Is it normal for bruises to itch: The request could not be satisfied

31.05.197701.11.2021 by alexxlab

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Why do you bruise easily? What you need to know

Do you ever feel like the main character in Hans Christian Andersen’s fairy tale “The Princess and the Pea,” in which the delicate princess wakes up “black and blue all over” after sleeping on a single pea covered by a tower of mattresses?

Your skin can reveal many clues about your health, so a tendency to bruise easily might make you worry.

Although finding frequent bruises can sometimes signal health problems, doctors say most cases are nothing to worry about.

Dr. Monique Tello, a primary care physician at Massachusetts General Hospital, encounters patients with “easy bruising anxiety” quite frequently.

“Thus far, in my ten years as an attending (physician), no one in my primary care practice has had any serious underlying condition,” Tello told TODAY. “Usually, they didn’t remember some bump, or were taking aspirin. Rarely, bruising can be a clue that there is a medical issue.”

Most bruises happen when you suffer an injury that fails to break the skin, but crushes the small blood vessels underneath. Blood then leaks and becomes trapped under the surface, leaving the telltale mark.

If you work out a lot, you might notice random bruising on your legs, primarily in fatty areas that are exposed, like your thighs or buttocks, said Dr. Abigail Waldman, a dermatologist at Brigham and Women’s Hospital.

Here are other possible causes of easy bruising:

Blood thinners

Besides injury, blood thinners — medications or supplements that slow down or decrease your blood’s clotting ability — may be the number one cause for easy bruising, Waldman said. They’re very common, ranging from aspirin to drugs like Coumadin. If you’re on blood thinners, it may take longer for bleeding to stop, leading to bigger bruises.

You might not even realize you’re taking something that thins your blood: Fish oil supplements, ginkgo biloba, alcohol and garlic have similar effects.

Other drugs

Steroids can lead to thinner skin, so you may notice bruising with just slight trauma. Chemotherapy can lower the number of platelets — the cells that help your blood to clot — in your body, the National Cancer Institute notes. A low platelet count means a higher risk of bruising.

Vitamin deficiency

Easy bruising might suggest you lack enough vitamin K, found in leafy green vegetables, broccoli and Brussels sprouts. Most people get enough of this fat-soluble vitamin in their diets, so you don’t need to take a supplement, Waldman said. But if you are deficient, it’s a sign you may not be absorbing vitamins correctly, she added. That may include people with Crohn’s disease or ulcerative colitis.

A severe lack of vitamin C — or scurvy — could also be the culprit because the vitamin is involved in building the walls of blood vessels, Waldman said. Scurvy is rare in the U.S. — symptoms include bleeding around hair follicles and bleeding gums.

Aging

As you age, your blood vessels become more fragile. “You can think of it like a hose that holds the blood,” Waldman said. “As you get older, you sort of have some leaks in the hose. So very small injuries can cause that area to open up and leak blood out into the skin, causing a bruise.”

Older skin is more fragile, too, and there’s less fat underneath it, leaving you with less cushion if you bump into something. All of those factors can lead to senile purpura, or bruises that show up after very slight injury in elderly people. The marks typically appear in areas that have had significant sun exposure, like the arms and the hands, Waldman said

“Unfortunately, there’s not a lot you can do to prevent it, except to try to avoid any even minimal injury. But sometimes it’s nice for patients just to have a diagnosis,” she added.

Cancer

In rare cases, easy bruising can be a sign of blood, bone marrow or lymph node cancers, Waldman said. These marks often show up as petechiae — very small red dots from bleeding under the skin — but can look like large bruises as well.

The bruises can be one clue of many, so doctors will ask about any accompanying bleeding from the gums, fevers, chills, night sweats, bone pain, Tello said.

“In my years of training, I rotated through oncology and ICU units where patients had had easy bruising as one of many signs of their underlying leukemia or bleeding disorder diagnosis originally,” she noted.

Liver disease

The liver’s many functions include producing clotting factors. When the organ is damaged and slows or stops producing the proteins needed for blood clotting, you will bruise or bleed easily, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

Genetic factors

The tendency to bruise easily can run in families. Genetic causes can lead to changes in your platelet count or the factors that are involved in clotting.

See a doctor if you have:

Significant pain and swelling. That could represent a larger bleed under the skin, especially if you’ve had a significant fall or injury, Waldman said.
A bruise that lasts longer than two weeks without changing. It may not be a bruise at all or be caused by an underlying problem.
Small blood spots accompanied by fever, chills, weight loss or any other systemic symptoms that are new.
Recurrent bruises without any clear causes.

There’s no one true definition of being an “easy bruiser,” but Waldman defines it as bruising with minimal or no injury. In most cases, bruises are not a cause for worry.

Putting ice on a bruise can help minimize swelling and some data suggests taking arnica orally can help prevent bruising, she noted. Your body will clear most bruises within a week.

Neuropathic Itch – Itch – NCBI Bookshelf

7.1. BACKGROUND AND INTRODUCTION

Dermatologists are increasingly aware that some cases of unexplained chronic itch are caused by underlying neurological disease, and some now seek neurological care for these patients, but few neurologists feel prepared to help. This overview is intended both to guide clinicians and to suggest research topics. A PubMed search referencing the terms “neuropathic itch” plus “neuropathic pruritus” on December 22, 2012, yielded only 101 primary and review citations. Other relevant papers are not retrieved by these search terms as they may not even contain the words “itch” or “pruritus,” but instead refer to “distressing sensory symptoms” or to self-injurious scratching (often by other names, e.g., “trigeminal tropic syndrome”). The fragmented literature attests to the current rudimentary state of awareness about neuropathic itch.

7.1.1. Definitions of Neuropathic Itch

The epistemology of neuropathic itch (NI) is based on that of neuropathic pain, which has so far worked well, no doubt because most peripheral itch neurons are a subset of peripheral pain neurons. NI is thus defined as perception of itch in the absence of pruritogenic stimuli (formerly known to dermatologists as pruritus sine materia). In other words, there is uncoupling of the stimulus-response curve for itch sensation since dysfunction or disease of itch-signaling neurons is causing them to fire without cause. At a practical level, NI can only be diagnosed after dermatological and systemic causes have been excluded, so dermatological evaluation should usually precede referral to a neurologist.

The International Forum for the Study of Itch (IFSI) recognizes four types of itch causality—dermatologic, systemic, neurologic, and psychiatric (Ständer et al. 2007) plus mixed and unknown causes. Etiology Category III (NI) is defined as “arising from diseases or disorders of the central or peripheral nervous system, e.g. nerve damage, nerve compression, nerve irritation” (Ständer et al. 2007, p. 87). From the neurological perspective, NI is primarily a modality-specific sensory hallucination, and the literature on other types of sensory hallucinations, e.g., tinnitus, the Charles Bonnet syndrome, phantom pain (recently reviewed in Sacks [2012]) can help inform understanding.

At the time of this writing, pain specialists are digesting 2012 revisions by the International Association for the Study of Pain (IASP) to their definition of neuropathic pain, which restricts it to “pain caused by a lesion or disease of the somatosensory system” (http://www. iasp-pain.org/Content/NavigationMenu/GeneralResourceLinks/PainDefinitions/default.htm#Neuropathicpain). This replaces the definition in the IASP’s Classification of Chronic Pain (Merskey and Bogduk 1994, p. 212) that defined neuropathic pain more broadly, specifically as “pain initiated or caused by a primary lesion or dysfunction in the nervous system.” In the 2012 version, “dysfunction” has been removed and a lesion or disease affecting the nervous system is now required. The requirement for a structural abnormality is problematic because in many patients, the causal lesions can often be hard to localize, meaning that they therefore no longer qualify as having neuropathic pain (Jensen et al. 2011, 2012; Oaklander et al. 2012). Regarding pruritus, the causal pathologies are even less defined than for neuropathic pain, so the author favors the less restrictive IFSI definition of neuropathic itch that permits “disorders” as well as “diseases” of the nervous system.

7.1.2. Neuroanatomy and Cell Biology

As is typical in neurology, discovering the anatomical pathways for normal itch sensation has been aided by studying patients with neurological diseases or injuries that caused their itch. The relevant methods include localization by neurological examination, imaging (Chapter 24), and rarely, anatomical or surgical pathology. Studying patients has demonstrated that NI is caused by lesions that specifically affect itch neurons, just as other neurological symptoms reflect the functions of the specific neurons damaged. As always, the cause of the lesion is less important than its location. A stroke, tumor, or multiple sclerosis plaque in the same brain region will generate similar signs and symptoms. As imaging methods advance, it should improve our understanding of the pathways and mechanisms of NI. Better visualization of white matter tracts is particularly relevant for network disorders such as NI. For instance, applying 7T magnetic resonance imaging (MRI) to the spinal cord of a patient with NI after cavernous hemangioma (see below) suggested the hypothesis that his late-onset central itch might be triggered by delayed white matter degeneration (Cohen-Adad et al. 2012).

Peripheral nervous system (PNS) lesions appear to be the most common causes of NI, most likely because these are more common than injuries to the well-protected central nervous system (CNS). Neuropathological study shows clearly that injury to specific neurons is necessary to produce itch, namely, to the subset of sensory small fibers that encode itch signals, which includes C-fiber and A-delta primary afferents with various transduction patterns (Chapter 9). Neuropathic itch is caused by the same type of neurological injuries and diseases that cause neuropathic pain as well. Many patients present with pain alone, or pain plus itch, but some report only itch, for unknown reasons. Lesions that primarily affect motor neurons, amyotrophic lateral sclerosis, for instance, are not associated with NI. Lesions anywhere in the PNS appear capable of causing NI, whether distally (axonopathy) or centered on the sensory ganglion (e.g., shingles) or the proximal nerve roots. Even the most distal PNS lesion can affect the spinal cord and then the brain to cause NI. While cutting a nerve reduces incoming sensory signals (after the injury barrage) and thus would be expected to reduce sensation, in some individuals later compensatory mechanisms paradoxically augment sensations coming from nerve-injured areas. The causes include abnormal firing of nearby preserved primary afferents, loss of tonic dorsal-horn inhibitory circuits (Basbaum and Wall 1976; Woolf and Wall 1982), and alterations in thalamic and cortical circuits (Chapters 23 and 26).

NI involves nonneural cells and mechanisms as well. Some diseases that cause NI also cause itch through other mechanisms (e.g., cutaneous inflammation as during shingles) or the mixed itch of uremic neuropathy. Also, scratching NI-affected skin can trigger additional pruritogenic cutaneous inflammation, irritation, ulceration, or scarring. Even under normal conditions, nonneural cells participate in itch signaling. Small fibers release neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P that have paracrine effects on nearby nonneural cells that augment itch. Keratinocytes express the heat-sensing vanilloid type 3 (TRPV3) receptor (Peier et al. 2002) and several neuronal sodium channels (Zhao et al. 2008) so they may contribute to or modulate normal and/or neuropathic itch. Secretions of injured small fibers stimulate mast cell degranulation, which not only initiates itch-signaling action potentials through histamine, serotonin, and tryptase-activated proteinase-activated receptor-2 receptors on primary afferent nerve endings, but additionally stimulates release of proinflammatory cytokines from T-cells to further augment inflammation and neuronal activation (Chapters 19 and 20).

7.1.3. What Is the Relationship between NI and Psychogenic Itch?

In the past, physicians routinely interpreted itch syndromes without evident cause (pruritus sine materia) as psychogenic. Recognition of NI and of how little we know about itch mechanisms is curbing this habit of blaming the patients rather than our own uncertainty. In practice, psychogenic itch diagnoses (Etiology Category IV itch; [Ständer et al. 2007]) are considered in two types of patients, those with or without major psychiatric diagnoses. For patients without psychiatric diagnoses, it is probably inappropriate for nonpsychiatrists to diagnose psychogenic itch. The psychiatric diagnoses associated with unexplained chronic itch—somatization disorder, obsessive compulsive disorder, and thought disorders—are serious illnesses with specific diagnostic criteria. If they are suspected, a psychiatrist should be consulted to diagnose and treat the patient. Even in patients with established major psychiatric diagnoses, new itch complaints will more often have dermatologic or medical causes. My few patients with obsessive-compulsive disorder plus postherpetic itch (PHI) have successfully avoided picking or scratching their itchy areas, recognizing the danger.

Psychotic patients with itch are the most difficult to evaluate because sensory hallucinations are a central symptom of psychosis. It is unclear whether or not psychiatric illness itself can trigger delusions of itch, although considering the prevalence of auditory and other hallucinations in some of the psychoses, this has be presumed possible. When psychotic patients develop unexplained itch, it is often attributed to their psychosis, despite the lack of any known specific association. Advanced imaging is now identifying abnormal brain structure and activity associated with somatic delusions and hallucinations in such patients, blurring the distinction between psychogenic and central neuropathic itch. MRI has identified reduced left fronto-insular gray matter volume in schizophrenic patients with somatic delusions as compared with schizophrenics without hallucinations and healthy controls (Spalletta et al. 2012). The thalamus, particularly the right ventral-anterior thalamic nucleus that projects to prefrontal-temporal cortex and the inferior frontal lobe, is significantly larger in hallucinating patients as well (Spalletta et al. 2012).

We all harbor illogical explanations and expectations regarding health symptoms, and some are widely accepted, e.g., health benefits of expensive organic food or colon cleanses. The most common irrational explanation for unexplained chronic itch is undiagnosed parasite infestation. It is difficult to determine in any specific patient how illogical (delusional) this is, given that the sensation of itch is thought to have evolved to signal parasite contact. Our brains have likely been hard wired to interpret itchy stimuli as insect contact until proven otherwise. However, some patients with unexplained chronic itch cling to the parasite explanation despite repeated testing showing no evidence of this, and sometimes even after other causes of itch are diagnosed.

Names for this syndrome include primary delusional parasitosis, Ekbom syndrome, and Morgellon’s syndrome. Some of these individuals have related convictions that there are tiny threads or fibers in or on their skin triggering their itch. They are a mixed bunch. Some have delusional explanation for itch that is caused by other identifiable causes (Fleury et al. 2008), whereas in others the causes of itch remain unknown, making it hard to exclude implausible explanations. Intellectual impairment and cultural and religious traditions can also make it hard for patients to evaluate the relative validity of their physicians’ explanations versus those suggested by the Internet, friends, and spiritual leaders. Low-level psychoses and schizophrenia are more prevalent than appreciated, and patients with delusional thinking and other mild psychotic symptoms often remain unrecognized even by physicians. Illogical beliefs and paranoid or conspiracy theories are part of all cultures, with no distinct border between “normal” and “delusional” thinking. Typically, such individuals remain in the community without exhibiting flagrant enough behavior to trigger psychiatric evaluation and diagnosis.

In my limited experience caring for patients harboring delusional explanations for obscure sensory symptoms, I have usually identified a neurological cause (although the patient often disagrees), a psychiatrist has confirmed the presence of mild thought disorder, and antipsychotic medications have lessened the delusions but not the sensory symptoms. Such patients are ill served by our fragmented health care system, which enables them to reject and conceal diagnoses that displease them—such as schizophreniform disorder plus atypical trigeminal neuropathy—and to decline treatment for such rejected diagnoses. Instead, they self-refer to new physicians who unwittingly repeat the cycle of unnecessary diagnostic testing and ineffectual treatments for their delusional diagnoses. Tragically, some patients impoverish themselves to “treat” their delusions, investing thousands of dollars on mold remediation, insect extermination, or unnecessary surgeries or medications.

Regardless of a patient’s own interpretation of the cause of their itch, it is their physician’s responsibility to look for “actionable” causes, including not only dermatological and systemic causes but also mastocytosis, restless leg syndrome, and neuropathic itch.

7.1.4. Animal Models of NI

Because itch is subjective, itch assessment in animals traditionally relied on measuring hair loss or wounds caused by scratching or other forms of self-injury directed toward skin that was experimentally irritated or denervated. Video systems now permit quantitation of even noninjurious scratch bouts. Although it can never be proven that scratching and similar behaviors (rubbing and biting) in animals are motivated by itch, the evidence for this overwhelming because a wide range of nonhuman animals scratch in response to the same provocations (dermatologic, systemic, and neuropathic) that cause human itching and scratching.

Until recently, human NI and associated lesions were usually attributed to psychiatric causes or pain (see trigeminal trophic syndrome below), so it is not surprising that self-injury to denervated skin in nerve-injured experimental animals was and still is often attributed to neuropathic pain rather than itch. Although neuropathic self-injury was noted from the very first nerve-injury experiments, it was first systematically studied in rodents and called “autotomy” by pain scientists Pat Wall, Marshall Devor, and colleagues, who developed a grading system for it (Wall et al. 1979). They and others initially interpreted autotomy as modeling anesthesia dolorosa type neuropathic pain, but from the beginning there was disagreement, especially from neurosurgeons who know that patients with neuropathic pain including anesthesia dolorosa protect rather than injure their painful areas (Levitt et al. 1992). Neurosurgical pioneer Will Sweet also pointed out that although dorsal rhizotomy was one of the main triggers for experimental autotomy in animals, it does not cause pain in humans (Sweet 1981). By the end of his career, Dr. Wall had come to believe that neuropathic autotomy in rodents more likely reflected neuropathic itch rather than pain (P. Wall, pers. comm.). He was additionally influenced by later reports of “autotomy” in nerve-injured humans who reported that their self-injurious scratching was motivated by itch and not by pain (Oaklander et al. 2002). Other scientists use the term “overgrooming” for pathological scratching at experimentally nerve-injured skin. These behaviors develop in some but not all rodents after experimental lesions throughout the PNS and in the spinal cord that damage pain/itch pathways (Yezierski et al. 1998). Genetic (Mogil et al. 1999) and dietary factors (Shir et al. 1997) influence whether or not rats develop autotomy after nerve injuries and demonstrate that NI is a complex disorder with both environmental and genetic causes.

Widespread NI caused by polyneuropathy has been modeled by treating neonatal rodents with systemic capsaicin, which permanently ablates TRPV1+ primary afferents and triggers 80% to 90% of rats to engage in self-injurious overgrooming (Maggi et al. 1987). Interestingly, this is largely restricted to the areas around the eyes, ears, and snout, consistent with the idea that these locations may be enriched in itch receptors, perhaps because their moistness and lack of keratinization attracts insects (Maggi et al. 1987). It is unclear whether or not neuropathies that damage axons only while preserving the cell bodies in the sensory ganglia also produce NI.

Focal NI caused by nerve injury has been modeled by studies of autotomy after sciatic nerve transection in rodents. Action potentials from the damaged nerve appear required to maintain autotomy, because chronic administration of local anesthetics to a sciatic nerve that completely suppresses sciatic action potentials does not trigger autotomy (Blumenkopf and Lipman 1991).

Dermatomal NI caused by ganglion lesions has been modeled by surgical extirpation of specific dorsal root ganglia. The resultant overgrooming centered on the denervated dermatome is associated with ectopic firing within the dorsal horn (Asada et al. 1996) and modulated by descending dopaminergic inhibition (Tseng and Lin 1998).

Dermatomal NI caused by radiculopathy is modeled by the autotomy that develops after lesioning rodent dorsal rootlets or roots. This seems to correspond to the rare phenomenon of self-injury after plexus injuries in humans (e.g., McCann et al. 2004). As in humans, there seems to be a rostro-caudal gradient, or at least for developing autotomy as this develops after dorsal rhizotomy of cervical and thoracic roots, but not lumbosacral nerve roots (Lombard et al. 1979).

NI caused by myelopathy has been linked by my group to a rat model of spinal-cord injury, involving micro-injection of quisqualate excitotoxin into the deep dorsal horn, which creates a small necrotic cavity (Dey et al. 2005). The dermatomal scratching and biting that some injected rats develop was interpreted as modeling neuropathic pain until we suggested it more closely modeled NI in humans with intramedullary cavernous hemangiomas (see below). We later found that injected rats that self-injure have deafferentation of their itchy dermatomes, implying that their small spinal cord injuries cause retrograde degeneration of primary afferent neurons as well as of intrinsic spinal neurons (Brewer et al. 2008). Thus, myelopathy-induced NI may not be purely central. This model also provided the information that only injected rats with lesions in the deep dorsal horn that spared the superficial lamina developed dermatomal self-injury (Yezierski et al. 1998). NI in these rats may thus be maintained by spontaneous activity in second order, lamina I, itch projection neurons responding to both loss of local inhibitory circuits (Ross et al. 2010) but also loss of normal peripheral input.

NI caused by brain lesions has not been systematically modeled in animals.

7.2. DIAGNOSIS AND MEASUREMENT

Itch, a subjective sensation, is diagnosed and measured based mostly on subject report. The following steps are recommended for clinical practice to establish the diagnosis of NI:

Eliminate dermatological and systemic causes including medications.
Establish inadequacy of conventional antipruritic treatments including antihistamines and anti-inflammatories.
Ask about known neurological disorder or nerve injury (e.g., shingles, degenerative spine disease, and peripheral neuropathy).
Refer to a neurologist for history, neurological examination, and testing for nuerological causality and treatment recommendations.

There are no diagnostic tests for NI, but the following types of measurement can help support a clinical diagnosis or rule out other possibilities. Clinical approaches to measurement rely on questionnaires and rating scales, which are subjective (Wahlgren 1995). One objective approach is to measure the consequences of itch, namely, the scratch response, although this is an indirect correlate modified by other variables including subject volition, attention, and motivation. Photographic or videographic documentation of scratching and associated lesions has clinical and research utility.

Neurophysiological studies, specifically nerve conduction study and electromyography (EMG) are often used to document peripheral nerve damage. However conventional electrodiagnostic testing is insensitive to small-fiber neuropathy; surface electrode nerve conduction studies only measure large (rapidly conducting) myelinated A fiber activity in mixed peripheral nerves, not the A-delta and C-fibers primarily involved in itch. With electromyography, abnormal “neurogenic” patterns only identify axonal injuries to motor axons. Abnormal studies can be clinically useful when they identify associated polyneuropathy or a focal nerve injury that also affects large-diameter sensory axons and/or motor axons, but normal studies do not rule out the presence of small-fiber nerve damage, or of subthreshold injuries, or injuries to nonstudied nerves (e.g., small sensory branches), and thus they lack negative predictive value for excluding small-fiber predominant nerve injuries. Microneurography or other special methods (Zotova and Arezzo 2013) may be required for electrophysiological diagnosis or confirmation of ectopic firing of peripheral itch axons.

Quantitative sensory testing is a more formal method of measuring sensory thresholds (most commonly thermal, mechanical, and vibratory) than examination, but despite its numerical results, the findings remain subjective and depend on subject motivation and alertness (Freeman et al. 2003). No diagnostically useful patterns have emerged for neuropathic pain conditions (Pappagallo et al. 2000). This method is mainly a research tool at present.

Radiological studies, specifically MRI or CT are optimal for detecting foraminal stenosis or other structural lesions that can impinge on cranial or spinal nerve roots to cause brachioradial pruritus or other radiculopathies. MR neurography and ultrasound are emerging techniques for visualizing nerves, especially in entrapment neuropathies.

Pathologic diagnosis of small-fiber polyneuropathy once required surgical biopsy of a sensory nerve. Now neurodiagnostic skin biopsy specially fixed and immunolabeled with axonal markers and/or autonomic function usually suffices (England et al. 2009). Skin biopsies have linked PHI to severe loss of distal unmyelinated axons (Oaklander et al. 2002) and to increased innervation in notalgia paresthetica (Savk et al. 2002; Springall et al. 1991) attributed to secondary inflammation. Neurodiagnostic skin biopsy is not routinely performed by dermatologists, and it must be planned in advance as it requires different fixatives and processing than those used for routine dermatopathological study. It involves removing a small piece of skin under local anesthesia, vertically sectioning and immunolabeling with a pan-axonal marker (i.e., PGP9.5) to permit evaluation and quantitation of sensory axons in the dermis and epidermis. Because normative densities differ at different body locations, and there is considerable interindividual variability, these biopsies are not useful diagnostically except rarely, when comparing biopsies from patients’ itch-affected and matching unaffected areas confirm focal small-fiber losses.

7.3. CLINICAL NI SYNDROMES

7.3.1. Widespread NI from Generalized Peripheral Nerve Damage (Polyneuropathies)

Widespread small-fiber predominant polyneuropathies (SFPN) typically include symptoms of burning pain, allodynia, hyperalgesia, sweating, and microvascular changes. Itch is currently not adequately recognized as part of this syndrome (). SFPN has metabolic (e.g., diabetes), infectious, rheumatologic, toxic, paraneoplastic, autoimmune, and hereditary causes, some of which are curable and thus a diagnosis mandates additional testing for cause (Amato and Oaklander 2004). Most small-fiber polyneuropathies are length dependent, beginning with foot pain that can progress proximally in a stocking-and-glove pattern. Occasional patients present with patchy, proximal, or total-body sensory symptoms caused by widespread ganglionopathy/neuronopathy; described below. If large (A alpha or beta) myelinated nerve fibers are also affected, there can be colocalizing hyporeflexia, weakness, and vibratory and proprioceptive deficits.

FIGURE 7.1

Widespread neuropathic itch caused by small-fiber polyneuropathy. A patient with chronic itch and scratching-induced lesions on her distal legs. She had negligible sweat production from the forearm, proximal leg, distal leg, and foot sites after iontophoresis (more…)

Toxic polyneuropathy caused by infusing hydroxyethyl starch (HES), a synthetic colloid widely used to increase intravascular volume in surgical, emergency, and intensive care patients, can cause widespread NI plus kidney and coagulation disorders. These are attributed to starch deposition in tissues including kidney and peripheral nerve (Kamann et al. 2007). Neuropathy symptoms typically include diffuse itching and sensorineural hearing loss (Klemm et al. 2007). It is debated whether or not newer formulations are safer (Hartog et al. 2011).

7.3.2. Focal NI from Nerve and Nerve-Root Lesions Including Brachioradial Pruritus and Notalgia Paresthetica

Any type of injury to itch-signaling peripheral afferent neurons can trigger itch in and near the receptive field of the injured neurons. As with neuropathic pain, it is entirely unknown why only a few patients with such injuries (which are common) develop clinically significant NI. One association is with neurofibromas, benign tumors that arise from Schwann cells. The itch is attributed to the abundant mast cells within these tumors (Johnson et al. 2000).

Radiculopathies involve damage to cranial or spinal nerve roots. These are established causes of neuropathic itch (see below) and other sensory symptoms including pain, and/or reduced sensations in the territory of affected nerve roots. If severe, patients can develop colocalizing motor deficits. Mechanical compression or irritation at the neural foramen (“pinched nerve”) is the most common cause; others include inflammation or neoplasm (e.g., meningioma and schwannoma) and even Tarlov cysts (Oaklander et al. 2013).

Plexopathies refer to lesions of the intertwining neural networks near the spine where axons within nerve roots re-sort into peripheral nerves. Symptoms reflect often patchy or incomplete combinations of nerve root and nerve damage. The brachial plexus is affected more often than the lumbosacral plexus, and motor fibers are affected along with sensory fibers. Movements that irritate the affected plexus can worsen sensory symptoms. Common causes include autoimmunity (e.g., in brachial plexitis, also known as neuralgic amyotrophy or Parsonage-Turner syndrome [van Alfen and van Engelen 2006]), tumor or radiation therapy, diabetes, and tissue entrapment. Additional causes of brachial plexopathy include Pancoast lung tumors, neurogenic thoracic outlet syndrome, and SEPT9 mutations, which cause recurrent attacks (Jeannet et al. 2001). In children, traction injuries during birth have been associated with self-mutilation of the affected arm (McCann et al. 2004). Although such children are preverbal, and others have interpreted such behaviors as a sign of psychopathology or neuropathic pain, the author continues to interpret them as painless self-injury caused by the conjunction of neuropathic itch and loss of protective nociceptive pain sensation from severe sensory-nerve injury (Brewer et al. 2008; Dey et al. 2005), as in the trigeminal trophic syndrome discussed below.

Mononeuropathy, meaning damage to a single nerve, is most often caused by trauma. While originally associated with military trauma, medical injuries are now a more common cause of traumatic nerve injury in developed countries. Less frequent causes include internal lesions such as impingement, entrapment, scarring, infection (e.g., leprosy), or inflammation. Because some causes are curable or require independent treatment (e.g., tumor and aneurysm), focal peripheral neuropathies of unclear etiology require additional evaluation to identify their cause. Symptoms can spread outside the dermatome of the affected nerve (e.g., in the complex regional pain syndrome) owing to electrical coupling in the skin between nociceptive afferents (Meyer et al. 1985), secondary irritation of nearby neurons within nerve trunks, nerve roots or the DRG, the dorsal horn, and occasionally even the sensory cortex of the brain. Furthermore, there are poorly understood links between contralateral anatomically matched primary afferents that allow some types of unilateral nerve injuries to produce “mirror-image” effects on the contralateral uninjured areas (Oaklander et al. 1998; Oaklander and Belzberg 1997; Oaklander and Brown 2004; Scott et al. 2000). Induction or exacerbation of symptoms by percussing the involved nerve (Tinel’s sign) can help with localization. Diagnostic aids include electrophysiological testing and advanced imaging modalities (see below).

Brachioradial pruritus is the historic term referring to NI originating from the cervical spinal nerves. NI characteristically presents with bilateral or less often unilateral itchy patches (with or without cutaneous stigmata of scratching) on the forearms, elbows, or upper outer arms (Massey and Massey 1986). Because of the location, and because most patients have worsening in the summer and improvement with protection against the sun (Veien and Laurberg 2011), ultraviolet exposure may be a contributory factor, but one third to one half of patients have radiological evidence of degenerative osteoarthritis of the spine compressing their cervical nerve roots (Abbott 1998; Goodkin et al. 2003; Veien and Laurberg 2011). As below, this same phenotype is less often caused by spinal cord lesions (myelopathy) including tumors (Kavak and Dosoglu 2002), so cervical MRI should be considered in patients without electrophysiological or other evidence of a peripheral lesion, particularly in patients with bilateral symptoms or signs or other symptoms suggestive of cervical myelopathy. A single-case report suggests efficacy of topical injection of botulinum toxin-A (Kavanagh and Tidman 2012).

Notalgia paresthetica is another well-known focal neuropathic itch syndrome. This historical term describes usually unilateral itchy areas on the back, near and below the scapula in the mid-thoracic dermatomes (Massey and Pleet 1979). These areas often exhibit the stigmata of chronic scratching as well, and dermatopathological examination reveals postinflammatory hyperpigmentation (Savk et al. 2002). Focal entrapment or irritation has been attributed to the location where nerves turn to traverse through the muscles of the back at an angle, and indeed, electromyographic study showed that seven of nine patients with notalgia paresthetica had evidence of chronic denervation of paraspinous muscles; localizing the causal lesion to the posterior rami of the spinal nerves (Massey and Pleet 1981). Radiological study also provides evidence of degenerative spine disease in up to 60% of studied patients so this same phenotype can equally be caused by radiculopathy (Raison-Peyron et al. 1999; Savk and Savk 2004, 2005), and no doubt by zoster sine herpete. Additionally, given the fact that even intramedullary lesions including spinal cord tumors can present as notalgia paresthetica (Johnson et al. 2000), thoracic MRI should be considered in notalgia paresthetica patients without electrophysiological evidence of a peripheral cause, particularly in those with bilateral symptoms or other signs and symptoms suggestive of myelopathy. Regarding treatment of notalgia paresthetica, there are case reports of efficacy of various neuropathic-pain medications including topical capsaicin and oxcarbazepine (Savk et al. 2001). Exercises to alter muscle configuration and presumably reduce nerve impingement have also been recommended (Fleischer et al. 2011; Savk and Savk 2004). Prospective study of injection of botulinum toxin type A in four patients with notalgia paresthetica, one with meralgia paresthetica and one with neuropathic itch of the foot showed mean reductions of itch by 28% at 6 weeks posttreatment (Wallengren and Bartosik 2010).

7.3.3. Focal NI from Sensory Ganglia Lesions (Neuronopathies/Ganglionopathies) Including Shingles

Attacks on the sensory ganglia (cranial and dorsal root ganglia) cause sensory symptoms centered on the peripheral distribution of these ganglia. Motor function is usually spared because motor axons bypass most sensory ganglia, although motor axons may undergo secondary bystander damage due to proximity to degenerating sensory axons within the nerve roots, plexi, or nerves. Multiple sensory ganglia can also be affected by generalized conditions to cause widespread or patchy symptoms (polyneuropathy). Because sensory ganglia lack a blood–nerve barrier, they are vulnerable to autoimmune attack such as in Sjögren’s, and paraneoplastic syndromes. Given the abundance of itch-associated primary afferents within the DRG (Han et al. 2012), the strong link between ganglionopathies and NI is no surprise.

Shingles (herpes zoster) is by far the most common type of sensory ganglionitis, and it is currently the best characterized cause of focal NI (). Although clinicians recognized that dermatomal itch was a common sequel of zoster, and there were scattered reports, one well-studied patient who scratched through her skull into the frontal lobe of her brain after V1 shingles, brought much wider awareness of PHI (Oaklander et al. 2002). A global epidemiologic study of 586 adults with prior shingles demonstrated that itch, usually mild or moderate, affected roughly one third of patients with acute shingles or PHN. Furthermore, shingles affecting the face, head, or neck was significantly more likely to trigger PHI than shingles affecting more caudal dermatomes (Oaklander et al. 2003).

FIGURE 7.2

Facial neuropathic itch caused by shingles (trigeminal trophic syndrome). A 21-year old woman with trigeminal trophic syndrome in the right V1 dermatome after cranial irradiation for pituitary adenoma followed by right V1 herpes zoster. Her ulceration (more…)

7.3.4. NI Syndromes Arising from Lesions within the Spinal Cord (Myelopathy)

These are well-recognized causes of NI. It is not always clear whether the causal lesions are affecting the PNS or CNS, because primary afferent neurons extend into the spinal cord. Many peripheral sensory neurons synapse segmentally on projection neurons (e.g., spinothalamic tract neurons; see Chapter 22), but the central axons of some unmyelinated fibers as well as of myelinated fibers ascend in the dorsal columns (Briner et al. 1988). Given the small size of the spinal cord, many lesions likely affect all these compartments (Brewer et al. 2008).

It is important to recognize that NI can be the presenting sign of spinal cord injury because this requires neurological evaluation and treatment if possible. Scattered reports associate NI with various causes of myelopathy including tumors (Johnson et al. 2000; Kavak and Dosoglu 2002), multiple sclerosis (Yamamoto et al. 1981), syringomyelia (Kinsella et al. 1992), and traumatic injury causing the Brown-Séquard syndrome (Thielen et al. 2008). These authors attributed their patient’s NI to axotomy of itch neurons crossing the ventral commisure en route to the contralateral anterolateral spinothalamic tract. Paramedian lesions may similarly downregulate the existing tonic inhibitory control of itch in the spinal cord, e.g., by bhlhb5 expressing neuron (Ross et al. 2010). There are more case reports of rostral than caudal lesions. One cervical ependymoma tumor extending between C4-C7 presented with brachioradial pruritus on both arms, elbows, and forearms as the only symptom (Kavak and Dosoglu 2002).

The best documented association is with inflammatory myelopathies. Among a series of 377 MS patients, 4.5% reported NI (Matthews 2005). Itch was even more common in myelopathy from neuromyelitis optica (NMO), a relapsing autoimmune/inflammatory demyelinating disorder of the spinal cord and brain (including the optic nerves) associated with aquaporin-4 autoantibody (AQP4-Ab) (Elsone et al. 2012). Twenty-seven percent among 44 patients with AQP4-Ab-positive NMO myelitis had NI attributed to their spinal cord lesion. Itch affected the trunk in 67%, the limbs in 75%, and the occiput in 25% of patients, most often accompanied by other colocalizing sensory symptoms (Elsone et al. 2012). About half had continuous pruritus whereas half had intermittent symptoms; median itch intensity was 6 of 10 (Elsone et al. 2012). The authors postulated that itch was more common in NMO than in MS because MS affects mostly white-matter tracts, whereas NMO primarily damages gray-matter neuronal cell bodies, including the lamina 1 second-order dorsal-horn neurons that process itch signals.

The second best documented association between spinal-cord injury and itch is with cavernous hemangiomas of the spinal cord (Cohen-Adad et al. 2012; Dey et al. 2005; Sandroni 2002; Vuadens et al. 1994). The author suggested that features of these rare lesions make them pruritogenic, specially their preferred location in the upper rather than the lower spinal cord and perhaps in the dorsal rather than ventral cord (although dorsal cavernomas may simply be those that are more operable and come to neurosurgical attention), plus the tendency of these lesions to trigger gliosis and bleeding. Cavernomas are probably pruritogenic for the same reasons that they are epileptogenic when in the brain; gliosis and hemosiderin deposition both excite ectopic action potentials (Dey et al. 2005). Of note, our rat model of NI from spinal cord cavernoma (see above) includes both these features, and the cervical syrinx associated with NI contained hemosiderin consistent with prior bleeding as well (Kinsella et al. 1992).

7.3.5. NI Syndromes Affecting the Head and Neck (Cranial Nerves and Ganglia)

Lesions of any cranial nerve that contain somatosensory representation, its ganglion, or its central projections can cause NI and/or neuropathic pain that localizes to the region innervated by that nerve’s sensory axons. In the head and neck, this includes VI (nervus intermedius) and IX in addition to V. At least one case of neuropathic self-injury to a tonsil has been associated with damage to IX (Stefaniu et al. 1973). Although any type of lesion or injury can trigger neuropathic sensory symptoms, the most common causes are vascular compression (e.g., tic douloureux) or zoster, which can affect VI and IX as well as all three branches of V (of which involvement of V₁ or herpes zoster ophthalmicus is most common).

Cranial neuropathies are disproportionately likely to trigger NI as compared to lesions affecting nerves innervating the lower torso, legs, and the sacrally innervated dermatomes. The reasons are unknown, but it has been hypothesized that they might be related to protecting the facial mucosa, a prime target of insect attack (Oaklander et al. 2003). In PHI, after shingles, data from several independent groups confirm that higher proportions of patients with shingles of the head or neck develop PHI than patients with zoster on the torso (Oaklander et al. 2003). A similar gradient in susceptibility to autotomy after dorsal rhizotomy is described in rats (Lombard et al. 1979). Despite its proximity to the brain, neuropathic itch of the face, head, and neck is more likely to be caused by lesions of peripheral rather than central neurons. The discussion above pertaining to ganglionopathies and radiculopathies applies equally to the cranial nerve ganglia.

7.3.6. Trigeminal Trophic Syndrome and Other Forms of Self-Injurious Behavior from NI

Group III itch according to the IFSI classification (Ständer et al. 2007) includes self-injurious scratching or mechanical stimulation of the receptive field innervated by injured sensory nerves. Such self-injury was for many years attributed by most to an aberrant response to neuropathic pain (Mailis 1996; Rapin and Ruben 1976) plus or minus coexisting psychopathology. Few patients were ever actually asked if they felt itch. Some authors mention vague descriptors of itch (e.g., aversive sensations and formication). Some patients had itch and pain, making it difficult to be certain which motivated their self-stimulation. However, given that pain triggers protective behaviors such as withdrawal, whereas itch triggers scratching, pain seems implausible as a motivation for self-injury. Publication of the case of a woman who scratched through her skull because of intractable PHI (without postherpetic pain) (Oaklander et al. 2002), helped demonstrate the self-injurious scratching was a marker of neuropathic itch colocalizing with loss of protective pain sensation. Also, see the discussion above of animal models regarding autotomy.

A contributing factor to such self-injurious behavior is many patients’ (and even their physicians’) unawareness that their cutaneous lesions are the consequence of their itch and not the cause of it. Teaching how to break the itch–scratch cycle is imperative. The confusing nomenclature for the skin changes caused by excessive scratching (e.g., prurigo nodularis, lichen planus, and macular amyloidosis) can obscure the true cause, which, in many cases, is chronic itch. Because scratching can occur while patients are sleeping or inattentive (Savin et al. 1973, 1990; Savin 1975), barriers to scratching (e.g., wearing mittens during sleep), and behavioral modification can be effective. Topical local anesthetics can also be helpful, testifying to the importance of remaining primary afferent signaling in maintaining this condition.

My explanation is that severe damage to primary afferent pathways can leave isolated remaining itch axons firing ectopically (without provocation) but in insufficient numbers to generate the powerful surround fields of inhibition that normally laterally inhibit itch in the dorsal horn (Oaklander et al. 2002). This is consistent with the fact that scratching, which augments nociceptive afferent firing in and around the receptive field, provides transient relief, and with reports that administering minute amounts of pruritogens to the skin using cowhage spicules produces itch disproportionate in intensity to the dose of pruritogen or to the size of the stimulated area (Sikand et al. 2011).

Trigeminal trophic syndrome (TTS) is a historical term referring to self-induced traumatic lesions of the head and face caused by the most severe forms of NI. The worst cases are literally disfiguring and even potentially fatal. Other historical names include trigeminal neuropathy with nasal ulceration, trigeminal neurotrophic ulceration, ulceration en arc, and trophic ulceration of the ala nasi (Jaeger 1950; Ziccardi et al. 1996). Attributed first to loss of a “trophic” substance normally supplied by axons, then to psychopathology during the Freudian era, TTS is now attributed to the disastrous conjunction of intractable neuropathic itch plus colocalizing loss of protective pain sensation caused by severe nerve injury. Some but not all patients have colocalizing neuropathic pain as well.

TTS was reported and studied in numerous publications including large case series by early twentieth century neurosurgeons including Harvey Cushing. It occurred then as an adverse effect of trigeminal rhizotomy, the only logical treatment for trigeminal neuralgia in the premedication era (Becker 1925; Cliff and Demis 1967; Cushing 1920; Harper 1985; Henderson 1967; Howell 1962; Jefferson and Schorstein 1955; Karnosh and Scherb 1940; Kavanagh et al. 1996; Knight 1954; Loveman 1933; McKenzie 1933; Philpott 1941; Schorstein 1943). TTS was also reported after other iatrogenic injuries to the trigeminal ganglion and root including injection of neurotoxins or thermal injury (Harris 1940; Walton and Keczkes 1985). Rare causes include infections such as syphilis, leishmaniasis, and leprosy (Thomas et al. 1991). Shingles currently appears to be the most common peripheral cause (). The TTS syndrome can also be produced by brain lesions, most often stroke (see below). There are scattered reports of self-injurious scratching inside the mouth or nose. One patient whose “burning mouth syndrome” of unknown etiology apparently included itch, although itch was not explicitly mentioned, used “mechanical manipulation” inside her mouth to “obtain relief” to the point of causing superficial lesions. Her symptoms (and erosions) resolved after gabapentin treatment (Meiss et al. 2002).

In addition to the treatments discussed below for NI, patients with self-injury from NI require additional treatment. Most important is to make sure that patients understand that their lesions are self-induced. Behavioral modification including barriers to protect the affected area and wearing mittens during sleep can impede scratching. TTS injuries may require treatment of infections, wound management, and surgical reconstruction of defects. This must be done with innervated flaps as grafts of denervated tissues from the affected areas are less viable and patients continue to damage them (McLean and Watson 1982). Other strategies to modulate peripheral activity in itch neurons, such as transcutaneous electrical stimulation (Westerhof and Bos 1983) are worth considering.

7.3.7. Neuropathic Itch Syndromes Arising from the Brain

Brain lesions that cause NI validate the concept of “central itch”; that lesions of second- and third-order CNS itch neurons are also capable of triggering it. They demonstrate that NI is a systems or network disorder caused by imbalances between excitatory and inhibitory transneuronal signaling, rather than by consequence of lesions in one specific location. Case reports demonstrate that any type of brain lesion that affects the brain’s itch neurons can cause central neuropathic itch, including TTS (King et al. 1982). Central lesions were said to cause about one fifth of cases of TTS (Spillane and Wells 1959).

Stroke is the most common brain lesion associated with NI, particularly infarctions of the lateral medulla (Wallenberg’s syndrome; ) or slightly more rostral strokes in the lateral pons where itch signals presumably ascend (Curtis et al. 2012; Dick and Gonyea 1990; Fitzek et al. 2006; Massey 1984; Savitsky and Elpern 1948; Shapiro and Braun 1987; Wallenberg 1901). Even today, some stroke specialists are not aware of these associations (Oaklander et al. 2009). Strokes that only cause weakened chewing or reduced facial touch with preserved pain sensation do not cause NI and TTS, only those that damage nociceptive pathways and cause profound sensory loss (Fitzek et al. 2006). Such lesions identify the location of ascending itch pathways (see Chapter 22). Neurophysiological study of nonhuman primates has established that itch-signaling spinothalamic tract neurons project to the ventral posterior lateral nucleus, ventrobasal complex, and the posterior thalamic nuclei (Davidson et al. 2012; Simone et al. 2004). Correspondingly, NI has also been associated with Dejerine-Roussy syndrome (also known as the posterior thalamic syndrome and retrolenticular syndrome), caused by lesions of the ventral posterior thalamus and internal capsule (King et al. 1982). Better known symptoms include hemianesthesia and hemi-pain contralateral to the lesion. One of few studies that correlated sensory disturbances with anatomical localization of infarctions of the posterior cerebral artery (it supplies the ventrolateral thalamic sensory nuclei and white-matter tracts to the somatosensory cortex) found that all patients with sensory findings had thalamic damage, and that among patients with sensory findings, 11 of 15 had infarctions in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries (Georgiadis et al. 1999). However, as in most such studies, itch was not specifically studied.

FIGURE 7.3

Focal neuropathic itch due stroke (trigeminal trophic syndrome). A woman with trigeminal trophic syndrome (TTS) as part of Wallenberg syndrome: (a) Location of her lateral medullary infarction on imaging and (b) excoriations of the itchy areas of her (more…)

Interestingly, Wallenberg’s original patient with TTS had shingles in his stroke affected area as well, so the exact cause of that patient’s NI remains uncertain (Wallenberg 1901; Wolf 1971). Less frequent brain lesions associated with NI include multiple sclerosis (Matthews 2005; Ostermann 1976; Yamamoto et al. 1981), tumors within or near the brain (Andreev and Petkov 1975; Summers and MacDonald 1988), and infections (Sullivan and Drake 1984). NI or scratch marks that spread beyond the dermatome of one individual trigeminal division suggest a causal lesion in the ganglion or brain rather than in the PNS.

Severe pruritus unresponsive to conventional treatments has been associated with several prion diseases including Creutzfeldt-Jakob disease (CJD) in humans. Scrapie (Petrie et al. 1989), which develops in sheep and goats in western Europe, is named for the characteristic injurious self-directed scratching and biting. This most often affects the rump, unlike the rostral predominance typical of other human and animal forms of NI. NI appears to occur only rarely in sporadic CJD (Shabtai et al. 1996) but was reported by 19% among 31 patients with familial CJD (Cohen et al. 2011). The itch was generalized in three patients, regional in two and localized in one patient. It was transient in one patient and continued throughout the disease in five patients. Diffusion weighted imaging associated the itch with reduced diffusion in several brain areas known to be affected by CJD, but most significantly with the midbrain periaqueductal gray. The authors postulated damage to inhibitory gating mechanism for itch however, because prions are deposited in the skin and in the peripheral nerves in CJD and other human prion diseases (Lee et al. 2005), the itch signals might also have conceivably been generated in the PNS.

In addition to the brain stem and posterior thalamus, higher brain areas participate in itch perception and processing (see Chapters 23 and 24). Positron emission tomography in normal adults implicates primary but not secondary somatosensory cortex (Brodmann 24) as well as the periaqueductal gray and cingulate gyrus in histamine-induced itch (Drzezga et al. 2001; Hsieh et al. 1994; Mochizuki et al. 2003). However, the secondary somatosensory cortex and insula have been implicated in electrically induced acute itch (Mochizuki et al. 2009). There are very rare reports of patients with small somatosensory-cortex lesions and somatotopically appropriate NI, usually associated with seizure (Maciejewski and Drop 2002) or subarachnoid hemorrhage (Canavero et al. 1997), consistent with cortical hyperactivity rather than degeneration.

7.3.8. Phantom Itch in Amputated Body Parts

Phantom itch is well described and even known to the public. It can occur after amputation of any innervated body part. Among the roughly 60% of women with phantom sensations after mastectomy, itch was the most common (Lierman 1988). The prevalence of phantom itch demonstrates the critical role of denervation in generating neuropathic itch; phantom itch is an extreme endophenotype of peripheral NI, which arise in the context of sensory deafferentation. Because the itchy area is missing and thus cannot be scratched, phantom itch is not associated with self-injury. It remains uncertain exactly which neurons fire excessively to generate phantom itch sensation. On the basis of the more plentiful studies of postamputation pain, possibilities include spontaneous activity of isolated peripheral nociceptors, perhaps those that are regenerating or entrapped in scar tissue (as with postburn itch) or neuromas. These can generate “stump” sensations perceived in remaining tissue as well as sensations perceived in prior receptive fields that have been amputated. Edge effects at the border of innervated and noninnervated tissues may also contribute. However, central mechanisms, whether originating in the spinal cord or brain, are paramount in phantom sensations including the Charles Bonnet syndrome after visual loss and tinnitus after hearing loss (Jastreboff 1990; Schultz and Melzack 1991). Phantom itch can only be studied in humans who can report it, but there are few or no studies of patients with phantom itch independent of phantom pain. It is likely that thalamic plasticity, including expansion of the representation of the proximal limb into thalamic region that used to represent the amputated part contributes, as well as unmasking of latent receptive fields (Dostrovsky 1999).

Treatment options primarily involve medications shown effective for phantom pain and other sensations, such as the gabapentinoids and tricyclics. Several methods involve increasing remaining afferent input. This includes behavioral therapies such as wearing a prosthesis to provide visual and functional input (Lierman 1988), mechanically stimulating the area or the contralateral body part and “mirror therapy” (Chan et al. 2007). Neuromodulation may have similar effects by triggering action potentials at various parts of the itch network independently of afferent input (Ahmed et al. 2011). One patient reportedly found relief from phantom itch and pain by scratching or massaging his prosthesis or the leg of another person (Weeks and Tsao 2010). The authors hypothesized that sensory mirror neurons permitted integration of this feedback into his own sensory circuits.

7.4. MANAGING AND TREATING NEUROPATHIC ITCH

The reflex and volitional scratching triggered by NI bring fleeting relief at best, and treatments effective for conventional itch such as antihistamines and anti-inflammatories are usually ineffective, so treatment is a challenge in most cases. Pharmacotherapy is worth considering for patients with disabling NI, particularly when scratching remains uncontrolled even after its origin is explained and behavioral modification is attempted. No medication has a U.S. Food and Drug Administration indication for neuropathic itch and no high-quality clinical trials have been conducted. No studies of NI are considered Class I according to evidence-based medical guidelines, such as those of the American Academy of Neurology. The information below comes from Class IV studies. Insurance companies can deny reimbursement as there is no good evidence for most treatments. It is self-evident that the best treatments are disease modifying, such as treatment of the cause of an itch-inducing peripheral nerve or root lesion. The remarks below refer to management of symptoms for patients who do not have this option. The efficacy of medications prescribed for neuropathic itch is variable.

7.4.1. Conservative Treatments

Options to consider in all patients include those that minimize secondary itch and inflammation caused by scratching, such as maintaining good skin hydration, as well as barriers to reduce scratching. Barriers should be used in most patients with self-injury from scratching NI, particularly while patients sleep and scratch (Savin et al. 1973). Options include a lockable helmet to protect the scalp in patients with V1 TTS, rigid surgical braces to protect the limbs and torso, and wearing mittens at night. Video recordings document that patients with severe itch engage in nocturnal scratching while sleeping and are unaware of their actions. Cognitive behavioral therapy may be required to help break the itch–scratch cycle or at least to substitute less destructive methods for scratching. Other behavioral changes to consider include protecting affecting areas from itch-triggering stimuli (e.g., contact with clothing) and instituting low levels of tonic mechanical stimulation. Wearing a close-fitting binder or wrap can be helpful in several ways. Exercises to reduce nerve impingement in notalgia paresthetica have also been recommended (Fleischer et al. 2011; Savk and Savk 2004). Consideration should also be given to ways to reducing barriers to axonal regeneration and healing, among which smoking cessation and regular exercise to improve tissue perfusion are paramount. However, many patients will require drug therapies as well.

7.4.2. Topical Application of Medications

Topical treatments that have no systemic absorption and hence no systemic adverse effects are appealing. Among them, the local anesthetics are paramount. These penetrate mucous membranes well (with some potential for systemic absorption) and thus should be considered for chronic itch affecting the mucosa. They are not administered to the eye because of the potential for suppressing protective pain sensation. On the skin, local anesthetics require an occlusive wrap or patch (e.g., 5% lidocaine patch) for penetration. Rare patients with significant self-injury require daily subcutaneous injection of long-active local anesthetics. Rarely, have caregivers or patients with V1 PHI been taught to perform supraorbital nerve blocks at home.

The utility of topical capsaicin (8-methyl-N-vanillyl-6 nonenamide) is uncertain. Punctate or miniscule experimental doses can cause itch (Sikand et al. 2011). When applied to larger areas, topical capsaicin induces predominantly pain, which inhibits itch. Over-the-counter products containing low-concentration capsaicin (usually 0.025%–0.075% w/w) have marginal efficacy against various pain conditions in clinical studies, but they require dosing three to five times daily. Systematic review found no convincing evidence for the use of low-dose topical capsaicin to treat pruritus in any medical condition, although the quality of most of the trials reviewed was poor (Gooding et al. 2010). Practically speaking, most patients find capsaicin application painful and few continue it. Scientifically speaking, capsaicin causes degeneration of distal TRPV1⁺ axon terminals (Simone et al. 1998), producing the same kind of axonal injuries that are associated with neuropathic pain and itch so there is at least potential for delaying or impeding axonal regeneration. A single-dose high-concentration patch containing 8% w/w is currently licensed in the European Union for treating peripheral neuropathic pain in nondiabetic adults and in the United States for treating PHN, but PHI was not studied. Case reports support utility of other topical treatments such as topical tacrolimus and gabapentin (Nakamizo et al. 2010).

7.4.3. Intradermal Injection of Botulinum Toxin Type A

BTX-A administered by local subcutaneous injection is increasingly used to treat peripheral neuropathic pain. Anti-itch effects are independent of its better known ability to weaken cholinergic neuromuscular transmission. The antipruritic benefits are based on inhibition of cutaneous mediators of neurogenic inflammation including substance P, CGRP, and glutamate, as well as inhibition of vanilloid receptor activity (Ranoux et al. 2008). For this reason, BTX-A is being explored in itch, and there is prospective evidence of efficacy in histamine-induced experimental itch (Gazerani et al. 2009). Isolated case reports (Kavanagh and Tidman 2012) and a very small study of four patients with notalgia paresthetica, one with meralgia paresthetica and one with neuropathic itch on the upper foot that showed a mean reduction of VAS by 28% at 6 weeks posttreatment (Wallengren and Bartosik 2010), suggest efficacy so this is worth considering. As of 2012, an industry-sponsored phase III trial of BTX-A (Xeomin) was registered with the US NIH’s ClinicalTrials.gov.

7.4.4. Systemic Pharmacologic Treatment

There are no controlled trials (Class I–III) of treatments for neuropathic itch; hence the recommendations below are based on Class IV evidence such as case reports or expert opinion. General recommendations include beginning with one of the medications discussed below, then raising the dose until relief is obtained or persistent adverse effects ensue. During a medication trial the dose should usually be raised to the maximum tolerated before discontinuing that medication and trying another; preferably from a different class. If partial relief is achieved from a well-tolerated medication, the second one added should be from a different class. Too often, patients are treated with low doses of multiple medications making it difficult to assess each one’s efficacy or to attribute adverse effects.

Current options include systemic administration of medications that reduce ectopic neuronal firing, such as cation-channel antagonists (e.g., anti-epileptic medications), or those that augment inhibitory circuits (e.g., tricyclics). While many of these are also effective for neuropathic pain, not all are. Opioids—which are effective for neuropathic pain—trigger pruritus, particularly when administered near the spinal cord (Jinks and Carstens 2000). Isolated case reports, mostly in TTS patients, support use of carbamazepine (Bhushan et al. 1999), gabapentin (Macovei et al. 1991), amitriptyline (Finlay 1979), and pimozide (Duke 1983; Mayer and Smith 1993). One patient with intractable trigeminal itching and scratching after stroke plus shingles found efficacy of bupivicaine and clonidine administered intrathecally through a high thoracic catheter (Elkersh et al. 2003). As in neuropathic pain (Challapalli et al. 2005; Ferrini and Paice 2004), continuous systemic administration of low doses of local anesthetics by continuous subcutaneous administration at home, is a powerful treatment option that is underutilized. Brief courses of intravenous local anesthetics can be used for an in-hospital trial with cardiac monitoring to determine if there is a dose that is effective without producing adverse effects (Watson 1973).

7.4.5. Neurosurgical Treatment Options

Prior to the mid-twentieth century development of effective drugs, surgery was the only treatment for morphine-unresponsive neuropathic pain (Warren 1828). The first neurosurgeon, Harvey Cushing, established that ablative neurosurgery (cutting nerves carrying sensation from painful areas) is usually ineffective and in some cases triggers intractable anesthesia dolorosa pain (Cushing 1920). In contrast, surgical decompression or removal of structural lesions causing sensory symptoms including NI is potentially curative, even in medically refractory cases. Occasional rare causes of focal NI such as tumors or vascular malformations may require nerve surgery for definitive treatment. These surgeries are currently underutilized, in part because they requires skilled diagnosis and lesion localization by history, examination, electrophysiological study, or imaging before surgery. Itch is not yet adequately recognized as a potential localizing sign for structural nerve and root injuries.

Augmentive neurostimulation using implanted bipolar electrodes has been proven effective for various neurological symptoms including neuropathic pain, and has been used for decades. Its major advantage compared to medications is that its tiny electrical currents only affect nearby cells, unlike drugs that that can spread through the body to cause diverse adverse effects. Neurostimulation has few if any systemic adverse effects. To date, there has been little or no research on potential benefits for NI. Stimulation locations used for neuropathic pain and that should be considered for refractory NI, include proximal to a focal nerve injury (Campbell and Long 1976), the dorsal column of the spinal cord, the motor cortex, and the thalamus or periaqueductal gray (Nguyen et al. 2011). The major disadvantage of neurostimulation has been the requirement for surgical implantation. However, neurons can increasingly be activated from outside the body by electromagnetic induction or direct current stimulation. Noninvasive transcranial magnetic stimulation (TMS) of the brain is an innovative alternative with much lower risk and cost. Repetitive TMS was FDA approved for treating major depression in 2008, and several small clinical trials suggest efficacy for chronic neuropathic pain (Leung et al. 2009), so TMS should be considered for NI.

7.4.6. Contraindicated Therapies

It is perhaps equally more important in avoiding ineffective or potentially injurious treatments as in finding effective ones. Oral treatments for normal itch (e.g., h2 blockers) are usually ineffective for NI, although worth trying due to their low cost and safety, plus some patients may have a component of conventional itch that can be ameliorated by such treatment, e.g., due to substance P release from ectopically firing injured nociceptive neurons (Hagermark et al. 1978). The uncertain utility of capsaicin as a treatment for NI is discussed above. Although local anesthetics are often effective when applied topically or given systemically, there is no evidence that nerve or nerve root blocks containing local anesthetics (and/or corticosteroids) have long-term benefits that justify their risk and cost, despite transient efficacy (Eisenberg et al. 1997; Goulden et al. 1998).

When Parents Should Worry about Bumps and Bruises

What can cause some of the bumps and bruises on a child? Ebony Hunter, M.D., is a pediatric emergency medicine physician at Johns Hopkins All Children’s Hospital. On this week’s On Call for All Kids, she helps parents understand about bumps and bruises and when to be concerned.

So many things can cause bumps and bruises on your child. Insect bites and trauma are the main two reasons we see children for bumps and bruising.

Regarding insect bites, what should parents do if their child gets one, or two, or many?

First and foremost, cleanse the area as soon as you notice the bite. You can clean with soap and water. You can apply a topical over-the-counter anti-itch cream such as hydrocortisone if your child is having severe itching and there are not contraindications. However, do not apply these creams around eyes, mouth or genital areas. Try to prevent the child from scratching. You may have to clip his or her nails really short to help with this.

Can insect bites get infected?

Absolutely! If you start noticing redness, swelling, warmth, increased pain and yellow fluid from the area, then it may be getting infected. I would recommend a health care provider look at it if your child is experiencing those symptoms so that he/she can determine if it is infected or not.

How can parents prevent insect bites?

You can use a repellent. There are multiple types of repellant available. Some are DEET based and some are essential oil based/natural. If you have reservations about applying DEET frequently to your child, then you can choose the natural essential oil-based repellent. Both work well.

What about bruising? What can cause that?

Usually any type of trauma to the body can cause bruising. Kids can bump a table or fall and obtain a bruise.

When should parents become worried?

If you notice a laceration/cut that has the skin separated, your child may need stiches. I would want a health care provider to look at that. Also, if you notice any deformity in the shape of the bone or the child refuses to use that area of the body, I suggest bringing the child in. The child may have a broken bone underneath the bruise.

What should we do for bruises that seem mild?

Rest the area, ice if your child allows it and elevate it. Trying to get a child to rest and ice an area can be difficult. For mild discomfort, you can give over-the-counter pain medication such as ibuprofen or acetaminophen if your child has no other contraindications to these medications. We do not recommend you ever give a child under 18 aspirin, however.

How long will bruising last?

Usually the bruising will get worse over the first 48 hours and turn various colors of red, blue, purple depending on your skin pigmentation. There may be some initial swelling that improves over the first 24 hours. Bruises usually take about one to two weeks max to fade.

Are there any bruises that parents or caregivers should worry about immediately?

Unfortunately, yes. Any bruise on a non-mobile (meaning not walking not crawling) baby is worrisome. Ear bruising and bruising in the genital area are always concerning. Any child with frequent unexplained bruising. I would recommend the child be brought to the emergency department immediately if you notice these. Also, if you notice that your child is starting to frequently bruise more so than previously recognized with normal day play and activities, that may be an indication or underlying illness and needs to be assessed.

On Call for All Kids is a weekly series featuring Johns Hopkins All Children’s Hospital experts. Visit HopkinsAllChildrens.org/Stories each Monday for the latest report. You also can explore more advice from Ebony Hunter, M.D.

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So many things can cause bumps and bruises on your child. Insect bites and trauma are the main two reasons we see children for bumps and bruising.

Regarding insect bites, what should parents do if their child gets one, or two, or many?

Can insect bites get infected?

How can parents prevent insect bites?

What about bruising? What can cause that?

Usually any type of trauma to the body can cause bruising. Kids can bump a table or fall and obtain a bruise.

When should parents become worried?

What should we do for bruises that seem mild?

How long will bruising last?

Are there any bruises that parents or caregivers should worry about immediately?

Dangers of Button Batteries and Kids

Posted on Oct 11, 2021 in General News

If a child swallows a button battery, it can cause severe damage if not removed promptly. Emergency medicine physician Ebony Hunter, M.D., shares what to do if your child ingests a button battery.

Dangers of Button Batteries and Kids

Posted on Oct 11, 2021 in General News

If a child swallows a button battery, it can cause severe damage if not removed promptly. Emergency medicine physician Ebony Hunter, M.D., shares what to do if your child ingests a button battery.

How to Manage Back Pain, Itchy Skin & Night Sweats

Cancer patients often deal with a long list of physical side effects. But unlike fatigue, nausea, neuropathy and other well-known physical challenges that typically come with fighting cancer, some common conditions don’t get as much public attention. That may make it more difficult for patients to anticipate the side effects, to seek proper treatment for them, or to even recognize that they may have been caused by cancer or its treatment. Take back pain, for example. Is it a muscle strain or a sign that cancer has spread? Or when it comes to itching, is it a symptom of dry skin or a result of the hormone therapy the patient is taking to treat her breast cancer? Night sweats is another common complaint—was it the spicy food or a side effect of treatment? Knowing the answers may help patients better manage these issues so they don’t disrupt their quality of life.

“ Cancer patients are whole people with whole histories, and sometimes it’s hard to know what is causing certain symptoms.” – Katherine Anderson, ND, FABNO – Chief of the Division of Naturopathic Medicine at Cancer Treatment Centers of America^® (CTCA)

Back pain

Back pain may be a symptom of conditions unrelated to cancer, such as a ruptured disc. But cancer patients who experience these aches and pains during rest or even after medication or physical therapy may want to talk to their doctor about whether the pain is cancer-related.

For some cancer patients, for example, back pain is a sign that the cancer has traveled beyond its origin—namely, to the bones and spine. That especially happens with some breast and prostate cancers, which typically spread first to the bones, but it also happens with other metastatic cancers, such as those of the colon, rectum, ovaries and lung. In fact, about 25 percent of lung cancer patients experience back pain. Because the disease typically isn’t suspected until it has progressed to advanced stages, back pain also may be one of the first symptoms that people with undiagnosed lung cancer notice.

To help relieve back pain that’s not related to cancer, Anderson says she typically suggests that patients use acupuncture as an alternative to opioids. She also prefers options like chiropractic care, generalized stretching, deep breathing techniques and natural anti-inflammatories, such as fish oil and curcumin, a plant-produced chemical.

Itchy skin

In general, itching is not a symptom of cancer, although it may be a sign of advanced cases of pancreatic and liver cancer, when the cancer has progressed enough to cause jaundice—a yellowing of the skin or eyes that occurs when the organs aren’t functioning properly. Most of the time, itching is a sign of much more benign conditions like allergies or dryness, although it may be caused by certain cancer treatments, such as chemotherapy, radiation or targeted therapy.

To help soothe itchiness, patients may try a number of remedies, which typically involve moisturizing and hydrating the skin. Anderson suggests that patients:

Use skin creams that don’t contain alcohols or fragrances
Use warm water instead of hot water while bathing
Use a mild, unscented soap
Use baking soda instead of deodorant
Drink plenty of water and get plenty of rest

Night sweats

Menopause and fever are the most common causes of night sweats, but other, external factors may be at play, like exercising or eating spicy foods too close to bedtime. Night sweats may also be caused by cancer treatments like chemotherapy and hormone therapy, or they may develop as a symptom of cancer itself.

The most common types of cancer associated with night sweats are lymphoma, leukemia, bone cancer, liver cancer and mesothelioma. “It’s unclear why some types of cancer cause night sweats, but they may occur because your body is trying to fight the cancer,” Anderson says. “If your night sweats are caused by cancer, you’ll likely experience other symptoms, too, like unexplained weight loss and fevers without infection. Also, they’ll typically stop once your cancer is treated.”

Some tips for managing night sweats include:

Placing a damp cloth or cold compress on your forehead
Wearing loose-fitting clothes made of cotton
Taking a cool shower before bed
Practicing relaxation and stress-reducing techniques like yoga and meditation before bed
Using a fan at night

A number of lifestyle changes may also help ease back pain, itchy skin or night sweats. For instance, obesity is a risk factor for back pain in both men and women, and Anderson says she notices night sweats more often in breast cancer patients who are overweight. “Changes in diet and movement are going to help you manage your weight, build muscle mass and improve immune function, and those benefits are going to have a cascade effect to other areas of your life,” she says.

Genital Itching – Symptoms, Causes, Treatments

Itching in the genital region can result from irritation, allergy, inflammation, infection or cancer. Irritation can occur as a result of exposure to chemicals in soaps, feminine hygiene products, perfumes, lubricants, douches, and creams. Similar chemicals can also cause allergies in some people, as can latex. In the case of irritation and allergy, avoiding exposure to the irritant or allergen may be all that is needed for the itching to resolve.

Sexually transmitted infections, such as herpes or trichomoniasis, can cause genital itching, as can other infections, such as yeast infections and bacterial vaginosis. Pubic lice, also called “crabs,” are sexually transmitted and typically cause genital itching. Scabies, which can be spread sexually or through other skin-to-skin contact, is a contagious skin disease that typically causes itching. Scabies is caused by very small mites and can affect any part of the body.

Tinea cruris, a fungal infection sometimes referred to as “jock itch” or “ringworm of the groin,” can also cause genital infection. People who have tinea cruris may also have athlete’s foot or ringworm.

Some noninfectious skin conditions, such as psoriasis, eczema, and lichen simplex chronicus, can involve the genital area. These itchy skin conditions often affect other areas of the body, as well. Other noninfectious causes of genital itching include changes associated with decreased hormone levels following menopause, as well as precancerous changes and cancers. The treatment of genital itching is highly variable depending on the cause of the itching.

Genital itching is unlikely to be part of a condition that requires emergent treatment; however, it can have several causes, some of which are easily treated and others that can ultimately lead to serious complications. If you have genital itching that lasts for a couple days or more or causes you concern,
seek prompt medical care.

Board Certified Vein and Vascular Specialists

We all get bruises when we bump into something or fall down. Often, we may not remember exactly where a bruise came from. If you suffer from bulging or discolored varicose veins, you may get bruises more easily in that area. That’s because bruising, sometimes called vein bruising, is part of the body’s healing process after injury or trauma. Individuals can also get bruises after both minor medical treatments and major surgery. Bruises should improve steadily and gradually fade. If they don’t, you may need to see your doctor.

Minor Bruises

Bruises you may get after minimally-invasive Cincinnati vein treatment are generally very minor. Because of advancements in vein procedures, issues like varicose veins, spider veins, and vascular disease can all be treated through quick, efficient medical techniques in our offices. As bruises fade, your legs look and feel better than ever, as you’ll notice in our Before & After photo gallery. Follow your aftercare instructions from our clinic, which may include resting your bruised leg, propping it above heart level, applying an ice pack (for only 10 minutes at a time) and wearing compression socks. Keep in mind that non-strenuous walking is also encouraged to re-establish proper circulation.

How to Recognize Serious Bruising

Bruises may be serious, and require medical care when bruising:

Has not improved at all, or has gotten much worse, after a week. There could be a larger accumulation of blood, called a hematoma, under the skin. In some cases, a hematoma will need medical care or may clear up on its own. Contact your doctor for instructions and s/he may request you to come to the office.
Causes severe pain or swelling.
Feels warm and tender to the touch, with a possible “pulling” sensation when you move your leg. This can be a sign of DVT or deep vein thrombosis, which is a blood clot, typically occurring deep within the leg. Call or go to your local emergency room for immediate, expert care.
Is seen on a body area where you typically never bruise.
Keeps re-appearing, after initial healing.
Covers a large area with no probable cause. This could be a sign of a minor medical issue, or something more serious. Blood disorders such as hemophilia, other blood clotting disorders, anemia, or leukemia are possible causes, so schedule a visit to your doctor for an evaluation.

Advanced Vein Treatments in Kentucky

If you need varicose vein treatment, such as laser vein treatment, to banish your vascular problems or prevent future vein bruising, we’re ready to help. At our VIA vein center, we are always here for you if you notice vein symptoms, including bruising, that concern you after any procedure. For expert vein care that will improve circulation, health, and appearance, contact us at Vascular and Interventional Associates in Crestview Hills, KY, today.

Brachioradial Pruritus – Neuropathic itch – Caring Medical Florida

Ross Hauser, MD., Danielle R. Steilen-Matias, PA-C

Among the many symptoms we see in our patients are problems of skin rashes and itching. The problems of itching can in itself be challenging. Is it a problem of the skin and skin rashes or is it a problem of neurology and a symptom more on its own? If you are reading this article the most important thing to you is that there is an answer to stop the itching no matter what is causing it.

In this article, we are going to present information on a very interesting case of “itching” in a patient that we treated. It was an uncontrolled itching from an unknown source. We found the source. It was coming from the patient’s neck and her cervical spine instability.

This is a Hauser Neck Center at Caring Medical case study. The patient herself speaks in the video. Below are explanatory notes of points made during the video.

A miserable, itchy patient.

Danielle R. Steilen-Matias, PA-C: Attending clinician.

When this patient came in she was miserable. Itching up and down her arms. She was not sleeping and had tried many treatments and remedies to get rid of the itching.
Initially, she thought the itching was from too much sun.
We spoke about a condition of bilateral (both arms) upper arm itching called brachial radial pruritus that can be traced to the cervical spine nerve roots.

Too much sun? Cervical spine and neck instability? Both?

Many people contact us after years of topical steroid cream, high doses of gabapentin, muscle relaxants, cortisone injection, among other treatments. They have complaints of insomnia, stress, anxiety, irritability, and depression.

When people have itching of unknown origins they will typically be sent off to the dermatologist. This probably happened to you. The initial treatments offered were probably more potent or heavy-duty prescription ointments and creams than those you had already bought over the counter or on the internet. When these treatments are not working or have been eliminated from being useful for you, the next step is of course to dig deeper and look for other things.

If you are often out in the sun, the sun becomes an easy culprit. As you will see in our patient story, she was told by her dermatologist to avoid the sun, after two months of sun avoidance and no relief our patient decided that the sun was not the problem.

A paper in the Journal of the American Academy of Dermatology (1) found that the itching described as brachioradial pruritus, could be from the sun, it could be from neck instability causing compression in the cervical root nerves among many causes. People could also be at greater risk if they had neck instability and problems in the cervical spine and spent a lot of time in the sun.

So it could be from too much sun, cervical spine and neck instability, and both. Here is what the research says:

“There has been controversy regarding the cause of brachioradial pruritus: is it caused by nerve compression in the cervical spine or is it caused by prolonged exposure to sunlight?…. The temporal course (the time of year you get it, spring compared to fall for instance) of the brachioradial pruritus and the histological changes in the skin similar to those caused by ultraviolet light, indicate that sunlight is an eliciting (can cause the itching) factor and that cervical spine disease can be a predisposing (puts you at higher risk) factor.”

Exacerbated by exposure to bright sunlight or ultraviolet radiation (UVR), and is associated with degenerative changes in the cervical spine.

As I state throughout this article, cases of Brachioradial pruritus are thought to be rare and when a case is considered strange and rare enough it is published in a medical journal. We are finding these cases to be more common in our patient population and these people’s stories well match the examples from independent clinics published in the medical literature. That being a terrible itch with no diagnosis and no effective treatment.

This is a case history presented by doctors at the Beth Israel Deaconess Medical Center, Department of Anesthesia, Critical Care, and Pain Medicine, Harvard Medical School. It was published in the medical journal Case Reports in Women’s Health. (2)

Diagnosis is difficult and is usually delayed for two-three years.

“Brachioradial pruritus is a specific subtype of neuropathic pruritus that commonly presents in women. This condition is a type of neurological itch that mostly involves the dorsal forearm. It is more common in fair-skinned females, is exacerbated by exposure to bright sunlight or ultraviolet radiation (UVR), and is associated with degenerative changes in the cervical spine. Diagnosis is difficult, and is usually delayed for two-three years.”

A patient who suffered brachioradial pruritus for many years and was misdiagnosed by multiple specialists

“(In this case history the doctors describe) a patient who suffered brachioradial pruritus for many years and was misdiagnosed by multiple specialists until she presented to our pain clinic. The patient had undergone invasive diagnostic testing by previous specialists but this had not led to a diagnosis. After a thorough history and exam, the diagnosis of brachioradial pruritus was considered and the patient was treated with anticonvulsant medications, as these have been shown to be effective in this condition. This case is of interest to all physicians treating female patients as consideration of this diagnosis can avoid unnecessary invasive diagnostic testing.”

What the doctors at Harvard Medical School describe is what we see in many people that come to our center. Difficult to understand problem. A difficult-to-understand problem is a difficult-to-treat problem. People lived with it. For some of our patients with cervical instability, that in the past they could get an itching rash when exposed to too much sun was an understood consequence of being outside. The idea that it was coming from a neck problem, may not be as well understood.

Digital Motion X-Ray (DMX) demonstrates cervical spine instability.

From those of you reading this article and researching your itching problem the idea that your problem is coming from the neck or nerves may not be a new one as you may have symptoms of neck pain and instability and itching is one skin manifestation of many you may suffer from. Please see our article: Skin Pain, Hot, and Cold Skin: Are fixing upper cervical neck instability problems the missing treatment?

The images of the patient’s neck will be explained below. Based on these images we could then suggest beyond a reasonable doubt that the patient’s itching was related to her cervical spine instability.

So now let’s explain:

What is a DMX digital motion x-ray?
What does the image below mean?
How does this address the problem of itching?

If you are watching along with the video we are at 1:40:

To confirm our suspicions that brachial radial pruritus, the severe itching in both her arms was coming from nerve compression in the cervical spine we ordered a digital motion x-ray of her neck.
A digital motion x-ray is an x-ray movie that allows us to see cervical segment instability or cervical ligament laxity in the neck that could cause or allow pinched, herniated, compressed nerves to occur. These nerves of course run through the cervical spine.
The image above on the left is an image of the patient leaning forward, head down. The image to the right is the patient with her head back, chin in the air.

What do the red lines mean?

The red lines should be reflected as a continuous line. The continuous nature would show us that the cervical vertebrae are lined up in their proper alignment, the neck is stable. That is not the case however in this patient. What we see is this.
- Left side image: with the patient looking down we see that the line displaces at C3/C4. The vertebrae are in motion or they are hypermobile, not where they are supposed to be. This is cervical instability and vertebrae in motion can press on the cervical nerve roots that pass between them and go down your arm. The condition also exists at C4/C5 and C5/C6.
- Right side image: with the patient looking up we see that the line displaces at C4/C5. The value of the DMX motion picture x-ray is that we can see that on certain movements the patient’s symptoms can worsen or can be lessened.

Irritating Itching, pruritis from spinal instability

A patient had a horrific itching in the arms. She went to doctors and nobody seemed to be able to help her.
Later it was revealed that the patient had dizziness, clicking, and grinding in her neck and she had cervical spine instability. Among her may symptoms her cervical spine instability was causing the itching. After treatment, we were able to resolve her itching issues. That was about ten years ago.

Itching and nerve irritation

Itching can be from any type of nerve irritation. You may have been given a diagnosis of pruritus. If you have sciatic-like problems you may have been diagnosed with lumbar radicular pruritus. In other words, the sciatic nerve is getting irritated and causing itching in the leg or in the arm. This is a diagnosis of brachial radial pruritus or brachial pruritus and if it involves the neck is often called cervical pruritus.

One side of the body itching

In other patients, we see one side of the body itching. This is an indication that the problem is coming from the neck. In people like this, we examine them with a Digital Motion X-Ray (DMX) to determine the amount of cervical spine instability and if this is indeed a factor in their unexplainable and difficult-to-treat itch sensation. If the itch is on the left side of the body DMX will typically reveal cervical spine instability on that side of the body. We typically focus, based on decades of experience in treating these chronic neck cases on the C1-C2 when there are symptoms of pruritus although cervical spine instability at multiple regions can cause many conditions including symptoms.

In the video above the title refers to the strange sensations that a patient may experience with cervical spine instability that cause compression on their nerves and spinal column. One of the reasons we call these symptoms strange is that many of the people we see have been looking for and chasing a viable treatment for problems that are neurologic-like in nature. We see many people with these challenges.

Multiple inconclusive diagnostic evaluations (dermatology, rheumatology, neurology, and psychiatry) and unsatisfactory multimodal conservative treatment attempts.

The concept of itching skin or Brachioradial Pruritis is still considered somewhat of a medical ailment in the medical community. Here is a case history reported by the Department of Orthopaedic Surgery, Hospital for Special Surgery, and published in the Journal of the American Academy of Orthopaedic Surgeons (3). This is what the attending physicians wrote:

“Brachioradial pruritus is a rare condition characterized by chronic localized itching of the dorsolateral (back and to the side) upper extremities. Although the exact pathophysiology is still unknown, cervical nerve compression is thought to be a cause.

(This case history presents) the case of a 56-year-old man with a 6-year history of disabling chronic bilateral upper extremity pruritus and pain as well as concurrent neck pain. The patient presented to our office after multiple inconclusive diagnostic evaluations (dermatology, rheumatology, neurology, and psychiatry) and unsatisfactory multimodal conservative treatment attempts.

His symptoms markedly impeded his ability to get restful sleep. Imaging of the cervical spine revealed multilevel cervical spondylosis, spinal stenosis with cord compression, and multilevel foraminal stenosis. The patient underwent successful multilevel anterior cervical decompression and fusion and was instantly symptom-free. The present case highlights that patients complaining of itching of the dorsolateral forearms of seemingly unknown etiology should undergo a workup of the cervical spine. If conservative treatment fails, surgical decompression may be considered in select patients.”

As you read in this case the patient’s itching was resolved by a cervical fusion surgery. Many people have very successful spinal fusions that helped resolve their symptoms. These are typically the people we do not see at our center. We see the people for whom cervical fusion is not considered a good risk, have had failed cervical fusion, or want to explore every option before having the surgery.

A patient story: I have been suffering from stinging, itching, pain in both arms. No one could help me and on my own I found the diagnosis of Brachioradial Pruritis. I usually suffer from this burning itch pain equally in both arms but recently one of my arm became so bad I now have bruises from holding and squeezing my arm to try to relieve the pain.

I have been on Neurontin for years and have the neck traction at home to help relieve the symptoms. I am sleep deprived from it and now it is affecting my daily life.

Here is a case where these pinched nerves, can cause a neuropathic itch

Research note: Neuropathic itch can be caused by many diseases in addition to cervical spine instability. As mentioned above, if you are reading this article and you have suffered from this challenge, it would probably be safe to say that you have been to a dermatologist and followed the path that your blood work and other testing took you until you received some type of treatment or treatments and that has not worked that well for you.

Let’s look at a 2011 and a 2020 study and we can see that the understanding of Neuropathic itch remains a challenge.

You may hear yourself being described in this research.

“

Many physicians including neurologists are unaware that neurological problems alone can cause chronic itch.”

In 2011 Anne Louise Oaklander, MD, Ph.D. of the departments of Neurology and Pathology, Massachusetts General Hospital, Harvard Medical School wrote in the journal Seminars in Cutaneous Medicine and Surgery: (4)

“Many physicians including neurologists are unaware that neurological problems alone can cause chronic itch. Neuropathic itch and pain are signaling abnormalities – the source of the problem is not where the symptoms are felt. Like neuropathic pain, the neuropathic itch is still poorly understood despite fundamental advances in understanding the mechanisms of itch in the normal nervous system.

Considered physiologically, the neuropathic itch is a pathological form of itch where the stimulus-response curve that governs normal sensation has become distorted and the itch sensation is out of proportion or even completely independent of any pruritogenic stimuli (something that would normally cause an itch.) In other words, the itch can be of unknown origin.

Like an electrical problem in the wiring harness of an automobile, the actual location and cause of neuropathic itch can be extremely difficult to pin down, but effective treatment may require anatomical and etiological identification of the neurological problem and institution of disease-modifying treatment. In some cases, this may be neurosurgical. (Some type of surgery to the nerves).

Neuropathic itch does not often respond to antihistamines, topical steroids, or other medications effective for the conventional itch. Furthermore, like other neurological symptoms, the itch can signal a potentially serious neurological problem that might need treatment. Most neurology textbooks and training do not discuss the localization and etiology of errant itch, so not all neurological consultations will be insightful. A dermatologist should first examine the patient to exclude conventional causes of itch before requesting neurological consultation.”

Now to 2020

A September 2020 French study (5) showed the confusion in identifying neurological itch and the confusion of treatment which is often ineffective.

Chronic pruritus can occur in the absence of skin diseases and may be secondary to various causes. In this study, patients who sought dermatological treatment were studied.
- The study had 197 patients with chronic pruritus without skin disease.
- The average age of the patient was about 67. Almost an even split between men and women.
The main causes identified were psychogenic pruritus (41.1% of patients). The disease was coming from emotional or psychological distress.
Neuropathic (36.5%),
Endocrine (12.2%),
Haematological (9.6%) (Blood type cancers)
and iatrogenic reaction to some type of medical treatment (7.1%) causes.
The cause was unknown in 20.8% of patients.
The total percent is more than 100 because some patients had several etiologies.
Concerning symptomatic treatments, emollients (creams and ointments) were prescribed for 40.6% of patients and topical steroids for 20.3%.
Among systemic treatments, gabapentinoids (33%), antidepressants (27.4%), and antihistamines (25.3%) were prescribed. The efficacy of these treatments was rarely complete. (Did not work that well).

The itch is coming from a syrinx

When we see patients with problems of cervical spine instability, Chiari malformation, and syrinx, these patients come in with more symptoms than they can even list. One problem they may have is the itch.

A case report comes from the Michael E. DeBakey VA Medical Center and the McGovern Medical School at The University of Texas Health Science Center at Houston. It was published in the PM & R: The Journal of Injury, Function, and Rehabilitation. (6)

“This case describes a 56-year-old man with known thoracic spinal cord injury undergoing evaluation for a pruritic rash on the dorsolateral aspect of his forearms with no upper extremity neuromuscular symptoms. Common diagnoses were considered and treated with little success. The diagnosis of brachioradial pruritus was made, and evaluation for possible causes revealed a large cervicothoracic syrinx. To our knowledge, brachioradial pruritus has not been described previously as the presenting sign of post-traumatic syringomyelia.”

As stated numerous times in this article, when doctors come upon a case that is strange, rare, even unexplainable, they publish a case history to tell other doctors about what they found.

Is the itching coming from nerve compression in the neck? What are we seeing in this image?

Looking for a narrowing of the nerve space

If you have cervical spine problems and itching is just one manifestation of your symptoms, you do not need a lengthy explanation of what cervical foraminal stenosis is. If your doctors are starting to explore a cervical spine connection to a vast array of neurological type symptoms that you are suffering from and this is “new territory,” in your medical journal, here is a brief explanation. Cervical foraminal stenosis is the narrowing of the openings between the bones of the cervical vertebrae. The tunnel that your nerves move through is getting narrower. As these tunnels close in the nerves can be compressed and nerve message traffic comes to a standstill. If your nerves are not able to transmit correct messages you get neuralgic symptoms including skin problems and uncontrollable itching.

The tunnels that we are talking about are called foramen, the closing of the tunnels either through boney buildup on the tunnel walls or the compression of the walls is called a stenosis.

At 2:45 of the video. We had our clue that this is where the itching was coming from.

We did a view of the neural foramina to see if she had any narrowing of the neural foramina.

What we were looking for is where the nerve roots exit the spinal column if there was:
- Nerve compression on certain movements.
- The existence of a cervical neural foraminal stenosis.
- In general, nerve compression could lead to pain, numbness, and itching. We want to note here that this patient did not have neck pain or numbness that extended into the arms. This is not typical of the patients we see.
- But we did see that as she moved her neck, the foramen openings at C4/C5 and C5/C6 were narrowing and pinching on the nerves. We had our clue that this is where the itching was coming from. Nerves at C4/C5 and C5/C6.

What did we do about it?

This patient received Prolotherapy treatments. After the first treatment, she was able to sleep. After the second treatment, the itching went away. Disclaimer: These results may not be typical. The treatments may not help some people. Cervical spine instability may not be the cause of your itching.

Caring Medical has published dozens of papers on Prolotherapy injections as a treatment in difficult-to-treat musculoskeletal disorders. Prolotherapy is an injection technique utilizing simple sugar or dextrose. Our research documents our experience with our patients. The treatment is explained further below, but first the patient’s story.

Before we get to the patient’s story, please be aware that her story is an individual experience reflecting on her experience with our treatments. Results may vary among different individuals. Not everyone will have the same level of success.

The patient’s story begins at 4:20 of the video

I have been having severe itching in my forearms for at least a month-and-a-half. Then it progressed to my upper arms and it started to be accompanied by nerve-ending pain and burning. If I scratched my skin, it made it much worse, severely worse.

I had researched a lot and found that I thought it might be what they called Brachioradial Pruritis which could come from your neck.

I like to work out and be active so I didn’t feel like I was having neck issues or that I was doing things to irritate my nerves.

I had had Prolotherapy treatments in the past with Ross Hauser, MD, and now with his physician assistant Danielle R. Steilen-Matias, PA-C. The treatments helped my with wrist and hip pain. So when I began to suspect my neck was a problem I thought of Prolotherapy. But first, I went to a neurologist. They agreed with me that we should look at my neck and get an EMG and some imaging studies. I had a slight bulging of the discs. The intimal treatment reaction to these findings was to increase my medications to try to help me sleep at night. That did not help. The only thing that did help was ice packs. But I knew I could not spend the rest of my life sleeping with ice packs. The doctors I was seeing could not help me. They told me to come back in six months so that they could monitor the progression or regression of symptoms. I told these doctors that this plan was not helping me, I have two six-year-olds who need me and I have to function.

After the first Prolotherapy treatment I had maybe two bouts of itching within two weeks but it wasn’t anything as severe as I’ve had before. After the second treatment, I had zero symptoms. I can sleep every night I’m not taking one thing for the pain.

The treatment of cervical spine instability at the Hauser Neck Center – Research on cervical instability and Prolotherapy

In the above article, we suggest that many of the problems related to among other symptoms, itching, skin sensations, burning nerve pain. can be treated by addressing cervical spine instability in the neck. There are many ways to treat this problem. Our preferred choice is regenerative medicine injections that begin with Prolotherapy.

In 2015, our research team at Caring Medical published findings in the European Journal of Preventive Medicine investigating the role of Prolotherapy in the reduction of pain and symptoms associated with increased cervical intervertebral motion, structural deformity, and irritation of nerve roots. Irritation of nerve roots causes many of the symptoms and challenges our patients face.

Prolotherapy addresses cervical spine instability by addressing problems with the structures that hold the neck in its rightful place. The cervical spine ligaments. Ligaments are bands of connective tissue that hold C1 to C2 and C2 to C3 and C3 to C4, etc. In the images above in the patient’s DMX, we saw that the vertebrae were not being held in their proper place. This is where we directed the Prolotherapy injections as demonstrated in the above video.

In our research study, twenty-one study participants were selected from patients seen for the primary complaint of neck pain. Following a series of Prolotherapy injections, patient-reported assessments were measured using questionnaire data, including range of motion (ROM), crunching, stiffness, pain level, numbness, and exercise ability, between 1 and 39 months post-treatment (average = 24 months).

Ninety-five percent of patients reported that Prolotherapy met their expectations in regards to pain relief and functionality. Significant reductions in pain at rest, during normal activity, and during exercise were reported.
Eighty-six percent of patients reported overall sustained improvement, while 33 percent reported complete functional recovery.
Thirty-one percent of patients reported complete relief of all recorded symptoms. No adverse events were reported.

We concluded that statistically significant reductions in pain and functionality, indicating the safety and viability of Prolotherapy for cervical spine instability. (6)

In 2014, we published a comprehensive review of the problems related to weakened damaged cervical neck ligaments in The Open Orthopaedics Journal. (7) We are honored that this research has been used in at least 6 other medical research papers by different authors exploring our treatments and findings and cited, according to Google Scholar, in more than 40 articles.

This is what we wrote in this paper: “To date, there is no consensus on the diagnosis of cervical spine instability or on traditional treatments that relieve chronic neck instability issues like those mentioned above. In such cases, patients often seek out alternative treatments for pain and symptom relief. Prolotherapy is one such treatment that is intended for acute and chronic musculoskeletal injuries, including those causing chronic neck pain related to underlying joint instability and ligament laxity. While these symptom classifications should be obvious signs of a patient in distress, the cause of the problems are not so obvious. Further and unfortunately, there is often no correlation between the hypermobility or subluxation of the vertebrae, clinical signs or symptoms, or neurological signs (such as excessive sweating or inability to sweat and temperature dysregulation or other skin sensations mentioned in this article) or symptoms.”

What we demonstrated in this study is that the cervical neck ligaments are the main stabilizing structures of the cervical facet joints in the cervical spine and have been implicated as a major source of chronic neck pain and in the case of many of the symptoms we mentioned above.

Summary and contact us. Can we help you? How do I know if I’m a good candidate?

We hope you found this article informative and it helped answer many of the questions you may have surrounding Brachioradial Pruritus – Neuropathic itch. Just like you, we want to make sure you are a good fit for our clinic prior to accepting your case. While our mission is to help as many people with chronic pain as we can, sadly, we cannot accept all cases. We have a multi-step process so our team can really get to know you and your case to ensure that it sounds like you are a good fit for the unique testing and treatments that we offer here.

Please visit the Hauser Neck Center Patient Candidate Form

References:

1 Wallengren J, Sundler F. Brachioradial pruritus is associated with a reduction in cutaneous innervation that normalizes during symptom-free remissions. Journal of the American Academy of Dermatology. 2005 Jan 1;52(1):142-5. [Google Scholar]
2 Berger AA, Urits I, Orhurhu V, Viswanath O, Hasoon J. Brachioradial pruritus in a 52-year-old woman: A case report. Case reports in women’s health. 2019 Oct 1;24:e00157.
3 Salzmann SN, Okano I, Shue J, Hughes AP. Disabling Pruritus in a Patient With Cervical Stenosis. JAAOS Global Research & Reviews. 2020 Mar;4(3). [Google Scholar]
4 Oaklander AL. Neuropathic itch. InSeminars in cutaneous medicine and surgery 2011 Jun (Vol. 30, No. 2, p. 87). NIH Public Access. [Google Scholar]
5 Robert M, Misery L, Brenaut E. Chronic Pruritus in the Absence of Skin Disease: A Retrospective Study of 197 French Inpatients. Acta Dermato-venereologica. 2020 Sep 14. [Google Scholar]
6 Skelton F, Frontera JE. Brachioradial pruritus as a harbinger of syrinx in chronic spinal cord injury: a case report. PM&R. 2017 Mar 1;9(3):311-3.
7 Hauser RA, Steilen D, Sprague IS. Cervical Instability as a Cause of Barré-Liéou Syndrome and Definitive Treatment with Prolotherapy: A Case Series. European Journal of Preventive Medicine. 2015;3(5):155-66. [Google Scholar]
8 Steilen D, Hauser R, Woldin B, Sawyer S. Chronic neck pain: making the connection between capsular ligament laxity and cervical instability. The open orthopaedics journal. 2014;8:326. [Google Scholar]

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90,000 Why does skin itch during pregnancy?

Itching during pregnancy is not very common. Most often, the skin begins to itch unbearably (as after mosquito bites) in the evening, closer to night, which can provoke insomnia and generally worsen a woman’s mood. Usually, itching does not harm the baby and goes away on its own after childbirth. However, it is still worth consulting with a gynecologist and dermatologist.

What does it come from?

The cause of itching during pregnancy in most cases is a violation of the liver: the production and outflow of bile, a general increase in the level of bilirubin in the blood.This is due to a hormonal disruption in the body of the expectant mother – a violation of the synthesis of estrogen, as well as due to the pressure of the fetus on the bile ducts. The fatty acids produced in large quantities enter the woman’s skin with the bloodstream and irritate the nerve endings, causing excruciating itching. Similar phenomena associated with stagnation of bile in the body can make themselves felt in the third trimester of pregnancy. Sometimes itching is accompanied by such dangerous diseases as diabetes mellitus.

Who is predisposed?

Usually itching during pregnancy occurs in women with chronic diseases of the biliary tract and high cholesterol levels in the blood.Such expectant mothers need to regularly (at least once a month) do a biochemical blood test to exclude toxic effects on liver cells.

How to fight?

A pregnant woman should tell her gynecologist about the discomfort associated with itchy skin. In some cases, itching can be a sign of the development of such a dangerous disease as hepatitis. The doctor will conduct appropriate examinations. If, according to an objective examination, itching does not pose any danger, it is often possible to get rid of discomfort by simply following a diet aimed at lowering cholesterol levels, limiting the use of fatty, spicy and salty foods that prevent the liver from coping with the function of bile secretion, as well as drinking plenty of fluids – it is necessary to eliminate dry skin.If diet does not work, your doctor may prescribe choleretic drugs suitable for pregnant women.

It is important to find the cause of the bothersome itching, excluding a whole group of skin diseases that can occur during pregnancy.

Itching in the abdomen and chest

This itch is worth mentioning separately. As a rule, the skin on the abdomen or chest itches in the second and third trimesters due to its stretching, because it is these parts of the body that increase in volume during pregnancy.In this case, it is very important not to scratch the skin – this will lead to the appearance of stretch marks, which, unlike itching, will not go away after childbirth. Regularly use moisturizers, anti-stretch marks, gently massage your breasts and abdomen with circular motions of your fingers, and do not take a hot shower.

You can get answers to any questions about pregnancy and childbirth from leading EMC experts in the classes of the School of Mothers.

Subscribe to our Instagram. You will find useful information about pregnancy and childbirth from the leading obstetricians and gynecologists of EMC.

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90,000 🦷 Cheek pain after anesthesia. This is fine?

The choice of anesthetic in each case is due to the characteristics of the disease and the individual indicators of the patient’s health. Thus, minor caries can be treated without anesthesia. Treatment of moderate caries, pulpitis and periodontitis must be carried out with anesthesia.The injection itself is absolutely not felt by the patient: before giving the injection, we use application anesthesia, which excludes the sensitivity of the cheek, palate or gums. Mandatory anesthesia is performed when removing teeth. The dosage of the pain reliever depends on the age, weight of the patient, the expected duration of the treatment procedure, and other factors.

In some cases, patients report discomfort several hours after the treatment.As a rule, there is a slight pain in the area of the injection and a slight swelling of the cheek. We hasten to assure you that this is a normal reaction of the body to medications, due to your personal threshold of sensitivity. These sensations do not pose any danger and do not require a visit to a specialist. Slight pain after tooth extraction, during which the gums were cut, is also completely normal. If necessary, our dentists recommend pain relievers that must be taken to eliminate unpleasant symptoms a few hours after treatment.

Another question is if the pain is intense enough, accompanied by an increase in body temperature and noticeable swelling. In this case, it is imperative to report the symptoms to the attending physician. You should not endure the pain and drink anesthetics if the pain persists for more than two days after the dental procedure.

In any case, do not worry if, for example, after a tooth extraction you have a fever or a slight swelling. In 99% of cases, this is nothing more than an individual reaction of the body to surgery.

Be healthy and contact specialists in a timely manner!

90,000 Dark circles under the eyes signal dangerous diseases

It is believed that bruises under the eyes appear due to lack of sleep, but in fact they can signal a serious disturbance in the body.

Insomnia and stress are the most common causes of dark circles and bags under the eyes. Sometimes in order for them to pass, it is enough to spend at least seven hours in bed.But sometimes they appear due to the fact that serious disorders occur in the body.

In fact, bruises under the eyes are blood vessels that show through the thin skin of the eyelids. They are manifested due to overwork, lack of fluid in the body, the use of alcoholic or energy drinks. Even the age of a person affects the intensity of dark circles.

Heredity

Bruising and dark circles are often inherited. The skin in these places may be too thin and light, due to which the vessels appear translucent.For such cases, greenish and bluish tints are characteristic in the area of the inner corner of the eye.

Some people have very thin skin and bruises from childhood. For others, it becomes thinner too quickly. In order to understand that this is heredity, one should remember whether the next of kin had bruises.

Age

Dark circles appear regularly with age. The thing is that over time, the body loses collagen and the subcutaneous fat layer becomes thinner.The skin becomes fragile and almost transparent, blood vessels do not begin to show through.

Dehydration

With a lack of water, the body directs it to the organs responsible for life. Because of this, less fluid enters the blood and lymph, and their flow slows down. Venous congestion occurs, which is most noticeable under the thinnest skin – in the eye area.

Kidney problems

Dark circles around the eyes may appear due to kidney problems.But kidney failure usually manifests itself with other symptoms – bags under the eyes, puffiness and swelling of the skin.

Diseases of internal organs

Dark circles around the eyes can signal various diseases of the internal organs of a person. They are provoked by cardiovascular diseases, due to which blood stagnation occurs. An additional alarming signal is a vascular headache.

Infection

Various intoxications or intestinal infections also affect the blue under the eyes.These conditions are usually accompanied by vomiting and diarrhea. Because of this, the body loses fluid faster, and with dehydration, the vessels become darker.

Allergy

Firstly, with allergies, the eyes itch and watery. Secondly, histamines, which the body secretes in response to an allergen, dilate blood vessels. They begin to show through the skin under the eyes.

If you rub your eyes during an allergy, thin blood vessels can burst and break. Then there will be the smallest bruises, which will increase the cyanosis.

Low hemoglobin

Anemia can also cause dark circles around the eyes. Hemoglobin carries oxygen from the lungs to organs and tissues. When combined with oxygen, it becomes bright scarlet. Giving up oxygen, hemoglobin darkens.

If there is little iron in the body, the amount of hemoglobin decreases. The one that remains begins to lose oxygen faster than usual. Because of this, the vessels turn dark blue and begin to show through the thin skin near the eyes.

Legs itchy until bruised

Why does the body itch and bruises appear on the legs

The appearance of bruises on the body after a blow or injury is usually the case, people are rarely surprised at their occurrence. However, you should be wary if a hematoma appears due to scratching or without mechanical action. This condition may indicate the development of a serious illness that requires immediate treatment.

Causes

The appearance of multiple bruises of different sizes is characteristic of hematological diseases.They occur after minor injuries or even after itching.

Hematoma on the skin

The disease of hemophilia affects the male half of the population, while women are carriers of the gene. The reason is related to the insufficiency of the coagulation factor. First, hemorrhages appear on the legs, especially the knees, hips, then the course becomes generalized with the development of internal hemorrhages.

Patients with impaired liver function note that the skin of the legs just above the knees and the inner thighs itch unbearably.It is characteristic of acquired coagulopathy against the background of cirrhosis, cholestasis, liver failure. First, single bruises appear, then, with negative dynamics, all over the body.

Other causes:

Varicose veins.
Thrombocytopenia.
Lack of vitamin K, C, R.
Increased vascular fragility.
Endocrinopathy, kidney disease.

Mechanism of occurrence

Hematoma on the leg

Patients wonder why the legs itch and then bruises appear, in order to understand such an important issue, you first need to understand the pathophysiological mechanism.The skin is abundantly braided by the vasculature and has many nerve endings. It acts as a litmus test for internal diseases.

In hepatic, renal, endocrine pathologies, the vascular wall becomes thinner, sometimes perforations appear (in diabetes mellitus). With an increase in bilirubin, uric acid, creatinine, the nerve receptors of the skin are irritated, and the body itches a lot. So any mechanical impact leads to a breakdown of the microvessel and a bruise (hematoma) appears.

With varicose veins, the walls of the veins are weakened, at first the increased pressure in them leads to expansion, then to the loss of a healthy shape.The veins expand and convoluted blood vessels appear. The thinned venous framework allows blood components to pass through, causing bruising.

Treatment

Hematoma

Considering the reasons why the legs itch and bruises on the skin appear, etiotropic therapy is prescribed. Prescription of medications:

for hemophilia – fresh frozen plasma, hemoconcentrates with clotting factors, administration of antihemophilic globulin, symptomatic therapy;
platelet blood transfusion;
replenishment of vitamins C, P, K;
topically: heparin-based ointments, badyagi; gel Troxerutin, Lyoton;
to relieve swelling and pain – Fastumgel, Voltaren;

Bruise after itching on the leg

Ointments and gels are applied to the surface of the thighs, legs, ankle and rub in with slow massage movements without injuring already weakened vessels.Additionally, antiallergic gels are prescribed, such as Fenistil, if the skin itches a lot.

For varicose veins, in addition to local therapy, oral phlebotonics and phleboprotectors are used: Detralex, Phlebodia. It is not recommended to stay in a hot bath for a long time, visit a sauna. For prevention, create an elevated position of the legs, perform the “tiptoe” exercise.

It must be remembered that medication is taken only after visiting a profiling specialist.Self-medication can cause irreparable harm to health, no matter where the skin itches and bruises appear, above the knees or below. Only a doctor will be able to thoroughly examine, prescribe the necessary tests, instrumental studies and choose an adequate treatment.

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itchy bruises of the feet | Physician Answers

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23-year-old woman asked:

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Yes: You had a tissue bruise…. blood has entered the tissue … local blood pigments can cause this.

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The legs are sensitive: the legs do not have a lot of padding, so it is easy to get a small bump and end up with a bruise. If it does not heal quite like a bruise on the shoulder … More details

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Allergies: Hard to tell without seeing the skin, but this does not sound like a typical allergic reaction.I would recommend going to a dermatologist because of t … More details

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Not sure, but: the only way to know is to test it to make sure it isn’t … bruises tend to grow briefly for 1-2 days, then change color … More details

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Need for examination: It is impossible to give a meaningful conclusion without examining you.You can try warm compresses for several days, as there is a blood clot in the tissues … More details

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Consult a dermatologist: there may be several things, in general it is necessary to rule out infection , cannot be identified on the Internet, medical history and physical examination by a dermatologist or your d ….

Why do my feet itch? 18 Possible Causes of Itchy Feet

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external itching of the thigh turns into a bruise | Doctors Answers

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Not sure, but the only way to find out is to check to make sure it doesn’t develop normally and goes away … Bruises usually enlarge briefly for 1-2 days, then change color … More details

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Consult a dermatologist: There may be several things, mainly infectious needs should be excluded, cannot be provided online, history and physical examination by a dermatologist or your d… More details

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A lump on the inner thigh: Any firm lesion that persists should be examined and examined by a doctor. Leave it up to your doctor, depending on the weather, to remove, biopsy, or leave alone.

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Furuncle / sebum cyst: It looks like you may have a deep sebaceous cyst or ingrown hair.Apply damp heat to the affected area if it does not reach her … More details

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See: doctor. It may not be bruising. or you can post a photo or consult for an accurate diagnosis and treatment

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Check it out: maybe as you suspect, maybe not.It is best to consult a doctor or dermatologist.

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Contact your PCP: Most bites are relatively harmless, leaving only an itchy patch of skin. However, some bites can carry disease. Lyme disease is a good example of this.

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Blood: A bruise is formed from a ruptured abscess on the affected area. Hopefully it hasn’t been squeezed to open up or self-medicate.

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Why do you bruise easily? What you need to know

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Neuropathic Itch – Itch – NCBI Bookshelf

7.1. BACKGROUND AND INTRODUCTION

7.1.1. Definitions of Neuropathic Itch

7.1.2. Neuroanatomy and Cell Biology

7.1.3. What Is the Relationship between NI and Psychogenic Itch?

7.1.4. Animal Models of NI

7.2. DIAGNOSIS AND MEASUREMENT

7.3. CLINICAL NI SYNDROMES

7.3.1. Widespread NI from Generalized Peripheral Nerve Damage (Polyneuropathies)

FIGURE 7.1

7.3.2. Focal NI from Nerve and Nerve-Root Lesions Including Brachioradial Pruritus and Notalgia Paresthetica

7.3.3. Focal NI from Sensory Ganglia Lesions (Neuronopathies/Ganglionopathies) Including Shingles

FIGURE 7.2

7.3.4. NI Syndromes Arising from Lesions within the Spinal Cord (Myelopathy)

7.3.5. NI Syndromes Affecting the Head and Neck (Cranial Nerves and Ganglia)

7.3.6. Trigeminal Trophic Syndrome and Other Forms of Self-Injurious Behavior from NI

7.3.7. Neuropathic Itch Syndromes Arising from the Brain

FIGURE 7.3

7.3.8. Phantom Itch in Amputated Body Parts

7.4. MANAGING AND TREATING NEUROPATHIC ITCH

7.4.1. Conservative Treatments

7.4.2. Topical Application of Medications

7.4.3. Intradermal Injection of Botulinum Toxin Type A

7.4.4. Systemic Pharmacologic Treatment

7.4.5. Neurosurgical Treatment Options

7.4.6. Contraindicated Therapies

When Parents Should Worry about Bumps and Bruises

Regarding insect bites, what should parents do if their child gets one, or two, or many?

Can insect bites get infected?

How can parents prevent insect bites?

What about bruising? What can cause that?

When should parents become worried?

What should we do for bruises that seem mild?

How long will bruising last?

Are there any bruises that parents or caregivers should worry about immediately?

Regarding insect bites, what should parents do if their child gets one, or two, or many?

Can insect bites get infected?

How can parents prevent insect bites?

What about bruising? What can cause that?

When should parents become worried?

What should we do for bruises that seem mild?

How long will bruising last?

Are there any bruises that parents or caregivers should worry about immediately?

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Brachioradial Pruritus – Neuropathic itch – Caring Medical Florida

A miserable, itchy patient.

Too much sun? Cervical spine and neck instability? Both?

Exacerbated by exposure to bright sunlight or ultraviolet radiation (UVR), and is associated with degenerative changes in the cervical spine.

Digital Motion X-Ray (DMX) demonstrates cervical spine instability.

Irritating Itching, pruritis from spinal instability

“

The itch is coming from a syrinx

Is the itching coming from nerve compression in the neck? What are we seeing in this image?

Looking for a narrowing of the nerve space

The treatment of cervical spine instability at the Hauser Neck Center – Research on cervical instability and Prolotherapy