Arachnoid cysts are cerebrospinal fluid covered by arachnoidal cells and collagen that may develop between the surface of the brain and the cranial base or on the arachnoid membrane, one of the three meningeal layers that cover the brain and the spinal cord. Primary arachnoid cysts are a congenital disorder whereas secondary arachnoid cysts are the result of head injury or trauma. Most cases of primary cysts begin during infancy; however, onset may be delayed until adolescence. Signs and symptoms
Patients with arachnoid cysts may never show symptoms, even in some cases where the cyst is large. Therefore, while the presence of symptoms may provoke further clinical investigation, symptoms independent of further data cannot—and should not—be interpreted as evidence of a cysts existence, size, location, or potential functional impact on the patient.Symptoms vary by the size and location of the cyst(s), though small cysts usually have no symptoms and are discovered only incidentally. On the other hand, a number of symptoms may result from large cysts:

Cranial deformation or macrocephaly (enlargement of the head), particularly in children
Cysts in the suprasellar region in children have presented as bobbing and nodding of the head called bobble-head doll syndrome. Cysts in the left middle cranial fossa have been associated with ADHD in a study on affected children. Headaches. A patient experiencing a headache does not necessarily have an arachnoid cyst.
Tendinopathy involves cellular apoptosis, matrix disorganization and neovascularization.Classic characteristics of "tendinosis" include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity, and a lack of inflammatory cells which has challenged the original misnomer "tendinitis".Histological findings include granulation tissue, microrupture, degenerative changes, and there is no traditional inflammation. As a consequence, "lateral elbow tendinopathy or tendinosis" is used instead of "lateral epicondylitis".Examination of tennis elbow tissue reveals noninflammatory tissue, so the term "angiofibroblastic tendinosis" is used.Cultures from tendinopathic tendons contain an increased production of type III collagen.Longitudinal sonogram of the lateral elbow displays thickening and heterogeneity of the common extensor tendon that is consistent with tendinosis, as the ultrasound reveals calcifications, intrasubstance tears, and marked irregularity of the lateral epicondyle. Although the term "epicondylitis" is frequently used to describe this disorder, most histopathologic findings of studies have displayed no evidence of an acute, or a chronic inflammatory process. Histologic studies have demonstrated that this condition is the result of tendon degeneration, which causes normal tissue to be replaced by a disorganized arrangement of collagen. Therefore, the disorder is more appropriately referred to as "tendinosis" or "tendinopathy" rather than "tendinitis".Colour Doppler ultrasound reveals structural tendon changes, with vascularity and hypo-echoic areas that correspond to the areas of pain in the extensor origin.Load-induced non-rupture tendinopathy in humans is associated with an increase in the ratio of collagen III:I proteins, a shift from large to small diameter collagen fibrils, buckling of the collagen fascicles in the tendon extracellular matrix, and buckling of the tenocyte cells and their nuclei.