Worsening nausea, vomiting, and dizziness • 20-pound weight loss in 2 months • mild hearing loss • reoccurring episodes of falls • Dx?

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Case Reports

Worsening nausea, vomiting, and dizziness • 20-pound weight loss in 2 months • mild hearing loss • reoccurring episodes of falls • Dx?

J Fam Pract. 2019 November;68(9):515-518

By

Daniel Murphy, MD

Michael Levy, MD, PhD

► Worsening nausea, vomiting, and dizziness for 2-months, resulting in a 20-pound weight loss
► Pruritus
► Ataxia
► Mild hearing loss, with reoccurring episodes of falls

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References

1. Hinson SR, Pittock SJ, Lucchinetti CF, et al. Pathogenic potential of IgG binding to water channel extracellular domain in neuromyelitis optica. Neurology. 2007;69:2221-2231.

2. Ratelade J, Zhang H, Saadoun S, et al. Neuromyelitis optica IgG and natural killer cells Produce NMO lesions in mice without myelin loss. Acta Neuropathol. 2012;123:861-872.

3. Saadoun S, Waters P, Bell BA, et al. Intra-cerebral injection of neuromyelitis optica immunoglobulin G and human complement produces neuromyelitis optica lesions in mice. Brain. 2010;133:349-361.

4. Takahashi T, Fujihara K, Nakashima I, et al. Anti-aquaporin-4 antibody is involved in the pathogenesis of NMO: a study on antibody titer. Brain. 2007;130:1235-1243.

5. Jarius S, Aboul-Enein F, Waters P, et al. Antibody to aquaporin-4 in the long-term course of neuromyelitis optica. Brain. 2008;131:3072-3080.

6. Hamid SHM, Whittam D, Mutch K, et al. What proportion of AQP4-IgG-negative NMO spectrum disorder patients are Mog-IgG positive? A cross sectional study of 132 patients. J Neurol. 2017; 264:2088-2094.

7. Peschl P, Bradi M, Hoftberger R, et al. Myelin oligodendrocyte glycoprotein: deciphering a target in inflammatory demyelinating diseases. Front Immunol. 2017;8:529.

8. Jurynczyk M, Messina S, Woodhall MR, et al. Clinical presentation and prognosis in MOG-antibody disease: a UK study. Brain. 2017;140:3128-3138.

9. Sellner J, Boggild M, Clanet M, et al. EFNS Guidelines on diagnosis and management of neuromyelitis optica. Eur J Neurol. 2010;17:1019-1032.

10. Kleiter I, Gahlen A, Borisow N, et al. Neuromyelitis optica: evaluation of 871 attacks and 1,153 treatment courses. Ann Neurol. 2016;79:206-216.

11. Watanabe S, Nakashima I, Misu T, et al. Therapeutic efficacy of plasma exchange in NMO-IgG-positive patients with neuromyelitis optica. Mult Scler. 2007;13:128-132.

12. Collongues N, Brassat D, Maillart E, et al. Efficacy of rituximab in refractory neuromyelitis optica. Mult Scler. 2016;22:955-959.

13. Collongues N, de Seze J. An update on the evidence for the efficacy and safety of rituximab in the management of neuromyelitis optica. Ther Adv Neurol Disord. 2016;9:180-188.

14. Kim SH, Huh SY, Lee SJ, et al. A 5-year follow-up of rituximab treatment in patients with neuromyelitis optica spectrum disorder. JAMA Neurol. 2013;70:1110-1117.

15. Kim SH, Kim W, Li XF, et al. Repeated treatment with rituximab based on the assessment of peripheral circulating memory B cells in patients with relapsing neuromyelitis optica over 2 years. Arch Neurol. 2011;68:1412-1420.

THE CASE

A 26-year-old Hispanic/African American woman presented to our clinic with a 2-month history of nausea and vomiting, along with dizziness. The nausea and vomiting persistently worsened, and she was only able to tolerate apples and berries. During this 2-month period, she lost 20 pounds and her symptoms progressed to include pruritus, ataxia, and mild hearing loss, with reoccurring episodes of falls.

THE DIAGNOSIS

On examination, she was found to be bradycardic with a heart rate of 47 beats/min, right- axis deviation, and inverted T waves in leads I, II, and augmented vector left. Her family history included the death of an aunt who was in her early 30s due to an unknown heart condition.

Echocardiogram identified mild mitral valve regurgitation with an ejection fraction of 55% to 60% (reference range: 55%-70%). Cardiology determined that her bradycardia was not the source of her symptoms. A neurologic exam identified 3+ hyperreflexia (indicating the reflex was increased), tandem gait instability, and left oculomotor dysfunction.

Brain magnetic resonance imaging (MRI) identified bilateral parietal white matter lesions where a demyelinating process could not be excluded (FIGURE 1A). The patient’s symptoms of nausea and vomiting continued, and she only tolerated peanuts and liquids. An MRI of the spine was negative.

Laboratory testing revealed that the patient was negative for human immunodeficiency virus (HIV), syphilis, Lyme disease, and lupus. Her thyroid-stimulating hormone level was 1.7 mIU/L (reference range: 0.4-4.2 mIU/L), and her vitamin B₁₂ level was 504 pg/mL (reference range: 160-950 pg/mL).

The patient’s lumbar puncture was negative for oligoclonal bands. The IgG synthesis rate/index cerebrospinal fluid (CSF) was –3.9, ruling out multiple sclerosis. Her CSF culture was negative, with a glucose level of 42 mg/dL (reference range: 70-110 mg/dL), colorless appearance, 1 white blood cell, and spinal albumin of 12.2 mg/dL (reference range: 8-42 mg/dL). The visual evoked potential was negative. The aquaporin-4 (AQP4) antibody was positive at 3.4 U/mL, and the myelin oligodendrocyte glycoprotein (MOG) antibody was positive.

Gastroenterology concluded a normal gastric accommodation and unremarkable computed tomography (CT) enterography. Moderate erosions were identified in the stomach with an erythematous gastropathy. The patient was placed on a proton pump inhibitor.

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