Non-alcoholic Wernicke’s Encephalopathy
Narra Rama Krishna, P Bhimeswara Rao, B Johny Prasad, Putcha Anusha
Additional Proffessor, Department of Radiodiagnosis, Katuri Medical College, Guntur, Andhra Pradesh, India. 2. Proffessor, Department of Radiodiagnosis, Katuri Medical College, Guntur, Andhra Pradesh, India. 3. Assistant Proffessor, Department of Radiodiagnosis, Katuri Medical College, Guntur, Andhra Pradesh, India. 4. Junior Resident, Department of Radiodiagnosis, Katuri Medical College, Guntur, Andhra Pradesh, India.
Correspondence Address :
Dr. Narra Rama Krishna,
Flat No: 30, 5 Floor, Venkateshestate Apartment,
½ Chandramouli Nagar, Guntur-500019,
Andhra Pradesh, India.
: The term dermatoglyphics was coined by Cummins and Midlo in 1926. It applies to a unique division of anatomy which includes study of palm and toe prints. Palm prints include much more information than finger print. Palmar studies are much easier to study and interpret as compared to fingerprints.
Aim: To study the palmar angles in carcinoma breast patients and in normal healthy individuals.
Materials and Methods: A cross-sectional study was conducted in which palm prints of 100 breast cancer patients were taken as cases and were compared with those of healthy females without breast cancer, taken as controls. The parameters in this study were palmar angles (‘atd’,‘dat’,‘tda’).The means of ‘atd’, ‘tda’ and ‘dat’ angles were compared between right and left hands of cases and controls to establish the symmetry.
Results: Mean ‘atd’ angles in cancer cases were (44.9±6.04) as compared to controls (43.2±5.74). The mean ‘atd’ angle was significantly higher in cancer cases as compared to controls (p<0.05). The ‘tda’ angle in carcinoma of breast patients was 76.4±6.80 and in control it was 77.7±5.27 and ‘dat’ angle in carcinoma breast patients was 58.9±6.83 and in control it was 59.2±5.58 The angles ‘tda’ and ‘dat’ did not vary significantly between cancer patients and controls.
Conclusion: These angles play a significant role in assessing the dermatoglyphic difference between the cancer breast patients and normal healthy females. It can be used as a screening tool in assessing the carcinoma breast cases.
|Keywords : Demyelination, Mammillary body, Thiamine deficiency|
A 55-year-old female patient presented with history of abnormal eye movements and unsteadiness of gait since 15 days. There was no history of alcohol intake. General condition of the patient was poor with emaciated appearance. Neurological examination showed ataxic gait. Ophthalmological examination revealed bilateral nystagmus.
Magnetic resonance imaging of the Brain revealed: Bilateral, symmetric T2W & FLAIR hyperintensity in medial thalami (Table/Fig 1) (a and b), periaqueductal gray matter (Table/Fig 2) (a and b), upper dorsal pons (Table/Fig 3) (a and b) and hypothalamus (Table/Fig 4) (a and b). Hyperintense signal noted on DWI (Table/Fig 5) (a),(Table/Fig 6) (a) with no reversal on ADC (Table/Fig 5) (b),(Table/Fig 6) (b). No blooming on GRE. T1W hypointensity noted in the bilateral medial thalami and periaqueductal gray matter (Table/Fig 7) (a and b). Ischemic foci noted in bilateral fronto-parietal lobes.
Laboratory investigations revealed thiamine (vitamin B1) deficiency – 1.6µg/dL (Normal range = 2.5-7.5 µg/dL).
Hence, a final diagnosis of non-alcoholic Wernicke’s encephalopathy was made and treatment with rapid intravenous thiamine (vitamin B1) replacement was given.
Wernicke’s encephalopathy is a rare neurological disorder caused by thiamine (vitamin B1) deficiency, either in chronic alcoholics or in the non-alcoholic setting. Thiamine (vitamin B1) deficiency in non-alcoholic Wernicke’s encephalopathy occurs due to malnutrition secondary to hyperemesis gravidarum, reduced thiamine intake following bariatric surgery, eating disorders, prolonged parenteral nutrition and chemotherapy. Thiamine deficiency leads to disrupted osmotic gradients across cell membranes, lactic acidosis with intracellular and extracellular oedema (1).
Non-alcoholic Wernicke’s encephalopathy is more common in adults however, it can occur in children also (2). In acute stages, demyelination and petechial haemorrhages occur. In chronic Wernicke’s encephalopathy, callosal necrosis and white matter rarefaction can be seen. Most commonly involved areas in brain are medial thalami, periaqueductal gray matter, tectum and hypothalamus. Less commonly involved areas are dorsal medulla, cranial nerve nuclei and splenium of corpus callosum (3). Patients present with a clinical triad of nystagmus, ataxia and confused mental status. Some patients may have polyneuropathy. Korsakoff psychosis is sequelae of Wernicke’s encephalopathy which includes severe retrograde amnesia, memory loss and confabulation (3),(4).
CT scan has a low sensitivity in the diagnosis of Wernicke’s encephalopathy. NECT may be normal in Wernicke’s encephalopathy or there may be subtle bilateral hypodensities in midbrain and medial thalami. Contrast enhanced CT scan may show subtle enhancement of the involved areas. On T2W & FLAIR MR images, bilateral symmetric hyperintensity is seen in the medial thalami, periaqueductal gray matter and tectum. Bilateral, asymmetric cortical hyperintensities can be seen in some cases. On T1W MR Image, hypointense signal is seen around the third ventricle and cerebral aqueduct. Hyperintense signal on T1W images in medial thalami may be seen in cases with petechial haemorrhages.
Gradient echo sequences will show microhaemorrhages as areas of blooming in the affected areas (5). DWI images show restricted diffusion in the areas with cytotoxic oedema. In areas with vasogenic oedema, hyperintense signal on DWI with no reversal on ADC is seen. On T1 post contrast images, enhancement of the periventricular and periaqueductal lesions will be seen (6),(7).
Differential diagnosis of Wernicke’s encephalopathy includes Artery of Percheron infarct, Deep cerebral venous thrombosis and viral infections like Influenza A and West Nile virus. Alcoholic Wernicke’s encephalopathy is characterized by history of alcohol intake, atrophy of mammillary bodies and cerebellar vermis on imaging, which is absent in nonalcoholic Wernicke’s encephalopathy (8).
MRI is the imaging modality of choice for early diagnosis of nonalcoholic Wernicke’s encephalopathy.
|TABLES AND FIGURES|
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