Category: science

Treating Neurodegenerative Diseases with BCI

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If you’d asked me a short few weeks ago whether I thought neurogenesis in humans continued throughout their lifetime (as so often the topic comes up in the most casual of conversations), I’d have, with 100 percent confidence, said “yes.”

That’s right friends, strangers, guy in that chair over there… Today, we’re talking about one of my favorite subjects! Brains.

Recently, I found out that adult hippocampal neurogenesis (AHN) in humans might not, in fact, be a real thing.1 This is shocking! So then I wondered: Could we potentially use brain computer interface (BCI) as an artificial neurogenesis therapy for individuals suffering the effects of neurodegenerative diseases—such as Alzheimer’s—psychiatric disorders, and age-related cognitive dysfunctions?

But what is AHN, why is it important, and how does BCI fit in?

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The Importance of Adult Hippocampal Neurogenesis in Humans

Neurogenesis is basically what it sounds like—the birth of new neurons. It starts in the womb and may continue until about 13 years of age2 or until death. Adult neurogenesis (what we’re focused on) has been corroborated in mice, songbirds, and non-human primates. While there is considerable evidence of adult neurogenesis in humans, this is where things get dicey. The methodology currently used isn’t ideal. For example:

  • Carbon dating cells can be mislabel wherein dying cells are labeled as dividing cells, giving a false positive for neurogenesis, and protein markers can mislabel cell types (glia for neuron)1
  • Studies don’t particularly account for cellular degradation in post-mortem samples, nor for cognitive health of the doner before death, which can lead to erroneous findings1

The extreme variation in findings in similar methodologies used is another head scratcher. This is why proving AHN in humans is so difficult. Finding a reliable way to measure potential AHN in real-time in living subjects via imaging seems to be the way to go but has thus far not been available.

Anyway, based on both animal and (contentious) human studies, adult neurogenesis is thought to take place in two areas of the brain: the subventricular zone, and the dentate gyrus of the hippocampus. AHN is thought to be responsible for things like learning, memory retention, and spatial memory (which is the ability to navigate your environment and remember how to get to the grocery store).

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  • Happy little neurons firing when you turn left into the… no left. LEFT!

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Now… neurodegenerative diseases, psychiatric disorders, and age-related cognitive dysfunctions all have something in common: in both human studies, and in studies1 using animal models in which it’s been shown AHN is present, those with the abovementioned ailments all showed decreased neurogenesis. Based on this, we could hypothesize that human AHN therapies could provide symptom alleviation (or potential condition improvement) in such conditions as depression, Alzheimer’s, and age-related memory loss. According to ADULT NEUROGENESIS IN HUMANS: A Review of Basic Concepts, History, Current Research, and Clinical Implications:

  • “Consecutive animal model studies have indicated the potential of neurogenesis-based targets in drug development for depression due to the implied role that neurogenesis plays in the mechanisms of actions of many antidepressant drugs.
  • “A neurogenic drug […] was found to reduce severity of the symptoms in patients with major depressive disorder (MDD) compared to placebo, but the robustness of the results was limited by small sample size and skewed test-control distribution of the study…
  • “Metformin—[an FDA-approved] drug for the treatment of Type 2 diabetes—was reported to induce neurogenesis in a rat model and in human neuronal cell cultures, but no clinical trials have been conducted to support these results. Prolonged treatment with this drug in humans with diabetes, however, was found to have an antidepressant effect and appeared to protect patients from cognitive decline.”1

If AHN in humans eventually is proven, endogenous cell replacement or neuronal progenitor/stem cell transplant therapies could be a viable source of treatment.6 However, regardless of the existence of AHN in humans, prevention of cognitive decline is a noteworthy effort. But what about alternate treatment solutions in the absence of AHN in humans?

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  • Oh. Uh, no, Dave. Electrolytes is not the answer.

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BCI as a Treatment for Cognitive Disorders

BCI has been growing in popularity for some time and has been applied to both clinical and practical use for decades: cochlear implants, the Utah array, deep brain stimulation. But it seems that a lot of BCI solutions, and even studies, tend toward mobility vs cognition. For instance, BCI studies in stroke patients primarily focus on mobile rehabilitation; however, one study3 found a link between motor, cognitive, and emotion functions that revealed promising evidence of the benefits of BCI in treating post-stroke cognitive impairments (PSCI). I want to point something important out here: BCI mobility rehabilitation has yielded very good results for patients; however, patients with a certain percent of PSCI can’t participate in this type of rehabilitation. Your brain must be able to send, receive, and decode signals for BCI to work, which is why cognitive rehabilitation is so important.

Part of what led to studying BCI in PSCI is that since the “effects of BCI-based neurofeedback training have been seen to improve certain cognitive functions in neurodevelopmental and neurodegenerative conditions such as [ADHD] and mild cognitive impairment (MCI) in elderly subjects, respectively, it is therefore also likely to generalise to other dysfunctions, including PSCI.” While more research is needed in this area, the foundation has undeniably been set. BCI could potentially act as a treatment in cognitive and some psychological disorders.

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A Look at Current BCI Projects

There are multiple companies in the BCI industry, though most seem focused on entertainment and mobility. For example, NextMind’s Dev Kit is a very cool product available for consumer purchase that allows individuals to interact with the digital world in a hands-free manner. I recommend watching the launch talk—very cool. While the Dev Kit is geared mostly toward entertainment—video games, interacting with the TV, and such—being able to move and communicate through digital space offers a lot of benefits for mobility- and speech-impaired individuals.

Kernel’s Flux, however, is a different beast. According to their website, “Kernel Flux is a turnkey magnetoencephalography (MEG) platform based on optically-pumped magnetometers (OPMs), which provides real-time access to the intricate brain activity underlying functions such as arousal, emotion, attention, memory, and learning.” It’s a tool that’s been used in studies to help determine areas of the brain affected by such conditions as Parkinson’s4 and mild MCI5 related to dementia of Alzheimer’s type (DAT). The conclusion of the latter study found that “MEG functional connectivity may be an ideal candidate biomarker for early, presymptomatic detection of the neuropathology of DAT, and for identifying MCI-patients at high risk of having DAT.”

If Kernel is providing the means of early detection in neurodegenerative diseases and conditions linked with cognitive decline, is it possible that same tool can be used to detect AHN in humans? And more importantly, if AHN isn’t really real, who is going to step up to the plate with BCI focused on the treatment of neurodegenerative diseases? Elon Musk? Heh. Wait…

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  • Surprise!

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Could Neuralink Produce a Synthetic Neurogenesis Therapy?

Neuralinkan elon musk company is working on cutting edge BCI technology. They’ve created an implant that uses tiny threads inserted into the brain to receive neuronal signals. The implant amplifies the signals, then converts them to digital code which is sent via Bluetooth to a mobile app. The threads can also send signals to stimulate neurons and identify some neurons by shape.

While Neuralink’s initial goal is to facilitate digital communication and interaction in paralysis patients, they’re ultimately hoping for potential restoration of motor function in said patients, treatment of cognitive and psychological disorders, restoration of vision, and more. I highly recommend watching the launch of N1 for a look at the science and engineering behind all of it, and I recommend watching the progress update to get a look at the Link and its specs. It. Is. Very cool. But what does it have to do with neurogenesis?

Well, “Progressive degeneration of specific neuronal types and deterioration of local neuronal circuitry are the hallmarks of degenerative neurological diseases, such as [Parkinson’s, Alzheimer’s, Huntington’s, and ALS].”6 Identification of these specific neuronal types is key in any neurogenesis therapy (kinda like gene therapy!), whether transplanting genetically engineered cells into target regions of the brain or using software programed to mimic specific neuronal signals in place of lost or damaged neurons.

Because Neuralink’s device can send, decode, and receive signals and identify neurons, and because we know specific neurons related to specific neurodegenerative diseases (i.e. Huntington’s degrades striatal medium spiny and cortical neurons), I opine that, yes, Neuralink’s device could definitely act as a synthetic type of neurogenesis therapy. There’s obviously an extreme amount of data that would have to be collected though, given that two of the same type of neuron in a person’s brain giving the same directive (or “action potential”) can do so in two different ways, and this varies from person to person. Neuralink’s data processing ability is pretty remarkable and quite robust, and since it’s already individually tuned (so to speak), it’s essentially made to be a target therapy.

Furthermore, with the ability to process so much data simultaneously, the Link could additionally help identify neurons or neural circuitry affected by neurological disorders or damage to provide effective treatment therapy. It could also help with schizophrenia, wherein erroneous information processing due to abnormal dendritic branching and synaptic connections could be corrected or overwritten.1

There’s an exceptional amount of potential with this device and, while it might sound like science fiction, it seems more to me like it’ll be reality within the next 10-20 years given where technology is at now and the rate of progress.

Whew! It took a long time, but we got there. Now, enjoy a Macaque playing Pong with his brain.

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Video (and MindPong) courtesy of Neuralink

Sources

1 ADULT NEUROGENESIS IN HUMANS: A Review of Basic Concepts, History, Current Research, and Clinical Implications

2 The controversy of adult hippocampal neurogenesis in humans: suggesting a resolution and way forward

3 BCI for stroke rehabilitation: motor and beyond

4 Hypersynchrony despite pathologically reduced beta oscillations in patients with Parkinson’s disease: a pharmaco-magnetoencephalography study

5 A multicenter study of the early detection of synaptic dysfunction in Mild Cognitive Impairment using Magnetoencephalography-derived functional connectivity

6 Neurogenesis as a potential therapeutic strategy for neurodegenerative diseases

The Doctor Is In

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Hallo there, sweethearts. If you feel like I may have ghosted you for a bit, I place the blame solely on Dave. He’s getting out of hand. You know how it goes. But I’m back now, and I have a special guest. No, Dave, it isn’t you. I swear. Right! Before we dive in—I don’t want you to get any ideas, I know how you are—here’s a friendly disclaimer:

The below represents the opinions of psychologist Jerry Vanzant Walker, III, Ph.D., and not the opinions or beliefs of the United States Air Force or the entire field of professional psychology.

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As you might have guessed by now, the special guest is Dr. Jerry Walker! You might remember months ago when I released a two-part series on mood and anxiety disorders (part I—part II). Well, this is a bit of a follow-up to that. We’ve focused on the science and on the individuals suffering these types of disorders, so now we’re getting another POV.

Now, if you’ve dealt with any chronic or recurring disease/disorder, I’d be willing to bet that going through the gauntlet of finding a doctor has been a fucking nightmare. That’s just the way it is, sadly. Trying to find medical help—whether mental or physical—can be extremely frustrating. There’s a disconnect somewhere. Whether we like doctors or not, we subconsciously place them on a pedestal. We expect them to know everything about anything that could be wrong with us because, I mean, doctor. You know? Well, surprise! That’s not how it works. Something we need to remember when seeking medical help is that medical professionals are people too. Calm your tits, Dave, I know it’s a revelation.

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Meet the Psychologist

Dr. Walker is a licensed psychologist who’s been working (both active duty and as a contractor) for the USAF for the past six years. He earned his BA in Psychology and BS in Communication Studies from the University of Texas—where he was also a male cheerleader—and earned his Ph.D. in Counseling Psychology & Human Systems from Florida State University. Dr. Walker always had a desire to serve the military. He started talking to recruiters while in high school, but his parents were adamant that he go to college first. The study of psychology always fascinated him, but in undergrad it became his passion. In grad school, his program’s Director of Clinical Training (a former Navy psychologist) asked if Dr. Walker had ever considered working for the VA or military.

After entering the Air Force for his psychology residency in San Antonio, Dr. Walker spent the remainder of his career at Langley Air Force Base in southeast Virginia. He works as an embedded psychologist and behavioral/human factors consultant for a large intelligence organization on the Langley Air Force Base. As if that weren’t enough, he also has a local part-time private practice. The work ethic is strong with this one.

Throughout his military career, Dr. Walker has run an outpatient substance abuse program, a 25-person multidisciplinary outpatient mental health clinic, a suicide prevention program for 11,000 personnel at a military installation, and a disaster mental health team which responded to eight crises. He has also served as the sole psychologist for 9,000+ American, British, Canadian, and Australian military personnel in a deployed location. Dr. Walker’s graduate research and personal proclivity toward resilience and performance enhancement—vs treatment or remediation of deficits—led him to pursue opportunities within the military to work with special operations forces and other communities which might benefit from having an in-house psychological consultant.

When he isn’t working, Dr. Walker spends time with his wife and son. He’s a bit of an outdoorsy guy who enjoys kickboxing, playing racquetball and guitar, and reading fantasy. I mean, he’s legit a real person. Not a cyborg or robot or Pleadian. Damn Pleadians.

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Diagnosis from a new POV

I’ve heard a good deal of horror stories when it comes to getting a diagnosis and finding the right treatment. I’d make a joke about one of the side effects of trying to get a correct diagnosis being a sharp pain in the ass, but I’m realizing it’s becoming my own personal cliché. Which you’d know if you read Rise and Run. So never mind. Joke aborted, shameless plug ended. In any case, I wanted to provide a new POV on the diagnosis process so that we can get a better understanding of, you know, the whole process.

According to Dr. Walker, diagnostics is a continual process that involves listening to what the patient says—or doesn’t say—and knowing the right questions to ask and how to ask them. “Most mental health professionals use the Diagnostic and Statistical Manual, 5th Edition (DSM-5) as a guide when making a diagnosis,” says Dr. Walker. “Mental health disorders are described generally in terms of clusters of symptoms, so in order for a patient to meet diagnostic criteria, they generally have to endorse a sufficient number of symptoms from various clusters or categories.”

Dr. Walker usually utilizes the first session to try to get a general sense of what the patient is experiencing and the timeline/progression of symptoms. “It may be several sessions before we are able to trace [an individual’s] presenting concerns to their etiology,” says Dr. Walker. When this happens, he will sometimes provide a general (e.g. Unspecified Anxiety Disorder) or tentative diagnosis until there is enough information to either rule in or rule out a diagnosis with more certainty. “Sometimes a patient won’t reveal certain symptoms or experiences they’ve had or are having until much later on in treatment, because they didn’t believe them to be relevant to their presenting concern,” Dr. Walker explains. “Additionally, we have to determine the extent and severity of functional impact of these symptoms, as this is a core component of mental health diagnoses.”

Dr. Walker notes that empathic listening is critical to both fostering a collaborative, working relationship with a patient and determining accurate diagnoses. “It also helps to have general working knowledge of the DSM-5, though I do keep a pocket reference book nearby in case I need to refer to the diagnostic criteria for some of the rarer disorders.”

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    You can see the empathy, right?

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Trick or Treatment

So, we’ve gone through the diagnosis process and now we get to the fun part. Treatment! Or, rather, a whole host of attempted treatments that are less than stellar, followed by a winner. At least, that’s generally the patient’s experience. I asked Dr. Walker about the path to treatment and whether the original diagnosis could change depending on what worked and what didn’t. “Contemporary psychological practice emphasizes the use of evidence-based practices (i.e. psychological treatment procedures that are widely supported by a series of sound research studies) for the treatment of specific mental health conditions,” Dr. Walker says. “Depending on the complexity, acuity, coping resources, insight, etc. of the patient and their mental health condition(s), treatment can vary widely in terms of scope and longevity.  I’ve helped folks ameliorate chronic PTSD in as little as four one-hour sessions. I’ve also worked with an individual with childhood-related PTSD and Borderline Personality Disorder on a weekly basis for nearly two years (with relatively minor ultimate progress).” There’s also an aspect of patient commitment and patient-therapist relationship impacting the efficacy of treatment: “The stronger these are, generally the better the outcome.”

I want you to pay close attention to this next bit. There’s an important message there. “Psychologists do not prescribe medication [usually] but they do advocate for their patients and refer them to prescribing mental health providers when appropriate,” Dr. Walker says. Advocate. That’s fantastic. It’s great if you can find a healthcare pro who will advocate for you, but I want to stress that it is even more important for you to advocate for yourself. The more proactive you are when dealing with health problems and the more you advocate for yourself, the more likely you’ll be able to find a healthcare pro or team that will be willing to advocate for you. What’s that, Dave? Oh, yes. Got distracted. Back to the path … of treatment! “Typically, a general class of medication will be selected for treatment of specific mental health conditions. There does seem to be some evidence that specific drugs within a class are more indicated for a specific condition than others,” Dr. Walker says. “They also may have different effects/side effects (e.g., Zoloft, an SSRI, has been deemed safe for use to treat depression during pregnancy, though Prozac, also an SSRI, is not).”

And, as it turns out, the original diagnoses can change based on medication responses/non-response. “There are some cases I’ve seen where a prescriber gives a medication that reveals the diagnosis was entirely different. An SSRI prescribed for depression set off a manic episode, wherein it was discovered the patient did not have unilateral depression but actually a bipolar disorder.”

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    Pictured: What happens when you don’t advocate for yourself.

Mental Health and Violence

One mental health conversation that pops up periodically (mostly sensationalized in the media) is mental health in relation to extreme acts of violence—after mass shootings or spree killings, for instance. “Believe it or not, acts of violence are rarely related to mental health disorders such as depression, PTSD, or schizophrenia as the popular media might have you believe,” says Dr. Walker. “In actuality, substance abuse has a far higher contribution to self-harm, domestic violence, child abuse, and sexual assault.” I can’t say that’s surprising. The way the media presents most mental health discussions is a detriment to both the understanding and perception of mental health issues. Come, plebes, let us take a journey in the Way Way Back machine because I want to reference a particular mass shooting. If we look at the case of Charles Whitman, he obviously knew something was wrong. He sought help. It was only after his death that an autopsy (requested in his suicide note) revealed a tumor that “conceivably could have contributed to his inability to control his emotions and actions,” according to the Connally Commission. So, I guess my question is: At what point during the diagnosis/treatment phase is it determined that a patient’s symptoms are from, say, chemical imbalance issues vs something like a tumor or brain injury? Well good news, kids, because that’s a question Dr. Walker and his ilk are trained to consider.

“In most of the diagnostic criteria in the DSM-5, there is a line that asks whether the presenting symptoms could be better explained by a medical condition or the effects of a medication,” explains Dr. Walker. “This requires the psychologist to have a basic working knowledge of neuroanatomy, psychopharmacology, and neuropsychology, which allows us to ask appropriate questions to rule out the possible influence of these variables on the [individual’s] presenting condition.” If the psychologist deems it appropriate, they will refer the individual to another provider for additional assessment/testing to clarify the root cause of the presenting symptoms. “This has happened several times in my career. I once referred a patient to his primary care physician to request an MRI based on the patient’s reported onset of severe headaches and display of pseudobulbar affect—random, uncontrollable laughing and crying. A patient with a mild traumatic brain injury from an automobile accident six years prior developed OCD. One time I had a patient present with hypomanic symptoms (super happy, talkative, goal-directed, restless, etc.) who, it turned out, was abusing Adderall he got from his roommate.” Dr. Walker doesn’t have admitting privileges or the ability to refer patients for certain medical tests, so in cases like those mentioned above, he consults with other medical providers and encourages them to investigate further.

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    ‘Member that scene from Infinity War? You’re welcome.

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Things, they are A-Changin’

Over the past few years, more people have joined the campaign to be open about mental health. “I get the feeling that there are a lot of misconceptions about mental health disorders, though I’ve seen mental health stigma gradually decrease in the general population over the last decade,” Dr. Walker says. “Mental health disorders are, by definition, abnormal. This has a negative connotation, but in truth all this means is that mental health disorders are not the predominant function of our brains or behavior.  As with any minority condition or trait, this makes understanding the experiences of someone with a mental health condition difficult for the majority who do not have this personal experience or exposure.”

As we talk about mental health issues more frequently and in a more open-minded and educated manner, we gradually begin to lessen the stigma. “The millennial generation seems to be more prone to talking about mental health issues and advocating for disenfranchised/minority members, including those who suffer from relatively rare mental health conditions like OCD, schizophrenia, and Bipolar Disorder,” says Dr. Walker.

If you or someone you know is struggling with any type of mental health issues, reach out, talk about it, and seek help. You are not alone.

Mood and Anxiety Disorders: Part Two (the People)

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Hallo, hallo, and happy Monday. Or just normal Monday. Dave says, “Melancholy Monday,” but we don’t really want to entertain anything Dave says. He’ll start to think he’s people. Welcome to part two of Mood and Anxiety Disorders. We’re past the science dump and onto the human side of these disorders. Three volunteers agreed to be interviewed. The questions for each interviewee were essentially the same in order to get a scope of how differently these disorders affect individuals.

From the top, I want to give a huge thank you to the participants—whose names I will be changing for privacy purposes.

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Internal Struggles

The first task I asked of my participants was to try to describe what their depressive and anxiety episodes felt like and whether they differed from day to day. The participants included one male (based in Alabama), and two females (one based in California, and one in Florida). So, going forward, the participants will be called Alabama, California, and Florida. It’s nice when I don’t have to be creative and make up actual names.

Both Alabama and Florida suffer from depression and anxiety. If you remember from the previous post, anxiety and depression tend to show up together—first one, then the other. The symptoms of these disorders also overlap quite a bit. While California suffers from anxiety, her chances of battling depression in the next few years are statistically higher than average.

So, what do depression and anxiety feel like, day to day, for our participants?

Alabama: The depression feels like you’re all alone, no one cares, and you’d be better off not being here. The anxiety makes me feel like I can’t breathe, like I’m going to cave in on myself. I don’t want to be around anyone. It’s different from day to day. Some days I don’t want to leave the house and others I’m just fine and seem normal to everyone, but inside I’m screaming.

Florida: My anxiety feels like someone is sucking the life out of me. Having anxiety and anxiety attacks are very scary. Recently I had three very bad attacks where I thought I was having a heart attack and needed to go to the hospital. I ate tums, drank cold water, laid down, and focused on my breathing. It lasted roughly 15 minutes, then the next one came on and the same thing happened. I had to take my prescribed medication. I eventually fell asleep and slept for several hours. I was okay after that.

My depression is a feeling of just being in a funk and not wanting to do anything or go anywhere. After my dad passed in December 2017, I became really depressed and was diagnosed with severe depression. If I was talking to someone, I would just burst into tears for no reason. I would sleep a lot and didn’t want to take a shower—it didn’t even cross my mind until my husband asked me if I took one that day. The depression and anxiety differ from day to day. Some days/weeks I do not leave my house, I don’t talk to anyone (I used to be a social butterfly and talk to a lot of people, now I don’t). I am withdrawn from life. I don’t sleep well and can fall asleep anywhere from 11 pm to 3 am. At night my mind races and I can’t get it to slow down (even with meds) enough to relax and fall asleep.

California: Anxiety has different types of feelings or levels. Some days it’s no big deal. When I’m dealing with a lot of stress at work, with the kids, etc., it’s harder to sleep. I find my mind can’t stop thinking about whatever the problem is. Sometimes, even if nothing is going wrong, I have anxiety about what could potentially go wrong.

Insomnia and losing the will to do anything are common symptoms of depression and anxiety. These two symptoms feed a cycle that exacerbates depressive episodes especially. You can see this in cases of insomniacs suffering depressive episodes, though they might not be clinically depressed. In the most basic of terms: Lack of sleep can fuck you up. The lack of will to do the things you normally love is crippling. At a certain point, it turns into a lack of will to do anything and the less you do, the worse the depressive episode can become.

Florida: Depression is every day, really. It is just learning to focus on you and say, “Today is going to be a good day,” and accomplish one task. Just doing one task a day helps me a lot and I end up doing more sometimes.

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External Struggles

Individuals suffering from depression and anxiety aren’t just battling internally. Getting medical help, getting understanding, the pressure of trying to hide the illness is sometimes brutal. I asked our participants when they first realized something was wrong, when they sought help, and what frustrations they encountered while seeking treatment.

Alabama: I was about 12 [when I realized something was wrong]. I was 15 when I started receiving help. Then I stopped, thinking I’d be fine. It wasn’t until ’09 that I received the proper help I really needed. It was a slow, tedious process to find out what would work best for me [in terms of medication]. The first med was Lexapro. It is evil. I became meaner and angrier and gained a shit-ton of weight on it. I was then put on Wellbutrin, and it has been the best thing for me.

California: I want to say in my early 20s I noticed an issue with [anxiety]. Shortly after having kids. I still haven’t sought professional help. I’ve just realized in the past year that I need to do so. I plan to next week. Since I haven’t been “clinically diagnosed,” I’ve self-medicated for years without even knowing. I always drink before bed so that my mind doesn’t keep me awake. I’ve smoked pot before, but all it does is make me paranoid, which makes the anxiety worse.

Florida: I initially had my first bout with depression when I was 16, after my grandmother committed suicide. I lost weight, was tired all the time, slept a lot, cried a lot. We were out of town for a week and all I did was cry and yell to “go home.” The next week I didn’t go to school because I was physically sick. The next time it happened I was in my early 20s and I just felt low and disconnected. I went back to the doctor right away and went back on meds. I have been on and off [medication] throughout my life. This stint has been the longest, since I had my back surgery in July 2014. I really don’t know what happened, but I just don’t feel like the same person after the surgery.

The frustrations of being diagnosed are always being asked, “Do you want to end your life? Do you want to hurt yourself or other(s)?” In my opinion, I wouldn’t be seeking help if I was suicidal. I have already been through it, and I know the devastation it causes for a family/others left behind. The thought has never crossed my mind—I never wanted my parents to have to endure the hurt of losing a child.

Throughout the process of getting diagnosed and finding the right medication, many individuals must fight certain perceptions of depression and anxiety. This added external pressure sometimes keeps sufferers from seeking help in the first place. Sometimes that turns out okay … And other times, not so much. Suicide is often associated with depression and there are plenty of clinical studies to back that up, but it’s different for every individual. For some individuals, suicide is never a conscious thought—it’s a snap decision (and I hesitate to really even call it a decision). For other individuals, it’s just not an option. And, for some individuals, it’s a plague of a thought. Regardless, it’s not comfortable when you seek help and the first question is, “Are you suicidal?” It is a question that needs to be asked, but it’s also a stigma associated with depression.

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Clearing up Misconceptions

Friends and family can be some of the biggest tools in an individual’s arsenal while going through depressive or anxious episodes. Tools … in the toolbox. Weapons in the arsenal. Mixing metaphors again. The point is, it’s very helpful when the people you surround yourself with understand what depression is, what anxiety is, and are able to be supportive. I asked our participants how their friends and families treat them and what the biggest hurdle is when dealing with these disorders

Alabama: My family treated me like I was angry all the time. Well, I was. Friends are more understanding—they know why and what has conspired in my life to cause [the depression] to be worse as I’ve gotten older. I have a few friends that can tell when a really bad episode will take place. My biggest hurdle dealing with these [disorders] are people not understanding why I feel the way I do. It’s like, “You can get over it and be fine.” Okay, that’s not the case. People call you crazy or a nutcase—which may be true, but they don’t know what causes it.

Florida: My mom suffers from both depression and anxiety also, my sister has been diagnosed with depression since my dad became ill, my dad was on depression and anxiety meds, my grandfather is on depression meds since my dad has passed. It is hereditary on both sides of my family, unfortunately. My husband has suffered from both also, so he is understanding. [My biggest hurdle is] trying to overcome it, trying to have a “normal” life again. I don’t like taking pills and having to keep track of when I need more and of doctor appointments. I just want things to be okay again. I hate being like this. It makes my brain run slower. I can’t think of the answers to questions as quickly, especially when someone asks what I want to do—I don’t really want to do anything. I isolate myself, so I don’t have to be forced into a situation where I have to respond because it’s exhausting. Also eating maybe 1.5 meals a day, having no appetite. Trying to smile or laugh daily. I can’t remember the last time I laughed, seriously. My depression has gotten a lot worse since I lost my dad, too.

California: [Friends and family] treat me normal, I guess. I talk to my mom about it more than anyone, and she sympathizes more than anyone. I think she has the same issue. [My biggest hurdle] is trying not to think something is wrong. Every time things are going right, I get scared because it’s too good.

Well, it’s about time to wrap this up, folks. The final question I asked our participants is what they want people to understand about depression and anxiety. I think it’s a fitting place to leave off with this question since it offers a neatly-packaged take-away to the series. You’re welcome.

Alabama: I want people to understand that we do suffer from an illness and have no control over it except with medication. This isn’t something that can be turned on and off like a light switch. Those who have loved ones who do suffer, try to be understanding—we don’t mean to be harsh or reclusive or angry. It’s the chemical imbalance we were born with, or perhaps a traumatic experience. Whatever the case, educate yourselves on our behalf so you’ll get a better understanding of why we act the way we do.

Florida: It is a real illness; it is not fake. Anyone who suffers from depression and/or anxiety didn’t ask for either one of these illnesses. They can be debilitating for some people and life-consuming. I would like them to answer these questions:

  1. Do you enjoy getting up and going to a job every day and socializing with people?
  2. Do you like making money? Could you survive on $500-1,200 a month?
  3. Do you like going to the doctor and being reminded to get medications and when to take them?
  4. Do you enjoy going anywhere and not having a breakdown? Being able to breathe and not gasping for air, or not crying at the drop of a hat?
  5. Do you like to be reminded to shower daily, to accomplish one task a day?

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    So… It’s nap-time, now, right?

Mood and Anxiety Disorders: Part One (the Science)

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Hallo, darlings. I feel like we had so much fun in our previous discussion on depression that we should do it again! My last post came from a personal place and was definitely one-sided. Well, I’ve decided we need to split the difference between the science behind depression and speaking with sufferers. And not just depression, but anxiety disorders as well. Mood and anxiety disorders have numerous overlapping symptoms and often having one will lead to eventually suffering from the other.

I mentioned last time that depression isn’t an emotion—it’s a state being. So now, I’ll back that up with the—drumroll, please, Dave—science around depression and anxiety. As with any kind of neuroscience, nothing is completely concrete here. Every day we are learning more about the brain. That said, the clinical studies included in this post reflect the most in-depth researched and medically accepted causes for depression and anxiety.

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Serotonergic and Noradrenergic Systems

The prevailing science behind depression and anxiety disorders centers around serotonin and norepinephrine dysfunction. When you first get on an antidepressant, chances are it’s an SSRI (selective serotonin reuptake inhibitor) or SNRI (serotonin and norepinephrine reuptake inhibitor), which is usually prescribed before MAOI (monoamine oxidase inhibitor) or atypical antidepressants. Depending on who you talk to, SSRIs—though having the least side effects—are probably the least viable option long term. In an overview in Depression and Anxiety, Charles B. Nemeroff, M.D., Ph.D., states: “There has been increasing evidence […] that antidepressants that inhibit both norepinephrine and serotonin reuptake (SNRI) are more effective in severe and refractory depression than those that inhibit uptake of a single monoamine neurotransmitter. In addition, patients with major depression treated with dual reuptake inhibitors may achieve remission more frequently than those treated with single monoamine reuptake inhibitors.” Conversely, depressive episodes for patients on SSRIs often hit harder. In the event you think you have depression and are about to look for treatment, be ready for a whirlwind of ups and downs before you get the right meds.

Of course, there’s more to it than just serotonin and norepinephrine dysfunction. In Role of Serotonergic and Noradrenergic Systems in the Pathophysiology of Depression and Anxiety Disorders, Nemeroff and Kerry J. Ressler explain: “There is abundant evidence for abnormalities of the norepinephrine (NE) and serotonin (5HT) neurotransmitter systems in depression and anxiety disorders. […] The underlying causes of these disorders, however, are less likely to be found within the NE and 5HT systems, per se. Rather their dysfunction is likely due to their role in modulating, and being modulated by, other neurobiologic systems that together mediate the symptoms of affective illness.”

It’s important not to think of depression and anxiety as something you can throw pills at and be done with. These illnesses are more complicated than that, and their origins are not singular. Continues Nemeroff and Ressler: “Disrupted cortical regulation may mediate impaired concentration and memory, together with uncontrollable worry. Hypothalamic abnormalities likely contribute to altered appetite, libido, and autonomic symptoms. Thalamic and brainstem dysregulation contributes to altered sleep and arousal states. Finally, abnormal modulation of cortical-hippocampal-amygdala pathways may contribute to chronically hypersensitive stress and fear responses, possibly mediating features of anxiety, anhedonia, aggression, and affective dyscontrol.” When dealing with depression and anxiety, it is important to rule out symptoms that are caused by a secondary problem.

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It’s in Your Genes … And Environment

I’m assuming we all know the nature vs nurture argument, especially pertaining to mental illnesses. And, as with most cases to which this argument can be applied, the likelihood of suffering depression or anxiety are both attributed to nature and nurture. Nemeroff and Elizabeth B. Binder, M.D., Ph.D, explain: “Susceptibility to depressive or anxiety disorders is now well established to be due to the combined effect of genes and the environment, with heritability estimates for these disorders ranging from about 30% to 40%. The CRF system, being highly responsive to the environment, has been posited to serve as a key interface between environmental stressors and the development of depression.”

Research based on Hopelessness Theory (HT) and Beck’s Theory (BT) further backs up this claim. The team behind Cognitive Vulnerability-Stress Theories of Depression: Examining Affective Specificity in the Prediction of Depression Versus Anxiety in Three Prospective Studies posits that: “The cognitive vulnerability-stress component of HT, a depressogenic cognitive style is hypothesized to interact with negative life events to contribute to increases in depressive symptoms. In HT cognitive vulnerability is conceptualized as a tendency to make negative inferences about the cause […] consequences, and meaning for one’s self-concept, of a negative life event. Similarly, BT posits a vulnerability-stress component in which dysfunctional attitudes are hypothesized to interact with negative events to contribute to elevations of depressive symptoms. In BT, cognitive vulnerability is conceptualized as depressive self-schemas containing dysfunctional attitudes, such as one’s worth derived from being perfect or needing approval from others.”

For non-sufferers, it is important to realize that depression and anxiety are not normal emotional responses. They are abnormal and out of the sufferer’s control. Saying something like, “Relax,” or, “You’re overreacting,” to someone who suffers from depression or anxiety only serves to alienate the sufferer more.

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Complex Illnesses

I wanted part one of this series to really show that depression and anxiety are not personality defects, not cries for attention, not someone being overly dramatic or sensitive. Although, sure, there are some of those types of people scattered about. Depression and anxiety stem from the very genetic level of the sufferer. And from there, it’s a cycle. You’re genetically predisposed to negativity and so you find it everywhere, which doubles down on depressive or anxious episodes.

Part two of this post is going to balance out the science with the human aspect. We’ll be getting a peek into the lives and struggles of individuals suffering from depression, anxiety, or both.

Be on the lookout for part two next Monday!

The Subject that’s Making a Killing

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Serial killers! We’re interested! Why? I’ve been meaning to write this post for a little over a week now, but I’m a writer so … procrastination is part of the job. Luckily, I’ve got Dave here to keep me on track. Sometimes. Well, when he feels like being a productive member of society.

So, serial killers—a topic that never goes out of style. In fact, we tend to make celebrities of serial killers. You want proof? Look no further than the numerous podcasts, books, documentaries, and movies that discuss the lives and works of these murderous bastards.

In his 2017 article, Why Americans are so Fascinated with Serial Killers, David Schmid says:

Without wanting to minimize the difference between celebrating fictional and real-life serial killers, the impact of Silence [of the Lambs] demonstrates vividly the American obsession with serial murder, which by the 1990s had developed to a point where the serial killer had become a dominant presence in our popular culture, a figure that inspired not only fear and disgust, but also a mixture of fascination and even a twisted kind of identification.

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Consider the fact that Charlize Theron played Aileen Wuornos, Jeremy Renner played Jeffrey Dahmer, that former teen heartthrob Zac Efron is set to play Ted Bundy. That attractive A-listers are playing such loathsome characters is a Hollywood gimmick to capitalize on people’s interest in serial killers. People tend to like—and are better able to sympathize with—attractive people. On top of that, we’re juxtaposing the character onto the actor, and if we like the actor, that only makes us more receptive to sympathizing with the character—you know, the serial killer.

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    Oh, God, Kermit! Why!

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But, what sparks that initial interest? Why do we all recognize the names John Wayne Gacy, Ted Bundy, and H.H. Holmes, the noms de guerre Son of Sam, Jack the Ripper, and Boston Strangler? Why are these boogeymen so prominent in our culture?

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Media Influence

Society’s interest in serial killers is not recent and, in fact, started well before the term ‘serial killer’ was coined. “When the crimes of H.H. Holmes […] came to light in 1894, it seemed that America had its very own version of Jack the Ripper. The fact that Hearst newspapers paid Holmes $10,000, an extraordinary sum at the time, for his confession testifies to the immense public interest in the case,” says Schmid. The mystery serial killers present forces us to ask our favorite question: Why?

This is a question media platforms were only too happy to answer. In his 2017 article, Our Curious Fascination with Serial Killers, Scott A. Bonn, Ph.D. explains, “Highly stylized and pervasive news media coverage of real-life serial killers and their horrible deeds transforms them into […] celebrity monsters.” Add in the fact that fictional serial killers are now just as pervasive in pop culture as actual serial killers and things start getting, dare I say, catawampus. “Exaggerated depictions of serial killers in the mass media have blurred fact and fiction. As a result, real-life killers such as Jeffrey Dahmer and fictional ones like Hannibal “The Cannibal” Lecter have become interchangeable in the minds of many people.”

This mingling of fact and fiction helps us distance ourselves from feeling threatened, as we can now place this larger-than-life monster in an entertainment context and forget that there’s around a dozen distinctly not-Hannibal-Lecter-type serial killers operating in the US at any given time. Much like going through a haunted house during Halloween, we can watch movies about serial killers and enjoy the thrill of fear, but ultimately that fear is removable, it’s distanced. It’s only entertainment.

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    Are you not entertained?!

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Prevailing Theories

One theory regarding our interest in serial killers is that the topic tickles our survival instinct. That instinct, when it comes to serial killers, revolves around that pesky question again: Why? According to Bonn:

The average person who has been socialized to respect life, and who also possesses the normal range of emotions such as love, shame, pity, and remorse cannot comprehend the workings of a pathological mind that would compel one to abduct, torture, rape, kill, engage in necrophilia, and occasionally even eat another human being. The incomprehensibility of such actions drives society to understand why serial killers do incredibly horrible things to other people who often are complete strangers. As such, serial killers appeal to the most basic and powerful instinct in all of us—that is, survival. The total disregard for life and the suffering of others exhibited by serial killers shocks our sense of humanity and makes us question our safety and security.

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Another theory is that, well, we’re kind of morbid. In Andrew Hankinson’s article, This is Why We are All so Obsessed with Serial Killers, criminologist Elizabeth Yardley explains: “It’s that train wreck, car crash sort of thing, where you don’t want to look but you do anyway. It’s something we call ‘wound culture.’ We’re drawn to the trauma and suffering of other people, and there’s an awful lot of that around serial murder.”

The idea that we want to see something gruesome—as long as it involves someone else—can be repugnant, but the evidence is there to support it. There are myriad videos of beheadings, automobile accidents, extreme sports accidents, and websites like Documenting Reality. Just googling a serial killer will pull up images of crime scenes and victims. Media, survival instinct, and wound culture may play roles in our interest in serial killers, but my own theory is that our interest strikes a little closer to home.

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    Wait, empathy can cause physical pain? No thanks, I’m out.

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There but for a Head Injury go I

It’s estimated that about one percent of the general population suffers from psychopathy and four percent from sociopathy. Sounds small, but that’s more than seven million people and more than 300 million respectively, worldwide. That’s a lot of goddamn … erm … off-kilter. Not all psychopaths and sociopaths are violent and—specifically in the case of sociopaths—violent tendencies have a lot to do with upbringing. I don’t want to dwell on the nature vs nurture aspect—because Jesus H. that would last a while—but many serial killers have the common thread of shitty, sad, abusive, and in some cases downright horrific childhoods (I’m simplifying this to a degree that I will allow heckling). Another common thread? Head wounds.

An abusive childhood and a head injury … Things that could happen to anyone. We tend to see these commonalities and dismiss the neurochemical or neurophysiological aspects of psychopathy and sociopathy. According to Bonn, “The serial killer represents a lurid, complex and compelling presence on the social landscape. There appears to be an innate human tendency to identify or empathize with all things—whether good or bad—including serial killers.” The more similar we are to an individual—whether real or perceived similarities—the easier empathy becomes.

This empathy leads us to question our own capabilities. Professor Alexandra Warwick states: “Being interested in why other people do things is always being interested in what we’re like ourselves. The projection onto others and the consideration of what that is, it’s absolutely about what we’re like. Are we capable of those things?” There’s something about tapping those dark thoughts that’s enticing. Everyone gets angry at one point or another and many people have reached the point of rage. For the most part, we shake it off and move on. But what if we didn’t? What if we couldn’t?

Our interest in serial killers is a mirror of our interest in our own darkness. “Arguably, the serial killer identity is a mirror reflection of society itself,” says Bonn. “As such, there are things the rest of us can learn about ourselves from the serial killer if we look beyond the superficial ‘monster’ image depicted in the mass media.”

Since the question “why?” isn’t likely to be answered anytime soon, society’s interest in serial killers probably won’t be on the wane for quite a while.

This is Your Brain on Ultrasonic Frequencies

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Hallo, you beauties. It’s been a while since I’ve done a post that needed some research, but—just for you—I dusted off Dave’s research boots and put him to work. Today, I’d like to discuss ultrasound! You’ve no doubt heard of ultrasound as it applies to medical imaging—peeping the unborn babes, assessing muscle trauma, generally viewing those soft, delicate inner tissues. Huh … That came off a little weird.

Anyway, I’m not talking about ultrasound as an imaging tool. I’m talking about ultrasound as a treatment. For instance …

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Ultrasonic Frequencies Stimulate Intact Brain Cells

In a 2010 study, scientists investigated “the influence of transcranial pulsed ultrasound on neuronal activity in the intact mouse brain [and in deeper subcortical circuits] used targeted transcranial ultrasound to stimulate neuronal activity and synchronous oscillations in the intact hippocampus.” Oh, kids, isn’t science fun?

This study aims at finding a non-invasive brain stimulation method that does not suffer from the limitations of current methods, which include low spatial resolution, low spatial precision, and genetic manipulation.

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    Not that there’s anything wrong with genetic manipulation.

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Using transcranial pulsed ultrasound on the motor cortex and hippocampus could have several medical applications, specifically regarding Parkinson’s and Alzheimer’s. Speaking of …

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Practical Applications

In 2016, the FDA approved a similar treatment—called focused ultrasound thalamotomy—to treat people suffering from essential tremor (ET). According to the Focused Ultrasound Foundation, focused ultrasound offers the following benefits:

  • It is a non-invasive, single treatment that enables patients to recover rapidly and quickly return to activities of normal life (usually the next day).
  • Compared to radiofrequency ablation or deep brain stimulation (DBS), focused ultrasound offers a reduced risk of infection, of damage to the non-targeted area, and of blood clot formation.
  • Focused ultrasound offers rapid resolution of symptoms.
  • In contrast to lesioning performed with stereotactic radiosurgery, focused ultrasound does not use ionizing radiation, thus avoiding the side effects of exposure to radiation.
  • Because it is non-invasive, focused ultrasound could be an option for medically refractory ET patients (those who do not respond well to medication) who do not want to undergo surgery.

So, focused ultrasound thalamotomy uses MRI to aim ultrasonic waves at the thalamus. According to W. Jamie Tyler (who took part in the 2010 study), “We can focus the ultrasound through the skull to a part of the thalamus about the size of a grain of rice.” Ahem: precision. From there, the ultrasound kills ET-causing neurons in the thalamus, according to Esther Landhuis’s article Ultrasound for the Brain.

Landhuis goes on to explain that scientists are branching out to focus on treating psychiatric disorders with an emerging technology called focused ultrasound neuromodulation. This technology can boost or suppress small groups of neurons to “potentially treat other movement disorders, as well as depression, anxiety and a host of intractable neuropsychiatric disorders.”

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    Note: Not a brain.

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Minimally Invasive is Still Invasive

When discussing surgery in general, the phrase “minimally invasive” is a good thing. Well, you know … It’s not a terrible thing. However, when it’s your brain you’re talking about, minimally invasive is still pretty fucking invasive. DBS, for example, is a minimally invasive form of neuromodulation. While DBS has been around longer, focused ultrasound offers a more precise, non-invasive means of treatment.

The brain is pretty special organ and it’s, you know, important to your being able to function.

Genome Editing Advancements

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I know, I know. It’s been days. But, you can relax now. I’m here. Oh, and Dave, of course. Dave is always here. Today we (but mostly I) are going to discuss the fun, exciting, and controversial topic of genetic manipulation! I’ll hold for applause. Specifically, we’re talking about genome editing. The first quarter of this year (that’s 2017, in case you’re reading this in the future or are a time traveler) has seen exciting news coming from the genetics field, and with the help of CRISPR (that’s clustered regularly interspaced short palindromic repeats) gene editing, advancements are being made pretty swiftly.

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CRISPR-Cas9

So, CRISPR jumped on the scene as a more affordable, more precise, and quicker way to manipulate genes. CRISPR is made up of an enzyme (that’s the Cas9 part, which is often dropped from the acronym) and a bit of guide RNA. I’m going to share with you my favorite description of the CRISPR process, which was written by Sarah Zhang in this article:

Cas9 is an enzyme that snips DNA, and CRISPR is a collection of DNA sequences that tells Cas9 exactly where to snip. All biologists have to do is feed Cas9 the right sequence, called a guide RNA, and boom, you can cut and paste bits of DNA sequence into the genome wherever you want. [… ] Cas9 can recognize a sequence about 20 bases long, so it can be better tailored to a specific gene. All you have to do is design a target sequence using an online tool and order the guide RNA to match. It takes no longer than few days for the guide sequence to arrive by mail.

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    When ethical boundaries aren’t an issue, you’ll love how easy it is to order your significant other a new whatever-it-is-you-don’t-like.

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The benefits of using CRISPR gene editing extend from the agricultural side of things to health and wellness in humans, our pets, and potentially our future children. According to this article in New Science, “David Ishee, a dog breeder from Mississippi, told the US Food and Drug Administration that he planned to use CRISPR gene editing to fix a mutation that makes Dalmatians prone to kidney disease.” Want more? In a Wired article by Amy Maxmen, we can see a bigger run down of the goings on with CRISPR:

Using the three-year-old technique, researchers have already reversed mutations that cause blindness, stopped cancer cells from multiplying, and made cells impervious to the virus that causes AIDS. Agronomists have rendered wheat invulnerable to killer fungi like powdery mildew, hinting at engineered staple crops that can feed a population of 9 billion on an ever-warmer planet. Bioengineers have used CRISPR to alter the DNA of yeast so that it consumes plant matter and excretes ethanol, promising an end to reliance on petrochemicals.

A lot of good could come from the ongoing study and use of CRISPR, but I know the one thing you’re all wondering…

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    No, Dave, the question has nothing to do with douches.

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The Question of Designer Babies

Will this breakthrough lead to the ability to produce designer babies? This is the $64,000 question, right? And, also… Is it ethical? When will it be possible? What are the consequences? Let’s start with the ethics aspect.

Previous studies using CRISPR gene editing in human embryos have been done using only abnormal embryos—as in, embryos that couldn’t actually become children. But, this route was ineffective. The embryos’ genetic abnormalities don’t give an accurate look at what might be achievable in healthy embryos. So, when all else fails, there must be a compromise.

At the Third Affiliated Hospital of Guangzhou Medical University, a team has switched from abnormal embryos to “normal embryos derived from immature eggs donated by people undergoing IVF,” according to Michael Le Page. “Immature eggs like these are usually discarded by IVF clinics, as the success rate is much lower than with mature eggs. However, children have been born from such immature eggs.”

Toeing the ethics line? Maybe. But, as is the case with a deceased organ donor’s organs, if one person isn’t using it, someone else can.

While using CRISPR gene editing could lead to designer baby manufacturing, we’re a long way from that. Which means we’re a ways off from discussing the consequences. For the most part, current embryonic studies are focused on isolating and editing genetic disorders. The aforementioned team at Third Affiliated Hospital, for instance, is focused on the genetic disorders causing favism and betathalassemia, both of which affect the blood.

At the current stage, these types of studies are running into their own problems—primarily mosaicism. Mosaicism is when, during cell division, both repaired and unrepaired DNA is present.

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    Bad timing for a broken egg joke?

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While progress is being made in the genome editing arena, there is still quite a road that needs to be traveled. Fortunately (or unfortunately, depending on your outlook) science in traveling that road on a high-speed rail instead of a horse-drawn carriage.

Mental and Social Woes of Suspicion

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Welcome back! Good to see ya, nice to meet’cha, let’s dive right in! Today’s topic is solely focused on suspicion and how it can affect your social and business life and mental processes. Of course, it’s only reasonable that I explain how this topic popped into my head.

You see, kiddies, I get extremely suspicious when certain people ask me questions. Whether it’s a stranger or an acquaintance, there are just some people I feel should not be asking me things—no matter how innocent the question. Take this conversation, for instance:

I’m in a break room, heating up food in a microwave. (OP=other person)
OP: Heating up your lunch?
Me: Yes.
OP: What are you having?
Me: …Soup
OP: What kind of soup?
Me: Homemade soup.
OP: Well, what’s in it?
Me: ::shrugs:: Vegetables and broth.

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    It was almost as discomforting as this image.

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Yes, I knew what she wanted when asking what kind of soup. And, yes, I knew exactly what was in it. Yes, Dave, seriously. I can put edible things together in a bowl and pour broth over it. Anyway, the problem was this: I didn’t want to answer. Similarly, I don’t want to answer when asked about my prior weekend or my plans for the upcoming weekend. I don’t know why. My only reasoning is: It’s none of this person’s business. The next minute, I’ll turn around and tell the withheld information to a different person. And, I’m not the only one who does this. If some of you have picked this up as unconscious bias, well done. That definitely has an underlying role here.

We are all prone to unconscious bias, and I believe the type of guarded suspicion some of us have when asked questions by certain people is a symptom of this. So, why are some people more prone to suspicion, and why do certain people seem to rub us the wrong way?

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    Shown here: Not the wrong kind of rub.

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Looking at the Science Behind Suspicion

Understanding suspicion through science is a ideal “where” to start with our conundrum. In order to figure out how people assess the credibility of others, scientists at the Virginia Tech Carilion Research Institute (VTC) investigated the parts of the brain that function in suspicion: the amygdala and the parahippocampal gyrus. The amygdala “plays a central role in processing fear and emotional memories and the parahippocampal gyrus […] is associated with declarative memory and the recognition of scenes,” according to an article featured on VTC’s website. The study went like this:

76 pairs of players, each with a buyer and a seller, competed in 60 rounds of a simple bargaining game while having their brains scanned [using an fMRI]. At the beginning of each round, the buyer would learn the value of a hypothetical widget and suggest a price to the seller. The seller would then set the price. If the seller’s price fell below the widget’s given value, the trade would go through, with the seller receiving the selling price and the buyer receiving any difference between the selling price and the actual value. If the seller’s price exceeded the value, though, the trade would not execute, and neither party would receive cash.

The outcome? According to Read Montague, director of the Human Neuroimaging Laboratory and the Computational Psychiatry Unit at VTC, and the leader of the study, “The more uncertain a seller was about a buyer’s credibility […] the more active his or her parahippocampal gyrus became.”

Knowing what parts of the brain are most active during a state of suspicion is the first step in understanding the emotion, as well as where the suspicion is based. Heightened activity in the amygdala would, theoretically, signify fear-based suspicion, while heightened activity in the parahippocampal gyrus would signify suspicion based on mistrust. Montague suggests the parahypocampal gyrus acts “like an inborn lie detector.”

“So, what?” you demand. “How is this actionable information and why should I care?” Good question! It just so happens that…

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    Not caring could make you turn out like Dave.

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Suspicion can Cost You Profit… and Worse

First of all, not everything is about you. So, let’s look at the bigger picture. Like most things, suspicion in moderation can be quite good. There is a line, though. Being overly suspicious—either from fear or mistrust—can have negative consequences on financial success. According to Meghana Bhatt, one of the study’s authors:

People [taking part in the study] with a high baseline suspicion were often interacting with fairly trustworthy buyers, so in ignoring the information those buyers provided, they were giving up potential profits. The ability to recognize credible information in a competitive environment can be just as important as detecting untrustworthy behavior.

Not only can individuals with high baseline suspicion have a harder time achieving financial success, they can have a harder time achieving success in their careers. This can lead to a host of new problems, including an increase in stress and anxiety, as well as depression.

Speaking of the mental aspects, studies in suspicion can have implications for psychiatric disorders. “The fact that increased amygdala activation corresponds with an inability to detect trustworthy behavior may provide insight into the social interactions of people with anxiety disorders, who often have increased activity in this area of the brain,” explains Montague.

In short, studies such as these can help pinpoint sources of certain psychiatric disorders, which can better help scientists nail down proper treatments. But, these types of studies could also help to create a treatment or healthy way in which to promote balance for those with high baseline suspicion. Perhaps a better question is: When my internal lie detector goes off, who should I trust?

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    Here’s an anxious kitten. You’re welcome.

Improving Quality of Life

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I’ve previously written a couple of blog posts on tech advancements aimed at aiding movement inhibited individuals. This is another one of those, focused singularly on Brain-Machine Interface (BMI, also called Brain-Computer Interface, BCI), which we’ve touched on before. The reason I’m putting a good deal of focus on these types of topics—aside from the badassness of it—is because of my own physical issues.

You see kiddies, when I was the tender age of 16, I had a horseback riding accident that left me with a rotated hip. That one injury has since plagued me with low-back movement issues that are painful, sometimes debilitating, and decrease quality of life. On top of that, I have pretty bad knee issues—which also stem from the original rotated hip problem. I’ve had three epidurals, two cortisone shots at the knee joint, and so much physical therapy I count it as my second job. The one thing I want to do, physically, compounds all the wounds.

I just want to run. I love to run. I love the way it makes me feel before, during, and after. But, even jogging ¼ mile kills my knees and stresses my back. So, what must it be like for someone who wants to walk, or even just stand? Life is a lot of things, but movement plays such a significant role in life that it’s something we think about lightly. You know, until we can’t do it anymore.

So, while robotics, neuroscience, and advancements in technology are blow-your-mind-like-a-big-league-hotdog awesome, combining the three to improve quality of life for thousands—millions?—of people is blow-your-mind-in-the-archaic-sense-of-the-word awesome. So, without further ado, let’s dig into the real meat of this blog.

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    Just look at those cute, evil faces.

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Allowing Locked-In ALS Patients to Communicate

I know what ALS is, but I had never previously heard of the “Locked-In” ALS condition. Thanks to my ignorance, you’ll all get a bit of definition time. You’re welcome. ALS patients suffering from the Locked-In condition are considered to be in the severe stage of ALS, wherein they are conscious and have brain function, but are unable to move. At all.

Science is working toward giving such patients as these a way to communicate again. According to the article Locked-In ALS Patients Answer Yes or No Questions with Wearable fNIRS Device, published earlier this month in Neuroscience News:

Using a wearable system developed by SUNY Downstate Medical Center researcher Dr. Randall Barbour, a team of investigators led by Professor Niels Birbaumer at the Wyss Center for Bio and Neuroengineering in Switzerland and University of Tübingen in Germany were able to measure the brain’s hemodynamic response to a series of ‘yes’ or ‘no’ questions, thus allowing these patients to communicate.

While other tech has been used for this goal—EEG, fMRI, etc.—fNIRS (that’s functional near infrared spectroscopic) imaging has proved to be the breakthrough tech needed. But, what does this mean? Well, this is potentially the first step in bettering quality of life for Locked-In ALS patients. Communication, like movement, is a substantial part of life. It’s why we have language areas in the brain, Dave! But, this isn’t the only advance being made with BMI. Next up…

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  • This is your brain on binary code. Any questions?

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BMI Opens Doors to Paralysis Patients

In Bruce Goldman’s article, Brain-Computer Interface Advance Allows Fast, Accurate Typing by People with Paralysis, published by Stanford Medicine, we get another look into BMI advancement. I fully anticipate all the readers here will visit the original article, which means I’m not listing all the scientists involved. Instead, I’m going to refer to them as “The Team.” You’re welcome. Again.

In this study, The Team worked with three paralysis patients, using an intracordical BMI (or in the case of this study, the term BCI is preferred) to send brain signals to a computer. Goldman explains that:

The investigational system used in the study, an intracortical brain-computer interface called the BrainGate Neural Interface System, represents the newest generation of BCIs […] An intracortical BCI uses a tiny silicon chip, just over one-sixth of an inch square, from which protrude 100 electrodes that penetrate the brain to about the thickness of a quarter and tap into the electrical activity of individual nerve cells in the motor cortex.

These are the nerve cells that send the signals the brain would give off during specific movement tasks (the right hand moving and clicking a computer mouse, for instance). The signals are decoded and converted in real time by a special algorithm, which then allows the patients to control a cursor on the screen in front of them to type out words at a higher speed and accuracy than seen in previous methods. According to Chethan Pandarinath, one of the lead authors of the research report, “We’re achieving communication rates that many people with arm and hand paralysis would find useful. That’s a critical step for making devices that could be suitable for real-world use.”

This is not only exciting, it’s groundbreaking for movement inhibited individuals. Going forward, this tech could help with general household tasks we take for granted—opening doors, changing the thermostat, controlling the TV—and who knows what else?—just by using your mind. This gives movement inhibited individuals access to and a modicum of control over their surroundings. That’s seriously impressive.

Krishna Shenoy, an integral part of The Team—and whose lab pioneered the algorithm for the BMI interface—expects that around five years from now, they may be looking at a “self-calibrating, fully-implanted wireless system [that] can be used without caregiver assistance, has no cosmetic impact, and can be used around the clock.”

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    Just think of this computer as Professor X… you know… cause it’s reading your mind!

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Improving on Improvements

Now, we head over to San Diego State University (SDSU) to learn about new electrodes with increased durability that last longer and transmit clearer signals than current electrodes. This news comes to us from the article Big Improvement to Brain-Computer Interface, published by ScienceDaily with source material provided by SDSU. Here’s a rundown of the study:

The Center for Sensorimotor Neural Engineering (CSNE)—a collaboration of San Diego State University with the University of Washington and the Massachusetts Institute of Technology—is working on an implantable brain chip that can record neural electrical signals and transmit them to receivers in the limb, bypassing [spinal cord] damage and restoring movement.

The improvement here is the material out of which the chip is made. Current “state-of-the-art” electrodes are made from thin-film platinum, but researchers with CSNE are utilizing glassy carbon. According to the article, “This material is about 10 times smoother than granular thin-film platinum, meaning it corrodes less easily under electrical stimulation and lasts much longer than platinum or other metal electrodes.” These electrodes are being used both along the surface of and inside the brain for more complete—single neuron and cluster—data.

A doctoral grad student in the lab is even taking things one step further. According to the article:

Mieko Hirabayashi is exploring a slightly different application of this technology. She’s working with rats to find out whether precisely calibrated electrical stimulation can cause new neural growth within the spinal cord. The hope is that this stimulation could encourage new neural cells to grow and replace damaged spinal cord tissue in humans. The new glassy carbon electrodes will allow her to stimulate, read the electrical signals of, and detect the presence of neurotransmitters in the spinal cord better than ever before.

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I used this to represent “single” vs “cluster.” Is it working?

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Every year, new advances in tech are being made. But, seeing tech advancements geared toward improving quality of life for movement inhibited individuals is… well… awesome.

Misconceptions about Night Terrors

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There’s little doubt that illnesses, diseases, disorders, and the like can be scary. Moreover, they can be quite terrifying when little is widely known about them. The parasomnia (sleep disorder) known as Night Terrors (NTs) (sometimes, Sleep Terrors) is one of these misunderstood disorders. I first heard about NTs in a grossly misleading psychology class in college. The class, Motivation and Behavior Psych, was much more closely related to neurobiology or neurochemistry—it’s the class that sparked my deep love of neuroscience.

Right. Back to the topic. NTs are often confused with nightmares. It’s pretty widely known that nightmares suck donkey testicles; they’re vivid, scary, uncomfortable, and usually leave lasting impressions upon waking. In my worst nightmare, I awoke to someone standing over me while I slept. It was so real that, when I actually woke up, I thought the person was there. I couldn’t move, I was scared to open my eyes. It was only when I realized my dogs were calmly sleeping that I knew no one else was in the room.

Vivid? Check. Terrifying? Check! Seared into my memory? Super check. Gargling on the sack of a donkey? You bet! The nightmare, Dave, not me. Seriously. NT? Absolutely not.

So, what’s the difference between NTs and nightmares, and why is it important to know? I’m glad you asked!

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  • ST classification table.png
    Here’s a fancy chart on NT classification.

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Core Differences

Differences between nightmares and NTs range from when during sleep they occur to electroencephalography (EEG) activity. The point here is, the two are fundamentally different. Nightmares, and even nightmare disorder, are “different from NT [and consist of] a lowered motor activity […] the person is not confused on waking up, remembers the nightmares in detail, and the disordered orientation immediately recovers”.² The authors of the article, “Treatment Approach to Sleep Terror: Two Case Reports,” give a robust definition of NT:

NT is classified under parasomnias characterized with sudden attacks of fear associated with the increase in autonomic signs following crying and loud shouting during the first few hours of sleep during the delta stage (associated with the NREM period). Clinically, the person wakes up screaming, scaring, or performing sudden and self-destructive acts (like jumping, running, crashing into something, harming the person beside). The person is non-responsive to the external stimulus during this period […] The person may predominantly experience cognitive impairment signs, such as disordered orientation and memory problems, confusion, and fear on waking up. In addition to these mental symptoms, somatic symptoms associated with the overstimulation of the autonomic system, such as palpitation, sweating, shaking, skin rubor, pupillary response, may appear. While adults generally cannot remember what they experienced the previous night, children can indistinctly remember their fear.²

I think that about sums it up. So, while nightmares generally occur during REM, NTs occur prior to REM, during NREM—or non-rapid eye movement. The result of two independent sleep studies stated that NT episodes “begin exclusively during [NREM] sleep, most frequently during slow-wave sleep (SWS), and should not be considered an acting-out of a dream” and that “consciousness is altered during sleepwalking/sleep terror episodes.”¹ NT is most common in children, with a prevalence of ~3-15 percent, and decreases significantly with age, although, “it seems probable that the notion of sleep terrors is largely unknown to people, therefore different types of nocturnal attacks can be reported as sleep terrors.”¹

Difficulty in obtaining more concrete statistics pertaining to NT is a big indication that NT is a misunderstood parasomnia.

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  • zumbie-1797970_640
    Not that having this chase you around is a good thing.

 

What Triggers NT?

Another great question! Both genetics and environmental stimuli play a role in NT:

It is well known that sleepwalking and night terrors run in families. Based on the study of familial incidence of sleepwalking and sleep terrors proposed that sleepwalking and night terrors share a common genetic predisposition, although the clinical expression of symptoms of these parasomnias may be influenced by environmental factors.”¹

The authors of “Treatment and Approach…” explain that “the risk of occurrence [of NT] among the first-degree relatives is ten folds more compared with those with no family history of NT.”²

Cases of NT have also been reported after stressful and/or significant life events, including divorce—personal or parental—death of a loved one, changing jobs or getting let go, changing schools, etc.

 

Why Does This Matter?

Part of why this matters is because additional research in NT could point to treatments aside from “making bedrooms safe” for NT sufferers or being prescribed benzodiazepine, which can cause rebounds or addiction. There is, of course, another reason it would be good to be knowledgeable about NT: “NT is highly associated with schizoid, borderline and dependent personality disorder, post-traumatic stress disorder, [and] generalized anxiety disorder.”²

Which is not to say NT sufferers have those disorders. In fact, when comparing individuals with NT to individuals who only demonstrate somnambulism (sleepwalking), only a percentage of sleepwalkers had been diagnosed as psychotic:

In contrast to sleepwalkers, [individuals with NT] demonstrate higher levels of anxiety, obsessive-compulsive traits, phobias, and depression. The Minnesota Multiphasic Personality Inventory (MMPI) profile suggests an inhibition of outward expression of aggression. A psychiatric diagnosis was established in 85 percent of patients with current night terrors. Although their psychopathology was more severe than in patients with sleepwalking, none of them was diagnosed as psychotic.”¹

Knowing the difference between NT, other arousal parasomnia, and regular ole nightmares can make a difference to the individual suffering from NT. Because a significant symptom of NT is sleepwalking, and because NT sufferers have increased mobility, they could cause damage to self or others.

 

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¹Szelenberger, Waldemar, Szymon Niemcewicz, and Anna Justyna Dąbrowska.

…. “Sleepwalking and Night Terrors: Psychopathological and Psychophysiological

…. Correlates.” International Review of Psychiatry 17.4 (2005): 263-70.

²Turan, Hatice Sodan, Nermin Gunduz, Aslihan Polat, and Umit Tural. “Treatment

…. …. Approach to Sleep Terror: Two Case Reports.” Noro Psikiyatri Arsivi 52.2 (2015): 204-06.