We report a case of spontaneous intracranial hypotension due to a cerebrospinal fluid leak at the C2 level, which was successfully treated by epidural fibrin glue patching. Epidural blood patching was performed twice, first with 6 mL of autologous blood and then with 10 mL, but the intracranial hypotension was unresponsive. Although successful treatment of postdural puncture headache and persistent leak after intrathecal catheterization by epidural patching with fibrin glue has been reported, fibrin glue has not been previously applied in spontaneous intracranial hypotension. Our observation suggests that epidural patching with fibrin glue should be considered in patients with spontaneous intracranial hypotension, if epidural blood patching fails to resolve the symptoms.

We report a case of spontaneous intracranial hypotension due to a cerebrospinal fluid leak at the C2 level, which was successfully treated by epidural fibrin glue patching. Epidural blood patching was performed twice, first with 6 mL of autologous blood and then with 10 mL, but the intracranial hypotension was unresponsive. Although successful treatment of postdural puncture headache and persistent leak after intrathecal catheterization by epidural patching with fibrin glue has been reported, fibrin glue has not been previously applied in spontaneous intracranial hypotension. Our observation suggests that epidural patching with fibrin glue should be considered in patients with spontaneous intracranial hypotension, if epidural blood patching fails to resolve the symptoms.Key words: intracranial hypotension, epidural patch, fibrin glue ( Headache 2000;40:844-847) In spontaneous intracranial hypotension due to a cerebrospinal fluid (CSF) leak in which the site has been identified, targeted therapy is indicated when bed rest or medications do not relieve neurological symptoms. 1 If targeted epidural patching with autologous blood is not effective, neurosurgical procedures are then considered. 2,3 Recently, we evaluated and treated a patient with intracranial hypotension in whom epidural blood patching failed to resolve the symptoms, but success was achieved by epidural patching with fibrin glue. CASE HISTORYA 38-year-old man was admitted for increasingly severe postural headache, dizziness, and nuchal soreness, which were relieved in the supine position. He had suffered from these symptoms for 10 months, and had received outpatient treatment with analgesics. During this time, bilateral chronic subdural fluid collections and diffuse pachymeningeal thickening had been diagnosed by gadolinium-enhanced magnetic resonance imaging (MRI) of the head. These conditions did not require surgical intervention, but he could not continue his job as a secretary because of the symptoms. In the last few months, he had spent much of his time in the recumbent position. Although he had no history of lumbar puncture or neurosurgical operations, a year and a half before, he had a traffic accident, possibly with neck hyperextension, which was treated medically.On examination, a lumbar puncture showed a CSF opening pressure of 20 cm H 2 O. Cisternography performed after indium-111 radionuclide injection into the lumbar subarachnoid space disclosed early accumulation in the urinary bladder and direct evidence of a CSF leak at the upper cervical spinal level at 2 hours. Computed tomography (CT) myelography confirmed the CSF leak on the left side of the C2 level ( Figure 1A). Although MRI studies no longer showed either the chronic subdural hematoma or the pachymeningeal thickening after the administration of gadolinium, the

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Ventricular fibrillation (VF) is a cause of death in bupivacaine-induced cardiovascular toxicity. We have examined the therapeutic effects of lidocaine on the threshold for bupivacaine-induced VF in in situ beating swine hearts. Twenty-four animals were allocated to one of three groups: 0.25% bupivacaine, 1% lidocaine or 0.25% bupivacaine with 1% lidocaine were infused into the left anterior descending coronary artery in increasing doses of 0, 1, 2, 4, 8 and 16 ml h-1 for 15 min, respectively. ECG and haemodynamic variables were monitored continuously during infusion. Regional myocardial function in the area supplied by the left anterior descending coronary artery was assessed using the sonomicrometry technique. VF did not occur in the lidocaine group. VF developed at higher infusion rates in animals given bupivacaine with lidocaine (in one animal at an infusion rate of 8 ml h-1 and in seven at 16 ml h-1) compared with animals given bupivacaine alone (in one at an infusion rate of 4 and in seven at 8 ml h-1). Although regional myocardial function decreased with increases in the infusion rate in each group, the depressant effects of the bupivacaine solution (medial inhibitory infusion rate of systolic shortening: IR50 = 2.43 (0.43) ml h-1) were significantly greater than those of the lidocaine solution (IR50 = 5.83 (0.87) ml h-1), but did not differ from those of the bupivacaine with lidocaine solution (IR50 = 3.54 (0.56) ml h-1). This study indicates that a combination of lidocaine and bupivacaine increased the threshold for bupivacaine-induced VF without further depressing myocardial contractility.