Difference between revisions of "2° Clinical case: Pineal Cavernoma"

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[[File:Bruxer SP2.jpg|left|300x300px]]
Bruxism, characterized by involuntary teeth grinding or clenching, often occurs during sleep and is influenced by neurophysiological factors. This condition can lead to Orofacial pain (OP) and is often treated without a full understanding of its underlying causes. Recent studies have explored the roles of neurotransmitters and the pharmacological impacts on bruxism, suggesting that the sensitization of the trigeminal nociceptive system and neural hyperexcitability may play significant roles in its pathophysiology.
Bruxism is more than just a dental issue; it involves complex neurophysiological processes. This article expands on traditional views by discussing dystonic phenomena and their relation to orofacial pain, moving beyond dental aspects to a broader neurophysiological perspective.
Dystonia in the cranial-cervical region, often manifesting as orofacial dystonia (OFD), can lead to various involuntary muscle contractions, impacting speech and eating. Bruxism is linked to genetic factors, central nervous system disorders, and even certain medications. Notably, the relationship between painful temporomandibular disorders (TMDs) and bruxism highlights a significant overlap with conditions like migraines and tension-type headaches.
The treatment of bruxism varies, focusing on alleviating pain and preventing dental damage. However, understanding the basic knowledge about its etiology is crucial, which includes dismissing morphological factors while emphasizing psychological and pathophysiological factors. Investigations into the neurobiological aspects of bruxism have shown that neurotransmitter systems like dopamine, serotonin, and norepinephrine play pivotal roles. Medications affecting these neurotransmitters can exacerbate or suppress bruxism, indicating a direct link between drug therapy and bruxism activity.
Furthermore, electrophysiological studies have provided insights into how pain influences mandibular reflexes, suggesting that orofacial pain could modify jaw reflexes through central mechanisms, affecting muscle responses during episodes of bruxism.
From a clinical perspective, understanding the basic knowledge of bruxism’s underlying mechanisms helps in formulating more effective treatment strategies. The role of the trigeminal nociceptive system in orofacial pain associated with bruxism is crucial for developing targeted therapies that address the neural aspects of the disorder.
The case study of a 32-year-old man, referred to as 'Bruxer', illustrates the complex interplay of neurological and dental factors in diagnosing and managing bruxism. This case emphasizes the need for a holistic approach in treating bruxism, one that incorporates both dental and neurophysiological insights to address the root causes of the disorder effectively.
[[Category:Pathology of temporomandibular joints, muscles of mastication and associated structures]]
[[Category:Pathology of temporomandibular joints, muscles of mastication and associated structures]]
[[Category:Sleep disorders]]
[[Category:Sleep disorders]]
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== Introduction to the bruxist case report==
 
'''Abstract:'''This chapter focuses on the clinical case of a 32-year-old man suffering from severe nocturnal and diurnal bruxism, coupled with chronic bilateral orofacial pain (OP), predominantly on the left side. Unlike the traditional approach that views bruxism solely as a dental issue, this case study adopts a broader neurophysiological perspective. It introduces the phenomenon of dystonia and its connection to bruxism, highlighting the overlapping effects of temporomandibular disorders (TMDs), headaches, and neurological factors such as hyperexcitability of the central nervous system (CNS).
 
The patient, after 15 years of bruxism treatment involving bite planes, presented with a worsening condition that included trunk and limb muscle stiffness, visual disturbances, and neurological abnormalities such as diplopia, nystagmus, and polykinetic tendon reflexes. The chapter contrasts dental and neurological findings, using a formal logical diagnostic framework to clarify the dominance of neurological over dental factors in this case.
 
Key diagnostic tools included electromyography (EMG), motor evoked potentials (MEPs), and jaw jerk reflex testing, which indicated trigeminal system involvement. The coherence demarcator (<math>\tau</math>), previously applied to the case of hemimasticatory spasm, was employed here to resolve conflicts between dental and neurological assertions, leading to a stronger focus on neurophysiological abnormalities.
 
The chapter concludes by proposing a neurophysiological path to decode the "machine language" of the CNS in bruxism, aiming to understand the condition not merely as a dental issue but as a possible manifestation of hyperreflexia and CNS hyperexcitability. The next diagnostic step will be elaborated in the following chapter, "Encrypted Code: Hyperexcitability of the Trigeminal System."
==Introduction to the bruxist case report==
As anticipated in the chapter '[[Bruxism - en|Bruxism]]' we will avoid indicating this disorder as an exclusive dental correlate and will seek a broader and essentially more neurophysiological description by making a brief excursus on dystonic phenomena, on 'Orofacial Pain' and only then will we consider the phenomenon 'bruxism' true and own. Subsequently we will move on to the presentation of the clinical case.   
As anticipated in the chapter '[[Bruxism - en|Bruxism]]' we will avoid indicating this disorder as an exclusive dental correlate and will seek a broader and essentially more neurophysiological description by making a brief excursus on dystonic phenomena, on 'Orofacial Pain' and only then will we consider the phenomenon 'bruxism' true and own. Subsequently we will move on to the presentation of the clinical case.   


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====Significance of contexts====
====Significance of contexts====


===== Dental Contest significance =====
===== Dental Contest significance=====




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<math>\Im_n </math> ?|and it is precisely here that the contexts conflict or rather the results may not be so decisive}}
<math>\Im_n </math> ?|and it is precisely here that the contexts conflict or rather the results may not be so decisive}}


===== Neurophysiological Contest significance =====
=====Neurophysiological Contest significance=====
In the '''neurological context''' we will therefore have the following sentences and statements to which we give a numerical value to facilitate the treatment, i.e. <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:
In the '''neurological context''' we will therefore have the following sentences and statements to which we give a numerical value to facilitate the treatment, i.e. <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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<math>\gamma_3=</math> Electrical silent period and contextual symmetry Figures 7, <math>\gamma_3=0\longrightarrow</math> Normality, negativity of the report
<math>\gamma_3=</math> Electrical silent period and contextual symmetry Figures 7, <math>\gamma_3=0\longrightarrow</math> Normality, negativity of the report




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