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  • 1. Journal of Community Medicine, January 2009, Vol .5 (1) Original Article Introduction Uraemic encephalopathy is an acute or subacute organic brain syndrome that regularly occurs in patients with acute or chronic renal failure when glomerular filteration rate declines below approximately 10% of normal and is characterised by diffuse dysfunction of cerebral hemispheres. Such patients display variable disorders of consciousness, psychomotor behaviour, thinking, memory, speech perception and emotion. The symptoms that are invariably reported may include sluggishness and easy fatigue, daytime drowsiness and insomnia with a tendency towards sleep-inversion, itching, inability to focus or sustain attention or to perform mental (cognitive) tasks and manipulation, inability to manage ideas and abstractions, disorientation and confusion with bizarre behaviour, hallucinosis, meningeal signs and preterminal coma and convulsions. Correspondence: Manoj K Bansal, U.N. Mehta Institute of Cardiology & Research Centre, Civil Hospital Campus, Ahmedabad- 380 016, Email: docmbansal@gmail.com Bansal EEG changes in uraemic encephalopathy EEG CHANGES IN URAEMIC ENCEPHALOPATHY Manoj K Bansal U.N. Mehta Institute of Cardiology & Research Centre, Civil Hospital Campus, Ahmedabad- 380 016 Abstract This study conducted among 38 patients suffering from uraemic encephalopathy due to chronic renal failure explores the pattern of early EEG findings and reveals the prognostic usefulness of the early EEG findings among the patients while they are still conscious and oriented. The severity of the abnormal EEG changes also is well correlated with the severity of the renal damage and the decline of renal functions as revealed by high blood urea and serum creatinine levels. Keywords: EEG, uraemic encephalopathy, prognostic usefulness
  • 2. EEG is a sensitive, though non-specific measure of certain electrophysiological functions of brain and is used as a non-invasive means of screening for focal structural abnormalities of the brain. In uraemia the same progression of EEG abnormalities occur with the same broad correlation with the clouding of consciousness. The progression of the renal damage to the stage of uraemic encephalopathy is reflected through EEG abnormalities as appearance of theta waves; disorganisation to disappearance of normal basic rhythms; diminished reactivity to the EEG to afferent stimulation and domination by generalised delta activity. Not uncommonly this is frontally predominant and may take on a markedly paroxysmal appearance. The EEG findings are less pronounced in CRF patients, as compared to ARF patients, and generalised abnormalities occur when clinical signs of encephalopathy are equivocal1,2 . In most uraemic patients with abnormal EEGs, dialysis results within improvements within 24 hours, except for the percentage of EEG frequencies above 9 Hz and below 5 Hz which remain unaffected by dialysis for 6 to 8 weeks, though return to normal with recovery of renal function. Usually by the time diagnosis of ARF is made the EEG findings are grossly abnormal and the percentage of EEG power less than 5Hz and less that 7 Hz which are standard measurements of the percentage of EEG power devoted to abnormal (delta) slow wave activity, are over twenty times the normal value. This study attempts to assess the prognostic usefulness of EEG findings in uraemic encephalopathy and their correlation with the renal and mental functions as scant studies globally have addressed this important issue and an extensive review of the literature revealed an absence of studies on this important issue in India. Material & Methods This study explores the EEG changes among 38 patients suffering from uraemic encephalopathy due to chronic renal failure at M.Y. Hospital which is the teaching hospital of M.G.M. Medical College, Indore. The important inclusion criteria were age 11 years and above; blood urea levels above 160 mg/dl; serum creatinine levels above 2.5 mg/dl; evident clinical signs of renal failure such as fatigue, sleep disorder lethargy, asterixis, peripheral neuropathy, restless leg syndrome, muscle cramps, nausea & vomiting and uraemic foetor; and, clinical signs of ureamic encephalopathy as evidenced by changes in metal functions, pursuant to their detailed history taking and systemic examination. EEGs were taken through standard
  • 3. technique on a 16 channel modern EEG machine. Adequate technical skills care was taken in assuring good electrical contact for avoidance of artifacts. The study attempts to study the EEG changes in uraemic patients; correlates EEG observations with clinical mental status of patients; and finally correlates these with the biochemical profile. Mean ± S.D, Z test and percentages have been applied for statistical significance. Results and Discussion The general profile revealed that all of the cases belonged to the age group of 11 to 70 years with 41 years as the mean age; an almost 2: 1 sex ratio; and predominantly middle socioeconomic groups. Out of these 38 cases of uraemic encephalopathy, the majority 31 (82%) had abnormalities in the EEGs and only 7 had normal EEGs as seen in table 1 with a ratio of about 4.5 in line with earlier findings in the United States, which had reported of EEG abnormalities among the majority (61.5%) of the 13 uraemic patients3 . What was an important was that in the majorities of the patients in the present study the EEG had revealed abnormalities while the patients were still conscious and orientated. Table-I EEG findings in patients of uraemic encephalopathy EEG Rhythm Uraemic encephalopathy (No. of cases) Total Mild Moderate Severe ALPHA Rhythm 1. Normal & well sustained 15 14 1 0 2. Not well sustained 9 5 3 1 3. Intermittently seen 14 0 8 6 . Not mentioned 0 0 0 0 BETA Rhythm 1. Normal (anterior dormant) 15 13 1 1 2. Excessive 11 1 4 6 3. Not mentioned 12 5 7 0 THETA Waves 1. Absent 8 8 0 0 2. Mild, intermittent 5 3 2 0 3.Paroxysmal 16 8 7 1 4.Continuous 9 0 3 6 The patients with uraemic encephalopathy were classified into mild, moderate and severe depending upon their symptoms. Those having symptoms of itching, sluggishness and easy fatigue, day time drowsiness and insomnia with a tendency towards sleep inversion were classified as mild; those with inability to focus or sustain attention or to perform mental (cognitive) tasks and manipulation, inability to manage ideas and abstractions were classified as moderate; and, the patients who were disoriented and
  • 4. confused with bizarre behaviour, hallucinosis and preterminal coma and convulsions were classified as having severe uraemic encephalopathy. Their significant correlation with EEG findings has been discussed subsequently. The EEG findings in patients with CRF are usually less than those observed in patients with ARF. These early EEG findings in the majority of the patients, while they were still conscious and oriented reveal the prognostic usefulness of EEGs in patients of uraemic encephalopathy4 . The majority of the cases had exhibited borderline abnormality 22 (57.9%); followed by those moderately abnormal 9 (23.7%) and lastly 7 (18.4%) had abnormal EEGs as shown in table 1. All of the 31 abnormal cases had revealed diffuse non-specific slow wave abnormalities (p<0.05) which mainly consisted of theta slow wave activity (4-7 cps), reflecting the predomination of diffuse slowing in encephalopathy or the progression from slowing of alpha waves mixed with bursts of theta activities to predominance of diffuse slowing5 . The theta slow wave abnormalities had become more conspicuous by the stimulatory procedure of hyperventilation. The appearance of this theta activity disorganizes the normal basic rhythm and eventually leads to its final disappearance. In uraemia the progression of EEG abnormalities is similar to other encephalopathies with the same broad correlation with clouding of consciousness. In most of our abnormal cases the basic alpha rhythm was not well sustained and was intermittently seen posteriorly. Irregular beta and theta activity was seen bilaterally. The most significant and ominous abnormality was the occurrence of delta wave activity (1-4 cps) in 5 (13%) cases with the diminution of the reactivity of the EEG to afferent stimulation and sometimes frontal predominance. It needs to be mentioned that delta activity consists of very slow waves less than 4 Hz and its presence outside sleep in adults is always abnormal. In most of the cases the basic rhythm got disorganised and finally disappeared being replaced by diffuse non-specific slow wave abnormality as discussed earlier1,5 . The severity of the abnormal EEG changes was found to be well correlated with the severity of the clinical features and with the renal damage
  • 5. as revealed by high blood urea and serum creatinine levels ranging from 175 to 240 mg/dl in these patients. These findings support the earlier international findings reporting of a good correlation between the percentage of EEG frequencies and power below 7 Hz and the decline of renal functions as estimated by serum creatinine, in line with the findings of Teschan, PE et al. (19796 ; 19837 ), and the slowing of EEG with increased creatinine concentrations8 and with the severity of renal failure9 . Bourne JR et al. (1975)8 had found that the slowing in the EEG was directly correlated with increased creatinine concentrations and Ginn, HE et al. (1975)9 had reported the EEG findings to be highly correlated with the severity of renal failure. Questionable epileptiform discharges were found in two patients. None of the patients had dialysis encephalopathy as none of them were on a maintenance dialysis. The EEG may help in management of uraemic encephalopathy by picking up early cerebral dysfunction in the preclinical stage. It also helps in correlating clinical status with one of the objective parameters of cerebral function and if EEG is obtained in a serial manner in a given patient it helps in prognostication. With the advent of modern computerised digital brain mapping methods it may be expected to decipher more subtle and specific electrophysiological changes and their correlation with clinical status, biochemical profile, dialysis status and prognosis. Conclusion The early EEG findings are prognostic useful in patients of uraemic encephalopathy while the patients are still conscious and oriented and the severity of the abnormal EEG changes correlate well with the severity of renal damage as revealed by high blood urea and serum creatinine levels ranging from 175 to 240 mg/dl. Thus the early EEG findings can be of prognostic usefulness among the patients while they are still conscious and oriented and the severity of the abnormal EEG changes can be a useful pointer of the severity of the renal damage and also to the decline of renal functions. Acknowledgements The author is grateful to Dr. A. Puranik, DM (Neuro) and Dr. (Prof.) A. Bajpai of MGM Medical College, Indore for their kind guidance in the study and to the DAV University, Indore for permitting me to publish these results of my MD thesis. Reference 1. Arieff, A. I., Neurological complications of renal insufficiency. In Brenner & Rector’s- The Kidney (ed. Brenner, B. M.), Saunders, Philadelphia, 2004, pp. 2227-2253.
  • 6. 2. Fraser, C. L., Arieff, A. I., Nervous system manifestations of renal failure. In: Diseases of the Kidney and Urinary Tract (ed. Schrier, R. W.), Lippincott Williams & Wilkins, Philadelphia, 2001, pp. 2769-2794. 3. Kennedy, A. C., Linton, A. L., Luke, R. G., Renfrew, S., Electroencephalographic changes during haemodialysis. Lancet, 1963, 1, 408-11. 4. Eriksson, K. J., Boyd, S. G., Tasker, R. C., Acute neurology and neurophysiology of haemolytic-uraemic syndrome. Arch Dis Child., 2001, 84, 434-5. 5. Misra, U. K., Kalita, J., Clinical Electroencephalography, Elsevier, New Delhi, 2005. 6. Teschan, P. E., Ginn, H. E., Bourne, J. R., Ward, J. W., Hamel, B., Nunnally, J. C., Musso, M., Vaughn, W. K., Quantitative indices of clinical uremia. Kidney International, 1979, 15, 676-97. 7. Teschan, P. E., Bourne, J. R., Reed, R. B., Electrophysiological and neurobehavioral responses to therapy: The National Cooperative Dialysis Study. Kidney International, 1983, 13 S, 58-65. 8. Bourne, J. R., Ward, J. W., Teschan, P. E., Musso, M., Johnston, H. B. Jr., Ginn, H. E., Quantitative assessment of the electroencephalogram in renal diseases. Electroencephalography and Clinical Neurophysiology, 1975, 39, 377-88. 9. Ginn, H. E., Teschan, P. E., Walker, P. J., Bourne, J. R., Fristoe, M., Ward, J. W., McLain, L. W., Johnston, H. B. Jr., Hamel, B., Neurotoxicity in uraemia. Kidney International, 1975, S 3, 357-60.
  • 7. 2. Fraser, C. L., Arieff, A. I., Nervous system manifestations of renal failure. In: Diseases of the Kidney and Urinary Tract (ed. Schrier, R. W.), Lippincott Williams & Wilkins, Philadelphia, 2001, pp. 2769-2794. 3. Kennedy, A. C., Linton, A. L., Luke, R. G., Renfrew, S., Electroencephalographic changes during haemodialysis. Lancet, 1963, 1, 408-11. 4. Eriksson, K. J., Boyd, S. G., Tasker, R. C., Acute neurology and neurophysiology of haemolytic-uraemic syndrome. Arch Dis Child., 2001, 84, 434-5. 5. Misra, U. K., Kalita, J., Clinical Electroencephalography, Elsevier, New Delhi, 2005. 6. Teschan, P. E., Ginn, H. E., Bourne, J. R., Ward, J. W., Hamel, B., Nunnally, J. C., Musso, M., Vaughn, W. K., Quantitative indices of clinical uremia. Kidney International, 1979, 15, 676-97. 7. Teschan, P. E., Bourne, J. R., Reed, R. B., Electrophysiological and neurobehavioral responses to therapy: The National Cooperative Dialysis Study. Kidney International, 1983, 13 S, 58-65. 8. Bourne, J. R., Ward, J. W., Teschan, P. E., Musso, M., Johnston, H. B. Jr., Ginn, H. E., Quantitative assessment of the electroencephalogram in renal diseases. Electroencephalography and Clinical Neurophysiology, 1975, 39, 377-88. 9. Ginn, H. E., Teschan, P. E., Walker, P. J., Bourne, J. R., Fristoe, M., Ward, J. W., McLain, L. W., Johnston, H. B. Jr., Hamel, B., Neurotoxicity in uraemia. Kidney International, 1975, S 3, 357-60.