ABSTRACT
PURPOSE: To report a case of intravascular lymphoma (IVL) mimicking a Vogt-Koyanagi-Harada disease (VKH). DESIGN: Case report. METHODS: A 38-year-old man was referred for blurred vision, headache, and hearing loss. Examination demonstrated vitritis and subretinal detachments in each eye. Cerebral fluid analysis showed lymphocytic meningitis. Cerebral MRI was normal. A diagnosis of VKH disease was made. RESULTS: Steroid treatment was introduced, after which all symptoms disappeared. Six months later, the patient returned with paraplegia and confusion. Cerebral MRI revealed hypodense periventricular lesions. A stereotaxic biopsy confirmed the diagnosis of IVL. The patient died a few months later. CONCLUSION: IVL may have many revealing aspects, including ophthalmologic symptoms.
Subject(s)
Lymphoma/diagnosis , Uveomeningoencephalitic Syndrome/diagnosis , Vascular Neoplasms/diagnosis , Adult , Biopsy/methods , Brain/pathology , Confusion/etiology , Diagnosis, Differential , Fatal Outcome , Fluorescein Angiography , Humans , Lymphoma/complications , Lymphoma/drug therapy , Lymphoma/psychology , Magnetic Resonance Imaging , Male , Paraplegia/etiology , Stereotaxic Techniques , Steroids/therapeutic use , Vascular Neoplasms/complications , Vascular Neoplasms/drug therapy , Vascular Neoplasms/psychology , Vision Disorders/diagnosis , Vision Disorders/etiologyABSTRACT
INTRODUCTION: Depression is known to have a bidirectional relationship with cardiovascular disease. Severe major depression associated with psychomotor retardation and immobility can be a risk factor for pulmonary embolism; the reverse pathway has not been reported. CASE REPORT: We report a case of a 61-year-old man diagnosed with multiple pulmonary thromboembolism finally attributed to a right pulmonary artery intraluminal sarcoma. One month after the onset of presenting symptoms, the patient suddenly developed an episode of severe, melancholic depression, which remitted in six weeks under treatment with venlafaxine 225 mg/day. DISCUSSION: Pathophysiological mechanisms implicated in the development of depression in our patient might resemble those postulated for post-myocardial infarction depression; in line with the "vascular depression" hypothesis, cerebral damage in the limbic circuitry caused by transient hypoxia, an inflammatory response or both may have contributed. CONCLUSION: Multiple pulmonary thromboembolism seems to have a bidirectional relationship with major depression, in a similar way as myocardial infarction does.