1/21. Transient thalamic changes on MRI in a child with hypernatremia.Severe hypernatremia has been associated with a wide variety of central nervous system lesions. Neurologic sequelae are the usual outcome in those cases in which a lesion has been documented neuroradiologically. The authors report a 7-month-old male with severe hypernatremia who developed obtundation after correction of the electrolyte imbalance. magnetic resonance imaging revealed bilateral thalamic signal changes that resolved on follow-up study, in accordance with complete clinical recovery. To the authors' knowledge, bilateral thalamic signal changes are previously unreported findings associated with hypernatremia. Pertinent literature and the clinical course of the authors' patient are the basis for questioning currently recommended guidelines for the rate of correction of hypernatremia.- - - - - - - - - - ranking = 1keywords = central nervous system, nervous system (Clic here for more details about this article) |
2/21. Therapeutic relowering of the serum sodium in a patient after excessive correction of hyponatremia.BACKGROUND: Inappropriate correction of chronic hyponatremia could lead to major neuropathological sequelae. In man, the risk of brain myelinolysis increases strikingly when correction of the serum sodium exceeds 10-15 mEq/l/24 h. No treatment is actually available for this iatrogenic brain injury. However, recent experimental data showed that rapid reinduction of the hyponatremia greatly reduces the incidence of brain damage and death in case of serum sodium overshooting. SUBJECTS AND methods: We tested this rescue manoeuver in a 71-year-old woman with nausea, confusion and severe (SNa 106 mEq/l) chronic hyponatremia related to thiazides. It was associated with hypokalemia (SK: 3.2 mEq/l). RESULTS: Treatment with isotonic saline produced inappropriately high SNa correction level of 21 mEq/l after the first 24 h. After initial improvement, the neurological status deteriorated after 72 h. Rapid reinduction of the hyponatremia was then ordered. Administration of hypotonic fluids (by oral and i.v. route) combined with dDAVP induced a prompt decline in the SNa (-16 mEq/l/14 h) with a final gradient of correction of deltaSNa 9 mEq/l. This manoeuver was well tolerated without untoward effects. The natremia then progressively normalized and the patient completely recovered without neurological sequelae. CONCLUSION: Hypotonic fluids may be safely administered to decrease the natremia after excessive correction of hyponatremia for potential prevention of myelinolysis.- - - - - - - - - - ranking = 0.59839837724672keywords = brain (Clic here for more details about this article) |
3/21. Acute hypernatremia and neuroleptic malignant syndrome in parkinson disease.neuroleptic malignant syndrome is a clinical syndrome characterized by fever, muscle rigidity, and mutism. Some patients with neuroleptic syndrome may have elevated creatine phosphokinase values and abnormal liver aminotransferase values. precipitating factors are important clues for prompt diagnosis. Typical precipitating factors include antipsychotic agents and major tranquilizers. In parkinson disease, drug withdrawal, menstruation, and hyponatremia are precipitating factors. We report a case of neuroleptic malignant syndrome in a patient with parkinson disease and hypernatremia. In addition, we hypothesized that sudden change of sodium concentrations in the central nervous system could trigger neuroleptic malignant syndrome in patients with parkinson disease. According to our experience, neuroleptic malignant syndrome is a clinical diagnosis and prompt diagnosis avoids unnecessary, expensive work-ups.- - - - - - - - - - ranking = 1keywords = central nervous system, nervous system (Clic here for more details about this article) |
4/21. Cranial MRI in neonatal hypernatraemic dehydration.Severe neonatal hypernatraemia is a life-threatening electrolyte disorder because of its neurological complications. These are brain oedema, intracranial haemorrhages, haemorrhagic infarcts and thromboses. There are few reports concerning the radiological findings in the central nervous system in severe neonatal hypernatraemia. Cranial MRI findings in hypernatraemia have been reported in an older child, but have not been described in newborn infants. We report the cranial MRI findings in a newborn infant with acute renal failure and severe hypernatraemia.- - - - - - - - - - ranking = 1.1994661257489keywords = central nervous system, nervous system, brain (Clic here for more details about this article) |
5/21. Severe hypernatremia after hypertonic saline irrigation of hydatid cysts.IMPLICATIONS: patients with iatrogenic hypernatremia and serum sodium levels >170 mmol/L either die or sustain severe central nervous system damage. We report the first case of an adult patient who survived an extreme iatrogenic acute hypernatremia (200 mmol/L) resulting from a hypertonic saline irrigation of multiple intraabdominal hydatid cysts. It is a unique report of an intraoperatively developed serum sodium increase without subsequent neurological damage.- - - - - - - - - - ranking = 1keywords = central nervous system, nervous system (Clic here for more details about this article) |
6/21. Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.- - - - - - - - - - ranking = 1keywords = central nervous system, nervous system (Clic here for more details about this article) |
7/21. Brain tumor presenting as anorexia nervosa in a 19-year-old man.Slow-growing brain tumors can produce disturbances of food intake and endocrine dysfunction. We report a case of slow-growing midline brain tumor in a patient with clinical presentation of anorexia nervosa (AN). A 19-year-old man was referred from a general practitioner to a psychiatric clinic due to illness behavior and psychopathological characteristics of AN. His body weight had decreased from 52 kg to 40 kg within 6 months. Laboratory tests showed hypernatremia (160 mmol/L), adrenal insufficiency (adrenocorticotrophic hormone, 11.4 pg/mL; 8 am cortisol, 1.4 microg/dL; 4 pm cortisol, 11.4 microg/dL) and hypogonadotropic hypogonadism (testosterone < 0.5 ng/mL, follicle-stimulating hormone < 0.1 mIU/mL, luteinizing hormone < 0.7 mIU/mL). Brain magnetic resonance imaging showed an extensive mass lesion at suprasellar, hypothalamic region, third ventricle, pineal region, lateral ventricle, and corpus callosum. Owing to central herniation during physical assessment, he died of unknown intracranial pathology. This case suggests that an intracranial tumor near the hypothalamus should be included in the differential diagnosis of AN. Any male adolescent with the clinical impression of AN should receive periodic re-evaluation, including neurological, endocrinological and, if necessary, neuroimaging study.- - - - - - - - - - ranking = 0.39893225149781keywords = brain (Clic here for more details about this article) |
8/21. Severe cerebral edema in a patient with anasarca and hypernatremia.We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.- - - - - - - - - - ranking = 0.39893225149781keywords = brain (Clic here for more details about this article) |
9/21. May the best friend be an enemy if not recognized early: hypernatremic dehydration due to breastfeeding.Hypernatremic dehydration is a serious condition in the newborn period. We present 5 infants with hypernatremic dehydration due to breastfeeding; one of them died because of brain edema during treatment.Hypernatremic dehydration in breast-fed newborns is secondary to insufficient lactation and all mothers should be encouraged about breastfeeding, taught the signs of successful breastfeeding, and the warning signs of dehydration. Here, we discuss hypernatremic dehydration in breastfeeding neonates, its causes and treatment.- - - - - - - - - - ranking = 0.19946612574891keywords = brain (Clic here for more details about this article) |
10/21. Brain apparent diffusion coefficient decrease during correction of severe hypernatremic dehydration.We report on the brain diffusion MR imaging findings in a neonate with severe hypernatremic dehydration, which resulted in cerebral edema (osmotic edema) and in apparent diffusion coefficient decrease, despite a careful and slow rehydration. This report provides in vivo insight into nervous cell response to osmotic challenge.- - - - - - - - - - ranking = 0.19946612574891keywords = brain (Clic here for more details about this article) |
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