Anxiety, before and during treatment

Correct answer: C. Anterograde amnesia

• A. Dissociative anaesthesia describes KETAMINE, in which the patient appears awake but is dissociated from the environment, with nystagmus, catalepsy and emergence phenomena on recovery.
• B. Benzodiazepines have NO analgesic property whatsoever. This is a practical point rather than a technicality — full local anaesthesia is still required, and a sedated patient who is inadequately anaesthetised will still respond to pain.
• C. CORRECT. ANTEROGRADE AMNESIA is impairment of the formation of NEW memories from the time of administration onward. The patient remains conscious, responsive and cooperative throughout — exactly as her husband describes — but does not consolidate a memory of the period. It is mediated through GABA-A potentiation affecting hippocampal consolidation, and it is most pronounced with TRIAZOLAM and MIDAZOLAM. Far from being an unwanted effect, it is a valued property in a phobic patient, because it prevents the appointment from reinforcing the fear.
• D. Retrograde amnesia is loss of memories formed BEFORE the event. Benzodiazepines do not cause it — memory for everything preceding the dose remains intact, which is why the patient still recalls arriving at the practice.

Note: The amnesia carries an obligation: post-operative instructions must be given in WRITING and repeated to a responsible escort, because the patient will not recall anything said to her during or shortly after the appointment. FLUMAZENIL is the reversal agent, a competitive antagonist at the benzodiazepine receptor — and its half-life is SHORTER than that of most benzodiazepines, so the patient must be observed for resedation after it is given.

Correct answer: B. An anxiolytic that is NOT a benzodiazepine — a 5-HT1A partial agonist with little sedation, no dependence, and no acute effect

• A. Antipsychotics carry extrapyramidal effects, tardive dyskinesia, orthostatic hypotension and xerostomia. Buspirone has none of that profile.
• B. CORRECT. BUSPIRONE is an anxiolytic for generalised anxiety disorder acting as a partial agonist at the 5-HT1A serotonin receptor. What matters clinically is what it does NOT do: little sedation, no meaningful potentiation of alcohol or other CNS depressants, no dependence or withdrawal syndrome, and — critically — NO ACUTE EFFECT. It takes two to four weeks to reach efficacy, which makes it useless for situational or procedural anxiety. So this patient's buspirone does nothing for today's appointment, and a separate plan is still required.
• C. Buspirone is specifically NOT a benzodiazepine, and rapid onset is precisely what it lacks — which is the clinically important point about it.
• D. The tricyclics are amitriptyline, imipramine and nortriptyline, used for depression and neuropathic pain. They cause marked xerostomia and an exaggerated response to injected vasoconstrictors, neither of which applies to buspirone.

Note: The dental relevance of buspirone is mostly NEGATIVE, which is why it appears in exam stems: no local anaesthetic dose modification, no vasoconstrictor restriction, minimal xerostomia, and no interaction of consequence. The trap is assuming that a patient already on an anxiolytic is covered for procedural anxiety. She is not.