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S P A S T I C I T Y D.S.N.V. - UniGE Motor disorder characterized by velocity dependent increase in tonic stretch reflexes and exaggerated tendon jerksMotor.

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Presentazione sul tema: "S P A S T I C I T Y D.S.N.V. - UniGE Motor disorder characterized by velocity dependent increase in tonic stretch reflexes and exaggerated tendon jerksMotor."— Transcript della presentazione:

1 S P A S T I C I T Y D.S.N.V. - UniGE Motor disorder characterized by velocity dependent increase in tonic stretch reflexes and exaggerated tendon jerksMotor disorder characterized by velocity dependent increase in tonic stretch reflexes and exaggerated tendon jerks

2 UPPER MOTONEURONE SYNDROME Negative phenomenaNegative phenomena - Weakness - Fatigability - Reduced MUs recruitment recruitment - Reduced dexterity D.S.N.V. - UniGE Positive phenomenaPositive phenomena - Tone increase - Stretch hyperreflexia - Clonus - Flexor-extensor spasms - Abnormal cutaneous r. - Babinski sign - Cocontraction/Dystonia

3 HigherCentres Spinal Cord Circuitry SkeletalMuscle PeripheralAfferents Pathways Descending D.S.N.V. - UniGE

4 SPASTICITY and UMN Syndrome Pathophysiological Mechanisms Defective InhibitionDefective Inhibition MNs MNs Postsynaptic MNs inhibition Presynaptic Ia inhibition Excitatory group II INs Defective ExcitationDefective Excitation Inhibitory Ia-INs Reciprocal Inhibitory Ib- INs Autogenetic Renshaw cells Recurrent D.S.N.V. - UniGE

5 SPASTICITY Ia Pre-synaptic Inhibition D.S.N.V. - UniGE

6 SPASTICITY Ia Reciprocal Inhibition D.S.N.V. - UniGE

7 SPASTICITY Interneuronal Excitability D.S.N.V. - UniGE

8 SPASTICITY and UMN Syndrome Pathophysiological Mechanisms Motor Units changesMotor Units changes –collateral sprouting –transynaptic degeneration –dendrite shortening –silent synapses activation –denervation supersensitivity Changes of Stiffnes andChanges of Stiffnes and muscle properties D.S.N.V. - UniGE

9 Muscle & Nerve suppl D.S.N.V. - UniGE

10 TREATMENT of SPASTICITY Therapeutic Objectives TECHNICAL:TECHNICAL: - Promote: TONE REDUCTION - Improve: RANGE of MOTION, JOINT POSITION - Facilitate: REHABILITATION FUNCTIONAL:FUNCTIONAL: - Improve: GAIT, HYGIENE, ADL, EASE of CARE - Reduce: SPASMS, PAIN D.S.N.V.- UniGE

11 PHARMACOLOGIC TREATMENT OF SPASTICITY Recommended when spasticity produces a clinical disability by interfering with posture, motor capacity, nursing, ADLRecommended when spasticity produces a clinical disability by interfering with posture, motor capacity, nursing, ADL Indicated when muscle overactivity is diffusely distributed (spinal > cerebral)Indicated when muscle overactivity is diffusely distributed (spinal > cerebral) Timed in the early stages to prevent permanent musculoskeletal deformities or contracturesTimed in the early stages to prevent permanent musculoskeletal deformities or contractures The goal is to decrease spinal reflex excitability by:The goal is to decrease spinal reflex excitability by: - reducing the release of excitatory neurotransmitters - potentiating the activity of inhibitory circuits D.S.N.V.- UniGE

12 NEUROTRANSMITTERS AND PHYSIOLOGICAL MECHANISMS INVOLVED IN SPASTICITY GABAGlycineGlutamateEAAsNoradrenalineSerotonine D.S.N.V. - UniGE

13 DIAZEPAM Aumenta laffinità del GABA per il suo recettore ionoforico (GABA a)Aumenta laffinità del GABA per il suo recettore ionoforico (GABA a) -Livello postsinaptico: aumento conduttanza Cl, iperpolarizzazione, inibizione postsinaptica -Livello presinaptico: aumento conduttanza Cl, depolarizzazione, inibizione rilascio aminoacidi eccitatori D.S.N.V. - UniGE

14 BACLOFEN Stimolazione recettori GABA b (metabotropici)Stimolazione recettori GABA b (metabotropici) - Livello postsinaptico: aumento conduttanza K, iperpolarizzazione cellulare, inibizione - Livello presinaptico: blocco dei canali del Ca, alterazione liberazione aminoacidi eccitatori D.S.N.V. - UniGE

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16 DIAZEPAM (2) CLINICAL EFFECTS:CLINICAL EFFECTS: eduction of resistance to stretch (increased range of motion) - Reduction of resistance to stretch (increased range of motion) - Reduction of deep tendon reflexes and of painful spasms SIDE EFFECTS:SIDE EFFECTS: - Sedation & drowsiness, Attention & memory impairment - Weakness amd motor incoordination - Tolerance, dependency (withdrawal phenoemena) INDICATIONS: SCI - MS (possible: TBI - CP - CVA)INDICATIONS: SCI - MS (possible: TBI - CP - CVA) EFFICACY SHOWN BY DOUBLE-BLIND PROTOCOLS IN SC LESIONS (POSSIBLE STRENGTH-GAIT DETERIORATION)EFFICACY SHOWN BY DOUBLE-BLIND PROTOCOLS IN SC LESIONS (POSSIBLE STRENGTH-GAIT DETERIORATION) D.S.N.V. - UniGE

17 BACLOFEN (2) CLINICAL EFFECTS:CLINICAL EFFECTS: Reduction of flexor-extensor spasms - Reduction of flexor-extensor spasms - Reduction of mono- polysynaptic reflexes - Reduction of sphincter hyperreflexia SIDE EFFECTS:SIDE EFFECTS: - Sedation, Drowsiness, Fatigue, Confusion, Dizziness - Hypotonia, Ataxia INDICATIONS: Spinal s pasticityINDICATIONS: Spinal s pasticity EFFICACY SUFFICIENTLY DOCUMENTED IN PATIENTS WITH SC LESIONS (LESS IN CEREBRAL)EFFICACY SUFFICIENTLY DOCUMENTED IN PATIENTS WITH SC LESIONS (LESS IN CEREBRAL)

18 INTRATHECAL BACLOFEN Consists of direct long-term delivery of baclofen to the intrathecal space via an implanted programmable pumpConsists of direct long-term delivery of baclofen to the intrathecal space via an implanted programmable pump Indicated in patients with severe spasticity, not managed by oral baclofen (inadequate BBB penetration, side effects) or other oral medicationsIndicated in patients with severe spasticity, not managed by oral baclofen (inadequate BBB penetration, side effects) or other oral medications Same clinical effects at much lower doses (1 %)Same clinical effects at much lower doses (1 %) - Selection- Selection - Screening - Implantation - Dose adjustment & maintenance D.S.N.V. - UniGE

19 INTRATHECAL BACLOFEN (2) Benefits have been documented by placebo-controlled studies in severely disabled nonambulatory patients with overactivity mainly in ther lower limbs and with flexor spasmsBenefits have been documented by placebo-controlled studies in severely disabled nonambulatory patients with overactivity mainly in ther lower limbs and with flexor spasms Reduction of spasticity, spasms and painReduction of spasticity, spasms and pain Sleep improvement and better bladder management IMPROVEMENT IN QUALITY OF LIFEIMPROVEMENT IN QUALITY OF LIFE COMPLICATIONS: infection, pump dysfunction, high cost and invasivenessCOMPLICATIONS: infection, pump dysfunction, high cost and invasiveness D.S.N.V. - UniGE

20 TIZANIDINA Attività 2-agonista (spinale e sopra-spinale)Attività 2-agonista (spinale e sopra-spinale) - riduce la liberazione di aminoacidi eccitatori nel midollo spinale - inibisce la via coerulo-spinale (questa via normalmente facilita i circuiti spinali) D.S.N.V. - UniGE

21 TIZANIDINE (2) CLINICAL EFFECTS:CLINICAL EFFECTS: - reduction of tonic stretch polysynaptic reflexes - reduction of co- contraction SIDE EFFECTS:SIDE EFFECTS: sedation, dizziness, dry mouth, but not weakness INDICATIONS: MS - SCI (possible: cerebral spasticity)INDICATIONS: MS - SCI (possible: cerebral spasticity) EFFICACY PROVEN BY PLACEBO-CONTROLLED STUDIES (> DIAZEPAM IN CEREBRAL). NO DEFINITE FUNCTIONAL CHANGESEFFICACY PROVEN BY PLACEBO-CONTROLLED STUDIES (> DIAZEPAM IN CEREBRAL). NO DEFINITE FUNCTIONAL CHANGES D.S.N.V. - UniGE

22 DANTROLENE Peripheral inhibition of calcium release from sarcoplasmic reticulum. Decreased excitation-coupling reaction.Peripheral inhibition of calcium release from sarcoplasmic reticulum. Decreased excitation-coupling reaction. CLINICAL EFFECTS:CLINICAL EFFECTS: Reduction of muscle tone, phasic reflexes and spasms Increased range of passive motion INDICATIONS: CVA - CP (possible: TBI - SCI -MS)INDICATIONS: CVA - CP (possible: TBI - SCI -MS) SIDE EFFECTS:SIDE EFFECTS: hepatotoxicity, GE symptoms, weakness, but less sedation D.S.N.V. - UniGE

23 ANTISPASTIC DRUGS Clonazepam, Ketazolam, TetrazepamClonazepam, Ketazolam, Tetrazepam Progabide, Gabapentin PiracetamClonidineL-threonineThymoxamine Cyproheptadine, Orphenadrine ONLY FEW CONTROLLED STUDIESONLY FEW CONTROLLED STUDIES MOSTLY OPEN OR ANECDOTICAL OBSERVATIONS D.S.N.V. - UniGE

24 Cochrane Database Syst. Rev. (2000) - To assess the effectiveness and safety of antispastic drugs in patients with SCI -9 out of 53 parallel and crossover studies (up to 1998) included 2 studies (placebo controlled) showed a significant effect of intrathecal baclofen in reducing spasticity (Ashworth - ADL) 2 studies (placebo controlled) showed a significant effect of intrathecal baclofen in reducing spasticity (Ashworth - ADL) 1 study (placebo controlled) showed a significant effect of tizanidine in improving Ashworth scale but not ADL1 study (placebo controlled) showed a significant effect of tizanidine in improving Ashworth scale but not ADL No significant evidence for the other drugs (Gabapentin, Clonidine, Diazepam, oral Baclofen)No significant evidence for the other drugs (Gabapentin, Clonidine, Diazepam, oral Baclofen) D.S.N.V. - UniGE

25 Neurolytic Agents Phenol and alcohol injections may be used to induce a focal chemodenervation by: - protein denaturation - non-selective tissue destruction (nerve coagulation - muscle necrosis) - Wallerian degeneration Motor nerve blockMotor nerve block Motor point block D.S.N.V. - UniGE

26 Phenol and Alcohol (1) INDICATIONS:INDICATIONS: focal spasticity - proximal muscles (lower limb) CLINICAL EFFECTSCLINICAL EFFECTS Reduction of muscle tone (and clonus) without impairment of strength and voluntary contraction. Long duration. SIDE EFFECTSSIDE EFFECTS sensory damage (dysesthesia, causalgia, neuralgic pain) tissue damage (edema, venous thrombosis) tissue damage (edema, venous thrombosis) NO CONTROLLED FUNCTIONAL DATANO CONTROLLED FUNCTIONAL DATA D.S.N.V. - UniGE

27 BOTULINUM TOXIN Potent neurotoxin 7 serotypes (A-G) with different antigenic properties reversible block of Acetylcholine release

28 D.S.N.V. - UniGE BOTULINUM TOXIN Mechanism of action

29 D.S.N.V. - UniGE

30 BTX e SPASTICITA Indicazioni Trattamento della spasticità focale, cioè di limitati gruppi muscolari la cui iperattività o ipertonia interferisce con lo svolgimento di specifiche attività funzionali statiche o dinamicheTrattamento della spasticità focale, cioè di limitati gruppi muscolari la cui iperattività o ipertonia interferisce con lo svolgimento di specifiche attività funzionali statiche o dinamiche Lo scopo è ottenere un effetto locale, in assenza di effetti sistemiciLo scopo è ottenere un effetto locale, in assenza di effetti sistemici Controindicazioni:Controindicazioni: - mancanza di unadeguata attività dinamica - presenza di contratture fisse o deformità D.S.N.V. - UniGE

31 BTX e SPASTICITA Possibili obiettivi E fondamentale la selezione dei pazienti e dei muscoli bersaglio e lidentificazione degli obiettivi terapeutici Prevenzione complicazioni (evitare chirurgia)Prevenzione complicazioni (evitare chirurgia) Controllo del doloreControllo del dolore Facilitazione delligiene e/o assistenzaFacilitazione delligiene e/o assistenza Miglioramenti funzionaliMiglioramenti funzionali - adattabilità ortesi, ampliamento ROM - incremento autonomia (controllo motorio, appoggio, autonomia) D.S.N.V. - UniGE

32 BTX e SPASTICITA Effetti principali Riduzione delliperattività muscolare:Riduzione delliperattività muscolare: - riflesso tonico da stiramento (Ashworth Scale) dolore dolore - range di movimento passivo Evidenze neurofisiologiche:Evidenze neurofisiologiche: - modificazioni attività riflesse spinali - effetti di tipo centrale ? D.S.N.V. - UniGE

33 BTX e SPASTICITA Effetti principali Modificazioni funzionali:Modificazioni funzionali: - scale di autovalutazione (patient/caregiver) - scale di valutazione funzionale (ADL, FIM, Rivermead) - test motori (Frenchay Arm test, reaching, tapping) - analisi EMG/Video del cammino INCERTEZZA SULLE MISURE DI OUTCOME D.S.N.V. - UniGE

34 BTX e SPASTICITA Problemi metodologici Sede diniezione: Quali criteri ??Sede diniezione: Quali criteri ?? valutazione clinica e/o infiltrazione EMG-guidata - pattern MUPs - localizzazione punto motore - turns amplitude analysis - stimolazione elettrica Childers et al., Finsterer et al., 1997 Childers et al., Finsterer et al., 1997 Numero iniezioni e volume diluizione ??Numero iniezioni e volume diluizione ?? D.S.N.V. - UniGE

35 BTX e SPASTICITA Problemi metodologici Dosaggio ??Dosaggio ?? - lentità (ma non la durata) del miglioramento funzionale può essere dose-dipendente Wissel et al., 1999; Hyman et al., 2000; Smith et al., 2000; Wissel et al., 1999; Hyman et al., 2000; Smith et al., 2000; Bakheit et al., 2000 Bakheit et al., problema della immunoresistenza - basse dosi in associazione a procedure riabilitative D.S.N.V. - UniGE

36 BTX e SPASTICITA Trattamenti concomitanti La stimolazione elettrica o lattività muscolare potenzia lattività della tossinaLa stimolazione elettrica o lattività muscolare potenzia lattività della tossina Hesse et al., 1995 e 1998, Eleopra et al Hesse et al., 1995 e 1998, Eleopra et al D.S.N.V. - UniGE

37 BTX e SPASTICITA Follow-up Efficacia nel tempo del trattamento ??Efficacia nel tempo del trattamento ?? - analogia con altre indicazioni 4Lagalla et al efficacia invariata a 3 anni in pz. con stroke dose invariata, > intervallo D.S.N.V. - UniGE

38 SURGICAL TECHNIQUES in Spasticity Objective: to treat permanently static or dynamic consequernces opf UMN sundrome in stable patientsObjective: to treat permanently static or dynamic consequernces opf UMN sundrome in stable patients Timing: early and before severe and fixed deformitiesTiming: early and before severe and fixed deformities Methods: specific interventions for individual muscle/jointsMethods: specific interventions for individual muscle/joints - TENDON LENGTHENING - INTRAMUSCULAR LENGTHENING - TENDON TRANSFER - NEURECTOMY

39 D.S.N.V. - UniGE Management of Spasticity REGIONALIT/BACLOFEN NERVE BLOCKS MEDICALTHERAPYPHYSICALTHERAPY Treat muscle overactivity with different strategies FOCALBTXINJECTIONSGENERALORALDRUGS Prevent: - provocative factors or noxious stimuli noxious stimuli (medication if necessary) - delayed consequences (surgery if necessary)


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