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First Author:Rima Bakhru, OD Second Author: Justine Simon, OD SUNY College of Optometry Title: The Role of Neuro-Optometric Rehabilitation For Visual Complications After Acoustic Neuroma Resection Abstract: Recent literature notes that upto 49% of patients report debilitating visual symptoms after acoustic neuroma resection. Neuro-optometric rehabilitation makes a significant impact in a patient experiencing diplopia and visual-vestibular dysfunction. I. Case History ● A 49 year old white female presents to the neuro-optometric rehabilitation clinic with the following chief complaints: ■ 1) Intermittent Diplopia/Visual Discomfort ● Mostly horizontal with small vertical component ● Worse when near centered gaze ■ 2) Constant Dizziness ● Triggered by: ○ Diplopia ○ Visually stimulating environments ○ Moving or turning head ○ Driving ■ 3) Blurred Vision/Oscillopsia ● Ocular History ■ Her ocular history is significant for corneal hypoesthesia and decreased tear production in the left eye, both post-surgical complications secondary to trigeminal nerve damage. These have resulted in ocular surface disease in the left eye. She also has a left ptosis from operative damage to the facial nerve. Previously, the patient had an excellent result s/p LASIK and presented wearing no distance vision correction. ● Medical History ■ The patient was first diagnosed with acoustic neuroma in late 2010 after presenting signs of left unilateral hearing loss and tinnitus began. Because of the rate of tumor growth into the cerebellopontine angle, surgery was advised. She underwent a partial left acoustic neuroma resection on 6/28/2012. In addition to the ocular complications noted above, other post-operative sequellae included: ○ Tinnitus ○ Complete left-sided hearing loss ○ Chronic vestibular dysfunction ○ Gait abnormality ■ ○ Facial Nerve Palsy ○ TMJ ○ Chronic Headaches As expected, the patient was significantly functionally impaired; Because of her constant diplopia and sense of disequilibrium she was no longer able to work or drive. Prior to presenting to our clinic, she had already completed 1.5 years of vestibular therapy 3/2014. At the time of presentation, she was also taking Klonopin 0.5 mg for dizziness, as well as celebrex and tramadol to address chronic head and jaw pain. II. Pertinent findings (Pre-Therapy) ● Clinical ○ Best-corrected visual acuity was 20/20-1 in each eye, though the patient reported constant blurred vision. Extraocular motility testing revealed a partial left abduction deficit of the left eye, with low frequency jerk nystagmus in extreme gazes. Unilateral cover test showed non-comitant esotropia and left hypertropia, leading to nearly constant diplopia that increased on left gaze and during head motion. Saccadic testing showed gross undershoots. Fixation was unsteady with several saccadic intrusions during a 10s period. Keystone visual skills revealed fragile binocular fusion. The patient also had left ptosis and superior punctate keratitis of the left eye. ● Physical ○ On physical examinations by the patient’s physiatrist, ataxic movement is noted “when fixation is lost by sudden turning or head movement”. In addition, the patient had gait abnormality, using a cane to ambulate. Radiology studies ○ The patient’s latest MRI in August of 2015 indicated that remaining lesion s/p resection had increased from 2mm to 5mm since 2012. The patient’s neurologist is unsure whether this is tumor regrowth or surgical scar tissue. III. Differential diagnosis ● Our examinations lead us to three diagnoses. The findings that correlate with each diagnosis are listed below. 1. Divergence Insufficiency/Binocular Instability 2^ Partial L Abducen’s Palsy ■ Non-comitant esotropia ■ Diplopia greater in distance, left gaze 2. Oculomotor Dysfunction ■ Slowed saccades ■ Nystagmus ■ Intrusion fixation 3. Visual-Vestibular Dysfunction ■ Diplopia and symptoms of disequilibrium that increase on head and eye movement ● Vertigo was ruled out as a differential diagnosis. Vertigo is defined by a patient’s perception of the environment spinning, which our patient did not report. Unlike visualvestibular dysfunction, vertigo does not occur because of poor quality of ocular input into the vestibulo-ocular reflex. Since true vertigo is usually of pure vestibular origin, neurooptometric rehabilitation usually does not help. IV. Diagnosis and discussion ● Acoustic neuroma is a benign, slow growing tumor of the sheath of the acoustic nerve located within the internal auditory canal, but can grow into the cerebellopontine angle. Early signs mimic inner ear disease: acute unilateral hearing loss, tinnitus and problems with dizziness and balance. Larger tumors and/or surgical resection can cause mechanical damage to the trigeminal, abducen’s, and facial nerve or even grow into the brainstem and cerebellum ● ● Significant mechanical damage to the ipsilateral peripheral vestibular apparatus is unavoidable. There is some recovery of function, but literature reveals a difference in the recovery process of “static functions” vs “dynamic functions” ■ Static functions ● more dependent on vestibular healing ● tend to improve spontaneously within months as part of the healing process ■ Dynamic functions ● do not improve on their own ● can lead to poor compensation mechanisms and long-term impairments and disabilities ● dynamic functions can heal in optimally with the right rehabilitative program It is widely accepted that visual compensation is an effective technique to enhance function in patients with permanent vestibular deficits. However, intermittent diplopia, unsteady fixation and inefficient eye movements lead to erroneous and confusing visual input into the balance system. Vestibular specialists have termed this phenomenon “retinal slip”. This retinal slip leads to a phase mismatch between vestibular and visual input to the vestibulo-ocular reflex. This manifests in patients as a sense of disequilibrium, dizziness, nausea and discomfort. V. Treatment, management ● The patient was given a distance spectacle prescription with 3BO and 1BD in March 2015. At 3 month follow-up, she reported her constant diplopia mostly resolved, still occurring towards the end of the day on days that she was fatigued. ● The patient completed about 6 in-office sessions of vision therapy and about 20 weeks of home therapy while on the wait-list for in-office neuro-optometric rehabilitative therapy. The following techniques were used: ○ For divergence insufficiency/binocular instability: ■ Brock string ■ VTS4 ■ Stereoscope therapy procedures ■ vectograms ○ For oculomotor dysfunction: ■ Large, moderate and small-angle saccadic exercises ■ Reading eye movements and compensation techniques ● Over this time period, the patient reported being able to read more comfortably and for longer. Her diplopia continued to decrease and her fusional ranges and facility increased. ● The patient is now being seen on a weekly basis in our clinic. We continue to work on fusion and ocular motility, with a focus on dynamic function. We are also using a visual-vestibular/intermodal protocol to enhance the VOR. The main principles of this protocol: ○ Visuomotor integration and using visual and postural and audio feedback ○ Tasks that require a patient to make spatio-perceptual calculations (Neuro Visual Rehabilitator, Sanet Vision Integrator, Space Localizer Technique) ● Research has shown that vestibular rehabilitation can be enhanced by therapy procedures that require active, and inter-sensory integration. Additionally, visual feedback has been shown to enhance postural stability VI. Conclusion ● It is important for patients who have undergone acoustic neuroma resection to be evaluated for visual and visual-vestibular symptoms by an optometrist who specializes in neuro-optometric rehabilitation. ● Other professionals involved with post-surgical care such as a neurologist or ear-nosethroat specialist may not be able to identify symptoms with visual cause ● Neuro-optometrists possess the unique skill set to manage diplopia caused by a noncomitant strabismus and identify and rehabilitate visual/binocular dysfunctions. ● Neuro-optometric rehabilitation can help teach patients visually compensate for permanent vestibular deficits. Bibliography 1. 2. 3. 4. 5. Bateman N, Nikolopoulos TP, Robinson K, O’Donoghue GM. Impairments, disabilities, and handicaps after acoustic neuroma surgery. Clin Otolaryngol Allied Sci. 2000;25(1):62-65. doi:10.1046/j.13652273.2000.00326.x. Cohen AH. Vision rehabilitation for visual-vestibular dysfunction: The role of the neuro-optometrist. NeuroRehabilitation. 2013;32(3):483-492. doi:10.3233/NRE-130871. Douglas R. Acoustic neuroma and its ocular implications. 2000:29-33. Lacour M, Bernard-Demanze L. Interaction between Vestibular Compensation Mechanisms and Vestibular Rehabilitation Therapy: 10 Recommendations for Optimal Functional Recovery. Front Neurol. 2015;5(January):1-15. doi:10.3389/fneur.2014.00285. Roland JT, Fishman AJ, Golfinos JG, Cohen N, Alexiades G, Jackman AH. Cranial nerve preservation in surgery for large acoustic neuromas. Skull Base. 2004;14(2):85-90. doi:10.1055/s-2004-828699.