Peripheral nervous system

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TOPIC 5 Peripheral nervous system

Neuromuscular block monitor

Test: Train of four (TOF) stimulation

Indications

Owig to the variable individual response and a narrow therapeutic window of muscle relaxants, a peripheral nerve stimulation test is recommended after their use. In particular:

• After long-acting neuromuscular block (NMB) drugs and prolonged infusions

• Pulmonary disease, obesity and neuromuscular disorders such as myasthenia gravis and Eaton-Lambert syndrome, myopathies

• When reversal agents are contraindicated, e.g. tachyarrythmias, liver and renal dysfunction.

How it is done

• Application of a supramaximal stimulus to a peripheral nerve, followed by measurement of the associated muscular response.

• The nerve stimulator device should generate a monophasic square wave constant current up to 80 mA, and last between 0.1 and 0.5 ms.

• The nerve chosen must be close to the skin, have a motor element and muscular contraction must be visible or accessible to monitoring.

• The negative electrode should be placed directly over the superficial part of the nerve and positive electrode placed proximally to avoid direct muscular stimulation.

• The generation of single, train of four, double burst and 50-Hz patterns of stimulation is necessary. Polarity of output should be marked, and battery powered for safety.

• Small surface electrodes are used to apply to overlying skin. Good electrical contact is essential.

• Monitoring in clinical practice is by visual and tactile responses.

Interpretation

• Different patterns of nerve stimulation are used to determine onset, offset and percentage of NMB.

• Relationship between receptor occupancy and evoked responses can be estimated.

Management principles

• Onset and offset of NMB is faster in central muscles with a good blood supply.

• The most accurate muscle to monitor during NMB onset and maintenance is the orbiclaris oculi as it will reflect the conditions of the central larynx and diaphragm muscles.

• It is best to monitor a peripheral muscle such as adductor pollicis during reversal as it has a longer recovery time than respiratory muscles and will provide a greater margin of safety.

• TOF ratio >0.9 correlates with the ability to protect the airway and swallow normally. However up to 75% of receptors still remain occupied at this point.

• Clinically significant residual paralysis is defined as TOF ratio <0.9.

Stimulus responses and abnormalities

Table 5.1 TOF stimulation responses

Physiological principles

Limitations and complications

• Visual and tactile evaluation of muscular contractile response is unreliable. More accurate methods include mechanomyography (MMG), electromyography (EMG) and accelerometry (AMG) but they remain research tools.

• When monitoring is not performed up to 45% of patients are inadequately reversed on arrival to recovery room.

• When the T4–T1 ratio is 1 up to 50% of receptors can remain occupied (Table 5.2).

• Because of wide individual variability in responses, some patients may exhibit weakness at a TOF ratio of 0.8–0.9.

• Hypothermia increases skin impedance thus interpretation of evoked responses may be misleading.

Table 5.2 Receptor occupancy and TOF responses after neuromuscular paralysis

Investigation of suxamethonium apnoea

Suxamethonium is metabolized by the enzyme plasma cholinesterase (ChE). Abnormalities of this enzyme may cause prolonged muscular paralysis of variable duration after suxamethonium administration. The high prevalence of variant ChE genes in the population may contribute to the measured variability in recovery time after suxamethonium administration.

The clinical picture can be caused by (Table 5.3):

• Abnormal enzyme structure and activity

• Altered plasma enzyme concentration.

Table 5.3 Causes of suxamethonium apnoea

Genetic variants	Acquired causes
Atypical A	Pregnancy
Fluoride resistant F	Liver disease
Silent S	Carcinomatosis
H (10% reduced concentration)	Cardiac failure
J (33% reduced concentration)	Uraemia
K (66% reduced concentration)	Myxoedema
	Burns
	Poor nutrition
	Drugs: procaine, lithium, magnesium, ketamine, OCP, ecothiopate, tacrine

OCP, Oral Contraceptive Pill

Test: Dibucaine and fluoride number

Indications

• Prolonged apnoea (muscle relaxation) post suxamethonium or mivacurium administration as detected by a neuromuscular TOF monitor.

Interpretation

Data presented as

• Dibucaine number and fluoride number (Table 5.4).

Table 5.4 Common cholinesterase genotypes and their effect upon dibucaine number, fluoride number and phenotype

Limitations

• Biochemical tests are a measure of phenotype. This does not allow accurate determination of underlying genotype.

• They cannot distinguish between primary and secondary deficiencies.

• The duration of neuromuscular block can be different with patients of identical genotypes.

• Biochemical test results may remain normal in the presence of some clinically affected variants.

• ChE activity is higher in small children than adults and results have to be analyzed according to age.

• Heterozygotes are usually clinically insignificant unless accompanied by another mutation or an acquired cause of plasma ChE deficiency.

Test: Molecular genetic testing

• The gene that codes for the ChE enzyme is located at the E1 locus on the long arm of chromosome 3.

• More than 20 mutations have been identified in the plasma cholinesterase gene. They include: normal plasma ChE (u); atypical hydrolyzing activity (a), fluoride resistant (f), silent (s).

• Some mutations code for decreased concentration with normal activity: H, J and K variants.

• One further rare variant allele is C5, which has higher than normal ChE activity. It manifests as suxamethonium resistance.

• Genes follow typical autosomal recessive inheritance, and some by linkage disequilibrium.

Myasthenia gravis (MG) testing

Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction (NMJ) characterized by fatigable muscle weakness. It has an incidence of 1 in 100 000; average age of onset 20–30 years in women and 40–50 years in men.

Indications

• The diagnosis is based upon a characteristic history and examination, positive serological and electrophysiological diagnostic tests.

• The characteristic history is of weakness and/or fatigue in the voluntary muscles, increasing during the course of the day, worsening after exertion and improving with rest. It may involve ocular muscles only.

Test: Edrophonium (tensilon) test

• The tensilon (edrophonium) test can be performed at the bedside, but is neither sensitive nor specific for MG. It should only be performed when the diagnosis is required urgently. Full cardiac monitoring and atropine is required in case of cardiovascular side effects. Initially 2 mg (max 10 mg) edrophonium is administered IV.

• Edrophonium inhibits acetylcholinesterase (ACh) and prolongs the duration of ACh available at the neuromuscular junction (NMJ).

• A response is usually seen within a few minutes. An objective improvement in muscle strength is noted in a positive test.

Test: Repetitive nerve stimulation (RNS)

How it is done

• The nerve supplying an affected muscle is stimulated 6–10 times at 2–3 Hz.

• Using surface electrodes over the muscle a compound motor action potential (CMAP) is recorded.

Interpretation

Data is presented as a compound motor action potential (CMAP) (Fig. 5.1).

Fig. 5.1 Compound motor action potential (CMAP) from a muscle showing the progressive reduction in amplitude seen with repetitive stimulation.

Physiological principles

• In normal muscles there is no change with repetitive stimulation.

• CMAP amplitude decreases by greater than 10% in a positive test.

• The decrement is often enhanced following exercise.

• RNS decrement is seen in 75% of generalized MG, 50% ocular MG.

• A decremental response alone is not specific for MG and can be seen in other motor neuron disorders.

Test: Single fibre EMG

How it is done

• Undertaken in equivocal patients.

• The muscle fibre potentials from the same motor unit are monitored after a single axon innervation.

Interpretation

Fig. 5.2 Seven discharges superimposed to show variability in time interval caused by insecure neuromuscular junction transmission.

Physiological principles

• Activation of a normal motor unit will show a consistent latency after nerve stimulation, normally <55 μs.

• An increased variability of latencies is seen in NMJ disorders, termed jitter.

• A positive test occurs when the interval, or jitter, is increased to >100 μs.

• This is the most sensitive test for MG with >95% sensitivity in generalized and ocular MG.

Further investigations

• Required if above tests are negative in a patient with a convincing clinical history.

• Coexistent autoimmune diseases must be excluded.

• Antibodies to other areas of the NMJ (e.g. Anti MuSK) are present in 50% of seronegative MG.

• Muscle biopsy can be useful.

• CT/MRI thorax is necessary for diagnosis of thymomas and thymic hyperplasia.

• MRI of the brain may be necessary if a structural brain lesion is suspected.

• Exclude underlying malignancy.

Peripheral motor and nerve function assessment

Test: Nerve conduction studies and electromyography (EMG)

To evaluate the integrity and function of the peripheral nervous system.

Indications

Diagnosis and assessment of the following:

• Neuropathy – metabolic (diabetes mellitus, uraemia, hypothyroid, hepatic, HIV immune causes, rheumatoid arthritis, systemic lupus erythematosus), traumatic, entrapment, idiopathic mononeuropathies, clinical suspicion of amyotrophic lateral sclerosis (ALS), inflammatory (e.g. post polio, Guillain Barré syndrome), hereditary (e.g. Charcot Marie Tooth)

• Myopathy – Hereditary or inflammatory (e.g. polymyositis, critical illness myopathy)

• Neuromuscular junction – myasthenia gravis, Eaton-Lambert syndrome.

Perioperative monitoring:

• Facial nerve monitoring during posterior fossa neurosurgery and middle ear surgery

• Spinal surgery: during cauda equina surgery the anal sphincter and leg muscles can be monitored.

How it is done

• The selected nerve is stimulated using a current that will excite all the axons in the nerve trunk. The electric output is a rectangular wave, duration 0.1–0.2 ms. Needle electrodes may be required when stimulating a deep nerve. Stimulation should be performed at two or more sites along the nerve.

• Propagated activity is recorded at a distance along the nerve or from the muscle using a surface or needle recording electrode. The muscle response after nerve stimulation is the compound muscle action potential (CMAP).

Interpretation

Data presented as:

• Latency. The time between stimulus and response includes nerve conduction time and neuromuscular transmission time.

• Amplitude. This depends upon the number of axons that conduct impulses, the number of functioning endplates and the muscle volume.

• Conduction velocity (CV). Normally 40–60 m/s

Abnormalities

Pathological findings include conduction slowing, conduction block, no response, low amplitude response. This can evaluate the degree of demyelination and axonal loss in nerves studied.

• Demyelination: reduces maximal CV and may produce conduction block.

• Axonal loss: small action potentials (amplitude) with normal CV.

• In normal muscle no electrical activity occurs at rest, motor neurons discharge on voluntary contraction, and responses can be recorded. (MUAP).

• Degeneration of motor neurons results in small potentials recorded from muscles at rest: fibrillations and positive sharp waves, and the number of motor units on contraction decreases.

• Myopathic muscle becomes wasted and fibres shrink, MUAPs are smaller than normal, contraction is weak despite normal motor conduction. Sometimes needle insertion itself provokes bursts of muscle APs.

Management principles

• Neurophysiological data strongly suggests that critical illness myopathy is more common than previously assumed.

• Electrophysiological measurements can be obtained from the phrenic nerve and diaphragm in cases of respiratory weaning failure.

Further investigations

• Single fibre Electromyography.

• Quantitative EMG, direct muscle stimulation and other detailed assessments.

Limitations and complications

• Neurogenic and myopathic weakness can be difficult to distinguish clinically.

• Absence of a sensory nerve AP may be due to Na channel dysfunction, not necessarily peripheral nerve degeneration.

• It is difficult to distinguish different neuromuscular disorders in the critically ill as they are unable to cooperate with testing. Referral to expert centres is recommended.

Local oedema, electronic devices, lines and monitors frequently prevents reliable sensory recordings in intensive care.

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