Head Injury Medication
- Author: David A Olson, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA more...
Medications commonly are used in the acute setting to control early seizures, reduce intracranial pressure, and correct electrolyte abnormalities. Nimodipine may be neuroprotective in the subset of patients with traumatic subarachnoid hemorrhages.
In the long-term setting, cognitive and motoric augmentation as well as the control of spasticity and emotional incontinence may require pharmacologic interventions.
These agents may help reduce intracranial pressure.
May reduce subarachnoid space pressure by creating osmotic gradient between CSF in arachnoid space and plasma. Not for long-term use. Initially assess for adequate renal function in adults by administering test dose of 200 mg/kg, given IV over 3-5 min; should produce urine flow of at least 30-50 mL/h of urine over 2-3 h. Same test in children should produce urine flow of at least 1 mL/kg/h over 1-3 h.
These agents may help prevent early seizures in head injury.
May act in motor cortex, where it may inhibit spread of seizure activity; activity of brainstem centers responsible for tonic phase of grand mal seizures also may be inhibited.
Individualize dose. Administer larger dose in evening if dose cannot be divided equally.
Magnesium is given in hypomagnesemic states to ensure that adequate stores are present during acute phase of head injuries.
Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for optimum metabolic response.
These agents may help reduce intracranial pressure that is refractory to other conventional measures.
Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties. Can produce all levels of CNS depression.
Calcium Channel Blocker
Nimodipine has been demonstrated to improve outcomes of patients with traumatic subarachnoid hemorrhages.
Indicated for improvement of neurological impairments resulting from spasms following subarachnoid hemorrhage caused by ruptured congenital intracranial aneurysm in patients who are in good neurological condition postictus.
While studies show benefit on severity of neurological deficits caused by cerebral vasospasm following subarachnoid hemorrhage, no evidence that drug either prevents or relieves spasms of cerebral arteries. Thus, actual mechanism of action unknown.
Therapy should start within 96 h of subarachnoid hemorrhage. If capsule cannot be swallowed because patient undergoing surgery or unconscious, a hole can be made at both ends of capsule with 18-gauge needle and contents extracted into a syringe. Contents then can be emptied into patients' in situ nasogastric tube and washed down tube with 30 mL isotonic saline.
These agents may help increase alertness and some aspects of cognitive functioning in patients with brain injury.
Stimulates cerebral cortex and subcortical structures.
These agents may increase alertness in patients with brain injury; also may help in occasional patients with posttraumatic parkinsonism.
Large neutral amino acid absorbed in proximal small intestine by saturable carrier-mediated transport system. Absorption decreased by meals, which include other large neutral amino acids. Only patients with meaningful motor fluctuations need consider low-protein or protein-redistributed diet. Greater consistency of absorption achieved when levodopa taken 1 h or more after meals. Nausea often reduced if levodopa taken immediately following meals. Some patients with nausea benefit from additional carbidopa in doses up to 200 mg/d. Half-life of levodopa/carbidopa approximately 2 h.
When more carbidopa required, substitute 1 25/100 tab for each 10/100 tab; when more levodopa required, substitute 25/250 tab for 25/100 or 10/100 tab.
Sustained release (SR) formulation of levodopa/carbidopa is absorbed more slowly and provides more sustained levodopa levels than immediate release (IR) dosage form; SR as effective as IR formulation when levodopa initially required and may be more convenient when fewer intakes are desired.
Patients with dissipating motor fluctuations and no dyskinesia often benefit from prolongation of short-duration response when switched from IR to SR; however, patients with meaningful fluctuations and dyskinesia often experience increase in dyskinesia when switched to SR formulation.
Doses and dosing intervals of SR form may be increased or decreased based on response; most patients have been treated adequately with 2-8 tab/d (divided doses) at intervals of 4-8 h while awake; higher doses (>12 tab/d) and intervals < 4 h have been used but usually are not recommended; if < 4-h interval used or if divided doses are not equal, give smaller doses at end of day. Allow at least a 3-d interval between dosage adjustments. May administer as whole or half tab, which should not be crushed or chewed.
Selective serotonin reuptake inhibitors
These agents have been of benefit in patients with head injuries and emotional incontinence.
Selectively inhibits presynaptic serotonin reuptake.
These agents may reduce painful cramping and detrimental muscle tightening.
Centrally acting muscle relaxant metabolized in liver and excreted in urine and feces.
May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at spinal level.
Stimulates muscle relaxation by modulating skeletal muscle contractions at site beyond myoneural junction and acting directly on muscle.
Depresses all levels of CNS, possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.
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