Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label hope like hell. Show all posts
Showing posts with label hope like hell. Show all posts

Sunday, December 19, 2021

Catecholamine-induced cardiotoxicity: A critical element in the pathophysiology of stroke-induced heart injury

 You don't want a heart injury after your stroke also so you better hope like hell that your doctors have a protocol to prevent that.

The latest here:

Catecholamine-induced cardiotoxicity: A critical element in the pathophysiology of stroke-induced heart injury

https://doi.org/10.1016/j.lfs.2021.120106Get rights and content

Abstract

Cerebrovascular diseases such as ischemic stroke, brain hemorrhage, and subarachnoid hemorrhage provoke cardiac complications such as heart failure, neurogenic stress-related cardiomyopathy and Takotsubo cardiomyopathy. With regards to the pathophysiology of stroke-induced heart injury, several mechanisms have been postulated to contribute to this complex interaction between brain and heart, including damage from gut dysbiosis, immune and systematic inflammatory responses, microvesicle- and microRNA-mediated vascular injury and damage from a surge of catecholamines. All these cerebrovascular diseases may trigger pronounced catecholamine surges through diverse ways, including stimulation of hypothalamic-pituitary adrenal axis, dysregulation of autonomic system, and secretion of adrenocorticotropic hormone. Primary catecholamines involved in this pathophysiological response include norepinephrine (NE) and epinephrine. Both are important neurotransmitters that connect the nervous system with the heart, leading to cardiac damage via myocardial ischemia, calcium (Ca2+) overload, oxidative stress, and mitochondrial dysfunction. In this review, we will aim to summarize the molecular mechanisms behind catecholamine-induced cardiotoxicity including Ca2+ overload, oxidative stress, apoptosis, cardiac hypertrophy, interstitial fibrosis, and inflammation. In addition, we will focus on how synchronization among these pathways evokes cardiotoxicity.

 

Thursday, March 4, 2021

Delirium REduction after Administration of Melatonin in acute ischemic Stroke (DREAMS): A Propensity Score Matched Analysis

I had not heard of this problem. You'll have to hope like hell that your doctor has and knows the protocol to prevent it.  

1 in 4 have delirium post stroke from this research:

Delirium – an overlooked complication of stroke

The latest here:

Delirium REduction after Administration of Melatonin in acute ischemic Stroke (DREAMS): A Propensity Score Matched Analysis

First published: 03 March 2021

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1111/ene.14792

Abstract

Background

Post‐stroke delirium (PSD) comprises a common and severe complication after stroke. Yet, treatment options for PSD remain insufficient. We investigated whether prophylactic melatonin supplementation may be associated with reduced risk for PSD.

Methods

Consecutive patients admitted to Tübingen University Stroke Unit, Germany, with acute ischemic stroke (AIS), who underwent standard care (between August and December 2017) and patients who additionally received prophylactic melatonin (2 mg per day at night) within 24 hours of symptom onset (between August and December 2018) were included. Primary outcomes were: (i) PSD prevalence in AIS patients, (ii) PSD risk and PSD‐free survival in patients with cerebral infarction who underwent melatonin supplementation compared to propensity‐score‐matched (PSM) controls. Secondary outcomes included time of PSD‐onset and PSD‐duration.

Results

Out of 465 (81.2%) with cerebral infarction and 108 (18.8%) TIA patients, 152 (26.5%) developed PSD (median time‐to‐onset [IQR]: 16 [8,32] hours; duration 24 [8,40] hours). Higher age, cerebral infarction (rather than TIA), higher NIHSS and aphasia on admission were significant predictors of PSD. After PSM (164 melatonin‐treated patients with cerebral infarction versus 164 matched‐controls), 42 (25.6%) melatonin‐treated patients developed PSD vs. 60 (36.6%) controls (OR [95% CI]: 0.597 [0.372‐0.958], p=.032). PSD‐free survival differed significantly between groups (p=.027), favoring melatonin‐treated patients. In patients with PSD, no between‐group differences in the time of PSD‐onset and PSD‐duration were noted.

Conclusions

Patients prophylactically treated with melatonin within 24 hours of AIS onset had lower risk for PSD than patients undergoing standard care. Prospective randomized trials are warranted to corroborate these findings.

 

Tuesday, July 21, 2020

Functional Electrical Stimulation Therapy for Retraining Reaching and Grasping After Spinal Cord Injury and Stroke

You'll just have to hope like hell that this is enough description of the protocol that your doctors and therapists can duplicate it. 

Functional Electrical Stimulation Therapy for Retraining Reaching and Grasping After Spinal Cord Injury and Stroke

Naaz Kapadia1,2,3,4*, Bastien Moineau1,5,6 and Milos R. Popovic2,3,4,5
  • 1Rehabilitation Engineering Laboratory, The KITE Research Institute, Toronto Rehabilitation Institute-University Health Network, Toronto, ON, Canada
  • 2Rehabilitation Sciences Institute, University of Toronto, Toronto, ON, Canada
  • 3CRANIA, University Health Network and University of Toronto, Toronto, ON, Canada
  • 4The KITE Research Institute, Toronto Rehabilitation Institute-University Health Network, Toronto, ON, Canada
  • 5Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, Canada
  • 6Myant Inc., Toronto, ON, Canada
Neurological conditions like hemiplegia following stroke or tetraplegia following spinal cord injury, result in a massive compromise in motor function. Each of the two conditions can leave individuals dependent on caregivers for the rest of their lives. Once medically stable, rehabilitation is the main stay of treatment. This article will address rehabilitation of upper extremity function. It is long known that moving the affected limb is crucial to recovery following any kind of injury. Overtime, it has also been established that just moving the affected extremities does not suffice, and that the movements have to involve patient’s participation, be as close to physiologic movements as possible, and should ideally stimulate the entire neuromuscular circuitry involved in producing the desired movement. For over four decades now, functional electrical stimulation (FES) is being used to either replace or retrain function. The FES therapy discussed in this article has been used to retrain upper extremity function for over 15 years. Published data of pilot studies and randomized control trials show that FES therapy produces significant changes in arm and hand function. There are specific principles of the FES therapy as applied in our studies: (i) stimulation is applied using surface stimulation electrodes, (ii) there is minimum to virtually no pain during application, (iii) each session lasts no more than 45–60 min, (iv) the technology is quite robust and can make up for specificity to a certain extent, and (v) fine motor function like two finger precision grip can be trained (i.e., thumb and index finger tip to tip pinch). The FES therapy protocols can be successfully applied to individuals with paralysis resulting from stroke or spinal cord injury.

Introduction

Application of functional electrical stimulation (FES) for therapeutic purposes in rehabilitation settings dates back to the 1960’s when Liberson et al. (1961) used an FES system to stimulate the peroneal nerve to correct foot drop by triggering a foot switch, a single-channel electrical stimulation device stimulated the common peroneal nerve via a surface electrode, producing ankle dorsiflexion during the swing phase of gait (Liberson et al., 1961). This led to the first commercially available FES system with surface stimulation electrodes. Since then FES technology has been researched extensively to evaluate its benefits in diverse neurological conditions, and using an array of application techniques (Baldi et al., 1998; Field-Fote, 2001; Popovic et al., 2005, 2011, 2012, 2016; Yan et al., 2005; Frotzler et al., 2008; Griffin et al., 2009; Daly et al., 2011; Kapadia et al., 2011, 2013, 2014a; Giangregorio et al., 2012; Malešević et al., 2012; Martin et al., 2012; Kawashima et al., 2013; Lee et al., 2013; Sadowsky et al., 2013; Ho et al., 2014; Kapadia N. et al., 2014; Popović, 2014; Sharif et al., 2014; Bauer et al., 2015; Howlett et al., 2015; Vafadar et al., 2015; Buick et al., 2016; Cuesta-Gómez et al., 2017; Fu et al., 2019; Straudi et al., 2020). The two common uses of FES are to replace function (i.e., as an orthotic device) and to retrain function (i.e., as a therapeutic device). In this article we will limit ourselves to the therapeutic application of FES.
In the therapeutic application (FES therapy), FES is used as a short-term treatment modality. The expectation is that, after training with the FES system, the patients will be able to voluntarily perform the trained activities without FES (i.e., patients are expected to regain voluntary function). To date, a few high-quality randomized controlled trials have been performed, proving the efficacy of FES therapy over other rehabilitation techniques (Sharififar et al., 2018; Yen et al., 2019). This paucity in multicenter randomized controlled trials and the limited access to systems that can properly deliver FES therapy might have affected its uptake in clinical settings (Ho et al., 2014; Auchstaetter et al., 2016). Fortunately, both these issues are being addressed as new FES systems that are specifically developed for FES therapy are being introduced, as well as large scale multicenter randomized controlled trials are being planned to further confirm the efficacy of this rehabilitation modality. This article will provide readers with the details on how transcutaneous multichannel FES therapy for the upper extremity can be applied in clinical trials and as such the same methodology can be used in clinical practice by physiotherapists and occupational therapists.
The FES methodology discussed here has been developed with the intent to be user friendly, robust and to be able to produce better functional gains than the presently available best-practice rehabilitation techniques. The FES system used in our laboratory is a surface stimulation system with up to 4 stimulation channels that can produce gross motor function as well as precision grips such as two finger pinch grip. However, the methodology of FES application discussed here is pertinent to any multichannel transcutaneous FES device. We have used transcutaneous FES to retrain reaching and grasping in individuals with both spinal cord injury and stroke (Thrasher et al., 2008; Kapadia and Popovic, 2011; Kapadia et al., 2011, 2013; Popovic et al., 2012; Hebert et al., 2017). The results obtained in both patient populations indicate functional improvements after 8–14 weeks of therapy (20–48 h of stimulation). Patients showed reduced dependency on caregivers, and some even became independent in their activities of daily living.
This article will extensively detail how FES was applied in these previously successful clinical trials to retrain reaching and grasping functions in individuals who sustained a spinal cord injury or a stroke.

Materials and Equipment

The FES system we used was a four channel surface stimulation device consisting of a software, a portable stimulator with a programmed chip card, self-adhesive stimulation electrodes, and various man-machine interfaces, such as push buttons, sliding potentiometers (Mangold et al., 2005), accelerometers (Widjaja et al., 2011), EMG/biofeedback sensor, joysticks (Sayenko et al., 2013), foot switches (Popovic et al., 2001b), gait phase detection system (Pappas et al., 2004) and brain–machine interface (Márquez-Chin et al., 2009). This FES system has been extensively used in clinical trials by researchers both in North America and in Europe. Its unique capability is the ability to program stimulation protocols customized to a patient’s needs in less than 10–15 min.

Software

The software of our FES system allows one to specify/alter all stimulation parameters: frequency, minimum and maximum intensity, pulse duration, ramp time, synchronization and order of stimulations, type of user interactions and number of repetitions. The sensory, motor, functional and maximum thresholds are set using the continuous stimulation mode where the stimulation frequency and pulse duration are pre-set to values of 40 Hz and 200 μs, respectively.

Methods

Clinical Applications

To date, approximately 150 spinal cord injury and 50 stroke patients have been treated using transcutaneous FES in our facilities, ranging from pilot clinical trials to randomized controlled trials. The FES system has been primarily used as a therapeutic device for retraining reaching and grasping. More recently FES was successfully applied to an individual with cervical spondylotic myelopathy to retrain upper extremity function with very promising results (Popovic et al., 2016).

Neuroprosthesis for Grasping in Spinal Cord Injury Patients (University Health Network REB # 02-032, REB # 09-007, REB # 09-008)

In case of patients with spinal cord injury the upper extremity retraining program is designed based on the level and extent of injury. For example, in C1–C5 cervical incomplete injuries initially FES might be used to retrain proximal function and then once the patient is able to position their arm in the working space then distal function can be trained. The FES protocols for retraining proximal function in SCI remain the same as stroke (please refer to the next section on stroke for details). In patients with low cervical injury (C6 and below), proximal upper extremity function might be preserved, and FES might then be used to retrain distal function right from the beginning. Also, it is important to note that again based on level of injury patient with SCI may have difficulty with both hand closing and opening and will typically need to be trained for both.
Over the years, various grasping protocols have been identified and designed allowing for a wide variety of grasping patterns to be trained with a great deal of fidelity. Currently, the grasping patterns that can be successfully retrained using a transcutaneous multi -channel FES system are:
(1) Palmar Grasp (holding a ball)
(2) Lateral Grasp (holding a tray)
(3) Tripod grip (thumb, index, and middle finger: holding a pen)
(4) Two finger opposition (thumb and index finger: holding a peg)
(5) Lateral Pinch (thumb and index finger: holding a credit card)
(6) Two finger lateral pinch (index and middle finger: smoker’s grip)
(7) Lumbrical grip (all four fingers with the thumb: holding a closed book).
It is important to mention that FES therapy has the capability to help stroke and spinal cord injury patients relearn how to voluntarily perform all of the above grasps bilaterally and simultaneously, using surface FES system.
We have conducted a number of clinical studies using this FES technology the most recent one being a randomized controlled trial in incomplete cervical SCI patients (Popovic et al., 2011). Individuals allocated to the intervention group in this trial received FES stimulation protocols specifically designed for their upper extremity functional deficits. Individualized stimulation sequences were developed for each patient. The commonly trained grasping patterns were power and precision grasp where power grasp was used mainly to grasp larger everyday objects and the precision grip was used mainly to manipulate smaller objects. Power grasp was generated by partly flexing the fingers and the thumb in flexion and slight opposition. Lateral pinch was generated by fully flexing the fingers followed by the thumb flexion. Muscles that were stimulated during therapy were the following:
• Wrist flexors: flexor carpi radialis and flexor carpi ulnaris;
• Wrist extensors: extensor carpi radialis (longus and brevis) and ulnaris;
• Finger flexors: flexor digitorum superficialis and flexor digitorum profundus;
• Finger extensors: extensor digitorum;
• Thumb abductors: median nerve, or abductor pollicis brevis and longus;
• Thumb flexors: flexor pollicis brevis and flexor pollicis longus;
• Thumb oppositors: opponens pollicis;
• Metacarpophalangeal flexors and interphalangeal joint extensors: lumbricals.
The FES protocol allowed for individuals with little to no voluntary movement at the wrist and fingers to be able to perform simple tasks while being stimulated with the FES. This is what differentiates FES from other therapies. In the early stages of FES therapy, all the movements were performed with the help of FES. The treatment plan and instruction to participants were as follows:
(1) “Imagine hand opening” (or any movement that the therapist would like to train).
(2) “Try to perform the movement using your own muscle strength.”
(3) After trying for about 10 s: “Now, try to perform the movement with the help of FES.”
Hence, emphasis was put on participants voluntarily attempting the movement while being stimulated with the FES. During therapy when the participants started showing an ability to voluntarily contract certain muscle groups FES for those muscle groups was reduced to a minimum and gradually withdrawn completely. The available channel was then used on other muscle groups that were still weak and needed to be trained. The order in which muscle groups were sequentially “reactivated” was subject-dependent. FES was always delivered while the participants were performing functional tasks, such as grasping a mug, pouring water, holding a pen, etc.
The distinctiveness of this intervention is that FES is not primarily intended for muscle strengthening. Instead, it is used to retrain the neuromuscular system to execute tasks that it is unable to carry out voluntarily. Movements were performed against gravity and sometimes against light manual resistance. The number of repetitions was determined based on individual participant’s strength and endurance. In general, all participants spent 30–45 min out of 1-h session performing activities of daily living with FES. The stimulation parameters used were the following: (a) balanced, biphasic, current regulated electrical pulses; (b) pulse amplitude from 8 to 50 mA (typical values 15–30 mA); (c) pulse width 250 μs; and (d) pulse frequency 40 Hz (Popovic et al., 2011). During the intervention, the therapist, at their discretion, adjusted the placement of electrodes and guided the hand movements. The therapist ensured that the movements were functional. Occasionally FES would be combined with conventional rehabilitation strategies including strengthening exercises, stretching exercises, etc.

Neuroprosthesis for Grasping in Stroke Patients (University Health Network REB # 02-032).

The most important difference between FES training in spinal cord injury and stroke patients; is that stroke patients have difficulty opening their hand as they often exhibit flexor synergy and high levels of tone in the finger flexors. In stroke patients therefore, the focus of the therapy is on hand opening and relaxing the fingers. In spinal cord injury patient’s the focus of the FES therapy is on finger flexion and grasping tasks as weakness of the finger flexors is a bigger problem. Below are the methods of FES application in clinical trials conducted in individuals who suffered a stroke (Popovic et al., 2005; Thrasher et al., 2008; Kapadia et al., 2013).
For individuals allocated to the FES therapy group, treatment began by proximal shoulder muscle training. The muscles that were stimulated were deltoid, biceps, and triceps. Typically, participants would recover proximal function first. As soon as they gained functional strength in the proximal muscles, FES for those muscles would be discontinued and applied to distal muscles of the forearm and hand. The most difficult and time-consuming task was to train voluntary extension of the fingers. This is crucial to be able to get one’s hand around the objects that need to be manipulated. Once the participants were able to successfully open their hand with FES assistance, low amplitude stimulation of the finger flexors was used to signal hand closing. Stimulation parameters used to stimulate the muscles and nerves were the same as used for individuals with spinal cord injury (See section on “Neuroprosthesis for Grasping in Spinal Cord Injury Patients).
In the early stages of the treatment, the arm/hand tasks were performed predominantly with the help of FES. As participants showed improvement stimulation was gradually reduced to a minimum and eventually phased out. Typical treatment session lasted for about 45 min, including the donning and doffing of electrodes. During all FES sessions the physiotherapist guided the movements and provided assistance as appropriate to carry out the intended movement in as close to physiological manner as possible.
Over the years the FES-reaching protocols have expanded to cover various functional reach patterns:
(1) Sideways reaching
(2) Sideways reaching with hand opening
(3) Forward reaching and retrieving
(4) Forward reaching and retrieving with hand opening
(5) Reaching over opposite shoulder
(6) Reaching over opposite shoulder to forward reaching to sideways reaching
(7) Reaching over opposite knee
(8) Hand to mouth
All of these protocols can easily be paired with the FES-grasping protocols for the spinal cord injury population to train reaching and grasping together.

Practical Considerations for Therapist

In most of the clinical trials, FES sessions of 45–60 min were delivered 3–5 days a week, for 8–16 weeks, for a total of about 40 sessions. In our clinical experience, we found that patients are able to tolerate a maximum of one 60 min session per day and within the session typically we are able to stimulate one movement pattern for approximately 10–15 repetitions before fatigue sets in, however, it is important to note that this frequency is individual based and may vary based on extent of injury, chronicity and status of neuro-muscular system. Self-adhesive surface stimulation electrodes were used during therapy. All the patients were treated by registered physiotherapists or occupational therapists. In all instances, each phase of the FES was triggered by the treating Physiotherapist or Occupational therapist using a push button. All FES sessions incorporated functional tasks during FES sessions. All FES training was in combination with conventional physiotherapy or occupational therapy techniques selected based on individual patient needs. Also, irrespective of the population, patients were required to concentrate and actively make an attempt to carry out the movement while being assisted by FES, as described above.
The stepwise directions to conduct an upper extremity FES training session with a transcutaneous multi-channel FES device are as follows:
(1) Identify the functions to be trained (reaching and/or grasping).
(2) Select the order of the tasks to be re-trained: typically, start with gross motor tasks (proximal muscles) in early stages of therapy followed by fine movement control (distal muscles).
(3) For each task identify the muscles to be stimulated: at any given time either only simple reaching or grasping tasks such as touching mouth or palmar grasp can be trained or more complex tasks such as reaching + grasping can be trained based on number of channels available for stimulation.
(4) First identify the optimal electrodes positioning: For a given function, find the motor point; the electrode position where a maximal contraction is obtained with minimum stimulation current delivered. We recommend finding the motor point using a smaller electrode, by trying several positions on the bulk of the muscles to be stimulated. This allows for finding an electrode position with minimal secondary and unintentional stimulation of other muscles and/or nerves. Once you find the optimal electrode position(s) for a muscle, mark it with a pen/marker, and identify position(s) for other muscles.
(5) Apply self-adhesive electrodes over the motor points of the muscles identified.
Note: In case one has a stimulator that has galvanically isolated stimulation channels, one can apply the following: all electrodes on one aspect of the forearm can be “grounded” using a single return/anode electrode, i.e., all muscles on the palmar aspect of the forearm can be grounded using one electrode just proximal to the ventral aspect of the wrist joint and similarly all electrodes on the dorsal aspect of the forearm can be grounded using one electrode over the dorsal aspect of the wrist. If the stimulator does not have galvanically isolated stimulation channels one should not use this “common ground” strategy.
If you use non-alternate and asymmetrical pulses waveform (with the negative depolarizing pulse always on the same electrode, and the positive balancing pulse at a lower amplitude), then you will have an “active” electrode to be positioned on the motor point, and a “passive” or return/anode electrode under which there is no effective stimulation (setting typically used for smaller muscles). If you use alternate and/or symmetrical pulse waveform, then both electrodes are “active” and will trigger contractions similarly (setting typically used for larger muscles). The choice between one or two active electrode(s) is based on the muscle size (one active electrode is preferable where there is no space on the bulk of the muscle to position two electrodes). Also, having a single “active” electrode ensures greater specificity of the muscle and muscle volume that is stimulated.
(6) Identify and record the different stimulation thresholds: Identify sensory threshold (when the patient feels the current for the first time), motor threshold (when a palpable or a visible contraction is produced), functional threshold (when the desired functional movement is produced) and maximum threshold (beyond which the patient does not tolerate an increase in current amplitude).
Note: It is important to define the thresholds with the same current characteristics (pulse width and frequency) as the one used during FES therapy, because it has an impact on the comfort and efficiency of the stimulation.
(7) Explain to the patient what to expect when the FES in turned on
Example: “First your hand will close and then it will open.”
(8) Turn on the stimulator and adjust the current intensities for all muscles to the levels determined previously (intensity should not exceed the determined maximum threshold). Trigger the FES protocol a few times so the patient has a clear understanding of what to expect with each phase of FES. Once the patient has a clear understanding of the protocol, select the functional object to be used during training. If needed, assist the patient to bring their hand close to/around the object to be manipulated.
(9) Instruct the patient that she/he has to make an active attempt to perform the intended movement.
Example: For a grasp/release task, ask the patient to close the hand to grasp the object and, after the patient has attempted for about 5–10 s, assist with FES. Once the patient is able to grasp the object with assistance from FES, complete the functional task, for example transfer object from point A to point B. Following successful object transfer, instruct the patient to release the object and after about 5–10 s of the patient unsuccessfully attempting to release the object trigger the FES sequence for hand opening.
(10) Repeat this protocol 10–15 times. Then, select another protocol and perform the next task for 5–7 min or as appropriate for that task. Execute 3–6 different protocols in a 1-h session, with active stimulation for 30–40 min (depending on patient’s fatigue and therapist’s expertise with the system). The 1-h therapy duration includes positioning of the electrodes and all relevant preparations for therapy initiation and therapy completion.
(11) Rest time should be given when the patient asks for it and/or when muscle fatigue sets in.
(12) When the therapy is completed, turn off the stimulator, remove the electrodes and inspect the skin underneath for any redness.
Note: Occasionally redness may be present from the electrode sticking on the skin, but it should dissipate in less than 24 h. Ask patient to monitor area and re-inspect at the next session.
The selection of stimulation sequences is done based on clinical assessments which typically include use of standardized assessment tools like Graded Redefined Assessment of Strength, Sensibility and Prehension, Toronto Rehabilitation Institute- Hand Function Test and Spinal Cord Independence Measure Self-care Sub-scores in spinal cord injury (Popovic et al., 2011) and Action Research Arm Test and Fugl Meyer assessment – upper extremity scores in stroke (Hebert et al., 2017).

Limitations

There are certain limitations to this technology. The limb muscles that are intended for FES treatment have to be accessible for placement of the stimulation electrodes (Popovic et al., 2001a). There should not be a major degree of lower motor neuron injury or nerve-root damage of the stimulated muscle. In a number of patients with spinal cord injury, there may be a variable amount of peripheral nerve damage (Doherty et al., 2002) (motoneurons and nerve-roots) that restricts the application of FES. Also, the patient has to be cognitively able to follow the instructions and actively participate in the therapy process. The patient should not have any contraindications for FES application like metal implants at the site of stimulation, pace-maker, open wound or rash at the site of electrode placement, uncontrolled autonomic dysreflexia, etc.
Besides, with programmable surface stimulation devices, one would need an inter-professional team including bio medical engineers who are proficient in programming the stimulation protocols. This programming limitation may not apply to the more sophisticated newer FES systems. Presently there are commercially available FES systems that can deliver FES therapies discussed in this article. The reader is encouraged to find a device that delivers FES therapies and is approved by the local regulatory body. Systems that do not have neuroplasticity and neuromodulation in their indication for use defined by the regulatory body should be avoided, as these stimulators are for muscle strengthening and improving range of motion, and not for FES therapy discussed in this article.

Results

To date, in our laboratory transcutaneous FES therapy has been successfully applied to over 200 patients with either stroke or spinal cord injury. Based on the outcomes of these studies, it can be said that short duration FES therapy combined with conventional occupational therapy and physiotherapy has the ability to produce positive changes in these patients (Popovic et al., 2005, 2011, 2016; Thrasher et al., 2008; Kapadia and Popovic, 2011; Kapadia et al., 2013). The underlying mechanism responsible for these changes include central modulation effects. Stimulation induces cortical plasticity by modulating the ascending pathways through the Ia muscle fiber afferents (Chipchase et al., 2011). Additionally, somatosensory inputs to the motor cortex are essential for motor learning and control, and play critical roles in the motor recovery process (Vidoni et al., 2010; Pan et al., 2018). Stimulation above the motor threshold increases excitability of corticomotor pathway by activating sensory axons and recruiting synaptic motoneurons and motor reflex (Chipchase et al., 2011). FES therapy in combination with conventional PT and OT techniques harnesses the benefits of neuroplasticity thereby improving function and enhancing participant independence with activities of daily living.
In the randomized controlled trial carried out in individuals with subacute (<6 months post injury) incomplete traumatic C3–C7 spinal cord injury, it was found that the individuals who received 40 h of FES therapy had far greater improvements on the Self Care Sub-scores of the Functional Independence Measure and Spinal Cord Independence Measure as compared to individuals who received 40 h of conventional occupational therapy (Popovic et al., 2011). These gains were retained, or further improvement was observed, in the FES therapy group at the time of 6 months follow up assessment (Popovic et al., 2011). To date we have obtained similar results in all individuals with sub-acute incomplete spinal cord injury who received 40 h of FES therapy (Figure 1).
FIGURE 1
www.frontiersin.org Figure 1. Self-care Spinal Cord Independence Measure scores for all individuals with incomplete sub-acute spinal cord injury (blue bar indicates score at baseline and red bar indicates gain after 40 × 1 h therapy, treatment group received functional electrical stimulation and control group received conventional PT/OT).
Similar results were obtained in the randomized controlled trial carried out in individuals with acute (2–7 weeks post) severe stroke with a total arm and hand score no more than 2 on the Chedoke McMaster Stages of Motor Recovery (less than 15 points on Fugl Meyer Assessment Upper Limb Sub-score) (Thrasher et al., 2008; Hebert et al., 2017; Marquez-Chin et al., 2017). The individuals who received 12–16 weeks of FES therapy for the arm and hand had statistically better improvement on the Self-care sub-score of the Functional Independence Measure (Figure 2), Fugl Meyer Assessment, Barthel Index, and Chedoke McMaster Stages of Motor Recovery as compared to individuals who received conventional occupational therapy and physiotherapy for the same duration. Detailed results of this study are published elsewhere.
FIGURE 2
www.frontiersin.org Figure 2. Self-care Functional Independence Measure scores for all individuals with sub-acute stroke (blue bar indicates score at baseline and red bar indicates gain after 40 × 1 h therapy, treatment group received functional electrical stimulation and control group received conventional PT/OT).
In another clinical trial in chronic severe pediatric stroke population (Kapadia N. et al., 2014), where all four participants received a total of 48 h of FES therapy, statistically significant improvements were observed on the Quality of Upper Extremity Skills Test as well as on various sub components of the Rehabilitation Engineering Laboratory Hand Function Test (this is the Toronto Rehabilitation Institute- Hand Function Test with a scoring system adapted for stroke).

Discussion

Short duration multichannel surface FES is a viable and safe treatment modality that can be successfully applied in patients with neurological conditions. It is important to note that we did not formally investigate safety and feasibility in our clinical trials mainly because transcutaneous FES has been applied in clinical trials for over 5 decades now without any reports of major adverse events. However, given that we have applied FES to over 200 patients over the past 15+ years we are able to confidently say that transcutaneous FES is both safe and feasible. Across all of our clinical trials we did not encounter any serious adverse events and we have been able to successfully retain our study participants for the duration of the research therapy. Discussed here is an in-depth application of transcutaneous multi-channel FES therapy of the upper extremity in spinal cord injury and stroke patients. In order to obtain maximum benefits of this therapy there are some general points to keep in mind.
The goal of this manuscript is not to explore the mechanism of improvement in individuals with stroke and spinal cord injury following FES as this is a methods paper and as such these mechanisms have been widely discussed in literature (Quandt and Hummel, 2014; Hara, 2015; Luo et al., 2020; Marquez-Chin and Popovic, 2020). We do, however, recommend some basic principles of FES application on the widely accepted belief that mechanism of improvement with this therapy is based on the principles of neuroplasticity (Nagai et al., 2016). First and foremost it is strongly recommended that therapy should be started as soon as the medical condition of the patient is stabilized, i.e., preferably in the acute or sub-acute phase post-injury. Secondly, active participation of the patient during treatment is critical. Along with the FES, patients have to make an active attempt to execute the target movement. Third, the movements carried out should be functional and should follow a physiological pattern as closely as possible (movements similar to those of able-bodied individuals). Fourth, therapy should be combined with conventional rehabilitation modalities (example: stretching and strengthening) to reap maximum benefits. Lastly, while no specific dosing study has been conducted, our group recommends delivering at least three 1 h sessions per week. However, our group does not recommend more than one session per day, as this often exhausts the patient and prevents them from actively participating in the second session. In total, at least 20 sessions are needed to obtain clinically relevant changes, however, it is often recommended that patients have 40 or more hours of therapy to maximize outcomes and experience greater gains in function.
It should be noted that, in certain very acute or chronic spinal cord injury cases, a strengthening phase is necessary prior to the functional training phase because the muscles are minimally responsive to stimulation at first (Popovic et al., 2002) due to initial spinal shock (Galeiras Vázquez et al., 2017) or due to long-term disuse (Popovic et al., 2002).
It is important to bear in mind that although FES therapy has not been extensively tested in individuals with cervical complete spinal cord injury, those that have been trained with the system have shown remarkable improvements that were much more profound than those produced with conventional therapy (Popovic et al., 2006). This evidence merits conducting more comprehensive clinical trials with FES therapy in cervical complete spinal cord injury patients.
In conclusion, the most attractive feature of multichannel surface stimulators is that they are non-invasive, often programmable and allow for various muscles/muscle groups to be stimulated simultaneously in physiological patterns. They have a high level of fidelity and are able to produce global upper-limb motions as well as fine finger movements like two pinch grip (thumb and index finger) and tripod grip (thumb, index, and middle finger) using surface stimulation electrodes.
The specific surface stimulator used in our clinical studies, is not widely available any longer, however, the methodological considerations discussed above remain the same irrespective of the type of stimulation device. Any stimulator that can produce protocols discussed in this article can be used for FES therapy. Although the new stimulators used for the FES therapy come with guidelines for locating motor points, therapists should be mindful that motor points can anatomically vary between individuals. If required, the first session should be dedicated to finding correct stimulation points, after which these can be marked down for future sessions.
As important as it is to assist weak muscles with FES during execution of functional tasks, it is equally important that once functional voluntary strength is recovered (at least 3/5 on Manual Muscle Testing), stimulation is withdrawn from those muscles and the patient is encouraged to voluntarily control the muscles themselves. The available FES channels can then be applied to other weaker muscle groups that still need retraining. In some cases, with severe spasticity, manual stretching of the tight muscles prior to stimulation may yield better results.

Data Availability Statement

The datasets generated for this study are available on request to the corresponding author.

Sunday, July 19, 2020

Early Do-Not-Resuscitate Orders and Outcome After Intracerebral Hemorrhage



I see nothing here that suggests that an objective damage diagnosis was done before the DNR was written. You better hope like hell this doesn't happen to you, you better be awake and cognizant to dispute this. You better not be transported to one of these fast DNR hospitals, you won't make it out alive. Is the DNR because of co-morbidities or because of the extremely difficult work of stopping the bleed and the hospital doesn't have the staff to accomplish that? Is this before or after the bleed is stopped?

Early Do-Not-Resuscitate Orders and Outcome After Intracerebral Hemorrhage


Abstract

Background

Do-not-resuscitate (DNR) orders are commonly used after intracerebral hemorrhage (ICH) and have been shown to be a predictor of mortality independent of disease severity(So you don't know the severity? WHAT THE FUCK ARE YOU DOING?). We determined the frequency of early DNR orders in ICH patients and whether a previously reported association with increased mortality still exists.

Methods

We performed a retrospective analysis of patients discharged from non-federal California hospitals with a primary diagnosis of ICH from January 2013 through December 2014. Characteristics included hospital ICH volume and type and whether DNR order was placed within 24 h of admission (early DNR order). The risk of in-hospital mortality was evaluated both on the individual and hospital level using multivariable analyses. A case mix-adjusted hospital DNR index was calculated for each hospital by comparing the actual number of DNR cases with the expected number of DNR cases from a multivariate model.

Results

A total of 9,958 patients were treated in 180 hospitals. Early DNR orders were placed in 20.1% of patients and 54.2% of these patients died during their hospitalization compared to 16.0% of patients without an early DNR order. For every 10% increase in a hospital’s utilization of early DNR orders, there was a corresponding 26% increase in the likelihood of in-hospital mortality. Patients treated in hospitals within the highest quartile of adjusted DNR use had a higher relative risk of death compared to the lowest quartile (RR 3.9 vs 5.2) though the trend across quartiles was not statistically significant.

Conclusions

The use of early DNR orders for ICH continues to be a strong predictor of in-hospital mortality. However, patients treated at hospitals with an overall high or low use of early DNR had similar relative risks of death whether or not there was an early DNR order, suggesting that such orders may not be a proxy for less aggressive care as seen previously.

This is a preview of subscription content, log in to check access.

References

  1. 1.
    Feigin VL, Lawes CMM, Bennett DA, Barker-Collo SL, Parag V. Worldwide stroke incidence and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurol. 2009;8:355–69.
    Article  Google Scholar 
  2. 2.
    van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9:167–76.
    Article  Google Scholar 
  3. 3.
    Rincon F, Mayer SA. The epidemiology of intracerebral hemorrhage in the United States from 1979 to 2008. Neurocrit Care. 2013;19:95–102.
    Article  Google Scholar 
  4. 4.
    Davis SM, Broderick J, Hennerici M, Brun NC, Diringer MN, Mayer SA, et al. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology. 2006;66:1175–81.
    CAS  Article  Google Scholar 
  5. 5.
    Hemphill JC, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32:891–7.
    Article  Google Scholar 
  6. 6.
    Morgenstern LB, Zahuranec DB, Sánchez BN, Becker KJ, Geraghty M, Hughes R, et al. Full medical support for intracerebral hemorrhage. Neurology. 2015;84:1739–44.
    Article  Google Scholar 
  7. 7.
    Becker KJ, Baxter AB, Cohen WA, Bybee HM, Tirschwell DL, Newell DW, et al. Withdrawal of support in intracerebral hemorrhage may lead to self-fulfilling prophecies. Neurology. 2001;56:766–72.
    CAS  Article  Google Scholar 
  8. 8.
    Hemphill JC, Newman J, Zhao S, Johnston SC. Hospital usage of early do-not-resuscitate orders and outcome after intracerebral hemorrhage. Stroke. 2004;35:1130–4.
    Article  Google Scholar 
  9. 9.
    Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a Guideline From the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Circulation. 2007;116:e391–413.
    Article  Google Scholar 
  10. 10.
    Zahuranec DB, Brown DL, Lisabeth LD, Gonzales NR, Longwell PJ, Smith MA, et al. Early care limitations independently predict mortality after intracerebral hemorrhage. Neurology. 2007;68:1651–7.
    CAS  Article  Google Scholar 
  11. 11.
    Beach MC, Morrison RS. the effect of do-not-resuscitate orders on physician decision-making. J Am Geriatr Soc. 2002;50:2057–61.
    Article  Google Scholar 
  12. 12.
    Xian Y, Holloway RG, Smith EE, Schwamm LH, Reeves MJ, Bhatt DL, et al. Racial/ethnic differences in process of care and outcomes among patients hospitalized with intracerebral hemorrhage. Stroke. 2014;45:3243–50.
    Article  Google Scholar 
  13. 13.
    Silvennoinen K, Meretoja A, Strbian D, Putaala J, Kaste M, Tatlisumak T. Do-not-resuscitate (DNR) orders in patients with intracerebral hemorrhage. Int J Stroke. 2014;9:53–8.
    Article  Google Scholar 
  14. 14.
    Zurasky JA, Aiyagari V, Zazulia AR, Shackelford A, Diringer MN. Early mortality following spontaneous intracerebral hemorrhage. Neurology. 2005;64:725–7.
    CAS  Article  Google Scholar 
  15. 15.
    Sembill JA, Gerner ST, Volbers B, Bobinger T, Lücking H, Kloska SP, et al. Severity assessment in maximally treated ICH patients: the max-ICH score. Neurology. 2017;89:423–31.
    Article  Google Scholar 
  16. 16.
    Naidech AM, Bernstein RA, Bassin SL, Garg RK, Liebling S, Bendok BR, et al. How patients die after intracerebral hemorrhage. Neurocrit Care. 2009;11:45–9.
    Article  Google Scholar 
  17. 17.
    Suarez JI, Zaidat OO, Suri MF, Feen ES, Lynch G, Hickman J, et al. Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team. Crit Care Med. 2004;32:2311–7.
    Article  Google Scholar 
  18. 18.
    Diringer MN, Edwards DF. Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage. Crit Care Med. 2001;29:635–40.
    CAS  Article  Google Scholar 
  19. 19.
    González-Pérez A, Gaist D, Wallander M-A, McFeat G, García-Rodríguez LA. Mortality after hemorrhagic stroke: data from general practice (the health improvement network). Neurology. 2013;81:559–65.
    Article  Google Scholar 
  20. 20.
    Béjot Y, Grelat M, Delpont B, Durier J, Rouaud O, Osseby G-V, et al. Temporal trends in early case-fatality rates in patients with intracerebral hemorrhage. Neurology. 2017;88:985–90.
    Article  Google Scholar 
  21. 21.
    Poon MTC, Fonville AF, Al-Shahi SR. Long-term prognosis after intracerebral hemorrhage: systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2014;85:660–7.
    Article  Google Scholar 
  22. 22.
    Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, Hope DT, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the international surgical trial in intracerebral haemorrhage (STICH): a randomised trial. Lancet. 2005;365:387–97.
    PubMed  PubMed Central  Google Scholar 
  23. 23.
    Ziai WC, Siddiqui AA, Ullman N, Herrick DB, Yenokyan G, McBee N, et al. Early therapy intensity level (TIL) predicts mortality in spontaneous intracerebral hemorrhage. Neurocrit Care. 2015;23:188–97.
    CAS  Article  Google Scholar 
  24. 24.
    Qureshi AI, Majidi S, Chaudhry SA, Qureshi MH, Suri MFK. Validation of intracerebral hemorrhage-specific intensity of care quality metrics. J Stroke Cerebrovasc Dis. 2013;22:661–7.
    Article  Google Scholar 
  25. 25.
    Tomlinson T, Brody H. Ethics and communication in do-not-resuscitate orders. N Engl J Med. 1988;318:43–6.
    CAS  Article  Google Scholar 
  26. 26.
    Richardson DK, Zive D, Daya M, Newgard CD. The impact of early do not resuscitate (DNR) orders on patient care and outcomes following resuscitation from out of hospital cardiac arrest. Resuscitation. 2013;84:483–7.
    Article  Google Scholar 
  27. 27.
    Fuchs L, Anstey M, Feng M, Toledano R, Kogan S, Howell MD, et al. Quantifying the mortality impact of do-not-resuscitate orders in the ICU. Crit Care Med. 2017;45:1019–27.
    Article  Google Scholar 
  28. 28.
    Zahuranec DB, Morgenstern LB, Sánchez BN, Resnicow K, White DB, Hemphill JC. Do-not-resuscitate orders and predictive models after intracerebral hemorrhage. Neurology. 2010;75:626–33.
    CAS  Article  Google Scholar 
  29. 29.
    Creutzfeldt CJ, Becker KJ, Weinstein JR, Khot SP, McPharlin TO, Ton TG, et al. Do-not-attempt-resuscitation orders and prognostic models for intraparenchymal hemorrhage. Crit Care Med. 2011;39:158–62.
    Article  Google Scholar 
  30. 30.
    Zahuranec DB, Fagerlin A, Sánchez BN, Roney ME, Thompson BB, Fuhrel-Forbis A, et al. Variability in physician prognosis and recommendations after intracerebral hemorrhage. Neurology. 2016;86:1864–71.
    Article  Google Scholar 
  31. 31.
    Kelly PJ, Furie KL, Shafqat S, Rallis N, Chang Y, Stein J. Functional recovery following rehabilitation after hemorrhagic and ischemic stroke. Arch Phys Med Rehabil. 2003;84:968–72.
    Article  Google Scholar 
  32. 32.
    Katrak PH, Black D, Peeva V. Do stroke patients with intracerebral hemorrhage have a better functional outcome than patients with cerebral infarction? PM R. 2009;1:427–33.
    Article  Google Scholar 
  33. 33.
    Sreekrishnan A, Leasure AC, Shi F-D, Hwang DY, Schindler JL, Petersen NH, et al. Functional improvement among intracerebral hemorrhage (ICH) survivors up to 12 months post-injury. Neurocrit Care. 2017;27:326–33.
    Article  Google Scholar