Faculty Bibliography

An elderly man experienced recurrent transient episodes of right arm weakness and expressive aphasia. He was initially treated with aspirin and then with coumadin. Thirteen days after initial presentation, he became febrile and had signs of meningitis. The illness progressed relentlessly to death 9 weeks after admission to the hospital. Necropsy showed prominent meningitis with vasculitis extending into the left frontal lobe. Polymerase chain reaction identified the organism as Listeria monocytogenes

The purpose of this theoretical study is to determine whether the absence of ventricular enlargement in pseudotumor cerebri (PTC) is consistent with the theory that PTC is caused by reduced absorption of cerebrospinal fluid (CSF), either from increased outflow resistance at the arachnoid villi or from obstruction of the dural venous sinuses. We model the brain as a thick spherical shell of parenchyma, enclosing a CSF-filled ventricular system, and surrounded by a thin cerebral subarachnoid space (CSAS). We treat the parenchyma as a porous solid matrix, filled with interstitial fluid and blood vessels. We subject the model to a uniform increase in CSF pressure (CSFP) and solve the equations of poroelasticity for the resulting displacements of parenchymal tissue. The effect of a rise in CSFP on ventricular size depends on the response of the cerebral blood vessels and the degree to which the pia is tethered to the dura. If the cerebral vessels decrease in caliber with increasing CSFP, a rise in CSFP causes the ventricles to contract and the CSAS to expand if the pial surface is free to move inward, but causes slight ventricular enlargement if the pia is tethered to the dura. If, instead, the vessels dilate, the ventricles contract and the CSAS becomes effaced. Small, normal, or slightly enlarged ventricles in PTC are consistent with the theory of reduced CSF absorption

Hydrocephalus is an abnormal accumulation of cerebrospinal fluid (CSF) in the cerebral ventricles, usually caused by impaired absorption of the fluid into the bloodstream. Despite obstructed absorption and continued secretion of CSF into the ventricles at a near normal rate, the ventricular CSF pressure (VCSFP) is often normal. We attempt to understand how hydrocephalus can exist with normal VCSFP by exploring the role of the brain parenchyma in absorbing CSF in hydrocephalus. We test three theories: (1) the ventricular wall is impermeable to CSF; (2) ventricular CSF seeps into the parenchyma, from which it is efficiently absorbed; and (3) ventricular CSF seeps into the parenchyma but is absorbed inefficiently. We model the brain as a thick spherical shell consisting of a porous, elastic, solid matrix, containing interstitial fluid and blood. We modify the equations of poroelasticity, which describe flow of fluid through porous solids, to allow for parenchymal absorption. For each of the three theories we calculate the steady state changes in VCSFP and in parenchymal fluid pressure caused by an incremental defect in CSF absorption. We also calculate the-steady state changes in fluid content, tissue volume, tissue displacement, and stresses caused by a small increment of VCSFP. We conclude that only the second theory-seepage of CSF with efficient parenchymal absorption-accounts for the clinical features of normal pressure hydrocephalus. These features include sustained ventricular dilatation despite normal VCSFP, increased periventricular fluid content, and localized periventricular white matter damage

The classical theory of spontaneous pulsation of the retinal veins is that during systole intraocular pressure exceeds venous pressure, causing the veins to collapse. We show that this theory is internally inconsistent and not in accord with experimental data. It is inconsistent in assuming both (a) that oscillations of intraocular pressure (IOP) occur because the veins cannot immediately discharge the systolic arterial inflow and (b) that retinal venous pressure (RVP) can fluctuate independently of IOP during the cardiac cycle. It is not in accord with experimental data, which shows that RVP always exceeds IOP and that fluctuations in the latter are instantly transmitted to the former. We present an alternative theory that does not have these problems. We assume the following. (1) Inflow to the retinal venous tree from the capillaries is constant, the pulsatile arterial flow having been completely damped by the arterioles and capillaries. (2) Outflow from the central retinal vein (CRV) varies during the cardiac cycle because oscillations of IOP, transmitted to the intraocular CRV, are of greater amplitude than oscillations in cerebrospinal fluid pressure, transmitted to the extraocular CRV. By showing that the radial blood flow distending the veins obeys a diffusion equation and by employing an 'equivalent cylinder' analysis of the branched venous tree to simplify the boundary conditions, we demonstrate that, with the above assumptions and the additional assumption of low amplitude of radial flow, the CRV will pulsate, and the pulsations will remain confined to a small segment near the exit point. The proposed theory can explain disappearance of pulsation with intracranial hypertension, intensification of pulsation in glaucoma, and variability in the linear extent and amplitude of pulsation among normal individuals. The theory may also be applied to other venous pulsations, such as the respiratory pulsation of the terminal portions of large veins entering the thorax or the cardiac cycle pulsation of the superior vena cava

OBJECTIVE: To determine whether either of two mechanical theories predicts the topographic pattern of neuropathology in cervical spondylotic myelopathy (CSM). The compression theory states that the spinal cord is compressed between a spondylotic bar anteriorly and the ligamenta flava posteriorly. The dentate tension theory states that the spinal cord is pulled laterally by the dentate ligaments, which are tensed by an anterior spondylotic bar. METHODS: The spinal cord cross section, at the level of a spondylotic bar, is modelled as a circular disc subject to forces applied at its circumference. These forces differ for the two theories. From the pattern of forces at the circumference the distribution of shear stresses in the interior of the disc-that is, over the transverse section of the spinal cord-is calculated. With the assumption that highly stressed areas are most subject to damage, the stress pattern predicted by each theory can be compared to the topographic neuropathology of CSM. RESULTS: The predicted stress pattern of the dentate tension theory corresponds to the reported neuropathology, whereas the predicted stress pattern of the compression theory does not. CONCLUSIONS: The results strongly favour the theory that CSM is caused by tensile stresses transmitted to the spinal cord from the dura via the dentate ligaments. A spondylotic bar can increase dentate tension by displacing the spinal cord dorsally, while the dural attachments of the dentate, anchored by the dural root sleeves and dural ligaments, are displaced less. The spondylotic bar may also increase dentate tension by interfering locally with dural stretch during neck flexion, the resultant increase in dural stress being transmitted to the spinal cord via the dentate ligaments. Flexion of the neck increases dural tension and should be avoided in the conservative treatment of CSM. Both anterior and posterior extradural surgical operations can diminish dentate tension, which may explain their usefulness in CSM. The generality of these results must be tempered by the simplifying assumptions required for the mathematical model

Hemorrhage secondary to anticoagulant therapy is well documented. We report a patient who presented with acute vertigo and unilateral deafness while on warfarin and was found to have a probable hemorrhage in the labyrinth, identified on MRI