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Objective: To use the ulnar compound muscle action potential (CMAP) to abductor digiti minimi (ADM) to identify the proportion of individuals with cervical spinal cord injury (SCI) who have lower motor neuron (LMN) abnormalities involving the C8-T1 spinal nerve roots, within 3-6 months, and thus may influence the response to nerve transfer surgery., Design: Retrospective analysis of prospectively collected data. Data were analyzed from European Multicenter Study About SCI database., Setting: Multi-center, academic hospitals., Participants: We included 79 subjects (age=41.4±17.7, range:16-75; 59 men; N=79), who were classified as cervical level injuries 2 weeks after injury and who had manual muscle strength examinations that would warrant consideration for nerve transfer (C5≥4, C8<3)., Interventions: None., Main Outcome Measures: The ulnar nerve CMAP amplitude to ADM was used as a proxy measure for C8-T1 spinal segment health. CMAP amplitude was stratified into very abnormal (<1.0 mV), sub-normal (1.0-5.9 mV), and normal (>6.0 mV). Analysis took place at 3 (n=148 limbs) and 6 months (n=145 limbs)., Results: At 3- and 6-month post-injury, 33.1% and 28.3% of limbs had very abnormal CMAP amplitudes, respectively, while in 54.1% and 51.7%, CMAPs were sub-normal. Median change in amplitude from 3 to 6 months was 0.0 mV for very abnormal and 1.0 mV for subnormal groups. A 3-month ulnar CMAP <1 mV had a positive predictive value of 0.73 (95% CI 0.69-0.76) and 0.78 (95% CI 0.75-0.80) for C8 and T1 muscle strength of 0 vs 1 or 2., Conclusion: A high proportion of individuals have ulnar CMAPs below the lower limit of normal 3- and 6-month post cervical SCI and may also have intercurrent LMN injury. Failure to identify individuals with LMN denervation could result in a lost opportunity to improve hand function through timely nerve transfer surgeries., (Copyright © 2023 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.)

Although many of the vasculitides within the classification of the American College of Rheumatology can have a component of granulomatous inflammation with giant cells, two (ie, giant-cell [temporal] arteritis and Takayasu arteritis) are characterized by infiltrates that are dominated by granulomatous and/or giant-cell-containing inflammation. Furthermore, granulomatous and/or giant-cell dominant infiltrates can characterize disseminated giant-cell arteritis, granulomatous vasculitis of the central nervous system, localized giant-cell arteritis, mesenteric inflammatory veno-occlusive disease, primary cutaneous phlebitis, and giant-cell phlebitis of mesenteric veins and/or omentum. Like the other systemic vasculitides, there is considerable clinicopathologic overlap between these giant-cell vasculitides. Indeed, they are likely closely related, but how they specifically relate to each other is not clear. Their accurate diagnosis is important; because serious morbidity and even death may occur, if proper treatment is delayed or if excessive immunotherapy is given.

The vasculitides commonly create diagnostic and management problems, and a biopsy diagnosis of vasculitis usually does not stand alone in the proper medical management of a patient. Indeed, a conclusive diagnosis usually cannot be made without correlation with the patient's clinical history, physical findings, and/or angiographic findings. Nonetheless, a definitive diagnosis depends on histologic examination because few vasculitic syndromes have specific clinical and laboratory findings. Moreover, the histopathologic diagnosis depends on pathologist experience, tissue selection, sample size, chronologic age of the biopsied lesion(s), and effects of prior treatment. In this issue of Seminars in Diagnostic Pathology the important systemic vasculities are reviewed and updated. These include: polyarteritis nodosa, microscopic polyangiitis (microscopic polyarteritis), cutaneous leukocytoclastic vasculitis, Wegener's granulomatosis, giant-cell vasculitides, localized vasculitis, and angiocentric lymphomas (lymphomatous vasculitis).

The term "small round-cell tumor" describes a group of highly aggressive malignant tumors composed of relatively small and monotonous undifferentiated cells with high nuclear to cytoplasmic ratios. This group includes Ewing's sarcoma (ES), peripheral neuroepithelioma (aka, primitive neuroectodermal tumor or extraskeletal ES), peripheral neuroblastoma ("classic-type"), rhabdomyosarcoma, desmoplastic small round-cell tumor, lymphoma, leukemia, small-cell osteosarcoma, small-cell carcinoma (either undifferentiated or neuroendocrine), olfactory neuroblastoma, cutaneous neuroendocrine carcinoma (aka, Merkel-cell carcinoma), small-cell melanoma, and mesenchymal chondrosarcoma. Their clinical presentations often overlap, thus making a definitive diagnosis problematic in some cases. Yet, a clear understanding of their clinicopathologic features usually allows for a confident diagnosis, especially if immunohistochemistry is used. The following is a review of the immunohistochemistry of this small round-cell tumor group.

Mediastinal germ-cell tumors (GCTs) usually occur within the anterior mediastinum, accounting for about 15% of all mediastinal cysts and tumors. They are associated with the thymus, presumably arising from extragonadal germ cells or thymic cells with germ-cell potential. Mediastinal seminoma develops primarily in young males with rare cases reported in females; likewise, embryonal carcinoma, endodermal sinus tumor or yolk-sac tumor, choriocarcinoma, and malignant mixed or combined GCTs also overwhelmingly affect males. Mature cystic teratoma affects males and females equally. The prognosis for mediastinal mature cystic teratoma and seminoma is very good. Nonseminomatous malignant GCTs of the mediastinum often present with advanced disease and do not respond as well to chemotherapy as their gonadal counterparts. Nonetheless, it is important to separate mediastinal GCTs from other undifferentiated malignant tumors, especially thymic carcinoma, which has a poor prognosis. Clearly, some patients with mediastinal GCTs respond very well to modern therapies.

It has been estimated that approximately 1 in 9 women (living to age 85 years) in the United States will develop breast cancer at some time in their lives; hence the interpretation of breast biopsies has become a large and important component of the surgical pathologist's practice. Indeed, there is great pressure on surgical pathologists to make accurate diagnoses of breast lesions because of their high incidence, the increased public awareness of breast disease, the greater use of screening mammography to detect early carcinomas, the development of multiple therapeutic options (which is often determined by tumor pathology), and the harsh medical-legal climate. The focus of this article will be to define the clinicopathologic features of two malignant breast lesions that are particularly prone to simulate benign lesions, and thus pose important diagnostic problems to surgical pathologists. The two lesions include spindle-cell carcinoma and low-grade duct carcinoma in situ.

The first requirement of a new prognostic indicator is that it should possess a clear biological significance. Indeed, much evidence shows that tumor growth and metastasis depend on neovascularization. Tumor angiogenesis (TA) refers to the growth of new vessels toward and within the tumor; unless tumor neovascularization occurs, cell proliferation reaches a steady state, and the tumor grows no larger than about 2 mm greatest diameter. Moreover, for tumor cells to metastasize, they must gain access to the vasculature from the primary tumor, survive the circulation, localize in the target organ, and induce angiogenesis in that target organ. TA is necessary both at the beginning and at the end of the metastatic cascade of events. Recently, my colleagues and I showed that a statistically significant correlation exists between incidence of metastases and microvessel density (MVD) of primary invasive breast carcinomas. Now, subsequent studies have shown that the association of prognosis with MVD exists not only in breast carcinoma but also in non-small-cell lung carcinoma, prostate carcinoma, and head-and-neck carcinoma. This article reviews the concepts and mechanisms of TA, the evidence supporting its role in growth and metastasis of solid tumors, and how measuring MVD within invasive tumors correlates with factor VIII-related antigen, blood vessel.

Interpretation of breast biopsies has assumed a large and important component of the surgical pathologist's practice. Currently, about 10% of women will develop breast carcinoma during their lifetime. This high incidence, coupled with increased public awareness of breast disease, greater use of screening mammography to detect early carcinomas, development of multiple therapeutic options (the latter often influenced by the pathology of the tumor), and a harsh medicolegal climate have placed greater demands on surgical pathologists for accurate interpretation of breast tissues. The focus of this report is to define the clinicopathologic features of five benign breast lesions that mimic malignant breast disease, and thus pose important diagnostic considerations to surgical pathologists.

Sarcomatoid carcinomas are typically (but not always) biphasic tumors containing both carcinomatous and sarcomatous components. Within the upper aerodigestive tract, they arise from the mucosa and are predominantly composed of pleomorphic spindled cells associated with squamous carcinoma, the latter often presenting focally at the tumor base. Although their histogenesis is still debated, most authors favor metaplastic origin of the sarcomatous cells from carcinoma cells. Indeed, when studied with electron microscopy and/or immunohistochemistry the sarcomatous cells are frequently found to retain epithelial features; however, the sarcomatous metaplasia can be so complete that malignant cartilage, bone, and/or muscle cells are formed. In addition, metastatic deposits may contain sarcomatous and/or carcinomatous components. Sarcomatoid carcinomas are potentially aggressive tumors and should be treated accordingly. Although it is difficult to predict biologic behavior in every case, patients whose tumors are deeply invasive tend to have a poor prognosis, whereas those with superficially invasive tumors usually have an excellent prognosis.

Although mass lesions of the salivary glands are readily accessible to examination by fine-needle aspiration, the use of this modality has been limited. In part, this may be related to the difficulty differentiating between benign and malignant neoplasms in some cytologic specimens. Marked atypia in reactive non-neoplastic epithelium also could result in a false-positive diagnosis. In addition, aspiration of hypocellular material from cystic neoplasms, eg, well-differentiated mucoepidermoid carcinoma, may lead to false-negative cytologic reports. However, the diagnostic specificities claimed by a number of authors for this method are excellent. Furthermore, aspirates of certain specific neoplasms may yield highly distinctive cellular samples, such as the uniform tumor cells and extracellular hyaline spheres in many adenoid cystic carcinomas. Another example is the characteristic transition between the epithelial and myoepithelial cells of pleomorphic adenomas, which may contain prominent myxoid matrical material. With the increasing recognition of such features, the reported levels of diagnostic accuracy are improving.