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2006 | 6 | 4 | 232-241
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Podstawy kliniczne zespołów cieśni

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EN
Clinical basis of entrapment neuropathies
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EN
Peripheral nerve entrapment is a condition of chronic injury of a nerve passing through a narrow, noncompliant anatomical canal. This leads to clinically apparent entrapment neuropathy with pain and paresthesias in distribution of the affected nerve, progressing to motor weakness and muscle atrophy. The most common peripheral nerve entrapment is carpal tunnel syndrome found in 0.5 to 3% of the population. In the US, patients with entrapment neuropathies make up 10 to 20% of all neurosurgical cases. Deformities resulting from bone fractures or arthritis may account for chronic nerve compression as found in the classic tardy ulnar palsy. Not unusually, nerves are compressed by atypical anatomical structures such as Struthers ligament (median nerve), arcades of Struthers (ulnar nerve) or arcade of Fröhse (radial nerve). Superficially located nerves are vulnerable to direct trauma during the routine daily activities as this is the case with the ulnar nerve at the elbow and with the superficial lateral femoral nerve in patients wearing tight jeans. Entrapment neuropathies are frequently associated with pregnancy and acromegaly, with metabolic disorders (diabetes mellitus, alcoholism, chronic hemodialyses) and with hereditary neuropathy with liability to pressure palsies (HNPP), the condition showing autosomal dominant inheritance and caused by the deletion of a segment of chromosome 17p11.2-12 which contains peripheral myelin protein-22 gene (PMP22). Following general considerations, the clinical symptoms and etiology of carpal tunnel syndrome, pronator teres syndrome, anterior interosseous nerve syndrome, entrapment of the ulnar nerve at the elbow and at the wrist and hand, posterior interosseous nerve syndrome, Wartenberg syndrome, thoracic outlet syndrome, entrapment of the suprascapular and musculocutaneous nerves, Roth syndrome, tarsal and anterior tarsal tunnel syndromes, neuropathies of peroneal nerves and saphenous nerve as well as Morton’s neuroma were reviewed in detail.
PL
Istotą zespołów cieśni jest uszkodzenie nerwu obwodowego będące następstwem ucisku w wąskim i niepodatnym na rozciąganie kanale anatomicznym. Występująca wówczas neuropatia z uwięźnięcia objawia się najpierw bólem i parestezjami w polu unerwienia danego nerwu, następnie osłabieniem czucia powierzchniowego, a w zaawansowanych przypadkach także niedowładami i zanikami mięśni. Najczęściej występującą neuropatię z uwięźnięcia - zespół cieśni nadgarstka stwierdza się u 0,5-3% populacji. W USA chorzy z zespołami cieśni stanowią 10-20% pacjentów spotykanych w praktyce neurochirurgicznej. Zespołom cieśni sprzyjają urazy kostno-stawowe, jak to ma miejsce w tzw. opóźnionym uszkodzeniu nerwu łokciowego. Niekiedy nerwy bywają uciskane przez nietypowe struktury anatomiczne, takie jak np. więzadło Struthersa (nerw pośrodkowy), arkady Struthersa (nerw łokciowy) czy arkada Frohse’a (nerw międzykostny tylny). Istotną rolę odgrywa także ucisk z zewnątrz, np. na nerw łokciowy w okolicy łokcia lub nerw skórny boczny uda przez ciasne dżinsy. Rozwojowi neuropatii z uwięźnięcia sprzyjają również zmiany hormonalne (ciąża, akromegalia), metaboliczne (cukrzyca, alkoholizm, przewlekła dializoterapia) oraz tzw. dziedziczna neuropatia ze skłonnością do uciskowych uszkodzeń nerwów, dziedziczona autosomalnie dominująco, a spowodowana delecją 17p11.2-12 wywołującą zmniejszoną ekspresję genu odpowiedzialnego za syntezę jednego z białek mieliny nerwów obwodowych (PMP22). W części szczegółowej omówiono objawy kliniczne i patogenezę zespołów: cieśni nadgarstka, mięśnia nawrotnego obłego, nerwu międzykostnego przedniego, cieśni nerwu łokciowego w okolicy łokcia, kanału Guyona, nerwu międzykostnego tylnego, Wartenberga, otworu górnego klatki piersiowej, nerwu nadłopatkowego, nerwu mięśniowo-skórnego, Rotha, kanału kostki przyśrodkowej, cieśni nerwu strzałkowego wspólnego, przedniego cieśni stępu, nerwu strzałkowego powierzchownego, nerwu udowo--goleniowego i nerwoból Mortona.
Discipline
Year
Volume
6
Issue
4
Pages
232-241
Physical description
References
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