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1.
Fed Pract ; 39(6): 261-265, 2022 Jun.
Article in English | MEDLINE | ID: mdl-36404940

ABSTRACT

Background: Rhabdomyolysis is caused by muscle overuse, trauma, prolonged immobilization, drugs, or toxins. As rhabdomyolysis progresses, swelling and edema can compress surrounding structures. Few cases of the phenomenon occurring as a sequela of substance use have been described. Case Presentation: We present a 68-year-old male patient with rhabdomyolysis following use of crack cocaine contaminated with fentanyl. The patient had 0/5 strength bilaterally and bilateral absent reflexes in the upper extremities. Sensation was markedly decreased, as he was unable to feel temperature, pinprick sensation, or general touch. Creatine phosphokinase level was elevated at 21,292 IU/L. On magnetic resonance imaging, there was abnormal signal in the lower neck bilaterally. It is presumed that muscular edema resulted in partial narrowing of the thoracic outlet bilaterally with corresponding mass effect on the traversing brachial plexus. Conclusions: This is the seventh case of brachial plexopathy secondary to rhabdomyolysis precipitated by opioid use that has been reported in the literature. Prospective studies should examine treatment for this condition.

2.
Case Rep Neurol Med ; 2016: 5720319, 2016.
Article in English | MEDLINE | ID: mdl-27529041

ABSTRACT

Neuro-Behçet disease (NBD) is a multisystem inflammatory disorder characterized by oral lesions, genital lesions, uveitis, and neurological deficits. If left untreated, it may lead to worsening neurological function and can be fatal. Here we present a case of a 52-year-old woman who was diagnosed with Behçet disease (BD) as a teenager and had a relatively mild disease course. Decades later after her initial DB diagnosis, she presented to our hospital with a chief complaint of headache. She did not have focal neurological deficits or any active mucosal lesions. Upon further investigation, the patient was found to have multiple inflammatory changes on neuroimaging and abnormal cerebrospinal fluid (CSF), consistent with the diagnosis of NBD. She was treated with intravenous corticosteroid therapy and her symptoms resolved. Although our patient presented with minimal symptoms decades after her initial diagnosis, any neurological complaint warranted a thorough investigation for a proper diagnosis and treatment given the multisystem involvement of BD.

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