Patent Application
20090204175
The invention relates to an electrostimulating apparatus and method.
In neurophysiology, the H reflex, or Hoffman reflex is known, which, although it is a reflex that is very similar to the monosynaptic reflex following a mechanical stretching of a muscle, may also be evoked through an electric stimulation conducted at the level of an afferent innervation. In the recent past, the H reflex in humans has been studied widely, as the features of the latter enable useful information to be obtained for defining the spinal excitability in humans both in physiological and pathological conditions. In particular, the modulation of the H reflex has been studied following serious clinical manifestations of a heterogeneous group of pathologies, comprising spasticity, dystonia and fibromyalgia. In these pathologies, an increase in spinal excitation at the level of a single metamer or of several metamers is recognised as a physiopathological common denominator that is activated by various central and peripheral influences, and the spinal excitation can be studied in vivo in humans by evaluating carefully the H reflex both in terms of latency and in terms of the amplitude of the reflex with respect to the dispensed stimulation. The H reflex is definable as the simplest of the spinal reflexes and can be evoked by electrically stimulating type Ia afferent fibres comprised in the muscle spindle endings. This stimulation is followed by a transmission of the evoked discharge afferent to the spinal cord, a production of a synchronised postsynaptic excitatory potential that is sufficient to discharge the motor neurons of a relevant pool with a transmission of the reflex discharge along the axons of the alpha-type motor neurons to the muscle. The excitability of the spinal motor neuron depends directly on the descending central path under the systemic influence, which is typically at the endocrine level and is mediated by circulating neurotransmitters, of projection of the peripheral reflex arch. The measurement of the minimum latency of the H wave, combined with the amplitude, width and threshold values of the latter, provides information on the conduction level of the reflex arch. The amplitude of the H reflex on the other hand enables to measure indirectly the quantity of alpha motor neurons that have been activated synchronously, modulated by various afferences. A weak voluntary contraction strengthens the H reflex, increasing the discharge of the motor neuron pool, but alters the latency of the reflex. In non-pathological circumstances, the H reflex can be recorded from the soleus muscle by stimulating the tibial nerve and from the flexor carpi radialis muscle by stimulating the median nerve through a low-frequency stimulus.
If it is not possible to reproduce a reflected response this can be ascribed to an afferent disturbance or to a low central excitability. The low central excitability does not necessarily indicate a specific pathology, as the test during a weak muscular contraction may reveal an intact reflex path with a normal latency. In the literature, there are reported various attempts to reduce the hyperexcitability of the motor neuron through Transcutaneous Electric Stimulation (TENS), although there is no univocal consensus on the effect that the latter could have on the Hoffman reflex. The spinal excitability is regulated by many influences that can be concisely classified as above the spinal cord, systemic (due to hormones and circulating neurotransmitters), propriospinal (intra-spinal connections) or reflected peripheral influences.
The reflected peripheral influences in turn comprise a combination of reflex arches, which are both monosynaptic and oligo- or multisynaptic and are integrated at a distinct spinal innervation level (metamer). The peripheral afferences come from the central branch of the cells of the spinal ganglia. The peripheral branch is connected to different types of receptor: the muscle spindles, the tendon receptors, the joint receptors and various types of cutaneous receptors. In particular, the afferences of the muscle spindles (fibres Ia) are the afferences that determine the most direct relations with the pool of the alpha motor neurons interacting in the so-called “Sherrington monosynaptic reflex”. Although the Sherrington reflex model is still an object of discussion, it can be stated that when a muscle is stretched the primary sensory fibres, i.e. the afferent neurons of the group Ia of the muscle spindles, respond both to the speed and degree of extension, sending the information at the spinal level. On the other hand, the secondary sensory fibres, i.e. the afferent neurons of the group 11, detect and send to the central nervous system (CNS) only the information relating to the degree of stretching. This information is transmitted monosynaptically to the alpha motor neuron that activates the extrafusal fibres in order to reduce the stretching and is transmitted polysynaptically, by means of an interneuron, to another alpha motor neuron that inhibits the contraction in the antagonist muscle. Further, at the same time, through two types of gamma motor neurons, known as static and dynamic motor neurons, the CNS is able to influence the afferences of the muscle spindles during movement. The muscle spindle is thus definable as the most important proprioceptor, having a fundamental role in the movement and the control of the reflex activity. The combined signal coming from a plurality of muscle spindles of each muscle provides the CNS with information, generating a fine adjustment of the muscular activation and thus acting as a sort of servo control. At the same time, the muscle spindles are controlled in a continuous manner by the gamma neurons that the CNS controls separately from the alpha motor neurons by controlling all muscle functions. The intrafusal fibres are typically excited by the stimulation below the extrafusal motor threshold: as soon as the motor threshold has been exceeded, the muscle contraction activates the tendon receptors, which provoke the effect of the muscle spindles.
WO 02/09809 discloses an apparatus for treating muscular, tendon and vascular pathologies by means of which a stimulation is applied to a patient, which stimulation comprises a series of electric pulses having a width comprised between 10 and 40 microseconds and an intensity that is variable in function of the impedance and conductance of the tissue subjected to stimulation, and comprised between 100 and 170 microamperes.
WO 2004/084988 discloses an electrostimulating apparatus owing to which it is possible, in function of the type of electric stimulation produced and of the configuration parameters adopted, to generate an induced bioactive neuromodulation, which is suitable for producing vasoactive phenomena on the microcircle and on the macrocircle. These phenomena are in turn mediated by phenomena connected to the direct stimulation of the smooth muscle and by essentially catecolaminergic phenomena, by means of stimulation of the postsynaptic receptors. The aforesaid apparatus is able to produce specific stimulation sequences that induce reproducible and constant neurophysiological responses. In particular, WO 2004/084988 discloses an activating sequence for activating the microcircle (ATMC) and a relaxing sequence for relaxing the muscle fibre (DCTR), which are able to stimulate various functional contingents, including the striated muscle, the smooth muscle and the peripheral mixed nerve. The aforesaid stimulation sequences are assembled on three basic parameters: the width of the stimulation, the frequency of the stimulation and the intervals of time during which different width/frequency combinations follow. The general operating model of the stimulation sequences reflects the digital-analogue transduction that occurs in the transmission of a nerve pulse.
The neuronal electric stimulation by modulation of frequency and amplitude, or FREMS™ (Frequency Rhythmic Electric Modulation System™), disclosed in the aforesaid WO 2004/084988 and in WO 2004/067087 (incorporated herein for reference), is characterised by the use of transcutaneous electric currents, which are produced by means of sequential electric pulses having variable frequency and width. The frequency may vary between 0.1 to 999 Hz, the width of the stimulation is comprised between 0.1 and 40 μs and the voltage, which is kept constantly above the perception threshold, is comprised between 0.1 and 300 V (preferably 150 V). By suitably combining the aforesaid frequency and width variations a specific sequence defined as DCTR is obtained, having a relaxing effect and comprising a series of subphases, called A, B and C. Frequency and width are constant in the subphase A, the frequency is constant and the width is variable in the subphase B, the frequency is variable and the width is constant in the subphase C.
Experimental studies have enabled the effects of FREMS to be evaluated and the capacity of the latter to evoke compound muscle action potentials (cMAP) to be evaluated, which are obtainable in the adductor hallucis muscle by stimulating the posterior tibial nerve, as well as the variation in amplitude of the aforesaid H reflex by using the latter as a conditioning stimulus. As disclosed in WO 2004/084988, the aforesaid experimental studies have also shown that the greatest amplitude of the cMAPs that is obtainable (0.60±0.02 mV) is approximately 15 times less than that of the cMAPs obtained with the known devices that dispense TENS current, i.e. amplitudes of the order of 9±0.6 mV with stimuli having a width typically comprised in a range of 200-1000 μs. It has been further observed that the maximum amplitude value of the cMAPs is obtained in the presence of a width/frequency ratio of 0.13 (40 μs/29 Hz).
A further type of sequence, called ATCM and suitably designed for obtaining a vasoactive effect, has a prevailing action on the motility of the microcircle, i.e. of the smooth sphincters of the arterioles and venules of the subcutaneous tissue. The ATCM sequence is divisible into three subsequences, called S1, S2, S3. The subsequences S1 and S3 are both distinguished by a frequency increase phase, with distinct time modes. The subsequence S2 is mainly constituted for producing variability in the width of the individual stimuli, in a gradually increasing frequency range, in such a way as to reduce the bioreaction, until the latter is stabilised. More in detail, the subsequence S1, having a relaxing effect and therefore having an effect that is very similar to the aforesaid DCTR sequence, comprises phases in which, after a first adaptation phase conducted at 1 Hz frequency, the frequency is gradually increased at a constant amplitude, thus decreasing the bioreaction in a gradual manner. Subsequently, the frequency is increased in a much more rapid manner until it reaches a target of 19 Hz. The subsequence S2 is then run, which is in turn divisible into four phases, called S2-A, S2-B, S2-C and S2-D. In the subsequence S2, after a phase (S2-A) conducted at a constant frequency in which the amplitude is rapidly increased until the instant 1, the frequency is gradually increased and consequently the bioreaction rapidly falls until the instant 2 (S2-B). At this point the amplitude is reset that again rises at a constant frequency until the instant 3 (S2-C). Subsequently, the frequency again increases gradually whilst the amplitude is kept constant and, consequently, the bioreaction gradually decreases until the instant 3 (S2-D). In this way the bioreaction is varied in a discontinuous manner, producing points of sudden slope variation, i.e. the points 1, 2 and 3. In practice, as disclosed in WO 2004/084988, a system is obtained producing a sequence of vasodilations and vasocontractions with sequential increases and decreases of haematic flow of the microcircle surrounding the stimulation zone. These vasodilations and vasocontractions produce a “pump” effect that is clearly produced by neuromodulation of the sympathetic neurovegetative system, which influences the vasoaction through the smooth muscle of the capillary vessels and the arterioles. In this way it can be shown that this subsequence, which is distinguished by alternating variations of the rheobase, therefore produces a vasoactive effect consisting of sequential vasodilation phases and vasoconstriction phases. This definitely produces a draining effect and, above all, makes the microcircle elastic and modulates the latter around a main carrying event that determines the average variation thereof.
An object of the invention is to improve known electrostimulating apparatuses.
Another object is to provide an electrostimulating apparatus that enables muscular hyperexcitability of spinal and/or cerebral origin in a patient to be treated.
A further object is to provide an electrostimulating apparatus and method that enables muscular hyperexcitability of spinal and/or cerebral origin in a patient to be treated.
In a first aspect of the invention, there is provided an electrostimulating apparatus, comprising a generating arrangement for generating electric pulses organised in sequences having preset values of typical parameters, said typical parameters comprising amplitude, width and frequency of said pulses, a plurality of stimulation channels such as to dispense said sequences to body zones of an organism in an independent manner, a varying arrangement suitable for varying at least one of said typical parameters so as to substantially prevent said organism from habituating to said electric pulses.
In a second aspect of the invention, there is provided a method for electrostimulating an organism, comprising:
These aspects of the invention are based on a new neurophysiological effect that was found during recent experimental studies conducted on the aforesaid FREMS. These studies have in fact shown that the amplitude of the H reflex sampled from the ipsilateral soleus muscle with or without conditioning of the FREMS applied to the short adductor hallucis muscle, is substantially decreased (by a value equal to 50%) during FREMS stimulation. The amplitude variation of the H reflex is significantly influenced by the variations of the width pulse/stimulation frequency ratio (w/f), in particular during the subphase C (r2=0.43; p<0.001). This result suggested that the FREMS is actually capable of modulating the amplitude of the H reflex, very probably through active recruitment of the muscle spindles.
Owing to these results it has been possible to make a new electrostimulating apparatus, by means of which a new electrostimulating method can be carried out for treating the spinal hyperexcitability that is secondary to cerebral or spinal damage and is the cause of spasticity in a patient. The new electrostimulating apparatus enables the aforesaid FREMS to be applied, with different sequences and simultaneously, in two antagonist neuromuscular districts of a motor limb that are connected to the same metamer and mutually connected through an afferent neuron/interneuron/alpha motor neuron loop (circuit). In this way, a synergic effect can be produced that inhibits the hypertonic contraction, which contraction is typically caused by the dysfunctions of the upper motor neuron and is therefore typical of the spastic phenomena that are secondary to cerebral or spinal damage of the central nervous system.
The invention can be better understood and implemented with reference to the attached Figures, which illustrate an exemplifying but non-limiting embodiment thereof, in which:
In the embodiment of the apparatus 1 shown in
In an embodiment that is not shown, there is provided an apparatus 1 comprising a number of stimulation channels 2 that is greater than four.
In another embodiment that is not shown, there is provided an apparatus 1 comprising a number of stimulation channels 2 that is less than four.
The apparatus 1 comprises a first control unit 3 and a second control unit 4, which interact with one another and are made of microprocessors of known type. The first control unit 3 controls a displaying device, for example a liquid crystal display 5, and an alphanumeric keyboard 6. By keying in on the latter a user of the apparatus 1 can direct the operation of the latter and set the parameters, which are displayable on the display 5, of the electric stimulations to be administered to a patient.
In an embodiment that is not shown, there is provided a remote-control device by means of which a patient connected to the apparatus 1 can control the operation of the latter without interacting with the keyboard 6. This embodiment is particularly useful inasmuch as it enables the patient to control the apparatus 1 by acting as a sensory feedback element relating to one or more operating parameters of the apparatus 1. The first control unit 3 controls a safety switch 9, which in turn controls an input supply voltage VA. In normal operating conditions, the switch 9 is closed and a voltage adjuster 16 (the function of which will be disclosed below) that is comprised in each stimulation channel 2 is thus supplied. In emergency conditions, for example in the event of apparatus faults, the first control unit 1 opens the switch 9 and thus interrupts the supply to the voltage adjuster 16. To the second control unit 4 a luminous device, for example a LED 10 of known type, is further connected. When a patient is connected to the apparatus 1 by means of the electrodes 7 and the apparatus 1, supplied by the voltage VA, administers an electric stimulation to the patient, the LED 10 lights up, thus indicating that the patient is subjected to the action of an electric current.
Through a serial communication interface 8, of known type, the first control unit 3 is connected to the second control unit 4, which controls the production of the electric pulses by adjusting the basic parameters thereof, i.e. amplitude, width and frequency, and comprises an analogue-digital converter (ADC) 11 and an integrated timing unit (ITU) 12. In the second control unit 4 there can be housed a support 20 (that is shown by means of a dotted line) on which the data are recorded that are necessary for the operation of the apparatus 1, such as, for example, the data relating to the stimulation sequences that are producible by the apparatus 1. The support 20 is readable through a data processing device (which is not shown), of known type, comprised in the apparatus 1 or arranged outside the apparatus 1 and interfaced with the latter. The data processing device, if it is comprised in the apparatus 1, may, for example, be positioned in the second control unit 4.
In an embodiment that is not shown, the support 20 is housed in the first control unit 3.
The analogue-digital converter 11 receives a feedback signal (in the form of voltage) relating to the pulse amplitude, and intervenes by producing an adjustment and/or an alarm signal if the pulse amplitude produced by the apparatus 1 is different from that set by the user. In particular, the analogue-digital converter 11 receives a reference voltage VT regulating the operation of the analogue-digital converter 11, a further reference voltage VR, which enables the correct operation of the analogue-digital converter 11 to be checked, and, from each of the stimulation channels 2, a feedback voltage VF.
The integrated timing unit 12 defines the width and frequency of the pulse by interacting with a timing control device 13. The latter controls the width and frequency of the produced pulse and, if one or the other of these parameters is not correct, produces and sends a width error signal ED and/or a frequency error signal EF, which are able to arrest the second control unit 4.
Similarly to what has been disclosed in relation to the first control unit 3, also the second control unit 4 controls safety switches 9, which are provided in a number equal to the number of stimulation channels 2 comprised in the apparatus 1. The safety switches 9 controlled by the first control unit 3 and by the second control unit 4 interact with one another and with the LED 10 through an “OR”-type logic port 18.
The electric signals defining the frequency and width of the pulse are produced by the integrated timing unit 12 and are sent directly to an outlet pulses generator 14. In the apparatus 1 the outlet pulses generators 14 and the stimulation channels 2 are provided in equal numbers. Pulse width is defined and adjusted by a digital-analogue converter (DAC) 15 interacting with the second control unit 4. The digital-analogue converter 15 produces a plurality of electric signals defining the pulse amplitude for each single channel 2, and each signal is sent to a voltage adjuster 16. The apparatus 1 comprises a number of voltage adjusters 16 that is equal to the number of stimulation channels 2. An outlet voltage VU, the value of which is comprised between 0 and 300 Volts, is produced by each voltage adjuster 16 and is sent to a corresponding outlet pulses generator 14. Each outlet pulses generator 14 produces a pulse having a preset, frequency and width and sends this pulse to a pair of outlet selectors 17A, 17B to which the electrodes 7 are connected. The pairs of outlet selectors 17A, 17B are provided in a number equal to the number of outlet pulses generators 14 comprised in the apparatus 1. Each outlet selector 17A, 17B comprises a plurality of switches 19, which are provided in a number equal to the number of electrodes 7 connected to the selector, by means of which switches the produced pulse can be alternatively transmitted to the corresponding electrode 7, or stopped. In each pair of outlet selectors 17A, 17B the electrodes 7 are associated functionally so as to form four pairs, the electrodes of each pair being indicated respectively as 7A, 7B, 7C and 7D. The electrodes 7 of each pair are connected to the corresponding outlet selector 17A or 17B.
In an embodiment that is not shown, outlet selectors 17A, 17B are provided comprising a number of pairs of electrodes 7 greater than four.
In another embodiment that is not shown, there are provided outlet selectors 17A, 17B comprising a number of pairs of electrodes 7 that are less than four.
When the apparatus 1 is in use, by acting on the switches 19, it is possible to select the electrodes 7 to which to send the pulse produced by the outlet pulses generators 14. It is thus possible to use independently both the pairs of electrodes 7A-7D comprised in two or more stimulation channels 2 and the pairs of electrodes 7A-7D comprised in a single stimulation channel 2.
As the second control unit 4, by means of the digital-analogue converter 15 and the integrated timing unit 12, is able to adjust the amplitude, width and frequency of the pulses produced in the stimulation channels 2 in an independent manner for each channel 2, the apparatus 1 is such as to be able to multiply the outlet pulses and space the latter in a preset manner.
Further, the integrated timing unit 12 enables the width of the outlet pulse to be increased in a preset manner. In particular, it is possible to obtain a percentage increase of the width of an electric stimulation pulse that is conducted in a plurality of phases, after the completion of which phases the width of the pulse remains constant. The percentage increase of the width of the pulse, the width of the pulse and the number of the phases are mutually correlated by the following formula:
T
i(Nf)=T0×(1+I%)Nf
where:
Nf=Number of phase;
Ti(Nf)=Width of stimulation pulse in function of the number of phase;
T0=Width of initial stimulation pulse;
I %=Percentage increase of pulse width.
In the embodiment of the apparatus 1 illustrated in
The integrated timing unit 12 further enables to vary in a pseudorandom manner the length of the period of time that elapses between two subsequent phases. In this way, it is possible to produce stimulation sequences in which the width of the pulses varies proportionately to the percentage increase in a random manner. This enables phenomena of biological accommodation to be prevented, i.e. the stimulated tissues in a patient are prevented from habituating to the pulses and thus becoming less sensitive to the latter.
In the embodiment of the apparatus 1 illustrated in
In order to prevent the aforesaid phenomena of biological accommodation, the apparatus 1 can also act by varying the frequency and the amplitude of the pulses. The frequency, as previously disclosed, is adjusted by the integrated timing unit 12, whilst the amplitude is adjusted by the digital-analogue converter 15.
As previously disclosed, there is provided an embodiment of the apparatus 1 equipped with a remote control, by using which the patient may act as a sensory feedback element with respect to operation of the apparatus 1. In fact, the patient can be suitably instructed to vary the amplitude during the electrostimulating treatment by acting on the digital-analogue converter 15 through the remote control so as to prevent the aforesaid phenomena of biological accommodation. For example, the patient can be instructed to vary the pulse amplitude when the pulse reaches a maximum (subjective) level of tolerability. Alternatively, the patient can be instructed to vary the pulse amplitude when the pulse reaches the sensitivity threshold.
In use, the apparatus 1 is connected to a patient affected by spastic phenomena and at least two distinct stimulation channels 2 are used, for example the aforesaid channels 2A and 2B, the electrodes 7 of which are applied respectively to a body region near the specific efferent nerve of a hypertonic muscle (agonist muscle) and at a further body region comprising the corresponding antagonist muscle. The hypertonic muscle is then stimulated through the DCTR relaxing sequence whilst, simultaneously, the antagonist muscle is stimulated through the ATMC vasoactive sequence. The latter enables a direct muscular stimulation as well as an interaction with the sympathetic afferents and the afferents of the neurovegetative system, such as to close the circuit comprising motor neuron, interneuron and afferent neuron. The aforesaid double, simultaneous and differentiated stimulation inhibits the contraction of the hypertonic agonist muscle and rhythmically excites the motor neuron that is in synergy with the antagonist hypotonic muscle, creating mutual inhibition through the channel of the interneuron. The aforesaid effect of inhibition of the contraction of the hypertonic muscle is obtained by stimulating the latter with a sequence that is suitable for producing a phase depression of the H reflex.
When necessary, by using a suitable number of stimulation channels 2, and therefore a suitable number of pairs of electrodes 7, it is possible to stimulate simultaneously more than two body zones of the patient, in particular 4, 8 or 16 body zones. The pulses dispensed to the various body zones may or may not have the same frequency, and may be dispensed in a simultaneous manner or in a spaced over time, i.e. sequential, manner.
When the apparatus 1 is used to stimulate electrically a plurality of body zones of the patient, it is possible, during treatment, to select a certain number of body zones and limit the stimulation to the latter. This is obtained by acting on the second control unit 4 so as to exclude, for a preset period of time, all the stimulation channels 2 except for those relating to the body zones that it is desired to stimulate.
All the parameters relating to the operating modes of the apparatus 1, including the aforesaid “preferential zones” stimulation mode, can be recorded on the aforesaid support 20, which thus enables operation of the apparatus 1 to be programmed.
The experimental results are set out below that have led to the creation of the electrostimulating apparatus 1 disclosed above and the subsequent confirmations provided by the clinical experimentation.
In order to verify the possibility of using the FREMS stimulation in the treatment of the muscular hyperexcitability of spinal and/or cerebral origin, sequences of electric pulses of the aforesaid DCTR-type were used that were produced by a Lorenz™ electrostimulating apparatus. In these DCTR sequences, the successive width variations (between 10 and 40 μs) and frequency variations (between 1 and 39 Hz) can induce compound action potentials (cMAP) if applied along the motor nerve of the muscle, in a similar way to what occurs with voluntary muscle recruitment by means of the temporal summation. In particular, it was wished to evaluate the possibility of influencing the motor spinal activity through a different regulation of the activation of the various types of muscle spindle. For this purpose, the variation of the amplitude of the H reflex was evaluated, which was obtained by evoking the latter between the soleus muscle and the abductor hallucis muscle, both partially innerved at the level of the first sacral vertebra (S1). As shown in
With reference to
Since this has highlighted the possibility of devising new therapies for certain motion disorders that are distinguished by an abnormal motor neuron excitability, the aforesaid hypotheses were subjected to clinical experimentation. The latter was conducted on hospitalized patients suffering from pathologies of the upper motor neuron, such as haemiplegia, paraplegia, quadriplegia or spastic tetraparesis. These pathologies were a consequence of the ischemic phenomena, central haemorrhagic (brain stroke or head injury) phenomena or spinal cord lesions.
The therapeutic protocol consisted of simultaneously stimulating the hypertonic muscle with DCTR sequences and the antagonist muscle with ATMC sequences. Reasonably alert patients having a reasonable sense of space and time and a decent or high degree of cooperation, not suffering from fixed contractions of the joints and from grade 2-4 muscle-tendon retractions on the modified Rankin Scale (mRS), were accepted for treatment. On the other hand, patients having an altered state of consciousness, patients who were not very or not at all cooperative, wearers of pacemakers or implantable defibrillators, and patients affected by pathologies that were such as not to allow the use of electrotherapies, were excluded. The patients were assessed clinically at the moment of recruitment, at the end of the treatment and at 15, 30 and 45 days from the end of the therapy. For the functional assessments specific clinical scales were used: Ashworth Scale, A.D.L. Index (Activities of Daily Living according to Barthel), Rankin Scale, Spasm Frequency Scale, Motricity Index, FIM (Functional Independence Measure). These clinical scales enable the degree of tone and spasticity of a patient to be assessed and the possibility of the latter to perform motor functions with the limbs, to walk independently and to be independent in activities of daily living (ADL). For the pain assessment, the VAS 0-100 scale was used. The patients were subjected to a daily treatment session for 15 consecutive sessions. At the initial assessment all the patients had a grade 2 Ashworth spastic hypertonia of the lower limbs. At the end of the first cycle of therapy a reduction of hypertonia was found, with a grade 1 Ashworth average assessment. These evidences show the clinical efficacy of the method and of the electrostimulating apparatus that have been previously disclosed.
| Number | Date | Country | Kind |
|---|---|---|---|
| MO2006A000087 | Mar 2006 | IT | national |
This application is the U.S. national phase of International Application No. PCT/IB2007/000637, filed 15 Mar. 2007, which designated the U.S and claims priority to Italy Application Nos. MO2006A000087, filed 17 Mar. 2006, the entire contents of each application is hereby incorporated by reference.
| Filing Document | Filing Date | Country | Kind | 371c Date |
|---|---|---|---|---|
| PCT/IB2007/000637 | 3/15/2007 | WO | 00 | 11/18/2008 |
