Cervical spondylosis is the most common cause of cremasteric dysfunction in patients over the age of 55. Almost everyone has developed at least microscopically visible cervical degeneration by age 30, and 95% of men and 70% of women can detect cervical degeneration on x-ray by age 60-65. Cervical degeneration frequently occurs in the lower cervical spine (especially C4-7), most commonly at C5-6, followed by C6-7 and C4-5. This process often begins with degeneration and collapse of the intervertebral discs, followed by narrowing of the intervertebral spaces, formation of bony redundancies, hypertrophy and even ossification of the ligamentum flavum, and sometimes hypertrophy and ossification of the posterior longitudinal ligament, followed by loss of normal cervical anterior convexity. During the progression of cervical spine degeneration, damage to the neural structures occurs, and in a few patients, damage to the function of the crestal medulla occurs and crestal cervical spondylosis occurs. The damage caused by cervical spondylosis to the crestal medulla may originate from three sources. 1. It may originate from static compression caused by invasion of the spinal canal by bony redundancy, hypertrophic ligaments or herniated discs, and patients with developmental spinal stenosis (10-13 mm sagittal diameter of the spinal canal) are more likely to experience static compression. Symptoms often occur when the crestal medulla is compressed by more than 30%. Patients with severe spinal stenosis are also at increased risk for cremasteric injury following trauma. 2. It may originate from dynamic compression caused during neck flexion and extension. The anterior-posterior diameter of the spinal canal is reduced by 2-3 mm during neck flexion, which can cause compression of the crestal medulla by the posterior vertebral cavity; the crepitus ligamentum and the anterior cavity can cause clamping of the crestal medulla during posterior neck extension. 3, cervical degeneration can cause compression of the arterial blood supply or venous return to the crestal medulla by the bone superfluous, thus leading to ischemic crestal medullary lesions.