Abstract
Dear Editor,Intracranial hypotension syndrome (IHS) typically presentswith postural headache, often associated with one or moreof the following symptoms: nausea, vomiting, dizziness,diplopia, photophobia, hearing impairment, neck stiffness,and blurred vision [1].This condition is secondary to reduction of cerebrospinalfluid (CSF) volume. Most patients with spontaneous IHShave a CSF leak in the spinal dural sac demonstrated bymyelographic magnetic resonance (MR) or by isotopicmyelography.Someauthorshavehypothesizedthatthemaincausative factor of IHS could be the unbalance betweennegative spinal epidural pressure and CSF pressure [2].Magnetic resonance imaging (MRI) of the brain withcontrast enhancement is the imaging study of choice forpatients suspected of IHS [3]. Characteristic radiologicabnormalities include diffuse thickening of the pachyme-ninges, contrast enhancement of the pachymeninges, subduralfluid collections or subdural hematomas that are frequentlybilateral, and downward displacement of the brainstem andcerebellar tonsils [3, 4]. Computed tomography myelography,spinal MRI, and radionuclide cisternography are the imagingstudies used frequently for the localization of the CSF leaksite [3, 5].Treatment of spontaneous IHS begins with bed rest andintravenous fluid administration to restore the depleted CSFvolume [3]. Pharmacological therapy includes intravenousor oral caffeine, theophylline, and steroids. In casesrefractory to conservative therapy, epidural blood patch(EBP) and/or surgical repair are indicated [6, 7].We report a patient affected by IHS whose myelo-MRIdisclosed cervical CSF leakage and who was successfullytreated with spinal lumbar blood patch.This patient presented persistent headache associated withphotophobia and hyperpyrexia. In the suspect of meningitis,he underwent a lumbar puncture; the cytochemical examrevealed only mild proteins’ increase. He performed a brainMRI withgadoliniumenhancement which evidenced a linear,diffusepachymeningealthickeningwithevidentenhancement(upper left in Fig. 1). The maximum intensity projectionreconstructions and myelographic effect showed probablepoints of liquoral leakage bilaterally at C1–C2 level and onthe right side of C2–C3 level (lower left in Fig. 1). On thelumbar spine, the dural sac appeared collapsed. Beforeconsidering direct repair of the fistula or cervical bloodpatch, following our hypothesis [2], we performed a L2–L3“focal” epidural blood patch by injecting 5 ml of fibrin gluemixed with 5 ml of autologous blood and 3 ml ofhydrosoluble contrast medium. After the procedure, thepatient had a remission of the symptomatology. Brain MRIperformed 1 week later showed a reduction a reduction ofthe pachymeningeal thickening.Brain MRI was repeated after 2 months and revealed anevident reduction of dural contrast enhancement (upperright in Fig. 1). Two years after the procedure, the patient isstill free of symptoms, and MRI is normal.The injection site of epidural blood patch has not yetbeen standardized. Some authors believe that the EBPshould be performed at the same spinal level of a CSF leak
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