Benzodiazepine
Enhances GABA-A receptor-mediated chloride influx, potentiating inhibitory neurotransmission in the CNS. This leads to anxiolytic, anticonvulsant, muscle relaxant, and sedative effects.
Panic disorder, seizure disorders (including absence and myoclonic seizures)
Generalized anxiety disorder (GAD), restless legs syndrome (RLS), alcohol withdrawal syndrome
Oral tablets, orally disintegrating tablets
Start at 0.25–0.5 mg orally twice daily; titrate slowly based on clinical response and tolerability
0.25–4 mg/day in divided doses
Long elimination half-life ranging from approximately 18 to 50 hours, leading to potential drug accumulation. Primarily metabolized by hepatic enzymes, with active metabolites contributing to duration of action.
Sedation, dizziness, impaired coordination, memory impairment, fatigue, cognitive slowing
Tolerance, physical dependence, withdrawal symptoms upon abrupt discontinuation, increased risk of falls and fractures, respiratory depression (especially when combined with other CNS depressants), cognitive decline with long-term use.
Monitor for excessive sedation, cognitive impairment, risk of falls (especially in elderly or cognitively impaired patients), signs of tolerance or dependence. Periodic assessment of hepatic function is advised in patients with liver disease.
Risk of concomitant use with opioids or other CNS depressants causing profound sedation, respiratory depression, coma, and death. Potential for abuse, dependence, and withdrawal.
Use with caution in elderly patients and those with dementia due to heightened risk of sedation, falls, and cognitive impairment. In hepatic impairment, reduced metabolism may increase drug levels and toxicity risk; careful monitoring and dose adjustments are required. Limit duration and dose to the minimum effective amount to reduce risks associated with long-term benzodiazepine therapy.