Intracranial hypotension: diagnosis by trial of Trendelenburg positioning and imaging

An 80-year-old woman with well-controlled hypertension, hypothyroidism, and an atraumatic fall 3 weeks prior, presented with complaints of altered mental status and left eye drooping for 1 day, without headache. On initial examination, she was noted to be lethargic with a partial left third nerve palsy, with preserved but sluggish pupillary light reflex. A CT head scan was done, revealing bilateral acute on chronic subdural hematomas with an admixture of hypodense material in the subdural space and some hyperdense components (Fig. 1). Given her third nerve palsy, there was concern for pathology other than the subdural hematoma. An MRI brain scan with and without contrast was done, and revealed diffuse pachymeningeal enhancement, in addition to bilateral frontoparietal subdural collections. (Fig. 2d–f) The collections were heterogeneous and thought to represent a mixture of proteinaceous CSF material and acute blood (Fig. 2d–f). A lumbar puncture was performed, with an opening pressure of 9 cmH2O. CSF studies showed: glucose 64 mg/dL, protein 129 mg/dL, 4444 red blood cells, 167 white blood cells (24 % neutrophils, 76 % lymphocytes), and a negative Gram’s stain. The pachymeningeal enhancement, new cranial nerve palsy, and elevated CSF white blood cell count were thought to be consistent with chronic subdural hematoma versus lymphoma, inflammatory process, or other malignant process. While CSF cultures, cytology and flow cytometry were pending, the patient’s course improved, and she was able to maintain upright posture and feed herself. However, within a day of this improvement, she was again noted to have fluctuating mental status, ranging from baseline intact mental status to lethargic and obtunded. She also developed a new right third nerve palsy, which intermittently resolved and recurred spontaneously. EEG monitoring was done and revealed only diffuse slowing with no epileptiform activity. In addition, she developed episodes of hypertension with bradycardia and irregular breathing, which are the symptoms of Cushing’s triad, a syndrome associated with increased intracranial pressure. Given a fluctuating course and concern for increased intracranial pressure with the signs of Cushing’s triad, imaging was reviewed again. On second review, further abnormalities were noted, including engorged cortical veins and venous sinuses and signs of brain sagging. Brain sagging describes the downward displacement of the brain that was demonstrated in our patient with: ventricles smaller than expected for age, increased anterior–posterior and decreased bipeduncular diameter of the mesencephalon, an effaced interpeduncular cistern, enlarged pituitary gland, and a sagging corpus callosum with a down-pointing splenium (Figs. 1, 2) These imaging findings raised concern for spontaneous intracranial hypotension (SIH). The patient was subsequently placed in Trendelenburg position, and her mental status improved dramatically. She did, however, have a persistent partial left third nerve palsy. Although this was thought to support the diagnosis of SIH, there was some concern that the clinical improvement may have been coincidental, as her mental status had been fluctuating throughout her hospital course. A CT myelogram was done, revealing CSF extravasations at T11/T12, supporting the diagnosis of SIH (Fig. 3). As the patient’s examination continued to fluctuate with position, a lumbar epidural blood patch was performed. The patient showed significant & Andrew C. Berry Aberry5555@gmail.com