An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy
Objectives: To assess the clinical profile and electroencephalography (EEG) abnormal patterns in patients with metabolic encephalopathy (ME). Methods: A cross-sectional observational study was conducted on 80 diagnosed patients of ME over a period of 24 months from January 2019 until January 2021. C...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2025-05-01
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| Series: | Journal of Family Medicine and Primary Care |
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| Online Access: | https://journals.lww.com/10.4103/jfmpc.jfmpc_1926_24 |
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| author | Ajay K. Mishra Shahenshah Ahmad Mahima Pandey Saboor Mateen Firdaus Jabeen Nazrul Haque Memon Z. Abubakkar Furqan A. Memon |
| author_facet | Ajay K. Mishra Shahenshah Ahmad Mahima Pandey Saboor Mateen Firdaus Jabeen Nazrul Haque Memon Z. Abubakkar Furqan A. Memon |
| author_sort | Ajay K. Mishra |
| collection | DOAJ |
| description | Objectives:
To assess the clinical profile and electroencephalography (EEG) abnormal patterns in patients with metabolic encephalopathy (ME).
Methods:
A cross-sectional observational study was conducted on 80 diagnosed patients of ME over a period of 24 months from January 2019 until January 2021. Causes of ME were determined. Glasgow coma score (GCS) was recorded. Routine biochemical investigations were done, and EEG patterns were recorded. The outcome measures were association of EEG patterns with the cause of ME.
Results:
The mean age was 39.62 ± 14.98 years, with 61.3% being men. The mean GCS was 13.28 ± 0.96. The cause of ME was single in 34 (42.5%) cases and multifactorial in 46 (57.5%) cases. Hyperammonemia was present in all patients. Abnormal EEG findings were observed in 7 (8.75%) patients in the form of slow posterior background rhythm. The patients with normal EEG had comparable mean GCS as those with abnormal EEG (13.30 ± 0.97 vs. 13.14 ± 0.90, P = 0.667). Abnormal EEG was observed in comparable proportion of patients with single cause of ME than multiple causes (11.8% vs. 6.5p = 0.714).
Conclusion:
ME is seen in a wide age group of patients with majority being in the age group of 21 to 40 years followed by 41 to 60 years. It carries a male predominance with multifactorial causes where hyperammonemia remains the most common metabolic abnormality. Cases may either have a single cause or multiple causes for metabolic abnormality. EEG abnormality was seen in only 8.7% cases with no statistical relation with causes of metabolic abnormality. |
| format | Article |
| id | doaj-art-62c6fc8405db440fb04c8db8caa368cf |
| institution | OA Journals |
| issn | 2249-4863 2278-7135 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Journal of Family Medicine and Primary Care |
| spelling | doaj-art-62c6fc8405db440fb04c8db8caa368cf2025-08-20T02:34:46ZengWolters Kluwer Medknow PublicationsJournal of Family Medicine and Primary Care2249-48632278-71352025-05-011451968197210.4103/jfmpc.jfmpc_1926_24An observational study of clinical profile and EEG changes in patients with metabolic encephalopathyAjay K. MishraShahenshah AhmadMahima PandeySaboor MateenFirdaus JabeenNazrul HaqueMemon Z. AbubakkarFurqan A. MemonObjectives: To assess the clinical profile and electroencephalography (EEG) abnormal patterns in patients with metabolic encephalopathy (ME). Methods: A cross-sectional observational study was conducted on 80 diagnosed patients of ME over a period of 24 months from January 2019 until January 2021. Causes of ME were determined. Glasgow coma score (GCS) was recorded. Routine biochemical investigations were done, and EEG patterns were recorded. The outcome measures were association of EEG patterns with the cause of ME. Results: The mean age was 39.62 ± 14.98 years, with 61.3% being men. The mean GCS was 13.28 ± 0.96. The cause of ME was single in 34 (42.5%) cases and multifactorial in 46 (57.5%) cases. Hyperammonemia was present in all patients. Abnormal EEG findings were observed in 7 (8.75%) patients in the form of slow posterior background rhythm. The patients with normal EEG had comparable mean GCS as those with abnormal EEG (13.30 ± 0.97 vs. 13.14 ± 0.90, P = 0.667). Abnormal EEG was observed in comparable proportion of patients with single cause of ME than multiple causes (11.8% vs. 6.5p = 0.714). Conclusion: ME is seen in a wide age group of patients with majority being in the age group of 21 to 40 years followed by 41 to 60 years. It carries a male predominance with multifactorial causes where hyperammonemia remains the most common metabolic abnormality. Cases may either have a single cause or multiple causes for metabolic abnormality. EEG abnormality was seen in only 8.7% cases with no statistical relation with causes of metabolic abnormality.https://journals.lww.com/10.4103/jfmpc.jfmpc_1926_24electroencephalographyglasgow coma scalemetabolic encephalopathy |
| spellingShingle | Ajay K. Mishra Shahenshah Ahmad Mahima Pandey Saboor Mateen Firdaus Jabeen Nazrul Haque Memon Z. Abubakkar Furqan A. Memon An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy Journal of Family Medicine and Primary Care electroencephalography glasgow coma scale metabolic encephalopathy |
| title | An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy |
| title_full | An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy |
| title_fullStr | An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy |
| title_full_unstemmed | An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy |
| title_short | An observational study of clinical profile and EEG changes in patients with metabolic encephalopathy |
| title_sort | observational study of clinical profile and eeg changes in patients with metabolic encephalopathy |
| topic | electroencephalography glasgow coma scale metabolic encephalopathy |
| url | https://journals.lww.com/10.4103/jfmpc.jfmpc_1926_24 |
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