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Showing posts with label Physiology. Show all posts
Showing posts with label Physiology. Show all posts

Sunday, September 3, 2017

Difference between UMN and LMN lesion: Physiology



UMN
LMN
Bulk
Normal till disuse atrophy
Prominent weakness and atrophy occurs early
Tone
Increased
Except in spinal shock where tone will be flaccid and recovers in around 2 weeks
Always HYPOTONIA
Power
Reduced, tends towards normal over period of time if adequate stimulation maintained
Severely decreased
Abnormal movement
Fasciculation are not usually seen
Fasciculation is due to degenerative process in anterior horn cell
Reflexes
Brisk
Decreased to absent

Plantar/ Babiknsi
Up going
Downgoing


The most important thing to know is the intactness of the muscle stretch reflex. The tone is maintained under the influence of gamma motor neuron by the alpha motor neuron and the bulk and power is the pure function alpha motor neuron. The reflex is complete if its loop is complete.
alpha motor neuron , gamma motor neuron, corticospinal tract muscle spindle, extrafusal, intrafusal muscle fibre
Muscle Reflex arc
Upper Motor Neuron lesions are the lesion occurring anywhere in the central nervous system from the brain upto the spinal cord before the alpha motor neurons arise from the spinal cord. The lesion could arise from the cerebral cortex, internal capsule, midbrain, pons, medulla and the cortico spinal tract in the spinal cord. The lesions can be anything from vascular, traumatic, degenerative, and inflammatory to infective.

The lesions occurring after the alpha motor neuron accounts for the lower motor neuron lesions. The lesions could arise in the nucleus of alpha motor neuron (Polio myelitis, Amylotrophic lateral Sclerosis, brown sequard syndrome), Lesions in the nerve (Traumatic resection, entrapement, neuritis), Lesion in the NMJ (Myasthenia gravis, Lambert Eaton Syndrome) and the muscle (Duchenne Muscular Dystrophy, Beckers Muscular Dystrophy )itself.

The two principle that determine the features of upper motor and lower motor neuron include the completeness of muscle reflex arc and the higher motor control over it.
The motor reflex arc consists of the Ia fibres carrying the signal from muscle spindle which prevents the excessive stretch of muscle by contracting it. The afferent fibres mono synaptically fires the alpha motor neurons at the anterior horn and causes the muscle contraction. This reflexes is controlled further by higher centre and is thus there is an inhibitory mediatory released via an intermediate neuron coming from the corticospinal tract. If this closed loop of nerve are intact the muscle tendon reflex is intact and so is the deep tendon reflex which is elicited using reflex hammer.
The tone is the inherent state of contraction of muscles to maintain the posture of the body. It is in medicated by the Gamma motor neuron coming together wit alpha motor neuron and innervates the intrafusal fibres of muscle spindle and thus increases the sensitivity of change in length of the muscle. It is also directly innervated from the corticospinal tract and thus is affected in response to UMN lesion.  Along with that the gamma motor neurons are spontaneously firing and thus influence the sensitivity of alpha motor neurons and thus affect the tone.

In lower motor neuron lesion, the alpha motor neuron and distal is injured. So the loop can not be complete and hence no reflex contraction of muscle in response to stretch of muscle spindle receptor. In upper motor neuron lesion, the higher inhibition over the reflex arc is lost. This causes the excessive firing from alpha motor neuron and hence exaggerated deep tendon reflex.
The lower motor neurone lesion will develop flaccid paralysis because there is no innervation to muscle fibre to cause its contraction and hence they easily go into disuse atrophy early and the bulk is reduced. Contrary to the Upper motor neuron lesion where the higher control of the muscle is lost but still the muscle can be contracted locally. So, constant use of muscle via passive movement can preserve the bulk of the muscle.

The tone in upper motor neuron lesion is exaggerated because the supraspinous modulation over the gamma motor neuron is lost and they are firing spontaneously.  This increases the tone of the muscle with increases sensitivity of muscle spindle to passive stretch and increased firing in the Ia fibres. This increased firing induces increased firing in alpha motor neuron and increased contraction.The tone is higher in the antigravity muscle and hence clasp knife rigidity is due to the greater bulk of the antigravity muscles and hence the paralysis is spastic type in upper motor neuron lesion.

However, in the lower motor neuron lesion , again the same nerve that complete the muscle reflex is incomplete and hence the normal tone is present due to absence of innervation in the muscle to bring about the contraction and hence the tone is flaccid and hence the paralysis flaccid paralysis.

In LMN lesion, the muscle become hypersensitive to neurotransmitter as it is denervated. Similarly the damaged lower motor erratically discharges the neurotransmitter stored within itself as the neuron degrades. So, both increased hypersensitivity and erratic release of neurotransmitter causes fasciculations. However, in UMN lesion, there is regular firing to prevent the atrophy of muscles.

Learn about Cranial nerve examinations 

Upper Motor neuron , Lower motor neuron, differnence
Difference between UMN and  LMN lesion in tabulated form.



Tuesday, August 22, 2017

Physiology behind Rigor Mortis

Rigor Mortis/ Postmortem Rigidity is the state of contracture that develops several hours after the death of the individual. In this condition the muscle contract and become rigid even in the absence of action potential.

The basic physiology of muscle contraction include (the numbering may not coincide with the image given below)
           In a resting muscle, Tropo-myosin covers the actin’s binding site for myosin.
2         When cytosolic calcium increases after the opening of Sarcoplasmic Ca++ channel following the        action potential, Free calcium binds with the Troponin –C.
3         Calcium binding to Troponin C exposes the Mysoin- Binding site in the actin.
4         The binding of actin and Mysoin occurs and  Myosin pulls the actin towards itself producing              active tension. ATP is not needed for Cross bridge linking.
5         The dissociation of actin and myosin is energy dependent. ATP is needed for this release of actin        myosin bond.
           Once the dissociation occurs, the ATP is hydrolysed to form ADP and Inorganic phosphate and the      myosin is put back to the high energy state with high affinity for actin being ready for next cycle       of cross bridging.

Diagramtic represenatation of skeletal musle contraction.
Steps of Skeletal Muscle contraction
Source:http://studylib.net/doc/9410005/steps-of-a-muscle-contraction



Lets us take a special Consideration on the point no 5 (not from diagram). The release of actin from myosin needs ATP is the most important thing to describe physiology of post mortem rigidity.

Immediately after the death, the inherent tone of the muscle is lost and the initial state of flaccidity is seen known as the stage of Primary Flaccidity. In this stage, the somatic death has occurred but not the cellular death. So, the cell responds to electrochemical stimuli.

Once death occurs at the cellular level, the membrane permeability to all ions are disrupted and large amount of calcium is released from the sarcoplasmic reticulum causing the binding of actin and myosin which brings about the contraction. This is the stage of Rigor Mortis and the cells no longer respond to electro-chemical stimuli.

The separation of actin from myosin need ATP which is depleted once the cell dies. So they cannot separate and hence the muscle remains contracted.

After several hours of death, the autolytic enzyme released from the lysosomes gradually degrade all the proteins including actin and myosin causing the loss of stiifness after 15-20 hours. And hence the stage of Secondary Flacidity develops.