Welcome back to our discussion of upper motor neuronal control systems. I'd like to turn now to the clinical picture of what you'll discover in an individual that has had damage to their upper motor neurons, or the connections between upper and lower motor neurons. So, my learning objective for you is that I want you to be able to discuss the signs associated with damaged upper motor neurons. Well, for those of you heading into the health professions, it will be critical for you to understand the difference between the signs and symptoms associated with lower motor neuron injury and those associated with upper motor neuron injury. And the problem here is time, and that is shortly after damaged are pro-motor neurons. The patient might present with signs and symptoms that resemble those associated with a lower model neuron injury. what is observed with people in the first few hours to days, possibly as long as a week, following damage to upper motor neurons is a phenomenon called spinal shock. Spinal shock refers to an apparent failure of lower motor circuits to provide output to skeletal muscle. As a result, the patients are profoundly weak, the muscles appear to be flaccid, and the tone of the reflexes appears to be significantly reduced. These are all signs and symptoms that might be interpreted as a lower motor neuron injury. However, over time, as those first few hours to days to probably, the second week after the injury, we see a quite different clinical picture. Those flaccid muscles have now become spastic. The low muscle tone has now increased significantly, such that there's actually pathological tone. Too much tone in those muscles. And those reflexes that, soon after the injury, were essentially flat. Now, are actually hypertonic. That is, they're hyper reflexive. So, let's compare our lower motor signs with our upper motor signs. Assuming now that some time has passed, and this initial period of spinal shock has abated. So what we would see is, in the upper motor neuron syndrome, yes we'd see weakness, which is also seen with lower motor neuron injury, but rather then seeing a decrease in reflexes, we would see spasticity. And spasticity involves an increase in muscle tone, an increase in deep tendon reflexes, and the phenomenon of clonus. Which means that, with a quick stretch of a joint, this is typically tested in the ankle joint one might see a oscillatory movement or beating around that joint, more than about 2 or 3 cycles. this is an, a sign associated with the spasticity of the muscles that flex and extend that joint. One might also see some special signs associated with damage to upper motor neurons. one such sign is called the Babinski's sign. The Babinski's sign is evident with the stroke of the sole of the foot, with a sharp object. Now for adults with an intact cortical spinal system, such a stroke from the heel of the foot, towards the ball of the foot. Leads to flexion of the toes, or a downward turning of the, of the toes. This is a normal plantar flexion response. Someone with damaged upper motor neurons, might have a very different sign with this heal to ball of the foot stoking with a sharp object. We would see an upward turn of the great toe and a fanning out or an extension of the remaining toes. So this is quite a different sign than what we observe with an intact nervous system. Now the problem with the Babinski's sign is that, is just not that good. That is It has relatively low specificity and sensitivity. So a patient of yours may have an upper motor neuron injury but may show a normal plantar response. So just be cautious in how you interpret a normal Babinski's reflex. If you see an abnormal Babinski reflex then you can have more confidence that indeed there may be damage to an upper motor neuronal system. I want you to appreciate how the spasticity and the special science contrast with what we see with damage to lower motor neuron injuries. So with lower motor neuron injury, we see decreased reflexes. We see decreased muscle tone. And over time, we'll see muscle atrophy. In the early stages of injury, we'll see this abnormal activity of muscle fibers in motor units that we call fasciculations and fibrillations. With upper motor neuron injuries, we tend not to see such a loss of muscle structure and integrity. so there may be some atrophy due to not much use of the affected body regions. But the atrophy will not be nearly as severe as what is seen, over time, with damage to lower motor neurons and the loss of innervation of that muscle tissue. So, remember, with damage to upper motor neurons the muscle is still innervated. The problem is that, the output of lower motor neurons is no longer governed and regulated in a normal fashion. And that's why we see the emergence of these special signs. That's why we see the development of spasticity. It seems as though the aggregate effect of the descending projections, especially those that come from the reticulospinal connections is to suppress the gain and the tone of our segmental reflexes. So once that overall suppressive influence is lost with damage, let's say, to the spinal cord what we see below the level of injury is the emergence of higher gain in those segmental reflexes. And that's why there's increased muscle tone in hyperactive reflexes and perhaps that's why clonus emerges with the rhythmical beating of the extensors and flexor muscles. Now, one final point I would make here about upper motor neuronal damage is that the kind of movement that is especially affected is the fine volitional movement that expresses skill. And I hope this makes sense to you, I think I've been trying to emphasize that much of the motor cortex and the cortical spinal system is concerned with the expression of skill with the distal extremities. So, it would make some sense then if there is damage to the motor cortex that the greatest loss would be in the expression of skill, with our hands, with our feet, with our lower oral facial structures. Now, if one had damage limited to the upper motor neuron systems of the brain stem, then we might expect there to be problems with postural controls, specifically. and if there were sparing of, lets say, the pyramidal system, one might expect there to be residual activities that could be performed with the distal extremities. So one can have a neuro anatomical framework for interpreting specifically the signs and symptoms of upper motor neuron injuries that are observed in any given patient. Well, I'm going to conclude this extended tutorial at this point about upper motor neurons. The one topic that's relevant that we have not yet discussed in this tutorial concerns the anatomy of the descending projections. And its that topic that I'd like to turn to in our next tutorial we'll have a chance to actually see the connections in cross sections of the brain stem. And identify the location of our critical pathways for upper neural motor control of lower motor activity. So, I'll see you then, and look forward to having that anatomical discussion.