Does catatonia have a specific brain biology?

2002 ◽  
Vol 25 (5) ◽  
pp. 580-581
Author(s):  
Bernhard Bogerts

Dr. Northoff's comprehensive comparison of clinical symptoms and neurobiological findings in catatonia with that of Parkinson's disease through integration of various levels of investigation, from neurochemistry up to the subjective experience, is a good example of the new strategies we need to improve our understanding of psychiatric disorders. His multimodal approach, leading to the hypothesis that different pathophysiologies of transcortical “horizontal modulation” and “bottom-up/top-down” – orbitofrontal/basal ganglia – “vertical modulations,” may explain many clinical aspects of catatonia and Parkinson's disease, and thereby fills an important gap in current theories of psychomotor syndromes. However, to analyze more specifically the pathophysiology of catatonia, comparison not only with Parkinson's disease, but also with schizophrenia and anxiety disorders would be helpful. As long as the pathohistological and molecular basis of catatonic syndromes is unknown, theories based mainly on functional considerations remain preliminary.

2013 ◽  
Vol 71 (9A) ◽  
pp. 591-595 ◽  
Author(s):  
Raimundo Nonato Campos-Sousa ◽  
Elizabeth Maria Aparecida Barasnevicius Quagliato ◽  
Kelson James Almeida ◽  
Inacio Augusto Dias de Castro ◽  
Viriato Campelo

Introduction Detrusor hyperactivity is the leading cause of urinary dysfunction in Parkinson's disease (PD). There are few studies correlating PD clinical aspects with this autonomic feature. Methods A cohort of 63 women with PD were prospectively examined for assessment of clinical aspects and disease severity using unified Parkinson's disease rating scale and Hoehn-Yahr scale, respectively. The urologic function was evaluated by the urodynamic study. Two groups were categorized at this time - groups with and without detrusor hyperactivity. After seven years, the same parameters were re-evaluated. Results Progression of the disease on mental scores was found in the group with detrusor hyperactivity. On follow-up, clinical symptoms and severity did not show significant worsening between the groups. Conclusion Detrusor hyperactivity is a frequent urodynamic finding in PD, and even though it is associated with dopaminergic dysfunction, it cannot be blamed as a factor of worsening motor performance, but is probably associated with poor cognitive and mental prognosis.


2012 ◽  
Vol 153 (52) ◽  
pp. 2060-2069 ◽  
Author(s):  
András Guseo

Parkinson’s disease is one of the most frequent progressive degenerative disorders with unknown origin of the nervous system. The commutation of the disease on Guam led to the discovery of a neurotoxin which was also found in other continents. This neurotoxin was identified in the common cyanobacteria (blue-green algae). Early clinical observations suggested some loose correlations with gastric and duodenal ulcer and Parkinson’s disease, while recent studies revealed a toxin, almost identical to that found in cyanobacteria in one strain of Helicobacter pylori, which proved to cause Parkinson like symptoms in animals. Therefore, it cannot be ruled out that there is a slowly progressive poisoning in Parkinson’s disease. The disease specific alpha-sinuclein inclusions can be found in nerve cells of the intestinal mucosa far before the appearance of clinical symptoms indicating that the disease may start in the intestines. These results are strengthened by the results of Borody’s fecal transplants, after which in Parkinson patients showed a symptomatic improvement. Based on these observations the Parkinson puzzle is getting complete. Although these observations are not evidence based, they may indicate a new way for basic clinical research, as well as a new way of thinking for clinicians. These new observations in psycho-neuro-immunology strengthen the fact that immunological factors may also play a critical factor facilitating local cell necrosis which may be influenced easily. Orv. Hetil., 2012, 153, 2060–2069.


Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 371
Author(s):  
Patrycja Pawlik ◽  
Katarzyna Błochowiak

Many neurodegenerative diseases present with progressive neuronal degeneration, which can lead to cognitive and motor impairment. Early screening and diagnosis of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are necessary to begin treatment before the onset of clinical symptoms and slow down the progression of the disease. Biomarkers have shown great potential as a diagnostic tool in the early diagnosis of many diseases, including AD and PD. However, screening for these biomarkers usually includes invasive, complex and expensive methods such as cerebrospinal fluid (CSF) sampling through a lumbar puncture. Researchers are continuously seeking to find a simpler and more reliable diagnostic tool that would be less invasive than CSF sampling. Saliva has been studied as a potential biological fluid that could be used in the diagnosis and early screening of neurodegenerative diseases. This review aims to provide an insight into the current literature concerning salivary biomarkers used in the diagnosis of AD and PD. The most commonly studied salivary biomarkers in AD are β-amyloid1-42/1-40 and TAU protein, as well as α-synuclein and protein deglycase (DJ-1) in PD. Studies continue to be conducted on this subject and researchers are attempting to find correlations between specific biomarkers and early clinical symptoms, which could be key in creating new treatments for patients before the onset of symptoms.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Marina Maffoni ◽  
Anna Giardini ◽  
Antonia Pierobon ◽  
Davide Ferrazzoli ◽  
Giuseppe Frazzitta

Parkinson’s disease (PD) is a neurodegenerative disease characterized by motor and nonmotor symptoms. Both of them imply a negative impact on Health-Related Quality of Life. A significant one is the stigma experienced by the parkinsonian patients and their caregivers. Moreover, stigma may affect everyday life and patient’s subjective and relational perception and it may lead to frustration and isolation. Aim of the present work is to qualitatively describe the stigma of PD patients stemming from literature review, in order to catch the subjective experience and the meaning of the stigma construct. Literature review was performed on PubMed database and Google Scholar (keywords: Parkinson Disease, qualitative, stigma, social problem, isolation, discrimination) and was restricted to qualitative data: 14 articles were identified to be suitable to the aim of the present overview. Results are divided into four core constructs: stigma arising from symptoms, stigma linked to relational and communication problems, social stigma arising from sharing perceptions, and caregiver’s stigma. The principal relations to these constructs are deeply analyzed and described subjectively through patients’ and caregiver’s point of view. The qualitative research may allow a better understanding of a subjective symptom such as stigma in parkinsonian patients from an intercultural and a social point of view.


2010 ◽  
Vol 22 (5) ◽  
pp. 848-859 ◽  
Author(s):  
Roshan Cools ◽  
Robert Rogers ◽  
Roger A. Barker ◽  
Trevor W. Robbins

Cognitive dysfunction in Parkinson's disease (PD) has been hypothesized to reflect a failure of cortical control. In keeping with this hypothesis, some of the cognitive deficits in PD resemble those seen in patients with lesions in the lateral pFC, which has been associated with top–down attentional control. However, there is no direct evidence for a failure of top–down control mechanisms in PD. Here we fill this gap by demonstrating disproportionate control by bottom–up attention to dimensional salience during attentional set shifting. Patients needed significantly more trials to criterion than did controls when shifting to a low-salient dimension while, remarkably, needing significantly fewer trials to criterion than did controls when shifting to a high-salient dimension. Thus, attention was captured by bottom–up attention to salient information to a greater extent in patients than in controls. The results provide a striking reinterpretation of prior set-shifting data and provide the first direct evidence for a failure of top–down attentional control, resembling that seen after catecholamine depletion in the pFC.


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