Clinical and Experimental Evidence of Cirrhosis-Related Parkinsonism

Clinical and Experimental Evidence of Cirrhosis-Related Parkinsonism

Omar El Hiba, Bilal El-Mansoury, Hicham Chatoui, Hind Benammi, Tiziano Balzano, Mohamed Merzouki, My Abdelmonaim El Hidan, Jayakumar Radhakrishnan, Lahoucine Bahi, Hamid Rguibi Idrissi, Nabila Saadaoui, Mounir Tilaoui, Tiago Fleming Outeiro, Michael D. Norenberg
DOI: 10.4018/978-1-6684-5156-4.ch007
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Abstract

The clinical significance of hepatic encephalopathy (HE) includes a variety of neuropsychiatric abnormalities arising from both chronic and acute hepatic failures. Cirrhotic patients manifest symptoms related to acquired hepatolenticular degeneration (parkinsonism in cirrhosis); the disease is characterized by extrapyramidal symptoms including hypokinesia, dystonia, and rigidity that are rapidly progressive and independent of the severity of cognitive dysfunction, while imaging techniques revealed T1-weighted hyperintense signals in the globus pallidus (GP) and substantia nigra (SN) along with manganese (Mn) deposition leading to the dysfunction of the dopaminergic, glutamatergic, as well as GABAergic neurotransmitter systems in the basal ganglia. Through the chapter, the authors emphasize the common neurological and cognitive features between Parkinson's disease/parkinsonism and HE with a special focus on the underlying pathophysiological mechanisms.
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Clinical Evidence Of Chronic Parkinsonism In Advanced Liver Disease

Dering thelast century, particularly the first half,considerable attention was dedicated to the characterization of cirrhosis-related brain disorders(Stadler, 1935; Van Woerkem, 1914; Wilson, 1971)through clinico-pathological approaches of single cases or small series. While, the first establishment of the term “acquired type of chronic hepatocerebral degeneration” was elaborated by Victor et al in 1965(Victor et al., 1965), which intended to make a distinction from Wilson disease; a primarily genetic liver disease associated to copper accumulation due to the gene ATP7B mutation encoding for a transmembrane copper-transporting ATPase, which impacts several organs including the brain(Członkowska et al., 2018).Since, different aspects were defined including a wide range of neuro-cognitive disorders arising from chronic liver failure, different from those associated to acute and transient episodes of HE (Victor et al., 1965 ;Finlayson & Superville, 1981; Levy et al., 1983; Toghill et al., 1967; Weissenborn & Kolbe, 1998). Most of these symptoms refersto BG dysfunctions with abnormal involuntary movements including tremor, myoclonus, choreoathetosis, dystonia, rigidity, and dysarthria along with ataxia, pyramidal tract signs, and dementia (Jog & Lang, 1995).

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