Assessment
David F. O'Connell in Dual Disorders, 2014
A disturbance in memory may be a sign of a cognitive disorder or may be secondary to other symptoms (such as poor attention span). Determine the following during a conversational interview: Can this patient remember such basic information as his/her birthday, social security number, and phone number?Does this patient seem excessively forgetful and apologetic about his/her poor memory?Can this patient remember prior events of the day (such as what he/she ate for breakfast)?
Plant-Based Natural Products Against Huntington’s Disease: Preclinical and Clinical Studies
Megh R. Goyal, Hafiz Ansar Rasul Suleria, Ademola Olabode Ayeleso, T. Jesse Joel, Sujogya Kumar Panda in The Therapeutic Properties of Medicinal Plants, 2019
Huntington’s disease (HD) is a chronic, progressive, neurodegenerative disorder, characterized by a combination of choreoathetotic movements and cognitive and psychiatric disturbances associated with neuronal death in corticostriatal circuits. Symptoms develop insidiously either as brief, jerky movements of the extremities, trunk, face, and neck (chorea) or as a change in personality and sometimes both [14]. Fine motor in-coordination and impairment of rapid eye movements are early features. Occasionally, choreic movements are less prominent than the predominance of bradykinesia and dystonia in the early onset of symptoms that occurs before age 20. With the progression of the disease, the severity of involuntary movements is higher with development of dysarthria and dysphagia, and patients exhibit a typical sporadic, rapid, involuntary limb movement, limb stiffness with impeded balance. The cognitive disorder manifests first as sluggish mental processing and difficulty in organizing complex tasks along with progressive dementia [16].
Delirium
K. Rao Poduri in Geriatric Rehabilitation, 2017
The relationship between dementia and delirium is an important part of any discussion of delirium. Cognitive impairment as risk factor for delirium has long been clear. Dementia is the single largest risk factor in the development of delirium, with about two-third of patients with delirium having underlying dementia [42]. However, what is perhaps more interesting is the role delirium plays in the progression of cognitive impairment. In clinical practice, an episode of delirium is often the impetus that leads to the work-up and diagnosis of dementia. This is often due to the lack of identification of a preexisting cognitive disorder, but there may be more to that. There is some evolving evidence that the two conditions are more interrelated and the pathologic processes that cause delirium may also contribute to dementia or at least its progression [43]. While it is not clear that delirium itself causes dementia, there is an associated decline in cognitive functional abilities in patients with dementia who experience delirium [44]. Delirium contributes to worsening functional and cognitive status in patients with dementia with acceleration in the rate of cognitive decline [45]. This new decline may be what leads to the “uncovering” of dementia in a patient who experienced an episode of delirium. A relatively common clinical scenario is for a patient who has experienced delirium to “never return to baseline” and to continue on a steeper rate of decline than seen previously.
Tranexamic acid for chronic subdural hematoma
Published in British Journal of Neurosurgery, 2021
Roger Lodewijkx, Steven Immenga, René van den Berg, René Post, Lucas G. Westerink, Rob J. A. Nabuurs, Anil Can, William Peter Vandertop, Dagmar Verbaan
One patient (case no. 3) experienced a seizure five days after initiation of TXA treatment. The TXA was stopped temporarily, the patient re-admitted, and scheduled for surgery. However, because of persisting fever due to a bladder infection, the operation was postponed. His symptoms diminished nevertheless, and he was discharged home without an operation. TXA was continued at discharge, six days after the seizure. At follow-up one month later, the symptoms had resolved and further follow-up was not necessary. One patient (case no. 5) reported memory loss, however, this was also present prior to initial presentation described as ‘cognitive disorder not otherwise specified’. The patient was referred to a neurologist for further analysis. One patient was operated 11 months after TXA treatment. Possibly this was related to his myelodysplastic syndrome, a hematologic disorder characterized by chronic anemia, neutropenia and thrombocytopenia.
Semantic Adaptation and Validation of the Stanford Hypnotic Susceptibility Scale, Form C, in the Chilean Population
Published in International Journal of Clinical and Experimental Hypnosis, 2021
Erik Álvarez-Mabán, Maritza Muñoz-Pareja, Bryan Chamorro-Velásquez, Daniel Montecinos-Recabal, Flor Pedreros-Cartes, Carla Sepúlveda-Leal
A total of 102 students from the School of Medicine at Universidad Católica de la Santísima Concepción (UCSC) voluntarily took part in the study; they belonged to nursing, nutrition and dietetics, physical therapy, medical technology, and medicine degree programs. The sample calculation was performed using a formula for estimating proportions, which considered a total population of 1,251 students, 95% security, 5% risk, 3% accuracy, 5% expected high hypnotizability, and 10% of expected losses, finally made up of a total of 194 people. A voluntary, nonprobability sampling was used. The inclusion criteria were (a) to be of legal age (18 years or older) (b) to be Chilean or to have lived in Chile for the past 5 years. The exclusion criteria were (a) the presence of any cognitive disorder that hinders the understanding of instructions, (b) psychotropic use, and (c) drug use. The response rate of the study was 52.6%.
New insights into the clinical management of advanced gastrointestinal stromal tumors
Published in Expert Opinion on Pharmacotherapy, 2021
Avapritinib is a highly selective inhibitor of KIT and PDGFRA receptors with an extremely powerful action on secondary resistance mutations (exons 17 and 18 of KIT) and on primary resistance mutation (D842V mutation in PDGFRA). Safety and efficacy results from patients treated in the fourth-line setting or with a PDGFRA exon 18 mutation and included in the pivotal NAVIGATOR study (NCT02508532) were recently reported [27]. Patients were reported to use avapritinib at the recommended Phase 2 dose of 300 mg or the maximum tolerated dose of 400 mg. Among the 111 patients treated in the fourth-line setting or above, the objective response rate was 22% (95% CI 14.4–30.4). The median PFS was 3.7 months (3.4–5.6). The most frequent treatment-related adverse events were nausea (59.3%), fatigue (47.1%), anemia (36.3%), and cognitive effects (41.2%). These cognitive effects included memory impairment, cognitive disorder, confusion state, and encephalopathy. The mechanisms involved in these neurological symptoms have not yet been elucidated. Unfortunately, a Phase III study comparing this molecule to regorafenib in the third line of treatment (https://clinicaltrials.gov/ct2/show/NCT03465722) did not meet the primary endpoint of an improvement in progression-free survival.
Related Knowledge Centers
- Mental Disorder
- Cognitive Skill
- Delirium
- Dementia
- Executive Functions
- Social Cognition
- Alzheimer's Disease
- Frontotemporal Dementia
- Huntington's Disease
- Dementia With Lewy Bodies