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Mẫu co cứng
Tài liệu này trình bày về điều trị co cứng, định nghĩa và các phương pháp điều trị tổng quan. Nó liệt kê các triệu chứng, nguyên nhân và các cách tiếp cận để giảm thiểu tình trạng co cứng thông qua liệu pháp và thuốc. Cuối cùng, bài viết cũng thảo luận về những yếu tố ảnh hưởng đến chức năng vận động và cách quản lý co cứng trong điều trị.
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Mẫu co cứng
- 1. Xö trÝ vµ®iÒu trÞ CO cøng ThS L¬ng TuÊn Khanh Trungt©mPHCN – BÖnhviÖnB¹chMaiHµ néi
- 2. Dµn bµi • §ÞnhnghÜa vµ c¸c mÉu co cøng • C¸c ph¬ng ph¸p ®iÒu trÞ
- 3. Tæng quan §Þnh nghÜa: “Co cøng lµ sù t¨ng lªn cña ph¶n x¹ tr¬ng lùc (tr¬ng lùc c¬) phô thuéc vµo tèc ®é kÐo gi·n kÌm theo sù phãng ®¹i cña c¸c ph¶n x¹ g©n x¬ng do cung ph¶n x¹ c¬ bÞ kÝch thÝch qóa møc, co cøng lµ mét thµnh phÇn n»m trong héi chøng N¬ron vËn ®éng trªn” LanceJW(1980)
- 4. • Lµ métrèi lo¹n tr¬ng lùc c¬ do nguyªn nh©n tæn th ¬ng TKTW ®Æc trng bëi t¨ng søc c¶n khi vËn ®éng thô ®éng mét ®o¹n chi thÓ • Tr¬ng lùc c¬ t¨ng do mÊt nh÷ng th«ng tin øc chÕ tõ trªn xuèng (bã líi tñy) g©y nªn t¨ng tÝnh kÝch thÝch cña thoi vËn ®éng c¬ vµ neuron alpha Tæng quan
- 5. §¬n vÞ vËn®éng tñy sèng – thoi thÇn kinh c¬
- 6. C¸c ®êng vËn®éng ®i xuèng
- 7. S¬ ®å c¸chÖ thèng tõ trung t©m trªn tuû ®i xuèng øc chÕ vµ kÝch thÝch c¸c ph¶n x¹ tuû (Sheean 1998)
- 8. C¸c vßng tuûkiÓm so¸t tÝnh dÔ bÞ kÝch thÝch cña ph¶n x¹ c¨ng gi·n c¬ (Pierrot-Deseilligny vµ MaziÌres -1985)
- 9. Tæn th¬ng N¬ronvËn ®éng trªn
- 10. C¸c yÕu tèlµm t¨ng co cøng • NhiÔm trïng ®êng niÖu • T¸o bãn • Mãng ch©n mäc quÆp vµo trong • LoÐt do t× ®Ì • NÑp chØnh h×nh hoÆc xe l¨n qu¸ chËt
- 11. C¸c mÉu cocøng Toµn thÓ Theo vïngKhu tró CTSN X¬ cøng r¶i r¸c TBMN CT tñy sèng
- 12. C¸c triÖu chøngliªn quan co cøng • ®au • Cøng ®ê • Rung giËt (clo nus) • C¬n co th¾t c¸c c¬ gÊp vµ duçi (fle xo r and e xte nso r spasm s) • ®iÒu hîp vµ kiÓm so¸t c¸c vËn ®éng tinh vi kÐm • BiÕn d¹ng khíp
- 13. C¸c nguyªn nh©ng©y c¬ cøng • Tai biÕn m¹ch m¸u n·o • B¹i n·o • ChÊn th¬ng sä n·o • Tæn th¬ng tñy sèng • C¸c bÖnh tho¸i hãa myelin (vd: X¬ cøng r¶i r¸c, x¬ cét bªn teo c¬…) • C¸c bÖnh tho¸i hãa thÇn kinh (vd: tho¸i hãa tiÓu n·o…) • C¸c bÖnh kh¸c
- 14. C¸c khiÕm khuyÕtphèi hîp víi co cøng • C¬ bÞ rót ng¾n (co rót) • YÕu c¬ • C¬ ho¹t ®éng qu¸ møc phô thuéc sù kÐo gi·n (stre tch- de pe nde nt m uscle o ve ractivity) bao gåm co cøng ®ång ®éng (spastic co -co ntractio n), co cøng lo¹n tr¬ng lùc (spastic dysto nia) Ba gi¶i ph¸p lµm gi¶m t¸c ®éng cã h¹i cña co cøng: 1. KÐo dµi c¬ (muscle lengthening) 2. TËp vËn ®éng (motor training) 3. Gi·n c¬ t¹i chç (local muscle relaxation)
- 15. C¸c vÊn ®Òn¶ysinh sau tæn th¬ng hÖthÇn kinh trung ¬ng (Gracies 1997) Tæn th¬ng c¸c trung t©m trung ¬ng T¸i s¾p xÕp ho¹t ®éng tuû sèngLiÖt C¸c ho¹t ®éng qu¸ møc kh¸c Co cøngBÊt ®éng ë t thÕ xÊu (rót ng¾n) Co rót HËu qña muénHËu qña sím
- 16. C¸c mÉu cocøng chi díi – Bµn ch©n duçi, nghiªng trong (Equino varus Fo o t) – Ngãn ch©n gÊp, qu¾p – Duçi gèi – Hai ®ïi khÐp – H¸ng gÊp
- 17. C¸c mÉu rèilo¹n vËn ®éng hay gÆp trªn l©m sµng KhÐp ®ïi: d¸ng ®i “c¾t kÐo” do c¬ cøng c¸c c¬ khÐp ®ïi, g©y ra ch©n ®Õ hÑp cña d¸ng ®i. Cøng gèi: Gèi duçi cøng liªn tôc, thêng phèi hîp bµn ch©n ngùa. Lu ý gãt ch©n kh«ng thÓ ®Æt lªn chç ®Ó ch©n cña xe l¨n.
- 18. LiÖt nöa ngêico cøng: cæ tay duçi, bµn tay n¾m chÆt, bµn ch©n biÕn d¹ng duçi vµ nghiªng trong (equinovarus)
- 19. Ngãn ch©n c¸iqu¸ duçi C¬ duçi dµi ngãn c¸i
- 20. Co cøng c¸cc¬ gÊp ngãn ch©n
- 21. C¸c mÉu cocøng thêng gÆp ë chi díi vµ lîi Ých cña ®iÒu trÞ MÉu co cøng C¬ liªn quan Lîi Ých ®iÒu trÞ Co cøng vµ co th¾t c¸c c¬ khÐp h¸ng C¸c c¬ khÐp h¸ng Gi¶m d¸ng ®I “c¾t kÐo” do co th¾t c¬ khÐp T¹o thuËn cho ch¨m sãc vïng hËu m«n sinh dôc vµ ®Æt èng th«ng tiÓu Giao hîp dÔ dµng h¬n GÊp h¸ng vµ gèi C¬ th¾t lng chËu, nhãm c¬ gÊp gèi (c¬ lîc, c¬ b¸n m¹c, c¬ b¸n g©n, c¬ nhÞ ®Çu ®ïi. C¶i thiÖn d¸ng ®i vµ tèc ®é ®i, phßng ngõa co th¾t gÊp vµ c¶i thiÖn t thÕ ngåi trªn xe l¨n Rung giËt gèi C¬ tø ®Çu ®ïi Gi¶m ®au, phßng ngõa c¸c c¬n co th¾t c¬ Bµn ch©n gÊp lßng vµ nghiªng trong C¬ sinh ®«i, c¬ dÐp, c¬ chµy tríc vµ c¬ chµy sau. C¬ gÊp dµi ngãn c¸i, c¬ gÊp dµi ngãn ch©n C¬ duçi dµi ngãn c¸i §iÒu chØnh gÊp mÆt lßng qóa møc, cho phÐp ch¹m gãt ch©n khi ®i vµ söa ch÷a nghiªng trong bµn ch©n, t¹o thuËn cho ®i nÑp. Phßng ngõa ngãn ch©n quÆp xuèng Cho phÐp ®i giµy dÐp dÔ dµng
- 22. C¸c mÉu cocøng chi trªn – KhÐp vai – GÊp khuûu – C¼ng tay quay sÊp – GÊp cæ tay – Bµn tay n¾m chÆt – Ngãn tay c¸i khÐp vµ gÊp vµo gan tay
- 23. MÉu co cøngchi trªn ë bÖnh nh©n TBMMN KhÐp, xoay trong khíp vaiKhÐp, xoay trong khíp vai GÊp khuûuGÊp khuûu SÊp c¼ng taySÊp c¼ng tay GÊp cæ tayGÊp cæ tay Bµn tay n¾m chÆtBµn tay n¾m chÆt Ngãn c¸i khÐp vµ gÊp vµoNgãn c¸i khÐp vµ gÊp vµo lßng bµn taylßng bµn tay
- 24. Lîng gi¸ cocøng 1. Kh¸m l©m sµng Tr¬ng lùc nhãm c¬ chÝnh (Thang ®iÓm Ashworth) TÇn sè co th¾t c¬ (rung giËt) TÇm vËn ®éng cña khíp (Thíc ®o gãc) VÞ trÝ cña gèi/bµn ch©n ë t thÕ ®øng Møc ®é ®au 2. §¸nh gi¸ chøc n¨ng C¸c chØ sè cña d¸ng ®i Thang ®iÓm ®¸nh gi¸ møc ®é ®éc lËp chøc n¨ng Thang ®iÓm ®¸nh gi¸ vËn ®éng
- 25. ChØ ®Þnh ®iÒutrÞ 1. Co cøng nÆng g©y ¶nh hëng chøc n¨ng: • ¶nh hëng ®Õn ®Æt t thÕ bÖnh nh©n trªn giêng hoÆc xe l¨n, - ¶nh hëng ®Õn vËn ®éng - ¶nh hëng ®Õn thùc hiÖn c¸c ho¹t ®éng ch¨m sãc sinh ho¹t hµng ngµy (Activitie s o f Daily Living - ADL), - ¶nh hëng ®Õn vÖ sinh b¶n th©n (vÝ dô co cøng c¸c c¬ khÐp h¸ng lµm ¶nh hëng ®Õn viÖc ®Æt th«ng tiÓu, co cøng c¸c c¬ gÊp bµn vµ ngãn tay g©y khã kh¨n cho viÖc më lßng bµn tay ®Ó lau röa, c¾t mãng tay) ... 2. Co cøng nÆng cã thÓ dÉn ®Õn nh÷ng biÕn chøng: C¸c biÕn chøng hay gÆp nh: loÐt da, ®au, co rót sím, biÕn chøng khíp (vÝ dô b¸n trËt khíp h¸ng do co cøng
- 26. ChiÕn lîc ®iÒutrÞ co cøng ë ngêi lín Phßng ngõa c¸c yÕu tè kÝch thÝch, khëi ph¸t co cøng Th¶o luËn nhãm víi bÖnh nh©n vÒ chiÕn lîc ®iÒu trÞ C¸c ph¬ng ph¸p ®iÒu trÞ §iÒu trÞ thuèc§iÒu trÞ vËt lý trÞ liÖu Theo vïng c¬ thÓT¹i chçToµn thÓ Thuèc uèng BTX hoÆc phong bÕ thÇn kinh b»ng phenol B¬m baclofen trong mµng cøng hoÆc phong bÕ phenol PhÉu thuËt thÇn kinh PhÉu thuËt chØnh h×nh Source: Royal College of Physicians, 2001
- 27. C¸c ph¬ng ph¸pVLTL vµ H§TL • §øng trªn bµn nghiªng quay§øng trªn bµn nghiªng quay (® Æc biÖt g i¶m co cø ng sau chÊn th¬ ng tñy sè ng )(® Æc biÖt g i¶m co cø ng sau chÊn th¬ ng tñy sè ng ) • C¸c bµi tËp kÐo gi·n ®Òu ®ÆnC¸c bµi tËp kÐo gi·n ®Òu ®Æn (phß ng ng õ a co ró t vµ duy tr× tÇm vËn ® é ng khíp).(phß ng ng õ a co ró t vµ duy tr× tÇm vËn ® é ng khíp). • NÑp hoÆc bã bét chu kúNÑp hoÆc bã bét chu kú (duy tr× m é t vÞ thÕ ø c chÕ ph¶n x¹ kÐo g i· n cña chi bÞ(duy tr× m é t vÞ thÕ ø c chÕ ph¶n x¹ kÐo g i· n cña chi bÞ co cø ng vµ phß ng ng õ a co ró t).co cø ng vµ phß ng ng õ a co ró t). • KÝch thÝch ®iÖnKÝch thÝch ®iÖn ((kÝch thÝch qua da, kÝch thÝch thÇn kinh, c¬ , cé tkÝch thÝch qua da, kÝch thÝch thÇn kinh, c¬ , cé t sè ng ) – cß n tranh luËn .sè ng ) – cß n tranh luËn .
- 28. Kü thuËt tËpluyÖn phôc håi chøc n¨ng tay vµ bµn tay
- 29. Kü thuËt tËpluyÖn phôc håi chøc n¨ng tay vµ bµn tay
- 30. C¸c thuèc uèng ThuècLiÒu ban ®Çu LiÒu tèi ®a/ngµy C¬ chÕ t¸c dông T¸c dông phô Baclofen Dantrolene Tizanidine Benzodiazepin 5 mg x 3 25 mg 2 - 4 mg 2 mg 80 mg (chia 4 lÇn) 100 mg x 4 36 mg 30- 60 mg T¸c dông trung -¬ng, chÊt gièng GABA, g¾n víi thô thÓ víi GABA ë tËn cïng tr-íc xinap -> øc chÕ dÉn truyÒn TK qua xinap øc chÕ qu¸ tr×nh gi¶i phãng Canxi khái l-íi sîi bµo t-¬ng cña sîi c¬ T¸c dông lªn thô thÓ α2 trung - ¬ng, cã t¸c dông chèng co cøng nhê t¸c dông øc chÕ tr-íc vµ sau xin¸p Cã mét t¸c ®éng trung -¬ng nhê lµm t¨ng hiÖu n¨ng øc chÕ cña GABA t¹i c¸c xin¸p trªn TKTW. Chãng mÆt, ngñ gµ, yÕu c¬, mÖt mái, buån n«n. Dõng ®ét ngét g©y ¶o gi¸c, co giËt YÕu c¬ toµn thÓ, buån ngñ, chãng mÆt, buån n«n, Øa ch¶y, nhiÔm ®éc tÕ bµo gan Kh« miÖng, buån ngñ, chãng mÆt, h¹ ¸p nhÑ, yÕu c¬ nhÑ, t¨ng men gan MÖt mái, buån ngñ, ngñ gµ, g©y nghiÖn
- 31. Tiªm Phenol • §ÆcbiÖt cã t¸c dông trªn nh÷ng bÖnh nh©n co cøng chi d-íi do§Æc biÖt cã t¸c dông trªn nh÷ng bÖnh nh©n co cøng chi d-íi do b¹i n·o vµ chÊn th-¬ng tñy sèng.b¹i n·o vµ chÊn th-¬ng tñy sèng. • Môc tiªuMôc tiªu: ng¨n hoÆc chÑn c¸c d©y thÇn kinh lín ®i tíi c¸c vïng: ng¨n hoÆc chÑn c¸c d©y thÇn kinh lín ®i tíi c¸c vïng “co cøng” ®Æc biÖt cña c¬ thÓ.“co cøng” ®Æc biÖt cña c¬ thÓ. • Nh÷ng h¹n chÕ:Nh÷ng h¹n chÕ: - ®au vµ dÞ c¶m m¹n tÝnh- ®au vµ dÞ c¶m m¹n tÝnh - phï nÒ ngo¹i vi- phï nÒ ngo¹i vi - tæn th-¬ng da, bong da- tæn th-¬ng da, bong da - vÕt th-¬ng nhiÔm trïng- vÕt th-¬ng nhiÔm trïng
- 32. Tiªm Botulinum toxine •Botulinum toxin type ABotulinum toxin type A (BD: Dysport hoÆc Botox).(BD: Dysport hoÆc Botox). • C¬ chÕ: ChÑn dÉn truyÒn qua b¶n vËn ®éng thÇnC¬ chÕ: ChÑn dÉn truyÒn qua b¶n vËn ®éng thÇn kinh-c¬kinh-c¬(ng¨n c¶n viÖc gi¶i phãng Acetylcholin –Ach- tõ c¸c ®Çu(ng¨n c¶n viÖc gi¶i phãng Acetylcholin –Ach- tõ c¸c ®Çu tËn ë mµng tr-íc xinap thÇn kinh).tËn ë mµng tr-íc xinap thÇn kinh). • ChÑn cã chän läc c¸c c¬ co cøngChÑn cã chän läc c¸c c¬ co cøng (do sö dông m¸y ®iÖn c¬(do sö dông m¸y ®iÖn c¬ hoÆc m¸y kÝch thÝch ®iÖn).hoÆc m¸y kÝch thÝch ®iÖn). • HiÖu qu¶ kÐo dµi kho¶ng 4-6 th¸ngHiÖu qu¶ kÐo dµi kho¶ng 4-6 th¸ng (xuÊt hiÖn c¸c chåi(xuÊt hiÖn c¸c chåi xinap thÇn kinh míi ®Ó nèi víi c¸c sîi c¬ - tr-¬ng lùc c¬ quay trëxinap thÇn kinh míi ®Ó nèi víi c¸c sîi c¬ - tr-¬ng lùc c¬ quay trë l¹i).l¹i). •
- 33. C¸c ph-¬ng ph¸pphÉu thuËt • C¸c ph-¬ng ph¸p ph¸ hñyC¸c ph-¬ng ph¸p ph¸ hñy c¾t bá tñy (myelotomy) hoÆc c¾t bá cét tñyc¾t bá tñy (myelotomy) hoÆc c¾t bá cét tñy (cordotomy).(cordotomy). • C¸c ph-¬ng ph¸p chØnh h×nhC¸c ph-¬ng ph¸p chØnh h×nh (kÐo dµi, gi¶i phãng hoÆc chuyÓn g©n).(kÐo dµi, gi¶i phãng hoÆc chuyÓn g©n). • C¸c ph-¬ng ph¸p ®Æc biÖt:C¸c ph-¬ng ph¸p ®Æc biÖt: -- c¾t chän läc c¸c rÔ sau ë trÎ b¹i n·oc¾t chän läc c¸c rÔ sau ë trÎ b¹i n·o - phÉu thuËt x-¬ng ®Ó söa ch÷a c¸c biÕn d¹ng- phÉu thuËt x-¬ng ®Ó söa ch÷a c¸c biÕn d¹ng
- 34. C¸c nh-îc ®iÓmchÝnh cña c¸c ph-¬ng ph¸p ®iÒu trÞ co cøng C¸c thuèc uèng G©y ngñ gµ, yÕu c¬ toµn th©n, rèi lo¹n ý thøc ®Æc biÖt liªn quan ®Õn ng-êi giµ Phong bÕ Alcohol vµ Phenol §au rèi lo¹n c¶m gi¸c, tæn th-¬ng m« PhÉu thuËt KÕt qu¶ kh«ng ®¶o ng-îc, th-êng sö dông khi c¸c ph- ¬ng ph¸p ®iÒu trÞ b¶o tån thÊt b¹i. Sources: Kirazli et al, 1998; Kong, Chua, 1999; Davis, 2000; Hesse et al, 2001; Corbett et al, 1972; Wilson, McKechnie, 1966; Basmajian et al, 1984; Ketel et al, 1984; Hulme et al, 1985; Gelber et al, 2001
- 35.
Editor's Notes
- #3 The material in the presentation kit is designed to give viewers an understanding of the use of botulinum in the management of focal spasticity in adults. The presentation covers definitions of spasticity in the overall spectrum of management of adult spasticity and some details of the development of Allergan’s BOTOX and mechanisms of action. The presentation goes on to look at doses, injection techniques and finally reviews some outcome studies and cost benefit analysis of the use of the drug. The presentation has been compiled from existing presentations available world wide, as well as the experience of Australian physicians over the past decade.
- #5 This presentation focuses on the use of botulinum in the reduction of focal adult spasticity. In rehabilitation medicine the focus of treatment is on reducing disability and handicap in individuals with spasticity and the presentation will emphasise goal setting and the aim of improving function following the use of botulinum as a treatment to be integrated into the other treatments the patient receives such that an optimal response
- #14 The listed conditions may all cause an upper motor neurone syndrome, leading to neurological deficits that can adversely affect patient function. It should be noted that the development of spasticity is not immediate, and that muscles are often initially hypotonic or even flaccid. Spasticity can gradually develop days or even months following the initial event. Spasticity is one component of the upper motor neurone syndrome that includes positive and negative symptoms. The positive symptoms include spasticity, clonus, hyper-reflexia, dystonia and rigidity and the negative symptoms include decreased dexterity, weakness, paralysis, fatigability and slowness of movement. Negative symptoms are important in a functional sense as these deficits can limit the degree of functional benefit achieved when there is reduction of spasticity. Reducing spasticity can initially lead to apparent loss of function due to impaired dexterity (loss of fine motor planning skills resulting from the CNS injury) and underlying muscle weakness. When these negative symptoms are exposed, individuals will often need specific therapy interventions to strengthen muscles and retrain the use of movement in order to achieve the goals of improved function.
- #15 The direct consequences of spasticity leading to muscle shortening, muscle weakness and the over-activity of the stretch reflex, are noted as disabling consequences of spasticity. Other effects include the development of contractures and it should be noted that spasticity can be painful. It can be emphasised that the overall concern in therapy is therefore to stretch shortened muscles, to strengthen antagonist muscles, to learn muscle relaxation techniques and to retrain the use of muscles in order to improve function. It is worth noting again in the presentation of this slide that reducing spasticity can unmask underlying weakness of muscles.
- #17 Whilst the pattern of spasticity is not specific to one cause, generalised spasticity, which is diffuse and affects multiple regions of the body is most often associated with traumatic brain injury and multiple sclerosis, regional spasticity affecting a large area of the body is most often associated with spinal cord injury, and focal spasticity, which is localised to a particular area, is often a characteristic of spasticity following stroke.
- #18 There are typical patterns of adult spasticity associated with the upper motor neurone syndrome. Lower limb spasticity commonly affects extensor muscles, which effectively increases leg length. This affects the swing phase of gait, such that an individual either has to circumduct the leg or “hitch” the hip during the gait cycle. This subsequently leads to difficulties in the speed of walking, balance and increased energy expenditure during the gait cycle. Hip adduction as seen on the left side picture results in a narrow base of support with the feet crossing midline during the swing phase of locomotion, like walking on a tight rope. Equinovarus will preferentially load the lateral boarder of the forefoot producing pain and instability as well as potential for skin breakdown.
- #20 A patient with hallux hyperextension is depicted here. Patients often do not practice full plantar weight bearing support (in an effort to reduce the reflex response to toe extension), have difficulty wearing normal shoes, and there is a propensity for skin breakdown and pain on the dorsal surface of the big toe due to constant pressure of the toe on the inner surface of the shoe.
- #22 Specifics of the muscles involved in the patterns of spasticity often encountered in the lower limb are presented, with some examples of the benefits of reducing spasticity around the knee, hip and ankle. It should be noted that not all muscle groups are affected in all patients and that the functional consequences of spasticity in a muscle group is also influenced by the strength of the antagonist muscle.
- #23 In the upper limb, there is very commonly a predominant flexor pattern, which can functionally lead to a symmetry of gait and reduced balance, problems with reaching and thus in some individuals, limiting the use of intact distal movement, where proximal spasticity leads to an internally rotated adducted shoulder and flexed elbow.
- #25 In this slide, the muscles involved in the patterns of spasticity from proximal to distal in the upper limb are presented, with functional benefits of spasticity reduction being outlined.
- #26 Pre-injection examination of the patient should include a neurological examination and some direct measures of the effects of the spasticity such as the use of the Ashworth Scale and/or Tardieu scale. Goniometry of joints surrounded by muscles with increased tone prior to injection can also be useful. From a rehabilitation perspective, measures of patient function are particularly important. These can include measures of gait parameters such as velocity of gait, step width and step length. Disability measures such as Functional Independence Measure and motor functions such as measured by the Motor Assessment Scale. Patient self report of the efficacy of the treatment is also important to record.
- #28 Modalities used in the treatment of spasticity are outlined. In general, the treatment measures are listed, commencing with the least invasive physical modalities and concluding with surgical intervention. The use of botulinum toxin as a treatment modality in focal spasticity can be emphasized as one that can be integrated with physical therapy, oral medications (if still needed), and surgical treatments. It should be emphasized that this integrative approach is often the most successful in maximizing functional recovery.
- #29 In using the range of modalities outlined in previous slides for the management of focal adult spasticity, it must be emphasised that there should be clear functional objectives of the treatment, which align the technical objectives of the immediate consequences of improved range of movement of a joint, with the improvement of function that will be a consequence of this improved range of movement. It should be emphasised here that the patient and/or care giver objectives and expectations must also be taken into account. In consultation between the treating physician and the patient and/or care giver is essential to ensure that the goals set are realistic and achievable. Other aspects of the patient’s condition, such as cognitive and emotional function may influence the final outcome.
- #30 The Royal College of Physicians have produced a management strategy for the treatment of adult spasticity, which again makes the point that the management strategy needs to involve the team and the patient and again considers spasticity in terms of generalised, focal and regional.
- #38 This slide gives broad overview of the main drawbacks involved in the medical treatment of spasticity. With particular reference to the treatment of focal spasticity, it could be further noted that, with the use of alcohol and phenol in nerve or motor point blocks, the injections can be technically more difficulty and time consuming than with the use of botulinum toxin, as greater accuracy is required in targeting the motor point, whereas botulinum toxin has a clear lack of tissue toxicity. Typically there is no pain related to injection of the botulinum product other than the needle stick. Thus, the use of Botulinum overcomes some of the procedural difficulties of using phenol. Patients can tolerate the procedure and there is no risk of sensory dysesthesias, and tissue necrosis as is associated with phenol injections.