Faces in the Crowd 2011 Film

Facesin the Crowd 2011 Film

StudentName’s

TheNeuropyschological Phenomenon in the Film

Facesin the Crowd 2011film focuses on Anna Merchant, an elementary school instructor whodevelops face blindness (prosopagnosia). She developed thisneuropsychological condition after she came face to face with aserial killer, who attempted to slay her. The incident took placewhen Anna was going to meet with Bryce, her boyfriend. While she wascrossing the bridge, she spotted a renowned serial-killer murdering awoman. In spite of her efforts to run away, the killer attacked her.Fortunately, she was able to escape murder by falling down thebridge. Unfortunately, Anna knocked her head resulting in braindamage, which was followed by face blindness. From this time, Annawas not able to recognize faces, even her boyfriend or her closestfriends. Anna was suffering from acquired prosopagnosia consideringthat the condition developed after she knocked her head from thefall. The development of the disorder followed brain injury of thebilateral occipito-temporal regions.

Prosopagnosiais a condition of face perception in which the capability ofrecognizing faces is damaged (Sacks, 2010). The brain damage resultsin a kind of amnesia which makes it impossible to recognize faces. However, individuals who suffer from prosopagnosia have the relativecapacity to distinguish other objects. Despite efforts by SamKerrest, the police detective, to compel Anna to memorize theserial-killer’s face, he did not succeed. She is incapable ofremembering faces, and this is poses extreme danger to her life. Thisis based on the reason that she was able to identify the killer’sface during the attack, and he is aware of it. Prosopagnosia is notcurable meaning that patients have to learning other ways of dealingwith the disorder. This can be by learning to recognize peoplethrough their clothing or other distinguishable features which do notchange. Anna’s inability to remember the killer made her live alife of disturbance and fear. However, she was able to learn uniquemarks, which helped her to tell individuals apart, through theassistance of Dr. Langenkamp. The current paper discusses thebrain-behavior connection for prosopagnosia. This entails analyzinghow the brain physiology, function, chemistry, damage, as well asother physiological features which causes prosopagnosia. The paperdiscusses methods, results, and conclusions obtained from currentresearch on the topic.

Causesof Prosopagnosia

Faceindividuation entails recognition of faces at personal level. Thebrain contains widespread neural network with various ventro-medialparts containing the right hemisphere. This region is supposed toplay a major responsibility in processing of faces. The regions areoccipital pole and the temporal pole, as well as the superiortemporal sulcus and inferotemporal cortex (The brain injuryassociation, 2013). In particular, the fusiform face area (FFA),which is situated in the ventral temporal cortex, plays a significantrole in responding to faces. Besides, the FFA is optimized to processstimuli in a holistic and configural manner (Richler, Cheung &ampGauthier, 2011). Spatial-temporal multivariate examination isemployed in mapping these brain regions employed in facialprocessing. Neuroscientific studies have shown that facialrecognition depends on programming the how the facial attributes areconfigured.

Ingeneral, prosopagnosia is caused by injury of aforementioned regionsof the brain, which results from head trauma or degenerativeillnesses. The temporal and occipital lobes are generally concernedwith memory and perception, particularly the fusiform gyrus which isfound in each temporal. This implies that fusiform gyrus is presentin both parts of the brain. The area is significant in facerecognition and it is referred to as fusiform face area (FFA) (Bate,2012). Fusiform gyrus is the brain area that is linked withprosopagnosia. Its function is to activate in reaction to faces.Fusiform gyrus functions in such a way that permits individuals todistinguish and differentiate faces in a detailed manner as comparedto other multifaceted non-living objects. Research indicates that ascompared to the left hemisphere of Fusiform gyrus, the righthemisphere is greatly concerned with the recognition of familiarfaces, that is face processing (The brain injury association, 2013).It is however uncertain if fusiform gyrusis is merely involved indistinguishing human faces or whether it is as well concerned withvisual stimuli.

Prosopagnosiaas Portrayed in the Literature

Aspreviously defined, prosopagnosia, also commonly known as faceblindness, is a type of cognitive condition of facial insight (Hole &ampBourne, 2010). Individuals suffering from the disorder have theinability to distinguish faces as a result of impairment. However,other aspects including intellectual functioning (such as makingdecisions) and visual processing (such as distinguishing objects)remain undamaged (Bruce &amp Young, 2012). Initially, the termdenoted a condition that was followed by severe injury of the brain(Bruce &amp Young, 2012). Individuals with this disorder areincapable of differentiating between faces of family or closefriends. They are also incapable of recognizing their faces in frontof a mirror. The result is social isolation, misery, as well as lossof opportunities. People suffering from prosopagnosia learn noveltechniques of distinguishing faces which rely on less-perceptiveobject distinguishing system (Hole &amp Bourne, 2010).

Prosopagnosiais of two types: congenital (developmental) and acquiredprosopagnosia. Congenital prosopagnosia is projected to affect equalto 2.5 percent of the population (Bate, 2012). In this case, personsfail to sufficiently develop the capacity to distinguish faces.Acquired prosopagnosia develops when occipito-temporal lobe isdamaged. This disorder is commonly found among adults. Acquiredprosopagnosia is classified into associative and apperceptiveprosopagnosia. Apperceptive prosopagnosia develops when the rightoccipital temporal brain area fails to function as a result ofinjury. While apperceptive prosopagnosia affects the manner in whichindividuals perceive faces due to damage of fusiform gyrus,associative prosopagnosia affects individual’s memory of faces dueto damage of temporal lobes (Sacks, 2010). Acquired prosopagnosiadevelops as a result of impairment of the procedure which lessensuncertainty regarding the locality of diagnostic signals for facialrecognition. This means that the holistic processing is impaired. Itis the capacity to distinguish various facial components as adistinct global representation.

Pureprosopagnosia is not caused by generalized visual or memoryperception problems, and it is not linked with mental disorder (Thebrain injury association, 2013). However, patients have specificproblems in recognizing faces. Certainly, their intellectualfunctioning still operates meaning that they are in a position ofaccessing their knowledge regarding someone after knowing their name,in addition to recognizing other kinds of objects. Pure prosopagnosiais nonetheless uncommon. People who develop face blindness afterbrain damage additionally develop other visual and cognitivedifficulties. This is evidenced by the fact that brain damage impactsvarious brain regions, and causes numerous difficulties (Grüter,Grüter &amp Carbon, 2008). The specific model of face processingtogether with other visual and cognitive problems differs from oneperson to the other. The majority of individuals experiencedifficulties to extract information in addition to distinguishing aface. They struggle to construe an individual’s age, gender, aswell as emotional manifestation. Nearly all individuals withprosopagnosia go through navigational difficulties in conjunctionwith the disorder. The main cause of this experience is visualproblems in processing distance or angle, as well as poor memory(Grüter, Grüter &amp Carbon, 2008). Individuals with prosopagnosiaalso suffer from common visual impairments including perception ofcurvature, luminance, contrast or color.

Asdemonstrated by neuropsychological tests, extracting analyticalinformation from individual faces is non inconsequential (Mayer &ampRossion, 2007). This is evidenced by observing individuals sufferingfrom prosopagnosia, regardless of them having no other apparentvisual system impairment and a maintained capability to distinguishindividuals using other aspects such as voice. According to Hole &ampBourne (2010), the dearth of face recognition is a serious disorder,and although it is very uncommon (affects below one percent of braininjured individuals) it received significant infamy from theneuropsychological review after the initial clinical observations,and after Bodamer introduced the aspect ‘prosopagnosia’ (Hole &ampBourne, 2010). The anatomical and clinical states of prosopagnosiahave attracted the interest of many cognitive neuroscientists whohave shed light on the neuro-functional mechanism of face processing(Richler, Cheung &amp Gauthier, 2011). According to their findings,anatomical explanations of the disorder maintain the role played byoccipito-temporal regions in processing faces. The dual dissociationillustrated by various researchers between the capacity todistinguish well-known and strange faces, recognizing facial identityand expression, or face identification and lip–reading haveassisted in separating the diverse functions of face processing(Mayer &amp Rossion, 2007).

Methodsand Results

Variousstudies have been conducted to investigate the condition ofprosopagnosia. A study carried out by Duchaine &amp Nakayama (2006)indicated that prosopagnosia patients regularly suffer from leftvisual area impairments. This associates to injury caused in theright hemisphere. The study employed a sample of 22 patients. Out ofthese, 16 suffered from injury in the right hemisphere, two had lefthemisphere injury, while the remaining four had bilateral injury(Duchaine &amp Nakayama, 2006). Another study was carried out withthe aim of investigating if face recognition impairment wasprincipally a perceptual or memory shortfall as investigated inbelated memory role. Face recognition roles were administered to 114patients who suffered from unilateral injury of the brain. Thefragment facial roles entail three experiments. The initialexperiment required patients to match diverse components of faceswith the resultant complete facial image. The second experimentinvolved matching the front view with the profile. The lastexperiment entailed conducting a memory examination. In this, apicture was shown to patients and removed rapidly. The patients werethen requested to distinguish the face seen amongst various facesthat were displayed. The findings of the study indicated that 19patients who had right brain injury, as well as shortage in thematching left visual region had the poorest performance in relationto the facial fragment roles (Grüter, Grüter &amp Carbon, 2008).Patients suffering from right hemisphere damage only performed betteras compared to the 19 patients mentioned above. From this, thegeneral conclusion of the study was that perceptual deficit was themain cause of recognition impairment of strange faces (Grüter,Grüter &amp Carbon, 2008). Patients who suffered from right braininjury experienced recognition impairment of faces as a result ofinability to process minute slight dissimilarities and to incorporatevisual signals.

Anotherexperiment was a delayed memory role, in which a facial picture wasrevealed to patients for an extended length of time. After theremoval of the picture from the patients’ sight, they wererequested to distinguish the face amongst different individuals. Thiswas done either instantly or within one to two minutes time. Theexperiment was carried out with the interpretation that if memory wasvital in facial recognition, therefore delayed memory roles weresupposed to bring about the highest levels of impairment (Richler,Cheung &amp Gauthier, 2011). The experiment results failed toindicate considerable differences in responses. This meant that therecognition impairment of faces linked with the damage of the righttemporal lobe was not mainly as a result of memory but prosopagnosiaprimarily perceptual in nature.

Accordingto Richler, Cheung &amp Gauthier (2011), prosopagnosia may arise dueto the issue of holistic processing. Individuals are unable toprocess complete faces, and adopt a part by part strategy. In this,patients’ process faces little by little whereby every part isobserved at a time. This makes the process of recognizing faces morelengthy and difficult, and disregards the spatial associationsbetween different features- the information that is essential foreffective recognition. Eye tracking technology has been employed toillustrate this extraordinary processing framework. The eye movementsof the participants are monitored using sensitive equipment. Whilethey are viewing the facial images on a computer, the equipmentenables the researchers to know the exact part of the face observedby the participant in the recognition process (Richler, Cheung &ampGauthier, 2011). The findings have revealed that prosopagnosiapatients use a lot of time observing exterior parts of the face suchas ears and hair, while avoiding the area of the eye. However, normalparticipants mostly observe internal parts of the face including themouth and nose, while giving more emphasis on the eyes (Richler,Cheung &amp Gauthier, 2011). The decreased reliance on the eyeregion is attributed to the interference of holistic processing of aperson’s face.

Accordingto research, both bilateral and right unilateral injury results inprosopagnosia (Grüter, Grüter &amp Carbon, 2008). For example, anassessment of prosopagnosic brain injury using PET and magneticresonance imaging (MRI) structural imaging showed that the rightregion of the patients brain resulted in the development of thedisorder, as the left brain region was undamaged (Grüter, Grüter &ampCarbon, 2008). Prosopagnosia patients experiencing shortages invisual fields suffer from visual impairment of the left regionincluding left superior quadronopia. This illustrates that theexacted injury is on the brain’s right region. Besides, it hasdemonstrated through structural imaging researches which employ MRIand CT scans that development of prosopagnosia takes place when thereis right side injury.

Conclusion

Thispaper has focused on Prosopagnosia, a Neuropyschological Phenomenonthat is evident in the Facesin the Crowd 2011film. Anna developed the disease after she fell over a bridgeresulting in brain injury. After developing the disease, she wasunable to recognize the faces of her family of her closest friendsdespite efforts to force her to do so. Prosopagnosia has been definedas a condition of face perception in which the capability ofrecognizing faces is damaged. Nevertheless, individuals who sufferfrom prosopagnosia have the relative capacity to distinguish otherobjects. Prosopagnosia results when the brain parts that areconcerned with face processing are impaired as a result of braininjury. These parts include the temporal and occipital lobes whosemain role is memory and perception. In particular, the impairment offusiform gyrus, which is fundamental for recognizing faces. It isresponsible for activating in reaction to faces. Fusiform gyrusfunctions in such a way that permits individuals to distinguish anddifferentiate faces in a detailed manner as compared to othermultifaceted non-living objects. As compared to the left hemisphereof Fusiform gyrus, the right hemisphere is greatly concerned with therecognition of familiar faces. People who develop face blindnessafter brain damage additionally develop other visual and cognitivedifficulties since, brain damage impacts various brain regions, andcauses numerous problems. Researchers have used various methods tostudy prosopagnosia including structural imaging such as MRI and CTscans, delayed memory roles, and use of computer sensitive equipment.The results of the studies have demonstrated that prosopagnosiapatients use a lot of time observing exterior parts of the face suchas ears and hair, while avoiding the area of the eye. Besides,patients who suffered from right brain injury experienced recognitionimpairment of faces. In general, prosopagnosia was found to beprimarily perceptual in nature.

References

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Bruce,V. &amp Young, A. (2012). Faceperception.Hove: Psychology Press.

Duchaine,B, &amp Nakayama, K. (2006). The Cambridge Face Memory Test: resultsfor neurologically intact individuals and an investigation of itsvalidity using inverted face stimuli and prosopagnosic participants.Neuropsychologia44 (4): 576–85.

Eugene,M. &amp Bruno, R. (2007). Prosopagnosia.The behavioral and cognitive neurology of stroke (1ed.). New York: Cambridge University Press.

GrüterT, &amp Grüter M, Carbon, C. C. (2008). Neural and geneticfoundations of face recognition and prosopagnosia. JNeuropsychol2 (1): 79–97.

Hari, R. &amp Kujala, M. V. (2009). Brain basis of human socialinteraction: From concepts to brain imaging. PhysiologicalReviews89(2), 453-479.

Hole,G. &amp Bourne, V. (2010). Faceprocessing: Psychological, neuropsychological and appliedperspectives. Oxford:Oxford University Press.

Richler,J. J., Cheung, O. S. &amp Gauthier, I. (2011). Holistic processingpredicts face recognition. PsycholSci 22(4): 464–71.

Sacks,O. ( 2010). Prosopagnosia,the science behind face blindness.The New Yorker.

Thebrain injury association (2013). Prosopagnosia:Face blindness after brain injury.Factsheet.