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Chapter 8 Post:Polio Syi{Drome, and Tendon Transfer As Surgical Management

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Chapter 8 Post:Polio Syi{Drome, and Tendon Transfer As Surgical Management CHAPTER 8 POST:POLIO SYI{DROME, AND TENDON TRANSFER AS SURGICAL MANAGEMENT Melissa Robrtaille, DPM, MS Many patients who were diagnosed with innerwations (Figures 1,2'). Asymmetric, flaccid poliomyelitis 30 to 40 years ago are curently experi- paralysis occurs as well as other lower motor neu- encing increased muscle fatigue, new weakness, and ron symptoms. Only I to 20/o of all those infectecl pain. This decline in muscle function frequently with the poliovirus develop paralysis. Also, in chil- affects the patient's ability to ambulate and necessi- dren, paralysis occurs in 1/1000 case, whereas in tates additional bracing, assistive devices and possibly adults, the frequency increases to l/75.It is impor- surgical treatment. The characteristics of post-polio tant to note that patients retain normal syndrome (PPS) and tendon transfers for the afferent/sensory ancl central neurologic control.' ffeatment of weakness and joint instability will be The threat of poliomyelitis in developed discussed. countries is practically non-existent today thanks to In order to understand the possible causes of the development of the Salk vaccine in 7955 PPS and to provide the best plan for its treatment, and the Sabine oral vaccine in 1961. Polio still knowledge of acute polio is necessary. Acute continues to be a problem in third wodd countries anterior poliomyelitis is a viral infection localized in where mass immunizations are not always the anterior horn cells of the spinal cord and available. Many of those who contracted the cefiain brainstem motor nuclei. Initial invasion of clisease were able to recover from the resulting the vir-urs occurs through the gastrointestinal and paralysis and went on to lead active, normal respiratory tracts and spreads to the central nen/ous lifestyles. The potential for recovery of muscle system through a hematogenolls route. Once there, function depends on the recovery of damaged but neurologic and functional loss occurs as anterior not clestroyed anterior horn cells. Most clinical horn cells are damaged, destroying the efferent recovery occurs during the first month after the pathway, and thus the muscle fibers lose their acute illness and is almost complete within 6 Figure 1. Norm.ll anterior horn cell r,ith its Figure 2. In acute poliomyelitis. the :rnterior horn nlot()f-nellfon - cells are clestroyed and the n-nscle fiber lose thek innen ations creating weakness or paralysis. 40 CHAPTER B months although limited recovery mav occur for In general, the patients most at risk for devel- about 2 years. oping new problems are those who experienced The extent of neurologic and ftinctional recov- more severe polio at onset, although some patients ery is determined in part by the phenomenon of with typical post-polio symptoms had seemingly terminai axon sprolrting were a motor neuron can mild polio with excellent clinical recovery. In re-inneruate muscles fibers which have lost their addition, persons who were older when they nerue supply. In addition to this re-inneruation, the contracted polio appear to be at an increased risk for remaining muscle fibers hyperlrophy to increase the new neurological symptoms. The onset of there new strength of the muscle group. As a result, the problems is most commonly insidious, but in many sulivors of acute polio may be left with a few, persons they are precipitated by specific events such significantly enlarged motor units doing the work as minor accident, period of bed rest, or weight previously performed by many units.' gain. Patients characteristically say ihat a similar A suruey in 1987 found there were more than event severzrl years earlier would not have caused 640,000 sulivors of paralyic polio in this country. the same decline in health and function. Likewise, Population based sulveys have indicated that as new problems may begin when coexisting medical many as 540/o of polio survivors develop new problems such as diabetes develop or worsen.2 symptoms. If we consider these estimates to be This seemingly new phenomenon was accllrate, over 400,000 people may experience the actually recognized over 100 years ago, with the late effects of polio. It is impofiant to realize that first descriptions of the disease reported in 1875 in there are many affected and the possibility of the French literature. Sporadic reports describing encountering this condition in the office setting is similar phenomenon appeared in the literature quite 1ike1y.3 thror-rghout much of the 20th century. It was not until the early 1980s, approximately 40 years after Post-Polio Syndrome the major epidemics of the 1940s and 1950s, that post-polio syndrome (PPS) became widely Today, many of those earlier polio surwivors are recognizecl.t developing new problenis ancl facing new chal- lenges. These problems typically occur about 30 to 50 years after their initial polio illness and inclucle new w-eakness, fatigue, pain, ftrnctional loss, and cold sensitivity.r The cause of these new symptoms is unclear, with many theories regarding the etiology of post-polio syndrome being proposed; hower.er, the pathologic changes that cause the symptoms of PPS have not been proven conclusively.' Although many of these etiologies continue to be the subject of debate, the most popular and consistent factors appear to be motor trnit dysfunction due to oveflise and /or premature aging of large motor units. Following anterior horn cell death, adjacent healthy zrnterior horn ce1ls assume the filnction of those ion cells. Subsequently, the metabolic demand placed on them is greater (Figure 3). It is hypothesizecl that these over-worked anterior horn cells succumb prematurely to the aging process due to greater than normal stress placed on them. Nthough this hypothesis is artrac- tive to many, it has not been supported by biopsy or Figure J. Folloning anterior horn cell death, direct, conclusive experiment al data.' adjacent healthy anterior horn cells assume the function of those ion cells. CHAPTER 8 4t Criteia for the diagnosis of PPS Because of muscle weakness, gait characteris- tics in post-polio patients are predictably abnormal. The criteria for the diagnosis of PPS used by most A study by Perry et al found that impaired ankle investigators and clinicians were first described by plantarflexion due to weakness of tricep surae was Mulder et a1 in 7972. Theses criteria include 1) a the most significant indicator of abnormal gait documented history of polio (can be confirmed pattern in these patients. This led to a reduced through medical records, neurologic examinations velocity and stride length, which was amplified in and electromyography showing large polyphasic fast gait.5 The significance of this relates to the motor unit action potentials and a decrease in the increased demand of the plantar flexors during the number of motor units on maximum recruitment in single suppolt phase of stance, since this is when weak muscles with fibrillations); 2') a period (usu- the greatest demand is placed on these muscles. a1ly >15 yrs) of neurologic and functional stability Forward momentum of the body over the supporl- after recovery from acute illness; 3) the gradual or ing foot stimulates action of the gastrocnemius and rarely abrupt onset of new weakness. New neuro- soleus muscles to control the rate of tibial advance- genic weakness is essential for making the ment and maintain stability at the ankle. Likewise, diagnosis of PPS and presumably reflects continu- calf muscle action is the only mechanism used for ing dysfunction of previously injured motor units. It knee stability in normal gait after early mid-stance. is important to make a distinction between new The consequence is that a patient with weak plan- neurogenic weakness versus disuse weakness, tar flexors has poor tibial control and an unstable which is not always apparent. This can be inferred ankle joint. Therefore, when the stability of the by the onset of diminished function despite main- lower extremity is threatened during single limb taining the usual level and intensity of activity. stance, the velocity is limited to decrease the Fina1ly, 4) the criteria is the exclusion of all other chance of falling. Also, the heel cannot rise until conditions that might cause the weakness or other the contralateral limb is loaded, so a significant health problems.t't' As previously mentionecl, the portion of stride length is lost.;7 symptoms of fatig,-re, joint pain, muscle pain, new New muscle weakness usually appears in weakness, and cold sensitiviry are vague and can muscles previously affected with the initial attack, have a number of differentials. The major dif'feren- however muscles that were believed to be spared tial diagnosis include focal neurologic disease such can be affected as well. Because the mechanism of as a radiculopathy, focal compressive neuropathy, neurologic compensation, previously described, is or spinal cord lesion and medical causes of neu- so effective, a muscle can retain normal strength ropathy such as diabetes, thyroid disease, uremia, even after 50o/o of the original motor neurons have a1cohol, and hereditary neuromuscular disease. been lost. This is why manual muscle testing in Attempts must be made to ru1e out other causes of some patients may be normal. These patients man- disease since the management of different diseases age to function at an extraordinarily high level of can vary greatly. performance on relatively few sutwiving motor units.s'e The neurologic examination in PPS is char- Physical exam and gait evaluation acteristic of a lower motor neuron lesion. The patients will have intact sensorium, flaccid paraly- Muscles innervated by the cervical and lumbar sis, diminished reflexes and absence of clonus or spinal segments are most often affected, and babinsky. Intact sensation helps distinguish PPS paralysis occurs twice as often in the lower extrem- from other common differentials such as neuropathy.
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