MRI changes in intracranial hypotension.

We report seven patients with the syndrome of intracranial hypotension who were referred to Memorial Sloan-Kettering, primarily because of suspicion of meningeal tumor or infection raised by the finding of meningeal enhancement on MRI. In three patients, symptoms occurred after lumbar puncture; in four, there was no clear precipitating event. Lumbar puncture after MRI in six patients revealed low CSF pressure (six patients) and pleocytosis or high protein, or both (four patients). Three patients had subdural effusions. Six patients had measurable descent of the brain on midsagittal images. Postural headache resolved in all seven patients, six of whom had follow-up MRIs. Meningeal enhancement resolved or diminished in all six. Subdural effusions resolved spontaneously in two and were evacuated (but were not under pressure) in one. Downward brain displacement improved or resolved in all patients. The clinical syndrome and MRI abnormalities generally resolve on their own. An extensive workup is not helpful and may be misleading. Patients should be treated symptomatically.

Magnetic resonance imaging measurements and clinical changes accompanying transtentorial and foramen magnum brain herniation.

Current concepts of brain herniation have depended largely on correlating clinical signs and symptoms with indirect radiographic studies and the results of postmortem neuropathology. This article describes measurements on midsagittal magnetic resonance imaging (MRI) scans that distinctly define normal and abnormal rostral-caudal relationships between the diencephalic-mesencephalic junction and the plane of the tentorial incisura, herein termed the incisural line. We similarly provide quantitative MRI scan measurements relating the cerebellum and the plane of the foramen magnum, termed the foramen magnum line. Measurements from 156 midsagittal and 63 coronal MRI scans performed on 123 normal adults, placed the iter of the aqueduct 0.2 +/- 0.8 mm (mean +/- SD) below the incisural line and the cerebellar tonsils 0.1 +/- 2.1 mm below the foramen magnum line. Defining 2 SD from these norms as abnormal, 23 patients with intracranial mass or obstructive lesions showed 4 distinct patterns of brain herniation, i.e., upward or downward transtentorial shift with or without accompanying cerebellar tonsillar herniation. Five patients with posterior fossa masses demonstrated displacement of the iter above the incisura ranging from 1.6 to 6.3 mm. Eighteen patients with supratentorial masses demonstrated displacement of the iter ranging from 2.0 to 11.0 mm below the incisura. Two-thirds of patients with upward and one-half of those with downward transtentorial shift had concurrent tonsillar herniation. In acute illnesses, MRI scan changes anticipated or confirmed clinical signs of brain herniation. In chronic cases, clinical and MRI scans correlated less well, with MRI sometimes revealing major degrees of anatomical herniation well in advance of clinical abnormalities.

Effect of conditioning lesions on regeneration of goldfish optic axons: time course of the cell body reaction to axotomy.

The time course of the cell body reaction to axotomy was determined in goldfish retinal ganglion cells by measuring cell body size and the amount of labelled protein conveyed by fast axonal transport to the optic tectum, both of which increase during regeneration of the optic axons. Following a single testing lesion of the optic nerve, the regenerating axons began to innervate the tectum at about 14 days after the lesion and the cell body reaction began to decline 2-3 weeks thereafter. If the testing lesion had been preceded by a conditioning lesion 2 weeks earlier, the time for the regenerating axons to arrive in the tectum was reduced by a week, because of the faster rate of axonal outgrowth, but the interval between their arrival and the beginning of the decline of the cell body reaction was unchanged. Electrophysiological measurements showed that synaptic transmission was initiated earlier when the axons reached the tectum faster. These results indicate that the mechanisms initiating the recovery of cell body metabolism are independent of those governing the rate of axonal outgrowth. The recovery of the cell body may begin shortly after synapses are established, regardless of whether they are correctly or incorrectly targetted. The correctness of the target may be a separate factor in determining how rapidly and completely the cell body recovers.