This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Related letter  • Related article  • Similar articles in this journal  Topic Collections  • Neurology, Other  • Alert me on articles by topic

Ronald J. Gurrera, MD

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

With their report¹ of cerebral salt-wasting syndrome in a patient with neuroleptic malignant syndrome (NMS), Dr Lenhard and colleagues have taken a potentially important step toward explicating the pathophysiology of NMS. Previous work² suggested that salt-wasting caused by profound diaphoresis might explain electrolyte and fluid imbalances in NMS and the frequent co-occurrence of severe diaphoresis, hyponatremia, and polydipsia in that disorder. However, Lenhard et al propose that elevated levels of adrenomedullary brain natriuretic peptide (BNP) caused the severe hyponatremia observed in their patient. This alternative mechanism is intriguing because it represents a more direct consequence of the dysregulated hyperautonomic state that is central to NMS.

Although BNP is synthesized and secreted primarily by heart tissue, particularly in response to volume overload,³ comprehensive clinical evaluation excluded relevant cardiac pathology in their patient.¹ Within the porcine nervous system, BNP concentrations are highest in spinal cord, followed by medulla-pons . . . [Full Text of this Article]

AUTHOR INFORMATION

RELATED LETTER

Salt-Wasting and Hyponatremia in Neuroleptic Malignant Syndrome—Reply
Thorsten Lenhard and Stefan Schwab
Arch Neurol. 2007;64(7):1058-1059.
EXTRACT | FULL TEXT  

RELATED ARTICLE

Cerebral Salt-Wasting Syndrome in a Patient With Neuroleptic Malignant Syndrome
Thorsten Lenhard, Sonja Külkens, and Stefan Schwab
Arch Neurol. 2007;64(1):122-125.
ABSTRACT | FULL TEXT