Mohammad Fouladvand, M.D.

Headache and blurring of vision
Singh, Anuradha; Kurzweil, Arielle; Fouladvand, Mohammad
Case-based neurology New York : Demos Medical, c2012,
— id: 5943, year: 2012, vol: , page: 235, stat: Chapter,

Diplopia due to skew deviation following neurotologic procedures
Cosetti M.K.; Fouladvand M.; Roland Jr. J.T.; Lalwani A.K.
2011 ;121(SUPPL 4):s184-s184, Laryngoscope
Introduction: Diplopia following cerebellopontine angle (CPA) surgery is usually attributed to neuropathy of III, IV or VI cranial nerves. Diplopia in the absence of cranial neuropathy following CPA surgery is rare. We present a series of patients who developed vertical diplopia from skew deviation following resection of tumors in the CPA or labyrinthectomy. Primarily associated with brainstem lesions, this vertical misalignment of the visual axis is postulated to result from unilateral disruption of supranuclear input from the otolithic organs. Methods: Retrospective review of patients with complaints of diplopia following CPA surgery. Patients underwent neuroophthalmologic consultation and examination, including opticokinetic testing, confrontational visual field assessment, color plate, pupillary reflex, slit lamp examination and Head Tilt Test. Results: Four patients with residual hearing preoperatively developed skew deviation immediately following surgical intervention, including translabyrinthine(n=1) and retrosigmoid (n=2) approaches to the CPA and labyrinthectomy (n=1). Neuroophthalmologic exam demonstrated intact extraocular movements, and 2-14 mm prism diopter hypertropia on both primary gaze and Head Tilt Testing. In all cases, skew deviation resolved spontaneously with normalization of the neuroophthalmologic examination within 10 weeks. Conclusion: Patients undergoing CPA surgery or labyrinthectomy can develop postoperative diplopia due to skew deviation as a consequence of acute vestibular deafferentation. Patients with significant hearing preoperatively, a probable marker for residual vestibular function, may be specially at risk for developing skew deviation. As vestibular ablation occurs routinely with each of these procedures, skew deviation likely occurs more frequently than is currently diagnosed. Complaints of diplopia should prompt neuro-ophthalmologic consultation to reliably diagnose skew deviation and exclude cranial neuropathy. Patients can be reassured as spontaneous resolution typically occurs within 10 weeks
— id: 135625, year: 2011, vol: 121, page: s184, stat: Journal Article,

Skew deviation after intratympanic gentamicin therapy
Ng, Diana; Fouladvand, Mohammad; Lalwani, Anil K
2011 Mar;121(3):492-494, Laryngoscope
Intratympanic gentamicin therapy for the treatment of episodic vertigo associated with Meniere's disease is generally well tolerated. Although auditory and vestibular symptoms following intratympanic gentamicin are well known, visual disturbance has not been previously described. In this report, we describe two patients with Meniere's disease who developed sudden onset of binocular vertical diplopia due to skew deviation after intratympanic gentamicin therapy. The skew deviation and diplopia resolved spontaneously and completely within 6 to 8 weeks without therapy. Development of diplopia due to skew deviation should be discussed as a potential complication in patients undergoing intratympanic gentamicin therapy. Laryngoscope, 2011
— id: 124109, year: 2011, vol: 121, page: 492, stat: Journal Article,

Ocular motor nerve palsies: implications for diagnosis and mechanisms of repair
Sharpe, James A; Wong, Agnes M F; Fouladvand, Mohammad
2008 ;171:59-66, Progress in brain research
Measurements of the dynamics of the eyes in ocular motor nerve palsies may aid diagnosis, characterize peripheral and central palsies, and reveal adaptive properties of the brain. Saccadic and vestibulo-ocular reflex (VOR) functions of patients with peripheral and central sixth, and peripheral third and fourth nerve palsies were studied by three dimensional magnetic field search coil oculography. Combined third and fourth cranial nerve microvascular ischaemic palsy in diabetes mellitus produced low ratios of intorsion to adduction amplitudes. Presumed isolated third nerve palsy caused higher ratios of adduction to intorsion and violations of Listing's law. The VOR in third, fourth, and sixth nerve palsies reveals adaptive equilibration of the action of paretic agonist and their non-paretic antagonist muscles in violation of Hering's law during head motion. Saccadic speeds in the field of paretic agonists are repaired in chronic peripheral palsies despite limited ductions, but remain reduced in central palsies. Limited intorsion with third nerve palsy is attributed to concurrent fourth nerve ischaemia in the distribution of the inferolateral trunk of the intracavernous carotid artery. Adaptive repair of the VOR after ocular motor nerve palsies reduces asymmetric retinal image slip and binocular disparity, and repair of saccadic velocity drives both eyes rapidly and simultaneously into the paretic field of motion
— id: 96087, year: 2008, vol: 171, page: 59, stat: Journal Article,

Developmental apraxia arising from neonatal brachial plexus palsy
Boylan LS; Fouladvand M
2001 Feb 27;56(4):576-577, Neurology
— id: 21316, year: 2001, vol: 56, page: 576, stat: Journal Article,

Ocular aspects of myasthenia gravis
Barton JJ; Fouladvand M
2000 ;20(1):7-20, Seminars in neurology
Ocular myasthenia gravis is a not uncommon autoimmune disorder causing diplopia, ptosis, and weakness of lid closure. The predilection of myasthenia for the ocular muscles may be related to differences between limb and extraocular muscles in either physiological function or antigenicity. Clinically, ocular myasthenia can mimic any form of pupil-sparing ocular motility disorder. Dynamic abnormalities of myasthenic eye movements may reflect the primary hallmarks of the disease, which are fatigability and variability in strength, or secondary adaptive effects by the central nervous system. Tests to confirm the diagnosis include edrophonium challenge, repetitive nerve stimulation, single-fiber electromyography (EMG) of the frontalis, and assays for antibody directed against the acetylcholine receptor: all are less sensitive for ocular myasthenia than for generalized myasthenia. There is a higher incidence of other autoimmune conditions in myasthenia, notably thymoma and thyroid dysfunction. The differential diagnosis includes other diseases of the neuromuscular junction, such as Lambert-Eaton syndrome and botulism. Treatment consists of symptomatic use of acetylcholinesterase inhibitors and immunosuppression with steroids or azathioprine. Between 50 and 70% of patients with ocular myasthenia will eventually develop generalized disease: there is some retrospective data that steroids or azathioprine may reduce this by about 75%. The role of thymectomy in ocular myasthenia remains unclear
— id: 38600, year: 2000, vol: 20, page: 7, stat: Journal Article,