ABSTRACT
A woman in her early twenties presented with cerebellar tonsillar herniation with syrinx in the cervicothoracic spinal cord manifesting as postural headache after suffering trauma to the hip. She was treated under a diagnosis of traumatic intracranial hypotension. Cranial magnetic resonance (MR) imaging demonstrated tonsillar herniation to the upper rim of the C1 lamina, associated with effacement of the basal cisterns and flattening of the pons against the clivus, sagging of the optic chiasm, and protrusion of the pituitary gland into the suprasellar cistern. Spinal MR imaging and computed tomography (CT) myelography showed cervicothoracic syrinx and arachnoid diverticulum. Three applications of epidural blood patches produced no improvement. Surgery identified cerebrospinal fluid leakage from two small holes in the spinal dural sac, slightly proximal from the origin of the left L1 root sleeve, and arachnoid diverticulum. These two holes were sutured and a few sheets of gelatin sponge were placed around the arachnoid diverticulum and sealed with fibrin glue. The cervicothoracic syrinx was reduced significantly and tonsillar herniation disappeared within 10 days. Simple surgical repair of the dural tears may rapidly improve symptoms and imaging findings in patients with tonsillar herniation caused by traumatic intracranial hypotension.
Subject(s)
Headache Disorders/etiology , Intracranial Hypotension/etiology , Intracranial Hypotension/pathology , Syringomyelia/etiology , Syringomyelia/pathology , Wounds and Injuries/complications , Accidental Falls , Arachnoid Cysts/etiology , Arachnoid Cysts/pathology , Dura Mater/injuries , Dura Mater/pathology , Dura Mater/surgery , Female , Humans , Intracranial Hypotension/physiopathology , Laminectomy , Lumbar Vertebrae/injuries , Lumbar Vertebrae/pathology , Magnetic Resonance Imaging , Neurosurgical Procedures , Spinal Nerve Roots/injuries , Spinal Nerve Roots/pathology , Syringomyelia/physiopathology , Time Factors , Treatment Outcome , Young AdultABSTRACT
We investigated the effects of pentoxifylline (PTX) on endotoxin-induced diaphragmatic dysfunction in vitro. Seventy-two rats were divided into 3 groups: a group in which endotoxin (20 mg/kg) was injected intraperitoneally (endotoxin-group), a group in which PTX (100 mg/kg) was injected intraperitoneally 30 min before injection of endotoxin (endotoxin-PTX group), and a group in which only saline was given (sham group). Left hemidiaphragms were removed 4 h after injection of endotoxin. We evaluated the diaphragmatic contractility by twitch characteristics and force-frequency curves in vitro. We measured serum TNF-alpha concentrations, diaphragm malondialdehyde (MDA) levels (an index of oxygen-derived free radical-mediated lipid peroxidation), and diaphragm cAMP concentrations. Diaphragmatic force generation capacity was signifi cantly reduced after injection of endotoxin. Serum TNF-alpha concentrations and diaphragmatic MDA levels were significantly elevated after injection of endotoxin. PTX administration significantly improved diaphragmatic contractility and prevented the elevation in TNF-alpha concentrations and MDA levels after injection of endotoxin. There were no significant changes in the diaphragm cAMP concentrations among the 3 groups. These results demonstrated that PTX administration prevented endotoxin-induced diaphragmatic dysfunction without changing diaphragm muscle cAMP concentrations. The protective effects of PTX against endotoxininduced diaphragmatic contractile deterioration might be caused by attenuating TNF-alpha-mediated oxygen-derived free radical production.
