Dr. Maggie Jan, OD, FAAO

1. Time Course Evaluation & Treatment of Post-TBI
Brain Tumor with Corresponding Visual Field Loss
Maggie Jan, O.D.
Southern California College of Optometry at Marshall B. Ketchum University
VA Long Beach – Traumatic Brain Injury & Low Vision Rehabilitation Residency
Background
In recent research, traumatic brain injury (TBI) has been theorized as a possible
risk factor contributing to the development of brain tumors.1
In this case, a patient
with no previous history of brain tumors and no family predisposition for tumors
experiences a TBI. Seven years after sustaining IED blast-related military brain
injuries, the patient presents with symptoms consistent with a cranial neoplasm.
This study tracks the patient’s symptoms and visual field defect juxtaposed with
corresponding MRI images identified during the time course of tumor treatment.
Treatment & Management
• Medical team starts the patient on Parlodel® (bromocriptine) drug therapy
aimed at reducing the prolactin-secreting tumor size.
• If tumor fails to respond to drug therapy, invasive surgical pituitary tumor
resection remains an option but will require hormone replacement therapy.
• Testosterone therapy for decreased libido, weight gain, gynecomastia.
• Initiated mental care, psychiatry for depression and anger. Mood-enhancing
drug Wellbutrin® (bupropion HCl) and trazadone prescribed for insomnia and
mood changes.
• The visual fields are taken concurrently as tumor treatment is initiated. During
the time course of the patient’s treatment, a series of four 24-2 Humphery
threshold visual fields are taken over one year (Figure 1b). Challenges
acquiring visual fields from TBI patients exist – decreased visual attention,
PTSD and claustrophobia make it difficult to test.
• No prescription needed for distance vision. Sun wear with polarization
prescribed for protection against glare and symptomatic photophobia
secondary to TBI. Rx reading glasses for accommodative dysfunction.
References
1. McKinney, P A. “Brain Tumours: Incidence, Survival, and Aetiology.” Journal of
Neurology, Neurosurgery & Psychiatry. 75, 2004.
2. Mumenthaler, Marco, and Heinrich Mattle. “Visual Field Defects.” Fundamentals of
Neurology: An Illustrated Guide. Stuttgart: Thieme, 2006.
3. Kaufman, David M. “Visual Field Loss.” Clinical Neurology for Psychiatrists.
Philadelphia: Saunders/Elsevier, 2007.
4. Silverstone B, Lang MA, Rosenthal BP, Faye EE, editors. “Signs and Symptoms
of Chiasmal Lesions.” The Lighthouse Handbook on Vision Impairment and Vision
Rehabilitation. Vol. 2. New York: Oxford University Press. p 188-190.
5. Center for Disease Control and Prevention (CDC). National Center for Injury
Prevention and Control. Report to Congress on traumatic brain injury in the United
States. Atlanta (GA): Centers for Disease Control and Prevention. 1999, Dec.
6. Center for Disease Control and Prevention (CDC). National Center for Injury
Prevention and Control. Report to Congress on Traumatic Brain Injury in the United
States: Understanding the Public Health Problem among Current and Former Military
Personnel. Atlanta (GA): Centers for Disease Control and Prevention. 2013, Aug.
7. Elder, Gregory A, and Adrian Cristian. “Blast-related Mild Traumatic Brain Injury:
Mechanisms of Injury and Impact on Clinical Care.” Mount Sinai Journal of Medicine:
a Journal of Translational and Personalized Medicine. 76(2), 2009: 111-118.
Conclusions
• Addition of visual efficiency training or vision rehabilitation could be potentially
valuable in the future for helping the patient compensate for field loss.
• Growths + minute changes to mass/volume in confined space of sella turcica
can affect integrity of surrounding structures such as optic nerve, visual
function, and hormone secretions.
• Tracking changes to visual field not only helps radiologists gauge potential
treatment efficacy but serves dual purpose of helping the patient visualize
health status while continuing to undergo the remaining time course of
scheduled treatment with slow recovery.
• Patient’s brain tumor development following acquisition of TBI could be
coincidental. Although neuronal disruption and inflammation processes has
been hypothesized as a possible risk factor in epidemiological studies1, no
link is proven currently. Further research into patients that have both TBIs
and tumors to see if tumors do develop over time. The study must control for
and rule out genetic predisposition and subjects with existing tumors.
• 10% to 20% of veterans returning from Iraq and Afghanistan operations are
estimated to have suffered a traumatic brain injury.7
In addition, according to
CDC statistics the incidence of TBIs in current and former military personnel
has tripled in the six years between 2005 and 20116. High incidence and
quantifiable impact on quality of life necessitates the need to manage and
treat patients with TBI.
Case Report
Patient History
• 37-year-old Caucasian male, active duty military soldier complaining of visual
changes, difficulty with peripheral vision, difficulty seeing objects or people
who “suddenly appear” to his right or left.
• Vision loss is accompanied with symptoms of severe headaches worse in
the morning, poor balance and dizziness, decreased attention, personality
changes such as increased irritability and anger, problems with memory and
word retrieval, insomnia, weight gain, and gynecomastia.
• Med Hx: TBI secondary to fall with loss of consciousness from explosions
accompanied with impact in Iraq 7 years ago. Frontal lobe contusion with
encephalomalacia. MRIs taken at the time of the acquired brain injury revealed
no cranial lesions or masses. No family history of tumors.
• Ocular Hx: Unremarkable
• Medications: None
Exam Findings
• Ocular findings are unremarkable, with exception of mild decrease in
accommodative amplitudes, photophobia, and abnormal confrontation visual
field with findings of neglect in the superior temporal and inferior temporal fields
of both eyes.
• Baseline Humphery Threshold Visual Field 24-2 Sita Fast: temporal visual field
loss detected OD & OS (Figure 1a). Field loss is repeatable and displays pattern
of bitemporal hemaniopsia.
• Lab studies: Blood serum analysis reveals high levels of ACTH, elevated
prolactin, low levels of testosterone.
• Radiology studies: MRI imaging reveals a mass in the right side of the pituitary
gland measuring approximately 7x11x11mm which invades the sphenoid sinus
(Figure 2).
Differential Diagnosis & Discussion
• Differential Diagnoses (DDx) for Visual field loss: Pituitary adenoma (primary
DDx), mid chiasm neoplasm, craniopharyngiomas, meningiomas, anterior
carotid artery aneurysm.2
• Cranial neoplasm located in the pituitary determined to be the cause of patient’s
bitemporal visual loss, hyperprolactinemia, and hypogonadism.4
• Visual Field Loss & Visual PathwayAnalysis: Nerve fibers originating in the nasal
retina of each eye converge at the optic chiasm before crossing over to opposite
sides of the brain for higher level processing.2
Thus a compression of the optic
chiasm affects the visual impulse from both nasal retina which corresponds to
loss of temporal visual field in both eyes.3
• Symptoms of a moderate TBI could impact speech, sensory, vision and cognitive
symptoms5. Patient’s symptoms of: headaches, vertigo, trouble with memory,
attention, concentration deficits, irritability related to acquired brain injury.6
Of
these TBI-related symptoms some may closely resemble characteristics of a
brain tumor.
• Visual symptoms most commonly experienced by patients with TBI include:
accommodative dysfunction, noncompensating vergences, large phorias or
tropias, and photophobia.
• In this case symptoms of headaches, inattention, and irritability overlap in both
conditions; fortuitously, addressing these common symptoms via treatment of
the brain tumor will not exacerbate the underlying TBI.
• The patient’s TBI is categorized as “moderate” due to loss of consciousness
greater than half an hour but less than six hours, without open intracranial
wound5. Even with identification and diagnosis of the traumatic brain injury,
there exists no method of reversal for physical damage resulting from brain
injury. Current TBI care is centered around providing treatment of symptoms
and functional rehabilitation rather elimination of the condition.
Figure
2:
T1
Post-­‐Gadolinium
MRI
Images
AXIAL
CORONAL
Acknowledgements to Major Jennifer Stoecklin Stowe, O.D.