Peripheral nerve sheet tumors (PNSTs) are exceedingly rare with the most tumors being benign. Schwannomas are one of the two types of PNSTs and have been classified as a slow-growing, benign neurogenic tumor composed of Schwann cells. Schwannomas have been shown to occur primarily in middle-aged patients with no gender prevalence. The variable clinical presentation of this tumor makes it a difficult diagnosis with symptoms being based on their location. Magnetic resonance imaging (MRI) is used to reveals the location, size, texture, and relationships with surrounding neuromuscular structures, with surgical excision being the primary treatment option with excellent outcomes. Our patient presented to the clinic due to left leg pain. MRI was utilized to diagnosis the tumor was a sural nerve tumor. The tumor was tan-pink in color and measured 6 cm in length and ranging from 0.4 cm to a central bulging aspect up to 2.5 cm for 3 cm with positive markers for S100. This case report explores patients’ clinical manifestations of a lower extremity schwannoma.

Anaplastic oligodendrogliomas (AOD) are rare brain tumors with variable overall survival accounting for approximately 1.3% to 4.4% of brain tumors and about 5% to 10% of the gliocytomas. Anaplastic oligodendrogliomas, or grade III oligodendrogliomas, describe rare primary malignant brain tumors with exceedingly variable overall prognosis. Gliomas originate from neural stem cells or glial progenitor cells that develop or maintain glial characteristics. These tumors occur most frequently in males during the 5th and 6th decade of life often presenting with new onset seizures. The WHO grading system distinguishes two histopathologic grades of Oligodendrogliomas: grade II (low-grade) and grade III (anaplastic oligodendroglioma or AOD). Here we present a case of anaplastic oligodendrogliomas and review the literature.

Schwannomas are benign peripheral nerve tumors, presenting as solitary tumors mostly in head and neck region followed by upper and lower extremities. Various variants of Schwannomas have been described as: cellular, plexiform, ancient and psammomatouse. Plexiform Schwannoma (PS) is an unusual and rare variant of Schwannoma. They are usually more cellular and therefore also qualify as cellular schwannomas. Surgical excision with complete tumor removal with safe margin is the usual mode of treatment of PS. Schwannomas, including the plexiform variant, are benign and do not recur when completely excised. PS can be easily confused, and misdiagnosed as plexiform neurofibroma (PN), and thus may be misinterpreted as a sarcoma arising in a plexiform neurofibroma. It is critical to differentiate a PS from a PN because the latter is pathognomonic of Neurofibromatosis (NF) and carries significant risk of malignant transformation. Here we present a case of planter PS and review the literature.

We present a case of a 15-month-old female patient with a laryngeal neurofibroma of the larynx associated with Neurofibromatosis Type 1 (NF 1) and how it affected her spoken communication ability. In this report, we review the literature describing the rarity of Neurofibromatosis type 1 and laryngeal neurofibromas, the locations of laryngeal neurofibromas, the differential diagnosis for laryngeal neurofibromas, spoken communication disorders associated with NF1, early intervention and the role of concomitant recurrent otitis media in our patient. Following a review of the literature, suggestions for early intervention and assessments of language and speech for children with NF1 is discussed.

Recognition of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) as a spectrum of neurodegenerative disease is rapidly evolving. Both disorders have been shown to overlap in their pathology, genetics, and clinical presentations. Recent investigations have identified genetic hallmarks that concretely bridge those highly heterogenic disorders as a spectrum. The discovery of hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9orf72), TAR-DNA binding protein (TDP)-43 proteinopathy, and their implicated functions in neurodegeneration and autoimmunity suggests possible underlying pathogenesis of ALS/FTD and toxic neurodegeneration at large. The autoimmunity aspect of C9orf72 is particularly exciting as it may elucidate a novel paradigm that not only encompasses the origin of neurodegeneration, but also that of autoimmunity. Here, we briefly review the latest findings of functions of TDP43 and C9rof72 and further discuss the possibility of an overarching theme in neurodegenerative diseases.