Central Nervous System Stimulants

29 29 GENERIC NAME PAGE Amphetamine 350 Caffeine 351 Doxapram 349 Fenfluramine 351 Methamphetamine 350 Methylphenidate 350 Modafenil 351 GENERIC NAME PAGE Pemoline 350 Pentylenetetrazol 349 Sibutramine 351 Phentermine 351 Theobromine 351 Theophylline 351 Central nervous system (CNS) stimulation is the primary action of a diverse group of pharmacological agents and an adverse effect associated with the administration of an even larger group of drugs. CNS stimulation consists of a range of behaviors including mild elevation in alertness, increased nervousness and anxiety, and convulsions. In general, any hyperexcitability associated with drug administration (as either a desired or an undesired effect) results from an alteration in the fine balance normally maintained in the CNS between excitatory and inhibitory influences. Thus, the bases for CNS stimulation by this class of drugs reside in adjusting the integration of excitatory and inhibitory influences at the level of the individual neuron. An agent that induces CNS stimulation appears to act by one or more of the following mechanisms: (1) potentiation or enhancement of excitatory neurotransmission, (2) depression or antagonism of inhibitory neurotransmission, and (3) altered presynaptic control of neurotransmitter release. Although the use of CNS stimulants (also known as analeptics or convulsants) has declined, certain compounds within this category do possess some clinical utility. Historically, general CNS stimulants were used primarily as respiratory stimulants in the treatment of acute overdosage with CNS depressants (e.g., barbiturates). Several factors have contributed to the almost complete lack of use of CNS stimulants in this clinical situation. First, since the stimulants were not specific antagonists of the depressant agents, they frequently were not effective in reversing severe pharmacologically induced CNS depression. Second, the duration of action of the CNS stimulant was generally shorter than that of the depressant. Third, the dose of most CNS stimulants required to reverse severe CNS depression was quite close to the dose that produced convulsions and cardiac arrhythmias. In such cases, the CNS stimulant often exacerbated the clinical picture by producing severe life-threatening complications. Another factor contributing to the decline in CNS stimulant use for drug-induced CNS depression has been the development of generally safer procedures for patient management. Supportive measures (e.g., maintenance of a patent airway, elevation of low blood pressure) often provide greater bene