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Apraxic agraphia can be caused by left hemispheric cerebral lesions in the area that contains the spatial representations of the movements required to write, from a lesion in, or connections to, the frontal premotor cortex that converts these spatial representations to motor programs (Exner's area). A right-handed woman with Marchiafava Bignami disease and lesions of the genu and splenium of her corpus callosum had apraxic agraphia without ideomotor apraxia of her left. A disconnection of Exner's area in the left hemisphere from the right hemisphere's premotor and motor areas may have led to her inability to write with her left hand.

A 74 year-old woman (MD), free of previous neurological history, presented with difficulty in handling cutlery, clothes, writing with what was initially described as an atypical apraxia in acts related to space. Initial neurological evaluation revealed mixed, asymmetric pyramidal, and extrapyramidal semiology. Νeuropsychological testing revealed dressing and constructional deficits, ideomotor apraxia and signs of executive dysfunction in absence of memory, language, and visual perception pathology. The final diagnosis was that of a corticobasal degeneration, where the rare occurrence of a progressively emerging syndrome of self-management loss within peripersonal space is observed.

Studies of patients with brain lesions have demonstrated that language and praxis are mediated by dissociable networks. However, language has the capacity to influence the selection of purposeful actions. The abilities to use language and to program purposeful movements are often mediated by networks that have anatomic proximity. With hemispheric injury, the diagnosis of apraxia is often confounded by the specific influence of language impairments on the ability to select and produce transitive gestures. We report a patient who illustrates this confound. This patient is a right-handed man who developed global aphasia and neglect after a right hemispheric stroke. His right hand remained deft, and when asked to produce specific transitive gestures (pantomimes), he often performed normally but did make some body part as object and perseverative errors. However, he did not demonstrate the temporal or spatial errors typical of ideomotor apraxia. He also had a perseverative agraphia. Our patient’s left hemisphere praxis system appeared to be intact, and the error types demonstrated during production of transitive gestures cannot be attributed to a degradation of postural and movement (praxis) programs mediated by his left hemisphere. The praxis errors types are most consistent with a deficit in the ability to select the necessary praxis programs. Thus, our patient appeared to have dissociation between language and praxis programs that resulted in body part as object and perseverative errors.

Loss of ability of the left upper limb (LUL) to correctly produce spatial and temporal components of skilled purposeful movements was reported 34 years ago in a woman with a callosal infarction. To learn about recovery, we recently reexamined this woman. This woman was tested for ideomotor apraxia by asking her to pantomime to command and to seeing pictures of tools. Whereas she performed normally with her right upper limb, her LUL remained severely apraxic, making many spatial (postural and movement) errors. Initially, she did not reveal loss of finger-hand deftness (limb-kinetic apraxia), and when tested again with the coin rotation task, her left hand performance was normal. Without vision, she could name objects placed in her left hand but not name numbers written in this hand. Since this woman had a callosal lesion, failure to recover cannot be accounted for by left hemisphere inhibition of her right hemisphere. Although failure for her LUL to improve may have been related to not using her LUL for skilled actions, her right hemisphere was able to observe transitive actions, and this failure of her LUL to produce skilled purposeful movements suggests her right hemisphere may have not had the capacity to learn these movement representations. Without vision, her ability to recognize objects with her left hand, but not numbers written on her left palm, suggests graphesthesia may require that her left hand did not have access to movement representations important for programming these numbers when writing.

Dysgraphia (agraphia) is a common feature of posterior cortical atrophy (PCA). However, detailed analyses of these spelling and writing impairments are infrequently conducted. LM is a 59-year-old woman with dysgraphia associated with PCA. She presented with a two-year history of decline in her writing and dressmaking skills. A 3D T1-weighted MRI scan confirmed selective bi-parietal atrophy, with relative sparing of the hippocampi and other cortical regions. Analyses of LM's preserved and impaired spelling abilities indicated mild physical letter distortions and a significant spelling deficit characterised by letter substitutions, insertions, omissions, and transpositions that was systematically sensitive to word length while insensitive to real word versus nonword category, word frequency, regularity, imagery, grammatical class and ambiguity. Our findings suggest a primary graphemic buffer disorder underlies LM's spelling errors, possibly originating from disruption to the operation of a fronto-parietal network implicated in verbal working memory.

Although ideomotor apraxia (IM) has been a topic of investigation since the early 20th century, progress in studying the disorder has been hindered by important (and sometimes unarticulated) differences in the underlying theoretical models of various investigative groups. As a result, it is difficult to draw conclusions about the expected performance of IM patients on various tests of praxis (e.g. pantomime, single object use, gesture imitation, and naturalistic action); the relationship of IM to ideational apraxia (IA); the degree to which specific error types are diagnostic of one or the other disorder; the relationship of semantic knowledge to gesture representations; and the role of spatiomotor systems external to the stored gesture representation system. Here an updated model of IM is presented, informed by recent physiological and functional neuroimaging literature, as a step towards resolving some of these concerns. The model is intended to lay the groundwork for future investigations of specific performance patterns in different subtypes of IM.

We describe the case of a 74-year-old man with selective apraxia for transitive gestures (gestures of object use) following a left temporo-parietal infarction. We document his neuropsychological progress over 2 years and assess his praxic abilities according to the best-developed cognitive model of praxis. Strikingly, PF was unable to pantomime transitive gestures in every test modality (verbal command, imitation, photographs of objects and handling actual tools), but could still execute symbolic (e.g. salute) and meaningless gestures. He was able to discriminate and recognize transitive gestures as well as controls. His praxic impairment has persisted through the years in the absence of dementia. His inability to use tools cannot be accounted for on the basis of a visual agnosia, impaired language comprehension or a classic ideomotor apraxia. Such a selective deficit of transitive gestures is incompatible with the cognitive model proposing that the production of all meaningful gestures (symbolic...

Limb apraxia occurs in progressive supranuclear palsy (PSP); however, its characteristics and relation to dementia are unclear. We compared 25 probable PSP patients on cognitive and ideomotor apraxia tests with 19 healthy controls. Eleven PSP patients were demented (D-PSP) and 14 not (ND-PSP). D-PSP patients did worse than controls and ND-PSP patients in all cognitive tests; and ND-PSP patients did worse than controls in all except the memory test. In the apraxia test, PSP patients committed mainly sequence errors and executed complex gestures badly. Apraxia correlated strongly with dementia. In PSP, limb apraxia seems mainly due to frontal deafferentation and lesions, but only when these are severe enough to cause dementia.

Corticobasal degeneration (CBD) is a progressive disorder that can be characterised by asymmetrical akinetic rigidity, involuntary movements, cortical sensory loss, alien limb syndrome and asymmetrical apraxia (Gibb et al., 1989; Rinnie et al., 1994). Diagnosis of praxic disabilities is thought to be essential for distinguishing CBD, in its early stage, from other akinetic-rigid syndromes. However, the nature of apraxia in CBD, and the relations between ideomotor and ideational apraxia, are not well understood. For example, if there is an ideational deficit in a given patient, does this deficit occur independently of any ideomotor disorder, or are the two impairments linked in some manner? In the present paper we report a case study of a patient with apraxia due to CBD. We examine whether the disorder is confined to production tasks, or whether there is also a related deficit in recognising the correct actions performed with objects (an ideational deficit). We also evaluate whether a disorder found for action with single objects dissociates from the ability to link multiple actions into more complex, everyday tasks. The performance of our patient showed an impairment in both action production and action recognition system, suggesting a component of ideational as well as ideomotor apraxia in CBD.