الفهرس 
Acknowledgement
Epidemiology and Burden of COPDOnly 14 pages are availabe for public view
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Abstract
This study was conducted in Assuit University Hospital at the Chest Diseases and Tuberculosis Department and the Neurology and Psychiatry Department during the period between May 2013 and October 2015. We enrolled 25 stable COPD patients their mean age was (57 ±5 years) among which were (14 male & 11 female) and 25 adult age and sex matched healthy controls with mean age (56 ± 5 years) among which were (13 male & 12 female).
The cases were requrited from Chest department and Pulmonology outpatients’ clinic. Samplying was done by convienient samplying technique. Patients and controls were subjected to careful history taking, detailed chest and neurological examination and some routine investigation were done to apply criteria of inclusion to the study. After being included and informed consent with signed both patients and controls undergone arterial blood samplying, pulmonary function testing, cortical excitability evaluation, peripheral nerve study, psychometric evaluation of cognitive function & Anxiety and depression, p-300 related evoked potiential study and 1H MRI spectroscopy to evaluate cerebral metabolities distribution.
The observed data were collected and analyzed using SPSS statistical software computer program version 20 (Statistical Package for Social Science), Medcalc v.11.6.and Open Epi V.3.01. Nonparametric tests were applied, patients’ results were compared to control. Patients’ neuropsychiatric results were correlated to gasometric and spirometric parameters.
Conclusion:
from the current study we can conclude that there is alteration in cortical excitability of COPD patients with an obvious “ceiling effect” or “state of enhanced inhibition” and this is mainly explained by the degree of chronic hypercapnia rather than the extent of chronic hypoxemia.
Also there is an evident impairment of diaphragmatic central corticospinal pathway evident in increased motor evoked potential latency, failure of facilitation and decreased compound motor action potential amplitude these data are toward cortical depression and closely correlated to chronic hypercapnia mainly.
Peripheral neuritis is a very common comorbidity in COPD patients. All types of neuropathy can take place. Sensory affection is more evident than motor affection. Axonal degeneration type is the commonest type of observation noticed. Most affections are subclinical. chronic hypoxemia is the corner stone of pathogenesis of neuropathy in COPD. The frequency of neuropathy in COPD was 36% for motor neuropathy and 80 % for sensory neuropathy (68% axonal sensory neuropathy & 12% demyelinating sensory neuropathy).
Moreover, cognitive dysfunction is a fixed finding that occurs in the course of COPD. It should be early monitored and followed up. Hypoxemia seems to play the principal role in cognitive disorders. Spirometric parameters decline (namely FEV1/FVC) seems to be closely related to occurrence of cognitive dysfunction in COPD. The frequency of cognitive disorder by WAIS-III was 54% and by MMSE was 72%.
Meanwhile Depression and anxiety is a very common comorbidity seen with COPD. It is a fixed observation in all studies done to observe it. They are closely related to dyspnea and improvement of dyspnea markedly improve those symptoms. The incidence of anxiety and depression is directly related to decline in spirometric parameters namely (FVC). The frequency of anxiety in COPD was 36% & of Depression was 44 %.
Magnetic Resonance Spectroscopy (MRS) gave us an insight to study the neurochemical changes that occur in COPD patients. chronic hypoxemia & hypercapnia seems to play the key role in the pathophysiology of neurochemical changes in COPD.
Recommendations:
1- Neurological comorbidities are frequently associated with COPD patients and we recommend early screening and treatment of those comorbidities.
2- chronic hypoxemia and hypercapnia together with the indices of severity of COPD seems to be correlated to the severity of the neurological comorbidities, so we recommend early oxygen therapy and proper management COPD to avoid those comorbidities.
Limitations of the study: We were not able to evaluate myopathy in COPD group we examined because most of the patient refused the technique at the start of the study and some of them became defaulters. MRI spectroscopy was only applied to small number of patients and controls Due to financial issues.
Future prospective: we recommend a complementary study to assess the improvement of neurological comorbidities after oxygen therapy, improving spirometric parameters and treatment with anxiolytics and antidepressant in COPD. Combining Functional MRI (ƒMRI) and perfusion MRI together with MRI spectroscopy will make us understand more the cerebral metabolic changes in COPD.