Intramedullary pressure in syringomyelia: clinical and pathophysiological correlates of syrinx distension.

OBJECTIVE: The pathophysiological effects of syrinx distension are incompletely understood. Although it is generally assumed that the accumulation of fluid within syrinx cavities can contribute to neurological dysfunction, there are no reports describing intramedullary pressure in syringomyelia. The purpose of the current study was to measure syrinx pressures in patients with progressive clinical deterioration and to correlate these data with neurological deficits and intraoperative physiological findings. METHODS: Intramedullary fluid pressure was measured manometrically in 32 patients undergoing syrinx shunting procedures. The data were correlated with syrinx morphology, intraoperative somatosensory evoked potentials, laser Doppler measurements of local spinal cord blood flow (six patients), and neurological findings before and after syrinx decompression. RESULTS: Syrinx pressures recorded under atmospheric conditions ranged from 0.5 to 22.0 cm H2O (mean = 7.7 cm). There was a significant elevation of the cardiac pulse (mean = 0.7 cm H2O) and the respiratory pulse (mean = 1.1 cm H2O) that was consistent with raised cerebrospinal fluid pressure. Syrinx pressures decreased to subatmospheric levels after surgical drainage. In 18 of 24 patients with predrainage somatosensory evoked potential abnormalities, syrinx decompression produced a consistent reduction of N20 latencies (mean change = 0.49 ms +/- 0.094 SE right, P = 0.002; 0.61 ms +/- 0.089 SE left, P = 0.001) and a similar but less consistent increase in N20 amplitudes (mean change = 0.17 mV +/- 0.103 SE right, P = 0.115; 0.31 mV +/- 0.097 SE left, P = 0.027). Measurements of local spinal cord blood flow revealed very low baseline values (mean = 12.2 arbitrary units +/- 13.9 standard deviation), which increased to intermediate levels (mean = 144.7 arbitrary units +/- 42.6 standard deviation) after syrinx decompression. Patients with syrinx pressures greater than 7.7 cm H2O tended to have more rapidly progressive symptoms, exhibited greater improvements after shunting, and had a higher incidence of postoperative dysesthetic pain. CONCLUSION: The current study is the first to measure intramedullary pressure in a human disease. Evidence is presented that distended syringes are associated with varying levels of raised intramedullary pressure that can accentuate or induce neurological dysfunction by the compression of long tracts, neurons, and the microcirculation. Symptoms referrable to raised intramedullary pressure are potentially reversible by syrinx decompression.

Continuous postoperative lCBF monitoring in aneurysmal SAH patients using a combined ICP-laser Doppler fiberoptic probe.

Cerebral vasospasm remains the principal cause of morbidity and mortality following successful clipping of intracranial aneurysms. Current management often requires subjective judgments concerning presumed abnormalities of cerebral blood flow. In this study, a combined intracranial pressure (ICP)-laser Doppler flowmetry (LDF) fiberoptic probe that permits continuous monitoring of local cerebral blood flow (lCBF) was used in the postoperative management of 20 aneurysm patients. Using this probe, lCBF was simultaneously recorded and integrated on a real time basis with other physiological parameters, including ICP, systemic arterial pressure, pulmonary arterial pressure, central venous pressure, and pulse oximetry. The combined probe also provided the ability to obtain precise and detailed information concerning the presence or absence of cerebral autoregulation and CO2 vascular reactivity, and allowed calculation of the cerebral vascular resistance. Continuous monitoring of lCBF in this manner complemented by transcranial Doppler and angiographic data permitted early detection of cerebral ischemia, helped to differentiate cerebral ischemia from edema and hyperemia, was useful in titrating blood pressure and fluid management, provided direct feedback about the effectiveness of instituted therapies, and determined early on when medical management was of no avail and that interventional neuroradiology was indicated. Evidence is presented that the presence of angiographic vasospasm and increased velocities on TCD do not always correlate with ischemia in the microcirculation and that direct measurements of lCBF are often at variance with calculations of cerebral perfusion pressure (CPP).

Laser-Doppler flowmetry in neurosurgery.

Laser-Doppler flowmetry (LDF) provides a reliable measurement of local cerebral blood flow (lCBF) as demonstrated by multiple validation studies. This article evaluates the clinical applications of LDF in neurosurgery. With the availability of modified probes, it is possible to carry out LDF monitoring of neurosurgical patients in the intensive care unit. Currently, there are multiple systemic and intracranial parameters that are interactive and separately monitored. A multi-channeled digital data acquisition system allows these data to be compiled in a single computer environment for the interpretation of lCBF changes. Guidelines are suggested for the clinical use of LDF monitoring, and the technical features of monitoring including the interpretation of data are summarized.

Anatomical basis of syringomyelia occurring with hindbrain lesions.

Hindbrain lesions that distort or compress the cervicomedullary junction are commonly associated with syringomyelia. As a basis for discussing pathogenetic mechanisms, the upper end of the central canal of the spinal cord was examined histologically in six aborted fetuses and 14 adults dying of natural causes; the results were correlated with magnetic resonance images in 40 normal subjects. The central canal of the medulla, which extends from the cervicomedullary junction to the fourth ventricle, was found to migrate dorsally, elongate in dorsoventral diameter, and dilate beneath the tip of the obex to form a large, everted aperture. This opening communicates directly with the subarachnoid space through the foramen of Magendie and is indirectly continuous with the main body of the fourth ventricle. In adults, the aperture of the central canal is located approximately 1.0 cm below the tela choroidea inferior and 3.5 cm below the midpoint of the fourth ventricle. Analysis of magnetic resonance imaging scans in 45 patients with syringomyelia and simple hindbrain lesions revealed two patterns of cavity formation: 1) lesions that obstructed the upper end of the central canal or its continuity with the subarachnoid space produced a noncommunicating type of syringomyelia; and 2) lesions that obstructed the basilar cisterns or the foraminal outlets of the fourth ventricle produced a communicating type of syringomyelia (hydromyelia) in association with hydrocephalus. Evidence is presented that syrinxes occurring with hindbrain lesions are not caused by a caudal flow of cerebrospinal fluid from the fourth ventricle into the central canal of the spinal cord.

Histopathology of experimental hematomyelia.

The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 microliters blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.