Update Article
Approach to a Case of Autonomic Peripheral
Neuropathy
D Chowdhury*, N Patel**
Abstract
Autonomic neuropathy is the term used to describe autonomic disturbances resulting from diseases of the
peripheral autonomic nervous system. This is a group of disorders in which the small, lightly myelinated and
unmyelinated autonomic nerve fibers are selectively targeted. Most often, autonomic neuropathies occur in
conjunction with a somatic neuropathy (i.e. with motor weakness and/or sensory loss), but they can occur in
isolation. Causes of autonomic neuropathies are immune-mediated, paraneoplastic, infectious, toxic and
drug-induced, hereditary, nutritional and idiopathic. Amongst all, diabetes mellitus is the most common
cause. Autonomic features, which involve the cardiovascular, gastrointestinal, urogenital, sudomotor, and
pupillomotor systems, occur in varying combination in these disorders. Orthostatic hypotension is often the
first recognized and most disabling symptom. Noninvasive, well-validated clinical tests of autonomic
functions along with a host of laboratory tests are of immense value to diagnose the presence and to demonstrate
the distribution of autonomic failure. Treatment aims to treat specific cause of the autonomic neuropathy (if
possible) and to control symptoms of autonomic dysfunction. Present review attempts to outline clinical
approach to a case of autonomic peripheral neuropathy. ©
R
apid adjustments in vital physiologic mechanisms
critical to survival are accomplished by the
autonomic nervous system (ANS). From anatomical
point of view, ANS is divided into two parts:
parasympathetic (craniosacral) and sympathetic
(thoracolumbar). Disorders of the ANS may result from
central nervous system (CNS) or peripheral nervous
system (PNS) causes. Peripheral neuropathies are the
most common cause of chronic autonomic insufficiency.1
Autonomic nerve fibers are the small, lightly myelinated
(type B, preganglionic fibers) and unmyelinated (type C,
postganglionic fibers). These fibers are affected in most
symmetrical peripheral neuropathies. This involvement
is mild or subclinical in many cases. However, in a group
of peripheral neuropathies, autonomic fibers are
predominantly involved.2 Autonomic neuropathy is the
term used to describe autonomic disturbances resulting
from diseases of the peripheral autonomic nervous
system.3 Present review attempts to outline clinical
approach to a case of autonomic peripheral neuropathy.
The review is presented in the form of questions, which
a clinician is likely to ask when confronted with a case
of autonomic neuropathy.
What are The Causes of Autonomic Peripheral
Neuropathy?
Various causes of autonomic neuropathies are
enumerated in Table 1. Diabetes mellitus is the most
common cause of autonomic neuropathy.2
How do Autonomic Neuropathy Manifest Clinically?
The autonomic nervous system (ANS) modulates
numerous body functions, and therefore, dysfunction of
this system can manifest with numerous clinical
phenotypes. Most often, they occur in conjunction with
a somatic neuropathy (i.e. with motor weakness and/or
sensory loss) as in Gullain-Barre syndrome (GBS), but
they can occur in isolation (as in pandysautonomia).
Various autonomic abnormalities seen in a case of
autonomic neuropathy are as follows:5
Cardiovascular:
Orthostatic hypotension (OH)- symptoms of
orthostatic giddiness. May be associated with
palpitations, nausea, pallor or tremulousness.
In severe cases, episodes of syncope can occur
after standing up from supine position.
*Associate Professor; **Senior Resident, Department of
Neurology, GB Pant Hospital, New Delhi 110 002.
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Labile hypertension
Brady and tachyarrhythmias- may present with
palpitations or syncope
Gastrointestinal:
Dysphagia, constipation, episodic diarrhoea,
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Table 1 : Causes of autonomic neuropathies
Immune-mediated
causes
Related to systemic
disease
Infectious causes
Toxic causes
Drug induced
Hereditary
Nutritional
Idiopathic
neuropathy
Acute pandysautonomia
Gullain-Barre syndrome (GBS)
Paraneoplastic
Lambert-Eaton myasthenic
syndrome (LEMS)
Connective tissue diseases
Postural orthostatic tachycardia
syndrome (POTS)
Inflammatory bowel disorder–
related causes
Chronic inflammatory demyelinating
polyneuropathy (CIDP)
Diabetic neuropathy
Acquired amyloid neuropathy
Uremic neuropathy
Hepatic disease- related causes
Botulism
Leprosy
Chaga's disease
Human immunodeficiency virus
Diphtheria
Alcohol
Heavy metals
Organic solvents
Acrylamide
Hexacarbons
Vincristine
Cisplatin
Taxols
Vacor
Amiodarone
Perhexiline
Pyridoxine
Hereditary sensory and autonomic
neuropathy (HSAN)
Fabry disease
Tangiers disease
Familial dysautonomia
Vitamin B12 deficiency
Idiopathic distal small-fiber
Chronic idiopathic anhidrosis
Note: Modified from (3) and (4)
fecal incontinence, gastroparesis (cause
persistent fullness and subsequent abdominal
pain and vomiting), early satiety, bloating
Urogenital:
Urinary retention or incontinence, bladder
urgency, bladder frequency, nocturia, enuresis,
incomplete bladder voiding, impotence, loss of
ejaculation, retrograde ejaculation, vaginal
dryness
Thermoregulatory:
Hypothermia, hyperpyrexia
Secretomotor:
Anhidrosis or hypohydrosis (mainly in feet),
hyperhidrosis (in feet/hands/head), gustatory
sweating, dryness of mouth/eyes, excessive
salivation
728
Pupillomotor:
Abnormalities of size (presents with blurred
vision, glare in bright sunlight, difficulty in
focusing, poor night vision)
Skin and joints:
Feeling of coldness, acrocyanosis, pallor,
mottling or redness (vasomotor changes)
Loss of hair, nail thickening/ discolouration
Charcot’s joints: misshaped, crepitus, excessive
range of movement, pain
In general, some symptoms, such as those of
orthostatic intolerance, are common in autonomic
neuropathies, whereas other symptoms, such as
complete anhidrosis, are rare as primary manifestation.
OH is often the first recognized symptom and typically
is the most disabling.
Most autonomic neuropathies have symptoms of
sympathetic as well as parasympathetic dysfunction.
However, some neuropathies may have only sympathetic
(pure adrenergic neuropathy) or parasympathetic (pure
cholinergic neuropathies like chronic idiopathic
anhidrosis and Lambert-Eaton myasthenic syndrome
(LEMS)) dysfunction.3
Many hereditary autonomic neuropathies,
neuropathies seen in connective tissue diseases, leprosy,
acquired immunodeficiency syndrome (AIDS),
diphtheria, lyme disease, uremia, chronic inflammatory
demyelinating neuropathy (CIDP) and alcoholic
neuropathies have mild autonomic dysfunction, which
is usually clinically unimportant. While in neuropathies
associated with diabetes, amyloidosis and in chronic
paraneoplastic autonomic neuropathies, autonomic
involvement is severe and clinically important. 3
Most autonomic neuropathies are chronic in nature
and have insidious onset of symptoms. Some
neuropathies, like acute pandysautonomia, GBS,
botulism, porphyria, drug-induced and toxic autonomic
neuropathies, have acute to subacute onset of the
symptoms.3
Detailed family history may yield information about
possible inherited forms of autonomic neuropathy. In
some cases, involvement may be subtle in certain family
members, thus escaping detection.
WHAT ARE THE SALIENT FEATURES OF
VARIOUS AUTONOMIC NEUROPATHIES?
Diabetic autonomic neuropathy : It typically presents
late in the course of diabetes and is generally
accompanied by other features of distal sensorimotor
polyneuropathy. There is an increase in overall mortality
and sudden death in patients with diabetic autonomic
neuropathy.2 Erectile failure is present in 30-75% of
diabetic men6 and can be the earliest symptom of diabetic
autonomic neuropathy.2 Constipation and diabetic
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© JAPI • VOL. 54 • SEPTEMBER 2006
gastroparesis are two important manifestations in
diabetics, seen in 60% 7 and 50% 8 of the patients
respectively.
Acute and subacute autonomic neuropathies : Autonomic
dysfunction of various degrees has been reported in 65%
of patients of GBS admitted to the hospital.9 Serious
cardiac arrhythmias tend to be more frequent in GBS
patients with severe quadriparesis and respiratory
failure.10
Acute pandysautonomia is characterized by the rapid
onset of combined sympathetic and parasympathetic
failure without somatic and motor involvement,
although reflexes are usually lost during the course of
the illness. About half of the patients have autoantibodies
to ganglionic acetylcholine receptors, which may play a
pathogenic role.10 Only 40% of the patients recover fully
to premorbid status.2 Like GBS, this illness may present
as post/ parainfectious event3 and these patients may
have mild sensory-motor signs and cytoalbuminological dissociation in cerebrospinal fluid.11
Because of these similarities, acute and subacute
pandysautonomias are sometimes considered as GBSvariants.11 Acute dysautonomias can be restricted to the
cholinergic system (acute cholinergic neuropathy).3
Dysautonomia is common in acute intermittent
porphyria, and autonomic overactivity predominates
over autonomic failure, although both are present and
often coexistent.3
Botulism presents with the acute development of
cholinergic failure, ptosis, ophthalmoplegia, bulbar
weakness and generalized neuromuscular paralysis.3
Dilated pupils, with poor response to light and
accommodation, are characteristic autonomic signs. The
illness begins with gastrointestinal manifestations.2
Typically, the symptoms begin 12-36 hours after the
ingestion of home-canned food contaminated by
Clostridium botulinum.3
Hereditary autonomic neuropathies : Hereditary sensory
autonomic neuropathy (HSAN) is a group of
neuropathies characterized by prominent sensory loss
with autonomic features but without significant motor
involvement. Currently, these neuropathies are divided
into five main groups (HSAN I-V). HSAN is distinctly
rare. Sensory loss in HSAN predisposes to unnoticed,
recurrent trauma that may lead to neuropathic joints,
nonhealing ulces, infections, and acral mutilations. Out
of five types, HSAN I is the only autosomal dominant
disorder and it is the most common familial sensory
neuropathy.10 Autonomic manifestations are most
prominent in type III HSAN (Riley-Day syndrome or
familial dysautonomia). The axon-reflex mediated,
vasomotor response (the flare) after intradermal
histamine is absent in all HSAN.12
Fabry’s disease is an X-linked recessive disorder. It is
characterized by severe, paroxysmal pains in the hands
© JAPI • VOL. 54 • SEPTEMBER 2006
and feet, a truncal reddish-purple maculopapular rash,
and angiectases of the skin and mucous membrane,
together with the painful distal peripheral neuropathy,
progressive renal disease, corneal opacities, and
cerebrovascular accidents.2,10 Autonomic manifestations
include decreased sweat, saliva and tear production,
impaired cutaneous flare response, and disordered
intestinal motility.2
Amyloid neuropathy : Autonomic dysfunction
commonly accompanies the polyneuropathy of both
primary (AL; associated with immunoglobulin light
chains) and hereditary (familial amyloid
polyneuropathy, autosomal dominant) amyloidosis.
These patients have other systemic features including
hepatomegaly, macroglossia, cutaneous ecchymosis,
cardiomyopathy, and nephrotic-range proteinuria.2,10
Paraneoplastic autonomic neuropathies : This occurs
frequently in association with anti-Hu antibodies. These
antibodies are commonly found in patients with smallcell lung carcinoma, but can also occur in non-small cell
lung carcinoma and malignancies of gastrointestinal
tract, prostate, breast, prostate, bladder, kidney, pancreas,
testis, and ovary. Autonomic neuropathy can be the sole
manifestation of an anti-Hu related paraneoplastic
disorder or part of general paraneoplastic syndrome.13,14
Autoantibodies specific for neuronal nicotinic
acetylcholine receptors in the autonomic ganglia also
have been found in patients with paraneoplastic
autonomic neuropathy.10 Malignancies associated with
these antibodies include small-cell lung carcinoma,
thymoma, bladder carcinoma, and rectal carcinoma.2
LEMS is an acquired presynaptic disorder of
neuromuscular transmission that cause weakness
similar to that of myasthenia gravis, cranial nerve
abnormalities, depressed or absent reflexes, and
autonomic changes like dry mouth and eyes, impotence,
constipation, and bladder symptoms. Abnormalities are
predominantly restricted to parasympathetic nervous
system. Majority of the cases are paraneoplastic.15,16
Miscellaneous : Acute, subacute and chronic autonomic
dysfunctions can occur in settings of connective tissue
diseases including systemic lupus erythematosus,
scleroderma, mixed connective tissue disease and
especially, Sjogren syndrome.2,3
In leprous neuropathy, focal anhydrosis occurs in
association with impaired pain and temperature
perception in the cooler parts of the body. These symptoms
are the earliest neurological manifestations of leprosy.17
Of all cytotoxic agents, clinically evident
dysautonomia occurs most consistently with vincristine.
The abnormalities generally reverse several months after
the drug is stopped.18
Postural orthostatic tachycardia syndrome (POTS) is
characterized by symptomatic orthostatic intolerance
(not OH) and an increase in heart rate to >120/min or
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729
by 30/min with standing, most commonly in young
adult women.1
WHAT ARE THE IMPORTANT POINTS/ TESTS
FOR CLINICAL EXAMINATION OF
AUTONOMIC NEUROPATHY?
Examination of skin, mucous membrane, nails and
joints may indicate presence of autonomic dysfunction.
Careful general examination may also give clue to the
etiology. For example, characteristic skin changes are
observed in leprosy and angiokeratoma of the trunk is
suggestive of Fabry’s disease. Occurrence of arthritis
and rash can suggest a connective tissue disorder.
Pupillary examination may reveal Argyl-Robertson
pupil, Horner’s syndrome or tonic pupils. Detailed
neurological evaluation with special emphasis on motor
and sensory system examination is important to detect
associated somatic peripheral neuropathy. Presence of
pyramidal, extrapyramidal, or cerebellar signs indicate
a separate neurological disorder of the autonomic
nervous system like multisystem atrophy or Parkinson’s
disease.
Noninvasive, well-validated clinical tests of
autonomic functions are very useful and widely used.
These tests are of immense value to diagnose the presence
and to demonstrate the distribution of autonomic
failure.19 These tests are summarized in Table 2.
A combination of these tests is usually required
because certain ones are sensitive to sympathetic
dysfunction and others to parasympathetic
dysfunction.20 No food, coffee, or nicotine is permitted
for 3 hours before the tests. Medications affecting ANS
are stopped for five half-lives.19
Measurement of lying, sitting and orthostatic blood
pressure to detect a postural decrease is one of the
simplest bedside clinical tests of autonomic function.
Sustained drops in systolic (>20 mm Hg) or diastolic
(>10 mm Hg) BP after standing for at least 2 min that are
not associated with an increase in pulse rate of >15 beats
per minute suggest autonomic deficit. In nonneurogenic
cause of OH (e.g. hypovolemia), the BP drop is
accompanied by a compensatory increase in heart rate
of > 15 beats per minute.1 Cold pressure test and isometric
exercise test have not been well validated clinically.20
Electrocardiography can be used to monitor heart rate
while examiner observes respiratory rhythm to
determine if normal respiratory variations are present.
Beat-to-beat BP and pulse monitoring is required to
record changes in these parameters during Valsalva
maneuver. Sympathetic skin response (SSR) can be done
in electrophysiology laboratory. Special laboratory
equipments are required for thermoregulatory sweat test
Table 2 : Autonomic function testing2,19,20
Tests
1.
2.
3.
1.
2.
3.
4.
1.
2.
3.
4.
1.
1.
2.
3.
1.
1.
730
Normal
Response
Tests for cardiac parasympathetic nervous system function
Heart rate variability with deep respiration
1. Maximum minus minimum heart rate
(respiratory sinus arrhythmia)
>/= 15 beats/min E:I ratio 1.2 (age-dependent)
Heart rate response to Valsalva maneuver
2. Valsalva ratio >/= 1.4
Heart rate response to standing
3. Increase 11-90 beats/min; 30:15 ratio >/=1.04
Tests for sympathetic adrenergic function
Blood pressure response to upright posture
1. Fall in BP </= 30/15 mm Hg
Blood pressure response to Valsalva maneuver
2. Phase1- BP rise, phase 2- gradual reduction to
plateau, phase 3- fall, phase 4- overshoot
Cold pressor test
3. Rise in BP by 15-20/10-15 mmHg
Isometric exercise test
4. Rise in systolic-diastolic BP >/= 15 mmHg
Tests for sympathetic cholinergic function
Thermoregulatory sweat testing (TST)
1. Normal pattern of colour change of the indicator
over all body and limbs
Quantitative sudomotor axon reflex test (QSART)
2. Pattern of normal sweating over all body and limbs
Sympathetic skin response (SSR)
3. Recordable response
Sweat imprint methods
4. Normal sweating all over body and limbs
Tests for lacrimal function
Schirmer’s test
1. Length of moistened area 11-15 mm
Pressor infusion test
Blood pressure response to infusion of noradrenaline
1. Rise in BP and slowing of heart rate
Blood pressure response to infusion of angiotensin II
2. Rise in BP and slowing of heart rate
Heart rate response to atropine and neostigmine
3. Rise in BP and slowing of heart rate
Cutaneous flare response
Cutaneous flare response to intracutaneous
1. One cm wheal after 5-10 minutes, surrounded
histamine or skin scratch
by red areola, which in turn surrounded by erythematous
flare that extends 1-3 cm beyond the border of wheal
Tests for pupillary denervation
Response to instillation of topical
1. Depends on agent used
pharmacological agents (e.g. cocaine)
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(TST) and quantitative sudomotor axon reflex test
(QSART). 19,21 They respectively assess capacity to
produce sweat qualitatively and quantitatively. 1
Quinirazine or Alizarine red is used as sweat indicator
powder in TST.19
How to Investigate a Case of Autonomic
Neuropathy?
Although clinical diagnosis is essential for diagnosing
autonomic neuropathies, special studies can be helpful
in identifying a particular autonomic neuropathy. In
most cases, the laboratory assists in identifying
subclinical or subtle changes.
Various tests for laboratory assessment of autonomic
neuropathy are enumerated in Table 3.
In pure autonomic neuropathies, because the involved
fibers are small myelinated and unmyelinated fibers,
nerve conduction study can be normal. Plasma
catecholamine measurements have been used as an
index to separate postganglionic from preganglionic
failure. In a disorder where the lesion is preganglionic,
resting supine NE is normal, but the response to the
standing will be reduced or absent. In a postganglionic
lesion, the supine values would be reduced if the lesion
is widespread. 21 Measurements of plasma
norepinephrine levels are low and do not rise on headup tilt table testing in pandysautonomia.19 For evaluation
of bladder dysfunction cystometrogram is required, while
barium studies are useful for gastrointestinal
Table 3 : Laboratory assessment of autonomic
neuropathy2
Chemistry, hematology, and pathology
Complete blood count and differential
Fasting blood glucose or glucose tolerance test
HIV testing
Immunoelectrophoresis of blood and urine
Plasma norepinephrine (supine and standing)
Porphyria investigations- urinary porphyrin concentration
Genetic testing for inherited neuropathies
Fat aspirate, rectal biopsy, or gingival biopsy for amyloid
Autoantibody assessment
Antinuclear antibody
Rheumatoid factor
Anti-Ro/SS-A, Anti-La/SS-B
Antibodies to P/Q-type calcium channel
Antibodies to acetylcholine receptor
Paraneoplastic antibodies- anti-Hu, Purkinje-cell cytoplasmic
antibodies type 2 etc.
Electrophysiological studies
Nerve conduction studies (including repetitive stimulation)
Qauntitative sensory testing
Table 4 : Symptomatic treatment of autonomic neuropathies2,3,22
Orthostatic hypotension
Gastrointestinal dysfunction
Genital dysfunction
Urinary tract dysfunction
Labile hypertension
and tachyarrhythmias
hyperhydrosis
-Plenty of fluids (up to 10 L/day)
-Adequate salt intake (up to 10 g/day)
-Mineralocorticoid: 9-α-fludrohydrocortisone (0.1-0.3 mg/day)
-α –receptor agonist: Midodrine (2.5 mg to 10 mg tds)
-Gastroparesis:
Control of blood sugars
Low fat content of diet
Prokinetics: Metochlopramide (10 mg p.o. 30 mins before meals)
Domperidone (10-20 mg qds)
Erythromycin (250 mg tds)
-Bowel Hypomotility:
Increased intake of high fiber diet with plenty of fluids
Stool softeners and osmotic laxative
-Bowel hypermotility:
Restriction of lactose and gluten
Cholestyramine, clonidine, somatostatin analogue, metronidazole
-Erectile failure:
PDE 5 inhibitors: Sildenafil (50 mg), Tadafil (20 mg) etc.
Caution: ischemic heart disease, hypotension,
significant OH, concomitant nitrates
Intracorporal injection of vasoactive substances e.g. papavarine and PGE
Transurethral delivery of vasoactive agents
Mechanical devices e.g. vacuum erection device, constricting rings
Penile prosthetic implants
-Vaginal lubricants & estrogen creams
-Timed voiding schedules
-Bladder contraction increased by Crede maneuver
-Clean intermittent self catheterization (For impaired detrusor activity)
-Cholinergic agents: Bethanecol (10-30 mg tds) in detrusor areflexia
-Anticholinergic agents: Tolterodine tartrate (2 mg bid) for overactive bladder
-Betablockers (propranolol)
-Anticholinergic Agents: trihexyphenidyl, glycopyrrolate
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731
dysfunction.20 Nocturnal penile tumescence can be
recorded in sleep laboratory.20
How to Treat a Patient with Autonomic Neuropathy?
Treatment aims to treat specific cause of the autonomic
neuropathy (if possible) and to control symptoms of
autonomic dysfunction. Adequate control of blood sugar
is very important in diabetic neuropathy. Steroids and
intravenous immunoglobulins are helpful in immunemediated neuropathies. Immediate withdrawal of
offending drug or toxin is necessary. As most of the
autonomic neuropathies are not completely reversible,
symptomatic management holds very important place
in these cases. It is summarized in Table 4.
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Announcement
XVII Annual Conference of Association of Physician of India Assam Chapter APICON Assam 2006 will
be held at Tezpur from 15th to 17th December 2006.
For further details please contact : Dr. P Barooah (President) or Dr. AC Saikia (Organizing Secretary), IMA
House P.O. Tezpur Dist. Sonitpur: Assam
Phone : 03712-221658,03712-252120;
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Email: Saikia_ atul@rediffmail.com
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