Medication Summary
Because a wide array of neurotransmitters are involved in the pathways of autonomic control, a wide array of medications exert an influence on this system. [4, 12, 13, 14]
The effectiveness of chlorpromazine and bromocriptine (a dopamine antagonist and a dopamine agonist, respectively) in the treatment of ADS illustrates the complexity of the neurotransmitter regulation pathways and the variability of the lesions that can cause the syndrome.
Propranolol, a lipophilic beta blocker, has successfully been used to control ADS. [15] Beta blockade has been shown to decrease hypertension and hemodynamic abnormalities. Beta blockade does not alter diaphoresis, which is mediated via sympathetic cholinergic neurons. As with all beta blockers, use caution when using in patients with diabetes and asthma.
Clonidine has been effective in normalizing plasma epinephrine and in reducing plasma norepinephrine levels, effectively decreasing blood pressure. Alpha-adrenergic and beta-adrenergic blockers prevent electrocardiographic changes and cardiac arrhythmias associated with TBI. However, clonidine is known to cause sedation.
Bromocriptine has been used to help combat the hyperthermia and diaphoresis that occur with ADS. [16, 17]
Dantrolene has been a useful treatment for extensor posturing but has shown minimal effect against other components of ADS. [16]
Morphine has been effective in abolishing ADS, as has naltrexone. Gabapentin has been found to be effective in controlling the autonomic symptoms and the dystonic posturing of ADS. [14]
Beta blockers
Class Summary
May block effect of vasodilators, decreasing platelet adhesiveness and aggregation, stabilizing the membrane, and increasing the release of oxygen to tissues.
Propranolol (Inderal)
Beta blockers oppose the multisystemic effects of excessive adrenergic tone.
Dopamine agonists
Class Summary
Inhibit noxious input to spinal cord.
Bromocriptine (Parlodel)
Central dopamine excess and central dopamine insufficiency are viewed as contributing to dysregulation of autonomic pathways. Agonists or antagonists may be helpful in treating ADS.
Chlorpromazine (Thorazine)
Mechanisms include blocking postsynaptic mesolimbic dopamine receptors, anticholinergic effects, and depression of RAS. Blocks alpha-adrenergic receptors and depresses release of hypophyseal and hypothalamic hormones. As a rule, however, dopamine antagonists are avoided in patients with TBI
Muscle relaxants
Class Summary
Modulate muscle contractions.
Dantrolene (Dantrium)
Stimulates muscle relaxation by modulating skeletal muscle contractions at a site beyond the myoneural junction and by acting directly on muscle itself. Most patients respond to 400 mg/d or less.
Opioids
Class Summary
Pain control is essential to quality patient care. Analgesics such as opioids ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.
Morphine (Duramorph, Astramorph, MS Contin, MSIR, Oramorph)
Opioid receptor system is involved in the regulation of central autonomic pathways. ADS has been found to be responsive to narcotics. As a rule, however, narcotics and other sedating medications are avoided in patients with TBI.
Naltrexone (ReVia)
Cyclopropyl derivative of oxymorphone that acts as a competitive antagonist at opioid receptors. ADS has been found to be responsive to naltrexone.
Anticonvulsants
Class Summary
These agents terminate clinical and electrical seizure activity of the brain.
Gabapentin (Neurontin)
Membrane stabilizer, a structural analogue of inhibitory neurotransmitter gamma-amino butyric acid (GABA), which paradoxically is thought not to exert effect on GABA receptors. Appears to exert action via the alpha(2)delta1 and alpha(2)delta2 auxiliary subunits of voltage-gaited calcium channels.
