Loss of consciousness subsequent to chronic nose-blowing

The case of a patient with OCD who blew his nose way too often: 

The case is described of a 50-year-old man, treated for 10 years in an outpatient psychiatric clinic for an obsessive compulsive disorder, who presented with acute loss of consciousness after forceful nose blowing. A CT scan revealed an intraparenchymal air collection with tension signs in the left frontal lobe and a bone defect in the roof of the ethmoid sinus. After emergency left frontal craniotomy and dura opening, the gaseous collection was evacuated by a ventricular catheter inserted into the brain and the bone defect was repaired with pericranium flap and muscle. The postoperative course was uneventful with neurocognitive improvement and regained motility. Spontaneous tension pneumocephalus is a rare life-threatening condition which is often caused by a bone defect near the tegmen tympani. This case illustrates both an unusual cause and a unique surgical treatment for spontaneous tension intraparenchymal pneumocephalus. It can be a dangerous entity with potential for early mortality and long-term morbidity if not promptly decompressed. The pathogenesis, diagnosis and surgical strategies for spontaneous tension pneumocephalus are briefly discussed. 


Mirone G, Rotondo M, Scuotto A, et al. Spontaneous intraparenchymal tension pneumocephalus triggered by compulsive forceful nose blowing. Emerg Med J. 2009;26(11):837-838

Beware of cheerleading

An article on the dangers of cheerleading and the critical height in which one can sustain a brain injury. And who said this sport was for wusses?

CONTEXT: Although playground surfaces have been investigated for fall impact attenuation, the surfaces that cheerleaders use have received little attention. 

OBJECTIVE: To determine (1) the critical height for selected surfaces used by cheerleaders at or below which a serious head impact injury from a fall is unlikely to occur, (2) the critical heights for non-impact-absorbing surfaces for comparison purposes, and (3) the effect of soil moisture and grass height on g(max) (which is defined as the multiple of g [acceleration due to gravity at the earth's surface at sea level: ie, 32.2 feet x s(-1) x s(-1)] that represents the maximum deceleration experienced during an impact) and the Head Injury Criterion (HIC) at the critical height for a dry grass surface. 

DESIGN: Observational study. SETTINGS: A local cheerleading gym, indoor locations within the authors' institution, and various outdoor locations. MAIN OUTCOME MEASURE(S): g(max), HIC, and critical height. 

RESULTS: Critical heights for the surfaces tested ranged from 0.5 ft (0.15 m) for concrete and vinyl tile installed over concrete to more than 11 ft (3.35 m) for a spring floor. Increases in grass height and soil moisture resulted in an increase in the critical height for grass surfaces. Only spring floors and 4-in (0.10-m)-thick landing mats placed on traditional foam floors had critical heights greater than 10.5 ft (3.20 m), thus providing enough impact-absorbing capacity for performance of 2-level stunts. 

CONCLUSIONS: The potential for serious head impact injuries can be minimized by increasing the shock-absorbing capacity of the surface, decreasing the height from which the person falls, or both. Cheerleaders and cheerleading coaches should use the critical heights reported in this study to compare the relative impact-absorbing capacities of the various surfaces tested, with critical height as an indicator of the impact-absorption capacity of the surface. The findings of this study can be used to select the most appropriate surface for the type of maneuver to be performed, based on the maximum height expected to be achieved by the cheerleader(s) during execution of the maneuver. Cheerleaders should not perform maneuvers at heights that exceed the critical height for the surface on which they are performing. 

Shields BJ, Smith GA. The potential for brain injury  on selected surfaces used by cheerleaders. J Athl Train. 2009;44(6):595-602

Weapon swallowing as a form of stress relief

Another fascinating case study. Patient with intellectual disability who swallowed sharp objects to reduce stress. If only this solution was a viable option to end world violence...

A 41-year-old male patient with intellectual disabilities presented after having swallowed approximately 20 sharp objects. While admitted to a psychiatric ward, surgeons removed a glove from his stomach endoscopically and pharmacologically facilitated the objects' complication-free bowel passage. The patient explained the swallowing as a means to release himself from tension induced by stress. His aberrant behavior also seemed to serve as a means to exert pressure on psychosocial workers. Other deviations included the pushing of sharp objects under the skin and multiple paraphiliae. As a child, the patient suffered from early psychological and physical traumatization. Both parents were allegedly physically abusive alcoholics.  Apart from possible alcohol embryopathy and traumatic brain damage, meningitis, which the patient had at the age of three, is discussed as the most likely reason for his oligophrenia, associated with left-sided, temporo-parietal atrophy and epilepsy. 

te Wildt BT, Tettenborn C, Schneider U, et al. Swallowing foreign bodies as an example of impulse control disorder in a patient with intellectual disabilities: A case report. Psychiatry (Edgemont). 2010;7(9):34-37

Compulsive carnival song whistling

Another fascinating research article!

Compulsive carnival song whistling following cardiac arrest: a case study

A. Rosaura Polak, Jasper W. van der Paardt, Martijn Figee, Nienke Vulink, Pelle de Koning, Miranda Olff andDamiaan Denys
BMC Psychiatry 2012, 12:75 doi:10.1186/1471-244X-12-75

Background

Compulsivity is the repetitive, irresistible urge to perform a behavior, the experience of loss of voluntary control over this intense urge and the tendency to perform repetitive acts in a habitual or stereotyped manner. Compulsivity is part of obsessive-compulsive disorder (OCD), but may occasionally occur as stand-alone symptom following brain damage induced by cardiac arrest. In this case report, we describe a patient who developed compulsivity following cardiac arrest. We review diagnostic options, underlying mechanisms and possible treatments.

Case presentation

A 65-year-old man presented at our clinic with continuous compulsive whistling following cardiac arrest. Neither obsessive-compulsive symptoms, nor other psychiatric complaints were present prior to the hypoxic incident. An EEG showed diffuse hypofunction, mainly in baso-temporal areas. Treatment with clomipramine resulted in a decrease of whistling.

Discussion

This case report illustrates de novo manifestation of compulsivity following cardiac arrest and subsequent brain damage and gives additional information on diagnostic options, mechanisms and treatment options. Differential diagnosis between stereotypies, punding, or OCD is difficult. Compulsivity following brain damage may benefit from treatment with serotonin reuptake inhibitors. This finding enhances our knowledge of treatments in similar cases.

Why it's ok for Richard to touch Joan

Denman A, Wilkinson R. Applying conversation analysis to traumatic brain injury: Investigating touching another person in everyday social interaction. Disabil Rehabil. 2011;33(3):243-252

PURPOSE: Touching others, particularly the opposite sex, is a relatively common and problematic behaviour evident in many people with traumatic brain injury (TBI), in particular males. Here, we analyse this behaviour in a man with TBI (Richard) who regularly engages in inappropriate touching of women. The article draws on video-recordings of two naturally occurring social interactions between Richard and Joan (one of his carers) to analyse all six instances within these interactions where Richard touches Joan. METHOD: The recordings were made by leaving a video-recorder in Richard's home where he is supported by members of a care team. The socio-linguistic method of conversation analysis was used to transcribe and analyse the data. RESULTS: The analysis shows that each of the six instances of the touching behaviour occurred not as a random or isolated event in the interaction but rather in accompaniment with talk as part of a particular conversational action. Specifically, the conversational action in each case was produced in an emphatic or heightened style, with this style constituted by Richard touching Joan as well as by his use of a number of other resources such as eye gaze and the use of stress. CONCLUSIONS: The analysis suggests that the touching behaviours in this case were linked not so much to physical opportunities (which were available through much of these interactions) but rather to what conversational action was being produced at that particular sequential context within the interaction. For example, several instances of touching occurred as part of emphatically produced conversational actions where a previous, non-emphatic, production of that action had not been accepted or responded to by Joan. Clinical implications, such as suggestions for prophylactic management on the part of those interacting with people with TBI, are discussed.

Maple syrup urine disease. Who knew?

I've been tasked with sorting through thousands of articles in order to contribute to a systematic review on the treatment of psychiatric disorders in traumatic brain injury patients. Through this process I've stumbled upon a few fascinating and sometimes "out there" articles. For the next couple of weeks I'll be posting up abstracts that really caught my eye. We begin with Mescka and colleagues 2011 study on maple syrup urine disease; it's not what you think.

Maple syrup urine disease (MSUD) is an autosomal recessive inborn error of metabolism caused by deficiency of the activity of the mitochondrial enzyme complex branched-chain alpha-keto acid dehydrogenase (BCKAD) leading to accumulation of the branched-chain amino acids (BCAA) leucine, isoleucine and valine and their corresponding branched-chain alpha-keto acids. Affected patients present severe brain dysfunction manifested such as ataxia, seizures, coma, psychomotor delay and mental retardation. The mechanisms of brain damage in this disease remain poorly understood.

Mescka, C., Moraes, T., Rosa, A., Mazzola, P., Piccoli, B., Jacques, C., Dalazen, G., Coelho, J., Cortes, M., Terra, M., Regla Vargas, C., & Dutra-Filho, C. (2011). In vivo neuroprotective effect of L-carnitine against oxidative stress in maple syrup urine disease Metabolic Brain Disease, 26 (1), 21-28 DOI: 10.1007/s11011-011-9238-x

Texting while walking

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NYC pedestrian fatalities are up from last year, most likely due to txting while walking according to a NYTimes article. If you're going to txt while you walk irregardless of the dangers inherently involved, at least keep the phone up at eye level in order to improve peripheral vision. It may just save your life.

What Exactly is the Higgs Particle?

In light of the recent discovery of the very likely "God particle" I refer you to an excellent write up explaining what it is in layman's terms. The piece is written by my friend, Michael Park, who is currently a graduate student studying theoretical particle physics at Rutgers University. Enjoy!

link: http://www.allvoices.com/contributed-news/12672054-what-is-the-higgs-particle

Hooray for Higgs!

Finally, it's been found! I hear there may be more than one Higgs? I'm fascinated by where this discovery will take the field if deviations from the Standard Model are seen. This quote from the NYTimes made me lol. "Along the way the Higgs boson achieved a notoriety rare for abstract physics. To the eternal dismay of his colleagues, Leon Lederman, the former director of Fermilab, called it the 'God particle,' in his book of the same name, later quipping that he had wanted to call it 'the goddamn particle.'” Congrats to those who worked tirelessly on finding the goddamn particle. Congrats to Science. God particle bless America!

Does abnormal NREM sleep impair declarative memory consolidation?

Finally got to uploading the review paper Robert Goder and I had written recently on sleep and memory. You can download it HERE. Essentially, we describe a possible mechanism by which abnormal NREM sleep processes (i.e. reduced slow-wave sleep and sleep spindles) contribute to declarative memory impairment and concomittant sleep disruption in certain neuropsychiatric disorders including Alzheimer's, schizophrenia, and fibromyalgia. Underneath, I posted what the tentative model looks like (click to enlarge). Would love to hear your thoughts. 

Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.

Reference:

Lu, W., & Göder, R. (2011). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Sleep Medicine Reviews DOI: 10.1016/j.smrv.2011.08.001

Not all hippocampal hemispheres are created equal

I got a chance to sit down and read Kohl et al.'s recently published Nature Neuroscience paper titled "Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity". This paper contributes to our advancing knowledge of the asymmetrical brain and further elucidates the true complexity of the hippocampus, a sea horse shaped brain structure important for learning and memory.

More specifically, the team found that an area important for encoding and retrieving associated information (CA3) in the left hippocampus produced more long-lasting signal transmission to synapses of an area of the hippocampus important for spatial learning and memory (CA1) compared to CA3 in the right hippocampus of adult mice. Essentially, the left CA3 > right CA3 for triggering plasticity in CA1.

To make their observations Kohl and colleagues used optogenetics in which genetic and optical methods are combined to control specific events in targeted cells of living tissue. In this case, they injected a virus into either the left or right CA3. This particular virus contained a gene which encoded yellow fluorescent protein and led to selective expression of that protein when found in excitatory cells of the appropriately engineered transgenic mice. They then used a laser light to evoke excitatory postsynaptic potentials in the striatum radiatum, an area of the hippocampus that contains fibers connecting CA3 to CA1.

"Brainbow" transgenic mouse hippocampus - Tamily Weissman

The authors explained that the hemispheric asymmetry in plasticity was caused by differential GluN2B gene expression at CA1 synapses targeted by the left and right CA3. They conclude that their result "raises the possibility that the left and right CA3 might be differentially active and hence produce input-specific differences in postsynaptic spines.

However, the question still remains. Why the left and not the right?

(As an aside, I recommend checking out a free iPhone app called 3D Brain. Description: Use your touch screen to rotate and zoom around 29 interactive structures. Discover how each brain region functions, what happens when it is injured, and how it is involved in mental illness. Each detailed structure comes with information on functions, disorders, brain damage, case studies, and links to modern research)

References:

Kohl MM, Shipton OA, Deacon RM, Rawlins JN, Deisseroth K, & Paulsen O (2011). Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity. Nature neuroscience, 14 (11), 1413-5 PMID: 21946328

Why Non-rapid Eye Movement (NREM) sleep is important for memory

So...after 4 months of being MIA I've finally emerged from the deep, dark, and lonely cave of academia to give a brief update on what I've been doing all this time. When I wasn't furiously working on my dissertation related to working memory and aging, I was making final revisions to a theoretical review paper on sleep and memory. I'm happy to announce that after countless hours of lost sleep (irony?) it's finally been accepted for publication! I'll link the article abstract once it's up. For now let's talk about why NREM sleep is important (and why I needed it so badly for the past few months).

During the early years of sleep research, NREM sleep was discovered to play a role in the restoration of physiological functions (Siegal, 2005). However, relatively recently it's been established to play an equally important function, that of sleep-dependent memory consolidation. Some may be asking, "what the bleep is NREM sleep?" Here's the technical answer according to the American Academy of Sleep Medicine. It consists of 3 stages (N1, N2, and N3, very original...) N1 consists of low amp electrical activity measured by electroencephalogram (EEG) where slow eye movements take place. During N2, you're unconscious, but easily awoken. Here, we find seemingly weird blips in electrical brain activity known as k-complexes and sleep spindles. Sleep spindles are super important for memory consolidation, as will be discussed later. N3 (or slow wave sleep) consists of delta waves and peak to peak amps >75uV found in frontal lobes, also very important for sleep-dependent memory consolidation. Now how does all of this electrical activity consolidate memory?

In the early 1970s Ekstrand and colleagues observed that slow wave sleep was positively correlated with the ability to retain a word pair-associate list, while rapid eye movement (REM) sleep was not. They went on to publish their findings in Science. Memorizing these word pairs depend on declarative memory system functioning. Declarative memory is hippocampal-based memory accessible through conscious recollection including facts and events. Ekstrand's findings and many other subsequent studies firmly established that slow wave sleep was indeed important for declarative memory consolidation (check out Diekelmann and Born, 2010 for a comprehensive review).

Another seminal study by Wilson and McNaugton (1994), also published in Science, observed an increased tendency for particular hippocampal place cells that fired during a spatial behavioral task to also fire during subsequent slow wave sleep in rats. This lay the foundation for discovering that memory traces consolidate from short-term to long-term memories by a process involving reactivation of sharp wave-ripples in the hippocampus during sleep.

In a more recent and very cool study, Born and colleagues (2007) had human subject learn card pair locations while smelling different odors simultaneously (the top left card paired with the scent of my feet, for example). When the researchers reintroduced those same smells during the subjects' slow wave sleep (my feet in the poor subject's face), memory for the card pair locations (top left card) tied to those smells (my feet) were enhanced at recall the next day. Also, through fMRI they saw reactivation of the hippocampus during slow wave sleep. In an alternative study, they used transcranial magnetic stimulation to essentially boost slow oscillations during NREM sleep, which not only increased slow wave sleep and sleep spindles, but also enhanced declarative memory consolidation.

From these findings they developed a model postulating that slow waves originating from the neocortex synced both hippocampal sharp waves and thalamocortical sleep spindles, resulting in primed cortical networks for long-term memory storage. The research team was the first to provide empirical support for a causal role of hippocampal memory reactivation for memory enhancement during sleep.

The key point I'm trying to emphasize here is that slow wave sleep and sleep spindle activity are essential for sleep dependent declarative memory consolidation.

The question I pose in my paper (with the invaluable help of Dr. Robert Göder) is what happens to declarative memory consolidation when slow wave sleep and sleep spindle activity, both taking place during NREM sleep, are disrupted? I've definitely experienced the detrimental effects first hand and hope to soon show you, with the latest research, how abnormal NREM sleep can really mess with memory consolidation. For now, I return to my cave to rest my weary head, praying that I don't become an unfortunate case of ABD (all but dissertation) due to lack of sleep.

References:

Siegel, J. (2005). Clues to the functions of mammalian sleep Nature, 437 (7063), 1264-1271 DOI: 10.1038/nature04285

Iber C, Ancoli-Israel S, Chesson A, Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events : Rules, Terminology and Technical Specifications, 1st ed. : Wenchester, Minois, American Academy of Sleep Medicine 2007.

Diekelmann, S., & Born, J. (2010). The memory function of sleep Nature Reviews Neuroscience DOI: 10.1038/nrn2762

Fowler MJ, Sullivan MJ, Ekstrand BR. Sleep and memory. Science 1973;79:302-304.

Wilson, M., & McNaughton, B. (1994). Reactivation of hippocampal ensemble memories during sleep Science, 265 (5172), 676-679 DOI: 10.1126/science.8036517

Rasch B, Büchel C, Gais S, & Born J (2007). Odor cues during slow-wave sleep prompt declarative memory consolidation. Science (New York, N.Y.), 315 (5817), 1426-9 PMID: 17347444

Marshall, L., Helgadóttir, H., Mölle, M., & Born, J. (2006). Boosting slow oscillations during sleep potentiates memory Nature, 444 (7119), 610-613 DOI: 10.1038/nature05278

How a stinky chemical offers neuroprotection for a seizing brain

What did Socrates, Plato, Hercules, and Ajax have in common? Other than greatness, they were also epileptics according to the 17th century French physician, Jean Taxil.

An epileptic seizure consists of abnormal excessive or synchronous neuronal activity in the brain which can lead to convulsions, loss of awareness, full body slump, or even the experience of deja vu. Unprovoked seizures are typically related to epilepsy and other seizure related disorders while unprovoked seizures have multiple contributing factors including, but not limited to traumatic brain injury, kidney failure, sleep deprivation, brain lesions, metabolic disturbances, stroke, and tricyclic antidepressants. Sometimes seizures are just idiopathic (unknown cause).

Is epilepsy really the "sacred disease" Hippocrates had once thought it was? Not really. Serious complications may arise such as difficulty learning, aspiration pneumonia, injury from falls, and even permanent brain damage (I recommend the book The Spirit Catches You and You Fall Down).

A recent study by Bell and colleagues published in the latest Nature Neuroscience investigated whether polyamines, organic compounds having two or more primary amino groups, acted as a neuroprotective factor against subsequent seizures. Past studies have shown that polyamines increase after a seizure, but their regulatory role in epileptic seizures remain a mystery. 

The authors exposed Xenopus laevis tadpoles (aka African clawed tadpoles) to pentylenetetrazol (PTZ), a well known convulsant, to see if polyamines would regulate neural excitability following a seizure. After a priming exposure, they again exposed the poor tadpoles to PTZ 4 hours later. What they found was quite remarkable. Compared to a control group (tadpoles that did not receive a priming exposure to PTZ), the seizure onset in the primed group during the second exposure was delayed a whopping 25%. Something was protecting them from having a subsequent seizure, but what was it?

The authors found that a stinky type of polyamine known as prutescine (more like "putrid-scine" ::rimshot::) was involved in decreasing seizure susceptibility. They suggest that when prutescine is released after the first seizure, it converts into GABA, an inhibitory neurotransmitter. The extracellular GABA then activates presynaptic GABA receptors on inhibitory interneurons, temporarily decreasing inhibitory drive and increasing seizure susceptibility (a kindling effect). The inhibitory neurons respond to this activation with a compensatory release of more GABA. When the prutescine and GABA levels return back to normal, the inhibitory frequency stays elevated. When another seizure occurs, the animal is well protected.

The findings of this study shed further light on the development of the seizing brain and bring the field closer to developing preventative measures for both short-term and long-term seizure susceptibility. Prutescine may indeed be the golden ticket to improving resiliency to seizures. Now all we need to figure out is what to do with that horrific stench. 

Bell MR, Belarde JA, Johnson HF, & Aizenman CD (2011). A neuroprotective role for polyamines in a Xenopus tadpole model of epilepsy. Nature neuroscience, 14 (4), 505-12 PMID: 21378970

Disorder promotes stereotyping

It'll be interesting to see how this all plays out. Shame on you Stapel!

Xenophobic exclusion has been ubiquitous throughout history. However, the explanation of such a phenomenon has been little understood. Interesting research conducted by Stapel and Lindenberg published in the latest Science has brought us closer to some answers. They found that people who are in a disordered environment (e.g. unclean subway station) exhibit greater discriminatory behavior (e.g. decision to sit further away from a black person compared to a white person). The authors suggest that when the brain faces disorder there is a natural drive for order. One way to reach order is through stereotyping. It's the brain's way of making sense of the world. Too bad it doesn't work all the time.

Editorial Expression of Concern

The report “Coping with chaos: How disordered contexts promote stereotyping and discrimination” by D. A.Stapel and S. Lindenberg (1) reported the effects of the physical environment on human stereotyping and discriminatory behavior. On 31 October 2011, Tilburg University held a press conference to announce interim findings of its investigation into possible data fraud in the body of work published by Stapel. The official report in Dutch (translated into English using Google software) indicates that the extent of the fraud by Stapel is substantial. Pending further details of the Tilburg Committee's findings, Science is publishing this Editorial Expression of Concern to alert our readers that serious concerns have been raised about the validity of the findings in this Report.

1. Bruce Alberts, Editor-in-Chief

Stapel DA, & Lindenberg S (2011). Coping with chaos: how disordered contexts promote stereotyping and discrimination. Science (New York, N.Y.), 332 (6026), 251-3 PMID: 21474762

Zollner Illusion

You are not drunk on St. Patty's Day beer (or maybe you are). Those lines are indeed parallel.