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Archive for the ‘cerebral circulation stroke’ Category

The  major  issue of contention is fear of conversion of pure ischemic stroke into hemorrhagic stroke .

But here is a catch if you worry about that  . . . who will worry about recurrent emboli from heart ?

References

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678170/pdf/nihms104070.pdf


anti coagulation following cardio embolic stroke

aha stroke guidelines 2007

aha stroke guidelines

Recommendation for heparin

aha antiplatlet agent

Recommendation for anti-platelet drugs

I think  the 2007   stroke guidelines are the latest .Even after going  through the guidelines  I am not really clear about the answer for the question posed in this article.

One more thing   I  (mis) understood was  ,  In acute stroke thrombolysis seems to be safe  . . . Heparin seems to be dangerous ?  Is that true ?  It defies logic for  me !

One possible explanation is thromolysis is a emergency single shot salvaging  process . While prolonged heparin will ooze blood into Infarct ! This is exactly is the reason  in   tPA   should not be   followed up with heparin  in acute strokes.(unlike STEMI  where a follow up heparin is a must )

Regarding prevention of recurrent emboli , we need to bother about whether it is predominately platelet rich or RBC rich

Readers may contribute to find the exact answer !

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Thrombolysis in acute stroke

  1. rtPA is indeed useful in acute Ischemic stroke
  2. Elderly need not be excluded (Even > 80y)
  3. Time window : It definitely works up to 4.5 hours and vary likely  to be effective up t0 6 hours.

We are gradually widening the time window  , which was  3 hours a decade ago .It may soon catch up with STEMI window of 12 hours ! ( Mitochondrially myocytes  are not vastly different from cerebro-cytes ! )

So ,  the current role of   of thrombolyis for stroke  is best answered by the editorial  accomplishing  this article !

“The role of stroke and emergency physicians is now not to identify patients who will be given rt-PA, but to identify the few who will not.”

Reference :   A Lancet Break through

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2960738-7/fulltext

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2960768-5/fulltext

Coming soon

  • By the way ,  rTPA is prohibitively costly for common world citizens . Please tell us about streptokinase in stroke ? Does the poor cousin match the rich ?
  • Do we have primary cerebral angioplasty ?

 

Please read the comment form Dr  Anthony Andrew Bell it is a must read !

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Is there  an  anginal equivalent  in cerebral circulation ?

Coronary Ischemia produce  angina . . . Cerebral  ischemia do not produce  corresponding   ischemic cerebral pain ! Why ?

Exertional angina  is the dominant  event when coronary artery is  stenosed  . When cerebral artery is stenosed   exertional  head ache do not occur .  So , how does brain respond to  exertional  ischemia ? (EST is also  a stress  to our  cerebral circulation  .  If only we record  EEGs  during treadmill we will  know the truth !)

But in the clinical setting  ,  we are not only surprised by lack of head ache during cerebral  ischemia   , even  exertional   giddiness  is not a common presentation . Instead ,  brain  primarily   respond to ischemia  with focal neurological  deficit instead  of  generating  pain within the skull. This is often referred  to as TIAs .

But,  chronic ischemia  has its effect in the form of lacunar  infarct with its  clinical counter part  – vascular  dementia.

Electrical rhythm  disturbance   like   Ischemic cerebral  arrhythmia are also  known to occur .

The reason for these coronary vs cerebral stenosis behavior is  not clear . Number of possible explanations can be offered.

  1. Paradoxically ,   in spite  of  brain  being a central neurological  command , by itself  has less pain receptors  especially to ischemia
  2. The hypoxic threshold for cerebral cells may exceed many fold to  that of myocytes.
  3. Cerebral  auto-regulation is more developed than coronary regulation.
  4. The circle of  Willis  , though   do not help  much when individual  cerebral arteries are  occluded  suddenly , it does  play  a role in balancing cerebral circulation  at times of chronic  low flow states and  ischemia .
  5. Finally , even in physiology  many of us are comfortable with  little  brain function. One estimate says we  hardly  use   2-3 % of  brain’s processing power (Like our computer  CPU) .Hence  intellectual , deterioration  are  very  late  phenomenon of cerebral ischemia.

 

Reference 

How often head ache occur in  acute stroke ?

It occurs in less than 15 %  in acute ischemia .( In chronic ischemia it is very rare ? non existent ?)

The exact source of pain is not clear .

A stretch induced pain , dull infarct zone pain, cerebral edema induced transient  ICT may also contribute .

http://onlinelibrary.wiley.com/doi/10.1111/j.1526-4610.2009.01440.x/abstract

It  was a real surprise ,  when I found this journal exclusive for  head aches !

 

What is the mechanism of vascular head ache ?

It is ironical  ,  more often an excess blood flow by inappropriate vasodilatation that cause many episodes of vascular head ache . These confirm the complexities of  ischemic vs non ischemic pain within the brain .

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