News about Medicine - Part 185

Giant Cell Arteritis (Temporal Arteritis) and Polymyalgia Rheumatica

Temporal arteritis Classification & external resourcesDefinition

Giant cell arteritis (also called temporal arteritis) is an inflammation of medium – and large-sized arteries. The disorder most frequently involves one or more branches of the carotid artery, particularly the temporal artery. The disorder is a systemic disease which can involve arteries in multiple locations.

Incidence And Prevalence

Giant cell arteritis has a high incidence in Scandanavia and in regions of the United States with large Scandanavian populations, compared to a lower incidence in southern Europe. The annual incidence rates in individuals 50 years of age and older range from 0.49 to 23.3 per 100,000 population. It occurs almost exclusively in individuals older than 55 years; however, well-documented cases have occurred in patients 40 years old or younger. It is more common in women than in men and is rare in blacks. Familial aggregation has been reported, as has an association with HLA-DR4. In addition, genetic linkage studies have demonstrated an association of giant cell arteritis with alleles at the HLA-DRB1 locus, particularly HLA-DRB1*04 variants. The disease is closely associated with polymyalgia rheumatica, which is more common than giant cell arteritis. In Olmsted County, Minnesota, the annual incidence of polymyalgia rheumatica in individuals 50 years of age and older is 52.5 per 100,000 population. Read the rest of this entry »

New Treatments for Bursitis

BursitisWhen inflammation of a bursa is superficial, such as of the shoulder, knee, elbow, or Achilles tendon, the diagnosis of bursitis is easily accomplished. Deep bursae, such as those around the hip joint and the ischial tuberosity, do not present with obvious swelling; a diagnosis must be inferred from local tenderness and exacerbation of pain by activation of the associated muscles. In difficult cases, the temporary elimination of pain after the local instillation of an anesthetic is a useful diagnostic tool. Bursitis seldom shows up on plain radiographs, and expensive imaging studies are not routinely advocated. If possible, one should aspirate the bursa because the finding of synovial fluid helps confirm the diagnosis of bursitis. If the fluid is not clear (as is the case in most instances of “irritated” bursitis), it should be sent for culture and examined for the presence of crystals. Read the rest of this entry »

Henoch-Schönlein Purpura

Henoch-Schönlein purpura - Wikipedia, the free encyclopedia

Henoch-Schönlein purpura, also referred to as anaphylactoid purpura is a systemic vasculitis syndrome characterized by palpable purpura (usually distributed over the buttocks and lower extremities), arthralgias, gastrointestinal signs and symptoms, and glomerulonephritis. It is a small vessel vasculitis.

Incidence And Prevalence

Henoch-Schönlein purpura is usually seen in children, age from 4 to 7 years; however, the disease may also be seen in infants and adults. It is not a rare disease, accounting for approximately 5 and 24 admissions per year at one pediatric hospital. The male to female ratio is 1.5:1. A seasonal variation with a peak incidence in spring has been noted.

Pathophysiology And Pathogenesis

The presumptive pathogenic mechanism for Henoch-Schönlein purpura is immune-complex deposition. A number of inciting antigens have been suggested including upper respiratory tract infections, foods, insect bites, and immunizations. IgA is the antibody class most often seen in the immune complexes and has been demonstrated in the renal biopsies of these patients. Read the rest of this entry »

Huntington’s Disease

George Huntington's 1872 paper described the disorder.Huntington’s disease is a movement disorder characterized by chorea and dementia. It is inherited in an autosomal dominant manner and occurs throughout the world, in all ethnic groups, with a prevalence rate of about 5 per 100,000. The gene responsible for the disease has been located on the short arm of chromosome No. 4. At 4p16.3 there is an expanded and unstable CAG trinucleotide repeat. Symptoms do not usually develop until after 30 years of age, by which time the patient has usually had children, and so the disease continues from one generation to the next. The cause of Huntington’s disease is unknown.

Clinical Findings

Clinical onset is usually between 30 and 50 years of age. The disease is progressive and usually leads to a fatal outcome within 15–20 years. The initial symptoms may consist of either abnormal movements or intellectual changes, but ultimately both occur. The earliest mental changes are often behavioral, with irritability, moodiness, antisocial behavior, or a psychiatric disturbance, but a more obvious dementia subsequently develops. The dyskinesia may initially be no more than an apparent fidgetiness or restlessness, but eventually choreiform movements and some dystonic posturing occur. Progressive rigidity and akinesia (rather than chorea) sometimes occur in association with dementia, especially in cases with childhood onset. CT scanning usually demonstrates cerebral atrophy and atrophy of the caudate nucleus in established cases. MRI and positron emission tomography (PET) have shown reduced glucose utilization in an anatomically normal caudate nucleus.

Chorea developing with no family history of choreoathetosis should not be attributed to Huntington’s disease, at least not until other causes of chorea have been excluded clinically and by appropriate laboratory studies. In younger patients, self-limiting Sydenham’s chorea develops after group A streptococcal infections on rare occasions. If a patient presents solely with progressive intellectual failure, it may not be possible to distinguish Huntington’s disease from other causes of dementia unless there is a characteristic family history or a dyskinesia develops. Read the rest of this entry »

Peripheral Neuropathies – Bell’s Palsy – part 4

Bell's PalsyBell’s palsy is an idiopathic facial paresis of lower motor neuron type that has been attributed to an inflammatory reaction involving the facial nerve near the stylomastoid foramen or in the bony facial canal. A relationship of Bell’s palsy to reactivation of herpes simplex virus has recently been suggested, but there is little evidence to support this.

The clinical features of Bell’s palsy are characteristic. The facial paresis generally comes on abruptly, but it may worsen over the following day or so. Pain about the ear precedes or accompanies the weakness in many cases but usually lasts for only a few days. The face itself feels stiff and pulled to one side. There may be ipsilateral restriction of eye closure and difficulty with eating and fine facial movements. A disturbance of taste is common, owing to involvement of chorda tympani fibers, and hyperacusis due to involvement of fibers to the stapedius occurs occasionally.

The management of Bell’s palsy is controversial. Approximately 60% of cases recover completely without treatment, presumably because the lesion is so mild that it leads merely to conduction block. Considerable improvement occurs in most other cases, and only about 10% of all patients are seriously dissatisfied with the final outcome because of permanent disfigurement or other long-term sequelae. Treatment is unnecessary in most cases but is indicated for patients in whom an unsatisfactory outcome can be predicted. The best clinical guide to progress is the severity of the palsy during the first few days after presentation. Patients with clinically complete palsy when first seen are less likely to make a full recovery than those with an incomplete one. A poor prognosis for recovery is also associated with advanced age, hyperacusis, and severe initial pain. Electromyography and nerve excitability or conduction studies provide a guide to prognosis but not early enough to aid in the selection of patients for treatment.

The only medical treatment that may influence the outcome is administration of corticosteroids, but studies supporting this concept have been criticized. Many physicians nevertheless routinely prescribe corticosteroids for patients with Bell’s palsy seen within 5 days of onset. The author prescribes them only when the palsy is clinically complete or there is severe pain. Treatment with prednisone, 60 or 80 mg daily in divided doses for 4 or 5 days, followed by tapering of the dose over the next 7–10 days, is a satisfactory regimen. It is helpful to protect the eye with lubricating drops (or lubricating ointment at night) and a patch if eye closure is not possible. There is no evidence that surgical procedures to decompress the facial nerve are of benefit.

Peripheral Neuropathies – Mononeuropathies – part 3

MononeuropathiesAn individual nerve may be injured along its course or may be compressed, angulated, or stretched by neighboring anatomic structures, especially at a point where it passes through a narrow space (entrapment neuropathy). The relative contributions of mechanical factors and ischemia to the local damage are not clear. With involvement of a sensory or mixed nerve, pain is commonly felt distal to the lesion. Symptoms never develop with some entrapment neuropathies, resolve rapidly and spontaneously in others, and become progressively more disabling and distressing in yet other cases. The precise neurologic deficit depends on the nerve involved. Percussion of the nerve at the site of the lesion may lead to paresthesias in its distal distribution.

Entrapment neuropathy may be the sole manifestation of subclinical polyneuropathy, and this must be borne in mind and excluded by nerve conduction studies. Such studies are also indispensable for the accurate localization of the focal lesion.

In patients with acute compression neuropathy such as Saturday night palsy, no treatment is necessary. Complete recovery generally occurs, usually within 2 months, presumably because the underlying pathology is demyelination. However, axonal degeneration can occur in severe cases, and recovery then takes longer and may never be complete. In chronic compressive or entrapment neuropathies, avoidance of aggravating factors and correction of any underlying systemic conditions are important. Local infiltration of the region about the nerve with corticosteroids may be of value; in addition, surgical decompression may help if there is a progressively increasing neurologic deficit or if electrodiagnostic studies show evidence of partial denervation in weak muscles. Generic Drugs Online

Peripheral nerve tumors are uncommon, except in Recklinghausen’s disease, but also give rise to mononeuropathy. This may be distinguishable from entrapment neuropathy only by noting the presence of a mass along the course of the nerve and by demonstrating the precise site of the lesion with appropriate electrophysiologic studies. Treatment of symptomatic lesions is by surgical removal if possible. Read the rest of this entry »

Peripheral Neuropathies – Polyneuropathies and Mononeuritis Multiplex – part 2

Neuropathies Associated With Systemic & Metabolic Disorders

A. Diabetes Mellitus: In this disorder, involvement of the peripheral nervous system may lead to symmetric sensory or mixed polyneuropathy, asymmetric motor neuropathy (diabetic amyotrophy), thoracoabdominal radiculopathy, utonomic neuropathy, or isolated lesions of individual nerves. These may occur singly or in any combination.

Sensory polyneuropathy, the most common manifestation, may lead to no more than depressed tendon reflexes and impaired appreciation of vibration in the legs. When symptomatic, there may be pain, paresthesias, or numbness in the legs, but in severe cases distal sensory loss occurs in all limbs. Diabetic amyotrophy is characterized by asymmetric weakness and wasting involving predominantly the proximal muscles of the legs, accompanied by local pain.

Online Canada Drugs Thoracoabdominal radiculopathy leads to pain over the trunk. In patients with autonomic neuropathy, postural hypotension, impaired thermoregulatory sweating, postgustatory hyperhidrosis, constipation, flatulence, diarrhea, impotence, urinary retention, and incontinence may occur, and there may be abnormal pupillary responses. Isolated lesions of individual peripheral nerves are common and in the limbs tend to occur at sites of compression or entrapment. Treatment is symptomatic. Entrapment neuropathies may be helped by surgical decompression.

Treatment of neuropathic pain is discussed above.

B. Uremia: Uremia may lead to a symmetric sensorimotor polyneuropathy that tends to affect the lower limbs more than the upper limbs and is more marked distally than proximally. The diagnosis can be confirmed electrophysiologically, for motor and sensory conduction velocity is moderately reduced. The neuropathy improves both clinically and electrophysiologically with renal transplantation and to a lesser extent with chronic dialysis. Buy Online Generic Viagra Read the rest of this entry »

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