together to make a diagnosis and establish a treatment plan. Treatment for most aphasias consists of speech-language therapy. This long-standing therapy has been shown to be effective in improving a person’s language abilities and developing compensatory ways to communicate. Some evidence exists for the use of certain medications in tandem with speech-language therapy to enhance the rate and extent of recovery. Therapeutic treatment is best when initiated early, is of sufficient intensity and frequency, and allowed to continue across several months, if needed.
One can expect some spontaneous recovery early after an injury to the brain; however, the extent of the recovery is hard to predict and varies due to several factors such as age, coexisting conditions, the extent and nature of the injury to the brain, and access to therapy. Therapy can include home therapeutic exercises for the person to complete with the help of a family member to increase the exposure to treatment.
Aphasia can be quite frustrating to the person with the condition and those with whom they wish to communicate. Communication is central to the human condition, and aphasia can bring about frustration, depression, anxiety, and isolation. The inability to communicate about one’s health, psychological well-being, and safety matters can seriously impact the person with the condition or people in their environment.
Unfortunately, people with aphasia cannot always receive the necessary therapy needed to achieve their best outcome due to financial constraints or the availability of a speech-language pathologist. Organizations such as the American Stroke Association and the Brain Injury Association of America work to advocate for people with aphasia.
Finally, an excellent resource can be found in the American Speech-Language-Hearing Association.
On December 1, 2020, the number of COVID-19 cases worldwide totaled over 63.6 million, with 13.6 million cases within the United States. Of this total, nearly 1.5 million deaths were attributed to COVID-19, with over 269,000 of the deaths occurring in the U.S.1
COVID-19 had primarily been thought to be a respiratory disease. In recent months, however, growing evidence shows that the disease may likely be a disease of the epithelium of the lungs, or the lining of the respiratory tract, and the endothelium, the lining of arteries and veins throughout the body.2
Because of this, complications of COVID-19 tend to strike some organ systems more frequently than others. Respiratory, cardiovascular, renal, gastrointestinal, and neurological systems appear to be the most commonly impacted. Infection can present a loss of the sense of smell (anosmia) or taste (ageusia), Guillain-Barre syndrome, encephalopathy, encephalitis, and acute cerebrovascular disease.3,4
While extensive longstanding research has not been conducted due to relative inexperience with the virus, information is emerging that strongly suggests the risk of neurologic damage. One study compared the rate of acute ischemic stroke in individuals with COVID-19 to a group of people with influenza, a known stroke trigger. The research found the likelihood of stroke with COVID-19 infection (1.6% of people) to be substantially higher than for influenza (0.2%). 3
Another study examined the risk of developing cerebrovascular disease with COVID-19 infection, which refers to disorders that affect the blood vessels and blood supply to the brain. The categories of cerebrovascular disease examined included cerebral ischemia, intracerebral hemorrhage, and leukoencephalopathy of the posterior reversible encephalopathy type. In total, 1.4% of 1,683 cases developed neurological complications over 50 days.2 Neurological injuries included arterial dissections, subarachnoid hemorrhage, microbleeds, and single or multiple hematomas -severe injuries that resulted in high rates of death or significant disability.
The study found that the injuries tended to occur in the vascular areas that serve the brainstem and posterior (back) portions of the brain. Blood clotting in these areas can be exceedingly significant and impact the arteries feeding blood to the brain.5
There is also emerging evidence that individuals with pre-existing neurological injury are at greater risk for developing neurological complications in the event of COVID-19 infection. A case report of post-COVID-19 autoimmune encephalitis, an inflammation of the brain and spinal cord, found potentially significant long-term neurological symptoms and consequences if undiagnosed or improperly treated. These included non-fluent aphasia, oculomotor dysfunction, myoclonus of the tongue and limbs, echolalia, perseveration, and hallucinations.6
Recovery patterns post-COVID-19 show symptoms persistence at the time of follow-up visit to range from 5% to more than 50% for neurological symptoms ranging from myalgia, vertigo, lack of appetite, headache, loss of taste, loss of smell, and fatigue.7
For the time being, it is reasonable to exercise caution in prediction about recovery from neurological deficits that accompany COVID-19 infection. There is evidence of recovery in some symptoms, such as the loss of taste or smell and significant long-term deficits associated with other complications such as stroke. However, we remain in the earliest stages in regards to understanding the near- and longer-term neurological consequences of COVID-19 infection. Recovery and symptom severity in the presence of newer interventions that impact viral replication rates and address inflammatory processes may be different, and hopefully better, than the currently available data.
Bibliography
Stroke is an acquired brain injury and is a leading cause of long-term disability in the United States. Almost 800,000 people in America will experience a new onset or recurrent stroke each year. Worldwide, stroke is the second leading cause of death and disability.
Stroke is often thought of as a disease that occurs in older people. While this is often the case, the incidence of ischemic stroke in people aged 20-54 has increased.
Slightly over one-third of people who experience a stroke are functionally dependent or die by three months post-discharge. Recovery after stroke can require the care of a team of individuals, including physicians, nurses, physical and occupational therapists, speech-language pathologists, recreational therapists, psychologists, nutritionists, social workers, and others.
Stroke rehabilitation in the era of COVID-19
As we consider the impact of the recent COVID-19 pandemic, a number of concerns arise regarding the rehabilitation dosing afforded to individuals who sustain a stroke.
Hospitals have, necessarily, reduced lengths of stay for non-COVID-19 diagnoses as they attempt to free up bed space for COVID-19 cases. As a consequence, rehabilitation therapies have become shortened or non-existent. Further, outpatient rehabilitation services have been suspended in many locations, leaving one to wonder how people who suffer from stroke will receive crucial treatment.
Factors impacting stroke recovery
We know that many factors impact a person’s functional outcome after a stroke. These include age, where a younger age is associated with a better outcome, and the timing of therapy, which is essential because therapy that is provided too early can be detrimental, and therapy that is delayed can negatively affect the outcome. The exact window of opportunity is not clear and most likely varies with several patient-specific factors.
We also know that the degree of the expertise of rehabilitation treatment impacts outcome; with more expertise comes better outcomes. And we know that both the frequency and intensity of therapy affect the degree of recovery of function a person will achieve and reduce the likelihood of hospital readmission. Simply put, more therapy is associated with better outcomes. Furthermore, higher intensity therapy is associated with more recovery.
Several factors seem to merge around interfering with a person’s ability to recover to their fullest potential. One factor is bundling payments, wherein a hospital is incentivized to discharge a person quickly and to attempt to reduce re-hospitalization. It has been demonstrated that bundled payment arrangements result in less use of tertiary care settings, such as rehabilitation. As well, payers have become accustomed to very short inpatient rehabilitation stays, followed by simple outpatient rehabilitation services.
It is clear that more attention must be paid to scientific evidence that strongly links better outcomes with more frequent therapy, therapy of higher intensity, therapy that is properly timed and of sufficient duration, and therapy that is provided by properly trained specialists in neurorehabilitation.
Finally, great care in payment structuring should be taken to avoid skimping on care for this vulnerable population.
As the COVID-19 crisis has enveloped the world, the risk to individuals living with a brain injury has yet to be fully appreciated. The risk of contracting the virus is likely elevated for individuals with brain injury.
People with a relatively recent injury, and people who have been living with injury may not have normally functioning immune systems and may have more co-morbid health conditions. As a result, they may be at higher risk for severe complications if they contract the COVID-19 virus.
As well, people without brain injury who experience a COVID-19 infection may emerge with damage to the brain.
We do not know whether neurologic symptoms that develop with infection from the virus will be permanent. These symptoms can include changes in a person’s sense of smell or taste, extreme fatigue, headache, or disorders of consciousness and may also include muscle damage. Some patients are emerging with symptoms similar to Guillain-Barre syndrome. People may additionally require prolonged treatment on ventilators. And these people will not only be physically debilitated, requiring rehabilitation, they may also have lung damage, heart damage, renal damage, and could add injury to the brain as well. Further, there are reports of a high prevalence of coagulopathies resulting in deep-vein thromboses, myocardial infarcts, and strokes. However, the prevalence cannot be fully distinguished from the increased risk seen in critically ill patients in general.
Unfortunately, there is very little research available at this point in time. What is available, however, speculates that, perhaps, the epithelial lining of capillaries in the brain may be damaged by viral budding within the capillaries, thereby potentially enabling the virus to invade the brain. A second mechanism postulates the entry of the virus via the cribriform plate near the olfactory bulb of the brain. And a third mechanism suggests the potential for easier entry via leaky blood-brain barrier function after brain injury.
For now, we can only hope that the neurologic symptoms are temporary. Further, we can only speculate on the course of the disease and how it will affect people living with brain injury. And we cannot know whether there will be only near-term consequences of viral infection or unknown, as of yet, long-term consequences.
If there is a heightened element of risk to a person living with brain injury for a more severe manifestation of the disease, it is all the more critical that they, and the people who love them, take every available precaution to prevent exposure.
(Note: In this guest blog from Chris Persel, Regional Director of Clinical Services and Director of Behavior Programming for CNS, he explains behavioral changes following brain injury and the value of behavior analysis).
The effects of neurological damage from events like trauma and stroke can be devastating to the individual and those close to them. Brain injury can result in lifelong physical, cognitive, and behavioral changes. The impact of behavior changes can profoundly alter how the injured person functions day to day, even impeding rehabilitative goals and impacting the ability to live independently. Changes in personality and behavior following traumatic brain injury (TBI) often represent the most significant barrier to a successful outcome including reintegration into the community whether for basic daily tasks, work or recreational/social activities.
Common behavior issues following brain injury include behavioral excesses (occurring too much) such as irritability (e.g., poor tolerance, short temper) and aggression (e.g., hitting, grabbing, kicking), property destruction (e.g., striking furniture, throwing items) and inappropriate vocalizations (e.g., cursing, yelling, threats). Also presenting a concern are behavior deficits (do not occur enough) such as compliance with tasks (e.g., cooperation with requests), social skills (e.g., overfamiliar discussions, uncharacteristically rude remarks), initiation (e.g., knowing when to begin tasks) and the academic and return to work skills (e.g., being on time, following directions) to be successful. Some of the most difficult behaviors can be dangerous to the patient and others around them. Treating these dangerous and challenging behaviors, which may include physical aggression toward others, self-injurious behavior, sexual disinhibition, and escape or elopement, requires a treatment commitment across the continuum of care.
In the early, acute stages of recovery from brain injury, many of the behavioral complications demonstrated are considered to be a normal phase of recovery. When these behaviors continue beyond those early phases, however, and form on-going negative patterns of interaction with others, very specialized treatment is required. These behaviors can be disturbing to families and staff, disruptive to therapy, and jeopardize patient safety. The future quality of life for the patient and their family depends on effective interventions, provided with a great deal of consistency and structure. Behavior analysts (professionals in Applied Behavior Analysis) add value to interdisciplinary rehabilitation teams by helping to develop both skill acquisition and behavior reduction programs throughout the patient’s recovery (i.e., acute, post-acute, long term care). Behavior analysts spend a great deal of time directly observing interactions, determining what may be motivating the difficult behaviors, and what responses may need to be strengthened and reinforced. The behavior analyst must then provide training to all those who may interact with the patient, including most importantly, the family. This skilled, specialized intervention establishes more effective and acceptable response patterns that allow the patient to have their needs met and be better understood without displaying problem behavior. The structured behavior plan can also help the patient develop positive, prosocial responses, and more efficient functional skills.
The effects of brain injury are highly individual, which then challenges the behavior analysts, family and others on the treatment team to continually evaluate the responses, goals, and outcomes throughout recovery (e.g., monitoring response to new medications).
Considering the risk to patients and families, the rising healthcare cost and the possibility of reduced services being available, a focus on efficient and effective interventions such as behavior analysis seems essential to a well-integrated, interdisciplinary rehabilitation treatment team. The quality of life for those affected by brain injury depends on having the opportunity to receive not just the standard rehabilitation one might get following knee surgery but rather specialized, experienced and effective treatment specifically designed to address the unique difficulties they face including difficult behavior.
The estimates for exactly how often MTBI or concussion happens vary widely. However, concussion is quite common, and the total number of concussions in a year vastly outnumbers all new diagnoses of cancer combined in the U.S. Many concussions go unrecognized and unreported, making it far more difficult to understand the frequency of concussions.
Generally, it is thought that the brain recovers well after a single concussion. However, concussions vary by the amount and nature of the forces applied to the brain. Further, some concussions are referred to today as “complicated concussions” because evidence of damage to the brain is apparent in CT or MRI scans, though the person suffering the concussion seems to recover reasonably well.
It is estimated that between 5% and 20% of individuals who sustain a concussion will have one or more symptoms that last a year or longer. It is not entirely clear why symptoms persist for some individuals and not for others.
We now know that endocrine dysfunction can be caused by a concussion in some individuals. We also know that sleep disorders can occur after concussion in some individuals or may be present before the injury. Both of these factors, along with other general medical conditions, can complicate a person’s recovery.
Several neurodegenerative diseases have been found to occur in greater incidence in association with a single concussion. These include conditions like Alzheimer’s disease, amyotrophic lateral sclerosis, multiple sclerosis, a variety of endocrine disorders, epilepsy, brain tumor, schizophrenia, depression, psychosis, and dementia. However, the causal link to concussion as either an initiator of disease or accelerator of the disease has yet to be precisely determined.
Aging and a person’s genetic make-up likely complicate the picture further and can contribute to both onset and acceleration of disease. We cannot predict accurately who will develop a neurodegenerative disease, though an important indicator can be found in a person’s family history. That said, we still have no way to guarantee who will and who will not develop such conditions.
The only clear point is that avoiding concussion is well-advised. Once one or more concussions occur, the individual should consider significant lifestyle modifications, many of which are common sense and advised for many other health conditions. The person should be alert to developing conditions by working closely with their physician.
These include avoiding the use of caffeine, alcohol, over the counter sleep aids, and recreational drugs. Diet should be well-balanced, avoiding high carbohydrate intake, and maintaining an appropriate body mass index (weight). Ideally, the diet should be rich in antioxidants and low fat (~17%). Daily exercise should be included in one’s routine, just as one includes other daily hygiene care. Exercise should be under the supervision and advice of a physician and should be 30-60 minutes of cardiovascular exercise at least six days per week. Sleep should be 7-9 hours daily, and a rigorous sleep routine of regular sleep and wake times should be protected. A physician should screen annually for endocrine and sleep disorders, in particular, sleep apnea. And sleep apnea should be managed with breathing support.
