Complexity is intimidating: Some beautiful brain tractography here.
The truly exciting prospect: Much as our view of another familiar phenomenon, peptic ulcers, radically changed with the discovery that most are caused by bacterial infection. See PubMed Health, “Helicobacter Pylori,” http://goo.gl/2Ou1wn.
It’s worth a look: David Van Essen’s circuit diagram of the visual system, UCSD Neurosciences.
this conflict poses a challenge: For another approach to this challenge, look here.
It is very hard to write well: A figure reproduced on many quality websites (it can be seen here on Medline Plus: https://goo.gl/jwIsNF) illustrates the concern. It mixes basic anatomical facts, such as the locations of the major lobes, with simplistic assignments of functions to specific areas (e.g., Wernicke’s) and one pure fiction: there is no “reading comprehension area.”
A good theory: Putnam (1972).
forty-three major anatomically distinguishable: Quick introduction, McGill University, The Brain, http://goo.gl/udSioK.
modern Brodmann map: Glaser et al. (2016). For a video about the study, see “The Ultimate Brain Map,” https://www.youtube.com/watch?v=UHDfvfYCY0U.
tuberculosis in the literature: As discussed in Susan Sontag’s classic Illness as Metaphor (Sontag 1978).
The late Oliver Sacks: “I am a clinical ontologist, one for whom the diagnostic question is: How are you? How do you be?” Sacks as quoted by Lawrence Weschler, “A Rare, Personal Look at Oliver Sacks’s Early Career,” Vanity Fair, April 28, 2015. In the same article, Weschler writes, “[Sacks] respects facts, he tells me, and he has a scientist’s passion for precision. But facts, he insists, must be embedded in stories. Stories—people’s stories—are what really have him hooked.”
found that she regularized: Marlene Behrmann (personal communication).
We then developed models: The first-generation model: Seidenberg & McClelland (1989); the second-generation model with division of labor: Plaut et al. (1996).
The impairment is due: Hodges et al. (1992). The cause is usually Pick’s disease, a type of frontotemporal dementia.
Also as predicted: Patterson et al. (2006).
Responding with a word: Funnell (1983).
One patient was reported: Saffran & Marin (1977).
David Plaut, Tim Shallice, and Geoff Hinton: Hinton, Plaut, & Shallice (1993) is an accessible and entertaining overview.
As a British neurologist noted: Leff (2004).
“pure alexia” is not pure: Behrmann, Nelson, & Sekuler (1998). This type of lesion would also affect an illiterate’s performance on such tasks.
Connections from areas in the temporal lobe: Presenting the components in this way omits crucial facts that are hard to diagram: that there are feedback in addition to feedforward connections, which create much more complex neural dynamics, and that the functions of the parts depend on and are changed by each other because they are interconnected.
“Language” was located: My colleague Tim Rogers has pointed out that language may have been situated beneath the eyes because of a patient with a language impairment who also exhibited exophthalmos, the eye-bulging symptom of Graves’ disease.
visual word form area is one: Behrmann & Plaut (2013).
The evolutionary story: Caramazza & Mahon (2003).
Swiss army knife: Pinker (2003).
increasingly sophisticated methods: Behrmann & Plaut (2013).
Spelling gets routed: On Stanislaus Dehaene’s neuronal recycling hypothesis, see Dehaene (2010).
study of eighty patients: Hillis et al. (2005).
processing of visual word forms: For a case study of a patient who could read following surgical excision of the VWFA, see Seghier et al. (2012).
it is activated by objects: Price & Devlin (2003).
study of nonimpaired readers: Mano et al. (2012).
More sensitive methods: Cox, Seidenberg, & Rogers (2015).
other brain areas also respond: McCandliss, Cohen, & Dehaene (2003).
More recently Behrmann and Plaut: Behrmann & Plaut (2013).
The term “visual word form area”: Sandak et al. (2004) referred to it as a “skill zone,” but the term is perhaps too general.
Holmes nearly said to Watson: “You could not possibly have come at a better time, my dear Watson,” he said cordially. Arthur Conan Doyle, “The Red-Headed League,” East of the Web.
subjects are quicker: Ziegler & Ferrand (1998).
The experiment was then repeated: Stoeckel et al. (2013).
The technique may seem odious: A British journalist experiences TMS: “Michael Mosley Has Areas of His Brain Turned Off. The Brain: A Secret History. BBC Four,” video uploaded to YouTube by BBC, December 24, 2010, https://www.youtube.com/watch?v=FMR_T0mM7Pc. Some methods of applying the stimulation improve rather than interfere with performance.
Signatures of developmental reading impairments: For recent reviews, see Peterson & Pennington (2012); Pennington & Bishop (2009); Goswami (2015).
The effect is to interfere: Turkeltaub et al. (2003).
poorer performance on visual tasks: The visual deficit hypothesis is discussed in the reviews I’ve cited here.
Suggestive evidence is emerging: Yeatman et al. (2012).
Visual impairments may be: This evidence in no way validates “visual training” programs sold by optometrists and others as treatments for reading difficulties. Anomalies in these white matter tracts may be the source of the noisy visual processing in the Sperling et al. (2005, 2006) experiments.
The initial left hemisphere: Hoeft et al. (2011).
The global impact of these conditions: Rueckl et al. (2015).
The product of the newer: Ashkenazi et al. (2013) summarize structural brain anomalies associated with reading and math impairments.
Two studies have reported: Several studies have reported changes in white matter in dyslexics following short-term interventions. The findings are suggestive, but see Bishop (2013) for a clear-eyed assessment.
increases in white matter volume: Myers et al. (2015).
The brain research is converging: Pugh et al. (2014).
Migration errors produce ectopias: See Peterson & Pennington (2012). For neural migration explained, with animations, see “Research Interests,” Rakic Lab, http://rakiclab.med.yale.edu/research. The occurrence of migration errors in dyslexia was discovered in the 1980s by neurologist Albert Galaburda, who conducted postmortem studies of the brains of dyslexics who had recently died. Now, decades later, structural anomalies can be observed, using structural neuroimaging, in dyslexics who are very much alive. See Galaburda et al. (2006) for the story of this research.
behavioral measures could provide: Robin Morris (Georgia State University) described this use of behavioral and imaging data in a meeting of the scientists involved in a large project on dyslexia and comorbid conditions that he leads (June 24, 2016).