Category: Newsworthy Notes


National Institute of Neurological Disorders and Stroke (NINDS) has been a supporter of Parkinson’s Resource Organization almost from PRO’s inception. With their permission, we have taken information from their website, which you can do as well. We encourage you to visit their site to learn the prognoses and treatments for the below listed diseases. A number of disorders can cause symptoms similar to those of Parkinson’s. People with symptoms that resemble Parkinson’s but that result from other causes are considered to have Parkinsonism, A-Typical Parkinson’s or Parkinson’s Plus. Some of these disorders include:

Multiple system atrophy.  Multiple system atrophy (MSA) refers to a set of slowly progressive disorders that affect the central and autonomic nervous systems. In MSA, the protein alpha-synuclein forms harmful filament-like aggregates in the supporting cells in the brain called oligodenreoglia. MSA may have symptoms that resemble PD. It may also take a form that primarily produces poor coordination and slurred speech, or it may involve a combination of these symptoms. Other symptoms may include swallowing difficulties, male impotence, constipation, and urinary difficulties.  The disorder previously called Shy-Drager syndrome refers to MSA with prominent orthostatic hypotension—a fall in blood pressure every time the person stands up.  MSA with parkinsonian symptoms is sometimes referred to as MSA-P (or striatonigral degeneration), while MSA with poor coordination and slurred speech is sometimes called MSA-C (or olivopontocerebellar atrophy).  Unfortunately, many of the symptoms of MSA either do not respond to PD medications or the response is minimal or short-lived.

Dementia with Lewy bodies.   Dementia with Lewy bodies is a neurodegenerative disorder associated with the same abnormal protein deposits (Lewy bodies) found in Parkinson’s disease but in widespread areas throughout the brain. Symptoms may range from primary parkinsonian symptoms such as bradykinesia, rigidity, tremor, and shuffling walk, to symptoms similar to those of Alzheimer's disease (memory loss, poor judgment, and confusion).  These symptoms may fluctuate, or wax and wane dramatically. Visual hallucinations are often one of the first symptoms, and individuals may suffer from other psychiatric disturbances such as delusions and depression. Cognitive problems also occur early in the course of the disease.  Levodopa and other antiparkinsonian medications can help with the motor symptoms of Dementia with Lewy bodies, but they may make hallucinations and delusions worse, and affected individuals may require treatment with atypical antipsychotic medications.

Progressive supranuclear palsy.  Progressive supranuclear palsy (PSP) is a rare, progressive brain disorder that causes problems with control of gait and balance.  The symptoms of PSP are caused by a gradual deterioration of cells in the brain stem. People often tend to fall early in the course of PSP. One of the characteristic features of the disease is an inability to move the eyes properly, which some people describe as having blurred vision. People with PSP often show alterations of mood and behavior, including depression and apathy as well as mild dementia. PSP is often misdiagnosed because some of its symptoms are much like those of PD, Alzheimer's disease, and other brain disorders.  PSP symptoms usually do not respond to medication, or the response is minimal and short-lasting. PSP is characterized by aggregation of a protein called tau.

Corticobasal degeneration / CorticoBasal Ganglia.  Corticobasal degeneration (CBD) results from atrophy of multiple areas of the brain, including the cerebral cortex and the basal ganglia. Initial symptoms may first appear on one side of the body, but eventually affect both sides. Symptoms are similar to some of the features found in PD, including rigidity, impaired balance, and problems with coordination. Often there is dystonia affecting one side of the body. Other symptoms may include cognitive and visual-spatial impairments, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (muscular jerks), and dysphagia (difficulty swallowing).  Unlike PD, CBD usually does not respond to medication.  Like PSP, it is characterized by deposits of the tau protein.

Pseudobulbar Palsy. Progressive bulbar palsy, also called progressive bulbar atrophy, involves the brain stem— the bulb-shaped region containing lower motor neurons needed for swallowing, speaking, chewing, and other functions. Symptoms include pharyngeal muscle weakness (involved with swallowing), weak jaw and facial muscles, progressive loss of speech, and tongue muscle atrophy. Limb weakness with both lower and upper motor neuron signs is almost always evident but less prominent. Individuals are at increased risk of choking and aspiration pneumonia, which is caused by the passage of liquids and food through the vocal folds and into the lower airways and lungs. Affected persons have outbursts of laughing or crying (called emotional lability). Stroke and myasthenia gravis may have certain symptoms that are similar to those of progressive bulbar palsy and must be ruled out prior to diagnosing this disorder. In about 25 percent of individuals with ALS, early symptoms begin with bulbar involvement. Some 75 percent of individuals with classic ALS eventually show some bulbar involvement. Many clinicians believe that progressive bulbar palsy by itself, without evidence of abnormalities in the arms or legs, is extremely rare. Pseudobulbar palsy, which shares many symptoms of progressive bulbar palsy, is characterized by degeneration of upper motor neurons that transmit signals to the lower motor neurons in the brain stem. Affected individuals have progressive loss of the ability to speak, chew, and swallow. Progressive weakness in facial muscles leads to an expressionless face. Individuals may develop a gravelly voice and an increased gag reflex. The tongue may become immobile and unable to protrude from the mouth. Individuals may have outbursts of laughing or crying

Wilson Disease. Wilson disease (WD) is a rare inherited disorder of copper metabolism in which excessive amounts of copper accumulate in the body.  The buildup of copper leads to damage in the liver, brain, and eyes. Although copper accumulation begins at birth, symptoms of the disorder only appear later in life. The most characteristic sign of WD is the Kayser-Fleisher ring – a rusty brown ring around the cornea of the eye that can best be viewed using an ophthalmologist’s slit lamp. The primary consequence for most individuals with WD is liver disease, appearing in late childhood or early adolescence as acute hepatitis, liver failure, or progressive chronic liver disease in the form of chronic active hepatitis or cirrhosis of the liver.  In others, the first symptoms are neurological, occur later in adulthood, and commonly include slurred speech (dysarthria), difficulty swallowing (dysphagia), and drooling.  Other symptoms may include tremor of the head, arms, or legs; impaired muscle tone, and sustained muscle contractions that produce abnormal postures, twisting, and repetitive movements (dystonia); and slowness of movements (bradykinesia). Individuals may also experience clumsiness (ataxia) and loss of fine motor skills.  One-third of individuals with WD will also experience psychiatric symptoms such as an abrupt personality change, bizarre and inappropriate behavior, depression accompanied by suicidal thoughts, neurosis, or psychosis. WD is diagnosed with tests that measure the amount of copper in the blood, urine, and liver.

Guam/Kii Peninsula Parkinsonism Dementia Complex. One of a number of diverse hereditary and sporadic neurodegenerative diseases that lead to motor symptoms that are characteristic of Parkinsonism. These disorders form a heterogeneous group that may have commonalities at a cellular level, as many are characterized by accumulations of misfolded proteins that aggregate into fibrillar deposits containing a substance called amyloid. Adding further complexity to the current classification and understanding of these neurodegenerative parkinsonian disorders is that some may involve deposits of one, two, or three different forms of amyloid. For example, the most common subtype of Alzheimer's disease (AD) - the Lewy body (LB) variant of AD - appears to involve accumulations of three types of amyloid: 1) LBs formed of alpha-synuclein fibrils, 2) senile plaques formed of aß fibrils, and 3) neurofibrillary tangles formed by tau protein. For these reasons, there is a growing need to ensure that the nomenclature used for the different parkinsonian disorders reflects our rapidly growing insights into the genetic and cell biological mechanisms underlying these conditions. This, in turn, will promote greater diagnostic accuracy, facilitate communications between researchers, clinicians and patients and enhance the pace of research to identify more effective therapies for these diseases.

Neurodegeneration With Brain Iron Accumulation-1. Neurodegeneration with brain iron accumulation (NBIA) is a rare, inherited, neurological movement disorder characterized by an abnormal accumulation of iron in the brain and progressive degeneration of the nervous system.  Symptoms, which vary greatly among patients and usually develop during childhood, may include slow writhing, distorting muscle contractions of the limbs, face, or trunk, choreoathetosis (involuntary, purposeless jerky muscle movements), muscle rigidity (uncontrolled tightness of the muscles), spasticity (sudden, involuntary muscle spasms), ataxia (inability to coordinate movements), confusion, disorientation, seizures, stupor, and dementia.  Other less common symptoms may include painful muscle spasms, dysphasia (difficulty speaking), facial grimacing, dysarthria (poorly articulated speech), and visual impairment.  Several genes have been found that cause NBIA.

Lyme Disease. Lyme disease is caused by a bacterial organism that is transmitted to humans via the bite of an infected tick. Most people with Lyme disease develop a characteristic skin rash around the area of the bite. The rash may feel hot to the touch, and vary in size, shape, and color, but it will often have a "bull's eye" appearance (a red ring with a clear center). However, there are those who will not develop the rash, which can make Lyme disease hard to diagnose because its symptoms and signs mimic those of many other diseases Anywhere from 7 to 14 days (or in some cases, 30 days) following an infected tick's bite, the first stage of Lyme disease may begin with flu-like symptoms such as fever, chills, swollen lymph nodes, headaches, fatigue, muscle aches, and joint pain. Neurological complications most often occur in the second stage of Lyme disease, with numbness, pain, weakness, Bell's palsy (paralysis of the facial muscles), visual disturbances, and meningitis symptoms such as fever, stiff neck, and severe headache. Other problems, which may not appear until weeks, months, or years after a tick bite, include decreased concentration, irritability, memory and sleep disorders, and nerve damage in the arms and legs.

Normal Pressure Hydrocephalus.  Normal pressure hydrocephalus (NPH) is an abnormal increase of cerebrospinal fluid (CSF) in the brain's ventricles, or cavities. This causes the ventricles to enlarge, putting pressure on the brain.  Symptoms include problems with walking, impaired bladder control leading to increased urinary frequency or incontinence, and progressive mental impairment and dementia.  The person may also have a general slowing of movements or may complain that his or her feet feel "stuck."  These symptoms may sometimes be mistaken for PD. They do not respond to Parkinson’s medications.  Brain scans, intracranial pressure monitoring, and other tests can help to diagnose NPH. NPH can sometimes be treated by surgically implanting a CSF shunt that drains excess cerebrospinal fluid into the abdomen, where it is absorbed.

Post-traumatic Parkinsonism.   Also known as post-traumatic encephalopathy or "punch-drunk syndrome," parkinsonian symptoms can develop after a severe head injury or frequent head trauma associated with boxing or other activities.  This type of trauma can also cause a form of dementia called chronic traumatic encephalopathy.

Essential tremor.  Sometimes called benign essential tremor or familial tremor, this common condition tends to run in families and progresses slowly over time.  The tremor is usually equal in both hands and increases when the hands are moving. It may involve the head but usually spares the legs.  Essential tremor is not the same as Parkinson’s disease and does not usually lead to it, although in some cases the two conditions may overlap in one person. People with essential tremor have no other parkinsonian features. Essential tremor does not respond to levodopa or to most other PD drugs, but there are medications to treat it.

Arteriosclerotic Parkinsonism.  Sometimes known as pseudo Parkinsonism, vascular Parkinsonism, or atherosclerotic Parkinsonism, arteriosclerotic Parkinsonism involves damage to the brain due to multiple strokes. Tremor is rare in this type of Parkinsonism, while dementia and difficulties with gait are common. Antiparkinsonian drugs are of little help to people with this form of Parkinsonism.

ENVIRONMENTAL CAUSES  Postencephalitic parkinsonism. Just after the first World War, the viral disease encephalitis lethargica affected almost 5 million people throughout the world, and then suddenly disappeared in the 1920s. Known as sleeping sickness in the United States, this disease killed one-third of its victims and led to post-encephalitic Parkinsonism in many others. This resulted in a movement disorder that appeared sometimes years after the initial illness. (In 1973, neurologist Oliver Sacks published Awakenings, an account of his work in the late 1960s with surviving post-encephalitic patients in a New York hospital. Using the then-experimental drug levodopa, Dr. Sacks was able to temporarily "awaken" these individuals from their statue-like state). In rare cases, other viral infections, including western equine encephalomyelitis, eastern equine encephalomyelitis, and Japanese B encephalitis, have caused parkinsonian symptoms.

Drug-induced Parkinsonism.  A reversible form of Parkinsonism sometimes results from use of certain drugs, such as chlorpromazine and haloperidol, which are typically prescribed for patients with psychiatric disorders. Some drugs used for stomach disorders (metoclopramide), high blood pressure (reserpine), and others such as valproate can cause tremor and bradykinesia.  Stopping the medication or lowering the dosage of these medications usually causes the symptoms to go away.

Toxin-induced Parkinsonism. Some toxins can cause Parkinsonism by various mechanisms. The chemical MPTP also causes a permanent form of Parkinsonism that closely resembles PD. Investigators discovered this reaction in the 1980s when heroin addicts in California who had taken an illicit street drug contaminated with MPTP began to develop severe Parkinsonism. This discovery, which showed that a toxic substance could damage the brain and produce parkinsonian symptoms, led to a dramatic breakthrough in Parkinson's research. (Editor’s Note: The book The Case of the Frozen Addicts May 2, 1995 by J. William Langston and Jon Palfreman is a wonderful read and accounting of how Dr. Langston of the Parkinson’s Institute (the then California Parkinson’s Foundation) discovered these addicts.)

Parkinsonism-dementia complex of Guam. This disease occurs among the Chamorro populations of Guam and the Mariana Islands and may be accompanied by a motor neuron disease resembling amyotrophic lateral sclerosis (Lou Gehrig's disease). The course of the disease is rapid, with death typically occurring within 5 years.

For more information and/or to personally discuss your questions, please contact the Parkinson's Resource Organization, located in Palm Desert, Ca. We strive to help you find the answers, resources, and help that you need. Our team is available for private consultation and interested in sharing all we know to insure quality of life for our clients, their families and caregivers.

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Updated: August 16, 2017