For reasons I don’t think I have to mention, the pictures below the fold are not for the squeamish. I asked the doctor to take pictures in the operating room, because I wanted to see the scope of this thing. It was pretty darned impressive. What is now there in place of the bone is a molded surgical plastic. There was some invasion of the dura, but because of the compression, there were too many veins and arteries on the surface to take the chance of removing it. Since this cancer is benign and slow-growing, the surgeon opted to leave it, and we’ll just follow it with regular MRIs. At some point I may need further surgery or radiation treatments, but there’s also a good chance I won’t have to do anything.
Post surgery, the rest of october. Progress is slow, but it’s still progress.
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This is a continuation of my progress from diagnosis to the day before surgery, and this one contains dates. There is also a link at the beginning to a zipfile of my MRIs, so if you’re interested in seeing what they look like and trying to figure out the connection between the areas of compression and the symptoms I listed, go ahead and download.
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Collected are some notes, and some information, and some thoughts I posted elsewhere to describe what’s going on with the lump in my head.
Brain growth symptoms
-Headaches (these have become progressively worse, more frequent, and more persistent – originally attributed to allergies)
-Tinnitus in left ear has become distinct and progressively louder
-Short-term memory impairment (had thought this was caused by Cymbalta, as it was a problem after several years at 120mg/day, or perhaps a worsening of my ADHD.) Worse than usual, resulting in repeating things I’ve said to the same people several times in a row, and forgetting things that were said to me shortly after they were said. Others have brought this to my attention, although I’m occasionally aware of it myself. I am also finding myself lost briefly even when performing routine tasks like preparing a recipe I have had memorized for years. I am also having trouble not only remembering what day or date it is, but reading a calendar. I can know the day and date and still look at the wrong week and think that I have events coming up that day that are actually a week or more in the future.
-Some expressive aphasia – also originally thought this was Cymbalta, because I experienced similar episodes of blanking out during the same period as above. This is markedly different from usual ADHD. Normal “word loss” experience is that my thoughts will flood with many words that have characteristics in common with the word I want, making it more difficult to sort through and find it. At this time, when I can’t think of a word, I can’t think of any words at all. I have periods of near silence in my brain, which is very disturbing, because even medicated, I have always had constant “brain chatter.” I am forgetting what I’m trying to say when I speak much more frequently than usual.
-Loss of balance – I don’t feel any specific muscle weakness, although it is more difficult to move my eyes up and to the right, but I am bumping into things as I walk, and have begun to tip over while standing still on occasion. I am beginning to feel occasional bouts of dizziness similar to the onset of syncope even while sitting, but have not lost consciousness.
-Both my typing and my handwriting have deteriorated over the last several months. Normally my typing is fast and accurate, but I am hitting the wrong keys almost as often as the right ones, and backspacing over typos in more than half of the words. My speed has gone down in part because of this and in part because I find myself blanking on what I was going to type. My handwriting has never been neat, and I’ve always had trouble inverting tails on letters, but recently I was taking copious notes and found that I was scribbling things that weren’t even letters, and lines of script wobble up and down.
-There are problems with word perception in the upper right quadrant of my field of vision. I can recognize letters and words as letters and words, but in order to read and comprehend, I find myself tilting my head to read with my left eye on the page.
-Several months ago my optometrist noted excessive eye pressure in both eyes, particularly the left, and sent me for a thorough evaluation for glaucoma. None was found, but my prescription for corrective lenses has changed more rapidly than normal over the past two years or so.
-I am having difficulty with my sense of direction and spatial relations. In the past I have been able to negotiate unfamiliar places with minimal reliance on maps. Because I haven’t traveled far from familiar routes in some time, I was unaware how bad this was until a recent trip to colleges in New England. I googled directions, printed out large and step-by-step maps, plotted out routes on full size paper maps, and still needed to have the GPS turned on and preprogrammed with the selected route, because I had gotten lost when map directions and GPS directions conflicted. When we arrived on campuses, I was unable to get a fix on where we were and where we needed to go even though the areas on maps were small. I have sewn and designed clothing for years, and suddenly found myself lost trying to draft a simple paper pattern, not sure what pieces need to be changed or how to change them even though I’ve done this and even taught it without any difficulty before.
From a site chock-full of good information and educational links, Brain Info, I want to share the following:
This is an image of the left hemisphere. The structures that are involved here have unique functions that are not duplicated on the right hemisphere. My lump is smack dab over area 17 and extends a bit down into 18, and has deformed most of the central area of the left hemisphere all the way to the outer edges of the temporal lobe. So let’s see what it says about what can result from damages to these areas that apply to me (in bold):
The left primary visual area receives fibers in somatotopic distribution from the left half of each retina. Thus, it receives the input necessary for a point-to-point representation of the right half of the visual field. Penfield and others had shown that stimulation in that area produced a flash, or “phosphene”. Resection of the area was known to produce a left homonymous hemianopsia, i.e., ,em>patient does not respond to visual stimuli in the right half of the visual field. The limits of such a visual field defect are determined by the “confrontation” method or by perimetry.
The secondary visual area is involved in the perception of visual patterns, viz, in the recognition of so-called “simultaneous patterns”, as opposed to the “sequential patterns” with which the premotor area is concerned. Stimulation of this area may produce formed images; ablation leads to abnormal control of eye movements and instability of vision, so that when patients read they may jump lines or begin reading in the middle of the page. Spatial perception is impaired, and the field of visual attention may be constricted, i.e., the patient may be able to see only one or two objects at a time, regardless of their size, background, or position in the visual field (simultagnosia). The following tests were used to demonstrate damage of the secondary visual area.
The temporo-parieto-occipital area is phylogenetically one of the newest areas of the human cortex and constitutes the “zone of overlap” between. the cortical portions of the auditory, somesthetic-kinesthetic, and visual analyzers. Penfield had reported that electrical stimulation of this area occasionally produced deja vu, a visuo-auditory hallucination or the “reliving” of an old experience. Destruction of the area produced a number of signs that Luria judged could be traced to a loss of “simultaneous schemata”, i.e., to loss of the memory for, or ability to recognize, patterns in a group of auditory, visual, and/or somesthetic stimuli occurring simultaneously. This concept was similar to that of other investigators. According to Goldstein the antero-occipital area played an important role in the “transformation of sequential recognition processes into instantaneous recognition.” According to Head the area was necessary for the organization of individual “traces” into over-all, “simultaneous systems.” Luria found that the most prominent signs of damage to this area were spatial disorientation, loss of the “predicative” aspect of speech, agraphia, and alexia.
1. Spatial disorientation was demonstrable by a number of tests.
a. Shown the north and south poles of a compass, the patient was unable to tell which pole represented East and which West.
b. In drawing a map he positioned landmarks according to associations that occurred to him impulsively rather than according to conventional geographic coordinates.
g. In attempting to write he might construct individual letters upside down or backwards.
2. The speech disturbances of semantic aphasia were said to arise from the facts that (1) the patient was unable to deal with grammatical constructions and sentences as a whole and (2) he lost the meanings of words that derive from their relationship to general frames of reference, i.e., he retained the denotative or “nominative” meanings of words but lost the connotative or “predicative” meanings.
Loss of the ability to handle grammatical constructions and to deal with sentences as a whole was shown by the following tests:
c. He might be able to name the days of the week in correct order, but be unable to recite them backwards or answer such questions as, “What day comes before Wednesday?” Luria regarded this as evidence that he could not conceptualize or operate on the series as a unit to derive information in the form required by the task.
3. Loss of the predicative aspect of words led to:
a. inability to comprehend metaphor
b. nominal aphasia. The form of nominal aphasia seen with temporo-parieto-occipital lesions differed from that produced by damage to the postero-inferior temporal lobe in that prompting helped. Often the examiner needed only provide the first letter of the word sought, and the patient recalled it. Luria concluded that in this case the patient had not lost the auditory schema of the word but the system of associations that, for the normal person, mediate the process of recall.
Some of the pressure is on the temporal lobe, resulting in some Auditory Aphasias. My problems seem to be more expressive than receptive:
1. The predominant sign of an expressive speech disorder in auditory apahasias is nominal aphasia. Spontaneous speech is frequently interrupted by word-searching. Intonation and grammatical structure may be normal, but the speech consists largely of opening phrases, e.g., “Well, you see …it’s like this…” and interjections, e.g., “Oh hell, I don’t know why I can’t get that”. Unlike the nominal aphasias that result from parietal or frontal lobe lesions, the nominal aphasia associated with temporal lobe lesions is is not alleviated by prompting. (this goes back and forth for me – the confusion of words that start with the same letters has never been helped before with prompting, but in certain cases lately a little prompting helps. Not always.)
2. Literal and verbal paraphasias occur. The articulation (motor aspect) of phonemes and words is intact, but the patient may substitute oppositional phonemes for one another, e.g., “p” for “b”, or substitute words from the same sphere of meaning.” e.g., “elbow” for “arm”. Literal paraphasias are considered compensatory in nature. The attempt to utter the word “car” may result in such inhibition of the “auditory schema” of “car” that it is easier for the patient to say “automobile” instead.
Some reading and writing difficulties apply as well:
The degree of reading and writing difficulty in auditory aphasias depends on the extent to which these functions involve auditory analysis.
1. Patients may understand the meaning of a passage even though they cannot read it aloud. They only have difficulty reading words that are unfamiliar and that must be sounded out to be understood.
2. A patient is usually able to write his name and other familiar words on the basis of “kinestheic schemata” but has difficulty with words that he would ordinarily repeat to himself as he writes. He can copy written material without difficulty but makes phonemic substitutions in writing to dictation, and is virtually unable to write spontaneously. (I can still write spontaneously, but it takes a heck of a lot more time and effort.)
Because the various structures of the left hemisphere are essential for communication between other structures, some Afferent Motor Aphasias seem to be present as well. I’m stumbling over words when I speak (in addition to stumbling in general) and biting my tongue and the inside of my mouth so often that there’s always something hurting in there.
Efferent Motor Aphasia doesn’t seem to be much of a problem except for some mild versions of what are symptoms of damage to Broca’s Area:
The predominant signs of damage to “Broca’s area” are also loss of the “automaticity of speech” with the emergence of perseveration. There may be a loss of “dynamic schemata” at the phonemic, word, or sentence level. If disruption occurs at the phonemic level the patient may be totally aphasic. If it is less severe, some speech is retained, but the patient loses his “feel for the language,” i.e., his speech lacks normal intonation and is composed of sentence fragments rather than connected phrases. The “predicative aspect” of speech suffers more than the “nominative aspect”, i.e., verbs and adjectival, adverbial, and prepositional phrases are affected more than nouns. This gives rise to the so-called “telegraph style” of speech, e.g., “I came… Moscow…hospital … doctor … questions…”
Right in the middle of all this is the Hippocampus. The associated functions are early memory storage, formation of long-term memory, and spatial navigation. The memory functions particular to the Hippocampus seem to be OK, but the spatial navigation’s a problem.
There’s enough cushion around the Amygdala that it might be minimally involved or not involved at all, but it does play a part in short-term memory. Mostly it’s involved with emotions, but this is hardly a time for me to be assessing connections between a physical cause and my emotional state!
The Entorhinal Cortex is above and in front of the Hippocampus, and plays a part in declarative memory (conscious recall – being able to remember “on demand”) which has been a problem all my life, so it’s hard to tell if it’s any worse. It also is associated with spatial memory, but less so than the Hippocampus, and more on the right hemisphere than the left. Lastly, it assists in self-localization, which consists of integrating sensory input to orient your physical location with your surroundings. I think I’m seeing that a lot, more in new environments than familiar ones, but I am walking around in circles at home, too.
The secondary visual area is involved in the perception of visual patterns, viz, in the recognition of so-called “simultaneous patterns”, as opposed to the “sequential patterns” with which the premotor area is concerned. Stimulation of this area may produce formed images; ablation leads to abnormal control of eye movements and instability of vision, so that when patients read they may jump lines or begin reading in the middle of the page. Spatial perception is impaired, and the field of visual attention may be constricted, i.e., the patient may be able to see only one or two objects at a time, regardless of their size, background, or position in the visual field (simultagnosia).
When I posted this the other day, I hadn’t highlighted “when patients read they may jump lines or begin reading in the middle of the page or the field of visual attention may be constricted, i.e., the patient may be able to see only one or two objects at a time, regardless of their size, background, or position in the visual field (simultagnosia)” because I hadn’t experienced them. Now I have. The second one, while I was driving.
I had no choice because it was an appointment I wouldn’t be able to reschedule for months, and it was only a short drive, so I thought it would be OK. Once I realized that I was perceiving only pieces of what I was seeing on the road, I started blinking rapidly – thought I might trick my brain into thinking it was seeing a series of pictures and put it together like a kinetoscope. It worked OK, but it’s not such a good technique to use behind the wheel. (I’d also be in trouble if there were any Weeping Angels around, but I think I’m safe on that one!) When things were moving slowly or there were fewer moving objects visible, it was easier, but still really hard.
I can’t even accurately describe it except like real life was a set of pictures in a flip-book and would stick on one page before flipping to the next. Blinking allowed me to see the next picture in the series faster. Not a strobe light effect, because things that were moving would seem as if they’d stopped for a moment.
And just imagine – if this lump had been on the right occipital lobe, I would be experiencing something entirely different.
So today, when I have plenty of time to think about this and feel sorry for myself, I’m also fighting anger because I’m remembering so many conversations and debates with people who think that there’s some kind of magic to neuroplasticity. Right here in my head is clear evidence that there are physical structures in the brain that have highly specialized functions that are not, and cannot be, duplicated elsewhere in the brain.
Problems in the the brain itself, an organ formed by genetic instructions and physical and psychological environmental influences just like every other part of our bodies, cannot be “corrected” by diet or exercise or acts of will. Functions that are simple or are duplicated in other areas of the brain can be partially rehabilitated – sometimes. Occupational and physical therapies can train an individual with a damaged or incorrectly formed brain to compensate, but only within limits based on the ability of the physical brain to relocate the function.
What function I regain post-surgery depends entirely upon how much permanent damage has been done, and to what areas. Once the lump is removed and my brain is no longer compressed, it may well be that certain areas were deprived of blood and nutrients and shut off from communication will not improve. A certain amount of neuroplasticity will allow new cell generation in partially damaged areas, but if some of the tissue is destroyed, it ain’t coming back. And if that tissue was wholly or mostly responsible for regulating the activities in which I’m currently impaired, that impairment won’t go away.
I may be able to re-learn certain things, but it won’t be as easy as it was before, and it will feel different when I’m trying to do it. I’ll keep on trying to be objective as I update things here, but I can’t guarantee I won’t get snippy if someone suggests I can fix something that’s impossible to fix.
Well, this is fun. The black text here is turning blue off and on. Not the whole of it, but certain areas of it. The closer it is to the other blue text (“Smilies” to the right and “Post Icons” at the bottom left) the more likely it is to turn that shade of blue. At least I can read that – yellow text would be awful.
It’s only that one shade of blue, too. I’ve checked, and I don’t get the same kind of flashes with any other color. So far. . .