THE SHORT LINGUAL FRENUM AS A RISK FACTOR FOR CEREBRAL VASCULOPATHIES

EJMHR European Journal of Medical and Health Research      Volume 1 | Number 3 |November-December 2023

THE SHORT LINGUAL FRENUM AS A RISK FACTOR FOR CEREBRAL VASCULOPATHIES

Dr. Antonio Ferrante, Dott. Roberto M. Crotti

Keywords: Short lingual frenulum, ankyloglossia, Stroke, cerebral ischemia,

Abstract: Introduction: The tongue is the first functioning organ in embryonic development. Its developmental abnormalities can lead to dysfunctions with distant damage. Cranio-cervical anatomy suggests that lingual dysfunction may contribute to damage in the cerebral arteriovenous flow. Objective: To evaluate the possible relationship between a short frenulum and cerebral vascular problems. Method: We conducted an epidemiological study comparing the presence of vascular problems in families where the examined subject had a short frenulum (a genetically transmitted condition) and families in which the examined subject had no frenulum abnormality. Results: The presence of a short lingual frenulum was correlated with the presence of episodes of vascular damage in approximately 80% of cases, while in families without this lingual alteration, the percentage of damage ranged from 10 to 13%. Conclusions: The significant influence that the presence of an altered lingual frenulum seems to have on the future possibility of developing vascular problems should lead to a more careful evaluation of the presence of an incorrect frenulum size.

Introduction: The tongue appears in the embryo at about four weeks in the so-called mesobranchial area. In the same area, the epiglottis, thyroid, submandibular, and sublingual glands also form. However, the tongue mainly originates from the occipital somites, which, along with the formation of the cervical vertebrae, participate in cerebral blood supply through the vertebral arteries. The tongue remains connected to the cervical vertebrae by immersing itself in the cervical fascia, which also contains the hyoid bone and related structures. Another peculiarity of the tongue is that it is the only organ innervated by six cranial nerves.(1) As Professor Marcello Brunelli, the discoverer of the function of cyclic AMP in short-term memory mechanisms (2), pointed out, the tongue is the only organ represented once and a half in each cerebral hemisphere. To understand how a lingual dysfunction may predispose to vascular damage, we must remember the cranio-cervical vascular system and the anatomy and physiology of the tongue and swallowing.

The most important element is probably the Vertebral Artery. This artery has a peculiarity: in its direct path to the skull, it penetrates the vertebral foramina from C6 to the Atlas (C1), after which it deviates backward and enters the Occipital Foramen, where it then anastomoses with the contralateral artery (the Basilar Trunk) near the Roots of the Hypoglossal Nerve. From it originate the Meningeal Branches, the Anterior and Posterior Spinal Arteries, and the Posterior Inferior Cerebellar Artery. The External Carotid Artery, which originates at the level of C3 and C4 and enters between the Posterior Belly of the Digastric Muscle and the Stylohyoid Muscle, is also important. Limiting ourselves to listing only the branches that may be affected by muscle dysfunction related to lingual function, we must mention:

The Ascending Pharyngeal Artery (Pharyngomeningeal), the Occipital Artery, which goes to the muscles of the occipital region superficially and to the meninges, the Medial Meningeal Artery, which ends with a Frontal Branch and a Parietal Branch that distribute internally to the Dura Mater of the respective areas. The Accessory Meningeal Artery.

Internal Carotid Artery. Originating just above the lateral edge of the Thyroid Cartilage, it penetrates the Temporal Bone through the Carotid Foramen, releasing four branches (e.g., Anterior Choroidal Artery, Anterior Cerebral Artery, Middle Cerebral Artery, and Posterior Communicating Artery).

Anterior Cerebral Artery, which gives rise to the Basilar Trunk. It releases Central Branches that penetrate the White and Gray Matter of the underlying nuclei and Cortical Branches that distribute to the Cortex of the Lobes.

Middle Cerebral Artery, which releases Cortical Branches and Central Branches.

Vertebral Vein (Brachiocephalic Venous Trunk). Originating from venous plexuses at the level of the Occipital Bone and C1, it descends within the Vertebral Foramina of the Vertebrae down to C6, after which it heads to its root. It provides blood drainage for the Spinal Cord and the Cervical Vertebral Column.

External Jugular Vein (Subclavian Vein). Its two roots, the Retromandibular Vein and the Posterior Auricular Vein, meet and converge approximately behind the Mandibular Angle.

Venous Sinuses of the Dura Mater. These are dilated venous structures located in the Dura Mater of the Skull, which receive various venous vessels. They then mostly drain into the Internal Jugular Veins.

Superior Cerebral Veins, draining the upper medial part of the Cerebral Hemispheres. They join to form the Superior Sagittal Sinus, which is located at the point where the Saggital Suture ends.

Analogous Inferior Cerebral Veins, which collect blood from the Occipital Lobes and Temporal Lobes. From the base of the Brain, it heads toward the Tentorium.

Sphenopalatine Vein, which drains the Nasal Cavity and communicates with the Ophthalmic Vein.

Internal Jugular Vein, which carries blood from the Brain and communicates with the Subclavian Vein. Its lower part is also called the Venous Angle.

Subclavian Vein, which becomes the Brachiocephalic Trunk in conjunction with the Internal Jugular Vein.

The preceding description demonstrates that not only arteries but also veins and venous sinuses may be affected by cranial dysfunction due to lingual dysfunction. The appearance of vascular phenomena in areas far from the tongue should therefore not be surprising. These considerations prompted the evaluation of the influence that a lingual dysfunction, such as a short frenulum, can exert on the cranio-cervical region.

THE LINGUAL FRENUM Along the midline, there is a thin fold of fibro-mucous membrane, the lingual frenulum, which connects the body of the tongue to the mucosa of the oral floor. The lingual insertion can be at the tip, and this pathological condition is called ankyloglossia, or it can be slightly closer (less than 2 cm) or further away (more than 2 cm) from the tip. The alveolar insertion can be marginal, at the base of the tooth, apical, at the apex of the tooth’s root, or subapical, below the apex of the tooth. The presence of a short lingual frenulum can be responsible for limited tongue mobility.

3.1. FUNCTIONAL ANATOMY The tongue, as a functional matrix, plays a plastic role on the palatal vault and the development of the maxillaries. A lingual dysfunction caused by an anatomical impediment such as a short frenulum can create disharmony in the stomatognathic system by altering the relationships between the bony bases and both anterior and posterior stability, causing abnormal tensions on the hyoid bone and, secondarily, cervical and postural issues.

In the resting position, the tip of the tongue comes into contact with the estereceptors, which were discovered only in 1999 to be present in large quantities at the opening in the palate of the nasopalatine nerve, the terminal branch of the second branch of the trigeminal nerve. Discovered by Professors Halata and Bauman, researchers in Comparative Anatomy (3), we have explained in numerous studies that demonstrated their particular importance in the production of neurotransmitters involved in brain function (4,5). In physiological swallowing, the tongue makes contact with the palate at this point (Palatal Spot) with its tip and raises the dorsum, pushing the bolus toward the pharynx (6). Recent research on the function of nasopalatine receptors has shown that their stimulation is also essential for muscle relaxation (7). The lack of contact between the tongue and the palatal receptors, on the contrary, leads to worsening muscle hypertonicity.

A short lingual frenulum, even in a static situation, causes a problem in the lingual and suprahyoid muscles similar to what a short muscle fascia does to the muscle it contains, i.e., contraction or hypertonia. In a dynamic situation, such as during swallowing, it has different effects on the muscles involved, in particular:

• It acts as an anterior anatomical restraint for the stylohyoid and digastric muscles, preventing them from moving the hyoid bone upward and backward, as should occur in physiological swallowing, thus pulling on the styloid and mastoid processes of the temporal muscle and blocking the hyoid bone anteriorly.
• It prevents the styloglossus and palatoglossus muscles from bringing the dorsum of the tongue into contact with the palatal vault.
• It does not allow the subhyoid muscles to perform their important stabilizing function on the hyoid bone, resulting in flexion of the cervical spine and head.

CEREBRAL VASCULOPATHIES In industrialized countries, cerebral vasculopathies are the third leading cause of death, after cardiovascular diseases and neoplasms, but they are the leading cause of chronic disability. The nosological category of cerebral vasculopathies includes both acute conditions, such as cerebral stroke and subarachnoid hemorrhage, and a variety of subacute or chronic clinical conditions, such as subcortical white matter pathologies, vascular etiology cognitive and behavioral disorders, vascular epilepsy, genetically-based vasculopathies, arteriovenous malformations, alterations of the arterial wall of the carotid and vertebrobasilar circulations, and post-stroke recovery and rehabilitation phases. In Italy alone, there are approximately 200,000 acute stroke events each year, with at least 80% being first events, resulting in a one-year mortality rate of 30% for ischemic forms and 50% for hemorrhagic forms. Acute cerebral vasculopathies cause more deaths (1.45 times) than myocardial infarction. In the case of arterial obstruction, ischemic stroke occurs (accounting for approximately 80% of stroke cases). In the case of a rupture of a cerebral artery, cerebral hemorrhage (10-15% of cases) or subarachnoid hemorrhage occurs, and these two situations cannot be differentiated based solely on clinical criteria; they require the use of imaging techniques such as brain CT and MRI. When neurological deficits completely resolve within 24 hours (generally within 60-90 minutes), it is referred to as a transient ischemic attack (TIA) if neuroimaging is negative, or as a completed infarct with full recovery when imaging reveals a vascular lesion consistent with clinical findings.

Despite constituting only about 2% of total body mass, the brain receives 15% of the cardiac output and continuously consumes 20% of the glucose and oxygen available to the entire body. The supply of these nutrients is essential because the brain parenchyma has no energy reserves. Cerebral circulation, through autoregulation systems involving changes in arteriolar resistance, is capable of maintaining relatively constant blood flow that satisfies neuronal energy and metabolic demands, even under conditions of systemic blood pressure variability. When an arterial vessel becomes occluded, blood flow is almost completely interrupted in the central (core) area of the irrigated territory, resulting in neuronal death. In the adjacent area (ischemic penumbra), blood supply is partially supported by collateral circulation, allowing nerve cells to remain vital but damaged and functionally compromised. Neuronal damage is caused by the cessation of metabolic processes, as well as by complex pathophysiological processes such as the release of excitatory neurotransmitters with excitotoxicity, electrophysiological alterations, production of free radicals, which can transform reversible ischemic penumbra into irreversible infarction.

An explanation of the relationship between lingual dysfunction and vascular problems comes from an understanding of the muscular structures.

MUSCULAR RELATIONS (8,9) The thoracic inlet is the region that connects the cervical and thoracic areas; it is crossed by blood and lymphatic vessels in their passage. If the return of cranial fluids to the thoracic cavity is even slightly inhibited by abnormal muscular hypertonicity at the level of the thoracic inlet, cranial movement activity is consequently altered by fluid congestion inside the cranial vault. At the thoracic inlet, the fibers of the sternocleidomastoid and trapezius muscles, along with their fasciae, have a significant impact on the functional mobility of bony structures, as well as on fluid circulation and fascial mobility. Even the infrahyoid muscles and their fasciae can interfere with the normal mobility of these regions, as well as the scalene muscles, which, although not acting directly on the cranial bones, can interfere with blood circulation through the subclavian artery and vein that pass between the fascial layers.

The external and anterior jugular veins are completely enveloped by the superficial layers of these fascial coverings, so an increase in fascial tension due to muscular hypertonicity can result in increased venous backpressure in the cranial vault.

CONSIDERATIONS From the biomechanical analysis of the swallowing process with a short frenulum, it is evident that there is a correlation between this and the state of hypertonia and hypertrophy of part of the infrahyoid musculature and the cervical tract. This evidence suggests that venous flow, although regulated by fine autonomous mechanisms, may encounter difficulties with a dual effect:

• At the arterial level, greater winding of the flow leads to increased sedimentation in areas of difficult passage, resulting in atherosclerotic deposits and increased intravascular pressure.
• At the venous level, the difficulty of passage leads to stagnation of reflux blood, increasing pressure in upstream structures.

DURAL RELATIONSHIPS The dural membrane adheres to the entire inner aspect of the cranial cavity, allowing the passage of various venous sinuses: the sagittal and transverse sinuses, the occipital sinus, the petrosal sinuses, and the straight sinus. The dural membrane transmits tensions originating from any of its points through its own structure, along a direction determined by the geometry of its anchoring points. It is not difficult to imagine how abnormal tensions in the membrane can interfere with the normal movement of cranial bones and the free circulation of blood through the venous sinus system. Interferences with venous sinus drainage can lead to increased intracranial venous backpressure, which reduces normal blood supply to the brain and can also cause a modest but significant increase in cerebrospinal fluid pressure, interfering with the normal movement of these vital fluids through the brain’s ventricular system and various subdural spaces.

TRIGEMINO-CARDIAC REFLEX Observations in humans have shown that overstimulation of the trigeminal nerve (10) can also cause severe bradycardia, hypotension, apnea, and gastric hypermotility. These effects have been attributed to the so-called “trigemino-cardiac reflex” (11,12,13).

The trigemino-cardiac reflex (TCR) is described as the sudden onset of cardiovascular effects (bradycardia, hypotension) that can be accompanied by apnea and gastric hypermotility during manipulation of one of the branches of the trigeminal nerve. It has been described in humans during craniofacial and maxillofacial surgery (Cha et al., 1999) and resection of pontocerebellar tumors (Schaller et al., 1999). Despite the powerful effects of the trigemino-cardiac reflex, there is limited information on the underlying physiological mechanisms.

CONSIDERATIONS The trigemino-cardiac reflex associates trigeminal stimulation with a drop in blood pressure in the cerebral vascular circulation. In the case of a real short frenulum, where the tongue does not reach to stimulate the emergence of the sphenopalatine branch of the trigeminal nerve, part of the trigeminal input is missing. This deficiency can be compensated by overstimulation of the periodontal trigeminal innervation, but it may not be sufficient, resulting in increased intravascular pressure in the cerebral circulation.

RESEARCH Two parallel studies were conducted in two regions of Italy. Patients were evaluated by specialists in orofacial rehabilitation and deglutition. An epidemiological study was conducted. All patients who came to our studies were asked if there were any cases of cerebral vascular diseases in their families, including parents, siblings, aunts, and grandparents. Responses to our question were very different between the group of patients who did not have frenulum problems and those who had a very short frenulum or ankyloglossia (the most severe condition in terms of tension and the ability to express correct motility).

In both studies, the control group consisted of patients undergoing therapy for incorrect swallowing but without lingual structural abnormalities.

The study group in Campania consisted of 40 subjects with a very short frenulum or ankyloglossia. For the control group, 40 subjects were randomly selected.

The study in Tuscany was conducted on 30 people with a real short frenulum according to the protocol described above. A control group of 30 subjects without lingual abnormalities was randomly selected.

Patient Ages: Given the relevance of family history, age was not considered as a significant factor.

RESULTS Of the 40 subjects with a short frenulum in the study conducted in Campania, 31 reported a family history of vascular events, while in the group without a short frenulum, only 4 subjects had a family history of such conditions.

In the study conducted in Tuscany, it was found that out of 30 patients with a real short frenulum, 24 had a family history of various types of vasculopathies, such as stroke, transient ischemic attack, and cerebral hemorrhage, accounting for 80% of the total. Among patients with a normal-sized lingual frenulum, the presence of familial vasculopathies was found in 4 out of 30 subjects (13.3%).

Given the significant value observed, we visited patients admitted to rehabilitation centers after suffering significant cerebral vascular problems. Seventy percent of them had a very short frenulum or ankyloglossia. Considering that approximately 8% of patients die during the first event, this confirms the magnitude of the damage that an altered frenulum can cause.

CONCLUSIONS The research has shown that there are anatomical conditions in which the hemodynamics of cerebral blood flow can be disturbed by an unsupported swallowing pattern with a lack of trigeminal stimulation through the palatal spot. In clinical practice, there is a higher incidence of cerebral vasculopathies when a real short frenulum is present. Furthermore, it leaves open the possibility of further investigations to determine whether appropriate frenulum treatment and swallowing rehabilitation can lead to changes in blood circulation.

 

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