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One study found the five year survival rate of patients Formerly called tapetochoroidal dystrophy purchase aurogra 100mg with mastercard, choroi- with grades 1 purchase aurogra 100 mg free shipping, 2 discount aurogra 100mg visa, and 3 to be 90% cheap aurogra 100mg with amex, 83% 100 mg aurogra otc, and 43% respec- deremia is a chronic form of retinal disease characterized tively. This means that five years after the diagnosis of by degeneration of the layers of the retina, which is the the tumor, 90 out of 100 people with grade 1 were still light-sensitive part of the eye. On the opposite spectrum, 43 out of 100 patients layers: the outer neural retina, consisting of nerve cells with grade 3 chondrosarcoma survived five years. Size of the a capillary layer (chorio capillaris); and the photorecep- tumor is also an important factor. Tumors greater than 4 tor (light-sensitive) layer that contain the rods and cones, in (10 cm) are more likely to become aggressive and which function as detectors to process light, color and spread. Resources The pigmentary changes in the RPE begin with fine BOOKS spotting and continue with areas of depigmentation and Bridge, Julia A. Cotran, Vinay Kumar, Stanley Choroidal vessels provide oxygen and nutrients to Robbins, and Frederick J. RPE, which lies directly beneath the retina, supports the ORGANIZATIONS function of photoreceptor cells. National Cancer Institute, National Institutes of and cones) convert light into the electrical impulses that Health. NCI Public Inquiries Office, Building 31, Room transfer messages to the brain where “seeing” actually 10A03, 31 Center Dr. Eventually, photore- GALE ENCYCLOPEDIA OF GENETIC DISORDERS 229 ceptor cells also degenerate, resulting in a loss of central Demographics vision. Choroideremia is believed to affect approximately The age at which choroideremia first appears varies; one in 100,000 individuals—primarily men—although initial symptoms (usually night blindness) may occur as women who are carriers may exhibit mild symptoms as early as three years of age and as late as 40 years. The disorder may be generally under-reported However, occurrence peaks between the ages of ten and because there was no diagnostic test for choroideremia 40. Loss of central vision usually occurs after the age of reasons that have yet to be determined, choroideremia 35. However, in nearly all patients with choroideremia, has affected an unusually large number of people; about visual acuity (acuteness or sharpness of vision) is well one in forty people have the disorder. Signs and symptoms Genetic profile A variety of other degenerations of the choroid may Choroideremia is an X-linked, recessive disorder, or look like choroideremia. Thus in females, the altered gene also seen in X-linked retinitis pigmentosa (one of a on one X chromosome can be masked by the normal gene group of genetic vision disorders causing retinal degen- on the other X chromosome. However, unlike retinitis pigmentosa, which or may not be symptomatic—have a 50% chance of pass- starts in early childhood, the onset of choroideremia is ing the X-linked abnormal gene to their daughters, who variable and is rarely seen in childhood. The distin- become carriers, and a 50% chance of passing the gene to guishing feature of choroideremia is the diffuse their sons, who are then affected by the disease. Fran chorio capillaris and RPE layers begins peripherally and Cremers of the University of Nijmegen in the spreads centrally, central macular function is preserved Netherlands isolated the gene believed to be responsible until late in the course of the disease. The gene for choroideremia was more frequently in men diagnosed with choroideremia. Although symptoms vary widely among affected individ- Although the choroideremia gene causes problems uals, men usually retain little or no useful vision beyond in the retina, choroid, and RPE, expression of this gene is the age of 60. Choroideremia may also manifest Choroideremia is characterized by extensive abnor- as a generalized disorder. The choroid (the vascular membrane located between the Isolated choroideremia retina inside the eye and the sclera) contains large In isolated choroideremia, which is the most com- branched pigmented cells and prevents light rays from mon form of the disorder, affected individuals display passing through areas of the eye outside of the pupils. Night blindness is usually the first noticeable symptom of choroideremia, usually occurring during childhood. Associated choroideremia Degeneration of the vessels of the choroid and func- Although relatively rare, associated choroideremia tional damage to the retina occur later in life and usually with mental retardation occurs in patients with a deletion lead to progressive central vision field loss and eventual of part of the X chromosome, including the region called blindness. Such a deletion may cause choroideremia with ment clumps tend to accumulate in the middle portion severe mental retardation or with mental retardation and and on the edges of the choroid. In these individuals, the mothers are is initially normal but may later evolve into tritanopia the carriers, showing the same deletions but not the (color blindness in which there is an abnormality in the severe clinical manifestations. However, female carriers sometimes show Choriocapillaris—Capillary layer of the choroid. Brownish granular pigmentation and changes in and serves to nourish the retina and absorb scat- the RPE and choroid may occur later. Retina—The light-sensitive layer of tissue in the Diagnosis back of the eye that receives and transmits visual signals to the brain through the optic nerve. Although there is no treatment for choroideremia because the disorder is so rare and has received relatively Retinal pigment epithelium (RPE)—The pig- little research attention, a diagnostic blood test developed mented cell layer that nourishes the retinal cells; by Canadian researchers allows early diagnosis of the located just outside the retina and attached to the disorder.

Coupled with the low back pain that usually is seen with dysfunction in this region discount aurogra 100mg with visa, patients with a gluteus minimus myofascial trigger point will report a distinctive pain pattern that resembles sciatic or discogenic radiation 100 mg aurogra with amex. Any dysfunction in these muscles Figure 5 Hamstring trigger point pain pattern and false-positive neurological testing order aurogra 100 mg line. Reproduced with permission from reference 75 Osteopathic considerations in neurology 81 should be identified and treated 100mg aurogra, with rechecking of Trendelenburg and/or muscle strength afterwards discount 100 mg aurogra visa. After the dysfunction is removed, the patient should be re-questioned to determine whether the pain pattern has resolved. The commonly employed straight leg-raising test is also fraught with confounders, ranging from sacroiliac joint and hip pain (from dysfunction or pathology) to myofascial trigger points in the hamstrings. Each of these is capable of restricting the total range of 75 motion during the test and creating local and referred pain. Correction of underlying somatic dysfunction in the sacroiliac joint, hip and hamstrings will provide a more accurate straight leg-raising test. Sacroiliac joint dysfunction is also capable of placing biomechanical stress on the 76 posterior sacroiliac ligament. This ligament has been shown to create a pain pattern similar to that of the gluteus minimus. Significant stress on this ligament, and the piriformis muscle as well, is seen after certain traumatically induced shearing forces into the sacroiliac joint, creating non-physiological somatic dysfunction (dysfunction that is not a normal part of the motions of this joint while walking, breathing and bending). Often resolution of low back pain with radiation down the leg is delayed until the sacral or innominate shearing dysfunction is corrected. Such somatic dysfunction has been documented by Greenman to be two of the top six diagnoses responsible for recurrent 77 low back pain otherwise unresponsive to conservative care. Piriformis muscle dysfunction is another diagnosis that should be ruled out in patients with a sciatic pain distribution. Travell and Simons document entrapment of the sciatic nerve (or more commonly the peroneal fibers within) with myofascial trigger points in this muscle and the osteopathic literature discusses the piriformis syndrome as having the 78 potential to maintain irritability of the underlying sciatic nerve. In the case of true entrapment, there may be some weakness in testing muscles innervated by the peroneal nerve and the Complementary therapies in neurology 82 Figure 6 Anatomic variations of relationship between the sciatic nerve and the piriformis muscle: neurologic implications of piriformis somatic dysfunction vary with structure as does treatment with injection therapy. Reproduced with permission from reference 78 patient may notice a slight foot drop when tired. Other critical diagnostic findings include ipsilateral external hip rotation and palpable hypertonicity generally with the potential for local myofascial trigger points (Figure 6). Tenderness over the sciatic nerve without these Osteopathic considerations in neurology 83 palpable changes in the piriformis muscle or its function would rule out piriformis 2 dysfunction as the cause of the symptoms. A final caveat in this discussion is offered based upon the multiple models applied to diagnosis and treatment in this region; co-existing and overlapping diagnoses are quite common here. A variety of effective OMT techniques can be applied to correct sacroiliac, gluteus 81 and piriformis dysfunction. Because of the potential for co-existing pathology, dysfunction in the presence of preliminarily positive neurological testing is most commonly treated with counterstrain, indirect myofascial release, or muscle energy techniques. For pelvic shearing somatic dysfunction, a gentle springing or, occasionally, a direct reversal of the traumatic shearing forces will provide dramatic relief. Care in positioning to avoid aggravation of any existing dysesthesia or pain is the rule. A more complete description of an osteopathic approach to lower motor neuron disorders will appear at the end of this chapter. Other common neurological tests and syndromes with somatic differentials As noted above, an important component of the osteopathic approach to patients presenting with signs and symptoms of what might be a neurological disorder involves ruling out and/or treating certain somatic dysfunctions considered to be important in the differential diagnosis or that might confound the neurological tests used. In definitive neurological disorders, the co-existence of somatic dysfunctions that produce similar symptoms makes the diagnosis and treatment of somatic dysfunction in these patients an important component to be considered. The constraints on the length of this chapter do not allow the use of the same level of detail as used in the previous section concerning radiculopathy and sciatica. Table 3, however, provides a partial list of entrapment neuropathies, neurological tests that might be altered by certain somatic dysfunctions, and pain and dysfunction patterns that are 4,40,51,82,83 similar to neurological disorders. While Table 3 Examples affecting differential diagnosis Condition Somatic dysfunction (SD) with similar presentation. Should be ruled out or, if present, treated first Examples of upper extremity entrapment neuropathies Median nerve carpal tunnel, pronator teres muscle, anterior interosseous membrane Ulnar nerve ulnar general: cubital tunnel, canal of Guyon, thoracic outlet, first rib, flexor digitorum muscle, flexor carpi ulnaris muscle ulnar deep motor branch: opponens digiti minimi muscle Complementary therapies in neurology 84 Radial nerve radial general: triceps brachii muscle radial sensory: brachialis muscle radial superficial sensory: supinator muscle radial deep: middle scalene muscle Musculocutaneous coracobrachialis muscle nerve Brachial plexus anterior and middle scalene muscles lower trunk: thoracic outlet, first rib, scalene trigger points, pectoralis minor muscle Examples of lower extremity entrapment neuropathies Sciatic nerve (sciatica) piriformis syndrome or trigger point Common peroneal fibular head posterior SD (fibular) nerve Posterior tibial nerve tarsal tunnel Examples of nerve entrapment neuropathies (cranial Greater occipital nerve semispinalis capitis muscle Cranial nerve VI petrosphenoidal ligament secondary to temporal SD (medial strabismus) Examples of altered neurological sign/test Muscle strength tests myofascial trigger point or prolonged strain in that phasic muscle Straight leg raising myofascial trigger point hamstrings Extraocular muscle petrosphenoidal ligament secondary to temporal SD testing Balance tests sternocleidomastoid myofascial trigger point temporal bone SD Sciatic posturing psoas syndrome Examples of similar pain or dysesthesia patterns L5, S1 radiculopathy gluteus minimus myofascial trigger point posterior sacroiliac ligament strain Migraine cephalgia trapezius myofascial trigger point sphenosquamosal pivot SD Carpal tunnel syndrome forearm myofascial trigger points Brachial plexopathy scalene trigger points, first rib SD Sciatica piriformis syndrome varying degrees of documentation exist for items listed, the couplings are clinically useful in teaching osteopathic students to broaden their differential diagnosis and it takes only a few extra minutes to evaluate and treat as needed to obtain a more accurate diagnosis.

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