2° Clinical case: Pineal Cavernoma

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2° Clinical case: Pineal Cavernoma

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.

Keywords

Bruxism - Refers to the medical condition characterized by the involuntary grinding or clenching of teeth, typically during sleep, which can lead to jaw pain and damage to teeth.

Orofacial Pain - Describes pain felt in the face and mouth area, often associated with conditions like bruxism, and includes symptoms such as jaw muscle pain and headaches.

Neurobiological Factors of Bruxism - Focuses on the underlying neurophysiological causes of bruxism, emphasizing how neurotransmitters and neural pathways contribute to involuntary teeth grinding.

Trigeminal Nociceptive System - Pertains to the part of the nervous system involved in transmitting pain from the face to the brain, crucial in understanding the pain associated with bruxism.

Dopaminergic Medication and Bruxism - Involves the impact of medications affecting dopamine levels in the body, which can influence the occurrence and severity of bruxism.

Mandibular Stretch Reflexes - Deals with reflex actions of the jaw muscles, which are affected by bruxism and can lead to changes in jaw muscle activity and tension.

Sleep Bruxism - Specifically refers to bruxism that occurs during sleep, distinguishing it from bruxism that might occur during waking hours, with different etiological factors and treatment approaches.

Treatment of Bruxism - Encompasses various strategies and interventions used to manage and alleviate the symptoms of bruxism, including dental guards, medication, and behavioral therapy.

Temporalmandibular Joint Dysfunction (TMD) - Relates to disorders of the jaw joint and chewing muscles, often linked to bruxism, causing pain and dysfunction in the jaw joint and surrounding tissues.

Pharmacological Effects on Bruxism - Describes how certain drugs can either exacerbate or suppress bruxism, indicating the importance of medication management in treating bruxism.

 

 

Introduction

As anticipated in the chapter '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.

Figura 1: The subject was a 32-year-old man suffering from pronounced nocturnal and diurnal bruxism and chronic bilateral Oorofacial pain

Dystonia is an involuntary, repetitive, sustained (tonic), or spasmodic (rapid or clonic) muscle contraction. The spectrum of dystonias can involve various regions of the body. Of interest to oral and maxillofacial surgeons are the cranial-cervical dystonias, in particular, orofacial dystonia (OFD). OFD is an involuntary, sustained contraction of the periorbital, facial, oromandibular, pharyngeal, laryngeal, or cervical muscles. OFD can involve the masticatory, lower facial, and tongue muscles, which may result in trismus, bruxism, involuntary jaw opening or closure, and involuntary tongue movement.

The etiology of OFD is varied and includes genetic predisposition, injury to the central nervous system (CNS), peripheral trauma, medications, metabolic or toxic states, and neurodegenerative disease. However, in the majority of patients, no specific cause can be identified. An association was found among painful temporomandibular disorders (TMDs), migraine, tension-type headache, and sleep bruxism, although the association was only significant for chronic migraine. The association between painful TMDs and sleep bruxism significantly increased the risk for chronic migraine, followed by episodic migraine and episodic tension-type headache.

Bruxism is the most frequently occurring oral movement disorder, and can occur in subjects while awake and during sleep. Both forms are likely to have different etiologies, and their diagnosis and treatment require different approaches. Treatment is indicated when bruxism causes pain in the masticatory system or leads to damage such as tooth wear or fractures of teeth, restorations, or even of implants. A focused review on the etiology of bruxism concluded that there is a limited role for morphological factors in the etiology of bruxism, while psychological factors (e.g., stress) and pathophysiological factors (e.g., disturbances in central neurotransmitter systems) are more prominently involved.

Orofacial pain (OP), including pain from TMDs, exerts a modulatory effect on mandibular stretch reflexes. Electrophysiological studies have shown that experimentally induced pain from injections of 5% hypertonic saline solution into the masseter muscle causes an increase in the peak-to-peak amplitude of the jaw jerk. This facilitatory effect appears to be related to an increased sensitivity of the fusimotor system, which at the same time causes muscle stiffness. In addition, a number of animal studies of experimentally-induced muscle pain have shown that activation of the muscle nociceptors markedly influences the proprioceptive properties of the muscle spindles through a central neural pathway, and that washing of the local algogenic substance causes a return to normal tendon reflexes.

However, few studies have attempted to characterize the pain associated with bruxism (i.e., to examine the neurobiological and physiological characteristics of the mandibular muscles). Some clinical cases and small-scale studies suggest that certain drugs linked to the dopaminergic, serotoninergic, and adrenergic systems can either suppress or exacerbate bruxism. Further, the majority of these pharmacological studies indicate that various classes of drugs can influence the muscular activity related to bruxism, without exerting any effect on OP.

Therefore, the sensitization of the trigeminal nociceptive system and the facilitating effect on mandibular stretch reflexes and CNS hyperexcitability are neurophysiopathogenetic phenomena that can be correlated to pain in the craniofacial region. However, up to now, no correlation has been reported between OP, dysfunction of the mesencephalic nuclei, and facilitation of trigeminal nociception, except for a clinical study on a patient affected by pontine cavernoma, which highlighted a relative facilitation of the trigeminal nociceptive system through the blink reflex.

Case report

As anticipated we will take up the same diagnostic language presented for the patient Mary Poppins so that it becomes an assimilable and practicable model, and we will try to superimpose it on the present clinical case called 'Bruxer'.

The subject was a 32-year-old man suffering from pronounced nocturnal and diurnal bruxism and chronic bilateral OP prevalent in the temporoparietal regions, with greater intensity and frequency on the left side. The patient came to our observation after being treated for 15 years by dental colleagues with a biteplane. A sort of muscular stiffening of the trunk and legs had recently been added to bruxism and orofacial pain. Come to our observation beyond the clinical signs of bruxism the patient, to neurological examination, showed a contraction of the masseter muscles with pronounced stiffness of the jaw, diplopia and loss of visual acuity in the left eye, left gaze nystagmus with a rotary component, papillae with blurred borders and positive bilateral Babynski’s, and polykinetic tendon reflexes in all four limbs.

From what has been exposed in the previous chapters from the 'Introduction' to the chapters 'Logic of medical language' and the last chapter 'Bruxism', in addition to the complexity of the arguments and the vagueness of the verbal language, we could find ourselves faced with a clinical situation in which seems to dominate one of the contexts considered.

«does the tennis match start again?»
(it looks like it but....)

Unlike the patient with 'Hemimasticatory Spasm', the clinical case of our poor 'Bruxer' shows a phenomenon of overlapping of propositions, assertions and logical sentences in the dental and neurological context and apparently neither of the two obtains an absolute and clear compatibility and coherence. This has repercussions in the clinic in which all the actors involved (medical examiners) are right and contextually wrong, making the diagnostic conclusion inadequate and dangerous, but let's see the process as a whole step by step.

Significance of contexts

In the dental context we will have the following sentences and statements to which we give a numerical value to facilitate the treatment, namely $\delta _{n}=[0|1]$ where it $\delta _{n}=0$ indicates 'normal' e $\delta _{n}=1$ abnormality and therefore positivity of the report:

$\delta _{1}$ Negative MR report of the TMJ in Figure 2, $\delta _{1}=0\longrightarrow$Normality, negativity of the report

$\delta _{2}$ Negative axiographic report for right condylar traces in Figure 3, $\delta _{2}=0\longrightarrow$ Normality, negativity of the report

$\delta _{3}$ Negative axiographic report for left condylar traces in Figure 4, $\delta _{3}=0\longrightarrow$ Normality, negativity of the report

$\delta _{4}$ Symmetric EMG interference pattern in Figure 5, $\delta _{4}=0\longrightarrow$ Normality, negativity of the report

• 

  Figura 2: $\delta _{1}=0\longrightarrow$ MR images of the temporomandibular joint (right side only shown for simplification) show no signs of meniscal derailment and/or inflammation. Negative result report.

• 

  Figura 3: $\delta _{2}=0\longrightarrow$A xiographic tracing performed with a paraocclusal tray showing a normal translational and mediotrusive trend of the right condyle. Negative result report

• 

  Figura 4: $\delta _{3}=0\longrightarrow$ Axiographic tracing performed with a paraocclusal spoon showing a normal translational and mediotrusive course of the left condyle

• 

  Figura 4: $\delta _{4}=0\longrightarrow$ Masseter muscle EMG tracing (upper/right and left masseter respectively).The test shows bilateral symmetry in motor unit recruitment

«We could, paradoxically, have the same rationale in the neurological context $\Im _{n}$ ?»
(and it is precisely here that the contexts conflict or rather the results may not be so decisive)

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. $\gamma _{n}=[0|1]$ where $\gamma _{n}=0$ indicates 'normality' and $\gamma _{n}=1$ 'abnormality and therefore positivity of the report:

$\gamma _{1}=$ Presence and symmetry of the Motor Evoked Potentials of the trigeminal roots in Figure 5, $\gamma _{0}=0\longrightarrow$ Normality, negativity of the report

$\gamma _{2}=$ Presence of jaw jerk with relative amplitude asymmetry in Figure6 $\gamma _{2}=1\longrightarrow$ Abnormality, negativity of the report* (the * was inserted to note an ambiguity in the report which we will describe in detail in the clinical discussion)

$\gamma _{3}=$ Electrical silent period and contextual symmetry Figures 7, $\gamma _{3}=0\longrightarrow$ Normality, negativity of the report

• 

  Figure 5: ${\gamma _{1}}=$ Motor Evoked Potentials of the trigeminal roots

• 

  Figure 6: ${\gamma _{2}}=$ Jaw jerk detected electrophysiologically on the right (upper traces) and left (lower traces) masseters. The morphology and duration of the silent periods called 'Esteroceptive Suppression' appear to be symmetrical.

• 

  Figure 7: $\gamma _{3}=$ Electrical silent period detected electrophysiologically on the right (upper superimposed traces) and left (lower superimposed traces) masseters

Demarcator of Coherence $\tau$

As we described in the chapter '1st Clinical case: Hemimasticatory spasm' the $\tau$ is a representative clinical specific weight, complex to research and develop because it varies from discipline to discipline and for pathologies, essential in order not to collide the logical assertions $\Im _{o}$ and $\Im _{n}$ in diagnostic procedures and fundamental to initialize the decryption of the machine language code. Basically it allows you to confirm the coherence of a union $\Im \cup \{\delta _{1},\delta _{2}.....\delta _{n}\}$ versus another $\Im \cup \{\gamma _{1},\gamma _{2}.....\gamma _{n}\}$and vice versa, giving greater weight to the seriousness of the allegations and the report in the appropriate context.

The demarcation weight $\tau$, therefore, gives more significance to the more serious assertions in the clinical context from which they derive and therefore beyond the greater or lesser positivity of the assertions $0\leq \delta _{n}\leq 1$ or $0\leq \gamma _{n}\leq 1$ which in any case are always verified and respected, these must be validated according to the intrinsic clinical severity by multiplying the average of the assertions ${\bar {\delta _{n}}}$ and ${\bar {\gamma _{n}}}$ for a $\tau =[0|1]$ where $\tau =0$ indicates 'low severity' while $\tau =1$ 'high severity'.

To summarize in our case 'Bruxer' we therefore have:

$\Im _{o}\cup ({{\bar {\delta }}_{n})}\tau _{o}+\Im _{n}\cup ({{\bar {\gamma }}_{n})}\ \tau _{n}=\Im _{d}$

where

${{\bar {\delta }}_{n}}=$ average of the value of clinical statements in the dental context and therefore ${{\bar {\delta }}_{n}}=0$

${{\bar {\gamma }}_{n}}=$ average of the value of clinical statements in the neurological context and therefore ${{\bar {\gamma }}_{n}}=0,33$

$\tau _{o}=0$ reporting of low severity of the dental context

$\tau _{n}=1$ reporting of high severity of the neurological context

where the 'consistency marker $\tau$ will define the diagnostic path as follows

$\Im _{o}\cup 0+\Im _{n}\cup 0,33=\Im _{d}\longrightarrow \Im _{d}=\Im _{n}\cup 0,33\longrightarrow \Im _{d}=\Im _{n}$

As can be seen in our clinical case 'Bruxer' we have a very slight diagnostic slope towards the neurological context which allows us, however, to glimpse more of a neurological component rather than a dental one.

«This procedure of formal logical syntax has allowed us to eliminate the interference of low clinical seriousness statements and quickly define a neurological rather than dental diagnostic path through the definition of$\Im _{d}=\Im _{n}$»

Once the myriad of normative data reported positively, which generate conflict between contexts, has been washed away, thanks to the coherence demarcator $\tau$ we have a much clearer and more linear picture on which to deepen the analysis of the functionality of the Central Nervous System ( CNS) than in our clinical case ' Bruxer' appears somewhat intrigued by the low diagnostic weight derived from the neurological assertions $\Im _{n}\cup 0,33$.

This average figure derives primarily from a hypothetical jaw jerk amplitude anomaly labeled with an asterisk (*). We will talk about it in the section dedicated to this trigeminal reflex.

Consequently we can concentrate on intercepting the tests necessary to decrypt the machine language code that the CNS sends outwards converted into verbal language which at first sight would seem to concern a sort of hyperreflexia of the tendon reflexes. and specifically the jaw jerk. To confirm this hypothetical intuition, a brainstorming of the type 'Cognitive Neural Network' abbreviated as 'RNC' presented for the diagnosis of the case of our 'Mary Poppins' in the chapter 'Encrypted code: Ephaptic transmission' is necessary.

However, through this first diagnostic process we have made progress because, contrary to the codified process in dental disciplines, we are undertaking a neurophysiological process to decrypt the machine language code of 'bruxism'.

In order not to weigh down the discussion, we will deal with the second diagnostic step of the Masticationpedia model in the following chapter entitled 'Encrypted code: Hyperexcitability of the trigeminal system'

Bibliography & references