Parkinsonism, secondary

Davis GC, Williams AC, Markey SP, Ebert MH, Caine ED, Reichert CM, Kopin IJ (1979) Chronic parkinsonism secondary to intrvenous injection of meperidine analogues. Psychiat Res 7 249-254. 

Idiopathic parkinsonism (Parkinson s disease, Lewy body parkinsonism) Secondary parkinsonism Drug-induced... 

Salazar Z, Tschopp L, Calandra C, Micheli F. Pisa syndrome and parkinsonism secondary to valproic acid in Huntington s disease. Mov Disord 2008 23(16) 2430-1. 

Ubiquitous mitochondrial monoamine oxidase [monoamine oxygen oxidoreductase (deaminating) (flavin-containing) EC 1.4.3.4 MAO] exists in two forms, namely type A and type B [ monoamine oxidase (MAO) A and B]. They are responsible for oxidative deamination of primary, secondary, and tertiary amines, including neurotransmitters, adrenaline, noradrenaline, dopamine (DA), and serotonin and vasoactive amines, such as tyramine and phenylethylamine. Their nonselec-tive and selective inhibitors ( selective MAO-A and -B inhibitors) are employed for the treatment of depressive illness and Parkinson s disease (PD). 

Roberts TM, Hutchinson TC, Paciga J, Chattopadhyay A, Jervis RE, VanLoon J, Parkinson DK. 1974. Lead contamination around secondary smelters estimation of dispersal and accumulation by humans. Science 186 1120-1123. 

The 140-residue protein AS is able to form amyloid fibrils and as such is the main component of protein inclusions involved in Parkinson s disease. Full-length 13C/15N-labelled AS fibrils and AS reverse-labelled for two of the most abundant amino acids, K and V, were examined by homonuclear and heteronuclear 2D and 3D NMR.147 Two different types of fibrils display chemical shift differences of up to 13 ppm in the l5N dimension and up to 5 ppm for the backbone and side-chain 13C chemical shifts. Selection of regions with different mobility indicates the existence of monomers in the sample and allows the identification of mobile segments of the protein within the fibril in the presence of monomeric protein. At least 35 C-terminal residues are mobile and lack a defined secondary structure, whereas the N terminus is rigid starting from residue 22. In addition, temperature-dependent sensitivity enhancement is also noted for the AS fibrils due to both the CP efficiency and motional interference with proton decoupling.148... 

Dystonia due to identifiable structural or biochemical abnormalities ( secondary dystonia) often occurs weeks or months after strokes or other focal lesions, which commonly involve the basal ganglia, but may also involve the thalamus or cerebellum. Dystonia is also seen in children with cerebral palsy and in patients with abnormalities of dopaminergic transmission. For instance, dystonia may develop in the context of Parkinson s disease, either as an early parkinsonian sign, or in response to dopaminergic drugs. A particularly interesting inherited disease results in a combination of dystonia and parkinsonian features at a young age, which responds dramatically to treatment with low-dose levodopa ( dopamine-responsive dystonia ). 

Parkinsonism is an extrapyramidal motor disorder, characterized by akinesia, rigidity and tremor with secondary manifestations such as excessive salivation, seborrhoea, mood changes (especially depression) and in certain patients, liver damage has been reported. It was first described by James Parkinson in 1817. 

Stimulation of the subthalamic nucleus or globus pallidus by an implanted electrode and stimulator has yielded good results for the management of the clinical fluctuations occurring in advanced parkinsonism. The anatomic substrate for such therapy is indicated in Figure 28-1. Such procedures are contraindicated in patients with secondary or atypical parkinsonism, dementia, or failure to respond to dopaminergic medication. 

Sleep disturbance secondary to other disorders is common in Parkinson s. One common symptom associated with Parkinson s disease is dementia (88,89). 

Secondary parkinsonism Parkinsonian symptoms infrequently follow viral encephalitis or multiple small vascular lesions. Drugs such as the phenothiazines and haloperidol (see p. 127), whose major pharmacologic action is blockade of dopamine receptors in the brain, may also produce parkinsonian symptoms. These drugs should not be used in parkinsonian patients. 

Some patients may experience hearing loss, which may accompany diabetes. Usually, type 2 diabetes is described in individuals with MELAS, although type 1 or insulin-dependent diabetes also may be observed. Palpitations and shortness of breath may be present in some patients with MELAS secondary to cardiac conduction abnormalities such as Wolff-Parkinson-White syndrome. Acute onset of gastrointestinal manifestations (e.g., acute onset of abdominal pain) may reflect pancreatitis, ischemic colitis, and intestinal obstruction. Numbness, tingling sensation, and pain in the extremities can be manifestations of peripheral neuropathy. Some patients may have the presentation of Leigh syndrome (i.e., subacute necrotizing encephalopathy). 

As more was written on the subject of negative symptoms the literature became blurred as to whether the symptoms discussed were related to state or trait (Sommers, 1985). To refine the concept, negative symptoms resulting from treatment (e.g., Parkinsonism related to neuroleptics), psychosis (e.g., elective mutism related to paranoia), institutionalization/monotonous routine, and/or related to depression were referred to as secondary negative symptoms (Carpenter et al., 1985). In contrast, primary negative symptoms were due to the illness itself. These enduring traits were labeled deficit symptoms (Carpenter et al., 1985). 

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