CASE REPORT
Guillain-Barr$ syndrome
Upper Airway Dysfunction-An Unusual Presentation of Guillain-Barr6 Syndrome From the Departments of Emergency Medicine* and
Joan Faloona, MD* Christine M Walsh-Kelly, MD t
Pediatrics,t Medical College of Wisconsin, Milwaukee. Received for publication February 26, 1991. Revisions received August 8 and October 22, 1991. Accepted for publication November 22, 1991.
We report the case of a 9-year-old boy who presented to the emergency department with dysphagia, respiratory distress, hoarseness, and generalized weakness. While in the ED, his respiratory status deteriorated, and he required intubation. At that time, he was found to have normal upper airway anatomy. He was admitted to the pediatric ICU and, within 24 hours, developed areflexia and muscle weakness; he was diagnosed with Guillain-Barrd syndrome. Atypical presentations of GuillainBarrd syndrome are discussed, and the necessityof considering this diagnosis when evaluating patients with evidence of cranial nerve dysfunction or upper airway distress is emphasized. [Faloona J, Walsh-Kelly CM: Upper airway dysfunction-An unusual presentation of Guilfain-Barrd syndrome. Ann EmergMedApril 1992;21:437-439.] INTRODUCTION Guillain-Barr6 syndrome is an acute demyelinating process. The classic clinical presentation is described as an ascending motor paresis with onset five days to three weeks after a viral illness. However, the literature is replete with "atypical" presentations of the syndrome, and our case is one of these.
CASE REPORT A 9-year-old boy presented to the emergency department complaining of a severe sore throat and generalized weakness. One day before admission, he had presented to another ED with a one-week history of sore t h r o a t and headache that had progressed to vomiting, weakness, and "fainting spells." A "beefy, r e d " p h a r y n x , "hot p o t a t o " voice, tachycardia, and dehydration were noted. 1V hydration and benzathine penicillin 1.2 million units were administered in the ED, and the patient was discharged on oral amoxicillin. His t h r o a t culture was negative for group A Streptococcus, and his medical history was noncontributory. On a r r i v a l in our ED, the patient was lethargic and ill appearing and had a blood pressure of 113/70 mm Hg; pulse, 115; respirations, 32; and temperature, 37 C. Ortho-static changes in pulse and blood pressure were noted. His voice was hoarse and muffled, and he refused to swallow his secretions because "it hurt." The pharynx was moderately •
APRIL]992
21:4 ANNALS OF EMERGENCY MEDICINE
437/125
GUILLAIN-BARRE SYNDROME Faloona & Walsh-KeUy
injected without exudate. Anterior neck tenderness without crepitus, swelling, or a d e n o p a t h y was noted, and there were signs of dehydration. Cardiac, pulmonary, and abdominal examinations were normal. Initial neurologic examination demonstrated generalized mild p e r i p h e r a l muscle weakness and intact gait, p u p i l l a r y responses, extraocular muscles, and facial muscles. The gag reflex was not assessed, and p e r i p h e r a l reflexes were not evaluated until several hours later. Oxygen was administered, vascular access was obtained, and a 20-mL/kg bolus of lactated Ringer's was given, after which the patient was more alert and h a d decreases in pulse to 100 and respirations to 22. Lateral neck and chest radiographs were normal. Complete blood count revealed a WBC count of 9,500 with a normal differential. Electrolytes were normal. Arterial blood gases revealed a PO2 of 135 mm Hg; Pco2, 45 mm Hg; and p H 7.40 on 2 L oxygen by nasal cannula. Urine and serum toxicologic studies and blood cultures were obtained, and l g IV ceftriaxone was given. The ear, nose, and throat consultation recommended direct laryngoscopy to evaluate the airway. Before this could be accomplished and three hours after arrival in the ED, the patient worsened acutely. He developed sudden r e s p i r a t o r y distress with m a r k e d tachypnea, decreased lung aeration, severe suprasternal retractions, diaphoresis, and minimal chest wall motion with respiration. R a p i d sequence intubation with atropine and succinylcholine was performed, and normal airway anatomy was noted. After l u m b a r puncture, the patient was admitted to the pediatric ICU and subsequently developed areflexia, paresis progressing to quadriplegia, and loss of facial motor function over the next 48 hours. Diagnostic investigation for Guillain-Barr6 syndrome, botulism, myasthenia, viral myositis, and heavy metal intoxication was extensive. Electrodiagnostic studies demonstrated a patchy, demyelinating p o l y r a d i c u l a r n e u r o p a t h y consistent with Guillain-Barr6 syndrome. The patient underwent plasmapheresis within 12 hours of arrival, and an additional seven treatments were administered over the next 14 days. The patient remained ventilator dependent for six days. Blood and cerebrospinal fluid bacterial cultures; urine and serum toxicologic studies; and cerebrospinal fluid, nasal, and rectal viral cultures were negative. The patient was discharged after 83 days with residnal truncal weakness, and he continues to undergo extensive motor and speech rehabilitation. The patient's presenting features of hoarseness and difficulty with secretions were attributed to cranial nerve involvement in the GuillainBarr6 process. DISCUSSION
Guillain-Barr6 syndrome is a demyelinating p o l y r a d i c u l a r n e u r o p a t h y characterized by an acute onset of symptoms that generally reach their nadir, plateau over a course of several weeks, and then spontaneously resolve. The classic
126/438
presentation is that of an acute ascending motor deficit and areflexia, p r i m a r i l y arising in the lower extremities. A nonspecific antecedent viral infection is noted in 75% of cases. Gastrointestinal and r e s p i r a t o r y infections are the most common; however, rubeola, rubella, mumps, and infectious mononucleosis have been associated with Guillain-Barr6 syndrome. 1 Numerous case reports of atypical presentations are available in the literature, including p r i m a r y cranial nerve dysfunctions, p r i m a r y sensory deficits, and/or descending paresis. 2 As Munstat and Barnes discuss, "the GuillainBarr6 syndrome is easy to diagnosis, but impossible to define.'3 Since Guillain first described and classified the syndrome in 1938, multiple revisions and reclassifications have been proposed. Many authors insist on stricter ~diagnostic criteria, whereas others call for b r o a d e r definitions. In 1978, the National Institute of Neurological and Communicative Disorders and Stroke called for clarification of the diagnostic criteria, including clinical, laboratory, and electrodiagnostic criteria. According to this clarification, two features are required for diagnosis: progressive motor weakness of more than one limb and associated areflexia. Other features supportive of the diagnosis include relative symmetry of symptoms and mild sensory deficits as well as cranial nerve deficits and autonomic dysfunction (heart block, tachycardia, hypertension, or hypotension). Cerebrospinal fluid demonstrates albuminocytologic dissociation with protein elevation usually noted at some point in the process if serial l u m b a r punctures are performed; cerebrospinal fluid cell counts should be less than 10 cells/mm. 4 Electrodiagnostic evidence of nerve conduction slowing or blockage, usually in a patchy distribution, is also present with Guillain-Barr6 syndrome. Rapid progression of signs and symptoms and full recovery of function (usually beginning two to four weeks after the nadir, but possibly delayed for months) are also characteristics of Guillain-Barr6 syndrome.4 The diagnosis of the syndrome requires that other causes of an acute p o l y r a d i c u l a r n e u r o p a t h y be ruled out. Differential diagnoses include toxins (organophosphates, arsenic, lead, disulfiram, and uitrofurantoin), infection (botulism, diphtheria, tetanus, and mononucleosis), neoplasias (Hodgkin's disease and lymphoma), metabolicendocrine (porphyria) and nutritional deficiencies, connective tissue disorders, sarcoid, myastheuia gravis, and multiple sclerosis. Patients presenting with p r i m a r y cranial nerve deficits often have a delayed diagnosis. There are varying reports on the incidence of cranial nerve dysfunctions, many as high as 50%.4,s Most frequently affected are cranial nerves VII, IX, and X, which result in facial weakness, dysphagia, or hoarseness.3, 5 Cranial nerves III, IV, and XI also may be affected and result in ophthalmoplegia or loss of accommodation.
ANNALS OFEMERGENOYMEDICtNE 21:4 APRIL1992
GUILLAIN-BARR
IE S Y N D R O M E
Faloona & Walsh-Kelly
One case r e p o r t describes a 7-year-old boy with b l u r r e d vision, headache, and paralysis of accommodation who subsequently developed weakness, areflexia, and elevated cerebrospinal fluid protein. 6 In 1965, Munstat and Barnes described five patients with Guillain-Barr6 syndrome presenting with cranial nerve dysfunction, three of whom had dysphagia, aspiration with nasal regurgitation, and dysphonia. Deficits of cranial nerves IX and X were noted. 3 A case r e p o r t in 1978 by Cohn and Silver described a 20-year-old patient who had a presentation similar to that of our patient. He had complained of a sore throat for two weeks, dysphagia, and hoarseness for one week before arrival at the ED. A cervical esophogram was attempted, and neuromuscular dysfunction of the swallowing mechanism was noted. At this time, he also r e p o r t e d vague numbness in his feet. Subsequently, areflexia, proximal muscle weakness, and paresis of cranial nerves IX and X were identified. These clinical findings in association with cerebrospinal fluid albuminocytologic dissociation were consistent with GuillainBarr6 syndrome. 5 Involvement of cranial nerves IX and X and subsequent vocal cord paresis were believed to be the etiology of both patients' hoarseness and r e s p i r a t o r y distress. Severe sore throat, a prominent presenting symptom of our patient, has not been r e p o r t e d in association with Guillain-Barre syndrome. Pain, however, reportedly precedes the onset of paralysis in approximately 50% of all patients with the syndrome. 7 The presence of sore throat, dysphonia, dysphagia, pharyngeal erythema, and respiratory distress in our patient suggested other, more common diseases: peritonsillar abscess, retropharyngeal abscess, infectious mononucleosis, epiglottitis, pneumomediastinum, airway foreign body, or bacterial tracheitis. Physical examination and lateral neck r a d i o g r a p h excluded all but airway foreign body. Ear, nose, and throat evaluation of the airway anatomy and function was prevented by the r a p i d onset of severe respiratory compromise, necessitating endotracheal intubation. Visualization of vocal cord paresis and absence of a gag reflex would have implicated a cranial nerve disorder for the dysphonia, swallowing dysfunction, and r e s p i r a t o r y distress. The pharyngeal erythema and sore throat, the sources of considerable confusion in this case, most likely resulted from an i n t e r c u r r e n t viral infection and were unrelated to the cranial nerve dysfunction. Guillain-Barr6 syndrome should be considered in any patient with dysphagia, dysphonia, and r e s p i r a t o r y distress, especially in the absence of the more common etiologies. In addition to examination of the p h a r y n x , a careful p e r i p h e r a l and cranial nerve examination should be performed to rule out neurologic dysfunction as the etiology.
APRIL1992
21:4
ANNALS OF EMER6ENCY MEDICINE
SUMMARY
A 9-year-old boy with dysphagia and r e s p i r a t o r y distress as presenting symptoms for Guillain-Barr6 syndrome subsequently developed r e s p i r a t o r y arrest and areflexia. Treatment included mechanical ventilation for six days and eight plasmapheresis treatments. Eighty-three days later, the child was discharged with residual truncal weakness requiring extensive motor rehabilitation. The possibility of dysfunction of cranial nerves IX and X should be considered when evaluating patients with complaints of dysphagia or dysphonia or with evidence of u p p e r airway obstruction. • REFERENCES 1. Peterman AF, Daly DD, Dion R, et al: Infectious neuronitis (6uillain-Barrb syndrome) in children. Neurology 1959;9:533. 2. Masueci EF, Kurtzke JF: Diagnostic criteria for the 6uillain-Barr6 syndrome. J Neurol Sci 1971;13:483-501. 3. Munstat TL, Barnes JE: Relation of multiple cranial nerve dysfunction to the 6uillainBarr6 syndrome. JNeurolNeurosurg Psychiatr1965; 28:115-120. 4. Ashbury AK, Cornblath DR: Assessment of current diagnostic criteria for GuillainBarr6 syndrome. Ann Neuro11990;27(suppl):521-524. 5. Cohn A, Silver S: Cranial nerve dysfunction as a primary manifestation of GuillainBarr6 syndrome. Ear Nose Throat J 1978;57:47-49. 6. DeRespinis PA, Shen J J, Wagner RS: 6uillain-Barr~ syndrome presenting as paralysis of accommodation. Arch Ophthalmo11989;107:1282. 7. Swaiman KF, Wright FS: The Practice of Pediatric Neurology. St Louis, CV Mesby, 1975, p 961.
Address for reprints: Christine M Walsh-Kelly, MB, Department of Pediatrics, Children's Hospital of Wisconsin, 9000 West Wisconsin Avenue, Mail Station 756, Milwaukee, Wisconsin 53226.
439/127
Guillain-Barr$ syndrome
Upper Airway Dysfunction-An Unusual Presentation of Guillain-Barr6 Syndrome From the Departments of Emergency Medicine* and
Joan Faloona, MD* Christine M Walsh-Kelly, MD t
Pediatrics,t Medical College of Wisconsin, Milwaukee. Received for publication February 26, 1991. Revisions received August 8 and October 22, 1991. Accepted for publication November 22, 1991.
We report the case of a 9-year-old boy who presented to the emergency department with dysphagia, respiratory distress, hoarseness, and generalized weakness. While in the ED, his respiratory status deteriorated, and he required intubation. At that time, he was found to have normal upper airway anatomy. He was admitted to the pediatric ICU and, within 24 hours, developed areflexia and muscle weakness; he was diagnosed with Guillain-Barrd syndrome. Atypical presentations of GuillainBarrd syndrome are discussed, and the necessityof considering this diagnosis when evaluating patients with evidence of cranial nerve dysfunction or upper airway distress is emphasized. [Faloona J, Walsh-Kelly CM: Upper airway dysfunction-An unusual presentation of Guilfain-Barrd syndrome. Ann EmergMedApril 1992;21:437-439.] INTRODUCTION Guillain-Barr6 syndrome is an acute demyelinating process. The classic clinical presentation is described as an ascending motor paresis with onset five days to three weeks after a viral illness. However, the literature is replete with "atypical" presentations of the syndrome, and our case is one of these.
CASE REPORT A 9-year-old boy presented to the emergency department complaining of a severe sore throat and generalized weakness. One day before admission, he had presented to another ED with a one-week history of sore t h r o a t and headache that had progressed to vomiting, weakness, and "fainting spells." A "beefy, r e d " p h a r y n x , "hot p o t a t o " voice, tachycardia, and dehydration were noted. 1V hydration and benzathine penicillin 1.2 million units were administered in the ED, and the patient was discharged on oral amoxicillin. His t h r o a t culture was negative for group A Streptococcus, and his medical history was noncontributory. On a r r i v a l in our ED, the patient was lethargic and ill appearing and had a blood pressure of 113/70 mm Hg; pulse, 115; respirations, 32; and temperature, 37 C. Ortho-static changes in pulse and blood pressure were noted. His voice was hoarse and muffled, and he refused to swallow his secretions because "it hurt." The pharynx was moderately •
APRIL]992
21:4 ANNALS OF EMERGENCY MEDICINE
437/125
GUILLAIN-BARRE SYNDROME Faloona & Walsh-KeUy
injected without exudate. Anterior neck tenderness without crepitus, swelling, or a d e n o p a t h y was noted, and there were signs of dehydration. Cardiac, pulmonary, and abdominal examinations were normal. Initial neurologic examination demonstrated generalized mild p e r i p h e r a l muscle weakness and intact gait, p u p i l l a r y responses, extraocular muscles, and facial muscles. The gag reflex was not assessed, and p e r i p h e r a l reflexes were not evaluated until several hours later. Oxygen was administered, vascular access was obtained, and a 20-mL/kg bolus of lactated Ringer's was given, after which the patient was more alert and h a d decreases in pulse to 100 and respirations to 22. Lateral neck and chest radiographs were normal. Complete blood count revealed a WBC count of 9,500 with a normal differential. Electrolytes were normal. Arterial blood gases revealed a PO2 of 135 mm Hg; Pco2, 45 mm Hg; and p H 7.40 on 2 L oxygen by nasal cannula. Urine and serum toxicologic studies and blood cultures were obtained, and l g IV ceftriaxone was given. The ear, nose, and throat consultation recommended direct laryngoscopy to evaluate the airway. Before this could be accomplished and three hours after arrival in the ED, the patient worsened acutely. He developed sudden r e s p i r a t o r y distress with m a r k e d tachypnea, decreased lung aeration, severe suprasternal retractions, diaphoresis, and minimal chest wall motion with respiration. R a p i d sequence intubation with atropine and succinylcholine was performed, and normal airway anatomy was noted. After l u m b a r puncture, the patient was admitted to the pediatric ICU and subsequently developed areflexia, paresis progressing to quadriplegia, and loss of facial motor function over the next 48 hours. Diagnostic investigation for Guillain-Barr6 syndrome, botulism, myasthenia, viral myositis, and heavy metal intoxication was extensive. Electrodiagnostic studies demonstrated a patchy, demyelinating p o l y r a d i c u l a r n e u r o p a t h y consistent with Guillain-Barr6 syndrome. The patient underwent plasmapheresis within 12 hours of arrival, and an additional seven treatments were administered over the next 14 days. The patient remained ventilator dependent for six days. Blood and cerebrospinal fluid bacterial cultures; urine and serum toxicologic studies; and cerebrospinal fluid, nasal, and rectal viral cultures were negative. The patient was discharged after 83 days with residnal truncal weakness, and he continues to undergo extensive motor and speech rehabilitation. The patient's presenting features of hoarseness and difficulty with secretions were attributed to cranial nerve involvement in the GuillainBarr6 process. DISCUSSION
Guillain-Barr6 syndrome is a demyelinating p o l y r a d i c u l a r n e u r o p a t h y characterized by an acute onset of symptoms that generally reach their nadir, plateau over a course of several weeks, and then spontaneously resolve. The classic
126/438
presentation is that of an acute ascending motor deficit and areflexia, p r i m a r i l y arising in the lower extremities. A nonspecific antecedent viral infection is noted in 75% of cases. Gastrointestinal and r e s p i r a t o r y infections are the most common; however, rubeola, rubella, mumps, and infectious mononucleosis have been associated with Guillain-Barr6 syndrome. 1 Numerous case reports of atypical presentations are available in the literature, including p r i m a r y cranial nerve dysfunctions, p r i m a r y sensory deficits, and/or descending paresis. 2 As Munstat and Barnes discuss, "the GuillainBarr6 syndrome is easy to diagnosis, but impossible to define.'3 Since Guillain first described and classified the syndrome in 1938, multiple revisions and reclassifications have been proposed. Many authors insist on stricter ~diagnostic criteria, whereas others call for b r o a d e r definitions. In 1978, the National Institute of Neurological and Communicative Disorders and Stroke called for clarification of the diagnostic criteria, including clinical, laboratory, and electrodiagnostic criteria. According to this clarification, two features are required for diagnosis: progressive motor weakness of more than one limb and associated areflexia. Other features supportive of the diagnosis include relative symmetry of symptoms and mild sensory deficits as well as cranial nerve deficits and autonomic dysfunction (heart block, tachycardia, hypertension, or hypotension). Cerebrospinal fluid demonstrates albuminocytologic dissociation with protein elevation usually noted at some point in the process if serial l u m b a r punctures are performed; cerebrospinal fluid cell counts should be less than 10 cells/mm. 4 Electrodiagnostic evidence of nerve conduction slowing or blockage, usually in a patchy distribution, is also present with Guillain-Barr6 syndrome. Rapid progression of signs and symptoms and full recovery of function (usually beginning two to four weeks after the nadir, but possibly delayed for months) are also characteristics of Guillain-Barr6 syndrome.4 The diagnosis of the syndrome requires that other causes of an acute p o l y r a d i c u l a r n e u r o p a t h y be ruled out. Differential diagnoses include toxins (organophosphates, arsenic, lead, disulfiram, and uitrofurantoin), infection (botulism, diphtheria, tetanus, and mononucleosis), neoplasias (Hodgkin's disease and lymphoma), metabolicendocrine (porphyria) and nutritional deficiencies, connective tissue disorders, sarcoid, myastheuia gravis, and multiple sclerosis. Patients presenting with p r i m a r y cranial nerve deficits often have a delayed diagnosis. There are varying reports on the incidence of cranial nerve dysfunctions, many as high as 50%.4,s Most frequently affected are cranial nerves VII, IX, and X, which result in facial weakness, dysphagia, or hoarseness.3, 5 Cranial nerves III, IV, and XI also may be affected and result in ophthalmoplegia or loss of accommodation.
ANNALS OFEMERGENOYMEDICtNE 21:4 APRIL1992
GUILLAIN-BARR
IE S Y N D R O M E
Faloona & Walsh-Kelly
One case r e p o r t describes a 7-year-old boy with b l u r r e d vision, headache, and paralysis of accommodation who subsequently developed weakness, areflexia, and elevated cerebrospinal fluid protein. 6 In 1965, Munstat and Barnes described five patients with Guillain-Barr6 syndrome presenting with cranial nerve dysfunction, three of whom had dysphagia, aspiration with nasal regurgitation, and dysphonia. Deficits of cranial nerves IX and X were noted. 3 A case r e p o r t in 1978 by Cohn and Silver described a 20-year-old patient who had a presentation similar to that of our patient. He had complained of a sore throat for two weeks, dysphagia, and hoarseness for one week before arrival at the ED. A cervical esophogram was attempted, and neuromuscular dysfunction of the swallowing mechanism was noted. At this time, he also r e p o r t e d vague numbness in his feet. Subsequently, areflexia, proximal muscle weakness, and paresis of cranial nerves IX and X were identified. These clinical findings in association with cerebrospinal fluid albuminocytologic dissociation were consistent with GuillainBarr6 syndrome. 5 Involvement of cranial nerves IX and X and subsequent vocal cord paresis were believed to be the etiology of both patients' hoarseness and r e s p i r a t o r y distress. Severe sore throat, a prominent presenting symptom of our patient, has not been r e p o r t e d in association with Guillain-Barre syndrome. Pain, however, reportedly precedes the onset of paralysis in approximately 50% of all patients with the syndrome. 7 The presence of sore throat, dysphonia, dysphagia, pharyngeal erythema, and respiratory distress in our patient suggested other, more common diseases: peritonsillar abscess, retropharyngeal abscess, infectious mononucleosis, epiglottitis, pneumomediastinum, airway foreign body, or bacterial tracheitis. Physical examination and lateral neck r a d i o g r a p h excluded all but airway foreign body. Ear, nose, and throat evaluation of the airway anatomy and function was prevented by the r a p i d onset of severe respiratory compromise, necessitating endotracheal intubation. Visualization of vocal cord paresis and absence of a gag reflex would have implicated a cranial nerve disorder for the dysphonia, swallowing dysfunction, and r e s p i r a t o r y distress. The pharyngeal erythema and sore throat, the sources of considerable confusion in this case, most likely resulted from an i n t e r c u r r e n t viral infection and were unrelated to the cranial nerve dysfunction. Guillain-Barr6 syndrome should be considered in any patient with dysphagia, dysphonia, and r e s p i r a t o r y distress, especially in the absence of the more common etiologies. In addition to examination of the p h a r y n x , a careful p e r i p h e r a l and cranial nerve examination should be performed to rule out neurologic dysfunction as the etiology.
APRIL1992
21:4
ANNALS OF EMER6ENCY MEDICINE
SUMMARY
A 9-year-old boy with dysphagia and r e s p i r a t o r y distress as presenting symptoms for Guillain-Barr6 syndrome subsequently developed r e s p i r a t o r y arrest and areflexia. Treatment included mechanical ventilation for six days and eight plasmapheresis treatments. Eighty-three days later, the child was discharged with residual truncal weakness requiring extensive motor rehabilitation. The possibility of dysfunction of cranial nerves IX and X should be considered when evaluating patients with complaints of dysphagia or dysphonia or with evidence of u p p e r airway obstruction. • REFERENCES 1. Peterman AF, Daly DD, Dion R, et al: Infectious neuronitis (6uillain-Barrb syndrome) in children. Neurology 1959;9:533. 2. Masueci EF, Kurtzke JF: Diagnostic criteria for the 6uillain-Barr6 syndrome. J Neurol Sci 1971;13:483-501. 3. Munstat TL, Barnes JE: Relation of multiple cranial nerve dysfunction to the 6uillainBarr6 syndrome. JNeurolNeurosurg Psychiatr1965; 28:115-120. 4. Ashbury AK, Cornblath DR: Assessment of current diagnostic criteria for GuillainBarr6 syndrome. Ann Neuro11990;27(suppl):521-524. 5. Cohn A, Silver S: Cranial nerve dysfunction as a primary manifestation of GuillainBarr6 syndrome. Ear Nose Throat J 1978;57:47-49. 6. DeRespinis PA, Shen J J, Wagner RS: 6uillain-Barr~ syndrome presenting as paralysis of accommodation. Arch Ophthalmo11989;107:1282. 7. Swaiman KF, Wright FS: The Practice of Pediatric Neurology. St Louis, CV Mesby, 1975, p 961.
Address for reprints: Christine M Walsh-Kelly, MB, Department of Pediatrics, Children's Hospital of Wisconsin, 9000 West Wisconsin Avenue, Mail Station 756, Milwaukee, Wisconsin 53226.
439/127
