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O'Connell et al. proposed that the vestibular bulbs be renamed the "clitoral bulbs" because of their consistent relationship to the clitoris and inconsistent relationship to the vestibule. Normally such proposed esoteric changes in anatomical nomenclature would get little notice by anatomists, yet alone the general public; however, many subsequent articles and books placed this change in the context of centuries of male anatomists and physicians downplaying female sexual anatomy and sexuality. Most prominent is a 2022 book by Rachel Gross, Vagina Obscura: An Anatomical Voyage. Here we review this "Anatomical Voyage" and find author bias in omitting/including erroneous facts in this book. We also present a critique of a 1995 article that appeared in Feminist Studies; Graphical Representations in Anatomy Texts, c1900-1991. This article, which has been repeatedly cited in the clinical literature, asserts that between circa 1950-1980 anatomy textbooks purposely eliminated depicting/labeling the clitoris in illustrations because the authors of the textbooks were reflecting societal norms that de-emphasized the importance of the clitoris. Unfortunately, the methods used by Moore and Clarke are not replicable; and further, their conclusions were not justified because of clear bias in their description and depiction of the anatomy sources they review.

Newborn anatomy, despite being distinctly different than adult anatomy, does not constitute a major component of a typical medical school course in gross anatomy. Accordingly, there is a perception that other than the well-known late 20th-century atlas and small textbook by Edmund Crelin on newborn anatomy, there is almost no information available for anatomists and clinicians to refer to on normal infant anatomy. This perception, as verbalized by Crelin in his books, is not correct. There is an amazing wealth of accurate descriptive and pictorial information on infant anatomy available from late 19th- and early 20th-century sources. One of these sources is a comprehensive 200-page chapter on pediatric anatomy by Richard Scammon that was published in 1923 and that is freely available. Because of some inconsistencies and inaccuracies we have identified in the Crelin works, we suggest that any anatomist or clinician who wishes to learn and teach about infant anatomy refer to Scammon's chapter before using any text or image from the Crelin books.

The inherent variable anatomy of the neonate and the uniquely-shaped maternal birth canal that is associated with the evolution of human bipedalism constitute risk factors for neonatal brachial plexus palsy (NBPP). For example, those neonates with a prefixed brachial plexus (BP) are at greater risk of trauma due to lateral neck traction during delivery than those with a normal or postfixed BP. Compared to adults, neonates also have extremely large and heavy heads (high head: body ratio) set upon necks with muscles and ligaments that are weak and poorly developed. Accordingly, insufficient cranial stability can place large torques on the cervical spinal nerves. In addition, the pelvic changes necessary for habitual bipedal posture resulted in a uniquely-shaped, obstruction-filled, sinusoidal birth canal, requiring the human fetus to complete a complicated series of rotations to successfully traverse it. Furthermore, although there are many risk factors that are known to contribute to NBPP, the specific anatomy and physiology of the neonate, except for macrosomia, is not considered to be one of them. In fact, currently, the amount of lateral traction applied to the neck during delivery is the overwhelming legal factor that is used to evaluate whether a birth attendant is liable in cases of permanent NBPP. Here, we suggest that the specific anatomy and physiology of the neonate and mother, which are clearly not within the control of the birth attendant, should also be considered when assessing liability in cases of NBPP.

Postpartum pelvic floor dysfunction (PFD) has been identified as a significant public health issue. The study aimed to (a) identify the impact of PFD on parous women’s occupations, (b) explore how PFD impacts daily life, and (c) determine the level of awareness regarding availability of PFD treatment. The preliminary study utilized a mixed-methods descriptive design. In total, 255 participants completed the Mothers and Children (MAC) survey, distributed electronically throughout the United States. Results indicated that PFD symptoms limit parous women’s occupational performance, specifically sexual activity and exercise. Despite results indicating PFD significantly detracted from participants’ daily life, 66.8% of participants reported having no awareness of pelvic floor rehabilitation to address PFD. Findings suggest that further research and increased advocacy within the field of occupational therapy are necessary to increase the awareness of PFD rehabilitation and mitigate the impact on women’s lives after childbirth.

Nuchal translucency (NT) is a hypo-echoic region of subcutaneous fluid accumulation in the posterior neck at the level of the cervical spine between the skin and soft tissues found at 10-14 weeks gestation. This ultrasound finding is important because increased NT measurements place the fetus at increased risk for chromosomal and structural abnormalities. It is a fascinating phenomenon that displays the intersection of anatomy, development, and imaging. In addition, with the ever increasing use of ultrasound in anatomy, NT is a readily demonstrable example of how important ultrasound has become to the practice of medicine. Articles on NT were obtained from OVID database and reviewed for their contribution to an understanding of the anatomical basis of NT. Whereas it is well established that the ultrasound finding of increased NT is a sensitive marker for Trisomy 21 at 10-14 weeks gestation, why this phenomena occurs has yet to be explained. The basis of nuchal edema is most likely multifactorial, a combination of delayed or disturbed lymphangiogenesis, cardiac and vascular abnormalities, and abnormal extracellular matrix components. Further research on the development of the fetal head and neck related to lymphatic development and fluid regulation during 8-14 weeks gestation will enable a greater understanding of how and why increased NT occurs compared to what is currently known. This could lead to early intervention to manage some of the repercussions of Trisomy 21 and other abnormalities related to NT.

Orbital and retro-orbital pain are relatively common clinical conditions that are associated with such disorders as trigeminal, lacrimal, and ciliary neuralgia, cluster headaches, paroxysmal hemicrania, inflammatory orbital pseudotumor, trochleitis, and herpetic neuralgia ophthalmicus, thus making the nerves supplying the orbit of great clinical importance. Surprisingly, how pain from this region reaches conscious levels is enigmatic. Classically, it has been assumed that pain reaches the ophthalmic division of the trigeminal nerve (V1 ) and travels to the descending spinal trigeminal nucleus. However, exactly where the receptors for orbital pain are located and how impulses reach V1 is speculative. In this project, we reviewed all of the reported connections between the orbital nerves and V1 in order to understand how pain from this region is transmitted to the brain. We found reported neural connections to exist between cranial nerve (CN) V1 and CNs III, IV, and VI within the orbit, as well as direct neural branches to extra-ocular muscles from the nasociliary, frontal, and supraorbital nerves. We also found reported neural connections to exist between the presumed carotid plexus and CN VI and CN V1 , CN VI and CN V1 and V2 , and between CN V1 and CN III, all within the cavernous sinus. Whether or not these connections are sympathetic or sensory or some combination of both connections remains unclear. An understanding of the variability and frequency of these neural connections could lead to safer surgical procedures of the orbit and effective treatments for patients with orbital pain.

Vacuum phenomenon (VP) is an anatomical entity of potential confusion in the diagnosis and evaluation of joint pathology. Observation of this phenomenon has been demonstrated on basic radiographs, computed tomography, and magnetic resonance imaging. Although VP is most often associated with degenerative joint disease, it is observed with other pathologies. Two problematic scenarios can occur: a false-positive diagnosis of serious pathology instead of benign VP and a false-negative diagnosis of benign VP with a more serious underlying process Despite this potential for confusion, criteria for distinguishing VP from other causes of joint pain and for evaluating a suspected case of VP have not been fully established. We reviewed the literature to determine underlying mechanism, symptomology, associated pathologies, and clinical importance of VP. The formation of VP can be explained by gas solubility, pressure-volume relationships, and human physiology. CT, GRE-MRI, and multipositional views are the best imaging studies to view VP. Although most cases of VP are benign, it can be associated with clinical signs and symptoms. VP outside the spine is an underreported finding on imaging studies. VP should be on the differential diagnosis for joint pain, especially in the elderly. We have proposed criteria for diagnosing VP and generated a basic algorithm for its workup. Underreporting of this phenomenon shows a lack of awareness of VP on the part of physicians. By identifying true anatomic VP, we can prevent harm from suboptimal treatment of patients.

The etiological basis of trigeminal neuralgia (TN) is unknown but vascular (arterial and venous) compression of the trigeminal nerve roots has emerged as the likely cause in most cases. Here we examine the evidence for the "brain sagging/arterial elongation hypothesis" with reference to the cerebral arteries and veins believed to cause the compression. Most often implicated are the superior cerebellar artery, the anterior and posterior inferior cerebellar arteries, and the superior petrosal vein including several of its tributaries. The reviewed data suggest that the theoretical support for a vascular compressive etiology of TN is weak, albeit the surgical outcome data are relatively convincing.

Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.

The nervus terminalis (NT; terminal nerve) was clearly identified as an additional cranial nerve in humans more than a century ago yet remains mostly undescribed in modern anatomy textbooks. The nerve is referred to as the nervus terminalis because in species initially examined its fibers were seen entering the brain in the region of the lamina terminalis. It has also been referred to as cranial nerve 0, but because there is no Roman symbol for zero, an N for the Latin word nulla is a better numerical designation. This nerve is very distinct in human fetuses and infants but also has been repeatedly identified in adult human brains. The NT fibers are unmyelinated and emanate from ganglia. The fibers pass through the cribriform plate medial to those of the olfactory nerve fila. The fibers end in the nasal mucosa and probably arise from autonomic/neuromodulatory as well as sensory neurons. The NT has been demonstrated to release luteinizing-releasing luteinizing hormone and is therefore thought to play a role in reproductive behavior. Based on the available evidence, the NT appears to be functional in adult humans and should be taught in medical schools and incorporated into anatomy/neuroanatomy textbooks.

The anatomical understanding of the pain generators in osteoarthritis (OA) is incomplete and the teaching about these pain generators in medical school anatomy/histology courses is minimal. This review covers the nociceptive innervation of synovial joints for the purposes of teaching. Studies that discuss the presence of neuropeptides involved in pain, such as Substance P (SP) and calcitonin-gene-related peptide, are the focus of this review. Nociceptive free-nerve endings and SP staining nerves are found in the accessory ligaments, synovium, subchondral bone, menisci, and periosteum. The vasculature may also play a role in pain generation through vasospasm or ischemia, but this has yet to be proven. Joint denervation may relieve joint pain showing that it is indeed articular nerves that are carrying pain impulses but denervation does not identify the precise source of the pain. It remains unclear which of the anatomical loci of pain generation are primary in OA and if sources of pain vary in different patients and in different joints.

The objective of the study is to ascertain the rationale for the diagnosis of postencephalitic parkinsonism (PEP) at Boston City Hospital's Neurological Unit (1930-1981). 5,270 discharge summaries were evaluated for the diagnoses of PEP. Sixteen cases of PEP were identified; the diagnosis of PEP was justified in approximately half of these cases based on the published criteria for distinguishing PEP from Parkinson's disease (PD). In conclusions, the absence of a clear justification for the diagnosis of PEP in many of the 16 cases suggests that the accepted relationship between encephalitis lethargica and PEP may be less definitive than currently believed.

Postencephalitic parkinsonism has been considered unique among disorders with parkinsonian features because it is believed to have a unitary etiology associated with the virus that presumably caused encephalitis lethargica. Careful analysis of the historical record, however, suggests that this relationship is more complex than commonly perceived. In most cases, the diagnosis of acute encephalitis lethargica was made post hoc, and virtually any catarrh-like illness was considered to have represented encephalitis lethargica, often after an oral history-taking that was undoubtedly subject to patient recall and physician bias. Also, postencephalitic parkinsonism and oculogyric crises were not recognized as sequelae to encephalitis lethargica until well after other sequelae such as movement disorders and mental disturbances had been identified (see previous paper). We suggest here that the relationship between encephalitis lethargica and postencephalitic parkinsonism is not simplistic, i.e., encephalitis lethargica was not solely responsible for the etiology of postencephalitic parkinsonism, thus aligning the latter with most other parkinsonian disorders that are now believed to have multiple causes.

This article and the subsequent one suggest that the currently accepted view of a simplistic (direct) relationship between encephalitis lethargica (EL) and postencephalitic Parkinsonism (PEP) is based on a incomplete evaluation of the epidemic period literature. In this article we provide a detailed analysis of the literature from the period that demonstrates that Parkinsonism was not initially part of acute EL symptomatology, that PEP was not typically the prevailing type of chronic EL and that oculogyric crises were never part of acute EL symptomatology and not initially associated with PEP. The second paper uses these finding, and also examines the clinical justifications for concluding that all patients with PEP had prior acute episodes of EL, to reevaluate the presumed direct etiologic relationship between EL and PEP.

Since encephalitis lethargica’s (EL) prevalence in the 1920s, epidemiologic and clinical debate has persisted over whether EL was caused by, potentiated by, or merely coincident with the Spanish influenza pandemic. Epidemiologic analyses generally suggest that the disorders were coincidental. Beginning in the 1970s, modern experiments on archival brain samples mainly failed to confirm a direct relationship between influenza and EL. These experimental studies have technical limitations, e.g., the appropriateness of antibodies, polymerase chain reaction (PCR) primers and controls, and the extreme paucity and age of available material. These factors render the case against influenza less decisive than currently perceived. Nevertheless, there is little direct evidence supporting influenza in the etiology of EL. Almost 100 years after the EL epidemic, its etiology remains enigmatic, raising the possibility of a recurrence of EL in a future influenza pandemic.