Markedly Prolonged Latency of Patellar Tendon Reflex in a Patient With Apparent Acute Motor Axonal Neuropathy

Dear Editor,

It is not easy to differentiate between the demyelinating and axonal forms of Guillain-Barré Syndrome (GBS). Some patients who are considered to have acute inflammatory demyelinating polyradiculoneuropathy (AIDP) in an initial nerve conduction study (NCS) can be diagnosed as acute motor axonal neuropathy (AMAN) or acute motor and sensory axonal neuropathy (AMSAN) in a follow-up study. Patients with acute motor conduction block (failure) neuropathy (AMCBN), a type of axonal GBS, or a reduction in the length - dependent compound motor action potential (CMAP) amplitude can be diagnosed as AIDP without the follow-study.1

Reduction in the length—dependent distal CMAP amplitude is often expected when the initial NCS is performed earlier than 7 days after disease onset. If there is only physiological conduction failure with mild axonal injury, the physiological conduction block is reversible in a follow-up study, which can be seen in patients with AMCBN.2, 3 In patients with more severe injury, conducting the initial NCS earlier than 7 days after disease onset will result in the CMAP amplitude being lower for proximal than distal stimulation of the lesion site before loss of distal nerve excitability.

However, a follow-up study conducted at the time of complete loss of nerve excitability at the distal part of the lesion can also show distal CMAP reduction, which is called length - dependent distal CMAP reduction.1, 4, 5 These findings are not consistent with a demyelinating lesion even though they appear as conduction blocks in the initial NCS. GBS pathology can occur at any portion of the peripheral nerve. AIDP is easily diagnosed if the lesion is prominent in the intermediate segment of the nerve fibers because it presents as a conduction block, and temporal dispersion and markedly slowed nerve conduction velocities. However, if the lesion is extremely distal or proximal, it is difficult to detect those demyelination features. In a patient with extreme distal demyelination, we need to stimulate more distally than the common site of routine NCS to reveal extreme distal conduction block. In a patient with an extremely proximal lesion, there is no specific abnormalities in routine NCS except for the lack of F-waves and H-reflexes, or markedly prolonged F-wave and H-reflex latencies. Greater than 120% prolongation of the F-wave or H-reflex latency is the criterion for demyelination. It is more difficult to differentiate AIDP from AMAN or AMSAN if the F-wave or H-reflex has no potentials. Functional selectivity also influences the results of electrophysiological tests.

Tendon reflexes induced by tapping the tendon with a mechanical hammer can only be observed and analyzed visually, but tendon reflexes can also be evoked using an electric hammer and displayed electrophysiologically, which is used to numerically analyze the characteristics of tendon reflexes. The tendon reflex is mediated by type Ia afferent fibers as the afferent arc and alpha motor fibers as the efferent arc, which are connected to agonist muscles through excitatory interneuron and antagonistic muscle through inhibitory interneuron in the spinal cord.6 Type Ia and alpha motor fibers are large myelinated fibers.

We tested the patellar tendon reflex using the method of Oh7 with an electric T-hammer on a patient with apparent AMAN and well-preserved deep tendon reflexes (DTRs). An active surface-recording electrode was placed on the rectus femoris midway between the anterior superior iliac spine and the superior border of the patella, and a reference-recording electrode was placed 5 cm distal to that line. The quadriceps tendon was tapped gently right below the patella using the electronic T-reflex hammer (sweep speed: 10 msec/div, sensitivity: variable, starting at 1 mV/div). The onset latency of the right patellar reflex that was measured 2 weeks after symptom onset was about 20.70 msec, which was markedly increased compared to that on the left side (about 4.55 msec) (Fig. 1).

Fig. 1
Patellar tendon reflex test right after IVIg injection (A) and after 2 weeks from IVIg injection (B). IVIg, intravenous immunoglobulin.

• Click for larger image
• Download as PowerPoint slide

After intravenous immunoglobulin (IVIg) treatment, the latency of the right patellar reflex that was measured 3 weeks after symptom onset was reduced to about 6.05 msec (Fig. 1) which was similar to that on the left side (4.85 msec). No T-wave chronodispersion was observed when several electrically induced patellar reflexes were superimposed.

We suggest that this marked prolongation of the right patellar reflex before receiving IVIg cannot be matched with axonal pathology such as that seen in AMAN or AMSAN. However, we can also suggest the possibility of reversible conduction failure or slowing in axonal GBS due to the rapid normalization of markedly prolonged patellar reflex and no marked chronodispersion of the patellar reflex in a follow-up study. We found that even in a patient with preserved DTR’s according to observation by the naked eye, the tendon reflex evoked by an electric T-reflex hammer can show some abnormalities.

We recommend thorough evaluations of all longitudinal and functional portions of the peripheral nerves including using the electrical tendon reflex test to differentiate the types of GBS.