more significant functional improvement in damaged areas as a result of msc treatment. msc treatment also has shown to have various neuroprotective effects, including reductions in apoptosis, inflammation and demyelination, as well as increased astrocyte survival rates. msc treatment also appears to improve the control of cerebral blood flow and blood–brain barrier permeability, as well as what is currently thought to be the most important mechanism of msc treatment after stroke, the activation of endogenous neuroprotection and neurorestoration pathways by the release of cytokines and trophic factors. although activation of endogenous neuroprotection and neurorestoration probably has a major part in the improvement of brain function after stroke, it is likely that the functional improvements as a result of msc treatment are due to combined action via multiple cellular and molecular mechanisms to affect neurorestoration and neuroprotection, rather than just a single mechanism. these effects are also modulated by key variables, including the number of and type of mscs used, timing of treatment relative to when the patient's stroke occurred, route of delivery of the mscs, as well as patient variables (e.g. age, underlying conditions). what this means for stroke patients and the limitations or concerns with mscs as a potential treatment if msc treatment becomes available for stroke patients, it is possible that current mortality and morbidity rates could substantially improve due to the direct enhancement of neuroprotection and neurorestoration mechanisms rather than only indirect facilitation or prevention of further damage, e.g. decompressive surgery. however, for msc treatment to be used effectively and safely in a clinical setting, more research needs to be conducted, specifically in the areas of determining the relative influences of key variables (especially patient variables) on patient outcomes as well quantifying potential risks, e.g. tumour formation. although ethical concerns are mostly limited to the use of embryonic stem cells, it may also be important to address any possible ethical concerns (however unlikely) over the use of somatic stem cells. training of muscles affected by the upper motor neuron syndrome muscles affected by the upper motor neuron syndrome have many potential features of altered performance including: weakness, decreased motor control, clonus (a series of involuntary rapid muscle contractions), exaggerated deep tendon reflexes, spasticity and decreased endurance. the term "spasticity" is often erroneously used interchangeably with upper motor neuron syndrome, and it is not unusual to see patients labeled as spastic who demonstrate an array of umn findings. it has been estimated that approximately 65% of individuals develop spasticity following stroke, and studies have revealed that approximately 40% of stroke patients may still have spasticity at 12 months post-stroke. the changes in muscle tone probably result from alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord, and the absence of an intact corticospinal system. in other words, there is damage to the part of the brain or spinal cord that controls voluntary movement. various means are available for the treatment of the effects of the upper motor neuron syndrome. these include: exercises to improve strength, control and endurance, nonpharmacologic therapies, oral drug therapy, intrathecal drug therapy, injections, and surgery. while landau suggests that researchers do not believe that treating spasticity is worthwhile, many scholars and clinicians continue to attempt to manage/treat it. another group of researchers concluded that while spasticity may contribute to significant motor and activity impairments post-stroke, the role of spasticity has been overemphasized in stroke rehabilitation. in a survey done by the national stroke association, while 58 percent of survivors in the survey experienced spasticity, only 51 percent of those had received treatment for the condition. nonpharmacologic therapies treatment should be based on assessment by the relevant health professionals, although there is evidence that caregivers utilise social media communities to source information related to stroke recovery. for muscles with mild-to-moderate impairment, exercise should be the mainstay of management, and is likely to need to be prescribed by a physiotherapist. muscles with severe impairment are likely to be more limited in their ability to exercise and may require help to do this. they may require additional interventions, to manage the greater neurological impairment and also the greater secondary complications. these interventions may include serial casting, flexibility exercise such as sustained positioning programs, and patients may require equipment, such as using a standing frame to sustain a standing position. applying specially made lycra garments may also be beneficial. interventions for age-related visual problems in patients with stroke with the prevalence of vision problems increasing with age in stroke patients, the overall effect of interventions for age-related visual problems is currently uncertain. it is also not sure whether people with stroke respond differently from the general population when treating eye problems. further research in this area is needed as current body of evidence is very low quality. physiotherapy physiotherapy is beneficial in this area as it helps post-stroke individuals to progress through the stages of motor recovery. these stages were originally described by twitchell and brunnstrom, and may be known as the brunnstrom approach. initially, post-stroke individuals have flaccid paralysis. as recovery begins, and progresses, basic movement synergies will develop into more complex and difficult movement combinations. concurrently, spasticity may develop and become quite severe before it begins to decline (if it does at all). although an overall pattern of motor recovery exists, there is much variability between each individual's recovery. as previously described, the role of spasticity in stroke rehabilitation is controversial. however, physiotherapy can help to improve motor performance, in part, through the management of spasticity. repetitive task training (rtt), which involves the active practice of task-specific motor activities, improves upper and lower limb function, with improvements being sustained 6-months post-treatment. more research is needed on the type and amount of training. unaddressed spasticity will result in the maintenance of abnormal resting limb postures which can lead to contracture formation. in the arm, this may interfere with hand hygiene and dressing, whereas in the leg, abnormal resting postures may result in difficulty transferring. in order to help manage spasticity, physiotherapy interventions should focus on modifying or reducing muscle tone. strategies include mobilizations of the affected limbs early in rehabilitation, along with elongation of the spastic muscle and sustained stretching. in addition, the passive manual technique of rhythmic rotation can help to increase initial range. activating the antagonist (muscle) in a slow and controlled movement is a beneficial training strategy that can be used by post-stroke individuals. splinting, to maintain muscle stretch and provide tone inhibition, and cold (i.e. in the form of ice packs), to decrease neural firing, are other strategies that can be used to temporarily decrease the extent of spasticity. the focus of physiotherapy for post-stroke individuals is to improve motor performance, in part, through the manipulation of muscle tone. oral drug therapies oral medications used for the treatment of spasticity include: diazepam (valium), dantrolene sodium, baclofen, tizanidine, clonidine, gabapentin, and even cannabinoid-like compounds.³ the exact mechanism of these medications is not fully understood, but they are thought to act on neurotransmitters or neuromodulators within the central nervous system (cns) or muscle itself, or to decrease the stretch reflexes. the problem with these medications is their potential side effects and the fact that, other than lessening painful or disruptive spasms and dystonic postures, drugs in general have not been shown to decrease impairments or lessen disabilities. intrathecal drug therapy intrathecal administration of drugs involves the implantation of a pump that delivers medication directly to the cns. the benefit of this is that the drug remains in the spinal cord, without traveling in the bloodstream, and there are often fewer side effects. the most commonly used medication for this is baclofen but morphine sulfate and fentanyl have been used as well, mainly for severe pain as a result of the spasticity. injections injections are focal treatments administered directly into the spastic muscle. drugs used include: botulinum toxin (btx), phenol, alcohol, and lidocaine. phenol and alcohol cause local muscle damage by denaturing protein, and thus relaxing the muscle. botulinum toxin is a neurotoxin and it relaxes the muscle by preventing the release of a neurotransmitter (acetylcholine). many studies have shown the benefits of btx and it has also been demonstrated that repeat injections of btx show unchanged effectiveness. surgery surgical treatment for spasticity includes lengthening or releasing of muscle and tendons, procedures involving bones, and also selective dorsal rhizotomy. rhizotomy, usually reserved for severe spasticity, involves cutting selective sensory nerve roots, as they probably play a role in generating spasticity. post-stroke pain syndromes chronic pain syndromes are common in about one half of stroke patients. central post-stroke pain (cpsp) is neuropathic pain which is caused by damage to the neurons in the brain (central nervous system), as the result of a vascular injury. one study found that up to 8% of people who have had a stroke will develop central post-stroke pain, and that the pain will be moderate to severe in 5% of those affected. the condition was formerly called "thalamic pain", because of the high incidence among those with damage to the thalamus or thalamic nuclei. now known as cpsp, it is characterized by perceived pain from non-painful stimuli, such as temperature and light touch. this altered perception of stimuli, or allodynia, can be difficult to assess due to the fact that the pain can change daily in description and location, and can appear anywhere from months to years after the stroke. cpsp can also lead to a heightened central response to painful sensations, or hyperpathia. affected persons may describe the pain as cramping, burning, crushing, shooting, pins and needles, and even bloating or urinary urgency. both the variation and mechanism of pain in cpsp have made it difficult to treat. several strategies have been employed by physicians, including intravenous lidocaine, opioids/narcotics, anti-depressants, anti-epileptic medications and neurosurgical procedures with varying success. higher rates of successful pain control in persons with cpsp can be achieved by treating other sequelae of stroke, such as depression and spasticity. as the age of the population increases, the diagnosis and management of cpsp will become increasingly important to improve the quality of life of an increasing number of stroke survivors. cause hemiplegic shoulder pain (shoulder pain on the stroke-affected side of the body) is a common source of pain and dysfunction following stroke. the cause (etiology) of hemiplegic shoulder pain remains unclear. possible causes may include shoulder subluxation, muscle contractures, spasticity, rotator cuff disorders or impingement, and complex regional pain syndrome. overall, the shoulder is very mobile, and relies on muscles and ligaments to support it, therefore, if a stroke damages the neurons that control those muscles and ligaments, the joint can be affected and pain may result. pharmacological therapies analgesics (ibuprofen and acetaminophen) may offer some pain relief for generalized hemiplegic shoulder pain. for people with spasticity associated shoulder pain, botulinum toxin injections into the shoulder muscles has also been shown to provide significant pain relief and improve range of motion. subacromial corticosteroid injections can be effective for people with shoulder pain related to injury/inflammation of the rotator cuff region. non-pharmacological treatment there are several non-pharmacological interventions which are recommended for prevention and treatment of post-stroke hemiplegic shoulder pain. these include proper positioning, range of motion exercises, motor retraining, and adjuvant therapies like neuromuscular electric stimulation (nmes) (e.g. functional electric stimulation (fes)). the use of slings remains controversial. functional electric stimulation (fes) is a nmes technique where nerves or muscles affected by stroke receive bursts of low-level electrical current. the goal of fes is to strengthen muscle contraction and improve motor control. it may be effective in reducing subluxation and the pain associated with subluxation. different slings are available to manage shoulder subluxation. however, the use of slings remains controversial and may increase the risk of adverse effects on symmetry and balance between the left and right shoulders, and can impact peoples' body image. shoulder subluxation glenohumeral (or shoulder) subluxation is defined as a partial or incomplete dislocation of the shoulder joint that typically results from changes in the mechanical integrity of the joint. subluxation is a common problem with hemiplegia, or weakness of the musculature of the upper limb. traditionally this has been thought to be a significant cause of post-stroke shoulder pain, although a few recent studies have failed to show