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Upper motor neuron - Wikipedia, the free encyclopedia

Mon Jun 22 00:58:25 +0000 2009

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originate in the motor region of the cerebral cortex or the brain stem and carry motor information down to the final common pathway, that is, any motor neurons that are not directly responsible for stimulating the target muscle
Upper motor neurons travel in several pathways through the CNS:
corticospinal tract
corticobulbar tract
tectospinal tract/colliculospinal tract
rubrospinal tract
vestibulospinal tract
reticulospinal tract

Mon Jun 22 00:56:55 +0000 2009

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Hoffmann's sign is often considered the upper limb equivalent of the Babinski's sign^[3] because it, like the Babinski sign, indicates upper motor neuron dysfunction.^[4] Its mechanism differs considerably from the Babinski which is also known as the plantar reflex; Hoffmann's sign involves a monosynaptic reflex pathway in Rexed lamina IX of the spinal cord, normally fully inhibited by descending input. The pathways involved in the plantar reflex are more complicated, and different sorts of lesions may interrupt them. This fact has led some neurologists to reject strongly any analogies between the finger flexor reflex and the plantar response.

Mon Jun 22 00:40:59 +0000 2009

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benign nerve sheath tumor composed of Schwann cells, which normally produce the insulating myelin sheath covering peripheral nerves.
Schwannomas are relatively slow growing. For reasons not yet understood, schwannomas are mostly benign and less than 1% become malignant, degenerating into a form of cancer known as malignant peripheral nerve sheath tumour, malignant schwannoma, or neurofibrosarcoma.

Sun Jun 21 23:56:08 +0000 2009

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Cause

The voltage-gated sodium channel Na_V1.7 is expressed in nociceptive and sympathetic neurons, where it aids in action potential creation and regulation. The mutations in this gene that have received study all alter the channels ability to inactivate. Sodium channel inactivation is vital for the proper cessation of action potentials. The decreased inactivation caused by these mutations, then, is expected to cause prolonged action potentials and repetitive firing. Such altered firing will cause increased pain sensation and increased sympathetic nervous system activity, producing the phenotype observed in patients with PEPD.^[2]

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