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Laurance Johnston, Ph.D.

Sponsor: Institute of Spinal Cord Injury, Iceland



1) Creatine: SCI Strength Enhancer

2) Vitamin D & SCI Bone Density

3) Ginkgo Biloba's Neuroprotective Effect

4) Fasting

5) Buyang Huanwu Decoction

6) Quercetin

7) Vitamin E

8) Chinese Skullcap

9) Acetyl-L-Carnitine

10) Herbal Formulation JSK

CREATINE: SCI STRENGTH ENHANCER: Creatine is a common nutritional supplement used by athletes to build-up muscles and strength. Several scientific studies suggest that creatine can also enhance strength in individuals with physical disability, including SCI. Furthermore, animal studies indicate that creatine exerts a neuroprotective effect after injury.

Our bodies contain more than 100 grams of creatine, mostly in our muscles, heart, brain, and testes. Physical activity stimulates primarily the liver to produce about two grams of creatine daily from three key amino acids: glycine, arginine, and methionine. The creatine is then sent through the blood and transported into muscle cells. 

Creatine can also be provided by diet, especially one rich in meat and fish. Vegetarian diets, however, often lack not only creatine, but also the methionine precursor needed for internal production. For comparison’s sake, a pound of meat contains about 40-times more creatine than a pound of milk.

Creatine-Generated Energy: Most muscle creatine is converted into the energetically powerful creatine-phosphate. The high-energy molecular bond connecting the creatine to the phosphate group is an energy source that can quickly fuel muscle activity. This fueling, however, is mediated through the creation of yet another powerhouse molecule called adenosine triphosphate (ATP).

ATP is extremely important because it is the body’s energy currency, expended to drive most biochemical processes. Like creatine-phosphate, ATP’s terminal phosphate group is connected by a high-energy bond that when severed provides energy needed for muscle contraction.

Under more constant or endurance working conditions, the body obtains ATP by metabolizing carbohydrates and fats, a relatively slow process that cannot generate immediately needed ATP energy.

When energy bursts are required, the body uses instead creatine-phosphate. Specifically, the phosphate group on this molecule is transferred to replenish spent ATP, transforming it into its energetically powerful form.  During rest periods, creatine-phosphate is then replenished by the ATP generated by the slower metabolic processes.

If intracellular creatine-phosphate levels can be increased, for example, through supplementation, it will take longer before the short-term energy source is depleted and a switchover to slower carbohydrate or fat metabolism is needed. 

Strength & Muscles: Creatine supplementation is most useful for physical activities that require intense bursts of energy - e.g., a bench press, a sprint, or games requiring energy bursts. It is less useful for endurance events, except when such events are enhanced by building-up muscle strength through creatine-stimulated weightlifting.

Creatine can build muscle mass by several mechanisms. For example, because weightlifting is exactly the sort of short-term, intense physical activity fostered by creatine, more repetitions and harder workouts can be achieved, building up muscle. In addition, however, creatine increases water uptake into the muscle, a process called cell volumizing that bulks up the muscles in a fashion that may not add much real strength.

Physical Disability & SCI: Studies suggest that creatine can enhance strength compromised by physical disability:

First, Dr. P. Jacobs and colleagues at the Miami Project  have shown that creatine promotes upper-extremity work capacity in quadriplegics ((Arch Phys Med Rehabil 83, 2002). In this study, 16 male quadriplegics with complete cervical C5-7 injuries were randomly assigned to receive either 20 grams/day of creatine or placebo maltodextrin (a common food ingredient) for seven days. Treatment was then discontinued for a three-week washout period, after which the treatment groups were reversed for another seven days - i.e., the initial placebo group now received creatine, and the initial creatine group now was given maltodextrin.

Work capacity was assessed before and after each dosing period using arm ergometry, a common SCI-rehabilitation exercise. Specifically, subjects faced a series of two-minute, increasing-intensity work stages with one-minute, intervening recovery periods.

After creatine supplementation, improvements were noted in various respiratory measurements, including oxygen uptake, carbon dioxide production, tidal volume (amount of air that enters the lungs), and breathing rate. For example, 14 of the 16 subjects demonstrated increased oxygen uptake, averaging 19 %. Improvements were also noted in peak power output and increased time to fatigue.

Second, Dr. K. Adams et al (Dallas, Texas) carried out a creatine-loading study in 10 subjects with SCI (Arch Phys Med Rehabil 81, 2000). The subjects had their peak-power production tested on an upper extremity exercise machine before and after creatine supplementation. Most improved their peak-power production, with quadriplegics and paraplegics averaging 21and 13% improvement, respectively.

Third, Drs. Stephen Burns, R. Kendall and colleagues (USA) examined the effects of creatine supplementation on muscle strength in eight subjects with quadriplegia. Average age was 48, seven were men, and seven had C6-level injuries. In a double-blind crossover study (a study design in which subjects unknowingly become controls and vice versa during the study), subjects were randomized to receive either creatine supplementation or a placebo Wrist and grasping strength were evaluated before and after supplementation. Unlike the preceding studies, results suggested that no additional strength accrued from creatine supplementation.

Finally, Drs. M. Tarnopolsky and J. Martin (Hamilton, Ontario) have shown that creatine can increase handgrip, knee-extension, and ankle strength in individuals with various forms of neuromuscular disease (Neurology 52, 1999).

Neuroprotection: Animal studies indicate that creatine exerts a neuroprotective effect in traumatic brain and spinal cord injury. For example, Dr. O. Hausmann et al (Zurich, Switzerland) demonstrated that four-weeks of creatine supplementation before experimental spinal cord injury reduced glial scar formation and enhanced functional recovery in rats. In another example, Dr. A. Rabchevsky and colleagues (Lexington, Kentucky) showed that creatine supplementation spared spinal cord gray matter in injured rats (gray matter contains neuronal cell bodies and dendrites and glial cells; white matter consists mainly of axons).

VITAMIN D & BONE DENSITY: As summarized in two key articles, research carried out by Dr. William Bauman and colleagues, Bronx VA Medical Center indicates that individuals with SCI are often vitamin-D deficient (Metabolism 44(12), 1995; & J Spinal Cord Med 28, 2005).

Like astronauts who lose bone density from the lack of weight-bearing activities, paralysis causes osteoporosis. As much as 50% of lower-extremity bone mass is lost during the first several years after injury, people with complete injuries losing the most. Hence, a deficiency in bone-enhancing vitamin D further aggravates an already serious SCI problem, in turn increasing fracture risk.

Bauman believes SCI predisposes one to vitamin-D deficiency for several reasons. For example, he speculates that due to limited mobility, someone with SCI may not get as much vitamin-D-producing sunlight as the general population. Supporting this idea, other scientists have demonstrated that pressure-sore-afflicted patients with SCI, who have access to the least sunlight, have the greatest vitamin-D deficiency.

Bauman also suggests that a lack maybe be caused when health-care professionals recommend reduced consumption of vitamin-D-fortified dairy products under the mistaken belief that the calcium in such foods will aggravate kidney problems. And, he believes that many SCI-associated medicines reduce the body’s vitamin-D stores.

In his 1995 study, Bauman compared vitamin-D levels in control subjects and in 100 veterans with SCI who averaged 20 years post-injury. Subjects with SCI were twice as likely to have vitamin-D levels less than that considered normal.

In his 2005 study, Bauman examined the effectiveness of several dosing regimens in elevating vitamin-D levels in people with chronic SCI. In one regimen, 40 subjects consumed 800 IU of vitamin-D per day for 12 months. Their mean age was 43; injury duration averaged 12 years; and 17 and 23 had quadriplegia and paraplegia, respectively. Before supplementation, 33 had below-normal vitamin-D levels; in contrast, after 12 months of supplementation, only 9 remained deficient.

Although average serum vitamin-D levels doubled in subjects, Bauman believes that even greater supplementation is needed to obtain nutrient serum levels needed for promoting optimal bone health in SCI.

Dr. Christina Oleson and colleagues (USA) assessed vitamin-D levels in individuals with SCI from the Birmingham, Alabama area. Because Birmingham is in the southern USA, solar exposure in the area includes more of the sun’s vitamin-D-producing ultraviolet UV-B rays compared to most other parts of the country. Hence, any vitamin-D deficiencies observed in this location would suggest that the problem is even greater in other, more-northern parts of the country.

Ninety-six patients between the ages of 19 and 55 with subacute (specifically, two to six months post injury) and chronic (i.e., at least a year after injury) injuries were recruited. All individuals had motor, complete injuries ranging from the cervical C3 to thoracic T10 level; specifically, 43% and 57% had tetraplegia and paraplegia respectively. Seventy percent were male, and 46% and 54% were white and African-American, respectively.

Vitamin-D levels were assessed in both the summer and winter, periods with greater and reduced vitamin-D production, respectively. Even in the study’s southern location in summer, 65% and 81% of subjects with subacute and chronic injuries, respectively, had subtherapeutic vitamin-D levels, predisposing them to a loss of bone density and a multitude of other vitamin-D-aggravated problems. As expected, the situation was even worse in winter with 84% and 96% of subjects with subacute and chronic injury, respectively, having subtherapeutic levels. Vitamin-D levels are believed to be higher in those with acute injury due to the residual stores of the vitamin accrued before injury. These stores are depleted over time because the injured individual tends to get outside in the sun less and consume a diet supplemented with less vitamin D (e.g., forgoing fortified milk) due to concerns of developing kidney stones. Due to darker skin pigmentation, vitamin-D deficiencies were greater in African Americans.

The investigators concluded “Vitamin D insufficiency and deficiency are found in the majority of patients with chronic SCI and in many with acute SCI. Initial screening for [vitamin D] should be performed early in rehabilitation. Periodic monitoring in the chronic setting is highly recommended.”

The problem of vitamin-D deficiency in individuals with SCI was further documented by Dr. Gregory Nemunaitis and colleagues (USA) in a 2011-published study. Specifically, vitamin-D levels were assessed in 100 patients with SCI who were consecutively admitted to acute inpatient rehabilitation. Of these patients, 93% had inadequate levels of the vitamin, with 21% classified as severely deficient.


Obtained from the leaves of a large deciduous tree originally from China, Ginkgo biloba is one of mankind’s most ancient medicines. Fossil records indicate the species has been around for over 200-million years, and some ginkgos at Chinese temples are more than 1,500-years old. Given the trees are highly disease and insect resistant and grow in urban environments where other trees can not, it is not surprising that they possess substances with medicinal properties.

In Europe, ginkgo is the most widely sold and prescribed plant-based medicine; in the U.S., it is one of the top ten best-selling herbal remedies. Supported by varying degrees of animal research and clinical studies, ginkgo may provide benefits for a variety of disorders, including:

bulletCerebral vascular insufficiency and impaired mental performance (e.g., senility);
bulletAlzheimer’s disease (AD);
bulletCochlear deafness;
bulletSenile macular degeneration;
bulletPeripheral arterial insufficiency;
bulletErectile dysfunction;
bulletDepression and anxiety;
bulletMultiple sclerosis (MS);
bulletTraumatic brain injury;

Ginkgo operates through several potential physiological mechanisms especially relevant for neuronal health. For example, it is an antioxidant, maintains cell-membrane integrity, enhances oxygen use and metabolism, augments neurotransmission, and inhibits a form of programmed cell death called apoptosis.

Using a rat model of acute injury, Turkish investigators showed that ginkgo extract inhibits post-injury lipid peroxidation, a biochemical process that mediates secondary damage to the injured cord (Koc et al. Res Exp Med 195, 1995). Ginkgo’s inhibition was even greater than methylprednisolone (MP), a glucocorticoid-steroid drug which is now routinely administered after injury to minimize neurological damage.

More recently, Chinese investigators demonstrated that ginkgo extract is neuroprotective in rats with experimental SCI (Ao et al. Spinal Cord, 44, 2006). Specifically, after cutting the spinal cord in half at the thoracic T-9 level, rats were given either ginkgo or saline. The ginkgo-treated rats had smaller injury-related cavities, less conduction-inhibiting demyelination, and less apoptotic neuronal cell death.  

FASTING: Recent paradigm-expanding research carried out by Drs. Ward Plunet and Wolfram Tetzlaff and colleagues at the University of British Columbia (Canada) suggests that fasting enhances nervous-system regeneration after SCI. Specifically, rats with experimental cervical injuries were randomized into two groups. The control animals had free access to food and water, while the experimental animals received food only every other day starting immediately after injury.

Compared to controls, fasted rats had improved gait and forelimb function. Fasting also preserved neuronal integrity, reduced the size of the injury-site lesion by more than 50%, and increased sprouting of axons. Finally, the blood level of a neuroprotective agent (called beta-hydroxybutyrate) increased 2-3 times on the fasting days. A similar neuroprotective effect has also been observed by other scientists for traumatic brain injury.

The investigators concluded that because every-other-day-fasting “is a safe, non-invasive, and low-cost treatment, it can readily be translated into the clinical setting of spinal cord injury and possibly other insults.”

Buyang Huanwu Decoction (BYHWD):

BYHWD is a Chinese herbal medicine that has been used for centuries to treat a variety of disorders, including paralysis. From a Traditional Chinese Medicine viewpoint, it’s used to “invigorate the body, promote blood circulation, and activate meridians (energetic channels).” The decoction is composed of extracts of a number of Chinese herbs or remedies, including astragalus, dong quai, red peony root, Rhizoma Chuanxiong (Lingusticum), earthworm, peach seed, and safflower.

Demonstrating that ancient wisdom often has much contemporary validity,  studies indicate that BYHWD, indeed, exerts some neuroprotective and regenerative effects. For example, animal research suggests that this herbal decoction can promote nerve regeneration after stroke and both peripheral-nerve and spinal-cord injuries.

In the case of SCI, Dr. An Chen et al (China) have evaluated BYHWD in a rat model of injury in which one side of the cord was transected at the cervical level. After transection, the rats were administered either the BYHWD or a distilled-water control for eight weeks via gastrogavage (i.e., through a stomach tube). After this time period, the number of surviving neurons on the cord’s injured side for both BYHWD- and water-treated groups were compared to the neuron level on the non-injured side (i.e., a baseline comparison). Compared to the uninjured side, 78% of the neurons remained with the BYHWD-treated rats compared to only 58% of the water-treated rats. In other words, the BYHWD decoction reduced injury-related neuronal loss from 42 to 22%.

In addition, cell bodies of surviving neurons atrophied by 64% in the water-treated controls compared with 35% in the BYHWD-treated rats. In other words, BYHWD enhanced the apparent robustness of the surviving neurons.  

Especially significantly, only in the BYHWD-treated rats did axons regenerate through the injury site. And, as would be expected with such regeneration, these rats recovered more forelimb function, the physical area affected by the experimental transection injury.

In another study, Dr. Lihong Fan and colleagues (China) evaluated the effects of BYHWD in a rabbit model of SCI. In this model, injury was generated by temporarily shutting off blood flow to the spinal cord’s lumbar region (i.e., ischemia), affecting hind-limb function. The rabbits were treated with either BYHWD or saline starting seven days before injury and continuing two days after injury. Hind-limb function was then measured using a scale ranging from 0 (complete paralysis) to 5 (normal function). Forty-eight hours after injury, the BYHWD-treated rabbits averaged 3.4 on this scale compared to 2.6 for the saline-treated controls.

With respect to peripheral nerve injuries, Dr. Yueh-Sheng Chen et al (Taiwan) demonstrated that BYHWD stimulates growth in regenerating nerves. In this study, a 10-millimeter gap was created in the rat sciatic nerve (a nerve that runs down the leg from the back) and then bridged by a silicon-rubber tube. Regeneration across the gap was compared in BYHWD-treated rats and control animals who received no BYHWD. Nerves regenerated across the gap in 89% percent of the BYHWD-treated rats compared to only 70% of controls.

Although these BYHWD-related improvements may appear modest, it is important to underscore that studies have shown that substantial physical function can be retained even if only a relatively small percentage of neurons survive the injury.

BYHWD may mediate its neuroprotective effects through several physiological mechanisms. For example, scientists have shown that BYHWD 1) stimulates the outgrowth and differentiation of neurites on neuronal stem cells (neurites are processes budding out from immature neurons, such as developing dendrites and axons); 2) inhibits apoptosis – a post-injury, programmed cell death of spinal-cord cells; and 3) decreases free radical generation and associated lipid peroxidation, biochemical processes that mediates secondary damage to the injured cord.


Quercetin is another commonly available nutritional supplement that has been shown to reduce neurological damage in animals after acute injury. Belonging to a family of molecules called flavonoids, quercetin imbues coloring to many foods, including apples, red onions, red grapes, tomatoes, raspberries and other berries, and broccoli. Evidence suggests that it provides benefits in cancer, prostatitis, heart disease, cataracts, allergies/inflammation, and respiratory disorders.


Like melatonin described previously, quercetin is an antioxidant. By scavenging free radicals, it inhibits the damage-perpetuating lipid peroxidation that occurs soon after injury. As discussed above, this peroxidation impairs neuronal and axonal membranes, resulting in further cell death.

Injury results in hemorrhaging. This process causes the hemoglobin within red blood cells to disintegrate, releasing oxidized iron. This reactive form of iron also promotes nervous-system-compromising lipid peroxidation. Quercetin has been shown to chelate or bind iron, preventing it from reacting with the lipids on neighboring cells. In addition to its antioxidant characteristics, quercetin has other properties that augment its neuroprotective potential. For example, it is 1) lipophilic (i.e., affinity for fat or lipid), allowing it to diffuse through cell membranes and scavenge free radicals within the cells, 2) anti-inflammatory, and 3) anti-edematous, i.e., inhibits damage-causing swelling.

Given such properties, Dr. E. Schultke and colleagues (Canada) assessed the impact of treating injured rats with quercetin. The rats were experimentally injured by exposing their cords through a laminectomy and clipping them at the thoracic level for five seconds. Different doses of quercetin or saline (i.e., control animals) were then injected into the body cavity (i.e., intraperitoneally) one hour after injury and every 12 hours thereafter for either 4 or 10 days. Recovery of hind-limb function was evaluated by a commonly used animal test called the BBB scale, which assesses functional recovery on a scale from 0 (no hind-limb movement) to 21 (normal walking).

Although no saline-treated controls walked, two-thirds of the quercetin-treated animals recovered some, albeit compromised, walking ability. Supporting the hypothesis that iron mediates damage, the tissue of the injured cords of saline-treated-control animals tested positive for iron, but no iron was detected in the cords of quercetin-treated animals. 

The investigators reported the results of a somewhat similar investigation in 2009. This study evaluated the effects of different quercetin treatment regimens on recovery in injured rats. Although no control animals regained sufficient hind-limb function to walk, approximately 50% of the rats treated with twice-daily doses of quercetin over three or 10 days were able to walk.  In general, the rats that were treated with quercetin for a longer duration recovered more function. Compared to controls, more spinal-cord tissue was preserved at the injury site in the quercetin-treated rats.

The investigators have also demonstrated quercetin’s potential neuroprotective effects in traumatic brain injury, a disorder exhibiting injury mechanisms somewhat comparable to SCI. In these experiments, rats with an experimentally created brain injury were treated intraperitoneally (again, into the body cavity) with either quercetin or saline one hour after injury and thereafter at 12 hour intervals. The amount of neurological damage was assessed by 1) electrophysiological measurements of nerve activity/conduction and 2) various biochemical markers of oxidative stress. These assessments indicated that quercetin-treated rats had less neurological damage compared to the saline controls.

Vitamin E

Evidence indicates that the commonly consumed nutritional supplement vitamin E may be neuroprotective after acute injury. Vitamin E is a generic term for a class of molecules called tocopherols, the most physiologically ubiquitous being alpha-tocopherol.


Alpha-tocopherol form of vitamin E


Vitamin E is found in a variety of foods, including vegetable oils, whole grains, dark green leafy vegetables, nuts and seeds, and legumes. Vitamin-E supplementation may provide a number of health benefits, such as promoting cardiovascular and eye health, and preventing cancer and age-related cognitive decline.

Like melatonin and quercetin discussed above, vitamin E is an antioxidant that protects cell membranes from the free radicals generated through lipid-peroxidation. Research suggests that vitamin E exerts its neuroprotective by inhibiting this damage-mediating process after injury, and, by so doing, helps to preserve neighboring neurons and axons.

Key studies include:

In 1987, Dr. Royal Saunders and co-investigators (USA) reported the results of treating experimentally injured cats with a combination of vitamin E (alpha-tocopherol) and another antioxidant, selenium, on lipid peroxidation. Before injury, cats were pretreated orally for five days with this combination. Compared to untreated injured controls, the spinal-cord tissue at the injury site of vitamin-E/selenium-treated cats had fewer molecules associated with destructive, lipid-peroxidation. The investigators concluded “the combination of alpha-tocopherol and selenium may protect injured spinal cord tissue…by limiting these posttraumatic membrane lipid changes.”

In 1988, Dr. Douglas Anderson (photo) and colleagues (USA) evaluated the effect of vitamin E on functional recovery in cats with experimental SCI. To produce the injury, the lumbar area of the spinal cord was exposed by a laminectomy and a compressing weight placed on it. The cats were treated orally with vitamin E (i.e., alpha-tocopherol) for five days before and after injury. Functional recovery was assessed by improvements in the cats’ ability to walk, run, and climb stairs.

Four weeks post-injury, vitamin-E treated cats recovered 72% of their pre-injury function compared to only 20% for similarly injured but untreated control cats. The investigators concluded that “pretreatment with alpha tocopherol was extraordinarily effective in promoting functional recovery in cats undergoing spinal-cord compression.” However, they noted that because vitamin E enters the central nervous system slowly, it must be administered before injury, and, hence, is probably not a viable possibility for treating SCI. (see Al Jadid study summarized below)

Reported in 1989, Dr. Kenichi Iwasa and associates (Japan) compared the recovery of rats fed a diet containing vitamin E at a level 25 times that fed to control animals. The high vitamin-E diet was consumed for eight to ten weeks prior to a compression injury produced by placing a weight on the thoracic area of the exposed cord.

Hindlimb function was assessed using a scale ranging from 0 (no voluntary movement) to 4 (complete recovery). One day after injury, the vitamin-E-treated rats had a hindlimb score of 3.5 compared to 2.4 for controls. In addition, vitamin-E supplementation enhanced the recovery of nerve conductivity and spinal-cord blood flow, and reduced the level of molecules associated with lipid peroxidation. Finally, microscopic examination of the injured cord tissue showed less damage, such as bleeding and edema, in vitamin-E-treated animals. The researchers concluded that “supplementation of the diets with vitamin E only had a dramatic effect in preventing motor disturbance.”  

In a somewhat similar study reported in 1990, this investigative team compared recovery in rats fed the aforementioned control diet with rats fed a vitamin-E deficient diet (specifically, 20-times less). In other words, this study is comparing controls to vitamin-E-deficient and not -supplemented animals. The results indicated that vitamin-E-deficient rats 1) had less recovery of hindlimb function, 2) less restoration of spinal-cord blood flow, 3) more compromised nerve conduction, 4) more bleeding and edema, and 5) a greater production of chemicals associated with lipid peroxidation.

Reported in a recent 2009 article, Dr. Al Jadid and colleagues (Saudi Arabia) reconfirmed vitamin E’s neuroprotective effects in rats with experimental SCI. Like previous studies, a compression injury was produced by placing a weight on the cord after exposing it with a laminectomy. Injured rats were divided into three groups: a a saline-treated control group, and two groups that received different levels of vitamin E.

Unlike earlier studies, apparently the rats were not pretreated with vitamin E; supplementation was started at the time of injury and continued for 14 days. This is a key difference in study design because pretreatment is obviously not a real-world therapeutic option. As mentioned above, because vitamin E was thought to enter the central nervous system slowly, it was not considered a viable candidate to administer after injury. This assumption is apparently not correct as demonstrated by Dr. Al Jadid’s research.

In this study, post-injury functional recovery was measured using an activity cage, which uses horizontal and vertical sensors to measure animal movements. In other words, injured rats who have recovered more function would trigger the sensors to a greater degree. Both vitamin-E supplemented groups rats had statistically significant improvements in function by the end of the study compared to controls. These results suggest that vitamin E, indeed, may be a useful SCI treatment option.

Chinese Skullcap

One of the 50 foundation herbs of Chinese herbology, Chinese Skullcap has been used to treat a multitude of ailments, including epilepsy, hepatitis, infections, inflammatory diseases, and cancer. Also known as Baikal Skullcap, Huang Qin, and by its scientific name Scutellarai baicalensis, Chinese Skullcap should not be confused with American Skullcap, which exerts different physiological influences.

Chinese Skullcap contains a variety of biologically active molecules, including flavonoids. Flavonoids, such as quercetin discussed before, provide the pigmentation in many of the plant foods we eat. Because they are strong antioxidants, scientists theorized that flavonoid-endowed Chinese Skullcap could protect neurons from post-injury oxidative stress and damage-mediating free radicals. Flavonoids contained within Chinese Skullcap have been shown to cross the blood-brain barrier; hence, they are able to get to the injured cord where they are needed.

Dr. Tae Yune and colleagues (Korea) examined the effects of Chinese Skullcap in rats with a contusion injury produced by dropping a weight on the exposed cord (36). The injured rats were treated orally with varying levels of Chinese Skullcap or water as a control beginning two hours after injury and then once daily for 14 consecutive days.

Functional improvement was measured by 1) the BBB locomotor score, which measures hind-limb functional recovery on a scale from 0 (no hind-limb movement) to 21 (normal walking); 2) the grid-walk test measuring foot-placement accuracy; and 3) footprint analyses after paws were dipped in dye. As measured by the BBB evaluation, hind-limb functional recovery was significantly higher in Skullcap-treated rats 14 to 35 days after injury. In addition, these rats made fewer mistakes on the grid-walk test, and footprint analyses demonstrated better forelimb-hindlimb coordination, including less toe drag.

This improved function could be the result of a number of physiological effects that Skullcap exerts on the injured cord.  For example, the investigators demonstrated that Skullcap inhibits the production of inflammatory molecules involved in the injury process, reduces oxidative stress, inhibits the programmed cell death of neurons and their support cells (a process called apoptosis), decreases the size of the injury-site lesion, and lessens the post-injury loss of myelin, the insulating, conduction-promoting material surrounding neurons.


The amino acid acetyl-L-carnitine is a frequently used nutritional supplement. It is a chemically modified form of L-carnitine, a substance abundantly found in red-meat and dairy products and also produced to some degree by the brain, liver and kidneys. Unlike many substances, acetyl-L-carnitine can pass through the blood-brain barrier and, by so doing, exert physiological, neuroprotective effects on nervous-system cells. For example, evidence suggests that acetyl-L-carnitine may be beneficial for age-related neurodegenerative conditions, such as Alzheimer’s dementia, memory difficulties, depression, etc.

Acetyl-L-carnitine also affects the functioning and viability of mitochondria, all-important organelles within cells responsible for generating the chemical fuel (i.e., ATP or adenosine triphosphate) used to drive most biochemical processes. Mitochondrial functioning can be severely compromised in injury-affected neuronal tissue, which, in turn, contributes to the secondary injury processes that magnify the damage after the initial traumautic insult.

In a series of investigations in animal models, Dr. Samir Patil and associates (USA) showed that acetyl-L-carnitine helps to preserve mitochondrial function after SCI. As a consequence of this preservation, there was less tissue damage at the injury site, and, as expected with this observation, more function was retained.

Herbal Formulation JSK

Anecdotal reports from China suggest that treatment with the JSK (Jiu-Sui-Kang) herbal formulation after SCI may enhance functional recovery by improving post-injury physiology and biochemistry. Although the specific composition of the proprietary JSK herbal formulation has not been disclosed, the formulation contains a number of Traditional Chinese Medicine herbs, including Ginseng, Chuanxiong Rhizoma, Glycyrrhizae Radix, Paeoniae Alba Radix, and Cinnamomi Cortex.

Dr. Caixin Su and colleagues (Canada) investigated JSK’s therapeutic potential in a commonly used rat model for acute SCI (ref). Rats injured by compression were randomly divided into a treatment group administered a daily dose of JSK solution or a control group receiving the same solution lacking the JSK. The locomotor ability of all rats were periodically assessed using the BBB locomotor rating scale which measures recovery of hind-limb function on a scale from 0 (complete loss of function) to 21 (normal function).

Using this scale, it was shown that JSK-treated rats had more preservation of function after injury compared to control rats. Specifically, the JSK-treated rats recovered to a 13.8 locomotor score compared to 11.2 for the controls, a statistically significant difference. In addition, experiments demonstrated that JSK-treated animals had 1) less tissue damage at the injury site, 2) less injury-related loss of body weight, 3) less injury-site deposition of fibrinogen, an inflammation molecule that inhibits neurite outgrowth, 4) less injury-associated cell death by apoptosis (defined in glossary), 5) a decreased production of Rho, a molecule that inhibits axonal growth  and regeneration (see Cethrin discussion elsewhere), 6) more axonal sparing, including preservation of the insulating myelin surrounding the axons, and 7) an increase in the expression of blood-circulation-enhancing molecules.

The investigators concluded that “JSK appears to target multiple biochemical and cellular pathways to enhance functional recovery and improve outcomes of SCI.”