olly
Extremely helpful member
- Joined
- Jan 10, 2008
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- 2,743
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- PALS
- Diagnosis
- 11/2007
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- uk
part1
Upper Motor Neuron Damage (UMN)
Historically, this has been associated with the corticospinal (pyramidal) tract. However, this is not quite accurate since voluntary motor pathways arising in the cerebral cortex can function by activating more primitive descending tracts from the brain stem. It is clear that the direct projections in the corticospinal tract are responsible for highly skilled movements, especially of the hands. In this section we will refer to direct and indirect corticospinal projections to distinguish the corticospinal tract itself from the indirect activation of other descending motor tracts by cerebral cortical input. Additionally, it must be understood that the motor cortex does not act independently, but rather under the influence of the premotor cortex (involved in planning and initiating movement) as well as "extrapyramidal" systems such as the basal ganglia and cerebellum (see below).
The classic picture of acute damage to UMNs includes contralateral paralysis of distal limb movements, while proximal limb movements are severely weakened and trunk movement minimally involved. Muscle tone (measured as passive resistance to manipulation) is depressed in this initial phase. The deep-tendon reflexes are also likely to be absent, recovering over time to normal or hyperactive levels. The superficial reflexes (abdominal and cremasteric) opposite the lesion are depressed or absent. A Babinski response is often present on the weak side.
Over weeks to months proximal strength improves to a significant degree, whereas distal movements make only a poor recovery. A rudimentary grasping capability is frequently all that remains in the hand. Extension, opposition, and individual finger movements remain severely affected or lost. Presumably, the recovery of proximal functions relates to some bilaterality of distribution of corticospinal fibers that innervate proximal muscles. The modest recovery of distal movements is suspected to relate to preserved motor pathways from the brain stem (presumably under extrapyramidal control).
Damage to the precentral gyrus (primary motor cortex) or isolated damage to the medullary pyramid produces a rather pure corticospinal tract lesion. In these cases, the weakness of distal muscles is severe but there is little appearance of other findings, such as spasticity and hyperreflexia that are hallmarks of most UMN lesions. Other UMN lesions also damage indirect descending connections between the cerebral cortex and spinal cord. This happens with lesions of the premotor cortex, corona radiata, internal capsule, cerebral peduncle, basal pons, and lateral columns of the spinal cord. Invariably, lesions in these areas also involve other pathways leaving the cerebral cortex that are intermixed with the direct corticospinal (pyramidal) projection. In addition to the weakness found in all of these patients, there is a decrease in tonic inhibition of reflexes and an increase in resting muscle tone. This is accompanied by hyperactivity of the deep-tendon reflexes and development of what is traditionally called spasticity.
Upper Motor Neuron Damage (UMN)
Historically, this has been associated with the corticospinal (pyramidal) tract. However, this is not quite accurate since voluntary motor pathways arising in the cerebral cortex can function by activating more primitive descending tracts from the brain stem. It is clear that the direct projections in the corticospinal tract are responsible for highly skilled movements, especially of the hands. In this section we will refer to direct and indirect corticospinal projections to distinguish the corticospinal tract itself from the indirect activation of other descending motor tracts by cerebral cortical input. Additionally, it must be understood that the motor cortex does not act independently, but rather under the influence of the premotor cortex (involved in planning and initiating movement) as well as "extrapyramidal" systems such as the basal ganglia and cerebellum (see below).
The classic picture of acute damage to UMNs includes contralateral paralysis of distal limb movements, while proximal limb movements are severely weakened and trunk movement minimally involved. Muscle tone (measured as passive resistance to manipulation) is depressed in this initial phase. The deep-tendon reflexes are also likely to be absent, recovering over time to normal or hyperactive levels. The superficial reflexes (abdominal and cremasteric) opposite the lesion are depressed or absent. A Babinski response is often present on the weak side.
Over weeks to months proximal strength improves to a significant degree, whereas distal movements make only a poor recovery. A rudimentary grasping capability is frequently all that remains in the hand. Extension, opposition, and individual finger movements remain severely affected or lost. Presumably, the recovery of proximal functions relates to some bilaterality of distribution of corticospinal fibers that innervate proximal muscles. The modest recovery of distal movements is suspected to relate to preserved motor pathways from the brain stem (presumably under extrapyramidal control).
Damage to the precentral gyrus (primary motor cortex) or isolated damage to the medullary pyramid produces a rather pure corticospinal tract lesion. In these cases, the weakness of distal muscles is severe but there is little appearance of other findings, such as spasticity and hyperreflexia that are hallmarks of most UMN lesions. Other UMN lesions also damage indirect descending connections between the cerebral cortex and spinal cord. This happens with lesions of the premotor cortex, corona radiata, internal capsule, cerebral peduncle, basal pons, and lateral columns of the spinal cord. Invariably, lesions in these areas also involve other pathways leaving the cerebral cortex that are intermixed with the direct corticospinal (pyramidal) projection. In addition to the weakness found in all of these patients, there is a decrease in tonic inhibition of reflexes and an increase in resting muscle tone. This is accompanied by hyperactivity of the deep-tendon reflexes and development of what is traditionally called spasticity.
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