The structure of the meninges, with particular attention to the architecture of the inner portions of the dura mater and the arachnoid mater, has been reviewed in reference to the probable existence of a "subdural" space. The dura is composed of fibroblasts and large amounts of extracellular collagen. The innermost part of the dura is formed by the dural border cell layer. This layer is characterized by flattened cells with sinuous processes, extracellular spaces containing an amorphous material, and the presence of junctions between its cells. The dural border cell layer is continuous with the inner (meningeal) portions of the dura and may be attached to the underlying arachnoid by an occasional cell junction. The arachnoid consists of an outer part, the arachnoid barrier cell layer, and an inner portion, the arachnoid trabeculae which bridge the subarachnoid space. Arachnoid barrier cells are electron-lucent, closely apposed to each other, and joined by many cell junctions; in this layer there is little extracellular space and essentially no intercellular material. Arachnoid trabecular cells cross the subarachnoid space in a random manner, have extracellular collagen associated with their flattened processes, and form structures of variable shapes and sizes. There is no evidence of an intervening space between the arachnoid barrier cell layer and the dural border cell layer that would correlate with what has been called the subdural space. When a tissue space is created in this general area of the meninges it is the result of tissue damage and represents, in most instances, a cleaving open of the dural border cell layer. In this situation, extracellular spaces in the dural border cell layer are enlarged, cell junctions are separated, and it is probable that cell membranes are damaged. A survey of reports describing the morphology of the inner and outer capsule of so-called subdural hematomas in humans reveals that dural border cells are found in both parts of the capsule. Also, experimental infusion of blood into this portion of the meninges in animals frequently dissects open the dural border cell layer. These data support the view that what has been called a subdural hematoma is most frequently a lesion found within the layer formed by dural border cells. It is suggested that the so-called subdural space is not a "potential" space since the creation of a cleft in this area of the meninges is the result of tissue damage. In this respect it shares no similarities with legitimate potential spaces (i.e., serous cavities) found at other locations in the body.(ABSTRACT TRUNCATED AT 400 WORDS)

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v, A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months.Spinal cord blood flow studies using the hydrogen clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature. KEY WORDS 9 cervical spondylosis 9 cervical myelopathy 9 spinal cord compression 9 magnetic resonance imaging 9 somatosensory evoked potentials 9 dog

Expanding cysts of the septum pellucidum, although rare, may be a cause of significant neurological dysfunction. Most become symptomatic as a result of obstruction of the interventricular foramina and produce headaches, papilledema, emesis, and loss of consciousness. Behavioral, autonomic, and sensorimotor symptoms occur when an expanding cyst impinges on the structures of the hypothalamoseptal triangle or impairs the deep cerebral venous drainage. Neuroophthalmological symptoms may develop as a consequence of hydrocephalus or direct compression of visual structures. The authors describe the case of a young boy with an expanding septum pellucidum cyst who presented with a sudden, severe headache and loss of consciousness. In addition, he had a history of hyperactivity and progressively declining school performance. All symptoms resolved following decompression of the cyst. Seventeen cases from the literature are reviewed. The pathophysiological mechanisms underlying the development of symptoms secondary to expanding septum pellucidum cysts are outlined, and the related clinical neuroanatomy is described. A model is proposed for the natural history of expanding septum pellucidum cysts that provides a rational basis for understanding their clinical behavior and response to intervention. In most cases, fenestration or shunting will relieve the obstructive hydrocephalus and mass effect caused by the cyst and will produce rapid symptomatic improvement.

This review considers the structure of the meninges, as seen at the electron microscopic level, with particular emphasis on the dura-arachnoid junction and whether a naturally occurring space is found at this interface. The classic view has been that a so-called subdural space is located between the arachnoid and dura and that subdural hematomas or hygromas are the result of blood or cerebrospinal fluid accumulating in this (preexisting) space. The dura is composed of elongated, flattened fibroblasts and copious amounts of extracellular collagen. A specialized layer of fibroblasts, the dural border cell layer, is found at the dura-arachnoid junction and is characterized by flattened fibroblasts, no extracellular collagen, extracellular spaces, and few cell junctions. These features combine to create a layer of the inner dura that is structurally weak when compared with external portions of the dura and the internally located arachnoid. The arachnoid layer is composed of larger cells with numerous cell junctions, no extracellular space, and no extracellular collagen. The occurrence of many tight junctions in this layer also serves as a barrier to the movement of fluids and ions. Fibroblasts specialized to form the arachnoid trabeculae attach to the inner surface of the arachnoid layer, bridge the subarachnoid space, and surround vessels in the subarachnoid space as well as attach to pia on the surface of the brain. Under normal conditions, there is no evidence of a naturally occurring space being extant at the dura-arachnoid junction. A space may appear at this point subsequent to pathological/traumatic processes that result in tissue damage with a cleaving opening of the structurally weakest plane in the meninges--through the dural border cell layer. Furthermore, when a space does appear, it is not "subdural" in location but rather within a morphologically distinct cell layer.