Workbook questions 5 - Motor lesions Flashcards
List five signs that distinguish upper / lower motor neurone lesions
Muscle Power - loss of voluntary control vs weakness
Muscle Tone - increased tone inc. ‘clasp knife’ and ‘cog wheel’ vs Flaccidity
Muscle Wasting - none vs wasting
Reflexes - Hyperreflexia vs hyporeflexia
Plantar response - Babinksi/ not
Give three other associated features of UMN lesion
- Drift of limbs. If the eyes are closed and the arms are held outstretched, the arm on the affected side will tend to drift downward.
This can be an important sign as it may appear before weakness is noted by the patient. This is known as Pronator Drift.
- Loss of abdominal reflexes. If the rectus muscles on one side are stroked the umbilicus “looks” to that side. In males the cremasteric reflex,
the elevation of the testis if the thigh is stroked, is also lost. - Sensory deficits involve quadrants or halves of the body.
Give three other associated features of LMN lesion
- Fasciculation seen as a faint quivering under
the skin from spontaneous contraction of motor units
as the nerve fibres degenerate. Fibrillation cannot be seen because it is the contraction of denervated individual muscle fibres caused by their increasing sensitivity to ACh. It is easily detected electromyographically. - Muscle contractures occur at the end stage of a LMN deficit as muscle cells are replaced by fibrous tissue.
- Associated sensory deficits are likely to have a peripheral nerve pattern.
What would be the consequence of a pure lesion of the cell body of the α-motoneurone a) acutely and b) chronically on the ability of the muscle to produce force? What disease(s) can give rise to this scenario?
Death of the cell body of an α-motoneurone will result in the muscle losing its neuronal innervation, hence all its ability to produce force both acutely and chronically. There will be no chance of recovery from this situation. In this regard, there is no difference between
the acute and chronic states.
Polio myelitis is a fitting example of a disease that selectively destroys α-motoneurone cell bodies. Limb muscles or those for respiration are equally vulnerable to this disease
What would be the consequence of a pure lesion of the axon of the α-motoneurone a) acutely and b) chronically on the ability of the muscle to produce force? What pathology is likely to result in this kind of scenario
Lesions of an axon of an α-motoneurone will result in the nerve dying and the muscle
losing its neural innervations, hence all its ability to produce force both acutely and chronically.
There will be no chance of recovery from this situation. In this regard, there is no difference between the acute and chronic states.
Presentational signs are exactly the same as those of
lesions affecting cell bodies. Any disease processes that selectively damage axons of α-
motoneurones will produce such an impairment of the motor system. The usual suspect in such a scenario has to be a complete transection of a peripheral nerve as a result of trauma to it.
Lesion of either cell bodies or axons of all α-motoneurones to a muscle result in
paralysis of that muscle. By what name is this kind of paralysis commonly known?
Flaccid paralysis
Imagine strong descending tonic synaptic inhibition on all α-motoneurones supplying a
muscle or limb. a) How will this affect the ability of that muscle to produce force? b) Under what physiological conditions does this scenario occur? c) What muscles are
exempt from this form of inhibition?
a) and b) α-motoneurones of all muscles of the body are said to be subject to constant and tonic inhibition from extrapyramidal descending (motor) system. Careful consideration of the physics
attending this subject predicts that motoneurones with large diameter cell bodies will be
relatively more severely inhibited than those with smaller diameter cell bodies.
As such ,when at rest, most α-motoneurones are under constant tonic inhibition, thus making them unable to
recruit their respective muscles, hence there is not much muscle force to speak of when muscles are at rest.
C) Muscles of respiration and those of extra-ocular muscles are not subject to the tonic descending inhibition from descending motor systems. The biggest benefit to be
derived from this arrangement is that when we are asleep, descending inhibition on the motor system is extremely heavy and leads to general paralysis of our bodies, however, our ability to
breathe whilst in deep sleep is not impaired. The rapid eye movements seen in REM sleep
explain this lack of descending inhibition to extra-ocular muscles. There are many debates as to the necessity of such movements.
Lesion of either cell bodies or axons of some but not all α-motoneurones to a muscle
result in partial paralysis of that muscle. How will this affect the ability of that muscle to produce maximum force?
This will result in reduction of maximum force production by the limb in question.
The severity of the resulting disability is quantified using the MRC scale for force production in which a score of 0 suggests complete paralysis (i.e.no force production at all) whilst that of 5 suggests that the muscle is able to produce maximum force that should be expected.
What would be the consequence of a pure lesion of either cell bodies or axons of α-motoneurones a) acutely and b) chronically on the appearance of the muscle they
supply?
a) There would be no obvious perceptible change in the appearance of the muscle soon after lesioning either cell bodies or axons of α-motoneurones
b) This is a little more involved and can be answered as follows (thorough treatment of the question):
Intermediate :The muscle will first exhibit spontaneous and continuous ripples referred to as fasciculations. It will also start to lose its bulk, though this could be subjective.
Long-term: The muscle will lose most of its bulk and the fasciculations will eventually
disappear as the muscle tissue dies through loss on neurotrophins that are normally produced by the nerve so as to keep the muscle tissue alive .
What is the explanation for the progressive changes that take place between acute and
chronic denervation of a muscle?
The denervated muscle up-regulates its production of nicotinic Ach receptors. These receptors are said to be super-sensitive and will detect minute amounts of Ach circulating in the blood
stream, (note that these Ach molecules would have escaped destruction by synaptic as well as
blood-borne circulating Ach-esterase). On being detected by these super-sensitive nicotinic receptors, these trace amounts of Ach produce unco-ordinated and random minute contractions of individual fascicles of the muscle, hence the fasciculations. The muscle will lose its bulk as a result of loss of trophic support which it receives from α-motoneurones supplying it.
Eventually, the muscle will die and only fat or connectivetissue would occupy the compartment of the
muscle.
Where would you expect to a find cell body of an α-motoneurone in the spinal cord and what would be the effect of directly activating it on a) muscle length and b) motor tone?
Cell bodies of α-motoneurones are found in the ventral horn of the grey matter of the spinal cord (lamina IX of Rexed)
a) Activating an α-motoneurone will result in shortening of the muscle it innervates, development of force and
b) an increase in the motor tone of the muscle in question
Where would you expect to find a cell body of a γ-motoneurones in the spinal cord and what would be the effect of directly activating it on a) muscle length and b) motor tone?
Cell bodies of γ-motoneurones are found in the ventral horn of the grey matter of the spinal cord (lamina IX of Rexed) intermingling with those of α-motoneurones
a) Activating γ-motoneurones will result in shortening of the intrafusal muscle fibres of the
muscle spindle sense organ it innervates. This in turn will result in opening of spiral endings of the sensory endings of the muscle spindle afferent on the intrafusal muscle fibre. Consequently,
this will result in activation of the muscle spindle afferent, and in turn, recruitment of the α— motoneurone via the stretch reflex. Activation of the stretch reflex will lead to activation of the muscle, hence shortening of its length. This long-loop pathway of activation of the muscle is
said to have occurred via the γ-loop.
b) Contraction of the muscle will result development of force and thus an increase in the motor tone of the muscle in question
Imagine a motor nucleus comprising of an equal mixture of cell bodies of α- and γ-motoneurones, what feature would help you to distinguish between these populations of
cells?
The motor nucleus of the grey matter of the spinal cord contains a mixture of cell bodies of α- and γ-motoneurones arranged topographically according to the muscles they supply in terms of flexors and extensors.
There is no way of telling them apart according to their topographical distribution within the spinal motor nucleus. The only distinguishing feature between them is that α-motoneurones tend to have large cell body diameters whilst γ-motoneurones have smaller
cell body diameters.
Imagine a motor nucleus comprising of an equal mixture of cell bodies of α- and γ-motoneurones, what would be the effect of a defined synaptic current impinging on it?
According to Ohm’s law, a defined excitatory synaptic input (current) to a motor nucleus will produce a large voltage change on a cell body with a smaller diameter than it would on a cell body with a larger diameter, hence lower cross-sectional resistance. Consequently, for a given
(fixed) synaptic current, smaller cell bodied motoneurones require less current and therefore, will be recruited earlier than their large cell-bodied equivalents which will require even more current before they are recruited.
What do you understand by the term “orderly recruitment” of motor units?
Taking the example of the upper limb, it is interesting to note that force development by the limb occurs on a continuously smooth scale, whereby the limb always starts by generating minimal
forces such as those required to lift a feather, followed by forces that will permit us to lift a pen and write with it, progressing to the sort of forces needed to lift a cup of tea, to lifting a brick and
finally “pumping iron” in the gymnasium. Thus, recruitment of motor units is always “orderly”, starting with motor units capable of only minimal forces and ending with motor units that generate the heaviest forces that the limb in question is capable of generating. This feature of
the motor system is explained by applying the principle of motoneurone recruitment-order based on cell body size
How useful is orderly recruitment of motor fibres in the physiological development of a) muscle or motor tone and b) muscle force?
Motor tone is generated by development of minimal forces by the smallest motor units
of the body. As it so happens, this minimal amount of motor tone is adequate to maintain ournormal posture. Given the small size of the motor units that generate motor tone (hence posture), the amount of energy required for this purpose is also minimal, thus making them less
liable to fatigue.
What is the sign of Babinski?
When the sole of the foot is stroked the normal response is to curl the toes in a plantar response. Following an upper motor neurone lesion this is replaced by an extension and fanning of the toes to give a dorsiflexion.
Which pathway is damaged in Parkinson’s Disease?
Parkinson’s disease is associated with the degeneration of cells in the substantia nigra, a collection of
melanin containing neurones in the midbrain, which secrete dopamine. These neurones project to the
putamen and pallidum (striatum) of the basal ganglia.
Normally dopamine exerts an excitatory influence upon neurones of the medial pallidal segment (the direct path) and an inhibitory effect upon cells in the lateral pallidal segment (the indirect pathway). Loss of
dopamine causes underactivity of the direct pathway and overactivity of the indirect pathway, which is
inhibitory upon the thalamus and cerebral cortex giving the hypokinetic symptoms of the disease.
