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In an interview with American television channel CBS, Microsoft Chairman Bill Gates said that for a long time he did not tell about his disease to anyone, even his children adding that he was afraid to scare them. He also said that for a long time he could not come to terms with his illness. “Most of all I was afraid that people would treat me as someone as a seriously ill person. I could imagine people talking about my health and illness whenever I entered a room. Besides, I also did not want to scare my children, my work would not have been taken seriously,” Gates has said.
Bill Gates also told that he gets a lot of letters from relatives of patients with Parkinson’s disease, and is glad that he could be an example for those people. Parkinson’s disease is a chronic illness caused by the death of neurons in certain parts of brain and spinal cord. Its symptoms include – shaking hands, low physical activity. All this is accompanied by frequent bouts of fear, confusion, insomnia, hallucinations, disturbance in space orientation. Patients all the time feel sleepy and sluggish, and are prone to repeating same questions. Currently, this disease is incurable, but there are certain techniques that improve the quality of life of patients.
Many famous people have suffered from Parkinson’s disease such as former U.S. President Ronald Reagan and actor Michael Fox. Fox, the Canadian born Hollywood star famous for his blockbuster trilogy “Back to the Future”. In 2009, he founded the Michael J. Fox Foundation to combat Parkinson’s.
The Mini-Mental State Examination (MMSE) and the
Montreal Cognitive Assessment (MoCA) are the most commonly used scales to test
cognitive impairment in Lewy body disease (LBD), but there is no consensus on
which is best suited to assess cognition in clinical practice and most
sensitive to cognitive decline.
Retrospective
cohort study of 265 LBD patients [Parkinson's disease (PD) without dementia
(PDnD, N = 197), PD with dementia (PDD, N = 40), and
dementia with Lewy bodies (DLB, N = 28)] from an international
consortium who completed both the MMSE and MoCA at baseline and 1-year
follow-up (N = 153). Percentage of relative standard deviation (RSD%)
at baseline was the measure of inter-individual variance, and estimation of
change (Cohen's d) over time was calculated. RSD% for the MoCA (21 %) was
greater than for the MMSE (13 %) (p = 0.03) in the whole group.
This difference was significant only in PDnD (11 vs. 5 %,
p < 0.01), but not in PDD (30 vs. 19 %, p = 0.37)
or DLB (15 vs. 14 %, p = 0.78).
In
contrast, the 1-year estimation of change did not differ between the two tests
in any of the groups (Cohen's effect <0.20 in each group). MMSE and MoCA are
equal in measuring the rate of cognitive changes over time in LBD. However, in
PDnD, the MoCA is a better measure of cognitive status as it lacks both ceiling
and floor effects.
Figure. (A) T2-weighted brain MRI showing cavum vergae. (B) 123I-FP-CIT-SPECT revealed a re-
duced uptake in both of the putamen, which was more prominent on the right. (C) 123I-metaiodoben-
zylguanidine scintigraphy showing normal cardiac uptake in the early and delayed phases. (D) A
FISH chromosome analysis indicating del(22) (q11.2q11.2)(TUPLE1-).
February 7, 2016 Abstract
We herein report the case of a 43-year-old man with a 4-year history of resting tremor and akinesia. His
resting tremor and rigidity were more prominent on the left side. He also presented retropulsion. His symp-
toms responded to the administration of levodopa. The patient also had a cleft lip and palate, cavum vergae,
and hypoparathyroidism. A chromosome analysis disclosed a hemizygous deletion in 22q11.2, and he was di-
agnosed with early-onset Parkinson’s disease associated with 22q11.2 deletion syndrome. However, the patient lacked autonomic nerve dysfunction, and his cardiac uptake of 123I-metaiodobenzylguanidine was nor-
mal, indicating an underlying pathological mechanism that differed to that of sporadic Parkinson’s disease.
Introduction
Chromosome 22q11.2 deletion syndrome (22q11.2DS) is
the second most common chromosomal abnormality next to
Down’s syndrome. It causes abnormalities in the midline
structures such as characteristic facial features, cleft lip and
palate, hypoparathyroidism, and cavum vergae. It also
causes mental retardation or schizophrenia (1).
Several cases of early-onset Parkinson’s disease (PD) as-
sociated with 22q11.2DS have been reported, but its patho-
logical mechanism is not yet clear. We herein report a case
of early-onset PD associated with 22q11.2DS, review the
previous cases in the literature, and discuss the possible
pathogenesis.
Case Report
A 43-year-old man presented with resting tremor, dis-
abling akinesia, and gait disturbance. He first noticed a rest-
ing tremor in his left arm at 39 years of age, for which a
nearby neurologist prescribed pramipexole (0.5 mg tid). His
tremor was not relieved, and the medication was discontinued. Short-stepped gait and bradykinesia developed at 41
years of age. He became depressed at 42 years of age, but
improved spontaneously over the following 3 months. How-
ever, the motor symptoms showed gradual progression, and
he eventually required help in getting dressed.
He received an operation for a cleft lip and palate in his
infancy. Hypocalcemia was diagnosed when he was 39 years
of age, and 1-alpha-calcidol was prescribed. Neither neuro-
logical diseases nor consanguinity were reported in his fam-
ily history. On examination, he was alert and did not show
signs of dementia. Although he was not aware of anosmia,
his odor identification rate in the Odor Stick Identification
Test for Japanese (2) was 25%, indicating decreased olfac-
tory recognition ability. His facial expression was mask-like,
and his speech was monotonous. The patient’s rigidity was
severe in the neck, moderate on the left side and mild in the
right extremities. A pill-rolling tremor of 4-6 Hz was no-
ticed predominantly on the left side. Finger- and foot-
tapping was decreased predominantly on the left side. His
gait was short-stepped, but independent. Retropulsion was
noticed. Orthostatic hypotension was not observed in the
head-up tilt test. Constipation was denied. No symptoms of
rapid eye movement (REM) sleep behavior disorder (RBD)were detected on the RBD screening questionnaire.
The results of an electrocardiogram, chest X-ray, and rou-
tine blood tests were normal. Brain CT and MRI (Figure A)
studies showed cavum vergae, but no calcification was de-
tected. The patient’s total Unified Parkinson’s Disease Rat-
ing Scale (UPDRS) part III score improved by 28% after
the intravenous infusion of 100 mg levodopa. The ioflupane
(123I)-FP-CIT-single photon emission computed tomography
(SPECT) (Figure B) showed the reduced uptake of both of
the putamen (specific binding ratio: R/L=1.81/2.28). The
heart to mediastinum (H/M) ratio obtained by 123I-
metaiodobenzylguanidine (MIBG) cardiac scintigraphy (Fig-
ure C) was 2.29 in the early phase and 2.60 in the late
phase. A fluorescence in situ hybridization (FISH) chromo-
some study (Figure D) disclosed del(22) (q11.2q11.2)
(TUPLE1-), and a genetic analysis revealed no mutations in the Parkin, PINK1, LRRK2 or SYNA genes. Mitsuaki Oki, Shin-ichiro Hori, Shinya Asayama, Reika Wate, Satoshi Kaneko and Hirofumi Lusaka To view more information: https://www.jstage.jst.go.jp/article/internalmedicine/55/3/55_55.5485/_pdf ~~~~~~~~ http://www.topix.com/health/parkinsons-disease/2016/02/early-onset-parkinsons-disease-associated-with-chromosome-22q11-2-deletion-syndrome
As
many as 74 drugs, including life saving ones used for treating cancer and HIV,
will see sharp rise in prices as the government has withdrawn customs duty
exemption on their imports. The Central Board of Excise and Customs (CBEC) last
week issued a notification withdrawing exemption of levy of basic customs duty
on as many as 74 drugs.
The
medicines on which customs duty will now be imposed include the ones used for
treating kidney stones, cancer chemotherapy and radiotherapy, life-threatening
heart rhythm disorders, diabetes, Parkinson's disease, bone diseases,
antibiotic to treat infections. Besides, drugs used for bacterial infections,
leukemia, anesthetic medication, human immunodeficiency virus (HIV) or hepatitis
B virus cells, allergies, arthritis, lupus and ulcerative colitis might a Also
drugs used in blood dilating medicine or for treating menopause, glaucoma,
anogenital warts, poisoning by a chemical or pesticide, growth failure in children
and adults who lack natural growth hormone would also attract customs duty.
"The withdrawal of exemption from basic customs duty for certain drugs and
medicines including life-saving drugs is intended to provide protection to the
domestic manufacturing industry and enhance the attractiveness of make in India
initiative," KPMG India Partner and Head of Indirect Tax Sachin Menon
said.
"An
increase has also been made in the customs duty rates of certain life saving
drugs such as abciximab, anti-rabies immunoglobin, FSH, procarbazine and
saquinavir to 35 per cent," Deloitte in India Senior Director MS Mani
said.
These
changes signify the intention of the government to promote domestic manufacture
of these items as imports would now become more expensive, Mani said. Menon
said the move seems to be in line with the government's objective to
rationalise the duty exemptions.lso see spurt in prices.
UNRAVELING THE MYSTERY OF ALPHA-SYNUCLEIN AT DRUG REHAB CENTER
Can a single protein help us to solve the mystery of Parkinson’s disease (PD)? The answer, scientists increasingly believe, may be yes. And the protein of interest? Identified more than two decades ago, it is alpha-synuclein (α-synuclein). In Parkinson’s disease, abnormal forms of this protein are found clumped together within dopamine neurons, the brain cells that help control smooth movement, as well as in other neurons.
The clumps, called Lewy bodies, are currently the only definitive confirmation we can get of a PD diagnosis, but they can only be seen at autopsy.
It turns out that Parkinson’s is not the only neurological disease to be identified with mysterious protein clumps in the brain. In both Alzheimer’s and Huntington’s diseases, for example, scientists have observed clumps of other proteins — known by the names beta-amyloid, tau, huntingtin and TDP-43 — in the brains of people who live with these conditions. And scientists have discovered that α-synuclein — the same protein that is found in PD — also clumps in a parkinsonism known as multiple system atrophy (MSA) and in dementia with Lewy bodies (DLB).
What can we learn from these clumps? Despite much research, it has been a challenge for scientists to understand normal α-synuclein and how it changes in Parkinson’s. But recent findings have cast new light on how the protein works and what its potential may be to help diagnose and treat the disease.
To find out more, we went to Dr. Dennis J. Selkoe, the Vincent and Stella Coates Professor of Neurologic Diseases at Harvard Medical School and Co-Director at the Center for Neurologic Diseases at Brigham and Women’s Hospital. As a neurological specialist, he cares for people with PD and DLB and conducts research with a special focus on α-synuclein. Together with colleague Tim Bartels, M.Sc., Ph.D., he has twice been awarded PDF funding to study the protein.
We sat down with Dr. Selkoe to talk about the mystery of α-synuclein and how science is coming closer to understanding its role. Here is what he told us.
Q. What is α-synuclein and why has it been linked to PD?
It is a naturally occurring protein that is found in all nerve cells of the body, as well as in red blood cells and other cells. Over the years, multiple discoveries from many scientific labs have greatly heightened interest in α-synuclein as a potential cause of PD. It has been linked to familial forms of PD (that is, mutations in the α-synuclein gene have been found to cause rare forms of inherited PD) and to genetic variants which increase risk for PD in the general population. It has also been shown to form clumps that are toxic to the dopamine neurons which are lost in PD. Moreover, the protein has been found to clump abnormally in two related diseases, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) — and even in some neurons in Alzheimer’s disease.
Q. How has our understanding of α-synuclein in PD changed over time?
In the 20 years or so since α-synuclein was discovered, there has been a major revision in our understanding of what normal α-synuclein looks like in the brain — that is, its structure and shape. For example, it was initially thought that strands of normal α-synuclein appeared alone, as individual molecules (monomers). Now it is known that normal α-synuclein is often folded into groups of four molecules, bound together in a natural cluster called a tetramer.
Research is helping scientists understand how the shape of α-synuclein in Parkinson’s might lead to the disease. The protein, when in groups of four (tetramers) can often protect itself from being damaged. But unfolded single strands (monomers) are at risk for damage that leads to clumping in Parkinson’s disease.
Q. How are these discoveries about the structure of α-synuclein helping us to better understand PD?
Our understanding of the size and shape of normal α-synuclein is helping us to understand what might go wrong in PD. For example, when studying α-synuclein tetramers, we found that there was strength in numbers — meaning their grouping into sets of four molecules allowed them to avoid the harmful aggregation (clumping) process that leads to PD. In other words, the tetramers resist the pressure to transform into toxic abnormal clumps. In contrast, excess α-synuclein monomers are known to promote the PD process — meaning they are much more likely than the normal tetramers to transform into the abnormal clumps, or aggregates, that prove toxic in PD.
We have seen this to be true for the rare genetic mutations in α-synuclein that cause PD. These mutations decrease the formation of healthy tetramers, which leaves more free monomers in the neuron. We believe that when this happens, it could trigger the transformation of normally shaped α-synuclein into the abnormal, unhealthy type.
Q. Could these findings point us toward newer or better therapies for PD?
In the future,research into α-synuclein will likely help us to develop drugs and antibodies that can stabilize healthy α-synuclein or help clear unhealthy forms from the brain, thus slowing down the loss of dopamine and other neurons in PD.
For example, we see potential in the concept of keeping α-synuclein in its healthy tetramer shape. In theory, if the protein remains as a tetramer, it may be safe from the process that leads to PD. But first, we have to find a way of stopping the tetramers from breaking up into monomers.
To accomplish this, we are screening existing drugs to find compounds that could help normal tetramers stay together and retain their shape, thereby avoiding the abnormal clumping of monomers that occurs in PD. We think that this might present an entirely new way of preventing the onset of PD and the related diseases, DLB and MSA. In all cases, we want to keep α-synuclein in its principal normal form (tetramers) and keep the level of the aggregation-prone monomers relatively low.
Currently, we rely on a doctor’s observation for a PD diagnosis. Could research on α-synuclein lead to better diagnostic tools for PD?
Yes, research could one day help scientists to routinely measure normal and abnormal forms of α-synuclein in cerebrospinal fluid (the liquid that bathes the brain and spinal cord) and perhaps even in blood, thus serving as tools to diagnose PD.
We may also find ways to visualize abnormal clumps of α-synuclein to diagnose PD through brain imaging. To get there, we need to find compounds that can be used in specialized brain scans — that could be injected intravenously and go to the brain to bind to abnormal α-synuclein aggregates. This would give us a way to detect the presence of Lewy bodies in cases of PD, DLB or MSA, both before and during the development of clinical symptoms of these diseases.
Q. When can people with PD expect treatments to be available that might “clear” the brain of too much α-synuclein?
This goal is now at the forefront of PD research. The approach involves addressing the problem of abnormal protein deposition — a crucial early step in the development of several degenerative brain diseases. Our goal in PD is analogous to worldwide efforts to prevent or slow the abnormal accumulation of the beta- amyloid protein as a treatment for Alzheimer’s disease.
As of today, there is no approved treatment that can prevent abnormal α-synuclein build-up or clear it from the brain. The good news is that there are now clinical trials afoot that are intended to do just that — to treat the build-up of the protein (e.g., with antibodies to α-synuclein that can be injected intravenously once a month). This development could present new hope for people who live with Parkinson’s disease.
Conclusion
For years, α-synuclein has been under intense investigation. While the protein remains somewhat mysterious, recent breakthroughs — about its size, shape and ability to spread in the brain — have allowed us insights into how it occurs normally — and what goes awry in PD.
Such discoveries are absolutely necessary for us to identify ways to more effectively diagnose, treat and perhaps one day prevent Parkinson’s disease.
Parkinson’s
disease (PD) is a progressive neurological illness affecting the basal
ganglia
causing neuronal cell death of the dopamine producing cells within the
substancia nigra as well as neuronal death in other parts of the brain
including the brainstem. Rest tremors, rigidity, gait impediments, and marked
slowness of movements (commonly referred as motor symptoms) are the hallmark of
this disease. However, there are also many other non-motor symptoms
involving sleep, cognition, behavioral problems, and autonomic dysfunction.
Among these dizziness is a common complaint among people living with PD making
up to 30% of those over the age of 65.
So what is dizziness?
Because the term dizziness is so imprecise due to the fact that it can refer to vertigo, syncope, disequilibrium, general weakness, or a non- specific feeling such as giddiness; It is often dismissed by healthcare providers as trivial if one complains of ‘dizziness’ purely as a non-specific symptom. First, we have to understand what we mean by feeling dizzy- some people think of this as the room spinning or a sense of self spinning- this is actually known as vertigo and implies a different cause (etiology). While a feeling of unsteady in your feet when walking and actually veering or falling to one side as opposed to just falling all over the place implies more than loss of balance but rather a structural abnormality within the brain or ear canal. Some people feel lightheaded instead- feeling faint, and may complain of feeling a sensation of swimmy headed/ water inside the head.
So as you can see there are a multitude of causes of ‘dizziness’ and in order to get the right treatment you must learn to be specific with your problem.
The Medical definition of dizziness is- either someone who is mentally confused or is having a feeling of whirling in the head with a tendency to fall.
In order for someone to walk normally without unsteadiness or loss of balance, one must have intact sensory input (eyes, ears, nerves in feet referred to proprioception as well as intact cerebellum; extrapyramidal system-one involved in PD; and cerebral cortex). As you can see there are a lot of places where we can have a deficit causing us to feel ‘unsteady’ and ‘dizzy’ making us prone to fall or become confused.
Causes of Dizziness in PD:
Neuro-otological- meaning inner ear problems
Cardiovascular disease
Drugs
Multisensory dizziness syndrome- meaning poor input from various sources i.e. eyes, ears, nerves, etc.
Cervical vertigo
Postural hypotension
Postural instability due to tremors/dyskenesiasPisa syndrome- antero-flexion of the trunk leading to loss of balance by shifting gravity forward- treat with brace, botox and medication adjustment.
Migraines- occipital (basilar migraines) may present only as dizziness and nausea without headache- common change in people who had migraines all of their lives. Stalevo and levodopa compounds are more likely to trigger. treatmnent migraine medications – e.g. maxalt, imitrex & preventive meds such as Topamax or keppra
BPPV-Benign Positional Vertigo- treated with vestibular therapy
Treatments of dizziness:
The most important thing to discovering and treating the cause of your problem is a good detail history. This includes:
What do you mean by dizziness? Is it vertigo or light-headedness or swimming sensation in head or a feeling of confusion, etc.?
Are you falling? Or simply unsteady?
When does it occur? (After medication, before medication?)
How long does it last?
What makes it better? What makes it worse?
Other symptoms? Ringing in ears? Hearing loss? Numbness in feet? Weakness? Headaches?
Chest pain?
Only when you stand still? Or walking?
Neuro-otological– it is important to have yearly check- ups of hearing and sight especially as we age. This is the number one cause of falls and unsteadiness in older people because the sensory input from these areas are no longer functioning as well as we would like. Especially in PD we already have vision problems including loss of contrast and difficulty moving eyes more so if you have PSP – vision is extremely limited in the vertical plane resulting in frequent falls because people are not able to see changes in sidewalks, like small steps. The other group who might have had essential tremor initially and then developed PD may suffer from significant hearing loss which is one of the hall marks of ET- which may then contribute to poor equilibrium.
Get hearing aids and/ or prisms to help with these types of problems that lead to disequilibrium. This means seeing an ENT doctor and possibly getting an MRI brain, an electronystagmogram (ENG)- this test helps distinguishes between abnormalities in the vestibular system, brainstem, and cerebellum, and having a hearing test done. Also may need to see a specialist called neuro-opthalmologist if your regular eye doctor is not able to detect any eye abnormalities but have trouble seeing resulting in falls.
Cardiovascular-of as we age we also have tendency to develop heart disease, women are not excluded from this- after menopause we have same risk as men. Furthermore, although it is still controversial and not well publicized most of the dopamine agonists do increase the risk for arrhythmias (this risk increases with age in my opinion and needs to be monitored especially if already have risks for heart disease or family history of such). I myself have developed a secondary heart degree block since I have been on my medications. This type of problem usually presents in the middle of the night but can occur anytime a person goes to the bathroom to void, they may experience near fainting or actual fainting- this is extremely serious and need to seek medical attention ASAP from cardiologist!
Drugs-most of the drugs used for PD because they work on the neurochemicals can potentially alter cognitive status especially if have underlying dementia or a Parkinson’s plus syndrome. But in PD patients these medicines can often cause sleepiness making one feel somewhat unsteady and dizzy particularly when in a moving vehicle it may trigger actual spinning sensation even when the vehicle comes to a sudden stop. This feeling is more common with benzodiazepines (e.g. klonopin, valium, etc.) The dopamine agonists are more likely to cause sedation, the one least likely is Neupro patch. One way of counteracting is taking medications like Provigil & Nuvigil (narcolepsy drugs often used in PD to help maintain alertness). However, one simple solution is when you feel this way lay down and take a small nap- problem solved. If unable to function because feeling unsteady, and spinning talk to your doctor about adjusting your medication especially if you are actually experiencing outright confusion and disorientation.
Multisensory dizziness syndrome– the biggest thing here is loss of proprioception- feeling or sensory input from the ground due to peripheral neuropathies. This is common from B12 deficiency, a common problem in PD easily corrected by checking blood work- levels should be in the 1000’s replaced only via IM B12 injections or nasal spray. Other common causes is diabetes – this is a risk that increases as we age plus as I mentioned in other blogs PD patients may be at higher risk of developing Diabetes due to insulin resistance cause by dopamine intake since it shuts down the pancreas. I suggest close monitoring of your sugars especially if had PD for a long period of time and/or have family history. * see how to tell if you are at risk of diabetes. Take B1- thiamine 100mg a day to protect against neuropathies. Another reason people may have sensory loss in their limbs is due to stenosis/herniated discs in neck and lumbar spine – frequent problems in PD. In order to avoid this from becoming chronic irreversible problem seek immediate medical attention if have pain, weakness or numbness shooting down a limb.
Cervical vertigo- as I said above cervical stenosis can cause problems of proprioception- since head and neck move together any compromise of the neck disrupts the input into the brain- this may be one of the biggest problems in PD since so many of us as we advance in our disease experience problems in our neck due to dystonia/ dyskenesias/ and increased rigidity. Not only will this affect sensory input coming in as well as going out but may also disrupt blood flow into the brain by compromising the vertebral arteries if there is abnormal positioning of the neck. Hence it is extremely important that if you are experiencing neck issues especially in light of dizziness, vertigo or unsteadiness- seek immediate medical attention to adjust medications, get Botox, DBS or neck surgery and even take a blood thinner in form of aspirin to maintain blood flow if not contraindicated. The advantage is that an aspirin a day may also be beneficial (possibly neuro- protective) in PD.
Postural hypotension –the #1 cause of dizziness and falls in PD patients. Most medications can cause low blood pressure upon arising quickly leading to loss of balance or falls as you first get up from sitting or lying down. Sometimes can be severe that it lasts several hours making gait difficult. When hypotension is medication related you will notice this symptom an hour -2 after medication intake and will improve as medication wears off. Usually most severe within first hour. Some patients if they have Parkinson’s plus syndromes like Shy dragger, LBD, or PSP may have symptoms from the beginning even before medication intake. These patients need to be on hypotension precautions like wearing support hose (ted hose, compression hose that go to their thighs), sleep with head of bed elevated at 45 degree angle (can get a bed tempurpedic mattress, or put a few bricks at head of bed), do not shower with hot water- only warm, drink cold water during an episode, and take medications like salt tablets, Northera, Midrodine, Fludrocortisone, and others like Rameron (because of increased BP potential). If you have advanced PD, you also may have this problem and may need to resort to similar symptoms. However, if you have early onset PD and are experiencing this type of side effects- one try adjusting medications or switching to another type. Sometimes taking meds on a full stomach helps decrease this side effects or taking meds early in am and going back to bed and sleeping symptoms off are some of the possible strategies to dealing with this issue. Talk to your doctor as soon as possible if you are experiencing light-headedness, dizziness, and disequilibrium and faint feeling upon arising. Also remember to get up slowly from sitting or lying down.
