You are on page 1of 9

Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.

com

Journal of Neurology, Neurosurgery, and Psychiatry, 1976, 39, 453460

Peripheral motor nerve function in diabetic


autonomic neuropathy
D. J. EWING', A. A. BURT, I. R. WILLIAMS, I. W. CAMPBELL,
AND B. F. CLARKE
From the University Departments of Medicine and Medical Neurology and the
Diabetic and Dietetic Department, Royal Infirmary, Edinburgh

SYNOPSIS Motor conduction velocity was measured in the median, ulnar, and common peroneal
nerves of 32 diabetics with clinical features of autonomic neuropathy. The responses to the Valsalva
manoeuvre and sustained handgrip, and the postural fall in blood pressure were used to assess the
integrity of the autonomic nervous system. Abnormalities in the three autonomic function tests were
significantly correlated with the forearm conduction velocity of the ulnar nerve, the conduction
velocity and motor latency of the common peroneal nerve, and the H reflex. These results show that,
in diabetics with autonomic neuropathy, abnormalities in the autonomic nervous system parallel
changes in the peripheral nerves. Any diabetic with peripheral neuropathy should be examined for
evidence of autonomic nervous system involvement.

Peripheral neuropathy is a well-recognized METHODS


complication of diabetes mellitus which can be PATIENTS Thirty-seven diabetics with features
detected even at diagnosis (Ward et al., 1971). suggestive of autonomic neuropathy were selected
With increasing duration of diabetes there is for study. All patients had normal levels of serum
increasing impairment of nerve conduction vitamin B12, except one who was excluded; four others
(Gregerson, 1967). Autonomic neuropathy is were excluded as complete nerve conduction data
likewise common, and, although it does not could not be obtained. The ages of the remaining 32
become clinically manifest until the later stages, patients ranged from 26 to 63 years (mean 48 10
tests of autonomic function show abnormalities years), and the duration of diabetes from two to
before the onset of symptoms (Sharpey-Schafer 33 years (mean 199 years). All but four were
and Taylor, 1960; Ewing et al., 1974; Murray et insulin dependent, and none had cardiac failure or
was receiving hypotensive therapy. None of the
al., 1975). patients was known to be an alcoholic, all had normal
This study compares autonomic and peripheral protein bound iodine values, and 18 had blood urea
nerve function in diabetics with clinical features levels within normal limits (less than 6.6 mmol/l).
suggestive of autonomic neuropathy to see Of the remainder 11 had blood urea levels between
whether the nerve damage known to occur in the 6.6 and 10.0 mmol/l, while only three had higher
peripheral motor nerves was paralleled by similar levels of 10.5, 10.6, and 12.1 mmol/l. All patients had
changes in the autonomic nerves. A preliminary one or more of the following features: impotence
report of nerve conduction in diabetic autonomic (25 patients); symptoms of postural hypotension
neuropathy has been published elsewhere (Ewing (seven patients); intermittent diarrhoea (nine
et al., 1973); this paper gives the findings in more patients); gastric fullness or delay in emptying (four
patients); a history of hypoglycaemic unawareness
detail and analyses them in relation to the (1 1 patients); gustatory sweating (two patients); and
autonomic function tests. reduced sweating in the legs (one patient). Ten
patients had symptoms of a peripheral neuropathy
I Address for correspondence: Dr D. J. Ewing, Department of including numbness and painful cramps in the legs
Medicine, Royal Infirmary, Edinburgh EH3 9YW. but without signs. Nineteen had signs of peripheral
(Accepted 13 January 1976.) neuropathy on clinical examination including absent
453
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

454 D. J. Ewing, A. A. Burt, L R. Williams, L W. Campbell, and B. F. Clarke

knee and ankle jerks and diminished sensation in the However, they had a significantly longer duration
lower limbs. of diabetes, their conduction velocity was slower
Autonomic function was assessed by the Valsalva and terminal latency longer.
manoeuvre, the response to sustained handgrip, and
the postural fall in blood pressure. The Valsalva RELATION BETWEEN THE CLINICAL FEATURES OF
manoeuvre was carried out using a standardized
technique as previously described (Ewing et al., 1973). AUTONOMIC AND PERIPHERAL NEUROPATHY
The heart rate response was measured by a simul- (Table 3) Five patients with impotence alone
taneous electrocardiograph (ECG). The results were had signs of a peripheral neuropathy in contrast
expressed as the Valsalva ratio (the ratio of thelongest with 14 of those with other features of autonomic
RR interval in the ECG after the manoeuvre to the neuropathy (x2= 5.15, P < 0.05).
shortest RR interval during the manoeuvre), a ratio
of 1.10 or less being defined as an abnormal response, CLINICAL FEATURES OF AUTONOMIC NEUROPATHY
1.11 to 1.20 as borderline, and 1.21 or more as a AND NERVE CONDUCTION (Table 4) When the
normal response. A standardized sustained handgrip MCV results were analysed in terms of the
test was also performed as described previously clinical features of autonomic neuropathy, there
(Ewing et al., 1974). A rise in diastolic blood pressure were significant differences between the groups
of less than 10 mmHg was defined as abnormal,
1 1-15 mmHg as borderline, and 16 mmHg or more as only in the terminal motor latency of the common
normal. Postural hypotension was defined as a fall in peroneal nerve (P < 0.02).
systolic blood pressure of 30 mmHg or more im-
mediately on standing up from the supine position. CLINICAL FEATURES OF PERIPHERAL NEUROPATHY
Motor conduction velocity (MCV) was measured AND AUTONOMIC FUNCTION TESTS (Table 5)
in the median, ulnar, and common peroneal nerves. Table 5 shows the results of the autonomic
The latency of the H reflex in the triceps surae was function tests when the subjects were grouped
measured after stimulation of the medial popliteal according to the clinical features of peripheral
nerve at the popliteal fossa. Surface electrodes were neuropathy.
used for stimulating with 1 cm silver discs placed
5 cm apart. Standard DISA surface recording elec-
trodes and a DISA two channel electromyograph NERVE CONDUCTION AND AUTONOMIC FUNCTION
were used in all studies, which were performed in the TESTS MCV and Valsalva manoeuvre (Table
same environment with skin temperatures maintained 6) The Valsalva ratio was significantly cor-
above 30C. related in the group as a whole only with the
The physical examination of the patients, the auto- forearm conduction velocity in the ulnar nerve
nomic function tests, and the nerve conduction (r=0.375, P<0.05); but, when the group was
studies were carried out by three independent divided into those with normal and abnormal
observers. Standard statistical methods were used to Valsalva ratios, those with abnormal ratios had
calculate the significance of the results. significantly more abnormal MCV measurements
in the forearm conduction velocity in the ulnar
RESULTS nerve (P<0.01), the motor latency (P<0.005),
and conduction velocity (P < 0.02) of the common
CLINICAL FEATURES OF AUTONOMIC NEUROPATHY peroneal nerve and the H reflex latency (P < 0.05).
AND AUTONOMIC FUNCTION TESTS (Table 1)
When the patients were grouped into those with MCV and response to sustained handgrip (Table
impotence alone and those with other features of 6) Within the whole group the rise in diastolic
autonomic neuropathy, there were significant blood pressure correlated significantly with the
differences between the results of the autonomic forearm conduction velocity in the ulnar nerve
function tests in the two groups. (r=0.356, P <0.05), the motor latency of the
common peroneal nerve (r=0.552, P < 0.01) and
CLINICAL FEATURES OF PERIPHERAL NEUROPATHY the conduction velocity of the common peroneal
AND NERVE CONDUCTION (Table 2) Patients nerve (r=0.390, P <0.05). When normal and
with symptoms and signs of a peripheral neuro- abnormal handgrip responses were separated,
pathy did not, as a group, differ significantly in there was a significant difference only in the motor
mean age from those having no such features. latency of the common peroneal nerve (P < 0.005).
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

Peripheral motor nerve function in diabetic autonomic neuropathy 455

ei e~i

-H -H-i -H

'tH -H -H -H

~~~~~f -H H1- -H

N0~~~~~~~0W

06 Ni e~) 0
-H - H110 -H
Li CR tn~~Hi Q N; 00

~ ~ ~ ~ ~ r t

1:4
t,
616 e'it

- ~0 L ~ IZ
~ 00

H00~
~~~~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~~~~0 0

ei~~~~~~~~~e

CA O~~~~~~~~0

V~~~~~~~~~~~~~~~~~~~~~~~~~~~~~-
CACo
U~~ ~ ~ ~ ~ ~ ~

.0

z~~~~~~~~~

C~~~Z
m

0)
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

456 D. J. Ewing, A. A. Burt, L R. Williams, L. W. Campbell, and B. F. Clarke

N en
-H -H on
en

-n t-n
6 0
CZ,
0~ oIR-H r-_
+00
L.
'I Z
6
0~
0:
0s
0~
N t-
C
U. 0:
01,
00
00c
"t c a

L
L. 0x rl
0~
01 n
U
z
\_ en_
-H

tt el;

U 0u
U
L;
0
z 0
0 0x
-H
O.
o4
LL +
6 ~oo+00
Z
4o
0

0
z _- 00
F- zw eO
"

t0t .!L. Ci
(
12-H
z4
-f
F- w
-z
u A. .2 E 110
C4
0 (L)
U
E 0 -
0. :00
0o
1 % - 0
vo0.
0E
.0 z
-H
&a r. -H0
<z Q-.
. 0
'--0 U
0 + U
U
w
O 0
en Nt
0
U

.0
._

0
0O
_04)
0 4) 0

U) eo
0

ES
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

Peripheral motor nerve fuinction in diabetic autonomic neuropathy 457

C
r-~ 00r

4h+0/) -4A-+ -H -H0En


0 0 ~~~~~~~~~~~~~ oooo7~~~~~~~~~~~~0W 9- v r_-.7 ~

00 r'
- -
0O 06 0-

0.
0~~~~~~~4C
~~~~~~~~~~~
N
C4 ~ ~ ~ ~ -

LL.~~~~~~~
z C E

0 O~~~~~~~~~~~~~

LU ro-
(A
0 0C3000 1
-H
Q ~~~ O
~00
r-- r 'I
42 W)~~~~~~~~~~~~~~~r~rorW)) 0
0-- ~~~~~~~~~~~~LU0
U
W)~~~~~~
0. ~~~~~~~~~~~~~~~LU
0 Ho- r + H -Ho0 -Hooo
Z
tc ~~~~~LU
* ~r-~
H00~~~~~~~~~.
00 ~ ~ ~ ~ ~ ~ ~ ..0V,W
~ ~
7 0
Z. 7. -H
I
7~ 00~ ~0 ~0'r- \00 or-
~~~
H
H U H r-0~ ~ ~ ~ ~ ~ ~ ~ ~ r-1r-O ~ r-
~
o~
~~
~ ~ ~ ~ ~ ~ ~ ~ L U H 0~~~~~~~~~~~~~~~-

Z~ < - H s- 0)~~~~~0
0O

7LU
LU
C.~~~~~~~~~~~~~~~~~~~~77~~~~~~~~~~~~~~~LU -
Z 0

0.0 ~~~00
~~~~ (10 iO0
CZ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~C

7U HU
D 1~~~~~~~~0o- r-
00 00 "C -

00~~~~~~~~~~~~ 0. ~ ~ ~ ~ ~ ~ ~ n
-~~~~~~~~~~~~ c

Ho > 0 +0 ++ 0 +02 .

0 U.,~~~~~~~~0~~*~o-7--~r.o

E0 0

7-~~~~~~~~~~~~o
0 0. 0~~~~~~~~~~~~~~~C a0
~~~~~
(.~~~~~~)
....o
0
0).-
C. .-~~~~~~~~~~~~~~~~~~~~~~~
-~~~~~~~~~~~~~~~~
~ ~
~ ~
Eo C
o 0 ;o. 0~~~~~~~~~~~~~~~~~~~~~~~~~~ 0(Z.

0~~~~~~~~~~~~~~~~~
0 0~~~~~~~~~~~~~~~~~~~~~~~> O
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

458 D. J. Ewing, A. A. Burt, I. R. Williams, I. W. Campbell, and B. F. Clarke

MCV and postural fall in blood pressure (Table more specifically at the peripheral and the auto-
6) The fall in systolic blood pressure also cor- nomic nervous systems independently. Martin
related significantly with the forearm conduction (1953b) showed abnormalities of sudomotor and
velocity in the ulnar nerve (r=0.466, P<0.01), vasomotor function in 20 patients with diabetic
the motor latency of the common peroneal nerve peripheral neuropathy, and another study at-
(r=0.681, P<0.001), the conduction velocity of tempted to assess the amount of autonomic nerve
the common peroneal nerve (r=0.573, P < 0.001), damage in patients with peripheral neuropathy
and also the H reflex latency (r=0.374, P < 0.05). by using the Valsalva manoeuvre (Bishnu and
Again, however, when those with a normal and an Berenyi, 1971). The present study, however, has
abnormal fall in systolic blood pressure were examined the relationship in more detail from the
separated, there was a significant difference only opposite viewpoint by measuring peripheral
in the motor latency of the common peroneal nerve function in patients with autonomic
nerve (P < 0.05). neuropathy.
As has been demonstrated previously (Ewing
Renal function, MCV, and autonomic function et al., 1973), the study shows that diabetics with
tests The level of the blood urea correlated impotence alone, which is often stated to be the
significantly, in the group as a whole, with the only manifestation of diabetic autonomic neuro-
forearm conduction velocity in the ulnar nerve pathy in some patients (British Medical Journal,
(r=0.447, P < 0.05), and the motor latency of the 1974), had more normal autonomic vascular
common peroneal nerve (r=0.452, P <0.01). It reflexes than those with other features of
was also significantly correlated with the sustained autonomic neuropathy. Similarly, the clinical
handgrip response (r=0.356, P<0.05) but not symptoms and signs of peripheral neuropathy
with the Valsalva ratio (r=0.286 NS) nor with were closely reflected by the changes in MCV.
fall in systolic blood pressure (r=0.214 NS). As might be expected, therefore, few patients with
impotence alone also had signs of a peripheral
DISCUSSION
neuropathy.
In addition, this study now provides more
This study shows that, in diabetics with auto- detailed information of the relation between
nomic neuropathy, abnormalities in the auto- MCV and autonomic vascular reflex responses.
nomic nervous system parallel changes in Whether one examines the regression relationship
peripheral nerves. Previous workers have between the individual values, or the differences
demonstrated that peripheral nerve function, as between groups with and without abnormal
determined by motor nerve conduction velocity, is autonomic function tests, it is clear that changes
impaired in diabetics and that, although this is in the common peroneal nerve and in the forearm
reflected by the presence of peripheral neuro- conduction velocity of the ulnar nerve are
pathy, some diabetics have early changes of MCV closely related. The three autonomic responses
without clinical evidence of a neuropathy (Mulder measured-the Valsalva manoeuvre, sustained
et al., 1961; Lawrence and Locke, 1961; Skillman handgrip, and postural fall in blood pressure-
et al., 1961). Others have documented abnormal are all cardiovascular reflexes. Although auto-
autonomic function tests in diabetics both with nomic neuropathy affects all systems of the body,
and without clinical features of autonomic neuro- it is the vascular responses that are both simplest
pathy (Sharpey-Schafer et al., 1960; Ewing et al., to measure non-invasively and easiest to quantify,
1974; Murray et al., 1975). It is surprising perhaps and they bear a close relation to symptoms
that there has been little attempt to relate the two, (Ewing et al., 1973). Their reflex pathways are
either in terms of clinical features, or in terms of not clear in their entirety, but probably involve
objective testing. Early authors considered auto- efferent fibres to the blood vessels in the lower
nomic neuropathy as one part of the spectrum of limbs in all three responses and this would
diabetic neuropathy (Rundles, 1945; Martin, therefore suggest that damage to the nerves
1953a); but, with the development of objective conveying the reflexes occurs in parallel with the
means of testing both nerve conduction and motor nerve damage measured by the nerve
autonomic function, later workers have looked conduction studies.
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

Peripheral motor nerve function in diabetic autonomic neuropathy 459

Peripheral neuropathy in diabetics is common 1974), the greater splanchnic nerves (Low et al.,
in the lower limbs, but rare in the upper limbs 1975), and the lumbar sympathetic ganglia (Kott
(Noel et al., 1971; Noel, 1973), and, although the et al., 1974).
neuropathy is predominantly sensory, changes in Diabetic peripheral neuropathy and diabetic
the motor fibres correlate well with the clinical autonomic neuropathy are often considered as
picture (Lamontagne and Buchthal, 1970) and distinct clinical entities, with their different
with changes in the sensory nerves (Gilliatt and symptomatology and features. They share,
Willison, 1962). On the basis of these observa- however, a common pathogenesis, and the
tions, it would be expected that the leg MCV present study shows that abnormalities occurring
gives a better correlation than the arm MCV with in the autonomic nervous system are paralleled
the autonomic function tests. by changes in the peripheral nervous system. In
Although the level of blood urea correlated practice, therefore, as diabetic peripheral neuro-
both with the MCV findings and the autonomic pathy has been more closely studied and
function tests, and could be presumed to be the understood, it means that any patient with
cause of both abnormalities, this does not stand peripheral neuropathy due to his diabetes should
up to critical analysis. In chronic renal failure be examined carefully for evidence of autonomic
the blood urea, although a crude index of renal nerve involvement.
function, is usually much higher than the levels
in this study before changes in MCV are detected. REFERENCES
Of those patients with normal blood urea values,
seven had clinical signs of peripheral neuropathy; Appenzeller, O., and Richardson, E. P. (1966). The
and although changes of autonomic function sympathetic chain in patients with diabetic and alcoholic
polyneuropathy. Neurology (Minneap.), 16, 1205-1209.
have been described in chronic renal failure Bishnu, S. K., and Berenyi, M. R. (1971). Circulatory
(Ewing and Winney, 1975), eight patients with reflex response in diabetic patients with or without
normal blood urea levels had abnormal auto- peripheral neuropathy. Journal of the American Geri-
nomic function tests. Impaired renal function, atrics Society, 19, 159-166.
although it cannot be incriminated causally, may British Medical Journal (1974). Editorial: diabetic
nevertheless contribute to the neuropathy. autonomic neuropathy, 3, 2-3.
Fibres mediating the autonomic responses are Chopra, J. S., Hurwitz, L. J., and Montgomery, D. A. D.
both myelinated and unmyelinated, while the (1969). The pathogenesis of sural nerve changes in
MCV is measured in large myelinated fibres diabetes mellitus. Brain, 92, 391-418.
ending at neuromuscular junctions. The most Dyck, P. J. (1971). The concept of secondary segmental
constant underlying lesion in the peripheral demyelination. Proceedings of the 2nd International
Congress of Muscle Diseases. Excerpta Medica Inter-
neuropathy of diabetes has been shown to be national Congress Series, no. 237, 74
segmental demyelination (Thomas and Lascelles, Ewing, D. J., Campbell, I. W., Burt, A. A., and Clarke,
1965, 1966; Locke, 1967). This is usually thought B. F. (1973). Vascular reflexes in diabetic autonomic
to be due to disturbance of the Schwann cells, neuropathy. Lancet, 2, 1354-1356.
but it has been suggested that segmental Ewing, D. J., Irving, J. B., Kerr, F., Wildsmith, J. A. W.,
demyelination may result from axonal dis- and Clarke, B. F. (1974). Cardiovascular responses to
turbance (Dyck, 1971; Thomas, 1971). Axonal sustained handgrip in normal subjects and in patients
with diabetes mellitus: a test of autonomic function.
loss has been demonstrated in more severe cases Clinical Science and Molecular Medicine, 46, 295-306.
(Chopra et al., 1969). Histological studies of Ewing, D. J., and Winney, R. (1975). Autonomic function
autonomic nerves in diabetics are limited, but in patients with chronic renal failure on intermittent
widespread changes have been noted in the haemodialysis. Nephron, 15,424-429.
sympathetic chain and ganglia in patients dying Faerman, I.. Glocer, L., and Celener, D. (1973). Auto-
from various complications (Appenzeller and nomic nervous system and diabetes. Histological and
Richardson, 1966; Olsson and Sourander, 1968). histochemical study of the autonomic nerve fibres of the
Damage has also been noted to the autonomic urinary bladder in diabetic patients. Diabetes, 22,
225-237.
fibres supplying the bladder wall (Faerman et al., Faerman, I., Glocer, L., Fox, D., Jadzinsky, M. D., and
1973); the corpora cavernosa (Faerman et al., Rapaport, M. (1974). Impotence and diabetes. Histo-
1974), the innervation of the oesophagus (Smith, logical studies of the autonomic nervous fibres of the
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

460 D. J. Ewing, A. A. Burt, 1. R. Williams, L W. Campbell, and B. F. Clarke

corpora cavernosa in impotent diabetic males. Diabetes, Noel, P. (1973). Sensory nerve conduction in the upper
23, 971-976. limb at various stages of diabetic neuropathy. Journal of
Gilliatt, R. W., and Willison, R. G. (1962). Peripheral Neurology, Neurosurgery, and Psychiatry, 36, 786-796.
nerve conduction in diabetic neuropathy. Journal of Noel, P., Lauvaux, J. P., and Pirart, J. (1971). Upper limb
Neurology, Neurosurgery and Psychiatry, 25, 11-18. diabetic neuropathy: a clinical and electrophysiological
Gregerson, G. (1967). Diabetic neuropathy: influence of study. Hormone and Metabolic Research, 3, 386-392.
age, sex, metabolic control and duration of diabetes on
motor conduction velocity. Neurology (Minneap.), 17, Olsson, Y., and Sourander, P. (1968). Changes in the
972-980. sympathetic nervous system of diabetes mellitus. A
Kott, I., Urca, I., and Sandbank, U. (1974). Lumbar preliminary report. Journal of Neurovisceral Relations,
sympathetic ganglia in atherosclerotic patients, diabetic 31, 86-95.
and non-diabetic. Archives of Surgery, 109, 787-792. Rundles, R. W. (1945). Diabetic neuropathy. General
Lamontagne, A., and Buchthal, F. (1970). Electro- review with report of 125 cases. Medicine (Balt.), 24,
physiological studies in diabetes mellitus. Journal of 111-160.
Neurology, Neurosurgery and Psychiatry, 33, 442-452. Sharpey-Schafer, E. P., and Taylor, P. J. (1960). Absent
Lawrence, D. G., and Locke, S. (1961). Motor nerve circulatory reflexes in diabetic neuritis. Lancet, 1,
conduction velocity in diabetes. Archives of Neurology 559-562.
(Chic.), 5, 483-489. Skillman, T. G., Johnson, E. W., Hamwi, G. J., and
Locke, S. (1967). Axons, Schwann cells and diabetic Driskill, H. J. (1961). Motor nerve conduction velocity
neuropathy. Bulletin of the New York Academy of in diabetes mellitus. Diabetes, 10, 46-51.
Medicine, 43, 784-791.
Low, P. A., Walsh, J. C., Huang, C. Y., and McCleod,
Smith, B. (1974). Neuropathology of the oesophagus in
diabetes mellitus. Journal of Neurology, Neurosurgery,
J. C. (1975). The sympathetic nervous system in diabetic and Psychiatry, 37, 1151-1154.
neuropathy-a clinical and pathological study. Brain,
98, 341-356. Thomas, P. K. (1971). The morphological basis for
Martin, M. M. (1953a). Diabetic neuropathy. A clinical alterations in nerve conduction in peripheral, neuro-
study of 150 cases. Brain, 76, 594-624. pathy. Proceedings of the Royal Society of Medicine, 64,
295-298.
Martin, M. M. (1953b). Involvement of autonomic nerve
fibres in diabetic neuropathy. Lancet, 1, 560-565. Thomas, P. K., and Lascelles, R. G. (1965). Schwann cell
abnormalities in diabetic neuropathy. Lancet, 1,
Mulder, D. W., Lambert, E. H., Bastron, J. A., and 1355-1357.
Sprague, R. G. (1961). The neuropathies associated with
diabetes mellitus. A clinical and electromyographic Thomas, P. K., and Lascelles, R. G. (1966). The pathology
study of 103 unselected diabetic patients. Neurology of diabetic neuropathy. Quarterly Journal of Medicine,
(Minneap.), 11, 275-284. 35, 489-509.
Murray, A., Ewing, D. J., Campbell, I. W., Neilson, Ward, J. D., Barnes, G. C., Fisher, D. J., Jessop, J. D., and
J. M. M., and Clarke, B. F. (1975). RR interval varia- Baker, R. W. R. (1971). Improvement in nerve con-
tions in young male diabetics. British Heart Journal, duction following treatment in newly diagnosed
37, 882-885. diabetes. Lancet, 1, 428431.
Downloaded from jnnp.bmj.com on May 26, 2013 - Published by group.bmj.com

Peripheral motor nerve


function in diabetic autonomic
neuropathy.
D J Ewing, A A Burt, I R Williams, et al.

J Neurol Neurosurg Psychiatry 1976 39: 453-460


doi: 10.1136/jnnp.39.5.453

Updated information and services can be found


at:
http://jnnp.bmj.com/content/39/5/453

These include:
Email alerting Receive free email alerts when new articles cite
service this article. Sign up in the box at the top right
corner of the online article.

Notes

To request permissions go to:


http://group.bmj.com/group/rights-licensing/permissions

To order reprints go to:


http://journals.bmj.com/cgi/reprintform

To subscribe to BMJ go to:


http://group.bmj.com/subscribe/

You might also like