What are the key clinical features that differentiate trigeminal neuralgia from other causes of facial pain?

Trigeminal neuralgia (TN) is primarily differentiated from other causes of facial pain by its characteristic clinical features:

• Paroxysmal, electric shock-like pain: TN presents with sudden, brief, severe, stabbing or electric shock-like pain attacks lasting seconds to two minutes, typically triggered by light touch or activities such as chewing, talking, or brushing teeth. This contrasts with other facial pains that tend to be more constant or dull (NG127) ¹.
• Distribution along one or more divisions of the trigeminal nerve: The pain is unilateral and follows the sensory distribution of the trigeminal nerve branches (V1, V2, or V3), which helps distinguish it from other facial pain syndromes that may not respect these anatomical boundaries (NG127) ¹.
• Refractory periods and trigger zones: TN often has identifiable trigger zones on the face or inside the mouth where minimal stimulation precipitates pain, and a refractory period follows an attack during which pain cannot be triggered again immediately. This feature is less common in atypical facial pain or other neuralgias (Türp and Gobetti, 1996).
• Absence of continuous background pain: Unlike atypical facial pain or persistent idiopathic facial pain, TN typically lacks a continuous dull ache between attacks, although some patients may develop a background pain over time (NG127) ¹.
• Response to carbamazepine: TN usually shows a dramatic response to carbamazepine, which is less typical for other facial pain disorders (NG127) ¹.
• Exclusion of other neurological signs: TN is a diagnosis of exclusion; the absence of sensory loss or other neurological deficits helps differentiate it from secondary causes such as multiple sclerosis or tumours (NG127) ¹.
• Differentiation from trigeminal autonomic cephalalgias (TACs): TN pain is shorter and triggered by sensory stimuli, whereas TACs (e.g., SUNCT, SUNA) involve autonomic symptoms like lacrimation and nasal congestion and have different attack patterns (VanderPluym and Richer, 2015).

In summary, the key clinical features that differentiate trigeminal neuralgia from other facial pain causes are its paroxysmal, shock-like unilateral pain triggered by specific stimuli, presence of trigger zones, lack of continuous background pain, and typical response to carbamazepine, alongside the absence of neurological deficits and autonomic symptoms seen in other conditions ¹ (Türp and Gobetti, 1996; VanderPluym and Richer, 2015).