A rare variation in popliteal artery branching: anterior tibial artery and fibular artery from the common tibiofibular trunk.

The popliteal artery is a continuation of the femoral artery and is the main arterial supply to the lower leg and foot. Variation in the branching of the popliteal artery typically occurs proximal or distal to where the vessel crosses the popliteus muscle. In the case of a routine dissection of a 92-year-old female cadaver, a variation of the popliteal artery was found where the branches are a posterior tibial artery and a common tibiofibular trunk. It is important to recognize the vascular variations that exist in the popliteal fossa to prevent any unforeseen complications during surgeries or procedures to the knee or lower leg.

Three-Headed Biceps Brachii Muscle: A Rare Site of Proximal Median Nerve Entrapment.

The biceps brachii muscle is a highly variable muscle in the anterior compartment of the arm, and the most common variants include additional heads or slips. The median nerve courses with the brachial artery in the medial arm near the biceps brachii muscle, crosses the elbow, and enters the forearm deep to the bicipital aponeurosis. While entrapment of the median nerve in the carpal tunnel is one of the most common neuropathies, more proximal entrapments by the bicipital aponeurosis or other variants have been reported. In a 94-year-old embalmed female cadaver received through the Humanity Gift Registry of Pennsylvania, a biceps brachii muscle with an additional slip that arose from the coracoid process was found, which bridged over the median nerve and blended with the investing fascia of the forearm flexors via aponeurosis. Because of the course of this muscular slip in the arm and its relationship to the median nerve, this may be an additional site of proximal entrapment of the median nerve. It is important to consider these rare sites of nerve entrapment when diagnosing patients with median nerve neuropathy.

Pterygoideus proprius muscle: stuck between the greater wing and lateral pterygoid plate.

The muscles of mastication derive from a common embryological source, and the presence of accessory muscles in the infratemporal fossa (ITF) is uncommon. Here, we present findings from postmortem dissection of the ITF revealing a unilaterally present muscle extending from the greater wing of the sphenoid to blend inferiorly with the medial and lateral pterygoid muscles before attaching to the lateral pterygoid plate. This muscle is most consistent with the pterygoideus proprius muscle initially described in 1858. Though the exact embryological origin and function of this muscle remain speculative, these topics are nonetheless worth investigating as it may provide insight regarding the ontogeny of muscles descending from the first pharyngeal arch. Additionally, presence of the pterygoideus proprius muscle may have clinical implications and impact surrounding structures such as the mandibular division of the trigeminal nerve, maxillary artery, pterygoid venous plexus, masticatory muscles, and temporomandibular joint (TMJ).

Cortical dysmorphology and reduced cortico-collicular projections in an animal model of autism spectrum disorder.

Autism spectrum disorder is a neurodevelopmental disability that includes sensory disturbances. Hearing is frequently affected and ranges from deafness to hypersensitivity. In utero exposure to the antiepileptic valproic acid is associated with increased risk of autism spectrum disorder in humans and timed valproic acid exposure is a biologically relevant and validated animal model of autism spectrum disorder. Valproic acid-exposed rats have fewer neurons in their auditory brainstem and thalamus, fewer calbindin-positive neurons, reduced ascending projections to the midbrain and thalamus, elevated thresholds, and delayed auditory brainstem responses. Additionally, in the auditory cortex, valproic acid exposure results in abnormal responses, decreased phase-locking, elevated thresholds, and abnormal tonotopic maps. We therefore hypothesized that in utero, valproic acid exposure would result in fewer neurons in auditory cortex, neuronal dysmorphology, fewer calbindin-positive neurons, and reduced connectivity. We approached this hypothesis using morphometric analyses, immunohistochemistry, and retrograde tract tracing. We found thinner cortical layers but no changes in the density of neurons, smaller pyramidal and non-pyramidal neurons in several regions, fewer neurons immunoreactive for calbindin-positive, and fewer cortical neurons projecting to the inferior colliculus. These results support the widespread impact of the auditory system in autism spectrum disorder and valproic acid-exposed animals and emphasize the utility of simple, noninvasive auditory screening for autism spectrum disorder.

Abnormal auditory brainstem responses in an animal model of autism spectrum disorder.

Auditory dysfunction is a common feature of autism spectrum disorder (ASD) and ranges from deafness to hypersensitivity. The auditory brainstem response (ABR) permits study of the amplitude and latency of synchronized electrical activity along the ascending auditory pathway in response to clicks and pure tone stimuli. Indeed, numerous studies have shown that subjects with ASD have ABR abnormalities. In utero exposure to the antiepileptic drug valproic acid (VPA) is associated with human cases of ASD and is used as an animal model of ASD. Previous studies have shown that VPA-exposed animals have significantly fewer neurons in the auditory brainstem and thalamus, reduced ascending projections to the auditory midbrain and thalamus and increased neuronal activation in response to pure tone stimuli. Accordingly, we hypothesized that VPA-exposed animals would have abnormal ABRs throughout their lifespans. We approached this hypothesis in two cohorts. First, we examined ABRs from both ears on postnatal day 22 (P22). Then, we examined monaural ABRs in animals at P28, 60, 120, 180, 240, 300 and 360. Our results suggest that at P22, VPA-exposed animals have elevated thresholds and increased peak latencies. However, by P60 these differences largely normalize with differences appearing only near hearing threshold. Additionally, our analysis revealed that maturation of ABR waves occurred at different trajectories in control and VPA-exposed animals. These results, together with our previous work, suggest that VPA exposure not only impacts total neuron number and connectivity, but also auditory evoked responses. Finally, our longitudinal analysis suggests that delayed maturation of auditory brainstem circuits may impact ABRs throughout the lifespan of the animal.

Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders-Denial is not an option.

Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM2.5), including combustion and friction ultrafine PM (UFPM) and industrial nanoparticles (NPs) starting in utero, are linked to early pediatric and young adulthood aberrant neural protein accumulation, including hyperphosphorylated tau (p-tau), beta-amyloid (Aß1 - 42), α-synuclein (α syn) and TAR DNA-binding protein 43 (TDP-43), hallmarks of Alzheimer's (AD), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). UFPM from anthropogenic and natural sources and NPs enter the brain through the nasal/olfactory pathway, lung, gastrointestinal (GI) tract, skin, and placental barriers. On a global scale, the most important sources of outdoor UFPM are motor traffic emissions. This study focuses on the neuropathology heterogeneity and overlap of AD, PD, FTLD, and ALS in older adults, their similarities with the neuropathology of young, highly exposed urbanites, and their strong link with sleep disorders. Critical information includes how this UFPM and NPs cross all biological barriers, interact with brain soluble proteins and key organelles, and result in the oxidative, endoplasmic reticulum, and mitochondrial stress, neuroinflammation, DNA damage, protein aggregation and misfolding, and faulty complex protein quality control. The brain toxicity of UFPM and NPs makes them powerful candidates for early development and progression of fatal common neurodegenerative diseases, all having sleep disturbances. A detailed residential history, proximity to high-traffic roads, occupational histories, exposures to high-emission sources (i.e., factories, burning pits, forest fires, and airports), indoor PM sources (tobacco, wood burning in winter, cooking fumes, and microplastics in house dust), and consumption of industrial NPs, along with neurocognitive and neuropsychiatric histories, are critical. Environmental pollution is a ubiquitous, early, and cumulative risk factor for neurodegeneration and sleep disorders. Prevention of deadly neurological diseases associated with air pollution should be a public health priority.

Characterization of the superior olivary complex of chimpanzees (Pan troglodytes) in comparison to humans.

The superior olivary complex (SOC) is a collection of nuclei in the hindbrain of mammals with numerous roles in hearing, including localization of sound sources in the environment, encoding temporal and spectral elements of sound, and descending modulation of the cochlea. While there have been several investigations of the SOC in primates, there are discrepancies in the descriptions of nuclear borders and even the presence of certain cell groups among studies and species. Herein, we aimed to clarify some of these issues by characterizing the SOC from chimpanzees using Nissl staining, quantitative morphometry and immunohistochemistry. We found the medial superior olive (MSO) to be the largest of the SOC nuclei and the arrangement of its neurons and peri-MSO to be very similar to humans. Additionally, we found neurons in the medial nucleus of the trapezoid body (MNTB) to be immunopositive for the calcium binding protein calbindin. Further, most neurons in the MNTB, and some neurons in the lateral nucleus of the trapezoid body were associated with large, calretinin-immunoreactive calyx terminals. Together, these findings indicate the organization of the SOC of chimpanzees is organized very similar to the SOC in humans and suggests modifications to this region among species consistent with differences in head/body size, restricted hearing range and sensitivity to low frequency sounds.

Noradrenergic axons hitch hiking along the human abducens nerve.

The abducens nerve (AN; cranial nerve VI) exits the brainstem at the inferior pontine sulcus, pierces the dura of the posterior cranial fossa, passes through the cavernous sinus in close contact to the internal carotid artery (ICA) and traverses the superior orbital fissure to reach the orbit to innervate the lateral rectus muscle. At its exit from the brainstem, the AN includes only axons from lower motor neurons in the abducens nucleus. However, as the AN crosses the ICA it receives a number of branches from the internal carotid sympathetic plexus. The arrangement, neurochemical profile and function of these sympathetic axons running along the AN remain unresolved. Herein, we use gross dissection and microscopic study of hematoxylin and eosin-stained sections and sections with tyrosine hydroxylase immunolabeling. Our results suggest the AN receives multiple bundles of unmyelinated axons that use norepinephrine as a neurotransmitter consistent with postganglionic sympathetic axons.

A portal quadrad with triple hepatic arteries.

The arterial support of the liver is most commonly from the celiac trunk via the proper hepatic artery (PHA). The PHA divides into left and right branches: the right hepatic artery (RHA) supplies the right and caudate lobes while the left hepatic artery (LHA) supplies the left and quadrate lobes. Aberrant hepatic arteries are relatively common, and the most frequent contributors are the superior mesenteric artery and left gastric artery. Herein we present findings from postmortem dissection of an abdominal cavity that revealed a rare combination of reported variations. Specifically, this subject had three extrahepatic arteries - a replaced LHA (rLHA), a PHA, and a replaced RHA (rRHA). The rLHA originated from the left gastric and the rRHA originated from the superior mesenteric artery. Knowledge of these variations is important for surgical and radiological procedures to avoid complications during treatment and improve patient outcomes.

Untrapped: bilateral hypoplasia of the trapezius muscle.

Agenesis or congenital hypoplasia of skeletal muscles occurs infrequently but may occur with specific conditions such as Poland syndrome. The trapezius muscle can vary in the extent of its bony attachments or may have additional slips, however congenital absence or hypoplasia is extremely rare. There are only a few reports of partial or complete absence of the trapezius muscle. Two cases of bilateral absence of the trapezius were both in males and were accompanied by the absence of additional muscle in the pectoral girdle. Herein, we describe a case of a 56-year-old male cadaver with bilateral hypoplasia of the trapezius. The muscle was largely represented by atrophied muscle fibers with an abundance of fibrotic or fatty connective tissue. This subject had very minor hypoplasia of the left pectoralis major muscle, but the remaining muscles of the pectoral girdle were normal. The spinal accessory nerve terminated in the sternocleidomastoid muscle on both sides, failing to reach the trapezius. We interpret these findings to be consistent with a minor variant of Poland syndrome.