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

| 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:

{{:F:Delta1}} Positive radiological report of the TMJ in Figure 2, <math>\delta_1=1\longrightarrow</math> Abnormality, 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:

\Im_n\cup\{1,1.....1\}=1</math> with contextual coherent affirmation of sentence <math>\Im_n</math> in which it is argued that the symptomatology of the patient Mary Poppins has a neuromotor cause and the clinical consequences of a masticatory occlusal type are nothing other than a consequence of the neuropathic damage.

}}

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.   

To recap we therefore have:

\tau_n=

\Im_d

where  

<math>\tau_o=0</math> low severity performance of the dental context<math>\tau_n=1</math>reporting of high severity of the neurological 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.   

In this clinical iter that we have presented, the choice of the clinician to follow the electrophysiological trigeminal roadmap from which the positivity of the <math>\bar{\gamma_n}=1</math> assertions have already been derived, therefore, having already defined a picture of serious anomaly of absence of the jaw jerk and of the silent period masseterino on the right side of the patient will have to understand if the damage is intracranial or extracranial.

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)}}

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.

{{Q2|These results indicate axon-sparing demielination.}}  

Muscle nerve damage would not be explained only because patients with Hemimasticatory Spasm (HMS) do not have sensory disturbances but also because they often only have spasms in one or two levator mandibular muscles. These observations argue against damage to the motor root or to the intracranial portion of the mandibular nerve where the motor bundles are closely grouped,<ref>Pennisi E, Cruccu G, Manfredi M, Palladini G. [https://pubmed.ncbi.nlm.nih.gov/1795166/ Histometric study of myelinated fibers in the human trigeminal nerve]. J Neurol Sci 1991;105:22-8.</ref> favoring damage to the individual muscle nerves that pass through the infratemporal fossa.

In EMG, these prolonged spasms fit perfectly into the description of cramps, that is, discharges of irregular motor units that progressively increase, leading to the recruitment of much of the muscle of synchronous discharges at speeds of 40 to 60 Hz.<ref>Kimura J. Electrodiagnosis in diseases of nerve and muscle: principles and practice, 2nd edn. Philadelphia: FA Davis 1989.</ref> Common to hemifacial spasm and cramps however, ectopic EMG activities can also be detected.

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[[Category:Articles about logic of language]]