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We report the case of a 50-year-old female survivor of Hodgkin lymphoma (HL), who developed dropped head syndrome (DHS). The patient was diagnosed with HL at 20 years of age, and underwent chemo-radiotherapy, which led to complete remission. Undergoing supplemental therapy for post-radiation hypothyroidism, she had twin babies. She noticed white stains on her neck at the age of 30, and the decolored area gradually expanded. Sixteen years after the radiotherapy (RT), her posterior neck muscle strength began to decline. She had to make considerable efforts to keep her neck straight, and came to experience a severe pain in the neck and shoulders. The patient visited our department due to DHS at the age of 50. She had leukoderma, muscle weakness, and muscle atrophy in the neck and para-spinal region, which were consistent with the area of RT. The strength was preserved in the other parts of the muscle, including the proximal upper limbs. Sensory nerve disorder was not detected. The serum creatine kinase level was slightly elevated. Cervical spine or cervical cord disease that can cause DHS was not detected by MRI examination. The MRI and CT images revealed marked atrophy in the posterior neck and para-spinal muscles. The electromyogram revealed myopathic changes, and the cause of her DHS was diagnosed as radiation-induced myopathy. DHS is a well-known late-onset radiation injury, and Japanese cases have been reported in elderly persons with laryngeal or lung cancer. However, there have been no Japanese case reports of radiation-induced DHS due to RT against HL in younger persons. The patient had visited several clinics and hospitals before she came to our hospital, but RT-induced DHS had been overlooked. Greater recognition and consideration is required for DHS as one of the various issues arising after long passage of HL survivors.

We report the case of a patient who had developed multiple cranial nerve palsies in the course of possible paraneoplastic neurological syndrome (PNS) associated with gallbladder cancer. Twelve days prior to visiting our hospital, a 69-year-old man began experiencing neurological symptoms, beginning with diplopia and progressing to ptosis of the left palpebra and subsequent complete closure of the eye within 8 days. Results of the initial medical examination indicated paresis of left oculomotor (III) and abducens (VI) nerves. MRI of the brain revealed no focal lesion that could have resulted in compression of the affected nerves, while further examination ruled out diabetes mellitus, infection, vasculitis, and other systemic autoimmune diseases as potential causes. Gadolinium-enhanced MRI revealed high intensity located in the oculomotor nerves, and steroid pulse therapy was performed based on the assumption of inflammatory diseases. Although slight improvement was observed with respect to the left extraocular paresis, subsequent emergence of bilateral facial nerve (VII) palsy, right abducens nerve palsy, and right oculomotor nerve palsy occurred in succession. PET/CT performed under suspicion of PNS, confirmed the presence of gallbladder cancer. Surgical extirpation of the cancer occurred 3 months following the appearance of left oculomotor paralysis, after which the patient underwent postoperative chemotherapy. All cranial nerve palsies resolved within 2 months after the operation, and both cancer and PNS have shown no recurrence for over 5 years. Pathological examination of the resected tumor revealed well-differentiated tubular adenocarcinoma showing some signs of epithelial-mesenchymal transition, typically an indicator of a poor prognosis. Nevertheless, lymph node metastasis did not progress beyond N2, and the cancer was completely removed by lymph node dissection. Therefore, the presence of multiple cranial palsies in this patient led to early detection of the asymptomatic gallbladder cancer and immediate administration of life-saving treatment.

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