When a client presents with noticeable weakness or other ‘hard’ neurological findings; abnormal sensation (temperature, light touch, pinprick), not just altered sensation or absent reflex, often I find clinicians jump to implicate a central nerve root involvement (dermatonal) without considering peripheral nerve compression or a somatic source. I think this just reflects the strong emphasis of our undergraduate training.
This case report looks at the cubital tunnel and flexor carpi ulnaris as a source of peripheral nerve compression. No mention in this report is made of the anatomical variation anconeus epitrochularis, that would cause the same situation and as no MRI was conducted we are none the wiser as to which muscle was actually involved. You can read more about this muscle variant in a previous blog.
This case report highlights a potential anatomical weak point where the involvement of a trigger point produces a myriad of symptoms that involve both somatic (in this case from the muscle, but could also be osseous, say in the case of a tumor) and neural (neuropraxia) symptoms of altered light touch/pressure & vibration.
One aspect that I found interesting and had not considered in my few experiences of this presentation was the mismatch in sensory testing. In response to his examination Dr. Yeo noted “Clinical examination showed numbness over his entire left ring and little fingers up to the level of the metacarpophalangeal joint. His sensation was tested and showed intact pinprick and temperature, but diminished vibration sensation”.
How can someone have numbness, reduced vibration sense and yet intact pinprick and temperature sensation? Read on if you believe that this statement was an editorial typo.
Nerve Function & Nerve Injury
Peripheral nerve fibres are classified by two systems. In 1937 Erlanger & Gasser, divided peripheral nerves based upon conduction velocity into A, B and C fibres. The A fibres were myelinated, with the largest diameters and had the fastest conduction rates. A fibers are divided into efferent (Aα & Aβ: extrafusal muscle fibres innervation, Aγ: intrafusal fibres- muscle spindle innervation) and afferent (Aα: skin, joint and muscle spindles, Aβ: Merkel discs, pacinian & Meissner corpuscles providing innervation for vibration, pressure & tissue deformation). B fibres were also myelinated but slightly thinner and slower and C fibres were unmyelinated and had the slowest conduction velocities.
The other classification system is that of Lloyds and based upon fibre diameter. Group I, II and III are all myelinated with the Group I being thickest and diminishing in diameter with increasing number, while IV is unmyelinated. The different classification systems, fibre diameters, conduction velocity and information transmitted are summarised in the adjoining picture.
The larger diameter fibres apart from being faster conducting have some important clinical features. Larger diameter fibres are;
More sensitive to pressure/compression
More sensitive to hypoxia
Are the most sensitive to thermal changes
Most sensitive to bacterial and viral toxaemia
C fibers are most sensitive to chemical agents and respond to thermal and nociceptive stimuli.
Nerve injuries were classified by Seddon in 1943 as neuropraxia, axontomesis and neurotemesis.
Neuropraxia (mild blunt trauma or compression) with associated biochemical nerve irritation, sensitisation, and compression by oedema. This is the most common form that I would see in a country based private practice. There is a disruption of nerve conduction which generally affects motor (power, reflex) > sensory (light touch, vibration, pressure) > temperature, nociception & ANS and is reversible usually over a 6-8 week period.
Axontomesis is a more severe injury that involves some nerve degeneration and subsequent nerve regeneration. Occurring at 3-4cm per month this process takes time to bridge the original injury site. Loss in both the motor and sensory nerves is more complete.
Neurotemesis is the most severe injury with not only loss of nerve conducting tissue but surrounding supportive connective tissues with the most severe end point being transection.
So getting back to the editorial typo, I maybe about to put my head on the literary chopping block, but it is a good way to learn, so please send me a few email axes if you have alternative thoughts.
In reviewing this case study and putting together the theory of nerve classifications, functions and injury we have a clinical situation of a muscle compression of the ulna nerve by FCU (or anconeus epitrochularis) causing a reduction in nerve conduction & function. Compression and hyproxia target the larger nerve fibres first, being the A fibre group. A fibre efferent: Aα/β motorneurones (reduced muscle strength in ulna nerve distribution); afferent: Aα/β light touch, pressure, proprioception (not mentioned) and vibration sensations.
While not applicable in this case study, it would be reasonable to expect also a loss of the normal reflex arc function, either due to disruption of the large Aα/β efferent extrafusal fibre or the Aγ afferent intrafusal fibres innervating the muscle spindle.
Notably, the small diameter C fibres were unaffected (temperature and nociception) in this case study.
Why the title ‘Miracle Muscles and Neuropraxia’? I had the experience of a lady presenting with a 2 week foot drop that I could hear her problem coming. She was presenting for a foot drop splint from her GP. After questioning her history and then performing an examination, I noted the presence of active trigger points in her extensor digitorum longus. I explained the possible link and asked her consent to treat with dry needling. On return a week later for follow-up I never heard her coming. She said her GP was amazed – but not as much as I was – first time round for me it seemed a miracle.
All the best,
Doug Cary FACP Specialist Musculoskeletal Physiotherapist (awarded by Australian College of Physiotherapy, 2009) PhD Candidate Curtin University Clinical Director AAP Education
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