Moving Physical Therapy Forward

You can listen to Joseph Brence, DPT talk about the need for PTs to have evidence to  support their therapy. This was talked about here in 1994 by Carr and Shepherd. Why should he have to repeat this 18 years later?
http://pttalker.com/2012/09/moving-physical-therapy-forward/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+PtTalker+%28PT+Talker%29
But then we might not get any therapy at all, for those like me who have large areas of dead brain, What will therapists provide as evidence? I remember my OT telling me that studies showed that survivors that didn't have this type of finger movement wouldn't recover finger movement. I still do not have finger movement  but she kept trying and I will eventually prove it can be done.

Researchers Compare Walking Ability of Post-Stroke Patients and Non-Disabled Adults

Something  we should have had for years, evidence-based practice.
http://www.ptproductsonline.com/news/2012-09-06_01.asp
Individuals with stroke have reduced walking activity, although it is unknown whether this deficit is due to a reduction in all aspects of walking activity or only in specific areas. Researchers from Delaware and Maine performed a study to examine the walking activity in post-stroke individuals compared with older adults without disability. The results were published in the September 2012 issue of Physical Therapy. 
Margaret A. Roos, PT, DPT, PhD, NCS, from the department of physical therapy at the University of Delaware, Newark, Del, led the cross-sectional study of 54 post-stroke participants and 18 older adults reported as having no disability. All participants wore a step activity monitor for 3 days, which calculated steps per day (SPD), bouts per day (BPD), steps per bout (SPB), total time walking per day (TTW), percentage of time walking per day (PTW), and frequency of short, medium, and long walking bouts.
The researchers classified 29 participants as household and limited community ambulators (HHA-LCA group) and 22 participants as unlimited community ambulators (UCA group). According to the results, the SPD, TTW, PTW, and BPD measurements were the greatest in the older, non-disabled adults and the lowest in the HHA-LCA group. In addition, walking in the short, medium, and long categories was found to be lowest in the HHA-LCA group, greater in the UCA group, and greatest in the non-disabled group.
The specific descriptors of walking activity presented can provide insight into walking deficits post-stroke that cannot be determined by looking at steps per day alone. The researchers stress the need to analyze the structure of walking activity, concluding that the deficits found during this study could be addressed through appropriate exercise prescription.

What is your stroke protocol?

Definition:  The plan for a course of medical treatment or for a scientific experiment.

Isn't this by definition what Physiatrists or PM&R doctors supposed to do? Or is yours like mine was; hand you off to the therapists with ET, evaluate and treat, nothing scientific there and no way to monitor progress against your goals. You did discuss your goals with your doctor, didn't you? 100% recovery. I had no goal discussion with my doctor.
Wouldn't you think that stroke rehab would have the same type of detail as below?

Check out what colon cancer has from  Medscape
http://emedicine.medscape.com/article/2005487-overview

Adjuvant chemotherapy for patients with resectable colon cancer

Stage 0 and I:

• Patients do not require adjuvant therapy

Adjuvant chemotherapy for resectable colon cancer

Stage IIA, B and C (node-negative)^{[1, 2, 3]} :
The value of adjuvant therapy in stage II disease is at best controversial; however, the following regimens may be used:

• Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d for 8 cycles or
• Leucovorin 500 mg/m² given as a 2-h infusion and repeated weekly for 6wk plus  5-fluorouracil (5-FU) 500 mg/m² given as a bolus 1h after the start of leucovorin and repeated 6 times weekly; every 8wk for 4 cycles or
• Leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU bolus 400 mg/m², then  1200 mg/m²/day for 2d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk

Stage II adjuvant chemotherapy in high-risk or intermediate-risk patients:
Adjuvant therapy for high-risk patients with stage II is an option, and common regimens include use of 5-FU and leucovorin with or without oxaliplatin or capecitabine.^[1]

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2d continuous infusion; repeat every 2wk or
• FLOX: 5-FU 500 mg/m² IV weekly plus  leucovorin 500 mg/m² IV weekly for 6wk (days 1, 8, 15, 22, 29, and 36) of each 8-wk cycle plus  oxaliplatin 85 mg/m² IV administered on days 1, 15, and 29 of each 8-wk cycle for 3 cycles or
• Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d for 8 cycles

Adjuvant therapy for resectable cancer

Stage III (node-positive)^{[2, 3]} :
The following regimens are acceptable adjuvant therapies for stage III disease for resectable colon cancer:

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk or
• FLOX: 5-FU 500 mg/m² IV weekly plus  leucovorin 500 mg/m² IV weekly for 6wk (days 1, 8, 15, 22, 29, and 36) of each 8-wk cycle plus  oxaliplatin 85 mg/m² IV administered on days 1, 15, and 29 of each 8-wk cycle for 3 cycles or
• Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d for 8 cycles or
• CapeOx: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² PO BID on days 1-14 every 3wk for 8 cycles or
• Leucovorin 500 mg/m² given as a 2-h infusion and repeated weekly for 6wk plus  5-FU 500 mg/m² given as a bolus 1h after the start of leucovorin and repeated 6 times weekly; every 8wk for 4 cycles or
• Leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU bolus 400 mg/m², then  1200 mg/m²/day for 2d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk

Neoadjuvant therapy for resectable metastatic disease

Neoadjuvant therapy for resectable metastatic disease is usually administered for approximately 2-3mo, limiting the development of hepatotoxicity.^[3] Regimens for adjuvant and neoadjuvant therapy are similar.

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk or
• FOLFIRI: Irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk
• CapeOx with or without bevacizumab: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² PO BID for 14d; repeat every 3wk plus bevacizumab 7.5 mg/kg IV every 3wk

Chemotherapy for advanced or metastatic disease

Stage IV:
Chemotherapy for advanced or metastatic disease includes the use of multiple drugs as single agents or as combination regimens.^{[4, 5, 6, 7, 8, 9]}
First-line chemotherapy for bevacizumab candidates:

• mFOLFOX6 plus bevacizumab: Bevacizumab 5 mg/kg over 30-90min on day 1 plus  oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4-6 cycles with reevaluation for maintenance therapy (1 g of calcium gluconate and 1 g of magnesium sulfate may be give over 15min preinfusion and postinfusion to reduce the risk of neurotoxicity) or
• FLOX plus bevacizumab: Bevacizumab 5 mg/kg over 30-90min on days 1, 15, and 29 plus  oxaliplatin 85 mg/m² on days 1, 15, and 29 plus  leucovorin 500 mg/m² on days 1, 8, 15, 22, 29, and 36 plus  5-FU 500 mg/m² on days 1, 8, 15, 22, 29, and 39 for 2 cycles followed by reevaluation or
• FOLFIRI plus bevacizumab: Bevacizumab 5 mg/kg over 30-90min on day 1 plus  irinotecan 180 mg/m² IV over 30-90 min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4-6 cycles with reevaluation for maintenance therapy or
• CAPEOX plus bevacizumab: Bevacizumab 7.5 mg/kg over 30-90min on day 1 plus  oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² PO BID for 14d; repeat every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• Capecitabine plus bevacizumab (in patients not able to undergo treatment with oxaliplatin or irinotecan): Bevacizumab 7.5 mg/kg on day 1 plus  capecitabine 1250 mg/m² PO BID for 14d; repeat cycle every 21d for 8 cycles, then  reevaluate for maintenance or
• DeGramont regimen plus bevacizumab (in patients not able to undergo treatment with oxaliplatin or irinotecan): Bevacizumab 5 mg/kg over 30-90min on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU bolus 400 mg/m², then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4-6 cycles with reevaluation for maintenance therapy or
• Bevacizumab plus 5-FU and leucovorin (Roswell Park) (in patients unable to undergo treatment with oxaliplatin or irinotecan): Bevacizumab 5 mg/kg over 30-90min on day 1 plus  leucovorin 500 mg/m² over 2h plus  5-FU 500 mg/m² bolus every 2wk for 4-6 cycles with reevaluation for maintenance therapy

First-line chemotherapy for patients who are not candidates for bevacizumab^{[7, 8, 9, 10]} :

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4 cycles or
• FLOX: Oxaliplatin 85 mg/m² on days 1, 15, and 29 plus  leucovorin 500 mg/m² on days 1, 8, 15, 22, 29, and 36, followed by 5-FU 500 mg/m² on days 1, 8, 15, 22, 29, and 39 for 2 cycles followed by reevaluation or
• FOLFIRI: Irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles or
• Capecitabine: Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d until progression or
• Roswell Park regimen: Leucovorin 500 mg/m² IV weekly for 6wk over 2h followed by 5-FU 500 mg/m² IV bolus weekly for 6wk; repeat cycle every 8wk or
• CapeOx: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² BID for 14d every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• mFOLFOX6 plus cetuximab (only for KRAS wild-type tumors): Cetuximab 400 mg/m² loading dose on day 1, then  cetuximab 250 mg/m² weekly plus  oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4 cycles, then reevaluate or
• FOLFIRI plus cetuximab (only for KRAS wild-type tumors): Cetuximab 400 mg/m² loading dose over 2h on day 1, then  cetuximab 250 mg/m² over 1h weekly plus  irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles, then reevaluate or
• Referral for clinical trial

Second-line chemotherapy for metastatic disease^{[11, 12, 13]} :

• FOLFIRI (if FOLFOX, CapeOx, CapeOx plus bevacizumab or FOLFOX plus bevacizumab used as first-line chemotherapy): Irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles, then reevaluate or
• FOLFIRI plus cetuximab (only for KRAS wild-type tumors and if FOLFOX, CapeOx, CapeOx plus bevacizumab or FOLFOX plus bevacizumab used as first–line chemotherapy): Cetuximab 400 mg/m² loading dose over 2h on day 1, then  cetuximab 250 mg/m² over 1h weekly plus  irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles and then reevaluate or
• mFOLFOX6 (if FOLFIRI or FOLFIFI plus bevacizumab used as first-line chemotherapy): Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4 cycles or
• CapeOx: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² BID for 14d every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• mFOLFOX6 plus cetuximab (only for KRAS wild-type tumors and if FOLFIRI or FOLFIRI plus bevacizumab used as first-line chemotherapy): Cetuximab 400 mg/m² loading dose on day 1 over 2h, then  cetuximab 250 mg/m² over 1h weekly plus  oxaliplatin 85 mg/m² IV over 2h day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2d continuous infusion; repeat every 2wk for 4 cycles and then reevaluate or
• Irinotecan 125 mg/m² over 90min weekly with reevaluation after 8wk or
• Cetuximab 400 mg/m² over 2h on day 1, then  250 mg/m² over 1h weekly with reevaluation after 8wk or
• Panitumumab 6 mg/kg over 60-90min every 2wk with reevaluation after 8wk or
• Modified FOLFOX6 plus bevacizumab (if FOLFIRI used upfront and bevacizumab never used as first-line chemotherapy; note higher dose of bevacizumab as second-line chemotherapy): Bevacizumab 10 mg/kg over 30-90min on day 1 plus  oxaliplatin 85 mg/m² over 2h on day 1 plus  leucovorin 400 mg/m² over 2h plus  5-FU 400 mg/m² IV bolus on day 1, followed by 5-FU 2400 mg/m² IV continuous infusion over 46h every 2wk for 4-6 cycles with reevaluation for maintenance therapy (1 g of calcium gluconate and 1 g of magnesium sulfate may be give over 15min preinfusion and postinfusion to reduce the risk of neurotoxicity) or
• CAPEOX plus bevacizumab (if FOLFIRI used upfront and bevacizumab never used as first-line chemotherapy; note higher dose of bevacizumab as second-line chemotherapy): Bevacizumab 15 mg/kg over 30-90min on day 1 plus  oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² BID for 14d every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• FOLFIRI plus bevacizumab (if FOLFOX or CAPEOX used upfront and bevacizumab never used as first-line chemotherapy): Bevacizumab 10 mg/kg over 30-90min on day 1 plus  irinotecan 180 mg/m² over 90min on day 1 plus  leucovorin 400 mg/m² over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1 followed by 5-FU 2400 mg/m² IV continuous infusion over 46h every 2wk for 4-6 cycles with reevaluation for maintenance therapy or
• Aflibercept 4 mg/kg IV infused over 1 hr q2weeks plus FOLFIRI in mCRC resistant to or has progressed after an oxaliplatin regimen; administer before any component of FOLFIRI regimen on the day of treatment
• Referral for clinical trial

Note: In the above regimens, cetuximab can be replaced with panitumumab at 6mg/kg every 2wk if anaphylaxis is experienced with cetuximab.
Third-line chemotherapy for metastatic disease:

• Panitumumab 6 mg/kg over 60-90min every 2wk for KRAS wild-type tumors only with reevaluation after 8wk or
• Any regimen incorporating an EGFR antibody for patients with KRAS wild-type disease using a cytotoxic backbone not previously tried or
• Referral for clinical trial

Summary of guiding principles in the treatment of metastatic colorectal cancer

• Importance of differentiating between M1a (1 organ site of metastatic disease) and M1b (more than 1 organ site) in view of curative potential of 1 organ site
• Selection of oxaliplatin or irinotecan as part of cytotoxic backbone upfront in metastatic disease is based primarily on toxicity profile
• Bevacizumab improves survival as first-line and second-line therapy and works with irinotecan- and oxaliplatin-based therapy
• Addition of bevacizumab to irinotecan, fluorouracil, and leucovorin (IFL) significantly improved the response rate, overall survival, and progression-free survival
• The addition of bevacizumab to fluorouracil-based combination chemotherapy results in statistically significant and clinically meaningful improvement in survival among patients with metastatic colorectal cancer
• Interruption in therapy is not ideal for patients; some form of therapy should always be continued after a stable disease state is obtained
• Single-agent maintenance bevacizumab may be a feasible option for patients receiving bevacizumab + CapeOx as induction therapy
• There are no data on maintenance anti-EGFR therapy
• Anti-EGFR antibody therapy should be given only to patients with KRAS wild-type tumors
• Anti-EGFR antibody therapy and bevacizumab should never be combined
• Progression-free survival (PFS) and overall survival (OS) in randomized clinical trials using both FOLFOX and FOLFIRI cytotoxic backbones has been improved only in those patients with KRAS wild-type tumors
• The data on BRAF status are still preliminary in terms of predictive value, but there is a suggestion that even in the setting of KRAS wild-type tumors, BRAF mutation abrogates the effect of anti-EGFR antibody therapy; it is, however, prognostic of a worse outcome
• Optimal use of all therapeutic agents improves survival in patients with metastatic disease
• It is reasonable to leave the primary therapy in place and start treatment for metastatic disease
• A multidisciplinary approach is necessary to deal with the complicated issue of potentially resectable or marginally resectable metastatic disease
• Pharmacogenomics profiling beyond KRAS mutation status is not yet standard of care

Etiologic work-up crucial after stroke

Etiology is the study of causation, or origination. The word is derived from the Greek αἰτιολογία, aitiologia, "giving a reason for". And after the workup they should put that into a stroke causation database so  everyone can read about it.
 http://www.news-medical.net/news/20120905/Etiologic-work-up-crucial-after-stroke.aspx

Connexin 36 Promotes Cortical Spreading Depolarization and Ischemic Brain Damage

What is the logical conclusion after this research and what theory can be tested  to help survivors?

Connexin 36 Promotes Cortical Spreading Depolarization and Ischemic Brain Damage

Abstract

Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs.

In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined.

Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia.

These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.

Tests for silent neck artery narrowing to curb stroke risk: Waste of resources

Well are there other options? like;
Do you want the lawnmower?
http://www.articlecity.com/videos/health/Lawnmower-For-Clogged-Arteries-175286465.php
Or Drano? I would be worried about this, sloughing off chunks
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=26404
 and the waste of resources here:
http://www.sciencecodex.com/tests_for_silent_neck_artery_narrowing_to_curb_stroke_risk_waste_of_resources-97904
This was the starting point of my stroke and could have been solved if when my Dad was diagnosed with 85% blockage his doctor had recommended that any children get tested, At the time of my stroke it was estimated at 85 % blockage(This was 3 years later) when an ultrasound was done and I found out that the right carotid was totally blocked. The blockage was never found during my hospital stay. I consider that a complete failure on my doctors part. I luckily did not have any further strokes during that 3 year window of high danger.

Who Best to Create a Sense of Urgency for Acute Stroke Treatment? Commentary on “Neurohospitalists Improve Door-to-Needle Times for Patients With Ischemic Stroke Receiving Intravenous tPA”

I'm sorry but the urgency  they are trying to create to speed up tPA time is the wrong focus. A separate and just as important focus should be to find multiple ways to stop the neuronal cascade of death. And that will have to come from survivors. 17 years to find  out that tPA is hard to implement is a colossal failure. Fire them and put survivors in charge if you want something done. 

http://nho.sagepub.com/content/2/4/117.full?etoc

In the 17 years since the efficacy of intravenous tissue plasminogen activator (tPA) for acute ischemic stroke was first established,¹ we have struggled to develop the infrastructures and systems of care that are necessary to deliver this therapy as quickly and efficiently as possible.

Speed matters. Although delays in presenting to the emergency department account for most of the unrealized potential of thrombolysis,² the time from when a patient arrives in the emergency department to when the tPA infusion begins—the door-to-needle time—presents a more readily accessible target for hospital-level interventions. Pooled data from 6 randomized trials³ and analyses of large observational data sets⁴ consistently show that faster door-to-needle times are associated with better patient outcomes. In fact, each 15-minute decrease in door-to-needle time is associated with a 5% lower odds of in-hospital mortality.⁴ Therefore, the American Heart Association: Target Stroke initiative has set a specific goal of raising the percentage of patients treated within 60 minutes from the current level of 29% to over 50%.⁴

Precisely how to actually achieve this goal involves evaluating a variety of factors, but certainly one important consideration is ensuring that appropriate staffing is available for these neurological emergencies. In this issue of The Neurohospitalist, Bhatt and Shatila examine the impact of neurohospitalists on door-to-needle times for acute ischemic stroke.⁵ The study includes data from 107 consecutive patients treated with intravenous (IV) tPA at 2 community hospitals between July 2009 and September 2011. The study was a natural experiment of sorts: halfway though the study period, coverage for acute stroke calls from the emergency department changed from a rotating schedule of 4 community neurologists with shared inpatient and outpatient responsibilities to a neurohospitalist model staffed by 2 inpatient-based neurologists. Occasional weekend coverage continued to be provided by locums tenens and community neurologists.

The primary finding was that among patients treated with IV thrombolysis for stroke, 51% (24 of 47) of those evaluated by neurohospitalists were treated in 60 minutes or less, compared with 15% (9 of 60) of those evaluated by nonneurohospitalists—a difference that may be due, at least in part, to the greater likelihood that a neurohospitalists is in hospital for an emergency in-person consultation.

Bhatt and Shatila are generally careful not to assert a causal relationship between a neurohospitalist’s involvement and faster door-to-needle times, with the notable exception of the article’s title. Such caution is warranted. First, there are likely to be unmeasured confounders and secular trends at play. For example, a t test comparing the mean performance of the 2 groups may obscure a secular trend of improved door-to-needle times over time. Other analytic methods such as interrupted time series analysis are often used to mitigate this possibility in other quality improvement studies. Next, relevant details on how the availability of neurohospitalists would actually impact the response time are unavailable. These details would be especially important to understand and evaluate because the acute stroke response involves interactions between multiple disciplines—not just the neurohospitalist—and since shared knowledge and best practices at the team- or hospital-level would be expected to diffuse to the care of all patients over time. Finally, upward of 90% of the observed difference was driven by the performance of the neurohospitalist with specific certification in vascular neurology—someone with both the experience and interest to shepherd the performance improvement seen here.

So can we attribute these improvements to neurohospitalist staffing, to vascular neurology training, or perhaps to the involvement of a motivated, invested, and accountable champion for change regardless of specialty? I would say that what probably matters most is the watchful eye and the sustained involvement of someone with an interest in improving these processes and outcomes—a motivated neurohospitalist may be ideally situated to take on this role.

New technique helps determine degree of muscle wasting in critically ill patients

While we as stroke patients may not be critically ill we do have muscle wastage that should be objectively measured and come up with ways to correct it. So ask your doctor what they are doing about this problem. I know I had this because my AFO got looser rather rapidly and my doctor never checked on it.
 http://www.alphagalileo.org/ViewItem.aspx?ItemId=123625&CultureCode=en
 Researchers have identified a new technique that can help determine the severity of muscle loss in critically ill patients. The breakthrough could lead to new research to help prevent muscle-wasting and new therapeutic interventions to help treat critically ill patients.
The results of the study will be presented today (2 September 2012) at the European Respiratory Society’s Annual Congress in Vienna.
Patients who are critically ill with multi-organ failure often have significant muscle wasting after recovering from their illness. This can delay their discharge from an intensive care unit and is a major cause of disability affecting quality of life once patients have left the hospital.
Until now, there has been no clinically useful way of measuring muscle wastage, or identifying patients who are at a high-risk of this. The researchers hypothesised that they could measure the rectus femoris, one of the four quadriceps muscles in the leg, to determine the level of muscle wasting.
63 patients were recruited to the study within 24 hours of admission to hospital. Muscle wasting was assessed using an ultrasound to measure muscle circumference of the rectus femoris. Researchers also monitored the number of failed organ systems during the patient’s time in intensive care, to assess which patients were at a high risk of muscle wasting.
The researchers determined that circumference measurements of the rectus femoris area by ultra sound can objectively track muscle loss early in critical illness. They also determined that the greatest reduction in muscle circumference was seen in patients with multi-organ failure. In patients with multi-organ failure, the circumference of the rectus femoris was reduced by approximately 21.53%. This compared with an approximate reduction of 7.2% in people with single organ failure.
Lead author, Dr Zudin Puthucheary from University College London, UK, said: “Our research has determined that measuring the rectus femoris using ultrasound is a useful tool to analyse the degree of muscle wasting in critically ill patients. This is clinically relevant as it can help healthcare professionals detect those at high-risk of muscle loss and provide interventions to help improve their quality of life. It is also an important discovery for research as it can help scientists track muscle response to different interventions, so we can find new solutions to addressing this problem in our critically ill patients.”

Fly through the brain of a mouse

Ok, not too useful for us but the eventual possibilities for understanding our brains are great.
http://www.newscientist.com/blogs/nstv/2012/09/matrix-like-fly-through-shows-brain-in-amazing-detail.html?

Aqua-wheelchair performs flips underwater

Ask your therapist for this. I could easily see the fantastic therapeutic stroke rehab possibilities. I would have been able to reduce the spasticity preventing me from raising my left arm. That alone  would make it cost feasible.
http://www.newscientist.com/blogs/nstv/2012/08/aqua-wheelchair-performs-flips-underwater.html?

Statins linked with development of cataracts

Another discussion point with your doctor, if you are keeping track I'll be indexing all of statin side effects under that name  for your ease of doctor questioning.
http://www.theheart.org/article/1434435.do?utm_medium=email&utm_source=20120903_TopTen&utm_campaign=newsletter
Statin users are more than 50% likelier to develop age-related cataracts, according to the results of a new study [1]. And type 2 diabetics who use statins are at even greater risk of cataracts, report investigators.

"The bioplausibility of these results lies in the fact that the crystalline lens membrane requires high cholesterol for proper epithelial cell development and lens transparency," write Dr Carolyn Machan (University of Waterloo, ON) and colleagues in the August 2012 issue of Optometry and Vision Science. "Increased cataract formation has been seen in both animals and humans with hereditary cholesterol deficiency, and the risk exists that statins can inhibit cholesterol biosynthesis in the human lens."

Asked to comment on the paper for heartwire, Dr Richard Karas (Tufts University School of Medicine, Boston, MA), called the findings "an interesting observation [that] isn't alarmist." There is, he says, a "suggestion" here that statins may increase the risk of cataracts, but this visual problem eventually afflicts everyone of a certain age anyhow, he says, adding that further study of this association will be required.

Waterloo Eye Study includes almost 6500 patients

The analysis included 6397 patients with and without diabetes. As the researchers note, diabetes is a risk factor for the development of cataracts, leading the group to analyze the prevalence of cataracts among patients with diabetes taking statins (n=452) and the prevalence among those taking statins but without diabetes (n=5884). The mean age of patients with diabetes was 14 years older than those without diabetes and included a slightly higher proportion of female subjects. The prevalence of statin use in patients 38 years of age and older was 56% for those with type 2 diabetes and 16% for those without diabetes.

In the study, known as the Waterloo Eye Study, diabetes was associated with an 86% higher risk of developing cataracts (odds ratio [OR] 1.86; 95% CI 1.34-2.59) across the lifespan after researchers controlled for multiple variables, including age, female sex, smoking, and blood pressure. A diagnosis of diabetes was also associated with an increased risk of different subtypes of cataracts: an 84% greater risk of nuclear sclerosis, a 38% higher risk of cortical cataract, and a 52% rise in posterior subcapsular cataract

Statin use was also associated with a significantly increased risk of developing age-related cataracts (OR 1.57; 95% CI 1.15-2.13) and some subtypes, including a 48% higher risk of nuclear sclerosis and a 48% rise in posterior subcapsular cataract but no increased risk of cortical cataract.

In an analysis of cataract prevalence among patients with and without diabetes taking statins, Machan and colleagues found that the prevalence of cataract increased at a faster rate in patients with diabetes who used statins. "Similar prevalence levels were seen in patients with diabetes who did not use statins and in patients without diabetes who did use statins," according to the researchers. "The prevalence of cataract increased at the slowest rate in patients without diabetes who did not use statins."

Are you on your own for stroke recovery?

Did your doctor and therapists not have a plan B? Then your plan B will have to be Steven Wolfs contention, 'Stroke patients need to rely more on their own problem solving to regain mobility', I can't give you any medical advice but if you read all the entries in my blog, wink,wink, you might be able to figure what to do to continue your recovery. Your recovery can continue as long as you keep working at it. I'm going to be doing this till the day I die.

Muscle action and explanation for stroke rehab

I'm sure your therapists throw a lot of muscle names at you. This site can explain what they are referring to and for those of the do-it-yourself plan  you can use it for your mental imagery and action observation.
http://www.getbodysmart.com/
My first lookup was the latissimus dorsi to find out which muscle is causing me so much grief in trying to raise my arm due to spasticity. And as Steven Wolf says, 'Stroke patients need to rely more on their own problem solving to regain mobility',  this would be a good start for your problem solving.

Red Meat Consumption and Risk of Stroke: A Meta-Analysis of Prospective Studies.

And even our American Heart Association promotes the conflating of corellation and causation. They should be working on figuring out how to stop the neuronal cascade of death. How about it, Ms. Nancy Brown?
http://www.ncbi.nlm.nih.gov/pubmed/22851546

Stroke. 2012 Jul 31. [Epub ahead of print]

Abstract

BACKGROUND AND PURPOSE:

Prospective studies of red meat consumption and risk of stroke have provided inconsistent results. We performed a meta-analysis to summarize the evidence regarding the effects of red meat (fresh, processed, and total) consumption on stroke risk. (Where's the hard work stopping neuronal death?)

METHODS:

Studies were identified by searching the PubMed database through May 26, 2012, and by reviewing the reference lists of retrieved articles. Prospective studies that reported relative risks (RR) with 95% confidence intervals (CI) for the association between red meat consumption and risk of stroke were eligible.

RESULTS:

Five articles including results from 6 prospective studies with 10ü630 cases of stroke and 329ü495 participants were included in the meta-analysis. For each serving per day increase in fresh red meat, processed meat, and total red meat consumption, the RR (95% CI) of total stroke were 1.11 (1.03-1.20), 1.13 (1.03-1.24), and 1.11 (1.06-1.16), respectively, without heterogeneity among studies (P>0.16). Among 4 articles with results for stroke subtypes, the risk of ischemic stroke was positively associated with consumption of fresh red meat (RR, 1.13; 95% CI, 1.00-1.27), processed meat (RR, 1.15; 95% CI, 1.06-1.24), and total red meat (RR, 1.12; 95% CI, 1.05-1.19); no statistically significant associations were observed for hemorrhagic stroke.

CONCLUSIONS:

Results from this meta-analysis indicate that consumption of fresh red meat and processed red meat as well as total red meat is associated with increased risk of total stroke and ischemic stroke, but not hemorrhagic stroke.

Eating small bar of chocolate cuts risks of stroke in men

I hate these articles, correlation does not prove causation. And it dumps all responsibility for preventing stroke damage on the patient. Rather than doing the hard research necessary to prevent the neuronal cascade of death. I expect better from our researchers and no one is calling out them on their taking the easy way out.
http://www.healthcareglobal.com/administration/eating-small-bar-of-chocolate-cuts-risks-of-stroke-in-men

According to a new study, eating a small bar of chocolate every week can considerably lessens the risk of stroke in men. The study conducted on more than 37,000 Swedish men showed that those eating chocolates were least likely to have a stroke.  

Other studies have suggested that eating chocolate can definitely improve the health of the heart.  The participants of the study were asked about their habits of eating and for a decade their health was monitored.  

Based on the amount of chocolate, they were split into four groups, with the bottom group eating, on average, no chocolate each week. Meanwhile, the top group had 63 grams, slightly more than an average bar. Study also found that those eating the most chocolate were 17% less likely to have a stroke.  

Prof Susanna Larsson, said, “The beneficial effect of chocolate consumption on stroke may be related to flavonoids in the chocolate.” “Flavonoids appear to be protective against cardiovascular disease through antioxidants, anti-clotting and anti-inflammatory properties,” said Prof Susanna.  

The study also stated that milk chocolate was ideal option in Sweden and the dark chocolate has been linked to benefits for the heart in the past.

Dr. Clare Walton, from the Stroke Association, UK said, “Past research has shown that eating dark chocolate might go some way to reduce your stroke risk if it’s eaten as part of a healthy, balanced diet.”  Or maybe richer/healthier persons can afford to buy dark chocolate.

Dr Walton also said, “This study suggests that eating a moderate amount of other types of chocolate could also be beneficial in men.”  It is sensible enough to understand that eat chocolates in moderation as it contains high sugar and fat content.

Chocolate is a raw or processed food produced from the seed of tropical Theobroma cacao tree. It mostly comes in dark, milk, and white varieties with cocoa solids and contributes to brown coloration.

My theory on motor recovery - stroke rehab

I put this out there with no professional background, borrowed from Cassalita and my original OT on eccentric vs. concentric contractions.Most therapists focus on functional recovery because that's what they are paid for. From some questions directed to me, a lot of survivors have a specific movement they want to recover - not necessarily functional. And no one is giving them any help in planning out how to recover that.  And as Steven Wolf says, 'Stroke patients need to rely more on their own problem solving to regain mobility', Prerequisites are a decent muscle anatomy or body-building book or anatomy software that shows the complete range of movement of the muscles you are interested in. My example is the bicep.
1. First you need to see where you have some control. straighten your arm out, see if you can exert force at any point in the contraction phase, this might entail having someone lift your arm up bit by bit to see if you have some muscle control at any point, try this standing and lying down. That determines if you have some concentric contractions. Then get the lower arm to 90 degrees to your body and try to lower it. You may need someone to pull on your hand to tell if you can resist. That determines if you have eccentric contractions.
2. If you have control at any point, start there and move it back and forth, thousands to millions of times.
3. If that doesn't produce anything it's time to go to the dead brain recovery options - these are not really proven yet and some can be quite dangerous(videos and mirrors)
    a. Mental imagery
    b. Passive movement
    c. Mirror therapy
    d. Thermal therapy
    e. Action observation
4. If 3 works go back and repeat 1 and 2.

Remember, this is not for personal use, ask your doctors and therapists for validation first.

If your doctor or therapist has given you something better, please post it, it must be worth a lot since it is not public information.

A Hybrid Controller with Chedoke-McMaster Stroke Assessment for Robot-Assisted Rehabilitation

See if your therapist has any way to use robotics or if they even know about this stuff.
http://www.sciencedirect.com/science/article/pii/S1877705812026227

Abstract

Amongst the major challenges in post-stroke rehabilitation are the repetitiveness nature of rehabilitation procedure, and the accessibility of therapists for long-term treatment. In manual rehabilitation procedure, the patient is subjected to repetitive mechanical movement of the affected limb by the therapist. In one of the techniques called active-assist exercise, the subject moves his affected limb along a specified trajectory with the therapist guiding the motion. The therapist gives some assistance to the subject to complete the course if deemed necessary and the procedure repeats. The significant advantages of using robots in assisting rehabilitation are its efficiency and it is fatigue free. The robots however need to be developed to have the capability of human therapist in providing the rehabilitation more naturally. In this paper, the work focuses on developing a new framework for the robot controller system. In particular, a low-level controller, which is in the form of force controller based on impedance control theory is discussed. The controller is capable of governing the active-assist exercise through autonomous guidance during the therapeutic procedure based on the Chedoke-McMaster stroke assessment method.

Endonuclease VIII-like 1 (NEIL1) promotes short-term spatial memory retention and protects from ischemic stroke-induced brain dysfunction and death in mice

Another one to talk to your researcher about.
http://www.pnas.org/content/early/2012/08/22/1204156109.short

Abstract

Recent findings suggest that neurons can efficiently repair oxidatively damaged DNA, and that both DNA damage and repair are enhanced by activation of excitatory glutamate receptors. However, in pathological conditions such as ischemic stroke, excessive DNA damage can trigger the death of neurons. Oxidative DNA damage is mainly repaired by base excision repair (BER), a process initiated by DNA glycosylases that recognize and remove damaged DNA bases. Endonuclease VIII-like 1 (NEIL1) is a DNA glycosylase that recognizes a broad range of oxidative lesions. Here, we show that mice lacking NEIL1 exhibit impaired memory retention in a water maze test, but no abnormalities in tests of motor performance, anxiety, or fear conditioning. NEIL1 deficiency results in increased brain damage and a defective functional outcome in a focal ischemia/reperfusion model of stroke. The incision capacity on a 5-hydroxyuracil–containing bubble substrate was lower in the ipsilateral side of ischemic brains and in the mitochondrial lysates of unstressed old NEIL1-deficient mice. These results indicate that NEIL1 plays an important role in learning and memory and in protection of neurons against ischemic injury.

Neuron-Specific Prolyl-4-Hydroxylase Domain 2 Knockout Reduces Brain Injury After Transient Cerebral Ischemia

I'm sure  your researcher can explain how this matches up with other hyperacute therapies and what the plan is going forward.
http://stroke.ahajournals.org/content/early/2012/08/24/STROKEAHA.112.669598.abstract

Abstract

Background and Purpose—Numerous factors involved in the adaptive response to hypoxia, including erythropoietin and vascular endothelial growth factor are transcriptionally regulated by hypoxia-inducible factors (HIFs). During normoxia, prolyl-4-hydroxylase domain (PHD) proteins hydroxylate HIF-α subunits, resulting in their degradation. We investigated the effect of neuronal deletion of PHD2, the most abundant isoform in brain, for stroke outcome.

Methods—We generated neuron-specific Phd2 knockout mice and subjected animals to systemic hypoxia or transient middle cerebral artery occlusion. Infarct volume and cell death were determined by histology. HIF-1α, HIF-2α, and HIF target genes were analyzed by immunoblotting and real-time polymerase chain reaction, respectively.

Results—Neuron-specific ablation of Phd2 significantly increased protein stability of HIF-1α and HIF-2α in the forebrain and enhanced expression of the neuroprotective HIF target genes erythropoietin and vascular endothelial growth factor as well as glucose transporter and glycolysis-related enzymes under hypoxic and ischemic conditions. Mice with Phd2-deficient neurons subjected to transient cerebral ischemia exhibited a strong reduction in infarct size, and cell death of hippocampal CA1 neurons located in the peri-infarct region was dramatically reduced in these mice. Vessel density in forebrain subregions, except for caudate–putamen, was not altered in Phd2-deficient animals.

Conclusions—Our findings denote that the endogenous adaptive response on hypoxic–ischemic insults in the brain is at least partly dependent on the activity of HIFs and identify PHD2 as the key regulator for the protective hypoxia response. The results suggest that specific inhibition of PHD2 may provide a useful therapeutic strategy to protect brain tissue from ischemic injury.

No. 2 Acupuncture treatment programs for post-stroke motor rehabilitation in community hospitals: study protocol of a multicenter, randomized, controlled trial

I moved this to get it out of the top post.
Why are people even reading this unsupported crap? I have more important posts you should be reading.
 See here for lack of evidence.  Why is the NIH even publishing this stuff?
http://www.ncbi.nlm.nih.gov/pubmed/22587973

Abstract

BACKGROUND:

Stroke is responsible for increasingly high rates of mortality and disability worldwide. Approximately two million people suffer from stroke for the first time in China each year. The high incidence (50%) of post-stroke disability brings a heavy burden to patients and their caregivers. Acupuncture has been widely used in the communities for post-stroke rehabilitation in China.(who cares? Is it effective?, research?) The objective of this trial is to apply our acupuncture research achievement to treatment and evaluation of post-stroke hemiplegic patients in community.

METHODS AND DESIGN:

A multicenter, randomized, controlled trial will be performed in Longhua Hospital and a number of community health service centers in Shanghai. A total of 124 patients (estimated sample size) with post-stroke hemiplegia will be randomly divided into an acupuncture group and a control group. The patients undergoing randomization should be stratified according to National Institutes of Health Stroke Scale score at baseline. Within the acupuncture group, different acupuncture protocols are administered to patients with flaccid paralysis or spastic paralysis based on the Ashworth Scale. Patients in the acupuncture group will also be treated with comprehensive rehabilitation therapy.(dual treatment,which one works?) The control group will be treated with comprehensive rehabilitation therapy only. The primary outcome measures are the Simplified Fugl-Meyer Motor Scale, the Modified Barthel Index, and the Burden of Stroke Scale. Secondary outcome measures are the modified Rankin Scale, the modified Ashworth Scale and the Stroke Scale of Traditional Chinese Medicine. Outcome measures will be performed after 4 and 8 weeks of treatment. The patients will be followed up after 6 months.

DISCUSSION:

The results of this study are expected to demonstrate that our standardized acupuncture protocol for treating and evaluating post-stroke hemiplegic patients will improve motor function and lessen the burden of post-stroke patients within the communities. This will provide the evidence to support successful translation of acupuncture therapy for post-stroke hemiplegic patients in community hospital use.

TRIAL REGISTRATION:

This trial was registered in Chinese Clinical Trial Registry with the registration number ChiCTR-TRC-11001347.