Research Interests
I am particularly interested in the auditory and visual perceptual impairments suffered by dyslexic children. These may be responsible for their auditory/phonological and visual /orthographic reading problems. My work over the last 25 years suggests that dyslexic children have impaired auditory and visual temporal processing which explains why they have difficulty acquiring the phonological and orthographic skills required for reading. Understanding these mechanisms has helped to explain why such seemingly bizarre treatments such as occluding one eye, wearing blue or yelllow coloured spectacles, playing music into the right ear, or eating omega 3 fish oils, may help some dyslexic children to overcome their problems.
The basic cause of dyslexics' temporal processing impairments is probably a congenital mild impairment of the development of magnocellular neurones; so I collaborate with Prof. Tony Monaco (Wellcome Inst. of Human Genetics) to find out whether this is linked with genes known to be associated with neurodevelopmental problems. We have discovered that in many dyslexics an allele of a new gene, KIAA 0319, causes underexpression of a surface active protein that helps to control neuronal migration early in the development of the brain in utero. With Prof. Angela Vincent (Inst. Mol. Medicine) we were also able to show that maternal antibodies may attack magnocellular neurones during foetal development.
Magnocellular neurones seem to be particularly vulnerable to lack of omega 3 essential fatty acids, especially eicosapentanoic (EPA) and docosahexanoic acid (DHA) which are normally found in oily fish. We have therefore conducted a number of randomised control trials that have shown that in appropriate subjects supplements of these long chain omega 3s can improve attention, concentration, reading and even antisocial behaviour in young offenders.
In addition I collaborate with Tipu Aziz and Alex Green (Oxford Functional Neurosurgery), Mitchel Glickstein (UCL) and Alan. Gibson (Barrow Neurological Inst., Phoenix, Arizona) on the neural control of movement, particularly in patients with movement disorders such as Parkinson's disease (PD). We insert stimulating electrodes into the movement control network from which we can record spontaneous electrical oscillations that correlate with the patients' involuntary movements. High frequency deep brain stimulation in these areas can often stop these oscillations and thus greatly improve the involuntary movements. We have recently discovered that another upper brainstem site, the pedunculopontine nucleus, plays an important role in controlling proximal muscles for posture and locomotion; this area is over-inhibited in many of the patients, which is a major cause of their inability to move, akinesia. If we stimulate the PPN directly at low frequencies we can often return these previously chairbound patients to an active life. We are currently attempting to develop an improved stimulator which will detect the aberrent oscilations that cause the symptoms and switch on individualised patterns of stimulation designed to combat that particular patient's abnormal activity.
In patients with intractable central neuropathic pain, the pain seems often to be caused by spontaneous oscillations in the 'central pain matrix' (periaqueductal, periventricular grey (PAG/PVG), thalamus, somatosensory cortex, anterior cingulate, insula, orbitofrontal cortex). We have found that if we drive the sensory thalamus or PAG/PVG by stimulating them at c.10 Hz we can often eliminate the oscillations and reduce the patients' feelings of pain very considerably. This stimulation also changes autonomic function; and the degree of pain reduction seems to correlate with the degree of blood pressure reduction that we achieve.
It seems possible that negative mood swings in depression may also be associated with spontaneous uncontrolled oscillations in the limbic system; hence we may be able to use stimulation of the anterior thalamus, cingulate or orbitofrontal cortex to relieve intractible depression
Teaching and Public Understanding of Science
I continue to carry out some
tutorial teaching (currently for Balliol College) because I enjoy it
and still believe that it is the best way to teach. I also still
give some University lectures, and also many lectures to schools and
general audiences about the fascination of Neuroscience, the
importance of animal experiments for advancing this and about Oxford
University and its admissions procedures. I believe strongly that
the benefits of Oxford's tutorial teaching should be made available to
all those with the ability to benefit from it, irrespective of income,
class, colour or creed (despite Chancellor Gordon Brown's allegations
of my 'elitism' over the Laura Spence affair!). I also
continue to try to relieve the load of rote learning endured by medical
students during their preclinical course; the course should
emphasise only what is important for clinical medicine, and encourage
students to go into greater depth only in areas which really interest
them. Thus we must preserve the strengths of the final Honours course
in which students can specialise in what they find most interesting.
Our job is to teach students how to teach themselves, to think clearly
and logically and to evaluate evidence critically, without being
overburdened with memorising facts which nowadays can so quickly and
easily be obtained from computerised reference sources.
I am grateful that I now no longer have much University or College
administration, and still deplore the current climate of
'accountability', which implies lack of trust in people's commitment to
do their job conscientiously, and has spawned such a
proliferation of forms to fill in that nobody reads.
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Neural Basis of
Dyslexia |