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Neuroimaging in Nuclear Medicine
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Anne Larsson Strömvall, Susanna Jakobson Mo
In another common neurodegenerative disorder, Parkinson´s disease (PD), clumps of protein called Lewy bodies (protein aggregates dominated by α-synuclein) accumulate inside neurons. Like in AD and FTD, neurons producing acetylcholine degenerate in PD. However, the hallmark of PD is loss of dopamine-producing nerve cells. In particular, dopamine-producing neurons located in the substantia nigra (see section 13.1.1) are affected. These cells normally produce lots of dopamine that is released in the striatum, regulating movements, but is also important in cognitive function. The typical movement symptoms of PD, Parkinsonism (i.e. slowness of movement, muscular stiffness/rigidity, balance impairment, and resting tremor) are largely associated with the loss of dopamine, and treatment with dopamine-like drugs (e.g. L-dopa) substitute for the loss of neurotransmitter and improve symptoms through action on the dopamine receptors. Parkinsonism may be seen in other conditions not associated with dopamine loss. Hereditary tremor, for example, is a relatively common neurological condition that may sometimes resemble early Parkinson’s disease, but is not a neurodegenerative disease and should not be treated with anti-Parkinson drugs (i.e. dopaminergic agents). Parkinsonism is also seen in so-called atypical Parkinson syndromes (Multisystem atrophy, Progressive supranuclear palsy, and Corticobasal syndrome). These are far less common, but share the loss of dopamine in the striatum with PD. However, in these diseases, also the dopamine receptors are lost, and therefore dopaminergic treatment is usually not helpful.
Applications of imaging genomics beyond oncology
Published in Ruijiang Li, Lei Xing, Sandy Napel, Daniel L. Rubin, Radiomics and Radiogenomics, 2019
Xiaohui Yao, Jingwen Yan, Li Shen
There are three types of FTD categorized by distinct syndromes, including behavioral variant frontotemporal dementia (bvFTD), primary progressive aphasia (PPA), and motor neuron dementia (FTD-MND). The FTD-MND has overlaps with other three neurological disorders including amyotrophic lateral sclerosis (ALS), corticobasal syndrome (CBS), and progressive supranuclear palsy (PSP). The term frontotemporal lobar degeneration (FTLD) has been used as the neuropathological concept of the FTD and currently been categorized as three subtypes according to specific proteinaceous inclusions including tau (FTLD-tau), TAR DNA-binding protein 43 (FTLD-TDP), and fused in sarcoma (FUS) inclusions (FTLD-FUS).
The New Zealand Genetic Frontotemporal Dementia Study (FTDGeNZ): a longitudinal study of pre-symptomatic biomarkers
Published in Journal of the Royal Society of New Zealand, 2023
Brigid Ryan, Ashleigh O’Mara Baker, Christina Ilse, Kiri L. Brickell, Hannah M. Kersten, Joanna M. Williams, Donna Rose Addis, Lynette J. Tippett, Maurice A. Curtis
Clinically, FTD presents as one of three major syndromes: behavioural variant FTD (bvFTD), characterised by behavioural change with executive dysfunction (Rascovsky et al. 2011); non-fluent variant primary progressive aphasia (nfvPPA), characterised by agrammatism and motor speech deficits (Gorno-Tempini et al. 2011); or semantic variant PPA (svPPA), characterised by semantic aphasia (Gorno-Tempini et al. 2011). In some cases, symptoms overlap with amyotrophic lateral sclerosis (ALS) and the atypical Parkinsonism disorders progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS) (Lashley et al. 2015).
Smart ankle bracelet-laser device to improve gait and detect freezing of gait in Parkinsonism patients: a case series
Published in Assistive Technology, 2022
Chompoonuch Ratanasutiranont, Kwan Srisilpa, Pichet Termsarasab, Peeraya Ruthiraphong
A 58-year-old Thai woman had a cardiac arrest due to a massive pulmonary embolism. After recovering from the condition, she began having difficulty walking. Upon clinical evaluation, she was diagnosed with right hemi-parkinsonism with corticobasal syndrome-like features (mild ideomotor apraxia and agraphesthesia of the right hand), and freezing predominantly in the right leg, secondary to hypoxic brain injury involving the bilateral basal ganglia, with more severe injury on the left ganglion. FOG had been a predominant symptom for 5 years and was refractory to 600 mg/day of levodopa and 4 mg/day of ropinirole. FOG had been significantly worse in the past 2 years, and resulted in multiple falls. In addition, she had some impairments in attention. Red lines on the floor in her house were used as external cues to reduce FOG. However, the fixed visual cues were useful only for ambulation at home. Mobile visual (gait aid laser) cues, such as walker or cane lasers, were not suitable because her attention deficit resulted in an inability to manually control the device to effectively project the laser line. She was referred to our rehabilitation clinic for gait management, which included fall reduction. After a few minutes of trialing the device, gait speed and stride length increased from an average of 0.44 m/s and 0.68 m with the laser off to 0.50 m/s and 0.73 m with the laser on. The TUG test time decreased from 39.60 to 21.70 seconds after the laser cue was turned on. FOG predominantly occurred during turning, which necessitated physical assistance to secure stability, as shown in Video 1. The maximum %FOG was 47% during walking with the laser off. However, with the laser on, %FOG showed a marked reduction to less than 5% (Video 2). The FOG monitoring data detected by the device are shown in Figure 4. No adverse effects were observed. She was not able to participate in the follow-up because of COVID-19-related reasons and family issues.