Can Peripheral Nerve Treatment Have An Impact On Balance And Gait?

The progressive loss of balance and stability is a complication of diabetes that many physicians unfortunately overlook. In reviewing balance and gait science, this author suggests that there may be an unrecognized opportunity for partial restitution via nerve decompression in patients with diabetes.

Falls are common in the adult and elderly. We often do not consider them in connection with diabetic neuropathy and usually ascribe falls to the frailty and sarcopenia of advancing age. Toosizadeh and colleagues recently reviewed the topic in depth and their article is highly recommended.¹

Sarcopenia refers to the degenerative loss of skeletal muscle mass, quality and strength associated with aging (0.5 to 1 percent loss per year after the age of 50) combined with low physical performance levels.¹ Diabetes is a known risk factor for sarcopenia.

Postural stability and balance, in addition to adequate strength, are necessary conditions for bipedal stance, gait and ambulation, and for avoiding falls with their associated fractures and injuries. Balance is affected by at least three sensory systems (vision, vestibular and touch) with proprioception added into the mix. Patients with diabetes may report balance difficulties but usually only if physicians specifically ask them. It is worth reviewing the extant knowledge of postural stability before exploring the changes associated with diabetes and methods by which we might improve stability.

Standing is a process of ongoing sensing of position and applications of correction to sway variances by activating appropriate muscles. Normally, multiple sensory cues including vision, vestibular sensation, proprioception, leg muscle spindle stretch and pedal tactile sensations are available to the nervous system for the detection of sway. Ankle and hip muscle action subsequently respond to correct position and keep one’s center of mass over the base of stance. Ankle motion controls anterior to posterior corrections and hips manage lateral adjustments.

Reduced or absent input from any of these sensory channels, but especially vision, results in increased sway excursions that require greater muscle activation to compensate. This is manifest by greater deviation of the center of mass from the center of pressure. Interestingly, in the case of loss of vision, light touch contact of just the tip of one finger to a stable environmental surface restores stability to the level associated with full vision. This light touch contact or haptic sensing employs the senses of touch and proprioception, the positional awareness of body parts.

The various studies of light touch suggest that the force and position information obtained by light touch contact provides cues to balance that we can combine with other cues, such as visual or vestibular information, to determine the current postural state and take action to move toward a desired, more stable state.² Such haptic touch information appears to control body sway more efficiently than if there were no contact.

Vestibular dysfunction is surprisingly common in the United States. Agrawal and colleagues report 35 percent of U.S. adults aged 40 years and older (69 million Americans) had vestibular dysfunction as measured by the modified Romberg test of standing balance.² Odds of vestibular dysfunction increased significantly with age, were 40.3 percent lower in individuals with more than a high school education and were 70 percent higher among people with diabetes mellitus. Study participants with vestibular dysfunction who were clinically symptomatic (i.e., reported dizziness) had a 12-fold increase in the odds of falling.

Vision is a highly significant factor in balance maintenance. This is reflected by the inclusion in the standard neurological exam of the Romberg test of standing balance both with eyes open and eyes closed. The extensive review by Iosa and coworkers of the development and decline of upright gait stability verifies the fundamental primary role for vision in maintaining upright balance and gait.^3,4 This confirms that vestibular, proprioceptive, acoustic and tactile information cannot fully compensate for the loss of visual information to produce a normal gait pattern.^3,4 One assumes this holds true for balance at rest as well. Removing or adding sensory cues from one sensory system during standing balance causes a change in the contribution of remaining sensory systems, a process referred to as sensory reweighting.⁵

A Closer Look At The Relationship Between Diabetes And Balance  
Balance and stability are a complex summation of inputs from several sensory sources. However, in patients with diabetes, the situation is different in a number of ways. This is true even in the absence of identifiable peripheral neuropathy. More significant balance loss is associated with cutaneous sensibility dysfunction, putting the individual at increased risk for falling and compromising foot mechanics. Cognitive dysfunction and postural hypotension from autonomic disturbances may also intrude.  

Frequently in patients with diabetes, increased imbalance occurs in dark or low-light situations. This implies that visual cues can mask the loss of touch and vestibular controls, and this state becomes more obvious when contributions from all three sensory systems are impaired. Abdul Razzak and Hussein indicate that patients with diabetes may be vulnerable to falls on unstable surfaces before any clinical signs of peripheral neuropathy arise, especially in poorly lit areas, and may employ complex postural tactics such as a global stiffening to maintain their balance.⁶ Toosizadeh and colleagues suggest that diabetes leads to a lack of plantar sensory feedback cueing to activate local muscular control.¹ When patients finally perceive increased sway via vision and vestibular systems, central systems respond with rigid posture responses, presumably to avoid falling.¹

There is evidence for impairment of strength as well as each of the balance senses in diabetes. Functional limitations may occur more in patients with diabetes and those with diabetic peripheral neuropathy. Dynamic balance stability decreases more for patients with diabetic neuropathy than for people with diabetes alone.^7,8 Additionally, higher medial-lateral excursions in patients with diabetic peripheral neuropathy (versus patients with diabetes or controls) will require greater muscular demands to control upright posture.^7,8

Strength. In one study, ankle dorsiflexion strength was about 60 percent less for patients with diabetic sensory peripheral neuropathy than controls.⁹ Additionally, the estimated number of functioning tibialis anterior muscle units was about 60 percent fewer in patients with diabetes (about 46) versus controls (about 111).

Proprioception. Objective tests of proprioception and muscle spindle activity in people with diabetes are rare.

Touch. Sensory loss in feet and hands can seriously cripple haptic sensing. Diabetes induces measureable evidence of significant touch changes.¹⁰

Vestibular. Diabetes commonly affects the vestibular system and limits the effectiveness of exercises for recovery of vestibular function.^11,12

Vision. Diabetic retinopathy is another microvascular impairment that often accompanies diabetic sensorimotor peripheral neuropathy and can limit the ability of vision to compensate for neuropathic sensory impairment.

Neuropathic pain. Pain requiring treatment occurs in up to 25 percent of patients with diabetes.¹³ Analgesic therapy with drugs such as opioids, gabapentinoids, serotonin reuptake inhibitors or tricyclic antidepressants can have side effects that can exacerbate executive dysfunction and potentiate dizziness.

As Deshpande and colleagues summarize, “Subtle changes in multiple sensory systems of older adults with Type 2 diabetes may reduce redundancy available for balance control in performing challenging activities much before overt diabetic sensory peripheral neuropathy development.”¹⁴

Key Insights On Interventions For Balance and Sarcopenia
Pharmaceutical therapies for frailty have focused on the use of replacement therapy to raise circulating basal levels of various hormones. Results have been disappointing except in the case of testosterone, which has shown some benefits.¹⁵ Withdrawal of psychotropics to minimize their cognitive and woozy side effects may be worthwhile.

Authors have proposed several exercise interventions as being beneficial for those with impaired balance. Armstrong and coworkers examined the potential for exercise to improve balance in diabetes.¹⁶ Cavegn and Riskowski reported that Tai Chi exercise can produce significant improvements in ankle proprioception and fitness and decreased plantar pressure in the forefoot, but noted no statistical benefit in balance or tactile sensation.¹⁷ Aranda and coworkers found that vestibular neuropathy with diabetes responds more poorly to Cawthorne–Cooksey rehabilitation exercises.¹²

What The Literature Reveals About Nerve Decompression And Balance
Accumulated information over the past two decades has suggested that nerve decompression, in addition to addressing diabetic sensorimotor peripheral neuropathic pain, can be helpful in protecting patients with diabetic neuropathy from diabetic hand and foot complications as well as balance and stability impairments. This counsel is based upon the hypothesis of Dellon that diabetic sensory peripheral neuropathy is not only a metabolic disease but also frequently induces secondary physical compression effects in several peripheral nerves.¹⁸ Such consequences are produced by proven nerve enlargement explained as secondary osmotic effects of hyperglycemia and intraneural accumulation of sorbitol via the hexokinase metabolic pathway.^19,20 Enlarged nerves can become entrapped at periarticular fibro-osseous tunnel sites that are shrunken and stiffened by the effects of advanced glycation end products on collagen. Surgeons can relieve these physical compressions by opening of the fibro-osseous tunnel roof with surgical division of the bridging compressive tissues.

Dellon recommends nerve decompression via external neurolysis of the tibial nerve and its plantar branches at the medial ankle, the common peroneal nerve at the fibular neck, and the deep peroneal nerve on the dorsal foot under the extensor hallucis brevis tendon.²¹ One may also release the superficial peroneal nerve as it exits the anterior or lateral leg compartments through a fascial foramen in the distal leg. The high incidence of carpal tunnel syndrome in diabetes is in theory analogous in the upper extremity. After nerve decompression, improved nerve conduction velocity and immediate partial restitution of electromyography motor evoked potentials have been evident.²²

Physicians have applied nerve decompression to help address several complications of diabetic neuropathy. Level 1 evidence from three studies now has proven the value of nerve decompression in treating diabetic sensorimotor peripheral neuropathic pain and the study authors have noted that sensory improvement commonly occurs as well.²³ Level 2 and Level 3 evidence also suggest that nerve decompression offers protection against diabetic foot ulcer recurrence and initial occurrence.^24-25 Researchers have looked at the value of nerve decompression in facilitating static balance and stability in two published studies.^26-27

Ducic and colleagues have investigated whether there might be a relationship between pedal sensibility and balance.^26,28 They measured sway during static standing with eyes open or closed, and compared this to pedal sensibility as measured by one-point and two-point static touch sensation with the Pressure Specified Sensory Device (PSSD, Sensory Management). In their study group of patients diagnosed with neuropathy diagnoses, two-thirds of the patients had diabetes. The study authors showed impaired hallux sensibility at a level consistent with axonal loss in 52 percent of the patients and completely absent hallux sensibility in the remaining 48 percent of the study participants. Similarly, at the heel, sensibility was normal in 6.5 percent of patients, was abnormal at a level consistent with axonal loss in 71 percent of the patients and was absent in the remaining 22.5 percent of the study participants.

After this documentation of the intuitive relationship between increasing loss of foot sensibility and deficit in balance, the authors subsequently followed up with an intervention study employing nerve decompression and testing whether balance improvement would result.¹⁹ The PSSD touch sensibility improved as did the degree of sway. Unilateral decompression for eight patients produced a nominal sway improvement but this finding was not statistically significant. Bilateral neurolysis, however, produced sway reduction with eyes open and eyes closed of 23 percent and 145 percent respectively. This was statistically significant even in the small study size with only six bilateral nerve decompression cases. This result is very encouraging Level 2 prospective evidence that we can expect nerve decompression to improve impaired balance in patients with diabetic sensorimotor peripheral neuropathy.

It is unsurprising that bilateral sensibility improvement correlates best to balance. One can easily suspect that side to side sway at least requires pedal pressure and sensibility information input from two points for comparison by the haptic system. Unilateral change would not improve pedal sensing without another reference point (i.e. the other foot’s input) to evaluate changes and trigger muscle response. If you can’t feel it, you can’t correct it.

A second study of surgical decompression by Macare van Maurik and coworkers examined balance in a larger group of 42 diabetic sensorimotor peripheral neuropathy cases after unilateral nerve decompression.²⁹ The patients in these cases all met Dellon’s surgical criteria for using nerve decompression to address pain. Postoperative sway at six and 12 months did not improve. This finding was consistent with the observation by Ducic and coworkers that although bilateral nerve decompression significantly decreased sway with eyes open and eyes closed, unilateral nerve decompression did not suffice.

Unfortunately, this study has several serious deficiencies of protocol and interpretation.²⁶ The authors incorrectly state that Ducic and colleagues’ study reports that bilateral nerve decompression failed to produce significant reduction in sway for both eyes open and eyes closed states, which is clearly opposite of the conclusion asserted by Ducic and colleagues.¹⁹ The Macare van Maurik discussion correctly indicates their own study found “no evidence that unilateral decompression of nerves in the lower extremity influences postural stability in patients with painful diabetic polyneuropathy.”²⁹ However, the abstract drops the key modifier “unilateral” in claiming there is “no evidence that surgical decompression of nerves of the lower extremity influences stability within one year after surgery in patients with painful diabetic polyneuropathy.” These errors in combination encourage an egregious misinterpretation of the findings by Ducic and coworkers, and suggest a repudiation of nerve decompression benefit.

Publication of the Macare van Maurik study has lead to the unfortunate opinion of some, who fail to consult the Ducic papers, that this was a negative result for nerve decompression.^26,29 In reality, it neither tests the Ducic finding of benefit when bilateral nerve decompression surgery occurs, nor supports their expansive assertion that the study finds no evidence that nerve decompression of compressed leg nerves in diabetic sensorimotor peripheral neuropathy influences stability.

What Are The Functional Effects Of Nerve Decompression?
There is meager evidence of nerve decompression’s effects on physical function other than balance. In 2010, Paxton and colleagues presented the results of ankle function after nerve decompression in a single patient with diabetic sensorimotor peripheral neuropathy.²⁷ They found that nerve decompression greatly improved the patient’s maximal ankle dorsiflexion and plantarflexion force, and the rate of force development.

Another pilot trial found that five of seven painful diabetic sensorimotor peripheral neuropathy cases improved in dynamometer tested extensor hallucis strength after common peroneal nerve neurolysis.³⁰ One might reasonably expect similar improvement in other lateral and anterior compartment muscles (like the peroneals and tibialis anterior) involved in ankle positioning and adjustments to improve stability. Such experiments need to occur.

Electrophysiologic improvement of motor evoked potentials of peroneal nerve innervated muscles tibialis anterior and peroneus longus is common after nerve decompression. Zhang and coworkers found leg nerve conduction velocity deficits to be improved by about half by nerve decompression.³¹ Anderson and colleagues have demonstrated that motor evoked potentials in common peroneal nerve innervated leg muscles usually improve intraoperatively at the time of nerve decompression.²²

In Conclusion
At this point in time, there is some limited clinical evidence to suggest that bilateral nerve decompression can improve the balance and gait problems associated with diabetes. This prospect has the support of intraoperative electrophysiologic recordings and the anecdotal experiences of practitioners who have performed nerve decompression. While more studies are necessary to further explore the potential impact of bilateral nerve decompression on balance and gait issues for patients with diabetes, recent advances in the understanding of neural cueing, feedback effects and the complex processes of balance and gait control allow us to propose that nerve decompression shows real potential in confronting the progressive, entrapment-related deterioration of balance, stability and gait in patients with diabetes despite the relentless advance of metabolic neuropathy in this patient population. We should recognize and actively pursue such opportunities.

Dr. Nickerson is a member of the Advisory Board of the U.S. Neuropathy Centers in Arizona. He is board-certified in orthopedic surgery.

References

1.     Toosizadeh N, Mohler J, Armstrong DG, Talal TK, Najafi B. The influence of diabetic peripheral neuropathy on local postural muscle and central sensory feedback balance control. PloS One. 2015;10(8):e0135255.
2.     Agrawal Y, Carey JP, Della Santina CC, Schubert MC, Minor LB. Disorders of balance and vestibular function in US adults: data from the National Health and Nutrition Examination Survey, 2001-2004. Arch Intern Med. 2009;169(10):938-944.
3.     Hallemans A, Beccu S, Van Loock K, Ortibus E, Truijen S, Aerts P. Visual deprivation leads to gait adaptations that are age- and context-specific: I. Step-time parameters. Gait Posture. 2009;30(1):55-59.
4.     Iosa M, Fusco A, Morone G, Paolucci S. Development and decline of upright gait stability. Frontiers Aging Neurosci. 2014;6:14.
5.     Wing AM, Johannsen L, Endo S. Light touch for balance: influence of a time-varying external driving signal. Philos Trans R Soc Lond B Biol Sci. 2011;366(1581):3133-3141.
6.     Abdul Razzak R, Hussein W. Postural visual dependence in asymptomatic type 2 diabetic patients without peripheral neuropathy during a postural challenging task. J Diabetes Complications. 2016;30(3):501-506.
7.     Lim KB, Kim DJ, Noh JH, Yoo J, Moon JW. Comparison of balance ability between patients with type 2 diabetes and with and without peripheral neuropathy. PMR. 2014;6(3):209-214; quiz 214.
8.     Brown SJ, Handsaker JC, Bowling FL, Boulton AJ, Reeves ND. Diabetic peripheral neuropathy compromises balance during daily activities. Diabetes Care;38(6):1116-1122.
9.     Allen MD, Choi IH, Kimpinski K, Doherty TJ, Rice CL. Motor unit loss and weakness in association with diabetic neuropathy in humans. Muscle Nerve. 2013;48(2):298-300.
10.     Zhang Y, Li J, Wang T, Wang J. Amplitude of sensory nerve action potential in early stage diabetic peripheral neuropathy: an analysis of 500 cases. Neural Regener Res. 2014;9(14):1389-1394.
11.     Su J, Zhang J, Wang M, Zhou H. [The clinical values of VEMP in the diagnosis of vestibular nerve impairment in the patients with type 2 diabetes mellitus]. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2015;50(12):1001-1004.
12.     Aranda C, Meza A, Rodriguez R, Mantilla MT, Jauregui-Renaud K. Diabetic polyneuropathy may increase the handicap related to vestibular disease. Arch Med Res. 2009;40(3):180-185.
13.     Tesfaye S, Boulton AJ, Dickenson AH. Mechanisms and management of diabetic painful distal symmetrical polyneuropathy. Diabetes Care. 2013;36(9):2456-2465.
14.     Deshpande N, Hewston P, Aldred A. Sensory functions, balance, and mobility in older adults with type 2 diabetes without overt diabetic peripheral neuropathy: a brief report. J Appl Gerontol. Aug 30 2015.
15.     Laosa O, Alonso C, Castro M, Rodriguez-Manas L. Pharmaceutical interventions for frailty and sarcopenia. Current Pharm Design. 2014;20(18):3068-3082.
16.     Armstrong MJ, Colberg SR, Sigal RJ. Moving beyond cardio: the value of resistance training, balance training, and other forms of exercise in the management of diabetes. Diabetes Spectrum. 2015;28(1):14-23.
17.     Cavegn EI, Riskowski JL. The effects of tai chi on peripheral somatosensation, balance, and fitness in Hispanic older adults with type 2 diabetes: a pilot and feasibility study. Evid-Based Complement Alternat Med. 2015;2015:767213.
18.     Dellon AL. A cause for optimism in diabetic neuropathy. Ann Plast Surg. 1988;20(2):103-105.
19.     Lee D, Dauphinee DM. Morphological and functional changes in the diabetic peripheral nerve: using diagnostic ultrasound and neurosensory testing to select candidates for nerve decompression. J Am Podiatr Med Assoc. 2005;95(5):433-437.
20.     Riazi S, Bril V, Perkins BA, et al. Can ultrasound of the tibial nerve detect diabetic peripheral neuropathy? A cross-sectional study. Diabetes Care. 2012;35(12):2575-2579.
21.     Dellon AL. Diabetic neuropathy: medical and surgical approaches. Clin Podiatr Med Surg. 2007;24(3):425-448, viii.
22.     Anderson JC, Tracy, BL, Paxton R, Yamasaki, DS. Acute improvement in intraoperative EMG following common fibular nerve decompression in patients with symptomatic diabetic sensorimotor peripheral neuropathy: 1. EMG results. J Neurolog Surg A. 2016, accepted 2016.
23.     Macare van Maurik JF, van Hal M, van Eijk RP, et al. Value of surgical decompression of compressed nerves in the lower extremity in patients with painful diabetic neuropathy: a randomized controlled trial. Plast Reconstr Surg. 2014;134(2):325-332.
24.     Aszmann O, Tassler PL, Dellon AL. Changing the natural history of diabetic neuropathy: incidence of ulcer/amputation in the contralateral limb of patients with a unilateral nerve decompression procedure. Ann Plast Surg. 2004;53(6):517-522.
25.     Nickerson DS, Rader AJ. Low long-term risk of foot ulcer recurrence after nerve decompression in a diabetes neuropathy cohort. J Am Podiatr Med Assoc. 2013;103(5):380-386.
26.     Ducic I, Taylor NS, Dellon AL. Relationship between peripheral nerve decompression and gain of pedal sensibility and balance in patients with peripheral neuropathy. Ann Plast Surg. 2006;56(2):145-150.
27.     Paxton RJ, Jones, AM, Hitchcock, LN, et al. Improved ankle muscle function after surgical nerve release in a patient with lower limb neuropathy. Rocky Mountain Chapter, American College of Sports Medicine meeting, 2010, Denver.
28.     Ducic I, Short KW, Dellon AL. Relationship between loss of pedal sensibility, balance, and falls in patients with peripheral neuropathy. Ann Plast Surg. 2004;52(6):535-540.
29.     Macare van Maurik JF, ter Horst B, van Hal M, Kon M, Peters EJ. Effect of surgical decompression of nerves in the lower extremity in patients with painful diabetic polyneuropathy on stability: a randomized controlled trial. Clin Rehab. 2015;29(10):994-1001.
30.     Barrett S, Levine T, Hank N, et al. A pilot trial of peripheral nerve decompression for painful diabetic neuropathy. American Academy of Neurology Convention, San Diego, March 16–23, 2013.
31.     Zhang W, Zhong W, Yang M, Shi J, Guowei L, Ma Q. Evaluation of the clinical efficacy of multiple lower-extremity nerve decompression in diabetic peripheral neuropathy. Br J Neurosurg. 2013;27(6):795-799.