Parkinson's disease Tremor

Is Parkinsonism a common feature of essential tremor?

Parkinsonism in essential tremor cases: a clinicopathological study

Rajput AH, Rajput EF, Bocking SM, Auer RN, Rajput A.

Mov Disord 2019; 34:1031-1040.



Essential tremor and Parkinson’s syndrome are two common movement disorders that may co-occur in some individuals. There is no diagnostic neuropathology for essential tremor, but in PD and other Parkinson’s syndrome variants, the neuropathology is well known. The spectrum of Parkinson’s syndrome variants associated with essential tremor, their clinical features, and course have not been determined in autopsy-confirmed cases.


To identify: diagnostic features of essential tremor/Parkinson’s syndrome, different Parkinson’s syndrome variants, and long-term clinical profile in such cases.


Patients that had an essential tremor diagnosis and a subsequent clinical or pathological diagnosis of Parkinson’s syndrome seen in our clinic during 50 years were included. The diagnosis of parkinsonism was made when bradykinesia, rigidity, and resting tremor were all clinically evident.


Twenty-one cases were included. All the common variants of parkinsonism co-occurred with essential tremor. The most common was PD (67%) followed by PSP. The pathological findings were not predicted clinically in 2 cases that had essential tremor/PD and in all 5 essential tremor/PSP cases.


In most essential tremor/Parkinson’s syndrome patients, the main motor features of parkinsonism-bradykinesia, rigidity, and resting tremor-were identifiable. All known degenerative Parkinson’s syndrome variants co-occurred in essential tremor patients.

This paper is cited in the neurochecklist:

Essential tremor (ET): clinical features

Abstract link

Internet Archive Book Images on Flickr.
Neurochecklists updates

20 recently updated practical neurology checklists

Neurochecklists is a comprehensive and practical neurology database

Handy and fully referenced, it is in a constant state of review and renewal

Below are just 21 of our recently updated neurology checklists


Cervical artery dissection: clinical features 

Epilepsy: blood and CSF features 

Huntington’s disease: clinical features 

Leber hereditary optic neuropathy: management 

Parkinson’s disease tremor


Behcet’s disease: clinical features

MND C9orf72 variant


Neuropathy: toxic and drug-induced 

Narcolepsy: clinical features


Epicrania fugax

West Nile virus: clinical features 

Thrombolysis: complications 

Migraine: CGRP monoclonal antibodies

Lambert Eaton myasthenic syndrome: clinical features


Alzheimer’s disease

Pes cavus

Immune checkpoint inhibitor toxicity: management

Adrenoleukodystrophy: phenotypes

Myotonic dystrophy type 2: management


Neurochecklists updates

30 recently revised and updated practical neurology checklists

Neurochecklists is proud of being comprehensive and practical.

But more than that, we take pride in keeping each checklist updated.

To do this, we keep a keen eye on all relevant developments in the literature.

And below are just a few of the checklists that we have recently revised.

They all reflect findings from the latest neurology publications.


Anti Ma2 syndrome

Cerebral aneurysms rupture risk factors

Cerebral vein thrombosis

CGRP monoclonal antibodies


Dural AV fistula management

Giant cell arteritis treatment

Gluten sensitivity neurology

IIH clinical features

King-Denborough syndrome


Migraine acute treatment

MND c9orf72

Multiple sclerosis clinical features


Normal pressure hydrocephalus

Ocular myasthenia gravis

Oculopharyngeal muscular dystrophy


Parkinson’s disease risk factors

Post stroke recrudescence

PSP variants

Psychogenic seizures

Rapid onset dystonia-parkinsonism

Retinal migraine

Seizure manifestations

Stiff person syndrome

Subacute combined degeneration

Suprascapular neuropathy




What are the 10 most eminently curable neurological disorders?

Neurologists are often at the receiving end of the jokes of other medical specialists. They facetiously remark that neurologists know a lot, but do very little to cure their patients. Admittedly we do our fair share of dispensing weak platitudes, and we do break bad news with embarrassing regularity. There is no doubt that, for many diseases, all we have in stock are symptomatic or palliative. This is sadly the case with many familiar disorders such as Alzheimer’s disease (AD), Huntington’s disease, Charcot Marie Tooth disease (CMT), Freidreich’s ataxia (FA), essential tremor (ET), and myotonic dystrophy.

Three treatment capsules close-up. Marco Verch Professional Photographer and Speaker on Flickr.

It is even true that at the extreme end of neurological practice, there are conditions that literally turn a deaf ear to all our entreaties, brush off everything we hurl at them, taunt us with reckless abandon, and run relentlessly mortal courses. Such is the dismal state of affairs with diseases such as rabies encephalitis, Creutzfeldt Jakob disease (CJD), and motor neurone disease (MND).


Hypodermic needle-IMG7418. Steven Depolo on Flickr.

But neurologists don’t just tap their patients knees, and then raise their hands up in despair. We do more than just lend our patients a listening ear, or a leaning shoulder to cry on. We do have at our disposal a vast armamentarium that can control many neurological diseases, even if we need to use these chronically. Such is the state of play with diseases such as migraine, epilepsy, multiple sclerosis (MS), narcolepsy, myasthenia gravis (MG), restless legs syndrome (RLS)Wilson’s disease, and Parkinson’s disease (PD).

Mapping the brain. NIH History Office on Flickr.

But beyond just treatment, what patients really want is total cure. And neurologists can lay claim to this as well. Some diseases of the nervous system  can indeed be permanently remedied, their victims requiring no long-term medications to maintain the cure. To prove this, here are our 10 most eminently curable neurological disorders, linked to their treatment checklists.


Bacterial meningitis

Viral encephalitis

Autoimmune encephalitis

Wernicke’s encephalopathy

Ischaemic stroke

Idiopathic intracranial hypertension (IIH)

Cervical compressive myelopathy

Guillain Barre syndrome (GBS)


Normal pressure hydrocephalus (NPH)


It is important to note that curable neurological disorders are also potentially serious, and do carry the risk for serious complications, and even death, if not treated early and adequately. You may check out our previous blog posts to see the dark side of these disorders:

on ‘Have we missed anyone out? Please drop us a hint!

By JustfixingawrongnumberOwn work, CC0, Link
Parkinson's disease

Does trunkal vagotomy protect against Parkinson’s disease?

Vagotomy and Parkinson disease: a Swedish register-based matched-cohort study

Liu B, Fang F, Pedersen NL, et al.

Neurology 2017; 88:1996-2002.



To examine whether vagotomy decreases the risk of Parkinson disease (PD).


Using data from nationwide Swedish registers, we conducted a matched-cohort study of 9,430 vagotomized patients (3,445 truncal and 5,978 selective) identified between 1970 and 2010 and 377,200 reference individuals from the general population individually matched to vagotomized patients by sex and year of birth with a 40:1 ratio. Participants were followed up from the date of vagotomy until PD diagnosis, death, emigration out of Sweden, or December 31, 2010, whichever occurred first. Vagotomy and PD were identified from the Swedish Patient Register. We estimated hazard ratios (HRs) with 95% confidence intervals (CIs) using Cox models stratified by matching variables, adjusting for country of birth, chronic obstructive pulmonary disease, diabetes mellitus, vascular diseases, rheumatologic disease, osteoarthritis, and comorbidity index.


A total of 4,930 cases of incident PD were identified during 7.3 million person-years of follow-up. PD incidence (per 100,000 person-years) was 61.8 among vagotomized patients (80.4 for truncal and 55.1 for selective) and 67.5 among reference individuals. Overall, vagotomy was not associated with PD risk (HR 0.96, 95% CI 0.78-1.17). However, there was a suggestion of lower risk among patients with truncal vagotomy (HR 0.78, 95% CI 0.55-1.09), which may be driven by truncal vagotomy at least 5 years before PD diagnosis (HR 0.59, 95% CI 0.37-0.93). Selective vagotomy was not related to PD risk in any analyses.


Although overall vagotomy was not associated the risk of PD, we found suggestive evidence for a potential protective effect of truncal, but not selective, vagotomy against PD development.

This reference is cited in the neurochecklist:

Parkinson’s disease (PD): protective factors

Abstract link

Modeling the Molecular Basis of Parkinson’s Disease. Argonne National Laboratory on Flikr.
Neurological infections Parkinson's disease

What has hepatitis C virus to do with Parkinson’s disease?

Hepatitis C virus infection as a risk factor for Parkinson disease: a nationwide cohort study

Tsai HH, Liou HH, Muo CH, Lee CZ, Yen RF, Kao CH.

Neurology 2016; 86:840-846.



To determine whether hepatitis C virus (HCV) infection is a risk factor for developing Parkinson disease (PD).


This nationwide population-based cohort study was based on data obtained from a dataset of the Taiwan National Health Insurance Research Database for the period 2000 to 2010. A total of 49,967 patients with viral hepatitis were included for analysis. Furthermore, 199,868 people without viral hepatitis were included for comparisons. Patients with viral hepatitis were further grouped into 3 cohorts: hepatitis B virus (HBV) infection, HCV infection, and HBV-HCV coinfection. In each cohort, we calculated the incidence of developing PD. A Cox proportional hazards model was applied to estimate the risk of developing PD in terms of hazard ratios (HRs) and 95% confidence intervals (CIs).


The crude HRs for developing PD was 0.66 (95% CI = 0.55-0.80) for HBV infection, 2.50 (95% CI = 2.07-3.02) for HCV infection, and 1.28 (95% CI = 0.88-1.85) for HBV-HCV coinfection. The association between HCV and PD remained statistically significant after adjustments for age, sex, and comorbidities (adjusted HR = 1.29, 95% CI = 1.06-1.56).


We conducted a large nationwide population-based study and found that patients with HCV exhibit a significantly increased risk of developing PD.

You may also check out

Hepatitis C virus infection: a risk factor for Parkinson’s disease.

Wu WY, Kang KH, Chen SL, et al.

J Viral Hepat 2015; 22:784-791.

These references are now included in the Neurochecklist:

Hepatitis C virus (HCV) neurology

Parkinson’s disease (PD): risk factors


Abstract link

By BruceBlaus - Own work, CC BY-SA 4.0, Link
By BruceBlausOwn work, CC BY-SA 4.0, Link
Parkinson's disease

What is the actual risk of developing Parkinson’s disease from pesticides?

 Risk of Parkinson disease after organophosphate or carbamate poisoning

Chuang CS, Su HL, Lin CL, Kao CH.

Acta Neurol Scand 2016; doi: 10.1111/ane.12707 (Epub ahead of print)



Parkinson’s disease (PD) is a common neurodegenerative disease. The aim of this study was to evaluate the risk of PD in patients with organophosphate (OP) or carbamate (CM) poisoning by using the Taiwan National Health Insurance Research Database.


We conducted a retrospective study involving a cohort of 45 594 patients (9128 patients with a history of OP or CM poisoning and 36 466 control patients) who were selected from the Taiwan National Health Insurance Research Database. The patients were observed for a maximum of 12 years to determine the rates of new-onset PD, and a Poisson regression model was used to identify the predictors of PD. The cumulative incidence of PD between the two cohorts was plotted through Kaplan-Meier analysis.


During the study period, the incidence rate ratio (IRR) of PD in the OP or CM poisoning patients was 1.36-fold [95% confidence interval (CI)=1.26-1.47] higher than that in the control patients in the multivariable model. The absolute incidence of PD was the highest for the group aged ≥75 years in both cohorts (77.4 vs 43.7 per 10 000 person-years). However, the age-specific relative risk was higher for the group aged <50 years (adjusted IRR=3.88; 95% CI=3.44-4.39).


Our results suggest that the likelihood of developing PD is greater in patients with organophosphate or carbamate poisoning than in those without poisoning. OP or CM poisoning may be an independent risk factor for PD.

This reference is now included in the Neurochecklist:

Parkinson’s disease (PD): risk factors


Abstract link

Tractor Fertilize Field Pesticide And Insecticide. Aqua Mechanical on Flikr.
Tractor Fertilize Field Pesticide And Insecticide. Aqua Mechanical on Flikr.
Parkinson's disease

Is sildenafil safe and effective for erectile dysfunction in Parkinson’s disease?

Sildenafil in the Treatment of Erectile Dysfunction in Parkinson’s Disease

Bernard BA,  Metman LV, Levine L, et al.

Mov Disord Clin Pract 2016; DOI: 10.1002/mdc3.12456 (Epub ahead of issue)



Erectile dysfunction (ED) is a common non-motor feature in patients with Parkinson’s disease (PD). Data regarding the tolerability and efficacy of anti-ED medication in the PD population are limited. The aim of this work was to assess the safety and efficacy of sildenafil in treatment of ED in men with PD.


This was a double-blind, placebo-controlled, cross-over study consisting of two 4-week arms separated by a 2-week washout period. Treatment sequence (placebo-sildenafil vs. sildenafil-placebo) was randomized. Sildenafil was started at 50 mg and adjusted to 25, 50, or 100 mg after 2 weeks, depending upon side effects. The Erectile Function domain of the International Index of Erectile Function (IIEF-EF; primary outcome measure) and the Parkinson’s Disease Quality of Life (secondary outcome measure) were obtained at baseline and end of each treatment period. The UPDRS was obtained at each study visit. The difference between group means was tested for statistical significance using t tests.


Twenty men participated and completed both treatment arms of the study. There was one instance of headache as a side effect. There was a significant effect of sildenafil on sexual functioning as measured by the IIEF-EF domain (P < 0.0001; mean for sildenafil = 23.2 ± 7.0; mean for placebo = 12.3 ± 7.5). There were no treatment effects for quality of life (P = 0.3) or PD symptoms (P = 0.86).


Sildenafil was safe and improved ED in this sample of men with PD. Overall, PD symptoms and quality of life were not impacted by use of sildenafil.


This reference is now included in the Neurochecklist:

Parkinson’s disease (PD): treatment of non-motor features


Abstract link

CC BY-SA 3.0, Lenke
CC BY-SA 3.0, Lenke