Neuro Landscape
A Brain Injury Blog by Centre for Neuro Skills
(CNS Regional Director of Clinical Services Dr. Gary Seale shares research that shows an increased risk for suicidal thoughts, suicide attempts, and even death by suicide following brain injury.)
Neuropsychiatric disorders regularly occur following brain injury and are often diagnosed within a year of the injury.1,2 Mood disorders, particularly major depressive disorder (MDD), are the most frequently diagnosed DSM-5 psychiatric disorders after brain injury.3 Mood disorders can develop with or without a preinjury history of psychiatric disorder, and can increase risk for suicidal thoughts.1-4
MDD Following Brain Injury
Prospective studies using structured clinical interviews report rates of depression between 13.9% and 23.2% within the first year of injury for mild brain injury.3 Reported rates of MDD for a wider range of injury severity are higher, ranging from 15.3% to 33%.5 Risk factors for MDD include preinjury depression, focal lateral lesions and left anterior lesions, and psychosocial stressors including social isolation and maladaptive coping. MDD following brain injury was associated with comorbid anxiety and self-reported lower quality of life at 1 year after the injury.6
Suicide Risk and Suicidality
Studies report an increased risk for suicidal thoughts, suicide attempts, and even death by suicide following brain injury.4,7-9 Makelprang followed a cohort of adults with traumatic brain injury (TBI) for 1 year after discharge from the hospital, and found that 25% of the sample reported suicidal ideation within the first year of injury.4 The strongest predictors of suicidal ideation after brain injury included prior history of suicide attempt, neuropsychiatric diagnosis (depression, bipolar disorder), and less than a high school education. Simpson and Tate reported a lifetime prevalence rate of 26.2% for suicide attempt in an outpatient sample with TBI.9 They also examined the clinical features of suicide attempts after TBI in an outpatient cohort followed over a 24-month period. Their data set included 43 patients who made a total of 80 suicide attempts; 30% of the attempts were preinjury and 70% postinjury. Over 55% of the sample made a single attempt, 25.6% made 2 attempts, and 18.6% made 3 or more attempts. Of those that made 3 or more attempts, the repeat attempts occurred within 13 months of the index attempt, and over one third making multiple attempts used the same method. Excessive alcohol intake within the prior 24 hours, psychological distress brought on by antecedent stressors (arguments, loss of a significant relationship, negative feedback, etc), and hopelessness combined with high suicidal ideation, were associated with suicide attempt after TBI.
Treatment and Prevention
Prevention and treatment interventions for suicidal ideation and attempt can include pharmacological and psychosocial approaches, substance misuse treatment, environmental modifications, and when necessary, emergency intervention.10,11 Given the multiple and complex challenges associated with this population, practitioners are encouraged to adapt and individualize treatment and prevention practices.11
In terms of pharmacological intervention, SSRIs, namely sertraline, have been found to be effective an first line treatment for depression.12 In addition to treating depressive symptoms, SSRIs may also improve other frequently reported TBI symptoms, such as irritability, aggression and poor impulse control. When prescribing medications following TBI, a conservative, approach to dosing (ie, “low and slow”) is recommended as individuals with TBI may be sensitive and susceptible to medication adverse effects.13
Psychosocial interventions, such as support groups, strengthening family relationships, and involving patients in social skills training have been effective in decreasing feelings of loneliness and isolation.10 In a controlled trial, Simpson et al randomized a group of adults with severe TBI and severe hopelessness or suicidal ideation to either an intervention group (n=8) or a wait list control group (n=9).14 The participants in the intervention group received a 20-hour, manualized cognitive behavior therapy program. Interventions assisted participants to live a positive lifestyle by promoting expression of thoughts and feelings, reframing/reappraising disturbing situations, acquire adaptive coping skills (ie, problem-solving, asking for help, etc), and promoting posttraumatic growth by making meaning of the brain injury. The treatment group demonstrated a significant reduction in hopelessness, and this effect was maintained at 3-month follow-up for 75% of participants.
Given that substance abuse, particularly alcohol abuse, is a risk factor for suicide attempt, substance abuse treatment can be an important component in a suicide prevention plan.9,10 Environmental modifications, such as restricting access to sharps, guns, toxic chemicals, and other means of self-harm, has been shown to be effective in reducing suicide.10
Use of “No Harm Contracts” could be an appropriate intervention for patients with brain injury. A no harm contract is an intervention intended to prevent self-harm.15 It is a written agreement between a clinician and a patient (ie, person receiving psychotherapy or mental health services) whereby the patient promises not to harm themself. Reviewers of the literature on the efficacy of No Harm Contracts argue a lack of quantitative evidence to support the use of such contracts.16 Conceptual and ethical issues related to the use of No Harm Contracts include:
However, alternatives to No Harm Contracts have shown limited or questionable utility. Some clinicians believe that the absence of extensive research concerning the efficacy of contracts in the prevention of suicide should not be used to conclude that contracts have no therapeutic benefit or usefulness in treating suicidal patients.17 Some potential benefits could include:
Like all therapeutic interventions and techniques, those that address suicidality must be tailored to each patient.
Dr Seale is the Regional Director of Clinical Services at the Centre for Neuro Skills. He is licensed in Texas as a psychological associate with independent practice, and is a Certified Brain Injury Specialist Trainer. He holds a clinical appointment at the University of Texas Medical Branch (UTMB) in Galveston in the Department of Rehabilitation Sciences.
References
(Polypharmacy is often overlooked in patients with significant traumatic brain injury. How can you best manage medication in these patients? CNS Chief Medical Officer Matthew Ashley, MD, JD, explains in this article).
The issue of polypharmacy is often overlooked in patients with significant traumatic brain injury (TBI). In the acute setting—which includes the emergency department, critical care unit, and hospital floor—attention is appropriately fixed on survival and medical stabilization. To that end, interventions range from neurosurgical to pharmacological. In a typical severe TBI scenario, it is not unusual for a patient to undergo multiple surgical procedures (eg, craniotomy/craniectomy, ventricular drains, various orthopedic procedures to address polytrauma, tracheostomy, gastrostomy tube placement).
The science behind the acute management of TBI is evolving, and any intervention that improves survival and reduces long-term morbidity is worthwhile. But as patients recover, many of the pharmacological interventions become counterproductive and should be discontinued. TBI is increasingly recognized as a chronic disease with chronic impairments. Therefore, the majority of care for the patient with TBI occurs post hospital. This care is often highly fragmented and many opportunities to reduce medications and avoid polypharmacy and comorbidity can be missed.
Many categories of medication frequently used in patients with TBI can contribute to polypharmacy. Some medications sedate and cloud the sensorium, potentially limiting recovery. This group includes antipsychotics, anxiolytics, antiepileptics, and opiates. Another group includes preventive medications, whether for deep venous thrombosis (DVT) and pulmonary embolism (PE), seizures, or headaches. Yet another group might be referred to as convenience medication; for example, as-needed antiemetics. There are also medications directed at specific and frequent associated conditions such as syndrome of inappropriate antidiuretic hormone secretion (SIADH), cerebral salt wasting, autonomic dysfunction, neurogenic bowel/bladder, and so on. This article will attempt to address each medication briefly. What is important for clinical practitioners to know is that every successive evaluation is an opportunity to reexamine the medication list for necessity.
Some of the most problematic contributors to polypharmacy are the most common: sedating medications. Antipsychotics, typically used in acute settings to manage behavioral complications of TBI, or in rare cases actual psychosis, are generally detrimental to TBI recovery in the long term, unless the patient is diagnosed with psychosis. Similarly, benzodiazepines are generally detrimental unless used for very specific and time-limited purposes such as obtaining diagnostics, performing procedures, and the like. In addition, like opiates, the addictive potential of these medications in a patient with TBI and associated impulsivity is high. Opiate medications are unfortunately frequently necessary in patients with TBI, at least temporarily, as there is frequently associated polytrauma. These medications carry known and varied risks as mentioned, including addictive potential. Awareness of the individual risks of each of these medications, as well as the cumulative effects of polypharmacy involving multiple agents, is paramount. Recovery from TBI is already difficult for a patient combating impaired sensation due to impairments in vision, proprioception, balance, spatial awareness, language, vertigo, and so on. Unnecessary sedation from medication does not improve the process.
Antiepileptic medication is frequently initiated prophylactically during acute care for any patient who has a TBI with intracranial bleeding, and continued use is appropriate for patients who do experience seizure disorder post TBI. However, in patients without a history of seizure post TBI, guidelines suggest that this is not recommended beyond 7 days.1 Many antiepileptics have significant drug-drug interactions, pharmacokinetic impact, and other adverse effects. Older antiepileptics such as carbamazepine, oxcarbazepine, phenytoin, and phenobarbital have significant effects on cytochrome P450 enzymes. This leads to pharmacokinetic effects and risk for changes in serum drug levels. Valproic acid can similarly affect circulating drug levels through other mechanisms. Newer antiepileptics have less dramatic effect on serum drug levels but many remain hepatically metabolized, and therefore drug levels should be monitored and dosage adjusted. Fortunately, levetiracetam, considered a first-line agent by many for management of epilepsy post TBI, does not frequently alter the serum level of other drugs in clinical practice. In addition to seizure prophylaxis or management, some of these medications are also commonly used for various other purposes in the TBI population, including headache prevention (eg, topiramate), behavioral intervention (eg, lamotrigine, valproic acid), or neurogenic pain management (eg, gabapentin, pregabalin). These can be effective and beneficial, but as patients improve clinically over time, ongoing use should be addressed.
Many patients with TBI suffer from immobility as a consequence, whether transiently or long term. In either instance, acute immobility confers risk for DVT/PE, which some patients do experience during their illness.2 Patients are commonly discharged on prophylaxis for treatment of DVT/PE. This may be with either heparin, low molecular weight heparin, warfarin, or one of the novel anticoagulants. All these medications carry their own adverse effect profiles, and many have significant polypharmacy risks due to drug-drug interactions and pharmacokinetic impacts. In cases where a patient’s mobility improves, prophylaxis should be discontinued appropriately. Other individuals with anticipated long-term immobility still do not benefit from prophylaxis indefinitely, because the risk for DVT/PE in this context wanes over time. Appropriate guidelines related to the duration of treatment for DVT or PE should be adhered to, with medication discontinued when appropriate.3
TBI is also frequently associated with other secondary complications. Disorders of homeostasis such as the SIADH or cerebral salt wasting can result in the addition of fluid restriction or the use of salt tabs and/or fludrocortisone. It is not uncommon for this condition to remain unresolved at the time of discharge from the hospital. However, most often this condition will resolve over time with recovery, and these interventions can then be discontinued.
Various other medications, used during acute care to manage hypertension, hyperglycemia, nausea/vertigo, and so on, are frequently prescribed at the time of discharge. With patient improvement, these can also unnecessarily contribute to polypharmacy. This list is exhaustive, but the primary objective here is to highlight the beneficial role of a care provider paying close attention during each visit to the medication list and the ongoing indications (or lack thereof).
Finally, as patients proceed through the recovery process, still other medications can be added. Antidepressants, headache prevention or abortive medications, antiepileptics, and many others may be clinically indicated, some even permanently. However, in all cases, vigilance on behalf of all treatment providers as to the polypharmacy concerns remains vital.
Dr Ashley is a neurologist and chief medical officer for the Centre for Neuro Skills.
References
1. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80(1):6-15.
2. Mohseni S, Talving P, Lam L, et al. Venous thromboembolic events in isolated severe traumatic brain injury. J Emerg Trauma Shock. 2012;5(1):11-15.
3. Ortel TL, Neumann I, Ageno W, et al. American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism. Blood Adv. 2020;4(19):4693-4738.
(Note: In this guest blog from Chris Persel, Director of Clinical Services and Director of Behavior Programming for CNS, he discusses CNS’ Rehabilitation Super Power: Intensity, Repetition, Consistency and Integrity).
Individuals that have experienced a neurological injury from a traumatic event, stroke or other mechanism require specialized, skilled rehabilitation to maximize recovery. Research and clinical experience informs us that receiving treatment as soon as possible and at the appropriate level is essential. However, funding resources and support for treatment can be extremely limited, making every minute available for rehabilitation valuable. The treatment program and therapeutic staff have a responsibility to make their impact meaningful and effective. Several elements are important to maximize this rehabilitation opportunity, including establishing enriched, demanding environments, capitalizing on principles of neuroplasticity, providing treatment intensity and maintaining consistent program integrity.
ENRICHED ENVIRONMENT
Enriched, demanding environments create a strong foundation for success. The treatment environment must be challenging and create a demand for the patient to respond. Patients require engagement in activities that present choices which elicit a response, empowers them to make decisions and compels them to demonstrate skills, rather than have others do things for them. Studies support positive outcomes from enriched environments, such as increased adult hippocampal neurogenesis, improved spatial learning ability1, and increased activity levels2. One review indicated that work tasks that stimulate verbal intelligence and executive functions helped sustain good cognitive functioning3, so treatment environments that provide that experience are essential.
NEUROPLASITICITY
A few key principles of neuroplasticity can guide rehabilitation treatment. “Use it or Lose it” indicates that neural circuits that are not actively engaged in task performance for an extended period of time begin to degrade. This means that experiences after brain injury, such as an active skill rehabilitation program, can protect neuronal circuitry that may otherwise be lost. “Use it and Improve it” outlines that treatment that drives specific brain function and performance will lead to enhancement of that function. For example: “Forcing” engagement in tasks using an impaired limb can lead to enhanced functioning in that limb (e.g. constraint-induced movement therapy). “Repetition Matters” stipulates that induction of neuroplasticity requires sufficient repetition of activities. This concept demonstrates the strength of residential rehabilitation treatment programs because they allow for performing increased repetitions of specific tasks in the exact setting where these skills need to be utilized. In fact, research supports the observation that neuroplastic change and functional improvement occur when large numbers of a specific task are performed, however, this change does not occur with fewer repetitions. Unfortunately, a large multicenter study found that over half of the upper limb and gait training rehabilitation sessions did not come close to meeting the number of repetitions needed to impact patient neuroplasticity. Thus, one item of focus for rehabilitation professionals should be the number of repetitions and the type of activity performed.
INTENSITY
For programs to optimize patient recovery, sufficient learning and treatment intensity is key to the induction of neuroplasticity. If clinical therapy combined with residential rehabilitation can provide “treatment” for up to 16 hours each day, seven days a week in a structured setting, they will have provided 480+ hours over a month’s time. Studies found that this level of intense therapy over a short amount of time can improve outcomes for stroke patients with aphasia4 and decrease risk of hospital readmission for all rehabilitation patients5. Intensive neurorehabilitation treatment in a rehabilitation facility, that encompasses at least 20 therapy hours per week, promotes the greatest functional recovery6 and there is no evidence of a ceiling effect of therapeutic intensity beyond which no further response is observed7.
INTEGRITY
For rehabilitation programs to maximize their impact, treatment must also be delivered with consistency and integrity. What is program integrity? It is consistently implementing an intervention/program as intended. This allows skills to be mastered more quickly and produces the most effective and efficient strategies for recovery. Why is this important? It reduces “wasting time, money, resources” while maximizing the hope and energy of all involved. Lack of treatment integrity can diminish the field as a whole which could erode future resources. Following consistent treatment pathways improves efficiency, reduces the conclusion that there is “No Progress” and better informs staff on when to adjust programs.
The power of rehabilitation success after neurological injury lies in the consistent application of intense, targeted interventions as a part of an enriched and challenging treatment environment.
(In this article, Brent E. Masel, M.D, Executive Vice-President for Medical Affairs for CNS and a Clinical Professor of Neurology at the University of Texas Medical Branch in Galveston, discusses how we might decrease the severity of strokes or even mitigate them completely).
Stroke is the 4th leading cause of death in the US, where there are approximately 800,000 strokes yearly. A stroke occurs every 40 seconds, and one person dies every four minutes from a stroke. Globally, one person in four people over age 25 will have a stroke in their lifetime. Interestingly, 60% of individuals who have a stroke are female. (There are lots of theories about this, but no one knows for sure). An individual surviving a stroke has a 5.5-year reduction in their life span.
Aside from prevention, what can we, as healthcare providers, do to reduce these numbers? People will still have strokes, but we can do something to decrease the severity of the stroke or even mitigate it completely.
We need to recognize the symptoms of a stroke so the individual may receive an intervention that may change the course of the event. The key is the acronym FAST: Face, Arms, Speech, Time.
There are indeed other signs that should be considered and taken seriously, including sudden weakness or numbness on one side of the body, difficulty finding words or speaking in clear sentences, sudden blurred vision or loss of sight in one eye, sudden memory loss or confusion as well as dizziness or sudden fall.
“Time is brain.” 1.9 million brain cells die for every minute the brain is deprived of blood. If we see these signs, the individual must immediately go to a hospital emergency room – by ambulance if possible. But what happens next, and what can be done?
Upon arrival, a “stroke team” will be activated. This team consists of specially trained doctors, nurses, and technicians who have a protocol to work as quickly as possible to find the best intervention for that patient. The patient will be evaluated and stabilized. Blood studies and a CT scan of the head will be done. If the patient can receive treatment approximately 4.5 hours after the onset of symptoms, they may be appropriate for IV medication, TPA, that can break up the clot. It is believed that after approximately 4.5 hours, the chances of reversing the stroke and not causing further damage with the clot busters are markedly reduced. Studies have shown that individuals receiving TPA at the appropriate time are 30% more likely to have little or no symptoms at 3 months than those who received a placebo.
Another treatment possibility is removing the clot mechanically. This isn’t easy and requires highly trained interventionalists. A wire must be threaded up the artery to the clot and then the clot is “grabbed” and removed. Unfortunately, only 10% of stroke patients are eligible for this procedure, as the clot must be in a large artery close to the neck. The ideal timing is six hours after the event occurred, but the procedure can be done up to 24 hours later. Studies have shown recanalization, opening of the artery, in 60-75% of cases.
(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.
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