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NEURALGIC AMYOTROPHY: A COMPLICATION OF NEURORADIOLOGICAL CONTRAST MEDIA
1400
myocardial depressant and a peripheral vasodilator.3It is important to recognise a case of red man syndrome so that the reaction is not mistaken for vancomycin allergy. After a red man reaction, subsequent doese may be given without adverse effect if administered at a slower rate. Although the current edition of the
suggests an aetiological role. The early reaction to each exposure to contrast medium favours a sensitivity reaction, despite the absence of classical fever, rash, and arthralgia. We can find no other report incriminating iohexol or meglumine as the cause of this type of neural reaction.In view of its ionised fraction, meglumine is the
British National Formulary states that a 500 mg dose should be given as an infusion over 20-30 min, Eli Lilly’s US package insert (August, 1984) suggests an infusion over at least 60 min. The prolonged infusion regimen may prove to be of value in reducing the incidence of red man syndrome.
more
as a
Public Health Laboratory, St George’s Hospital, London SW17 0QT
R. HOLLIMAN
1. Garrelts JC, Peterie JD Vancomycin and the "Red Man’s Syndrome". N Engl J Med 1985; 312: 245. 2. Wold JS, Turnipseed SA. Toxicology of vancomycin in laboratory animals. Rev Infect Dis 1981, 3: S224-29. 3. Cohen LS, Wechsler AS, Mitchell JH, Glick G. Depression of cardiac function by streptomycin and other antimicrobial agents. Am J Cardiol 1970; 26: 505-11
DEAFNESS AND TOPICAL ANTIBIOTIC SPRAYS
SIR,-The report by Dr Morrell and colleagues (May 18, p 1167) of profound deafness diagnosed 11 months after preterm birth and the treatment of presumed cord infection with topical and systemic aminoglycosides reinforces the warnings given in the data sheet for ’Tribiotic’ spray. The dosage of topically applied neomycin should not exceed 15 mg/kg daily in children (a one second spray delivers about 15 mg), and even more cautious use is advised in infants. Concurrent use with other aminoglycosides is not recommended because of possible summation of toxic effects. 3M Health Care Ltd, Loughborough, Leicestershire LE11 1EP
H.E. LEWIS
likely cause.
Department of Neurology, Hull Royal Infirmary, Hull HU3 1.
J. M. S. PEARCE A. AL JISHI
2JZ
Spillane JD. Localised neuritis of
Lancet 1943; ii: 532-35. 2. Parsonage MJ, Turner JWA. Lancet 1948; i: 973-78.
the shoulder girdle:
a
report of 46
cases in
the MEF
Neuralgic amyotrophy: The shoulder-girdle syndrome.
3. Schaumburg HH, Spencer PS, Thomas PK. Disorders of peripheral nerves Philadelphia: FA Davis, 1984: 221-2. 4. Tsairis P. Brachial plexus neuropathies. In. Dyck PJ, Thomas PK, Lambert EH, eds Peripheral neuropathy. vol I Philadelphia: Saunders, 1975: 659-81. 5. Schott GD. A chronic and painless form of idiopathic brachial plexus neuropathy J Neurol Neurosurg Psychiatry 1983; 46: 555-57. 6. Lasser EC Adverse reactions to intravascular administration of contrast media Allergy 1981; 36: 369-73.
MENINGORADICULITIS ASSOCIATED WITH INFECTION BY BORRELIA BURGDORFERI
SiR,—Neurological abnormalities after a tick-bite were described in France in 1922.1 However, it was not until 1975 that Steere et al2 recorded the entire clinical spectrum of what is now called Lyme disease. The aetiological agent, Borrelia burgdorferi, is a spirochaete whose principal vector in Europe is the tick Ixodes ricinus.3 Erythema chronicum migrans is the most distinctive symptom associated with Lyme syndrome. However, the clinical course of the disease in Europe differs notably from that seen in the USA. Peripheral nerve involvement and lymphocytic meningoradiculitis (Bannwarth’s syndrome) are prominent in European series and questionshave been raised as to the uniqueness of the agent involved.
NEURALGIC AMYOTROPHY: A COMPLICATION OF NEURORADIOLOGICAL CONTRAST MEDIA
SIR,-Neuralgic amyotrophy I ,2 is an acute, painful disorder of the plexus, in which the shoulder girdle muscles waste, with inconspicuous impairment of sensation and tendon reflexes. Usually there is no antecedent illness.3Immunisation and heroin abuse have been responsible for some cases and others are familial. We report a case of neuralgic amyotrophy associated with
brachial
administration of contrast media. A 36-year-old man was admitted for investigation of three attacks of focal epilepsy. Apart from an extensor plantar response on the left side, there were no abnormal signs, and he had no history of injury, infection, surgery, or immunisation within 3 months. A computerised tomographic scan with meglumine (’Urografin’) enhancement (Dec 13, 1984) revealed an extensive area of atrophy over the right frontoparietal convexity with no evidence of a vascular malformation. A right carotid arteriogram with iohexol (’Omnipaque’) contrast on Dec 17, excluded a lesion of the anterior cerebral artery. The patient complained of muscle aching, malaise, and anorexia on the day after the CT scan. He had recovered in 36 h. The angiography was therefore covered with intravenous hydrocortisone 100 mg before and at the end of the procedure. An identical reaction recurred for 24 h after angiography. He was discharged on phenytoin 100 mg twice daily. 3 months later the epilepsy had not recurred. He told us that on the fourth day after angiography he had had excruciating pain in the right shoulder, sparing the neck. This had persisted for 10 days continuously, disturbing sleep. He had found it difficult to raise his right arm and his wife had noted that his shoulder blade stuck out. Examination revealed winging of the right scapula with sparing of the deltoid and spinati; reflexes were intact and there was no sensory deficit. Neuralgic amyotrophy was diagnosed. He retained good function of the arm. In the absence of evidence ofa local injury of the brachial plexus a systemic factor seems a likely cause. Although the radiological procedures may have been fortuitous, the temporal relationship
We report here two cases of meningoradiculitis admitted to hospital in Tours, central France. Both patients had significant B burgdorferi antibody titres, indicating that their unusual clinical course belongs to the Lyme complex. A 34-year-old woman was admitted in September, 1984, because of sudden facial-nerve paralysis limited to the right side. Several days earlier she had had rachialgia and dysaesthesias in the lower limbs. She had been bitten by a tick on the right flank 4 weeks earlier. At the site of the bite a macular erythema 5 cm in diameter had developed that lasted for 3 weeks. Right axillary adenopathy was noted. Apart from the Bell’s palsy, neurological examination was normal. CSF contained 102 cells/1 (98% lymphocytes), protein 2-88 g/1, glucose 3 mmolll. Electrophoresis of CSF showed an increase of IgG at 0-145 g/l (normal below 0 - 04 g/1) with an IgG/albumin ratio of 0-44 (normal below 0-25). Erythrocyte sedimentation rate (ESR) was 61 mm/h.
Other blood tests were normal. The patient was not treated and recovered
completely within 5
weeks. The second
patient was a 48-year-old man also admitted in September, 1984, with a similar history of sudden right facial-nerve paralysis preceded for several days by radiculoneuropathies of the lower limbs accompanied by arthralgias of the knees, ankles, and phalangeal joints of both hands. The patient reported a history of
B
burgdorferi antibody titres
in
cases
I(a) and 2(b).
myocardial depressant and a peripheral vasodilator.3It is important to recognise a case of red man syndrome so that the reaction is not mistaken for vancomycin allergy. After a red man reaction, subsequent doese may be given without adverse effect if administered at a slower rate. Although the current edition of the
suggests an aetiological role. The early reaction to each exposure to contrast medium favours a sensitivity reaction, despite the absence of classical fever, rash, and arthralgia. We can find no other report incriminating iohexol or meglumine as the cause of this type of neural reaction.In view of its ionised fraction, meglumine is the
British National Formulary states that a 500 mg dose should be given as an infusion over 20-30 min, Eli Lilly’s US package insert (August, 1984) suggests an infusion over at least 60 min. The prolonged infusion regimen may prove to be of value in reducing the incidence of red man syndrome.
more
as a
Public Health Laboratory, St George’s Hospital, London SW17 0QT
R. HOLLIMAN
1. Garrelts JC, Peterie JD Vancomycin and the "Red Man’s Syndrome". N Engl J Med 1985; 312: 245. 2. Wold JS, Turnipseed SA. Toxicology of vancomycin in laboratory animals. Rev Infect Dis 1981, 3: S224-29. 3. Cohen LS, Wechsler AS, Mitchell JH, Glick G. Depression of cardiac function by streptomycin and other antimicrobial agents. Am J Cardiol 1970; 26: 505-11
DEAFNESS AND TOPICAL ANTIBIOTIC SPRAYS
SIR,-The report by Dr Morrell and colleagues (May 18, p 1167) of profound deafness diagnosed 11 months after preterm birth and the treatment of presumed cord infection with topical and systemic aminoglycosides reinforces the warnings given in the data sheet for ’Tribiotic’ spray. The dosage of topically applied neomycin should not exceed 15 mg/kg daily in children (a one second spray delivers about 15 mg), and even more cautious use is advised in infants. Concurrent use with other aminoglycosides is not recommended because of possible summation of toxic effects. 3M Health Care Ltd, Loughborough, Leicestershire LE11 1EP
H.E. LEWIS
likely cause.
Department of Neurology, Hull Royal Infirmary, Hull HU3 1.
J. M. S. PEARCE A. AL JISHI
2JZ
Spillane JD. Localised neuritis of
Lancet 1943; ii: 532-35. 2. Parsonage MJ, Turner JWA. Lancet 1948; i: 973-78.
the shoulder girdle:
a
report of 46
cases in
the MEF
Neuralgic amyotrophy: The shoulder-girdle syndrome.
3. Schaumburg HH, Spencer PS, Thomas PK. Disorders of peripheral nerves Philadelphia: FA Davis, 1984: 221-2. 4. Tsairis P. Brachial plexus neuropathies. In. Dyck PJ, Thomas PK, Lambert EH, eds Peripheral neuropathy. vol I Philadelphia: Saunders, 1975: 659-81. 5. Schott GD. A chronic and painless form of idiopathic brachial plexus neuropathy J Neurol Neurosurg Psychiatry 1983; 46: 555-57. 6. Lasser EC Adverse reactions to intravascular administration of contrast media Allergy 1981; 36: 369-73.
MENINGORADICULITIS ASSOCIATED WITH INFECTION BY BORRELIA BURGDORFERI
SiR,—Neurological abnormalities after a tick-bite were described in France in 1922.1 However, it was not until 1975 that Steere et al2 recorded the entire clinical spectrum of what is now called Lyme disease. The aetiological agent, Borrelia burgdorferi, is a spirochaete whose principal vector in Europe is the tick Ixodes ricinus.3 Erythema chronicum migrans is the most distinctive symptom associated with Lyme syndrome. However, the clinical course of the disease in Europe differs notably from that seen in the USA. Peripheral nerve involvement and lymphocytic meningoradiculitis (Bannwarth’s syndrome) are prominent in European series and questionshave been raised as to the uniqueness of the agent involved.
NEURALGIC AMYOTROPHY: A COMPLICATION OF NEURORADIOLOGICAL CONTRAST MEDIA
SIR,-Neuralgic amyotrophy I ,2 is an acute, painful disorder of the plexus, in which the shoulder girdle muscles waste, with inconspicuous impairment of sensation and tendon reflexes. Usually there is no antecedent illness.3Immunisation and heroin abuse have been responsible for some cases and others are familial. We report a case of neuralgic amyotrophy associated with
brachial
administration of contrast media. A 36-year-old man was admitted for investigation of three attacks of focal epilepsy. Apart from an extensor plantar response on the left side, there were no abnormal signs, and he had no history of injury, infection, surgery, or immunisation within 3 months. A computerised tomographic scan with meglumine (’Urografin’) enhancement (Dec 13, 1984) revealed an extensive area of atrophy over the right frontoparietal convexity with no evidence of a vascular malformation. A right carotid arteriogram with iohexol (’Omnipaque’) contrast on Dec 17, excluded a lesion of the anterior cerebral artery. The patient complained of muscle aching, malaise, and anorexia on the day after the CT scan. He had recovered in 36 h. The angiography was therefore covered with intravenous hydrocortisone 100 mg before and at the end of the procedure. An identical reaction recurred for 24 h after angiography. He was discharged on phenytoin 100 mg twice daily. 3 months later the epilepsy had not recurred. He told us that on the fourth day after angiography he had had excruciating pain in the right shoulder, sparing the neck. This had persisted for 10 days continuously, disturbing sleep. He had found it difficult to raise his right arm and his wife had noted that his shoulder blade stuck out. Examination revealed winging of the right scapula with sparing of the deltoid and spinati; reflexes were intact and there was no sensory deficit. Neuralgic amyotrophy was diagnosed. He retained good function of the arm. In the absence of evidence ofa local injury of the brachial plexus a systemic factor seems a likely cause. Although the radiological procedures may have been fortuitous, the temporal relationship
We report here two cases of meningoradiculitis admitted to hospital in Tours, central France. Both patients had significant B burgdorferi antibody titres, indicating that their unusual clinical course belongs to the Lyme complex. A 34-year-old woman was admitted in September, 1984, because of sudden facial-nerve paralysis limited to the right side. Several days earlier she had had rachialgia and dysaesthesias in the lower limbs. She had been bitten by a tick on the right flank 4 weeks earlier. At the site of the bite a macular erythema 5 cm in diameter had developed that lasted for 3 weeks. Right axillary adenopathy was noted. Apart from the Bell’s palsy, neurological examination was normal. CSF contained 102 cells/1 (98% lymphocytes), protein 2-88 g/1, glucose 3 mmolll. Electrophoresis of CSF showed an increase of IgG at 0-145 g/l (normal below 0 - 04 g/1) with an IgG/albumin ratio of 0-44 (normal below 0-25). Erythrocyte sedimentation rate (ESR) was 61 mm/h.
Other blood tests were normal. The patient was not treated and recovered
completely within 5
weeks. The second
patient was a 48-year-old man also admitted in September, 1984, with a similar history of sudden right facial-nerve paralysis preceded for several days by radiculoneuropathies of the lower limbs accompanied by arthralgias of the knees, ankles, and phalangeal joints of both hands. The patient reported a history of
B
burgdorferi antibody titres
in
cases
I(a) and 2(b).