BACKGROUND AND PURPOSE:The corpus callosum is an important predilection site for traumatic axonal injury but may be unevenly affected in head trauma. We hypothesized that there were local differences in axonal injury within the corpus callosum as investigated with diffusion tensor imaging (DTI), varying among patients with differing severity of traumatic brain injury (TBI).
It seems legitimate to propose a categorization that takes into consideration a primary malformation (nidus or fistula) that evolves with time and in which angioarchitectural changes occur. Recognition of the factors originally responsible for the shunt (e.g., genetic hereditary or genetic nonhereditary) allows a different classification of SCAVSs.
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.
Endovascular treatment of SCAVFs stabilizes, normalizes, or improves neurological symptoms in all patients at long-term follow-up, with no bleeds or rebleeds. Embolization of SCAVFs with glue is a safe treatment that compares favorably with other approaches and significantly improves the poor natural history of the disease.
The short term prognosis of hemorrhagic SCAVSs is good, and there is no need for emergency treatment. MRI delineates the cord and makes the diagnosis of the lesion but angiography remains the gold standard for analysis of the vasculature. The angio-architecture reflects the ageing of the lesion but there is not a precise correlation between angio-architecture and clinical symptoms, except for pseudoaneurysms which relate to the hemorrhagic portion of the lesion.
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