Leslie Henderson

The severity and nature of motor impairment in Asperger's syndrome: a comparison with Specific Developmental Disorder of Motor Function

BACKGROUND The aims of this study were to measure objectively the extent and severity of motor impairment in children with Aspergers syndrome and to determine whether the motor difficulties experienced by such children differed in any way from those classified as having a Specific Developmental Disorder of Motor Function (SDD-MF). Criteria derived from ICD 10-R were used to identify 11 children with Aspergers syndrome and a matched group of 9 children with a Specific Developmental Disorder of Motor Function. Children in both groups were required to have a verbal IQ of 80 or greater on the WISC IIIR. METHOD The Autism Diagnostic Interview (Revised; Lord, Rutter, & LeCouteur, 1994) was used to identify features of AS in the first group and to exclude them in the latter. The Movement Assessment Battery for Children (Henderson & Sugden, 1992) provided a standardised test of motor impairment. A Gesture Test based on that by Cermak, Coster, and Drake (1980) was used to assess the childs ability to mime the use of familiar tools and to imitate meaningless sequences of movements. RESULTS All the children with Aspergers syndrome turned out to meet our criterion for a diagnosis of motor impairment, five of the six most severely motor impaired children in the whole study being from this group. Performance of the Asperger group was also slightly poorer on the Gesture Test. The profile of performance on each test was examined in detail but no evidence of group differences in the pattern of impairment was found. CONCLUSIONS This study is consistent with others suggesting a high prevalence of clumsiness in Aspergers syndrome. Our findings also attest to the widespread prevalence of motor impairment in developmental disorders and the problems such co-morbidity poses for attempts to posit discrete and functionally coherent impairments underlying distinct syndromes.

Antisaccades and remembered saccades in Parkinson's disease.

Antisaccades were studied in ten patients with mild to moderate Parkinsons disease and ten age-matched normal controls. Remembered saccades and reflex saccades were assessed for comparison. In the population of patients who showed the previously reported abnormalities of remembered saccades, antisaccades were indistinguishable from those of controls in latency, gain and peak velocity. This finding implies that antisaccades are mediated through pathways which are unaffected by Parkinsons disease, and which are therefore presumably distinct from pathways mediating other voluntary saccades.

Saccadic abnormalities in psychotic patients. I. Neuroleptic-free psychotic patients.

Most of the previous research reporting abnormalities of rapid re-fixation eye movements (saccades) in patients with schizophrenia has used patients receiving neuroleptic medication. In this study non-neuroleptically medicated schizophrenics were compared with other psychiatric patients using a variety of saccadic paradigms to determine the specificity of saccadic dysfunction. The patient groups consisted of schizophrenics (N = 18), bipolar affectives (N = 18), anxiety neurotics (N = 10) and normal controls (N = 31), none of whom had received neuroleptic medication for the preceding 6 months. Four behavioural paradigms, reflexive, predictive, remembered and ANTI were used to elicit saccades. The primary abnormality in the schizophrenic group was a significantly increased rate of distractibility in the ANTI (saccades made towards the target rather than in an opposite direction) and REM (saccades made prior to the imperative cue) paradigms. The major neuropsychological variable predictive of these errors was Wisconsin card sort perseverative errors. These data, in conjunction with findings from previous neurological research, would seem to provide converging evidence towards dysfunction of prefrontal cortex in schizophrenia.

Saccadic abnormalities in psychotic patients. II. The role of neuroleptic treatment

The effects of dopamine-antagonistic neuroleptic (NL) medication on saccadic eye movements were compared in matched groups of 40 NL-treated and 18 NL-free schizophrenic patients and in 18 NL-treated and 14 NL-free bipolar affective patients. Manipulation of the saccadic paradigm yielded data on four types of saccade: those reflexively elicited by novel stimuli (REFLEX saccades), those directed towards the remembered location of a target now extinguished (REM) or towards the location where a predictably alternating target is expected to appear (PRED), or ANTI saccades, directed away from the stimulus to the mirror image location. Extensive psychiatric, neurological and neuropsychological assessments were also carried out on all subjects. The saccades of NL-treated patients, regardless of diagnosis, were less spatially accurate than those of NL-free patients, with a greater tendency to fall short of the target when generated towards the locus of a mentally represented target. This effect was greatest with a predictably alternating target, especially during periods when target visibility was withdrawn, only a temporal cue remaining. This pattern of impairment which is also found in early stages of Parkinsons disease is likely to be due to deficiency of striatal dopamine. Its best clinical predictors were disease duration, and Webster-Parkinsonism scores. Failure to suppress reflexive saccades to the stimulus in the REM and ANTI paradigms were more closely associated with schizophrenia than with NL treatment and were best predicted by negative symptoms and Wisconsin perseverative errors, both of which are widely regarded as indicators of frontal lobe dysfunction.

Eye movements and spatial working memory in Parkinson's disease.

Abstract Mechanisms of spatial working memory and eye movement control were investigatedin eight mild to moderate Parkinsons disease patients (PDs). Subjects were presented with asequence of four targets which had to be memorized and then recalled by moving their eyes tofixate the four locations in the correct order. Two variations on this procedure were used inwhich either a different sequence of lights was presented on each trial, or an identical sequenceof lights was repeated on each trial. In both conditions subjects made memory-guided eyemovements in the dark, without any visual cues to eye movement accuracy or the locations of thepreviously illuminated lights. Analysis of the amplitude of the primary eye movement and finaleye position for each step in the sequence showed that PDs made several discrete saccadic eyemovements of reduced amplitude before reaching the final eye position (multi-stepping). When anovel target sequence had to be memorized on each trial, the final eye position reached by PDsfor each location was also found to undershoot relative to controls. In contrast, when an identicalsequence of targets was repeated on each trial, PDs final eye position was found to be normal,although primary movement amplitudes were still reduced. PDs showed no multi-stepping andnormal final eye position gain under conditions for which the target lights in the sequence wereilluminated during movement execution. PDs also made an increased proportion of overt errorsin target sequence recall. Parallel neuropsychological testing in PDs and controls revealed thaterror rates in the sequential memory-guided saccade task were significantly correlated withperformance in a task thought to be sensitive to spatial working memory dysfunction. Thefindings suggest that short-term spatial memory representations are disrupted in the early stagesof PD.

Toward an Understanding of Developmental Coordination Disorder

We consider three issues concerning unexpected difficulty in the acquisition of motor skills: terminology, diagnosis, and intervention. Our preference for the label Developmental Coordination Disorder (DCD) receives justification. Problems in diagnosis are discussed, especially in relation to the aetiology-dominated medical model. The high degree of overlap between DCD and other childhood disorders appears to militate against its acceptance as a distinct syndrome. In this context, we emphasize the need to determine whether incoordination takes different forms when it occurs alone is combined with general developmental delay or with other specific disorders in children of normal intelligence. Studies of intervention have mostly shown positive effects but do not, as yet, allow adjudication between different sorts of content. We suggest that the study of DCD and its remediation would benefit greatly from the employment of the simple but rich paradigms developed for the experimental analysis of fully formed adult movement skills.

Scales for rating motor impairment in Parkinson's disease : studies of reliability and convergent validity

Study 1 examined the reliability of the ratings assigned to the performance of five sign-and-symptom items drawn from tests of motor impairment in Parkinsons disease. Patients with Parkinsons disease of varying severity performed gait, rising from chair, and hand function items. Video recordings of these performances were rated by a large sample of experienced and inexperienced neurologists and by psychology undergraduates, using a four point scale. Inter-rater reliability was moderately high, being higher for gait than hand function items. Clinical experience proved to have no systematic effect on ratings or their reliability. The idiosyncrasy of particular performances was a major source of unreliable ratings. Study 2 examined the intercorrelation of several standard rating scales, comprised of sign-and-symptom items as well as activities of daily living. The correlation between scales was high, ranging from 0.70 to 0.83, despite considerable differences in item composition. Inter-item correlations showed that the internal cohesion of the tests was high, especially for the self-care scale. Regression analysis showed that the relationship between the scales could be efficiently captured by a small selection of test items, allowing the construction of a much briefer test.

On the existence of an attention-demanding process peculiar to simple reaction time: Converging evidence from Parkinson's disease

Abstract Patients with Parkinsons disease tend to be slower at simple reaction-time (S.R.T.) tasks than age-matched controls. Some previous studies have shown an S.R.T. impairment where no prolongation of choice reaction time (C.R.T.) could be detected. Furthermore, S.R.T. and C.R.T. have been found to be pharmacologically dissociable in Parkinsons disease, with the S.R.T. deficit resistant to dopaminergic therapy. Such a deficit implies the existence of an underlying process which normally confers a specific advantage on S.R.T. performance but which may be selectively impaired in Parkinsons disease. Using a high-compatibility tactile R.T. task, we show that control subjects are more impaired in S.R.T. by the imposition of a secondary, oral reading task than Parkinsonian subjects. Indeed, under dual-task conditions, the usual Parkinsonian disadvantage in S.R.T. is abolished. In contrast, the deleterious effect of the secondary task on C.R.T. did not differ between the two groups. These findings converg...

Remembered saccades with variable delay in Parkinson's disease

The effect of increasing delay on the metrics of remembered saccades was studied in 10 subjects with mild Parkinsons disease, none of whom was receiving treatment with L‐dopa, and nine age‐matched control subjects. Delays of 1 msec, 250 msec, 1000 msec, 2500 msec, and 5000 msec were used, and reflexive saccades used as a control condition. Results were analyzed for the gain of the primary saccade and the accuracy of the final eye position (FEP gain). Reflexive saccades were normal in subjects with Parkinsons disease, but remembered saccades showed marked hypometria of primary saccade gain at all delays. FEP gain was unimpaired in Parkinsons disease, and primary saccade gain and FEP gain did not vary as a function of delay. Hypometria of primary saccades is compatible with dysfunction in striato‐collicular inhibitory pathways in Parkinsons disease, arising as a functional consequence of dopamine deficiency in the basal ganglia. Maintenance of an accurate FEP gain suggests no deficit in oculomotor spatial working memory in Parkinsons disease, at least at delays of up to 5 sec.

Critical notice. Information processing approaches to acquired dyslexia

By far the most common traumatic cause of language disturbance is the cerebro-vascular accident (stroke). In this condition the blood supply to a region of brain tissue is interrupted, often due to the formation of an obstruction within the vasculature or to a larger clot forming in tissue after hemorrhage. In rarer cases a similar outcome may be due to hemorrhage caused by a gunshot wound or to closed head injury. The tissue that is deprived of blood dies. As a result of degeneration of the blood vessels water floods into the tissue, producing swelling that may affect the entire brain for a time. However, adaptation of the surrounding vascular system usually permits the fluid to drain away, together with much of the dead and now liquified tissue. This leaves the patient effectively with a hole in the brain, or at least an area of reduced tissue density, and as a consequence there may be some gross spatial readjustment of the surrounding tissue. With the dissipation of the swelling the patient becomes conscious but quite widespread changes in the state of the brain tissue may continue for some time thereafter. Typically the area of damage is large and difficult to define with precision due to the complex processes that give rise to it. For this reason, it is not, perhaps, surprising that attempts to relate patterns of impairment to the site of injury have yielded inconsistent outcomes. Despite these difficulties, naive psycho-anatomy (the term is Brain’s, I 96 I) has been the dominant tradition in the study of speech and reading disorders. Yet this approach has shown little success in accommodating the discrepancy between the effects of cortical stimulation and excision, on the one hand, and of cerebro-vascular accidents, on the other. Indeed, Penfield and Roberts (1959) have argued that there is no evidence for any cortical area that its removal causes permanent aphasia, though by convention surgeons avoid extirpation of Broca’s area. In some cases of acquired dyslexia the extent of brain damage can be estimated from computed tomograms. (These are two dimensional X-ray images of a horizontal section of the brain, produced by axial scanning of the intact brain). In an Appendix to Deep Dyslexia, Marin reviews such radiological evidence on five of the patients discussed in the book. All the patients had damage to the left hemisphere but the site of the damage varied considerably. Broca’s area, for instance, appeared to be spared in two cases. In all cases cortical and subcortical damage was very extensive and, as Marin observes, in some intuitive way out of proportion to the relatively minor language impairment.