The Neuroradiology Journal 21: 521-526, 2008
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Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and Cortical Laminar Necrosis) A Case Report and Review of the Literature A. BURGETOVA*, M. VANECKOVA*, Z. SEIDL*,**, O. DOLEZAL*** * Department of Radiology, First Faculty of Medicine, Charles University in Prague; Czech Republic ** Medical College, Prague 5; Czech Republic *** Department of Neurology, First Faculty of Medicine, Charles University in Prague; Czech Republic
Key words: osmotic demyelination syndrome, magnetic resonance imaging, cortical laminar necrosis, coagulative necrosis
SUMMARY – Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are disorders frequently associated with serum osmotic imbalance. The prognosis is very variable from complete regression of clinical symptomatology to signs of significant quadruparesis, a vegetative state and death. We report the case of a 25-year-old man with a diagnosis of osmotic demyelination syndrome. The patient was young healthy man with no history of chronic alcoholism or malnutrition. He underwent head trauma associated with consumption of alcohol, being diagnosed with cerebral commotion. Four days later he presented with generalised epileptic convulsions with unconsciousness. Laboratory findings showed significant hyponatremia and hypochlorinemia. Following the rapid correction of osmotic conditions of serum, spastic quadruparesis and coma developed. MRI of the brain showed finding of CPM and EPM, cortical laminar necrosis (CLN) and coagulative necrosis in the putamina. Our case is suggestive in the rare MRI appearance of myelinolysis in addition to CLN and coagulative necrosis in the basal ganglia following the rapid correction of serum osmolarity. We suggest that this finding is prognostically very unfavourable. In the reported patient clinically initial neurological deficit progressed to a vegetative state within one month.
Introduction CPM and EPM are disorders frequently associated with serum osmotic imbalance. Serum natrium is usually significantly decreased and rapid correction of this imbalance is considered to be an etiological factor as well. The pathophysiology is related to the physiological balance of osmoles in the brain 1. The clinical picture usually begins with an alteration of consciousness or epileptic seizure. The prognosis is very variable from complete regression of the clinical picture, residual memory failure or motility impairment to signs of severe quadruparesis, locked in syndrome, vegetative state or death 2.
CPM was originally reported by Adams et Al in 1959 in a now classical study on the histopathology of central pontine myelinolysis 3. Subsequent reports showed that myelinolysis may also involve other brain regions; similar lesions were described in cerebellum, putamen, thalamus, lateral geniculate body, cortex and other extrapontine locations 4. Previously, studies of CPM and EPM were based on autopsy and histopathology alone 5. The development of imaging methods, CT and MRI and their new variability of imaging (DWI) has significantly contributed to the in-depth assessment of these conditions and accurate diagnosis. MRI is more sensitive than CT, and therefore it is the imaging modality of choice. 521
Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and ... A. Burgetova
A
B
Figure 1 A) Axial T2WI, central pontine high signal. B) Axial T1WI, low signal in the central pons. C) DWI, high signal in the central pons.
Case Report
C
522
A 25-year-old man presented with head trauma while under the influence of alcohol and was diagnosed with cerebral commotion. Neurological examination and CT head scan after trauma were normal and the patient was discharged from the hospital. Four days later at home he presented a grand mal epileptic seizure accompanied with distressed breathing. The patient was admitted to the hospital with significant neurological findings - central spastic quadruparesis and unconsciousness. Serum sodium was 98 mEq/l and serum Cl 71 mEq/l. Electroencephalography showed normal findings and the cytological and biochemical examination of CSF was normal. Hyponatremia was promptly corrected. Early CT examination revealed slight, diffuse cerebral edema and a very small subdural hematoma in the left frontoparietal location. Subsequent CT scans performed two and five days
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A
The Neuroradiology Journal 21: 521-526, 2008
B
Figure 2 A) Axial T2WI, hyperintensities in both caudate nuclei, putamina and thalamus. B) Axial T1WI, high signal in the putamina, low signal in both caudate nuclei and thalamus.
A
B
Figure 3 A) Axial T2WI, high signal in cortex and subcortical region, B) Axial T1WI, high signal in the cortex.
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Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and ... A. Burgetova
Figure 4 Axial T1WI after contrast administration: enhancement in the cortex (cortical laminar necrosis).
later showed regression of brain edema, but the clinical condition did not improve and the patient progressed to a vegetative state. Two weeks after admission the patient was transferred to our Institution (the General Faculty Hospital in Prague). At this time CT of the brain showed decreased attenuation within the pons, within the basal ganglia and slight decreased attenuation in the cortex. MRI at one month following onset of the patient’s symptoms showed T2-increased signal lesion and T1-decreased signal lesion within the pons with typical trident shape on axial images (figure 1 A,B). DWI sequence revealed increased signal intensity (figure 1C), and low ADC values in the same area. There were imaged hyperintensities on T2-weighted and FLAIR sequences within both caudate nuclei and thalamus, associated with decreased signal intensities on T1-weighted sequences (figure 2 A,B). In addition bilateral symmetrical increased signal changes were revealed in the putamina on T1W and T2-weighted sequences (figure 2 A,B), and signal changes in the deep layers of the cerebral cortex and adjacent white matter, T2W and T1W- laminar high signal lesions (figure 3 A,B), with an enhancement after con524
trast administration (figure 4). These findings were consistent with coagulative necrosis of the putamina and cortical laminar necrosis. Follow-up MRI in five months showed similar changes, and brain atrophyhad developed. The patient continues to be in a vegetative state. Results This patient has been described because of the rare MRI appearance of CPM and EPM in addition to cortical laminar necrosis and coagulative necrosis of the basal ganglia. It is presumable that the cause of clinical progression was the rapid correction of serum osmolarity. Discussion CPM was initially described in patients with a history of alcoholism and malnutrition 3. This condition, however, has also been found in chronically debilitated patients (liver diseases, chronic kidney failure, diabetes mellitus, recurrent vomiting and drowsiness), transplant recipients and patients with severe burns 6,7. A frequent iatrogenic precursor of the syndrome
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is a rapid correction of serum osmolarity, usually, but not necessarily, in patients presenting hyponatremia 2,8,9, hypokalemia or hyperglycemia. The characteristic histopathological finding of CPM is a symmetrical central zone of myelin destruction in the pons with sparing of peripheral axons 5. Extrapontine myelinolysis mostly occurs in the bundles of myelinated fibers in the gray matter (basal ganglia, and thalamus), and in the white matter surrounded by massive gray matter (deeper layers of the cortex and adjacent white matter, white matter of the cerebellar folia, and internal,external, and extreme capsules) 10. On CT the lesions have the hallmark of decreased attenuation. MRI is more sensitive than CT, and therefore it is the imaging modality of choice. MRI findings of CPM and EPM include signal hyperintensities within the pons (typical trident shape on axial images) and extrapontine areas of myelinolysis on T2-weighted and FLAIR sequences and decreased signal intensities on T1-weighted sequences. There is no expanding phenomenon. Diffusion is restricted, and DWI-MR reveals early changes: increased signal intensity and low ADC values in pathological areas. DWI sequences can be useful for speedy diagnosis, and yield additional information by demonstrating that the edema is of cytotoxic and not vasogenic type 11,12. Thus DWI-MR allows differentiation of myelinolysis from other diseases which may have similar clinical and imaging features, such as tumors, acute disseminated encephalomyelitis, and multiple sclerosis 13,14. Low ADC values related to cytotoxic edema similar to that of
The Neuroradiology Journal 21: 521-526, 2008
myelinolysis appear in acute arterial stroke. Cortical laminar necrosis (CLN) is often connected with anoxic-ischaemic insult, but has been reported to be associated also with metabolic disturbance, drugs, infections, status epilepticus and hypoglycemia 15,16. Histopathologically, CLN is characterized by pannecrosis of the cortex involving neurones, glial cells, and blood vessels 17. Radiologically, CLN is defined as the cortical laminar high signal on T1WI with contrast enhancement 18,19. Findings of cortical laminar necrosis in addition to pontine and extrapontine myelinolysis have already been reported in the literature 20,21. In these cases the significance of the changed osmolarity of the blood as a cause has been discussed. We suggest that the cause of all cerebral changes and the clinical progression in our reported patient was just the serum osmotic imbalance and the rapid correction of serum osmolarity. Conclusion The prognosis of CPM and EPM varies. It is highly presumable that the MRI appearance of myelinolysis is related to cortical laminar necrosis, and coagulative necrosis of the putamina is prognostically very unfavourable. Acknowledgement This study was supported by grants MZO/ 00064165 and MSMOO21620849.
References 1 Brown WD: Osmotic demyelination disorders: central pontine and extrapontine myelinolysis. Curr Opin Neurol 13: 691-697, 2000. 2 Chua GC, Sitoh YY, Lim CC et Al: MRI findings in osmotic myelinolysis. Clinical Radiology 57: 800-806, 2002. 3 Adams RD, Mancall VM: Central pontine myelinolysis. Arch Neurol Psychiatry 81: 154-72, 1959. 4 Gocht A, Colmant HJ: Central pontine and extrapontine myelinolysis: a report of 58 cases. Clinical Neuropathology 6: 262-270, 1987. 5 Tomlinson BE, Pierides AM, Bradley WG: Central pontine myelinolysis. Quarterly Journal of Medicine 179: 373-86, 1976. 6 Lampl C, Yazdi K: Central pontine myelinolysis. Eur Neurol 47: 3-10, 2002. 7 Ann C, McKee, Marc D et Al: Central pontine myelinolysis in severely burned patients: relationship to serum hyperosmolality. Neurology 38: 1211-1217, 1988.
8 Karp BI, Laureno R: Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 72: 359373, 1993. 9 Brunner JE, Redmond JM, Haggar AM et Al: Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: A prospective magnetic resonance study. Ann Neurol 27: 61-66, 1990. 10 Okeda R, Kitano M, Sawabe M et Al: Distribution of demyelinating lesions in pontine and extrapontine myelinolysis- three autopsy cases including one case devoid of central pontine myelinolysis. Acta Neuropathol 69: 259-66, 1986. 11 Ruzek KA, Campeau NG, Miller GM: Early Diagnosis of Central Pontine Myelinolysis with Diffusion-Weighted Imaging. AJNR Am J Neuroradiol 25: 210-213, 2004. 12 Chu K, Kang DW, Ko SB et Al: Diffusion- weighted MR findings of central pontine and extrapontine myelinolysis. Acta Neurol Scand 104: 385-388, 2001.
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Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and ... A. Burgetova
13 Cramer SC, Stegbauer KC, Schneider A et Al: Decreased diffusion in central pontine myelinolysis. Am J Neuroradiol 22: 1476-9, 2001. 14 Dervisoglu E, Yegenaga I, Anik Y et Al: Diffusion Magnetic Resonance Imaging may provide prognostic information in osmotic demyelination syndrome: Report of a case. Acta Radiol 47: 208-212, 2006. 15 Saito Y, Ogawa T, Nagaishi JI et Al: Laminar cortical necrosis in adrenal crisis: Sequential changes on MRI. Brain Dev 30: 77-81, 2008. 16 Heinrich A, Runge U, Kirsch M et Al: A case of hippocampal laminar necrosis following complex partial status epilepticus. Acta Neurol Scand 115: 425-8, 2007. 17 Donaire A, Carreno M, Gómez B et Al: Cortical laminar necrosis related to prolonged status epilepticus. J Neurol Neurosurg Psychiatry 77: 104-6, 2006. 18 Siskas N, Lefkopoulos A, Ionnidis I et Al: Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology 45: 283-288, 2003. 19 Komiyama M, Nishikawa M, Yasui T: Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology 39: 474-479, 1997.
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20 Susa S, Daimon M, Morita Y et Al: Acute intermittent porphyria with central pontine myelinolysis and cortical laminar necrosis. Neuroradiology 41: 835- 839, 1999. 21 Shoji M, Kimura T, Ota K et Al: Cortical laminar necrosis and central pontine myelinolysis in a patient with Sheehan syndrome and severe hyponatremia. Intern Med 35: 427-31, 1996.
Manuela Vaneckova, MD, PhD MRI Unit, Department of Radiology First Faculty of Medicine Charles University in Prague Katerinska 30 128 08 Praha 2, Czech Republic Tel.: +420 224965454 Fax: +420 224965058 E-mail: [email protected]
www. centauro. it
Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and Cortical Laminar Necrosis) A Case Report and Review of the Literature A. BURGETOVA*, M. VANECKOVA*, Z. SEIDL*,**, O. DOLEZAL*** * Department of Radiology, First Faculty of Medicine, Charles University in Prague; Czech Republic ** Medical College, Prague 5; Czech Republic *** Department of Neurology, First Faculty of Medicine, Charles University in Prague; Czech Republic
Key words: osmotic demyelination syndrome, magnetic resonance imaging, cortical laminar necrosis, coagulative necrosis
SUMMARY – Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are disorders frequently associated with serum osmotic imbalance. The prognosis is very variable from complete regression of clinical symptomatology to signs of significant quadruparesis, a vegetative state and death. We report the case of a 25-year-old man with a diagnosis of osmotic demyelination syndrome. The patient was young healthy man with no history of chronic alcoholism or malnutrition. He underwent head trauma associated with consumption of alcohol, being diagnosed with cerebral commotion. Four days later he presented with generalised epileptic convulsions with unconsciousness. Laboratory findings showed significant hyponatremia and hypochlorinemia. Following the rapid correction of osmotic conditions of serum, spastic quadruparesis and coma developed. MRI of the brain showed finding of CPM and EPM, cortical laminar necrosis (CLN) and coagulative necrosis in the putamina. Our case is suggestive in the rare MRI appearance of myelinolysis in addition to CLN and coagulative necrosis in the basal ganglia following the rapid correction of serum osmolarity. We suggest that this finding is prognostically very unfavourable. In the reported patient clinically initial neurological deficit progressed to a vegetative state within one month.
Introduction CPM and EPM are disorders frequently associated with serum osmotic imbalance. Serum natrium is usually significantly decreased and rapid correction of this imbalance is considered to be an etiological factor as well. The pathophysiology is related to the physiological balance of osmoles in the brain 1. The clinical picture usually begins with an alteration of consciousness or epileptic seizure. The prognosis is very variable from complete regression of the clinical picture, residual memory failure or motility impairment to signs of severe quadruparesis, locked in syndrome, vegetative state or death 2.
CPM was originally reported by Adams et Al in 1959 in a now classical study on the histopathology of central pontine myelinolysis 3. Subsequent reports showed that myelinolysis may also involve other brain regions; similar lesions were described in cerebellum, putamen, thalamus, lateral geniculate body, cortex and other extrapontine locations 4. Previously, studies of CPM and EPM were based on autopsy and histopathology alone 5. The development of imaging methods, CT and MRI and their new variability of imaging (DWI) has significantly contributed to the in-depth assessment of these conditions and accurate diagnosis. MRI is more sensitive than CT, and therefore it is the imaging modality of choice. 521
Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and ... A. Burgetova
A
B
Figure 1 A) Axial T2WI, central pontine high signal. B) Axial T1WI, low signal in the central pons. C) DWI, high signal in the central pons.
Case Report
C
522
A 25-year-old man presented with head trauma while under the influence of alcohol and was diagnosed with cerebral commotion. Neurological examination and CT head scan after trauma were normal and the patient was discharged from the hospital. Four days later at home he presented a grand mal epileptic seizure accompanied with distressed breathing. The patient was admitted to the hospital with significant neurological findings - central spastic quadruparesis and unconsciousness. Serum sodium was 98 mEq/l and serum Cl 71 mEq/l. Electroencephalography showed normal findings and the cytological and biochemical examination of CSF was normal. Hyponatremia was promptly corrected. Early CT examination revealed slight, diffuse cerebral edema and a very small subdural hematoma in the left frontoparietal location. Subsequent CT scans performed two and five days
www. centauro. it
A
The Neuroradiology Journal 21: 521-526, 2008
B
Figure 2 A) Axial T2WI, hyperintensities in both caudate nuclei, putamina and thalamus. B) Axial T1WI, high signal in the putamina, low signal in both caudate nuclei and thalamus.
A
B
Figure 3 A) Axial T2WI, high signal in cortex and subcortical region, B) Axial T1WI, high signal in the cortex.
523
Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and ... A. Burgetova
Figure 4 Axial T1WI after contrast administration: enhancement in the cortex (cortical laminar necrosis).
later showed regression of brain edema, but the clinical condition did not improve and the patient progressed to a vegetative state. Two weeks after admission the patient was transferred to our Institution (the General Faculty Hospital in Prague). At this time CT of the brain showed decreased attenuation within the pons, within the basal ganglia and slight decreased attenuation in the cortex. MRI at one month following onset of the patient’s symptoms showed T2-increased signal lesion and T1-decreased signal lesion within the pons with typical trident shape on axial images (figure 1 A,B). DWI sequence revealed increased signal intensity (figure 1C), and low ADC values in the same area. There were imaged hyperintensities on T2-weighted and FLAIR sequences within both caudate nuclei and thalamus, associated with decreased signal intensities on T1-weighted sequences (figure 2 A,B). In addition bilateral symmetrical increased signal changes were revealed in the putamina on T1W and T2-weighted sequences (figure 2 A,B), and signal changes in the deep layers of the cerebral cortex and adjacent white matter, T2W and T1W- laminar high signal lesions (figure 3 A,B), with an enhancement after con524
trast administration (figure 4). These findings were consistent with coagulative necrosis of the putamina and cortical laminar necrosis. Follow-up MRI in five months showed similar changes, and brain atrophyhad developed. The patient continues to be in a vegetative state. Results This patient has been described because of the rare MRI appearance of CPM and EPM in addition to cortical laminar necrosis and coagulative necrosis of the basal ganglia. It is presumable that the cause of clinical progression was the rapid correction of serum osmolarity. Discussion CPM was initially described in patients with a history of alcoholism and malnutrition 3. This condition, however, has also been found in chronically debilitated patients (liver diseases, chronic kidney failure, diabetes mellitus, recurrent vomiting and drowsiness), transplant recipients and patients with severe burns 6,7. A frequent iatrogenic precursor of the syndrome
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is a rapid correction of serum osmolarity, usually, but not necessarily, in patients presenting hyponatremia 2,8,9, hypokalemia or hyperglycemia. The characteristic histopathological finding of CPM is a symmetrical central zone of myelin destruction in the pons with sparing of peripheral axons 5. Extrapontine myelinolysis mostly occurs in the bundles of myelinated fibers in the gray matter (basal ganglia, and thalamus), and in the white matter surrounded by massive gray matter (deeper layers of the cortex and adjacent white matter, white matter of the cerebellar folia, and internal,external, and extreme capsules) 10. On CT the lesions have the hallmark of decreased attenuation. MRI is more sensitive than CT, and therefore it is the imaging modality of choice. MRI findings of CPM and EPM include signal hyperintensities within the pons (typical trident shape on axial images) and extrapontine areas of myelinolysis on T2-weighted and FLAIR sequences and decreased signal intensities on T1-weighted sequences. There is no expanding phenomenon. Diffusion is restricted, and DWI-MR reveals early changes: increased signal intensity and low ADC values in pathological areas. DWI sequences can be useful for speedy diagnosis, and yield additional information by demonstrating that the edema is of cytotoxic and not vasogenic type 11,12. Thus DWI-MR allows differentiation of myelinolysis from other diseases which may have similar clinical and imaging features, such as tumors, acute disseminated encephalomyelitis, and multiple sclerosis 13,14. Low ADC values related to cytotoxic edema similar to that of
The Neuroradiology Journal 21: 521-526, 2008
myelinolysis appear in acute arterial stroke. Cortical laminar necrosis (CLN) is often connected with anoxic-ischaemic insult, but has been reported to be associated also with metabolic disturbance, drugs, infections, status epilepticus and hypoglycemia 15,16. Histopathologically, CLN is characterized by pannecrosis of the cortex involving neurones, glial cells, and blood vessels 17. Radiologically, CLN is defined as the cortical laminar high signal on T1WI with contrast enhancement 18,19. Findings of cortical laminar necrosis in addition to pontine and extrapontine myelinolysis have already been reported in the literature 20,21. In these cases the significance of the changed osmolarity of the blood as a cause has been discussed. We suggest that the cause of all cerebral changes and the clinical progression in our reported patient was just the serum osmotic imbalance and the rapid correction of serum osmolarity. Conclusion The prognosis of CPM and EPM varies. It is highly presumable that the MRI appearance of myelinolysis is related to cortical laminar necrosis, and coagulative necrosis of the putamina is prognostically very unfavourable. Acknowledgement This study was supported by grants MZO/ 00064165 and MSMOO21620849.
References 1 Brown WD: Osmotic demyelination disorders: central pontine and extrapontine myelinolysis. Curr Opin Neurol 13: 691-697, 2000. 2 Chua GC, Sitoh YY, Lim CC et Al: MRI findings in osmotic myelinolysis. Clinical Radiology 57: 800-806, 2002. 3 Adams RD, Mancall VM: Central pontine myelinolysis. Arch Neurol Psychiatry 81: 154-72, 1959. 4 Gocht A, Colmant HJ: Central pontine and extrapontine myelinolysis: a report of 58 cases. Clinical Neuropathology 6: 262-270, 1987. 5 Tomlinson BE, Pierides AM, Bradley WG: Central pontine myelinolysis. Quarterly Journal of Medicine 179: 373-86, 1976. 6 Lampl C, Yazdi K: Central pontine myelinolysis. Eur Neurol 47: 3-10, 2002. 7 Ann C, McKee, Marc D et Al: Central pontine myelinolysis in severely burned patients: relationship to serum hyperosmolality. Neurology 38: 1211-1217, 1988.
8 Karp BI, Laureno R: Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 72: 359373, 1993. 9 Brunner JE, Redmond JM, Haggar AM et Al: Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: A prospective magnetic resonance study. Ann Neurol 27: 61-66, 1990. 10 Okeda R, Kitano M, Sawabe M et Al: Distribution of demyelinating lesions in pontine and extrapontine myelinolysis- three autopsy cases including one case devoid of central pontine myelinolysis. Acta Neuropathol 69: 259-66, 1986. 11 Ruzek KA, Campeau NG, Miller GM: Early Diagnosis of Central Pontine Myelinolysis with Diffusion-Weighted Imaging. AJNR Am J Neuroradiol 25: 210-213, 2004. 12 Chu K, Kang DW, Ko SB et Al: Diffusion- weighted MR findings of central pontine and extrapontine myelinolysis. Acta Neurol Scand 104: 385-388, 2001.
525
Osmotic Demyelination Syndrome (Central Pontine and Extrapontine Myelinolysis with Coagulative Necrosis of the Putamina and ... A. Burgetova
13 Cramer SC, Stegbauer KC, Schneider A et Al: Decreased diffusion in central pontine myelinolysis. Am J Neuroradiol 22: 1476-9, 2001. 14 Dervisoglu E, Yegenaga I, Anik Y et Al: Diffusion Magnetic Resonance Imaging may provide prognostic information in osmotic demyelination syndrome: Report of a case. Acta Radiol 47: 208-212, 2006. 15 Saito Y, Ogawa T, Nagaishi JI et Al: Laminar cortical necrosis in adrenal crisis: Sequential changes on MRI. Brain Dev 30: 77-81, 2008. 16 Heinrich A, Runge U, Kirsch M et Al: A case of hippocampal laminar necrosis following complex partial status epilepticus. Acta Neurol Scand 115: 425-8, 2007. 17 Donaire A, Carreno M, Gómez B et Al: Cortical laminar necrosis related to prolonged status epilepticus. J Neurol Neurosurg Psychiatry 77: 104-6, 2006. 18 Siskas N, Lefkopoulos A, Ionnidis I et Al: Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology 45: 283-288, 2003. 19 Komiyama M, Nishikawa M, Yasui T: Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology 39: 474-479, 1997.
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20 Susa S, Daimon M, Morita Y et Al: Acute intermittent porphyria with central pontine myelinolysis and cortical laminar necrosis. Neuroradiology 41: 835- 839, 1999. 21 Shoji M, Kimura T, Ota K et Al: Cortical laminar necrosis and central pontine myelinolysis in a patient with Sheehan syndrome and severe hyponatremia. Intern Med 35: 427-31, 1996.
Manuela Vaneckova, MD, PhD MRI Unit, Department of Radiology First Faculty of Medicine Charles University in Prague Katerinska 30 128 08 Praha 2, Czech Republic Tel.: +420 224965454 Fax: +420 224965058 E-mail: [email protected]
