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Upper motor neuron corticospinal facial changes

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    Hypertonia and hyperreflexia are classically described responses to upper motor neuron injury. However, acute hypotonia and areflexia with motor deficit are hallmark findings after many central nervous system insults such as acute stroke and spinal shock. Historic theories to explain these contradictory findings have implicated a number of potential mechanisms mostly relying on the loss of descending corticospinal input as the underlying etiology. Unfortunately, these simple descriptions consistently fail to adequately explain the pathophysiology and connectivity leading to acute hyporeflexia and delayed hyperreflexia that result from such insult. This article highlights the common observation of acute hyporeflexia after central nervous system insults and explores the underlying anatomy and physiology. Further, evidence for the underlying connectivity is presented and implicates the dominant role of supraspinal inhibitory influence originating in the supplementary motor area descending through the corticospinal tracts.
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    Upper motor neuron

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    Neuroanatomy, Upper Motor Nerve Signs Article

    NCBI Bookshelf. Marc Christopher Emos ; Sanjeev Agarwal. A vast network of nerve tracts in the central nervous system CNS which spans the cerebral cortex, brainstem, cerebellum, and spinal cord control the initiation and modulation of movements. The primary tract which carries signals for voluntary movement is known as the pyramidal tract. The pyramidal tract divides further into the corticospinal tract and the corticobulbar tract. UMN lesions are designated as any damage to the motor neurons that reside above nuclei of cranial nerves or the anterior horn cells of the spinal cord. These symptoms can include weakness, spasticity, clonus, and hyperreflexia.
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    Upper motor neuron lesion

    NCBI Bookshelf. Sunderland MA : Sinauer Associates; Injury of upper motor neurons is common because of the large amount of cortex occupied by the motor areas, and because motor pathways extend all the way from the cerebral cortex to the lower end of the spinal cord. Damage to the descending motor pathways anywhere along this trajectory gives rise to a set of symptoms called the upper motor neuron syndrome. This clinical picture differs markedly from the lower motor neuron syndrome described in Chapter 16 and entails a characteristic set of motor deficits.
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    They are found in the cerebral cortex and brainstem and carry information down to activate interneurons and lower motor neurons , which in turn directly signal muscles to contract or relax. UMNs in the cerebral cortex are the main source of voluntary movement. They are the larger pyramidal cells in the cerebral cortex. There is a type of giant pyramidal cell called Betz cells and are found just below the surface of the cerebral cortex within layer V of the primary motor cortex. The cell bodies of Betz cell neurons are the largest in the brain, approaching nearly 0.
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