Metastasis of cervical esophageal carcinoma to the temporal bone — a study of the temporal bone histology

Imauchi, Yutaka; Kaga, Kimitaka; Nibu, Ken‐ichi; Sakuma, Nobuyuki; Iino, Yukiko; Kodera, Kazuoki

doi:10.1016/s0385-8146(00)00109-7

Cited by 26 publications

(11 citation statements)

References 8 publications

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“…Form the review of the literature, we should differentiate between esophageal squamous cell carcinoma (SCC) and (gastro)esophageal adenocarcinoma. PNI, the underlying histologic mechanism for PNS, is a known feature of SCC and our review supports the propensity of SCC for PNI (Tanaka et al, 1998;Ning et al, 2015;Sheng et al, 2015) and neural involvement in general (Thomas et al, 1968;Delamarre et al, 1981;Tachimori et al, 1995;Imauchi et al, 2001). On the other hand, only a few studies have focused on neural involvement in GEJ adenocarcinoma.…”

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confidence: 82%

Gastroesophageal junction carcinoma and brachial plexopathy: An anatomic explanation via perineural spread

2016

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Perineural spread (PNS) is a frequently missed or underestimated form of tumor extension to neighboring or even distant structures. A number of neoplasms are widely known for propensity for perineural invasion (PNI) and PNS. These include squamous cell carcinoma (Capek et al., 2015a;Roh et al., 2015), adenoid cystic carcinoma (Singh et al., 2015), or desmoplastic melanoma (Frydenlund and Mahalingam, 2015) in the head and neck area and prostate (Hashimoto et al., 2015) and pancreatic (Bapat et al., 2011) cancer as examples of visceral tumors. In our practice, we have observed a number of cases of extensive PNS of tumors not usually associated with PNS such as rectal (Capek et al., 2015b), bladder (Aghion et al., 2014), or cervical (Howe et al., 2013 cancer. Some of these cases went unrecognized for several years despite being symptomatic due to a relatively low level of suspicion. We present a patient with progressive upper extremity weakness and Horner's syndrome with a history of gastroesophageal junction (GEJ) carcinoma, in whom the mechanism was unrecognized. This is the first reported case of PNS in GEJ carcinoma and its anatomic basis.A 61-year old man was diagnosed with GEJ adenocarcinoma in May 2013 after an episode of dysphagia. The tumor was resected in September 2013 and the patient was staged as pT3, N3, M0, and underwent chemoradiotherapy. Interval scans showed no evidence of disease until October 2014, when he developed right adrenal gland and mediastinal metastases for which he was treated with another cycle of chemoradiotherapy. In June 2015, he developed a new left supraclavicular tumor mass and subsequently presented to our institution in November 2015 ( Fig. 1) with a pathological fracture of the T12 vertebra causing compression of the conus medullaris. On examination a left Horner's syndrome was noted, but according to the patient that had been present for at least one year. The preoperative imaging studies revealed other probable metastases in the T1 and C6 vertebrae and in the adrenal glands. A thoracolumbar spine fusion surgery was planned in an acute fashion, but the day before the spinal surgery the patient developed acute onset weakness of the left upper extremity. Neurology service established the diagnosis of a left brachial plexopathy and the patient subsequently underwent the planned T10-L2 interbody fusion with T12 corpectomy, T11-L1 laminectomies, and bilateral T12 rhizotomy. Pathology confirmed the metastatic nature of the T12 body lesion. After the surgery, his left brachial plexopathy was evaluated in detail; the supraclavicular mass was firm, non-mobile, and tender to palpation. Percussion of it produced radiating dyesthesias to the shoulder. The deltoid was 4/5 (MRC scale), external rotators were 3/5, biceps brachii, brachioradialis, and supinator were 4/5. He had decreased sensation on the lateral side of the arm, forearm, and hand. The left biceps brachii reflex was decreased. The remainder of the examination was unremarkable. A chest radiograph demonstrated an elevated left ...

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confidence: 82%

Gastroesophageal junction carcinoma and brachial plexopathy: An anatomic explanation via perineural spread

2016

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“…To our knowledge, our case represents the fourth reported case of acute epidural hematoma secondary to skull metastasis and the only case of epidural hematoma secondary to esophageal carcinoma metastasis to the skull, although one case of cervical esophageal cancer metastasizing to the temporal bone has been reported. 5 In the present case, the mechanism of spread from the esophagus and affected lymph nodes to the skull is unclear. Hematogenous spread from the primary lesion, perineural or perivascular spread through skull foramina, 9 as well as invasion through the skull sutures 10 have all been proposed to explain the routes of metastatic spread to the skull.…”

Section: Discussionmentioning

confidence: 70%

“…4 Although metastatic involvement of the skull has been observed in carcinoma of the breast, prostate, and lung among others, 1 skull metastasis arising from esophageal carcinoma is exceedingly rare. 5 In addition, acute hemorrhage secondary to skull metastases has rarely been described. Acute epidural hematoma resulting from skull metastases has been reported in only three cases.…”

Section: Discussionmentioning

confidence: 99%

Acute Epidural Hematoma Secondary to Skull Metastasis from Esophageal Carcinoma

Ellis

McDonald

2007

Can. j. neurol. sci.

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“…The solid tumours known to cause LC are breast cancer, lung cancer, primary brain tumours, melanoma and non-Hodgkin's lymphoma 2. Oesophageal cancer predominantly metastasises to the lymph nodes, liver, lungs, adrenal glands, stomach, kidneys and bones 3…”

Section: Discussionmentioning

confidence: 99%

Leptomeningeal carcinomatosis from oesophageal cancer, presenting as meningitis

et al. 2016

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SUMMARYA 47-year-old woman presented with headache, neck pain, dizziness, nausea and vomiting for 4-5 days. She also had a history of weight loss and difficulty in swallowing. On physical examination, she had nuchal rigidity with a positive Kernig's sign. Cerebrospinal fluid analysis revealed mild pleocytosis but some atypical cells were also noted. Cytopathological analysis of the atypical cells showed high nuclear/cytoplasmic ratios and eccentric nuclei with prominent nucleoli, consistent with malignancy. A CT scan of the head and neck showed multiple lytic lesions involving the left calvarium, and diffuse thickening and enhancement of meninges over the left cerebral area. Extensive osteolytic lesions were also noted on the vertebral bodies, pedicles and lamina, at multiple levels of the cervical spine. An endoscopy revealed a mass at the gastro-oesophageal junction, and biopsy confirmed moderately differentiated adenocarcinoma of the oesophagus. The patient was started on chemotherapy along with radiation therapy. BACKGROUND

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Metastasis of cervical esophageal carcinoma to the temporal bone — a study of the temporal bone histology

Cited by 26 publications

References 8 publications

Gastroesophageal junction carcinoma and brachial plexopathy: An anatomic explanation via perineural spread

Gastroesophageal junction carcinoma and brachial plexopathy: An anatomic explanation via perineural spread

Acute Epidural Hematoma Secondary to Skull Metastasis from Esophageal Carcinoma

Leptomeningeal carcinomatosis from oesophageal cancer, presenting as meningitis

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