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Home > JPO > 1993 Vol. 5, Num. 2 > pp. 52-54

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Neurological Aspects of Prosthetic/Orthotic Practice

John H. Bowker, MD

ABSTRACT

Many patients referred for orthotic or prosthetic services will have associated neurologic deficits. These must be recognized by the practitioner prior to the design and fitting of an orthosis or prosthesis to avoid costly and potentially harmful errors in design and application. Commonly seen deficits are loss of protective sensation, impaired proprioception and spasticity. Any one of these may be associated with fixed soft tissue or bony deformity. A working knowledge of sensory and motor examination, combined with careful history-taking, will greatly enhance the clinical skills of the prosthetist/orthotist in this challenging aspect of practice.

Introduction

A wide variety of disorders as well as trauma may result in neurological problems requiring prosthetic and orthotic services. Sensory and/or motor loss may exist alone or be complicated by spasticity or deformity, profoundly affecting the orthotic solution for something as seemingly simple as foot dorsiflexion paralysis.

The experienced prosthetist/orthotist realizes patients with virtually any type of disease or injury require careful evaluation for associated primary or secondary neurological aspects of their condition. When a detailed examination is performed prior to the design and fitting of an orthosis or prosthesis, costly and potentially harmful errors in design and application can be avoided(1).

Clinical Examination

When evaluating sensory function, patient history is extremely important. Patients with a sudden onset of sensory loss are usually aware of the loss unless a head injury or cerebrovascular accident occurred. Gradual loss related to peripheral neuropathy, as in diabetes, may be minimized or even denied by the patient. Those patients who have experienced congenital sensory loss, as in the case of spina bifida, have never experienced normal sensation (Figure 1) .

From a prosthetic/orthotic perspective, it is of utmost importance to determine if the body segment encompassed by a device has at least "protective" sensation, that is the ability to feel excessive pressures that will eventually lead to skin destruction. A simple and inexpensive test kit is available to determine if a part has normal, protective or absent sensation.

A simplified Semmes-Weinstein filament set' contains three filaments that specifically detect these particular sensation thresholds. In this concise test, each filament tip-starting with the thinnest-is applied in turn to the skin. Increasing pressure is applied until the patient can sense its presence. (The patient's eyes should be closed.)

In cases of limb paralysis, it is important to distinguish between flaccid and spastic types. Flaccid paralysis results from damage to lower motor neurons as in poliomyelitis, lumbosacral nerve trauma, spina bifida, isolated peripheral nerve injury or diabetes mellitus. Flaccid limbs, in the absence of contracture, are easily supported by orthoses in weightbearing postures. Many of these patients' limbs are also insensate, with the exception of those patients whose conditions affect only the motor cells of the anterior horn of the spinal cord, such as poliomyelitis or Guillain-Barre syndrome.

Spastic paralysis, in contrast, results from spinal cord injury, traumatic brain injury, cerebrovascular accident, multiple sclerosis or cerebral palsy, all of which involve damage to upper motor neurons of the brain and/or spinal cord. The resulting increased tone can sometimes be reduced without significant sedation with the use of antispastic drugs such as baclofen. The limiting factor in bracing spastic limbs remains, of course, the severity of reflexive muscle tone.

For example, in the equinovarus gait of the hemiplegic, if the foot becomes plantigrade during midstance, the spasticity is considered mild and an anklefoot orthosis (AFO) with moderately anterior trimlines will suffice to hold the foot plantigrade throughout the gait cycle.

If the foot remains in equinovarus throughout the gait cycle, an AFO may not be able to maintain a fully plantigrade position. When an AFO is indicated, it is essential the heel remains seated properly in the brace and shoe. If it does not, the patient's gait will be unsafe since the unstable foot and functional leg length discrepancy will make falls likely. If a patient with marked spasticity is otherwise a good candidate for ambulation, consider percutaneous fractional lengthening of the Achilles tendon coupled with a split anterior tibial tendon transfer (SPLATT) procedure (2). Such surgical intervention will make effective orthotic fitting feasible.

The presence of proprioception, or the ability to sense limb motion and weightbearing, will help determine if a patient will become a functional walker. Inability to sense floor contact and joint position will make safe ambulation difficult, if not impossible, even if other types of sensation are present.

In addition to severe spastic equinovarus, another condition in which bracing should be approached with caution is deformity secondary to neuropathic (Charcot) foot and ankle joints. Loss of sensory function plays a major role in the disintegration of bony structure and increases the risks of skin necrosis.

If treated early, prolonged casting of neuropathic foot fractures and fracture-dislocations followed by long-term circumferential bracing will usually result in a foot that can be fitted with a custom-made or in-depth shoe with custom-molded insert. Seen late, a severe and fixed deformity will likely not be amenable to casting or an orthosis. In fact, if "corrective" forces are orthotically applied in the face of rigid deformity, skin breakdown is to be expected. Charcot changes following simple ankle fractures sometimes result in severe, irreducible deformity (see Figure 2a and Figure 2b ). Surgical correction in carefully selected cases has been successful.

Lack of protective sensation obviously requires precise fitting and appropriate cushioning of shoes (see Figure 3 ) as well as orthoses and prosthetic sockets (see Figure 4a and Figure 4b ). Areas of skin pressure, blistering or abrasion by shear forces can be produced by loosely fitting shoes or by "pistoning" in loose prosthetic sockets, especially at the Syme or transtibial levels.

Conclusion

Patients with a wide variety of neurological deficits resulting from trauma or disease will see the orthotist or prosthetist for definitive management. A working knowledge of sensory and motor examination will assist greatly in the proper design and fitting of an orthosis or prosthesis and help avoid costly and potentially harmful errors in design and application.


John H. Bowker, MD, is professor and associate chairman of the department of orthopaedics and rehabilitation at the University of Miami School of Medicine, and director of ampputee and diabetic foot services at Jackson Memorial Medical Center, Miami, Fla.

References:

  1. Hoppenfield S. Orthopaedic neurology: a diagnostic guide to neurologic levels 1977; JB Lippincott Co., Philadelphia. Pa.
  2. Waters RL, Perry J, Garland D. Surgical correction of gait abnormalities following stroke. Clinical Orthopaedics and Related Research 1978; 131:54-63.


 

Home > JPO > 1993 Vol. 5, Num. 2 > pp. 52-54

 

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