ON THE BRAIN - Harvard Medical School
ON THE BR AI Nthe harvard mahoney neuroscience institute letterHumor, Laughter, and Those Aha MomentsSpring 2010Vol. 16, No. 2Acontentsd u c k wa l k s into a bar. . . . It’s a joke!Hearing just the first few words, yourbrain springs into action. The path ofneuronal activity is a complex one that enlistsvarious brain regions: the frontal lobe, to processthe information; the supplementary motor area, totap learned experience to direct motor activitiessuch as the movements associated with laughter;and the nucleus accumbens, to assess the pleasureof the story and the reward that the “aha!” brings.When the punch line hits home, your heart raterises, you jiggle with mirth, and your brain releases“feel good” neurotransmitters: dopamine, serotonin,and an array of endorphins.Jokes work because they defy expectations. Thesurprise aspect of these tales kicks in the frontallobe’s search for pattern recognition. The punchline moment shifts one’s orientation away frominformation processing toward an emotionalresponse arising deep within the nucleusaccumbens. This response is then tagged for anoverall relevance check. If the prefrontal cortex,which is part of the frontal lobe, deems theinformation attention worthy, it dedicates moreprocessing power to it, along with consciousawareness. If the information remains relevantthrough the punch line, the brain shifts its responseto its pleasure-and-reward center, which in turntriggers a guffaw.“It’s important to make a distinction betweenhumor and laughter,” says Carl Marci, MD, anassistant professor of psychiatry at Harvard MedicalSchool and the director of social neurosciencein the Psychotherapy Research Program atMassachusetts General Hospital. “Humor is anevoked response to storytelling and shiftingexpectations. Laughter is a social signal amonghumans. It’s like a punctuation mark.”To Titter Is HumanHumans experience the humor of a joke in threephases. First, the listener encounters some type ofincongruity: a punch line that seems out of placecompared with the joke’s set-up. Then, following acognitive construct called surprise and coherence,the listener tries to resolve this incongruity. Finally,the listener’s brain determines the joke’s sense—or lack thereof—and decides whether or not thejoke is funny.“The body sends a signal to the brain that says,‘Hey, that’s clever, that’s worth it,’ and we laugh,”says Marci.So incongruity and dashed expectations formthe foundation of what’s funny. But, as any comicwill tell you, timing is everything. Most successfuljokes are funny because the incongruity occurswithin the few beats that exist between the set-upand the punch line. The following joke providesan example:Gymnast: Can you teach me to do the splits?Gymnastics instructor: How flexible are you?Gymnast: Well, I can’t come in on Thursdays.We suss out the humor of this joke using theconcept behind what scientists call the incongruityresolution theory. The set-up gets us thinking inone direction, then the punch line comes alongcontinued on page 21 Humor, Laughter,and ThoseAha Moments4 Creating Immunityto Addiction5 Deciphering theTeenage Brain7 Manual ofMental DisordersBeing Revised
Humor, Laughter, and Those Aha Momentscontinued from page 1and jars us into realizing there is a completelydifferent way to interpret the situation. By resolvingthe incongruity—in this case, the double meaningof ”flexible”—we are suddenly surprised. Ourproverbial funny bone gets tickled, and we snicker.Studies have shown that the prefrontal cortexplays a vital role in the flexible thinking requiredto “get” a joke. This region of the frontal lobe,located forward of the brain’s motor regions,processes sensory information gathered by oureyes, ears, and other senses, then combines thisinformation in a manner that helps us form useful,behavior-guiding judgments. The region alsooversees the processing needed for planningcomplex cognitive behaviors, showing personalitycharacteristics, and moderating social behavior.And it is the prefrontal cortex that helps us makesense of a joke’s punch line by sending signalsalong connections to both the supplementarymotor area and the nucleus accumbens, producinga strong sense of surprise and eliciting laughter. Inshort, our prefrontal cortex is on the case as soonas we hear the first mention of that gymnast andthat trainer.Laughter is thought to have predated humanspeech, perhaps by millions of years, and mayhave helped our early ancestors clarify intentionsduring social interactions. But as language beganto evolve, laughter may also have provided anemotional context for conversations — a signal ofacceptance.Scientists have described laughter’s evolutionas one that preserved shared expressions ofrelief marking the passing of danger. Certaincontemporary researchers think that jokes linkwith this: We laugh out of relief when we recognizethe surprise element of the joke.Humans, however, are not the only species tolaugh; when tickled, some primates, includingapes, gorillas, orangutans, and chimpanzees, willgiggle, hoot, and scrunch their faces in a laugh-likemanner. Yet scientists have no evidence that theseother primates have a sense of humor. In fact,many researchers doubt they do. Unlike thebrains of humans, the brains of primates are notthought to have evolved in a manner that wouldallow them to process the incongruities introducedin a joke.Why We Laugh“Laughter was a safe, early social signal to formhuman bonds,” says Marci. “Before we could speak,laughter told early humans that ‘Everything’s okay,you can come over to my side.’”A Powerful ContagionAlthough the neural mechanisms of depression,anger, and fear have been tracked by scientists foryears, only recently have investigators begun tolook at how the brain processes humor.ON THE BRAIN
The brains of depression sufferers, for example,show decreased activity in the regions that areengaged during the processing of somethinghumorous. Researchers are studying whether thisdecrease in activity somehow impairs the brain’sability to process humor. If indeed researchers findprocessing abnormalities in parts of the brain thathandle humor, then some speculate it might bepossible to boost activity in these key regions tolessen the symptoms of depression.“The core deficit in depression is an imbalancebetween the frontal lobe and reward centers of thebrain,” says Marci. “If those areas are important forlaughter, then someone who is depressed willlaugh less.”Marci has in fact investigated humor’s role inmood disorders. In 2004, he published a study inthe Journal of Nervous and Mental Disease on the effectsof laughter during psychotherapy. Among thestudy’s participants, Marci found that for patientsbeing treated for depression, anxiety, and othermood disorders, laughter was less about humorand more about communicating emotions. Onaverage, these patients laughed about fifteen timesin each fifty-minute psychotherapy session. Todetermine whether laughter had an effect on thepatients, Marci measured the skin conductance,basically a measure of sweat, of both patients andpsychiatrists. Skin conductance increases with thenervous system activity that controls bloodpressure and heart rate, which together signal anaroused state. When clinicians did not laugh withpatients, conductance measures still indicated bothparties were aroused. But when patients andpsychiatrists laughed together, the arousal measuresfor each group doubled.“ It’s important to make a distinction between humor and laughter. . . . Humor is an evoked response to storytelling and shifting expectations. Laughter is a social signal among humans. It’s like a punctuation mark.”The contagion of laughter, Marci says, suggestspatients felt that the emotions they expressedwere being validated. It also supports the notionthat empathy is a shared experience. That laughteris catching is a reason television sitcoms uselaugh tracks: taped laughter invites audienceparticipation.The findings, Marci adds, also suggest thatmirror neurons, which are linked to empathicbehavior, are often involved in laughter. Mirrorneurons are a subset of neurons that fire bothwhen we perform an action and when we observethat same action performed by others.Once Daily, with GustoLaughter may also confer health benefits. For thepast forty years, studies have shown that good,hearty laughter can relieve tension and stress;boost the immune system, by reducing stresshormones and increasing activity among immunecells and antibodies; and help reduce the risk ofheart attack and stroke, by improving blood flowand blood vessel function.Laughter and humor can be a tonic for thebrain, as well. Triggering the brain’s emotional andreward centers spurs the release of dopamine,helping the brain to process emotional responsesand enhancing our experience of pleasure; ofserotonin, to buoy our mood; and of endorphins,to regulate our pain and stress and to induceeuphoria.The next time you hear a joke, whether you getit or not, let yourself go and enjoy a good, heartylaugh. It’s good for you!on the brain
Creating immunity to addictionimagine the day when a person addicted tococaine can walk into a clinic, get a series ofshots —and never crave cocaine again. While thisrelief is not yet on pharmacy shelves, a vaccinethat helps significantly block cocaine’s addictiveaction may not be that far away.According to Kevin Hill, MD, such a therapeuticapproach would alleviate one major frustration forclinicians in addiction psychiatry. “Although we’vebeen excited to think that pharmacogenomics,brain imaging, and other potential avenues totherapy could help us make progress againstaddiction,” he says, “so far, we haven’t been able tomake the strides we’ve hoped for.”Hill, an instructor in psychiatry at HarvardMedical School and the psychiatrist-in-charge atMcLean Hospital’s Alcohol and Drug AbuseTreatment Program, has been closely followingresearch on a vaccine called TA-CD —Therapy forAddiction-Cocaine Dependence. As with vaccinesfor pneumonia, the flu, and measles, TA-CDstimulates an immune response, prompting thebody to produce antibodies that bind to cocainemolecules as they enter the bloodstream. Usually,the immune system automatically jumps intoaction on encountering foreign substances, such asbacteria or viruses. Cocaine, however, can enterundetected. As is often the case with street drugsand even drugs with therapeutic value, cocainemolecules are too tiny for the immune system todetect. In addition, cocaine’s size allows it to slipeasily into the brain.The TA-CD vaccine cuts out cocaine’s tiny-sizeadvantage. When coupled with an antibody,cocaine becomes too large to cross the bloodbrain barrier and create the euphoric high thathelps foster addiction.To be effective, the vaccine must be deliveredin five shots over a three-month period, withfollow-up boosters every two months. This regimenand the efficacy of the vaccine have been establishedby a husband-and-wife research team at BaylorCollege of Medicine. Thomas Kosten, a psychiatrist,and Therese Kosten, a neuroscientist, vaccinatedfifty-eight volunteers suffering from cocaineaddiction and found that 38 percent producedenough antibodies to blunt the stimulant’s effects.More than half of the participants reduced theircocaine use by up to 50 percent.“The Kostens found that the vaccine workedreally well for people who developed a sufficientnumber of antibodies,” says Hill.on the brainA Hunger for PleasureAlthough the number of cocaine users in theUnited States has declined slightly since 2000,cocaine remains popular. An estimated 5.3 millionAmericans over age 12 abused cocaine in 2008.And in 2009, more than 1 million used crack, thestreet name for cocaine that has been processed asrock crystal. When heated, crack forms smoke thatcan be inhaled.Cocaine stimulates the brain’s production ofdopamine, a neurotransmitter associated withpleasure. Normally, a neuron releases dopamine inresponse to a pleasurable sensory signal, thenrecycles the chemical back into the cell to end thisresponse. Cocaine prevents dopamine reuptake,which causes the neurotransmitter to build up in thesynaptic regions between neurons. It is this excessivebuild-up of dopamine that creates euphoria.“With increased use of cocaine,” says Hill, “andconcurrent rise in the amount of dopamine inthe synapses, the brain’s physiology can changeover time and essentially create a hunger for thedrug.”That hunger is addiction. Addiction alters thebrain’s reward system, which includes the ventraltegmental area, the nucleus accumbens, and theprefrontal cortex. With prolonged use of the drug,neurons produce less dopamine. Between doses,euphoria is replaced by fatigue, depression, anxiety,and agitation. To reclaim their high, users requirelarger amounts of the drug. As their intake increases,addicts experience mood disturbances, irritability,restlessness, and even paranoid psychosis, whichcomes with auditory hallucinations and an inabilityto remain grounded in reality.Hurdles RemainExcitement within the research and clinicalcommunities about the Kosten study is temperedby the understanding that some vaccinated subjectsdid not make enough antibodies to blunt cocaine’seffects. Researchers are still seeking the scientificmechanism behind the vaccine as well as theformula needed to trigger effective levels ofantibodies.How addicts take cocaine can pose an obstacleto the vaccine’s effectiveness. People who smokecrack cocaine, for example, might not develop thenecessary antibodies because they heat the drugbefore inhaling it. Hills says the high temperatureof the cocaine molecules stimulates an inflammatoryreaction that prevents antibodies from binding to
Deciphering the teenage brainthe cocaine. Thus the cocaine molecules remainsmall enough to enter the brain.Users also might foil the vaccine’s effects bytaking so much of the drug that the body cannotmount a sufficient immune response.“Patients are very clever,” says Hill, “and oftenare ambivalent about treatment— and their desireto maintain abstinence.”A Treatment ToolThe TA-CD vaccine is not a preventive measure, butrather a therapeutic option only. Hill says thevaccine is geared toward hard-core rather thanrecreational users. The success of the treatmentdepends largely upon the user having a strongdesire to stop taking cocaine.Says Hill, “The National Institute on Drug Abuseis excited about this vaccine, researchers areexcited about it, and clinicians are excited about it.But I’m skeptical about any drug therapy being apanacea. The brain is a complicated organ.”Hill instead believes any effective treatment forcocaine abuse must combine medications withbehavioral therapies. Currently, no medications areapproved by the U.S. Food and Drug Administrationfor treating cocaine addiction. Several, however,are being studied, including acetylcysteine, used totreat acetaminophen overdose; baclofen, employedagainst certain types of alcohol dependence; andvigabatrin, an epilepsy treatment that may helprelieve cocaine and amphetamine dependence. Acocaine substitute, vanorexine, is being investigatedas a mitigator of cocaine’s withdrawal symptoms andas a block to its euphoric effects, just as methadoneis for heroin.Because addiction is a behavior, cognitivebehavioral therapy and motivational therapy canhelp with the social, emotional, and psychologicalproblems associated with continued drug use.Cognitive behavioral therapy aims to addressdysfunctional emotional and behavioral problemsby encouraging goal setting. Motivational therapy,by comparison, encourages patients to develop anegative view of their drug abuse and a desire tochange their behavior.As scientists continue work on a cocainevaccine, Hill remains cautiously optimistic.“Treating addiction requires a variety ofbehavioral and pharmacological approaches,” saysHill. “It’s probably the same with a cocaine vaccine.To be successful, it should be part of a comprehensivetreatment program.”as many parents can attest, the teenage yearsare a time of trial and triumph, a time forlearning and adapting, and, for many teens, a timefor risk-taking. This latter characteristic can beespecially disturbing to parents and teachers. Nomatter their intelligence or level of engagementwith peers and parents, teenagers simply makeperplexing, disturbing, and sometimes dangerousdecisions. Why are they such caldrons ofcontradiction?“Teens are in a discovery mode,” says FrancesJensen, MD, an HMS professor of neurology.“They’re experiencing new things, and their brainsare developing accordingly. There’s simply a lotgoing on in their brains.”Jensen, who directs epilepsy research atChildren’s Hospital Boston, found herself taking aprofessional interest in the developmental arc ofthe teenage brain as she watched her two sonsreach adolescence and “morph into other beings.”That domestic prod led her to share her knowledgeand research findings in public forums withparents and teachers as well as teens.Throughout the past decade, a growing numberof scientists have been using powerful technologieslike functional magnetic resonance imaging (fMRI)to investigate how young brains change. Thisresearch has shown that for teenagers, brain cellsrapidly form new connections with other neurons,allowing information to move quickly and learningto accumulate. This high degree of connectivitydoes not exist for all regions of the teenage brain,which may help explain teens’ impulsive behaviorand poor decision-making. Studies have, in fact,shown that the adolescent brain is only about 80percent developed, findings that Jensen says makecontinued on page 6on the brainThis is the fifthin a series onhow internal andexternal forcesaffect the brain.
Deciphering the Teenage Braincontinued from page 5it clear that teenagers are not just “young adultswith fewer miles.”Not Fully OnlineFrom childhood through adolescence, the brain’sbillions of neurons and synapses form and re-formconnections, giving it the plasticity needed forlearning. Throughout the development continuum,says Jensen, the brain is like a sponge, soaking upexperiences. That is why children and teenagerscan master such skills as foreign languages andmusical instruments more easily than adults can.The teenage brain matures from back to front.The posterior regions, especially those above thespinal column, are largely responsible for motorcontrol. Their earlier maturation helps account forthe quick acquisition of locomotion and othermovement skills by young people. Maturation ofmany sensory regions also occurs early, enabling agrowing person to learn from the surroundingworld. The maturing of the forward regions of thebrain, particularly the frontal lobe, doesn’t occuruntil late adolescence or early adulthood; someresearchers say the region’s maturation may not becomplete until age 30.The frontal lobe is the seat of executive function,a term for the cognitive processes that allow us toplan, make decisions and judgments, formulateinsight, and assess risk. The delayed maturation ofconnections to the frontal lobe, Jensen says,contributes to teenagers’ risk-taking. “Their frontallobes,” she says, “are simply not yet fully online.”The percentage of neurons in the adolescentbrain that are myelinated is also lower than that inthe adult brain. Myelin is the insulating coatingthat helps neurons pass signals along rapidly. Asthe brain matures, the number of myelinatedneurons grows, forming a dense mass — the brain’swhite matter. To underscore the developmental trackthat myelination takes, Jensen points to fMRI studiesthat show myelinated cells beginning to appear inthe brains of people in their early twenties.Statistics also bear out the link betweenteenagers and such health- and life-imperilingbehavior as dangerous driving, unsafe sex, poordietary habits, and experimentation with alcoholand drugs. One area in which teens’ recklessnessand inexperience collide is motor vehicle crashes:Per mile driven, 16- to 19-year-olds are four timesmore likely to crash
a strong sense of surprise and eliciting laughter. In short, our prefrontal cortex is on the case as soon as we hear the first mention of that gymnast and that trainer. Why We Laugh “Laughter was a safe, early social signal to form human bonds,” says Marci. “Before we could speak, laughter told early humans that ‘Everything’s okay,
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