Cerebral atrophy in Parkinsonism

Abstract

A review of the literature concerned with involvement of the cerebral cortex in Parkinsonism shows that this subject has received only little attention. Apart from the indirect evidence of degeneration of cortico-pallidal fibres, most reports deal with cases of Parkinsonism complicated by dementia or other neuronal degenerations. Criteria for the radiological diagnosis of cerebral atrophy are critically reviewed, and the standards adopted in this study for the diagnosis of enlargement and asymmetry of the ventricles, and of cortical atrophy, are defined. The pneumo-encephalograms of 250 cases of Parkinsonism, obtained by a standard technique during stereotactic operations, are compared with the pneumo-encephalograms of 56 patients over the age of 50 years, who suffered from various neurological diseases. Cortical atrophy was found in 57.2% of the patients with Parkinsonism, in contrast to only 26.8% of the patients of the control series. Enlargement of the lateral ventricles occurred with comparable frequency in the two series. Asymmetry of the size of the lateral ventricles, and widening of the third ventricle was found more often in the controls than in the Parkinsonian cases. A statistical analysis of the relationship of cortical atrophy and ventricular enlargement to various aetiological and clinical features of Parkinson's syndrome was carried out with the aid of a computer. No significant correlation between increased dimensions of the lateral ventricle, or of the third ventricle, and any of the symptoms of Parkinsonism could be demonstrated. Unilateral ventricular enlargement did not correspond with the severity or lateralisation of clinical symptoms in patients where the disease affected mainly one side of the body. A prevalence of cortical atrophy in females in contrast to a predominance of ventricular enlargement in males cannot be explained. Cortical atrophy was found more often in patients with presumed “arteriopathic” Parkinsonism than in those with the idiopathic and post-encephalitic forms of the disease. It was not influenced by the duration of the illness. Statistical analyses demonstrated a significant relationship between cortical atrophy and the degree of rigidity, the severe gait disorders, and the patients' general incapacity, whereas the correlation with tremor and akinesia reached significant levels only if the total incidence of these symptoms, irrespective of degree, was compared with the number of patients who did not suffer from them. In patients with pre-operative intellectual defects ventricular enlargement was found more often than cortical atrophy. After thalamotomy, the rate of recovery from rigidity and from general incapacity was found to be lower in patients with radiological signs of cortical atrophy, whereas the incidence of transient post-operative mental confusion and of permanent defects of memory and intellect was higher in these cases. The possible fallacies and limitations of pneumo-encephalography in the diagnosis of cortical atrophy are recognised and discussed, but it is concluded that the results of this investigation should stimulate further study of the contribution of the cerebral cortex to the pathogenesis of Parkinson's disease.