Post-dural-puncture headache (PDPH) is a complication of puncture of the dura mater (one of the membranes around the brain and spinal cord). The headache is severe and described as "searing and spreading like hot metal", involving the back and front of the head and spreading to the neck and shoulders, sometimes involving neck stiffness. It is exacerbated by movement and sitting or standing and is relieved to some degree by lying down. Nausea, vomiting, pain in arms and legs, hearing loss, tinnitus, vertigo, dizziness and paraesthesia of the scalp are also common.PDPH is a common side effect of lumbar puncture and spinal anesthesia. Leakage of cerebrospinal fluid causes reduced fluid levels in the brain and spinal cord. Onset occurs within two days in 66% of cases and three days in 90%. It occurs so rarely immediately after puncture that other possible causes should be investigated when it does.Using a pencil point needle rather than a cutting spinal needle decreases the risk. The size of the pencil point needle does not appear to make a difference. PDPH is estimated to occur in between 0.1% and 36% people following dural puncture. Signs and symptoms
PDPH typically occurs hours to days after puncture and presents with symptoms such as headache (which is mostly bi-frontal or occipital) and nausea that typically worsen when the patient assumes an upright posture. The headache usually occurs 24–48 hours after puncture but may occur as many as 12 days after.
The PAX7-FOXO1 fusion is often amplified in tumors (about 70 percent of all PAX7-FOXO1 fusion positive tumors) and the PAX3-FOXO1 fusion is rarely amplified (only in 5 percent of all PAX3-FOXO1 fusion positive tumors). About 60 percent of all ARMS cases are positive for PAX3-FOXO1 fusion gene, 20 percent are positive for PAX7-FOXO1 fusion gene, and the remaining 20 percent are fusion negative ARMS cases. Both fusion genes are composed of either the PAX3 or PAX7 DNA binding domains and the FOXO1 transactivation domain. This fusion causes a dysregulation of transcription and acts as an oncogene promoting cancer formation. Pathology
ARMS cells are often small with little cytoplasm. The nuclei of the cells are round with normal, dull, chromatin structures. The ARMS cells often clump together and have fibrovascular septae that interrupts the aggregates. The fibrovascular septae that disrupts the aggregates often give the tumor the physiology of the alveoli found in the lungs. In a few cases, there may not be any fibrovascular septae and this gives the tumor a more solid phenotype and no alveoli physiology. Immunostaining for myogenin and for MyoD can be used to determine ARMS from other rhabdomyosarcoma tumors and immunostaining for AP2β and p-cadherin can distinguish fusion positive ARMS from fusion negative. Embryonic origin and epidemiology
ARMS usually occurs in the skeletal muscles and is postulated to be derived from precursor cells within the muscle tissue. During embryonic development ARMS occurs in the mesoderm which is the precursor for the skeletal muscle tissue.