Workbook questions 5 - Motor lesions Flashcards Preview

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Flashcards in Workbook questions 5 - Motor lesions Deck (45):

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

1. 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.

2. 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.

3. Sensory deficits involve quadrants or halves of the body.


Give three other associated features of LMN lesion

1. 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.

2. Muscle contractures occur at the end stage of a LMN deficit as muscle cells are replaced by fibrous tissue.

3. 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 ( 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

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


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

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.


What structures are damaged to give a chorea?

Choreiform movements e.g. hemiballismus arise because neurones in the indirect pathway of the basal
ganglia are damaged in some way, so that the direct pathway is fully expressed.

The usual deficit is due to a
lesion in the sub-thalamus which leads to a disinhibition of the thalamus and high activity in the cortex
leading to the abnormal movement.

In Huntington's disease an inherited disorder (autosomic dominant) of the synaptic connections between the
striatum and the subthalamic nucleus disrupt the indirect pathway.


What would be the effect of giving a drug like levodopa to a patient with a chorea? Explain your answer?

The symptoms of a chorea arise because the direct pathway becomes overactive so that the thalamic motor
nuclei are disinhibited giving excessive activation of the motor cortex.

Giving these patients the precursors of dopamine would make the situation worse by increasing the activity in the direct and reducing activity in
the indirect pathways


Parkinson’s Disease is a common motor disorder with a characteristic clinical profile of florid presentational
features. List these

Hypertonia - Gross hypertonia - rigidity or the resistance to passive movement is a characteristic feature of the disorder. The resistance is felt throughout the range of movement typically with ratchet like interruptions
described as cog-wheel rigidity.

Hypokinesia - i.e. slowness of voluntary movement and reduction of automatic movement e.g. arm swinging on walking, is the major feature of Parkinsonism. It is demonstrated in slowness of voluntary movement such as finger pinching, wrist turning or rapid toe tapping.

Coordination - Co-ordination of movement is preserved but hypokinesia should not be
confused with a lack of co-ordination.

Facies - The patients face is relatively immobile - mask like - with widened palpebral fissures (eyes wide open) and infrequent blinking.

Tremor - Resting 'pill rolling' tremor which gets worse with stress (counting
backwards) but often improves during voluntary movement.

Gait & Posture - Patients find it difficult to get up from a chair and tend to adopt a flexed
posture on standing. They find it difficult to start walking and take small steps (festinating gait) with reduced arm swinging. They are unsteady
on changing direction and find it difficult to stop


In most typical cases of Parkinson’s Disease, would you expect the patient to be affected on one or both sides of the brain? If only one side is affected how would you know fromexamination of the limbs?

The basal ganglia affect motor commands which descend in the corticospinal and rubrospinal tracts.

These tracts cross over in the tegmentum (rubrospinal) and in the medulla (corticospinal) to affect muscles on the contralateral side. Although the effects of basal ganglion dysfunction are bilateral initially they often show on the contralteral side.

At onset, this disease tends to be characterised by unilateral tremor at rest, cogwheel rigidity, hypertonia, bradykinesia and a shuffling gait.


How is Parkinson’s disease usually treated?

There are currently two options for the management of Parkinson’s Disease and these are pharmaco-therapy or surgical. The first line of approach is pharmacologically-based and the aim here being to treat motor symptoms. The first-line drug used here is Levodopa (L-Dopa). There are
dopamine agonists and Monoamine Oxidase Inhibitors (MAO-B) Parkinson's is treated by the oral administration of Levodopa the precursor of dopamine, the neurotransmitter lost. In severe cases the improvement may be dramatic


What are the side effects of long term treatment?

Levodopa does not halt the progression of the disease. Although at first it may alleviate the symptoms ultimately it fails as the disease proceeds.
After about two years 'Levodopa induced dyskinesia' - involuntary choreic - movements may appear. These can be controlled by reduction of the drug dose but the hypertonia may reappear


What new approach to treatment is being developed to overcome the condition?

There is currently a lot of progress in treating severe forms of Parkinsonian patients with deep brain stimulation in brainstem regions that include the subthalamic nucleus. This remains experimental

Stem-cell therapy - i.e. the insertion of basal ganglionic stem cells


What form of poisoning could lead to Parkinson's disease?

Drugs-induced Parkinson syndrome: certain antipsychotic drugs e.g. haloperidol thioridazine

Toxins- Carbon monoxide poisoning may lead to mental impairment (possibly as a consequence of
the hypoxia). Residual Parkinson symptoms are seen on recovery


Features of Cerebellar Ataxia

Nystagmus - Nystagmus is common in cerebellar ataxia and when present can
indicate the site of the lesion in the cerebellum

Coordination - Cerebellar ataxia is associated with poor coordination. Other signs of incoordination are seen in (1) the amplitude of
movement so that a limb may overshoot its target (dysmetria or past
pointing). In (2) difficulty in performing fine repetitive movements such
as finger pinching, wrist turning or toe tapping (dysdiadochokinesis).
Fine co-ordination is particularly affected.

Dysarthria - Speech is slow and monotonous and patients find difficulty in repeated
sounds (scanning dysarthria)

Tremor - Resting tremor is not a feature of this disease, however an intention
tremor is seen when performing a task when movements are
decomposed into a succession of separate movements rather than
one smooth act.

Hypotonia - Hypotonia is common in cerebellar ataxia and is seen in defective
posture maintenance, when patients may be unable to stand with the
feet together. If the problems affect the vestibular centres of the cerebellum they may fall over if they close their eyes.
The limbs are floppy and easily displaced by a relatively small force. Tendon tapping may lead to several oscillations of the limb

Gait and posture - The patient walks with a broad based staggering gait and is
unbalanced if asked to walk 'heel to toe'. The arm swing on walking
may be increased.


What does the inability to perform repeated movements of the hands, or tongue/mouth tell you about the function of the cerebellum in motor control

The cerebellum matches motor output with motor intention and corrects any errors. If this function is lost, any error in motor performance is not corrected and can get worse and worse as the movement is repeated


Why is it more difficult for the patient to balance when he closes his eyes?

Damage to the vestibular centres in the cerebellum can be over-ridden by visual inputs. Losing these by
closing the eyes causes the patient to lose balance. A positive Romberg sign.


Does the patient tend to fall towards or away from the side of his lesion? Answer this
question with reference to the vestibulospinal tracts.

The vestibulospinal tracts which descend ipsilaterally receive input from the vestibular system and from the
cerebellum, to affect postural muscles. Cerebellar damage leads to postural loss on the same side as the
lesion - patient falls toward the lesion.


In what keyways does the movement impairment of Parkinson’s disease differ from that of cerebellar ataxia?

Parkinson's disease appears as a problem of motor planning and initiation. Patients show a hypertonicity and resting tremor, both of which disappear when movement is initiated.

Cerebellar ataxia is a problem of the execution of movement. The tremor is intentional seen only during the


What does the presence of a resting tremor in Parkinsonism and an intention tremor in
cerebellar ataxia tell you about the role of the basal ganglia and the cerebellum in the planning and the precise execution of movement?

Basal ganglia are in the planning circuits - resting tremor -difficult to execute movements etc. tremor
disappears or gets better once movement begins. Cerebellar ataxia gives difficulty of execution - past pointing, intention tremor etc.


For a patient with a complete transection of the
spinal cord at A (T11 six months earlier).

Is sensation around the umbilicus lost?

No - Remember that the lower thoracic dermatomes
slope downward. The umbilicus is innervated from


For a patient with a complete transection of the
spinal cord at A (T11 six months earlier).

The patellar reflex is: WEAK /

Exaggerated - a typical UMN response because
their spinal segment (L3/4) is below the lesion.


For a patient with a complete transection of the
spinal cord at A (T11 six months earlier).

Muscle tone in the arms is FLACCID /

Muscle tone in the arms will be normal because
their spinal segments (C5 - T1) are above the lesion


For a patient with a complete transection of the
spinal cord at A (T11 six months earlier).

Muscle tone in the legs is FLACCID /



For a patient with a complete transection of the
spinal cord at A (T11 six months earlier).

Co-ordination in the legs would be -

Untestable because voluntary movement is lost.


For a patient with a complete transection of the
spinal cord at A (T11 six months earlier).

Lightly stroking the sole of the foot with e.g.a key would cause the great toe to

Dorsiflex in a typical Babinski response


This person has cervical arthritis. Explain the where and how of the likely nerve injury.

How might this injury be treated?

The spinal nerves emerge between vertebrae close to the apophyseal joints which will be enlarged and
encroach on the intervertebral foramina to compress the nerves.

A cervical collar is used to limit movement.


A patient when 15 years old, presented with a mild slurring of her speech which
resolved itself without treatment. When she was in early pregnancy – aged 21 – she awoke one morning to find herself blind in her right eye. The next day she was experiencing tingling in the left side of her face, difficulty in swallowing, and her speech was again slurred. In addition, she developed weakness numbness and hypereflexia of the right leg, which gave a positive Babinski sign.

Can these symptoms and signs be explained by a single neurological lesion? Comment on the nature of the disorder and her future.

A lesion which would give these signs would have to involve her visual pathways and other sensory pathways (e.g of CN V), the motor pathways (CN. X,XI & XII) in the head and her long tracts (corticospinal tracts). This is an unlikely to be due to a single lesion. Scattered neurological signs are typical of a
demyelinating disorder where patches of damage occur.

In patients where the neurological signs & symptoms do not point to an isolated lesion multiple sclerosis is normally the explanation.

In multiple sclerosis patients show remission and may go many years between attacks. Each attack, however, leaves some disability, which compound to lead ultimately to severe disability.


What does the sudden appearance of neurological signs suggest (right sided hemiplegia following a cerebral

A stroke. Stroke is the sudden onset of neurological signs that persist for more than 24 hours. (If they
resolve sooner than this the tern transient ischaemic attack (TIA) is used). Strokes arise from some kind ofcerebral vascular event that leads to ischaemia – either thrombosis or an embolism


In a man with right sided hemipledia - "The right arm would suddenly and aimlessly be throw about knocking over anything in its path."

What structures have been affected in this patient?

What is this condition called?

The contralateral subthalamic nucleus.

A chorea of this kind arises because the indirect pathway of the basal ganglia, which passes through the subthalamic nucleus is disturbed.

Hemiballismus – a unilateral chorea.


Which specific brain site must damaged in a parkinsonian type presentation?

The basal ganglia, specifically cells within the substantia nigra, the globus pallidus and putamen of the
direct route within the basal ganglia


In a hypokinetic movement disorder with the pattern Parkinsons disease (as the result of hypoxia from CO poisoning) - will the disorder progress?

Probably not.

Classical Parkinsons is progressive as cells in the substantial nigra continue to die. The Parkinsonian
features of poisoning arise from an isolated event and are unlikely to be progressive..

Interestingly whilst classical Parkinsons is treated with L-dopa. These patients are not improved by Ldopa
suggesting that the damage is different


Why might the hyperbaric oxygen treatment have limited the damage in CO poisoning?

The CO bound to haemoglobin is only slowly replaced by O2 at normal partial pressures. Increasing
the pressure to 3x atmosphere shortens the duration of tissue anoxia by displacing the CO much more quickly
so reducing hypoxic injury.