State-of-the-Art Diagnosis of Peripheral Nerve Trauma: Clinical Examination, Electrodiagnostic, and Imaging


EMG finding

Occurrence/cause

Timing

Normal

Central nervous system lesion (e.g., intracranial hemorrhage)

Always

Not a severe nerve lesion

Until the occurrence of pathological spontaneous activity

Pathologic spontaneous activity

Axonotmesis, neurotmesis, myopathy

Begins 10–14 days after a lesion, ends after full recovery, may persist for decades if recovery is incomplete

Polyphasic motor unit action potentials (MUAPs)

Partial axonotmesis, myopathy

Begins 6 weeks after an incomplete lesion, ends after recovery, some may persist

Large MUAPs (may be polyphasic)

Partial axonotmesis

Begins 6–12 months after an incomplete lesion, persists after recovery

Increased (>20/s) discharge rate of single motor units

Neurapraxia, partial axonotmesis

Begins immediately after the lesion, accompanies weakness




Table 2.2
NCS findings in a nerve supplying a weak muscle and their diagnostic meaning













































NCS finding

Occurrence/cause

Timing

Normal compound muscle action potentials (CMAPs)

Central nervous system lesion (e.g., intracranial hemorrhage),not a severe nerve lesion, myopathy

Always

Normal (CMAPs)

Stimulation distal to the lesion only

Ends 4–7 days after the lesion (due to Wallerian degeneration of axons)

Normal CMAPs upon nerve stimulation distal to the lesion, low CMAPs upon proximal stimulationa

Neurapraxia (also called “conduction block”)

Begins with the lesion, ends with recovery

Axonotmesis

Ends 4–7 days after the lesion (due to Wallerian degeneration of axons)

Innervation anomaly

Always

Low CMAPs at all stimulation sites,

low sensory nerve action potentials (SNAPs)

Axonotmesis

Begins 4–7 days after the lesion (due to Wallerian degeneration of axons), ends with full recovery

Mildly reduced nerve conduction velocity (NCV) (leg, 30–40 m/s; arm, 40–50 m/s)

Axonotmesis

Parallels low CMAPs

Pre-existing polyneuropathy

No relationship to the nerve trauma

Severely reduced NCV (leg, <30 m/s; arm, <40 m/s)

Demyelinating neuropathy, not caused by nerve trauma

No relationship to the nerve trauma


aNote that this finding is often labeled “conduction block,” although conduction block is only one of its potential causes


The tables indicate that the electrodiagnostic findings and their time course may provide valuable information about both the site and the type of a suspected nerve lesion. Table 2.3 is intended to help the reader plan a sensible timing for the diagnostic tests and to “decode” their results.


Table 2.3
Electrodiagnostic findings after a nerve trauma over time







































































   
Type of lesion

Time after trauma
 
Neurapraxia

Partial axonotmesis

Total axonotmesis, neurotmesis

Immediately

EMG

No PSA, DR ↑ MUAPs n

No PSA, DR ↑, MUAPs n

No PSA, no MUAPs

NCS

∆CMAP

∆CMAP

∆CMAP

4–7 days

EMG
 
No PSA, DR ↑, MUAPs n

No PSA, no MUAPs

NCS

CMAPs ↓

No CMAPs

10–20 days

EMG

PSA, DR ↑, MUAPs n

PSA, no MUAPs

NCS

CMAPs ↓

No CMAPs

>6 weeks

EMG

n

PSA, DR ↑, polyphasic MUAPs

PSA, small polyphasic (“nascent”) MUAPs

NCS

n

CMAPs ↓

No CMAPs

Years

EMG

n

MUAPs ↑

(PSA), MUAPs ↑

NCS

n

CMAPs (↓)

CMAPs ↓


DR discharge rate (of motor units!), MUAP motor unit action potential, PSA pathologic spontaneous activity, CMAP compound muscle action potential, ∆CMAP normal CMAPs upon nerve stimulation distal to the lesion, low CMAPs upon proximal stimulation (see Table 2.2), n normal, pathologically increased, pathologically decreased

Some time intervals after the trauma are noteworthy [8].

Immediately after a severe lesion an EMG may be valuable: If motor unit action potentials (MUAPs) are recorded, the lesion is incomplete, and thus neurotmesis is ruled out. If pathologic spontaneous activity (PSA) is recorded within the first 10 days or if abnormally polyphasic or enlarged MUAPs are found within the first 4 weeks, a pre-existing neuropathy (or, rarely, a myopathy) is documented. It should also be noted that PSA may persist for years. Thus, the occurrence of PSA not necessarily indicates a recent lesion. The recency of a lesion can be inferred from PSA only if the PSA was not found in an early recording but does appear later on.

If increased discharge rates of motor units are found at any time, a central nervous system lesion is ruled out.

An NCS may make particular sense within the first 4 days, namely, before Wallerian degeneration (see Chap. 1) becomes apparent [11]. Only during this time, the distal part of the lesioned nerve can be stimulated electrically. This results in a normal compound muscle action potential (CMAP) following stimulation distal to the lesion and a low CMAP following stimulation proximal to the lesion, a finding that reliably localizes the nerve lesion. After the completion of the Wallerian degeneration, namely, after 11 days [11], all CMAPs are low or have disappeared, irrespective to where the lesion is located. If a low CMAP upon distal stimulation is found within the first 4 days, a pre-existing lesion is documented. Conversely, a normal CMAP during that time documents the integrity of that nerve before the trauma. This finding, as well as the absence of PSA early on EMG, can be particularly helpful in the evaluation of potentially iatrogenic nerve lesions.

A major shortcoming of the established electrodiagnostic methods is that they do not help to make the important distinction between neurotmesis and total axonotmesis; the latter denominates a condition of a nerve characterized by all of its axons suffering from axonotmesis.

Figure 2.1 illustrates a common clinical situation and how a good knowledge about the benefit of electrodiagnostic procedures and the meaning of the respective findings are important for appropriate treatment decisions.

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Fig. 2.1
A 74-year-old man experienced plegia of his left foot extensors immediately after surgery on his lumbar spine. As a complication of the surgery was suspected, the patient underwent a second operation 1 day after the first one, which did not resolve the problem. First electrodiagnostic examination was done 2 days after the first surgery: (a) motor nerve conduction study (NCS) recordings from his left extensor digitorum brevis muscle, stimulation of the peroneal nerve at the dorsum of the foot (upper trace), and below and above the fibular head (lower traces). Compound muscle action potentials (CMAPs) upon distal stimulation are low, indicating a pre-existing lesion, and CMAPs upon proximal stimulation are absent, which shows that there is an additional lesion that can be localized at the fibular head (Table 2.3, “immediately”). (b) The electromyogram (EMG) of the anterior tibial muscle shows pathologic spontaneous activity (PSA), which also demonstrates a pre-existing lesion. (c) Increased (>20/s) discharge rates of motor units show that at least 80% of the motor units of the muscle are not functional [31]. These results point to the site of the actual lesion and show the pre-existing one. The type of the lesion cannot be inferred. A subsequent electrodiagnostic examination was done 20 days after surgery: (d) NCS as in (a) all CMAPs are absent, showing that the type of the lesion is axonotmesis (or neurotmesis) (Table 2.3, “10–20 days”). (e) The electromyogram (EMG) of the anterior tibial muscle shows pathologic spontaneous activity (PSA), showing that the type of the lesion is axonotmesis that took place at least 10–14 days before this recording was made. (f) Discharge rates of motor units are normal, showing a functional recovery of many motor units of this muscle since the recording (c) was made. These results do not permit to localize the lesion but show that the lesion type is partial axonotmesis, more pronounced in the extensor digitorum brevis than in the anterior tibial muscle. It should be noted that the second operation could have been avoided if the first electrodiagnostic examination had taken place immediately



2.4 Imaging



2.4.1 High-Resolution Ultrasound


Ultrasound imaging of peripheral nerves is done since a quarter of a century [13]. Initially, this was done virtually exclusively by radiologists and orthopedic surgeons. Neurological studies on this subject were published from the beginning of this millennium [2]. Since then technology had made extreme progress, especially the spatial resolution of ultrasound was dramatically improved. However, the penetration depth of ultrasound is still limited. This is the main shortcoming of ultrasound, especially if compared with magnetic resonance imaging (MRI) [29]. As a consequence of the methodological improvements, the number of publications on “ultrasound” and “peripheral nerve” increased from less than one per year before 2000 to 60 PubMed entries in 2015.

To date, the clinical significance of ultrasound imaging of peripheral nerves in general is not without controversial discussion [5], while its role in the diagnosis of traumatic nerve lesions is yet better defined [7, 20, 27, 37]. This is because the major diagnostic issue in traumatic lesions is to determine both the type and the morphology of the lesion and not so much to localize the lesion. As a major point, the important distinction between neurotmesis and total axonotmesis, which cannot be made with electrodiagnostic methods, can readily be made with ultrasound. When the diagnostic value of ultrasound was studied prospectively in 65 patients with nerve trauma, the use of ultrasound strongly modified the diagnosis and the therapy in 58 % of cases. It specifically contributed to the following:



  • Distinction between neurotmesis and axonotmesis


  • Identification of etiology


  • Demonstration of multiple sites of nerve damage

The contribution of ultrasound was clearly the highest in cases with neurophysiological evidence of complete axonal damage [27]. Figure 2.2 illustrates a typical clinical situation in which ultrasound imaging clearly demonstrates a peripheral nerve’s neurotmesis.

A394139_1_En_2_Fig2_HTML.jpg


Fig. 2.2
A 64-year-old woman got a lipoma removed from her cubital fossa. Immediately after surgery she experienced plegia of her finger extensors. Four weeks after, there still was plegia of all muscles innervated by her radial nerve distal to the extensor carpi radialis brevis muscle. Upon EMG examination of the plegic muscles, there was abundant spontaneous activity but no MUAPs. High-resolution ultrasound imaging (upper, provided by Peter Pöschl, Regensburg) clearly shows a transected nerve, with (A, B) and (C, D) marking the nerve stumps. This finding is confirmed by visual inspection during subsequent surgery (lower)

Ultrasound can be used to study the development of neuromas, both before and after nerve surgery. Unfortunately, the information that can be drawn from such imaging is of limited value so far, as there is no relation between enlargement of neuroma and nerve function unless the size of the neuroma exceeds a cutoff beyond which prognosis is negative [9].

Before nerve surgery, ultrasound can be used to detect the location of proximal and distal nerve stumps. They can be marked on the skin preoperatively to help the surgeon better tailor the procedure to the damaged nerve’s needs and save time that otherwise would be needed for the search for the stumps [20].

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Sep 23, 2017 | Posted by in NEUROLOGY | Comments Off on State-of-the-Art Diagnosis of Peripheral Nerve Trauma: Clinical Examination, Electrodiagnostic, and Imaging
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