Difference between revisions of "5° Clinical case: Spontaneous Electromyographic Activity"

== Abstract ==

   

In this chapter we will address another subject, much discussed but also much followed and proposed as a diagnostic test in particular in patients with Orofacial Pain (OP) and Temporomandibular Disorders (TMDs), that of electromyography in a muscle in resting conditions which causes immediately the usual Hamletic question:

For this reason we will present a clinical case reporting Orofacial Pain (OP) and Temporomandibular Disorders (TMDs) which, unfortunately, had encountered diagnostic difficulties in previous medical experiences.

65-year-old female patient reporting mainly Orofacial Pain (OP) in the left emirate of the face and in particular pain radiating from the masseters to the TMJ and left temporalis muscle. After about 2 years from an episode of sudden loss of consciousness at the moment in which his dentist performed a trochlear for periodontology of the lower left immigrant. From that moment on, sudden pains of the unthoracic type began and then spread to the whole left hemiface even when chewing. Colleagues saw the correlation with chewing and analyzed following the RDC protocol and defined the patient as suffering from Temporomandibular Disorders (TMDs)

Once it came to our attention, we followed all the gnathological tests (axiography, ATMs images, and surface EMGs) which did not testify for a TMDs but for an undefined but substantially neurological picture. The reason for this interpretation was precisely the execution of the surface EMG which returned the following results. The electromyographic picture of the masseters was determined following a logical sequence shown in figure 1. As can be observed, the lateral asymmetry of the EMG activity with surface electrodes of the masseters in a relaxed state (fig.1A) with the jaw maintained in rest position it was such as to require a needle EMG of the left masseter. The activity recorded with this technique (fig.1B) showed a discharge with a stable frequency of 20 Hz which presupposed a study of the motor unit. The study of the motor units of the left masseter (fig.1C) automatically selected 26 motor units whose shape, duration, spikes and turns of each unit were analysed. The data are reported in the table (fig.1D) Statistically, the following parameters can be detected: average amplitude of<math>\approxeq348\mu V</math>, a duration of <math>8.7 msec</math>, <math>23%</math> of polyphasic units. This clinical picture represents the typical pathophysiological phenomenon in which the patient reports pain but very often the diagnosis remains "difficulty in muscle relaxation", "atypical orofacial pain" or even better "fibromyalgia" and consequently the drug therapy remains symptomatic. Precisely these conditions should give the doctor the opportunity to deepen his research by carrying out and knowing at least in general terms the constituents of a coaxial needle EMG analysis, before referring the patient to a neurologist specialist.

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The EMG examination of skeletal muscles consists of four steps:

In one subject, the insertion activity appears as high-frequency positive and negative spikes in a single group and are typically a representation of muscle fiber damage or mechanical stimulation due to needle penetration into the muscle. In our patient this activity occurred with a duration of 80 mS and was referable to a normal picture. Also note the phenomenon of plaque activity. If a needle electrode is held stationary at one point in the muscle, normal muscles at rest show absolutely no electrical activity except in the region of the neuromuscular endplate. These consist of two components: low amplitude (on the order of 10-50 μV) and low duration (1-2 msec) which to the loudspeaker EMG resemble the sound of sea shells on the ear. In our case (fig.1A) the total absence of plaque activity in the right masseter can be explained by the recording performed with surface electrodes which partially reduce the energy of the signal but the activity recorded on the left masseter, again with surface, has a width of<math>\approxeq100\mu V</math> . For the same reasoning, this activity should not be considered as plate activity since, as can be seen in fig. 1B, recording of the left masseter performed with a coaxial electrode, the amplitude is <math>\approxeq 400\mu V</math>. Sometimes plaque potential spikes are indistinguishable in waveform from fibrillation potentials which also show initial negativity when recorded near the plaque. Another curious element is the similarity of the discharge model between the discharges of the neuromuscular spindles and of the plate potentials, so much so that some authors<ref>{{cita libro  

  }}</ref> hypothesized that these potentials could originate from the intrafusal muscle fibers. The discussion and the electrophysiological meaning to be given to the electrical activity observable in fig. 1B.

[[File:EMG a punta+.jpeg|thumb|'''Figur 2:''' Attività spontanea con scariche a punta positive in un muscolo denervato]]

In the first 2 weeks after denervation, the sensitivity of a muscle fiber to acetylcholine (ACh) increases up to 100-fold. This phenomenon known as “denervation hypersensitivity” may explain the spontaneous firing of denervated muscle fibers in response to minute ACh quanta.<ref>{{cita libro  

Repetitive firings of the same motor unit occur in bursts at regular intervals of <math>0.1-10sec</math> with <math>2-10</math> spikes firing at in each burst <math>30-40 Hz</math>. Fasciculation potentials are typically associated with anterior horn cell pathologies but are also seen in radiculopathies, entrapment neuropathies, and muscle pain fasciculation syndrome. Figure 4 shows a clear example of fasciculations of the orbicularis oculi muscle which, compared with the traces of the clinical case (fig. 1B and C), shows a total morphological diversity and temporal representation. This diversity would strengthen the exclusion of a denervation pathology.                                                                                                                                                                                                     

A motor unit can be defined by amplitude, rise time, duration and phases as will be further described in the chapter 'Electromyography'. The recorded amplitude varies widely with the position of the electrode tip relative to the discharged ion current source, so a skilled operator selects a motor unit potential with a rise time of <math>\approxeq 500\mu sec</math> to be certain of proximity to the source. The amplitude in the normal range goes from hundreds to <math>\mu V</math> a few <math>m V</math> and the duration from <math>5-10 msec</math>. For the facial muscles, in particular, we refer to the values reported by Buchthal<ref>Buchtal F: An introduction to electromyography Scandinavian University Books. Copenhagen 1957</ref> whose range is <math>4,2-7,5 msec</math> for a maximum <math>75</math> age of years. Biphasic or triphasic motor unit potentials are also present in normal muscles with an average of motor units <math>5-15%</math>with <math>4</math> or more phases           

            

[[File:EMG polifasico.jpeg|left|thumb|'''Figura 5:''' Tracciato MUAP polifasico]]

   

Increasing the contraction greatly increases the motor units which start firing very rapidly and this precludes the identification of individual motor unit potentials. This phenomenon has been given the name of interference pattern. The density of the spikes and the average amplitude of the summed responses are determined by a series of factors such as: the descending output from the cortex, the number of motor neurons capable of firing, the firing frequency of each motor unit, the waveform of individual potentials and the probability of phase cancellation (collision). In our clinical case, the interference pattern recorded on the masseters was normal in both amplitude and frequency.  

From the detailed analysis of the EMG tracing relating to the clinical case described, we can confirm the absence of organic damage to the motor unit and/or muscle fibers for the various reasons explained, such as: the absence of spontaneous activity, the normal morphology of the motor unit and interferential recruitment. The presence of EMG activity recorded on the left masseter still remains to be interpreted (fig.1) which, referring to the concepts described above, cannot be called "spontaneous activity" because it is not an expression of denervation, nor "lack of muscle relaxation" as the patient is unable to relax the muscle voluntarily or with stretching manoeuvres, nor of “EMG activity at rest due to psychic disorder as the psychometric tests are negative.{{q2|This activity seems to respond to a pacemaker of central origin which fires at a stable frequency on second order motor neurons (trigeminal motor nucleus). Unfortunately it is difficult to say whether this activity is due to a functional disorder of the motor neuron II or of the cortical and/or subcortical system.|}}

An experimental study was proposed, with the consent of the patient, in which an attempt was made to pharmacologically uncouple the brainstem neuronal activity from the cortical one. Simultaneously with the pharmacological uncoupling, the EMG activity with a coaxial needle on the left masseter was monitored and contextually the blink reflex. The experimental model, which we are going to explain briefly, was created through two essential elements, namely: the choice of the specific anesthetic for the purpose of the study (propofol) and the control of the electrophysiological activity of the brainstem through the blink reflex  

The effects of anesthetics produce loss of consciousness, memory, changes in spontaneous activity, attenuation of protective reflexes, loss of postural reflexes and also adverse effects such as hallucinations, euphoria and amnesia. Furthermore they may affect the level or homeostasis of neurotransmitters in the brain such as dopamine, noraepinephrine and acetylcholine (ACh).<ref>Angel A. : Central neuronal pathways and the process of anaesthesia. British Journal of Anaesthesia 1993; 71:148-163</ref> Ach was the first neurotransmitter to be described and cholinergic neurons are widely distributed in the brain. Cholinergic mechanisms are known to be important in the striatum where a balance between dopamine and ACh release ensures normal motor output,<ref>Iversen SD.: Behavioural evaluation of cholinergic drug. Life Sciences 1997; 60: 1145-1152</ref> hippocampus and frontal cortex where ACh plays an important role in the regulation of consciousness, memory etc.

Propofol is thought to potentiate the inhibitory effect of GABAA receptors and to have a different action from barbiturates or benzodiazepines. An elegant study<ref>Kikuchi T, Wang Y, Sato K, Okumura F.: In vivo effects of propofol on aceylcholine release from the fronatl cortex, hippocampus and striatum studied by intracerebral microdialysis in freely moving rats</ref> carried out through intracerebral microdialysis in mice demonstrated that propofol, with doses of 50 mg/kg, decreased the release of ACh from the frontal cortex by 85%, by 72% by the hippocampus and by 19% by the striatum.

The blink is a reflex that is evoked by hitting the eyebrow region on one side of the forehead. Electrophysiologically it is possible to evoke it by applying an electrical stimulus on the eyebrow arch in correspondence with the supraorbital foramen. The responses are recorded through two surface electrodes positioned on the orbicularis oculi muscle on each side and the motor potentials can be mainly represented by two events, namely the ipsilateral R1 response to stimulation and the bilateral R2. These responses represent a monosynaptic and polysynaptic circuitry for R1 and R2 respectively. The R1 response was considered to follow a trigeminal pathway in the pons while the R2 via a pathway adjacent the reticular formation reaches the facial nuclei.<ref>Ongerboer de Visser BW, Kuypers HG (1978): Late blink reflex changes in lateral medullary lesions. An electrophysiological and neuro-anatomical study of Wallenberg's syndrome. ''Brain'' '''101''': 285-294. </ref><ref>Ongerboer de Visser BW (1983b): Comparative study of corneal and blink reflex latencies in patients with segmental or with cerebral lesions. In: Desmedt JE , editor. ''Advances in neurology''. New York: Raven Press. p 757-772.</ref><ref>Ongerboer de Visser BW (1983b): Comparative study of corneal and blink reflex latencies in patients with segmental or with cerebral lesions. In: Desmedt JE , editor. ''Advances in neurology''. New York: Raven Press. p 757-772.</ref>

The main neural circuitry of the blink reflex is located in the brainstem but recent work, using functional magnetic resonance imaging (fMRI), has demonstrated that two main areas in the posterior lobe of the cerebellar hemisphere, mainly on the side ipsilateral to the stimulation, are activated during the blink reflexes in humans.<ref>Dimitrova A, Weber J, Maschke M, Elles HG, Kolb FP, Forsting M, Diener HC, Timmann D. Eyeblink-related areas in human cerebellum as shown by fMRI. Hum Brain Mapp. 2002 Oct;17(2):100-15.</ref>

The experiment consisted in simultaneously monitoring the presence of the blink relex (R1 and R2) and the EMG activity of the left masseter with a needle electrode at the time of Propofol infusion at doses of <math>2 mg/kg </math> which determined a slight dissociation - alert and with eyes open . In this way it can be stated, with a good approximation, that the drug released the mesencephalic-bulbar functions.  

[[File:EMG Propofol.jpeg|center|thumb|600x600px|'''Figure 6:''' EMG result of the experimental procedures. For better understanding follow text]]

The EMG activity present in the examined subject cannot be defined as "Spontaneous activity" because it does not show characteristics of organic damage to the muscle fibers and/or the second motor neuron. If it were muscle fiber damage, the EMG activity would have remained even after <math>2 mg/kg </math> administration of propofol. Indeed, it was observed that doses of <math>2 mg/kg </math> propofol failed to reverse the fasciculations induced by administration of 1 mg/kg of succinylcholine.<ref>Kararmaz A. Kaya S, TurhanogluS, Ozyilmaz A.: Effects of high-dose propofol on succinylcholine-induced fasciculations and myalgia. Acta Anaesthesiol Scand 2003; 47:180-184</ref> The EMG activity present in the subject cannot be described as "Incapacity to relax" because the term is too generic to refer to conditions of psychic disturbances and dystonic disorders. In oromandibular dystonias, in fact, there are phases of EMG silence when the patient is asked to deviate the jaw to one side in an attempt to stretch the muscle involved. This effect is determined by an additional input from the muscle proprioceptive fibers.

These authors suggested three mechanisms that may explain the increased sensitivity to vibration: the loss of the normal inhibition of the Ia afferents, a "central" alteration, and an alteration of the excitability of the neuromuscular spindles resulting from an overactivity of motor neurons. Loss of normal inhibition was also found in other experiments; in dystonics, in fact, there is a rapid curve of the recovery cycle of the blink reflex and of the H wave.<ref>Tolosa E, Montserrat L, Bayes A.: Blink reflex studies in focal dystonias: enhanced excitability of brainstem interneurons in cranial dystonia and spasmodic torticollis. Mov Disord. 1988;3(1):61-9</ref>

The patient responded positively to the administration of "SIRDALUD" at doses of 4 mg three times a day more than to the administration of diazepam. Tizanidine (Sirdalud) is in fact a molecule that acts centrally as a myotonolitic agent and is pharmacologically and chemically different from diazepam and baclofen. This is a potent inhibitor of  <math>\alpha</math> e <math>\gamma</math> motoneurons for  stiffness experimentally induced in mice and polysynaptic activity in cats. In the decorticated or decerebrated cat, tizanidine preferentially inhibits the tonic component of the reflex activity. The actions of tizanidine result from its agonist activity at noradrenergic subunit receptors and may also involve inhibition of the release of excitatory amino acids from spinal interneurons (EAAs).<ref>Coward DM: The drug treatment of spasticity. Sandoz 1997</ref> The action on muscle tone, the lower sedative effect compared to diazepam and baclofen and the resulting lower muscle weakness are the characteristics that led to the choice of this drug over the others (EAAs)

To reach a clear and meaningful clinical conclusion we need to ask ourselves the following question: