A 16-Year-Old Girl With Bilateral Visual Loss and Left Hemiparesis Following an Immunization Against Human Papilloma Virus

Journal of Child Neurology

As reported by the One Click Group 2/26/2010

Francis J. DiMario, Jr, MD, Mirna Hajjar, MD, and Thomas Ciesielski, MD

Received August 11, 2009. Received revised August 26, 2009. Accepted
for publication August 26, 2009.
From the University of Connecticut School of Medicine, Farmington,
Connecticut, and the Departments of Pediatrics1 at Connecticut
Children’s Medical Center, Hartford, Connecticut (FJD); and the
Departments of Neurology (MH) and Pathology (TC) at Hartford Hospital, Hartford, Connecticut.

The authors have no conflicts of interest to disclose with regard to this
article.
Address correspondence to: Francis J. DiMario Jr, Division of Child
Neurology, Connecticut Children’s Medical Center, 282 Washington St,
Hartford, CT 06106; e-mail: fdimari@ccmckids.org.

We report the course of a 16-year-old girl who presented with near complete visual loss associated with chiasmal neuritis and a biopsy proven tumefactive demyelinating lesion on magnetic resonance imaging (MRI) in association with a recent immunization against human papilloma virus.

Visual loss is a symptom that can occur from lesions anywhere along the visual pathways. Binocular visual loss can be further localized depending on
the size and location of the scotoma identified on examination. Lesions affecting the chiasm, in particular, may produce bitemporal visual field loss and the additional involvement of the optic nerves and/or retrochiasmatic
visual pathways will induce more complete degrees of blindness. There are a multitude of etiologies that produce this latter pattern of visual loss; however, the pace of progression, the anatomic localization of the process, and the precipitating circumstances will aid in pathophysiologic
classification as compressive or noncompressive. Noncompressive
etiologies involving the chiasm include processes within the spectrum from acute to a more chronic temporal course. This slower time course is characteristic of infiltrative lesions, granulomatous diseases, axonal dieback
phenomenon secondary to multiple sclerosis,1 and visual loss is a symptom that can occur from lesions anywhere along the visual pathways. Binocular
visual loss can be further localized depending on the size and location of the scotoma identified on examination.

Lesions affecting the chiasm, in particular, may produce bitemporal visual field loss and the additional involvement of the optic nerves and/or retrochiasmatic visual pathways will induce more complete degrees of
blindness. There are a multitude of etiologies that produce this latter pattern of visual loss; however, the pace of progression, the anatomic localization of the process, and the precipitating circumstances will aid in pathophysiologic
classification as compressive or noncompressive. Noncompressive
etiologies involving the chiasm include processes within the spectrum from acute to a more chronic temporal course. This slower time course is characteristic of infiltrative lesions, granulomatous diseases, axonal dieback
phenomenon secondary to multiple sclerosis,1 and Leber hereditary optic neuropathy. Acute noncompressive lesions of the optic chiasm have been described in infectious settings with Lyme disease,2 Epstein-Barr virus,3,4
varicella zoster virus5 and mumps,6 systemic lupus erythematosus, 7,8 and demyelinating processes (eg, neuromyelitis optica and multiple sclerosis).

MORE…

PG

Author: Leslie Carol Botha

Author, publisher, radio talk show host and internationally recognized expert on women's hormone cycles. Social/political activist on Gardasil the HPV vaccine for adolescent girls. Co-author of "Understanding Your Mood, Mind and Hormone Cycle." Honorary advisory board member for the Foundation for the Study of Cycles and member of the Society for Menstrual Cycle Research.