SqCC is typically a centrally located lung carcinoma with four variants recognized by the World Health Organization 2004 classification: clear cell, small cell, papillary and basaloid [
1,
9]. It is staged most commonly according to the seventh edition of the TNM classification of malignant tumors [
10]. The stage of the tumor is an important determinant of prognosis and the key determinant to guiding treatment [
11]. This case represents a rare occurrence of an intracranial metastatic SqCC lesion producing destruction of the parietal bone to invade beyond the skull and into the extracranial soft tissue. It also highlights an unusual presentation of lung cancer. It is extremely rare for intracranial metastases from lung carcinomas to produce destruction of bone. The authors were unable to find a published case of this occurring from an SqCC anywhere in the literature. Destruction of bone from a metastatic brain lesion originating from a primary lung carcinoma has been reported by Foco
et al. in the only published case of adenocarcinoma metastaticum that produced destruction of the frontal bone [
12]. Secondary metastases from Ewing’s sarcoma, carcinoma of the prostate, breast, thyroid and neuroblastoma have been reported to lead to destruction of the bone on rare occasions [
13,
14]. The mechanism of invasion of bone tissue from metastatic lesions has not been fully elucidated. Bone tissue is highly resistant to destruction and most of the information regarding bone destruction is derived from studies focusing on breast cancer, multiple myeloma and prostate cancer, which metastasize to the bone rather than directly invade it [
15]. Injuries to the periosteum have been implicated in making the bone more prone to malignant tumor invasion [
16]. Studies that looked at oral SqCCs directly invading the mandible proposed a role for interleukin (IL)-6 in the activation of osteoclastic activity and subsequent bone resorption [
17]. A recent model by Roato
et al. concluded that NSCLC bone-invading cells produce IL-7, which is known to promote osteolytic lesions [
18]. All of these pathological processes may be involved in this case. The prognosis of patients with stage four SqCC is extremely poor with a median survival of four months [
10]. Patients with brain metastases from any primary source have a median survival of one month from diagnosis if not treated [
4]. As a result, treatment in this population should be focused primarily on palliation. Management of patients with intracranial metastatic lesions extending extracranially is poorly studied. There is a demonstrated role for surgical resection followed by whole brain radiation therapy with doses of 30Gy to 40Gy in patients with a single intracranial metastatic lesion, particularly if the lesion appears capsulated and there are no extracranial lesions. The proposed benefits include improved neurocognitive function, elimination of mass effects and removal of the source of perifocal edema. Open surgical or stereotactic radiosurgery can be employed [
5]. Palliative radiotherapy without surgery has also been used with or without dexamethasone. A case report by Velnar
et al. outlined surgical removal of a meningioma, portions of the skull and portions of soft tissue in a tumor that invaded through the skull, however, this was for a benign lesion [
19]. Platinum-based chemotherapy agents, such as cisplatin and carboplatin, are reported to have a 29% response rate against intracranial metastatic brain lesions arising from SqCC and may be employed in patients with well-controlled neurologic symptoms. A 10% to 38% response to gefitinib and erlotinib was demonstrated in brain metastases from NSCLC that express EGFR [
6]. This patient was offered palliative radiotherapy but declined due to the travel and time commitments associated with accessing the treatment. Surgical resection was not considered an option. He opted for palliative medical management only.