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This video is from an online webinar from the Hypermobility Collective June 10, 2025 talk hosted by Manhattan Pain Medicine, where Dr. Arthur Jenkins discusses the state of the art and understanding of the causes and treatments for the dysautonomia (dysfunction of the autonomic nervous system) caused by ligament weakness in the region where the skull meets the spine (the craniocervical junction, also know as occiput to C2, which encompasses instability in the ligaments and joint capsules where the skull meets the first cervical [C1] and second cervical [C2] vertebral bodies). The major nerves and blood vessels that pass through this region are especially susceptible to injury or compression because excessive movement of the spine compared to the skull, in rotation, or bending movements, can stretch or pinch these structures, making nerves misfire or stop working, and making blood vessels narrow because of stretch or compression. The typical symptoms that people with these instability-related nerve and vascular dysfunction include: dizziness or lightheadedness when standing (also known as Postural Orthostatic Tachycardia Syndrome, or POTS) neck pain, especially at the top of the spine brain fog or memory problems swallowing problems constipation blurry vision, often dependent on head position auditory changes like intermittent tinnitus breathing problems, including "air hunger" or difficulty "catching their breath" bladder and sexual dysfunction Many patients have been told these are not treatable, or in some cases, that these symptoms are "all in their head". Patients are often reluctant to admit to the symptoms, for fear of being ignored, ridiculed, or otherwise "gaslit", which increases the anxiety that is already being caused by their own body malfunctioning. While the typical patient who suffers from this condition has a long history of hypermobility of other joints, many patients who present with these symptoms have no history of hypermobility, but do have a history of either trauma to the head and neck, or a history of COVID-19 infection. The mechanism of this ligament instability seems to be, at least in many patients, to involve an autoimmune (the body's own blood defenses attacking their own cells) weakening of ligaments, and this is often worsened after an infection like COVID-19. There are several different ways that problems in this area can be addressed, including eliminating movement at levels that are unstable (fusion), removing parts of bones, muscles, and other structures that are directly pinching structures (decompressions), and stretching out blood vessels and protecting them from compression through endovascular procedures (venoplasty or venous stenting). Dr. Jenkins works with surgeons who specialize in each of these techniques to determine if one approach is better for a particular patient, or in some cases, if multiple procedures will ultimately need to be performed to enhance recovery, and if so, in what order makes the most sense for each patient. Many patients with these conditions have other congenital or vascular conditions, including transitional spinal anatomy, congenital spinal stenosis, vascular conditions like May-Thurner Syndrome, Thoracic Outlet Syndrome, and Median Arcuate Ligament Syndrome, among MANY others. Dr. Jenkins knows to screen for these condition, and to manage the prioritization of the different but related conditions, to maximize the patient's recovery and minimize the risks of treatment. What Dr. Jenkins has found, by listening to his patients, discussing with other medical and surgical researchers, and by presenting and publishing his research, is that each patient requires a tailored workup that addresses their needs, that a robust support network is necessary for the patient and the surgical team, and that this is often a long-term relationship as we help patients to manage their condition to minimize it's impact on their lives.