Trigeminal Neuralgia

Known Symptoms

Classic symptoms:
- Unilateral, severe, brief (seconds to minutes), lancinating pain in the V1 (ophthalmic), V2 (maxillary), or V3 (mandibular) divisions.
- Pain triggered by light tactile stimuli (e.g., washing the face, brushing teeth, talking, wind exposure).
- Pain-free intervals between attacks.
Red flags:
- Bilateral pain, sensory loss, or constant background pain (suggests secondary causes).
- Corneal reflex impairment or other neurological deficits.

Known Causes

Primary (Classical) TN: Most commonly caused by neurovascular compression of the trigeminal nerve root entry zone by an adjacent blood vessel (e.g., superior cerebellar artery), leading to demyelination and aberrant nerve signaling.
Secondary TN: Associated with structural lesions such as tumors (e.g., vestibular schwannoma), multiple sclerosis (demyelinating plaques), or vascular malformations.
Pathophysiology: Ectopic impulses and ephaptic transmission between nerve fibers result in hyperexcitability and paroxysmal pain.

Care

Prevention: No known primary prevention; early diagnosis and treatment may reduce chronicity.
Follow-up:
- Regular monitoring of pain control and medication side effects.
- MRI surveillance if secondary cause is suspected or symptoms evolve.
- Long-term neurological and functional assessments.
- Patient education on trigger avoidance and emergency care for acute exacerbations.

Known Symptoms

Classic symptoms:
- Unilateral, severe, brief (seconds to minutes), lancinating pain in the V1 (ophthalmic), V2 (maxillary), or V3 (mandibular) divisions.
- Pain triggered by light tactile stimuli (e.g., washing the face, brushing teeth, talking, wind exposure).
- Pain-free intervals between attacks.
Red flags:
- Bilateral pain, sensory loss, or constant background pain (suggests secondary causes).
- Corneal reflex impairment or other neurological deficits.

Known Causes

Primary (Classical) TN: Most commonly caused by neurovascular compression of the trigeminal nerve root entry zone by an adjacent blood vessel (e.g., superior cerebellar artery), leading to demyelination and aberrant nerve signaling.
Secondary TN: Associated with structural lesions such as tumors (e.g., vestibular schwannoma), multiple sclerosis (demyelinating plaques), or vascular malformations.
Pathophysiology: Ectopic impulses and ephaptic transmission between nerve fibers result in hyperexcitability and paroxysmal pain.

Care

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