http://cmbi.bjmu.edu.cn/heart973net/db-disease/Praxis%20Medicin e%20-%20autonomic%20nervous%20system%20dis.files/cpmref.files/cpmref_mai n.htm

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for anyone curious about bethanechol chloride and other treatment

options, this is a solid source my doctor put me on to, even before I

joined this group.

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[image][image] [image][image]

Key Points

[image]

[image]

[image][image] The autonomic nervous system regulates body

temperature, circulation, respiration, digestion,

metabolism, and bladder and sexual function.

[image][image] Autonomic nervous system disorders are

important

but underrecognized causes of symptoms.

[image][image] The symptoms of autonomic nervous system

dysfunction often are nonspecific. Autonomic

nervous system dysfunction may be hard to confirm

by clinical examination.

[image][image] Laboratory testing is valuable to confirm

autonomic nervous system dysfunction.

[image][image] Autonomic nervous system dysfunction can be

restricted to one organ or may be widespread,

involving all organs innervated by the autonomic

nervous system.

[image][image] Treatment is largely symptomatic and is

directed

to the specific symptoms of the autonomic nervous

system dysfunction.

[image]

Structure and Function

[image]

[image]

[image]

The autonomic nervous system (ANS) consists of two main divisions:

sympathetic and parasympathetic (Fig. 1). Both have various centers

in the brain, with descending pathways to the brain stem and spinal

cord. Sympathetic nerve fibers leave through the thoracic and upper

lumbar spinal nerve roots and enter the ganglia of the

paravertebral sympathetic chain. Postganglionic fibers then travel

with peripheral nerves and arteries to supply various organs and

structures. Parasympathetic fibers leave the central nervous system

(CNS) through some of the cranial and sacral spinal nerves to reach

the parasympathetic ganglia, which are smaller than the sympathetic

ganglia and are located close to their effector organs.

[Click here to view full sized image] Figure 1

The peripheral autonomic

nervous system.

view larger image

[image]

The classic transmitters of the peripheral ANS are acetylcholine

and noradrenaline (Fig. 2). Neuropeptides have been identified as

important cotransmitters.

[Click here to view full sized image] Figure 2

Classic neurotransmitters of

the autonomic nervous

system. A[image]adrenaline;

ACh[image]acetylcholine; NA

[image]noradrenaline.

view larger image

[image]

The ANS regulates bodily activities that are not under ordinary

voluntary control (eg, temperature, circulation, respiration,

digestion, metabolism, and the activity of the genitourinary

system). The two divisions of the ANS often function as physiologic

antagonists, and it is the balance of their activities that

maintains good function in an organ.

[image]

Heart rate mainly is controlled by parasympathetic (vagus) nerves,

with less input from the sympathetic nerves. Blood pressure mainly

is regulated by the sympathetic system. Both are reflexly activated

by the baroreceptors. The gastrointestinal tract is innervated by

the enteric nervous system, to which both ANS divisions contribute.

This system controls gut motility, secretions, and blood flow. The

storage and elimination of urine depend on the integrated activity

of the bladder and the urethral sphincters. Both sympathetic and

parasympathetic nerve fibers contribute. The ANS also controls

sexual function: penile or clitoral engorgement, glandular

secretion, emission, and ejaculation. In the eyes, the ANS supplies

the pupils, the ciliary muscles controlling accommodation, and the

tear glands. Autonomic fibers to the skin innervate the sweat

glands and blood vessels and are thus important in temperature

regulation.

[image]

Clinical Evaluation

[image]

[image]

[image]

Symptoms suggesting autonomic dysfunction are listed in Table 1.

The clinical examination for autonomic dysfunction is limited. One

of the few reliable signs is orthostatic hypotension (systolic

blood pressure fall > 20 mm Hg, diastolic blood pressure fall >

10

mm Hg, or both when the patient goes from lying to standing). The

postural fall may be immediate or delayed and occasionally becomes

apparent only after exercise. Careful examination of the pulse rate

on standing may show a lack of tachycardia in a patient with

disordered cardiac innervation, but usually an electrocardiogram is

required to detect this feature. Abnormally reacting pupils may be

readily detected, but dryness of the eyes, mouth, or skin is often

difficult to ascertain clinically.

[image]

Table 1 Symptoms of autonomic dysfunction

Postural faintness or loss of consciousness

Gastrointestinal dysfunction

Bloating

Diarrhea

Constipation

Rectal incontinence

Bladder dysfunction

Sexual dysfunction

Poor erections

Impaired ejaculation

Decreased or increased sweating

Dry mouth or dry eyes

Blurring of near vision

Cold or discolored extremities

[image]

Tests of ANS function

[image]

[image]

[image]

Tests of autonomic function (Table 2) are gradually becoming more

readily available in laboratories dedicated to ANS testing [1

[image]].

[image]

Table 2 Tests of autonomic nervous system function

Function Type of

test

Heart rate Measures the reduced heart

rate response to

standing, to deep breathing, and to Valsalva

maneuver

Blood pressure Uses a continuous noninvasive monitor that

records

blood pressure following changes of posture on a

tilt table and/or from lying/standing and/or

during Valsalva maneuver, also prolonged

tilt-table testing for vasovagal syncope

Sweating Determines the

areas of sweating by the change in

color of heat-sensitive powders on the skin after

whole-body warming

Evaluates responses to injected or iontophoresced

sweat-stimulating chemicals (acetylcholine or

pilocarpine)

Uses bioelectric skin potentials (sympathetic skin

responses)

Gut motility Transit times are evaluated

radiologically by

barium meal studies, radiopaque pellets, and

chemical markers

Bladder Uses a

urodynamic battery of tests

Cystometrography

Urethral pressure profiles

Uroflowmetry

Pudendal nerve conduction studies

Sphincter electromyography

Sexual function Evaluates nocturnal erections by penile

tumescence

testing in a sleep laboratory

Measures blood pressure in the penis using Doppler

techniques

Determines prolactin levels; if elevated, a

pituitary prolactinoma is present

Uses intracavernous papaverine injections to

produce erections in patients with psychogenic or

neurogenic impotence but not with arterial

insufficiency

Pupils Shows

brisk constriction with dilute pilocarpine

in Adie[image]s pupils

Produces pupillary dilatation with

hydroxyamphetamine drops in Horner[image]s

syndrome when damage lies in the central nervous

system

Lacrimation Uses Schirmer strips (a thin

band of absorbent

paper is inserted into the lower eyelid for 5

min); moistening of less than 5 mm is abnormal

[image]

Clinical Syndromes

[image]

[image]

[image]

Clinical disorders of the ANS can be conceptualized in a manner

similar to other neurologic disorders. They may involve the CNS or

the peripheral nervous system, or both; they may be focal or

restricted (eg, Horner[image]s syndrome) or involve the ANS

diffusely; therefore, they are called generalized dysautonomias

(eg, pure autonomic failure). Dysautonomias also can be considered

primary (degenerative disorders) or secondary to traumatic,

vascular, or other identifiable causes.

Orthostatic Hypotension

[image]

[image]

Orthostatic hypotension has many causes, only some of which involve

the ANS (Table 3). Patient history and examination often reveal the

cause, but some individuals require extensive medical and

neurologic investigations to establish the etiology.

[image]

Table 3 Disorders associated with orthostatic

hypotension

Central nervous system disorders

Multiple system atrophy

Parkinson[image]s disease

Wernicke[image]s encephalopathy

Posterior fossa tumors

Brain stem lesions

Spinal cord lesions

Peripheral nervous system disorders

Diabetes mellitus

Pure autonomic failure

Acute dysautonomia

Peripheral neuropathies (acute or chronic)

Medications

Antihypertensive agents

Diuretics

Antianginal medications

Phenothiazines

Levodopa

Impaired circulation

Hypovolemia

Anemia

Electrolyte disturbances (metabolic or hormonal)

Adrenal insufficiency

Pheochromocytoma

Orthostatic hypotension of the elderly

[image]

Vasovagal (Neurocardiogenic) Syncope

[image]

[image]

Vasovagal syncope is an acute hemodynamic event that consists of

bradycardia and hypotension resulting in a marked reduction in

cardiac output and cerebral perfusion. Episodes may be triggered by

the sight of blood or needles or by other stimuli ([image]reflex

syncopes[image]) but often occur spontaneously. The cause is

unknown. There appears to be a sudden excess of vagal impulses to

the heart (producing bradycardia) and a concomitant withdrawal of

sympathetic vasoconstrictor impulses to the blood vessels

(producing hypotension) [2]. Recording the pulse and blood pressure

during a prolonged tilt of 60?or more on a tilt table often

reproduces these events and is a useful diagnostic test [3].

[image]

Multiple System Atrophy

[image]

[image]

Multiple system atrophy (MSA) is a progressive neurologic disorder

with prominent autonomic dysfunction [4,5]. When ANS features

predominate, the term Shy-Drager syndrome is used. When

parkinsonian features predominate, the disorder is often designated

striatonigral degeneration. When ataxia and corticospinal tract

involvement are prominent, the disorder is often labeled

olivopontocerebellar atrophy. All conditions are thought to be

variants of a widespread CNS degenerative disorder, the cause of

which is unknown. MSA is relentlessly progressive, with death

occurring within 7 years of onset.

[image]

Pure Autonomic Failure

[image]

[image]

Pure autonomic failure is a chronic disorder that produces mainly

orthostatic hypotension, male sexual dysfunction, and bladder

dysfunction. Some patients develop, over time, the somatic

neurologic features of MSA.

[image]

Parkinson[image]s Disease

[image]

[image]

About 10% of patients with Parkinson[image]s disease have

dysautonomic symptoms. Orthostatic hypotension may be unmasked or

worsened by the medications used to treat Parkinson[image]s

disease.

[image]

Diabetes Mellitus

[image]

[image]

Diabetic patients can develop various dysautonomias: restricted or

generalized, symptomatic, or those detected only by special tests

[6,7[image]]. They often are associated with generalized peripheral

neuropathy. Orthostatic hypotension can be a serious problem.

Cardiac innervation also can be affected, producing a resting

tachycardia, a fixed heart rate, and reduced heart rate variations

on lying to standing. This abnormal cardiac innervation may

contribute to the sudden and unexplained deaths in patients with

diabetic autonomic neuropathy. Gastric atony causes abdominal

distention, nausea, and vomiting. Midgut and lower gut dysfunction

causes diarrhea that is often intermittent, worse at night, and

associated with abdominal cramps and anorectal incontinence. It is

uncertain whether bacterial overgrowth or autonomic neuropathy is

the more important cause; improvement with antibiotics suggests the

former. Sexual dysfunction affects up to 40% of diabetic men. The

principal cause is probably autonomic neuropathy, but vascular

factors may contribute. Sexual function in diabetic women is

thought to be normal. Some patients develop atonic bladders caused

by the loss of bladder sensation and detrusor and sphincter

dysfunction. Urinary tract infections with fibrosis and scarring

worsen the situation. Decreased sweating distally in the limbs is

common in patients with diabetic polyneuropathy but is of little

importance. Gustatory sweating (excessive sweating on the face or

torso when eating, sometimes only specific foods) can be

troublesome. Hypoglycemic unawareness, with a lack of sweating and

tachycardia, also is caused by dysautonomia.

[image]

Orthostatic Hypotension of the Elderly

[image]

[image]

Orthostatic hypotension of the elderly is an underdiagnosed cause

of dizziness, unsteadiness, syncope, and falls. Causes are

multifactorial, including aging changes in the ANS, medications,

prolonged recumbency, and concurrent illness.

[image]

Chronic Alcoholism

[image]

[image]

Many alcoholic patients are asymptomatic, but tests of autonomic

function often reveal abnormalities. There is a divergence of

opinion about the occurrence and frequency of orthostatic

hypotension in alcoholics [8]. It has been reported to be frequent

in those with Wernicke[image]s encephalopathy and chronic liver

disease. Hypothermia is common and has been attributed both to the

vasodilator effects of alcohol and to dysfunction of hypothalamic

thermoregulatory mechanisms. Decreased sweating contributes to

accidental hyperthermia in hot climates. Erectile impotence is

frequent in alcoholics, but it more often results from psychogenic

or endocrinologic causes than ANS dysfunction.

[image]

Spinal Cord Lesions

[image]

[image]

Autonomic abnormalities vary with the time after the injury or

disease onset and with the extent and cause of the damage. Trauma

is the most common cause, but similar problems occur in patients

with myelopathies caused by multiple sclerosis, acute or subacute

transverse myelitis, vascular disease, syringomyelia, and spinal

cord compression. A complete transection of the spinal cord above

T6 destroys the descending vasomotor pathways to the abdominal

vascular bed and legs; thus resting blood pressure is low, and

orthostatic hypotension can be a problem. In patients with lesions

below T6, blood pressure disturbances are less severe.

[image]

Autonomic dysreflexia is a frequent problem in quadriplegics or

paraplegics. This disorder consists of episodic hypertension

accompanied by bradycardia, sweating above the level of the spinal

cord lesion, and headache. These attacks often are precipitated by

distention of the bladder or bowel, stimulation of the skin below

the level of the lesion, or reflex spasms of the lower limb

muscles. Other autonomic abnormalities in quadriplegics and

paraplegics include bladder and male sexual dysfunction and reduced

bowel motility. Damage to the lower spinal cord or cauda equina

produces variable weakness and sensory loss in the legs and sacral

area, atonic bladder with urinary retention, anorectal

incontinence, and sexual dysfunction.

[image]

Peripheral Neuropathies

[image]

[image]

Autonomic dysfunction occurs in many patients with Guillain-Barr

[image] syndrome and includes hyperactivity or hypoactivity of

sympathetic and parasympathetic functions. Major fluctuations in

blood pressure are common. Hypotension can be caused by even low

doses of vasoactive drugs; therefore hypertension must be treated

cautiously. Sinus tachycardia is frequent, and various cardiac

arrhythmias may occur; the latter may be responsible for sudden

death in some patients. Bladder dysfunction and paralytic ileus

also may occur. The dysautonomic abnormalities are at their maximum

during the peak period of paralysis.

[image]

Acute dysautonomias present with varying combinations of

sympathetic and parasympathetic abnormalities [9]. They are thought

to be similar in cause to Guillain-Barr[image] syndrome (an acute

immune-mediated phenomenon) but with the brunt of the damage being

to the autonomic rather than the somatic nerves.

[image]

Dysautonomic symptoms and signs are uncommon in most chronic

polyneuropathies. The major exception is amyloid neuropathy [10].

This neuropathy occurs in certain types of familial amyloidosis or

in immunocyte dyscrasias with amyloidosis. The ANS dysfunction is

relentlessly progressive, with death occurring within 5 years of

diagnosis, which is made by biopsy of nerve, rectal mucosa, or

abdominal wall adipose tissue.

[image]

Peripheral Nerve Injuries

[image]

[image]

A major nerve lesion causes hypohidrosis, vasomotor impairment, and

trophic skin changes in the cutaneous distribution of the nerve.

Sometimes, excessive vasoconstriction in response to emotion or

cold occurs. Causalgia is a distinct syndrome that follows a

partial or complete lesion of a peripheral nerve. It consists of

these autonomic disturbances as well as severe pain. The

sympathetic nervous system is thought to be involved in causing

these symptoms, although the mechanism is unclear.

[image]

Reflex Sympathetic Dystrophy

[image]

[image]

Reflex sympathetic dystrophy (RSD) includes entities such as

shoulder-hand syndrome and Sudeck[image]s atrophy. The clinical

features resemble causalgia, but it is best to restrict causalgia

to denote the syndrome that follows a nerve injury. The most common

cause of RSD is a limb fracture. Other local causes include soft

tissue trauma, tendinitis, bursitis, and shoulder dislocation.

Visceral injury or diseases such as myocardial infarction and

carcinoma of the lung also can cause RSD, as can CNS lesions such

as cerebral infarctions. In approximately one third of patients,

there is no identifiable antecedent event or cause. Despite the

vasomotor and sweating abnormalities that implicate involvement of

the peripheral ANS, there is no firm evidence that this disorder

involves the ANS; the responses to treatments such as chemical

sympathectomy with intravenous guanethidine and surgical

sympathectomy are inconsistent [11].

[image]

Treatment

[image]

[image]

[image]

In many patients with disorders of the ANS no specific treatment of

the underlying disease is available; therefore treatments are aimed

at relieving symptoms [12].

Orthostatic Hypotension

[image]

[image]

Patients who are symptom free can be left untreated. Medications

that can cause or aggravate orthostatic hypotension should be

stopped (see Table 3). Patient education is important; patients can

do many things for themselves to help control symptoms [13]. They

should learn to sit awhile on the side of their bed before

standing. Before rising from a chair, they should exercise their

feet and legs. Elevating the head of the bed improves early morning

blood pressure, and some patients have been maintained

satisfactorily for years by this method solely. Salt content of the

patient[image]s diet should be increased unless there is a

contraindication, such as congestive heart failure. Elastic

stockings, if they extend to include the thighs, may help;

custom-fitted ones that extend to the midabdomen are even more

effective but are very uncomfortable. Orthostatic hypotension is

often worse after meals; thus patients should be aware of the

increased danger of standing and exercising at that time. Alcohol

with meals may add to the hypotension.

[image]

Drugs for treating orthostatic hypotension are listed in Table 4.

Doses should be titrated depending on the response. Fludrocortisone

is the drug of choice for most patients; supine hypertension,

hypokalemia, and congestive heart failure are side effects.

Midodrine is a recent and very promising medication [6]. Side

effects include supine hypertension, gastrointestinal complaints,

and urinary urgency. If these two medications, alone or in

combination, prove unsatisfactory, then treatment becomes a

trial-and-error approach using other medications listed in Table 4.

[image]

Table 4 Medications for the treatment of orthostatic

hypotension*

Mode of action

Agent

Dosage

Fluid expansion

Fludrocortisone 0.05 mg twice daily

to

0.2 mg three times per

day

Vasoconstriction

Fludrocortisone As above

Midodrine

2.5[image]10 mg three

times per day

Prevention of

Indomethacin 25 mg

three times per

vasodilation

day

Flurbiprofen 50 mg

three of four

times per day

Metoclopramide 5[image]10 mg

three

times per day

Prevention of diuresis Desmopressin acetate 10 [image]g twice

daily

nasal spray

Prevention of

Octreotide

50[image]100 [image]g

splanchnic

vasodilation

subcutaneously twice

daily

*Some drugs have more than one mode of action.

[image]

Gastrointestinal Dysfunction

[image]

[image]

In patients with gastroparesis, acceleration of gastric emptying

can be achieved with metoclopramide. Other treatments include

bethanechol, domperidone, and cisapride (Table 5). These

medications may improve coexisting constipation; stool bulk

expanders, laxatives, or enemas also can be used. Diarrhea can be

treated with antibiotics, such as tetracycline, as well as routine

antidiarrhea agents, such as codeine and loperamide. Profound

rectal incontinence in some patients with severe ANS dysfunction,

particularly in those with spinal cord damage, can be a major

problem. Continual leakage often produces sacral ulcers. A

colostomy should be considered in this situation.

[image]

Table 5 Medications for the treatment of

gastrointestinal

autonomic symptoms

Clinical sign

Agent

Dosage

Gastroparesis

Metoclopramide

5[image]20 mg 30 min

before meals and at

bedtime

Bethanechol

10[image]50 mg three

times per day

Domperidone

15[image]20 mg three or

four times per day

Cisapride

5[image]10 mg three or

four times per day

Constipation Laxatives

Enemas

Diarrhea

Tetracycline

250 mg four times per

day

Codeine

15[image]30 mg three

times per day

Loperamide

2 mg two or three times

per day

Diphenoxylate

2.5[image]5 mg three or

hydrochloride atropine

sulfate

four times per day

Clonidine

200 [image]g four times

per day

[image]

Bladder Dysfunction

[image]

[image]

Superimposed urinary tract infections must be treated. Urodynamic

tests can help to determine the type of chronic neurogenic bladder

dysfunction (the failure to store or to void). Failure to store

urine is caused by either detrusor hyperreflexia or sphincter

weakness (Table 6). Detrusor hyperreflexia may respond to a

muscarinic cholinergic blocking agent, although inability to void

may then become a side effect that could then be dealt with by

intermittent catheterization. Tricyclic antide-pressants reduce

bladder contractility and increase sphincter activity; therefore

imipramine taken at night can improve urine storage during sleep.

a-adrenergic agonists may increase urinary sphincter activity, but

urinary drainage, such as a condom catheter in men or an indwelling

catheter in women, often is required when sphincter hypoactivity is

severe.

[image]

Table 6 Medications for the treatment of autonomic

bladder

dysfunction

Disorder

Agent

Dosage

Failure to store urine

Detrusor

Propantheline 15[image]30 mg

four

hyperreflexia

times per day

Oxybutynin chloride 5 mg two to four times

per day

Sphincter

Ephedrine

25[image]50 mg four

hypoactivity

times per day

Both

Imipramine

10[image]25 mg every

night

Failure to void urine

Detrusor hypoactivity

Bethanechol

10[image]50 mg three

times per day

Urethral sphincter

Prazosin

1[image]5 mg three

spasm

times per day

[image]

Failure to void urine results from bladder-sphincter dyssynergia

and other causes (see Table 6). Detrusor hypofunction can be

managed by suprapubic tapping or compression and with bethanechol.

Prazosin sometimes reduces urethral sphincter spasm. When these

treatments fail, the best alternative is intermittent

catheterization, which is much safer than an indwelling catheter.

When this option is not practical, as, for example, in a patient

with reduced manual dexterity, an indwelling catheter can be used

in women and in some men, or surgical division of the urethral

sphincters followed by condom catheter drainage can be used in men.

[image]

Male Sexual Dysfunction

[image]

[image]

Satisfactory erections often can be achieved with papaverine or

prostaglandin E1 injections into the corpora cavernosa of the penis

[14]; or intraurethral insertion of a pellet that contains

prostaglandin E1 (alprostadil). Penile prostheses are either

semirigid and malleable or inflatable. Both types of prostheses are

associated with an impressively high degree of user satisfaction.

However, the recently released oral agent sildenafil (Viagra;

Pfizer, New York, NY) is rapidly replacing many of the older

remedies because it is more convenient and painless [15[image],16].

[image]

Key References

[image]

[image]

Recently published papers of outstanding interest, as identified in

References and Recommended Reading, have been annotated.

[image]

[image]Younger DS, Rosoklija G, Hays AP: Diabetic peripheral

neuropathy. Semin Neurol 1998, 18: 95-

104. [PubMed abstract]

[Related articles]

[image]

An excellent review of the diagnosis and management of

clinicopathologic neuropathic syndromes occuring with diabetes.

[image]

[image]Kloner RA: Viagra: What every physician should know. Ear Nose

Throat J 1998, 77: 783- 786.

[image]

This article covers the basic medical considerations involved when

prescribing sildenafil (Viagra).

[image]

[image]

References and Recommended Reading

[image]

[image]

Recently published papers of particular interest have been

highlighted as:

[image]

[image] Of interest

[image]

[image] Of outstanding interest

[image]

1.[image]Low PA: Laboratory Evaluation of Autonomic Function. In

Clinical Autonomic Disorders,

edn 2. Low PA, ed. New York:

Lippincott-Raven; 1997: 179-

208.

[image]

2.Kaufmann H: Neurally mediated syncope: Pathogenesis, diagnosis,

and treatment. Neurology 1995, 45: S12- S18.

[image]

3.Benditt DG, Ferguson DW, Grubb BP, et al.: Tilt table testing for

assessing syncope. J Am Coll Cardiol 1996, 28: 263- 275.

[PubMed

abstract] [Related articles]

[image]

4.Schatz IW, Bannister R, Kaufmann H: Consensus statement on the

definition of orthostatic hypotension, pure autonomic failure

and

multiple system atrophy. Clin Auton Res 1996, 6: 125- 126.

[image]

5.Wenning GK, Ben-Shlomo Y, Magalh?es M, et al.: Clinical features

and natural history of multiple system atrophy: Ananalysis of

100

cases. Brain 1994, 117: 835- 845.

[image]

6.Hilsted J, Low PA: Diabetic Autonomic Neuropathy. In Clinical

Autonomic Disorders, edn 2. New York: Lippincott-Raven; 1997:

487-

508.

[image]

7.[image]Younger DS, Rosoklija G, Hays AP: Diabetic peripheral

neuropathy. Semin Neurol 1998,

18: 95- 104. [PubMed

abstract] [Related

articles]

[image]

8. JD: Causes and Evaluation of Male Sexual Dysfunction. In

Clinical Autonomic Disorders, edn 2. New York:

Lippincott-Raven;

1997: 269- 276.

[image]

9.Low PA, McLeod JG: Autonomic Neuropathies. In Clinical Autonomic

Disorders, edn 2. New York: Lippincott-Raven; 1997: 463- 486.

[image]

10.Reilly MM: Genetically determined neuropathies. J Neurol 1998,

245: 6- 13. [PubMed abstract] [Related articles]

[image]

11. PR: Reflex Sympathetic Dystrophy. In Clinical Autonomic

Disorders, edn 2. New York: Lippincott-Raven; 1997: 537- 544.

[image]

12.Freeman R, Miyawaki E: The treatment of autonomic dysfunction. J

Clin Neurophysiol 1993, 10: 61- 82. [PubMed abstract]

[Related

articles]

[image]

13.on D, TL: Recent advances in the treatment of

orthostatic hypotension. Neurology 1995, 45: S26- S32.

[PubMed

abstract] [Related articles]

[image]

14. JD: Management of male sexual dysfunction. In Clinical

Autonomic Disorders, edn 2. Low PA, ed. New York:

Lippincott-Raven; 1997: 803- 807.

[image]

15.[image]Kloner RA: Viagra: What every physician should know. Ear

Nose Throat J 1998, 77:

783- 786.

[image]

16.Mobley DF, Baum N: When patients request the impotence pill.

Postgrad Med 1998, 104: 55- 66. [PubMed abstract] [Related

articles]

[image]

[image]

Select Bibliography

[image]

[image]

Low PA, ed.: Clinical Autonomic Disorders. New York:

Lippincott-Raven; 1997.

[image]

on D, Low PA, Polinsky RJ, eds.: Primer on the Autonomic

Nervous System. San Diego: Academic Press; 1996.

[image]

[image][image] [image][image]

[image]

[image]

©2000 Praxis Press Inc.

Content from Current Medicine Inc. ©2000, all rights

reserved.

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