RESUMEN

Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease (MND), is a progressive neurodegenerative disease that affects both upper and lower motor neurons, which results in loss of muscle control and eventual paralysis [1]. Currently, there are as yet unresolved challenges regarding efficient drug delivery into the central nervous system (CNS). These challenges can be attributed to multiple factors including the presence of the blood-brain barrier (BBB), blood-spinal cord barrier (BSCB), as well as the inherent characteristics of the drugs themselves (e.g. low solubility, insufficient bioavailability/bio-stability, 'off-target' effects) etc. As a result, conventional drug delivery systems may not facilitate adequate dosage of the required drugs for functional recovery in ALS patients. Nanotechnology-based strategies, however, employ engineered nanostructures that show great potential in delivering single or combined therapeutic agents to overcome the biological barriers, enhance interaction with targeted sites, improve drug bioavailability/bio-stability and achieve real-time tracking while minimizing the systemic side-effects. This review provides a concise discussion of recent advances in nanotechnology-based strategies in relation to combating specific pathophysiology relevant to ALS disease progression and investigates the future scope of using nanotechnology to develop innovative treatments for ALS patients.

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Three cases of posttraumatic cystic myelopathy occurring early in the postinjury period are reported. A patient with C5 tetraplegia developed bilateral upper extremity paresthesias and right upper extremity weakness 2 and a half months postinjury necessitating immediate syringo-subdural shunting. A patient with C6 tetraplegia complained of left upper extremity paresthesias 2 months postinjury. A syringoperitoneal shunt was placed 19 months postinjury due to new onset intermittent weakness of the right upper extremity. A patient with C4 tetraplegia developed right upper extremity paresthesias, sensory loss, and weakness 56 days postinjury; it was treated conservatively. Two years postinjury he required surgery because of progression of symptoms. A review of the literature reveals that posttraumatic cystic myelopathy has been found to be an incidental pathologic finding at autopsy within 2 months postinjury. However, sensory and motor loss have not been clinically described as an early complication of spinal cord injury. We conclude that posttraumatic cystic myelopathy should be considered in the differential diagnosis of motor or sensory loss occurring early in the postinjury period.

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This case illustrates the importance of intraoperative monitoring of neuronal function to help separate tumor tissue from neural tissue in a 54-year-old patient with left shoulder pain resulting from a desmoid tumor. Preoperative nerve conduction and electromyographic studies showed a lesion in the lateral cord of the brachial plexus, which was found to be intimately involved with the tumor mass and was splayed into a very thin effaced sheet of neural tissue. Stimulation of the tumor/nerve tissue mass proximal to the lesion was impossible due to the invasion of the brachial plexus by the tumor. The technique that was adapted for this unusual presentation was to stimulate the tumor/nerve tissue mass itself and record compound muscle action potentials distally. With the technique described, a subtotal resection of an aggressive fibromatosis enmeshed in the proximal brachial plexus was possible, and excellent relief of pain symptoms and retention of functional capabilities of the involved extremity were achieved.

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