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Home > RNJ > 2005 > September/October > Understanding Guillain-Barré Syndrome and Central Nervous System Involvement

Understanding Guillain-Barré Syndrome and Central Nervous System Involvement
Mary Ann Gregory, BA • Robert J. Gregory, PhD • John V. Podd, PhD

 

Guillain-Barré syndrome is a rare neurological disease that causes paralysis and may necessitate hospitalization for some patients in its acute stages. It primarily affects the peripheral nervous system, though recent research has shown that for some patients, the central nervous system is involved. The acute phase often requires intensive care services. Recognition is growing that recovery is not as smooth and free of symptoms as previously thought. Following “recovery” some people endure long-term residual symptoms, such as fatigue and pain. Nursing input can be of value by providing support, information, explanations, and empathy to reassure patients and families. A greater understanding of the nature and course of the disease and its ramifications can lead to more effective nursing management and a faster rehabilitation process.

Nurses, particularly rehabilitation nurses, need up-to-date information about rare neurological diseases, such as Guillain-Barré syndrome (GBS), to deal effectively with the transition from acute stages to rehabilitation and long-term recovery. The historical and general classification of GBS as a neuropathy that only influences the peripheral nervous system (PNS) is no longer tenable. This article reviews research on GBS. Recent findings show that in some cases, this disease affects the central nervous system (CNS). Further, it appears that residual long-term effects are more likely to persist than previously thought. Neuropsychological testing, greater attention to follow up, and further research could prove valuable in future studies to explore these effects. Through an understanding of GBS, nursing care can lead to more effective and efficient rehabilitation and recovery.

Overview

GBS is “an acute immune mediated disease of the PNS with a wide range of clinical symptoms and great variability in outcome” (Visser, Schmitz, Meulstee, van Doorn, & van der Meche, 1999). The major diagnostic feature of GBS is abnormally increased protein in the spinal fluid, even in the presence of a normal cell count (Guillain, Barre, & Strohl, 1999). This disease has only one or two case(s) per 100,000 population diagnosed per year. The syndrome, however, is the most common cause of paralysis from a peripheral nerve disorder in developed nations (Steinberg, 2000). One hypothesis about the etiology of GBS is that it results from an attack by the immune system on the spinal nerve roots, the peripheral nerves, and the cranial nerves, which results in a focal inflammation and damage to the myelin sheaths and axon fibers (Coyle, 2002). Steinberg (2000) discusses GBS as a family of disorders called acquired autoimmune demyelinating peripheral neuropathies that occurs in both demyelinating and axonal forms. A wide range of variants and subtypes have been charted according to the nerve molecules or gangliosides attacked by the disease (Steinberg, 2000).

GBS is a disabling condition that in its mildest forms leads to muscle weakness and abnormal sensations. GBS is associated with sensory, motor, and autonomic abnormalities, such as pain, fatigue, and urinary dysfunction. It is predominantly a motor neuropathy in which the majority of cases are bilateral and symmetrical (Parry, 1993). In some severe cases, GBS can cause paralysis and even death, but Steinberg (2000) found that 98% of patients survive, though full recovery, if it occurs, may take months of rehabilitation.

Healthcare providers typically treat GBS patients as though the CNS is not involved, perhaps because paralysis created by peripheral nerve damage masks other symptoms. Steinberg (2000) believed that the CNS does not appear to be affected by GBS. In at least a percentage of GBS patients, however, recent studies have shown that the CNS is affected. Parry (1993) found both clinical and laboratory evidence of CNS involvement. The controversy raised by these conflicting views is examined in terms of the human nervous system and the various ways that GBS damages the PNS, and the CNS. It should be remembered that GBS can be disabling, yet people with long-term fatigue and pain can—and do—respond to rehabilitation measures.

Long-Term Damage

Long-term damage from GBS can seriously disrupt patients’ lives. In one study, neurological examinations of 122 patients who had GBS revealed that 14 patients showed severe residual signs and 69% showed some sensory deficit several years after contracting GBS (Bernsen, de Jager, Schmitz, & van der Meche, 2001). Another study found persistent disability in GBS patients 11–35 months after onset (Lennon, Koblar, Hughes, Goeller, & Riser, 1993). Although 70% of the 140 GBS patients examined by Kleopa and Brown (2000) made a complete neurological recovery, some patients experienced long-term disabilities, such as residual weakness, pain, fatigue, psychosocial dysfunction, and multiple relapses. Parry (2000), in a discussion of the severity of residual effects, noted that fatigue and pain are problems for a large number of patients. A recent study conducted in New Zealand found fatigue was the most common residual problem, affecting 93% of 44 patients diagnosed with GBS, but other common issues for patients included pain and motor-related problems (Bourke, 2001). An earlier survey in New Zealand described the deep psychosocial impact GBS has and the need for professional assistance to deal with this disorder (Renaud, 2000). The problems mentioned above have an immense impact on the lives of people with GBS.

The Nervous System

Tuck and McLeod (1981) found that in all of the cases of GBS studied, the autonomic nervous system (ANS) was affected in various ways, including urinary dysfunction, rectal dysfunction, hypotension, hypertension, sinus tachycardia, arrhythmia, and hyponatremia. ANS involvement usually is not life-threatening, but cardiac arrhythmias that occur, in serious forms of GBS, can be (Lichtenfeld, 1971; Truax, 1984; Tuck & McLeod, 1981). In contrast with the autonomic neuropathy which is a common feature of GBS, the CNS (brain and spinal cord) involvement is less common.

GBS does not usually involve spinal cord damage, though small collections of perivascular lymphocytes may be found in the spinal cord (Haymaker & Kernohan, 1949; Parry, 1993). Some areas of the brain, however, can be affected and possibly damaged by GBS and its variants. CNS involvement, though rare, needs to be taken into account in diagnosis, treatment, and rehabilitation.

Parry (1993) found that computed tomography (CT) and magnetic resonance imaging (MRI) scans and pathological specimens show abnormalities in the conduction of the CNS pathways. Seven CNS abnormalities have been reported. First, GBS with papilledema may raise intracranial pressure that could cause damage to the CNS (Joynt, 1958; Morley & Reynolds, 1966; Peterman, Daly, Dion, & Keith, 1959; Reid & Draper, 1980; Ropper & Marmarou, 1984; Sullivan & Reeves, 1977; Weiss, Bajwa, & Mehler, 1991). Second, optic neuritis, a CNS disorder, has been associated with GBS (Pall & Williams, 1987; Phanthumchinda, Intragumtomchai, & Kasantikul, 1988; Toshwinal, 1987). Third, in at least two reported cases, an onset of acute disseminated encephalomyelitis and GBS occurred simultaneously. Encephalopathy is the most commonly reported CNS abnormality (Amit, Glick, Itzchak, Dgani, & Meyer, 1989; Amit, Shapira, Blank, & Aker, 1986). Fourth, although there is little clinical evidence of spinal cord myelopathy in GBS, fatal cases have revealed small collections of perivascular lymphocytes in the spinal cord (Parry). Fifth, some patients dying of GBS have meningeal involvement or inflammation. Sixth, some people with GBS experience supranuclear eye movement disorders and ataxia, although these symptoms are more likely associated side effects rather than direct CNS involvement. The final CNS manifestation is the inappropriate secretion of antidiuretic hormone (ADH), which may be due to hypothalamic involvement or, more probably, to autonomic neuropathy (Parry).

CNS involvement in chronic inflammatory demyelinating polyneuropathy (CIDP), a GBS subtype, is more common than in classic GBS. Clinical, electrophysiological, CT, and MRI evidence shows central demyelination in CIDP (Mendal et al., 1987; Ohake, Komori, Hirose, & Tanabe, 1990; Rubin, Karpati, & Sterling-Carpenter, 1987; Thomas et al., 1987). A number of studies have found CNS lesions in patients with ClDP (Dyck et al., 1975; McCombe, Pollard, & McLeod, 1987; Mendell et al., 1987). Ormerod, Waddy, Kermode, Murray, and Thomas (1990) discuss a CNS disorder with clinical features that resembles multiple sclerosis (MS) in patients with CIDP. They found 5 of 30 patients with CIDP had minor clinical evidence of CNS involvement and concluded that such involvement is infrequent but that subclinical evidence is common. Bouchard et al. (1999) found five percent of patients with CIDP to have symptomatic involvement of the CNS, which correlated with higher levels of disability.

Ropper (1983) is not convinced that the CNS is involved in these diseases. Rather, he suggests that the “dysfunction of peripheral mechanisms may simulate brain-stem signs.” He urges neurologists to resist attributing all unusual clinical signs to the CNS, as the pathophysiology of the PNS is not completely understood. His arguments against CNS involvement in GBS, however, have been weakened by more recent research (Bouchard et al., 1999; De la Monte et al., 1986; Kalita, Misra, & Bansal, 2001; Maier, Schmidtbauer, Pfauster, Schmutzhard, & Budka, 1997; Omerod et al., 1990; Parry, 1993; Thomas et al., 1987) using diverse clinical methods to show that in severe cases there is involvement of the CNS in GBS.

Implications for Nursing

The Case of Andy

At age 50, Andy (pseudonym) held a strenuous professional position that demanded his attention, time, and energy. After a bout of flu, he noticed both his lower legs throbbed. When his wrists began hurting as well, he consulted his physician who diagnosed peripheral neuropathy. Following a neurological work-up, his physician determined that Andy had GBS. A neurologist confirmed the diagnosis and placed Andy in intensive care, where he soon found himself unable to walk and in considerable pain.

Physicians used immunoglobulin (IVIg) to protect Andy’s nerves (a larger center might have used plasmapheresis). Tests, such as breathing capacity, blood pressure, and blood chemistry, were used to monitor progress (or deterioration). When Andy’s ability to breathe became limited, use of broncho-dilators and special breathing techniques were added. His heart began beating irregularly, and he had elevated blood pressure. His legs were elevated. Medications and elastic stockings helped. Andy complained of pain and had trouble communicating his needs and wants. His family tried to talk with him about their distress without him. This acute stage was worrisome for them.

In the third month, Andy entered rehabilitation, where he was encouraged to have physiotherapy. He began to move about in a wheelchair, then to walk, albeit initially with foot-drop. He fed and cared for himself, but tired easily. Andy’s family visited, but also wanted him to come home soon.

GBS affects the PNS, which, in turn, affects the entire body. Andy was exhausted, sleeping 12–14 hours a night and dozing during the day. When asked, he complained of tingling pains in his extremities and body. When family or visitors, while engaging in conversation, also turned on the television in his room Andy seemed confused, and became angry for no apparent reason. He complained that no one understood what was going on with him and retreated to sleep.

At this point, Andy was only beginning to come to grips with his “near-death” experience, and his many emotions related to helplessness. Being a “macho” male, he did not share his feelings, and sometimes seemed confused, disoriented, and helpless. Others found it difficult to interact with him, or empathize because they perceived that he did not look ill.

Over the next several months, Andy seemed to lack judgement, foresight, and the ability to plan ahead. He tended to be compliant and rarely showed initiative. Although family tried to talk with him, his tendency to complain about pains and funny pins and needles, or “electrical,” feelings left them unsure about whether to offer sympathy or push him to get on with recovery so he could go home and return to work.

Andy was discharged to home after about 5 months and soon began a part-time return to less strenuous work. He still complained of neurological pain and had considerable fatigue and emotional outbursts, but he was on the road to recovery.

Nursing Care

Andy’s case is a composite. Every GBS patient is different, but a nurse can scan the information presented and note a progression from onset, to acute care, to stages of rehabilitation, and finally, to long-term recovery. Each phase requires different forms of care, initially focusing on close cooperation among physicians and other medical staff to maintain life and to prepare for the best possible outcome.

Frequent assessments and monitoring of Andy’s body and functions were essential during acute care. For example, in respiratory care, understanding of the conceptual aspects of care, specific assessment techniques of and preparation for any deterioration is most important (Pulmonary concepts of critical care, n.d.). For cardiac functioning, a range of nursing assessments may be needed, but resources in the literature (e.g., Schwarz, Bailey, & Ciarlariello, 2003) and on the Internet may be helpful. Gastrointestinal functioning should be monitored particularly for deviations from the norm.

Andy was carefully turned, moved frequently, fed, and toileted during the initial month. Nursing staff saw to it that physiotherapeutic care was initiated early. This movement and care is extremely important, because the pain that accompanies GBS is often excruciating, and patients may not be able to express their distress. Speech therapy may be useful for those whose speech is affected. Communication can be enhanced through use of cards available from the Guillain-Barré Syndrome Foundation International, a major source of information for patients, family members, physicians, and the general public.

Nurses can—and should—explain what is taking place to patients, family members, and those involved in the rehabilitation process. In this case, it is essential that the nurse in charge reassure Andy that people with GBS do survive and recover to help to prevent and to resolve anxiety and depression (Dattilio, 2002). Provision of information about anatomy and physiology facilitates understanding and enhances further communication (Gregory, 1998), both for patients and family members.

Nurses might assume that since he “looked” okay, Andy was well on the road to recovery. They might admonish him when he claimed fatigue, push him to walk when he claimed to be tired, and make him aware that they were busy. GBS is a serious neurological disease, and appearances of physical well-being should not be interpreted as reality. Nurses should receive information about the physiological limits of GBS.

Occupational, speech, and physical therapy should be added to Andy’s routine as soon as possible to help speed the recovery process. A knowledge of cardiac function and carefully-paced exercise routines can help nurses who work more closely with physiotherapy.

Nurses confronted with persons recovering from GBS need to recognize that these patients have undergone a major neurological insult (Gregory, 1995) and that they have a relatively invisible disability. During the acute phase and hospitalization, nurses may have to provide almost total care to patients. Encouraging patients to walk, toilet, or eat on their own during the acute stages does not work if their nervous systems have stopped functioning effectively. Encouragement does not necessarily lead to greater results. Pain management, including opioids or analgesics, frequent repositioning, gentle movement, and physical therapy will help to prevent pain, pressure sores, muscle soreness, and other complications. Matching expectations to the gradual improvement of patients’ nervous systems is an art that depends on communication, careful planning, intensive case management, and empathy. Several excellent and insightful books by patients about their experiences with GBS should be read by nurses who deal with patients with this disorder to gain insight into what may take place during recovery (Baier & Schomaker, 1985; Heller & Vogel, 1986; Safranski, 2004; Wilcox, 2000).

In addition to neurological and physiological deficits, patients with CNS involvement may have some subtle cognitive deficits, weak executive functioning or inappropriate decision-making skills, emotional volatility, confusion, loss of short-term memory, or other impairments. Knowledge, clarity, focus, and empathy are helpful in directing, managing, and supporting patients, even if family members feel patients have recovered. Although patients’ appearance may be normal, nurses who realize there are residual effects can offer valuable support and education to patients and families that can enable them to cope. Planning and pacing a series of steps through the recovery process may be particularly worthwhile, so that patients do not overexercise or try to do too much too quickly. Fatigue and pain are indicators that can guide the process. Both patients and nurses need to listen to and respect the signs and symptoms that emerge. Through nursing intervention, families will be better equipped to understand and support patients.

In line with the thesis expressed in this article, CNS effects may be present to varying degrees. According to DeVos (1989) “brain dysfunction occurs more often in general hospital patients than is commonly recognized.” Stratton and Gregory (1995) cautioned that “it is common for the behavior of TBI (traumatic brain injury) patients to be agitated, inappropriate, or difficult.” If GBS patients do happen to have CNS involvement, those around them, including family, friends, and nurses, may become frustrated with them and their behavior. Nurses, in addition to their role in hospital care, can be of particular value in the recovery phase for those with GBS who may have cognitive or emotional dysfunction. The nurse who understands the reasons for seemingly difficult behavior, who can manage patients during their hospitalization, and who can provide explanations to assist patients and family members understand what is happening, can thereby assist all involved to adjust their expectations and can deal with patients more effectively. For example, patients expect their lives to quickly return to normal but they find that fatigue, pains, and tingling sensations may continue for months or years. Others find communication with family members and friends strained, because others fail to understand the ongoing effects of GBS. Still other patients may become depressed and need help (Gregory, 2003).

Nursing skill and ability to facilitate patients’ recoveries depends on levels and specialization of training, experience in practice, and empathy. Familiarity with standard textbook information (Del Bene & Polak, 2002) offers nurses basic background information that will give them greater confidence in providing care. Further knowledge of strategies and tactics for dealing with patients with similar or related diseases, such as depression and MS, may enrich the range of treatment options (Burgess, 2002). Gregory (1998) described the important role nurses can play by simply teaching GBS patients and their families about basic physiology and anatomy terms associated with the neurological system. By accurately describing the nervous system and explaining what happens to the body during the acute and later phases of GBS, nurses offer useful long-term tools to enhance patients’ understanding and coping skills during and after hospitalization. Another strategy that can prove valuable is to have people who have largely recovered from GBS meet with those who are still struggling through its earlier phases. They can share common experiences, answer questions, act as role models, and otherwise assist the rehabilitation process. Such knowledge facilitates communication and understanding and thereby enables both families and patients to make better use of services.

Conclusion

Research indicates that GBS is primarily a neuropathy of the PNS. In some cases, and possibly more frequently than has been recognized, GBS affects the CNS. The effects vary and usually occur only in more severe forms of the syndrome. CNS involvement in the variant form, CIDP, has been noted in many studies, and the case for CNS involvement in this variant form is supported. People who suffer severe forms of the disorder need neurological assessments, such as MRI and CT scans, to identify CNS involvement. Neuropsychological tests currently in use typically are not able to distinguish between CNS damage and PNS damage, because they are not sufficiently sensitive, and peripheral damage may confound results. It is important for the possibility of CNS damage to be included in the diagnosis, treatment, rehabilitation, and literature on GBS.

With the advances in brain imaging and with more research into nervous system diseases, the effects of GBS will become more clearly understood. The possibility that common antigens in the PNS and the CNS are damaged by the same immunologically mediated attack is especially interesting for the medical field. This review of research has uncovered credible links, in some cases, between GBS and the CNS. Application of nursing care based on understanding the connections and links can help improve the rehabilitation process.

About the Authors

Mary Ann Gregory, BA (Hons), is a graduate student at the School of Psychology, Massey University in Palmerston North, New Zealand.

Robert J. Gregory, PhD, is a Senior Lecturer at the School of Psychology, Massey University in Palmerston North, New Zealand.

John V. Podd, PhD, is an Associate Professor at the School of Psychology, Massey University in Palmerston North, New Zealand.

Questions or comments about this article may be directed to Mary Gregory, School of Psychology, Massey University, Palmerston North, New Zealand, or via e-mail to MaryGregory566@hotmail.com.

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