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Saebo, Inc. is a medical device company primarily engaged in the discovery, development and commercialization of affordable and novel clinical solutions designed to improve mobility and function in individuals suffering from neurological and orthopedic conditions. With a vast network of Saebo-trained clinicians spanning six continents, Saebo has helped over 100,000 clients around the globe achieve a new level of independence.
In 2001, two occupational therapists had one simple, but powerful goal – to provide neurological clients access to transformative and life changing products.
At the time, treatment options for improving arm and hand function were limited. The technology that did exist was expensive and inaccessible for home use. With inadequate therapy options often leading to unfavorable outcomes, health professionals routinely told their clients that they have “reached a plateau” or “no further gains can be made”. The founders believed that it was not the clients who had plateaued, but rather their treatment options had plateaued.
Saebo’s commitment – “No Plateau in Sight” – was inspired by this mentality; and the accessible, revolutionary solutions began.
Saebo’s revolutionary product offering was based on the latest advances in rehabilitation research. From the SaeboFlex which allows clients to incorporate their hand functionally in therapy or at home, to the SaeboMAS, an unweighting device used to assist the arm during daily living tasks and exercise training, “innovation” and “affordability” can now be used in the same sentence.
Over the last ten years, Saebo has grown into a leading global provider of rehabilitative products created through the unrelenting leadership and the strong network of clinicians around the world. As we celebrate our history and helping more than 100,000 clients regain function, we are growing this commitment to affordability and accessibility even further by making our newest, most innovative products more accessible than ever.
Post by D. Chloe Chung
“I was so anxious to do what is right that I forgot to do what is right.” – Jane Austin
You’re giving an important presentation tomorrow for work in front of a big crowd. You know you’re well-prepared, but when you imagine yourself standing at the podium, facing strangers whose eyes are fixed on you, you start to feel nauseated – your palms sweat and your heart hammers in your chest. You’re experiencing acute anxiety, a state of negative emotions and heightened arousal, often accompanied by increased alertness. This definition may sound similar to that of ‘fear’, which is produced as an acute response to immediate threats. There is considerable overlap between the brain circuitry regulating anxiety and fear, but anxiety is distinct from fear because it can be internally triggered or anticipatory – just like when you were merely imagining that presentation for work. Much of our understanding of anxiety stems from what we have learned about how the brain processes and learns fear responses.
Recent research efforts have emphasized the importance of communication between multiple brain areas in evoking anxiety. One of the established models of the neural circuitry of anxiety proposes that anxiety arises due to active neural communication between brain regions, including the amygdala, a brain structure involved in fear learning. The amygdala (the central extended amygdala [CeA]) sends projections to the bed nucleus of the stria terminalis (BNST), a cluster of nuclei involved in threat monitoring. The amygdala and the BNST also communicate with other brain regions such as the ventral hippocampus (vHPC) and the prefrontal cortex (PFC). According to this model, these four regions are connected by neural projections and work with one another in an orchestrated manner to evaluate whether or not a situation is threatening. The brain activity in this group of regions that we’ll refer to as the ‘anxiety detection’ regions can be either anxiogenic or anxiolytic, meaning they can perpetuate or reduce anxiety, respectively.
Downstream, the motor cortex, regions of the brainstem, and the neuroendocrine system receive, interpret, and evaluate possible anxiety signals from the brain regions involved in anxiety detection. These downstream regions then initiate anxiety responses by triggering defensive and risk-avoiding behaviors and altering biological functions such as heart and respiration rate. Excessive anxiety can occur when the brain’s anxiety pathways misinterpret incoming signals. For instance, repeated exposure to ‘threatening’ situations may cause anxiogenic pathways to become abnormally hyperactive, and therefore more sensitive to threatening stimuli. This can cause an imbalance in the neural circuitry that processes anxiety, shaping the brain to become more reactive and susceptible to experiencing anxiety.
While we know the amygdala (specifically the CeA) is particularly important for anxiety regulation, the exact mechanisms are difficult to disentangle. Recent research has helped to shed light on some of the specific circuitry involved. A recent study in the Journal of Neuroscience used a novel rat model and deleted a gene called ErbB4 – implicated in various neurological disorders – in a group of amygdala neurons that release somatostatin, a peptide implicated in fear responses. In behavioral tests, rats without this gene exhibited higher anxiety levels, due to increased somatostatin levels in the amygdala. The abnormal activity of somatostatin neurons in the CeA also disrupted the inhibition of somatostatin neurons in the BNST, rendering these neurons hyperactive and ultimately causing heightened anxiety. A peptide called dynorphin has been identified as a key molecular player in this amygdala-BNST anxiety circuit. The authors demonstrated that the amount of dynorphin produced by somatostatin neurons in the amygdala was increased, and led to disinhibition of the BNST, contributing to the induction of anxiety-related behaviors. In other words, both somatostatin and dynorphin work together to play an important role in increased anxiety in mice without ErbB4. The good news is that dynorphin could be a potential target for anxiety treatment.
Another area of anxiety research concerns the stress neuropeptide, corticotropin-releasing factor. It’s known to regulate the BNST’s ability to elicit anxiety, but it was unclear where the corticotropin-releasing factor was coming from until recently. A study published by Pomrenze et al. showed that corticotropin-releasing factor is majorly produced and released by a group of neurons located in the lateral amygdala and the dorsolateral BNST. Using designer drugs that can either inhibit or activate neurons expressing the corresponding receptors via viral transduction, the authors found that neurons that project from the lateral amygdala to the BNST and release corticotropin-releasing factor are critical in mediating anxiety. Removal of these neurons reduced anxiety behaviors, confirming the importance of corticotropin-releasing factor in evoking anxiety responses.
Modern life is full of stressors and many people are prone to experiencing intense anxiety at some point in their lives. In fact, anxiety is a part of a normal emotional spectrum and can even be beneficial at times, increasing our vigilance and enabling our survival. However, chronic anxiety can severely interfere with day-to-day living and become pathological, resulting in generalized anxiety disorder (GAD) or other anxiety-related disorders. Anxiety disorders like GAD are common, impacting one in every five adults. Considering how many individuals are affected by pathological anxiety, there is a need for highly effective anti-anxiety drugs or behavioral interventions. It is critical to understand the brain circuitry underlying anxiety to develop effective treatment options for chronic anxiety disorders.
Since anxiety results in heightened arousal, many anxiety medications manipulate neurotransmitters to slow the nervous system down, decreasing arousal. Medications such as selective serotonin reuptake inhibitors (SSRIs) and Buspirone work to increase serotonin in the nervous system, which can, in turn, decrease arousal. Medication options for phobias such as social anxiety tend to decrease the effect of norepinephrine, a neurotransmitter connected to the ‘fight or flight’ fear response. Cognitive-behavioral therapy (CBT) and consulting with certified therapists can also improve anxiety. CBT is a popular and effective strategy that guides individuals to replace anxiety-provoking interpretations of situations with benign ones. For individuals with less severe anxiety symptoms, CBT can sometimes work as well as some medications, depending on the person and the extent of their anxiety. CBT can also be combined with other therapeutic approaches to effectively treat anxiety depending on the severity of symptoms. Regular physical exercise and breathing exercises can also be effective in reducing anxiety symptoms.
To manage acute daily anxieties, remembering how the brain circuitry of anxiety works might be helpful – the anxiety regions of the brain first assess whether the situation is threatening or not, and then subsequently trigger the anxiety response. This means that we can practice psychological tricks to aid the brain in better assessing non-threatening situations as just that – non-threatening. Similar to CBT, by taking a step back and evaluating the situation, we can develop habits that lead to new responses and potentially avoid an unnecessary anxiety response in the future. Making an effort to be aware of our anxious thoughts or worries and replacing them with more realistic ones can also be beneficial in helping our brain to relearn our responses to potentially threatening situations. Since the human brain is plastic (i.e. it adapts to changes in our internal and external environments), conscious efforts can result in a shift in the anxiety circuitry. Another key factor in mitigating anxiety is an awareness of the surrounding environment. Anxiety-inducing neural circuitry can be over-activated when we’re repeatedly exposed to certain stressors in our environment, resulting in feelings of anxiety in situations that are not immediately threatening. Hence, eliminating or minimizing such stressors in our environment can help.
Calhoon GG, Tye KM. Resolving the neural circuits of anxiety. Nature Neuroscience (2015) 18(10): 1394-404. DOI: 10.1038/nn.4101.
Ahrens S, Wu MV, Furlan A, Hwang GR, Paik R, Li H, Penzo MA, Tollkuhn J and Li B. A central extended amygdala circuit that modulates anxiety. Journal of Neuroscience (2018) 38(24): 5567-5583. DOI: 10.1523/JNEUROSCI.0705-18.2018
Pomrenze MB, Tovar-Diaz J, Blasio A, Maiya R, Giovanetti SM, Lei K, Morikawa H, Hopf FW and Messing RO. A corticotropin releasing factor network in the extended amygdala for anxiety. Journal of Neuroscience (2019) 39(6): 1030-1043. DOI: 10.1523/JNEUROSCI.2143-18.2018
Hofmann SG, Asnaani A, Vonk IJJ, Sawyer AT, and Fang A. The Efficacy of Cognitive Behavioral Therapy: A Review of Meta-analyses. Cognitive Therapy and Research (2012) 36(5): 427-440. DOI: 10.1007/s10608-012-9476-1
Kaczkurkin AN, Foa EB. Cognitive-behavioral therapy for anxiety disorders: an update on the empirical evidence. Dialogues in Cinical Neuroscience (2015) 17(3):337-46. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4610618/
After injury, survivors and their family members often experience a variety of strong emotions. Many people describe feeling frustrated, angry, or sad about changes following the injury. Others talk about feeling worried or scared about what will happen in the future. Some people notice that their emotions change quickly, “like a roller coaster.” Feeling misunderstood is also common. Strong emotions can weaken your ability to solve problems, handle challenges effectively, and get along with others. Recognizing, understanding, and controlling your feelings can be very difficult.
This is part of a series of articles focusing on intense feelings and how to manage them effectively. In this article, we’ll present Parts I and II. Part I covers understanding and identifying your emotions. Part II covers barriers to communicating about your feelings. Part III, a separate article, will focus on ways to manage intense emotions effectively.
The first step in controlling your emotions is recognizing how you feel and noticing when your emotions get in the way. If you can figure out how you’re feeling early on, you can get your feelings under control faster and more easily. Then you’ll be able to feel better and reach your goals more efficiently.
Take a moment to think about how you feel. Below, check off the sentences that describe you:
Review the items you’ve checked and the ones you haven’t to better understand your feelings. The more items you’ve checked, the more likely it is that you are experiencing many different and strong emotions. Is there a pattern to the items you’ve checked? Show your checklist to someone you know and trust. Do you agree on the items that should be checked?
Once you recognize how you feel, you can take steps to help yourself cope with the emotions effectively. Talking about your feelings is an important first step to feeling better. But, many people have trouble talking about their feelings.
In Part II (below), we’ll talk about common barriers that keep people from talking with others about their feelings.
Talking about your feelings may be difficult. People often say they worry about what others will think of them. Others say they don’t know who to turn to or who they can trust. Think about what gets in the way of talking to others about your feelings. The following questionnaire will help you figure out the answer. Circle T (True) or F (False) to figure out the challenges you face in talking about your emotions.
T F 1. My feelings change from day to day.
T F 2. Nobody understands what I am going through.
T F 3. I feel uncomfortable around other people.
T F 4. I’m worried about what others think of me.
T F 5. Nobody cares about me.
T F 6. I have a hard time describing my feelings.
T F 7. I don’t want to burden people with my feelings.
T F 8. I feel uncomfortable talking about my feelings.
T F 9. I don’t know where to turn for help.
T F 10. I can’t hide my feelings like I used to.
T F 11. I’m afraid to show my true feelings.
T F 12. I don’t want to upset people by talking about my feelings.
T F 13. I’m afraid to let my guard down.
T F 14. I keep my feelings bottled up.
T F 15. I don’t know how I’m feeling.
T F 16. I don’t feel anything anymore.
Look over your answers with family, friends, or trusted professionals. Think about the main issues that are getting in the way of talking about your feelings.
Each of these issues may get in the way of you talking to others about your feelings. Remember that talking to others about your feelings is a big step toward feeling better. Often, you need support from others to be able to deal with difficult emotions, so you can handle your responsibilities effectively.
Asking for help lets people know that you value their support and involvement and offers chances to build relationships. Talk to trusted family, friends, and professionals about your feelings and about ways to cope with strong emotions. They may be able to give you some good ideas about ways to cope with your feelings.
We’ve talked to lots of survivors and their families to find out ways they cope with strong feelings. Here are a few strategies that have worked for other people. Look over this list and pick out which ones you think will work for you and your family:
Virginia Commonwealth University’s TBI Model System includes a research project to better understand how to look at emotional adjustment after brain injury. Participants for this study need to have had a traumatic brain injury and be at least 18 years old. If you have questions about the project or would like to be involved, please call Jenny Marwitz at: (804) 828-3704 or toll free (866) 296-6904, or email her at firstname.lastname@example.org.
After injury, survivors and their family members often experience a variety of strong emotions. Many people describe feeling frustrated, angry, or sad about changes following the injury. Others talk about feeling worried or scared about what will happen in the future. Some people notice that their emotions change quickly, “like a roller coaster.” Feeling misunderstood is also common. Strong emotions can weaken your ability to solve problems, handle challenges effectively, and get along with others.
Recognizing, understanding, and controlling your feelings can be very difficult. The first step in controlling your emotions is recognizing how you feel and noticing when your emotions get in the way. If you can figure out how you’re feeling early on, you can get your feelings under control faster and more easily. Then you’ll be able to feel better and reach your goals more efficiently.
Take a moment to think about how you feel. On the list below, mark the sentences that describe you:
Review the items you’ve checked and the ones you haven’t to better understand your feelings. The more items you’ve checked, the more likely it is that you are experiencing many different and strong emotions. Is there a pattern to the items you’ve checked? Show your checklist to someone you know and trust. Do you agree on the items that should be checked?
Once you recognize how you feel, you can take steps to help yourself cope with the emotions effectively. We’ve talked to lots of survivors and their families to find out ways they cope with strong feelings. Here are a few strategies that have worked for other people. Look over this list with trusted family, friends, or professionals and pick out which ones you think will work for you and your family:
Sometimes people have trouble helping themselves feel better. Often, you can benefit from support and guidance from others. Talk with trusted family, friends, or professionals about your feelings. Also, consider joining a support group, so you can learn from others about how they’ve dealt successfully with similar emotions.
This column was written by Laura Taylor and Jeff Kreutzer from the VCU TBI Model System Family Support Research Program. The program teaches families how to deal with stress and intense emotions. For more information about the program, please contact Laura at 804-828-3703, toll free at 866-286-6904, or by email at email@example.com.
Virtual reality can help patients with movement issues, but only if it is done correctly and tailored to individual patients, says Robert Ferguson, a neurorehabilitation clinical specialist who focuses on such therapy.
Clinicians “are reading the research and they are applying it wrong,” he explains, in Medscape Medical News. “The evidence suggests that it’s not about the virtual reality, it’s about how you use the research. You need to know how the equipment and programs work so you know how to modify them for your individual patient.”
A more methodological approach to virtual reality therapy is needed.
“It shouldn’t be that we just throw someone into a virtual reality environment,” states Nancy Baker, ScD, an occupational therapist at Tufts University in Medford, Mass. “If you want it to be therapeutic, it has to be thoughtfully applied.”
Ferguson, who manages the stroke rehabilitation program at the University of Michigan Health System in Ann Arbor, presented a number of cases during his talk on virtual reality and occupational therapy recently at the American College of Rheumatology 2019 Annual Meeting.
He described asking a stroke survivor who appeared to be unable to handle problems on the left side of her body to “climb” a virtual reality rock wall. Ferguson watched as the patient sat in a chair and moved her arms in a climbing motion in response to the computer-generated field in front of her.
At first, the woman only seemed to climb to her right. But as she learned the rules of the game, Ferguson manipulated the rock wall she was seeing, ultimately encouraging her to explore the wall to her left. By the end of the session, her brain — which until then had ignored problems on the left side of her body — had led her to “climb” the wall to her left, per Medscape.
Another patient, an avid bowhunter, was trying to regain balance after a leg amputation. Ferguson constructed a virtual reality game in which the patient had to defend a castle using a bow and arrows.
“He told me, ‘it’s the hardest therapy I’ve ever done, but it’s also the most fun’,” Ferguson shares.
“The thing about immersive virtual reality environments is that we need to connect it to a goal,” he told the audience. “The virtual reality is not the treatment; it’s an adjunct treatment to what you’re doing. You need to know what your goal is and how you are going to get the patient to that goal.”
“When we use immersive virtual reality — the kind of virtual reality that makes people feel as though they are in the virtual world — meta-analyses and systemic reviews suggest that people are more engaged and more motivated,” Ferguson tells Medscape Medical News.
“We are seeing some immediate and longer-term improvements in both cognitive performance and motor function, but we are not sure how long-lasting those effects are,” he adds.
Baker, who focuses on musculoskeletal disorders and chronic pain, shares that she has been working to launch research programs looking at the effect virtual reality can have in therapy.
“The thing about chronic pain is that people lose the ability to do the things they love to do, and it can be hard to motivate them in occupational therapy,” she continues. “In a virtual reality environment, you can put them in a real-seeming space, so they can do the things they like to do.”
Research to this point indicates that virtual reality is a reasonable addition to a comprehensive rehabilitation program, as long as therapists take into account a patient’s goals, abilities, and preferences, Ferguson concludes.
“The problem is that significant heterogeneity and small study sizes limit the power of the conclusions,” he adds. “That’s why we need more research.”
[Source: Medscape Medical News]
By CHARLES N. (NICK) SIMKINS, Attorney at Law
Although we live in a society where people freely discuss toilet paper, hemorrhoids, and all sorts of quite personal issues, without bashfulness or hesitation, the problem of sexual dysfunction following lightning strike, electric shock, or traumatic brain injury is so “hush hush” that not even the treating physicians inquire about possible sexual dysfunction in their usual history-taking from the patient. It is well known and well recognized, in all of the literature and research, that sexual dysfunction can be the result of chronic pain, medications, injury to the brain, psychological injury, depression, and a whole host of common problems that those surviving electric shock, lightning strike, or traumatic brain injury may have, yet it seems to be a well-kept secret and people are left to deal with problems related to sexual dysfunction on their own.
In a society where sexuality seems so important in our humor, television commercials, politics, and sometimes the very core of our culture, it is a shame that people are left to suffer on their own, without knowing why, and without knowing that there may be some kind of care, treatment, or therapy that could be of help. This article is an attempt to pull back the curtain of darkness in an effort to give comfort to those in that it is not “their fault,” and maybe to educate so that people can get real and available help.
Let me be clear that it was not my idea to write an article about sexual dysfunction following injury. I must confess that when I was first asked to write an article about sexual dysfunction following injury, my first thought was “whoa, sex is a very sensitive subject,” and then I thought, “whoa, whoa, talking about sex is a very, very sensitive subject,” and then I thought “whoa, whoa, whoa, writing about sexual dysfunction is going to be a really sensitive subject and there is no way that I am going to do that.”
As I thought about responding to the request to write this article about sexual dysfunction following injury, I realized that in my over 25 years of representing persons and families surviving various types of injury, including traumatic brain injury, lightning strike, or electric shock injury, that one of the very real consequences of those injuries, directly or indirectly, has been sexual dysfunction. But I still thought, no way am I going to write about this, and there is no way that I want to be introduced at seminars, or be known, as an expert in sexual dysfunction.
Suffice it to say that those who know me best would not consider me as the poster child for openness in discussion of sexual issues. Then, I thought it was perhaps the type of attitude that I had in terms of reluctance to discuss sexual issues or sexual dysfunction issues, that formed part of the weave of the cloak of darkness and silence that surrounds the very real issue and problem of sexual dysfunction following injury.
It just so happened that right about this time, I came across a booklet put out by Pfizer, Inc., U.S. Pharmaceuticals entitled “Putting Sexual Health Into Practice”, that was published in August, 1999 for physicians. As I read through the booklet, I began to think that maybe an article of this type could be help to some people.
At page one of the booklet, under the heading of “Breaking the Silence Around Sexual Health”, it says:
Having a healthy sex life is one factor that may contribute directly to the quality and longevity of an individual’s life, according to the Duke First Longitudinal Study of Aging. In a World Health Organization (WHO) Report, sexual health is defined as the integration of the somatic, emotional, intellectual, and social aspects of sexual being, in ways that are positively enriching and that enhance personality, communication, and love. The international group of experts convened by WHO take the position that the notion of sexual health implies a positive approach to human sexuality, and the purpose of sexual healthcare should be the enhancement of life and personal relationships and not merely counseling and care related to procreation or sexually transmitted diseases. But sexual health, primarily in men, is frequently overlooked as an integral part of overall health. ? For various reasons, millions of men are not discussing the sexual health problems with their physicians. By keeping these issues to themselves, they suffer silently.
In a survey of 500 adults, 94 percent of those polled said that sexual satisfaction added to the quality of life at any age. Marianne J. Legato, M.D., commented, “As human beings our sexuality is inextricably linked to our overall health, happiness, and sense of wellness.” Furthermore, the American Medical Association lists “participating in desired sexual activity” as one of many important activities of daily living.”
At page three of this booklet and remembering that it is a booklet written for doctors, it says:
One of the most rewarding aspects of treating sexual health is that you can impact two lives. Often, a sexual problem can make partners feel that they are no longer attractive or that the problem is a reflection on them.
The fact is that the world health organization and the American Medical Association consider sexual function to be in the category of an important daily activity. There are many studies that relate a number of health benefits to a healthy sexual life. There may be millions of people in the United States and around the world who are suffering from some aspect of sexual dysfunction as a result of injury and maybe at least one of those people could benefit from receiving at least the knowledge that they are not alone.
For those persons who may be shy, reserved, or reluctant to bring up sexual issues with their doctor, at the end of this article is a form that can be filled out in advance of the doctor’s appointment, and simply handed to the doctor to sort of help break the ice about any discussions with regard to sexual issues.
This has been the most difficult article that I have ever written, and I have tried to be as careful as I could so as not to offend anyone. While some aspects of this article may focus on male issues, that is simply because much of the available literature and research deals with male sexual dysfunction as opposed to female. Every word in this article is intended to help women as much as men.
As basic as is the human sexual desire and function, we all know, from research, medical literature and, most of all, life and experience, that the sexual function is a highly complicated process. It depends upon emotion, feelings, timing, mood, words, and so many other factors, and when injury and consequences are added to the mix, the process can become impossible.
The purpose of this article is not only to discuss these issues, but more importantly, to accomplish one or more of the following:
Since the beginning of time, and at whatever stage of the civilization humanity was, and whether people lived outside, in a cave, in a hut, in a barn, or in a mansion, the common historical thread of a man was that he could always do what had to be done in order to get food for himself and his family, to do what was needed to be done to have shelter for himself and his family, and at the same time, to have the energy and imagination to dream and plan for better days for himself and his family. Women and men are taught and raised to be self-reliant, and if fortunate, are able to go through their entire lives taking care of themselves, raising their children, paying their bills, and persevering regardless of their lot in life.
When injury strikes, all of this changes because all of a sudden, instead of being self-reliant, the family may now have to rely on an insurance clerk to mail a check on time to pay their bills, or rely on a doctor to send a certain report to an insurance carrier to get bills paid and the focus of the family’s financial security may literally shift from the wage earner to the mailbox. This alone may have an impact on a person’s sexual function. While this is going on, and just as suddenly, the entire focus of the family’s social life may change, or disappear, and now the time that was spent working, enjoying social and leisure activities, enjoying children, is replaced with time in therapy, sitting in doctors’ offices, worrying and wondering about when things will get back to normal.
With all of this going on, it is no wonder that the delicate balance of life that leads to human sexuality is upset and disturbed, but the suffering in silence, in terms of any sexual dysfunction issues, only adds to the cycle of frustration, problems, and everything else that is going on.
In the United States, men seem to have, on one level or another, the image of themselves as the “Marlboro Man,” with a very macho image of themselves. Women may equate their own sexuality with attractiveness, beauty, and personality, all of which may suffer when there is sexual dysfunction following injury. Men and women may be reluctant to even discuss issues related to sexual dysfunction with their treating physicians, and they are left to suffer in silence.
Sometimes, regardless of what our problem may be, we think we suffer alone. There is comfort, as well as knowledge, knowing that many other people are in the same situation, and it is the purpose of this article not only to distribute that information about the possible causes of sexual dysfunction, but to let people know that there may be help in the form of medical treatment, care, or therapy that can alleviate some of these problems. In this situation of sexual dysfunction, in order for the person to be able to get help, there must be a bridge between the person’s knowledge of their own sexual dysfunction, and the doctor’s knowledge of the patient’s sexual dysfunction. That bridge is sometimes not built because of shyness or reservation, on the part of either the doctor or the patient, or both, and part of the purpose of this article is to help build that bridge, and one of the recommendations, at the end of this article, is a written form that can be filled out in advance and given to the doctor.
Several years ago, Dr. George Zitnay, then president of the National Head Injury Foundation, testified before congress, and started his prepared remarks with the following statement:
Ladies and gentlemen, I am here today to talk about the largest and most important sex organ in the human body – the brain.
As Dr. Zitnay spoke those words, everyone in the hearing stopped talking and paid strict attention to what he had to say.
Amazingly enough, all of the following have one thing in common:
What all of these have in common is that any or all of these can have an impact upon a person’s sexual functioning. For example, many medications have, as a side effect, a potential impact on a person’s libido which may not be known to the patient or their family.
Following the injury, it may be weeks or months before the person experiences the romance of a sexual encounter, which may not be the same as it was before the injury. This may lead to embarrassment, and depending upon how the situation is dealt with, may lead to humiliation, particularly on the part of the man. This humiliation may, in and of itself, lead to stress, and in and of itself, lead to an avoidance of the next romantic sexual encounter, which may then engender some feelings of guilt on the part of the uninjured spouse. This may snowball and become a vicious cycle of frustration for both parties.
Where the woman experiences a lack of libido, for any number of reasons related to the injury, the man may feel unloved and unwanted, which leads to stress, arguing, and again, can snowball and become a vicious cycle of frustration for both parties.
The uninjured spouse may then begin to think that the injured spouse no longer cares about them, or no longer has romantic feelings, and is unable to provide an explanation for the cause of the problem. It may very well be that as of that point in time, no one in the health care system has taken the time to explain to either of the parties that any aspect of the injuries may have an impact upon sexual function.
In the book Neuropsychological Assessment, Third Edition, by Dr. Muriel D. Lezak, at page 42, she writes:
One significant personality change that is rarely discussed but is a relatively common concomitant of brain injury is a changed sexual drive level. A married man or woman who has settled into a comfortable sexual activity pattern of intercourse two or three times a week may begin demanding sex two and three times a day from the bewildered spouse. More frequently, the patient loses sexual interest or capability. This leaves the partner feeling unsatisfied and unloved, adding to other tensions and worries associated with cognitive and personality changes in the patient. For example, some brain damaged men are unable to achieve or sustain an erection, or they may have ejaculatory problems secondary to nervous tissue damage. Patients who become crude, boorish, or childlike as a result of brain damage no longer are welcomed bed partners and may be bewildered and upset when rejected by their once affectionate mates. Younger persons brain damaged before experiencing an adult sexual relationship may not be able to acquire acceptable behavior and appropriate attitudes. Adults who were normally functioning when single often have difficulty finding and keeping partners because of cognitive limitations or social incompetence resulting from their neurological impairments. For all of these reasons, the sexual functioning of many brain damaged persons will be thwarted. Although some sexual problems diminish in time, for many patients they seriously complicate the problems of readjusting to new limitations and handicaps, by adding another stage of frustrations, impulses, and reactions.
There may be an escalating cascade of problems which can be, for example:
One of the concepts in psychology is the concept of what is called a stroke as being a unit of recognition, or a form of stimulation. This is far different from the medical concept of a stroke, and this discussion is related solely to the psychological concept of stroke. In psychology, strokes can be physical, verbal, or non-verbal, and as a person grows older, new ways are discovered to receive and exchange strokes. For example, some may enjoy making presentations at church, or at local groups, because they enjoy the recognition, and the recognition would, in psychology, be called a stroke. The need for stimulation becomes at least, in part, a need for recognition, and this is a very basic human need and, as stated in the book entitled Transactional Analysis by Woollams, Brown & Huige, at page 16:
Since the need for strokes is inherent in each person, exchanging strokes is one of the most important of all human activities.
Further, at page 16:
Since strokes are necessary for survival, a person will do whatever she thinks necessary in order to receive the strokes she needs. A person will develop a style of giving and receiving strokes based on her life position.
Again, remember that the concept of strokes in this context is a psychological term. Now think about the psychological concept of strokes in the context of a relationship between a loving couple, having sexual relations prior to injury. Human sexuality certainly encompasses far more than just the act of sex between two people. When we think of the delicate balance necessary for human sexuality, in terms of mood, physical, mental, emotional, and timing, and then remember that all of this must exist in a multiple of two, the psychological concept of what are called strokes is very applicable.
With the intimacy of the couple’s knowledge of each other, they have developed a concept of strokes for each other, and how they receive strokes in the world, through their work, recreational activities, and things. Now, with injury, all of this has changed not only for the injured person, but then in consequence, also for the uninjured person. Just looking at this psychological concept of strokes alone, one could think that there must be a proper balance of strokes, from an emotional point of view, in order for there to be a loving sexual relationship, and if that emotional framework becomes unbalanced and distorted, as it does, that alone can impact on the sexual function.
Consider, for example, a young couple who would typically enjoy going out to dinner, a little dancing, and each other’s personality, filled with a sense of humor, as a prelude to sexual relations. Now, following injury, a partner is in pain, has very little sense of humor, does not enjoy eating in the noisy atmosphere of a restaurant, and it is easy to see that the emotional framework of this couple has become unbalanced and distorted, and without help, the relationship may become further unbalanced and distorted through the silence of sexual dysfunction.
As I researched and thought about what to say and include in this article, I was amazed to discover that just about every medical textbook that I reviewed had at least some information about sexual dysfunction, whether neurology, psychiatry, orthopedics, neuropsychology, or other areas, somewhere in each book there was some discussion about relationships between trauma, medications, emotions, injury, or something to sexual dysfunction.
I decided to include this section with just quotes from the medical literature not, in any way, to try and teach the medical substance of the quotes, but rather, for the purpose of making the reader aware of how extensively this topic is discussed in some of the very same medical books that may well be on your doctors’ shelves. This knowledge may help people feel a little more comfortable about discussing issues of sexual dysfunction with a doctor.
It is also important to remember that there are physicians, specialists, and health care providers who specialize in working with people with sexual dysfunction and people have the right to request such referrals.
Rehabilitation of the Adult and Child with Traumatic Brain Injury, Second Edition, by Rosenthal, Griffith, Bond, and Miller, 1990. At page 206, the chapter is entitled “Sexuality and Sexual Dysfunction.”
Human sexuality conceptually embraces the composite of those factors that result in our capacity to love and procreate. A related aspect of sexuality is the individual’s perception and expression of “womanliness” or “manliness.” By these terms, it is predictable that a catastrophic event such as brain injury will almost ineluctably affect the sexuality of the survivor. Sexual disabilities may include disturbances of any of the component functions of sexuality: sexual drive, interests, beliefs, attitudes, behaviors, identity, activities, responses, and fertility.
In this chapter, they refer to:
Disabilities resulting from physical or organic factors as primary dysfunction, and secondary sexual dysfunctions resulting from brain trauma are those disturbances of psychosocial abilities or sexual responses due to the mental deficits in psychologic reactions consequent to the injury. Secondary sexual dysfunctions may arise in the partner, if one exists, as the consequences of reactions to the disabled person and the altered life situation.
Current evidence indicates that secondary factors account for the great majority of sexual dysfunctions in brain injured subjects. However, more recent data suggest that primary factors may be less rare than previously surmised . . . In contrast to the growing body of general information on psychosocial aspects of brain trauma, very little has been written about sexuality.
Sexual responses – erection, vaginal lubrication, ejaculation, orgasm, and fertility – are not altered as a direct consequence of brain injury unless the hypothalamic-pituitary function has been disturbed or disrupted. The resulting endocrinopathies have received increasing attention, with recognition that testicular and ovarian hypofunction can occur. Some women with mesial temporal lobe foci of seizures have recently been reported to have hypogonadotropic hypogonadism. Women often become temporarily amenorrheic following severe trauma, but menses should ordinarily resume within 4 to 6 months. Persistent amenorrhea should alert the clinician to the possibility of pituitary dysfunction. Similarly, men frequently have transient impotence, but the ability to achieve an erection should reappear after several months.
Trauma to the craniofacial area, primary or secondary sexual organs, and orthopedic injuries resulting in amputation, contractures, deformities, and chronic pain are potential sources of dysfunction . . . Abdominal or pelvic vascular injuries can compromise circulation to the genitalia, producing impotence or other alterations in sexual responses.
Recurrent medical complications, sustained bed rest, and inactivity with its many consequences cause deconditioning and other effects that impinge upon sexual activity. A multitude of drugs produce side effects that influence sexual acts and responses . . .
Finally, pre-existing disorders may become additive factors contributing to the primary sexual dysfunction. Cardiac, vascular, pulmonary, or other types of diseases may already have compromised sexual function of the elderly before injury.
In the book Principals of Neurology by Adams, Victor, and Ropper, Sixth Edition, at page 517, under the heading of “Altered Sexuality” it states:
The normal pattern of sexual behavior in both male and female may be altered by cerebral disease quite apart from impairment due to obvious physical disability or to diseases that destroy or isolate the segmental reflex mechanisms.
Hypersexuality in men or women is a rare but well-documented complication of neurologic disease. Kleist pointed out that lesions of the orbital parts of the frontal lobes may remove moral-ethical restraints and lead to indiscriminate sexual behavior, and that superior frontal lesions may be associated with a general loss of initiative which reduces all impulsivity, including sexual.
At page 518:
In our clinical work we find that hyposexuality, meaning loss of libido, is most often due to a depressive illness. Certain chemical agents – notably antihypertensive, anticonvulsant, serotoninergic antidepressant and neuroleptic drugs – may cause a loss of libido. A variety of cerebral diseases may also have this effect.
At page 545, under the heading of “Disturbances of Sexual Function,” it says:
Sexual function in the male, which is not infrequently affected in neurologic disease, may be divided into several parts: (1) sexual impulse, drive, or desire, often referred to as libido; (2) penile erection, enabling the act of sexual intercourse (potency); and (3) ejaculation of semen by the prostate through the urethra, whereby impregnation of the female may be accomplished.
The arousal of libido in men and women may result from a variety of stimuli, some purely imaginary. Such neocortical influences are transmitted to the limbic system and thence to the hypothalamus and spinal centers.
The difference aspects of sexual function may be affected separately. Loss of libido may depend upon both psychic and somatic factors. It may be complete, as in old age or in medical and endocrine diseases, or it may occur only in certain circumstances or in relation to a certain situation or individual.
. . . sexual desire may be present but penile erection impossible to attain or sustain, a condition called impotence, in which nocturnal erections are usually preserved. The commonest cause of impotence is a depressive state.
Comprehensive Textbook of Psychiatry, Volume I, Sixth Edition, by Kaplan and Sadock, at page 1296:
Innervation of the organs of sexuality is mediated primarily through the autonomic nervous system. It is generally assumed that the parasympathetic system activates the process of erection via impulses that pass through the pelvic splanchnic nerves (S2, S3, S4) which caused the smooth muscles of the penile arteries to dilate.
Recent evidence implicates the sympathetic (adrenergic) system as being responsible for ejaculation . . . In women, the sympathic system facilitates smooth muscle contraction of the vagina, urethra, and uterus that occurs during orgasm.
The autonomic nervous system functions outside of voluntary control and is influenced by external events (for example, stress, drugs) and internal events (hypothalamic, limbic, and cortical stimuli). It is not surprising, therefore, that erection and orgasm are so vulnerable to dysfunction.
At page 1298:
Experimentation with animals has demonstrated that the limbic system is directly involved with elements of sexual functioning. In all mammals the limbic system is involved in behavior required for self-preservation and the preservation of the species.
A vast array of neurotransmitters are produced by the brain. They include dopamine, epinephrine, norepinephrine, and serotonin. All have effects on sexual function. For example, an increase in dopamine is presumed to increase libido. Serotonin produced in the upper pons and mid-brain is presumed to have an inhibitory effect on sexual function.
At page 1300, it says:
Seven major categories of sexual dysfunction are listed in DSM-IV: (1) sexual desire disorders, (2) sexual arousal disorders, (3) orgasm disorders, (4) sexual pain disorders, (5) sexual dysfunction due to a general medical condition, (6) substance-induced sexual dysfunction, and (7) sexual dysfunction not otherwise specified.
At page 1300:
The sexual cycle is divided into four phases: desire, excitement, orgasm, and resolution. The essential feature of the sexual dysfunctions is inhibition in one or more of the phases, including disturbance in the subjective sense of pleasure or desire or disturbance in the objective performance. Either type of disturbance can occur alone or in combination. Sexual dysfunctions are so diagnosed only when such disturbances are a major part of the clinical feature. They can be lifelong or acquired, generalized or situational, and due to psychological factors or due to combined factors. If they are attributable entirely to a general medical condition, substance use, or adverse effects of medication, then sexual dysfunction due to a general medical condition or substance-induced sexual dysfunction is diagnosed.
With the possible exception of premature ejaculation, sexual dysfunctions rarely are found separate from other psychiatric syndromes. Sexual disorders may lead to or result from relational problems, and patients invariably develop an increasing fear of failure and self-consciousness about their sexual performance. Sexual dysfunctions are frequently associated with other mental disorders, such as depressive disorders, anxiety disorders, personality disorders, and schizophrenia. In many instances, sexual dysfunctions may be diagnosed in conjunction with the other psychiatric disorders. In some cases, however, it is but one of many signs or symptoms of the psychiatric disorder.
A sexual disorder can be symptomatic of biological problems, intrapsychic conflicts, interpersonal difficulties, or a combination of these factors. The sexual function can be affected by stress of any kind, by emotional disorders, and by a lack of sexual knowledge.
At page 1302:
Hypoactive sexual desire disorder is experienced by both men and women; however, they may not be hampered by any dysfunction once they are involved in the sex act. Conversely, hypoactive desire may be used to mask another sexual dysfunction. Lack of desire may be expressed by decreased frequency of coitus, perception of the partner as unattractive, or overt complaints of lack of desire. In some cases there are biochemical correlates associated with hypoactive desire. A recent study found markedly decreased levels of serum testosterone in men complaining of this dysfunction when they were compared with normal controls in a sleep-laboratory situation. Also, a central dopamine blockage is known to decrease desire.
Patients with desire problems often have good ego strengths and use inhibition of desire in a defensive way to protect against unconscious fears about sex. Lack of desire can also be the result of chronic stress, anxiety, or depression. Abstinence from sex for a prolonged period sometimes results in suppression of the sexual impulse. It may also be an expression of hostility or the sign of a deteriorating relationship.
The presence of desire depends on several factors: biological drive, adequate self-esteem, previous good experiences with sex, the availability of an appropriate partner, and a good relationship in nonsexual areas with one’s partner. Damage to any of those factors may result in diminished desire.
Male erectile disorder is also called erectile dysfunction and impotence . . . In acquired male erectile disorder the man has successfully achieved vaginal penetration at some time in his sexual life but is later unable to do so.
The percentage of all men treated for sexual disorders who have impotence as the chief complaint ranges from 35 to 50 percent. The incidence of psychological as opposed to organic impotence has been the focus of many recent studies. Physiologically, impotence may be due to a variety of medical causes. In the United States it is estimated that two million men are impotent because they suffer from diabetes mellitus; an additional 300,000 are impotent because of other endocrine diseases; 1.5 million are impotent as a result of vascular disease; 180,000 because of multiple sclerosis; 400,000 because of traumas and fractures leading to pelvic fractures or spinal cord injuries; and another 650,000 as a result of radical surgery, including prostatectomies, colostomies, and cystectomies. In addition, the clinician should be aware of the possible pharmacological effects of medication on sexual functioning. The increased incidence of organic etiologies for this dysfunction in the past 15 years may, in part, reflect the increased use of psychotropic and antihypertensive medications. Statistics indicate that 20 to 50 percent of men with erectile dysfunction have a medical basis for their problem.
Sexual dysfunction due to a general medical condition. The category covers sexual dysfunction that results in marked distress and interpersonal difficulty when there is evidence from the history, the physical examination, or the laboratory findings of a general medical condition judged to be causally related to the sexual dysfunction.
Male erectile disorder due to a general medical condition. The incidence of psychological as opposed to organic male erectile disorder has been the focus of many studies. Statistics indicate that 20 to 50 percent of men with erectile disorder have an organic basis for the disorder. The medical causes of male erectile disorder are listed in Table 21.1a-10 which include, as general categories, infectious and parasitic diseases, cardiovascular disease, renal and urological disorders, hepatic disorders, pulmonary disorders, genetics, nutritional disorders, endocrine disorders, neurological disorders, pharmacological contributants, poisoning, surgical procedures, and miscellaneous including “any severe systemic disease or debilitation condition.” Side effects of medication may impair male sexual functioning in a variety of ways. Castration does not always lead to sexual dysfunction, depending on the person. Erection may still occur after castration.
A number of procedures, benign and invasive, are used to help differentiate medically caused impotence from psychogenic impotence. The procedures include monitoring nocturnal penile tumescence (erections that occur during sleep), normally associated with rapid eye movement; monitoring tumescence with strain gauge; measuring blood pressure in the penis with a penile plethysmograph or an ultrasound (Doppler) flow meter, both of which assess blood flow in the internal pudendal artery; and measuring pudendal nerve latency time. Neurological impairment of penile function may be indicated if vibratory perception is increased in the penis. Other diagnostic tests that delineate organic bases for impotence include glucose tolerance tests, plasma hormone assays, liver and thyroid function tests, prolactin and follicle-stimulating hormone (FSH) determinations, and cystometric examinations. Invasive diagnostic studies include penile arteriography, infusion cavernosography, and radioactive xenon penography. Invasive procedures require expert interpretation and are used only for patients who are candidates for vascular reconstructive procedures.
A good history is crucial in determining the etiology of the male erectile disorder. If a man reports having spontaneous erections at times when he does not plan to have intercourse, having morning erections or only sporadic erectile dysfunction, or having good erections with masturbation or with partners other than his usual one, then organic causes for his impotence can be considered negligible, and costly diagnostic procedures can be avoided. In those cases in which a medical basis for impotence is found, psychological factors often contribute to the dysfunction, and psychiatric treatment may be helpful. In some diabetics, for instance, erectile dysfunction may be psychogenic. In general, the psychological conflicts that cause impotence are related to an inability to express the sexual impulse because of fear, anxiety, anger, or moral prohibition.
Many developmental factors have been cited as contributing to erectile disorder. Any experience that hinders the ability to be intimate, that leads to a feeling of inadequacy or distrust, or that develops a sense of being unloving or unlovable may result in impotence. In an ongoing relationship, erectile dysfunction may reflect difficulties between the partners, particularly if the person cannot communicate his or her needs or angry feelings in a direct and constructive way. Successive episodes of impotence are reinforcing, with the man becoming increasingly anxious about his next sexual encounter. Regardless of the original etiology of the dysfunction, his anticipatory anxiety about achieving and maintaining an erection interferes with his pleasure and sexual contract and with his ability to respond to stimulation, thus perpetuating the problem.
Hypoactive sexual desire disorder due to a general medical condition. Desire commonly decreases after major illness or surgery, particularly when the body image is affected after such procedures as mastectomy, ileostomy, hysterectomy, and prostatectomy. Illness that deplete a person’s energy, chronic conditions that require physical and psychological adaptation, and serious illnesses that may cause the person to become depressed can all result in a marked lessening of sexual desire in both men and women.
In some cases, biochemical correlates are associated with hypoactive sexual desire disorder.
Other male sexual dysfunction due to a general medical condition. The category is used when some other dysfunctional feature is predominant (for example, orgasmic disorder) or no feature predominates. Male orgasmic disorder may have physiological causes and can occur after surgery on the genitourinary tract, such as prostatectomy. It may also be associated with Parkinson’s disease and other neurological disorders involving the lumbar or sacral sections of the spinal cord. The antihyptensive drug guanethidine monosulfate (Ismelin), methyldopa (Aldomet), the phenothiazines, the tricyclic drugs, and fluoxetine (Prozac), among others have been implicated in retarded ejaculation. Male orgasmic disorder must also be differentiated from retrograde ejaculation, in which ejaculation occurs but the seminal fluid passes backward into the bladder. Retrograde ejaculation always has an organic cause.
Acquired female orgasmic disorder is a common complaint in clinical populations. One clinical treatment facility described nonorgasmic women as about four times more common in its practice than patients with all other sexual disorders. In another study 46 percent of the women complained of difficulty in reaching orgasm, and 15 percent described an inability to have orgasm.
Male orgasmic disorder. In male orgasmic disorder (previously inhibited male orgasm and called retarded ejaculation) the man achieves climax during coitus with great difficulty, if at all. A man suffers from lifelong orgasmic disorder if he has never been able to ejaculate during coitus. The disorder is diagnosed as acquired if it develops after previous normal functioning.
Almost every pharmacological agent, particularly those used in psychiatry, has been associated with an effect on sexuality. In men those effects include decreased sex drive, erectile failure (impotence), decreased volume of ejaculate, and delayed or retrograde ejaculation. In women decreased sex drive, decreased vaginal lubrication, inhibited or delayed orgasm, and decreased or absent vaginal contractions may occur. Drugs may also enhance the sexual response and increase the sex drive, but that effect is less common than are adverse effects.
Talk about the male ego being associated with sex, and the male ego being associated with the ability to make a living, as 19th century as that may sound. When the man is all of a sudden transformed from the wage earner, and head of the family, to someone who is reliant upon the system for his living, or a workers compensation carrier for money, this does tremendous damage to the male ego.
Under the heading of Treatment of Sexual Dysfunction:
Various corrective therapies are now used to treat sexual dysfunctions . . .
In addition to making the determination of which type of therapy to use, the clinician must evaluate whether or not the disorder has a physiological cause. It is assumed that prior to entering psychotherapy, a patient will have had a thorough medical evaluation, including a medical history, physical examination, and appropriate laboratory studies when necessary. If a medical cause for the disorder is found, treatment should be directed toward ameliorating the cause of the dysfunction.
Page 1319, under the heading of Biological Treatment Methods, it says:
Pharmacotherapy. Penile injections produce a transient increase in penile blood flow, which allows the patient to become tumescent or gain an erection. The physician usually administers a test dose of the drug, and if the patient responds favorably, he is then taught to inject himself. Hormone therapy is listed, antiandrogens and antiestrogens, male prosthesis (at page 1320): Surgical treatment is rarely advocated, but improved penile prosthetic devices are available for men with inadequate erectile response who are resistant to other treatment methods or who have medically caused deficiencies.
The course and prognosis of secondary sexual dysfunctions vary widely, depending on the etiology . . . Dysfunctions due to neurological disease may run protracted, even progressive, courses. The treatment approach similarly varies widely, depending on the etiology. When reversal of the underlying cause is not possible, supportive and behaviorally oriented psychotherapy with the patient (and perhaps the partner) may minimize distress and increase sexual satisfaction (for example, by developing sexual interactions that are not limited by the specific dysfunction). Support groups for people with specific types of dysfunction are available.
Organic Psychiatry, the Psychological Consequences of Cerebral Disorder by Dr. William A. Lishman, Third Edition, 1988. At page 271 under the heading of Sexual Disorder in Epilepsy:
Sexual disorder attracted little attention in epileptic patients until relatively recently. Several reports, however, now stress the frequency of sexual disturbance in patients with temporal lobe epilepsy. Hyposexuality has emerged as the commonest abnormality, with perversions of sexual interest and outlet occurring in a much smaller number.
Gastaut and Collomb (1954) were the first to draw attention to hyposexuality after specific inquiry in 36 patients with temporal lobe epilepsy. More than two-thirds showed marked diminution or absence of interest, appetite or sexual activity. Other forms of focal and generalized epilepsy appeared to be unassociated with such problems. There was often a remarkable lack of sexual curiosity, fantasies or erotic dreams, yet little to suggest inhibition since the patients talked easily and without reserve about such matters. Indeed they appeared to be quite indifferent about the subject.
By detailed interviews it was established that 41% of the male temporal lobe epileptics were hyposexual, compared to 8% of the males with generalized epilepsy. The corresponding figures for females were 38% and 5% respectively. On restricting attention to patients over the age of 15 and where adequate information was available these differences were accentuated, reaching statistically significant levels. Among the males the disorder was manifest as a global lack of interest, failure of erections and nocturnal emissions, and absence of fantasies or dreams of a sexual nature. The females remained totally passive in sexual relations and failed to reach orgasm . . . The lack of concern evidenced by the patients, and their failure to make complaints, probably accounted for the problem having attracted so little attention in the past. Toone et al (1989) found that temporal lobe epileptics and other focal epileptics recruited from general practice were equivalently impaired, both more often lacking sexual interest and activity than patients with primary generalized epilepsy.
From the Textbook of Clinical Neurology by Goetz and Pappert, at page 369, under the heading of “Sexual Dysfunction” it says:
Treatment of organic impotence includes treatment of secondary psychological problems and reducing or eliminating aggravating factors such as poor sleep, chronic pain, malnutrition, alcohol use, and some medications. Yohimbine can be used orally to increase penile arterial vasodilatation and enhance relaxation of the cavernous trabeculae. Direct injection of papaverine (direct smooth muscle relaxant), phentolamine, or prostaglandin E1 into the corpora cavernosa may be effective but poses the risks of priapism and scarring of the tunica albuginea. A vacuum device may also be used to enhance corporal filling.
In the book Head Injury and Post Concussive Syndrome by Rizzo and Tranel, at page 312, under the heading of “Sexual Disorders” it says:
Symptoms of sexual dysfunction can be noted after TBI. These symptoms can be grouped into changes in sexual interest or performance and the development of inappropriate or unusual sexual behaviors. A syndrome of apathy can extend to apathy in sexuality, with diminished desire and reduced frequency of sexual intercourse. Impotence can also develop after TBI. Finally, inappropriate sexual behavior and speech have been noted, especially in patients with significant frontal lobe dysfunction. This can include suggestive remarks or unwanted sexual advances toward health professionals. Increased interest in pornography has also been noted.
Under DSM-IV Classification, it says:
When sexual apathy is a target of evaluation and interest, the appropriate classification comes under the sexual dysfunction due to head trauma category. The subclassification would be 608.89 Male (or 625.80 Female) hypoactive sexual desire due to head trauma. Male impotency following TBI would be denoted by 607.84, male erectile disorder due to head trauma.
Inappropriate sexual behavior problems can be clinically important enough for diagnosis. Inappropriate sexual behaviors believed to be due to frontal lobe damage would be designated as personality change due to head trauma – disinhibited type.
Under the heading of “Differential Diagnosis” it says:
Disorders of sexual desire can be primary (i.e., present prior to head trauma or unrelated to the injury). Medications can have significant effect on sexual interest and performance. A variety of causes for impotence should be reviewed, including vascular disorders, diabetes, and psychological disorders impairing male sexual function.
The only way that your doctor is going to have the information about your situation following injury is if it is provided by you, or someone on your behalf. Since the doctor may not inquire about it, as a part of the history, and since it is important to provide complete information, the following is suggested. It is suggested that you actually make a copy of this form, fill it out, and hand it to your doctor at your next appointment to start the conversation that may lead to a more fulfilling life for you and your partner.
Dear Dr. _________:
Since my injury, I have noticed a change in my sexual functioning, and I am providing you with this information, and any other information that you might need to evaluate my situation. Can you help me, or refer me to a doctor or health care provider who could help me with this change in my sexual functioning?
Then, provide in that same letter, the following information:
Any other information that you think would be helpful for the doctor should be written down and given to the doctor.
This should help break the ice about any discussion of sexual dysfunction.
This article is dedicated to my friend, Mr. Steve Marshburn, founder and president of Lightning Strike & Electric Shock Survivors International. If this article dealing with sexual dysfunction after injury is of any help or comfort to anyone, such persons owe a great debt of gratitude to Mr. Steve Marshburn. When God chose Steve Marshburn to be at the forefront of the fight for better understanding, medical care, and legal representation for persons and families surviving electric shock and lightning strike injury, obviously He chose wisely. The courage, persistence, determination, and wisdom of my friend, Mr. Steve Marshburn, can never be underestimated.
It has been a real privilege working with Steve and Joyce Marshburn over the years. When Steve told me that many members had requested an article and information on sexual dysfunction following injury, and asked me to write such an article, I was somewhat taken aback with shyness and awe at the complexity of the task. But, as anyone who knows Steve Marshburn knows, no one ever says no to Steve Marshburn.
CHARLES N. (NICK) SIMKINS, is a trial lawyer specializing exclusively in representing persons and families surviving traumatic brain injury, spinal cord injury, and brain dysfunction, and electric shock and lightning strike survivors. Mr. Simkins has served as a consultant to Lightning Strike and Electric Shock Survivors International, is an elected board member of the Brain Injury Association, editor of the National Head Injury Foundation book entitled “Analysis, Understanding, and Presentation of Cases Involving Traumatic Brain Injury,” author of “Can Long Term Cognitive and Emotional Problems be Caused by Electric Shock and Lightning Strike Accidents, or Is Anything That I Know About Brain Injury Applicable to Electric Shock and Lightning Strike Victims?,” Editor, Melvin Belli Society Newsletter, and he has represented injured persons and served as a consultant for trial lawyers throughout the United States on cases involving traumatic brain injury, brain dysfunction, and electric shock and lightning strike injuries. During his career, Mr. Simkins, whose office is in Northville, Michigan, has achieved numerous seven-figure plus verdicts and settlements in cases involving traumatic brain injury, brain dysfunction, and issues related to post traumatic stress disorder.
Charles N. (Nick) Simkins
Attorney at Law
200 North Center St.
Northville, Michigan 48167
Facsimile: (248) 349-8982
East Hanover, NJ. November 26, 2019. Kessler Foundation is participating in a phase II multi-site study of an innovative treatment to improve hand function in stroke survivors. Olga Boukrina, PhD, research scientist in the Center for Stroke Rehabilitation Research, is the site’s principal investigator. The study is funded through a five-year $3.2 million grant from the National Institutes of Health awarded to the principal investigator, Jayme S. Knutson, PhD, director of Research and associate professor of Physical Medicine and Rehabilitation at the MetroHealth System and Case Western Reserve University.
This is the first multi-site clinical trial of contralaterally controlled functional electrical stimulation (CCFES), a new rehabilitation intervention for hand recovery following stroke developed by Knutson and colleagues. With CCFES, electrical stimulation is applied to the muscles of the weak hand through surface electrodes, causing the weak hand to open, a function that is often lost in stroke survivors. The patient controls the stimulation to their weak hand through a glove with sensors worn on their opposite, unaffected hand. Opening their unaffected hand delivers a proportional intensity of electrical stimulation that opens their weak hand, and enables them to practice using their hand in therapy. Researchers will enroll 129 patients who are 6 to 24 months post stroke who have upper extremity hemiparesis and limited hand movement.
The effectiveness of CCFES will be compared with two other treatments — cyclic neuromuscular electrical stimulation (CNMES), which has pre-set duration and intensity of stimulation and operates independent of patient control, and traditional task-based training without stimulation. Participants will be randomly assigned to one of the three treatment options for 12 weeks. The research teams will administer the treatments and conduct blinded outcome assessments. The durability of functional improvements will be evaluated at 6-month follow-up. Study sites include the MetroHealth System (Jayme Knutson, PhD), the Cleveland Clinic (Ela Plow, PT, PhD), Emory University (A.M. Barrett, MD), and Johns Hopkins University (Preeti Raghavan, MD).
“Because hand function is integral to so many activities of daily living, advances that improve function can have significant effect on the lives of stroke survivors,” said Dr. Boukrina. “This study will help determine the optimal method for restoring hand function. We anticipate that putting the patients in control of stimulating their weak hand with CCFES may activate neuroplastic changes that lead to greater and longer lasting functional gains.”
Neuroplasticity is the brain’s ability to restructure its neural connections at any given moment. It allows nerve cells to adjust their formation in response to novelty and challenged.
This video talks about the key principles of neuroplasticity and the 6 simple ways to increase neuroplasticity.
Read the article for the studies: http://siimland.com/how-to-increase-n…
Brain Training Playlist: https://www.youtube.com/watch?v=r0168…
Table of Contents What is Neuroplasticity: 00:14 Neuroplasticity Explained: 00:49 Benefits of Neuroplasticity: 01:54 The Key to Increase Neuroplasticity: 02:22 Strategies to Increase Neuroplasticity: 02:32 #1 Whole-Brain Holistic Thinking: 02:40 #2 Practice FLOW: 04:08 #3 Expose Yourself to Novelty: 05:25 #4 Meditation: 05:45 #5 Exercise: 06:20 #6 Intermittent Fasting: 06:43 Nutrients for Neuroplasticity: 07:04 Concluding Remarks: 08:12 Become Limitless: 08:52
What if your brain at 77 were as plastic as it was at 7? What if you could learn Mandarin with the ease of a toddler or play Rachmaninoff without breaking a sweat? A growing understanding of neuroplasticity suggests these fantasies could one day become reality. Neuroplasticity may also be the key to solving diseases like Alzheimer’s, depression, and autism. In this program, leading neuroscientists discuss their most recent findings and both the tantalizing possibilities and pitfalls for our future cognitive selves.
PARTICIPANTS: Alvaro Pascual-Leone, Nim Tottenham, Carla Shatz
MODERATOR: Guy McKhann
MORE INFO ABOUT THE PROGRAM AND PARTICIPANTS: https://www.worldsciencefestival.com/…
This program is part of the BIG IDEAS SERIES, made possible with support from the JOHN TEMPLETON FOUNDATION.
FOLLOW us on Twitter: https://twitter.com/WorldSciFest
TOPICS: – Opening film 00:07 – What is neuroplasticity? 03:53 – Participant introductions 04:21 – Structure of the brain 05:21 – Is the brain fundamentally unwired at the start? 07:02 – Why does the process of human brain development seem inefficient? 08:30 – Balancing stability and plasticity 10:43 – Critical periods of brain development 13:01 – Extended human childhood development compared to other animals 14:54 – Stability and. plasticity in the visual system 17:37 – Reopening the visual system 25:13 – Pros and cons of brain plasticity vs. stability 27:28 – Plasticity in the autistic brain 29:55 – What is Transcranial magnetic stimulation (TMS) 31:25 – Phases of emotional development 33:10 – Schizophrenia and plasticity 37:40 – Recovery from brain injury 40:24 – Modern rehabilitation techniques 47:21 – Holy grail of Neuroscience 50:12 – Enhancing memory performance as we age 53:37 – Regulating emotions 57:19
PROGRAM CREDITS: – Produced by Nils Kongshaug – Associate Produced by Christine Driscoll – Opening film written / produced by Vin Liota – Music provided by APM – Additional images and footage provided by: Getty Images, Shutterstock, Videoblocks
This program was recorded live at the 2018 World Science Festival and has been edited and condensed for YouTube.