eMedicine Specialties > Physical Medicine and Rehabilitation > Traumatic Brain Injury
Post Head Injury Autonomic Complications: Treatment & Medication
Updated: Jul 24, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Rehabilitation Program
Physical Therapy
Severe episodes of ADS may preclude or delay any of the components of a contemporary, multidisciplinary rehabilitation program. Physical therapy sessions may have to be held episodically because labile blood pressure, ICP, heart rate, and temperature may preclude participation. Of course, it is preferable to continue not only with passive range of motion (PROM) but also with as much of the functional program as possible; monitor these symptoms during therapy.
Occupational Therapy
Continue occupational therapy as regularly as possible, with the same considerations as for physical therapy.
Speech Therapy
Patients with ADS usually have severe impairment of alertness. Thus, speech therapy may not yet be appropriate.
Medical Issues/Complications
Severe muscle rigidity can result in muscle rupture or in rhabdomyolysis. Fever is viewed as a source of secondary injury in individuals with TBI, because marginal cerebral blood flow fails to provide for normal brain cooling. This may result in a brain temperature that is higher than the measured core temperature. The resulting increase in metabolic demand may not be met by increasing blood flow, so local areas of hypoxia and further neuronal dysfunction and death ensue.
Hypertension and tachycardia could theoretically increase the risk of developing hemorrhage from injured blood vessels. Prolonged, severe diaphoresis may result in dehydration and in electrolyte abnormalities.
Surgical Intervention
Surgery is not part of the treatment for ADS.
Consultations
Consultation from infectious disease experts is appropriate, but it is not always necessary in this context.
Medication
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.3,8,9,10
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.11 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.12,13
Dantrolene has been a useful treatment for extensor posturing but has shown minimal effect against other components of ADS.12
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.10
Beta blockers
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.
Adult
40-80 mg PO bid initially; increase to 160-320 mg/d (some patients require up to 640 mg/d)
Pediatric
0.5 mg/kg/d PO divided bid/qid; increase gradually q3-7 d; dosage range is 2-4 mg/kg/d divided bid; not to exceed 2 mg/kg/d
Co-administration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; A-V conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; slowly withdraw drug, and closely monitor patient
Dopamine agonists
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.
Adult
1.25 mg (one half of 2.5-mg tab) PO bid with meals; increase by 2.5 mg/d q2-4 wk prn
Dosing range is 10-40 mg/d
Safety not demonstrated at doses >100 mg/d
Pediatric
Not established
Toxicity may increase with ergot alkaloids; amitriptyline, butyrophenones, imipramine, methyldopa, phenothiazines, and reserpine may decrease bromocriptine effects
Documented hypersensitivity; ischemic heart disease and peripheral vascular disorders
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal or hepatic disease
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
Adult
25-50 mg PO q4-6h
25-50 mg IM q6-8h if symptoms persist for 2-3 d
Pediatric
Not established
Other CNS depressants, anticholinergics, or anticonvulsants; antihypertensives may cause additive effect; co-administration with epinephrine may cause hypotension
Documented hypersensitivity; bone marrow suppression, narrow-angle glaucoma, severe liver disease, or cardiac disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause pseudoparkinsonism; akathisia is a common extrapyramidal reaction in elderly patients; lowers seizure threshold and increases risk of seizures in patients with history of seizures
Muscle relaxants
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.
Adult
Begin with 25 mg PO qd; increase to 25 mg bid/qid; then increase by 25-mg increments to as high as 100 mg bid/qid prn
Pediatric
Begin with 0.5 mg/kg PO bid; increase to 0.5 mg/kg bid/qid; then increase by increments of 0.5 mg/kg to 3 mg/kg bid/qid if necessary; not to exceed 100 mg qid
Toxicity may increase with the co-administration of clofibrate and warfarin; co-administration with estrogen may increase hepatotoxicity in women older than 35 y
Documented hypersensitivity; active hepatic disease (eg, hepatitis, cirrhosis)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hepatotoxicity (use only for recommended indications); caution in impaired pulmonary function and severe cardiac insufficiency; may cause photosensitivity with exposure to sunlight
Opioids
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.
Adult
Initial dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC; re-assess hemodynamic effects of dose
Pediatric
Infants and children: 0.1-0.2 mg/kg dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose
Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hypotension, respiratory depression, nausea, emesis, constipation, urinary retention, atrial flutter, and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Naltrexone (ReVia)
Cyclopropyl derivative of oxymorphone that acts as a competitive antagonist at opioid receptors. ADS has been found to be responsive to naltrexone.
Adult
25 mg PO initially; if no withdrawal signs within 1 h, administer another 25 mg
Maintenance dose: 50-150 mg PO 3 times/wk
Pediatric
Not established
Inhibits effects of opiates
Documented hypersensitivity; acute hepatitis or liver failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hepatic impairment
Anticonvulsants
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.
Adult
900-1800 mg PO in divided doses, not to exceed 3600 mg/d; renally excreted, dosage adjustment necessary for patients with renal dysfunction
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Antacids may significantly reduce bioavailability of gabapentin (administer at least 2 h following antacids); may increase norethindrone levels significantly; cimetidine, hydrocodone, and morphine may increase gabapentin AUC; naproxen may increase gabapentin absorption
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Common adverse effects include drowsiness, dizziness, somnolence, and unwanted eye movements; children may experience emotional ability hostility, thought disorder, and hyperkinesia; caution in elderly and patients with severe renal impairment; abrupt withdrawal may precipitate seizures
More on Post Head Injury Autonomic Complications |
| Overview: Post Head Injury Autonomic Complications |
| Differential Diagnoses & Workup: Post Head Injury Autonomic Complications |
 Treatment & Medication: Post Head Injury Autonomic Complications |
| Follow-up: Post Head Injury Autonomic Complications |
| References |
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References
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Further Reading
Keywords
autonomic dysfunction syndrome, ADS, dysautonomia, paroxysmal sympathetic storm, autonomic storm, neurostorming, diencephalic seizure, acute midbrain syndrome, brainstem attack, hypothalamic-midbrain dysregulation syndrome, hyperpyrexia associated with muscle contraction, paroxysmal autonomic instability with dystonia, PAID, traumatic brain injury, TBI, hydrocephalus, brain tumor, subarachnoid hemorrhage, intracerebral hemorrhage
