Thursday 10 November 2016

Update Post Avastin, 18 months post diagnosis

My husband, diagnosed May 2015, with inoperable tumor in his right frontal lobe, had the usual radiation/temodar protocol, post radiation chemo only four months. Important to note; 60% of his brain was radiated because of the placement of the tumor(s). After much urging from his UCLA neuro-onc, he had four infusions of Avastin, starting end of August 2016. The results were not what we had hoped, he got weaker after each infusion, to the point that he was back in his wheelchair after being ambulatory post shunt in early July. He is just now clawing his way back from the effects of Avastin, which also include fatigue, and fogginess. It is too soon to tell if Avastin will have any beneficial effects for him. His post Avastin MRI showed a sizable reduction of his tumor and much less inflammation. It also showed possible necrosis.  Two weeks ago he had a major seizure, his neuro-onc can't explain it. I also asked my husband's neuro-onc if he was experiencing aphasia and her response said no, that the EEG showed a slowness of the brain. I'm not sure what that means.  I asked if conflating thoughts, ideas, imagining experiences that didn't occur, word confusion be defined as slowness? And doesn't an EEG just map one moment of time? Would the results of an EEG be different without medication, morning vs afternoon, etc? I need help understanding and also to set my expectations on remapping and what I thought was a pliable brain.  I thought these symptoms would have been a left temporal lobe issues, not right. Does anyone have a similar experience to share?
BTW, his tumor is MGMT methylated and IDH1 non-mutated.

4 comments:

  1. I can't answer your question, but I wonder whether the "slowness of the brain" on EEG is simply presence of abnormally slow waves which is a standard symptom of tumors (see for example http://emedicine.medscape.com/article/1139025-overview#a3)

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  2. AGM,
    The comment of marian is correct. The finding of "diffuse slowing" on EEG is extremely common and not terribly meaningful. The list of conditions which can give this finding is extremely long, and it might be expected in any condition giving the neurologic deficits you described, with or without a tumor. Essentially, that finding gives no additional useful information.

    The reason for doing the EEG, I suspect, was to evaluate the seizure and his risk for more seizures. They were likely looking for any "epileptogenic activity." If they didn't find this, it *might* suggest lower risk for future seizures. Had they found this, it would have pointed to a particular area on the brain, and might have led to useful information. Essentially, the test seems to have yielded little information of real use.

    It's certainly possible to obtain an EEG over 24 hours (or more). This is mostly useful for sorting out difficult-to-control epilepsy, and would likely not be terribly useful if he's only had one major seizure.

    I'm sorry he's having such trouble. This is a very distressing disease to have to deal with, as we all here have found.

    Steve

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  3. My husband had focal seizures and multiple EEGs never showed anything specific. They were abnormal, with slowing on the side of his tumor, but we were told by multiple doctors that was as expected because of the tumor and treatments.

    Unfortunately, a post Avastin MRI is very hard to read, even for the true experts. My husband was having difficulties, including focal seizures, post Avastin and we were repeatedly assured it was not recurrence, but something causing edema. Even his NO and Duke told us this, but it was tumor growth, Just took a while to show itself on the MRI due to the Avastin. Don't stop pushing to figure out what's going on!!

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  4. Thank you all. Here is the latest review of my husband's MRIs. Please see the last paragraph.

    There has been no significant interval change in the ill-defined heterogeneously enhancing mass within the right frontal lobe with extension into the genu of the corpus callosum and right temporal lobe white matter. Serial measurements are provided
    below.

    10/26/2016: 46 x 16 mm (971-23)
    9/28/2016: 46 x 16 mm (8-63)
    8/24/2016: 62 x 24 mm (12-86)
    7/2/2016: 64 x 25 mm (20-90)
    6/22/2016: 64 x 24 mm (8-58).
    5/18/2016: 68 x 23 mm (8-54)
    4/20/2016: 68 x 24 mm (8-54)
    3/23/2016: 66 x 25 mm (8-50)
    2/24/2016: 69 x 26 mm (15-27)
    1/27/2016: 69 x 28 mm (900-23)
    12/30/2015: 67 x 27 mm (14-24)
    12/2/2015: 66 x 26 mm (901-30)

    No significant change in the extent of confluent FLAIR/T2 hyperintense signal surrounding the enhancing region, as well as involving the bilateral frontotemporal cerebral white matter. Stable mass effect upon the frontal horn of the right lateral
    ventricle

    Right parietal approach ventricular drainage catheter is in stable position. The ventricles are stable in size and configuration. The basal cisterns are patent.

    No acute intracranial hemorrhage or hydrocephalus. There is no abnormal restricted diffusion to suggest recent infarction. Incidental note is made of a partially empty sella turcica. The major intracranial vessels demonstrate normal flow voids. The mastoids and paranasal sinuses are well aerated.

    Impression
    IMPRESSION:

    No significant change when compared to September 28, 2016 in the ill-defined heterogeneous with irregular enhancement centered within the right frontal lobe.

    However, decreased enhancement and mass effect when compared to July 2, 2016, raising the possibility of radiation necrosis.

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