Post-traumatic trigeminal neuropathy

 

Symptoms and Clinical Presentation of Post-Traumatic Trigeminal Neuropathy

Clinically, traumatic trigeminal neuropathy is primarily manifested by impaired sensation in the innervation zone of the affected branches of the trigeminal nerve. Motor disorders occur if the motor root or motor branches of the mandibular division (V3) are involved.

 

Sensory Disturbances and Pain

Symptoms include:

• Paresthesia: Abnormal sensations like tingling, "pins and needles," crawling, or itching in the affected facial area.
• Hypoesthesia or Anesthesia: Decreased or complete loss of sensation (touch, pain, temperature) in the distribution of the injured nerve branch.
• Pain: Constant aching, burning, or sharp pain of varying intensity in the affected area. This is sometimes referred to as traumatic trigeminal neuropathic pain (TTNP).
• Dysesthesia or Allodynia: Unpleasant abnormal sensations or pain provoked by normally non-painful stimuli.
• Soreness with percussion of some teeth may occur if alveolar nerves are involved.
• Electroexcitability of dental pulp (tested by an electric pulp tester) in teeth innervated by the damaged trigeminal branch may be reduced or absent.

There may be a loss or decrease in all types of superficial sensitivity (light touch, pain, temperature) in the zone of innervation of the affected trigeminal nerve branch.

Motor Deficits (if V3 motor branch affected)

If the motor root of the trigeminal nerve or its motor branches within the mandibular division (V3) are damaged, weakness or paralysis of the muscles of mastication can occur. This may lead to:

• Difficulty chewing.
• Deviation of the jaw upon opening if there is unilateral weakness of the pterygoid muscles.
• Atrophy of the masseter or temporalis muscles over time.

 

Neuropathy of Specific Trigeminal Branches

Sometimes, neuropathy is observed in individual terminal branches of the trigeminal nerve:

• Mental Nerve Neuropathy (Chin Neuropathy): A branch of the inferior alveolar nerve (from V3). Characterized by paresthesia, pain, and sensory disturbances in the region of the lower lip and chin on the corresponding side ("numb chin syndrome"). This can be caused by mandibular fractures, dental procedures, or sometimes systemic malignancy (if presenting without obvious trauma).
• Lingual Nerve Neuropathy: A branch of V3 providing sensation to the anterior two-thirds of the tongue, floor of mouth, and lingual gingiva. Injury (often during wisdom tooth extraction or other floor-of-mouth surgery) causes numbness, altered taste (as chorda tympani fibers travel with it), and pain in these areas.
• Buccal Nerve Neuropathy: A sensory branch of V3 innervating the skin over the buccinator muscle and buccal mucosa. Injury can cause sensory loss in the cheek.
• Superior Alveolar Nerve Neuropathy: Branches of the maxillary nerve (V2) supplying upper teeth, gums, and maxillary sinus lining. Neuropathy here is characterized by a persistent, long course of pain or altered sensation in the upper teeth or maxilla.
• Palatine Nerve Neuropathy (Greater and Lesser Palatine Nerves): Branches of V2 via the pterygopalatine ganglion, supplying the hard and soft palate. Neuropathy is characterized by burning sensations and dryness in the area of half of the palate on the affected side. There may be a decrease or lack of sensitivity in the palatine nerve's innervation zone.
• Infraorbital Nerve Neuropathy: Terminal branch of V2. Often injured by orbital floor ("blowout") fractures or midface trauma, causing numbness of the cheek, side of the nose, upper lip, and upper gingiva.

 

Diagnosis of Post-Traumatic Trigeminal Neuropathy

To establish the type and severity of damage to the trigeminal nerve in traumatic neuropathy, a clear diagnosis of the level of its damage is required. The diagnostic process typically includes:

 

Clinical Neurological Examination

A detailed examination by a neurologist or neurosurgeon, assessing:

• Sensory function (light touch, pinprick, temperature) in all three divisions (V1, V2, V3) of the trigeminal nerve on both sides of the face.
• Corneal reflex (V1 afferent, VII efferent).
• Motor function of the muscles of mastication (masseter, temporalis, pterygoids) if V3 motor involvement is suspected.
• Palpation for tenderness over nerve exit points (supraorbital, infraorbital, mental foramina) or fracture sites.

 

Electrodiagnostic Studies

• Electroneurography (ENG/NCS): Can be used to assess the integrity of sensory branches (e.g., supraorbital, infraorbital, mental nerves) by recording sensory nerve action potentials (SNAPs). Motor NCS can evaluate the motor branches to the masseter or temporalis.
• Electromyography (EMG): Needle EMG of the muscles of mastication can detect signs of denervation or reinnervation if the motor root of V3 is affected.
• Trigeminal Reflexes (e.g., Blink Reflex): Can help localize lesions within the trigeminal pathways.

Imaging Studies

• CT Scan of the Brain and Skull Bones: Essential for identifying facial bone fractures (mandible, maxilla, orbital floor, skull base) that may have injured trigeminal nerve branches. Dental CT (CBCT) can be useful for jaw and dental injuries.
• MRI of the Paranasal Sinuses and Orbits, or Brain MRI with focus on cranial nerves: To visualize the trigeminal nerve and its ganglia, detect soft tissue injuries, hematomas, inflammation, or compressive lesions like tumors. High-resolution sequences (e.g., FIESTA, CISS) are valuable.

 

Treatment of Post-Traumatic Trigeminal Neuropathy

Disruption of nerve impulse transmission in neuropraxia (the mildest form of nerve injury where axonal continuity is preserved) usually lasts an average of 6–8 weeks, with full spontaneous recovery being typical. Treatment for more significant traumatic trigeminal neuritis or neuropathy is selected individually in each case and aims to alleviate symptoms, promote nerve recovery, and manage complications. It often includes a combination of conservative procedures.

 

General Principles and Conservative Management

• Addressing the Cause: If there's ongoing compression (e.g., by bone fragments, displaced dental implant, hematoma), surgical decompression may be necessary. Removal of a problematic dental implant that has caused damage (compression) to one of the branches of the trigeminal nerve is important.
• Pain Management:
  • Non-steroidal anti-inflammatory drugs (NSAIDs) like nalgesin (naproxen), ibuprofen, meloxicam, etc.
  • Analgesics.
  • Medications for neuropathic pain (sometimes referred to as "antipsychotics" in older texts, but more accurately anticonvulsants or antidepressants with analgesic properties): Carbamazepine (Finlepsin), gabapentin, pregabalin (Lyrica), amitriptyline.
• Observation for Neuropraxia: If neuropraxia is suspected, a period of observation for spontaneous recovery is often appropriate.

 

Pharmacological Treatment

In addition to pain medications:

• Corticosteroids: A short course of systemic corticosteroids may be considered in the acute phase to reduce inflammation and edema around the injured nerve.
• Vitamins: B-complex vitamins (group "B"), Vitamin C ("C"), and Vitamin E ("E") are often prescribed as supportive therapy for nerve health, though evidence for significant benefit in traumatic neuropathy varies.
• Homeopathic Remedies: Some patients explore these options.

 

Rehabilitative and Adjunctive Therapies

These aim to manage symptoms and support recovery:

• Acupuncture: Can be very effective in treating trigeminal neuropathy, particularly for pain relief and reducing paresthesias. It is aimed at:
  • Providing anti-inflammatory effects.
  • Removing edema and swelling of the nerve trunk.
  • Achieving a desensitizing effect (modulating pain perception).
  • Increasing the general resistance and adaptive capacity of the body.
  • Facilitating adaptive and compensatory reactions.
  • Promoting the most complete restoration of lost conduction of impulses along the nerve trunk.
• Nerve Stimulation: Transcutaneous Electrical Nerve Stimulation (TENS) may be used for pain relief.
• Muscle Stimulation: If motor branches are affected, electrical muscle stimulation may help maintain muscle viability during reinnervation.
• Physiotherapy: May include modalities like low-level laser therapy, ultrasound, or specific exercises if masticatory muscles are involved. The elimination of paresthesia and pain (neuralgia) on the skin of the face and in the teeth during treatment of trigeminal neuropathy can be accelerated with physiotherapy.
• Desensitization techniques and cognitive-behavioral therapy: For managing chronic neuropathic pain.

Surgical Intervention

Surgical treatment is considered if:

• There is a known nerve transection or severe disruption.
• Persistent compression by bone fragments, foreign bodies, or scar tissue is identified.
• Conservative management fails to provide adequate relief for severe, debilitating pain or significant functional loss, and there is no evidence of spontaneous recovery after an appropriate observation period.

Surgical options may include:

• Exploration and Decompression/Neurolysis: Freeing the nerve from entrapment or compression.
• Nerve Repair (Neurorrhaphy): Direct suturing of severed nerve ends.
• Nerve Grafting: Using a segment of another sensory nerve (e.g., sural nerve) to bridge a gap if direct repair is not possible.
• Removal of offending foreign bodies or compressive lesions.

The duration of treatment and its frequency for traumatic neuropathy of the trigeminal nerve will be dictated by the ongoing assessment of the nerve's functional state and the restoration of sensation in the facial skin and oral mucosa.

 

Differential Diagnosis of Facial Pain and Numbness

Post-traumatic trigeminal neuropathy symptoms must be differentiated from other conditions causing facial pain or sensory disturbances:

Condition	Key Differentiating Features
Post-Traumatic Trigeminal Neuropathy	Clear history of trauma to face/jaw/teeth or related surgery/procedure. Sensory loss, paresthesias, +/- pain in specific trigeminal branch distribution. Motor weakness if V3 motor root involved. EMG/NCS confirms peripheral nerve lesion.
Trigeminal Neuralgia (Tic Douloureux)	Paroxysmal, severe, electric shock-like pain, often triggered by light touch or specific movements. Usually no constant sensory loss between attacks initially. Often due to vascular compression.
Atypical Facial Pain / Persistent Idiopathic Facial Pain	Chronic, often constant, poorly localized facial pain, may not follow clear nerve distribution. No objective neurological deficits. Diagnosis of exclusion.
Dental Pathology (Pulpitis, Periapical Abscess, Cracked Tooth Syndrome)	Pain often localized to a tooth, may be throbbing, sensitive to temperature or percussion. Dental examination and imaging are key. Can refer pain.
Temporomandibular Joint (TMJ) Dysfunction	Pain in jaw joint, ear, or side of face, often with clicking, popping, or limited jaw movement. Can refer pain to trigeminal areas.
Sinusitis (Maxillary, Frontal, Ethmoid)	Facial pain/pressure over affected sinus, nasal congestion/discharge, fever. CT of sinuses diagnostic. Can irritate trigeminal branches.
Herpes Zoster Ophthalmicus/Maxillaris/Mandibularis (Shingles)	Vesicular rash in a trigeminal dermatome, followed by acute pain (herpetic neuralgia) and potentially postherpetic neuralgia.
Migraine or Cluster Headache with Facial Pain	Headache is primary symptom. Migraine often unilateral, throbbing, with associated features. Cluster headache severe, orbital/periorbital, with autonomic signs.
Tumors Affecting Trigeminal Nerve or Ganglion (e.g., Schwannoma, Meningioma)	Often gradual onset of progressive sensory loss, pain, or weakness. MRI is crucial.

 

Prognosis and Potential Complications

The prognosis for post-traumatic trigeminal neuropathy depends on the type and severity of the nerve injury:

• Neuropraxia: Generally excellent prognosis with full recovery, typically within 6-8 weeks to a few months.
• Axonotmesis: Recovery is possible through axonal regeneration (slowly, about 1 mm/day) but may be incomplete, especially if the distance for regeneration is long or if scar tissue forms. Persistent sensory deficits or pain can occur.
• Neurotmesis: Poor prognosis for spontaneous recovery. Surgical repair may offer some improvement, but outcomes are variable and often incomplete.

Potential complications include:

• Chronic neuropathic pain (traumatic trigeminal neuropathic pain - TTNP).
• Persistent numbness or bothersome paresthesias.
• Anesthesia dolorosa (pain in an area that is numb - rare but very difficult to treat).
• Motor weakness and atrophy of masticatory muscles if V3 motor root is severely affected.
• Impaired quality of life due to pain or sensory loss.
• Corneal complications if V1 (ophthalmic division) sensation is lost (neurotrophic keratitis).

 

Prevention of Iatrogenic Trigeminal Nerve Injury

While accidental trauma is often unavoidable, iatrogenic injuries (caused by medical/dental procedures) can be minimized:

• Thorough knowledge of facial and dental anatomy by surgeons and dentists.
• Careful surgical technique during procedures near trigeminal nerve branches.
• Precise administration of local anesthetic injections, avoiding direct intraneural injection.
• Use of appropriate imaging pre-procedure to identify nerve pathways when indicated.
• Minimizing trauma during tooth extractions or implant placements.

 

When to Consult a Specialist (Neurologist, Neurosurgeon, Oral & Maxillofacial Surgeon)

Following facial or dental trauma or procedures, consultation with a relevant specialist is important if an individual experiences:

• Persistent or worsening facial numbness, tingling, or pain.
• New onset of weakness in chewing muscles.
• Symptoms that do not resolve within the expected timeframe for neuropraxia (e.g., > 8-12 weeks).
• Severe, debilitating pain.
• Suspicion of ongoing nerve compression or significant nerve injury.

Early evaluation by a neurologist, neurosurgeon specializing in peripheral nerves, or an oral & maxillofacial surgeon with expertise in nerve injuries can lead to accurate diagnosis, appropriate management, and potentially improved outcomes.