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Oculomotor Nerve Palsy as a Manifestation of Immune Thrombocytopenic Purpura: A Case Report
Immune thrombocytopenic purpura (ITP) is caused by alterations in the immune system resulting in platelet destruction. It often manifests clinically with bleeding or on routine lab work revealing thrombocytopenia in asymptomatic individuals. Neurologic manifestations of this condition are sparsely d...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cureus
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617074/ https://www.ncbi.nlm.nih.gov/pubmed/36320952 http://dx.doi.org/10.7759/cureus.29723 |
Sumario: | Immune thrombocytopenic purpura (ITP) is caused by alterations in the immune system resulting in platelet destruction. It often manifests clinically with bleeding or on routine lab work revealing thrombocytopenia in asymptomatic individuals. Neurologic manifestations of this condition are sparsely documented in the literature. Among the symptoms reported were case reports of ischemic strokes, transient ischemic attacks, mononeuropathy multiplex, and polyneuropathy as neurological complications from immune thrombocytopenic purpura. Isolated cranial nerve palsies are uncommon. The following case describes a patient with immune thrombocytopenic purpura who presented with an isolated cranial nerve III palsy. A 55-year-old presented with pain in the right eye that was found in a downward and lateral gaze paralysis. There was no evidence of central or peripheral neurovascular etiology on imaging. However, workup revealed isolated thrombocytopenia with platelets <2000/ml(3). Other possible etiologies, such as human immunodeficiency virus (HIV) and infectious etiologies, were evaluated and excluded. Thrombotic thrombocytopenia purpura was excluded with the results from ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) activity. The patient was appropriately transfused with platelets and was treated with methylprednisolone, which improved his platelets. At the time of discharge, the patient continued to have cranial nerve III palsy and was referred to follow up with hematology on an outpatient basis. In prior case reports where ITP presented as neurological deficits, there was evidence of intraneural microhemorrhage. Our case is unique in that the primary neurologic presentation without central nervous system pathology eventually led to the diagnosis of ITP. The symptoms were attributed to microhemorrhages that were not detected in imaging studies. Further studies are warranted to explore any correlation or causative association between ITP and neurological symptoms. This case report highlights the need to consider uncommon but possible manifestations of conditions that may initially appear seemingly irrelevant to the patient’s chief complaint. |
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