HTLV-1 uveitis and Graves' disease presenting with sudden onset of blurred vision

The Lancet ◽  
2022 ◽  
Vol 399 (10319) ◽  
pp. 60
Author(s):  
Koju Kamoi ◽  
Kaoru Uchimaru ◽  
Arinobu Tojo ◽  
Toshiki Watanabe ◽  
Kyoko Ohno-Matsui
2021 ◽  
Vol 20 (4) ◽  
pp. 182-188
Author(s):  
Sun Young Lee ◽  
Mi-Ra Park

Purpose: We report a case of multiple sclerosis with bilateral optic neuritis that was atypical in terms of both the clinical signs and symptoms.Case summary: A 34-year-old female visited the department of neurology with a complaint of sudden-onset, left lower extremity weakness and numbness that had developed 3 weeks prior, and bilateral blurred vision that had commenced 2 weeks prior. The patient was diagnosed with multiple sclerosis and prescribed high-dose intravenous methylprednisolone for 3 days, but the blurred vision did not improve. The patient was referred to the ophthalmology department. The initial best-corrected visual acuity was 0.04 in both eyes, and the relative afferent pupillary defect test was positive for the left eye. The Ishihara color test scores were 1/17 for both eyes. No optic disc swelling was evident on fundus examination. Brain and spine magnetic resonance imaging (T2-weighted) performed during the initial visit revealed lesions of high signal intensity in the frontal, subcortical white matter; the optic chiasm; the left retrobulbar optic segment; the medulla; and the spinal C2-5 processes. Aquaproin-4 immunogloblin G antibody (AQP4-IgG Ab) was not detected in serum. One month after prescription of the oral steroid, the vision improved to 1.0 in the right and 0.8 in the left eye. The patient was lost to follow-up after prescription of interferon-beta for 4 years, without recurrence.Conclusions: Binocular optic neuritis accompanied by severe visual loss is a rare form of multiple sclerosis. A thorough diagnosis (with a focus on exclusion) is required, as is appropriate treatment.


2019 ◽  
Vol 18 (6) ◽  
pp. E184-E190 ◽  
Author(s):  
Jaims Lim ◽  
Hussain Shallwani ◽  
Kunal Vakharia ◽  
Adnan H Siddiqui

Abstract BACKGROUND AND IMPORTANCE Few studies describe the use of adenosine-induced cardiac systole for treatment of cerebrovascular pathologies. We describe a midbrain arteriovenous malformation (AVM) treated with transvenous embolization using adenosine-induced asystole to achieve transient systemic hypotension with the purpose of furthering discussion on the technique and operative considerations for adenosine use in endovascular AVM treatments. CLINICAL PRESENTATION A 29-yr-old man presented with sudden onset of severe bilateral headache, blurred vision, and numbness on the right side of his face and tongue. Noncontrast head computed tomography revealed fourth ventricle hemorrhage. Diagnostic cerebral angiography revealed a high-flow midbrain AVM with a posterior wall perforator from the basilar artery terminus and a draining vein into the straight sinus. Transarterial AVM embolization was successful. The patient was discharged with no residual neurological deficits but returned 1 wk later with slurred speech and left-sided dysmetria. Repeat angiography revealed partial AVM filling. Attempts at transarterial embolization were unsuccessful. Thus, transvenous AVM embolization with adenosine-induced cardiac asystole and systemic hypotension was performed. A total of 60 mg of adenosine was administered, followed by 2 additional doses of 60 and 40 mg; and complete cardiac asystole with a mean arterial pressure of 40 mmHg was maintained, resulting in successful embolization of the AVM. No residual filling was visualized on postembolization arterial angiography runs. The patient was neurologically stable and discharged on postoperative day 2. CONCLUSION With appropriate and safe dosing, adenosine-induced asystole and systemic hypotension may be a feasible, safe option to reduce flow and assist endovascular transvenous embolization of high-flow AVMs.


2020 ◽  
Vol 12 ◽  
pp. 1759720X2095173
Author(s):  
Judith Rademacher ◽  
Denis Poddubnyy ◽  
Uwe Pleyer

Uveitis is the most frequent extra-articular manifestation of axial spondyloarthritis (SpA), occurring in up to one-third of the patients. In the majority of patients, uveitis is acute, anterior and unilateral and presents with photosensitivity, sudden onset of pain and blurred vision. Topical steroids are an effective treatment; however, recurrent or refractory cases may need conventional disease-modifying antirheumatic drugs or biological treatment with monoclonal tumor necrosis factor (TNF) inhibitors, thus also influencing treatment strategy of the underlying SpA. Though the exact pathogenesis of SpA and uveitis remains unknown, both seem to result from the interaction of a specific, mostly shared genetical background (among other HLA-B27 positivity), external influences such as microbiome, bacterial infection or mechanical stress and activation of the immune system resulting in inflammation. Up to 40% of patients presenting with acute anterior uveitis (AAU) have an undiagnosed SpA. Therefore, an effective referral strategy for AAU patients is needed to shorten the diagnostic delay of SpA and enable an early effective treatment. Further, the risk for ophthalmological manifestations increases with the disease duration in SpA; and patients presenting with ocular symptoms should be referred to an ophthalmologist. Thus, a close collaboration between patient, rheumatologist and ophthalmologist is needed to optimally manage ocular inflammation in SpA.


2021 ◽  
pp. 634-639
Author(s):  
Shizuka Takahashi ◽  
Kentaro Nishida ◽  
Hirokazu Sakaguchi ◽  
Kohji Nishida

We report a novel case of vitreous hemorrhage associated with suspected rupture of 2-disc-diameter retinal arterial macroaneurysm on the optic disc. A 90-year-old woman presented with blurred vision (sudden onset) in her left eye. Examination of the fundus revealed acute onset vitreous hemorrhage of unknown origin without retinal detachment. She underwent vitrectomy, but after excision of the dense vitreous hemorrhage, a 2-disc-diameter hematoma appeared on the optic disc and was removed promptly. Because the bleeding at the base of the hematoma was of arterial origin and pulsating, the first vitrectomy could not achieve hemostasis. Five days after the first surgery, we performed a second vitrectomy. This revealed a subretinal hemorrhage along the superior and inferior arcade vessels and a macular hole, which was almost completely closed with an inverted internal limiting membrane flap. Unfortunately, the macular hole reopened 41 days after the second surgery. In patients presenting with only a large hematoma on the optic disc, it might be prudent to leave the hematoma. However, this large retinal arterial macroaneurysm was on a rare location on the optic disc, making it doubly difficult for the surgeons to diagnose and choose the best option intraoperatively. The differential diagnosis for dense vitreous hemorrhage of unknown origin should include a large retinal arterial macroaneurysm on the optic disc.


2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Manasa Gunturu ◽  
Shiva Kumar Gosi ◽  
Swetha Kanduri ◽  
Vishnu Garla

Varicella-zoster virus (VZV) has been known to cause various eye disorders in both immunocompetent and immunocompromised patients. We present a case of a forty-nine-year-old female patient with acquired immunodeficiency syndrome (AIDS) who presented with headache, fever, and blurred vision. Cerebrospinal fluid (CSF) analysis was consistent with VZV meningitis. Magnetic resonance imaging (MRI) of the brain showed enhancement of the right optic nerve indicative of optic neuritis. She responded well to acyclovir and steroids and discharged on the same. Four weeks after discharge, she presented with sudden onset blindness in the left eye. A cerebral angiogram revealed left retinal artery occlusion and was treated with tissue plasminogen activator (tPA). Funduscopic examination showed patchy areas of necrosis in the periphery which were rapidly progressive, diagnostic of posterior outer retinal necrosis (PORN). She was started on ganciclovir and cidofovir and experienced significant improvement in her visual acuity.


2018 ◽  
Vol 2018 ◽  
pp. 1-3 ◽  
Author(s):  
Nick Si Rui Lan ◽  
P. Gerry Fegan

Thyrotoxic periodic paralysis is an infrequent manifestation of hyperthyroidism and an uncommon cause of muscle weakness in western countries. The diagnosis should be considered in the differential when a patient presents with transient and recurrent weakness associated with hypokalaemia. We present a case of a 26-year-old Asian male presenting with sudden onset muscle weakness affecting predominantly his lower limbs on a background of weight loss. Physical examination demonstrated symmetrical proximal muscle weakness with normal sensation and reflexes. Initial biochemical investigations revealed hypokalaemia, hypomagnesaemia, and hyperthyroidism. Intravenous electrolyte replacement was administered in the emergency department. The patient’s symptoms resolved during inpatient admission. Subsequent TSH receptor antibody testing and radionuclide thyroid scan confirmed a diagnosis of Graves’ disease. The patient was discharged on antithyroid medication with no further episodes of weakness on follow-up. Therefore, thyrotoxic periodic paralysis can be the presenting feature of previously undiagnosed Graves’ disease and should be considered in the differential diagnosis in patients presenting with weakness.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Emily V Nosova ◽  
Emily Japp ◽  
Sheldon T Brown ◽  
Alan J Cohen ◽  
Pietra D Greenberg

Abstract Relevance: A rare yet distinct cause of sudden onset paralysis is severe hypokalemia associated with thyrotoxicosis. This is thought to be associated with mutations in genes encoding cellular potassium channels. We report a case of acute onset paralysis with profound hypokalemia and a new diagnosis of Graves’ thyrotoxicosis in a previously asymptomatic African American, HIV+ man on highly active antiretroviral therapy (HAART) for over 8 years. Clinical case: A 49-year-old man with hypertension and HIV presented with acute paralysis of his bilateral upper and lower extremities. His initial potassium was 1.8 mEq/L (3.5-5.0). Prior to sudden onset loss of motor strength, he denied any preceding palpitations, tremor, anxiety, diaphoresis, hyper-defecation, weight loss, heat or cold intolerance, neck pain, increase in neck girth or difficulty swallowing, proptosis or other ocular symptoms. He has no family history of thyroid disease. He had an enlarged palpable thyroid without nodules and no audible bruit. There was no periorbital edema or proptosis, and no signs of dermopathy. A thyroid ultrasound showed a hyperemic and diffusely enlarged thyroid gland without nodules. Labs included a TSH of 0.007 mCU/mL (0.43-3.8), Free T4 2.1 ng/dL (0.71-1.85), Total T3 229.6 ng/dL (58-194), and thyrotropin receptor antibody 2.6 IU/L (0-1.75). The CD4+ count was 146 in 2010 with a slow gradual rise to 673 in 2019, and HIV viral load was undetectable. There were no offending medications or supplements identified. With aggressive potassium repletion, the serum potassium improved to 4.6 mEq/L and he regained normal strength within several hours. He was started on Methimazole 10mg daily and propranolol 10mg TID. At one month, the thyroid function tests normalized. Methimazole 10mg daily was continued and propranolol was tapered off. He remains euthyroid. Genetic testing is pending. Conclusions: Graves’ disease is the most common thyroid disease triggered by immune reconstitution in HIV + individuals on HAART. The incidence of thyroid disease in HIV patients on HAART is higher in women and Africans with a 1.5-2 fold increase compared with the general population [Muller et. al, Eur Thyroid J 2019;8:173-185]. Despite a higher incidence of hyperthyroidism in women, over 95% of cases of hypokalemic periodic paralysis have been reported in men, with a 10-fold higher incidence among Asians compared to Westerners. There has been one prior case report of Thyrotoxic Periodic Paralysis in an HIV + patient and this was in a Polynesian male (Brown JD et al. Hawaii Med J 2007). To our knowledge, this is the first case report of an African American HIV+ patient with this disorder. An association with mutations in the Kir2.6 gene (encodes a potassium channel, is expressed in skeletal muscle, and is transcriptionally regulated by thyroid hormone) has been proposed [Ryan et. al, Cell 2010 January 8; 140(1):88-98].


1995 ◽  
Vol 14 (11) ◽  
pp. 1016 ◽  
Author(s):  
MOSES GROSSMAN ◽  
PARVIN H. AZIMI ◽  
Sylvia M. Delius Maxwell
Keyword(s):  

2014 ◽  
Vol 20 (6) ◽  
pp. 754-755 ◽  
Author(s):  
Stefan Kipfer ◽  
David W Crook

Predilection sites for infratentorial multiple sclerosis lesions are well known and frequently involve the fasciculus longitudinalis medialis leading to classical internuclear ophthalmoplegia. We report a very rare oculomotor disorder due to a demyelinating central nervous system (CNS) lesion in the medial part of the lower pontine tegmentum. A 36-year-old man presented with sudden onset of blurred vision. Clinically there was limited eye adduction and abduction to either side, which corresponds to bilateral horizontal gaze palsy. Brain magnetic resonance imaging (MRI) showed a demyelinating CNS lesion affecting the fasciculus longitudinalis medialis, abducens nuclei or abducens fibres in the medial part of the lower pontine tegmentum. Furthermore there were six further demyelinating white matter lesions fulfilling all Barkhof criteria for multiple sclerosis. Demyelinating CNS lesions causing isolated bilateral horizontal gaze palsy are exceptional and usually associated with further focal neurological deficits, which was not the case in the presenting patient. This is a unique video report of isolated bilateral horizontal gaze palsy as the initial manifestation of demyelinating CNS disease, which lead to definite diagnosis of relapsing remitting multiple sclerosis.


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