5.12 Miscellaneous Therapies

5.12.1 Zinc Supplementation

“Zinc is an essential element for humans that constitutes less than 0.1% of body weight, yet is vitally important for normal nucleic acid and protein metabolism” (McClain et al., 1986). Serum hypozincemia and increased urinary zinc excretion are common following head injury and are thought to be an adaptive responsive to inhibit the proliferation of infective organisms. Levels of serum albumin, the major transport carrier for zinc, are also markedly depressed following brain injury and likely help to explain a portion of the reductions in serum zinc levels.  Urinary excretion of zinc appears to be proportional to the severity of head injury (Levenson, 2005). Zinc is an important trace mineral in protein synthesis. Moderate zinc deficiency has been associated with cell death.

Individual Studies

Table 5.26 Zinc Supplementation in ABI Patients

PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al., 2002).
D&B = Downs and Black (1998) quality assessment scale score.

Discussion

A single RCT was identified which examined the effect of parenteral zinc supplementation following ABI (see Table 5.24).  Improvements in protein synthesis and neurological recovery were noted in patients who received supplementation.  Surprisingly, there were no differences in either the serum or cereobrospinal fluid zinc concentrations between the groups.

Conclusions

Based on a single RCT there is Level 1 evidence that zinc supplementation in ABI patients has a positive effect on neurological recovery as measured by the Glasgow Coma Scale. However, no significant improvement in mortality rates could be attributed to zinc supplementation.

5.12.2 Growth Hormone

Anabolic agents have been proposed as a means to improve lean body mass (Behrman et al., 1995). Its been reported that growth hormone mobilizes fat stores as an energy source and enhances whole body and liver mitochondrial protein stores (Maddaiah et al., 1973; Marimee & Rabin, 1973).  It is believed that growth hormones exert their effects via insulin-like growth factor-1 (IGF-1), which is synthesized in the liver (Phillips & Vassilopoulou-Sellin, 1980). Several studies in non-stressed postoperative patients have demonstrated improvements in nitrogen balance following the use of growth hormone (Ponting et al., 1988; Manson et al.,1988; Manson & Wilmore, 1986). The effects of growth hormone on the nutritional parameters of injured patients have not been well established.

Individual Studies

Table 5.27 Growth Hormone Treatment on Nutrition Post-ABI

D&B = Downs and Black (1998) quality assessment scale score.
PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al., 2002).

Discussion

In a study conducted by Behrman et al. (1995) they found GH treatments administered to patients resulted in higher IGF-I and GH concentrations; however it was not found to improve nitrogen balance.  In a RCT conducted by Hatton et al. (2006) they found individuals who were administered IGF-I/GH had a higher nitrogen balance per day (1.20+/-0.84) than those in the control group (-3.90+/-0.87), p<0.0001.

Conclusions

Based on two RCTs, there is conflicting evidence that IGF-I is effective in enhancing growth hormone in those who have sustained an ABI.

5.12.3 Increased Nitrogen Feeds

Following a brain injury, the incidence of metabolic changes can influence cell turnover use of substrate and body composition (Twyman, 1997). Twyman (1997) noted that urinary urea nitrogen levels increase by a factor of three compared with normal levels within 10 days after severe head injury. On average, about 5 to 10 g of urea nitrogen are excreted daily from an individual; however ABI patients’ lose a mean of 21 g urinary urea in a single day (Twyman, 1997). Following brain injury, nitrogen loses result from the conversion of endogenous protein to energy with the extra stress demand (Grahm et al., 1989). Hadley et al. (1986) also reported that attainment of a positive nitrogen balance is complicated because increasing the amount of nitrogen feeding will not be retained, rather it will cause an increased amount of nitrogen excretion. “Positive nitrogen balance in brain injured patients usually does not occur until the catabolic stimulus begins to subside” (Hadley et al., 1986).

Individual Studies

Table 5.28 Nitrogen Balance

PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al., 2002).
D&B = Downs and Black (1998) quality assessment scale score.

Conclusions

Based on a single RCT, there is Level 2 evidence that high nitrogen feedings of approximately 2 g protein/kg are necessary to restore the substantial nitrogen loses that occur post-ABI.

5.12.4 Branched-Chain Amino Acids

Branched-Chain Amino Acids (BCAAs), which include leucine, valine and isoleucine, make up roughly 35% of the human body’s essential amino acids (AAs) and approximately 14% of skeletal muscle AAs,(Aquilani et al., 2005). Following intake of a meal, the amino acid skeletal muscle uptake is comprised of 50% or more BCAAs (Aquilani et al., 2005). Aquilani et al. (2005) observed many studies suggesting AAs are more than just nutritionally beneficial, but also may substantially impact cognitive functions (Table 5.29). Possible mechanisms explaining the improvements in cognitive function associated with BCAAs may be “a direct action of the BCAAs on brain functions by providing substrates and an indirect action by increasing brain insulin availability” (Aquilani et al., 2005).

Individual Studies

Table 5.29 Branched-Chain Amino Acid Treatment in ABI patients

PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al. 2002).
D&B = Downs and Black (1998) quality assessment scale score.

Conclusions

There is Level 2 evidence that supplementation of BCAAs in post-ABI patients enhances recovery of cognitive function, without negatively effecting tyrosine and tryptophan concentration.