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Unravelling the causes of cerebral damage in subarachnoid haemorrhage: might biomarkers help?

Correspondence to:
Correspondence to:
Dr Alejandro A Rabinstein
Mayo Clinic College of Medicine, 200 First Street SW, Mayo W8, Rochester, MN 55905, USA; rabinstein.alejandro@mayo.edu

Keywords: axonal; neurofilament; outcome; subarachnoid haemorrhage; vasospasm

The first 150 words of the full text of this article appear below.

Aneurysmal subarachnoid haemorrhage (SAH) is very often associated with significant functional sequelae. The causes of cerebral injury in this condition are multiple, including the immediate effects of the initial bleeding (vasoparalysis, possible ischaemia, brain oedema, and sudden rise in intracranial pressure), early or delayed hydrocephalus, delayed ischaemia due to vasospasm, systemic complications (such as infections and hyponatraemia), and iatrogenic complications (for example, occlusion of penetrating arterial branches during clipping or coiling of the ruptured aneurysm).¹ In this issue of the journal, Petzold et al (see page 753–9) present their provocative findings suggesting that secondary axonal degeneration may be responsible for poor recovery after SAH.²

The authors serially collected cerebrospinal fluid (CSF) samples from 17 patients with SAH and hydrocephalus requiring external ventricular drainage. Using these samples, they measured the concentration of neurofilament high chain (NfH), a previously validated marker for axonal degeneration. They found that CSF . . . [Full text of this article]

Related Article

Axonal damage and outcome in subarachnoid haemorrhage

A Petzold, G Keir, A Kay, M Kerr, and E J Thompson
J. Neurol. Neurosurg. Psychiatry 2006 77: 753-759. [Abstract] [Full Text] [PDF]