Saifuddin et al. examined MRI images of 231 men and  273 women with a mean age of 46 and found the mean position of the conus to be at the lower third of L1, with a mean variation from the middle one-third of T12 to the upper one-third of L3. There were no significant variations related to gender or increasing age.[2]

Wilson et al. studied MRI images of 184 children ranging from neonates to 20-year-olds. They found that the position of the conus in the 0 to 2 year age group was from T12 to L2-L3 with an average being L1-L2. For the 19 to 20 year age group, the range was L1-L2 with the average being L1-L2. Based on these findings, they concluded that the conus does not ascend throughout childhood as previously believed but attains the adult position sometime during the first few months of life. A conus located at L2-L3 or above is considered normal for any age.[3]

Lesions around the vertebral L2 level can affect the conus medullaris and is known as conus medullaris syndrome. Symptoms include sudden onset severe back pain, perianal anesthesia, symmetric lower extremity motor weakness with hyperreflexia, and early onset bowel and bladder dysfunction.[14] Known causes of conus medullaris syndrome include spinal fracture, disc herniation, tumors, trauma, epidural abscess, and infarction. It is essential to clinically differentiate this condition from cauda equina syndrome whose causes are similar but characterized by severe unilateral radicular pain, saddle anesthesia, asymmetric lower extremity motor weakness with hyporeflexia, and late-onset bowel and bladder dysfunction.[14] As a rule of thumb, conus medullaris syndrome causes both upper and lower motor neuron features, whereas cauda equina syndrome causes predominantly lower motor neuron features. The annual incidence of both conditions is between 1.5 to 3.4 per million. Diagnosis is made via an urgent MRI with T1 and T2 sequences within an hour of presentation. Orthopedic and neurosurgical consultation is necessary as treatment is primarily surgical, with decompression via laminectomy/discectomy or sequestrectomy.[15] According to Kingwell et al., there is no robust evidence to support urgent surgical intervention over non-operative management in terms of neurologic outcomes.[16] Also, the timing of surgery does not affect neurologic recovery for traumatic cases. However, surgery may be preferable due to patient preference, shorter hospital stay, availability of nursing care, and earlier rehabilitation. Posterior decompression and stabilization are generally more viable options due to reduced morbidity and surgeon familiarity. It offers equivalent outcomes as anterior decompression and non-operative management, however anterior decompression may be beneficial in terms of bladder recovery, particularly in cases of surgical delay.

Tethered cord syndrome is a condition caused by an abnormal filum terminale that prevents the conus medullaris from ascending and restricts the mobility of the spinal cord. As a result, the spinal cord gets abnormally stretched, with neurologic symptoms referable to the lower cord.[17] It is typically diagnosed during periods of rapid growth in adolescence but may go undiagnosed until adulthood. MRI shows a low lying conus, i.e., below the L2 vertebra or a thickened filum terminale. However, Tubbs and Oaks studied a cohort of patients of tethered cord syndrome in whom the conus was in the normal range and suggested that this condition might be tautness of the cord rather than pure distal elongation.[18] Frequently, it is associated with spinal anomalies like diastematomyelia, dermal sinuses, and lipomas. Treatment is via surgical release and halts the progression of symptoms. According to Liu et al., spinal anesthesia should be avoided in adults with tethered cord syndrome to prevent long term neurologic damage. 

Intramedullary lesions of the conus medullaris are numerous. Neoplastic lesions include glial tumors such as ependymoma, astrocytoma, and glioblastoma multiforme; non-glial tumors include primitive neuroectodermal tumor and hemangioblastoma along with lymphoma, melanoma, and metastases. Non-neoplastic lesions include granulomas such as tuberculosis and sarcoidosis, parasitic infections such as cysticercosis and schistosomiasis, demyelination in multiple sclerosis, vascular lesions such as vascular malformations, cavernoma, and amyloid angiopathy and dysembryogenetic lesions such as lipoma, dermoid cyst, epidermoid cyst, and teratoma.[19][20][21]

The incidence of intramedullary tumors in the conus is roughly 10%, with the most common being myxopapillary ependymoma (50%), followed by lipoma, hemangioblastoma, and astrocytoma (11.5% each). Patients present with symptoms such as lower extremity pain, lower back pain, sensory disturbance, bowel and bladder problems, motor weakness, and saddle anesthesia. Sacral nerve root compression can cause severe perineal pain. Conus tumors can cause sacral nerve root compression similar to sciatica or cauda equina syndrome due to degenerative disc disease. Urinary abnormalities are present in 91% of patients and include decreased urge to void, sphincter dyssynergia, and detrusor areflexia. Treatment of all tumors is primarily surgical, with complete resection achieved in roughly 81% of patients. The highest resection rate is 90% for ependymoma and hemangioblastoma, and it is 50 to 76% for astrocytomas.[21][22] In-Ho Han et al. studied surgical outcomes for 26 patients and found that the modified Japanese Orthopedic Association (JOA) score worsened in 26.9% of patients, remained stable in 38.5%, and improved in 34.6%. Out of 21 patients who had leg and lower back pain, the mean visual analog scale (VAS) score for pain improved from 5.4 to 1.8.[23] 

The artery of Desproges Gotteron can get compressed by L5-S1 disc herniation and lead to conus medullaris syndrome. It is also frequently involved in arteriovenous fistulas, which can be treated by microsurgery or embolization.[24]