INTRODUCTION
Normal volitional control of movement depends on the balanced relationship of the cortical, subcortical, cerebellar, spinal, and peripheral nervous systems. Neurologic dysfunction can result from compromise at any point in this balance resulting in motor or sensory impairment, or both. This chapter reviews essential features of common diseases encountered in neurorehabilitation, including amyotrophic lateral sclerosis, Guillain-Barré syndrome, polio and post-polio syndrome, and Parkinson’s disease, with a focus on diagnosis, treatment, and rehabilitation for each disorder.
AMYOTROPHIC LATERAL SCLEROSIS
ESSENTIALS OF DIAGNOSIS
Most widely known motor neuron disease.
Insidious onset and rapidly progressive course.
Most common presentation is painless asymmetric limb weakness and atrophy.
Diagnosis is primarily clinical, based on the presence of upper and lower motor neuron signs.
In its classic form, amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disease affecting both upper and lower motor neurons that results in destruction of the anterior horn cells, motor cranial nerve nuclei, and corticospinal–bulbar tracts. Patients most commonly present with painless asymmetric limb weakness, but other symptoms associated with upper and lower motor neuron degeneration include spasticity, pathologic reflexes, and muscular atrophy. The worldwide prevalence is 5–7 in 100,000, and men are more commonly affected than women at a ratio of 1.5:1.0. The disease onset is typically between 40 and 60 years of age (mean: 58 years).
A group of atypical motor neuron diseases has been studied that usually but do not always evolve into ALS. These disorders—progressive muscular atrophy (PMA), progressive lateral sclerosis (PLS), and progressive bulbar palsy (PBP)—are distinct but interrelated disorders, perhaps representing variants within a spectrum of ALS disease.
PMA is a sporadic disease affecting only the anterior horn cells without involvement of the upper motor neurons (UMNs). Hence, those affected exhibit only lower motor neuron (LMN) signs. As such, the most common presenting symptom of PMA is distal limb weakness with muscle atrophy. The natural history of PMA and ALS demonstrate such a high degree of similarity as to often be indistinguishable, and in one study of PMA subjects, 35% of patients developed UMN signs, mirroring the classic ALS phenotype.
PLS is also a rare sporadic motor neuron disorder. The initial manifestations of the disease are dominated by UMN features. The chief complaint is progressive asymmetric spasticity, most commonly in the legs followed by the arms or bulbar muscles. The disease progression appears to be slower than in ALS, occurring over years to decades. The life expectancy of patients with PLS is also better than that of ALS patients, ranging between 7 and 14 years. Ultimately, approximately 45% of PLS patients go on to develop LMN symptoms and progress to ALS.
In rare instances motor neuron disease is limited to the bulbar muscles. Patients with this condition most often present with dysarthria or dysphagia, or both.
Although the cause of ALS is unknown, it may share common biologic mechanisms with disorders such as Parkinson’s, Alzheimer’s, and other neurodegenerative diseases. One widely held hypothesis postulates an interaction between genetic susceptibility and environmental exposure in sporadic ALS. Investigations are currently underway to find susceptibility genes or materials within the environment that predispose certain individuals to sporadic ALS. Evidence supports several different causative mechanisms leading to the demise of motor neurons: nucleic acid changes, oxidative damage, mitochondrial dysfunction, growth factor expression, protein aggregation, inflammatory cascades, derangement of cytoskeletal elements and axonal transport, excitotoxicity, and apoptosis. How these mechanisms work to achieve motor neuron death is unknown, but a variety of factors, either in sequence or in combination, most likely predispose certain individuals to develop the ALS phenotype.
The initial clinical symptoms of ALS can vary greatly. Clinical diagnosis relies on the demonstration of UMN and LMN signs, although either may be absent early in the course of the disease. Signs of LMN involvement include muscle weakness, atrophy, diminished or absent deep tendon reflexes, and fasciculations. Identification of UMN signs can be more subjective as they can be transient, developing and then disappearing as the more clinically dominant LMN features manifest. In addition, signs indicative of UMN pathology—sustained clonus, hyperactive deep tendon reflexes, spasticity, and a Babinski sign—may not manifest clinically in some patients with ALS. Additional UMN features to be aware of are forced yawning, retained reflexes in an atrophied and weakened limb, pseudobulbar affect, and pathologic reflexes (eg, Hoffman sign’s and a heightened jaw, gag, or snout reflex). Pseudobulbar affect is an interesting feature in what is primarily known as a pure motor disorder, and refers to uncontrollable episodes of laughing, crying, or other emotional displays.
The most common presentation of ALS is a patient with a combination of UMN and LMN features. Typically patients present to the physician with persistent, unexplained weakness and atrophy. These signs are frequently painless and asymmetric at onset. Neurologic examination may reveal hyperreflexia, increased muscle tone, and clonus. Some patients may not have sought early medical evaluation or may have done so, but their physicians did not recognize the significance of the symptoms. In these instances their disease may evolve from limb-dominant ALS to bulbar-dominant ALS. Such patients present with dysarthria, dysphagia, and aspiration. Head drop is often seen and results from weakness in the neck extensors, causing a chin-on-chest deformity that requires cervical bracing.
Other signs and symptoms associated with ALS are loss of manual dexterity, cachexia, fatigue, and diffuse musculoskeletal complaints. Fasciculations, particularly in the setting of weakness, should raise a strong suspicion of motor neuron disease. Wasting and fasciculations on examination of the tongue indicate LMN involvement of the cranial nerves. Muscle cramping is frequently elicited during manual muscle testing but can occur anywhere in the body, including the trunk. Ventilatory difficulties and paradoxical abdominal movements usually indicate diaphragmatic weakness and necessitate pulmonary function testing.
The presence of cognitive and behavioral deficits in ALS was recognized in the 19th century; however, for many years this was overlooked as an area of clinical investigation and research. These deficits can exist in both sporadic and familial forms of the disease and are frequently the initial symptoms. Cognitive impairment is most prominent in the domain of executive function and language. This impairment may appear in a clinical setting as disorganization, mental inflexibility, word finding difficulty, and fluent semantic dementia. Behavioral difficulties are displayed in social and personal interactions. Patients may be unable to receive and interpret nonverbal cuing, and they may become disinhibited or withdrawn.
General laboratory workup includes a chemistry panel, complete blood count (CBC), and creatine kinase concentration. Based on the patient’s history and presentation, additional laboratory evaluation may include antibody testing to assess immune-mediated causes and serology testing to rule out infectious etiologies. If there is a family history of motor neuron disease, DNA mutational analysis is warranted. A muscle biopsy can be done if myopathy is suspected, but findings are not diagnostic for ALS.
Electrodiagnostic testing improves diagnostic accuracy and should be performed on every patient suspected of having a motor neuron disease. Testing offers insight into the rate of progression and helps to exclude other diagnoses that may mimic ALS. Nerve conduction studies (NCS) with electromyography (EMG) can confirm a pattern of active or chronic denervation and demonstrate fasciculation potentials in multiple muscles innervated by multiple segments in multiple regions. Although these findings are not diagnostic of ALS, they have been shown to be a consistent pattern. Most often NCS indicates a normal sensory response, normal or low motor amplitudes, and up to a 25% decrease in conduction velocities. Needle EMG shows a pattern of decreased recruitment, normal to large motor unit action potentials, and abnormal spontaneous activity such as positive sharp waves, complex repetitive discharges, and fibrillation potentials. Single-fiber EMG and repetitive stimulation can also be included in this study.
Magnetic resonance imaging of the brain and spinal cord can exclude other diagnoses such as cord compression, syrinx, tethered cord, stroke, or tumor. Pulmonary function testing is invaluable in assessing the patient’s current level of respiratory impairment. For a patient who presents with bulbar muscle weakness, referral to speech therapy for a video-assisted swallow evaluation is warranted to determine the risk of choking or aspiration.
For a patient with a combination of UMN and LMN signs, the differential diagnostic considerations are limited. ALS may mimic hereditary spastic paraparesis if the patient exhibits spastic paraparesis. Myasthenia gravis must also be considered in a patient with a bulbar presentation of ALS. Other disorders deserving of consideration include inflammatory myopathies, X-linked spinobulbar muscular atrophy, head and neck cancer, and syringobulbia.
As ALS progresses, patients experience complications consistent with continued neurodegeneration of the motor system. Respiratory problems are the most common serious complication of ALS. Dysfunction in the upper airway and expiratory muscles leads to impaired swallow and inadequate cough. This decreased ability to clear secretions and protect the airway leads to an increased risk of aspiration with swallowing. Weakness in the inspiratory muscles, including the diaphragm and external intercostal muscles, results in retention of carbon dioxide. Nocturnal hypoventilation is a common problem in patients with ALS, a consequence of reduced neural output to the respiratory muscles coupled with decreased ventilatory drive that occurs during sleep. Ultimately this restrictive lung disease leads to respiratory failure, necessitating cough-assistive devices, mechanical ventilation, and tracheostomy.
The use of noninvasive positive-pressure ventilation (NIPPV) has been shown to be beneficial by improving duration and quality of life. NIPPV can serve as an effective temporizing measure before the progression of weakness and onset of bulbar symptoms make more invasive ventilation such as tracheostomy or laryngeal diversion necessary for continued survival. Because of the multiple adverse effects on the respiratory system, a pulmonary specialist is an integral part of ALS management. Frequent monitoring of pulmonary function provides valuable information on disease progression and prognosis. In addition, objective measurements of pulmonary function may help patients and families address crucial decisions concerning more invasive interventions or end-of-life issues.
Bulbar muscle weakness as a result of motor neuron involvement in the brainstem causes dysfunction in the lips, tongue, pharyngeal and laryngeal muscles. Swallowing and cough can be impaired, making clearance of oral secretions and ingestion of adequate nutrition difficult. In addition, deficits in speech production can make attempts at communication frustrating. Early referral to speech therapy for a comprehensive evaluation of speech and swallowing function can address these issues by providing patients with compensatory strategies to maintain intelligible speech and adequate oral nutrition. Recent development of sophisticated computer-based augmentative communication devices has greatly enhanced the ability to communicate when phonation is no longer possible.
Dysphagia can be addressed initially by instruction in compensatory swallowing techniques such as chin tuck, head turn, and double swallow. This instruction is essential in helping to maintain oral nutrition and decrease the risk of aspiration. ALS patients often have difficulty with certain dry foods and thin liquids. Modifying the diet by thickening liquids, moistening solids, and changing food texture can help. The addition of high-calorie liquid supplements helps to maintain caloric requirements and stave off weight loss and cachexia. Because malnutrition can precipitate increased fatigue, muscle breakdown, and risk of death, a referral to a registered dietician can be invaluable in maintaining appropriate nutrition through diet and supplementation. When nutrition can no longer be maintained orally, the option of enteric feeding must be broached with the patient and family. Placement of a feeding tube must be strongly considered with weight loss greater than 10%, increase in the time required for oral feedings, and the occurrence of aspiration pneumonia. Feeding tubes have been shown to stabilize weight, decrease fatigue, and prolong survival.
Spasticity is treated if it impairs function, prevents bracing, or causes pain.
Currently, no treatment options are able to reverse or arrest the progression of ALS. Consequently, the management of ALS revolves around slowing the inexorable progression of symptoms, minimizing complications, maintaining independent patient function, and ensuring meaningful quality of life. Optimal management of patients with ALS and their families is an arduous task and cannot be accomplished singly. The interdisciplinary approach provides management of patient care issues by a team composed of physicians, therapists, social workers, and mental health professionals. Physiatrists offer the training and expertise to direct the rehabilitation team as well as to oversee the goals of treatment. A comprehensive program of rehabilitation is essential in maximizing functional capacity, maintaining function, optimizing mobility within the home and community, and preventing physical deformity.
Riluzole remains the only Food and Drug Administration (FDA)-approved pharmacologic treatment available that has been proven to affect the natural history of ALS and slow its progression. A Cochrane Database review in 2007 concluded that riluzole at a dose of 100 mg daily prolonged median survival by 2–3 months. Other studies suggest an even greater benefit ranging from 4 to 20 months. Unfortunately, this drug comes at considerable expense and may not be affordable for all ALS patients. The most common side effects are asthenia, nausea, and reversible hepatotoxicity, requiring monitoring of liver function. In recent years there has been an increase in ALS research as well as clinical trials for promising medications that have the potential to slow progression of the disease. The search for potential therapeutic targets based on motor neuron degeneration may lead to novel treatments for ALS.
As in all other motor neuron diseases, the essential condition in ALS is musculoskeletal weakness, which ultimately causes the majority of complications. Exercise training is not absolutely contraindicated, and a program of aerobic, strengthening, and endurance exercise prescribed with a commonsense approach can yield physical benefits such as improved cardiovascular endurance and increased muscle efficiency. Patients may also experience improvements in pain, appetite, sleep, and psychological well-being. Ideal therapeutic modalities include aquatherapy, stationary bicycling, and other low-impact activities. However, patients should be advised not to exercise to exhaustion and should be educated on the symptoms of overwork weakness, such as increased muscle cramping, fasciculations, and prolonged shortness of breath.
It is important to discuss end-of-life issues with ALS patients and their families. Physicians should outline available treatment options and choices, and a social worker should be involved, when possible, to help the patient designate a durable power of attorney as well as to assist in drafting a living will.
Sadly, ALS remains a rapidly fatal disease, with a median survival of 3–5 years. However, longer survival is not unseen. About 15% of ALS patients survive 5 years after initial diagnosis, and 5% survive past 10 years. Younger age at symptom onset, male gender, and limb-dominant symptoms all offer improved chances at long-term survival. Poor prognostic factors include older age at symptom onset, bulbar and pulmonary dysfunction early in the clinical course, a short period from symptom onset to diagnosis, and the presence of frontotemporal dementia.
GUILLAIN-BARRÉ SYNDROME
ESSENTIALS OF DIAGNOSIS
Most common cause of acute neuromuscular paralysis.
Recognized as a syndrome of disorders with various subtypes.
Characterized by progressive onset of symmetric limb weakness.
Cranial nerve involvement occurs in 45–75% of patients, most often after the limbs are affected, and severe pain in 50%.
Weakness of oropharyngeal and respiratory muscles affects 40% of presenting patients.
Can be confirmed with electrodiagnostic testing, which also differentiates demyelinating from axonal forms.
With the eradication of poliomyelitis in the Western world, Guillain-Barré syndrome (GBS) has become the most common cause of acute neuromuscular paralysis, with an annual incidence of 1–2 per 100,000. The male-to-female ratio is 1.5:1. Most patients are older males, although GBS has been reported in all age groups. In the United States the disease appears to have a bimodal distribution, with the first peak occurring in young adulthood (15–35 years of age) followed by a second peak in elderly people (50–75 years of age).
GBS is characterized by a progressive, symmetric weakness of the limbs. Reflexes are typically absent or greatly diminished, and sensory deficits may be present. Today it is recognized that GBS is not a single disorder but a syndrome of several subtypes of acute immune-mediated polyneuropathies. The term acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is often used synonymously with GBS, and it accurately describes the histopathologic features seen in this disease. AIDP is the most common subtype, accounting for 95% of GBS cases in Europe and North America. Although rare, accounting for only 5–10% of all US cases, axonal subtypes also occur, as an acute motor axonal neuropathy (AMAN) or an acute motor sensory axonal neuropathy (AMSAN). The prevalence of axonal subtypes is higher in South America and Asia, comprising 30% of GBS cases in those regions. Miller-Fisher syndrome (MFS) is a subtype of GBS that manifests in a unique triad of ataxia, areflexia, and ophthalmoplegia.
GBS is considered to be a postinfectious, immune-mediated disease that attacks peripheral nerves, leading to progressive, symmetric onset of limb weakness. Up to two thirds of patients report an infectious illness in the weeks before symptom onset. Respiratory infections are most often reported, followed by gastrointestinal infections. The most commonly identified infectious agent is Campylobacter jejuni, but other causative agents include cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumonia, and Haemophilus influenza. There is also a well-recognized association between GBS and acute human immunodeficiency virus (HIV) infection.
The typical patient with GBS, which in most cases is the AIDP subtype, presents 2–4 weeks after a relatively benign upper respiratory or gastrointestinal illness with complaints of bilateral weakness in the lower extremities and dysesthesias in the fingers. The classic clinical picture of weakness is one that is ascending and symmetric in nature with involvement of the lower extremities occurring before the upper extremities. Proximal muscles may be involved earlier in the course than distal muscles. Signs of axial involvement may also be seen, with weakness in the trunk and bulbar muscles. The patient may complain of difficulty standing or walking secondary to ophthalmoparesis or proprioception deficits. Shortness of breath may be present due to respiratory muscle weakness.
The onset of weakness is typically acute, with progression over days to weeks. Maximal weakness usually occurs by 2 weeks. By 4 weeks, 98% of all cases have reached maximal weakness. The severity of weakness over the course of GBS can be variable, from mild paresis to complete tetraplegia.
Involvement of cranial nerves is observed in 45–75% of patients with GBS. Most frequently, cranial nerves III–VI and IX–XII are affected. Common symptoms with cranial nerve involvement include ophthalmoplegia, dysphagia, dysarthria, diplopia, and facial droop. In most cases, facial symptoms appear after the limbs and trunk are affected. The Miller-Fisher variant is unique in that cranial nerve deficits appear first, with minimal weakness in the limbs.
Loss of sensation is variable and is usually mild. Sensory symptoms often precede muscle weakness, manifested as paresthesias or numbness beginning in the toes and fingertips and migrating proximally. Distal loss of proprioception, light touch, and vibration sense may also be observed.
Pain can be a significant complaint, and on initial presentation approximately 50% of patients rate their pain as severe. The most common locations of pain are in the shoulder girdle, buttocks, thighs, and back. Characterized as deep, aching, and throbbing in nature, pain initially may be nociceptive from acute nerve inflammation, but it can evolve during the course of the illness into neuropathic pain as sensory nerve degeneration followed by regeneration occurs. Neuropathic pain persists indefinitely in 5–10% of patients.
Involvement of the autonomic nervous system has also been observed in patients with GBS. Autonomic dysfunction in the sympathetic and parasympathetic systems can manifest with hypertension, cardiac arrhythmias, tachycardia, bradycardia, facial flushing, orthostatic hypotension, and diaphoresis. Urinary retention and constipation can also occur. The likelihood of dysautonomia is higher in patients with severe weakness and respiratory failure.
Upon presentation, 40% of patients complain of weakness in oropharyngeal or respiratory muscles. Typical symptoms include shortness of breath, dyspnea on exertion, difficulty swallowing, and slurred speech. These patients must be monitored for respiratory failure with sequential measurement of forced vital capacity every 2–4 hours initially because up to one third will require ventilatory support at some point during the course of the disease.
The diagnosis of GBS is generally made based on clinical features. Laboratory studies such as CBC and chemistry panel are less useful but are utilized to exclude other potential diagnoses.
Lumbar puncture for cerebrospinal fluid (CSF) studies is recommended and routinely performed in patients presenting with rapidly progressive weakness. The characteristic finding on CSF analysis is albuminocytologic disassociation, which is an elevated CSF protein level greater than 0.55 g/L with normal white blood cell count (<5–10 × 106 cells/L). The elevated CSF protein is believed to reflect widespread inflammation within the nerve roots. However, a normal CSF protein level does not rule out GBS, as the level in 10% of patients may be normal. Additionally, CSF protein may not rise until 1–2 weeks after the onset of weakness.
MRI is sensitive but not specific in GBS diagnosis. The use of gadolinium with resulting nerve root enhancement is strongly suggestive of GBS; however, this nonspecific feature is commonly seen in inflammatory conditions where the blood–nerve barrier has been disrupted.
Electrodiagnostic testing is the most useful confirmatory test for GBS, able to differentiate between the more common demyelinating form (AIDP) and axonal forms (AMAN, AMSAN). Details of these findings are presented in Chapter 17.
Severe, early symptoms of GBS significantly increase the risk of complications during hospitalization. The care of acutely affected patients involves close monitoring of respiratory and cardiovascular status. Depending on the patient’s initial presentation and course, management of these issues may best be accomplished in an intensive care unit (ICU). Severe muscle weakness may affect the diaphragm and intercostal muscles to such an extent that intubation and ventilatory support may be indicated. Autonomic dysfunction can lead to blood pressure fluctuations and cardiac arrhythmias, complicating the use of vasoactive and sedative medications. In addition, bladder areflexia and adynamic ileus can occur with derangement of the parasympathetic system.
Because of the high percentage of cranial nerve involvement in patients with GBS, symptoms of dysarthria and dysphagia may precede aspiration and lead to pneumonia. The prolonged immobilization that can occur with weak or paralyzed muscles is a significant risk factor for development of deep vein thrombosis and pressure ulcers.
The management of GBS consists of supportive care, disease-modifying treatment, and rehabilitation. Patients should be admitted to a hospital for close monitoring until the course of the disease has reached a plateau or undergone reversal. Continued progression may result in a neuromuscular emergency with complications related to respiratory insufficiency and cardiac arrhythmia. Primarily because of respiratory failure, about one third of GBS patients require ICU admission. Chemical prophylaxis to prevent deep vein thrombosis along with frequent repositioning for pressure relief will minimize problems related to immobility. Continued care is also needed to minimize complications from neurogenic bowel and bladder, and pain.
Immunomodulatory therapy is beneficial in patients with GBS, hastening recovery. Intravenous immunoglobulin (IVIG) and plasma exchange have proven equally effective. IVIG is usually the preferred treatment because of greater availability and convenience. Administration is for 5 consecutive days at 0.4 g/kg per day. Plasma exchange administered five times over the course of 2 weeks is beneficial when started within 4 weeks of symptom onset. The exact mechanism of action is unclear but likely involves removal of autoantibodies, complement, immune complexes, or other humoral factors involved in the pathogenesis of GBS.
Given the marked degree of weakness, potential complications, protracted recovery, and possible long-term functional deficits, rehabilitation of patients with GBS should begin in the acute phase. Patients with persistent functional impairments may require transfer to an inpatient rehabilitation unit. Initial therapeutics should begin with range of motion, positioning, and splinting followed by early mobilization to minimize the effects of prolonged bed rest. As strength improves the patient can be advanced to ambulation and self-care activities utilizing adaptive equipment and assistive devices. After discharge, outpatient therapy and a home program are essential in continued functional gains and a return to independence.
Although rare, death may occur from acute complications such as respiratory distress syndrome, cardiac arrest, sepsis, pneumonia, and venous thromboembolic disease. Most often, mortality is due to complications of prolonged intubation and paralysis or from severe autonomic instability. GBS-related deaths usually occur in ventilator-dependent patients, and mortality is increased in elderly patients, particularly those with underlying pulmonary disease and the need for mechanical ventilation. Although most patients (up to 85%) with GBS make a full and functional recovery, 2–12% will die from complications related to GBS, and a significant percentage of survivors will have persistent symptoms.
After symptoms reach a plateau, which usually occurs within 4 weeks from onset, the recovery phase of GBS begins. This period typically lasts from 6 to 12 months, but for some patients it may take up to 3 years. Although the exact prevalence is uncertain, up to 50,000 persons in the United States may have long-term functional deficits from GBS. Estimates indicate 15–20% of patients will have moderate residual deficits, and 1–10% will be left severely disabled. Long-term sequelae of GBS include persistent fatigue, weakness, imbalance, and residual sensory changes. Approximately 7–15% of patients have permanent neurologic sequelae, including bilateral foot drop, intrinsic hand muscle wasting, sensory ataxia, and dysesthesia. Patients may also exhibit long-term differences in pain intensity, fatigability, and functional impairment compared with healthy controls. In a small percentage (~10%) of patients, an acute relapse occurs after initial improvement or stabilization after treatment.
POLIO & POST-POLIO SYNDROME
ESSENTIALS OF DIAGNOSIS
Polio:
Results from infection with an RNA virus that invades the motor cells of the anterior horn cells (LMN) and spinal cord.
Common symptoms include fever, malaise, headache, and myalgias.
Patients may also report gastrointestinal and respiratory symptoms.
Paralysis is asymmetric, with involvement of lower extremities greater than that of upper extremities.
Post-polio syndrome:
Confirmed history of paralytic polio followed by partial or fairly complete neurologic and functional recovery and a period of stability for at least 15 years.
Onset of two or more of the following symptoms since achieving stability: unaccustomed fatigue, new weakness in muscles previously affected or in unaffected muscles, joint pain, functional loss, cold intolerance, or new atrophy.
No other medical explanation for the new health problems.
Poliomyelitis is a disease caused by an RNA virus that invades the motor nerve cells of the anterior horn cells (LMNs), and spinal cord, producing weakness in affected bulbar or spinal myotomes, or both. Before the advent of the Salk trivalent inactivated polio vaccine in 1956, and the Sabin trivalent oral live vaccine in 1962, polio was the most common viral infection of the central nervous system, affecting more than 600,000 children per year worldwide.
Polio has been eradicated in the United States since 1979; however, there may remain as many as 1.5 million polio survivors in this country, and millions more worldwide, where a small percentage of initial cases continue to be reported. Post-polio syndrome (PPS) is a neurologic disorder that occurs in polio survivors 20 or more years after recovery from the initial infection. New-onset weakness is the hallmark symptom. PPS has been reported to affect anywhere from 20% to 60% of polio survivors.
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