Tumors of the cerebellopontine angle (CPA) are frequent; acoustic neuromas and meningiomas represent the great majority of such tumors. However, a large variety of unusual lesions can also be encountered in the CPA. The site of origin is the main factor in making a preoperative diagnosis for an unusual lesion of the CPA. In addition, it is essential to analyze attenuation at computed tomography (CT), signal intensity at magnetic resonance (MR) imaging, enhancement, shape and margins, extent, mass effect, and adjacent bone reaction. CPA masses can primarily arise from the cerebellopontine cistern and other CPA structures (arachnoid cyst, nonacoustic schwannoma, aneurysm, melanoma, miscellaneous meningeal lesions) or from embryologic remnants (epidermoid cyst, dermoid cyst, lipoma). Tumors can also invade the CPA by extension from the petrous bone or skull base (cholesterol granuloma, paraganglioma, chondromatous tumors, chordoma, endolymphatic sac tumor, pituitary adenoma, apex petrositis). Finally, CPA lesions can be secondary to an exophytic brainstem or ventricular tumor (glioma, choroid plexus papilloma, lymphoma, hemangioblastoma, ependymoma, medulloblastoma, dysembryoplastic neuroepithelial tumor). A close association between CT and MR imaging findings is very helpful in establishing the preoperative diagnosis for unusual lesions of the CPA.
Residual activation of the cortex was investigated in nine patients with complete spinal cord injury between T6 and L1 by functional magnetic resonance imaging (fMRI). Brain activations were recorded under four conditions: (1) a patient attempting to move his toes with flexion-extension, (2) a patient imagining the same movement, (3) passive proprio-somesthesic stimulation of the big toes without visual control, and (4) passive proprio-somesthesic stimulation of the big toes with visual control by the patient. Passive proprio-somesthesic stimulation of the toes generated activation posterior to the central sulcus in the three patients who also showed a somesthesic evoked potential response to somesthesic stimulation. When performed under visual control, activations were observed in two more patients. In all patients, activations were found in the cortical areas involved in motor control (i.e., primary sensorimotor cortex, premotor regions and supplementary motor area [SMA]) during attempts to move or mental imagery of these tasks. It is concluded that even several years after injury with some local cortical reorganization, activation of lower limb cortical networks can be generated either by the attempt to move, the mental evocation of the action, or the visual feedback of a passive proprio-somesthesic stimulation.
A fast computation and accurate analytical model for off-body propagation is derived in this paper. The paper discusses the off-body model propagation from an external source to a receiver located on the body. The model is developed for normal incident plane wave by describing the human body with a circular cylinder. We show that the total received electric field around the human body can be written as a creeping wave in the shadow region and as a Geometrical Optics result for the lit region. It is also shown that at 60 GHz, the shadow boundary width is negligible. The model shows perfect agreement with the experimental results conducted on a perfectly conducting cylinder. Measurements of the creeping wave path gain have been also conducted on a real body to assess the validity of the cylinder assumption. The results have shown a path gain of about 5 dB/cm for TM case and 3 dB/cm for TE case. The standard deviation between the measurements and the cylindrical model is about 3.5 dB for both TM and TE cases.
The lower cranial nerves innervate the pharynx and larynx by the glossopharyngeal (CN IX) and vagus (CN X) (mixed) nerves, and provide motor innervation of the muscles of the neck by the accessory nerve (CN XI) and the tongue by the hypoglossal nerve (CN XII). The symptomatology provoked by an anomaly is often discrete and rarely in the forefront. As with all cranial nerves, the context and clinical examinations, in case of suspicion of impairment of the lower cranial nerves, are determinant in guiding the imaging. In fact, the impairment may be located in the brain stem, in the peribulbar cisterns, in the foramens or even in the deep spaces of the face. The clinical localization of the probable seat of the lesion helps in choosing the adapted protocol in MRI and eventually completes it with a CT-scan. In the bulb, the intra-axial pathology is dominated by brain ischemia (in particular, with Wallenberg syndrome) and multiple sclerosis. Cisternal pathology is tumoral with two tumors, schwannoma and meningioma. The occurrence is much lower than in the cochleovestibular nerves as well as the leptomeningeal nerves (infectious, inflammatory or tumoral). Finally, foramen pathology is tumoral with, outside of the usual schwannomas and meningiomas, paragangliomas. For radiologists, fairly hesitant to explore these lower cranial pairs, it is necessary to be familiar with (or relearn) the anatomy, master the exploratory technique and be aware of the diagnostic possibilities.
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