丹尼爾·吉布斯 王昊堃

Recently， while out walking my dog Jack， I encountered a blond woman pushing a toddler in a stroller while walking her dog. I stopped to chat， asking her how old her son was now， and she responded amiably. About a year and a half ago， three women on our block gave birth within a month of each other. One woman has blond hair and two have dark hair. They all have dogs. As soon as we had ended our chat and I was walking on， I realized that she had the wrong dog. The blond on our block has a black lab1， and this dog was some kind of curly-haired terrier2. I then realized that the woman I had approached was a complete stranger， not one of my neighbors.

On the face of it， this wouldn’t be a particularly noteworthy incident， given the context of the COVID pandemic that has so many of us wearing masks. It has become a common， shared experience， these awkward social moments in which we’ve failed to recognize people we know， or we’ve been on the receiving end3 of someone we know looking right past us as if we’re strangers. But the moment held more for me.

I am a retired neurologist. I also have early-stage Alzheimer’s disease. During my 25 years practicing general neurology in Portland， Ore.， I took care of many patients with dementia， including Alzheimer’s disease. I never suspected that I too might get Alzheimer’s， but then about 15 years ago I started to lose my sense of smell and began to experience stereotypical phantom odors called phantosmias4. Problems with smell can be early symptoms of neurodegenerative5 diseases like Alzheimer’s， but it was another six or seven years before I started to have issues with my memory. The neuropathology6 of Alzheimer’s disease， the beta-amyloid plaques7 and tau-containing neurofibrillary tangles， are found first in olfactory centers in the brain， years before cognitive impairment begins. As part of a research study， I underwent amyloid and tau PET8 scans of my brain in 2015 and again in 2018， and the scans confirmed the diagnosis and progression of Alzheimer’s disease.

Being a neurologist with a neurological disorder has provided me some special insights. For example， seeing beta-amyloid on my first amyloid PET scan located not only in the prefrontal cortex9 and precuneus10 but also in olfactory processing centers such as the piriform cortex11 and orbital frontal cortex12 was really exciting because it provided a logical explanation for my olfactory problems. The PET scans also gave me some hints as to the cause of my trouble recognizing my neighbors.

Face blindness， or prosopagnosia13， is a neurological condition resulting in trouble identifying human faces. It is usually caused by damage to the fusiform gyrus14 in the posterior temporal lobe15 and anterior16 portion of the occipital lobe17. Neurologist-author Oliver Sacks famously introduced this condition to popular culture in his 1985 book The Man Who Mistook His Wife for a Hat. Sacks wrote about his own severe face blindness in a wonderful， August 23， 2010， article in the New Yorker. One of my neurologist colleagues has such severe face blindness that she needs to hear someone speak before reliably making an identification. Like Sacks， she’s had it all her life. Up to 2.5 percent of people are born with congenital18 face blindness， mostly inherited in an autosomal19 dominant pattern.

Acquired face blindness may be caused by head trauma， strokes or tumors affecting the fusiform gyrus. A more insidious20 form of face blindness occurs in many people with Alzheimer’s disease， even in the early stages. The tau-containing neurofibrillary tangles of Alzheimer’s disease usually first occur in the medial21 portion of the anterior temporal lobes. With time， these neurofibrillary tangles can spread backwards into the fusiform gyrus.

Although my cognitive impairment is still mild， I have been having increasing trouble recognizing faces， even of people I know well. Many of my neighbors are hard for me to recognize until I hear their voices or see the dog they are walking. Before the pandemic， I would often be embarrassed by not recognizing or misidentifying an acquaintance while walking my dog.

Our masks are now covering important facial features used for facial recognition. A recent study from York University in Toronto and Ben-Gurion University in Israel confirmed this by demonstrating “quantitative and qualitative changes in the [visual] processing of masked faces” that “could have significant effects on activities of daily living.” Perhaps everyone now is experiencing a degree of face blindness.

The ability to accurately identify other people by recognizing their faces is important to our social， emotional and cultural behaviors. Our brains appear to learn how to recognize the faces of other people of our race during childhood. A study in 2019 showed that there is a critical period for this learning. Children learn how to recognize faces of the group they are raised with， up until about age 12. White children will become adept at distinguishing white faces， but unless they are exposed to other racial faces， they will have trouble distinguishing people of other races.

Similarly， an Asian child raised in an Asian country without exposure to white faces will not be able to distinguish white faces. An Asian child adopted and raised in a predominantly white country will distinguish white faces but not Asian faces. A child who grows up in a racially heterogeneous22 setting will be able to distinguish faces of all of those races. This learning process slows down and then is gone by age 12.

To me this implies that there are pathways in the brain， probably in the fusiform gyrus， that are developing new neuronal23 connections during childhood as we learn what makes one face look different from another， but that this plasticity24 is lost by age 12. It strikes me that while face masks are drawing our attention to the subject of face blindness， more relevant may be the impact of our children’s social exposure that supports how they see others， literally， in our diverse communities.

I’ll need to attend closely to those masked faces to overcome my combined disadvantage of neurological face blindness and masked face blindness， the first caused by abnormalities of the brain and the second simply due to the blocking of visual cues. My best option may be to pay closer attention to the dogs. Even for me， pets are easy to identify because of shape， size， color of coat and sometimes temperament or behavior. I’ll also need to expand my mental dog gallery now to include that curly terrier and his friendly human companion with the baby stroller. Next time we pass on the street， we’ll be strangers no more.

最近，我在遛狗狗杰克時(shí)，遇見(jiàn)了一位同在遛狗的金發(fā)女士，她推著嬰兒車，車?yán)镒粋€(gè)看樣子正在學(xué)步的小男孩。我停下來(lái)與她交談，問(wèn)她兒子多大了，她友善地回應(yīng)了我。大約一年半前，我們街區(qū)有三位女士在一個(gè)月內(nèi)先后生了孩子，她們當(dāng)中一人是金發(fā)，兩人是黑發(fā)，并且三人都養(yǎng)狗。就在我們剛剛結(jié)束聊天、我繼續(xù)往前走時(shí)，我意識(shí)到這只狗并不是她的。我們街區(qū)那位金發(fā)女士養(yǎng)了一只黑色的拉布拉多，而這只是一種卷毛小獵狗。我恍然大悟，剛剛與我交談的女士完全是個(gè)陌生人，并非我那三位鄰居之一。

表面看來(lái)，在許多人因新冠疫情都要佩戴口罩的情況下，這并不是一件多么值得注意的事。我們沒(méi)能認(rèn)出認(rèn)識(shí)的人，或是認(rèn)識(shí)的人沒(méi)能認(rèn)出我們，如同面對(duì)陌生人，這些社交場(chǎng)合的尷尬瞬間已經(jīng)成了人人都有的經(jīng)歷。但這一刻對(duì)我來(lái)說(shuō)卻有著非同尋常的意義。

我是一名退休的神經(jīng)學(xué)家，患有早期阿爾茨海默病。我在俄勒岡州波特蘭市從事普通神經(jīng)學(xué)研究已有25年，其間治療過(guò)許多患有包括阿爾茨海默病在內(nèi)的癡呆病人。我從未想到自己會(huì)患上阿爾茨海默病。然而，大約15年前，我開(kāi)始失去嗅覺(jué)，典型的癥狀就是會(huì)聞到實(shí)際上并不存在的臭味，這叫“嗅幻覺(jué)”。嗅覺(jué)出現(xiàn)問(wèn)題可能是阿爾茨海默病之類的神經(jīng)退行性疾病的早期癥狀，而我的記憶開(kāi)始出現(xiàn)問(wèn)題是六七年之后的事了。阿爾茨海默病的神經(jīng)病理學(xué)表明，在人體發(fā)生認(rèn)知障礙的幾年前，大腦嗅覺(jué)中樞就已經(jīng)存在β-淀粉樣斑塊和含tau蛋白的神經(jīng)原纖維纏結(jié)。我在2015和2018年先后做了兩次“派特”，檢測(cè)腦部的淀粉樣蛋白和tau蛋白含量，這也是一次研究的組成部分。掃描確診我患上了阿爾茨海默病，并且顯示病情在惡化。

作為一名神經(jīng)學(xué)家，患上神經(jīng)功能障礙倒是讓我有了一些獨(dú)到的認(rèn)識(shí)。比如，我的第一張淀粉樣蛋白派特圖顯示，β-淀粉樣蛋白不僅位于前額皮層和楔前葉，同時(shí)還存在于梨狀皮層和眶額皮層等嗅覺(jué)處理中樞。我對(duì)此格外興奮，因?yàn)檫@樣，我的嗅覺(jué)問(wèn)題就解釋得通了。派特掃描還給了我一些線索，幫助我找到認(rèn)不出鄰居的原因。

臉盲，也叫面容失認(rèn)癥，是一種神經(jīng)系統(tǒng)疾病，具體表現(xiàn)為辨別人臉困難，通常由后顳葉和枕葉前部梭狀回?fù)p傷導(dǎo)致。眾所周知，神經(jīng)學(xué)家兼作家?jiàn)W利弗·薩克斯在其1985年的著作《錯(cuò)把妻子當(dāng)帽子》中將這一疾病引入大眾文化。2010年8月23日發(fā)行的《紐約客》曾刊登過(guò)薩克斯的一篇精彩文章，其中就寫到他自己患有嚴(yán)重的臉盲癥。我的一位神經(jīng)學(xué)家同事也有嚴(yán)重的臉盲癥，她需要聽(tīng)到對(duì)方說(shuō)話才能確認(rèn)此人的身份。和薩克斯一樣，臉盲癥伴隨了她一生。高達(dá)2.5%的人患有先天性臉盲癥，其中大多數(shù)是常染色體顯性遺傳所致。

導(dǎo)致后天臉盲癥的原因可能是頭部創(chuàng)傷、中風(fēng)或腫瘤影響到了梭狀回。臉盲癥還會(huì)以一種更加隱蔽的方式存在于許多阿爾茨海默病患者體內(nèi)，甚至病程早期就已存在。阿爾茨海默病的含tau蛋白的神經(jīng)原纖維纏結(jié)通常首先出現(xiàn)在前顳葉中部。隨著時(shí)間推移，這些神經(jīng)原纖維纏結(jié)會(huì)向后蔓延至梭狀回。

我的認(rèn)知障礙不算太嚴(yán)重，但在認(rèn)人方面卻越來(lái)越困難，甚至包括熟人。許多鄰居我已經(jīng)很難辨認(rèn)，除非聽(tīng)到他們的聲音或看到他們遛的狗。疫情之前，我在遛狗時(shí)，常會(huì)因?yàn)檎J(rèn)不出或認(rèn)錯(cuò)人而感到尷尬。

戴上口罩，識(shí)別人臉?biāo)璧膸醉?xiàng)重要面部特征便被遮住了。加拿大約克大學(xué)和以色列本·古里安大學(xué)近期的一項(xiàng)研究演示了“大腦對(duì)戴上口罩的人臉進(jìn)行（視覺(jué)）處理時(shí)量和質(zhì)的變化可能給日常生活中的各類活動(dòng)帶來(lái)顯著影響”，由此證實(shí)了這一點(diǎn)。或許我們每個(gè)人都正在體驗(yàn)一定程度的臉盲。

通過(guò)辨認(rèn)人臉來(lái)準(zhǔn)確識(shí)別人，這一能力對(duì)于我們的社交、情感及文化行為都非常重要。我們的大腦似乎在幼年時(shí)就學(xué)著如何辨認(rèn)同一種族其他人的臉了。2019年的一項(xiàng)研究表明，辨認(rèn)人臉的學(xué)習(xí)有一段關(guān)鍵時(shí)期。一直到12歲左右，兒童都在學(xué)習(xí)如何辨認(rèn)他們成長(zhǎng)過(guò)程中身邊人的臉。白人兒童會(huì)變得擅長(zhǎng)辨認(rèn)白種人的臉，而辨認(rèn)其他種族人的臉就會(huì)有難度，除非與其他種族的人共處。

同樣，一個(gè)在亞洲國(guó)家長(zhǎng)大的亞洲兒童，如果不與白種人共處，就不會(huì)辨認(rèn)白種人的臉。一個(gè)亞洲兒童被領(lǐng)養(yǎng)并在以白種人為主的國(guó)家長(zhǎng)大，就會(huì)辨認(rèn)白種人的臉，卻不會(huì)辨認(rèn)亞洲人的臉。一個(gè)在多種族混居環(huán)境中長(zhǎng)大的孩子將會(huì)辨認(rèn)所有相關(guān)種族人的臉。學(xué)習(xí)辨認(rèn)人臉的過(guò)程在12歲之前會(huì)逐漸減緩，直至消失。

對(duì)我來(lái)說(shuō)，這意味著大腦中——很可能就在梭狀回中——存在著一些通路，我們?cè)诤⑼瘯r(shí)期學(xué)習(xí)辨認(rèn)不同人臉的區(qū)別時(shí)，這些通路就在不斷建立新的神經(jīng)元連接，不過(guò)這種可塑性到12歲就消失了?？谡忠鹆宋覀儗?duì)臉盲這個(gè)話題的關(guān)注，但我認(rèn)為更有意義的或許是，在這個(gè)多元化的社會(huì)里，接觸的群體與環(huán)境對(duì)孩子們發(fā)展認(rèn)人能力的影響。

我得密切注意那些戴著口罩的路人，以便克服我的兩個(gè)弱點(diǎn)：一個(gè)是因大腦異常導(dǎo)致的神經(jīng)學(xué)意義上的臉盲，而另一個(gè)僅僅是因面部特征被遮擋導(dǎo)致的臉盲。對(duì)我來(lái)說(shuō)，最佳的選擇或許是給予狗狗們更密切的關(guān)注。因?yàn)榧幢銓?duì)于我這種認(rèn)臉有困難的人，也可以根據(jù)體形、塊頭、皮毛顏色，以及脾氣或行為，輕易辨認(rèn)出不同的寵物。同時(shí)，我也要擴(kuò)充我腦海中的狗狗圖庫(kù)，把那只卷毛小獵狗加進(jìn)去，還有它那位友善的推著嬰兒車的人類伙伴。下次在大街上相遇，我們便不再是陌生人。

（譯者為“《英語(yǔ)世界》杯”翻譯大賽獲獎(jiǎng)?wù)撸?/p>

1 lab = labrador拉布拉多獵犬。? 2 terrier?犬，一種活潑的小狗。

3 be on the receiving end遭受，承受（不愉快的事）。? 4 phantosmia嗅幻覺(jué)，指患者通常會(huì)聞到排泄物或下水道的味道。? 5 neurodegenerative神經(jīng)退行性的。? 6 neuro-pathology神經(jīng)病理學(xué)。? 7 beta-amyloid plaque β-淀粉樣斑塊。? 8 = Positron Emission Computed Tomography正電子發(fā)射型計(jì)算機(jī)斷層顯像，是核醫(yī)學(xué)領(lǐng)域比較先進(jìn)的臨床檢查影像技術(shù)。

9 prefrontal cortex前額皮層。? 10 precuneus楔前葉。? 11 piriform cortex梨狀皮層。? 12 orbital frontal cortex眶額皮層。? 13 prosopagnosia面容失認(rèn)癥。? 14 fusiform gyrus梭狀回，大腦顳葉及枕葉之間的皮層，最主要的作用是識(shí)別人臉。普通人看到人臉時(shí)，其神經(jīng)活躍度會(huì)變高。? 15 posterior temporal lobe后顳葉。? 16 anterior前部的。? 17 occipital lobe枕葉。

18 congenital先天性的。? 19 autosomal常染色體的。? 20 insidious潛伏的。? 21 medial中間的，平均的。

22 heterogeneous各種各樣的，混雜的。

23 neuronal神經(jīng)元的，神經(jīng)細(xì)胞的。? 24 plasticity可塑性，適應(yīng)性。

1152501186208