The fiber density in the deltoid, extensor digitorum communis, and first dorsal interosseous muscles was measured using SFEMG in 11 patients with acute and chronic inflammatory demyelinating polyneuropathy. The fiber density was increased in 58% of the muscles studied. The deltoid muscle was the most abnormal of the 3 muscles studied. There was no correlation with the clinical syndrome, with conduction block or slowed motor conduction, or with the distribution of weakness. Changes were noted even in patients studied within 3 weeks of presentation, suggesting that reinnervation begins soon after the onset of the disease. Key words: SFEMG fiber density Guillain-Barre syndrome polyneuropathy MUSCLE 81 NERVE 15~168-171 1992
FIBER DENSITY IN ACUTE AND CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY MAYA GANTAYAT, MB, MICHAEL SWASH, MD, FRCP, MRCPath, and MARTIN S. SCHWARTZ, MD
S i ngl e fiber EMG (SFEMG) studies in chronic inflammatory demyelinating polyneuropathy (CIDP) in the extensor digitorum communis muscle have shown an increased fiber density in 37% of a group of 19 patients." An increased fiber density usually has been regarded as a feature of reinnervation, and thus, of axonal rather than demyelinating n e ~ r o p a t h i e s . ' : ~ In " ~ this report, we describe measurements of the fiber density in proximal and distal upper limb muscles in a group of patients with the acute (AIDP) and chronic (CIUP) progressive forms of inflammatory demyelinating polyneuropathy. Previous SFEMG studies of peripheral neuropathie~~.".".'~,'" have been confined to single muscles in the upper or lower limbs, but it is of interest to study the changes in proximal and distal muscles in this disease in which weakness is often strikingly proximal in the acute phase, but may be proximal o r distal when the disease enters a more chronic phase.
From the Atkinson Morley's Hospital (Drs. Gantayat and Schwartz) and The Royal London Hospital (Drs. Gantayat, Swash, and Schwartz), London, United Kingdom Acknowledgment: Dr. Gantayat was supported by a BOYSCAST Fellowship awarded by the Government of India (1990). Address reprint requests to Dr. M.S. Schwartz, Atkinson Morley's Hospital, Wimbledon, London, SW20 ONE, UK. Accepted for publication February 25. 1991
CCC 0148-639X/92/020168-04
$04 00
0 1992 John Wiley & Sons, Inc.
168
Fiber Density in Polyneuropathy
PATIENTS AND METHODS
Seven men and 4 women, aged 24 to 77 years, were studied; 6 had acute AIDP and 5 had CIDP. T h e criteria for diagnosis were both clinical and electrophysiological as recommended by Asbury et al.,'*3 Prineas and M ~ I ~ e o dand , ~ Albers and Kelly.' T h e duration of symptoms in the 6 patients with the AIDP ranged from 3 to 7 weeks and, in the 5 patients with CIDP, it ranged from 3 months to 3 years ('Table 1). I n these patients, the strength of the deltoid, extensor digitorum communis (EDC), and first dorsal interosseous (1st DI) muscles was assessed in the right arm using the MKC scale. Motor and sensory nerve conduction studies and F wave studies were made in the upper and lower limbs; in particular, motor nerve conduction and F wave responses were examined in the right arm. T h e latter studies are summarized in Table 2. In each patient, the fiber density was measured in the right deltoid, EDC, and 1st DI muscles, using a SFEMG electrode (Dantec 13K387) and a Dantec Neuromatic 2000M EMG apparatus. 1s,'4 T h e fiber density was considered abnormal when higher than 1.8, a value 3 SD above the mean in a control population younger than 75 (our laboratory normal data). Conventional concentric needle EMG studies were also carried out in these muscles. RESULTS
T h e electrophysiological findings are summarized in Tables 1 and 2. T h e nerve conduction studies
MUSCLE & NERVE
February 1992
-
~
~~~~
Table 1. Clinical data and fiber density in 3 arm muscles SFEMG fiber density
MRC muscle power
Case
Age1 sex
GBS type
Duration
Deltoid
EDC
1st DI
Deltoid
EDC
1st DI
1 2 3 4 5 6 7 8 9 10 11
60lM 73lM 71lM 30lM 24lM 49lF 57lM 691F 39lF 771F 60lM
Acute Acute Acute Acute Acute Acute Chronic Chronic Chronic Chronic Chronic
3 weeks 3 weeks 3 weeks 5 weeks 6 weeks 7 weeks 12 weeks 1 year 3 years 3 years 3 years
2.3* 1.9 2.4* 2.4' 2.4* 2.1' 2.4' 2.3' 2.4* 2.3* 3.7'
1.6 1.8 2.5* 1.7 1.5 2.2* 1.9* 2.8* 1.7 2.1* 2.7'
1.6 1.9 2.5' 2.1* 1.7 2.1* 1.8 2.9* 2.3' 1.5 NR
445 5 4+ 5 4+ 45 3 4+
4+ 4+ 5 45 5 5 4+ 4+ 3 4-
4+ 4+ 5 3 5 4+ 4+ 4441
5 3 SD above mean of normal control data. NR: No Dotentials recordable.
and F responses were abnormal in the median nerves in all the patients studied, and in the ulnar nerves in 9 of the 11 patients. The most abnormal findings were noted in the 5 patients with CIDP (Tables 1 and 2). There was evidence of conduction block in 50% of the nerves studied. In the 11 patients, the mean fiber density was 2.5 (range 1.9 to 3.7) in the deltoid, 2.2 (range 1.5 to 2.8) in the EDC, and 2.0 (range 1.5 to 2.9) in the 1st DI muscle (Table 1). In the deltoid muscle, the fiber density was increased in all the 11 patients, in the EDC in 6 patients, and in the 1st DI in 6 patients, but no potentials could be recorded in this muscle in 1 patient with CIDP (case 11). There was no constant relationship between the fiber density, clinical features, duration of the dis-
ease, age, or muscle strength. In addition, the changes in fiber density did not correlate with the abnormalities found in motor conduction velocity or F-wave responses. Even in those patients in whom the motor conduction velocities were very slowed, the fiber densities in the 3 muscles showed similar changes to those found in the other patients. In case l l , however, conduction was markedly abnormal and the fiber density was much greater (3.7) than in the other patients. In 2 patients (cases l and 5), with AIDP, the fiber density was increased only in the deltoid muscle. In the patients with AIDP, concentric needle EMG studies showed fibrillation potentials, which were more prominent in the deltoid than in the other 2 muscles. In these cases, a slight increase in
Table 2. Motor nerve conduction studies in right arm. Median nerve
Case 1 2 3 4 5 6 7 8 9 10 11
DML (ms) 5.2* 4.6* 8.4' 4.6'
5.0* 5.6* 5 2' 4.8* 11.6' 15.2* 11.6*
Ampl. (mV)
Ulnar nerve
cv
Distal
Prox.
(ms-')
F (ms)
8.5 4.5 5.2 3.0 16.0 4.0 2.5* 7.0 1.2' 0.25* 1.O'
7.0 4.5 13t 2.5 13.5 2.0t 0.5t 5.2 0.3t 0.04t
43 42 39* 45 46 52 40* 59 23* 8* 20
27.6 24.2 A* 30.4 A* 28.2 28.8 28.6 A* A' 59.0*
0.5t
DML (ms) 3.8 4.0 4.4" 5.0k 5.4' 3.6 3.6 8.0* 20.4* 12.8*
5.0*
Ampl. (mV)
cv
Distal
Prox.
(m"-')
8.0 6.2 2.0* 1.7' 7.0 6.0 2.5* 5.5 1.2* 0.25*
6.0 5.5 1.3t 1.ot 3.5t 6.0 1.7t 5.0 0.6t A' 0.5
45 50 45 43 36* 50 50 50 18* A* 24*
0.5*
F (ms) 33.2* 33.0' A* 39.2* 34.2" 27.6 32.2' 29.0 A* A'
50.0*
~~
'Abnormal values, jconduction block A = absent response
Fiber Density in Polyneuropathy
MUSCLE & NERVE
February 1992
169
polyphasic motor unit action potentials was noted in deltoid muscles, but not in the other 2 muscles. In the patients with CIDP, polyphasic potentials were more prominent, particularly in cases 8 and 11. DISCUSSION
Our data show that a modest increase in fiber density may be a feature of proximal and distal muscles in acute and chronic idiopathic demyelinating polyneuropathy. It is of interest that the increase in fiber density was not more prominent in the chronic cases, and that there was no relation between fiber density and the extent of the abnormalities in motor nerve conduction. Thiele and Sta1be1-g'~suggested that the fiber density may be used to assess axonal damage in polyneuropathy, basing this concept on studies of the EDC muscle in patients with diabetes") and uremic neuropathy in whom the fiber density in this muscle was normal, and another group of patients with alcoholic neuropathy in whom the fiber density in the EDC was raised to a mean value of 2.03. Subsequent studies of the changes in fiber density in the tibialis anterior muscle in patients with diabetic polyneuropathy have shown that the fiber density is i n ~ r e a s e dparticularly ,~ in those patients with symptomatic polyneuropathy.9 In patients with asymptomatic diabetic polyneuropathy, the mean fiber density in the tibialis anterior muscle was 2.17, and was 2.49 in those with symptomatic neuropathy. These modest elevations in fiber density in affected distal muscles in metabolic neuropathy contrast with the much higher values found in patients with anterior horn cell disorders,I2 and in the hereditary motor and sensory neuropathies,'2,'9 in which the primary abnormality is associated with axonal degenerati~n."'~ In AIDP, weakness is often prominent in proximal muscles at presentation but later may involve both proximal and distal muscles, or predominantly affect distal muscle^.'-^'^ Our data show that the fiber density may be increased in the
proximal muscles within 3 weeks of presentation, a feature that may relate to early reinnervation of these muscles in some cases. In studies of amyotrophic lateral and radiculopathies, SFEMG studies may reveal an increased fiber density even when concentric needle EMG studies are normal. Our finding of increased fiber density early in the course of AIDP, at a time when sparse fibrillations were present, but polyphasic motor unit action potentials were not prominent, is consistent with the observation that SFEMG is more sensitive in detecting early reinnervation than concentric needle EMG. AIDP is associated with demyelination rather than with axonal degeneration, but these EMG findings indicate that there is axonal dysfunction early in the course of the disease that is rapidly repaired. Stalberg" found that, in 2 patients with AIDP, the macro-EMG motor unit potentials were of increased amplitude only 1 week after the onset of the neuropathy, but that the fiber density at this time was normal. In CIDP, the macro-EMG potentials were often of very markedly increased amplitude, with a corresponding increase in tiber density." Stalberg suggested that the early increase in macro-EMG amplitude might be due to loss of small motor units, but our finding of an increased SFEMG fiber density 3 weeks after onset indicates that reinnervation may commence very soon after the onset of the disease. The increase in fiber density in our patients could not be correlated with the distribution of weakness, probably because of the varying severity, time-course, and distribution of involvement of the innervations of the muscles assessed. In CIDP, when there is long-standing weakness, there may be secondary axonal degeneration"' and higher fiber density values, as in our case 11. These observations suggest that quantitative SFEMG and concentric needle EMG studies of both proximal and distal muscles are useful in evaluating the distribution and evolution of the abnormalities in the peripheral nervous system in patients with peripheral neuropathy.
REFERENCES
1. Albers JW, Kelly JJ Jr: Acquired inflammatory demyelinating polyneuropathies: Clinical and electrophysiological features. Muscle Nerve 1989;12:435-451. 2. Asbury AK, Arnason BG, Karp HR, McFarlin D E : Criteria for diagnosis of Guillain- Barre syndrome. Ann Neurul 1978;3:565-566. 3 . Asbury AK, Cornblath DR: Assessment of current diag-
170
Fiber Density in Polyneuropathy
nostic criteria for Guillain-Barre syndrome. Ann Neurol 1990;27(suppl):S21 4 2 4 . 4. Bril V , Werb M: SFEMG in tibialis anterior muscles of patients with diabetic peripheral neuropathy. Muscle Nerue 1986;9:563. 5. Oh SJ: Single fiber EMG in chronic demyelinating neuropathy. M u . d e Nervr 1989;12:371-377.
MUSCLE & NERVE
February 1992
6. Oppenheimer DR, Spalding JMK: Late residue of acute idiopathic polyneuritis. J Neurol Neurosurg Psychrutry 1973;36:978-988. 7 . Prineas JW, McLeod JG: Chronic relapsing polyneuritis. J Neurol Scr 1976; 27 :427-458. 8. Ropper AH, Wijdichs EFM, Shahani BT: Electrodiagnostic abnormalities in 1 13 consecutive patients with GuillainBarre syndrome. Arch Neurol 1990;47:881-887. 9. Schwartz MS, Stalberg E, Schiller HH, Thiele B: T h e reinnervated motor unit in man. J Neurol Sci 1976;27:303312. 10. Shields RW Jr: Single fiber electromyography is a sensitive indicator of axonal degeneration in diabetes. Neurology l987;37: 1394.
Fiber Density in Polyneuropathy
11. Stalberg E: Macroelectrornyography in reinnervation. Mu.cle Nerue 1982;5:s135- S 138. 12. Stalberg E, Schwartz MS, Trontelj J V : Single fibre electromyography in various processes affecting the anterior horn cell. J Neurol Sci 1975;24:403-415. 13. Stalberg E, Trontelj JV: Single Fiber Electromyogruphy. Old Woking, Surrey, UK, Mirvalle Press, 1979. 14. Swash M, Schwartz MS: A longitudinal study of changes in motor units in motor neuron disease. J Neurol Sci 1982;56:185- 197. 15. Thiele B, Stalberg E: Single fiber EMG findings in polyneuropathies of different aetiology. J Neurol Neurosurg Psychiatry 1975;38:881-887.
MUSCLE & NERVE
February 1992
171
FIBER DENSITY IN ACUTE AND CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY MAYA GANTAYAT, MB, MICHAEL SWASH, MD, FRCP, MRCPath, and MARTIN S. SCHWARTZ, MD
S i ngl e fiber EMG (SFEMG) studies in chronic inflammatory demyelinating polyneuropathy (CIDP) in the extensor digitorum communis muscle have shown an increased fiber density in 37% of a group of 19 patients." An increased fiber density usually has been regarded as a feature of reinnervation, and thus, of axonal rather than demyelinating n e ~ r o p a t h i e s . ' : ~ In " ~ this report, we describe measurements of the fiber density in proximal and distal upper limb muscles in a group of patients with the acute (AIDP) and chronic (CIUP) progressive forms of inflammatory demyelinating polyneuropathy. Previous SFEMG studies of peripheral neuropathie~~.".".'~,'" have been confined to single muscles in the upper or lower limbs, but it is of interest to study the changes in proximal and distal muscles in this disease in which weakness is often strikingly proximal in the acute phase, but may be proximal o r distal when the disease enters a more chronic phase.
From the Atkinson Morley's Hospital (Drs. Gantayat and Schwartz) and The Royal London Hospital (Drs. Gantayat, Swash, and Schwartz), London, United Kingdom Acknowledgment: Dr. Gantayat was supported by a BOYSCAST Fellowship awarded by the Government of India (1990). Address reprint requests to Dr. M.S. Schwartz, Atkinson Morley's Hospital, Wimbledon, London, SW20 ONE, UK. Accepted for publication February 25. 1991
CCC 0148-639X/92/020168-04
$04 00
0 1992 John Wiley & Sons, Inc.
168
Fiber Density in Polyneuropathy
PATIENTS AND METHODS
Seven men and 4 women, aged 24 to 77 years, were studied; 6 had acute AIDP and 5 had CIDP. T h e criteria for diagnosis were both clinical and electrophysiological as recommended by Asbury et al.,'*3 Prineas and M ~ I ~ e o dand , ~ Albers and Kelly.' T h e duration of symptoms in the 6 patients with the AIDP ranged from 3 to 7 weeks and, in the 5 patients with CIDP, it ranged from 3 months to 3 years ('Table 1). I n these patients, the strength of the deltoid, extensor digitorum communis (EDC), and first dorsal interosseous (1st DI) muscles was assessed in the right arm using the MKC scale. Motor and sensory nerve conduction studies and F wave studies were made in the upper and lower limbs; in particular, motor nerve conduction and F wave responses were examined in the right arm. T h e latter studies are summarized in Table 2. In each patient, the fiber density was measured in the right deltoid, EDC, and 1st DI muscles, using a SFEMG electrode (Dantec 13K387) and a Dantec Neuromatic 2000M EMG apparatus. 1s,'4 T h e fiber density was considered abnormal when higher than 1.8, a value 3 SD above the mean in a control population younger than 75 (our laboratory normal data). Conventional concentric needle EMG studies were also carried out in these muscles. RESULTS
T h e electrophysiological findings are summarized in Tables 1 and 2. T h e nerve conduction studies
MUSCLE & NERVE
February 1992
-
~
~~~~
Table 1. Clinical data and fiber density in 3 arm muscles SFEMG fiber density
MRC muscle power
Case
Age1 sex
GBS type
Duration
Deltoid
EDC
1st DI
Deltoid
EDC
1st DI
1 2 3 4 5 6 7 8 9 10 11
60lM 73lM 71lM 30lM 24lM 49lF 57lM 691F 39lF 771F 60lM
Acute Acute Acute Acute Acute Acute Chronic Chronic Chronic Chronic Chronic
3 weeks 3 weeks 3 weeks 5 weeks 6 weeks 7 weeks 12 weeks 1 year 3 years 3 years 3 years
2.3* 1.9 2.4* 2.4' 2.4* 2.1' 2.4' 2.3' 2.4* 2.3* 3.7'
1.6 1.8 2.5* 1.7 1.5 2.2* 1.9* 2.8* 1.7 2.1* 2.7'
1.6 1.9 2.5' 2.1* 1.7 2.1* 1.8 2.9* 2.3' 1.5 NR
445 5 4+ 5 4+ 45 3 4+
4+ 4+ 5 45 5 5 4+ 4+ 3 4-
4+ 4+ 5 3 5 4+ 4+ 4441
5 3 SD above mean of normal control data. NR: No Dotentials recordable.
and F responses were abnormal in the median nerves in all the patients studied, and in the ulnar nerves in 9 of the 11 patients. The most abnormal findings were noted in the 5 patients with CIDP (Tables 1 and 2). There was evidence of conduction block in 50% of the nerves studied. In the 11 patients, the mean fiber density was 2.5 (range 1.9 to 3.7) in the deltoid, 2.2 (range 1.5 to 2.8) in the EDC, and 2.0 (range 1.5 to 2.9) in the 1st DI muscle (Table 1). In the deltoid muscle, the fiber density was increased in all the 11 patients, in the EDC in 6 patients, and in the 1st DI in 6 patients, but no potentials could be recorded in this muscle in 1 patient with CIDP (case 11). There was no constant relationship between the fiber density, clinical features, duration of the dis-
ease, age, or muscle strength. In addition, the changes in fiber density did not correlate with the abnormalities found in motor conduction velocity or F-wave responses. Even in those patients in whom the motor conduction velocities were very slowed, the fiber densities in the 3 muscles showed similar changes to those found in the other patients. In case l l , however, conduction was markedly abnormal and the fiber density was much greater (3.7) than in the other patients. In 2 patients (cases l and 5), with AIDP, the fiber density was increased only in the deltoid muscle. In the patients with AIDP, concentric needle EMG studies showed fibrillation potentials, which were more prominent in the deltoid than in the other 2 muscles. In these cases, a slight increase in
Table 2. Motor nerve conduction studies in right arm. Median nerve
Case 1 2 3 4 5 6 7 8 9 10 11
DML (ms) 5.2* 4.6* 8.4' 4.6'
5.0* 5.6* 5 2' 4.8* 11.6' 15.2* 11.6*
Ampl. (mV)
Ulnar nerve
cv
Distal
Prox.
(ms-')
F (ms)
8.5 4.5 5.2 3.0 16.0 4.0 2.5* 7.0 1.2' 0.25* 1.O'
7.0 4.5 13t 2.5 13.5 2.0t 0.5t 5.2 0.3t 0.04t
43 42 39* 45 46 52 40* 59 23* 8* 20
27.6 24.2 A* 30.4 A* 28.2 28.8 28.6 A* A' 59.0*
0.5t
DML (ms) 3.8 4.0 4.4" 5.0k 5.4' 3.6 3.6 8.0* 20.4* 12.8*
5.0*
Ampl. (mV)
cv
Distal
Prox.
(m"-')
8.0 6.2 2.0* 1.7' 7.0 6.0 2.5* 5.5 1.2* 0.25*
6.0 5.5 1.3t 1.ot 3.5t 6.0 1.7t 5.0 0.6t A' 0.5
45 50 45 43 36* 50 50 50 18* A* 24*
0.5*
F (ms) 33.2* 33.0' A* 39.2* 34.2" 27.6 32.2' 29.0 A* A'
50.0*
~~
'Abnormal values, jconduction block A = absent response
Fiber Density in Polyneuropathy
MUSCLE & NERVE
February 1992
169
polyphasic motor unit action potentials was noted in deltoid muscles, but not in the other 2 muscles. In the patients with CIDP, polyphasic potentials were more prominent, particularly in cases 8 and 11. DISCUSSION
Our data show that a modest increase in fiber density may be a feature of proximal and distal muscles in acute and chronic idiopathic demyelinating polyneuropathy. It is of interest that the increase in fiber density was not more prominent in the chronic cases, and that there was no relation between fiber density and the extent of the abnormalities in motor nerve conduction. Thiele and Sta1be1-g'~suggested that the fiber density may be used to assess axonal damage in polyneuropathy, basing this concept on studies of the EDC muscle in patients with diabetes") and uremic neuropathy in whom the fiber density in this muscle was normal, and another group of patients with alcoholic neuropathy in whom the fiber density in the EDC was raised to a mean value of 2.03. Subsequent studies of the changes in fiber density in the tibialis anterior muscle in patients with diabetic polyneuropathy have shown that the fiber density is i n ~ r e a s e dparticularly ,~ in those patients with symptomatic polyneuropathy.9 In patients with asymptomatic diabetic polyneuropathy, the mean fiber density in the tibialis anterior muscle was 2.17, and was 2.49 in those with symptomatic neuropathy. These modest elevations in fiber density in affected distal muscles in metabolic neuropathy contrast with the much higher values found in patients with anterior horn cell disorders,I2 and in the hereditary motor and sensory neuropathies,'2,'9 in which the primary abnormality is associated with axonal degenerati~n."'~ In AIDP, weakness is often prominent in proximal muscles at presentation but later may involve both proximal and distal muscles, or predominantly affect distal muscle^.'-^'^ Our data show that the fiber density may be increased in the
proximal muscles within 3 weeks of presentation, a feature that may relate to early reinnervation of these muscles in some cases. In studies of amyotrophic lateral and radiculopathies, SFEMG studies may reveal an increased fiber density even when concentric needle EMG studies are normal. Our finding of increased fiber density early in the course of AIDP, at a time when sparse fibrillations were present, but polyphasic motor unit action potentials were not prominent, is consistent with the observation that SFEMG is more sensitive in detecting early reinnervation than concentric needle EMG. AIDP is associated with demyelination rather than with axonal degeneration, but these EMG findings indicate that there is axonal dysfunction early in the course of the disease that is rapidly repaired. Stalberg" found that, in 2 patients with AIDP, the macro-EMG motor unit potentials were of increased amplitude only 1 week after the onset of the neuropathy, but that the fiber density at this time was normal. In CIDP, the macro-EMG potentials were often of very markedly increased amplitude, with a corresponding increase in tiber density." Stalberg suggested that the early increase in macro-EMG amplitude might be due to loss of small motor units, but our finding of an increased SFEMG fiber density 3 weeks after onset indicates that reinnervation may commence very soon after the onset of the disease. The increase in fiber density in our patients could not be correlated with the distribution of weakness, probably because of the varying severity, time-course, and distribution of involvement of the innervations of the muscles assessed. In CIDP, when there is long-standing weakness, there may be secondary axonal degeneration"' and higher fiber density values, as in our case 11. These observations suggest that quantitative SFEMG and concentric needle EMG studies of both proximal and distal muscles are useful in evaluating the distribution and evolution of the abnormalities in the peripheral nervous system in patients with peripheral neuropathy.
REFERENCES
1. Albers JW, Kelly JJ Jr: Acquired inflammatory demyelinating polyneuropathies: Clinical and electrophysiological features. Muscle Nerve 1989;12:435-451. 2. Asbury AK, Arnason BG, Karp HR, McFarlin D E : Criteria for diagnosis of Guillain- Barre syndrome. Ann Neurul 1978;3:565-566. 3 . Asbury AK, Cornblath DR: Assessment of current diag-
170
Fiber Density in Polyneuropathy
nostic criteria for Guillain-Barre syndrome. Ann Neurol 1990;27(suppl):S21 4 2 4 . 4. Bril V , Werb M: SFEMG in tibialis anterior muscles of patients with diabetic peripheral neuropathy. Muscle Nerue 1986;9:563. 5. Oh SJ: Single fiber EMG in chronic demyelinating neuropathy. M u . d e Nervr 1989;12:371-377.
MUSCLE & NERVE
February 1992
6. Oppenheimer DR, Spalding JMK: Late residue of acute idiopathic polyneuritis. J Neurol Neurosurg Psychrutry 1973;36:978-988. 7 . Prineas JW, McLeod JG: Chronic relapsing polyneuritis. J Neurol Scr 1976; 27 :427-458. 8. Ropper AH, Wijdichs EFM, Shahani BT: Electrodiagnostic abnormalities in 1 13 consecutive patients with GuillainBarre syndrome. Arch Neurol 1990;47:881-887. 9. Schwartz MS, Stalberg E, Schiller HH, Thiele B: T h e reinnervated motor unit in man. J Neurol Sci 1976;27:303312. 10. Shields RW Jr: Single fiber electromyography is a sensitive indicator of axonal degeneration in diabetes. Neurology l987;37: 1394.
Fiber Density in Polyneuropathy
11. Stalberg E: Macroelectrornyography in reinnervation. Mu.cle Nerue 1982;5:s135- S 138. 12. Stalberg E, Schwartz MS, Trontelj J V : Single fibre electromyography in various processes affecting the anterior horn cell. J Neurol Sci 1975;24:403-415. 13. Stalberg E, Trontelj JV: Single Fiber Electromyogruphy. Old Woking, Surrey, UK, Mirvalle Press, 1979. 14. Swash M, Schwartz MS: A longitudinal study of changes in motor units in motor neuron disease. J Neurol Sci 1982;56:185- 197. 15. Thiele B, Stalberg E: Single fiber EMG findings in polyneuropathies of different aetiology. J Neurol Neurosurg Psychiatry 1975;38:881-887.
MUSCLE & NERVE
February 1992
171
