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visayanbraindoctor
Member since Jun-04-08 · Last seen Dec-05-16
Good Day to All! Ma-ayong adlaw sa tanan. And my thanks to CG.com for this excellent website. Salamat CG.com. Opinions:

1. World Chess Championship

The true Chess World Champions are the holders of the Traditional Title that originated with Steinitz & passed on in faithful succession to Lasker, Capablanca, Alekhine, Euwe, Botvinnik, Smyslov, Tal, Petrosian, Spassky, Fischer, Karpov, Kasparov, Kramnik, Anand, and Carlsen. The sacredness of this Title is what makes it so valuable.

And how does one become the true Chess World Champion? In general, by beating the previous Titleholder one on one in a Match! Matches are preferred over Tournaments because of the Tradition of the WC Succession & because the chance for pre-arranging a Tournament result is more likely. The only exceptions to this rule:

A. In case where the Candidates and World Champion participate in an event that all the participants agree to be a World Championship event because of extraordinary circumstances.

Thus, the 1948 World Championship Tournament was justifiable because of the death of the Title holder Alekhine.

Likewise, the 2007 WC Tournament was justifiable under the extraordinary circumstances of the Chessworld trying to heal its internal rift over the 1993 Kasparov Schism. Anand himself became the World Champion in this 2007 Tournament & not in 2000 when he won a knock-out FIDE Tournament. Caveat: Some chess fans deem the 2007 WC Tournament as illegitimate, considering that Anand became the World Champion only in 2008, when he beat the previous Titleholder Kramnik in a WC match. From this perspective Anand only became the Undisputed World Champion in 2008.

Karpov lost his Title to Kasparov in 1985, & never regained it in the 1990s events that FIDE labeled as 'world championships'. All solely FIDE Champions that emerged outside WC Traditional Succession elaborated on above, strong as they were, were not true World Champions (eg., Bogolyubov 1928, Khalifman 1999, Ponomariov 2002, Kasimdzhanov 2004, Topalov 2005).//

B. In case the previous Titleholder defaults an event that the Chessworld largely deems as a World Championship event in the Tradition of the World Championship Succession. Thus, Karpov was the true successor to Fischer who defaulted their WC Match in 1975.

2. The strongest chess events in different eras of chess history?

Because of the brain's limitations explained below, the best professional (amateurs don't matter much in top level chess) chess players of each generation beginning in the Lasker era have always played at a similar level - near the maximum allowed by human standards. Now there are larger cohorts of chess professionals post WW2 than preWW2 thanks to government state funding in the Soviet era and presently corporate funding. The result is that large preWW2 tournaments had numerous 'bunnies', relatively weak players. By the Kasparov era, super-tournaments that featured most of the top ten, and no bunnies, had became more common. However, the top 4 or 5 since Lasker's time have always been very strong.

Consequently the smaller the top-player-only tournament, the stronger it gets. For any era. If there was a double round robin tournament in 1914 featuring Lasker, Capablanca, Alekhine, and Rubinstein, and no other, it would be as strong as any present day super-tournament.

Now weed out everyone except the two strongest players in the world. What we (usually) get is the chess World Championship match.

There has been talk of elite tournaments, composed only of the strongest top masters and no weaker bunnies replacing the World Championship match in prestige, probably because of the assumption that they would be the strongest chess events possible. False assumption. The strongest chess events in chess history generally have been World Championship matches. Even the strongest masters in each generation usually do not match the world champion and challenger in chess strength. In a World Championship match, the contestant has to meet the monster champion or challenger over and over again, with no weaker master in between. Capablanca vs Lasker 1921 was just as strong a chess event as the recent Carlsen vs Anand 2013, and far stronger than Zurich 2014. (Imagine having to play 14 straight games with a computer-like errorless Capablanca at his peak.)

3. The strongest chess players in chess history?

IMO the 1919 version of Capablanca & the 1971 version of Fischer, both of whom played practically error-free chess, are it; updated in opening theory, they should beat anyone in a match.

If computers were self-aware, I have no doubt that they would unanimously choose the 1916 to 1924 Capablanca as the strongest chess player in history. And please no red herring remark that Capa played only 'simple' chess. This young Capablanca played some of the most complicated, sharp, double edged, and bizarre positions possible; and played them without making a single losing error (and by all accounts with unsurpassed quickness), something that has always befuddled my mind when I got to peruse through his games.

We have to take this question in the context of the limits of the human Anatomy and Physiology. A concrete example would be the one hundred meter dash. The human body is designed such that the limit it can run is about 9 seconds. In order for a human being to run faster, we would have to redesign the human anatomy into that of say a cheetah. One can rev up the human Anatomy and Physiology, say with steroids, but this regimen would hit an eventual Stonewall too; the same way that we could rev up human proficiency to learn openings with computer assistance.

Since the Nervous System has physiological limits (example of a limit- neuronal action potential speed don't go up much more than 100 m/s) and so limits the human chess playing ability, increasing the number human chess players, thus expanding the normal curve of players, simply creates more possibilities of players playing like a Fischer in his prime, but will not create a mental superman who plays chess at computer levels. This explains why human and computer analysis indicate that Lasker was playing on a qualitatively similar level as more recent WCs.

'Worse' in chess, any computer assistance ends once the opening is over. After a computer-assisted opening prep, every GM today has to play the game the way Lasker did a hundred years ago, relying on himself alone, with the same fundamental chess rules and chess clock. An Encyclopedic opening repertoire is not a necessity to be a top player. In fact, there are World Champions who did not do deep opening prep; they just played quiet but sound openings that got them into playable middlegames and then beat their opponents in the midlegame or endgame. Just look at Capablanca, Spassky, Karpov, and now Carlsen.

Because of subconscious adherence to the narcissistic generation syndrome, the belief that everything that is the best can only exist in the here and now, many kibitzers would not agree to the above theses. While it is true that there have been more active chess professionals and consequently larger cohorts of top chess masters on a yearly basis since WW2 thanks to Soviet state funding and present corporate funding, the very top chess masters since Lasker's time have always played at a similar level- within the limits imposed by the human brain. There is no physical law that bars a pre-WW2 chess master from playing chess as well as today's generation. The human brain has not changed in any fundamental manner in the past tens of thousands of years.

4. The greatest chess players in history?

A related question is who is the greatest chess player in history. The answer depends on the criteria one uses. Since I place great emphasis on the ability to play world class chess for the longest period of time, Lasker would be it. He was playing at peak form from 1890 age 22 (when he began a remarkable run of match victories over Bird, Mieses, Blackburne, Showalter, and culminating in his two massacres of Steinitz) until 1925 at age 57 (when he nearly won Moscow after winning new York 1924). Kasparov (high plateau from 1980 to 2005) and Karpov (high plateau from 1972 to 1996) would follow. (At their very peak though, I believe that Kasparov was stronger than Karpov, and both were stronger than Lasker; and the peak Capablanca and Fischer were stronger than any of them.)

5. Computers vs Humans, who is stronger?

Another related question is how history's top masters would fare against computers. It's obvious from Kasparov's time that computers would totally crush them all. Opening knowledge would not matter much. Computers swamp human opponents in the middle game, simply by calculating more variations more rapidly by several orders of magnitude. Peak Capablanca probably would have the best score among humans. Talk about another level of playing is fans' subjective and IMO wrong words for their favorite players, unless one talks about chess computers. Chess computers do play at a higher level.

6. On the game and chess players young and old, past and present:

The proposition that an older player would not be able to adjust to the openings and methods of a younger generation is false, as evidenced by the observation of strong masters whose careers happened to span generations beating the tar out of weaker masters of the next generations. Lasker provides a classic example; he was beating Mieses, Blackburne, and Steinitz in the 1890s, and crushing masters versed in the hyper-modern teaching of controlling the center indirectly- Reti, Bogolyubov, and Euwe in the 1920s. In more recent times, we have Victor the Terrible, who learned most of his chess in the 1940s and 1950s, whom we have seen competing successfully with the so-called computer generation even at an advanced age.

This 'inter generational knowledge/theory leveling phenomenon' holds true today and will probably still hold true two decades from now. As of the end of 2015, Kramnik, Anand and Topalov, and a couple of years ago Gelfand are living smoking gun proofs that the speculation that the older generation cannot adopt to newer openings is false. Older players have always adapted and will always adapt to the latest openings in the vogue. The present day young players will do the same 20 years from now, faced with a future generation of rising chess players.

The notion that computers are more advantageous to younger players IMO is not quite right. Younger players should have more energy and stamina in studying chess openings and endgames for long hours everyday compared to older players without computers, but the use of computers would tend to make the learning process easier for every one including the older ones.

As a corollary, computers also make it easier today for very young players in their early teens to peak at a younger age than in past eras, although they tend to level off in their early 20s to their high plateau, defined by their inborn talents and determination.

In brief. computers tend to level chess learning for everyone, young and old.

This is not a rigid rule. The best games I have ever seen played by a 12-13 year old are Capablanca's; and Tal, Karpov, and Kasparov reached their high plateau in their early 20s in a computer-less era, similar to computer age Carlsen. However let it be noted that Carlsen reached his peak sidestepping intensive computer-prepped tactical openings and beating his competitors in the old fashioned way in the middlegame and endgame. These masters peaked early not because of computers by because of their immense chess talent. Perhaps normal rules do not apply to these geniuses.

Another false notion is that the nature of the middlegame today is somehow different from the middlegame in the past. The easiest way to prove the wrongness of this proposition is by observing CG's daily puzzles. Do not peek at the names of the players that played these puzzles, and don't look at the dates. Can you glean from the middlegame play and combinations in the puzzles the date they were played? You can't. You would not know if it was played in 2016, 2000, 1950, or 1900. Chess combinations don't just suddenly change their stripes just because a hundred years have passed.

Another observation is that when the best masters of the past, Lasker, Capablanca, and Alekhine met the occasional 'modern' structures of the Sicilian Scheveningen and Dragon, KID, Modern Benoni, Benko Gambit, they played strategically perfectly, in just the way these opening structures should be played. So how did these masters play openings and the resulting middlegame structures that are deemed incomprehensible to them by some of today's dogmatically 'modern' kibitzers? The answer is that chess rules and principles have not changed. Center, rapid development, open files and diagonals, holes, weak pawns, piece activity, initiative and attack, positional sacrifices and all types of combinations were as familiar to them as to us.

Note that it is the frequencies of a few middlegame pawn structures that have changed since WW2. Not the Ruy Lopez or QGD, but obviously Sicilians and KIDs are much more common post-WW2. Since so many games nowadays begin with the Sicilian and KID, people associate these with being 'modern' (which is a rather vague undefined term IMO). But certainly Lasker and Capablanca understood the middlegame principles behind them and when they did get these positions they played them excellently, like the top masters they are.

Moreover, Keres is another smoking gun, bomb proof evidence of the fallacy of Watson's speculation that 'the best players of old were weaker and more dogmatic than the best players today', and Larsen's assertion that he would crush everyone in the 1920s. The glaring fact is that Keres is a pre-WW2 master who began his career in the late 1920s, and played competitively up to the 1970s, and he did learn (and contributed) to the newer opening variations (the most famous of which is the Keres attack which he invented in 1943). The ideal way for Watson and Larsen to prove their statements is to beat a top pre WW2 master such as Keres. They failed. Tellingly enough an aging Keres beat both a rising Watson and a peak Larsen when they happened play each other.

7. On ratings:

Elo ratings reflect relative and not absolute chess strength.

Chessplayers are naturally arranged in populations partitioned by geopolitical regions & time periods that have infrequent contacts with one another. Within such a population, players get to play each other more frequently, thus forming a quasi-equilibrium group wherein individual ratings would tend to equilibrate quickly; but not with outside groups. With caveats & in the proper context, FIDE/Elo ratings are simply fallible descriptors & predictors of an active player's near-past & near-future performances against other rated players, & only within the same quasi-equilibrium group.

As corollaries: the best way to evaluate a player's strength is to analyze his games & not his ratings; one cannot use ratings to accurately compare the quality of play of players from the past and present, or even the same player say a decade ago and today; & care should be taken in the use of ratings as a criterion in choosing which players to seed into the upper levels of the WC cycle. All the above often entail comparisons between players from different quasi-equilibrium groups separated by space and/or time.

Regarding inflation deniers, they imply that Elo ratings reflect absolute and not relative chess strength. Professor Elo himself would condemn their view. If the top 20 players were to suffer a serious brain injury and begin playing like patzers, but play no one else for the next decade, they would more or less retain their 2700s ratings, although they would be playing terrible patzerish chess.

8. Best Qualifiers?

The credible, fair, tried & tested Zonals - Interzonals - Candidates (with known strong players directly seeded into the Interzonals & Candidates; & here ratings may be used with caveats) over the random World Cup and the elitist Grand Prix. If possible long Candidate matches and 16 to 24 game World Championship matches. However, with the passing of the state-funded chess era of Soviet times, I begin to doubt if the strict money guzzling qualification process above can be re-installed.

9. The 1993 Chess Rift and Kramnik:

Regarding the Rift in the chessworld after Kasparov split in 1993, I believe that Kramnik has done more than any other individual in helping heal it by concrete actions - agreeing to a WC Match with Topalov in 2006 & not walking out when he could have done so with the support of most of the world's top GMs after getting accused of cheating; & agreeing to Defend his Title in a WC Tournament in 2007, the first time a living Titleholder has agreed to do so in chess history. My eternal gratitude to him.

10. Finances of a would-be Challenger:

Regarding all kinds of problems chessplayers outside of Europe & the USA face in their quest for the Title, Capablanca & Anand have proven it's possible for a non-European non-USA chessplayer to be World Champion; but apparently only if you have the chess talent of a Capablanca or Anand! For others, I guess they would have to try to get monetary support & good seconds somewhere to have some hope for a Title shot.

11. Ducking a World Championship re-match:

Alekhine vs. Capablanca - Not definitively resolved. If pushed, I would tend to favor Capablanca given that pre-WW 2, there was no definitive cycle to choose the Challenger &, after all is said and done, it was the Champion who set the conditions & who chose his Challenger. AAA could & should have chosen Capa; & there was ample time, more than a decade, to do so before WW2. On the other hand, Capa's pride may have caused him to behave arrogantly & thus offend AAA. The issue is very much debatable. //

Kramnik vs. Kasparov - For me, it's resolved. Kudos to Kramnik for trying his best to install a decent Qualifying Event. Kasparov for his reasons clearly did not want to go through the Qualifying Event that he himself had pledged before losing his Title; & did not even seem serious in playing the solely FIDE champions. Why? I can only speculate that Kasparov would rather retire than risk a loss in a Qualifier or a match to either a FIDE champion or to Kramnik. If he regained his Title, he would be the greatest Champion in history, but there was risk involved. If he retired, he would still be the greatest Champion in history, but there would be no risk involved. Kasparov chose the latter & no one should blame him for that decision; & more so don't blame Kramnik!

12. Predictions for Hypothetical World Championship Matches:

Lasker vs. Pillsbury, Rubinstein, Maroczy - Lasker wins 2, loses 1 match //

Lasker vs. Capablanca (inexperienced) 1914 - Lasker close win //

Capablanca (not overconfident & not having TIAs) 1929 to 1937 vs. Alekhine or any other master - Capa win //

Alekhine (sober & prepared) vs. Capablanca (w/ severe HPN & numerous past strokes), Botvinnik, Keres, Fine, Reshevsky, Flohr 1939 - Alekhine win //

Alekhine (alcoholic, ill, & depressed) vs. Botvinnik 1946 - Botvinnik win //

Fischer (inactive for 3 years) vs. Karpov 1975 - Karpov win//

Kasparov vs. Shirov 2000 - Kasparov win. (But GKK should still have given it to Shirov. And don't blame Kramnik. Had Kramnik declined, GKK would have chosen another; & Shirov would still be frustrated.)

---

I have opened a <'multi-experimental' forum> below. Its nature is that of several secret social and psychological experiments, whose objectives and parameters, and the rules that follow, are strictly defined and which I may or may not reveal. Readers of this forum might be able to deduce some of these rules. Accordingly messages shall be retained or removed with or without explanation, even those from my dear friends here in CG, although I am making it clear here that absolutely no offense is intended to any one in this experiment. I may or may not respond to certain questions and messages, also according to the rules. To my friends: Please bear with me in this matter. There can be a certain amount of disinformation and propaganda in the messages that are retained.

The title of this <'multi-experimental' forum> is:

Biased Journal of a Fourth World Brain Operator

Some abbreviations

ASDH = Acute Subdural Hematoma, SDH incurred recently, usually less than a week

BT: Blood Transfusion

CAB = Continuous ambubagging

CiH = the public City Hospital

CNS = Central Nervous System

Craniectomy = neurosurgical procedure that involves removing a portion of the skull

CSDH = Chronic Subdural Hematoma, SDH that is more than two weeks old

CSF = Cerebrospinal Fluid

CVA = Cerebrovascular accident = stroke

EBRTL: Equally briskly reactive to light.

EDH = Epidural Hematoma, blood above the dura mater, the outer covering of the brain, and beneath the skull.

ETT = Endotracheal tube (for airway purposes)

EXTUBATION: the removal of a tube especially from the larynx after intubation—called also detubation.

FWB = Fresh Whole Blood

HCP = Hydrocephalus, too much CSF in the brain's ventricular system

INTUBATE: To put a tube in, commonly used to refer to the insertion of a breathing tube into the trachea for mechanical ventilation

MF = Motorcycle Fall

NGT = Nasogastric tube (for feeding purposes)

NOD = Nurse on duty

NRTL: Non reactive to light.

NSS: Normal Saline Solution

Oracle = personification of the CT (computed tomography) scan.

ProvH = the public Provincial Hospital

PrvH = Private Hospital. There are three main ones. So PrvH 1, PrvH 2, PrvH 3.

SDH = Subdural Hematoma, blood beneath the dura mater.

SOL = Space Occupying Lesion

SQ = Subcutaneous tissue layer of the skin or scalp

SRTL: Slowly or sluggishly reactive to light.

Tracheostomy = a surgical procedure to create an opening through the neck into the trachea (windpipe)

Uneventful day = Most likely still a busy day, making daily rounds in the hospitals, following up post-op patients, seeing patients in the OPD, answering referrals, admitting all kinds of patients in the hospitals; nevertheless a day in which nothing interesting has caught my attention.

Witching Hour Admissions or Referrals = 12 midnight to 5am.

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Chessgames.com Full Member

   visayanbraindoctor has kibitzed 8774 times to chessgames   [more...]
   Dec-05-16 twinlark chessforum
 
visayanbraindoctor: <twinlark> Admittedly, I don't know much of anything about National Front's Marie Le Pen. (I didn't even know how she looks like.) Here is a video from her interview with BBC. A must see IMO, as she clearly enunciates her views. (Now I know how she looks like.) ...
 
   Dec-05-16 Annie K. chessforum
 
visayanbraindoctor: ‘Here’s another theory,’ Bodhi added. ‘The essential soul of Elam is not in your body. Your body is just a radio that receives broadcasts from your essence somewhere more or less permanently preserved in the Tela. You die. Elam’s fundamental essence transmits broadcasts ...
 
   Dec-03-16 visayanbraindoctor chessforum
 
visayanbraindoctor: 3 December 2016. 24F, passenger on an SUV, hit a truck. She came in GCS 7 with anisocoria, right pupil larger than the left. This is a real emergency. The intracranial hematoma presses on the temporal lobe's uncus, which begins to herniate into the tentorial notch, ...
 
   Nov-30-16 Carlsen - Karjakin World Championship (2016) (replies)
 
visayanbraindoctor: My thoughts regarding the quick game tiebreakers: 1. Ideally the Champion must have beaten the old one to be Champion. 2. I hate these FIDE quick game tie-breaks to decide the Classical Champion. My suggestion (which I have previously posted on other pages) if the World ...
 
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Kibitzer's Corner
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Oct-26-16
Premium Chessgames Member
  visayanbraindoctor: 21 October 2016.

48M, motorcycle fall, driver, by himself, GCS 12. CT scan showed brain fungating out of an open right frontal depressed fracture.

Pre-op I had one unit of FWB BT'ed.

(Left frontal craniectomy, evacuation of contused brain, repair of dura with periosteum, bone transplant to left hemi-abdomen SQ layer. 10/21/16 10:15 am to 12:20 pm. No BT.)

I got a big shock. Pre-op the patient's head was heavily and tightly bandaged, and I did not remove it for fear he would bleed from the underlying scalp laceration.

During the operation, I found out that the depressed fracture was located on the left frontal bone, not on the right as the CT scan showed. Fortunately I had done a bicoronal incision, a cut from ear to ear behind the hairline following the coronal suture, which exposed both frontal bones. If I had just made a right sided incision, I would have had to make another one on the other side.

Afterward I went to the hospital where the CT scan was done and informed the radiologist about this potentially disastrous incident. He told me they would check the CT scan machine's settings.

Oct-26-16
Premium Chessgames Member
  visayanbraindoctor: 23 October 2016.

Entry 1.

At witching hour I was informed <19 October 2016. 34M, a Caucasoid male from UK, motorcycle fall, driver by himself, GCS 3.> had died.

Entry 2.

58M, pedestrian, hit by a motorcycle. GCS 7. Right hemiparesis.

(Left parietal craniectomy, evacuation of epidural hematoma, bone transplant to left hemi-abdomen SQ layer. 10/23/16 3:47 to 4:20 pm. No BT.)

He was more awake post-op. He'll probably survive.

Oct-26-16
Premium Chessgames Member
  visayanbraindoctor: 24 October 2016.

50M, motorcycle fall, backrider, hit by a truck. GCS 6, and aspirated.

I had intubated the patient yesterday in the ward. The family procured OR needs only today.

(Bifrontal craniectomy, evacuation of acute subdural hematoma right hemisphere, bone transplant to left hemi-abdomen SQ layer. 10/24/16 11:33 am to 12:42 pm. No BT.)

(Tracheostomy. 10/24/16 12:52 to 1:04 pm.)

Still comatose post-op, I told the family that they had to get him into a private ICU equipped with a ventilator machine, or he would probably die, because there were none in the public CiH. As it was, they were manually ambubagging him continuously.

Oct-26-16
Premium Chessgames Member
  visayanbraindoctor: 25 October 2016.

<50M, motorcycle fall, backrider, hit by a truck. GCS 6, and aspirated.

(Bifrontal craniectomy, evacuation of acute subdural hematoma right hemisphere, bone transplant to left hemi-abdomen SQ layer. 10/24/16 11:33 am to 12:42 pm. No BT.)

(Tracheostomy. 10/24/16 12:52 to 1:04 pm.)

Still comatose post-op, I told the family that they had to get him into a private ICU equipped with a ventilator machine, or he would probably die, because there were none in the public CiH. As it was, they were manually ambubagging him continuously.>

The relatives had no money to transfer to private hospital ICU with a ventilator. The patient died early morning.

Oct-26-16
Premium Chessgames Member
  visayanbraindoctor: 26 October 2016.

14M, motorcycle fall, driver, by himself.

I had admitted him 3 days ago, and he seemed fine, GCS 15, with only a small parietal epidural bleed of about 20 cc. No need to operate.

This morning, he suddenly deteriorated to GCS 7. I had 150 cc of Mannitol given fast drip, and repeated the CT scan. The EDH had grown to about 60 cc.

The family had no money for an operation in the private hospital that 14M was admitted in. So I had to transfer him to the public CiH, after warning them that the transfer might result in a potentially fatal delay.

I went simultaneously with the patient in the afternoon to the public CiH. Then I had to wait in the hospital for 6 hours, for the other scheduled operations to finish. I gave another dose of Mannitol 4 hours after the last one was given. Fortunately the patient did not further deteriorate pre-op.

(Left parietal craniectomy, evacuation of epidural hematoma, bone transplant to left hemi-abdomen SQ layer. 10/26/16 7:15 am to 7:45 pm. No BT.)

Oct-29-16
Premium Chessgames Member
  visayanbraindoctor: 29 October 2016.

A large scalp laceration on a small child can result in life-threatening exsanguination. But not in adults, or so I believed. So when 26F (on a tricycle that got hit by a truck) was referred to me with BP 60/40 and HR more than 120 (signs of hypovolemic shock), I assumed the blood loss was coming from injured internal organs or limb fractures.

I had 300cc of NSS fast dripped, and with BP back to 100 systolic, I proceeded to clean and suture a 25cm scalp avulsion on 26F's fronto-parietal scalp in the ER in four minutes (the ER ROD had previously had the area shaved, and then decided she could no suture it herself, referring to me instead).

There did not seem to be any further sign of abdominal or chest injury, nor were there any fractures. I referred to a General Surgeon just to make sure.

The GS concluded the same thing. I had 1 unit FWB BT'ed. Later CXRs and abdominal ultrasound turned out negative.

So, contrary to my old opinion, a large bleeding scalp laceration may cause life-threatening hypotension even in adults.

Oct-31-16
Premium Chessgames Member
  Jonathan Sarfati: Important to know this about scalp lacerations. I didn't realize that a skin injury alone could lead to such catastrophic loss.
Nov-01-16
Premium Chessgames Member
  visayanbraindoctor: <Jonathan Sarfati: Important to know this about scalp lacerations. I didn't realize that a skin injury alone could lead to such catastrophic loss.>

In children, huge scalp lacerations are often life threatening, but this is the first one I have seen such a case in the ER in an adult. Perhaps the fact that the woman was small of stature contributed to it. I estimate that she is under 5 feet tall and thin.

The scalp is the most vascular part of our integumentary system. There are large arteries that richly vascularize it, and if severed can cause profuse bleeding. If you see a person (especially a child) in the street bleeding badly from a scalp injury, it would probably help if you wrap some tight dressing/ bandage around his head, just to minimize more blood loss. (Until a doctor can definitively suture it in the hospital, which would stop the bleeding permanently.) I think such a procedure can save lives in some scalp injury cases.

Nov-02-16
Premium Chessgames Member
  ketchuplover: I think the creation of chess rating systems has been at least slightly detrimental to the PURE enjoyment of chess.

If you reply please do so in my forum. Thank you.

Nov-03-16
Premium Chessgames Member
  ketchuplover: Thanks for your erudite response. I asked Judit Polgar a similar/related question as part of the global chess festival. I coulnd't get online the day of the festival and still haven't seen her response.

Hope the coverage of Carlsen v. Karjakin here is worthy of a WC match.

Nov-04-16
Premium Chessgames Member
  visayanbraindoctor: <ketchuplover> Waay sapayan. You're welcome.
Nov-04-16
Premium Chessgames Member
  visayanbraindoctor: 4 November 2016.

28M, motorcycle fall, driver, by himself.

He was admitted a week ago in CiH, awake at GCS 15. CT scan showed a depressed fracture on his left frontal bone, with underlying pneumocephalus (air in the brain).

I assessed the family of the danger of meningitis or brain abscess, since peumocephalus indicates a communication between the brain and the exterior. It may resolve uneventfully with antibiotic treatment, but occasionally can also result in CNS infection. The family opted for conservative management. Two days ago, the patient began to experience fever and bouts of disorientation, possible signs of CNS infection. His relatives changed their minds.

(Left frontal craniectomy, repair of dura for CSF leak, bone transplant to left hemi-abdomen SQ layer. 11/4/16 3:03 to 4:02 pm. No BT.)

I found out that the patient has a dural tear that was leaking CSF into his frontal sinus. (Therefore bacteria from his frontal sinus and nasopharynx can also travel into the brain through the same hole.) I covered it with periosteum, hoping it would stop the leak. I will have to keep him in the hospital for at least another week, on 3rd generation cephalosporin antibiotic and observation for more CSF leak.

Nov-12-16
Premium Chessgames Member
  visayanbraindoctor: 8 November 2016.

42M, sudden decrease in sensorium (GCS 9) and right hemiparesis while woking in a mining area. His fellows workers did not know exactly why that happened, but a CT scan showed a basal ganglia hemorrhage of 50 cc. (Basal ganglia hemorrhages comprise approximately 60% of hypertensive hemorrhagic strokes, and usually result in permanent hemiparesis if the patient survives.)

(Left temporo parietal craniectomy, cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemi-abdomen SQ layer. 11/8/16 9:21 to 10:21 pm. No BT.)

Originally, the patient was admitted in PriH 2 four days ago. The family had no money to pay for the Operating Room fee, and so could not be scheduled for an operation. I advised them to transfer to the public CiH. He was deteriorating fast (only GCS 7) by the time I was able to operate on him.

Pre-op I found out that the head nurse had placed the bipolar forceps in a locked cabinet. It was night already, and she had gone home. I had the OR staff contact her. Someone went to her house to retrieve the keys.

I used to operate basal ganglia hemorrhages in the public hospital without bipolar in the past (until the City Government ordered for a bipolar cautery), but it's unsafe using only monopolar cautery.

Post-op patient 42M woke up. I did not have any problem since the hemorrhage had dissected from the deep gray matter through the white matter and was located only about 3 cm beneath the cortical surface. When I did a little cortisectomy, old clotted blood spilled out.

Nov-12-16
Premium Chessgames Member
  visayanbraindoctor: 9 November 2016.

<42M, sudden decrease in sensorium (GCS 9) and right hemiparesis while woking in a mining area. His fellows workers did not know exactly why that happened, but a CT scan showed a basal ganglia hemorrhage of 50 cc. (Basal ganglia hemorrhages comprise approximately 60% of hypertensive hemorrhagic strokes, and usually result in permanent hemiparesis if the patient survives.)

(Left temporo parietal craniectomy, cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemi-abdomen SQ layer. 11/8/16 9:21 to 10:21 pm. No BT.)>

When I made rounds this morning, 42M was fully awake, although still on ETT. He looked at me curiously when I approached him at bedside.

After dinner (around 9 pm), the ward nurses texted me. 42M was desaturating (O2 sat in the 80s), and hypotensive (BP 80 systolic). I ordered for them to suction secretions through the ETT and start Dopamine. This is an inotropic to increase BP; if BP falls below 70, many of these patients suffer cerebral perfusion problems and get an infarct from lack of oxygen.

The patient died after about two hours anyway. I suspect something went wrong with his ETT. (Got kinked, got clogged with mucus plug, got pushed endobronchially, or got pulled out.) Next time I will definitely do a tracheostomy in these basal ganglia patients.

Nov-12-16
Premium Chessgames Member
  visayanbraindoctor: 10 November 2016.

Weird first in a lifetime experience for me. I attended a court hearing (reckless imprudence case), testifying for one of my post craniectomy patients, WITHOUT a subpoena, upon the request of the relatives.

They talked with me two days ago, saying that my patient's case had gone to the court (he got run over by a motorcycle, and I had to do craniectomies on both sides of the skull, plus a tracheostomy, in order to save his life).

'Doc, you have to go to court.'

'Where's the subpoena?'

'The judge failed to issue one.'

'What?! I'm not going. You'll be taking me away from my private clinic, and private patients who pay me 500 hundred pesos for a consultation. Besides, I've done my duty and he lives. My oath to do good to my patients does not extend to attending court hearings.'

'OK. We'll pay you 1500 in order to compensate for your loss of income.'

That perked up my ears. I always do charity cases even if I'm not paid if public hospital patients have an objective need for my services; but you gotta admit money makes the world go rounder.

So I went to the Regional Court and testified.

'Yes, Your Honor, the patient would have died if I did not operate on him.'

'His injuries are compatible with him falling down after being hit by a motorcycle and banging his head on the road's surface.'

'Complications? Well, Sir, he incurred a right frontal contusion hematoma, which burst his frontal lobe and also resulted in a large acute subdural hematoma. So he would have residual left hemiparesis.'

'Why? Because the right motor cortex controls the left side of the body.'

The judge then had me call out the patient from the audience. Since I had not yet returned his frontal bones from where I buried them in his left abdominal subcutaneous tissue, there were two large depressions on the front of his head. The crowd in the court aahed and oohed with fascination.

This judge was a curious one. He held me up for maybe 5 more minutes asking about the Neurological aspects of brain injury. The questions obviously had nothing much to do directly with the case anymore. Finally he thanked me for the lecture and told me I could go. I thanked him too for the opportunity to educate the audience, and then left immediately for my morning rounds before he could change his mind, and ask more questions.

Nov-12-16
Premium Chessgames Member
  visayanbraindoctor: 12 November 2016.

37M, motorcycle fall, driver, by himself.

He was referred to me four days after the accident. His CT scan showed a huge 70 cc epidural hematoma. I was surprised he was still GCS 14 (drowsy, not comatose). If such cases survive for more than 3 days, they usually will survive without an operation.

However, the slightest trauma outside the hospital will kill them. If the brain swells just a little, with 70 cc of intracranial blood, there is no leeway that would prevent fatal brain herniation. Since these blood clots take two months to resolve safely, the patient is in danger of sudden death for this span of time if he leaves the hospital for home.

(Right parieto temporal craniectomy, evacuation of epidural hematoma, bone transplant to left hemi-abdomen SQ layer. 11/12/16 12:22 to 12:59 pm. No BT.)

Nov-23-16
Premium Chessgames Member
  visayanbraindoctor: 14 November 2016.

They come in pairs. Another case similar to <29 October 2016. So when 26F..

A large scalp laceration on a small child can result in life-threatening exsanguination.>

This time it was a 29M, motorcycle fall, driver, hit a van.

He had an avulsion and multiple lacerations on the left temporal scalp, which resulted in a transected superficial temporal artery transection. (Press your finger on your temple, just above and in front of your ear. If you feel a pulsation, that's your superficial temporal artery, one of the large arteries that supply the scalp.)

When I arrived at PrH1 ER, one of the nurses was pressing his fingers on the patient's temple, but he was only half-succeeding. Blood would still spurt out of the torn artery as he kept on adjusting his fingers. The BP was only 60/40. Another case of hypovolemic shock secondary to blood loss. I swiftly applied local anesthesia and sutured all the scalp lacerations, beginning with the transected artery. I had fluids fast dripped and started Dopamine.

29M, unlike 26F above, was a bgger than normal sized East Asian male, so why did he get hypotension? Was it only from a scalp avulsion? Well, he also had a left femoral fracture. A femoral fracture can cause hypotension by itself. In his case, he also had a bleeding scalp artery to add to the exanguination.

After fluids and Dopamine, his BP went back to above 90 systolic, which is on the safe side. I am planing to transfuse 3 units of blood, but he'll be OK now that the bleeding has been controlled and the drop in BP reversed.

Nov-23-16
Premium Chessgames Member
  visayanbraindoctor: 21 November 2016.

Entry 1.

28M, sudden decrease in sensorium (GCS 9) and left hemiparesis. CT scan showed a right a basal ganglia hemorrhage of about 30 cc (which often is small enough to be treated conservatively), but significant brain swelling, which is indicative of cerebral ischemia.

(As mentioned previously, basal ganglia hemorrhages comprise approximately 60% of hypertensive hemorrhagic strokes, and usually result in permanent hemiparesis if the patient survives. This guy is surprisingly young, but he is obese and already a chronic hypertensive, predisposing him to hypertensive hemorrhages.)

Unfortunately there was a 36 hour delay as the patient was first admitted in the pubic CiH. The family decided to transfer him to a private hospital, after scrounging around for money. I operated at midnight, not waiting for the dawn, as I was afraid he would herniate before then.

(Right temporo parietal craniectomy, cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemi-abdomen SQ layer. 11/21/16 1:00 to 2:35 am. No BT.)

When I opened up and removed some of the blood clot, I found out that his brain was not pulsating.

(In basal ganglia bleeds, I never remove all of the blood clot, but just around a third to two thirds of it, as there is almost invariably a firmly clotted portion that acts as a tamponade to the ruptured micro-aneurysms on the lenticulo-striate arteries that cause the hemorrhage in the first place. Releasing the tamponade causes rebleeding, usually disastrous for the patient.>

Bad prognosis. His brain could already be infarcted.

Entry 2.

I was called near midnight to PrH 2 ER. Two males in their 20s got shot in the head.

One of them was already dead when I arrived. The other was still alive. 28M was shot through the left occiput, with the bullet exiting through the midfrontal area between the eyes. (He also had gunshots on his right neck and left arm. The one on the left arm probably perpetrated into the lung because there was decreased breath sound on his right.)

In such cases, even without gunpowder burns, you know which is the point of entry because upon palpation, it feels as if the skull caved inwards. The point of exit feels as if the skull burst outwards.

28M was GCS 6, and died in less than two hours.

Nov-23-16
Premium Chessgames Member
  visayanbraindoctor: 22 November 2016.

<28M (Right temporo parietal craniectomy, cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemi-abdomen SQ layer. 11/21/16 1:00 to 2:35 am. No BT.)>

Post-op 28M woke up, eyes open. He was struggling to sit up. This does not mean that he's safe. Severely ischemic brains can still transform to infarcts.

My fears were realized when he deteriorated after 20 more hours. Repeat CT scan showed a massive right hemisphere infarct on the middle cerebral artery (MCA) territory. That's just incompatible with life; and in cases they do survive, they become completely disabled and often aphasic or abulic as well.

I don't think such patients are even self-aware anymore. Layman's term for them is 'vegetable'.

Nov-29-16
Premium Chessgames Member
  visayanbraindoctor: 23 November 2016.

Entry 1.

<28M (Right temporo parietal craniectomy, cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemi-abdomen SQ layer. 11/21/16 1:00 to 2:35 am. No BT.)>

28M suddenly deteriorated, from GCS14 to GCS 5 (decorticate posturing). A repeat CT scan confirmed a massive right hemisphere infarct middle cerebral artery territory. 28M will die after all.

Nov-29-16
Premium Chessgames Member
  visayanbraindoctor: 24 November 2016.

In the public CiH surgery ward, there are no mice or rats, or even cockroaches. That's because of the female cat that lives in the nurses station. She keep on giving birth to kittens year after year. The cat hunts the rodents, the kittens catch the cockroaches and play with them until they die. The nurses keep their lunch food covered so the cats won't steal them, and show the mama cat breastfeeding to human moms, as an example of a correct breastfeeding attitude.

A couple of months ago, the cat gave birth to three kittens. Yesterday, the cardiac board kept at the back of the nurses station fell on one of them (colored gray), crushing it to death. Mama cat licked the body and tried to breastfeed it, probably wondering why her kitten would not respond. The nurses finally shooed her off, got the body out of the station and gave it to the orderlies for disposal, cleaned up the blood on the floor.

Only two kittens left (an orangy one and a black one). They were terrified and hid in a cabinet. Today, they came out but have not resumed play behavior with each other.

Can kittens feel psychologically traumatized? These kittens certainly act like they were.

Nov-29-16
Premium Chessgames Member
  visayanbraindoctor: 25 November 2016.

19M, motorcycle fall, driver, hit another motorcycle.

He arrived in PrH2 comatose (GCS 6) two days ago. I intubated him in the ER. He was severely aspirated, and I suctioned out mixed gastric fluid and blood from his trachea.

He had an open depressed fracture on his right frontal bone that was oozing out blood and brain. I had an elastic bandage wrapped around his head in order to control the bleeding.

Surprisingly enough, these patients with large holes on their skull don't often die of brain herniation. The contused brain and hematomas typically fungate right out of the hole, so that the remaining normal brain does not get squashed. It was the same for 19M. The plan in such cases is to replace the blood loss pre-op; and during the operation remove contused brain and intracranial hematoma, and repair the dural defect.

Unfortunately, because 19m was severely aspirated, I did not expect him to survive. Because he was young and his family was cooperative, I decided to be aggressive. They could not afford a private hospital operation, so I transferred 19M to the public CiH next day while he was on continuous ambubagging.

I had two units of blood transfused pre-op.

(Right fronto- temporal craniectomy, evacuation of contusion-hematoma, repair of dura with periosteum and temporalis muscle flap. 11/25/16 10:23 to 11:26 am. No BT.)

(Tracheostomy. 11/25/16 11:40 to 11:50 am.)

Post-op I had another unit of FWB transfused. 19M was running temperatures above 40, indicative of sepsis.

19M died anyway 12 hours after the operation.

Nov-29-16
Premium Chessgames Member
  visayanbraindoctor: 26 November 2016.

While riding a PUV from CiH back to my apartment, we came upon a smashed up motorcycle on the highway. There was a pool of blood beside it, and a police officer and bystanders around the scene.

I checked my cell phone. So much blood on the road's surface indicated an open skull injury, which tends to gush out copious amounts of blood.

No referrals. The driver probably was DOA. ERs don't call me in if the patient arrives already expired.

Dec-03-16
Premium Chessgames Member
  visayanbraindoctor: 2 December 2016.

52M, motorcycle fall, driver, alone.

In most of bihemisphere injuries, one side does not have significant contusions or hemorrhages, and so I operate only on the side where the injuries are creating dangerous mass effects. In 52M's case there were significant hemorrhages in both cerebral spheres, and so I decided to open up both sides of the skull.

(Right fronto - parietal and left frontal craniectomies, evacuation of acute subdural hmatoma, bone transplant to left hemi-abdomen SQ layer. 12/2/16 9:10 to 10:28 am. No BT.)

Dec-03-16
Premium Chessgames Member
  visayanbraindoctor: 3 December 2016.

24F, passenger on an SUV, hit a truck.

She came in GCS 7 with anisocoria, right pupil larger than the left. This is a real emergency. The intracranial hematoma presses on the temporal lobe's uncus, which begins to herniate into the tentorial notch, where the midbrain is located. Cranial Nerve III (oculomotor nerve) runs through this notch as well, on the midbrain. If compressed, the ipsilateral pupilloconstrictor muscle, which it innervates, relaxes and the pupil dilates.

I had the patient rushed to the OR stat, and operated without blood prepared. That's alright with me because I usually don't get much bleeding on my operations. The priority is to get the blood clot out ASAP.

(Right fronto-temporal craniectomy, evacuation of epidural hmatoma, bone transplant to left hemi-abdomen SQ layer. 12/3/16 8:35 to 9:31 pm. No BT.)

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