CSI MEDBLOGS: FURTHER INVESTIGATION OF CT BRAINS TURNS UP NEW ASTOUNDING EVIDENCE

Terri Did Not Suffer Her Brain Damage Outside The Hospital--It Occurred While She Was Hospitalized

According to a time-line of physicians and therapists reports, posted on The Empire Journal, Terri's injury occurred on 2/25/90:

2/25/1990

 

Terri's Injury

 

 

 

2/25/1990

X-Ray Report Dr. Hameroff

Images taken of cervical spine, no acute bony pathology - straightening of normal cervical lordosis

 

 

 

2/25/1990

Neuro Consult Dr. DeSousa

Deeply comatose.  No evidence of acute process in CT scan.  Evidence of myoclonic seizures.  Rule out acute myocardiac infarction, seizures as cause.  Neck is somewhat stiff as is all of the muscles of the body.  No jugular venous distension.  WBC 26,300, drug screen negative

 

 

 

2/25/1990

CT Scan Report Dr. Hameroff

Normal

 

 

 

2/26/1990

EEG Report Dr.  DeSousa

Abnormal EEG indicative of generalized suppression and slowing

 

 

 

2/27/1990

DeSousa Report

Brainstem Auditory Evoked Response shows no significant disruption of the brain stem acoustic pathway - study within normal limits

 

 

 

2/27/1990

CT Scan Report Dr. Greenberg

Normal CT Scan

 

 

 

2/28/1990

EEG Report Dr. DeSousa

Generalized diffuse slowing.  Some fast frequency rhythms which were not obvious during previous recording.  May have been slight improvement over last EEG.

 

 

 

3/19/1990

EEG Report Dr. DeSousa

Markedly abnormal EEG, no significant improvement from previous records

 

 

 

3/30/1990

CT Scan Report Dr. Abramson

CT Scan shows noncommunicating hydrocephalus, changes occurred since 2/27 exam

If you look carefully at this time line you will see that Terri had "NORMAL" CT's of the brain on 2/25 and 2/27.

STOP THE PRESSES

There is categorically and absolutely NO WAY Terri could have suffered MASSIVE ANOXIC INJURY TO THE BRAIN ON 2/25 AND HAVE NORMAL CT SCAN ON 2/27

NO WAY

Brain edema begins to occur about 20 minutes after infarction and by 24 hours her brain (if she HAD suffered a massive anoxic event) would have been MASSIVELY SWOLLEN -- something that could NEVER be missed and NEVER called normal.

NEVER.

If Terri's brain CT was NORMAL 2 days after she entered the hospital then there is NO POSSIBLE WAY she suffered a massive infarction or global ischemia on 2/25.

THIS IS ALL WRONG

Now look at 3/30. Suddenly she develops NONCOMMUNICATING HYDROCEPHALUS.

WHAT?

Did anyone ask HOW? How did she develop noncommunicating hydrocephalus suddenly on 3/30/90 with 2 normal CT scans on 2/25 and 2/27??

CONCLUSIONS?

1. IF this is an accurate report (normal CT brain on 2/27 -- injury on 2/25) then  TERRI DID NOT suffer an event of massive ischemia on 2/25. THERE IS NO RADIOLOGIST OR NEUROLOGIST OR NEUROSURGEON IN THE WORLD THAT WOULD DISPUTE THIS. it is impossible. The ct ON 2/27 WOULD HAVE BEEN grossly ABNORMAL.

2. IF TERRI DID NOT SUFFER ANOXIC DAMAGE ON 2/25 THEN THE REASON FOR HER BRAIN ATROPHY WAS CAUSED BY SOMETHING THAT OCCURRED after 2/25 namely in the hospital during February or march of 1990.

3. How does one develop NONCOMMUNICATING HYDROCEPHALUS in ONE MONTH? By a blood clot obstructing the CSF outflow from the brain at the Foramen of Magendie.

4. How does one get #3.

BY BEING HIT ON THE HEAD AND SUFFERING INTRACRANIAL HEMORRHAGE.

So Terri WAS HIT ON THE HEAD OR DROPPED ON HER HEAD DURING LATER FEBRUARY OR EARLY MARCH WHILE IN THAT HOSPITAL.

Posted by Doctor CBB on March 24, 2005 at 03:56 AM | Permalink | Comments (89) | TrackBack (9)


Watchdog Note: A possible reason for the NONCOMMUNICATING HYDROCEPHALUS is that it may not have been spotted, the hospital equipment may have been older, or it may have developed over a longer period of time, but still may be the result of a blow to the back of the head, and the mechanism for NONCOMMUNICATING HYDROCEPHALUS may have been in place when TS entered the ER.

 

 

Source:

http://codeblueblog.blogs.com/codeblueblog/2005/03/csi_medblogs_fu.html