UMN lesion and LMN lesions

- Saroj kumar jha

13-Nov-15

Mass of muscle: Actually the motor nerves always secrete small amount

of neurotransmitters at NMJ that acts as trophic stimulators (growth factors) for

muscle bundle supplied by that nerve. In case of LMN lesion, the alpha motor

neurons fail to release Ach at NMJ so the muscle mass gradually reduces. This is

called Denervation atrophy. Also Disuse atrophy is there due to lack of innervations.

But the case is not the same with UMN lesion where the lower motor neuron(alpha

motor neuron) is intact and secretes Ach at NMJ that maintains the mass of muscle.

So the mass of muscle in case of UMN is not reduced so much as compared to LMN

lesion. But Disuse atrophy is there also in UMN lesion .

Tone of muscle: Tone of muscle is maintained by the intactness of gamma

motor neuron which is a component of lower motor neuron. In case of LMN lesion,

the supply of gamma motor efferent to muscle spindle is cut, so it results in reduced

afferent signals(gamma afferent) from gamma afferent to alpha motor neurons that

results in decreased tone of the muscle. The point to be noted here is: Even if the

gaama afferent is correct the alpha motor neuron cannot fire for the contraction of

muscle that results in hpotonia or flaccidity. But in case of UMN lesion, the gamma

afferent and efferent is all intact along with alpha motor neurons. Also, there is no

inhibitory influence from upper motor neuron to alpha motor neuron which results

in overfiring and ultimately hypertonia or rigidity results.

Tendon reflex: Areflexia or Hyporeflexia in case of LMN lesion due to less

firing of gamma afferents, gamma efferents and alpha motor neurons. But in case of

UMN lesion, there is over firing of gamma afferents, gamma efferents and alpha

motor neurons due to inhibition of inhibitory supply from UMN that results in

Hyperreflexia. Clonus may be present. i.e. slight stretch in tendon may produce

exaggerated reflex response due to over firing.

Power of muscle: Power of muscle is highly reduced in case of LMN

lesion due to damage in LMN that is due to reduced firing of LMN. But in case of

UMN lesion, the LMN can efficiently fire so the power is maintained but reduced

slightly as there ia loss in control from UMN.

Babinski reflex: This reflex is by the influence of UMN. Normally when

there is scratch on the lateral border of sole of foot, there is withdrawl reflex i.e.

there is dorsiflexion. In case of UMN lesion, there is plantarflexion and fanning of

toes. This case is also seen in babies without UMN lesion, due to incomplete

development of UMN in terms of myelination. There is reversal of spinal reflex i.e.

there is strong plantarflexion that leads the baby to learn and start walking. While

walking due to plantar flexion the baby is able to stand. Otherwise, due to normal

withdrawl reflex the baby would fall each time he/she takes his/her foot onto the

ground. In case of LMN lesion these signs Babinski’s sign are simply absent.

Note: i)Tone is the resistance felt when flexion or extension is produced.

ii)Spasticity is special case of hypertonia/rigidity in which there is phenomenon of

clasp-knifing i.e. sudden loss of rigidity while performing flexion and/or extension. In

case of UMN lesion, ther is rigidity felt when extending forearm due to over function

of gamma afferents, muscle spindle stretch reflex. But the resistance is lost when the

Golgi tendon organ is stimulated due to tremendous increasing in tension in a

tendon while extending the forearm. Hence clasp knife reaction is due to switch of

muscle spindle reflex to golgi tendon organ reflex.

iii)Lead pipe rigidity: mainly seen in parkinsons disease due to degeneration of

nigrostriatal pathway which leads to interruption of inhibition to alpha motor

neurons by extrapyramidal tract. Since, extrapyramidal tract response is less( i.e. due

to slightlt less inhibition, there is slightly more overfiring, there is not so severe

rigidity that would lead to activation of golgi tendon organ. So, there is continuous

rigidity in flexing or extending unlike clasp-knife relex i.e. the resistant in constant as

is when we try to bend a lead pipe.

iv) Cog wheel rigidity: lead pipe rigidity + tremors i.e. rigidity intervened by tremors.

Fasciculation and Fibrillation: Absent in UMN lesion and present in LMN

lesion. Whem you tap muscle mechanically, muscles show some involuntary

contractions called as fasciculation, and the same phenomenon when

demonstrated electrically is called fibrillation.

When a nerve is cut(LMN lesion) and a particular target cell loses all its Ach

signaling, the cell nuclear machinery thinks that there is less receptor and it

synthesizes more no of receptors. Due to more no of receptors slight tapping

of muscle mechanically stimulates the wide no receptors and action potential

is generated that results in fasciculation and if this is detected only

electrically it is called fibrillation. This oversensitivity of muscle is called

Denervation hypersensitivity. But this is absent in case of UMN lesion

because in this case the lower motor neuron fires continuously and ther is no

increase in no of receptors , so no hypersensitivity and no fasciculation an

dfibrillatin in case of UMN lesion because slight tapping of muscle opens only

small no of receptors incapable of firing to threshold and subsequent muscle

contraction.

THANK YOU!