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Gerstmann Syndrome (Dysgraphia, Dyscalculia, Finger Agnosia, and Left-Right Disorientation)
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Damage to a part of the brain called the angular gyrus, located near where the parietal and temporal lobes meet, appears to be enough to produce this syndrome. However, there are reports of people developing some of the symptoms even with brain damage in different areas (Bhattacharyya et al., 2014). For example, dyscalculia can be a symptom of damage to many different brain locations, including frontal, temporal, parietal, and subcortical structures, although the angular gyrus is probably the most frequently implicated (e.g., Grafman et al., 1982; Willmes, 2008). Importantly, Gerstmann syndrome is commonly associated with damage to the dominant hemisphere of a person's brain (Tucha et al., 1997). In right-handed people, the left side of the brain is usually dominant, and because most people are right-handed, Gerstmann syndrome is usually associated with damage to the left half of the brain. Therefore, Gerstmann syndrome is most frequently associated with left-sided damage of the angular gyrus… but there are exceptions to all of this (Lebrun, 2005). In fact, there are a lot of exceptions to the guidelines of this syndrome, which brings us to an important question.
Seizure and cognitive outcomes of posterior quadrantic disconnection: a series of 12 pediatric patients
Published in British Journal of Neurosurgery, 2020
Yao Wang, Chao Zhang, Xiu Wang, Lin Sang, Feng Zhou, Jian-Guo Zhang, Wen-Han Hu, Kai Zhang
Nevertheless, seizures continue following all disconnection operations, including PQD, due to incomplete disconnection.12 Postoperative DTI sequences can help judge whether the disconnection was complete so that we can appraise seizure outcomes and postoperative complications. During PQD, the optic radiation, corpus callosum and some projection fibres were severed, resulting in some special complications after PQD, including hemiplegia and visual impairment. Impairments in visual function have been reported in the majority of patients, mostly consisting of partial/complete ipsilateral hemianopia, visual hemi-inattention and strabismus.2,13–15 In accordance with our data, hemianopia after PQD due to complete optic radiation disruption cannot be restored even after several years. Furthermore, 3 patients (25%) had some extent of hemiplegia after PQD. The primary reasons for the hemiplegia were inaccuracy of the location of the postcentral sulcus or forward deviation when the parietal lobe was disconnected, resulting in partial disconnection of the corticospinal tract. A rare complication, Gerstmann syndrome, was observed in 1 patient who underwent PQD in the dominant hemisphere. At present, the cause of Gerstmann syndrome remains unclear. Previous reports have suggested that the cause of Gerstmann syndrome includes damage of the parietal lobe, long-distance tracts between distinct brain areas or tracts connecting different regions in the parietal lobe.16–18 Interestingly, 6 patients in our study underwent PQD in the dominant hemisphere, while only one experienced Gerstmann syndrome. The reasons for this outcome require further study.
Posterior cortical atrophy: clinical, neuroimaging, and neuropathological features
Published in Expert Review of Neurotherapeutics, 2023
John Best, Marianne Chapleau, Gil D. Rabinovici
Following Benson’s initial report, additional case series were published highlighting the clinical and radiographic features of PCA. Presenting symptoms classically include a variety of deficits in higher-order visual processing but can also include a number of nonvisual deficits which localize toposterior parietal regions. The most frequent visual symptoms are spatial perception deficits (i.e. where objects are in space) as well as object perception deficits (i.e. visual agnosia). Patients develop features of Gerstmann Syndrome, including agraphia (inability to write), acalculia (impaired mental calculations), finger agnosia (loss of ability to name and distinguish fingers), and right-left dissociation. Features of Balint syndrome, including oculomotor apraxia (impaired voluntary and purposeful eye movements), optic ataxia (inability to accurately reach toward an object under visual guidance), and simultanagnosia (the inability to simultaneously process and integrate multiple visual inputs), are also commonly present. Visual field defects are often detected, especially when formally assessed with perimetry. Function in other cognitive domains is generally preserved until more advanced stages of the disease, although visual memory can be impacted early in the disease course [2]. The syndrome’s name is derived from the profound atrophy, hypometabolism and hypoperfusion of parieto-occipital and parieto-temporal visual association cortices noted on structural and functional brain imaging [1,3]. Neuropathologic series of patients diagnosed with PCA during life and followed to autopsy have found that the PCA clinical syndrome is most frequently associated with Alzheimer’s disease (AD) neuropathologic changes and is therefore sometimes referred to as the ‘visual variant of AD’ The most common alternative pathologies are Lewy Body Disease and corticobasal degeneration [4,5]. Prion disease has been described with an initial PCA presentation but is exceedingly rare [4].