Ponad 7000 publikacji medycznych!
Statystyki za 2021 rok:
odsłony: 8 805 378
Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu
© Borgis - Nowa Medycyna 1/2022, s. 20-35 | DOI: 10.25121/NM.2022.29.1.20
*Jan Namysł, Krystyna Garstka-Namysł
Cauda equina syndrome – rehabilitation after anal sphincter paralysis
Zespół ogona końskiego, rehabilitacja po porażeniach zwieraczy odbytu
INNOMED – A Centre for the Treatment of Paresis in Poznań
Streszczenie
Porażenie zwieraczy odbytu lub pęcherza w wyniku zespołu ogona końskiego lub urazu rdzenia kręgowego powoduje znaczne pogorszenie jakości życia dotkniętych tym stanem chorych.
O ile chirurgiczne odbarczenie ucisków na nerwy realizowane jest w trybie pilnym, to specjalistyczna, kierunkowa rehabilitacja, konieczna dla stworzenia warunków do poprawy kontroli nad czynnością zwieraczy, jest wdrażana nie tylko ze znacznym opóźnieniem, ale w większości przypadków wcale, pozostawiając chorych z przekonaniem, że nie ma dla nich pomocy. Tym przekonaniom przeczą nie tylko randomizowane badania naukowe, ale również poprawa kontroli nad czynnością zwieraczy uzyskiwana przez chorych z porażeniem mięśni miednicy w wyniku zespołu ogona końskiego, dzięki zabiegom elektrostymulacji i ćwiczeniom EMG-biofeedback, poprzedzonym badaniem elektromiograficznym z dwukanałową elektrodą doodbytniczą. Terapia jest realizowana w warunkach domowych, po przeszkoleniu w gabinecie, a jej postępy monitorowane w czasie okresowych badań EMG, których wyniki stanowią podstawę dla korekty parametrów stymulacji, stosownie do postępów w zakresie reinerwacji i świadomej kontroli napięcia zwieraczy.
Summary
Paralysis of the anal sphincters or the bladder due to cauda equina syndrome or spinal cord injury significantly reduces the quality of life of the affected patients.
Although surgical decompression to relieve pressure on the nerves is an urgent procedure, specialised, targeted rehabilitation to create conditions for improving control over sphincter function is either significantly delayed or even avoided in most cases, leaving these patients convinced that their problem cannot be resolved. However, these beliefs are contradicted not only by randomised trials, but also by the improved sphincter control achieved in patients with pelvic paralysis secondary to cauda equina syndrome, which is made possible by electrostimulation and EMG biofeedback exercises preceded by electromyography with a two-channel rectal electrode. The therapy is conducted in a home setting, after an in-office training, and its progress is monitored by periodic EMG, which provides the basis for adjusting stimulation parameters to the progress in reinnervation and voluntary control of sphincter tone.



Introduction
Paralysis of the anal sphincters and/or other muscles involved in ensuring continence as a result of damage to the cauda equina nerves usually occurs due to weight lifting in a bent position, sudden movement or trauma to the lumbar region (1, 2). L4/5, followed by L3/L4, L5/S1 are the most common levels of disc prolapse, sequestration or hernia (3). Much less frequently reported causes include epidural hematoma, infections, primary and metastatic tumours, spinal anaesthesia (4), constipation (5) or, as described in this paper, failed chiropractic manipulations in a person with pre-existing spinal degeneration and pain. Cauda equina nerve paralysis can give rise to a variety of symptoms, depending on the location and degree of damage, the time from the event to surgical nerve decompression, as well as treatment extent and method.
Disturbed conduction of both somatic and autonomic nerves controlling the activity of pelvic floor muscles following injury may occur. The efficiency of both these groups of nerves is important for the proper, voluntary and physiological bowel emptying. Due to the high number of combinations of damage and types of treatment provided, there is a large variety and severity of symptoms in different patients. These include e.g. loss of natural reflexes due to sensory impairment, disturbed bioelectrical activity responsible for smooth rectal muscle peristalsis and retention of faecal masses, paralysis of striated muscles forming the sphincter mechanism and loss of voluntary control over sphincter activity, gas and liquid stool incontinence, feeling of incomplete bowel emptying and persistent moisture in the anus, perianal itching and burning sensation. They are often accompanied by neurogenic bladder known as neurogenic lower urinary tract dysfunction, manifested by detrusor areflexia or atony, urinary retention, urinary retention in the bladder, and loss of control over bladder sphincter tone, causing urinary incontinence or the need for catheterisation.
Severe sciatica and “red flag symptoms” such as urinary retention, perineal sensory disturbances, difficulty passing stools, etc., can be the manifestation of many different diseases and should be diagnosed as soon as possible in an emergency department with easy access to Spinal Surgery Unit (6). The lack of perineal reflex and the bulbocavernosus reflex, absent or impaired perineal sensation, and loose anal sphincter are important indicators of sphincter involvement. Rapid imaging diagnosis is of great importance in reducing the negative effects of disc prolapse, as the delicate, unmyelinated preganglionic fibres of cauda equina in and around the midline and the sacral nerves are much more susceptible to compression than motor nerves. The clinical features of motor weakness and sensory impairment in the lower limbs depend on the degree of compression of the intervertebral disc on the motor nerves, and their damage may be minimised by rapid decompression. Hence, the manifestations of lower limb paralysis are much easier to rehabilitate and resolve faster than the symptoms of sphincter paralysis (7).
Patients with anal sphincter paralysis have a severely impaired sense of bowel filling or do not feel the need to use the toilet in the way they did before the paralysis occurred. Urine is drained through a Foley catheter or clean intermittent catheterisation (CIC). Panty liners or incontinent briefs are needed. Emptying the intestines becomes possible only after increasing the involvement of the abdominal press, which is associated with a high risk of secondary damage to the peripheral nerves, the use of lubricants, enemas or manual evacuation. These methods are however highly problematic and significantly reduce the quality of life. The use of abdominal press is particularly harmful, as it can give rise to adverse effects and complications, such as stretching of the muscles and secondary damage to motor nerve axons, resulting in further weakening of the contractile capacity, worsening of haemorrhoidal disease and discoordination of intestinal smooth muscles responsible for peristalsis, the puborectalis muscle and sphincters.
Under normal conditions, the sphincter tone increases in response to increased intra-abdominal pressure. The use of abdominal press to initiate and maintain bowel movement leads to a dyssynergia of the mechanisms underlying peristalsis and faecal continence.
The external anal sphincter (EAS) and the walls of the anal canal are innervated by the inferior rectal nerves, which are part of the voluntarily controlled mixed somatic pudendal nerve. The pudendal nerve consists of motor and sensory nerves S2-S4 as well as the sympathetic and parasympathetic fibres arising from the ventral branches of the spinal nerves. The striated muscles, skin and organs are sensorially innervated by the branches of the sacral plexus (8). Smooth muscles and glands are innervated by the pelvic autonomic system: pelvic branches of the sympathetic trunk, pelvic parasympathetic visceral nerves and the inferior hypogastric plexus (9).
The contractile activity of EAS is closely related to the activity of the neighbouring groups of levator ani muscles and the puborectalis muscle innervated by the pudendal and coccygeal nerves, as well as the activity of smooth bowel muscles. The coordination of this muscle activity is controlled by complexes of multiple interneurons that integrate the activity of neurons (10). Some of them are found in the brain and spinal cord, while other are located in the autonomic ganglia. The intestinofugal neurons, whose cellular bodies are located in the Auerbach’s plexus, are also important in controlling local reflexes (11). This plexus creates a network of connections of thousands of ganglia located in the muscle, extending from the upper oesophagus to the internal anal sphincter (IAS) (12). Due to the complex structure of the nervous system controlling the activity of the pelvic floor muscles and the intercorrelations, even partial damage to somatic or autonomic nerves significantly disturbs the neuromuscular function responsible for continence and proper bowel movement. Qualified rehabilitation is needed in order to restore this function.
Rehabilitation approaches for sphincteric paralysis
In addition to pharmacotherapy, diet and other interventions to facilitate bowel movements, rehabilitation using both electrostimulation and biofeedback exercises is also needed. Both methods have been known and used for years in patients with impaired muscle function control and incontinence. Their positive role has been confirmed in many randomised clinical trials (13-17). Since each of these approaches has its own indications and limitations, both methods should be used in patients with neurogenic muscle dysfunction. Electrostimulation is the only method to provide the nervous system with stable tensions, is used in the processes of reinnervation and normalisation of the bioelectrical activity of the muscles, and is essential in all neurogenic muscle dysfunctions. Its parameters, which mainly include pulse frequency (Hz), pulse duration (μs), current intensity (mA), session time (minutes), duration of contraction and relaxation breaks (seconds), should be shaped based on the results of sphincter EMG using a two-channel rectal electrode. It is impossible to assess the ability to voluntarily control sphincter tone and identify appropriate electrostimulation parameters without dynamic EMG performed in the semi-recumbent, lying position, before and after the sphincter stimulation or before and after biofeedback exercise. Assessing pudendal nerve latency with St. Mark’s electrode or accurate location of the affected motor units in multichannel EMG, provided that it delivers objective data for scientific research, does not provide the information needed for the rehabilitation process. Biofeedback exercises also use a rectal electrode for neuromuscular re-education and enhancement of central tone control. Visualization of muscle tone, the bioelectric activity of which is generally modulated without voluntary control, is an invaluable tool in the treatment of impaired muscle tone control. Biofeedback is mainly used on an outpatient basis, during medical appointments to assess the current ability to control muscle tone and teach patients how to focus on tensing the sphincters, without harmful co-contraction of the gluteal muscles, abdomen or femoral adductors. Patients in whom the extent of nerve damage and interneuronal tone regulation and distribution mechanisms have resulted in an inability to maintain stable muscle tone on contraction, inability to perform post-exercise relaxation or discoordination should use both daily electrostimulation sessions and biofeedback therapy. Both therapies can be successfully used at home, after thorough training in the doctor’s office. While electrostimulation sessions can (and must) be implemented in patients with complete or severe loss of control over muscle activity, the ability to generate at least 5-8 microvolts and mental fitness to operate the device are the basic conditions for home-based biofeedback exercises. Palpation used by some physiotherapists to stimulate sphincters in patients whose ability to generate muscle tone does not exceed 2-3 microvolts, as confirmed in EMG, is pointless. Such low contraction activity does not motivate the body to strengthen the muscles. Neither touch nor independent attempts to tighten the muscles affected by the flaccid paralysis provide electrical stimulation with parameters that could stimulate contraction of the denervated muscles. This can be achieved only with electrostimulation.
Regular, long-term (many months), correctly performed stimulation sessions and biofeedback exercises enable regeneration of the damaged nervous system and restoration of central control over muscle activity to a much greater extent than commonly believed. Not only somatic nerves, but, as extremely rarely reported, also autonomic nerves can be regenerated. The fact that the internal anal sphincter is not controlled voluntarily does not mean that it will not respond to stimulation. Electrostimulation supports the processes of reinnervation in peripheral nerve injuries (18) as a result of pregnancy and childbirth, episiotomy, muscle injuries caused by lifting, iatrogenic effects of pelvic surgery or radiotherapy, as well as after spinal cord injuries (19). Due to the long time (months to years) needed to initiate reinnervation and reconstruction of synaptic connections involved in controlling the tone of multiple muscles ensuring continence, the therapy is home-based. This not only applies to the affected muscles, but also to neural pathways that control their activity, providing both types of tissues with “electricity supply” necessary to maintain their vital processes. This type of stimulation improves blood supply in the treated area, increases the synthesis of growth factors (NGF, VEGF) and neurotrophins (BDNF, CNTF) and the chances of survival of oligodendrocytes and Schwann cells, as well as it may activate their precursor cells and enable myelin regeneration (20). Furthermore, stimulation increases survival and differentiation of oligodendrocytes, inhibits myelin degeneration and the activity of apoptotic markers (21). The belief that electrical stimulation is useless in patients with spinal cord injuries and may disturb possible reinnervation is outdated and, according to current knowledge, should be put aside (22), and patients should be informed about the need for this treatment approach.
Case reports

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
  • Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
  • Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
  • Aby kupić kod proszę skorzystać z jednej z poniższych opcji.

Opcja #1

29

Wybieram
  • dostęp do tego artykułu
  • dostęp na 7 dni

uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony

Opcja #2

69

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 30 dni
  • najpopularniejsza opcja

Opcja #3

129

Wybieram
  • dostęp do tego i pozostałych ponad 7000 artykułów
  • dostęp na 90 dni
  • oszczędzasz 78 zł
Piśmiennictwo
1. Harrop JS, Hunt GE, Vaccaro AR: Conus medullaris and cauda equine syndrome as a result of traumatic injuries: management principles. J Neurosurg Neurosurg Focus 2004; 16: 19-23.
2. Issada T, Le H, Park J, Kim DH: Cauda equina syndrome in patients with low lumbar fractures. J Neurosurg Neurosurg Focus 2004; 16: 28-33.
3. Singh P, Batish VK, Sarup S et al.: Sphincter involvement in lumbar disc herniation, Med J Armed Forces India 2000; 56(2): 117-121.
4. Ozgen S, Beyken N, Dogan IV et al.: Cauda equina syndrome after induction of spinal anaesthesia. J Neurosurg Neurosurg Focus 2004; 16: 24-27.
5. Lawrentschuk N, Nguyen H: Cauda equina syndrome secondary to constipation: an uncommon occurrence. ANZ J Surg 2005; 75: 498-500.
6. Coscia M, Leipzig T, Cooper D: Acute cauda equina syndrome: diagnostic advantage of MRI. Spine 1994; 19: 475-478.
7. Rydevik BL, Brown M, Lundborg G: Pathoanatomy and pathophysiology of spinal nerve root compression. Spine 1984; 9(1): 7-15.
8. Kołodziejczak M, Sudoł-Szopińska I: Podstawy anatomiczne leczenia operacyjnego chorób proktologicznych – budowa odbytnicy, kanału odbytu i układu mięśni zwieraczy. Nowa Medycyna 2008; 4: 10-14.
9. Fitzgerald CM, Hynes CK: Female Perineal/Pelvic pain: The rehabilitation approach. [In:] Smith HS (ed.): Current Therapy in Pain. W.B. Saunders 2009: 227-233.
10. Gutierrez-Mecinas M, Singer J, Weruaga E (eds.): The Importance of Interneurons in Neuronal Circuitry. Frontiers Media SA, Lausanne 2022: 8, 41.
11. Townsend CM, Popiela T (red.): Chirurgia Sabistona. Elsevier Health Sciences 2010: 168.
12. Furness JB, Callaghan BP, Rivera LR, Cho HJ: The enteric nervous system and gastrointestinal innervation: integrated local and central control. Adv Exp Med Biol 2014; 817: 39-71.
13. Schwandner T, Hemmelmann C, Heimerl T et al.: Triple-target treatment versus low-frequency electrostimulation for anal incontinence: a randomized, controlled trial. Deutsches Arzteblatt International 2011; 108: 653-660.
14. Kalkdijk-Dijkstra AJ, van der Heijden JAG, van Westreenen HL et al.: Pelvic floor rehabilitation to improve functional outcome and quality of life after surgery for rectal cancer: study protocol for a randomized controlled trial. Trials 2020; 21(1): 112.
15. Bols EM, Berghmans BC, Hendriks EJ et al.: A randomized physiotherapy trial in patients with fecal incontinence: design of the PhysioFIT-study. BMC Public Health 2007; 7: 355.
16. Mazur-Bialy AI, Kołomańska-Bogucka D, Opławski M, Tim S: Physiotherapy for Prevention and Treatment of Fecal Incontinence in Women-Systematic Review of Methods. J Clin Med 2020; 9(10): 3255.
17. Mundet L, Rofes L, Ortega O et al.: Kegel Exercises, Biofeedback, Electrostimulation, and Peripheral Neuromodulation Improve Clinical Symptoms of Fecal Incontinence and Affect Specific Physiological Targets: An Randomized Controlled Trial. J Neurogastroenterol Motil 2021; 27(1): 108-118.
18. Willand MP: Electrostimulation enhances reinnervation after nerve injury. Eur J Transl Myol-Basic Appl Myol 2015; 25(4): 243-248.
19. Duffell LD, Donaldson NN: A Comparison of FES and SCS for Neuroplastic Recovery After SCI: Historical Perspectives and Future Directions. Front Neurol 2020;11: 607.
20. Li G, Fan ZK, Gu GF et al.: Epidural Spinal Cord Stimulation Promotes Motor Functional Recovery by Enhancing Oligodendrocyte Survival and Differentiation and by Protecting Myelin after Spinal Cord Injury in Rats. Neurosci Bull 2020; 36(4): 372-384.
21. Phillips AA, Squair JW, Sayenko DG et al.: An Autonomic Neuroprosthesis: Noninvasive Electrical Spinal Cord Stimulation Restores Autonomic Cardiovascular Function in Individuals with Spinal Cord Injury. J Neurotrauma 2018; 35: 446-451.
22. Marcante PG, Baba A, Carraro U et al.: Modulation of trophism and fiber type gene expression in denervated muscle activated by different patterns of electrical stimulation. Role of muscle fiber regeneration revisited in 2017. Biology, Engineering and Medicine 2017; 2(1): 1-9.
23. Ahn UM, Ahn NU, Buchowski JM et al.: Cauda equina syndrome secondary to lumbar disc herniation – a meta-analysis of surgical outcomes. Spine 2000; 25(12): 1515-1522.
24. Kohles SS, Kohles DA, Karp AP et al.: Time-dependent surgical outcomes following cauda equina syndrome diagnosis – Comments on a meta-analysis. Spine 2004; 29(11): 1281-1287.
25. Qureshi A, Sell PJ: Cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome. Eur Spine J 2007; 16: 2143-2215.
26. Dahlin LB: The role of timing in nerve reconstruction. Int Rev Neurobiol 2013; 109: 151-164.
27. Barker TP, Steele N, Swamy G et al.: Long-term core outcomes in cauda equina syndrome. Bone Joint J 2021; 103-B(9): 1464-1471.
28. Pollard C, Kennedy P: A longitudinal analysis of emotional impact, coping strategies and post-traumatic psychological growth following spinal cord injury: a 10-year review. Br J Health Psychol 2007; 12(Pt 3): 347-362.
29. Leonard BE: Inflammation and depression: a causal or coincidental link to the pathophysiology? Acta Neuropsychiatr 2018; 30(1): 1-16.
30. Gould E, Woolley CS, McEwen BS: Short-term glucocorticoid manipulations affect neuronal morphology and survival in the adult dentate gyrus. Neuroscience 1990; 37(2): 367-375.
31. Kern H, Carraro U: Home-Based Functional Electrical Stimulation of Human Permanent Denervated Muscles: A Narrative Review on Diagnostics, Managements, Results and Byproducts Revisited 2020. Diagnostics (Basel) 2020; 10(8): 529.
32. Greenhalgh S, Finucane L, Mercer C, Selfe J: Assessment and management of cauda equina syndrome. Musculoskelet Sci Pract 2018; 37: 69-74.
otrzymano: 2022-01-12
zaakceptowano do druku: 2022-02-02

Adres do korespondencji:
*Jan Namysł
Wielkopolskie Centrum Terapii Niedowładów INNOMED w Poznaniu
ul. Przepiórcza 9/1A, 60-162 Poznań
tel.: +48 601-519-667
jan@innomed.pl

Nowa Medycyna 1/2022
Strona internetowa czasopisma Nowa Medycyna