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

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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:

<math>\Im_n </math>  we will have the same rational process:|and it is precisely here that the contexts conflict}}

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

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The <math>\tau</math> is a representative clinical specific weight, complex to research and fine-tune because it varies from discipline to discipline and for pathologies, essential in order not to make logical assertions collide <math>\Im_o</math> and <math>\Im_n</math> in the diagnostic procedures and essential to initialize the decryption of the logic communication code. Basically it allows you to confirm the consistency of a union <math>\Im\cup\{\delta_1,\delta_2.....\delta_n\}</math> with respect to another <math>\Im\cup\{\gamma_1,\gamma_2.....\gamma_n\}</math> and vice versa, giving greater weight to the severity of the statements and the report in the appropriate context.   

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.   

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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.   

{{Q2|The response in the right masseter was clearly delayed but relatively symmetrical in amplitude between sides. (Fig. 9)}}

The trigeminal root was stimulated transcrally through high voltage, low impedance through an electrical stimulator (Neuropack X1, Nihon Kohden Corporation, Tokyo, Japan)) with the anode electrode positioned at the apex and the cathode approximately 10 cm laterally from the apex along a line vertex acoustic meatus. The electric field is believed to excite the trigeminal motor nerve fibers via the trancranial route, near their exit from the skull.<ref name="fris1992" /><ref>G Frisardi, P Ravazzani, G Tognola, F Grandori. [https://pubmed.ncbi.nlm.nih.gov/9467995/ Electric versus magnetic transcranial stimulation of the trigeminal system in healthy subjects. Clinical applications in gnathology.] J Oral Rehab.1997 Dec;24(12):920-8.doi: 10.1046/j.1365-2842.1997.00577.x.</ref> Also in this case, the response in the right masseter was markedly delayed (3.5 ms on the right side 2 ms on the left and dispersed. amplitude of the M-wave.

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.