Neurological complications in hyperemesis gravidarum.

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Title: Neurological complications in hyperemesis gravidarum.
Authors: Zara, Gabriella, Codemo, Valentina, Palmieri, Arianna, Schiff, Sami, Cagnin, AnnaChiara, Citton, Valentina, Manara, Renzo
Source: Neurological Sciences. Feb2012, Vol. 33 Issue 1, p133-135. 3p. 1 Color Photograph.
Subjects: Morning sickness, Neurological disorders, Vitamin B1, Electrolytes, Ophthalmic plastic surgery, Hypothalamus, Afferent pathways, Magnetic resonance imaging
Abstract: Hyperemesis gravidarum can impair correct absorption of an adequate amount of thiamine and can cause electrolyte imbalance. This study investigated the neurological complications in a pregnant woman with hyperemesis gravidarum. A 29-year-old pregnant woman was admitted for hyperemesis gravidarum. Besides undernutrition, a neurological examination disclosed weakness with hyporeflexia, ophthalmoparesis, multidirectional nystagmus and optic disks swelling; the patient became rapidly comatose. Brain MRI showed symmetric signal hyperintensity and swelling of periaqueductal area, hypothalamus and mammillary bodies, medial and posterior portions of the thalamus and columns of fornix, consistent with Wernicke encephalopathy (WE). Neurophysiological studies revealed an axonal sensory-motor polyneuropathy, likely due to thiamine deficiency or critical illness polyneuropathy. Sodium and potassium supplementation and parenteral thiamine were administered with improvement of consciousness state in a few days. WE evolved in Korsakoff syndrome. A repeat MRI showed a marked improvement of WE-related alterations and a new hyperintense lesion in the pons, suggestive of central pontine myelinolysis. No sign or symptom due to involvement of the pons was present. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Neurological complications in hyperemesis gravidarum.
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  Data: <searchLink fieldCode="DE" term="%22Morning+sickness%22">Morning sickness</searchLink><br /><searchLink fieldCode="DE" term="%22Neurological+disorders%22">Neurological disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Vitamin+B1%22">Vitamin B1</searchLink><br /><searchLink fieldCode="DE" term="%22Electrolytes%22">Electrolytes</searchLink><br /><searchLink fieldCode="DE" term="%22Ophthalmic+plastic+surgery%22">Ophthalmic plastic surgery</searchLink><br /><searchLink fieldCode="DE" term="%22Hypothalamus%22">Hypothalamus</searchLink><br /><searchLink fieldCode="DE" term="%22Afferent+pathways%22">Afferent pathways</searchLink><br /><searchLink fieldCode="DE" term="%22Magnetic+resonance+imaging%22">Magnetic resonance imaging</searchLink>
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  Data: Hyperemesis gravidarum can impair correct absorption of an adequate amount of thiamine and can cause electrolyte imbalance. This study investigated the neurological complications in a pregnant woman with hyperemesis gravidarum. A 29-year-old pregnant woman was admitted for hyperemesis gravidarum. Besides undernutrition, a neurological examination disclosed weakness with hyporeflexia, ophthalmoparesis, multidirectional nystagmus and optic disks swelling; the patient became rapidly comatose. Brain MRI showed symmetric signal hyperintensity and swelling of periaqueductal area, hypothalamus and mammillary bodies, medial and posterior portions of the thalamus and columns of fornix, consistent with Wernicke encephalopathy (WE). Neurophysiological studies revealed an axonal sensory-motor polyneuropathy, likely due to thiamine deficiency or critical illness polyneuropathy. Sodium and potassium supplementation and parenteral thiamine were administered with improvement of consciousness state in a few days. WE evolved in Korsakoff syndrome. A repeat MRI showed a marked improvement of WE-related alterations and a new hyperintense lesion in the pons, suggestive of central pontine myelinolysis. No sign or symptom due to involvement of the pons was present. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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              Text: Feb2012
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