Human intelligence is reflective in nature. Reflection is the ability of the brain to consciously manipulate the given information and rehearse options prior to action. When guessing well is the game and pressure is on the brain, people who display reflective intelligence and foresight in thought and action, have distinct advantage as leaders. Such people have higher survival instinct and more mindful disposition. The brain of such people spontaneously responds to problems and obstacles by retrieving and contemplating information which is relevant to action options. Journal writing, meditation, case study analysis and investigative learning enhance reflective intelligence by many folds. People with leadership qualities have been found to be doing these activities more often than others who remain followers.

Reflective intelligence of human brain has also been found to increase by provoking deliberate critical and creative thinking. Provoking critical analysis and creative thinking engages natural ability of the human brain to detect relationships between seemingly unrelated objects, link seemingly unrelated information into useful revelation, and create innovative products with new information. While people with leadership tendencies have been extensively found to be in indulging in lateral & critical thinking, innovative inventions, and analyzing errors in positions by interactive discussions, followers have often been found to tread the beaten path and avoiding social interacting on controversial positions.

A capacity for reflective intelligence does not translate into intelligent behavior and thought automatically. The constructive and reflective dimensions of human intelligence need to be consciously cultivated and continuously exercised if its true potential is to be realized. The constructive and reflective intelligence have to developed and refined to a degree where the person is naturally inclined to use it every time, in his every action and thought. Leaders have a natural disposition to cultivate and maximize such constructive and reflective intelligence by indulging in meta-cognition, reflection on specific thinking strategies, seeking social opportunities for sharing of challenging ideas and optimizing physiological intelligence by choosing to exercise, eat only healthy food, and live in conducive environment which allows adequate light, fresh air and no distractions.

Followers don’t care what their thinking strategies or general disposition is. They do not feel the need to acquire the knowledge about nurturing intelligence. They react to situations in their environment by spontaneous reaction, without applying critical thinking and without analyzing their position. They would more often indulge in gossip, rather than meaningful exchange of ideas on challenging topics. They have less tolerance for views of others which are divergent from their own. They give a damn to what they eat or space where they live, they live only for sensory pleasures which provide immediate gratification.

Emotion involves the processing of sensory information through neural and glandular systems that alter mind and body states while arousing the prefrontal cortex to what is worth thinking about. Emotion is closely connected to arousal and operation of physiological, social and reflective capacity of the human brain. The brain of humans with leadership qualities are conscious of their emotions and are able to control and mediate their responses to their own emotions. This is an essential quality which differentiates leaders from followers. This is also called Emotional Intelligence.

The brain of leaders is able to harness the power of emotion which helps the leaders to make judgments after receiving stimuli from environment and get motivated by challenges. The leader’s brain is continuously screening sensory information, guided by emotions, to understand which task is worthy of attention and commitment of its infinite resources. In other words, when the human brain of people with leadership qualities gets emotionally excited about some task, it helps the leader to efficiently engage in accumulation of knowledge about that task, to engage in meaningful social interaction to find other human brains with common goals, and to engage in reflective reasoning to solve problems encountered in accomplishing that task — all this leads to enhanced physiological growth and refinement of neural networks in human brain. Thus, it can be inferred that brain of humans with leadership traits have more refined neural networks.

References

Gardner, H. (1997). Leading Minds – An Anatomy of Leadership. London: Harpers Collins.

Dickmann, M. H. & Blair, N.S. (2001). Connecting Leadership to the Brain. Thousand Oaks: Corwin Press.

The fMRI showed that connections between specialized cells in different parts of the brain are used together to exchange information and coordinate simple tasks. However, four activation patterns emerged when 60 commonplace nouns were to be thought of in the mind. The patterns are grouped by how the noun could be sorted: things that are manipulated; things that are eaten; things that represent shelter, or an entryway into shelter; and finally, words that are long. Interestingly, when ‘eating’ nouns were thought of, the brain area associated with eating was activated, which works on coordination and movement of the lower facial muscles. Why these four seemingly simple groupings? It has to do with evolution and the hierarchy of needs.

Maslov’s Hierarchy of Needs pyramid puts human needs in groups based on survival and physiological needs at the bottom with social needs at the top. Humans evolved to survive with the lower needs being met before moving onto higher level needs. The brain works the same way. Things that are manipulated represent concrete physical things, those than exist in reality rather than abstract thought. These words relate to those that are held and used with the hands. Eating and shelter words have to do with physiological and safety needs. So why separate long words into a distinct pattern?

Long words were not useful or needed for much of human history. Human communication grew from meeting the lowest needs on the Maslov pyramid. Eating, shelter, and safety through tools and other object manipulation was needed first and foremost. Culture and civilizations, which came about much later in human history, met the needs of the lowest levels and humans were free to form societies, participate in leisure activities, and think of abstract concepts. Here, longer words emerged that could convey complex, associated and connected things. The long words used in the study represent technological objects that are often compound words from existing simpler words, or modern words (“telephone”, “refrigerators”, “airplane”). These words and word lengths weren’t needed for survival and are grouped different in the brain.

Reference

Just, M., Cherkassky, V., Aryal, S., & Mitchell, T. (2010). A Neurosemantic Theory of Concrete Noun Representation Based on the Underlying Brain Codes PLoS ONE, 5 (1) DOI: 10.1371/journal.pone.0008622

Sensory stimulation such as listening to speech or watching colors or emotional stimulation by getting hugs or eye contact can change the physiological development of infant brain by changing the quality and quantity of the electrical wiring between brain cells. This promotes the growth of dendrites in the brain making stronger and richer neural connections.

Different parts of infant brain get stimulated in different ways when infant brain experiences different emotions leading to connections between different synapses. Infants who experienced playful teaching by happy adults or teachers in a fun environment showed considerable neural activity in areas of brain which specialized for positive emotion. When such infants grow up into adulthood, they are more like to feel positive and stay positive even when they experience a negative or stressful event in their environment. Such stimulation of the infant brain can determine whether the infant will grow into peaceful & happy adult or a violent antisocial troublemaker.

Therefore it is prime responsibility of the adult teachers to stimulate the infant brains in various playful ways to bring about the optimum physiological, emotional, social and mental development of the infant’s brain and body. Playful teaching is a dynamic and constructive behavior which is essential for infant’s healthy growth, development, and learning, especially during the first three years of life.

Lack of play in teaching methods stifles creativity and healthy development. A playful method of teaching allows the child to discover his own strengths, his own body, and his environment by allowing him to experience by experimenting. Opposite of playful method of teaching is the instructional method of teaching in which child is directed how to do things. When the child learns by playful techniques, he develops a head full of knowledge and a heart full of confidence. On the other hand, the instructional method of teaching makes a child feel less confident and less clever because he is given this subtle message by his instructional teacher that he is incapable, he does not know, he needs the teacher to teach him.

As you read below, you will discover how a playful teacher can stimulate the infant brain to result in multifaceted growth of the infant human life.

To develop the gross motor skills and body awareness in an infant, the playful teacher should encourage the child to participate in various physical sports which allow him to walk, climb, kick, jump, climb and catch. This will help the infant to develop higher control of large muscles of the body which coordinate the movement.

To develop higher control of smaller muscles of the body which coordinate fine motor movements, the playful teacher should encourage the infant to indulge in activities such as sketching, painting, sculpting, block building and cutting.

In order to encourage innovation and creative thinking abilities in the child, the playful teacher should allow free reign to fantasy and imagination of the preschool infant. They should encourage the child to playfully re-enact events or take on roles, and use props to replace an original object. They should allow the child to make their own story suiting their personal desires, without putting pressure on them to win any contest and without judging the child. While re-enacting events or playing role of someone else, child learns to visualize and imitate codified rules. While narrating his story as in role playing, child learns creative thinking and learns how to express his story and plan to others more effectively. This helps in building the confidence level of the child.

The playful teacher can develop analytical reasoning and problem solving skills of a child by asking him to arrange and organize what he can see, touch, hear or smell. He should encourage the child to play with another child and help another child in the process to solve the problem which another child may be seemingly facing. By helping another child, the child will learn the skill of problem solving and joy of mastery.

Much before the infant can learn to speak himself any meaningful words, his ears begin to be conditioned by language input of the playful teacher or caring adult. To develop the speech and language skills of the child, the playful teacher should frequently talk to the infants and condition their ears to differentiate between different sounds. By repeated talking to the infant, ability for speech is developed by forming new neural connections which help infant to combine sounds in order to form words. To teach the language skills to older infant, playful teacher should use music and poems to make the child understand comprehension and correct use of those words.

Thus, it can be inferred that a playful teacher can unlock the world for an infant with care. What stimulation the infant brain will get and thus what the child will know, think and feel, will depend on the playful teacher. What playful teacher does not offer, the child will not know.

Since Lotze’s time, empathy has become an area of contemporary psychological and neuroscientific research. In psychology, empathy refers to the ability to understand another person’s mental and emotional experience. While a great deal of psychology research created a conceptual understanding of empathy, it was in the early 1990s that researchers first gained insight into the biological mechanisms that may underpin empathy. Researchers at the University of Parma, Italy, discovered that when macaque monkeys observe another individual’s (monkey or human) actions, the neurons that normally fire when the monkey him/herself performs the same action also fires in response to watching another person. The finding of these neurons, known as ‘mirror neurons,’ suggests that these monkeys use the same neural mechanism to represent their own and others’ actions, creating a neurophysiological link between one’s own experience and that of another individual. Humans also seem to have mirror neurons in brain areas analogous to those observed in the macaques. Several studies confirm that when humans observe another person’s intentional action and/or emotional expressions, they activate brain areas that are also engaged when the person would perform the action or experience the emotion him/herself.

It is worth mentioning that the relative role of mirror neurons in human empathy is currently of heated debate among researchers in neuroscience and psychology. The mirror neuron theory suggests that because of the immediate overlap in neural activation in response to our own and other individual’s actions, we are able to imagine another individual’s subjective experience. Yet, much of the time we are either inaccurate about or apathetic towards another individual’s experience. Mirror neurons do not explain why humans empathize with others more or less easily, nor whether we are more or less accurate in imagining their internal mental experience.

Although there is much more to learn about how humans experience empathy, the discovery of mirror neurons are a major contribution to our understanding. For now, the next time you pass someone on the street and feel sad because they look sad, you may have a better understanding as to why this happens. As the old saying goes, “I feel your pain.”

References

Rizzolatti, G., & Craighero, L. (2004). The Mirror-Neuron System. Annual Review of Neuroscience, 27 (1), 169-192 DOI: 10.1146/annurev.neuro.27.070203.144230

Rizzolatti, G. (1996). Premotor cortex and the recognition of motor actions Cognitive Brain Research, 3 (2), 131-141 DOI: 10.1016/0926-6410(95)00038-0

Decety, J., & Meyer, M. (2008). From emotion resonance to empathic understanding: A social developmental neuroscience account Development and Psychopathology, 20 (04) DOI: 10.1017/S0954579408000503

Glossolalia, or speaking in tongues, has fascinated thinkers ever since the “tongues of angels” descended upon early believers as a gift from the Holy Ghost in the New Testament of the Bible. This unusual mental state, characterized by utterances that sometimes sound like an untranslated psalm from Mars, typically occurs during instances of religious excitation, and is primarily associated with Pentecostal religious practices. It has commonly been considered a form of ecstatic trance accompanied by verbal utterances not found in any language.

Tongue speakers typically claim that the outbursts are non-voluntary, but others can sometimes produce instances of glossolalia on demand. Glossolalia has typically been considered a psychopathology, although little has been known about what occurs in the brain during this behavior. Plato asserted that these occurrences were caused by divine inspiration. He suggested that God took possession of the mind while man was sleeping or possessed, and during such a state, God inspired man with utterances that he can neither understand nor interpret.

Research performed in the 1980s at Denison University by the late anthropologist Felicitas Goodman led to a theory that glossolalia was a trance state caused by rhythmic discharges from the reticular formation, an area of the brain stem that plays a role in sleep and dreams. Goodman believed that this represented an alternative neural pathway for language, but more recent research has cast light on activity in other areas of the brain.

In 2006, Andrew Newberg and associates conducted the first functional neuroimaging study of cerebral changes during the act of glossolalia. In the study, published in Psychiatry Research: Neuroimaging, Newberg and other researchers at the University of Pennsylvania managed to run single photon emission computed tomography (SPECT) scans to measure regional cerebral blood flow in the brains of five people during episodes of active glossolalia. (As controls, the investigators took scans of people singing gospel songs.)  Despite the prevailing notion in the biomedical community of glossolalia as psychopathology, the researchers discovered that “the limited number of reported studies have suggested that people who speak in tongues show no differences in personality traits from other population groups.” Indeed, an earlier study in Britain of glossolalia among the clergy found that those who sometimes spoke in tongues showed more emotional stability and less depression than a control group.

In an earlier neuroimaging study of meditation states, Newberg and coworkers had observed increased activity in the frontal lobes, a finding consistent with scans of other attention-focusing activities.  But in the case of glossolalia, Newberg, the director for the Center for Spirituality and the Mind at the University of Pennsylvania School of Medicine, discovered that activity the frontal lobes decreased, including activity in the brain’s primary language processing centers: “Our finding of decreased activity in the frontal lobes during the practice of speaking in tongues is fascinating because these subjects truly believe that the spirit of God is moving through them and controlling them to speak. Our brain imaging research shows us that these subjects are not in control of the usual language centers during this activity, which is consistent with their description of a lack of intentional control while speaking in tongues.”

Another area of activity during glossolalia is the left superior parietal lobe (SPL), a region behind the frontal lobes that plays an important role in processing sensory input. In the meditation scans, during which subjects describe a loss of the sense of self, there was a significant decreases in SPL activity. However, glossolalia patients showed no such decreases, a finding consistent with their assertion that they experience no loss of individual boundaries, or submerging of the sense of self, while speaking in tongues.

The study also found increased activity in the limbic system, the seat of emotional responses, but the researchers declined to speculate on “altered emotional activity during glossolalia.”

One of the curious aspects of the study, as pointed out on the Neurocritic Blog, is that the subjects were capable of entering the state of glossolalia more or less on cue. This finding seems to call into question the “spontaneous utterance” aspect of glossolalia.

Spiritual or religious aspects notwithstanding, the study strongly points to the act of speaking in tongues as a verifiable language phenomenon that invites further study.

References

Francis, L. (2003). Personality and Glossolalia: A Study Among Male Evangelical Clergy Pastoral Psychology, 51 (5), 391-396 DOI: 10.1023/A:1023618715407

Goodman, Felicitas D. (1969). Phonetic Analysis of Glossolalia in Four Cultural Settings. Journal for the Scientific Study of Religion, 8 (2), 227-239.

NEWBERG, A., WINTERING, N., MORGAN, D., & WALDMAN, M. (2006). The measurement of regional cerebral blood flow during glossolalia: A preliminary SPECT study Psychiatry Research: Neuroimaging, 148 (1), 67-71 DOI: 10.1016/j.pscychresns.2006.07.001

Richardson, James T. (1973). Psychological Interpretations of Glossolalia: A Reexamination of Research. Journal for the Scientific Study of Religion, 12 (2), 199-207.

Published by BioMed Central, JMCR “is a peer-reviewed open access journal that will consider any original case report that expands the field of general medical knowledge.” To submit a case report for publication, please review the JMCR submission checklist.

Introduction

We describe the case of a 79-year-old Caucasian woman with a transient basilar occlusion monitored by transcranial Doppler, with subsequent recanalization and clinical shrinking deficit. [The basilar artery is one of many cerebral vessels that supply the brain, however, unlike the others, it is singular and supplies the brainstem]. This is the first case of transient basilar occlusive disease diagnosed and monitored by transcranial Doppler. This case is important and needs to be reported because transient basilar occlusion may be easily diagnosed if transcranial Doppler is performed.

Case Presentation

A 79-year-old woman affected by chronic atrial fibrillation and not treated with oral anticoagulants, cardioverted to sinus rhythm during a gastric endoscopy. She then showed a sudden-onset loss of consciousness, horizontal and vertical gaze palsy [unable to move eyes up-down or sideways], tetraparesis [paralysis of all four extremities] and bilateral miosis [constriction of the pupil] and coma. Two hours later, the symptoms resolved quickly, leaving no residual neurologic deficits. Transcranial Doppler examination showed a dampened flow in the basilar artery in the emergency examination and a restored flow when the symptoms resolved.

Conclusion

This is the first case of transient basilar occlusive disease diagnosed and monitored by transcranial Doppler. We believe that transcranial Doppler should be performed in all cases of unexplained acute loss of consciousness, in particular, if associated with signs of brainstem dysfunctions.

My Comments

I’ll take this opportunity to describe an invaluable utility in neurology — transcranial Doppler (TCD). This real-time ultrasonic examination measures blood flow through intra-cranial vessels using a probe over the patient’s head. It is inexpensive, quick, and, most importantly, noninvasive. It has been used used in the following clinical applications:

• Sickle Cell Disease — assessing stroke risk
• Intracranial Vasospasm — especially in subarachnoid hemorrhage
• Arterial Stenosis and Occlusion — including testing for recanalization post-treatment
• Monitoring for Sources of Emboli and Heart Shunts during Procedures — detecting microemboli
• Brain Death (Cerebral Circulatory Arrest) — often an adjunct modality
• Testing for Cerebrovascular Autoregulation — testing patients prior to carotid endarterectomy surgery
• Testing for Flow Changes with Cognitive Tasks — akin to MRI and fMRI

In our present case, the patient’s constellation of symptoms (sudden-onset loss of consciousness, horizontal and vertical gaze palsy, tetraparesis and bilateral miosis and coma) is highly indicative of a brainstem lesion most likely of vascular origin. The reticular activating system, a neural network in the brainstem that controls arousal, was presumably affected causing loss of consciousness. The gaze palsy may be explained by involvement of the midbrain and pons. If the cortico-spinal tracts were affected, then tetraparesis is possible. Lastly, a lesion involving hypothalamospinal fibers can triggering bilateral miosis (as in Horner’s syndrome). It is the basilar artery that supplies these territories and its occlusion is associated with the famed locked in syndrome.

In considering acute basilar artery occlusion, cerebral angiography is the gold standard diagnostic test where a neuroradiologist enters the femoral artery with a catheter and reverses his/her way up the brain to illustrate its circulation. However, since the patient’s symptoms resolved and angiography is not without risk including stroke, TCD was performed and revealed “dampened flow” suggestive of recanalization in the case of intracranial artery occlusion. In other words, the presumed embolus that once occluded the basilar artery underwent breakdown (fibrinolysis) and blood flow was re-established. Given that the neurological symptoms completely resolved in less than 24 hours from onset, we would label this event as a transient ischemic attack (TIA).

Diagnosis: Brainstem TIA most likely due to basilar artery embolism diagnosed by TCD

This case illustrates one of the great utilities of TCD — looking at the posterior-circulation of the brain (vertebral-basilar arteries) in acute events for diagnostic purposes. However, the latest application of TCD lies in treating disease, particularly stroke. The TCD ultrasound waves have shown to improve the delivery and penetration of rtPA (the FDA approved clot busting therapy for stroke) inside the clot. This utility, called sonothrombolysis, coupled with special catheters are being studied for acute strokes and look promising.

Case Reference

Nicoletti, G., Albano, G., Sanguigni, S., Tardi, S., Malferrari, G., Del Sette, M., Bruno, F., & Nicolai, A. (2010). Transient basilar artery occlusion monitored by transcranial color Doppler presenting with a spectacular shrinking deficit: a case report Journal of Medical Case Reports, 4 (1) DOI: 10.1186/1752-1947-4-13

Additional References

Kassab, M., Majid, A., Farooq, M., Azhary, H., Hershey, L., Bednarczyk, E., Graybeal, D., & Johnson, M. (2007). Transcranial Doppler: An Introduction for Primary Care Physicians The Journal of the American Board of Family Medicine, 20 (1), 65-71 DOI: 10.3122/jabfm.2007.01.060128

Rubiera M, & Alexandrov AV (2010). Sonothrombolysis in the management of acute ischemic stroke. American journal of cardiovascular drugs : drugs, devices, and other interventions, 10 (1), 5-10 PMID: 20104930

We would like to hear from program participants and organizers, especially on the less-known or fewer-attended conferences. As major conferences draw near (e.g., AAN, AES), we will offer reminders, customized coverage, and interactive commentary from participants, presenters, and speakers.

Note to medical residents: Here is your opportunity to use your residency allotment/stipend for conference travel. Remember to plan early to arrange for call schedules and rotation requirements. Also, should you have an interesting case or a research project with any findings, your abstract submissions will undoubtedly be accepted in conference proceedings and/or poster-presentations at most venues.

List of 2010 Neurology, Neurosurgery, and Neuroscience Conferences (chronological):

Dates: January 08, 2010 – January 10, 2010
Conference: American Society for Peripheral Nerve (ASPN) 2010 Annual Meeting
Sponsor(s): American Society of Plastic Surgeons, American Association for Hand Surgery, American Society for Peripheral Nerve, American Society for Reconstructive Microsurgery
Venue/Location: Boca Raton Resort and Spa, Boca Raton, Florida, USA
Registration Fees: $375-$845 (ASPN conference only).

Dates: January 10, 2010 – January 15, 2010
Conference: Alzheimer’s Disease Beyond Abeta (A4)
Sponsor(s): Schering-Plough Research Institute, Takeda Pharmaceutical Company Limited
Venue/Location: Copper Mountain Resort, Copper Mountain, Colorado, USA
Registration Fees: $440-$765.

Dates: January 16, 2010 – January 19, 2010
Conference: The Surgical Management of Spinal Disorders
Sponsor(s): BroadWater
Venue/Location: The Pines Lodge, Beaver Creek, Colorado, USA
Registration Fees: $645-$945.

Dates: January 21, 2010 – January 22, 2010
Conference: Advances in Chronic Pain Management
Sponsor(s): British Journal of Hospital Medicine
Venue/Location: Institute of Physics, London, England, United Kingdom
Registration Fees: £345-£862.50.

Dates: January 22, 2010 – January 24, 2010
Conference: 3rd European Neurological Conference on Clinical Practices: Neurovascular and Neurodegenerative Diseases
Sponsor(s): Romanian Society of Neurology
Venue/Location: JW Marriot Grand Hotel, Bucharest, Romania
Registration Fees: €100-€650 (free for neurology residents).

Dates: January 24, 2010 – January 29, 2010
Conference: Neuronal Control of Appetite, Metabolism and Weight
Sponsor(s): Takeda Pharmaceutical Company Limited
Venue/Location: Keystone Resort, Keystone, Colorado, USA
Registration Fees: $440-$765.

Dates: January 28, 2010 – January 29, 2010
Conference: 5th Annual NeuroICU of the Future Symposium
Sponsor(s): UCLA Neurosurgery
Venue/Location: UCLA Neuroscience Research Building Auditorium, Los Angeles, California, USA
Registration Fees: $175-$500.

Dates: January 31, 2010 – February 04, 2010
Conference: 5th Mayo Clinic International Spine Symposium
Sponsor(s): Mayo School of Continuous Professional Development
Venue/Location: Mauna Lani Bay Hotel, Big Island, Kohala Coast, Hawaii, USA
Registration Fees: $895-$1295.

Dates: February 01, 2010 – February 02, 2010
Conference: 4th Drug Discovery for Neurodegeneration Conference
Sponsor(s): Alzheimer’s Drug Discovery Foundation
Venue/Location: Houstonian Hotel, Houston, Texas, USA
Registration Fees: $200-$650 (free for the media).

Dates: February 10, 2010 – February 12, 2010
Conference: 43rd Annual Recent Advances in Neurology
Sponsor(s): University of California, San Francisco School of Medicine
Venue/Location: Ritz Carlton Hotel, San Francisco, California, USA
Registration Fees: $300-$495.

Dates: February 15, 2010 – February 16, 2010
Conference: 6th Annual Update Symposium on Clinical Neurology and Neurophysiology
Sponsor(s): The Adams Super Center for Brain Studies Tel Aviv University, Joseph Sagol Neuroscience Center at the Chaim Sheba Medical Center, Tel Hashomer
Venue/Location: Metropolitan Hotel, Tel Aviv, Israel
Registration Fees: $550-$650.

Dates: February 16, 2010 – February 19, 2010
Conference: 6th Interventional/Neurointerventional Conference
Sponsor(s): Dotter Interventional Institute, Oregon Health & Science University
Venue/Location: Park City Marriott Hotel, Park City, Utah, USA
Registration Fees: $250-$650

Dates: February 18, 2010 – February 19, 2010
Conference: Dementias 2010: 12th National Dementias Conference
Sponsor(s): British Journal of Hospital Medicine
Venue/Location: Institute of Engineering and Technology, Savoy Place London, London, England, United Kingdom
Registration Fees: £450-£763.75.

Dates: February 18, 2010 – February 20, 2010
Conference: Neurology Update and Stroke Intensive 2010 [PDF]
Sponsor(s): University of Miami Miller School of Medicine
Venue/Location: The Alexander All-Suite Oceanfront Beach Hotel, Miami Beach, Florida, USA
Registration Fees: $315-$650.

Dates: February 22, 2010 – February 26, 2010
Conference: 48th Annual Dr. Kenneth M. Earle Memorial Neuropathology Review
Sponsor(s): Armed Forces Institute of Pathology
Venue/Location: Bethesda North Marriott Hotel & Conference Center, Bethesda, Maryland, USA
Registration Fees: $350-$1175.

Dates: February 26, 2010 – February 28, 2010
Conference: 3rd International Congress on Gait and Mental Function
Sponsor(s): Kenes
Venue/Location: Omni Shoreham Hotel, Washington, District of Columbia, USA
Registration Fees: $330-$700.

Dates: February 28, 2010 – March 04, 2010
Conference: International Congress XXIII on Endovascular Interventions
Sponsor(s): International Congress Foundation
Venue/Location: The Phoenician Resort, Scottsdale, Arizona, USA
Registration Fees: $550-$1250.

Dates: March 04, 2010 – March 06, 2010
Conference: 2nd East Mediterranean Epilepsy Congress
Sponsor(s): International Bureau for Epilepsy, International League Against Epilepsy
Venue/Location: Dubai, United Arab Emirates
Registration Fees: €100-€460.

Dates: March 05, 2010 – March 07, 2010
Conference: Neuroimaging and Head & Neck Radiology Update at Mount Tremblant
Sponsor(s): University of Ottawa’s Office of Continuing Medical Education
Venue/Location: Mount Tremblant, Quebec City, Canada
Registration Fees: $125-800 (CDN).

Dates: March 17, 2010 – March 20, 2010
Conference: 1st International Congress on Epilepsy, Brain & Mind
Sponsor(s):
Venue/Location: Prague, Czech Republic
Registration Fees: €100-€330 (free for invited speakers and student discount available).

Dates: March 19, 2010 – March 21, 2010
Conference: 3rd Vienna Symposium on Surgery of Peripheral Nerves
Sponsor(s): Vienna Medical Academy of Postgraduate Education & Research
Venue/Location: General Hospital Lecture Halls, Vienna, Austria
Registration Fees: €250-€400.

Dates: March 21, 2010 – March 25, 2010
Conference: 6th World Congress for Neurorehabilitation
Sponsor(s): World Federation for NeuroRehabilitation
Venue/Location: Hofburg, Vienna, Austria
Registration Fees: €170-€530.

Dates: March 22, 2010 – March 26, 2010
Conference: 20th Annual Rotman Research Institute Conference – The Frontal Lobes
Sponsor(s): Baycrest
Venue/Location: Toronto, Ontario, Canada
Registration Fees: $300-$1050 (CDN).

Dates: March 24, 2010 – March 27, 2010
Conference: 11th International Geneva/Springfield Symposium on Advances in Alzheimer Therapy
Sponsor(s): Southern Illinois University, School of Medicine, University of Geneva, Medical School Dept. of Rehabilitation and Geriatrics
Venue/Location: Geneva, Switzerland
Registration Fees: $180-$980.

Dates: March 25, 2010 – March 27, 2010
Conference: European Association of Neurosurgical Societies (EANS) Annual Meeting 2010)
Sponsor(s): Kenes
Venue/Location: Groningen, Netherlands
Registration Fees: €250-€480.

Dates: March 25, 2010 – March 26, 2010
Conference: Olfaction and Issues 2010
Sponsor(s): Takayama
Venue/Location: Paris, France
Registration Fees: €395-€895.

Dates: March 25, 2010 – March 28, 2010
Conference: Advances in Pediatric Neuropsychology: From Toddlers Through School-Aged Children
Sponsor(s): UC San Diego School of Medicine
Venue/Location: Hilton San Diego Resort, San Diego, California, USA
Registration Fees: $195-$445.

Dates: April 10, 2010 – April 17, 2010
Conference: 62nd Annual Meeting of the American Academy of Neurology (AAN) 2010
Sponsor(s): American Academy of Neurology
Venue/Location: Metro Toronto Convention Centre, Toronto, Ontario, Canada
Registration Fees: $70-$645 (free for students).

Dates: April 11, 2010 – April 15, 2010
Conference: Towards Defining the Pathophysiology of Autistic Behavior (Z4)
Sponsor(s): Keystone Symposia
Venue/Location: Snowbird Resort, Snowbird, Utah, USA
Registration Fees: $390-$715.

Dates: April 11, 2010 – April 15, 2010
Conference: Synapses: Formation, Function and Misfunction (Z3)
Sponsor(s): Keystone Symposia
Venue/Location: Snowbird Resort, Snowbird, Utah, USA
Registration Fees: $390-$715.

Dates: April 15, 2010 – April 16, 2010
Conference: 7th Dutch Society of Neuroradiology International Conference Course
Sponsor(s): University Medical Center Groningen
Venue/Location: University Medical Center Groningen, Groningen, Netherlands
Registration Fees: €130-€470.

Dates: April 20, 2010 – April 23, 2010
Conference: International Forum on Quality and Safety in Health Care
Sponsor(s): BMJ Publishing Group Ltd.
Venue/Location: Nice, France
Registration Fees: £382-£1396

Dates: April 23, 2010 – April 25, 2010
Conference: International Congress on Neurology and Rehabilitation (ICNR) 2010
Sponsor(s): Maharashtra Association of Neurology, World Federation for NeuroRehabilitation
Venue/Location: Hotel Holiday Inn, Goa, India
Registration Fees: 3,000-12,000 (INR).

Dates: May 01, 2010 – May 06, 2010
Conference: 78th AANS Annual Meeting
Sponsor(s): American Association of Neurological Surgeons
Venue/Location: Philadelphia Marriott, Philadelphia, Pennsylvania, USA
Registration Fees: $150-$750 ($100 for students and neurosurgery resident members).

Dates: May 02, 2010 – May 07, 2010
Conference: 11th International Child Neurology Congress (ICNC) 2010
Sponsor(s): Egyptian Society of Child Neuropsychiatry
Venue/Location: Grand Hyatt Hotel, Cairo, Egypt
Registration Fees: €380-€650.

Dates: May 05, 2010 – May 08, 2010
Conference: The American Academy of Neurological and Orthopaedic Surgeons 34th Annual Scientific Meeting & Workshops
Sponsor(s): American Academy of Neurological and Orthopaedic Surgeons
Venue/Location: The Brown Palace, Denver, Colorado, USA
Registration Fees: ?

Dates: May 11, 2010 – May 14, 2010
Conference: Association of British Neurologists (ABN) Annual Meeting
Sponsor(s): Association of British Neurologists
Venue/Location: Bournemouth International Centre, Bournemouth, England, United Kingdom
Registration Fees: £100-£300.

Dates: May 12, 2010 – May 15, 2010
Conference: 12th Congress of the European Federation of Autonomic Societies (EFAS)
Sponsor(s): European Federation of Autonomic Societies
Venue/Location: Giardini Naxos, Taormina, Italy
Registration Fees: €235-€525.

Dates: May 15, 2010 – May 20, 2010
Conference: 48th American Society of Neuroradiology (ASNR 2010) Annual Meeting
Sponsor(s): American Society of Neuroradiology
Venue/Location: Hynes Convention Center, Boston, Massachusetts, USA
Registration Fees: $185-$1600.

Dates: May 19, 2010 – May 22, 2010
Conference: 3rd International Epilepsy Colloquium: Surgery of Extratemporal Lobe Epilepsy [PDF]
Sponsor(s): Case Western Reserve University
Venue/Location: Renaissance Cleveland Hotel, Cleveland, Ohio, USA
Registration Fees: ?

Dates: May 25, 2010 – May 28, 2010
Conference: 19th European Stroke Conference (ESC)
Sponsor(s): European Stroke Organisation
Venue/Location: Barcelona, Spain
Registration Fees: €300-€700 (free for students).

Dates: May 26, 2010 – May 29, 2010
Conference: 12th Congress of the Pan Arab Union of Neurological Societies
Sponsor(s): Syrian Society of Neurosciences
Venue/Location: Damascus, Syrian Arab Republic
Registration Fees: €100-€250.

Dates: May 27, 2010 – May 30, 2010
Conference: 3rd International Congress on Neuropathic Pain (NeuPSIG 2010)
Sponsor(s): Kenes
Venue/Location: Athens, Greece
Registration Fees: €150-€495.

Dates: May 27, 2010 – May 28, 2010
Conference: Alzheimer’s Disease: Update on Research, Treatment, and Care
Sponsor(s): Shiley-Marcos Alzheimer’s Disease Research Center, UCSD
Venue/Location: Omni San Diego Hotel, San Diego, California, Guyane
Registration Fees: $299-$425 (discount for UCSD affiliates).

Dates: May 31, 2010 – June 01, 2010
Conference: 2nd International Conference – Advances in Clinical Neuroimmunology
Sponsor(s): Biuro Organizacji Konferencji i Zjazdów
Venue/Location: Gdansk, Poland
Registration Fees: €200-€300.

Dates: June 05, 2010 – June 09, 2010
Conference: Sleep 2010
Sponsor(s): Associated Professional Sleep Societies
Venue/Location: San Antonio, Texas, USA
Registration Fees: ?

Dates: June 08, 2010 – June 11, 2010
Conference: Canadian Neurological Sciences Federation 45th Annual Congress
Sponsor(s): Canadian Neurological Sciences Federation
Venue/Location: Quebec City, Canada
Registration Fees: ?

Dates: June 13, 2010 – June 17, 2010
Conference: 14th International Congress of Parkinson’s Disease and Movement Disorders
Sponsor(s): The Movement Disorder Society
Venue/Location: Sheraton Buenos Aires Hotel and Convention Center, Buenos Aires, Argentina
Registration Fees: $300-$850.

Dates: June 14, 2010 – June 17, 2010
Conference: The 2nd Joint Symposium of the International and National Neurotrauma Societies 2010
Sponsor(s): National Neurotrauma Society, Virginia Commonwealth University School of Medicine
Venue/Location: Paris Las Vegas Hotel, Las Vegas, Neveda, USA
Registration Fees: $225-$700.

Dates: June 19, 2010 – June 23, 2010
Conference: 20th Meeting of the European Neurological Society
Sponsor(s): European Neurological Society
Venue/Location: Berlin, Germany
Registration Fees: ?

Dates: June 20, 2010 – June 23, 2010
Conference: ISPNO 2010 – 14th International Symposium on Pediatric Neuro-Oncology
Sponsor(s): Vienna Medical Academy
Venue/Location: Vienna, Austria
Registration Fees: €240-€595.

Dates: June 25, 2010 – June 26, 2010
Conference: Aging and Sleep 2010
Sponsor(s): International Association of Sleep Research in Gerontology
Venue/Location: Lyon, France
Registration Fees: €150-€290.

Dates: June 25, 2010 – June 28, 2010
Conference: NeuroTalk 2010 – From Nervous Functions to Treatment
Sponsor(s): BIT Life Sciences
Venue/Location: Singapore Expo Convention and Exhibition Center, Singapore.
Registration Fees: $549-$1,799.

Dates: June 27, 2010 – July 01, 2010
Conference: 9th European Congress on Epileptology
Sponsor(s): International Bureau for Epilepsy, International League Against Epilepsy
Venue/Location: Rhodes, Greece
Registration Fees: €150-€720.

Dates: July 03, 2010 – July 07, 2010
Conference: 7th Federation of European Neurological Societies (FENS) Forum of European Neuroscience
Sponsor(s): European Federation of Neurological Societies
Venue/Location: Amsterdam, Netherlands
Registration Fees: €100-€475.

Dates: July 10, 2010 – July 15, 2010
Conference: 7th International Congress on Neuroendocrinology
Sponsor(s): International Neuroendocrine Federation
Venue/Location: Rouen, France
Registration Fees: €250-€500 (free for select students).

Dates: July 10, 2010 – July 15, 2010
Conference: 10th Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD)
Sponsor(s): Alzheimer’s Association
Venue/Location: Honolulu, Hawaii, USA
Registration Fees: ?

Dates: July 30, 2010 – July 31, 2010
Conference: 4th Annual Brain Endoscopy Course
Sponsor(s): University at Buffalo Neurosurgery, State University of New York
Venue/Location: Lecture & Practical Lab, Buffalo, New York, USA
Registration Fees: $500 (free for residents and fellows).

Dates: August 04, 2010 – August 07, 2010
Conference: American Society of Electroneurodiagnostic Technologists (ASET) 2010 Annual Conference
Sponsor(s): American Society of Electroneurodiagnostic Technologists
Venue/Location: Kentucky International Convention Center, Louisville, Kentucky, USA
Registration Fees: $285-$600.

Dates: August 25, 2010 – August 27, 2010
Conference: 12th European Congress on Epilepsy and Society
Sponsor(s): International Bureau for Epilepsy, International League Against Epilepsy
Venue/Location: Porto, Portugal
Registration Fees: ?

Dates: August 28, 2010 – September 01, 2010
Conference: 23rd Congress of The European College of Neuropsychopharmacology (ECNP)
Sponsor(s): The European College of Neuropsychopharmacology
Venue/Location: Amsterdam, Netherlands
Registration Fees: €60-€950 (waived for poster presenters).

Dates: September 11, 2010 – September 15, 2010
Conference: XVIIth International Congress of Neuropathology
Sponsor(s): Austrian Society of Neuropathology
Venue/Location: Salzburg Congress, Salzburg, Austria
Registration Fees: ?

Dates: September 12, 2010 – September 16, 2010
Conference: 14th International Conference on Intracranial Pressure and Brain Monitoring
Sponsor(s): European Federation of Neurological Societies
Venue/Location: Tübingen, Germany
Registration Fees: €250-€450.

Dates: September 14, 2010 – September 18, 2010
Conference: 20th Congress of the European Sleep Research Society
Sponsor(s): European Sleep Research Society
Venue/Location: Lisbon, Portugal
Registration Fees: €200-€550.

Dates: September 25, 2010 – September 28, 2010
Conference: 14th Congress of the European Federation of Neurological Societies (EFNS 2010)
Sponsor(s): European Federation of Neurological Societies
Venue/Location: Geneva, Switzerland
Registration Fees: €295-€635.

Dates: September 28, 2010 – October 01, 2010
Conference: 2nd World Parkinson Congress
Sponsor(s): World Parkinson Coalition
Venue/Location: Glasgow, Scotland, United Kingdom
Registration Fees: £125-£500.

Dates: October 01, 2010 – October 04, 2010
Conference: 6th international Symposium on Neuroprotection and Neurorepair
Sponsor(s): Fraunhofer
Venue/Location: Yachthafenresidenz Hohe Düne, Rostock, Germany
Registration Fees: ?

Dates: October 04, 2010 – October 09, 2010
Conference: XIX Symposium Neuroradiologicum – The World Congress of Neuroradiology
Sponsor(s): University of Bologna
Venue/Location: Bologna, Italy
Registration Fees: ?

Dates: October 13, 2010 – October 16, 2010
Conference: ECTRIMS/RIMS 2010: 26th Congress of the European Committee for Treatment and Research in Multiple Sclerosis and the 15th Conference of Rehabilitation in Multiple Sclerosis
Sponsor(s): European Committee for Treatment and Research in Multiple Sclerosis
Venue/Location: Copenhagen, Denmark
Registration Fees: ?

Dates: October 13, 2010 – October 16, 2010
Conference: 7th World Stroke Congress, organized by the World Stroke Organization (WSO)
Sponsor(s): Kenes
Venue/Location: Seoul, Republic of Korea
Registration Fees: $50-$875.

Dates: October 26, 2010 – October 30, 2010
Conference: 10th International Congress of Neuroimmunology
Sponsor(s): International Society of NeuroImmunology
Venue/Location: Palau de Congressos de Barcelona, Barcelona, Spain
Registration Fees: ?

Dates: October 28, 2010 – November 02, 2010
Conference: 29th International Congress of Clinical Neurophysiology
Sponsor(s): International Federation of Clinical Neurophysiology
Venue/Location: Portopia Hotel, Kobe, Japan
Registration Fees: JPY 20,000-75,000.

Dates: October 28, 2010 – October 31, 2010
Conference: The 4th World Congress on Controversies in Neurology (CONy)
Sponsor(s): ComtecMed
Venue/Location: Barcelona, Spain
Registration Fees: €385-€590.

Dates: October 28, 2010 – October 31, 2010
Conference: European Headache and Migraine Trust International Congress (EHMTIC 2010)
Sponsor(s): Kenes
Venue/Location: Nice, France
Registration Fees: €225-€650.

Dates: October 28, 2010 – October 31, 2010
Conference: 14th World Society of Pain Clinicians Congress (WSPC 2010)
Sponsor(s): Kenes
Venue/Location: Beijing, China
Registration Fees: ?

Dates: October 31, 2010 – November 04, 2010
Conference: 38th Annual Meeting of the International Society for Pediatric Neurosurgery
Sponsor(s): International Society for Pediatric Neurosurgery
Venue/Location: Jeju, Republic of Korea
Registration Fees: ?

Dates: November 09, 2010 – November 12, 2010
Conference: 7th Interdisciplinary World Congress on Low Back & Pelvic Pain
Sponsor(s): University of California at San Diego
Venue/Location: Hyatt Regency Century Plaza, Los Angeles, California, USA
Registration Fees: ?

Dates: November 13, 2010 – November 17, 2010
Conference: Neuroscience 2010
Sponsor(s): Society for Neuroscience
Venue/Location: San Diego, California, USA
Registration Fees: ?

Dates: December 03, 2010 – December 07, 2010
Conference: 64th Annual Meeting of the American Epilepsy Society
Sponsor(s): American Epilepsy Society
Venue/Location: San Antonio, Texas, USA
Registration Fees: ?

Dates: December 09, 2010 – December 12, 2010
Conference: The 7th International Congress on Mental Dysfunctions & Other Non-Motor features in Parkinson’s Disease (MDPD 2010)
Sponsor(s): Kenes
Venue/Location: Barcelona, Spain
Registration Fees: €300-€680.

Dates: December 16, 2010 – December 19, 2010
Conference: 59th Annual Conference of Neurological Society of India (Neurocon) and Congress of Neurological Surgeons (CNS)
Sponsor(s): Neurological Society of India
Venue/Location: Birla Science and Technology Centre, Jaipur, India
Registration Fees: ?

“Time is brain” in the treatment of stroke. If a quick and accurate diagnosis is not made, patients can experience serious complications, including permanent disability or death. Typical stroke symptoms include dizziness, one-sided weakness, numbness, and speech problems. The gold standard for stroke diagnosis is an MRI, but these are costly, time-consuming exams, and the wait time may be several hours in some cases, potentially leading to loss of brain function and limiting treatment options. Now, researchers have shown that three simple eye-movement tests are more accurate than an MRI, anyway. The study included 101 patients complaining of severe dizziness; all had at least one risk factor for stroke. More than half presented to the emergency room for treatment, while others were already admitted in the hospital. The eye movement test accurately diagnosed all of the strokes and all but one of the inner-ear conditions, while MRI misdiagnosed 12% of the strokes.

Patients were assessed and evaluated by neuroimaging within 72 hours of the onset of dizziness. The three-step eye exam is known as HINTS (Head-Impulse-Nystagmus-Test-of-Skew) and evaluates (1) the ability of the patient to keep the eyes stable as the head is rotated rapidly side-to-side, (2) the jerkiness of eye movements as the patient follows the doctor’s finger left and right, and (3) the vertical misalignment of the eyes. Patients also underwent an MRI. If the eye movement tests indicated a stroke, but the MRI did not, patients received a follow-up MRI. Overall, the HINTS exam was 100% sensitive and 96% specific for stroke, correctly diagnosing all 69 ischemic strokes and 24 out of 25 inner ear problems among the study population. The initial MRI scan misdiagnosed 8 of the 69 stroke patients, but these were confirmed with repeat scans.

The current study is limited by its small size and restricted population, but the results are promising. While the health care system searches for ways to contain costs but improve quality of care, a quick and easy -– and basically free — eye exam could prove useful in diagnosing stroke victims, especially when costly MRI’s could fail to diagnose stroke in a timely matter. More research is needed before the results of this latest study can be generalized to a larger population, but it is possible that physicians could move back to an age of simple, straightforward bedside diagnosis and stop relying on expensive diagnostic equipment.

References

Newman-Toker, D., & Pronovost, P. (2009). Diagnostic Errors–The Next Frontier for Patient Safety JAMA: The Journal of the American Medical Association, 301 (10), 1060-1062 DOI: 10.1001/jama.2009.249

Kruschinski, C., & Hummers-Pradier, E. (2008). Diagnosing Dizziness in the Emergency and Primary Care Settings Mayo Clinic Proceedings, 83 (11), 1297-1298 DOI: 10.4065/83.11.1297-a

Newman-Toker, D., Kattah, J., Alvernia, J., & Wang, D. (2008). Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis Neurology, 70 (Iss 24, Part 2), 2378-2385 DOI: 10.1212/01.wnl.0000314685.01433.0d

Kattah, J., Talkad, A., Wang, D., Hsieh, Y., & Newman-Toker, D. (2009). HINTS to Diagnose Stroke in the Acute Vestibular Syndrome. Three-Step Bedside Oculomotor Examination More Sensitive Than Early MRI Diffusion-Weighted Imaging Stroke DOI: 10.1161/STROKEAHA.109.551234

Researchers at the Feinstein Institute identified two specific brain pathways that influence the severity of dystonia symptoms. All individuals who carry the mutations and symptoms for dystonia have an abnormal pathway between the cerebellum and the thalamus, but a normal second pathway between the thalamus and the cortex. Indeed, it is the people who carry the mutations but have no symptoms of dystonia that have this abnormal second pathway. Scientists believe that the different brain pathways are formed at an early stage of brain development. This phenomenon gives a whole new meaning to the logical fallacy of “two wrongs make a right.” When one wrong is committed (genetic mutation), another wrong will cancel it out (the abnormal thalamus and cortex connection).

The finding can bring many implications. For one thing, the study could lead to new treatments and prevention options for patients with dystonia. Additionally, it could provide better understanding to other neurological illnesses, especially those involving movement, such as the more popular, Parkinson’s disease. Conceivably, the abnormal brain wiring may be similar to the electrical stimulation used in treating movement disorders. The preferred surgical treatment for these disorders is the chronic electrical stimulation of the brain, known as deep brain stimulation (DBS). It has been shown that DBS improves motor symptoms, although we do not exactly know how stimulation works in a physiological level. Do abnormal brain circuits between the thalamus and cortex act like the DBS therapy? Does the irregular wiring of the brain, due to developmental problems, improve dystonia, in the same way as our known therapies?

The developmental changes in brain wiring could be the same as foreign electrical stimulation, in that they both modify transmission in movement through an unknown mechanism.

Reference

Johnson MD, Miocinovic S, McIntyre CC, & Vitek JL (2008). Mechanisms and targets of deep brain stimulation in movement disorders. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 5 (2), 294-308 PMID: 18394571

One of the strongest divides in thinking across cultures is the different perspectives about ‘the individual’ in East-Asian and Western-European/American cultures. Western-Europeans and Americans emphasize individuals as unique entities from others, while East-Asian cultures emphasize the individual in relation to other people and their environmental context. These viewpoints can be traced to the cultures’ unique philosophies concerning the individual. After all, Descartes noted “I think therefore I am,” which he used to prove that if one wonders whether or not they exist, they therefore must exist because they are capable of this and other such internal thoughts. Confucian philosophy, on the other hand, emphasizes that a person cannot fully exist alone, and that a person only reaches the highest form of existence once he/she mentally severs the divide between themselves, others and the environment.

Though these distinctions seem esoteric, they do in fact permeate contemporary psychology. For example, a classic finding in western psychology is that people are better at remembering adjectives related to themselves than adjectives related to a family member or strangers. When this study was replicated in China, however, Chinese participants remembered adjectives related to themselves and a family member equally well.

Based on the above and other similar findings in psychological research conducted across cultures, cognitive neuroscientists questioned whether the brain would respond differently to information about oneself, a family member, and strangers across individualistic and collectivist cultures. Past studies in American samples found that the ventral medial prefrontal cortex (vmPFC) shows stronger activation to viewing adjectives that describe the individual compared to adjectives describing a family member and strangers, highlighting the vmPFC’s role in representing the individual.  In a Chinese sample, however, the vmPFC is strongly active when participants view adjectives about themselves and a family member, though not for strangers.

Taken together, these divergent findings fit with each cultures’ conceptualization of the individual — independent in Western-European/American cultures, and intertwined with others in your environment in East-Asian cultures. Of course, this research should not be used to over-generalize differences in thinking across cultures. Indeed, there is also a great deal of research highlighting the commonalities in cognition across cultures. That said, acknowledging the subtle differences may help people in contemporary society — which is increasingly culturally diverse — appreciate the nuances in thought and behavior among the people we come across in our day to day lives.

References

Klein, S.B., Loftus, J. & Burton, H.A., (1989). Two self-reference effects: the importance of distinguishing between self-descriptiveness judgments and autobiographical retrieval in self-referent encoding. Journal of Personality and Social Psychology, 56, 853-865.

Qi, J., & Zhu, Y. (2002). Self-reference effect of Chinese college students. Psychological Science (in Chinese), 25, 275-278.

ZHU, Y., ZHANG, L., FAN, J., & HAN, S. (2007). Neural basis of cultural influence on self-representation NeuroImage, 34 (3), 1310-1316 DOI: 10.1016/j.neuroimage.2006.08.047

There is considerable evidence that age is the single strongest risk factor for the development of POCD – outside of actually having surgery, of course! This means that the older a surgery patient is, the more likely they are to develop POCD. There is also evidence that prior cognitive impairment, lower education, and pre-surgery depression also place adults at risk for POCD following both cardiac and major non-cardiac surgery. Perioperative events (e.g., strokes and other neurological events) and postoperative pain are additional risk factors for POCD.

As mentioned previously, age is the most consistent predictor of POCD. Those who are older are more susceptible to POCD and for longer periods after surgery. For patients undergoing coronary artery bypass graft (CABG) surgery, the best studies show that 33% of patients have POCD at one week post-surgery. This rate falls to 4% at three months. Other studies show rates as high as 50-60% at one week and 13-20% at three months. However, these have been criticized for less-than-ideal methods. For major non-cardiac surgeries, the trend with POCD in older adults is similar, if with somewhat lower rates. For most studies, about 20% of noncardiac older patients exhibit POCD at one week following surgery with virtually no POCD at three months. However, some studies show higher rates (up to 50% at hospital discharge and 30% at three months post-discharge) of POCD in older adults following noncardiac surgery.

Past research showed widely variable rates in POCD. This inconsistency is due to major variations in the methods. Many researchers focused solely on subjective cognitive complaints or intelligence or general cognition as measured by a screening test such as the Mini Mental Status Examination. The problem is that these measures are insensitive to subtler cognitive changes. Intelligence tests generally have high test-retest reliability even with fairly major cerebral events (in other words, it usually takes major damage to the brain to significantly affect general intelligence). Brief general cognitive tests are usually quite reliable over time but they are insensitive to change because they are so shallow and broad. Minor or specific declines are important to measure because they can cause impairment in everyday functioning.

Even though POCD research has varied in quality, researchers and doctors are confident that POCD is a real effect. Any older adults (POCD researchers typically use age 60 as the threshold for “old adulthood”) who are undergoing major cardiac or non-cardiac surgery should be aware that mild to moderate cognitive deficits can occur following surgery. The cause is generally unknown. The good news is that there is little evidence that these deficits in general last longer than a few months.

References

&NA;, . (2006). The Role of Postoperative Analgesia in Delirium and Cognitive Decline in Elderly Patients Survey of Anesthesiology, 50 (5), 263-264 DOI: 10.1097/01.sa.0000238941.61799.e6

Lewis, M., Maruff, P., Silbert, B., Evered, L., & Scott, D. (2006). Detection of Postoperative Cognitive Decline After Coronary Artery Bypass Graft Surgery is Affected by the Number of Neuropsychological Tests in the Assessment Battery The Annals of Thoracic Surgery, 81 (6), 2097-2104 DOI: 10.1016/j.athoracsur.2006.01.044

&NA;, . (2008). Predictors of Cognitive Dysfunction After Major Noncardiac Surgery Survey of Anesthesiology, 52 (3), 135-136 DOI: 10.1097/01.SA.0000307885.46705.f5

&NA;, . (2007). Postoperative Cognitive Dysfunction After Noncardiac Surgery Survey of Anesthesiology, 51 (6) DOI: 10.1097/sa.0b013e31815c0ff1

Rasmussen, L. S., Larsen, K., Houx, P., Skovgaard, L. T., Hanning, C. D., & Moller, J. T. (2001). The assessment of postoperative cognitive dysfunction. Acta Anaesthesiol Scand, 45, 275-289.

Based on brain imaging studies, the medial prefrontal cortex (MPFC) seems to play a pivotal role in the self. For example, the MPFC is more active when participants make judgments about themselves, compared to other semantic judgments (i.e. I am a good friend vs. you need water to live). Similarly, MPFC is recruited when subjects retrieve memories about themselves compared to a fictional character. Interestingly, the MPFC is also recruited when participants passively rest while undergoing an fMRI scan. Until recently, most fMRI scans required that participants perform cognitive tasks during scanning, and researchers mapped statistically significant brain activation to cognitive components of the task. However, a recent trend in brain imaging is to identify the neural circuitry active during humans’ resting state, or when they are not performing tasks and instead are free to think about whatever they want. During such scans, a few brain areas are active, including the MPFC. It has been hypothesized that the MPFC activation represents the ongoing self-related processing during a conscious state, orchestrating the ‘authorship’ of our daily experiences.

However, such interpretations are controversial. Most notably, skeptics argue that 2identifying the neuroanatomy during rest does not reveal anything about the cognitive content that corresponds with it. Although previous studies identify the MPFC as crucial in self judgments and reflection, this is not enough evidence to suggest that during our day-to-day experience, it is the hub unifying and personalizing our conscious experience.

Skepticism aside, the findings reflect the reality that cognitive neuroscience is beginning to address questions previously believed to be unanswerable. In his recent book, “Proust was a Neuroscientist,” Jonah Lehrer elegantly draws connections between the philosophies of great artists that now, hundreds of years later, garner empirical support from the neurosciences. Virginia Woolf, one of the profiled artists, attempted to translate the contents of her resting state into written narration. Today, scientists are trying to identify the brain mechanisms underlying this narrative content. As Lehrer argues, it may be that in this pursuit, science could learn from art, and hopefully create studies that better isolate the content of the self and it’s related brain architecture.

References

Gusnard, D. (2001). Medial prefrontal cortex and self-referential mental activity: Relation to a default mode of brain function Proceedings of the National Academy of Sciences, 98 (7), 4259-4264 DOI: 10.1073/pnas.071043098

Kelley, W.M., Macrae, C.N., Wyland, C.L., Caglar, S., Inati, S. & Heatherton, T. F. (2002). Finding the self? An event-related fMRI study. Journal of Cognitive Neuroscience, 14(5), 785-794.

Pfeifer, J., Lieberman, M., & Dapretto, M. (2007). ?I Know You Are But What Am I?!?: Neural Bases of Self- and Social Knowledge Retrieval in Children and Adults Journal of Cognitive Neuroscience, 19 (8), 1323-1337 DOI: 10.1162/jocn.2007.19.8.1323

The human brain is exceedingly complex. There are about 100 billion neurons within the human central nervous system (brain and spinal cord) with an estimated 100 trillion synapses (connections between neurons). However, the brain grows and prunes synapses constantly, so that number is fluid. In addition there are probably 1 trillion glial cells that serve as support among other roles to the neurons. This web of densely-connected cells produces all behavior, thoughts, movements, and emotions. The human brain is the most complex organ on earth and one of the most complex things in the universe, especially gram for gram.

Because it is so complex, the brain does not always function properly. Sometimes various chemicals or substances act as teratogens, which interfere with the normal development of a fetus and often result in serious and permanent neural deficits, such as fetal alcohol syndrome. Other times, genetic abnormalities like trisomy 21 produce Down’s Syndrome. Other abnormal brain developmental pathways can result in anything from mild, even grossly unnoticeable deficits, to death. For the most part and for most people, however, the human brain develops normally and functions as nature intended.

The researchers at the Blue Brain Project are working towards simulating the entire human brain with its billions of neurons and trillions of synapses. How feasible is the project? Currently it takes the equivalent of one computer — one microprocessor — to model a single neuron. The goal of the project is to accurately model individual neocortical columns (a cylindrical volume with a diameter of 0.5 mm and height of 2 mm that contains about 10,000 neurons) in series and then extrapolate that model out to the entire cortex, which should simplify the overall model and reduce needed computing power. Currently to model a single neocortical column the researchers utilize a supercomputer with 10,000 processors. As you can imagine, modeling the entire brain of 100 billion neurons is a mind-boggling task. However, with advances in computer hardware and software, we are moving closer to such models, especially as researchers are able to simplify the overall brain model by modeling it at a more macro level than individual neurons.

One reason the researchers give for wanting to model the entire human brain is so they can hopefully better understand brain diseases and abnormal brain development. Imagine being able to simulate a brain of someone with Down’s Syndrome, or better yet, the development of a brain of someone with Down’s Syndrome! We could then hopefully understand exactly what goes wrong and when and try to correct it genetically or through some other means. Or, researchers could model the brain of an autistic child to try and understand how it functions. There are myriad possibilities.

However, is creating a complete model of the human brain ethical? Would the model develop into a self-aware and potentially sentient entity? If the model has self-awareness would it be ethical or moral to turn off the simulation? Would the model or simulated brain be considered alive? What are the potential pitfalls, if any, to creating a fully-functional brain simulation? What happens if treatments or policies are created based on the simulated brain and those treatments prove deleterious or the models miscalculated? Could we plug a simulated brain into a body and create a new “person”?

I think this research is exciting and ground-breaking should it come to full fruition. On the other hand, I do not believe we should proceed without serious ethical discussions. This is not just cloning a sheep or a rat, this is creating a full simulation of the human brain that would ostensibly grow, develop, feel, and mature.

What is the brain computer interface (BCI)?

BCI encompasses a wide range of technological ideas that allow our brains to directly communicate and control external devices via a computer. It is well-established that our brain transmits signals via electrical impulses (whether it be signals that control limb movement or signals that encode the color of a flower). These electrical impulses are recorded by electrodes placed either on the scalp or within the brain tissue, and converted into binary signals that can be interpreted by computer programs. These computer programs use the decoded signal to control a wheelchair, a mouse on a computer screen or even a robotic arm that can grasp objects. Alternatively, the BCI can work in the opposite direction. Signals generated by a computer can be converted to electrical impulses and sent to the brain. The brain then interprets these impulses as a smell, a color, a movement or even a visual outline. Either way, the BCI is the first technology to directly utilize the electrical signals generated by the brain tissue to control external devices and vice versa.

The importance of BCI devices

At first thought, spending large amounts of money for a device that can be thought of as an interactive video game may seem superfluous. However, this technology may afford severely disabled persons the opportunity to communicate while simultaneously restoring their independence and mobility. Conditions such as amyotrophic lateral sclerosis (ALS or more commonly Lou Gehrig’s Disease), muscular dystrophy and spinal cord injury often leave individuals without the ability to move, while their cognitive function is unaffected. Persons with ALS, muscular dystrophy and spinal cord injury are still capable of creating motor plans within the cerebral cortex, although the signals are not transmitted to the muscles. Scientists are working to capture the signals created in the cortex and utilizing them to control external devices.

BCI – where are we now?

Although the concept has been around for nearly 40 years, scientists have made significant advancements in BCI technology over the past 10 years. BCI technology has recently been used to drive a robotic arm for self-feeding in a monkey. The animal was initially trained using a joystick to control the robotic arm. The joystick was eventually weaned and motor activity from the cortex was recorded via an implanted electrode. Signals from the cortex were decoded in real-time to control the movement of the robotic arm. The monkey was then able to feed himself via the robotic arm, using only his conscious thought.

While these trials are impressive, they are not the focus of the majority of BCI research. The next most important step is creating devices that improve functional ability in humans with disabilities. Researchers at Brown University are currently conducting clinical trials in humans with the ultimate goal of restoring “the communication, mobility and independence of people with severe paralysis.” BCI devices that acquire signals through EEG technology or implanted invasive techniques are currently being used by disabled individuals to control wheelchairs, type on a computer and even send text messages.

While the media has glorified the use of BCI devices, there are many limitations to the current BCI technology. In order to make BCI devices a tangible reality for a large portion of persons with disabilities, specific roadblocks need to be passed. The current technology permits only a few words per minute to be “typed” using BCI devices. The speed and accuracy of the decoding and signal analysis would need to be greatly enhanced to permit real-time communication. The current technology is also limited the BCI control of robotic extremities to small movements in a confined space. For a practical real-world application, the methodology and timing of signal extraction would need to be improved vastly beyond the present day possibilities. To date, much of the BCI devices are operated in research settings, with few practical devices being used outside of the laboratory. The goal of many scientists working on the technology is to create user-friendly devices that can be operated in an individual’s home without supervision. Presently, there are very few of these types of devices available.

The future of BCI

The future for BCI technology is boundless. This technology will offer future generations with disabilities the ability to communicate and interact with their environment in ways that we have viewed as impossible for millennia. In addition to restoring mobility to disabled persons, the technology also offers a potential method to overcome blindness, deafness and other sensory-affected conditions. In a world that is continually more “plugged in” day after day, the exchange of information has become nearly completely digital. This environment fosters the development of BCI technology and continues to expand the possibilities of BCI applications.

References

Hochberg, Leigh. Hope for people with paralysis. Brain-Computer Interface, Developed at Brown, Begins New Clinical Trial. Brown University Press Release. Jun 10 2009.

Birbaumer N. Brain-computer-interface research: coming of age. Clin Neurophysiol. Mar 2006;117(3):479-483. doi:10.1016/j.clinph.2005.11.002

Vaughan TM, Heetderks WJ, Trejo LJ, et al. Brain-computer interface technology: a review of the Second International Meeting. IEEE Trans Neural Syst Rehabil Eng. Jun 2003;11(2):94-109. doi:10.1109/TNSRE.2003.814799

Velliste M, Perel S, Spalding MC, Whitford AS, & Schwartz AB (2998). Cortical control of a prosthetic arm for self-feeding Nature, 453 (7198), 1098-1101 DOI: 10.1038/nature06996

In a seminal paper published in Science, Eisenberger, Lieberman, and Williams created feelings of social exclusion in participants using a task known as “Cyberball.” Cyberball is a virtual ball-tossing game, in which participants believe that they are playing catch with other players. However, there is an interesting caveat. Although participants believe they are playing in a live game, the game is in fact a predetermined simulation, in which after several tosses amongst all players, the virtual players systematically stop throwing the ball to the participant. The researchers found that when participants played Cyberball during a fMRI brain imaging scan, the dorsal anterior cingulate cortex (dACC), an area known to code for the negative sensations related to physical pain, activated when participants stopped being tossed the ball, as did the ventrolaterateral prefrontal cortex (VLPFC), an area known to regulate the distress associated with physical pain.

But how sweeping is it to say that social and physical pain share the same neuroanatomy? It is important to stress that the networks are not entirely overlapping. Physical pain researchers have already identified what they call, “the pain matrix,” or, the neuroanatomy that underpins the experience of physical pain. In addition to the dACC, this matrix includes the thalamus, insula, the cerebellum, frontal cortex and primary and secondary somatosensory cortices. Nevertheless, pain researchers suggest that there are two physiological aspects of pain — the actual somatosensory experience and the perceived unpleasantness of that experience. Importantly, a great deal of research has identified the dACC to play a role in the felt unpleasantness of physical pain, whereas the somatosensory cortex and insula are associated with the sensory discrimination of pain.

Why might the human brain rely on one region, the dACC, to compute the felt unpleasantness associated with both physical injury and social distress? One explanation relies on the observation that humans, and other mammals, rely on social bonds for survival. The unpleasantness associated with physical injury acts like an alarm notifying the animal of ensuing threat to survival. Through the course of evolution, the same alarm system may have been hijacked to also notify the mammal of threat to their social bond, and hence survival. Indeed, young mammals’ distress vocalizations in response to separation from their caregivers rely on functioning cingulate gyrus, and destroying the ACC in macaques lends reduced affiliating social behavior.

All in all, it seems that feeling “hurt” can apply to both physical and social injury, and the feelings similarly rely on activation of the dACC. Although words may never break your bones, words and other forms of social rejection, could surely hurt you.

References

Eisenberger, N. (2003). Does Rejection Hurt? An fMRI Study of Social Exclusion Science, 302 (5643), 290-292 DOI: 10.1126/science.1089134

Hariri, A., Bookheimer, S., & Mazziotta, J. (2000). Modulating emotional responses: effects of a neocortical network on the limbic system. NeuroReport, 17(11), 43-48.

Panksepp, J. (1998). Affective neuroscience: The foundations of human and animal emotions. Oxford University Press.

MacLean, P.D. (1993). Perspectives on cingulate cortex in the limbic system. In Neurobiology of Cingulate Cortex and Limbic Thalamus: A Comprehensive Handbook (Vogt, B.A. and Gabriel, M., eds), pp. 1-15, Birkhauser.

Hadland, K. (2003). The effect of cingulate lesions on social behaviour and emotion Neuropsychologia, 41 (8), 919-931 DOI: 10.1016/S0028-3932(02)00325-1