Lockjaw (Trismus): A Complete Guide to Causes, Diagnosis, and Treatment

Table of Contents

• Key Points
• Background: Why This Review Matters
• How Normal Chewing Works
• The Brain's Control of Chewing
• How the Researchers Reviewed the Evidence
• A New Way to Classify Trismus
• Neurological Causes with Structural Damage
• Neurological Causes Without Structural Damage
• Non-Neurological, Structural Causes
• Non-Neurological, Non-Structural Causes
• Full Differential Diagnosis List
• Diagnosis: How Doctors Tell These Causes Apart
• Treatment Approaches Covered by the Review
• What This Means for Patients
• Limitations of This Review
• Practical Recommendations
• Frequently Asked Questions
• Source Information

Key Points

• Trismus, or lockjaw, is a symptom of an underlying problem, not a diagnosis, and it is often under-recognised, especially in sedated or critically ill patients.
• Causes are classified as neurological or non-neurological, and each as structural or non-structural, guiding diagnosis and treatment.
• Diagnosis relies on clinical assessment plus MRI, CT, EEG, EMG, and trigeminal reflex testing to identify the cause.
• Treatment options reviewed include medication, botulinum toxin type A, physical therapy, surgery, and rehabilitation, matched to the mechanism.
• Red flags such as rapidly worsening jaw closure, fever, facial swelling, recent dental surgery, or new medication need urgent evaluation.

Background: Why This Review Matters

Trismus, commonly known as "lockjaw," is a clinical condition in which a person cannot open their mouth normally. The restriction is persistent and involuntary, and it comes from tonic contraction (sustained tightening) or spasm of the masticatory muscles — the muscles used for chewing.

How common trismus is remains uncertain. The authors state clearly that prevalence (how many people have it) varies depending on which patient group is studied and what is causing the problem. Trismus is also frequently under-estimated, because there are no standardised screening protocols (no routine, agreed-upon checks) and because it is hard to distinguish from other reasons a person might not open their mouth widely. This is a particular problem in sedated patients or those who are critically ill and cannot report symptoms.

Because of these gaps, the authors argue that clinicians need three things: a clearer understanding of the mechanisms behind trismus, a structured way to classify its causes, and an evidence-based algorithm (a step-by-step decision guide) for managing it. Their stated goal is to help doctors recognise trismus early, choose targeted treatments, and ultimately improve patient outcomes.

How Normal Chewing Works

Mastication (chewing) is the process that mechanically breaks food into small particles so they can be swallowed and digested by enzymes. It depends on a set of structures the authors call the stomatognathic system, which includes bones, joints, teeth, muscles, glands, and sensory receptors working together.

The mandible (lower jaw) is the only movable bone of the facial skeleton. It joins the skull on both sides at the temporomandibular joints (TMJs) — the jaw joints — which have a condyle–disc structure allowing both rotational and translational movement. That design lets the jaw open, close, move sideways, and jut forward. A fibrocartilaginous articular disc (a cushion of tough cartilage) keeps the bony surfaces aligned and spreads mechanical stress evenly. By contrast, the maxilla (upper jaw) is fixed and supports the upper dental arch.

Teeth are arranged symmetrically and are specialised by shape:

• Incisors — sharp edges for cutting.
• Canines — robust cusps for piercing food and guiding jaw movement.
• Premolars and molars — broad, cuspidated surfaces for grinding and crushing the food bolus (the ball of chewed food).

The four main masticatory muscles are the masseter, temporalis, and the medial and lateral pterygoid muscles. The masseter and temporalis mainly raise the jaw, while the pterygoid muscles enable the more complex sideways and forward movements. Accessory muscles, such as the buccinator and the suprahyoid group, help position the food and stabilise the jaw.

Saliva and the tongue are also essential. Saliva lubricates the mouth, softens food, and starts enzymatic digestion through amylase and lipase, while also helping food particles stick together into a bolus suitable for swallowing. The tongue continuously repositions food between the chewing surfaces and shapes the bolus. Its intrinsic and extrinsic muscles make it indispensable not just for chewing, but also for swallowing and speech.

The Brain's Control of Chewing

Chewing is largely automatic, but it is not simple. It is a highly coordinated, rhythmic motor behaviour that depends on three interacting systems: a central pattern generator, modulation from the cortex (the brain's outer layer), and sensory feedback from the mouth.

The basic rhythm of chewing appears to be generated in the brainstem by a central pattern generator — a network of neurons that produces rhythmic output without needing conscious effort. The key rhythm-generating elements sit in the dorsal division of the main sensory nucleus of the trigeminal nerve (the fifth cranial nerve, which carries sensation and motor signals for the face and jaw). Neurons in this region have intrinsic oscillatory properties, meaning they fire in rhythmic cycles on their own. Electrophysiological recordings and calcium imaging studies have confirmed that they drive rhythmic activation of the trigeminal motor nucleus.

The trigeminal motor nucleus, located in the pons (part of the brainstem), contains separate groups of jaw-opening and jaw-closing motoneurons (nerve cells that directly command muscles). These are clustered separately, with the jaw-closing group being significantly larger and made up mostly of motoneurons for the masseter and temporalis muscles.

Cortical structures matter too. The cortical masticatory area — located in humans within or next to the primary motor cortex — is the only cortical region whose inactivation significantly impairs chewing. Other regions contribute to controlling orofacial movement, including the primary somatosensory cortex, premotor cortex, supplementary motor area, insular cortex, anterior cingulate cortex, and amygdala.

Sensory feedback is indispensable for fine-tuning. Periodontal mechanoreceptors (pressure sensors in the ligament that anchors each tooth to the jawbone) provide detailed information about food contact and forces inside the mouth. They come in two subtypes: fast-adapting receptors, found mainly in the molars and active during the early phase of jaw closure, and slow-adapting receptors, found in the incisors and active throughout the entire closing phase. When these receptors are inactivated, the chewing sequence breaks down, including the ability to regulate bite force and fine oromotor control.

Muscle spindles — stretch sensors particularly rich in the deep layers of the masseter — also contribute to orofacial proprioception (the sense of where the jaw is and how hard it is working). Notably, spindles are absent in jaw-opening muscles but plentiful in jaw-closing muscles.

The authors stress that understanding this neuroanatomy is not academic. It is the prerequisite for interpreting what goes wrong in trismus and for designing targeted diagnostic and treatment strategies.

How the Researchers Reviewed the Evidence

This is a narrative review, not a systematic review. The authors followed SANRA (the Scale for the Assessment of Narrative Review Articles) recommendations as a quality guide.

They searched six databases: MEDLINE, Scopus, PubMed, Web of Science, EMBASE, and the Cochrane Library. Their search terms included "trismus," "jaw dysfunction," and "treatment of trismus," with specific terms such as "botulinum toxin type A" and "BoNT-A" added for trismus treatment. Boolean operators (AND, OR) were used to refine results. Terms related to tetanus, such as "tetanus trismus" and "tetanus lockjaw," were also included.

Studies were included if they:

1. Were published in peer-reviewed journals.
2. Provided clinically relevant data, case reports, case series, or expert reviews on the etiology (cause), pathophysiology (disease mechanism), diagnosis, or management of trismus.
3. Reported interventions such as pharmacological therapy, botulinum toxin type A, physical therapy, surgery, or rehabilitation.

Both neurological and non-neurological causes were considered, including structural and non-structural factors.

Studies were excluded if they:

• Were not published in English.
• Focused solely on animal models or in vitro (laboratory dish) experiments without translational relevance to patients.
• Lacked direct clinical applicability, including editorials, letters, conference abstracts, non-peer-reviewed publications, and anecdotal reports without sufficient clinical or scientific detail.

Because this is a narrative review, the authors note these criteria were used as a guide rather than a rigid filter. They deliberately allowed flexibility to include seminal, highly cited, or otherwise clinically significant references, even when those papers did not meet every inclusion criterion. They also manually searched the reference lists of retrieved articles for additional studies.

A New Way to Classify Trismus

The authors propose a refined etiological classification of trismus. The first split is between neurological and non-neurological causes. Each of those categories is then divided into structural and non-structural causes. Neurological causes are further divided according to whether they involve the central nervous system (CNS — the brain and spinal cord) or the peripheral nervous system (PNS — the nerves outside the brain and spinal cord).

The organising principle is that all forms of trismus, whatever the trigger, ultimately result from dysfunction of the masticatory system. This is the framework the authors use throughout the review, and the one their diagnostic algorithm is built on.

Neurological Causes with Structural Damage

Structural lesions — physical damage — to the central nervous system can cause trismus, particularly when they disrupt the motor pathways involved in chewing.

In diffuse axonal injury (DAI), a subtype of traumatic brain injury (TBI), widespread shearing of white matter tracts (the brain's long-distance nerve fibres) compromises both voluntary and reflex-based control of orofacial movements. This often shows up as increased tone in the masticatory muscles, contributing to trismus. Post-stroke trismus is most frequently associated with lesions affecting the corticobulbar tract (the nerve pathway running from the cortex to motor nuclei in the brainstem). Damage along this pathway leads to disinhibition of brainstem motor nuclei — a loss of the normal braking signals — resulting in hyperactivity and sustained contraction of the jaw-closing muscles.

Brainstem lesions from any cause — demyelinating, neoplastic (tumour-related), inflammatory, or traumatic — can interfere with the descending inhibitory control that normally regulates masticatory motor output. When that inhibitory modulation is lost, muscle tone rises abnormally, producing persistent and often severe jaw closure.

Peripheral nerve damage can also cause trismus, through neuroinflammatory and hyperexcitability mechanisms. Trauma or accidental injury during dental surgery to the trigeminal mandibular division (V3) — for example during nerve blocks or tooth extractions — can disrupt axonal integrity (the nerve fibre's structure) and trigger inflammatory cascades. These release mediators such as bradykinin and adenosine triphosphate, which promote peripheral sensitisation (heightened nerve sensitivity). This works by modulating ion channel activity, in particular increasing T-type calcium channels and hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels in trigeminal ganglion neurons. The result is abnormal neuronal excitability and spontaneous ectopic discharges — nerve firing when it should not.

That abnormal activity travels along motor fibres and causes sustained contraction of the masseter, temporalis, and pterygoid muscles. Direct nerve compression or post-traumatic fibrosis (scarring) can further impair normal inhibitory signalling between opposing jaw muscles, worsening the trismus.

The authors draw a key distinction: central lesions primarily affect supranuclear pathways (above the brainstem motor nuclei), while structural PNS damage shows how localised neuropathic changes — ion channel dysregulation, ectopic firing, and inflammatory fibrosis — can directly generate and sustain trismus.

Neurological Causes Without Structural Damage

Several neurological conditions produce trismus without structural damage, including Parkinson's disease (PD) and atypical parkinsonian syndromes such as progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). In these conditions, dysregulation of the masticatory muscles can promote trismus.

Trismus can also be a manifestation of oromandibular dystonia (OMD), particularly the jaw-closing subtype, or in severe cases part of status dystonicus (a life-threatening episode of continuous, severe muscle contraction). Epileptic status, through sustained hyperactivation of cortical and subcortical motor circuits, can precipitate involuntary contraction of the masticatory muscles. Storage diseases, often genetic, are another group — including copper storage disease (Wilson's disease) and iron-related neurodegeneration.

Medication adverse effects or poisoning are an important non-structural neurological category and include phenothiazines and metoclopramide. The review also lists malignant syndrome (including neuroleptic malignant syndrome), functional disorders, hemimasticatory spasm, and uremic encephalopathy (brain dysfunction from kidney failure) in this group.

Tetanus deserves special attention. Tetanus causes involuntary contractions of skeletal muscles, including the masseter and other jaw-closing muscles. Clinically, this produces the characteristic "lockjaw" of tetanus, which often appears before the disease's systemic (whole-body) manifestations. The severity and duration of tetanus-related trismus correlate with how much toxin-mediated neuronal inhibition has occurred. Early recognition is critical, because it allows prompt treatment with antitoxin therapy, supportive care, and muscle relaxants. The authors note that tetanus-induced trismus is a useful model for studying toxin-mediated hypertonia in the peripheral nervous system.

Heavy metal exposure — particularly lead and mercury — can also cause neurotoxicity that disrupts normal motor neuron function, leading to increased muscle tone and spastic contractions, including in the masticatory muscles. The review also lists trigeminal neuralgia, hypocalcaemia and hypomagnesemia (low blood calcium and magnesium), anaesthetic medications such as succinylcholine, halothane, and etomidate, and muscle contractures among the non-structural causes.

The practical message: when structural brain or nerve lesions have been ruled out, doctors should take a detailed medication and exposure history, use neurophysiological tests (EEG — electroencephalography; EMG — electromyography; and trigeminal reflex testing), and finally evaluate for botulinum toxin exposure. This integrated approach separates organic (drug-induced) causes from functional or psychogenic causes and from tetanus, guiding the right diagnostic and treatment path.

Non-Neurological, Structural Causes

Non-neurological causes cover a broad range of structural and inflammatory conditions that restrict jaw movement through mechanical obstruction, fibrosis, or joint dysfunction.

Congenital malformations — conditions present from birth — include trismus pseudo-camptodactyly syndrome and arthrogryposis multiplex congenita. These involve musculoskeletal abnormalities or fibrous contractures that restrict jaw mobility from the outset.

Temporomandibular joint disorders are a major non-neurological cause in dental and maxillofacial practice, covering joint dysfunction and ankylosis (stiffening or fusion of the joint).

Other structural causes listed by the authors include:

• Tumours of the oral cavity, oropharynx, or the masticator space.
• Trauma, including fractures of the mandible or maxilla.
• Orofacial infections — peritonsillar abscess, dental abscess, and osteomyelitis (bone infection).
• Post-surgical oedema (swelling) or hematoma (blood collection) after dental or maxillofacial procedures, and surgical complications generally.
• Soft tissue injuries causing hematoma or oedema.
• Radiation therapy, and fibrosis due to prolonged immobility.
• Burns.
• Complications of dental extraction, especially an impacted third molar (wisdom tooth).
• Rheumatoid arthritis, scleroderma, and temporal arteritis.

Non-Neurological, Non-Structural Causes

This category covers conditions that reduce jaw opening without a structural block or nerve lesion. The authors list myofascial pain syndrome (pain originating in the muscles and connective tissue of the jaw) and malignant hyperthermia — a rare, life-threatening reaction to certain anaesthetic agents characterised by dangerously high body temperature and muscle rigidity. Malignant syndrome appears in this group as well.

The clinical point is that these conditions require a different diagnostic route from structural or neurological causes. They are identified largely through history and examination rather than through imaging alone.

Full Differential Diagnosis List

The review's Table 1 sets out the complete differential diagnosis — the full list of conditions doctors should consider when a patient presents with trismus.

Neurological causes — central nervous system (structural):

• Traumatic brain injury (TBI), including diffuse axonal injury (DAI)
• Brain tumours
• Stroke (ischemic or haemorrhagic)
• Multiple sclerosis
• CNS infections: meningitis and encephalitis

Neurological causes — peripheral nervous system (structural):

• Trigeminal nerve lesions

Neurological causes — central nervous system (non-structural):

• Status epilepticus
• Parkinson's disease and atypical parkinsonian syndromes
• Storage disease (for example, Wilson's disease)
• Medication adverse effects or poisoning (phenothiazines, metoclopramide, and others)
• Functional disorder
• Malignant syndrome
• Status dystonicus and oromandibular dystonia (OMD)
• Hemimasticatory spasm
• Uremic encephalopathy

Neurological causes — peripheral nervous system (non-structural):

• Tetanus
• Trigeminal neuralgia
• Heavy metal poisoning (lead or mercury)
• Hypocalcaemia, hypomagnesemia
• Anaesthetic medications (succinylcholine, halothane, etomidate)
• Muscle contractures

Non-neurological causes (structural and non-structural):

• TMJ disorders (dysfunction or ankylosis)
• Tumours of the oral cavity or oropharynx, or of the masticator space
• Trauma
• Orofacial infections (peritonsillar abscess, dental abscess, osteomyelitis)
• Fractures of the mandible or maxilla
• Post-surgical oedema or hematoma following dental or maxillofacial procedures
• Surgical complications
• Soft tissue injuries causing hematoma or oedema
• Radiation therapy
• Fibrosis due to prolonged immobility
• Burns
• Complication of dental extraction (impacted third molar)
• Rheumatoid arthritis
• Scleroderma
• Temporal arteritis
• Congenital malformation: trismus pseudo-camptodactyly syndrome, arthrogryposis multiplex congenita
• Myofascial pain syndrome
• Malignant hyperthermia

Diagnosis: How Doctors Tell These Causes Apart

Diagnosis of trismus is primarily based on clinical assessment and physical examination. Instrumental investigations then help identify the underlying etiology (cause).

The authors emphasise that a thorough clinical evaluation should be combined with two kinds of testing. The first is neuroimaging — MRI and CT scans — to look for structural lesions. The second is neurophysiological testing that targets the trigeminal nerve, such as trigeminal reflex studies. Together, these help accurately define the mechanism behind the trismus, improve diagnostic precision, and guide individualised treatment.

When structural lesions of the CNS or PNS have been excluded, a further sequence is recommended:

1. Take a detailed anamnestic history (the patient's full medical and medication history) and pharmacological history.
2. Perform neurophysiological investigations — EEG, EMG, and trigeminal reflex testing.
3. Evaluate for botulinum toxin exposure.

This integrated approach lets doctors separate organic (drug-induced) causes from functional or psychogenic causes and from tetanus-induced trismus, and then choose the right diagnostic and treatment strategy.

The authors also flag a practical problem in diagnosis: it is difficult to distinguish trismus from other causes of limited mouth opening, particularly in sedated or critically ill patients. That is why their algorithm prioritises red flag conditions — urgent, potentially life-threatening causes that must be identified and treated quickly.

Treatment Approaches Covered by the Review

The authors propose a stepwise diagnostic and management algorithm. It prioritises red flag conditions, guides differential diagnosis, and supports treatment decisions in both outpatient and hospital settings — including surgical and critical care considerations.

The treatment approaches assessed in the reviewed literature include:

• Pharmacological therapy (medication).
• Botulinum toxin type A (BoNT-A) — a purified bacterial toxin given in very small doses to relax overactive muscles. BoNT-A appears in the article's keyword list and was a dedicated search term in the review.
• Physical therapy.
• Surgical procedures.
• Rehabilitation strategies.

For tetanus specifically, the review notes that early recognition is critical because it enables prompt treatment with antitoxin therapy, supportive care, and muscle relaxants. The severity and duration of tetanus-related trismus track with the extent of toxin-mediated neuronal inhibition, which is why speed matters.

The authors frame the whole algorithm around one aim: matching the treatment to the mechanism. A patient whose trismus comes from an overactive jaw-closing muscle after corticobulbar damage is not treated the same way as a patient with a dental abscess, a tetanus infection, or a drug reaction.

What This Means for Patients

The most important message is that trismus is a symptom, not a diagnosis. It is a sign that something is wrong with the chewing system, and the underlying cause could range from a minor dental problem to a neurological emergency.

Because prevalence data are lacking and screening is not standardised, trismus is likely under-recognised. Patients who notice they cannot open their mouth as widely as before — especially if the change is persistent or worsening — should treat it as a reason to seek medical assessment, not something to wait out.

The new classification matters to patients because it gives clinicians a structured route to the right answer. Neurological versus non-neurological, structural versus non-structural — this framework prompts the right questions, the right imaging, and the right referrals. In practice, that means fewer patients being treated for the wrong cause.

It also means treatment can be targeted. If the problem is a structural block such as an abscess or a fractured jaw, the solution is structural. If the problem is a hyperactive nerve pathway, the solution may involve medication or botulinum toxin. If the problem is tetanus, the priority is antitoxin therapy and intensive support.

Limitations of This Review

Several limitations deserve honest acknowledgement.

• This is a narrative review, not a systematic review. The authors state this explicitly. The inclusion and exclusion criteria were used as a guide, not as a rigid filter, and the authors deliberately included some highly cited or clinically significant papers that did not meet every criterion.
• Because it is non-systematic, the selection of studies involves judgement. Different reviewers might have chosen different papers.
• The prevalence of trismus remains uncertain. There are no standardised screening protocols, so nobody knows exactly how many people are affected or how the numbers break down by cause.
• Trismus is often under-estimated, especially in sedated or critically ill patients who cannot report symptoms reliably.
• The proposed classification and the stepwise algorithm are new proposals from the authors. The review does not report that they have been validated in prospective clinical trials — the article describes a framework, not a tested protocol with outcome data.

None of this makes the framework useless. It means the framework should be read as expert synthesis and a practical guide, not as proof of superiority over existing approaches.

Practical Recommendations

Based on the review, the following practical points apply to patients and the clinicians caring for them.

1. Treat reduced mouth opening as a clinical sign, not a nuisance. If you cannot open your mouth as widely as usual, and the change persists, get assessed.
2. Know the red flags. Rapidly worsening jaw closure, fever, facial swelling, recent dental surgery or trauma, recent tetanus exposure, or a new medication start should prompt urgent evaluation.
3. Bring a full medication list. Drug-induced trismus is a real category — phenothiazines, metoclopramide, and anaesthetic agents such as succinylcholine, halothane, and etomidate are all listed. So are lead and mercury exposure.
4. Report recent procedures. Dental extractions (especially impacted wisdom teeth), nerve blocks, and maxillofacial surgery are recognised triggers.
5. Expect imaging and nerve testing. MRI, CT, EEG, EMG, and trigeminal reflex studies may be used to find the cause.
6. Ask whether botulinum toxin type A is appropriate. BoNT-A is one of the treatment options reviewed for trismus.
7. Follow through with rehabilitation and physical therapy. Prolonged immobility itself causes fibrosis, so keeping the jaw moving under professional guidance matters.
8. If tetanus is suspected, act immediately. Early recognition allows antitoxin therapy, supportive care, and muscle relaxants — the earlier, the better.

Frequently Asked Questions

What is trismus, or lockjaw?

Trismus, commonly called lockjaw, is a condition in which a person cannot fully open their mouth because the chewing muscles stay tightly contracted. The restriction is persistent and involuntary, caused by sustained tightening or spasm of the masticatory muscles. It is a symptom, not a diagnosis, meaning an underlying cause should be identified. It is often under-recognised, especially in sedated or critically ill patients who cannot report symptoms.

What causes trismus?

Causes are split into neurological and non-neurological, then structural and non-structural. Neurological causes include stroke, traumatic brain injury, Parkinson's disease, tetanus, medication effects, and heavy metal poisoning. Non-neurological structural causes include temporomandibular joint disorders, tumours, trauma, infections, radiation therapy, and dental extraction complications. Non-neurological non-structural causes include myofascial pain syndrome and malignant hyperthermia. A full medication and exposure history helps separate these categories.

How do doctors diagnose trismus?

Diagnosis is primarily based on clinical assessment and physical examination, combined with instrumental tests. Doctors may use MRI and CT scans to look for structural lesions, and neurophysiological testing targeting the trigeminal nerve, such as trigeminal reflex studies. If structural lesions are excluded, they take a detailed medical and medication history, perform EEG, EMG, and trigeminal reflex testing, and evaluate for botulinum toxin exposure. This separates drug-induced, functional, and tetanus-related causes.

What treatments are available for trismus?

Treatment approaches reviewed include pharmacological therapy, botulinum toxin type A (BoNT-A), physical therapy, surgical procedures, and rehabilitation strategies. For tetanus specifically, early recognition is critical because it allows prompt treatment with antitoxin therapy, supportive care, and muscle relaxants. The aim is to match treatment to the underlying mechanism, so a patient with an overactive jaw-closing muscle is not treated the same way as one with a dental abscess or a drug reaction.

When should I seek urgent care for lockjaw?

Seek urgent evaluation for rapidly worsening jaw closure, fever, facial swelling, recent dental surgery or trauma, recent tetanus exposure, or a new medication start. These are red flag features that may indicate urgent, potentially life-threatening causes. If tetanus is suspected, act immediately, because early recognition allows antitoxin therapy, supportive care, and muscle relaxants. Reduced mouth opening that is persistent or worsening should be assessed rather than waited out.

What should I bring to my appointment for trismus?

Bring a full medication list, because drug-induced trismus is a real category. Phenothiazines, metoclopramide, and anaesthetic agents such as succinylcholine, halothane, and etomidate are listed, as are lead and mercury exposure. Also report recent procedures: dental extractions, especially impacted wisdom teeth, nerve blocks, and maxillofacial surgery are recognised triggers. Expect that imaging and nerve testing may be used to find the cause.

When should a patient with lockjaw (trismus) seek a second opinion?

Trismus is a symptom, not a diagnosis, and its causes range from a dental abscess to a neurological emergency, so the underlying reason matters more than the jaw restriction itself. A second opinion is reasonable when no clear cause has been identified, when structural brain or nerve lesions have been excluded but symptoms persist, or when the proposed treatment does not match the suspected mechanism. Because the classification and stepwise algorithm are new proposals not yet validated in prospective trials, an independent review of the diagnosis and records can help confirm the cause. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: An update on trismus: etiology, diagnosis and treatment.

Authors: Falletti M, Cuccarelli M, Evangelisti E, Zampogna A, Patera M, Truini A, Romeo U, Suppa A.

Affiliations: Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy; Department of Anesthesia and Intensive Care Unit, Campus Bio-Medico University Hospital Foundation, Rome, Italy; IRCCS Neuromed Institute, Pozzilli, Italy; Department of Oral and Maxillofacial Sciences, Sapienza University of Rome, Rome, Italy.

Journal: Frontiers in Neurology, volume 17, article 1758417.

DOI: 10.3389/fneur.2026.1758417

Publication timeline: Received 1 December 2025; revised 27 February 2026; accepted 10 March 2026; published 24 March 2026; corrected 20 April 2026.

Article type: Review (narrative, non-systematic). Open access under a Creative Commons Attribution License (CC BY).

Keywords: botulin toxin, lockjaw, malignant syndrome, tetanus, trismus.

Editors and reviewers: Edited by Gabriele Siciliano (University of Pisa, Italy). Reviewed by Farzin Sarkarat (Gulf Medical University, United Arab Emirates) and Daiana Cristina Pereira Santana (Federal University of Bahia, Brazil).

This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and does not replace personalised medical advice. If you or someone you care for has trouble opening the mouth, speak to a qualified clinician.