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   Diseases of the Peripheral Nervous System Part 1
  </title><meta content="noodp, noydir"name=robots><meta content="Anatomy of the Peripheral Nervous System The peripheral nervous system (PNS) comprises all of the cranial nerves (except the first and second), the nerve roots, the spinal ganglia, the segmental nerves, the nerve plexuses, and the limb nerves. The role […]"name=description><link media="screen, projection"href=http://what-when-how.com/wp-content/themes/thesis_182/style.css rel=stylesheet><link media="screen, projection"href=http://what-when-how.com/wp-content/themes/thesis_182/custom/layout.css rel=stylesheet><link rel="shortcut icon"href=http://what-when-how.com/wp-content/uploads/2011/08/favicon.ico><link title="what-when-how RSS Feed"href=http://feeds.feedburner.com/what-when-how rel=alternate type=application/rss+xml><link href=http://what-when-how.com/xmlrpc.php rel=pingback><link href=http://what-when-how.com/xmlrpc.php?rsd rel=EditURI title=RSD type=application/rsd+xml><link href=http://what-when-how.com/wp-includes/wlwmanifest.xml rel=wlwmanifest type=application/wlwmanifest+xml><body><div class=full_width id=header_area><div class=page><ul class=menu></ul><div id=header><p id=logo><a href=http://what-when-how.com> what-when-how </a><p id=tagline>In Depth Tutorials and Information</div></div></div><div class=full_width id=content_area><div class=page><div id=content_box><div class=hfeed id=content><script language=javascript>//	navigator.CustomTag = null;</script><div class="post-223927 post type-post status-publish format-standard hentry category-acp-medicine post_box top"id=post-223927><div class=headline_area><h1 class=entry-title>Diseases of the Peripheral Nervous System Part 1</h1></div><div class="format_text entry-content"><script>google_ad_client = "ca-pub-3548356617924720";
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    google_ad_height = 90;</script><script src=//pagead2.googlesyndication.com/pagead/show_ads.js></script><h2>Anatomy of the Peripheral Nervous System</h2><p><strong> The peripheral nervous system (PNS) </strong> comprises all of the cranial nerves (except the first and second), the nerve roots, the spinal ganglia, the segmental nerves, the nerve plexuses, and the limb nerves. The role of the PNS is simple but vital: to link the central nervous system to the external environment and the milieu interieur of the body.<p><strong> Peripheral nerves are composed of fascicles </strong> of endoneurium, containing several thousand axons and various supporting cells [see Figure 1 ]. Each endoneurial fascicle is enveloped by the perineurium (several concentric layers of fibroblast-like cells). Nerve trunks are composed of several endoneurial fascicles bound together by the epineurium (a loose framework of collagen and fibroblasts). There are two complementary networks of blood vessels in nerves: (1) an epineurial system of arterioles and venules, which are tributaries of the major limb vessels, and (2) a series of capillary-like microvessels in the endoneurium. The anastomoses between these two networks are extensive, resulting in a robust supply system.<p><strong> Each axon is a longitudinal extension of a neuron cell body. </strong> The functioning and maintenance of axons depend on the cell body’s biochemical and genetic machinery. An energy-dependent bidirectional system of axonal transport shuttles structural and signaling molecules between the cell body and the axon terminal. Motor, sensory, and autonomic axons are intermingled in most nerves, but the cell bodies are grouped separately in the spinal cord and brain stem (motor), the dorsal root ganglia (sensory), and the paravertebral and somatic ganglia (autonomic).<div style=float:left;margin-top:3px;margin-bottom:3px;padding-top:3px;padding-bottom:3px;><script>google_ad_client = "ca-pub-3548356617924720";
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    google_ad_height = 280;</script><script src=//pagead2.googlesyndication.com/pagead/show_ads.js></script></div><br clear=all><p><strong> Roughly one quarter of the axons in </strong> the PNS are myelinated. Myelin is produced and maintained by Schwann cells, the most important of the supporting cells in the endoneurium. During development, Schwann cells elaborate increased amounts of cy-toplasmic membrane to form a spiral around some axons. The cytoplasmic membrane forms the lamellar wrapping of myelin. A single Schwann cell myelinates 0.2 to 1.8 mm of cytoplasmic membrane along the length of a single axon, meaning that the myelin along the entire length of a single axon is the collective product of the actions of several hundred consecutive Schwann cells. The more numerous unmyelinated axons are also intimately associated with Schwann cells. Normal development of axons and normal development of Schwann cells are interdependent, and many details of their complex interactions are known.<h2>Clinically Significant Features of the Peripheral Nervous System</h2><p><strong> To early anatomists </strong> , dividing the nervous system into central and peripheral parts was intuitively reasonable. This division is not arbitrary; several differences between the PNS and the CNS are of clinical importance. The most apparent difference between the two is the functional simplicity of the PNS. In essence, the PNS is a simple relay system carrying motor, sensory, and autonomic signals between the CNS and somatic structures. The clinical correlate is the limited repertoire of symptoms and signs produced by malfunction of the PNS. One can infer relatively little about the cause of a peripheral nerve disorder from the symptoms and signs alone.<p><strong> A second distinctive feature of the </strong> PNS is its accessibility. Unlike the brain and the spinal cord, which are well protected by bony cases, most of the major peripheral nerves reside for much of their course only a short distance beneath the skin. This accessibility simplifies direct study of the electrical and histologic characteristics of the peripheral nerves. Clinical evaluation of PNS diseases has been greatly facilitated by nerve conduction studies and nerve biopsies, which can be performed with essentially no risk to the patient.<p><strong> Regenerative capacities differ between the </strong> PNS and the CNS. In the mature CNS, little or no regrowth of axons occurs after injury. However, an injured peripheral nerve can often regenerate over long distances and reestablish functional connections. Thus, many peripheral nerve disorders have the potential for significant recovery of function with treatment.<p><strong> The difference in regenerative </strong> capacity was long thought to be related to some intrinsic property of PNS neurons. However, it appears that the critical issue is the environment to which neurons are exposed.1 If a bundle of CNS nerve fibers (e.g., the optic nerve or the spinal cord) is transected and then immediately re-anastomosed, there is little axonal outgrowth. However, if the proximal end of the same lesion is anastomosed to a peripheral nerve graft, axonal sprouts will extend many millimeters through the peripheral nerve graft and may even establish functional connections with target CNS neurons.<p><strong> The cellular and molecular basis for this difference </strong> between PNS and CNS supporting tissues is not fully understood. The Schwann cell (which is exclusive to the PNS) appears key, although other cells (e.g., fibroblasts and macrophages) are probably involved. It is thought that the Schwann cell and the extracellular milieu of the peripheral nerve provide a favorable environment for axonal growth, attracting and perhaps guiding axonal sprouts. Two major classes of molecules influence the growth and development of sprouting axons in vitro: growth factors and adhesion molecules. Some of these molecules (e.g., nerve growth factor, N-cadherin, and laminin) have been well characterized.1<h2>General Approach to Peripheral Nerve Diseases</h2><h3>Clinical manifestations</h3><p><strong> PNS disorders produce combinations of motor </strong> , sensory, and autonomic symptoms. These symptoms are primarily determined by the class of nerve fibers affected (e.g., motor or sensory fibers) and by the location of the lesions, rather than by the etiology of the process. Motor symptoms include weakness (a common presenting complaint), muscle atrophy, fasciculations, and cramps; the last two motor symptoms may be discovered only by specific questioning of the patient. Sensory symptoms include the loss of certain types of sensation and the presence of prickling, pins-and-needles, and burning sensations. The patient’s own description of the quality and distribution of sensory symptoms is often more revealing than the sensory examination.<p><strong> Pain is a common symptom in peripheral nerve disorders, </strong> and it often occurs in association with other neuropathic symptoms. If pain is the only symptom, its cause is probably related to structures other than the peripheral nerves. Autonomic symptoms are heterogeneous and are often discovered only by direct inquiry because they may not seem especially neurologic to the patient. Common autonomic symptoms are orthostatic faintness or dizziness, excessive or diminished sweating, impotence or ejaculatory failure, and impaired gastrointestinal motil-ity (particularly, delayed gastric emptying).<p><a href=http://what-when-how.com/wp-content/uploads/2012/04/tmp5F3.jpg target=_blank> <img alt="Peripheral nerves are composed of several fascicles of endoneurium, each enveloped by perineurium and bound together by loose connective tissue, the epineurium. Each fascicle of endoneurium contains up to several thousand axons. Blood is supplied to the endoneurium by a network of capillary-like microvessels derived from arterioles and venules in the epineurium, which in turn are branches of major limb vessels. "style="border-top-width: 0px; display: inline; border-left-width: 0px; border-bottom-width: 0px; border-right-width: 0px"title="Peripheral nerves are composed of several fascicles of endoneurium, each enveloped by perineurium and bound together by loose connective tissue, the epineurium. Each fascicle of endoneurium contains up to several thousand axons. Blood is supplied to the endoneurium by a network of capillary-like microvessels derived from arterioles and venules in the epineurium, which in turn are branches of major limb vessels. "border=0 height=768 src=http://what-when-how.com/wp-content/uploads/2012/04/tmp5F3_thumb.jpg width=1008> </a><p><strong> Figure 1 Peripheral nerves are composed of several fascicles of endoneurium, each enveloped by perineurium and bound together by loose connective tissue, the epineurium. Each fascicle of endoneurium contains up to several thousand axons. Blood is supplied to the endoneurium by a network of capillary-like microvessels derived from arterioles and venules in the epineurium, which in turn are branches of major limb vessels. </strong><h2>Laboratory tests</h2><p><strong> Laboratory investigations are often required </strong> to clarify the nature of a peripheral nerve disorder. In addition to testing used in the evaluation of other types of neurologic diseases (e.g., lumbar puncture), techniques for the direct study of peripheral nerve physiology and histology are available. Neurophysiologic testing (especially nerve conduction studies) can be considered a routine part of the evaluation of any patient with polyneuropa-thy. Nerve biopsy, on the other hand, is best reserved for patients with disabling neurologic symptoms and signs.<h3>Nerve Conduction Studies</h3><p><strong> Nerve conduction studies can provide support </strong> for a diagnosis of neuropathy and are a relatively objective way to follow the course of the disease. These studies may also allow a clinician to infer whether a disease is affecting primarily axons or their myelin sheaths—an important distinction in the differential diagnosis of polyneuropathy. Nerve conduction studies provide an indication of the numbers of functioning large myelinated motor and sensory axons in various nerves and the speed of impulse transmission in these fibers. The procedure consists of depolarizing a short segment of nerve with a brief electric shock and recording the resultant volley of action potentials as they propagate down the nerve. Both motor and sensory fibers are activated by this procedure; the motor and sensory responses are distinguished from each other by recording either from a cutaneous branch of the nerve (sensory) or from an innervated muscle (motor). If the nerve conduction studies show decreased motor and sensory amplitudes but preserved conduction velocities, the underlying pathologic process is probably loss of or destruction of axons. By contrast, if amplitudes are relatively preserved but there is marked slowing of conduction velocity or conduction block, an abnormality of the myelin sheath is likely.<h3>Needle Electromyography</h3><p><strong> Needle electromyography is a complementary </strong> investigation that is usually performed at the same time as nerve conduction studies. In a patient with peripheral neuropathy, electromyogra-phy is helpful in detecting small degrees of axon loss that may go undetected by nerve conduction studies. Electromyography can also be helpful in pinpointing the precise location of the lesion in a mononeuropathy. The procedure entails recording electrical activity in muscle by use of a needle electrode inserted into the muscle. Muscles are examined at rest and during mild voluntary contraction. If the electrical activity produces an abnormal pattern, the electromyographer can determine whether a patient’s weakness is the result of a diseased muscle or a diseased motor nerve.<h3>Nerve Biopsy</h3><p><strong> Nerve biopsy can be diagnostically useful in </strong> carefully selected patients. Nerve biopsy can provide a specific diagnosis (e.g., necrotizing vasculitis) but more often gives less specific information that can be useful in combination with the other clinical data. Apart from alteration in the number or size of axons, the most common abnormality found by nerve biopsy is inflammation, usually related to altered immune function. On occasion, a disease that affects both the CNS and the PNS (e.g., metachro-matic leukodystrophy) can be conveniently diagnosed by nerve biopsy. The sural nerve is preferred in most instances because sural nerve biopsy results in a small area of generally well-tolerated sensory loss along the lateral side of the foot.<p>Proper pathologic examination of a nerve biopsy specimen requires techniques that are often available only in specialized laboratories. When such facilities are not available locally, the patient should be referred to an appropriate center.<h2>Treatment of neuropathic symptoms</h2><p>The symptoms of neuropathy may be treatable even if the cause of the neuropathy is untreatable or unknown. With simple measures, many patients can have meaningful relief of symptoms.<p><strong> The ankle-foot orthosis is a simple device that </strong> compensates for footdrop. The main benefit offered by an ankle-foot orthosis is greater stability at the ankle, resulting in better balance and overcoming the tendency to catch the toes on edges of steps, curbs, and carpets. A lightweight, properly fitted ankle-foot orthosis that slips into the shoe is usually the most comfortable. Patients with weakness of wrist and finger extensors may be helped by a brace that keeps the wrist and fingers in a neutral position. Unfortunately, this type of splint is of little help when there is significant concomitant weakness of intrinsic hand muscles.<p><strong> Pain, particularly in the feet </strong> , often accompanies the sensory disturbances of neuropathy. Paradoxically, in polyneuropathies with prominent pain, the neurologic deficits are often minor and there is a dissociation between the actual disability and the level of the patient’s distress. Patients may interpret pain as a sign of a serious disorder that threatens their independence or their life. Sometimes, simple reassurance, emphasizing how little neurologic function has been lost, helps the patient cope effectively with neuropathic pain.<p><strong> Nonpharmacologic measures may be as effective as medications </strong> . Careful attention should be paid to footwear. Loose-fitting, soft-soled shoes and thick socks are advisable. Neuropathic pain tends to be aggravated by extremes of temperature—especially heat—and open-toed sandals may give relief. Prolonged weight bearing often worsens neuropathic pain; patients whose work requires them to be on their feet may be helped by frequent short sitting breaks.<p><strong> Foot soaking produces short-lived relief </strong> in many patients. Soaking the feet in ankle-deep cold tap water (without ice) for 15 to 20 minutes can be particularly helpful at bedtime. Although the relief is short-lived, it may be sufficient to allow the patient to fall asleep and to sleep well. For some patients, warm water is better than cold water, and others find that alternating cold and hot water (so-called contrast soaks) provides the best relief. Daily inspection of the feet for undetected injuries—an important habit that patients with neuropathy should develop—can be conveniently combined with nightly foot soaks.<p><strong> Medications can be useful in the management of </strong> neuropathic pain, but the goals of therapy should be realistic. Complete pain relief is unlikely. Therefore, the aim of therapy should be to make the pain more tolerable without adding intolerable side effects of medication. Of the many drugs that can be tried for neuropathic pain, tricyclics (especially amitriptyline) and carba-mazepine are still most frequently used, although gabapentin is increasingly used as a first-line agent. Lancinating, paroxysmal pains may be more likely to respond to carbamazepine (200 mg t.i.d.), whereas amitriptyline (10 to 30 mg at bedtime) is the preferred agent for the more common, continuous burning numbness. Several randomized, controlled trials in patients with neuropathic pain of various etiologies have shown a clear benefit of gabapentin over placebo in several measures of pain relief.2 Effective dosages of gabapentin vary considerably; in most patients, a good initial dosage is 300 mg three times a day, which can be titrated upward over several weeks to 1,800 to 3,600 mg daily or higher, according to response.<p><strong> At least 1 month of treatment should be undertaken </strong> before any conclusions are drawn about the usefulness of a drug for neuropathic pain. In addition to tricyclics, carbamazepine, and gabapentin, salicylates and other simple analgesics give relief to some patients. As is the case with other types of chronic pain, the usual practice has been to avoid narcotics, but a new appreciation for the potential benefits of opioids in managing chronic neuropathic pain is developing.3 Second-line drugs for neuropathic pain include baclofen, mexiletine, valproic acid, and topiramate. Topical capsaicin ointment causes depletion of the neurotrans-mitter substance P in the dorsal horn of the spinal cord and helps some patients. For most patients, however, the expense and inconvenience of topical capsaicin outweigh any benefits.<p><strong> In some patients </strong> , the pain remains refractory to all of these measures. These patients present difficult management problems. Concurrent depression can complicate the situation, and psychiatric referral may be worthwhile. Referral to a multidisci-plinary pain management center can also be considered.<h3>Peripheral Nerve Diseases</h3><p><strong> It is helpful to divide PNS diseases into </strong> those that affect single nerves (mononeuropathies) and those that involve the PNS diffusely (polyneuropathies). A mononeuropathy may involve any cranial or limb nerve. In general, mononeuropathies occur in otherwise healthy patients, cause troublesome symptoms but no major disability, and often improve spontaneously with time.<h2>Cranial mononeuropathies</h2><p><strong> Neuropathies can arise in any individual </strong> cranial nerve [see Table 1]. The seventh (facial), fifth (trigeminal), and third (oculomotor) cranial nerves account for most cranial mononeu-ropathies encountered in clinical practice.<h3>Facial Neuropathy</h3><p><strong> Acute, idiopathic facial neuropathy </strong> (Bell palsy) is the most common cranial neuropathy, with an annual incidence of about 25 per 100,000 persons. The main symptom is unilateral facial weakness that begins abruptly and is often preceded by or accompanied by pain behind the ear. In some patients, a mild upper respiratory tract infection may have occurred up to 2 weeks earlier. The facial weakness usually reaches its zenith within 24 hours after onset and is of the lower motor neuron type, affecting both the upper and the lower face. Some patients experience altered taste on one half of the tongue and hyperacusis. Patients often complain of numbness of the face, but sensory loss is not found.<p><strong> Table 1 Common Cranial Neuropathies </strong><p><table border=1><tbody><tr><td><p><strong> Cranial Nerve </strong></p><td><p><strong> Effects of Lesion </strong></p><td><p><strong> Causes </strong></p><tr><td><p>Olfactory (I)</p><td><p>Loss of smell</p><td><p>Trauma, olfactory groove meningioma</p><tr><td><p>Optic (II)</p><td><p>Loss of vision (monocular or bitemporal hemianopsia)</p><td><p>Optic neuritis, pituitary tumor, ischemic optic neuropathy, optic nerve glioma, Leber disease</p><tr><td><p>Oculomotor (III)</p><td><p>Weakness of adduction, elevation, and depression of eye Ptosis</p> <p>Dilated, nonreactive pupil</p><td><p>Trauma, microvessel ischemia, compression by aneurysm or mass, brain stem stroke or tumor, orbital tumor</p><tr><td><p>Trochlear</p> <p>(IV)</p><td><p>Weakness of depression and intorsion of eye</p><td><p>Trauma, microvessel ischemia, brain stem stroke or tumor, orbital tumor</p><tr><td><p>Trigeminal (V)</p><td><p>Weakness of chewing and other jaw movements Loss of facial sensation and corneal reflex</p><td><p>Trigeminal neuralgia (tic douloureux), sclero-derma and other connective tissue diseases, tumor of petrosal bone</p><tr><td><p>Abducens (VI)</p><td><p>Weakness of abduction of eye</p><td><p>Trauma, raised intracranial pressure, microvessel ischemia, brain stem stroke or tumor, orbital tumor</p><tr><td><p>Facial (VII)</p><td><p>Weakness of half of face Loss of taste Hyperacusis</p><td><p>Bell palsy, Lyme disease, sarcoidosis, herpes zoster, cerebellopontine angle tumor, pontine stroke or tumor</p><tr><td><p>Vestibulo-cochlear (VIII)</p><td><p>Unilateral deafness</p> <p>Vertigo</p> <p>Nystagmus</p><td><p>Vestibular neuronitis, acoustic schwannoma</p><tr><td><p>Glossopha-ryngeal</p> <p>(IX)</p><td><p>Dysphagia</p> <p>Weakness of elevation of</p> <p>palate Loss of gag reflex</p><td><p>Motor neuron disease, jugular foramen tumor, nasopharyngeal carcinoma, metastases to skull base, glossopha-ryngeal neuralgia</p><tr><td><p>Vagus (X)</p><td><p>Dysphagia Dysarthria</p> <p>Weakness of elevation of</p> <p>palate Loss of gag reflex</p><td><p>Motor neuron disease, jugular foramen tumor, metastases to skull base, nasopharyngeal carcinoma</p><tr><td><p>Accessory (XI)</p><td><p>Weakness of sternocleido-mastoid and trapezius muscles</p><td><p>Trauma (surgical and other), jugular foramen tumor</p><tr><td><p>Hypoglossal (XII)</p><td><p>Weakness of tongue</p><td><p>Motor neuron disease, skull base tumor, carotid artery dissection or trauma</p></table><p><p><strong> When the history and examination </strong> are typical of Bell palsy and the condition is mild and nonprogressive, no tests are needed. Severe or progressing cases should be referred to a neurologist to confirm the diagnosis and decide whether intervention is needed. Occasionally, sarcoidosis, Lyme disease, and herpes zoster (shingles) present as facial neuropathy; testing to exclude these conditions may be appropriate. When the neurologic examination reveals more than a unilateral facial neuropathy or when the weakness has evolved over weeks or months, an alternative diagnosis should be sought, such as a cerebellopontine angle tumor or a brain stem lesion.<p><strong> The natural history of untreated </strong> Bell palsy is generally favorable: 85% of patients recover fully within 1 year. However, some clinical features are associated with a poorer prognosis, including old age, complete facial palsy, and the presence of hyperacu-sis or altered taste. Hemifacial spasm (a syndrome of painless, brief, involuntary contraction of the facial muscles) occasionally develops after Bell palsy and other types of facial neuropathy.<p><strong> Although there is general agreement that </strong> the pathogenesis of Bell palsy involves facial nerve inflammation, there is debate about whether the condition is a postinfectious autoimmune phenomenon or the result of a direct viral infection of the facial nerve. Herpes simplex virus type 1 has been implicated by the presence of its DNA in facial nerve specimens from 11 of 14 patients with Bell palsy but not in patients with other causes of facial neuropathy, including herpes zoster.<p><strong> Because of the presumed role of an inflammatory response, </strong> Bell palsy is often treated with glucocorticoids. Several studies have suggested that glucocorticoid therapy speeds recovery. However, a meta-analysis of the few placebo-controlled trials concluded that clear evidence for the efficacy of glucocorticoids had not been demonstrated.5 Nevertheless, for patients seen within a few days after onset of Bell palsy, it is reasonable to follow the common practice of prescribing a short, tapering course of glucocorticoids (e.g., prednisone, 60 mg/day for 5 days, tapering to zero over the next 10 days). A controlled trial of acy-clovir plus prednisone versus prednisone alone found a modest but significant improvement in clinical outcome in the acyclovir-treated group.6 On the basis of this study, the combination of acyclovir and prednisone can reasonably be considered for most patients with Bell palsy, although the natural history of the condition is generally benign, regardless of treatment.<p><strong> Prevention of corneal desiccation </strong> with an eye patch is important for patients who cannot fully close the eye. Facial nerve decompression was once widely used, but the procedure has been largely abandoned because its efficacy is unproved. Injections of botulinum toxin are helpful in treating hemifacial spasm.</p><script>google_ad_client = "ca-pub-3548356617924720";
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    google_ad_height = 90;</script><script src=//pagead2.googlesyndication.com/pagead/show_ads.js></script></div></div><div id=comments></div><div class="prev_next post_nav"><p class=previous>Next post: <a href=http://what-when-how.com/acp-medicine/diseases-of-the-peripheral-nervous-system-part-2/ rel=prev> Diseases of the Peripheral Nervous System Part 2 </a><p>Previous post: <a href=http://what-when-how.com/acp-medicine/the-dizzy-patient-part-4/ rel=next> The Dizzy Patient Part 4 </a></div></div><div id=sidebars><div class=sidebar id=sidebar_1><ul class=sidebar_list><li class="widget widget_nrc"id=related-links-by-category><h3>Related Links</h3> <ul><li class=serif><span class=cat-name> <a title="ACP Medicine"href=http://what-when-how.com/category/acp-medicine/> ACP Medicine </a> </span> <ul><li class=cat-item id=related-cat-post-226874><a title="On Being a Physician"href=http://what-when-how.com/acp-medicine/on-being-a-physician/> On Being a Physician </a><li class=cat-item id=related-cat-post-226872><a title="Contemporary Ethical And Social Issue in Medicine"href=http://what-when-how.com/acp-medicine/contemporary-ethical-and-social-issue-in-medicine/> Contemporary Ethical And Social Issue in Medicine </a><li class=cat-item id=related-cat-post-226870><a title="Reducing Risk of Injury and Disease Part 1"href=http://what-when-how.com/acp-medicine/reducing-risk-of-injury-and-disease-part-1/> Reducing Risk of Injury and Disease Part 1 </a><li class=cat-item id=related-cat-post-226866><a title="Reducing Risk of Injury and Disease Part 2"href=http://what-when-how.com/acp-medicine/reducing-risk-of-injury-and-disease-part-2/> Reducing Risk of Injury and Disease Part 2 </a><li class=cat-item id=related-cat-post-226864><a title="Diet and Exercise Part 1"href=http://what-when-how.com/acp-medicine/diet-and-exercise-part-1/> Diet and Exercise Part 1 </a></ul></ul><li class="widget thesis_widget_google_cse"id=google-custom-search><h3>:: Search WWH ::</h3> <style>@import url(http://www.google.com/cse/api/branding.css);</style> <div class=cse-branding-bottom style=background-color:#FFFFFF;color:#000000><div class=cse-branding-form><form action=http://www.google.com/cse id=cse-search-box target=_blank><div><input name=cx type=hidden value=partner-pub-3548356617924720:u0h0be-i8eq><input name=ie type=hidden value=ISO-8859-1><input name=q size=60><input name=sa type=submit value=Search></div></form></div><div class=cse-branding-logo><img alt=Google src=http://www.google.com/images/poweredby_transparent/poweredby_FFFFFF.gif></div><div class=cse-branding-text>Custom Search</div></div></ul></div><div class=sidebar id=sidebar_2><ul class=sidebar_list></ul></div></div></div></div></div><div class=full_width id=footer_area><div class=page><div id=footer><p><a href=http://what-when-how.com/help-unprivileged-children/ rel=nofollow> Help Unprivileged Children </a>  ¶  <a href=http://what-when-how.com/careers/ rel=nofollow> Careers </a>  ¶  <a href=http://what-when-how.com/privacy-statement/ rel=nofollow> Privacy Statement </a>  ¶  <a href=http://what-when-how.com/copyright-information/ rel=nofollow> Copyright Information </a></p><script>var sc_project=4900976; 
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