Importance Parkinson disease is the second most common neurodegenerative disease worldwide. Although no available therapies alter the underlying neurodegenerative process, symptomatic therapies can improve patient quality of life. Objective To provide an evidence-based review of the initial pharmacological management of the classic motor symptoms of Parkinson disease; describe management of medication-related motor complications (such as motor fluctuations and dyskinesia), and other medication adverse effects (nausea, psychosis, and impulse control disorders and related behaviors); and discuss the management of selected nonmotor symptoms of Parkinson disease, including rapid eye movement sleep behavior disorder, cognitive impairment, depression, orthostatic hypotension, and sialorrhea. Evidence Review References were identified using searches of PubMed between January 1985 and February 2014 for English-language human studies and the full database of the Cochrane Library. The classification of studies by quality (classes I-IV) was assessed using the levels of evidence guidelines from the American Academy of Neurology and the highest-quality data for each topic. Results Although levodopa is the most effective medication available for treating the motor symptoms of Parkinson disease, in certain instances (eg, mild symptoms, tremor as the only or most prominent symptom, aged Conclusions and Relevance Strong evidence supports using levodopa and dopamine agonists for motor symptoms at all stages of Parkinson disease. Dopamine agonists and drugs that block dopamine metabolism are effective for motor fluctuations and clozapine is effective for hallucinations. Cholinesterase inhibitors may improve symptoms of dementia and antidepressants and pramipexole may improve depression. Evidence supporting other therapies for motor and nonmotor features is less well established.

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=JAMA&articleId=1861807&pdfFileName=jrv140005.pdf

Pharmacological Treatment of Parkinson Disease: A Review

Amyotrophic lateral sclerosis

Objective
To update evidence‐based medicine recommendations for treating nonmotor symptoms in Parkinson's disease (PD).

https://onlinelibrary.wiley.com/doi/pdf/10.1002/mds.27602

Update on treatments for nonmotor symptoms of Parkinson's disease—an evidence-based medicine review

During the past 25 years, there has been an explosion of information regarding the occurrence of gastrointestinal dysfunction in Parkinson’s disease. In this review, the clinical features of gastrointestinal dysfunction in Parkinson’s disease will be described and information regarding the potential role of the enteric nervous system and the gut microbiome in the genesis of Parkinson’s disease will be addressed. Recognition is growing regarding the role that gastroparesis and small intestinal dysfunction may play in Parkinson’s disease, especially with regard to erratic responses to anti-Parkinson medication. The presence of enteric nervous system involvement in Parkinson’s disease is now well established, but whether the enteric nervous system is the starting point for Parkinson’s disease pathology remains a source of debate. The potential role of the gut microbiome also is beginning to emerge. Gastrointestinal dysfunction is a prominent nonmotor feature of Parkinson’s disease and dysfunction can be found along the entire length of the gastrointestinal tract. The enteric nervous system is clearly involved in Parkinson’s disease. Whether it is the initial source of pathology is still a source of controversy. There also is growing recognition of the role that the gut microbiome may play in Parkinson’s disease, but much more research is needed to fully assess this aspect of the disorder.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(15)00007-1.pdf

Gastrointestinal Dysfunction in Parkinson’s Disease

Drooling in Parkinson's disease: A review

Background: Either botulinum tox- ins (BoNTs) A and B have been used for improving drooling in different neurological conditions. Methods: Consecutive patients affected by Amyotro- phic Lateral Sclerosis (ALS) or Parkinson's Disease (PD) accompanied by severe drooling were random- ized to receive botulinum neurotoxin type A (BoNT-A) or B (BoNT-B) injections into the salivary glands. Fol- lowing the first treatment, when sialorrhea returned to baseline (at least three months after the first injection), subjects were re-treated with the other serotype. Ultrasound-guided injections into parotid and sub- mandibular glands were bilaterally performed: total doses were 250 U BoNT-A (Dysport) and 2500 U BoNT-B (Neurobloc). Objective (cotton roll weight) and subjective (ad hoc clinical scales) evaluations were performed at baseline, after 1 and 4 weeks, and every 4w eeks until drooling returned to baseline. Results: Twenty-seven patients (15 ALS and 12 PD) were enrolled, fourteen completed the study. BoNT-A and BoNT-B treatments gave both subjective and objective improvements in all patients. The latency was significantly shorter after BoNT-B treatments (3.2 6 3.7 days) compared to BoNT-A (6.6 6 4.1 days; P 5 0.002). The mean benefit duration was similar at 75 and 90 days for BoNT-A and BoNT-B, respectively (P 5 NS). The only toxin-related side effect was a change to saliva thickness. Conclusions: Either 250 U Dysport or 2500 U Neuro- bloc have similar effectiveness and safety in control- ling sialorrhea. BoNT-B has a shorter latency and comparable duration. Cost analysis, considering the doses used in this study protocol favored BoNT-B treatment. V C 2011 Movement Disorder Society

Botulinum toxin A versus B in sialorrhea: A prospective, randomized, double‐blind, crossover pilot study in patients with amyotrophic lateral sclerosis or Parkinson's disease

We evaluated whether the addition of delayed phase imaging (DPI) gadobenate dimeglumine-enhanced MRI to dynamic postcontrast imaging improves the characterization of small hepatocellular carcinoma (HCC) and the differentiation between HCC, high grade dysplastic nodules (HGDN), and low grade dysplastic nodules (LGDN). Twenty-five cirrhotic patients with 30 nodules (16 HCC, 8 HGDNs, and 6 LGDNs; maximum size of 3 cm) were included in this retrospective study. The diagnostic reference standard was histology. All the patients underwent MRI both prior to and following intravenous administration of gadobenate dimeglumine. The lesions were classified as hypointense, isointense, hyperintense on DPI for qualitative assessment. In the quantitative analysis the relative tumor-liver contrast to noise ratio (CNR) of the lesions on DPI was calculated. All HCCs were hypointense on DPI while only 8 (57.1%) of 14 DNs were hypointense and only 1 of 6 (16.6%) LGDNs was hypointense. There was a statistically significant difference in the hypointensity on DPI between HCCs and DNs (p = 0.003) in the qualitative analysis but not in the CNR values while there was a strong statistically significant difference in the hypointensity on DPI in the qualitative (p = 0.00001) and quantitative analysis (p < 0.05) between LGDNs and the group obtained by unifying HGDNs and HCCs. DPI is helpful in differentiating HCCs and HGDNs from LGDNs. Demonstration of hypointensity on DPI should raise the suspicion of HGDN or hypovascular HCC in the case of nodules with atypical dynamic pattern.

Differentiating hepatocellular carcinoma from dysplastic nodules at gadobenate dimeglumine-enhanced hepatobiliary-phase magnetic resonance imaging

T.n.11 hepatic vein transit time (hvtt) of ii generation ultrasound contrast agent (usca): new tool in assessment of portal hypertension. preliminary results

Hepatic Vein Transit Time (hvtt) Of Ii Generation Ultrasound Contrast Agent (usca): New Tool In Assessment Of Portal Hypertension? Preliminary Results: 384

This case demonstrates that clinical and pathological suspicion of NTM could be sufficient to start an empiric treatment even when microbiological isolation is unavailable. Moreover, disseminated mycobacteriosis may underlie an occult aggressive neoplasm.

Non‐tuberculous mycobacteriosis of the liver responsive to empiric therapy

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