axon reflex

8/3/2019 Axon Reflex

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AXON REFLEXES:


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A reflex is an involuntary, immediate, automatic andstereotyped response to a specific sensory stimulation.

Sir Thomas Lewiss explanation of the flare component of

the triple response.

This response, consisting sequentially of the red line,flare, and wheal, can readily be produced by scratchingthe skin with a blunted point.


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According to Lewis, the flare was due to dilatation ofneighboring arterioles, this in turn having been triggeredby a local nervous system.


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Reflex arc

There is a sensory receptor at the starting point of reflexarc, an effector at the final point and an integration centerbetween them.

An afferent pathway connects the sensory receptor to theintegration center. An efferent pathway connects theintegration center to the effector. There is one or moresynapses in a reflex arc.

Sensory receptors and neurons:

Sensory neurons which transmit impulses toward thecentral nervous system from sensory receptors.

Central process is known as central branch, axonalbranch, central axon and axon.


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Peripheral process is also known as peripheral branch,dendritic branch, peripheral axon, and dendrit.

When a sensory receptor is stimulated it initiates a signalthat is carried to the central nervous system by processes

of sensory neurons.Physiopathology:

It is included in physiopathological processes fromregulation of skin blood flow and sweating to inflammation

and pain, from itch to asthma bronchiale and allergicrhinitis.

It is proposed that axon reflexes are responsible fromsome effects of acupuncture which is a complementarytechnique for analgesia.


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The effect of axon reflex to skin blood vessels ismonitored measuring the skin blood flow by laser doppler.

Axon reflex test are useful for monitoring the effects ofaxon reflexes on sweat glands.

Measurements of effects of axon reflexes are importantfor neuropathies like as pre-diabetic and diabeticneuropathy.


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Clinical importance:

Axon reflex mechanism therapy is effective for itch andpain.

Axon reflex mechanism is important for physiopathologyof allergic rhinitis and sinusitis & inflammation.

In bronchial asthma release of sensory neuropeptidessuch as substance P, neurokinin A, and calcitonin gene-related peptide are potent inducers of airway smoothmuscle contraction, bronchial oedema, extravasation ofplasma, mucus hypersecretion, and possibly inflammatorycell infiltration and secretion by axon reflex mechaism.


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REPETITIVE NERVESTIMULATION


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INTRODUCTION:

Nerve stimulation techniques as tests for neuromusculartransmission.

It began with Jolly (1895) who applied faradic currentrepeatedly at short intervals by using a kymographicrecording and visual inspection of skin displacement.

He found that the size of the muscle responsedeteriorated rapidly in patients with myasthenia gravisduring the faradization.

His equipment consisted of a double-coil stimulatorcapable of eliciting only submaximal responses and amechanical, rather than electrical, recorder.


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Regardless of the cause, the end plate potentials thatoccur in the muscle fibers are mostly too weak tostimulate the muscle fibers in myasthenia gravis.

Faradic current failed to elicit a response in the volitionallyfatigued muscle prior to testing. Conversely, afterfaradization, muscle responded poorly to subsequentvolitional contraction.

Based on these findings, he concluded that the

myasthenics had motor failure of the peripheral, ratherthan central, nervous system.


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The use of supermaximal stimulation and the recording ofthe muscle action potential have increased the reliabilityand sensitivity of nerve stimulation techniquesconsiderably.

Later studies have established optimal frequency ofstimulation, proper control of temperature, appropriateselection of muscles, and various activation procedures to

enhance an neuromuscular block.


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Microelectrode studies provide direct recording of end-plate potentials from Muscle

Other electrophysiologic methods assess theneuromuscular junction only indirectly.

such an approach allows quantitation of the motor

response to paired stimuli, tetanic contraction, orrepetitive stimulation at fast and slow rates


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Use:

Transmission defects affect a variety of disease states,such as

myasthenia gravis,

myasthenic syndromes, botulism,

amyotrophic lateral sclerosis,

poliomyelitis,

and multiple sclerosis.


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METHODS ANDTECHNICAL FACTORSBelly-Tendon Recording

Belly-tendon recording consists ofstimulating the nerve with supramaximal intensity andrecording the muscle action potential with the activeelectrode (G1) placed over the motor point and thereference electrode (G2) on the tendon.


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The initially negative potential thus recorded representsthe summated electrical activity from the entire musclefiber population, discharging relatively synchronously.

The area under the negative phase changes primarily withthe number of muscle fibers activated. The magnitude ofthe unit discharge from individual muscle fibers also altersthe size of the compound muscle potential, especially inmyogenic disorders.


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Movement-Induced Artifacts

Movement-related artifacts abound during repetitivestimulation of the nerve.

The recording electrode may continuously slide awayfrom the muscle belly, or the stimulating electrodes maygradually slip from the nerve, causing subthresholdactivation.


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Changes in limb position and the spatial relationship ofmuscle and recording electrodes, does alteration inamplitude of the recorded response

Firm immobilization of the limb together with visualinspection of the contracting muscle under studyminimizes the movement induced variability.


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Alteration in thumb position from abd to add. after each shockgave rise to a smooth reduction in amplitude with concomitantincrease in duration of successive potentials. The area under thewaveform showed relatively little change from the 1st to the 5th

response.


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Artifacts cause abrupt, irregular changes in the amplitudeor shape of the evoked response.

Some movement artifacts, however, induce a smooth,progressive alteration of amplitude that closely mimics themyasthenic response.

Nevertheless, close scrutiny often disclosesaccompanying changes in duration or other aspects ofWaveform.


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Temperature and Other Factors

Exposure to warm sunlight may precipitate ptosis anddiplopia in myasthenic patients.

Similarly, electrophysiologic abnormalities of weakmuscles may appear only after local warming.

Physiologic mechanisms that account for the improvedneuromuscular transmission with cooling include-

1. Facilitated transmitter replacement in the presynapticterminal


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2. reduced amount of transmitter release at theneuromuscular junction by the first of a train of impulses,leaving more quanta available for subsequent stimuli

3. decreased hydrolysis of acetylcholine (ACh) by acetylcholinesterase, allowing sustained action of the transmitteralready released from the axon terminal

4.increased postsynaptic receptor sensitivity to Ach

5.reduced rate of removal of calcium ions (Ca2+) from thenerve terminal after stimulation.


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Elevated body temperature up to 42 C causes noabnormality in healthy subjects, but enhances thedecrement on repetitive nerve stimulation in patients withmyasthenia gravis.

From 35 to 28 C increases the amplitude of thecompound muscle action potential and enhances theforce of the isometric twitch and tetanic contraction.

Patients with the myasthenic syndrome also experiencedistinct improvement after cooling


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Cooling reduces the decrement to repetitive nervestimulation but causes increase in amplitude.


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The effect of cholinesterase inhibitors also influences theresults of repetitive stimulation.

Administration of anticholinesterase drugs within a fewhours before the test reduces the probability of obtaininga decremental response.

With an overdose of anticholinesterase drugs, a singlenerve impulse may cause a repetitive muscle response,and repetitive stimuli at a high rate give rise to adecremental response.


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COMMONLY USEDNERVES AND MUSCLES

Distal Versus Proximal Muscle

Patients with myasthenia gravis rarely have a decremental

response in clinically unaffected muscle.

Weak proximal or facial muscles show a higher incidence ofelectrical abnormality than stronger distal muscles.

Studies of the distal musculature provide technically morereliable results than those of more proximal muscles in the limbor facial muscles.


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RECOVERY CURVES BYPAIRED STIMULATIONShort Interstimulus Intervals

A second stimulus delivered within a few millisecondsevokes a smaller response, indicating refractoriness ofthe nerve and muscle (see Fig.)

The second potential then progressively recovers, withsome overlap of the two responses at intervals of lessthan 15 ms.

In typical cases of myasthenia gravis, the first stimulus

elicits a maximal or near-maximal muscle response. Therecovery curve also follows a normal pattern for shortinterstimulus intervals up to 15 ms.


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Fig: Compound action potentials from the thenar muscles elicited by pairedshocks delivered to the median nerve at the wrist. Time intervals rangedfrom 2 to 30 ms between conditioning and test stimuli.


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Long Interstimulus Intervals

Despite the release of a greater amount of acetylcholine(ACh), the second muscle potential normally shows no

increment from the already maximal first response.

Most patients with myasthenia gravis or botulism alsohave minimal change at this interstimulus range. In

contrast, patients with myasthenic syndrome show anincrement at interstimulus intervals ranging from 15 to 100ms as one of the most characteristic electrophysiologicfeatures.

The decremental response in myasthenia gravis begins atintervals of about 20 ms but becomes more definite atintervals between 100 and 700 ms. The response reachesthe trough at an interstimulus interval of about 300-500 ms


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DECREMENTAL RESPONSEAT SLOW RATES OFSTIMULATIONNormal Muscles

Repetitive stimulation at a rate of 1-5 Hz depletes the

immediately available acetylcholine (ACh) store, withoutsuperimposed facilitation from neurosecretorymechanisms.

In normal muscles, decrement at stimulation of 2-3 Hz, if

present, does not exceed 5-8 percent.


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In myasthenia gravis, the amplitude drops maximallybetween the first and second responses of a train,followed by a further but lesser decline up to the fourth orfifth potential.

Occasionally, the recovery may even exceed the originalvalue by 10-20 percent, especially after several secondsof repetitive stimulation.

More characteristically, continued stimulation induces a

long, slow decline after a transient increment.


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Fig: slight decrement at slow rates of stimulation up tofive per second, and progressively more prominent

increment at faster rates of 10-30 per second.


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INCREMENTAL RESPONSE

AT FAST RATES OF STIMULATIONNormal Muscles

Supramaximal stimulation normally activates all musclefibers innervated by the nerve.

This precludes any increment in response to greateramounts of acetylcholine (ACh) released by subsequentstimuli.

In normal adults, muscle action potentials remain stableduring repetitive stimulation at a rate of up to 20-30 Hz.Some healthy infants, however, may show a progressivedecline in amplitude at this rate.


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In the myasthenic syndrome single stimuli typically elicit astrikingly small compound muscle action potential (SeeFig.)The amplitude varies over a wide range amongdifferent subjects.

Repetitive stimulation given at 20-50 Hz induces aremarkable increment of successive muscle actionpotentials to a normal or near normal Level

An incremental response, though characteristic of the

myasthenic syndrome and Botulism.


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The histogram plots the amplitude of the hypothenar muscle potential elicitedby single maximal stimuli to the ulnar nerve. The scale on the abscissadenotes normal strength (0), 75 percent (1), 50 percent (2), 25 percent (3),and complete paralysis (4) in MG patient.


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EFFECT OF TETANIC

CONTRACTION

Use of Prolonged Stimulation

A short train of several shocks at a slow rate suffices forroutine evaluation of neuromuscular transmission.

Prolonged stimulation at a rapid rate adds diagnosticinformation in the evaluation of infantile Botulism

Tetany develops after electrical stimulation of a 20-30 strain at 50 Hz or a continuous run for a few minutes at 3Hz.


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CHANGES IN MYOGENICDISORDERS

A train of stimuli causes an apparent decrement of thecompound muscle action potentials in a number of

myogenic disorders, such as

McArdle's disease,

myotonia,

pararnyotonia congenita, and

periodic paralysis.


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axon reflex

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