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Knee Pain
Published in Benjamin Apichai, Chinese Medicine for Lower Body Pain, 2021
The lateral collateral ligament originates from the lateral femoral epicondyle, joins the bicep femoris tendon, and then ends at the head of the fibula. It is a cord-like ligament about 66 mm long and 3.4 mm wide (Meister et al. 2000).
Ankle instability
Published in Maneesh Bhatia, Essentials of Foot and Ankle Surgery, 2021
Ankle sprains can be broadly classified according to the anatomical region: lateral, syndesmotic and medial. Lateral injuries can also be classified as low or high ankle sprains. High ankle sprains refer to disruption of the syndesmosis and should be differentiated from low ankle sprains (lateral ligament complex) because they are higher energy injuries and are associated with prolonged disability. Medial ankle ligament injuries (deltoid) usually occur in combination with syndesmosis injuries, or ankle fracture-dislocations (6), and less frequently in isolation.
Introduction: Background Material
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The CSF also circulates in four cavities, or ventricles, in the brain: two large lateral ventricles on either side in the cerebrum, a small third ventricle along the midline in the diencephalon, and a fourth ventricle of intermediate size along the midline at the back of the pons and the upper half of the medulla. The central canal of the spinal cord is continuous with the fourth ventricle. The CSF is produced from the blood mainly by the choroid plexuses in parts of the ventricles. Each of these plexuses consists of a layer of epithelial cells that is continuous with the ependymal cell layer that lines the ventricles. The epithelial cells surround blood capillaries and form tight junctions that act as a blood-CSF barrier, allowing only some substances to pass. In addition to its cushioning effect, the CSF provides buoyancy to the brain, circulates nutrients and chemicals, and removes waste products from the brain. Regulating the volume of the CSF plays an important role in regulating cerebral blood flow.
Center of pressure velocities in patients with body lateropulsion: three case report series of Wallenberg’s syndrome
Published in Physiotherapy Theory and Practice, 2022
Hideaki Matsuo, Masafumi Kubota, Mayumi Matsumura, Mami Takayama, Yuri Mae, Yuki Kitazaki, Soichi Enomoto, Asako Ueno, Masamichi Ikawa, Tadanori Hamano, Ai Takahashi, Misao Tsubokawa, Seiichiro Shimada
Wallenberg’s syndrome, also known as a lateral medullary syndrome, is a neurological condition caused by a lateral medullary infarction. This syndrome’s symptoms are ipsilateral Horner syndrome, ipsilateral limb ataxia, superficial sensory disturbance of the ipsilateral face and contralateral limbs, dysarthria, dysphagia, and vertigo. Body lateropulsion (BL), a postural disorder characterized by the body involuntarily tilting to one side, is one of the Wallenberg syndrome’s predominant symptoms (Dieterich and Brandt, 1992, 2019; Kim et al., 2007; Maeda et al., 2005; Pérennou et al., 2008; Thömke et al., 2005; Yamaoka, Kishishita, Takayama, and Okubo, 2018). Lesions of the descending lateral vestibulospinal tract or the ascending dorsal spinocerebellar tract may induce BL (Kim et al., 2007; Maeda et al., 2005; Thömke et al., 2005). Pérennou et al. (2008) reported that patients having brainstem strokes showed severe visual vertical tilts and BL and minor or no tilts of vertical posture. This suggests that vestibular nuclear lesions interfere with postural control via direct vestibulo-spinal mechanisms rather than via a higher-order representation mechanism (Kim et al., 2007; Pérennou et al., 2008, 2014). Although pathological mechanisms that cause BL are better understood, features of postural control are not fully understood. Therefore, demonstrating these features during the recovery process of patients with BL may assist in developing effective physical therapy programs and plans of care.
Association between lateral epicondylitis and the risk of herpes zoster development
Published in Postgraduate Medicine, 2021
Chao-Yu Hsu, Der-Shin Ke, Cheng-Li Lin, Chia-Hung Kao
Lateral epicondylitis (LE), also known as tennis elbow or lateral elbow tendinopathy, is a painful condition involving the elbow. LE may be associated with biomechanic exposure, [1] cardiovascular disease risk factors, [2] hyperglycemia, [3] or psychosocial risk factors. [4] It is a commonly encountered problem in primary care clinics, and affects an estimated 1% to 3% of adults. [5] A report determined that the incidence of LE remained constant from 2007 to 2014. The annual incidence of LE per 10,000 patients was 14.5 in 2007 and 15.5 in 2014. [6] Gruchow et al. reported that the prevalence of LE among tennis players was 14.1%. [7] LE does not only occur in athletes but also in people with physically strenuous jobs that involve the overloading of the elbows. Kim et al. investigated the prevalence of upper extremity musculoskeletal diseases among fruit tree farmer and determined that 40.9% of participants developed LE. [8] LE is one of the most common work-related conditions.
Factors associated with musculoskeletal injuries in an infantry commanders course
Published in The Physician and Sportsmedicine, 2021
Shani Svorai Band, Michal Pantanowitz, Shany Funk, Gordon Waddington, Nili Steinberg
Repetitive ankle sprains and/or inadequate rehabilitation following a sprain may contribute to the development of Chronic Ankle Instability (CAI), a term used to describe the experience of persisting limitations resulting from an acute ankle sprain or repetitive sprains [11]. In the general population, lateral ankle sprains are a common injury, with a large proportion of individuals developing long-term symptoms that contribute to the progress of CAI [12]. Special care should be addressed to screening for CAI among combat soldiers, as this phenomenon was reported to increase the risk for all types of other lower-limb musculoskeletal injuries [13,14]. Yavnai and colleagues [15] showed that combat soldiers who had pre-course low subjective ankle stability were at higher musculoskeletal injury risk. Furthermore, soldiers – like athletes with CAI – may demonstrate impaired postural stability, increased postural sway, peroneal muscle weakness, and prolonged peroneal muscle reaction time, all of which could be explained by somatosensory deficits that might increase the risk for musculoskeletal injuries [11,16–19].