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Examination of the Nervous System
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
Tim Fowler, John Scadding, Nick Losseff
Gait apraxia describes problems walking. In dressing apraxias, patients cannot put their clothes on correctly. Constructional apraxias produce problems in copying designs or arranging patterns on blocks.
Clinical management
Published in Alistair Burns, Michael A Horan, John E Clague, Gillian McLean, Geriatric Medicine for Old-Age Psychiatrists, 2005
Alistair Burns, Michael A Horan, John E Clague, Gillian McLean
This is usually slow in onset and gradually progressive. Early on, the patient walks with the feet ci�se together and takes small steps: hips and knees are often flexed. There are frequent pauses followed by another series of steps. As the disorder progresses, initiating walking becomes more and more dif- ficult, as if the feet are glued to the floor. When the patient is examined in a chair or on the bed, neurological signs may be minimal and the patient may be able to mimic walking movements. Dementia may be present and it may not. Not all demented patients develop gait apraxia.
Motor imagery and gait control in Parkinson’s disease: techniques and new perspectives in neurorehabilitation
Published in Expert Review of Neurotherapeutics, 2022
Giovanna Cuomo, Valerio Maglianella, Sheida Ghanbari Ghooshchy, Pierluigi Zoccolotti, Marialuisa Martelli, Stefano Paolucci, Giovanni Morone, Marco Iosa
Essential components of MI are visual and kinesthetic imagery, which refer to the mental proprioceptive perception of muscle contractions and changes [17]. Kinesthetic motor imagery involves the imagination of the sensation of the movement, not just the visualization of the movement as in visual MI, so kinesthetic MI yielded more activity in motor-associated structures and the inferior parietal lobule, suggesting that these two modalities of imagery could be mediated through separate neural systems, whereas visual MI activated predominantly the occipital regions and the superior parietal lobules, so they may contribute differently during processes of motor learning and neurorehabilitation [18]. Gait in MI tasks involves fronto-parietal areas and subcortical areas such as basal ganglia, brainstem, and cerebellum as the actual movements do [19]. Inhibitory and excitatory signals from the brainstem and spinal cord modulate the muscle tone in locomotion*** [19–24]***. Limbic system and basal ganglia have a role in the gait emotional expression [25]. Supplementary motor area appears fundamental to initiate and stop motor gait: lesions in this area result in gait apraxia [26]. Posterior-parietal areas contribute to motor planning and visual feedback, while cerebellum supports proprioception and balance [27,28]. Individual differences in gait imagery abilities might lead to differences in the pattern of brain activation, but the same areas of the gait network are involved [17].
Unusual gait disorders: a phenomenological approach and classification
Published in Expert Review of Neurotherapeutics, 2019
Vijayashankar Paramanandam, Karlo J. Lizarraga, Derrick Soh, Musleh Algarni, Mohammad Rohani, Alfonso Fasano
The concept of HLGD was introduced in 1993 to explain the gait disorder of patients without ‘middle level’ (e.g. cerebellar) or ‘lower level’ (e.g. neuropathic) gait disorders. Unfortunately, the initial description of HLGD was accompanied by an artificial distinction of five forms that also included PPFOG and ‘cautious gait’ (which is a compensatory gait). Thus, other classifications were preferred undermining the popularity of the HLGD concept. Other limitations of similar classifications arise from the distinction based on the presumptive site of anatomical damage. For example, if the dominant feature is severe balance impairment, the terms ‘frontal disequilibrium’ or ‘subcortical disequilibrium’ have been proposed. Frontal disequilibrium is supposed to be caused by frontal lobe dysfunction and is associated with a ‘difficult-to-describe stepping disorder’. In contrast, subcortical disequilibrium is supposed to arise from midbrain, basal ganglia and/or thalamic dysfunction (also known as ‘thalamic astasia’) [1,3,7]. Even though these classifications of gait disorders might be interesting, we recommend avoiding the misnomer ‘gait apraxia’ and to only use HLGD to describe the typical features of lower body parkinsonism caused by disorders of the frontal lobe or its connections with deeper brain structures.
Rapidly progressive dementia in a nonagenarian with acute disseminated encephalomyelitis
Published in Acta Clinica Belgica, 2022
After an initial postictal state clinical assessment showed serious cognitive deficits and several types of apraxia (apraxia of speech, constructional apraxia, gait apraxia, conceptual apraxia, ideomotor apraxia and oculomotor apraxia) with mild frontal disinhibition symptoms, dysarthria, dysphagia, ataxia, nystagmus, bilateral miosis, pyramidal signs with right-sided hemiparesis, cranial nerve involvement with deviated tongue protrusion to the right and left facial paralysis and mild extrapyramidal symptoms.