Mornings were good for some time. Now they are terrible. I don't feel like getting up. I swear. I just feel tired and lazy. It's the break of routine I had. That's it . A few days of unexpected and intense rainfall. An aberration in the nature of things . And whatever I wanted achieved is off. How do we change? How does a community change how does a nation the world? Individually.
Really. That's new. By tech
By routine. By doing something again and again. Small change. Don't litter.
Thursday, September 27, 2012
THE MINDS "I" OR TRYING TO MAKE SENSE OF IT ALL
I have been reading or trying to read Douglas Hofstadter book "I AM A STRANGE LOOP". I tried "GEB", the conversations were nice ,yet i am phobic of maths and was overwhelmed soon. The present one is more readable and yet as i approach Godel Encounters Fibonacci i have started to give reasons to re read the earlier parts and this will lead to an abrupt cessation of perusal of the book. I will deem it difficult and not pragmatic enough to be read. And as i write this there is a frisson( as the author puts it repeatedly) to get to the part which also entices me, that being how does the self, me or" I" arise from a collection of atoms,molecules which do not have the ability to even understand that they are a part of this big"I". They are clueless ,the same as in any other species or object yet they give rise to a property that not only wants to know the purpose of the collection but also how each part contributes. This introspective ability, this judgemental capacity, this cognition of self and non self,these tears ,these remembrances, the ability to plan, check, cross check and wonder........
Why only with this species, why did we evolve in this manner? Is there any other path? Was it concieved when the universe began ? Or did this chance occur serendeptiously?
We take the aura or I out and its just dust nothing else. Magic. Yes it seems and no one has an understanding how it came about. Some one tries and i get scared of maths. Thats abominable, i am too lazy, the effort will have to be more. Keener. Its astounding that that the whole humanity nearly takes it for granted this abstract concept of "I". If its just a process and not a concrete object and this process depends upon 1.5 kg of goo, then this is liable to dysfunction easily. Either by way of the goo being spoilt or the process malfunctioning. Also this process would have a basic sound framework and newer processes would be developed as the organism evolves. Hey i am shooting in the dark, let me finish the book.
Why only with this species, why did we evolve in this manner? Is there any other path? Was it concieved when the universe began ? Or did this chance occur serendeptiously?
We take the aura or I out and its just dust nothing else. Magic. Yes it seems and no one has an understanding how it came about. Some one tries and i get scared of maths. Thats abominable, i am too lazy, the effort will have to be more. Keener. Its astounding that that the whole humanity nearly takes it for granted this abstract concept of "I". If its just a process and not a concrete object and this process depends upon 1.5 kg of goo, then this is liable to dysfunction easily. Either by way of the goo being spoilt or the process malfunctioning. Also this process would have a basic sound framework and newer processes would be developed as the organism evolves. Hey i am shooting in the dark, let me finish the book.
Monday, May 7, 2012
GOODBYE AND HELLO AGAIN !
It always ends this way. Its meant to be so. Even death. Probably. Goodbye and hello new world. Relentless is the pace. Its like riding the tiger. One does not get off.
A new college, afresh patient load, an empty consulting chamber. I am not familiar. Unwanted. Trying to be a somebody. Keep on trying. JUST FINISHED FRANNY AND ZOOEY. TRYING TO UNDERSTAND PETER ATKINS GALILEOS FINGER.Do individuals ,such as the undersigned , find physics confusing because its so full of maths? Probably, but its a treat to read that book. At times when one understands what he is trying to convey it is breathtaking. Especially the chapter on symmetry will require a re-re reading on my part. Probably it would be best to go slow. I wish i could write science like him. and so many others. Read it out to my children and they also stare in awe. He puts a twist to the story and the implications are gigantic, and the universe in its awe inspiring dimensions as well as the discoveries made makes one feel very very small and insignificant. Yet its recommended and a must read,for all.
A new college, afresh patient load, an empty consulting chamber. I am not familiar. Unwanted. Trying to be a somebody. Keep on trying. JUST FINISHED FRANNY AND ZOOEY. TRYING TO UNDERSTAND PETER ATKINS GALILEOS FINGER.Do individuals ,such as the undersigned , find physics confusing because its so full of maths? Probably, but its a treat to read that book. At times when one understands what he is trying to convey it is breathtaking. Especially the chapter on symmetry will require a re-re reading on my part. Probably it would be best to go slow. I wish i could write science like him. and so many others. Read it out to my children and they also stare in awe. He puts a twist to the story and the implications are gigantic, and the universe in its awe inspiring dimensions as well as the discoveries made makes one feel very very small and insignificant. Yet its recommended and a must read,for all.
Thursday, April 26, 2012
Got my leave, bid me farewell
ITS HAPPENING.The wheels of time(kala) churn away and we mortal beings wonder how it came to this stage.I hang up my uniform in 2 days time. 23 years. Really i dont believe it. Ihave not changed, i am still confused, unsure and uncertain. I have a feeling of being a vagrant.Never have i been anyplace i can sincerely call my own. Always passing though, waiting for the next flight as ordered.
Who am i? The reflection in the mirror or the shadow i cast.Am i the person who wears the uniform and looks stern or the man in rags supplicating to all.Am i the words or the music? These seem stupid thoughts but, they rustle up in my mind. 45 years and the rustle is louder. My farewell speech was a poem from GITANJALI by Rabindranath Tagore. It was so appropriate, as if written for my goodbye.
Who am i? The reflection in the mirror or the shadow i cast.Am i the person who wears the uniform and looks stern or the man in rags supplicating to all.Am i the words or the music? These seem stupid thoughts but, they rustle up in my mind. 45 years and the rustle is louder. My farewell speech was a poem from GITANJALI by Rabindranath Tagore. It was so appropriate, as if written for my goodbye.
Farewell
I have got my leave. Bid me farewell, my brothers!
I bow to you all and take my departure.
Here I give back the keys of my door
---and I give up all claims to my house.
I only ask for last kind words from you.
We were neighbors for long,
but I received more than I could give.
Now the day has dawned
and the lamp that lit my dark corner is out.
A summons has come and I am ready for my journey.
I bow to you all and take my departure.
Here I give back the keys of my door
---and I give up all claims to my house.
I only ask for last kind words from you.
We were neighbors for long,
but I received more than I could give.
Now the day has dawned
and the lamp that lit my dark corner is out.
A summons has come and I am ready for my journey.
Rabindranath Tagore
Wednesday, April 4, 2012
Forgets names but has a new appreciation for polka music
Editors: Noseworthy, John H.
Title: Fifty Neurologic Cases from Mayo Clinic, 1st Edition
Copyright ©2004 Oxford Unversity Press (Copyright 2004 by Mayo Foundation for Medical Education and Research)
> Table of Contents > Case 1: Forgets names but has a new appreciation for polka music
Case 1: Forgets names but has a new appreciation for polka music
CASE 1
History
At age 52 years, a left-handed man began experiencing difficulties stating the names of familiar people and objects. Initially, he had no apparent problems with memory or other cognitive functions or changes in behavior. By age 54, difficulties with verbal comprehension had developed, but he still worked as a farmer and had no problem working or driving. At age 55, he developed a profound interest in listening to polka music, sometimes doing so for 12 hours or more at a time. By age 57, he was not able to read or write or to recognize most familiar faces and objects.
His father and paternal aunt had become forgetful late in life. His son has congenital apraxia of speech that has improved markedly with speech therapy.
Examination
Neurologic examination at age 53 revealed an alert, cooperative man whose language was fluent. He had difficulty naming simple objects and famous faces. Reading, writing, memory, and constructional praxis were all preserved. Over the next 4 years, his aphasia worsened, as did recognition of words, objects, and faces (associative agnosia). His verbal memory and attention also declined; yet, on examination at age 57, his recall of where objects were hidden in the office and his ability to draw figures remained intact.
Investigations
The cerebrospinal fluid examination was normal. Serial magnetic resonance imaging demonstrated progressive left, and then right, anterior temporal lobe atrophy (Figure). Initial neuropsychologic testing at age 53 demonstrated problems with divided attention, mental manipulation, executive functioning, and verbal learning and recall; his performance on language function tests (e.g., Boston Naming Test [BNT] score of 16/60) was particularly poor. Subsequent testing sessions showed progression in all cognitive domains, particularly language (BNT, 3/60 at age 56); yet, his copy of the Rey-Osterreith Complex Figure was almost perfect.
P.2
FIGURE. Representative T1-weighted coronal magnetic resonance images of patient from age 53 to 57 years. Note the progressive atrophy of the left amygdala and temporal cortex beginning at age 53. Atrophy in the right amygdala and temporal cortex was subtle at age 54, but it was clearly progressive over the years. (From Boeve BF, Geda YE. Neurology 2001;57:1485.By permission of the American Academy of Neurology.)
P.3
DIAGNOSIS CASE 1 Asymmetric cortical degeneration syndrome: semantic dementia
Commentary by Dr. Bradley F. Boeve
The terms “semantic dementia,†“semantic aphasia and associative agnosia,†“primary progressive aphasia,†“chronic progressive aphasia,†“temporal variant of frontotemporal dementia,†and “focal or asymmetric cortical degeneration syndrome†have all been applied to patients who exhibit a degenerative neurobehavioral disorder with progressive impairment predominantly or exclusively in the domain of language. When impairment is isolated to language, the term “primary progressive aphasia†is appropriate; when impairment is present in object naming (i.e., anomia) and word meaning (i.e., agnosia), with other aspects of language and cognition relatively intact, the term “semantic dementia†is apt. The initial symptom is typically “forgetfulness for names,†and although paraphasic errors, dyslexia, dysgraphia, visual agnosia, and executive dysfunction usually evolve with time, many patients perform daily activities remarkably well over the initial 2 to 5 years of symptoms. Progression can vary, with symptoms reflecting the topography of progressive cortical dysfunction. Typically, degeneration spreads posteriorly in the ipsilateral temporal lobe, with involvement eventually extending to the perisylvian, frontosubcortical, and sometimes superior parietal regions in the dominant hemisphere. When the contralateral hemisphere is affected, a remarkably consistent finding is progressive atrophy in the opposite anterior temporal lobe. If and when sufficient nondominant hemisphere frontotemporal cerebral dysfunction ensues, problematic neuropsychiatric features can evolve, such as socially inappropriate, disinhibited, and even criminal behavior. Misidentification errors, prosopagnosia, and ultimately multimodal associative agnosia become apparent as the nondominant temporal lobe atrophies.
Semantic dementia is one of the focal or asymmetric cortical degeneration syndromes and is associated with anterior temporal lobe dysfunction. Other clinical syndromes include progressive nonfluent aphasia associated with dominant hemisphere frontal opercular or insular dysfunction; frontotemporal dementia associated with dorsolateral prefrontal, orbitofrontal, or anterior cingulate dysfunction (or a combination of these); corticobasal syndrome associated with parietofrontal cortical dysfunction; and posterior cortical atrophy associated with parieto-occipital cortical dysfunction. Although the nomenclature
P.4
for these syndromes and the disorders that underlie them can be confusing, the conceptual perspective is the same—symptomatology is dictated more by the topography of dysfunction than by the underlying histopathologic disorder.
The pathologic substrates for semantic dementia have tended to be associated with either nonspecific neurodegenerative changes (e.g., “dementia lacking distinctive histopathology†or “frontotemporal lobar degeneration†with or without ubiquitin-positive inclusions) or a disorder within the tauopathy spectrum (e.g., Pick's disease, corticobasal degeneration, or argyrophilic brain disease). Alzheimer's disease rarely presents in this manner. Mutations in the tau gene have been identified in some patients who present with semantic dementia. No therapy has been identified that alters the pathophysiologic mechanism of the disorders that manifest as semantic dementia, nor have pharmacologic manipulations led to a marked and sustained symptomatic benefit in any patient. Speech therapy is reasonable for patients early in the course of the disease.
A striking and poorly understood observation is the remarkable evolution of artistic talent in rare persons with frontotemporal dementia, of whom some have had semantic dementia. Some patients have produced paintings more elaborate than their past renderings, whereas others have developed interests in listening to or playing forms of music that previously had not been considered interesting. This phenomenon seems completely contrary to degenerative brain disease. Whether compensatory mechanisms in relatively unaffected neuronal networks or disinhibition of affected neuronal networks (or both) explains this phenomenon is not known. Further study in semantic dementia and other focal or asymmetric cortical degeneration syndromes may not only improve our understanding of degenerative brain disease but also provide insight into the neurologic underpinnings of artistic appreciation and expression.
REFERENCE
Neary D, Snowden J, Gustafson L, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 1998;51:1546-54.
Title: Fifty Neurologic Cases from Mayo Clinic, 1st Edition
Copyright ©2004 Oxford Unversity Press (Copyright 2004 by Mayo Foundation for Medical Education and Research)
> Table of Contents > Case 1: Forgets names but has a new appreciation for polka music
Case 1: Forgets names but has a new appreciation for polka music
CASE 1
History
At age 52 years, a left-handed man began experiencing difficulties stating the names of familiar people and objects. Initially, he had no apparent problems with memory or other cognitive functions or changes in behavior. By age 54, difficulties with verbal comprehension had developed, but he still worked as a farmer and had no problem working or driving. At age 55, he developed a profound interest in listening to polka music, sometimes doing so for 12 hours or more at a time. By age 57, he was not able to read or write or to recognize most familiar faces and objects.
His father and paternal aunt had become forgetful late in life. His son has congenital apraxia of speech that has improved markedly with speech therapy.
Examination
Neurologic examination at age 53 revealed an alert, cooperative man whose language was fluent. He had difficulty naming simple objects and famous faces. Reading, writing, memory, and constructional praxis were all preserved. Over the next 4 years, his aphasia worsened, as did recognition of words, objects, and faces (associative agnosia). His verbal memory and attention also declined; yet, on examination at age 57, his recall of where objects were hidden in the office and his ability to draw figures remained intact.
Investigations
The cerebrospinal fluid examination was normal. Serial magnetic resonance imaging demonstrated progressive left, and then right, anterior temporal lobe atrophy (Figure). Initial neuropsychologic testing at age 53 demonstrated problems with divided attention, mental manipulation, executive functioning, and verbal learning and recall; his performance on language function tests (e.g., Boston Naming Test [BNT] score of 16/60) was particularly poor. Subsequent testing sessions showed progression in all cognitive domains, particularly language (BNT, 3/60 at age 56); yet, his copy of the Rey-Osterreith Complex Figure was almost perfect.
P.2
FIGURE. Representative T1-weighted coronal magnetic resonance images of patient from age 53 to 57 years. Note the progressive atrophy of the left amygdala and temporal cortex beginning at age 53. Atrophy in the right amygdala and temporal cortex was subtle at age 54, but it was clearly progressive over the years. (From Boeve BF, Geda YE. Neurology 2001;57:1485.By permission of the American Academy of Neurology.)
P.3
DIAGNOSIS CASE 1 Asymmetric cortical degeneration syndrome: semantic dementia
Commentary by Dr. Bradley F. Boeve
The terms “semantic dementia,†“semantic aphasia and associative agnosia,†“primary progressive aphasia,†“chronic progressive aphasia,†“temporal variant of frontotemporal dementia,†and “focal or asymmetric cortical degeneration syndrome†have all been applied to patients who exhibit a degenerative neurobehavioral disorder with progressive impairment predominantly or exclusively in the domain of language. When impairment is isolated to language, the term “primary progressive aphasia†is appropriate; when impairment is present in object naming (i.e., anomia) and word meaning (i.e., agnosia), with other aspects of language and cognition relatively intact, the term “semantic dementia†is apt. The initial symptom is typically “forgetfulness for names,†and although paraphasic errors, dyslexia, dysgraphia, visual agnosia, and executive dysfunction usually evolve with time, many patients perform daily activities remarkably well over the initial 2 to 5 years of symptoms. Progression can vary, with symptoms reflecting the topography of progressive cortical dysfunction. Typically, degeneration spreads posteriorly in the ipsilateral temporal lobe, with involvement eventually extending to the perisylvian, frontosubcortical, and sometimes superior parietal regions in the dominant hemisphere. When the contralateral hemisphere is affected, a remarkably consistent finding is progressive atrophy in the opposite anterior temporal lobe. If and when sufficient nondominant hemisphere frontotemporal cerebral dysfunction ensues, problematic neuropsychiatric features can evolve, such as socially inappropriate, disinhibited, and even criminal behavior. Misidentification errors, prosopagnosia, and ultimately multimodal associative agnosia become apparent as the nondominant temporal lobe atrophies.
Semantic dementia is one of the focal or asymmetric cortical degeneration syndromes and is associated with anterior temporal lobe dysfunction. Other clinical syndromes include progressive nonfluent aphasia associated with dominant hemisphere frontal opercular or insular dysfunction; frontotemporal dementia associated with dorsolateral prefrontal, orbitofrontal, or anterior cingulate dysfunction (or a combination of these); corticobasal syndrome associated with parietofrontal cortical dysfunction; and posterior cortical atrophy associated with parieto-occipital cortical dysfunction. Although the nomenclature
P.4
for these syndromes and the disorders that underlie them can be confusing, the conceptual perspective is the same—symptomatology is dictated more by the topography of dysfunction than by the underlying histopathologic disorder.
The pathologic substrates for semantic dementia have tended to be associated with either nonspecific neurodegenerative changes (e.g., “dementia lacking distinctive histopathology†or “frontotemporal lobar degeneration†with or without ubiquitin-positive inclusions) or a disorder within the tauopathy spectrum (e.g., Pick's disease, corticobasal degeneration, or argyrophilic brain disease). Alzheimer's disease rarely presents in this manner. Mutations in the tau gene have been identified in some patients who present with semantic dementia. No therapy has been identified that alters the pathophysiologic mechanism of the disorders that manifest as semantic dementia, nor have pharmacologic manipulations led to a marked and sustained symptomatic benefit in any patient. Speech therapy is reasonable for patients early in the course of the disease.
A striking and poorly understood observation is the remarkable evolution of artistic talent in rare persons with frontotemporal dementia, of whom some have had semantic dementia. Some patients have produced paintings more elaborate than their past renderings, whereas others have developed interests in listening to or playing forms of music that previously had not been considered interesting. This phenomenon seems completely contrary to degenerative brain disease. Whether compensatory mechanisms in relatively unaffected neuronal networks or disinhibition of affected neuronal networks (or both) explains this phenomenon is not known. Further study in semantic dementia and other focal or asymmetric cortical degeneration syndromes may not only improve our understanding of degenerative brain disease but also provide insight into the neurologic underpinnings of artistic appreciation and expression.
REFERENCE
Neary D, Snowden J, Gustafson L, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 1998;51:1546-54.
The strangulation of the mind
Sir, it may be construed as bitterness as i leave the armed forces in a few months.Yet, i will say that i was very proud of the ethos and the pragmatism the Indian Army has displayed. Your front page news about the events of 16th Jan 2012 has dented this pride to such an extent that i am ashamed. It is not sensationalism as many have commented ,but a sorry state of politico-defence relations and more importantly blatant miscommunication on part of the Army. In an organisation where even a menu change in the officer messes requires permission of the seniormost dining officer,it is shameful that the elected government was not informed about large scale troop movements around Delhi.This erodes the very office of DGMO. Yet., i feel this was a skirmish bound to happen. It is the nature of the protected cloistered cantonment mindset. A phrase i think was quoted by Hussain Haqqani in an article a few years ago in your paper. The more one is insulated the more are the chances of a regression in intelligence and a stunting of rational thought. This point is made in Matt Ridleys book "The Rational Optimist", in which he mentions about the regression seen in Tasmanian natives as they never interacted closely with other civilizations. Archaeologist Rhys Jones called it a strangulation of the mind. The same afflicts the Army. The only solution is to engage in administration by appointing officers who are promising who work with the beaurucracy and politicians on a regular basis and engage as well as enjoy the hustle bustle of the democratic process. Its time we in the army stopped considering ourselves as unique and above board. We serve this nation first and foremost ,not an ideology or an organisation.
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