See also the Oxford Dyslexia Unit.
Click on the superscripts to find the reference.
As many as 10% of 8-10 yr olds experience exceptional difficulties learning to read. 4 times as many boys as girls are affected, and most have a close relative with similar problems. Many are mixed handed with difficulties telling left from right and sequencing the days of the week, months of the year etc. Neuropathological and brain imaging studies have shown clear differences between dyslexics' and good readers' brains, particularly in the left, language, hemisphere. Thus dyslexia has an organic neurological basis and, contrary to previous strongly held beliefs, it is not 'purely psychological'.
Dyslexics' difficulties with reading derive from the extra demands that learning to read makes, compared with learning to speak. Reading requires the child to identify and order letters visually and to match them with the phonemic sound segments that they represent, whereas speech naturally segments into syllables, not phonemes. So children learning to read have to be taught how to subdivide words further into phonemes, and how these correspond to letters. Many dyslexics seem to have slight difficulties with hearing the subtle acoustic differences that are used to distinguish phonemes so even though they may have had little obvious difficulty learning to speak, their inability to analyse the phonemic structure of words quickly, prevents them learning to read easily1.
Likewise parsing fine optical detail is not usually required to recognise natural visual scenes; but the visual pattern of print has to be accurately segmented into separate letters when reading in order to match them with phonemes. Many dyslexics complain that letters seem to merge and move around. This is often because their eye control is insufficiently stable for accurate visual segmentation2 . In summary dyslexic children often show not only impaired ability to segment syllables auditorily into their separate phonemes, but also inability to visually sequence small letters accurately. These impairments may be individually mild, but they can accumulate to impede reading.
Both phonological and visual segmentation draw upon the ability of the nervous system to time sensory events precisely. A specific magnocellular cell type which may express a distinctive surface antigen vulnerable to autoimmune attack, probably plays a crucial role in these functions. Dyslexics seem to inherit genes that compromise development of this cell line3; in post mortem dyslexic brains the magnocellular layers of the thalamic visual and auditory relays, the lateral and medial geniculate nuclei, are found to be abnormal when compared with controls. Flicker and motion sensitivity both depend upon the visual magnocellular system, and we have shown that these are reduced in dyslexics1. Also the EEG potentials evoked by flickering visual stimuli depend on the activity of the magnocellular component of visual processing; and we have found that these are also reduced in many dyslexics. The visual magnocellular system also plays a leading part in controlling eye movements; hence dyslexics' ocular instability and poor ability to sequence letters visually may be the result of the abnormal development of their magnocellular system. We have found that we can often help children to overcome their ocular instability by means of fixation exercises or in some cases reading with only one eye4. Also some children are helped by using either blue or yellow filters, probably because these alter the balance of magnocellular and parvocellular activity. We have found that we can more than double children's reading progress by treatment of their visual instability using these techniques5.
Analogous to the visual magnocellular system, there is probably an auditory timing system whose development may also be impaired in dyslexics6. Thus their phonological problems may result not only from their visual sequencing difficulties but also from their problems hearing the acoustic cues that distinguish phonemes. In fact individuals' auditory and visual timing sensitivity explains a very large proportion (over 2/3rds) of their differences in reading ability. Thus auditory sensitivity to sound frequency predicts phonological skill independently of IQ or visual/orthographic ability, and visual motion sensitivity predicts orthographic skill independently of IQ or auditory/phonological ability, and this is true of both good and bad readers. Therefore we are developing tests of low level auditory and visual timing skills for use with preschool children to try to identify those with problems early so that we can start helping them before they begin to fail and lose self confidence.
Since we have been studying and helping thousands of children in the free clinics that we run in Oxford and Reading we have accumulated a large number of families with one or more dyslexic children. We have therefore teamed up with Professors Monaco and Fisher at the Wellcome Inst. of Human Genetics to identify genes that may be associated with reading difficulties. So far we have genotyped more than 1500 individuals and located genes that probably contribute to dyslexia on chromosomes 15 and 6. The latter may be KIAA 0319 which we've now shown to help control the migration of neurones to their correct places in the brain during cerebral development in utero7
Funding: Dyslexia Research and Wellcome Trusts.
STEREOTAXIC SURGERY FOR MOVEMENT DISORDERS AND PAIN - THE OXFORD MOVEMENT DISORDERS GROUP
The overall aim of the Oxford Movement Disorders Group is to
elucidate
the brain mechanisms that cause movement disorders in Parkinsonian and
other patients in order to improve their neurosurgical treatment.
Clearly such knowledge should assist the development of medical
treatments
as well.
The symptom that is most
disabling and most resistant to either medical or surgical treatment is
akinesia. We have found in MPTP treated monkeys that an important
cause of akinesia is overinhibition of upper brainstem structures such
as the pedunculopontine nucleus (PPN)8, which control axial
and proximal
muscles. If we overcome this inhibition using local bicuculline or
electrical
stimulation of the PPN the animals begin moving again. We
aim
to transfer these results to relieving akinesia in humans with
Parkinson's
disease, multiple system atrophy (MSA) and Progressive supranuclear
palsy
(PSP).
We have also been recording
basal ganglia field potentials (FPs) in patients with movement
disorders
during and after stereotaxic surgery, and shown that involuntary
movements
and dystonias are associated with uncontrolled spontaneous low
frequency
FP oscillations9. When these
areas are lesioned or overdriven
by high frequency electrical stimulation the oscillations cease and
this
eliminates the unwanted movements. We aim to elucidate how these
oscillations arise, how they correlate with the movement disorders and
how they differ in different structures, such as GPi, STN and
PPN.
Knowledge of each target's ‘signature’ should enable us to
optimise
our choice of target and our techniques for eliminating uncontrolled
oscillations
in each.
We have also found
characteristic spontaneous FP oscillations in the sensory
thalamus in patients with intractable central neuropathic pain from a
variety
of different origins (post stroke, post herpetic, post trigeminal
neuralgia,
phantom limb pain)10. These seem to be
associated with the feeling
of pain, and if we can reduce them by local stimulation at high
frequencies
or by driving the periventricular grey at low frequencies the patients'
pain is improved also.
Funding: MRC, Norman Collison Trust .
Last modified: 1.6.06