Diffuse vertebral body edema due to calcified intraspongious disk herniation.

We describe the case of a patient with a recent history of high back pain, with magnetic resonance imaging (MRI) of the thoracic spine showing intervertebral disk herniation into the spongious bone of the vertebral body of T9 that might have caused diffuse, low signal intensity on fluid-attenuated inversion recovery T1-weighted (FLAIR-T1W) images, high signal intensity magnetic resonance (MR) on T2-weighted (T2W) images and T2-weighted fat-suppressed images (T2W-FSIs) and marked enhancement on the vertebral body of T9 with gadolinium on T1-weighted fat-suppressed images (T1W-FSIs) images. Those findings suggested diffuse edema and might be indistinguishable from tumoral or inflammatory diseases, but the plain films and the reformatted sagittal computed tomography scans of the thoracic spine were helpful to show a calcified part of the intervertebral disk migrating into the vertebral body of T9. The patient made full recovery from the symptoms after conservative treatment and at the follow-up MRI showed normalization of the bone marrow signal intensity of the vertebral body of T9.

Thoracic spine arachnoid ossification with and without cord cavitation. Report of three cases.

Thoracic spine arachnoid ossification is a relatively rare disease that affects mainly women and causes sensory, motor, and sphinctal symptoms associated with inferior limb pain. Based on three cases, the authors comment on pathogenic and surgery-related aspects of the disease. The patient in Case 1 was followed over the course of 23 years. Spinal cavitation is highlighted in Case 2, and yellow, gross, half-ring ossification is described in Case 3. Calcium deposits usually occur in the middle and lower thoracic spine where the majority of trabeculated arachnoid cells are located. Operative treatment does not interrupt the ossification process, which continues over time, causing progressive deterioration in the patient. Spinal cavitation can occur due to spinal cord tethering, stretching, and central cord edema formation, accompanied by cerebrospinal fluid blockage and pulse pressure changes. The results of surgical intervention are poor, offering short-term recovery with later deterioration. Multiple pathogenic factors are involved in this clinical syndrome including metabolic changes.

Paracoccidioidomycosis of the central nervous system: CT findings.

A retrospective analysis of six cases of central nervous system paracoccidioidomycosis, all but one proven by biopsy and surgery, was carried out to study the CT and clinical data and pathological correlation. Most of the patients were from the country. Headache, vomiting, seizures and hemiparesis were the most frequent symptoms. Papilloedema was present in four patients with raised intracranial pressure. Five patients had chronic lung disease and two with advanced systemic disease, skin and mucous membrane lesions were also observed. The neurological disturbance was sometimes the presenting features and the diagnosis was discovered incidentally after surgery. Both solitary and multiple parenchymal lesions were observed and the cerebral hemispheres were more commonly involved in four patients. Local meningeal involvement was observed in one with a single cortical granuloma. We emphasise the usefulness of CT, showing a rounded or lobulated mass with an isodense or radiolucent centre after contrast enhancement, surrounded by an irregular wall of varying thickness. There was always moderate oedema, extending peripherally. Other infections or neoplastic diseases may present similar findings. Preoperative diagnosis should rest on integration of clinical data, chest films, laboratory and neuroimaging studies.

CT features of cellulosae and racemosus neurocysticercosis.

Of 210 cases of cerebral neurocysticercosis studied with CT since 1982, three cases proved to be due to the rare Cysticercus racemosus (surgical verification) rather than to the much more prevalent infestation by Cysticercus cellulosae. We attempted to establish CT criteria for differentiating the more severe and always fatal form of C. racemosus. The CT appearance occasionally encountered in C. racemosus resembles a "bunch of grapes"; this appears to be the only criterion of differential value.

Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates.

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.