Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 3, 2011, pp. 490-490

Neurology India, Vol. 59, No. 3, May-June, 2011, pp. 490

Correspondence

It is posterior reversible encephalopathy, and not stroke, after intravenous gamma globulin

G. R. K. Sarma

Department of Neurology, St. John's Medical College Hospital, Bangalore, India

Correspondence Address: G. R. K. Sarma Department of Neurology, St. John's Medical College Hospital, Bangalore India grk_sarma@yahoo.com

Date of Submission: 22-Jan-2011
Date of Decision: 24-Apr-2011
Date of Acceptance: 19-Apr-2011

Code Number: ni11148

PMID: 21743203

DOI: 10.4103/0028-3886.82702

Sir,

I read with interest the case report titled "Stroke after intravenous gamma globulin" by Saeed et al., ^[1] in your recent issue of Neurology India. However, I would like to suggest that the clinical and radiological picture is not consistent with cerebral infarction in this patient. The computed tomography (CT) and magnetic resonance images (MRI) provided show bilateral, predominantly white matter lesions in the occipital regions with clear sparing of the cortical mantle. This strongly argues against an arterial infarction, which typically involves both gray and white matter. In addition, the rapid clinical improvement noted in this patient also argues against bilateral occipital infarctions, which typically have poor outcome. The clinical and radiological picture in this patient is characteristic of "posterior reversible encephalopathy syndrome (PRES)." The authors could have included DWI and ADC images to support their argument that it is a case of cerebral infarct.

PRES, initially described by Hinchey et al. in 1996 ^[2] is defined by the association of neurological signs (headache, vomiting, visual disturbance, confusion and seizures) and radiological abnormalities of occipital white matter, usually bilateral, characterized by cerebral edema with hypodense signals on CT scan and hyperintense signals on T2-weighted MR images. Several reports of PRES in association with IVIg therapy have been documented. Although a latency of 3 ^[3] -4 ^[4] days between IVIg infusion and onset of PRES has been reported, neurological signs may appear in the first hours of treatment. Complete recovery of neurological symptoms occurs within 2 days ^[5] to several weeks. Vasogenic edema, cerebral vasospasm and serum hyperviscosity ^[5] have been proposed as probable mechanisms of PRES. In the present patient, hyperviscosity has been demonstrated, and may account for the PRES. In conclusion, PRES should be suspected in patients with neurological signs, especially visual disturbance, after IVIg infusion and be confirmed by MRI studies, including DWI and ADC sequences.

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