In idiopathic CTS, many factors can originate increased nocturnal intratunnel pressure:. If the pressure exceeds 40—50 mmHg, this will interfere with the venous return of the intraneural microcirculation and cause diminished intraneural oxygen supply and venous stasis, with permeability problems originating from the endoneurial edema. An increase in pressure of 30 mmHg for 2 h leads to progressive weakening of the slow and fast axonal transportation.
This is corrected when the patient repositions his wrist and makes finger movements, thereby enabling drainage of the edema. After the compression has been relieved, there is a rapid improvement in the symptoms. Intermediary stage — The symptoms are both nocturnal and diurnal. Abnormalities of the microcirculation are constantly present, with epineural and intrafascicular interstitial edema, which causes increased endoneurial fluid pressure.
This interstitial edema causes absence of cell flow and thickening of the connective envelope, notably in relation to the epineurium. Destruction of the myelin sheath and nodes of Ranvier also occurs, based on saltatory conduction of inflows to the surface of the myelinated nerve fibers. After the compression has been relieved, rapid improvement of the symptoms occurs through reestablishment of the intraneural microcirculation. Unlike the restoration, repair of the myelin sheath requires weeks to months and causes intermittent symptoms and persistent electrophysiological abnormalities.
Advanced stage — Symptoms are constantly present, especially signs of sensory or motor deficit, translated as disruption of a greater or lesser number of axons axonotmesis. Wallerian degeneration exists at the level of the disrupted axons. The connective envelopes form the site for reactive fibrous thickening. After release of the nerve, the recovery depends on nerve regeneration, which takes several months and may be incomplete.
The significance of the recovery will depend on the patient's potential for axonal regeneration, particularly with regard to age, the existence of polyneuropathy and the severity of the compression. In reality, even with compression of all the nerve fibers within the same nerve, they will not be at the same stage of injury. It has been demonstrated that the peripheral nerve fibers in the region of the nerve trunk are affected before the more central fibers and, likewise, the myelinated fibers in relation to the smaller fibers and the sensory fibers in relation to the motor fibers.
In chronic CTS cases, worsening may occur over a period of months or years. All forms of polyneuropathy, including those relating to diabetes mellitus, promote CTS with structural and functional alterations of the median nerve, which makes the nerve more sensitive to all compressive phenomena.
Hereditary neuropathy with hypersensitivity to pressure is a hereditary sensory-motor form of neuropathy that is focal and recurrent. The first symptoms only rarely appear before the age of 20 years. It is characterized by occurrences of crises with paralysis and paresthesia in well-defined areas of the nerve trunk.
These crises, which are generally secondary to mild trauma or prolonged compression, often regress. Recurrence is frequent. Paralysis may become definitively established. At the electrophysiological level, this condition is characterized by myelinopathy with stretching of the distal motor latency. Biopsies of the nerve show zones of focal thickening of myelin in the form of sausages tomacula. The treatment is symptomatic.
The concept of double compression of the nerve is attributed to Upton and MacComas 22 and is based on the fact that proximal compression on the path of a nerve makes it more susceptible than if the compression was located more distally, because of cumulative effects on anterograde axonal transportation. This may occur in practice in cases of association between proximal compression of the nerve route at the vertebral level or thoracic outlet syndrome and distal CTS.
Careful clinical examination, aided by an electrophysiological study, will determine where the compression site is proximal or distal , i.
Treatment applied to the main compression site is generally sufficient for such patients. Compression of the nerve layer should be borne in mind if the results are incomplete or there is therapeutic failure in the medical or surgical treatment. In the great majority of cases, CTS is called idiopathic.
Secondary CTS may be related to abnormalities of the container or content. Furthermore, dynamic CTS is frequently found under pathological conditions relating to manual work. Repetitive manual activities and exposure to vibrations and cold temperatures were the least important.
Other factors involved were obesity and smoking. Any condition that modifies the walls of the carpal tunnel may cause compression of the median nerve. The pressure inside the carpal tunnel increases during wrist extension and flexion. No increase in the prevalence of CTS in cases of working on computers for more than 15 h per week has been observed. A tendency toward increased prevalence has been demonstrated in cases of working on computers for more than 20 h per week.
Exposure to vibration is one of the lesser predisposing factors. The clinical approach toward patients with acroparesthesia of the hand consists of five stages:. It should be noted first of all that there is no gold standard for a positive diagnosis of CTS. The median nerve is accessible in front of the wrist flexion crease and behind the long palmar tendon or in the middle of the wrist.
The typical form taken by nocturnal acroparesthesia comprises tingling, numbness, swelling or hypoesthesia, with or without pain reaching at least two of the first three fingers, palm and back of the hand excluded. The most specific tests are the score of Katz et al. A combination of four abnormal tests compression test, monofilament test, score of Katz et al.
If these four tests are normal, the probability that the patient might have CTS is 0. From the analysis on the times when symptoms appear and investigation of signs of neurological deficit, symptoms can be classified into early, intermediate and advanced states. Paresthesia can occur at night, in the morning or throughout the day. For sensitivity, the Weber test, which analyzes how the pulp of the fingers discriminates between two points, is very practical.
Starting from a distance of 6 mm, the sensitivity is considered to be abnormal. At the motor level, this study included the thumb opposition strength and investigated thenar amyotrophy. ENMG consists of a stimulation stage and a detection stage.
It is bilateral. The stimulation-detection stage makes it possible to study the sensory and motor nerve conduction of the median nerve and highlight the elective weakening in passing through the carpal tunnel. It also enables analysis on the amplitude and duration of the sensory and motor responses. This exploration is completed by measurements of the nerve conduction of the homolateral ulnar nerve and by studies on the contralateral side.
The earliest and most sensitive electrical abnormality is a decrease in the sensory conduction velocity possibly identified through the centimeter measurement method between the palm of the hand and the fingers and wrist.
This examination is operator-dependent. The skin temperature and age have an influence on the results. ENMG does not provide supplementary evidence in diagnosing CTS in relation to the clinical evaluation, when the clinical diagnosis seems evident.
None of these etiologies modified CTS treatment. In two cases out of the , the abnormalities required specific treatment. It was concluded that systematic radiographic examinations made insufficient contribution to be justified.
Radiographs of the wrist face, lateral and carpal tunnel views are useful in the following situations: Echography is operator and material-dependent. In the initial forms, the median nerve may conserve normal morphology. However, a median nerve of normal appearance does not rule out CTS. Echography may help in making an etiological diagnosis for morphological analysis of the content. The area of the median nerve is determined better on ultrasound at the level of the distal radius or the pisiform bone, which is considered to be the site of the proximal carpal tunnel and the expected location for maximum edema of the nerve.
If an elliptical shape is assumed, the area of the nerve in the proximal carpal tunnel should not be greater than 10 mm. MRI is rarely indicated, but may be useful for etiological diagnoses in the following situations:. Detailed anatomical knowledge is fundamentally important for medical practice, given that anatomical variations, when unknown, may give rise to severe complications in surgical procedures. Clinical comprehension of a disease is only attained when its physiopathology and etiology are known; from this knowledge, possible treatments can be analyzed.
Thus, although CTS is mostly idiopathic, other causes need to be determined in order to progress with adequate prevention and treatment. Another difficulty in clarifying this syndrome is the absence of any gold standard for confirmation. Hence, the diagnosis is primarily clinical and most of the tests that can be applied for evaluating its severity vary in sensitivity and specificity.
Nonetheless, such tests are of great value for ruling out other possible pathological conditions. Rev Bras Ortop. National Center for Biotechnology Information , U. Journal List Rev Bras Ortop v. Published online Aug Author information Article notes Copyright and License information Disclaimer. Jefferson Braga Silva: rb. Received Jul 10; Accepted Aug Published by Elsevier Editora Ltda.
This article has been cited by other articles in PMC. Abstract Carpal tunnel syndrome CTS is defined by compression of the median nerve in the wrist. Anatomy Limits The carpal tunnel is a non-extendible osteofibrous tunnel defined as the space located between the flexor retinaculum, which forms the roof, and the carpal sulcus, which forms the base. Content The median nerve is accompanied by four tendons from the superficial flexors of the fingers, four tendons from the deep flexors of the fingers and the long flexor of the thumb.
Anatomical variations Anatomical variations may explain the variations in symptoms and give rise to risks of iatrogenic injuries. Anatomical variations in the nerves A bifid median nerve caused by high division is observed in 1—3. Variations of the palmar cutaneous branch of the median nerve The palmar cutaneous branch usually begins 4—7 cm above the wrist crease and follows along beside the median nerve for 1. Intratunnel positioning of the ulnar nerve It is extremely rare to find the ulnar nerve inside the tunnel.
Areas of the hand innervated by the median nerve The area sensitized by the median nerve comprises the palmar face of the three radial fingers and the radial half of the ring finger; and on the dorsal face, the last two phalanxes of the first three fingers and the radial half of the fourth finger.
Muscle and tendon variations Long palmar muscle There is a variation of the long palmar muscle with an intratunnel tendon, called the deep long palmar muscle, which is inserted in the deep face of the palmar aponeurosis and may give rise to constriction of the median nerve. Lumbrical muscles Extension of the intratunnel insertion or abnormal insertion over the superficial flexor of the index finger may be observed, but it remains unproven whether these occurrences might be responsible for compression of the median nerve.
Physiopathology and etiology Ultrastructural nerve anomalies and clinical correlations From a physiopathological point of view, compressive syndromes combine the phenomena of compression and tension.
Lundborg 20 proposed the following clinical—anatomical classification: Early stage — Initial, characterized by intermittent symptoms that only occur at night. Associated pathological conditions Polyneuropathy All forms of polyneuropathy, including those relating to diabetes mellitus, promote CTS with structural and functional alterations of the median nerve, which makes the nerve more sensitive to all compressive phenomena.
Etiologies In the great majority of cases, CTS is called idiopathic. Secondary carpal tunnel syndrome Abnormalities of the container Any condition that modifies the walls of the carpal tunnel may cause compression of the median nerve. Dynamic carpal tunnel syndrome The pressure inside the carpal tunnel increases during wrist extension and flexion.
Exposure to vibration Exposure to vibration is one of the lesser predisposing factors. Challenge tests The median nerve is accessible in front of the wrist flexion crease and behind the long palmar tendon or in the middle of the wrist.
The time taken for the symptoms to appear in seconds is noted. The test is positive if paresthesia appears in the area of the median nerve. Tetro et al. Appreciating the severity: Lundborg's anatomoclinical classification From the analysis on the times when symptoms appear and investigation of signs of neurological deficit, symptoms can be classified into early, intermediate and advanced states.
Echography Echography is operator and material-dependent. Final remarks Detailed anatomical knowledge is fundamentally important for medical practice, given that anatomical variations, when unknown, may give rise to severe complications in surgical procedures.
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The stimulation-detection stage makes it pos- out CTS. Echography may help in making an etiological diag- sible to study the sensory and motor nerve conduction of the nosis for morphological analysis of the content. The area of median nerve and highlight the elective weakening in pass- the median nerve is determined better on ultrasound at the ing through the carpal tunnel.
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