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#1
10.01.2003, 13:56
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Онемение рук по утрам
Здравствуйте, у меня вопрос. У моей мамы по утрам немеют руки, иногда нормальная чувствительность восстанавливается лишь через час. Вы не подскажете какие обследования стоит сделать помимо ЭКГ. Заранее спасибо.
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#3
06.07.2005, 16:02
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Цитата:
 . Этому вопросу 2 года уже
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#4
06.07.2005, 16:12
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Цитата:
 А по существу? Тему возобновила по просьбам трудящихся... В Ангарске сидит за компом ГОСТЬ форума, зарегистрироваться почему-то не может.
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#5
06.07.2005, 16:53
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Часто онемение кистей является проявлением синдрома запястного канала, сенсорной полинейропатии. Для инструментального подтверждения проводят ЭМГ (электромиографию) с исследованием скорости проведения по двигательным и чувствительным нервам верхних конечностей.
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#6
07.07.2005, 09:47
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А ведь действительно, довольно частая жалоба, правда место топику не в кардиологии, конечно
.Отчего немеют руки? Полностью согласен с Игорем Николаевичем насчет туннельного синдрома и полинейропатии. Так же часто онемения связывают с "остеохондрозом" ШОП, поражением сосудов верхних конечностей (назначая РВГ  ). Интересен вариант остеоартроза суставов кисти.Лично мне из всего перечисленного наименее вероятным кажется "сосудистый" генез проблеммы при отсутсвии билатерального различия АД и пульсации  .А вот что по поводу дегенративных заболеваний ШОП и остеоартроза?
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#7
07.07.2005, 10:44
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Спасибо за поддержание темы...
Я - как "передаст" - доктор из Ангарска отправил мне мыло с благодарностью. Как раз по поводу того, что часто встречающаяся жалоба. Одного не пойму - почему у него не получается зарегистрироваться...
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#8
07.07.2005, 11:05
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Про регистрацию - это надо ступенчато весь процесс проконтролировать (лень человеческую опускаем). Может, письмо для регистрации не пришло, может адрес мыльный неправильный...
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#9
07.07.2005, 11:39
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Да вот пожалуйста - с пару недель имею легкое чувство онемения в области инневации локтевого нерва, иногда - покалывание. Чувствительность вроде норма
. Когда кручу баранку - усиливается, появляются умеренные боли в локте, через пару часов проходят, остается онемение в области гипотенара и мизинца. При резком активном сгибании в локте - неприятное ощущение в локте, усиление онемения, покалывания. Сила во всех пальцах не изменена, отведение, приведение, сгибание и т.п. как и раньше. Не лечусь никак . Подозреваю, что сие из-за нарушения техники при отжимании на брусьях, поскольку был грешок. Хотя по идее должно было разболеться плечо 
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#10
07.07.2005, 11:46
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Да чего далеко ходить, сама имела покалывание в кончиках пальцев и чувство мурашек не так давно... в области иннервации локтевого нерва тоже... на брусьях не отжималась. Терапия - упражнения на шейный отдел позвоночника (щадящие) и массаж воротниковой зоны (тоже щадящий).
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#11
07.07.2005, 12:11
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Цитата:
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#12
07.07.2005, 12:25
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Ulnar Neuropathy
Prevalence and Pathophysiology Ulnar neuropathy is not as common as carpal tunnel syndrome, but no data are available to indicate its prevalence. As the ulnar nerve passes through the ulnar groove at the elbow, it is subject to several types of compressive injuries. Even with the most careful electrophysiologic techniques, and with surgical exploration, it may be difficult to localize or precisely explain the neuropathy. Potential causes of ulnar entrapment, in approximate order of frequency, are as follows: cubital tunnel syndrome, external compression, previous fracture and scarring, recurrent subluxation of the nerve, and entrapment. A cubital tunnel syndrome35 can occur where the nerve passes the aponeurosis of origin of the flexor carpi ulnaris (Figure 2). In certain persons the aponeurosis is drawn taut over the nerve, particularly with elbow flexion. The point of constriction is 1.5 to 3.5 cm distal to the epicondyle. External compression can occur from repeatedly resting the elbow on a flat surface, especially if the ulnar groove is shallow. The comatose or anesthetized patient is at risk for prolonged pressure on the ulnar nerve37. Previous fracture may damage the elbow, and scarring can constrict the nerve. Recurrent subluxation of the nerve, which can roll anteriorly over the medial epicondyle, may contribute to ulnar neuropathy. However, nerve subluxation also occurs in asymptomatic persons. Finally, entrapment may occur distal to the cubital tunnel (more than 4 cm beyond the epicondyle) in the flexor-pronator aponeurosis. Assessment Patients with ulnar-nerve compression typically note numbness in the little finger and medial side of the hand. Pain and tenderness may occur at the elbow and radiate toward the hand. An increase in paresthesias with elbow flexion is a reliable sign of ulnar entrapment. Weakness, if it occurs, may affect many functions of the hand, including finger abduction, thumb abduction, pinching of the thumb and forefinger, and eventually, power grip. Musicians and others who require very fine control of the digits may note a decline in performance with minimal ulnar compression38. The techniques used for electrodiagnostic testing resemble those used for carpal tunnel syndrome36. Usually both motor and sensory testing are conducted. The location of the abnormality is sought by assessing conduction velocity across the elbow segment; the intrinsic muscles of the hand are used to determine motor velocity, and the little finger is used for sensory testing. Although the presence of an ulnar lesion is commonly established, the exact location of the lesion is unclear in one third to one half of cases, especially less severe cases39,40. If the site can be established by careful sequential measurements over short segments,41 there are therapeutic implications, since the nature of a surgical approach may depend on exact localization. Measurements of slowly conducting myelinated fibers can provide additional sensitivity42. A well-planned individualized test improves diagnostic usefulness43. Differential Diagnosis Several other entities need to be considered in a patient with numbness of the little finger and possible motor weakness. The ulnar nerve can be compressed at the wrist rather than the elbow by repeated trauma to the palm (often occupational) or by a ganglion or tumor. Rarely, the brachial plexus is involved by a metastatic tumor or by the thoracic outlet syndrome. Compression of the cervical nerve root can cause radiating paresthesia in the hand; the C-8 root can best be distinguished from the ulnar nerve by the pattern of muscle weakness. Treatment Conservative therapy for ulnar-nerve compression is limited. Steroid injections and oral antiinflammatory agents are not useful. If there is a source of external trauma, it must be eliminated. Frequent or prolonged flexion of the elbow should be avoided. The patient may try wearing a loose, bivalved cast at night to prevent elbow flexion; however, many patients cannot tolerate this approach. A surgical procedure is reserved for those with disability, particularly weakness. If the weakness is early and mild, especially if Tinel's sign is present or electrodiagnostic testing suggests cubital tunnel syndrome, a simple release may be performed. There is no consensus regarding other procedures. Some authorities prefer epicondylectomy,whereas others favor nerve transposition. The results of surgery are more commensurate with the degree of preoperative motor or sensory loss than they are with the choice of procedure. Generally, the results are satisfactory. Persistent postoperative symptoms, consisting of local tenderness and painful paresthesias, occur in a few patients.
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#13
07.07.2005, 12:28
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Carpal Tunnel Syndrome
Clinical Features Carpal tunnel syndrome is produced by compression of the median nerve at the wrist (Figure 1). Affected patients report numbness, tingling, and pain in the hand, which often worsens at night or after use of the hand. The pain may radiate proximally into the forearm and arm. Examination in the early stages often reveals no abnormality. With more severe nerve compression the patient will have sensory loss over some or all of the digits innervated by the median nerve (thumb, index finger, middle finger, and ring finger) and weakness of thumb abduction. Assessment Clinical assessment includes Phalen's test (appearance or worsening of paresthesia with maximal passive wrist flexion for one minute) and Tinel's sign (paresthesia in the median territory elicited by gentle tapping over the carpal tunnel). Tinel's sign has a sensitivity of 60 percent and a specificity of 67 percent; the corresponding values for Phalen's test are 75 percent and 47 percent5,6,7. When conducted in the proper setting, these tests can provide useful information. There have been scattered attempts to quantitate the sensory examination and improve its diagnostic yield1. In a clinical setting, an assessment of strength, sensory loss, and pain is sufficient to monitor the progress of the syndrome. Electrodiagnostic testing is important for the accurate diagnosis of carpal tunnel syndrome and should be carried out in most cases. The electromyographer uses sensory fibers to measure the nerve conduction velocity from the finger or palm to the wrist and motor conduction velocity from the wrist to the thenar muscles. The sensitivity of sensory conduction testing can be improved by making sequential measurements at short distances over the course of the nerve in the palm -- the palmar serial sensory study8. Approximately half the patients with carpal tunnel syndrome have abnormalities of the contralateral median nerve. Values in these patients therefore need to be compared with reference values obtained in normal subjects and with the ulnar or radial sensory latency values. Electromyography of thenar muscles innervated by the median nerve is also usually done. Electrodiagnostic testing is particularly useful for the differential diagnosis and in the presence of coexisting disease. Radiculopathy due to disease of the cervical spine, diffuse peripheral neuropathy, or proximal median neuropathy can pose clinical questions that electrodiagnostic testing can settle. No other test has a higher diagnostic accuracy in patients with a final diagnosis of carpal tunnel syndrome. In that sense electrodiagnostic testing is the laboratory gold standard, but to make a final diagnosis one must have clinical data, including the patient's response to treatment. Inevitably there are false positive and false negative results. Many of the apparent false positive results occur in patients who have measurable abnormalities of nerve conduction but no symptoms. This is illustrated by the high rate of abnormalities in the contralateral hands of patients with carpal tunnel syndrome. As testing becomes ever more complex and sophisticated,9 it is easier to find some subtest whose results are beyond the normal range. Rarely, patients who have typical symptoms have normal nerve conduction tests but respond to carpal tunnel release10. With currently used criteria the number of patients with such false negative results should be below 8 percent8. Most electromyographers consider the following results abnormal (with control for the patient's age and limb temperature): an absolute sensory latency of more than 3.7 msec, a difference of 0.4 msec or more between values obtained for the median nerve and those obtained for the radial or ulnar nerve, a motor conduction latency of more than 4.0 msec, and an incremental change of 0.4 msec in the palmar serial sensory study with the use of measurements made at standard distances11. Thermography shows clear abnormalities in carpal tunnel syndrome but is not reliable for the diagnosis of bilateral cases and has limited value in the differential diagnosis12. Computed tomography and magnetic resonance imaging have not been widely used for carpal tunnel syndrome and have no role in management at this time. Prevalence Carpal tunnel syndrome is common. A study of the syndrome in Rochester, Minnesota, which examined medical records, included symptoms compatible with the syndrome, and excluded other illnesses, calculated incidence of 125 per 100,000 population for the period 1976 through 198013. A survey of physicians in California estimated that 515 of every 100,000 patients sought medical attention for carpal tunnel syndrome in 1988; the syndrome in half of these patients was thought to be occupational in origin14. In the Netherlands, 8 percent of a random sample of 715 persons awoke with nocturnal paresthesias of the hand, and one third of the subjects were subsequently shown to have carpal tunnel syndrome, for a prevalence of 220 per 100,00015. When workers covered by a compensation system were surveyed in the state of Washington, the incidence of carpal tunnel syndrome was 15 times higher than that in the general population. A much higher percentage of men were affected (60 percent vs. 25 percent), and the peak age at onset was lower (37.4 years vs. 51 years)16. In some occupations, such as shellfish packing, the incidence was more than 200 times higher than that in the base-line Minnesota data. The highest reported incidence of carpal tunnel syndrome in an industrial setting, based on the numbers of carpal tunnel releases performed, was 15 percent among a group of meatpackers in Illinois17. Efforts have been made to define the exact occupational exposures that increase the incidence of carpal tunnel syndrome. These efforts have been hampered by a lack of consensus on diagnostic criteria. For example, a surveillance case definition established at a conference sponsored by the National Institute for Occupational Safety and Health was based on a combination of clinical and neurophysiologic data,18 but when tested in the field this definition had a sensitivity of only 0.67 and led to the misclassification of 38 percent of patients19. The incidence of carpal tunnel syndrome is increased among electronic-parts assemblers, frozen-food processors, musicians, and dental hygienists. The use of highly repetitive wrist movements, vibrating tools, awkward wrist positions, and great force seems to be correlated with the disorder (Table 1); however, not all experts agree. Some maintain that the causes of carpal tunnel syndrome in the workplace are not yet known and find correlations with age, obesity, and other nonergonomic factors21. A review of 49 relevant studies of all musculoskeletal disorders of the upper extremity in the workplace found that only 3 appeared to be well designed22. Clearly, further rigorous study is needed.
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#14
07.07.2005, 12:30
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Differential Diagnosis
The diagnosis of carpal tunnel syndrome is most reliably made by an experienced clinician6 after a review of the patient's history and a physical examination. Cervical radiculopathy may be identified by the occurrence of proximal radiation of pain above the shoulder, paresthesias with coughing or sneezing, or a pattern of motor or sensory disturbances beyond the territory of the median nerve. Ulnar neuropathy must be considered since no more than half the patients with carpal tunnel syndrome can reliably report the location of their paresthesias23. Thoracic outlet syndrome, discussed below, is occasionally a concern. Transient cerebral ischemia, not a rare occurrence, can be recognized by the absence of pain during an episode of numbness. Overuse syndrome (cumulative trauma syndrome) is a common diagnostic problem in occupational settings. Since 1989 these disorders have accounted for more than 50 percent of all occupational illnesses in the United States24. Overuse syndromes include muscle pain, tendinitis, fibrositis, epicondylitis, and attendant psychological conditions that may contribute to disability. The high frequency of this group of disorders is believed to be a result of automation and specialization in the workplace, with concentration of the workload on a few smaller groups of muscles (Table 2). Carpal tunnel syndrome probably accounts for a minority of the cases of overuse syndrome. The collection of relevant data has been hampered by the lack of consensus among researchers in the field22. It does appear that the incidence of both carpal tunnel syndrome and overuse syndrome increases in parallel in workers who are at risk25. Pathophysiology Under normal circumstances the tissue pressure studied by wick techniques within a compartment of a limb is 7 or 8 mm Hg. In carpal tunnel syndrome, the pressure is often 30 mm Hg -- near the level at which nerve dysfunction occurs26,27. With wrist flexion or extension pressures may increase to 90 mm Hg or more, which can also produce ischemia. The increase in pressure within the canal is usually caused by nonspecific flexor tenosynovitis. Diabetes, pregnancy, rheumatoid arthritis, and hypothyroidism are the commonest medical conditions associated with carpal tunnel syndrome, found in a total of 22 percent of cases in a meta-analysis1. Amyloidosis, acromegaly, and mycobacterial infections are important rare causes. Several studies have shown that the carpal canal is smaller in patients with carpal tunnel syndrome than in control subjects,28 although not all investigators agree with this finding29. Chronic focal compression of a nerve trunk can cause focal demyelination by mechanical stress, deforming the myelin lamellae. A distinctive pathologic change is found with chronic compression and has been studied experimentally and in some nerves in humans1. Ischemia also has a role in carpal tunnel syndrome; it can account for the intermittent paresthesias that occur at night or with wrist flexion. Clinical carpal tunnel syndrome frequently (but not always) spares both autonomic and sensory function, which are carried out by ischemia-sensitive small nerve fibers. This finding points to a more important role for compressive demyelination than for ischemia. Treatment The mainstays of nonsurgical treatment are avoidance of the use of the wrist, placement of a wrist splint in a neutral position for day and night use, and antiinflammatory medications. These treatments are especially useful in patients with an acute flare-up and in those with minimal and intermittent symptoms. There have been no recent prospective trials of the effect of splinting alone. A study of the response of a group of patients to splinting plus injections of local steroid into the carpal canal indicated that only 22 percent were free of symptoms at the end of the yearlong trial,30 although steroid injections have had a good record of success during short-term treatment, with good or complete relief in 81 percent of patients31. An age of more than 50 years, duration of disease for more than 10 months, and constant paresthesias are all indicators that conservative management will not succeed32. Surprisingly little information is available regarding the redesign of workstations and its effect on the reversal of symptoms or the prevention of carpal tunnel syndrome. Ergonomic redesign is widely practiced but rarely described in medical terms. Surgical treatment consists of sectioning the volar carpal ligament. The decision to proceed with surgery should be based on several considerations. The symptoms should have failed to respond to splinting, steroid injections, and oral antiinflammatory medications; the symptoms should limit the patient's activities; and the diagnosis should be based on a clinical examination and nerve conduction tests. Patients with acute carpal tunnel syndrome may need immediate decompression, as may patients with moderate or marked pain, sensory loss, or weakness. The procedure is usually done on an outpatient basis. It has a good record of success. In a Mayo Clinic follow-up series, the results were good to excellent in 80 percent of the patients, with 40 percent regaining normal function33. The condition of 5 percent of the patients, however, worsened. Other retrospective studies report good results in 82 to 98 percent of patients. Patients can return to an office job within a week of surgery, but it may be four to six months before carpenters, construction workers, or athletes can return to work. Many patients with work-related carpal tunnel syndrome need to change jobs. If a patient does not respond to carpal tunnel surgery, it is important to verify that the distal ligament has been properly sectioned. In nearly half of such patients, the release is found to be incomplete34. Entrapment Neuropathies of the Upper Extremities Treister M. R., Lucas G. L., Pavlovic D., Cala S., Jankovic N. Extract | Full Text N Engl J Med 1994; 330:1389-1390, May 12, 1994.
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#15
07.07.2005, 12:51
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Thoracic Outlet Syndrome
Prevalence and Pathophysiology Neurogenic thoracic outlet syndrome with measurable neurologic deficit is very rare. Patients who note tingling in the hands with shoulder abduction or elevation are relatively common. Neurogenic thoracic outlet syndrome is caused by abnormal bands crossing the brachial plexus, often inserting on a rudimentary cervical rib47. The pathogenesis of reversible, positionally dependent paresthesia is unknown; often the symptoms occur after a whiplash injury, and cervical-muscle spasm may have a role. Assessment Weakness of all the intrinsic muscles of the hand and sensory loss over the ulnar side of the hand and forearm are the classic features of neurogenic thoracic outlet syndrome47. A change in pulse volume with arm abduction is found in 15 percent of normal persons and is not a reliable indicator of the syndrome. Electrodiagnostic testing usually shows no abnormalities in patients with the more common reversible paresthesias and no evidence of focal demyelination in the rare patients with neurogenic thoracic outlet syndrome. Treatment Patients with reversible paresthesias usually respond well to a program of physical therapy, which increases the range of motion of the neck and shoulders, strengthens the rhomboid and trapezius muscles, and induces a more erect posture. Exploration of the brachial plexus carries some risk48 and should be reserved for rare patients with documented worsening of neurologic functions. Summary The three syndromes described in this article were chosen from about a dozen nerve-compression disorders that affect the arm from scapula to digits. They illustrate the range of problems encountered. None of the other syndromes are as common, and in some instances (pronator syndrome and anterior interosseous syndrome), localized inflammation is at least as common a cause of neuropathy as is compression. Some syndromes of nerve compression have important implications for musicians, athletes, and those who place stress on the upper limbs through heavy or repeated use. Well-designed prospective trials are clearly needed to expand our knowledge of the prevention and treatment of the entrapment neuropathies. Much more needs to be known about the long-term natural history of these disorders, since prevention is usually possible. Entrapment Neuropathies of the Upper Extremities Treister M. R., Lucas G. L., Pavlovic D., Cala S., Jankovic N. Extract | Full Text N Engl J Med 1994; 330:1389-1390, May 12, 1994.
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Линейный вид
