11/17/2014 1 Clinical applications of botulinum neurotoxin in the treatment of spasticity Petr Kaňovský Department of Neurology Palacky University Medical School University Hospital Olomouc, Czech Republic Spasticity has firstly been characterised by William John Little (1810 - 1894) in the description of cerebral palsy: “Pathology has gradually taught that the fetus in utero is the subject to similar diseases to those which afflict the economy at later periods of existence. This is especially true if we turn to the study of the special class of abnormal conditions, which are called deformities...“ On the influence of abnormal parturition, difficult labours, premature birth and asphyxia neonatorum, on the mental and physical condition of the child, especially in relation to deformities by WJ Little, MD, Senior Physician to the London Hospital, founder of the Royal Orthopaedic Hospital, Visiting Physician to Asylum for Idiots, Earlswood Transactions of the Obstetrical Society of London 1861, 3: 293 Spasticity is defined as an increase in the muscle tone, which depends on the increase of the tonic stretch reflex and on the velocity of the passive movement. The hyperexcitability of the stretch reflex has been supposed as its origin (Lance 1980, Brown 1994, Sheean 2004) Spastic muscle contraction is, in fact, a kind of pathological tonic muscle response appearing as the consequence of phasic increase of muscle tone The muscle response on the phasic increase of its tone can be tested in two ways: 1) Passive movement in different velocities 2) Tapping on the muscle tendon (reflex examination) Stretch reflex is managed by the very fast Ia afferent fibres originating in the muscle spindles. Stretch reflex depends on the velocity of passive movement and on the length of the muscle The increased response of stretch reflex is caused by the central hyperexcitability, which is one of the basic characteristics of the “spastic movement disorder“ Spasticity is not caused by the isolated lesion of corticospinal pathway itself. The selective lesion of corticospinal pathway causes a flaccid paralysis. Only the lesion of other descendent inhibition pathways (tectospinal, olivospinal, nigrospinal, rubrospinal), together with the re-organisation of spinal neuronal feed-back circuits, causes the increase of muscle tone typical for spasticity. Current model of the evolution of spastic hypertonus and spastic muscle contraction: The reduction of inhibitory inputs from the cortex and basal ganglia leads to the disordered modulation of monosynaptic affarentation via primary Ia afferent fibres and polysynaptic afferentation from the exteroreceptores. This disorder of modulation causes the hyperexcitability of spinal alpha motor neurons. Spinal interneurons are the “key player“ in this “modulatory“ phase, because of their ability of pre-synaptic and reciprocal inhibition (via Ia fibers). Ventromedial pontine reticular formation has an additive inhibitory input to the spinal interneurons. Vestibular nuclei (via vestibulospinal tracts) have, on the contrary, an additive inhibitory input to the spinal interneurons. Brown 1994, Sheean 2004, Kanovsky 2005, Rosales & Kanovsky 2011 Spasticity treatment options and methods: I. Non-surgical A. Non-pharmacological B. Pharmacological II. Surgical III. Chemodenervation with botulinum toxin A
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11/17/2014
1
Clinical applications of botulinum neurotoxin
in the treatment of spasticity
Petr Kaňovský
Department of Neurology
Palacky University Medical School
University Hospital
Olomouc, Czech Republic
Spasticity has firstly been characterised by William John Little (1810 - 1894) in the description of cerebral palsy:
“Pathology has gradually taught that the fetus in utero is the subject to similar diseases to those which afflict the economy at later periods of existence. This is especially true if we turn to the study of the special class of abnormal conditions, which are called deformities...“
On the influence of abnormal parturition, difficult labours, premature birth and asphyxia neonatorum, on the mental and physical condition of the child, especially in relation to deformities
by WJ Little, MD, Senior Physician to the London Hospital, founder of the Royal Orthopaedic Hospital, Visiting Physician to Asylum for Idiots, Earlswood
Transactions of the Obstetrical Society of London 1861, 3: 293
Spasticity is defined as an increase in the muscle tone, which depends
on the increase of the tonic stretch reflex and on the velocity of the
passive movement. The hyperexcitability of the stretch reflex has been
supposed as its origin (Lance 1980, Brown 1994, Sheean 2004)
Spastic muscle contraction is, in fact, a kind of pathological tonic muscle
response appearing as the consequence of phasic increase of muscle tone
The muscle response on the phasic increase of its tone can be tested in two
ways:
1) Passive movement in different velocities
2) Tapping on the muscle tendon (reflex examination)
Stretch reflex is managed by the very fast Ia afferent fibres originating in
the muscle spindles. Stretch reflex depends on the velocity of passive
movement and on the length of the muscle
The increased response of stretch reflex is caused by the central
hyperexcitability, which is one of the basic characteristics of the “spastic
movement disorder“
Spasticity is not caused by the isolated lesion of corticospinal pathway
itself. The selective lesion of corticospinal pathway causes a flaccid
paralysis.
Only the lesion of other descendent inhibition pathways (tectospinal,
olivospinal, nigrospinal, rubrospinal), together with the re-organisation
of spinal neuronal feed-back circuits, causes the increase of muscle tone
typical for spasticity.
Current model of the evolution of spastic hypertonus and spastic
muscle contraction:
The reduction of inhibitory inputs from the cortex and basal ganglia
leads to the disordered modulation of monosynaptic affarentation via primary
Ia afferent fibres and polysynaptic afferentation from the exteroreceptores.
This disorder of modulation causes the hyperexcitability of spinal alpha motor
neurons.
Spinal interneurons are the “key player“ in this “modulatory“ phase,
because of their ability of pre-synaptic and reciprocal inhibition (via Ia
fibers).
Ventromedial pontine reticular formation has an additive inhibitory input to
the spinal interneurons. Vestibular nuclei (via vestibulospinal tracts) have, on
the contrary, an additive inhibitory input to the spinal interneurons.
Brown 1994, Sheean 2004, Kanovsky 2005, Rosales & Kanovsky 2011
Spasticity treatment options and methods:
I. Non-surgical
A. Non-pharmacological
B. Pharmacological
II. Surgical
III. Chemodenervation with botulinum toxin A
11/17/2014
2
Study Year Invertion Outcome Measures Quality
(JADAD)
Brashear 2002 ONA or Placebo Functional disability, muscle tone, global assessment,