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Spinal CordAnatomical and Physiological Features
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The spinal cord is a long, thin tubular structure which is continuous with the caudal part of the medulla and is enlarged in the cervical and lumbar regions. The cervical enlargement stretches from C4 to T1 vertebrae and handles sensory input and motor output to the upper limbs. The lumbar enlargement, located between L2 and S3, corresponds to the lumbar plexus and handles sensory input and motor output to the lower limbs.
The female reproductive system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Knowledge of the series of changes that the cervix undergoes throughout reproductive life is central to the understanding of cervical neoplasia (Figure 15.3). Before puberty, the cervix is an inactive organ; the ectocervix is lined by squamous epithelium and the endocervix by columnar epithelium. After puberty, hormonal stimulation causes cervical enlargement with eversion of the squamocolumnar junction into the vagina. Exposure to the vaginal environment leads to metaplasia whereby the columnar epithelium changes into first immature and then mature squamous epithelium as a protective response. This zone of metaplastic squamous epithelium is known as the ‘transformation zone’, and is the region where almost all neoplasia of the cervix arises. After the menopause, the cervix shrinks and the transformation zone returns to within the endocervical canal.
Specific Synonyms
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Cervical enlargement (B&K, p. 63) Cervical intumescence (MarMar, p. 87)Upper enlargement (M&M, p. 15)
Perrault syndrome with amenorrhea, infertility, Tarlov cyst, and degenerative disc
Published in Gynecological Endocrinology, 2019
Dania Al-Jaroudi, Saed Enabi, Malak Sameer AlThagafi
LAR2 mutation typically manifests as PS type 1 [6, 8, 14]. Until 2018, there were only 15 cases harboring mutations in this gene, with 1 case displaying Type 2 PS [6]. Mutations in HSD17B4 have been described which manifest with distinct neurological symptoms including cerebellum dysfunction. This includes cerebellum atrophy on MRI [3]. The reported cases of TWNK mutations show distinct MRI findings including diminished cervical enlargement in the spinal cord, decreased grey matter, and increased white matter. Moreover, dysfunction and dys-synchrony of the auditory nerve, and partial atrophy of the vestibulocochlear nerves occurred in patients with TWNK mutations [2]. Patients with CLPP mutations display neurological symptoms, and show a unique MRI pattern that includes specific abnormalities of the subcortical and deep cerebral white matter and the middle blade of the corpus callosum [5]. ERAL1 mutations have also been identified with no specific features that differ from Type 1 or Type 2 PS [4].
What role should spinal cord MRI take in the future of multiple sclerosis surveillance?
Published in Expert Review of Neurotherapeutics, 2020
Maria A. Rocca, Paolo Preziosa, Massimo Filippi
However, spinal cord imaging can be challenging. The spinal cord is a thin structure, with the widest region at the level of the cervical enlargement of only ≈12-15 millimeters [9]. It lies within the spinal canal, is surrounded by cerebrospinal fluid (CSF) and by a thick layer of bone or cartilaginous discs between the vertebral bodies and it is relative close to heart and lungs [9]. The pulsating CSF flow, arterial pulsation, but also heart beating and breathing, cause the spinal cord to significantly move within the spinal canal, with an amplitude that diminishes with distance from the head.
Physiological distribution of 18F-FDG in the spinal cord: A systematic review
Published in The Journal of Spinal Cord Medicine, 2021
Zahra Kiamanesh, Farnaz Banezhad, Zakieh Nasiri, Farshad Emami, Giorgio Treglia, Ramin Sadeghi
Several mechanisms have been proposed as the cause of physiological 18F-FDG uptake variations in the spinal cord including: Hypermetabolism of the cervical enlargement in spinal cord segments C6-C8 (correspond to the C3-T2 vertebral body levels) and the lumbar enlargement in spinal cord segments L4-S1 (correspond to the T9-T12 vertebral body levels), which are responsible for supplying the neuronal activity of the upper and lower limbs.3,23–25White matter does not accumulate 18F-FDG in comparison with the gray matter. Therefore, it can be concluded that abundant amount of gray matter in the spinal cord enlargements at the C4-C8 and L4-S1 vertebral levels, involving in neuronal transmission for upper and lower extremities, could be responsible for the relative hyperactivity.3,6,24,25Some investigators brought up a hypothesis that the sensory stimuli (e.g. tactile or thermal) from the extremities to the spinal cord can be the reason of regional hypermetabolism.24,25Inadequate clearance of 18F-FDG from the Adamkiewicz artery (largest medullary segmental artery originated from aorta around the T9 to T11 thoracic vertebrae on the left side) is another explained mechanism.3,31In a study performed on rats with arthritis, acute or chronic arthritis in the extremities can cause a significant increase in metabolic activity of the relevant cord levels.32,33 This can also be true in human being although not specifically investigated.3,24Technical limitations like partial volume effect are another proposed mechanism that may be a cause of underestimation of SUVmax in spinal segments except for cervical and lumbar enlargements.24Several factors can be helpful in differentiation between physiologic and malignant spinal cord 18F-FDG uptake including SUVmax, and location in the spinal cord.