Question

What causes trigeminal neuralgia? Explain in your own words and give examples.

Answer 1

TRIGEMINAL NEURALGIA

DEFIITION

• Trigeminal neuralgia (TN) is defned as sudden, severe, brief, stabbing, and recurrent pain within the distribution of one or more branches of the trigeminal nerve.

TYPES OF TRIGEMINAL NEURALGIA :

• TYPICAL TRIGEMINAL NEURALGIA
• ATYPICAL TRIGEMINAL NEURALGIA
• PRE- TRIGEMINAL NEURALGIA
• MULTIPLE SCLEROSIS RELATED TRIGEMINAL NEURALGIA
• SECONDARY OR TUMOR RELATED TRIGEMINAL NEURALGIA
• TRIGEMINAL NEUROPATHY OR POST- TRAUMATIC TRIGEMINAL NEURALGIA
• FAILED TRIGEMINAL NEURALGIA

1.Typical trigeminal neuralgia

• Most common form, previously termed CLASSICAL, IDIOPATHIC and ESSENTIAL TRIGEMINAL NEURALGIA.
• Nearly all cases of typical trigeminal neuralgia are caused by blood vessel compressing the trigeminal nerve root.

2.Atypical trigeminal neuralgia

• it is characterized by a unilateral, prominent constant and severe aching and burning pain superimposed upon otherwise typical symptom.
• Some believe that atypical trigeminal neuralgia is due to vascular compression upon specific part of the trigeminal nerve( the portio minor) while other theorize atypical trigeminal neuralgia as more severe progression of typical trigeminal neuralgia

3. Pre trigeminal neuralgia

• Days to years before the first attack of TN pain, some sufferers experience odd sensations of pain, ( such as toothache) or discomfort ( parasthesia).

4.Multiple Sclerosis related trigeminal neuralgia

• symptoms of MS related TN are identical to typical TN.
• Bilateral TN is more commonly seen in people with MS. MS involves formation of demyelinating plaques within the brain.

5.Secondary or tumour related trigeminal neuralgia

• It may be related to cancerous or non cancerous tumours.

6.Failed trigeminal neuralgia

• In certain cases, all medications, surgical procedures prove ineffective in controlling TN pain.Such individual also suffer from additional trigeminal neuropathy as a result of destructive intervention they underwent.

ETIOLOGY OR CAUSES

Neurovascular confict

• Artery or vein  is usually compressing the trigeminal nerve near the pons injuring myelin sheath and causing erratic hyperactive functioning of the nerve.
• Focal arachnoid thickening, angulation, adhesion, traction, tethering or torsion, fibrous ring around the root,cerebello‑pontine angle (CPA) tumors, brain stem infarction, aneurism, and arteriovenousmalformation (AVM) can also cause TN.
• reduced basal ganglia μ‑opioid receptor
• altered gray matter (GM) in sensory, and motor cortexhas
• The dysfunction of multiple modulatory mechanisms

Bio resonance hypothesis

• This theory states that when the vibration frequency of a structure surrounding the trigeminal nerve becomes close to its natural frequency, the resonance of the trigeminal nerve occurs. The bioresonance can damage trigeminal nerve fibers and lead to the abnormal transmission of the impulse, which may finally result in facial pain.
• Trigeminal nerve fibers are damaged when the vibration frequency of nerve and surrounding structures becomes close to each other

Trigeminal convergence-projection theory

• In the trigeminal convergence-projection theory, it has been hypothesized that continuous or recurrent nociceptive inputs from head and neck converge on spinal trigeminal nucleus (subnucleus caudalis), where the release of neurotransmitters and vasoactive substances may be promoted.
• This release decreases the threshold of adjacent second- order neurons that receive input from sites other than nociceptive sources.
• The signals from these excited second-order neurons may be transmitted to the thalamus, limbic system, and somatosensory cortex and interpreted as pain.

Areterial elongation hypothesis

• according to this theory arterial elongation can cause nerve compression and ause trigeminal neuralgia

Vascular theory

• Arterial compression with venous conflict can cause TN
• Persistant primitive trigeminal artery ,its aneurysm and vertebro basilar ectasia can also cause TN

PATHOLOGY

Ignition theory

• Vascular contact leads to instability and atrophy
• Nerves become hyperexcitable and generate abnormal discharges
• Spontaneous firing results in burning and paresthesias
• Cascade propagation to the trigeminal nucleus is perceived as burst of pain.
• Intense flares from synchronization of bursts “ephaptic crosstalk” and increased ions or neurotransmitters in the interstitial space

DIAGNOSIS

• Neuro examination  findings are usually normal.

• Rapid spreading of pain, bilateral affliction, or involvement of other cranial nerves suggests a systemic cause

• multiple sclerosis

• expanding cranial tumors

• Nerve compression on MRI often not visualized

• Blood work indicated if medical therapy is contemplated or to exclude collagen vascular diseases

TREATMENT

MEDICAL

 Based on current evidence, therapy with carbamazepine is initiated and patients are switched at the earliest opportunity to the controlled-release (CR) formulation, which has fewerside effects

 If carbamazepine causes troublesome side effects, reduce the dose and add baclofen.

 Alternatively oxcarbazepine or addon therapy either with lamotrigine or with phenytoin may be tried.

 In refractory cases gabapentin is probably the most promising drug.

 Pregabalin, topiramate or even the “older” anticonvulsants valproate and phenytoin may be tried in recalcitrant cases.

SURGERY

 Medically resistant patients who are physically able to withstand neurosurgery, particularly with typical CTN, are prime candidates for surgery

 The decision to opt for surgery is based on response to and side effects from medical treatment, the patient’s age and profession, and the surgical facilities and expertise available.

 Surgery may be aimed peripherally at the affected nerve or centrally at the trigeminal ganglion or the posterior fossa

SURGICAL MANAGEMENT:

PERIPHERAL INJECTION:

It has been known that injection of destructive substance into peripheral branches of the trigeminal nerve, produces anaesthesia in the trigger zones or in areas of distribution of spontaneous pain.

A) LONG ACTING ANAESTHETIC AGENTS: Without adrenaline such as bupivacaine with or without corticosteroids may be injected at the most proximal possible nerve site.

(B) ALCOHOL INJECTION: 0.5 – 2 ml of 95 % absolute alcohol can be used to block the peripheral branches of the trigeminal nerve. Aim is to destroy the nerve fibres. It produces total numbness in the region of distribution of the nerve that was anaesthetized. Complication: Necrosis of the adjacent tissue Fibrosis Alcohol induced neuritis

PERIPHERAL NEURECTOMY (NERVE AVULSION):

• Oldest & most effective peripheral nerve destructive method Can be repeated & relatively reliable technique. It acts by interrupting the flow of a significant number of afferent impulses to central trigeminal apparatus.
• Performed commonly on infraorbital, inferior alveolar, mental and rarely lingual. Disadvantage: May produce full anaesthesia deep hypoesthesia

Braun’s trans antral approach:

• An intra oral incision is made from the maxillary tuberosity to the midline in the maxillary vestibule.
• The descending palatine branch of the trigeminal nerve is identified & traced to the sphenopalatine ganglion.
• The maxillary nerve is sectioned from the foramen rotundum to the inferior orbital fissure.
• The antral mucoperiosteal flap in the vestibule is repositioned & sutured back. A 3 cm window is made in the antero – lateral wall of the maxillary sinus

INFERIOR ALVEOLAR NEURECTOMY:

(i) Extra oral approach

The extra oral approach: Done through Risdon’s incision After reflection of masseter, a bony window is drilled in outer cortex & nerve is lifted with nerve hook & avulsed from its superior attachment & mental nerve is avulsed anteriorly through the same approach.

(ii)Intra oral approach

• Done via Dr Ginwalla’s incision Incision is made along with the anterior border of ascending ramus, extending lingually & buccally & ending in a fork like an inverted Y.
• Incision is then deepened on the medial aspect of ramus. The temporalis & medial pterygoid muscles are split at their insertion & inferior alveolar nerve is located.
• The nerve is ligated at two points in the most superior part visible & divided between the ligature. The superior end is cauterized & the lower end is held securely using a hemostat.
• The mental nerve is also similarly ligated in two points close to the mental foramen & divided between two.
• The remaining nerve is held at the inferior alveolar end & wound around the hemostat & excised from the canal.

LINGUAL NEURECTOMY:

• An incision is made in the anterior border of the ramus slightly towards the lingual side.
• The lingual aspect is exposed & the lingual nerve identified in the third molar region just below the periosteum. The nerve can be either avulsed or ligated, cut and the ends may be cauterized.

CRYOTHERAPHY:

• Barnard first used cryotheraphy in 1981 for the treatment of the trigeminal neuralgia.

• After identifying the affected nerve , it is then exposed to the cryoprobe intraorally.

• Direct application of cryotheraphy probe at temperatures colder than -60 C are known to produce Wallerian degeneration without destroying the nerve sheath itself.

• Nerve is exposed for 2 mm freeze followed by 5 mm thaw cycle.

• The freeze – thaw cycle is repeated at least 3 times.