Treatment Modalities

The National Acute Spinal Cord Injury Studies (NASCIS) I and II published in the 1990s demonstrated significant benefit in administering high doses of methylprednisolone early after a spinal cord injury (within 8 hours). The dose is 30 mg/kg IV over 15 minutes, followed by 5.4 mg/kg/h via continuous intravenous infusion over 24 hours (12,13).

In cases of failure of the listed approaches and procedures, resuscitative/sta-bilizing measures of increasingly heroic nature are attempted:

1. Heavy sedation to achieve paralysis

2. Increased rate of mannitol infusion, 1 g/kg, followed by 0.25 g/kg every 6 hours; serum osmolality maintained around 320 mOsm, consider alternating with furosemide at 1 mg/kg

3. Hyperventilation of the patient to achieve a Pco2 of 3 to 3.5 kPa and induce a high-dose barbiturate coma; the latter may serve as an excitotox-icity-limiting measure (14).

In the acute setting, use of phenytoin and nifedipine has been suggested. Phenytoin reduces the incidence of early posttraumatic seizures, and nifedip-ine is a potential neuroprotective agent. As a calcium channel blocker, nifedipine is expected to minimize the toxic effect of calcium ion flux in exci-totoxicity cascade. The possibility of an allergic response to phenytoin and apparent lack of dramatic improvement with nifedipine are likely to limit the use of these drugs in the field (15).

The long-term management of patients who suffered head trauma in the agricultural or other industrial setting is oriented toward a hard-to-achieve twofold goal: restoration of normal tonicity and restoration of cognitive function. Both of these consequences of brain trauma are disabling, and patients need a thorough and systematic evaluation of their employment prognosis. In our experience, in hypertonicity, spasticity, or dystonia with attendant muscle spasms both baclofen and tizanidine are preferred medications because of their more favorable side-effect profiles. Intrathecal baclofen is an excellent option for many patients and is usually tolerated well. A more direct approach that requires multiple injections and excellent knowledge of anatomy (as well as the ability to identify anatomical variations on the fly) is injection of botu-linum toxins types A and B. Other medications may include benzodiazepines (e.g., diazepam) and dantrolene. In all cases the physician must evaluate for tremor, dystonia, parkinsonism, myoclonus, and hemiballism, as all of these are common (more that 10% of head trama cases) and tend to persist long-term in head injury patients (16-18).

Cognitive enhancement is a much more vaguely defined goal and, as a result, most of the research performed in the area is either small-sample or poorly controlled. Anecdotal data suggests that methylphenidate, levodopa, amantadine, memantine, and donepezil may be useful. Amantadine is also an excellent fatigue-controlling agent and has few side effects. The use of the atypical members of the stimulant family, modafinil and adrafinil, is even less studied, although these medications show some promise. European colleagues often use piracetam and related compounds. These medications are not readily available in the United States, except for levetiracetam, which has not been studied in the cognitive restoration setting but may be of use in controlling seizures in some patients. Some consultants report the use of a semi-synthetic analogue of vasopressin (desmopressin) for the purposes of restoration of cognitive acuity. None of these approaches is in widespread use in the United States and should be considered experimental at best (16-18).

The physician must always remember that an initial grading of "mild" does not necessarily mean a mild outcome of any given brain injury. Recent studies have demonstrated that following mild head injury, only 54% to 79% of patients are able to return to full preinjury employment. Another study of 148 patients with mild head injury discovered that after 1 year, 26% had moderate disability and 3% had severe disability. Significant neuropsycho-logical dysfunction, primarily of attentional and memory domains, may persist after mild head injury alone. Irritability, posttraumatic headache (often complicated by the analgesic rebound headache), and fatigue are often the defining complaints in all cases of brain injury, regardless of the initial grading. Another concern is the issue of posttraumatic epilepsy that is diagnosed in about 4% of patients who sustained head injuries. As in other cases, 24-hour EEG monitoring is likely to detect or rule out seizure activity (19-23).

The main goal in the long-term care of spinal cord trauma patients is to prevent medical complications, a complex goal that requires administration of empiric antibiotics as indicated, maintenance of adequate perfusion (mean arterial pressure must remain above 70 mm Hg at all times), prophylaxis of deep vein thrombosis and pulmonary embolism, as well as bladder and bowel care to prevent distention, discomfort, impaction, and infection.

Pain and anxiety control is often required but may be difficult. Narcotics must be used judiciously or avoided because of adverse bowel and bladder effects. Drugs causing depression of the CNS (e.g., benzodiazepines) should be used with caution due to the possibility of respiratory failure (24,25).

Gastrointestinal prophylaxis against ulcers is mandatory. Patients with spinal cord injury have a high incidence of stress ulcers, which can also be exacerbated by the concomitant use of steroids in the acute phase. The use of antiinflammatory drugs should be very cautious since even highly promoted cyclooxygenase-2 (COX-2) inhibitors possess the intrinsic risk of promotion of GI ulceration (24).

Psychological and emotional support throughout the patient's disease course is necessary and is best provided informally and continuously by the caregivers; however, formal intervention by specialists may be required (24,25).

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