Gogi, or word meaning aphasia, refers to selective impairment of kanji pprocessing. Kanji is text from ideographs as opposed to kana, which is phonologic writing, with a 1:1 correspondence between sound and script for each mora or syllable. Gogi aphasia was first described by Imura T (Aphasia: characteristic symptoms in Japanese. Psychiatria et Neurologia Japonica 47: 196-218 1943). Gogi aphasic patients have preservation of kana processing, difficulty in comprehension, in the retrieval of content words (ie lexical items), and fluent oral repetition. One author compares it to the mixed form of transcortical aphasia (Goldstein K, Die transcortikalen aphasien. Fishcer, Jena, 1917), to Luria's semantic aphasia, or Geschwind, Quadfasel and Segarra's isolation of the speech area. A patient reported by Sasanuma and Monoi (after a traumatic hemorrhage) (Neurology 1975) could repeat without comprehension. He did poorly on sentencite comprehension, auditory comprehension but had preserved comprehension of numbers. He had fluent speech with normal prosody and loss of content words. He made numerous "unrelated" errors on confrontation naming. He pwherformed at 95 % on the Controlled Oral Word Association Test (Japanese version). He produced well formed but semantically empty sentences, and could repeat orally normally. Reading was impaired in kanji and kana in term s of comprehension, but he could read most kana words aloud but not kanji. Japanese on and kun reading of kanji requires semantic knowledge to read. Also, Japanese text does not have word boundaries except semanticallepy deduced by kana and kanji words, so one has to rely on semantics to know the correct boundaries (which take the place of commas, periods and spaces in English). Gogi aphasics who lack comprehension place pauses at the wrong loci eg in the middle of a morpheme. Writing was impaired in both kana and kanji with kanji worse. Writing to dictation in kana was relatively preserved, whereas kanji was awful. Kanji errors were made in which kanji chthe aracters which are ideograms were treated as though they were phonetic with phonetic errors in substitutions made. Number concept and calculation was preserved. Reviewing the literature, all but one of six cases spared "parietal" signs such as angular gyrus symptoms, constructional apraxia, or visuomotor impairment. The author posits impairment of kana processing, in contrast as being in Broca's area, whereas Gogi aphasia may represent impaired second or third temporal gyri or underlying white matter but sparing the "Wernicke-Broca" complex(Neurology 25: 627-632, 1975).
Kuku is a mnemonic rhyme by which Japanese learn the multiplication tables via ther auditory route. Patients with impaired kuku learning relearned multiplication tables using the visual route. (Kashiwagi et al. Neduropsychologia 1987).
For those English speakers who want to impress your audiences when you give a lecture, kana is further divided into katakan (imported words) and hiragana (nonimported or native words). Generally there is no difference in performance in the two types.
Another article analyzed error types in kana and kanji . Patients with kanji aphasia had "word (graphical) confusion" whereas kana aphasics had "phonologic confusion." However there were significantly less vowel errors than consonant errors in kana, and those vowel errors that occurred also had a substitution error in the preceding consonant. Patients with kana aphasia typically had apraxia of speech (80%) whereas patients with kanji aphasia did not. (Sasanuma S, Fujimura O. An analysis of writing errors in Japanese aphasic patients: kanji v. kana words).
Yet another article compared writing Arabic numerals, kani and kana in brain damaged patients (Tamara I, Kikuchi S, OtsukiM, Tashiro K. Cognitive Neuroscience and Neuropsychology Neuroreport 14:861-865, 2003). 4 patients with Gerstmann's syndrome and 4 with Wernicke's aphasia were studied. Wernicke's aphasics could write Arabic numerals, but Gerstmann's patients could write kanji numbers better than Arabic numbers. The authors speculate that Arabic numerals are somesthetic and linked to concept of number processing and bypass phonological analysis.
Sugishita M, Otomo K, Kabe S, Yunoki K. A critical appraisalof neuropsychological correlates of Japanese ideogram (kanji) and phonogram (kana) reading (Brain 1992; 115:1563-1585) looked at 23 patients with Broca aphasia, 13 Wernicke's and 7 with alexia and agraphia and did not find a relationship between aphasia pattern and lesion site, contrary to previous smallcase series.
Thursday, May 29, 2008
Saturday, May 24, 2008
Introduction to Luria
I have just read two and a half books of the half dozen or so I bought written by Alexander Romanovich Luria. Luria expands behavioral neurology well beyond what "classical" behavioral neurology. Whereas here we have been captive to anatomy and classical syndromes, Luria incorporates much more discussion of unknown Russian authors, known but underestimated Russian neurophysiologists, Pavlovian theory, developmental neurology, cross cultural neurology, politics, and evolutionary neurology. Need I add that Luria does discuss all the classical Western behaviorists from the time of Wernicke and before, and adds more bedside examination devices than I knew existed? The next few blogs will discuss this giant of neurology who happened to live in the Soviet Union. As a tidbit, the epilog written in "The Making of a Mind" takes us through the political contexts of the twists and turns in Luria's fascinating career, including purges, and makes sense of events that have caused some to label him as a "Soviet" neuropsychologist.
Interhemispheric relations and the functions of the minor hemisphere
Luria AR , Simernitskaya EG. Neuropsychologia 1977; 15: 175-178.
The authors propose a novel theory of brain reorganization wherein active, intentional memorization is governed by the dominant hemisphere, and involuntary or incidental memory depends upon the nondominant hemisphere. They introduce their relucatance to divide the hemispheres into verbal and nonverbal realm, but to further parse. He quotes Goldstein (1948) regarding the dedifferentiation of figure and background, and Bernstein NA (M0scow, 1948 in Russian) for the disorganization of movement.
The subjects were given lists of 10 unrelated 2 and 3 syllable words and asked to memorize them. The percentage retrieved was an indication of voluntary memory. In the second experiment subjects were asked to count the number of words with the letter K or thenumber of letters in the series. Then, retrieval was assessed as a measure of passive memory. The subjects were fifteen patients with left hemisphere lesions, fifteen with right hemisphere lesions, and fifteen normal controls (college students). The results showed that left hemisphere lesions were particularly impaired on active memorizing, whereas the right hemisphere patients were severely impaired on passive memorization. The right hemisphere lesion group showed catastrophic results on passive memorization. The authors speculate the findings indicated the concentration of attention on the conscious non memory task blocked the retrieval of background traces.
Caplan B (Hemispheric dominance for intentional and automatic processes: a test of the Luria and Simernitskaya hypotheses Neuropsychologia 22:247 1984) proposes the results were more consistent with material specific deficits following unilateral lesions.
The authors propose a novel theory of brain reorganization wherein active, intentional memorization is governed by the dominant hemisphere, and involuntary or incidental memory depends upon the nondominant hemisphere. They introduce their relucatance to divide the hemispheres into verbal and nonverbal realm, but to further parse. He quotes Goldstein (1948) regarding the dedifferentiation of figure and background, and Bernstein NA (M0scow, 1948 in Russian) for the disorganization of movement.
The subjects were given lists of 10 unrelated 2 and 3 syllable words and asked to memorize them. The percentage retrieved was an indication of voluntary memory. In the second experiment subjects were asked to count the number of words with the letter K or thenumber of letters in the series. Then, retrieval was assessed as a measure of passive memory. The subjects were fifteen patients with left hemisphere lesions, fifteen with right hemisphere lesions, and fifteen normal controls (college students). The results showed that left hemisphere lesions were particularly impaired on active memorizing, whereas the right hemisphere patients were severely impaired on passive memorization. The right hemisphere lesion group showed catastrophic results on passive memorization. The authors speculate the findings indicated the concentration of attention on the conscious non memory task blocked the retrieval of background traces.
Caplan B (Hemispheric dominance for intentional and automatic processes: a test of the Luria and Simernitskaya hypotheses Neuropsychologia 22:247 1984) proposes the results were more consistent with material specific deficits following unilateral lesions.
Luria's frontal lobe syndrome: psychological and anatomical considerations
Canavan AGM, Janota I, Schurr PH. JNNP 1985; 48: 1049-1053. Authors cast doubt on Luria's "frontal lobe syndrome" except in cases of more global cerebral dysfunction.
Complexmotor function in humans: validating and extending the postulates pf Alexandr R. Luria
Bhimani AA, Hlustik P, Small SL, Solodkin A. Cog Behav Neurol 2006; 19:11-20.
The authors use functional imaging to elaborate the neural circuitry of 3 of Luria's motor tests, modified for convenience with fMRI. The fist-palm-edge test, modified to fist, scissors, gun test, activated M1, S1 and the Supplementary motor area. The hand imitation task activated the right more than the left IFC (inferior frontal cortex) , as well as S1 and PL. The piano key task activated the SMA, pre SMA and LPMCd (lateral premotor cortex).
In the discussion the authors noted the contralateral M! activated without fail during movement, but ipsilateral activation was seen for simple movements. The paino key task had LESS ipsilateral M! activation than did fist-scissors-gun. (Familiarity diminished activation, and all subjects had typing experience per authors). However all 3 tasks had some ipsilateral activation. S1 activation was thought necessary to the requirement for proprioception activation. PL (parietal lobe) was extensively activated for the hand imitation task, as in other studies the area is shown tobe important for visuomotor transformation (Luria, Higher Cortical Functions), mental imagery rotation (Bonda et al. J Neurophysiol, 1996), and mechanisms of imitation (Iacoboni M et al. Science 1999; 286:2526-2528).
HI task is thought by Rizolatti to be part of the continuum of learning language through imitation (Trends in Neurosci 1998). The deficit was for static not dynamic HI which may be separately affected. Left preference was not seen, unlike cases in literature (Poizner et al.) nor in PK task perhaps due to familiarity. The piano key task had more activation of the pre SMA, perhaps due to self pacing.
The cerebellar cortex was crucially activated in all 3 tasks. Activation however, was generally ipsilateral.
The authors use functional imaging to elaborate the neural circuitry of 3 of Luria's motor tests, modified for convenience with fMRI. The fist-palm-edge test, modified to fist, scissors, gun test, activated M1, S1 and the Supplementary motor area. The hand imitation task activated the right more than the left IFC (inferior frontal cortex) , as well as S1 and PL. The piano key task activated the SMA, pre SMA and LPMCd (lateral premotor cortex).
In the discussion the authors noted the contralateral M! activated without fail during movement, but ipsilateral activation was seen for simple movements. The paino key task had LESS ipsilateral M! activation than did fist-scissors-gun. (Familiarity diminished activation, and all subjects had typing experience per authors). However all 3 tasks had some ipsilateral activation. S1 activation was thought necessary to the requirement for proprioception activation. PL (parietal lobe) was extensively activated for the hand imitation task, as in other studies the area is shown tobe important for visuomotor transformation (Luria, Higher Cortical Functions), mental imagery rotation (Bonda et al. J Neurophysiol, 1996), and mechanisms of imitation (Iacoboni M et al. Science 1999; 286:2526-2528).
HI task is thought by Rizolatti to be part of the continuum of learning language through imitation (Trends in Neurosci 1998). The deficit was for static not dynamic HI which may be separately affected. Left preference was not seen, unlike cases in literature (Poizner et al.) nor in PK task perhaps due to familiarity. The piano key task had more activation of the pre SMA, perhaps due to self pacing.
The cerebellar cortex was crucially activated in all 3 tasks. Activation however, was generally ipsilateral.
Monday, May 19, 2008
Hallucinations and related conditions
from S Tekin and JL Cummings, Clinical Neuropsychology, fourth edition, ed by Heilman KM and Valenstein E, chapter 17. An overview of semiology and terminology:
Unusual syndromes
Hallucinations with eye disorders: trauma, cataracts, macular degeneration, choroidal revascularization, retinal detachment, retinal traction, central retinal vein occlusion, and serous retinopathy. Moore's lighting streaks are vertical bands of light in temporal fields during eye movements. Saccades may cause flick phosphenes which are streaks of light in the central visual field. Photopsias are light with geometric structure. Phantom vision may occur after visual loss or enucleation. Hallucinations are rare after visual loss in the young.
The Charles Bonnet syndrome are visual hallucinations in normal elderly usually due to deprivation often with insight, usually pleasant formed images lasting for a few seconds to all day and disappearing with eye closure. Age, poor vision and binocular vision loss are risk factors. They are worse in demented patients and can be precipitated by beta blockers.
Entopic phenomena are actual visual phenomena, not hallucinations, occurring due to particles in the vitreous, macular edema or elements of one's own retinal circulation (Scheere's phenomena). Vitreous deposits (floaters) occur as amoeba shaped or shadow like forms.
Optic neuritis or compressive ischemic optic neuropathy may cause unformed visual hallucinations, including phosphenes, which occur in dim lighting often with horizontal saccades. Sudden sounds can cause auditory visual synesthesia.
Peduncular hallucinosis as part of the top of the basilar syndrome are vivid and full of motion including small (Lilliputian) people, animals, or kaleidoscopic views of landscapes. They occur in the evening or night and last a few seconds or minutes over days to weeks. Visual acuity and fields are normal. They are pleasant. Associations are abnormal SWS, impaired EOM's, and abnormal balance between serotonin and dopaminergic stimulation.
Release hallucinations occur with homonymous hemianopsia in 13 % of such patients, and consist of complex visual patterns, colored patterns or formed images in the area of the defect, and last minutes to hours. The "picture within a picture " sign was described in someone with a right parietal lesion, who saw people "milling around" only in the lower left quadrantanopic field.
Epileptic hallucinations are brief and stereotyped and in the occipital cortex are usually unformed, consisting of colored lights, weaving patterns, zig-zag lights, spots or amaurosis. Complex or formed visual hallucinations usually originate in the parietal or temporal association cortex. Epileptic hallucinations usually occur in one quadrant or hemifield and may be associated with motion, often rapid motion contralateral to the seizure focus. Headache may follow a seizure.
Migraines cause unformed flashes of light, or color, scintillating scotomas and zig zag lines called "fortification spectra." Reproductions of self or body parts in external space are called autoscopic phenomena. Migraine fortification spectra tend to be linear and black and white and last longer than epileptic phenomena, which tend to be multicolored circular or spheroid patterns.
Migraine visual phenomena tend to move across one fourth or one half the visual field and to grow in size as they do. Blurring of part or all of the field with scintillating lights around a scotoma is more common than fortification spectra.
Narcoleptics have hypnagogic and hypnopompic hallucinations which may be formed or unformed and associated with sleep paralysis.
In Parkinson's disease, hallucination are realistic nonthreatening images of people or animals and may be treatment associated. In Lewy body dementia hallucinations (by definition) occur in the first year.
Hallucinations in AD are as high as 67 % in facilities (much lower at home) and are associated with aggressive behavior. Such patients may also have visual processing deficits.
In DT's, patients usually see animals but may see Lilliputian hallucinations.
LSD usually causes visual hallucinations exacerbated by eye closure, geometric colors or audiovisual synesthesia. In general hallucinosis correlates with serotoninergicity. Other drugs include PCP, mescaline, cocaine, and meth (ecstasy) cause hallucinations.
Eidetic imagery is vivid internal imagery expressed onto the outside.
In depression, hallucinations are mood congruent, whereas in schizophrenia they are not.
Musical hallucinations occur in deafness, encephalitis, epilepsy, , and temporal lobe lesions.
Tactile hallucinations occur after amputations including children born without limbs. If they have the feeling of amputated limbs moving they are called kinesthetic hallucinations.Formication hallucinations (of bugs crawling) occur in DT's, schizophrenia, complex partial seizures, the use of hallucinogens, or if unilateral,with thalamic or parietal lesions.They also can be paraneoplastic in origin.
Narcoleptics may experience auditory hallucinations such as collections of sounds or melodies or tactile ones such as pinching, rubbing, light touching, or feeling above the bed and seeing one's own body below. They are complex and realistic.
Olfactory hallucinations may be part of an aura or complex partial seizure, and emanate from the olfactory bulb, posterior medial frontal cortex, olfactory cortex, uncus or anterior temporal lobe.
Gustatory hallucinations are especially common with uncinate gyrus seizures with a bitter, sweet, salty or tobacco like metallic or indescribable strange taste. They occur in 4 % of TLE, and parietal opercula seizures. Visceral hallucinations are common in TLE.
Drugs can cause hallucinations. Notably, digoxin can cause a yellow green tinge and sildafenil a blue tinged hallucination.
Unusual syndromes
Hallucinations with eye disorders: trauma, cataracts, macular degeneration, choroidal revascularization, retinal detachment, retinal traction, central retinal vein occlusion, and serous retinopathy. Moore's lighting streaks are vertical bands of light in temporal fields during eye movements. Saccades may cause flick phosphenes which are streaks of light in the central visual field. Photopsias are light with geometric structure. Phantom vision may occur after visual loss or enucleation. Hallucinations are rare after visual loss in the young.
The Charles Bonnet syndrome are visual hallucinations in normal elderly usually due to deprivation often with insight, usually pleasant formed images lasting for a few seconds to all day and disappearing with eye closure. Age, poor vision and binocular vision loss are risk factors. They are worse in demented patients and can be precipitated by beta blockers.
Entopic phenomena are actual visual phenomena, not hallucinations, occurring due to particles in the vitreous, macular edema or elements of one's own retinal circulation (Scheere's phenomena). Vitreous deposits (floaters) occur as amoeba shaped or shadow like forms.
Optic neuritis or compressive ischemic optic neuropathy may cause unformed visual hallucinations, including phosphenes, which occur in dim lighting often with horizontal saccades. Sudden sounds can cause auditory visual synesthesia.
Peduncular hallucinosis as part of the top of the basilar syndrome are vivid and full of motion including small (Lilliputian) people, animals, or kaleidoscopic views of landscapes. They occur in the evening or night and last a few seconds or minutes over days to weeks. Visual acuity and fields are normal. They are pleasant. Associations are abnormal SWS, impaired EOM's, and abnormal balance between serotonin and dopaminergic stimulation.
Release hallucinations occur with homonymous hemianopsia in 13 % of such patients, and consist of complex visual patterns, colored patterns or formed images in the area of the defect, and last minutes to hours. The "picture within a picture " sign was described in someone with a right parietal lesion, who saw people "milling around" only in the lower left quadrantanopic field.
Epileptic hallucinations are brief and stereotyped and in the occipital cortex are usually unformed, consisting of colored lights, weaving patterns, zig-zag lights, spots or amaurosis. Complex or formed visual hallucinations usually originate in the parietal or temporal association cortex. Epileptic hallucinations usually occur in one quadrant or hemifield and may be associated with motion, often rapid motion contralateral to the seizure focus. Headache may follow a seizure.
Migraines cause unformed flashes of light, or color, scintillating scotomas and zig zag lines called "fortification spectra." Reproductions of self or body parts in external space are called autoscopic phenomena. Migraine fortification spectra tend to be linear and black and white and last longer than epileptic phenomena, which tend to be multicolored circular or spheroid patterns.
Migraine visual phenomena tend to move across one fourth or one half the visual field and to grow in size as they do. Blurring of part or all of the field with scintillating lights around a scotoma is more common than fortification spectra.
Narcoleptics have hypnagogic and hypnopompic hallucinations which may be formed or unformed and associated with sleep paralysis.
In Parkinson's disease, hallucination are realistic nonthreatening images of people or animals and may be treatment associated. In Lewy body dementia hallucinations (by definition) occur in the first year.
Hallucinations in AD are as high as 67 % in facilities (much lower at home) and are associated with aggressive behavior. Such patients may also have visual processing deficits.
In DT's, patients usually see animals but may see Lilliputian hallucinations.
LSD usually causes visual hallucinations exacerbated by eye closure, geometric colors or audiovisual synesthesia. In general hallucinosis correlates with serotoninergicity. Other drugs include PCP, mescaline, cocaine, and meth (ecstasy) cause hallucinations.
Eidetic imagery is vivid internal imagery expressed onto the outside.
In depression, hallucinations are mood congruent, whereas in schizophrenia they are not.
Musical hallucinations occur in deafness, encephalitis, epilepsy, , and temporal lobe lesions.
Tactile hallucinations occur after amputations including children born without limbs. If they have the feeling of amputated limbs moving they are called kinesthetic hallucinations.Formication hallucinations (of bugs crawling) occur in DT's, schizophrenia, complex partial seizures, the use of hallucinogens, or if unilateral,with thalamic or parietal lesions.They also can be paraneoplastic in origin.
Narcoleptics may experience auditory hallucinations such as collections of sounds or melodies or tactile ones such as pinching, rubbing, light touching, or feeling above the bed and seeing one's own body below. They are complex and realistic.
Olfactory hallucinations may be part of an aura or complex partial seizure, and emanate from the olfactory bulb, posterior medial frontal cortex, olfactory cortex, uncus or anterior temporal lobe.
Gustatory hallucinations are especially common with uncinate gyrus seizures with a bitter, sweet, salty or tobacco like metallic or indescribable strange taste. They occur in 4 % of TLE, and parietal opercula seizures. Visceral hallucinations are common in TLE.
Drugs can cause hallucinations. Notably, digoxin can cause a yellow green tinge and sildafenil a blue tinged hallucination.
Monday, May 12, 2008
Regional frontal injuries cause distinct impairments in cognitive control
Alexander MP, Stuss DT, Picton T el al. Neurology 2007; 68: 1515-1523. 42 patients and 38 CS performed a modified Stroop test. Lesions in the left ventrolateral area produced errors of commission (ie utilization behavior) whereas lesions of the right ant cing, SMA, pre SMA or DL area caused a slowed reaction time (errors of omission).
Comment- a wonderful example of an advanced ablation paradigm article that is current, parcelling out frontal lobe function.
Aphasia: progress in the last quarter of a century
Hillis AE. Neurology 2007; 69: 200-213. (Views and reviews).
Summary: Dax, Broca and Wernicke made observations that Geschwind then summarized and reclassified in the 1960's. His BDAE held throught the CT/ MRI era.
In the 1980s, PET, fMRI and MEEG revolutionized our thinking. They showed bilateral involvement during language tasks, although the left hemisphere has more activation. These activated areas include remote locales such as inferior and anterior temporal cortex and basal ganglia and thalamus. The cognitive processes involved in language tasks in increasingly complex models were mapped out, involving PDP systems, linguistics, mathematics, and neuroscience. Third, analysis of dementia allowed analysis of semantic dementia after lobar degeneration, which does not occur after stroke.
Minutiae discovered include the constant finding of activation of the midfusiform area during reading, and the left midfusiform area during naming and other lexical tasks. Inhibition with cortical stimulation among presurgical epileptic patients of this area or the posterior basal temporal area disrupts kanji (represents meanings not sounds) and picture naming (semantic to phonologic conversions are necessary) but not comprehension of kana (sounds of words), copying or tool use (Usui, Brain 2003). Infarction of this area caused impaired oral reading and naming.
Classic aphasiology is reviewed. In Broca's aphasia, "nonfluency"can refer to decreased length of phrases, impaired melodies and articulatory agility, decreased words per minute, or agrammatism. Most patients have islands of preserved fluency especially of overlearned speech. This confounds classification. Comprehension of complex forms or noncanonical phrases (eg. passive voice) or comparisons of word order or meaning are damaged (Is a horse larger than a dog?) as is spelling of familiar words, and use of phonics to spell unfamiliar words. She criticizes the argument htat a single underlying impairment can cause Broca's syndrome, but allows that it is a vascular syndrome. She also discusses the conundrum of Broca's area lesion causing speech apraxia, and warns against excessive inflexibility in "localization," since individuals vary in their makeup. Hypoperfusion of surrounding tissue without infarction is another source of error.
Wernicke's aphasia consists of fluent jargons, neologisms, and lack of awareness of the deficit. Melody is preserved. Writing parallels speech (meaningless). It relates to posterior division of the MCA .
ACA lesions cause TCM aphasia (or watershed strokes between ACA and MCA).
Conduction aphasia has fluent accurate spontaneous speech with phonemic paraphasias, with conduit 'approche. Author rebuts Geschwind that the arcuate fasciculus is important, citing lesions in SMG or deep parietal white matter and on lesion studies showing lack of reliability of arcuate fasciculus lesions causing conduction aphasia.
Author discusses pure alexia and takes the classic disconnection explanation, emphasizing the co-occurrence with optic aphasia and the similarity of the neurologic lesions. She discusses semantic errors in such patients noting that they are partial.
Hillis discusses aphasia secondly, from the pov of the distributed semantic networks implied in addition to the previously described vascular syndromes. These account for category selectivity in naming, eg.
Treatment is discussed briefly, but author notes that intense treatment 4 days per week for a short time is more effective than spread out sessions over alonger period (Bhogal, Stroke, 2003).
Summary: Dax, Broca and Wernicke made observations that Geschwind then summarized and reclassified in the 1960's. His BDAE held throught the CT/ MRI era.
In the 1980s, PET, fMRI and MEEG revolutionized our thinking. They showed bilateral involvement during language tasks, although the left hemisphere has more activation. These activated areas include remote locales such as inferior and anterior temporal cortex and basal ganglia and thalamus. The cognitive processes involved in language tasks in increasingly complex models were mapped out, involving PDP systems, linguistics, mathematics, and neuroscience. Third, analysis of dementia allowed analysis of semantic dementia after lobar degeneration, which does not occur after stroke.
Minutiae discovered include the constant finding of activation of the midfusiform area during reading, and the left midfusiform area during naming and other lexical tasks. Inhibition with cortical stimulation among presurgical epileptic patients of this area or the posterior basal temporal area disrupts kanji (represents meanings not sounds) and picture naming (semantic to phonologic conversions are necessary) but not comprehension of kana (sounds of words), copying or tool use (Usui, Brain 2003). Infarction of this area caused impaired oral reading and naming.
Classic aphasiology is reviewed. In Broca's aphasia, "nonfluency"can refer to decreased length of phrases, impaired melodies and articulatory agility, decreased words per minute, or agrammatism. Most patients have islands of preserved fluency especially of overlearned speech. This confounds classification. Comprehension of complex forms or noncanonical phrases (eg. passive voice) or comparisons of word order or meaning are damaged (Is a horse larger than a dog?) as is spelling of familiar words, and use of phonics to spell unfamiliar words. She criticizes the argument htat a single underlying impairment can cause Broca's syndrome, but allows that it is a vascular syndrome. She also discusses the conundrum of Broca's area lesion causing speech apraxia, and warns against excessive inflexibility in "localization," since individuals vary in their makeup. Hypoperfusion of surrounding tissue without infarction is another source of error.
Wernicke's aphasia consists of fluent jargons, neologisms, and lack of awareness of the deficit. Melody is preserved. Writing parallels speech (meaningless). It relates to posterior division of the MCA .
ACA lesions cause TCM aphasia (or watershed strokes between ACA and MCA).
Conduction aphasia has fluent accurate spontaneous speech with phonemic paraphasias, with conduit 'approche. Author rebuts Geschwind that the arcuate fasciculus is important, citing lesions in SMG or deep parietal white matter and on lesion studies showing lack of reliability of arcuate fasciculus lesions causing conduction aphasia.
Author discusses pure alexia and takes the classic disconnection explanation, emphasizing the co-occurrence with optic aphasia and the similarity of the neurologic lesions. She discusses semantic errors in such patients noting that they are partial.
Hillis discusses aphasia secondly, from the pov of the distributed semantic networks implied in addition to the previously described vascular syndromes. These account for category selectivity in naming, eg.
Treatment is discussed briefly, but author notes that intense treatment 4 days per week for a short time is more effective than spread out sessions over alonger period (Bhogal, Stroke, 2003).
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