Neurology with dementia with Lewy bodies
John O'Brien, Ian McKeith, David Ames, Edmond Chiu in Dementia with Lewy Bodies and Parkinson's Disease Dementia, 2005
cognitively impaired DLB patient may be difficult. In particular, it is important not to overinterpret cortical problems such as apraxia or paratonic rigidity as representing parkinsonism, since this could lead to the inappropriate prescription of antiparkinsonian medications. The parkinsonism of DLB does not differ fundamentally from that seen in PD, although axial features, with postural instability, tend to be over-represented. More work is needed to establish the rate of progression and the response to treatment of the extrapyramidal syndrome in DLB. Further study of more subtle neurological features, such as saccadic eye movement abnormalities and myoclonus, may be of help in the differential diagnosis of DLB and could also shed further light upon the temporal and spatial evolution of the pathophysiological process.
Antidepressant Medications
Gary W. Jay in Practical Guide to Chronic Pain Syndromes, 2016
The major adverse effects of TCAs are secondary to cholinergic/muscarinic receptor blockade, histaminergic blockade (H1, H2), as well as blockade of the dopaminergic system. The anticholinergic side effects predominate and can include blurred vision, xerostomia, sinus tachycardia, constipation, urinary retention, confusion, and memory dysfunction. Histaminergic blockade can induce sedation, weight gain, dizziness, and hypotension. It also potentiates the effects of other CNS depressants. Alpha-1 adrenergic blockade can be associated with postural hypotension and dizziness. Blockade of dopaminergic receptors can induce extrapyramidal syndrome, dystonia, akinesia, neuroleptic malignant syndrome, tardive dyskinesia, and endocrine changes. Tachycardia and prolonged PR and QRS intervals with membrane stabilization can occur. The QT interval can become prolonged (1, 2).
Antidepressant Medications
Gary W. Jay in Clinician’s Guide to Chronic Headache and Facial Pain, 2016
The major adverse effects of TCAs are secondary to cholinergic/muscarinic receptor blockade, histaminergic blockade (H1, H2), as well as blockade of the dopaminergic system. The anticholinergic side effects predominate and can include blurred vision, xerostomia, sinus tachycardia, constipation, urinary retention, confusion, and memory dysfunction. Histaminergic blockade can induce sedation, weight gain, dizziness, and hypotension. It also potentiates the effects of other CNS depressants. Alpha-1 adrenergic blockade can be associated with postural hypotension and dizziness. Blockade of dopaminergic receptors can induce extrapyramidal syndrome, dystonia, akinesia, neuroleptic malignant syndrome, tardive dyskinesia, and endocrine changes. Tachycardia and prolonged PR and QRS intervals with membrane stabilization can occur. The QT interval can become prolonged (1, 2).
Dyskinesia is most centrally situated in an estimated network of extrapyramidal syndrome in Asian patients with schizophrenia: findings from research on Asian psychotropic prescription patterns for antipsychotics
Published in Nordic Journal of Psychiatry, 2021
Seon-Cheol Park, Gyung-Mee Kim, Takahiro A. Kato, Mian-Yoon Chong, Shih-Ku Lin, Shu-Yu Yang, Ajit Avasthi, Sandeep Grover, Roy Abraham Kallivayalil, Yu-Tao Xiang, Kok Yoon Chee, Andi Jayalangkara Tanra, Chay Hoon Tan, Kang Sim, Norman Sartorius, Naotaka Shinfuku, Yong Chon Park, Toshiya Inada
To facilitate the clinical and pharmacological approaches for extrapyramidal syndrome, estimating their latent structure is needed. Network analysis is an analytical method to estimate the map of a collection of interrelated symptoms and explicate dynamic causal architectures of symptom clusters [8]. From a topological perspective, a network’s structure consists of nodes (symptoms) and edges (inter-connections). According to graph theory, different spatial and functional characteristics that demonstrate information about the relationships between the nodes within an estimated network are represented [9,10]. Since centrality is based on the overall interconnections of a symptom within an estimated network, central symptoms may have greater influence than peripheral symptoms. It is speculated that intertwined symptoms are more easily activated by symptoms that are centrally situated within the entire network. In terms of centrality, node strength, closeness, and betweenness are defined as the sum of all associations of a given node with all other nodes, the measure of how close a symptom is to all other symptoms, and the shortest length of a path connecting any two nodes, respectively [11,12]. Thus, the network structures of psychopathology among patients with schizophrenia have been estimated below. Alogia and avolition have been the most central domains among the negative symptoms of schizophrenia. Furthermore, blunted affect, alogia, and asociality have been the most central domains in female patients with schizophrenia, whereas alogia and avolition have been the most central domains in their male counterparts [13]. Moreover, the latent structure of negative symptoms has been estimated as an association of the five domains – anhedonia, avolition, asociality, blunted affect, and alogia [14].
Purkinje cell (PC) antibody positivity in a patient with autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy
Published in International Journal of Neuroscience, 2022
Li Xu, Wenbiao Xian, Jin Li, Xiaoli Yao, Youming Long
A 52-year-old Chinese female patient presented with limb tremor and bradykinesia in the last week of September 2018. Initially, she was diagnosed with anxiety and was treated accordingly for three months. However, her condition worsened, with the development of other clinical symptoms, including cognitive dysfunction, psychiatric/behavioral abnormalities, and serious insomnia. The brain MRI scan revealed mild white matter degeneration. At that point, she was diagnosed with Parkinsonism and was treated with an anti-Parkinson’s agent (Madopar 62.5 mg three times a day) for 6 days; however, she showed no improvement. Then, she was transferred to our hospital. After admission, she reported a 2-week history of headache prior to the onset of her motor symptoms, which she did not notice. Up until that time, neurological dysfunction in this patient had mainly manifested as cognitive decline, pyramidal tract signs, and impairments of the extrapyramidal system. Dopamine metabolism in the bilateral basal ganglia as well as fludeoxyglucose (FDG) metabolism in the brain was normal as determined by positron emission tomography-computed tomography (PET-CT) scans. A contrast-enhanced brain MRI of this patient showed bilateral hyperintensity in the semioval centers on axial images and perivascular linear enhancement oriented radially to the ventricles on sagittal images (Figure 1), which was characteristic of GFAP astrocytopathy [3]. The pressure of the lumbar puncture was 150 mmH2O. CSF analysis showed that glucose, chloride, red blood cell (RBC), and white blood cell (WBC) levels were normal, while the protein level was 1302.9 mg/L (normal: 250–450 mg/L); the CSF sample was positive for OBs. A predominance of lymphocytes, accompanied by some monocytes and few eosinophils, was shown by CSF cytology. An infectious disease screen of CNS (antibodies against viruses, gram, and acid-fast stains) and CSF cultures of pathogenic microorganisms was negative. GFAP-IgG (1:100) was strongly positive in both her CSF and serum specimens. In addition, NMDAR-IgG (1:10) and ITPR1-lgG (1:10) were also positive in her CSF specimen (Figure 2) and the other antibodies mentioned above were negative.
Related Knowledge Centers
- Anatomy
- Corticobulbar Tract
- Pyramidal Tracts
- Medulla Oblongata
- Reticular Formation
- Motor System
- Large-Scale Brain Network
- Medullary Pyramids
- Corticospinal Tract
- Anterior Grey Column