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.