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communicationHemispheric Cerebral Edema

Hemispheric Cerebral Edema

 

(A) T2-weighted magnetic resonance image showing marked diffuse brain edema of the left hemisphere with mass effect effacing the normal cortical architecture and sulci (arrows). Note pressure on the left ventricle with slight midline shift. The right hemisphere is normal. (B) Diffusion-weighted magnetic resonance image demonstrating area of cortical diffusion decay in the left hemisphere (arrow), indicating an active process.
(A) T2-weighted magnetic resonance image showing marked diffuse brain edema of the left hemisphere with mass effect effacing the normal cortical architecture and sulci (arrows). Note pressure on the left ventricle with slight midline shift. The right hemisphere is normal. (B) Diffusion-weighted magnetic resonance image demonstrating area of cortical diffusion decay in the left hemisphere (arrow), indicating an active process.

A 67-year-old previously healthy man was admitted in November after a seizure.

Examination showed normal vital signs, right hemiparesis and facial palsy, global aphasia, and right upper motor neuron signs but no meningeal irritation.

Results from chest X-ray, electrocardiogram, and laboratory tests were normal.

Neuromaging revealed left hemispheric cerebral edema without evidence of vascular occlusion on computed tomographic angiography (Figure).

Electroencephalography demonstrated epileptiform activity over the left hemisphere.

He was initially treated with intravenous phenytoin, methylprednisolone, acyclovir, and ceftriaxone.

Extensive serology tests for infectious agents were negative. Autoantibodies were not found. Nasal swab screening by polymerase chain reaction testing was positive for influenza A and negative for influenza B and respiratory syncytial virus, confirmed by serologic testing (complement fixation test titer >64). He had not received an influenza vaccination.

A course of oseltamivir (Tamiflu) was administered.

Cerebrospinal fluid (1 mL removed, replaced with normal saline) was normal, including polymerase chain reactions for enteroviruses, herpes simplex viruses, varicella zoster, and influenza A.

The patient slowly improved clinically and on imaging over 2 weeks and was transferred for rehabilitation.

He recalled a minor febrile illness a few days prior.

Our patient presented with symptomatic marked left hemispheric edema, which is a rare occurrence, usually associated with obvious trauma or a major vascular event, both absent here. Single patients had been reported with unilateral brain edema after focal status epilepticus or fulminant hepatic failure. Unilateral hemispheric viral encephalitis is another cause, albeit exceedingly rare.

In our patient, varied infectious causes have been ruled out, and the identification of influenza A virus in the nasal swab may provide a clue to the underlying diagnosis, even though infection was largely subclinical. The diagnosis is further supported by the patient’s recovery and absence of any other identifiable cause.

Influenza A virus infection can be associated, albeit rarely, with a wide spectrum of central nervous system syndromes, including acute encephalitis.1 Children are more often affected, but adult patients have been reported,2 and influenza-associated encephalopathy or encephalitis deserves wider recognition.

Influenza-associated encephalopathy or encephalitis occurs at the height of the influenza illness; however, sometimes symptoms of influenza may be subtle. Convulsions and altered consciousness are common presentations,2 but cerebrospinal fluid may be normal, and virus RNA is rarely detectable, even in autopsied brain tissue.2 Thus, the pathogenesis of influenza-associated encephalopathy or encephalitis remains uncertain, but cerebral edema and enhancing lesions in the temporal and parietal regions have been reported,2 although usually not limited to one hemisphere. Most patients recover, but serious sequelae are common.1

To read this article in its entirety please visit our website.

-Ina Dubin, MD, Yosef Drahy, MD, Ami Schattner, MD

This article originally appeared in the August 2017 issue of The American Journal of Medicine.

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