Sunday, March 6, 2016

Can cognitive behavioral therapy for insomnia also treat fatigue, pain, and mood symptoms in individuals with traumatic brain injury?

Hi All! I haven't updated in quite a while because work as a rehabilitation psychologist has taken up most of my time. However, I was able to get a paper published recently in the journal NeuroRehabilitation. It was based on work done during my postdoc. The aim was to investigate whether cognitive behavioral therapy for insomnia would treat not only insomnia, but fatigue, pain, and mood in individuals with traumatic brain injury. It was a small case study, but I included a lot of rich detail for each case. I plan to continue with this line of research on a much larger scale. Here is the abstract. Let me know if you would like a copy of the paper and I can send it right over.


Individuals with traumatic brain injury (TBI) often develop sleep disorders post-injury. The most common one is insomnia, which can exacerbate other post-injury symptoms, including fatigue, impaired cognition, depression, anxiety, and pain. Cognitive Behavioral Therapy for Insomnia (CBT-I) is a manualized treatment that effectively treats insomnia with secondary effects on cognition, mood, and pain in various populations.


This paper reviews the use of CBT-I for three participants with TBI of different severities.


Pre- and post-treatment assessments of insomnia, fatigue, depression, anxiety, and pain were conducted. Mood was further assessed at follow-up. Minimal clinically important difference (MCID) scores derived from the research literature were used to establish clinically meaningful symptom improvement on self-report questionnaires.


The reduction in insomnia severity scores for all three participants were not large enough to be considered a clinically significant improvement following CBT-I, although trends toward improvement were observed. However, all participants showed clinically significant reductions in anxiety at post-treatment; the effects persisted for 2 participants at follow-up. Reductions in depression symptoms were observed for 2 participants at post-treatment, and treatment effects persisted for 1 participant at follow-up. One participant endorsed clinically significant improvements in fatigue and pain severity.


We conclude that CBT-I may provide secondary benefits for symptoms commonly experienced by individuals with TBI, especially mood disturbances.

Lu W, Krellman JW, & Dijkers MP (2016). Can Cognitive Behavioral Therapy for Insomnia also treat fatigue, pain, and mood symptoms in individuals with traumatic brain injury? - A multiple case report. NeuroRehabilitation, 38 (1), 59-69 PMID: 26889799

Sunday, July 26, 2015

The relationship between self-reported sleep disturbance and polysomnography in traumatic brain injury

Check it out. My work during postdoc that was just published early online in Brain Injury. Feel free to contact me for a PDF copy.

PRIMARY OBJECTIVE: To characterize sleep architecture and self-reported sleep quality, fatigue and daytime sleepiness in individuals with TBI. Possible relationships between sleep architecture and self-reported sleep quality, fatigue and daytime sleepiness were examined.
METHODS: Forty-four community-dwelling adults with TBI completed the Pittsburgh Sleep Quality Index (PSQI), Multidimensional Assessment of Fatigue (MAF) and Epworth Sleepiness Scale (ESS). They underwent two nights of in-laboratory nocturnal polysomnography (NPSG). Pearson product-moment correlation coefficients and hierarchical linear regression was used to analyse the data.
RESULTS: Based on the PSQI cut-off score of ≥ 10, 22 participants were characterized as poor sleepers. Twenty-seven participants met criteria for clinically significant fatigue as measured by the GFI of the MAF. Fourteen participants met criteria for excessive daytime sleepiness as measured by the ESS. Poor sleep quality was associated with poor sleep efficiency, short duration of stage 2 sleep and long duration of rapid eye movement sleep. There was little-to-no association between high levels of fatigue or daytime sleepiness with NPSG sleep parameters.
CONCLUSIONS: A high proportion of the sample endorsed poor sleep quality, fatigue and daytime sleepiness. Those who reported poorer sleep quality evidenced a shorter proportion of time spent in stage 2 sleep. These findings suggest that disruptions in stage 2 sleep might underlie the symptoms of sleep disturbance experienced following TBI.

Lu W, Cantor JB, Aurora RN, Gordon WA, Krellman JW, Nguyen M, Ashman TA, Spielman L, & Ambrose AF (2015). The relationship between self-reported sleep disturbance and polysomnography in individuals with traumatic brain injury. Brain injury, 1-9 PMID: 26204319

Monday, June 8, 2015

Stroke prevention with the Mediterranean diet

Fad diets abound, but none appear to be as positively impactful to health as the Mediterranean diet. Even the likes of Jennifer Garner, Elizbath Hurley, and Catherine Zeta-Jones adhere it, and they are all very attractive. Although it won't help increase attractiveness, it may contribute to preventing strokes.

The diet consists of eating primarily plant-based foods such as fruits, vegetables, whole grains, legumes, and nuts. The health benefits of eating such foods were confirmed in an epidemiological and longitudinal study known as the as the Seven Countries Study, which began in 1956 and was finally published in 1970. Ancel Keys, a biologist and director of the study, publicized the diet in 1975, but it didn't gain recognition until the 1990's.

In a recent review paper by Lakkur and Judd (2015), published in the journal Stroke, the authors looked at the different components of the popular diet and examined which foods were found to be truly effective for preventing strokes. After reviewing the research literature, they saw that consuming fruits, vegetables, fish, olive oil, and white meat were proven to be effective while eating tree nuts/peanuts, legumes, dairy, red/processed meat, and wine were not. The diet studies referenced in the review paper were published between 2011 to 2014, so we can assume that the studies were conducted somewhat recently (although one may be surprised how long of a lapse can take place between study-end and publication).

However, there are a few limitations that Lakkur and Judd point out regarding their write-up. The first limitation is that they could not account for the possibility that subjects who "choose to adhere to healthier dietary patterns may also engage in other health-promoting behaviors such as physical activity and may be more likely to maintain a healthy weight". Secondly, the types of strokes (hemorrhagic or ischemic) were not described in many of these studies. Lastly,  "there was a lack of racial and ethnic diversity in many of the epidemiological studies and many racial and ethnic minorities were not well represented", much like the aforementioned case of my "attractive actors only" reference pool.

Nonetheless, this paper makes a compelling point that eating like the Greeks, Italians, and Spaniards will help stave off having a stroke. What's even better is that you don't have to be gassy or drunk while doing it.


Lakkur S, & Judd SE (2015). Diet and Stroke: Recent Evidence Supporting a Mediterranean-Style Diet and Food in the Primary Prevention of Stroke. Stroke; a journal of cerebral circulation PMID: 25967574

Original image taken from

Wednesday, June 3, 2015

Motion blindness found in some dyslexics

Several years ago, I worked as a clinician at a treatment program for adults with learning disabilities, many of whom were diagnosed with dyslexia; a disorder that negatively impacts a person's ability to read, perceive speech, remember language, and recognize/manipulate language-based sounds. Many of my patients had difficulties advancing in their jobs, struggled to pay the rent or perform daily financial tasks that required reading, and thus relied on others to get by. The countless stories I listened to were heart-breaking, especially when one highly motivated and bright young adult became tearful while relaying to me his strong desire to advance in his career and to make something of himself, but struggled because he couldn't find a way around having to read on the job, no matter what compensatory strategies he used.

Approximately 5 to 17% of the entire population are estimated to have dyslexia. Some famous individuals with dyslexia include Albert Einstein, Whoopi Goldberg, Orlando Bloom, Cher, and Scott F. Fitzgerald. As dyslexia can be inherited, a few of these individuals may have had alterations in a gene known as DCDC2, for which deletion of this gene has been found to be a risk factor for dyslexia. It turns out, they may have also had issues with motion detection. 

Cicchini and colleagues (2015), in a recent study published in The Journal of Neuroscience, found that dyslexic individuals who inherited this particular phenotype were found to have impairments for motion processing at high spatial frequencies compared to dyslexics who had the DCD2 gene. 

The authors recruited 10 young adult subjects for the experimental group (dyslexics without the DCD2 gene) and 11 for the control group (dyslexics with the DCD2 gene). They then had the subjects fixate on the center of a computer screen while reporting whether they saw patterned black and white lines move from left to right or top to bottom. 

Those who lacked the DCD2 gene virtually demonstrated motion blindness. The authors propose that these deficits may be due to anatomical deficits of the lateral geniculate nucleus magnocellular cells (important for vision) as a consequence of DCD2 deletion. 

It's a good thing Legolas didn't seem to share the same genetic fate as the experimental group. Otherwise, he'd really be screwed. Legolost? ::rimshot, crickets chirping::


Cicchini GM, Marino C, Mascheretti S, Perani D, & Morrone MC (2015). Strong Motion Deficits in Dyslexia Associated with DCDC2 Gene Alteration. The Journal of neuroscience : the official journal of the Society for Neuroscience, 35 (21), 8059-64 PMID: 26019324

Tuesday, June 2, 2015

Possible link between Alzheimer's disease and disrupted sleep-dependent memory consolidation?

It has been well established that certain kinds of sleep consolidate certain kinds of memory. Mander and colleagues (2015) discovered that in older adults, beta-amyloid (the main component of amyloid plagues found in Alzheimer's disease) appears to disrupt slow wave activity in the medial frontal cortex during NREM sleep, which then impairs hippocampus-based memory consolidation.

It would also be interesting to investigate possible disruptions in thalamic sleep spindle activity to see how this may further contribute to memory impairment in this population. I wrote about this possibility in my Sleep Medicine Review's paper a few years ago.

Here is Mander et al.'s abstract, which appears under the advanced online publication section of Nature Neuroscience:

Independent evidence associates β-amyloid pathology with both non-rapid eye movement (NREM) sleep disruption and memory impairment in older adults. However, whether the influence of β-amyloid pathology on hippocampus-dependent memory is, in part, driven by impairments of NREM slow wave activity (SWA) and associated overnight memory consolidation is unknown. Here we show that β-amyloid burden in medial prefrontal cortex (mPFC) correlates significantly with the severity of impairment in NREM SWA generation. Moreover, reduced NREM SWA generation was further associated with impaired overnight memory consolidation and impoverished hippocampal-neocortical memory transformation. Furthermore, structural equation models revealed that the association between mPFC β-amyloid pathology and impaired hippocampus-dependent memory consolidation was not direct, but instead statistically depended on the intermediary factor of diminished NREM SWA. By linking β-amyloid pathology with impaired NREM SWA, these data implicate sleep disruption as a mechanistic pathway through which β-amyloid pathology may contribute to hippocampus-dependent cognitive decline in the elderly.

Mander, B.,A., Marks, S.,M., Vogel, J.,W., Rao, ,Vikram, Lu, ,Brandon, Saletin, J.,M., . . . Walker, M.,P.Beta]-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.

Lu, W., & Göder, R. (2012). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Sleep Medicine Reviews, 16 (4), 389-394 DOI: 10.1016/j.smrv.2011.08.001

Sunday, February 22, 2015

A Short Neuroscience-themed Poem

Sounds of playful children yelling into the deep caverns of my mind
Rattling me into wakefulness
These vivid voices echoing
Bouncing with energy and curiosity
Traveling through the dense gray matter via the Neurostransmitter Railway
Leaving Hippocampus Station
Mr. Amygdala accompanies them making sure they travel safely
It is here that I remember my childhood

From a Xanga post written several years ago.

God and The Anonymous Economic Game

Some anthropologists argue that the idea of God first arose in larger societies, for the purpose of curbing selfishness and promoting cooperation. Outside a tightly knit group, the reasoning goes, nobody can keep an eye on everyone’s behavior, so these cultures invented a supernatural agent who could. But does thinking of an omniscient God actually promote altruism? The University of British Columbia psychologist Ara Norenzayan wanted to find out.

In a pair of studies published in Psychological Science, Norenzayan and his student Azim F. Shariff had participants play the so-called “dictator game,” a common way of measuring generosity toward strangers. The game is simple: you’re offered 10 $1 coins and told to take as many as you want and leave the rest for the player in the other room (who is, unbeknown to you, a research confederate). The fair split, of course, is 50-50, but most anonymous “dictators” play selfishly, leaving little or nothing for the other player.

In the control group of Norenzayan’s study, the vast majority of participants kept everything or nearly everything — whether or not they said they were religious. “Religious leaders always complain that people don’t internalize religion, and they’re right,” Norenzayan observes.

But is there a way to induce generosity? In the experimental condition, the researchers prompted thoughts of God using a well-established “priming” technique: participants, who again included both theists and atheists, first had to unscramble sentences containing words such as God, divine and sacred. That way, going into the dictator game, players had God on their minds without being consciously aware of it. Sure enough, the “God prime” worked like a charm, leading to fairer splits. Without the God prime, only 12 percent of the participants split the money evenly, but when primed with the religious words, 52 percent did.

When news of these findings made headlines, some atheists were appalled by the implication that altruism depends heavily on religion. Apparently, they hadn’t heard the whole story. In a second study, the researchers had participants unscramble sentences containing words like civic, contract and police — meant to evoke secular moral institutions. This prime also increased generosity. And unlike the religious prime, it did so consistently for both believers and nonbelievers. Until he conducts further research, Norenzayan can only speculate about the significance: “We need that common denominator that works for everyone".

From a Xanga entry written several years ago.


Shariff AF, & Norenzayan A (2007). God is watching you: priming God concepts increases prosocial behavior in an anonymous economic game. Psychological science, 18 (9), 803-9 PMID: 17760777

Friday, September 19, 2014

The neuroscience behind scratching an itch

The beautiful experience of alleviating an itch, the vigorous scratching of skin cells, and the white flakes that float away slowly and gently like a whimsical dream.

If only those with chronic itching problems could describe their conditions in such a serene way. In the latest edition of Nature Neuroscience, Diana Bautista and colleagues (2014) review the literature on the underlying mechanism of the itch at the molecular and cellular level within the peripheral and central nervous systems. They describe what drives acute and chronic itching and even quote the famous Buddhist Nagarjuna in their abstract.

"There is a pleasure when an itch is scratched. But to be without an itch is more pleasurable still".

They provide the reader with a few examples of neurological disorders where chronic itching can become a problem:

1. multiple sclerosis
2. diabetic neuropathy
3. shingles

They also boldly state that the act of itching serves no biological purpose.

Because I currently do not have institutional access to any research journals, I can only surmise that this article is an incredibly interesting read (although there is a greater likelihood that the details would go over my head). But alas, I now suffer from an inability to rid myself of this nagging itch to read Bautista et al.'s article so that I can write a decent blog post about it.

You can check out the first page here.

You can also enjoy this Times read on the mysteries of the itch and how a molecule known as a neuropeptide natriuretic polypeptide b (Nppb) plays a crucial role in the itching process.


Bautista, D., Wilson, S., & Hoon, M. (2014). Why we scratch an itch: the molecules, cells and circuits of itch Nature Neuroscience, 17 (2), 175-182 DOI: 10.1038/nn.3619

The above image is from

Thursday, August 21, 2014

How to prevent a possible concussion from the ALS ice bucket challenge

The ice bucket challenge has swept the nation in an effort to raise awareness for ALS. However, there seems to have been a number of concussions (or mild traumatic brain injuries) sustained from performing a seemingly altruistic act. Although some people may find the below video funny, concussions are a serious issue and can lead to serious consequences including executive dysfunction. Symptoms can include short loss of consciousness, feeling dazed and confused, loss of immediate memory, headaches, blurry vision, slurred speech, concentration difficulties, fatigue, and sleep disturbance.

Two recent meta-analyses (one examining neuropsychological performance while the other examining fMRI data) have in fact supported the claim that executive functioning can be negatively impacted after a mild traumatic brain injury (Carr et al., 2014; Eierud et al., 2014), although, there has been long-standing controversy regarding whether a mild traumatic brain injury can lead to long-term effects (Rohling et al., 2012).

Nevertheless, appropriate guidelines should be established regarding how to safely execute the ice bucket challenge. Thus, I propose the following recommendations (this is by no means an exhaustive list):

1) At least two people should be holding the bucket
2) There should be absolutely no throwing or dropping of the bucket
3) The ice cubes should be crushed
4) The distance from bucket to head should be no greater than 3 ft high

...and finally

5) Don't be an idiot about it

I've treated too many unfortunate individuals who've sustained traumatic brain injuries to find the humor in "ice bucket challenge fails" (as shown above). All of this is supposed to support the treatment of a serious medical condition, not cause one. It's interesting that in raising awareness for ALS, we now have to raise awareness for traumatic brain injury.

You can find the full Karr et al. (2014) paper here.


Eierud C, Craddock RC, Fletcher S, Aulakh M, King-Casas B, Kuehl D, & LaConte SM (2014). Neuroimaging after mild traumatic brain injury: Review and meta-analysis. NeuroImage. Clinical, 4, 283-94 PMID: 25061565

Karr JE, Areshenkoff CN, & Garcia-Barrera MA (2014). The neuropsychological outcomes of concussion: a systematic review of meta-analyses on the cognitive sequelae of mild traumatic brain injury. Neuropsychology, 28 (3), 321-36 PMID: 24219611

Rohling, M., Larrabee, G., & Millis, S. (2012). The “Miserable Minority” Following Mild Traumatic Brain Injury: Who Are They and do Meta-Analyses Hide Them? The Clinical Neuropsychologist, 26 (2), 197-213 DOI: 10.1080/13854046.2011.647085

The above image is from

Saturday, July 12, 2014

Night-to-night variability of sleep in traumatic brain injury

It's been a while since I've posted something substantial. My apologies to all 20 followers of TQLC. Academia and clinical cases have been taking up most of my time. However, some exciting news! My paper on variability of respiration during sleep in traumatic brain injury (TBI) has recently been accepted into Neurorehabilitation. 

In the paper my colleagues and I examined the sleep processes of individuals with TBI using polysomnography. Polysomnography is a tool used to measure biophysical changes during sleep and diagnose disorders such as obstructive sleep apnea in which breathing repeatedly stops and starts during sleep, a big problem for individuals with TBI. The contraption is quite uncomfortable (as you can see by the image) and takes some getting used to. Thus, we looked at the "first-night effects" of polysomnography on our subjects to see if the measurements from night-to-night were reliable. 

We found that polysomnography was quite reliable on the first night compared to the second night, especially for diagnosing obstructive sleep apnea. This isn't typically the case for the general population so we were a bit surprised. There are a few possible explanations for why individuals with TBI don't seem to experience such first-night effects. One reason is that after a TBI, sleep becomes disrupted due to biological changes in the brain that regulate sleep processes. Thus, when our sample entered the sleep lab, their sleep remained poor on night 1 AND night 2 with little change. 

A second possible explanation may be that they were unaffected by novel external environmental stimuli such as the uncomfortable sensors they had to wear or the fact that they weren't in their own bedroom. This explanation is supported by the fact that individuals with TBI tend to have higher amounts of slow-wave sleep (the deep, restful kind). However, our subjects still tended to complain of sleep disturbances and daytime fatigue. Quite the mystery and something that needs to be further explored. I would love to hear your thoughts.

Here is a link to the uncorrected abstract.


Lu W, Cantor J, Aurora RN, Nguyen M, Ashman T, Spielman L, Ambrose A, Krellman J, & Gordon W (2014). Variability of respiration and sleep during polysomnography in individuals with TBI. NeuroRehabilitation PMID: 24990025

Monday, June 30, 2014

An influential reading

A question posed over at neuroecology. "So what readings have influenced you?"
My response: 
Joseph Goldstein’s Insight Meditation: The Practice of Freedom. It inspired me to further investigate why we, as humans, contribute to our own suffering and how to awaken from this dilemma. Thus, I became a psychologist interested in studying sleep processes.

Sunday, March 9, 2014

Lack of sleep impairs emotion recognition

This is a re-post of an entry I had written exactly 4 years ago. I liked it so much I decided to share it again. The ability to read emotions is an important part of the human experience; the only way to successfully navigate through complex social environments. It comes in handy especially if you don the title of psychotherapist or professional poker player. Without it, you are rendered socially inept. You enter the world of the autistic individual.

Thanks to Charles Darwin we now know that it’s not just the eyes that are “the windows to the soul”. He first wrote about the subject of facial expressions in his 1898 book titled The Expression of the Emotions in Man and Animals (the link includes the work in its entirety). In it he described the emotions conveyed in the face as being both universal and “species-specific”.

Saturday, February 15, 2014

Blasting long-term potentiation with a Mega Buster

Mega Man (1987) was one of the most entertaining games that I remember ever playing on Nintendo. You were Dr. Light's boy android (think Astro Boy or Pinocchio) and your mission was to defeat the multitude of robot bosses threatening to destroy the world. However, the only way to defeat them was to 1) consider how to counteract their special abilities with your own abilities and 2) memorize their attack patterns, often taking hours of learning (and frustration) before you got it right. Once successful, you would acquire that particular bosses' special ability, thus expanding your arsenal, and move on to fight another epic battle (not unlike Highlander). While reading Alvarez-Salvado and colleagues' (2014) paper on fMRI and long-term potentiation (LTP), it reminded me of this game. The vivid childhood memory was triggered by my reading of their abstract in which they wrote:

Neurons are able to express long-lasting and activity-dependent modulations of their synapses. This plastic property supports memory and conveys an extraordinary adaptive value, because it allows an individual to learn from, and respond, to changes in the environment.

Without this critical process of the brain, neither I nor Rock (the boy android) could have defeated Dr. Wily's evil robots and ultimately save the world from utter destruction. In Alvarez-Solvado and his colleagues' paper, they discuss how both cellular changes and network interactions in the brain are needed to encode a pattern of neuronal activity into long-term memory through synaptic plasticity. They go on to state that although the field of neuroscience already knows a great deal about the relationship between cellular changes and long-term memory, less is known about how regulation of network interactions effect plasticity. Thus, they were interested in looking at this mechanism a bit further using their version of a Mega Buster; a combination of high resolution functional magnetic resonance imaging (fMRI) and in vivo electrophysiology, in rats.

The team triggered LTP-induced network reorganization between the hippocampus (a seahorse shaped brain structure involved in learning and memory) and neocortical ("new brain") structures such as the prefrontal cortex (involved in executive functions such as planning and organization) and the sub cortical nucleus (involved in voluntary movement). They found that there was an enhancement of connection between these two brain regions via stimulation of the perforant pathway. The perforant pathway is a connective route between the entorhinal cortex to all fields of the hippocampus (think about the entorhinal cortex as the major highway between the hippocampus and the neocortex and the perforant pathway as the exit off the entorhinal cortex highway leading to the hippocampus). The perforant pathway plays a significant role in spatial memory and learning.

Image of perforant pathway from Learning and Memory16: 504-507

More specifically, Alvarez-Solvado et al. observed, through their high-res imaging, a fast increase in communication between the hippocampus and the prefrontal cortex mediated by N-methyl-D-aspartate (NMDA) receptors, the predominant molecular device for controlling synaptic plasticity and memory. From this finding they suggest that there may be two memory buffers functioning in parallel during memory encoding. They also observed that when LTP-induction was triggered on one side of the hippocampus, there was functional activation on the other side of hippocampus as well, supported by white matter structures that connect hemispheres of the brain. They believe this finding may represent bilateral coordination of associational networks with a role in pattern separation and sequence learning, all critical skills to have if you want to beat a game like Mega Man (and accomplish more important things, of course).

Alvarez-Salvado E, Pallarés V, Moreno A, & Canals S (2014). Functional MRI of long-term potentiation: imaging network plasticity. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 369 (1633) PMID: 24298154

Daumas S, Ceccom J, Halley H, Francés B, & Lassalle JM (2009). Activation of metabotropic glutamate receptor type 2/3 supports the involvement of the hippocampal mossy fiber pathway on contextual fear memory consolidation. Learning & memory (Cold Spring Harbor, N.Y.), 16 (8), 504-7 PMID: 19638469

Sunday, February 9, 2014

Forever alone disorder

Valentines Day is soon upon us. However, quite a few individuals, also known as otakus, could care less. During college I met some people who you might consider otakus or dorks. They never left their dorm rooms because they were just THAT into their video games. They would play for hours/days, completely disinterested in socializing with real people, partying, attending classes, and sometimes even eating. Although I didn't know it at the time, there was a name for this kind of strange and extreme "loner" behavior. For those of you who are unfamiliar with hikikomori, it is a recently recognized type of mental illness that has been rampant in locations like Japan. It refers to adolescent or young adult males who completely withdraw from social life and remain completely isolated, typically staying in their rooms for months on end. The criteria include:
1) spending most of the day and nearly every day confined to home 
2) marked and persistent avoidance of social situations
3) symptoms interfering significantly with the person’s normal routine, occupational (or academic) functioning, or social activities or relationships
4) perceiving the withdrawal as 
5) duration at least six months
6) no other mental disorder that accounts for the social withdrawal and avoidance. 
It is quite a serious issue and is linked to autism, pervasive developmental disorder, societal and cultural influences. 
I have heard of some cases happening here in the US  and Spain as well. Ovejero and colleagues (2013) provide a case study in which a young Spanish man was socially isolated for four years. He kept his room in an orderly fashion, was well groomed, and kept active within his home (although the article does not specify how he spent his time, I would put my money on World of Warcraft). There was no evidence of any other psychological disorder (e.g. schizophrenia, social phobia, anxiety, depression). The man stated that he was ashamed to leave his room because he had no teeth. He explained that his fear of needles prevented him from receiving dental prostheses. 
Below are some videos that nicely depict hikikomori. The first video is an illustration as to what the life of an individual "suffering" from hikikomori may look like.The second video is a commentary on hikikomori. The critical question that I have in mind is whether hikikomori should really be considered a disorder since the individual isn't really suffering per se. They actually quite enjoy being by themselves. Perhaps the "disorder" is due to the fact that they are not "productive" citizens of society. However, what if they were able to generate an income through something like internet services? I've heard of people who make a living by playing video games and streaming their performance live while receiving donations from dedicated viewers and fans (

Video 1:

Ovejero S, Caro-Cañizares I, de León-Martínez V, & Baca-Garcia E (2013). Prolonged social withdrawal disorder: A hikikomori case in Spain. The International journal of social psychiatry PMID: 24101742

First image taken from

Sunday, September 1, 2013

Just a mild electric current through the brain to increase memory gain

Have you ever watched that compelling infomerical selling the incredible electrical muscle stimulator, the Tone-A-Matic, promising beautiful rippling abs to couch potatotes all around the world? Ever hope something similar would work for the brain? Well folks, you're in luck!

There has been mounting evidence that transcranial direct current stimulation can improve cognitive functioning (Boggio et al., 2006; Brasil-Neto et al., 2012; Javadi et al., 2012, 2013). However, many of the studies used single stimulation sessions with only transient effects.

Meinzer and colleagues (2013), from Charite University in Germany, looked to fix this very issue. They investigated the effects of anodal transcranial direct current stimulation over multiple days on 20 very lucky people. They found that mild electrical stimulation to the brain, right after the learning sessions, enhanced language learning over time for both familiar and novel words. But wait! That's not all. They also observed that the effects lasted over an extended period of time. They suggest that this technology could possibly benefit stroke patients during rehabilitation. 

I, for one, truly need this in my life. Especially right after learning someones name. Maybe a cheap DIY 9-volt electrical stimulator would work just as well? Then again, knowing my luck, maybe not. I'll stick with using mnemonics, for now. 


Boggio PS, Ferrucci R, Rigonatti SP, Covre P, Nitsche M, Pascual-Leone A, & Fregni F (2006). Effects of transcranial direct current stimulation on working memory in patients with Parkinson's disease. Journal of the neurological sciences, 249 (1), 31-8 PMID: 16843494

Brasil-Neto JP (2012). Learning, memory, and transcranial direct current stimulation. Frontiers in psychiatry, 3 PMID: 22969734

Javadi AH, Cheng P, & Walsh V (2012). Short duration transcranial direct current stimulation (tDCS) modulates verbal memory. Brain stimulation, 5 (4), 468-74 PMID: 21962975

Javadi AH, & Cheng P (2013). Transcranial direct current stimulation (tDCS) enhances reconsolidation of long-term memory. Brain stimulation, 6 (4), 668-74 PMID: 23137702

Meinzer M, Jähnigen S, Copland DA, Darkow R, Grittner U, Avirame K, Rodriguez AD, Lindenberg R, & Flöel A (2013). Transcranial direct current stimulation over multiple days improves learning and maintenance of a novel vocabulary. Cortex; a journal devoted to the study of the nervous system and behavior PMID: 23988131