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.

Saturday, April 6, 2019

Somatosensory Deficits After Ischemic Stroke

Useless, useless, useless.  You mean that you missed the Margaret Yekutiel  book about this from 2001, 'Sensory Re-Education of the Hand After Stroke'?  And still didn't write a protocol on how to fix this?  How long do stroke survivors have to put up with such fucking incompetency?

Somatosensory Deficits After Ischemic Stroke

Time Course and Association With Infarct Location
Originally publishedhttps://doi.org/10.1161/STROKEAHA.118.023750Stroke. 2019;0

Background and Purpose—

About 50% to 80% of stroke survivors present with somatosensory deficits. Somatosensory deficits because of an ischemic stroke are determined by the infarct location. However, a detailed understanding of the long-term effect of lesions on somatosensory performance is lacking.

Methods—

This prospective observational study enrolled 101 ischemic stroke patients. For voxel-based lesion-symptom mapping, magnetic resonance imaging fluid-attenuated inversion recovery imaging infarct lesions were segmented within 5 days after stroke. Standardized tests such as the National Institutes of Health Stroke Scale and the Rivermead Assessment of Somatosensory Performance were performed during acute stage, after 3 and 12 months. This included bilateral testing for multiple tactile and proprioceptive somatosensory modalities (pressure, light touch, sharp-dull discrimination, temperature discrimination, sensory extinction, 2-point discrimination, and joint position and movement sense). We further study the association of acute somatosensory deficit with functional outcome 12 months after stroke assessed by the modified Rankin Scale using univariate and multiple linear regression analysis also including acute motor deficit assessed by the arm research action test.

Results—

Sixty patients (59.4%) showed impairment in at least one somatosensory modality. Light touch was most frequently affected (38.7%), whereas temperature was least frequently affected (21.8%). After 3 months, significant recovery was observed in all somatosensory modalities, with only minor additional improvements after 12 months. Voxel-based lesion-symptom mapping revealed significant associations of lesions in the primary and secondary somatosensory and insular cortex with somatosensory deficits. Acute somatosensory deficit was associated with functional outcome at 12 months. However, including the acute motor deficit, somatosensory deficit was no longer an independent predictor of functional outcome.

Conclusions—

Our study confirms that somatosensory deficits are frequent in acute ischemic stroke but largely recover over time. Infarct lesions in the primary and secondary somatosensory cortex and insula show a robust association with somatosensory impairment. Long-term disability is influenced by somatosensory deficits but driven by motor symptoms.(Where the fuck is the protocol that will cure these deficits?)

Footnotes

Correspondence to Simon S. Kessner, MD, Department of Neurology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, D-20246 Hamburg. Email

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