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Nutritional Deficiencies
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Deepa Bhupali, Fernando D. Testai
Neurologic manifestations: Cognitive decline: patients present with different degrees of cognitive involvement (lethargy, stupor, and coma) and seizures. Symptoms may evolve rapidly (delirium) or have a more protracted course (dementia).Apraxia: ideomotor apraxia may be seen in formal neurocognitive evaluation. The callosal necrosis causes interhemispheric disconnection, which manifests clinically by nondominant (usually left-sided) apraxia, alien hand phenomenon, and hemialexia without agraphia.
Motor Aspects of Lateralization: Evidence for Evaluation of the Hypotheses of Chapter 8
Published in Robert Miller, Axonal Conduction Time and Human Cerebral Laterality, 2019
Ideational apraxia is a motor disorder at a higher level than ideomotor apraxia. Patients typically are impaired in sequencing actions requiring the use of various objects in the correct order and sequence, in order to achieve a goal. According to Poeck (1986)this disorder is rare, but, when it occurs is chiefly in cases of lesions of the language-dominant hemisphere.
Signs and Symptoms in Psychiatry
Published in Mohamed Ahmed Abd El-Hay, Essentials of Psychiatric Assessment, 2018
Ideomotor apraxia: patients cannot perform on command acts that can be performed spontaneously. This results from lesions in the supramarginal gyrus presumably involving the fibers of the left arcuate fasciculus or in the left premotor cortex. Commands should include those for: orofacial (e.g., drink through a straw, lick lips, blow out a match);limb (e.g., hammer a nail, a military salute, waving goodbye);whole body movements (trunk apraxia): there is inadequate positioning of the body in bed or chair (e.g., stand like a boxer).
Body representation in people with apraxia post Stroke– an observational study
Published in Brain Injury, 2021
Donncha Lane, Alessia Tessari, Giovanni Ottoboni, Jonathan Marsden
Apraxia has been attributed to a conceptual or production problem when performing a desired action (13–15). The conceptual component of complex movements involves knowledge of action sequences and/or knowledge of tool use with the deficit in these commonly known as ideational apraxia. Ideomotor apraxia is a deficit in the production of both known, meaningful gestures (including transitive movements that involve tool use, or intransitive movements such as communication gestures) and novel, meaningless gestures. Ideomotor Apraxia is usually diagnosed by asking people to perform meaningful or meaningless gestures either by imitating the examiner (i.e. using visual cues) or pantomiming (i.e. following verbal commands).
The reliability and validity of the Turkish version of the apraxia screen of TULIA in multiple sclerosis patients
Published in Disability and Rehabilitation, 2022
Zeynep Yıldız, Fadime Doymaz, Fatih Özden
Apraxia occurs when CNS lesions damage the anterior cingulate, corpus callosum, and/or posterior parietal cortex, core tractus solitaries, hypothalamus, amygdala, insular cortex, and anterior cingulate cortex and parietofrontal pathways. In the case of ideomotor apraxia, patients cannot conduct movements purposefully. Individuals with apraxia are able to do automatic movements. For instance, patients with apraxia can brush their teeth. However, they cannot carry out this task when asked to do a different movement with the toothbrush. Furthermore, in the case of ideational apraxia, patients fail to complete automatic movements [7,8].
A case of intravascular large B cell lymphoma with brain involvement mimicking progressive multifocal leukoencephalopathy
Published in International Journal of Neuroscience, 2023
Elisabetta Belli, Chiara Milano, Ilaria Pesaresi, Ilaria Trivelli, Antonio Tavoni, Eugenio Ciancia, Greta Alì, Virna Zampa, Chiara Pizzanelli, Gabriele Siciliano, Giulia Ricci
Over the following few weeks, a rapid and progressive deterioration of her neurological conditions appeared, with apraxia, emotional lability, and mental confusion. During this period, she came to our attention and was admitted to our Neurology Unit. At neurological examination, the patient was alert and partially oriented; she presented with motor and verbal perseveration and ideomotor apraxia. No cranial nerves alterations or strength deficits in superior limbs were evident, but she was unable to walk and even to lift inferior limbs against gravity due to bilateral weakness with marked pain. Blood tests confirmed reduced levels of haemoglobin and platelets, consistent with the diagnosis of myelofibrosis, and elevated value of LDH (4538 U/L, normal values 135-214 U/l), while CPK levels were normal. The first brain MRI showed multiple large and confluent lesions which mainly involved supratentorial white matter with an asymmetrical pattern. They appeared hyperintense on T2-weighted images, slightly hypointense on T1-weighted images and did not show significant contrast enhancement or mass effect. Diffusion-weighted images (DWI) revealed multiple foci of restricted diffusion (Figure 1a–c). Such MRI findings were highly suggestive of PML. Since we found a report in literature of PML occurred during Ruxolitinib therapy [2], the treatment she took for 45 days – without any effects on the disease progression – was immediately stopped. Nevertheless, JC and BK virus were not detected in the cerebrospinal fluid (CSF) and all the other CSF tests were unremarkable. Human immunodeficiency virus test was negative and CD4 and CD8 T-lymphocyte counts were normal. Despite discontinuation of Ruxolitinib, her neurologic condition further worsened, with severe tetraparesis, diffuse muscular pain and progressive reduced level of consciousness. Moreover, during the following days, several subcutaneous nodules appeared on her upper and lower limbs: a musculoskeletal MRI of the lower extremities showed imbibition of fat tissue and diffuse muscle oedema (Figure 2a, b). In order to better characterize the subcutaneous lesions and the muscle involvement, we decided to perform a skin and quadriceps femoris biopsy. Muscle biopsy revealed the presence of several rounded and sharply angulated atrophic fibres, along with split fibres and necrotic fibres with phagocytosis. Adipose substitution of muscular tissue and atypical lymphoid elements in the lumen of medium-calibre vessels were observed. Succinate dehydrogenase (SDH), cytochrome c oxidase (COX), and reduced nicotinamide adenine dinucleotide (NADH) histochemical assays showed decreased staining in all muscle fibres.