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identify areas that correspond to specific nerves or to directed neurologic examination, in order to identify the
dermatomes (useful for root or spinal level injuries). clinical abnormalities and establish a differential diagnosis.
For this reason, the evaluation is commonly referred as the
Sensory disorders may also include positive
(irritative) symptoms which that should be explored: clinical neurophysiological examination.
(1) paresthesia (spontaneous feeling of needles, tingling, Clinical neurophysiological examination is currently the
numbness, and electric shock); (2) dysesthesia and gold standard for diagnosis and determination of prognosis
hyperalgesia (inaccurate interpretation of a sensory in peripheral nerve injuries, [15,16] in order to localize and
stimulus which is perceived as different and with an quantify clinical and subclinical preoperative damage and
affective unpleasant sensation); and (3) neuropathic postoperative recovery. As such, it yields key information
pain (spontaneous pain consequent to a lesion in the on the type of involved fibers (sensory vs. motor), on
afferent somatosensory fibers coming from the cutaneous the underlying pathophysiology (demyelination vs. axonal
territory of a nerve). loss), on axonal loss quantification, and consequently on
Motor signs and symptoms as a consequence of a reduced prognosis.
number of functional motor units include: (1) hyposthenia: The core neurodiagnostic studies are nerve conduction
reduced muscle strength as described by the use of the studies and electromyography (EMG). These tools test the
British Medical Research Council scale that recognizes integrity and physiological function of peripheral sensory
five grades of muscle strength: 0, neither contraction and motor fibers and the muscles.
nor movement are visible; 1, minimal contraction visible
or flickering (residual functioning motor units) without In order to reveal axonal loss (presence of denervation
movement; 2, active movement possible only without potentials), the optimal timing of a neurodiagnostic study
gravity (i.e. in a horizontal plane); 3, active movement is 2‑3 weeks after injury. [17,18] Neurodiagnostic studies
obtained against gravity; 4, active movement against should be repeated 3 months or more following trauma
mild resistance (4‑), moderate resistance (4) or strong or surgical repair to assess the ratio of denervation to
[14]
resistance (4+); and 5, normal strength; (2) muscular reinnervation. [19]
hypotrophy or atrophy: reduced volume of the muscle Nerve conduction studies
belly for both axonal damage and disuse; it will reach its Nerve conduction studies are the first line studies in
maximum state in 3‑4 months with a potential strength instrumental evaluation of nerve injuries. They are the
reduction of 80%. If denervation persists, a proliferation most basic and easily performed types of neurodiagnostic
of fibroblasts characterizes the histological picture, studies, and also used for screening prior to any additional
as new collagen is deposited in both the endo‑ and testing. [20]
perimysium, and atrophied muscle fibers are replaced
by thickened connective tissue; (3) absence or reduction Nerves and muscles are excitable structures and their
of osteotendinous (phasic) reflexes and of muscular potentials can be induced and recorded by external
tone (tonic reflex) due to involvement of both afferent electrodes. When the nerve is stimulated, a compound
sensory fibers from muscular spindles and efferent motor muscle action potential (CMAP) can be recorded from
neuron axons of the somatic arc reflex; (4) hyposthenia, the muscle, and a nerve action potential (NAP) can be
hypotrophy, and hypotonia configure the picture of recorded from the nerve. Amplitude and latency of the
partial or total flaccid paralysis of the group of muscles evoked response and conduction velocity are analyzed. [21]
innervated by the affected nervous structures (roots,
plexus, nerves); (5) positive symptoms (fasciculations The amplitude of the evoked response estimates the
and cramps) are rare in peripheral nerve injuries, but quantity of depolarized motor or sensory fibers, while
are often seen in radiculopathies; and (6) deformities: in conduction velocity measures the speed of the fastest (and
chronic and severe cases, muscle paresis reduced joint large caliber) motor or sensory myelinated axons.
movement in conjunction with healthy muscles may lead Sensory NAPs (SNAPs) are also helpful in differentiating
to deformities (cavus foot, claw‑hand) and ankylosis. between preganglionic (radiculopathies) and postganglionic
No clinical evaluation can distinguish neurapraxia from lesions; postganglionic lesions produce abnormal SNAP
axonotmesis, and no clinical or neurophysiological due to Wallerian degeneration of the axons distal to
examination can distinguish axonotmesis from neurotmesis. the peripheral injury, whereas in preganglionic lesions
To obtain the correct diagnosis and a plan appropriate to axon degeneration occurs in the dorsal root and in the
treatment, both neurophysiological and imaging studies ascending central pathway, leaving peripheral fibers intact
and clinical re‑evaluation over time are often required. and SNAP unmodified, despite anesthesia in the examined
cutaneous territory. [21]
CLINICAL NEUROPHYSIOLOGICAL Caution should be paid to interpretation of pure or
STUDIES prevalent motor diseases. Although changes in the CMAP
are frequently used to preliminarily diagnose peripheral
The neurophysiological or neurodiagnostic study represents nerve injuries, they are not specific and may reveal,
an extension of the clinical examination; accordingly, spinal disease of the anterior horn cells (myelopathy,
neurodiagnostic tests should always be combined with a amyotrophic lateral sclerosis, etc.), myopathy (muscular

Plast Aesthet Res || Vol 2 || Issue 4 || Jul 15, 2015 151