Delayed leukoencephalopathy after carbon monoxide poisoning presenting as subacute dementia.

We herein report the case of a 65-year-old woman who presented with the subacute onset of dementia and subsequently developed abnormal behavior and a gait disturbance. Her condition transiently improved; however, within one month, she became drowsy and poorly responsive, with limb chorea and urinary incontinence. Her history of frequently using charcoal led us to diagnose her with carbon monoxide (CO) poisoning. The findings of this case and a literature review suggest that subacute dementia due to CO poisoning recovers late, after a year or more, in patients above sixty years of age, and both hyperbaric oxygen and corticosteroid pulse therapy should be considered in such cases, even after one month.

Isolated thalamic agraphia with impaired grapheme formation and micrographia.

Two patients with isolated thalamic agraphia are described. Both showed kanji (Japanese morphograms) agraphia due to impaired character recall, grapheme deformity and micrographia (progressive reduction in character size during writing) after a lesion that involved the ventral lateral and ventroposterolateral nuclei. Single photon emission computed tomography with a (99m)Tc-ethylcysteinate dimer revealed hypoperfusion in the left precentral gyrus (Brodmann Area 6) and anterior supramarginal gyrus in both. Six months later, the extent of blood flow reduction decreased in the supramarginal gyrus in both patients and the precentral gyrus in patient 1. By this time, the writing impairment improved to nearly the normal range. Our study suggests that kanji agraphia (corresponding to lexical agraphia in Western countries) with poor grapheme formation and micrographia arises from a lesion in the ventral lateral and ventroposterolateral nuclei in the left thalamus. The accompaniment of poor grapheme formation and micrographia may reflect disruption of the cortico-subcortical motor circuit involving the putamen, thalamus, premotor cortex and sensorimotor cortex. It is also suggested that multiple cortical sites can be a target for secondary dysfunction that yields agraphia in a thalamic lesion, and that the recovery of reduced cortical blood flow does not always proceed in parallel with that of agraphia.

Parietal dysgraphia: characterization of abnormal writing stroke sequences, character formation and character recall.

OBJECTIVE: To characterize various dysgraphic symptoms in parietal agraphia. METHOD: We examined the writing impairments of four dysgraphia patients from parietal lobe lesions using a special writing test with 100 character kanji (Japanese morphograms) and their kana (Japanese phonetic writing) transcriptions, and related the test performance to a lesion site. RESULTS: Patients 1 and 2 had postcentral gyrus lesions and showed character distortion and tactile agnosia, with patient 1 also having limb apraxia. Patients 3 and 4 had superior parietal lobule lesions and features characteristic of apraxic agraphia (grapheme deformity and a writing stroke sequence disorder) and character imagery deficits (impaired character recall). Agraphia with impaired character recall and abnormal grapheme formation were more pronounced in patient 4, in whom the lesion extended to the inferior parietal, superior occipital and precuneus gyri. CONCLUSION: The present findings and a review of the literature suggest that: (i) a postcentral gyrus lesion can yield graphemic distortion (somesthetic dysgraphia), (ii) abnormal grapheme formation and impaired character recall are associated with lesions surrounding the intraparietal sulcus, the symptom being more severe with the involvement of the inferior parietal, superior occipital and precuneus gyri, (iii) disordered writing stroke sequences are caused by a damaged anterior intraparietal area.