Canadian biopsychologist, John Pinel developed an acoustic neuroma, but it was not diagnosed by his family physician. Because of his training and experience as a biopsychologist, Professor Pinel was able to diagnose his own tumor. The tumor was subsequently excised, but not without life-threatening complications. Professor Pinel subsequently designed his own program of rehabilitation based on recent research on neuroplasticity, and his recovery was excellent. In this article, Professor Pinel relates his tumor-related experiences. Two aspects of Professor Pinel's experiences are emphasized. First, he emphasizes ways in which he reacted to his tumor and treatment that were unconventional because of his years of experience as a professor of biopsychology. Second, he emphasizes important insights that he learned from his personal brain-related experiences—things that he did not fully appreciate, despite his considerable experience as a teacher and researcher of biopsychology.

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  Several cases, aphasic or non-aphasic, with anterior cerebral lesions were reported in order to reconsider the symptomatology of non-fluent aphasia. Included in this study were 10 cases with pure anarthria, 3 cases with Broca's area aphasia, 3 cases with transcortical motor aphasia, and 2 cases with atypicalBroca's aphasia.
  Among the various elements contributing to non-fluent verbal outputs in aphasics, anarthia is the most prominent feature and has the most definite anatomical correlate. The responsible lesion for anarthria is the lower portion of the middle third in the precentral gyrus. Within the precetral gyrus, the posterior portion is more important than the anterior portion. Damage to insula or Broca's area does not produce phomemic nor phonetic distur bances.
  Besides anarthria, neurobehavioral and neurolinguistic symptoms such as an aspontaneity of speech, word-finding difficulties, and an inability to construct sentences, are also important factors contributing to non-fluency. In some cases, the disturbance of the selection of words in running speech or deficits in verbal planning would play an important role in producing non-fluent speech. Therefore, the origins of non-fluent utterances could not be attributed only to anarthria or the reduction of impulse to speak.

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  In this paper, the author selected a mild Broca's aphasic, a 47-year-old female, and aimed to analyze her articulation problems including (1) disability in “speech sequential motion rate”(sequential repetition of/pataka/), (2) devoicing in repetitive production of voiced consonants, and (3) difficulty in devoicing of close vowels /i/and/_??_/under the given environment of speaking Japanese, using computerized software for acoustic analysis of speech. MRI revealed a clear lower density area in the frontal lobe. She showed “substitution” due to delay in voice on set time, substituting/p/for/b/,/t/for/d/and/k/for/g/, and “devoicing of close vowels” did not occur in the early stage of speech therapy. However, the above-mentioned phonetic problems disappeared after her abilities to read aloud and perform the tasks of sequential motion rate had improved. The author used the term AOS for some characteristic articulation problems which were caused by her poor regulative function of the timing of articulatory and laryngeal activity. Drills in repetition tasks of/pataka/or/badaga/and complex multisyllabic words such as/hakubutukan/(“museum” in Japanese)and sentence-reading tasks proved helpful for the improvement of articulation problems in this Braca's aphasic patient. Software for acoustic analysis of speech was a useful tool for evaluating the recovery of her speech disorders.

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  We reported a case impaired across a range of auditory input processing and spoken word production tasks.
  The patient is a 90-year-old right-handed male suffering from a cerebral infarction. MRI revealed a small lesion lying scattered in the left superior temporal gyrus and lower parietal lobe.
  His speech was grammatically well formed, but often interrupted by pauses because of selfcorrected phonemic errors. Prolonged, extraordinary pitch and distortion were exhibited. On confrontation naming, he could retrieve lexical representation ; however, similar sound errors were revealed. Surprisingly, in repetition he occasionally replied semantic paraphasias or formal paraphasias. Also, performance showed reverse word frequency and was affected by word imageability. He was entirely unable to repeat nonwords. Reading comprehension was spared. Reading aloud of kana words and nonwords was well preserved. These features share a number of similarities with deep dysphasia.
  His auditory word comprehension was nearly preserved. However, in auditory lexical decision tasks he tended to reject all stimuli that he could not recognize with certainty. Auditory phoneme discrimination of TLPA was in the nearly normal range. These features resemble “word form deafness.”
  Upon examining the patient's phonological awareness, we found rhyme judgment, homophone judgment and syllable deletion were all poor. He was unable to make associations with phonological representations accurately based on elementary speech sounds. We nevertheless concluded that he recognized a word because he captured the contour or supra-segmental features of words.
  The features of both his input and output suggest that the underlying mechanism of his impairments is inability of segmentation of sound structure.

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  How can we apply the knowledge and techniques obtained from speech science to the clinical issues of speech disorders including apraxia of speech? In this paper, I introduced some topics relating to the question. First, three-layered hierarchy of the speech production processes(phonological, phonetic, and articulatory levels) was defined. Second, models corresponding to the process for each level were presented, and mechanisms of speech disorders were described based on these models. I pointed out the difficulty in diagnosis of speech disorders only by hearing impression because speech production processes in the hierarchy are influenced each other with a complex manner. Lastly, I introduced some techniques to observe articulatory movements and brain function which might improve the understanding of mechanisms of speech disorders. Cooperative promotions for developing new observation methods, constructing theoretical models and accumulating clinical data can improve the understanding mechanisms and clinical issues in the speech disorders.

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  [Background] There are few therapeutic approaches for patients with corticobasal degeneration(CBD). We report a case of CBD whose physical and cognitive symptoms were partially ameliorated by SSRI.[Case] A right-handed, 80-year-old man, with 6 years educational level was studied. He had several episodes of fall from 2001. Speech disturbance became worse at the end of 2002. He was diagnosed as pseudo-bulbar palsy caused by cerebral infarctions at a hospital. His dysarthria and dysfunction of left upper arm got worse gradually, and he was admitted to our hospital in May, 2004. Neurologically, he had dysarthria, impairment of vertical eye movement, hyper-activity of jaw jerk reflex, decreased gag reflex, paratonic rigidity, increased deep tendon reflex, and mild retropulsion. He had disorder of attention, executive function, mental speed, and construction. MRI disclosed the right central sulcus being wider than the left. There were cerebral blood flow reduction at the periphery of right central sulcus and right basal ganglia as shown by SPECT. His symptoms met the CBD criteria of the ministry of Health, Labour and Welfare of Japan, and the Boeve's criteria. When he took SSRI(Paroxetine 10mg), his walking speed and balance were improved. Cognitive functions were also improved in the 2-or-3-month follow up evaluation; MMSE from 20 to 25, digit span backward from 3 to 4, trail making test part B from ‘incomplete’ to complete(16' 29" ), Rey's complex figure copy from 22. 5 to 29, immediate recall from 9. 5 to 15, delayed recall from 8. 5 to 13. 5.[Discussion] We considered that the patient's physical and cognitive dysfunctions were ameliorated by the replacement of serotonin which decreased in the brain of CBD.

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  We report on a case of aphasia that developed owing to injury to the left hemisphere. The aphasia improved slowly, but worsened mainly in using phonemes and kana after injury to the right hemisphere due to recurrence one year later. There appeared untranscribable jargon and logoclonia. Improvement is hardly in evidence even after a lapse of two years. The clinical course from the onset of the disease indicates that the homologue area in the contralateral hemisphere might be concerned with recovery of aphasia after the acute phase.
  This case and past cases in the literature show a possibility that functional recovery of aphasia is achieved by the homologue area in the contralateral hemisphere. We studied untranscribable jargon and logoclonia appearing after new injury of the right hemisphere from the viewpoint of disturbed action control of speech.

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  We have evaluated perioperative neuropsychological symptoms in 11 patients who underwent tumor resection with the aid of intraoperative language area mapping. SLTA, Rey's AVLT, ROCFT, KWCST, and RCPM were repeatedly conducted through perioperative periods. Preoperative general assessment of neuropsychological function was effective to detect subclinical symptoms and eventually contributed to the planning of tasks for the intraoperative mapping. During intraoperative mapping, positive response was affected by preoperative neuropsychological function. For cortical mapping, repetition should be included in the tasks. Timing of electrical stimulation and task was important for accurate mapping.

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