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olly

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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.
 
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part2


Spasticity is an increased in muscle tone that is detected during passive movement of the limbs. The muscles at rest do not have excessive tone but any brisk stretch of a muscle group (particularly the flexors in the upper extremity and the extensors in the lower extremity) will result in a "catch" at about midlength of the muscle followed by a sudden release of the catch and relaxation of the muscle. The last two components, the catch and release, have been likened to a closing pen knife, which is the origin of the term "clasp-knife" spasticity. The overactive muscle stretch reflexes that are resonsible for spasticity are also the mechanism behind the hyperactive deep-tendon reflexes. The giving away or release portion of the clasp-knife phenomenon is presumed to be caused by increased firing of the inhibitory Golgi tendon organs, which produce an overactive reflex that inhibits the muscle.

If the lesion extends beyond the confines of the traditional corticospinal path, more descending pathways are involved and a greater degree of spasticity is noted; there also is a poorer recovery from weakness. This is presumably because of loss of more inhibitory influences on the segmental reflex arc and loss of more facilitatory influences on the motor neuron effector systems.

After very acute lesions of the descending motor systems there is often initial flaccid weakness that is sometimes followed by stereotyped movements and postures (decorticate posture, decerebrate posture or generalized withdrawal reactions)(Fig. 10-1). Acute destructive lesions of the descending motor pathways cause a transient shock state of flaccid paralysis with loss of reflexes. When progressively greater amounts of the descending pathways are involved, a longer period of shock ensues. Acute cortical destruction may result in only hours to days of shock, whereas acute transection of the spinal cord can cause a shock state that persists for many weeks to months before spastic hyperreflexia and rudimentary spinal reflex behavior return. The precise pathophysiology of spinal shock is not clear, but it may complicate the evaluation of the patient following acute injury. It is always difficult to predict the final extent of the neurological injury in the setting of shock. Chronic or slowly progressive destruction of the descending motor pathways is not associated with a shock state. Presumably, this is because compensatory reorganization of the motor function occurs in equal pace with the losses.

Lesions that extensively destroy the cerebral cortex and basal ganglia, and preserve at least some of the diencephalon (like those caused by severe hypoxia) may result in stereotyped motor responses that involve flexion of the upper extremities and extension of the lower extremities. Noxious stimulation is usually necessary to elicit this reflex activity, which has been called decorticate posturing (Fig. 10-1). It has been thought, on the basis of experimental data, that release of the rubrospinal motor system is, at least in part, responsible for decorticate posturing.

Transection of the brain stem, for example by stroke, at the level of the midbrain or pons is followed after a period of neuraxis shock by severe spasticity and reflex extension and pronation of the upper extremities with extension of the lower extremities and trunk on noxious stimulation (see Fig. 10-1). This response is called decerebrate posturing and depends on preservation of the vestibular nuclei in the caudal brain stem, with the extension being produced by vestibulospinal pathways.

Lesions transecting the lowest portion of the brain stem or the upper spinal cord result in quadriplegia and severe spasticity after a period of shock. Later in the clinical course, reflex flexion movements of the limbs can be elicited by noxious stimulation (see Fig. 10-1). These probably represent primitive spinal withdrawal responses.

As a rule, UMN lesions affect large areas of the body below the level of injury. It is often difficult to localize the specific level of damage by the pattern of weakness. Associated neurologic findings may clarify the level. For example, cranial nerve involvement or involvement of nerves or nerve roots may indicate a brain stem or spinal cord level of involvement, respectively, while cortical findings such as language difficulties, visual field abnormalities, dyspraxias, or other disorders of higher integrative function suggest cortical damage. In most UMN lesions, the whole side of the body below the lesion is affected (hemiparesis or hemiplegia). However, in the cerebral cortex the motor representation for the arm, face, and trunk lie within the supply of the middle cerebral artery, whereas the leg lies within the distribution of the anterior cerebral artery (Fig. 10-2). Loss of middle cerebral cortical perfusion therefore causes a greater degree of weakness of the upper extremity than of the lower extremity. Occlusion of the anterior cerebral artery, an uncommon event, is associated with greater weakness in the leg than in the arm.

Because sensory and motor systems are near one another through the spinal cord, most of the brain stem and the cerebral hemispheres, it is common to have some sensory as well as motor symptoms. The sensory abnormality (see Chapt. 9) may help localize the lesion. Pure involvement of UMNs without any sensory damage is most often seen with small lesions (usually vascular) in the posterior limb of the internal capsule or in the base of the pons
 
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Olly, interesting information, but it appears to be referring to acute upper motor neuron lesions, such as stroke, rather than slowly progressive chronic assault of UMN such as PLS.
Just making it clear in case someone reads it and thinks that the recovery is referring to a chronic disorder.
 
hi aly,its actual an article on examining the motor sysyem.........will post site.

if your corrct i did find that some of the information is very consistant with umn desease.
from all the years of information i have gathered and how umn desease effects each person individualy depends on where and to what degree of damage there is.

for instance,damage can be hemifocal/one side or both.
there maybe incomplete lesions or severe acute leading to spinal shock..........while minor incomplete lesions do produce typical umn signs in the case of an acute lesion producing spinal shock there would be con tradictory signs..........this happend to me which produced hypotonia in the left lower leg

http://www.dartmouth.edu/~dons/part_1/chapter_10.html
 
So--if I'm reading this right, then I should only have a positive Babinski and hyper reflexes on one side? Then I'm more confused than ever--because mine are in both--as is the spasticity.

I'm still confused about muscle tone--because the muscle tone in my legs looks much better than it should, I think--they are very tense at all times. My 28 yo daughter's legs have more 'flab' stuff than mine--and I'm at least 50 lbs overweight.

Think I'll come read this again when I can assimilate it a little more.
 
Patty. I started off with just one side showing clinical spasticity, now it's on both sides, so either or.
I have negative babinski bilaterally, but positive pathological reflexes and spastic catches. My most affected side clinically is the least symptomatic side. It's just all weird and poorly understood by the Doctors.

I am not sure I understand your comment about what you expect your muscle tone to look like? UMN signs often cause hypertonia rather than hypotonia.

I am confused all the time and my Hubby never agrees with anything much my Doctor says, proof that they don't know squat, lol, better not have him know that.
 
Caroline, thank you for posting this study. I appreciate how you manage to come up with so much good material!
 
Definitely--thank you for posting this Olly. I think my brain is defective today. I am usually pretty good understanding medical speak!

Aly--I thought olly's article mentioned hypotonia--and I thought my issues were UMN=-so did the doc--but I don't have hypotonia in my legs---they are like lead they are so stiff and hard (the muscles) all the time. Makes walking look like a duck waddling or something. The only thing all 3 docs I've seen agree on is that I shouldn't be walking unaided.
 
That would probably be clinical hypertonia then

Patty, my brain just can't get a grip of medical stuff I read. It's the same with bibleverses, short term memory etc. It drives me crazy as I don't understand why. I missed my plane to USA by 4 hours. It's upsetting and rather scary. :(
 
Aly--if you take Neurontin--it's FAMOUS for killing sort term memory. It destroyed mine years ago. I wouldn't give that drug to my worst enemy. They prescribed it for my trigeminal neuralgia.

It caused massive swelling in my legs--to the point I was unable to walk at all--and I was getting lost driving to the grocery store. I still have horrid short term memory--but it improved drastically when I stopped the Neurontin--can't remember it's generic name. Gab something or another.
 
I has it years ago for my epilepsy. Limotrigine was way worse, now I am on tegretol again. It is probably what causes me not to store information very well. I have TLE, which is notorious for causing memory stuff, but seems to be worse.

When I was going through customs in LA, I was asked when I last came to USA. Took mw a while to remember I went to Hawaii earlier in the year, what month......no idea, for how long.........couldn't remember. I look nothing like my passport photo, so took them awhile to let me in. Arghhhhhh

Gabapentin. Hubby's good at epilepsy so I have tried all the new stuff, ended up back on the old, cheap drug, figures
 
Great news ladies! I've been taking gabapentin since July for the random muscle cramping I'd been getting. My regular neuro had given me Baclofen, but I really couldn't tell any difference with it. The gabapentin does seem to help. I can turn and make all sorts of movements without getting a cramping pain that halts me mid-move. Makes turning or shifting positions possible. I'll have to be on the lookout for memory issues. Hummm, my caretaker may already be seeing signs!
 
What was that Deb, I have forgotten already. :0
 
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