Difference between revisions of "1° Clinical case: Hemimasticatory spasm"

[[File:Spasmo emimasticatorio.jpg|left|300x300px]]

| autore = Gianni Frisardi

| autore2 = Giorgio Cruccu

| }}

From what has been exposed in the previous chapters from the 'Introduction' to the '[[Logic of medic language]]' chapters, beyond the complexity of the arguments and the vagueness of the verbal language, we found ourselves faced with a dilemma that of the context in which the patient is referred and in these cases for our poor Mary Poppins it seems to dominate the dental context, given the positive assertions reported by the clinical and laboratory tests performed on the patient.

*A set of {{:F:Im}} sentences, and a <math>n\geq1</math> number of other <math>(\gamma_1,\gamma_2,.....\gamma_n \ )</math> statements they are logically incompatible if, and only if, the union between them <math>\Im\cup\{\gamma_1,\gamma_2.....\gamma_n\}</math> it is inconsistent

Now, for the '''dental context''' we will have the following sentences and assertions to which we give a numerical value to facilitate the treatment and that is <math>\delta_n=[0|1]</math> where <math>\delta_n=0</math> indicates' normality' and <math>\delta_n=1</math> 'abnormality' and therefore positivity of the report:

Once we have washed away the myriad of positively reported normative data, which generate conflicts between contexts, thanks to the coherence marker <math>\tau</math> we have a much clearer and more linear picture on which to deepen the analysis of the functionality of the Central Nervous System. Consequently we can concentrate on intercepting the tests necessary to decrypt the machine language code that the SNC sends out converted into verbal language.

With a little effort and patience on the part of passionate readers who have followed the entire logical path, sometimes apparently off topic, we have reached a clinical picture in which the code to be decrypted is inherent in neuromotor damage. Consequently, the access keys to the code, the one that figuratively corresponds to the exact decryption algorithm, would correspond to the right choice of the neuromotor damage detector test.   

  }}</ref>   

The right masseter nerve was electrically stimulated in the infratemporal fossa (see clinical procedure chapter: [[Encrypted code: Ephaptic transmission]]) with a technique similar to that described by Macaluso & De Laat (1995).<ref>Macaluso G, De Laat A. [https://pubmed.ncbi.nlm.nih.gov/8773249/ H-reflexes in masseter and temporalis muscle in man. Experimental] Brain Research. 1995;107:315–320. [PubMed] [Google Scholar] [Ref list]</ref> Square cathode pulses (0.1 ms) generated by an electrical stimulator (Neuropack X1, Nihon Kohden Corporation, Tokyo, Japan) were delivered through a Teflon-coated monopolar needle electrode (TECA 902-DMG25, 53534) with a tip non-isolated (diameter 0.36 mm; area 0.28 mm2) inserted 1.5 cm through the skin below the zygomatic arch and anterior to the temporomandibular joint in the infratemporal fossa with electrical shocks of 0.5 - 5 mA, and 0.1 ms. The anode was a surface non-polarizable Ag-AgCl disc electrode (OD 9.0 mm) positioned over the ipsilateral ear lobe. Electrical stimulation of the masseter nerve never produced pain, and the subjects only perceived muscle contraction. The correct position of the stimulation electrodes was monitored throughout the experimental session by checking online the size of the M wave in the masseter muscle. The signals were recorded by placing surface electrodes on the masseter and temporal muscles and filtered at 10-2000Hz and by concentric needle electrodes inserted into the anterior temporal muscle.   

Having highlighted, through the execution of the <math>M-wave</math> and <math>_bRoot-MEPs</math> test, a delay in the conduction speed of the trigeminal nerve fibers generates the suspicion that it is a focal demyelination. This indicates that the problem is to be referred to the nervous component rather than to the muscular one, therefore, our attention should focus on the type of focal demyelination, extent of damage and presumably localization of the damage. The differential diagnosis at this point focuses on the type and area of the demyelinating damage, for example, if it is a damage exclusively referred to the masseterine motor nerve or the motor nerve of the temporal muscle is also involved, important for treatment with botulinum endotoxin. To resolve this doubt it is necessary to evoke a heteronymous <math>H-wave</math> response from recording on the temporal muscle.

The arrangement is similar to that previously described with regard to the <math>M-wave</math> with the variant that the temporal muscle is recorded simultaneously with the stimulation of the masseterine nerve in the intratemporal fossa by a bipolar needle electrode. The stimulation must be gradually adapted in order to evoke both a <math>M-wave</math> from the masseter that a heteronymous <math>H-wave</math> from the temporal muscle.

As previously mentioned and in order not to burden the topic, the detailed description of the 'Hephaptic' phenomenon will be treated in the chapter '[[Encrypted code: Ephaptic transmission]]' in order to better understand the physiological responses of heteronymous <math>H-wave</math> by pathological ones.

[[File:Hephaptic edited.jpeg|center|thumb|600x600px|'''Figure 10:''' On the left side indicated with EMG the recording of the motor unit discharge on the right masseter at the time of the spasm is shown while on the right below indicated with M-wave we can see two motor potentials evoked by the electrical stimulation in infratemporal fossa recorded on the masseter. With H-wave it is possible to note the recording of the heteronomous H-wave on the temporal ipsilateral to the stimulation.]]

Following this step by step path we have demonstrated a peripheral motor nerve injury as originally proposed by Kaufman.<ref name="kauf">Kaufman MD. [https://pubmed.ncbi.nlm.nih.gov/7436363/ Masticatory spasm in facial hemiatrophy]. Ann Neurol 1980;7:585-7.</ref> Conduction studies have shown a slowing of conduction in the extracranial course of masticatory nerve fibers without a reduction in the amplitude of <math>M-wave</math> and obviously EMG signs of chronic denervation. The temporal muscle biopsy appeared histologically normal.