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.

Monday, July 18, 2016

Brain Stimulation Therapy for Central Post-Stroke Pain from a Perspective of Interhemispheric Neural Network Remodeling

I have not focused on this since I didn't have it. Does your doctor know anything about this?
http://journal.frontiersin.org/article/10.3389/fnhum.2016.00166/full?
Takashi Morishita* and Tooru Inoue
  • Department of Neurosurgery, Faculty of Medicine, Fukuoka University, Fukuoka, Japan
Central post-stroke pain (CPSP) is a debilitating, severe disorder affecting patient quality of life. Since CPSP is refractory to medication, various treatment modalities have been tried with marginal results. Following the first report of epidural motor cortex (M1) stimulation (MCS) for CPSP, many researchers have investigated the mechanisms of electrical stimulation of the M1. CPSP is currently considered to be a maladapted network reorganization problem following stroke, and recent studies have revealed that the activities of the impaired hemisphere after stroke may be inhibited by the contralesional hemisphere. Even though this interhemispheric inhibition (IHI) theory was originally proposed to explain the motor recovery process in stroke patients, we considered that IHI may also contribute to the CPSP mechanism. Based on the IHI theory and the fact that electrical stimulation of the M1 suppresses CPSP, we hypothesized that the inhibitory signals from the contralesional hemisphere may suppress the activities of the M1 in the ipsilesional hemisphere, and therefore pain suppression mechanisms may be malfunctioning in CPSP patients. In this context, transcranial direct current stimulation (tDCS) was considered to be a reasonable procedure to address the interhemispheric imbalance, as the bilateral M1 can be simultaneously stimulated using an anode (excitatory) and cathode (inhibitory). In this article, we review the potential mechanisms and propose a new model of CPSP. We also report two cases where CPSP was addressed with tDCS, discuss the potential roles of tDCS in the treatment of CPSP, and make recommendations for future studies.

Introduction

Stroke is a vascular disorder of the brain causing various symptoms including motor weakness, sensory disturbances, balance problems, and spasticity. Pain after stroke can be caused by various conditions secondary to spasticity, and a recent study reported that as many as 39.0% of stroke patients experienced new-onset chronic pain after stroke (Klit et al., 2011). Among various pain etiologies, central post-stroke pain (CPSP) is an especially debilitating, severe disorder characterized by intractable pain with abnormal sensations such as burning and allodynia, which severely affect the quality of life (QOL).
CPSP was first described by Dejerine and Roussy as a consequence of stroke-related lesions in the thalamus (Dejerine and Roussy, 1906); however, lesions in other brain structures in the somatosensory pathway may result in CPSP (MacGowan et al., 1997; Klit et al., 2009). In the somatosensory pathway, lesions in the ventrocaudalis portae nucleus of the thalamus and lateral medulla particularly predispose patients to CPSP (Sprenger et al., 2012). The prevalence of CPSP has been reported to be 1–12% (Andersen et al., 1995; MacGowan et al., 1997; Lampl et al., 2002; Weimar et al., 2002; Widar et al., 2002; Appelros, 2006; Kuptniratsaikul et al., 2009; Lundström et al., 2009).
Even though the mechanisms of CPSP remain unclear, CPSP has been considered to be a maladapted network reorganization problem after stroke (Hosomi et al., 2015), as CPSP usually occurs in a delayed fashion from weeks to months after the initial insult (Nasreddine and Saver, 1997). To explain the abnormal network conditions of CPSP, various circuit models have been proposed (Klit et al., 2009; Hosomi et al., 2015). In this article, we review the potential mechanisms and propose a new model of CPSP. We also report two cases where CPSP was ameliorated with transcranial direct current stimulation (tDCS) and discuss the potential roles of tDCS in the treatment of CPSP and future studies.

More at link.

1 comment:

  1. Not sure exactly what kind of pain I had, but a lot of it on whole left side in first few weeks, then months as movement returned. The recovery process for me in 3 years since stroke is to get something moving (spontaneous or e-stim), exercise it for 5-6 weeks as pain subsides, then get the next movement going & repeat. Still have some pain resting and more when muscles are stretched, but getting better & better as spasticity subsides, which is why I keep at rehab, since still improving, but have a long way to go. Like you, a friend at same PT facility I go to to exercise has similar level of spasticity, except right side, not left, and he never had pain. Go figure.

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