alzheimers, confusion, dementia, LBD, parkinson's disease

Could I have Lewy Body Dementia?: by Dr. De Leon

I used to fear that taking medication would change my personality; now i fear that it won’t.” ~David Levy

In the last month and a half I have been dealing with (upper respiratory) infection after infection which have really got me thinking about the causes. Plus the severe dysautonomia which I have experienced recently, being a neurologists, I thought oh my!- this is one of the things that happens and usually the reason (recurrent infections) why people with Lewy body dementia (LBD) succumb to the illness leading to their demise.

I don’t have LBD however, i thought it would be a good time to discuss the clinical presentation of this illness compared to Parkinson’s. Funny thing though, I was commenting this observation with my BFF whom i was traveling with and I said jokingly – “ I know i am not demented” so can’t have that awful disease. She looked at me and responded ‘no not like all the people we have met with disease.’ I gestured in agreement. “but, your personality…” I immediately sat up becoming paranoid, ‘what’s wrong with my personality?’ I asked. She just smiled at me.

Sure I have become more outspoken but that is a factor of my getting older i assume not because of anything organic but just to make sure i had to ask a few people that known me for a long time and the conclusion- i am same crazy, stubborn, energetic, outspoken girl. ( ooh-thank God, what a relief- and don’t ask me to remember cliches because I have always gotten mixed up!)

But unfortunately the reality is that there are too many people out there who do suffer from this terrible disease which is a combination of Parkinson’s and frontal dementia/ Alzheimer’s.  I have seen too many friends and patients spiral down quickly.

So, I would like to talk about what we know about LBD and how we may improve the lives of the patients and caregivers. unfortunately, there is no cure and no specific treatment for this disease as with many other neurological illnesses.

This is the 3rd most common type of dementia affecting ~5% of those older than 75 years of age.

Symptoms which are features of both Alzheimer and Parkinson’s make it a particular challenge in diagnosing. However, the KEY  to diagnosis is the presence of pronounced visual hallucinations, psychiatric overtones and autoimmune problems from day one which then leads to a rapid and pronounced cognitive impairment, along with rigidity, freezing, and severe Rem behavior (often preceding) cognitive symptoms.

Interestingly, Sleep disturbances like REM behavior occurs in about 60% of  parkinson’s patients while an upwards of  80% is seen in MSA ( multi-system atrophy) and LBD.

Most people live on average of 5-8 years after diagnosis but some have lived up to 20 years.

Clinically:  Patients have vacillating or oscillating symptoms fluctuating from near normal to severely abnormal.  These episodes of downward spiral are typically triggered by infection and medications. These patients often have periods where they  return to normal or high function making some people think they are malingering or feigning illness. There is particular variation in cognition; well one day and confused and forgetful the next ..may appear as if doing on purpose which has infuriated and frustrated many a caregiver.  They also exhibit decreased attention, increased sleepiness, and alertness with patterns of normalcy interspersed  with decreased need for sleep, increased alertness and attentiveness. (like a yo-yo and in a step down progression each time rebounding less and less frequently back to normal).

Evolution of disease:

Prominent visual hallucinations, confusion, decreased concentration and alertness, sleep problems followed by apathy, (aphasia) speech impediments, swallowing trouble and paranoid delusion. initial treatment with Namenda makes cognition worse and worsens significantly with dopamine agonists and anticholinergic medications. Frequent falls are common often due to orhtostatic problems and fainting from autonomic dysfunction.

Subsequently, they become very weak developing frequent infections like pneumonia and other immunological infections leading to demise. by this time speech is usually very soft whisper almost inaudible or absent. This is the end stage phase


What are the risk factors?

  • older age >60
  • male gender
  • family history of PD or LBD
  • sleep disorder increases risk of  LBD five -fold
  • same risk factors as stroke (HTN, DM, Cholesterol) – linking it to a possible vascular etiology; interestingly not smoking just like in PD it seems to confer a positive benefit- however this does not mean you should take up smoking!
  • strokes
  • low education
  • attention deficit disorder


  • clinical
  • Dat scan shows low dopamine uptake
  • precision ct scan reveals abnormal uptake in the occipital and parietal lobes


  • This is symptomatic and supportive-treat dementia aggressively with medicines like  Exelon, Aricept or Razadyne.
  • use of antipsychotics like seroquel and clozaril
  • initiate speech therapy early on to improve not only swallowing but also speech and communication; consider feeding tube if necessary as well.
  • PT to prevent falling
  • monitor HTN, sugars
  • prevent infections as much as possible- constant vigilance, get vaccines if needed ahead of time
  • stay hydrated
  • treat with bp meds and orthostatic meds
  • most importantly try to establish a scheduled sleep pattern and use meds to help sleep.
  • discuss end of  life plans, hospice, dNr ( donot resucitate, etc)

@copyright 2017

all rights reserved Maria De Leon


dementia, parkinson's disease, Parkinson's Health, Parkinson's symptoms, Parkinson's treatment

Apathy: How to Combat: By Dr. De Leon

“Science may have found a cure for most evils; but it has found no remedy for the worst of them all- the apathy of human beings.” Helen Keller

It has been a few weeks since I have written. Why? Pure apathy or is it indifference! In our vocabulary we tend to use the words apathy, indifference, and impassivity interchangeably. However, are they really the same thing and if so what does it mean for us in our living with Parkinson’s disease? Why do we feel this way? Is it normal? And is there anything we can do to combat this feelings of inertia that seem to take over us from time to time. if not addressed and treated properly can lead to severe disruption of life as well as to isolation and depression.

Thus, I have chosen this particular topic for discussion now that my inertia has passed away. This is also a subject which has generated much interest in our community as per the choice award topics of interest gather by the former PDF ( Parkinson’s Disease Foundation). perhaps before we spend countless hours and research money on the subject we need to define exactly what we mean. As I said earlier, most of us equate apathy to indifference but they are not the same thing particularly when it is defined in terms of a neurological illness.

Apathy and indifference both denote a lack of responsiveness and interest to things that may normally stimulate, excite or cause great emotions. apathy comes from the Greek root word pathos meaning emotion ( a=pathos) without feelings or emotions. this is a deep rooted neurological problem that involves the frontal lobe of the brain which deal with personality, and executive functions. Not only do you not have much feelings or interest but you DON’T CARE! in neurology as I stated before when we use the word apathy we are saying there is a neurological problem in the wiring of the brain that has gone awry. Usually more common than not when we as neurologists see this behavior outside of structural injuries in brain (e.g. head injury,  stroke, etc.) is primarily related to dementia.

What most of us in PD experience commonly however, is not apathy but indifference. The difference between the two is the personal behavior attached to this feeling.  People with true apathy simply don’t give a hoot about anything and don’t know they are apathetic. As opposed to being indifferent or having inertia or decrease in concern or emotions; we are completely aware of the problem we want to change it and don’t want to feel this way but we lack the fortitude to do anything about it. This is the state where I have found myself recently and I am sure many of you as well.  I want to go out and socialize, get showered, write, exercise but don’t have enough stamina to make myself do these things because the energy involved to achieve these tasks supersedes our reward. Remember that the basal ganglia is also a center for reward and pleasure and if you don’t have enough dopamine to think and do necessary activities to stay alive then you wont have any surplus to go in search of feel good activities. the reason I experienced this has been due to a decrease in my dopaminergic intake due to cardiac issues being evaluated. however, once I took my regular doses of medications my concern for things that are pleasurable like socializing and writing have returned.

So what does this mean for you? evaluate your feelings? is it you feeling like you don’t care and rather not invest energy in things you normally would love to do like read or go to movies or is it your loved one saying what is wrong with you? you don’t seem to care? and it makes no difference to you, you are content in your lack of participation. You could careless if you never brush your hair or shower again in your life.

Independent of which feeling is plaguing you most, I want you to know that there are treatments available for both.

Apathy vs. indifference?

Both require evaluation by your physician/neurologist/MDS


  • evaluate for new brain abnormalities i.e. stroke ( just because you have PD does not mean you can have other diseases), rule out thyroid disease and other metabolic abnormalities.
  • Get new or follow up mini-mental status exam (MSE) or  CogTest
  • neurobehavioral evaluation (needed in some cases)
  • Treatments:
  1. medications for dementia if present -e.g. Exelon (Rivastigimine) – only drug approved for PD dementia, but can also use  Namenda (memantine), Aricept (Donepezil), and Razadyne (galantamine). in my experience combination of Namenda plus Exelon or one of the other works best in retarding dementia particularly if introduced early on. thus I suggest yearly screening for this especially if had had PD >10 years because dementia risk increases with age and disease process. 40-50% develop PD patients develop dementia eventually.
  2. anti-narcoleptics- Provigill, Nuvigil ( non-addictive- focus on alertness, no blood monitoring required, do not interfere with other PD meds.
  3.  stimulants- a whole host which are amphetamines and amphetamine derivatives like Adderall, Ritalin. These are controlled substances and usually require closer monitoring some may even require blood monitoring.
  4. increase dopamine – but if dementia present this may make cognition worst


  • evaluate for depression
  • adjust PD medications (usually go up)
  • rule out thyroid disease/other metabolic issues
  • get neuropsych/behavioral evaluation if not sure if depression vs. dementia
  • Treatments
  1. if depression treat with antidepressants ( e.g. Zoloft, Lexapro, Effexor, Remeron, etc.)
  2. fatigue may also be a cause- treat with amantadine, and evaluate sleep.
  3. may also need sleeping meds.
  4. participation in activities like art, singing, exercise, dancing, biking etc. can increase natural dopamine, serotonin, and endorphins among other. these will in turn allow you break that indifference. So don’t give in to it get a buddy who can help out to over come these challenges but don’t forget to talk to physician first.

Now that you are an expert on the subject, you and your family can discuss more accurately with your physicians as to the cause of your lack of interest and participation in previous activities which brought you joy. Soon you will be on your way to finding your passion once more. Find one thing that bring you joy and pursue it …..

Carpe Diem!

alzheimers, CBGD, dementia, LBD, parkinson's disease, parkinsons dementia, PSP

An Overview of Syndromes with Dementia & Parkinson’s – Diagnosis, Treatment & Prognosis. By Dr. De Leon

There has been much speculation since actor Robin Williams died regarding the circumstances that led to his demise.  Many wonder whether his neurological disease Lewy Body Dementia (LBD) diagnosed only after autopsy triggered his suicide.  One will never know for certain what drove this brilliantly talented man to the edge of desperation putting an end to his own life.

However, because of the tragic loss of such beloved celebrity who initially had been given a diagnosis of PD while living only to confirm  another less common disease LBD after his death,  the question still lingers in everyone’s mind could they or their loved ones be afflicted with such  disease and not know it?- such a strange word for so many…

Thus, I would like to discuss the topic of dementia in its various forms and its relation to Parkinson’s disease.

First, I would like  to put everything in perspective- dementia is defined as loss of previously acquired cognitive skills including language and complex motor skills, of which Alzheimer’s is by far the most common type affecting well over 5 million American or about 1/9 patients 65 or older.

Dementia is then subdivided in to cortical (pertaining to higher-cerebral- cortex and cognitive function such as memory and language) and subcortical (involving the structures ‘underneath’ the cerebral cortex –i.e. the connections between the different lobes). Subcortical dementia is a clinical syndrome characterized by mental slowness, depression, apathy, impaired cognition and forgetfulness.

Unlike Alzheimer’s (cortical dementia) where there is an actual loss of neurons- in Parkinson’s dementia since it’s a subcortical dementia, the neurons are preserved only the chemicals are diminished, and the wiring is faulty making retrieval cumbersome and slow. In Alzheimer’s, as in other forms of cortical dementia, the information once lost is gone- reason why giving cues does not help to remember as it does for those suffering subcortical dementia where Parkinson’s dementia is the prototype.  Therefore, in subcortical dementias like  seen in Parkinson’s the possibility exists of being able to create new pathways between the various structures of the brain thus potentially thwarting the progression nor severity of disease.  this is why it is EXTREMELY important to obtain early diagnosis by a neurologists because although there is no cure for dementia of any type subcortical ones can be slowed down significantly or halted if correct diagnosis is given and treatment started early. One of the biggest therapeutic advantages to a better prognosis and quality of life is the institution of non-traditional modalities such as exercise and art therapy in addition to traditional treatments.

Some neurologists / movement disorder specialist including myself believe there is a spectrum of disease in which you have Alzheimer’s on one end of the spectrum with Parkinson’s at the other end  …with about 2 million people. Then you can have as many diseases as you can think of with various combinations ..including all the Parkinson’s plus syndromes (MSA, PSP, etc. closer to PD) & dementia syndromes like Fronto-temporal dementia, pick’s disease, etc.



Lewy body dementia lies at the crux of the see-saw smack down the middle. Then there are those rare patients who also truly have BOTH Parkinson’s and Alzheimer’s but those are even more rare. The reality is that many patients have mixed symptoms most frequently due to vascular disease. This is why it is imperative to ALWAYS have a brain scan at onset of diagnosis or if things don’t match up. More PD patients are in fact more likely to have a variation of Parkinson’s and vascular dementia then Alzheimer’s or other PD Syndromes. This is because most Alzheimer patients are typically otherwise extremely healthy and have no other risk factors while (thus usually look normal in appearance and mannerism at presentation) those with Parkinson’s disease can have and usually do have other illnesses including risks for stroke ( which I believe is greatly enhanced by medication effect especially in woman as a study of PD women showed higher incidence of stroke compared to men- most likely due to uncontrolled hypertension caused by dopamine and dopamine agonists).

So how do you diagnose?-

First, we must remember that of all the dementias, Alzheimer’s is by far the most common followed by vascular dementia caused by strokes. Of course by far Parkinson’s is the more common of the movement disorders second only to essential tremors. After understanding of this knowledge, it is both a matter of recognition of patterns (comes only through extensive training and years of seeing patients in a particular field- hence need for neurologists/MDS) and a numbers game in diagnosing- meaning that common things happen commonly. Yet, a GOOD NEUROLOGISTS ALWAYS HAS THE RARE DISEASES IN THE BACK OF THEIR MIND when things are not presenting, progressing or responding as they should!

Second, listening to the patient and taking a good history is key which means that you as a patient or caregiver MUST try to give as concise and detailed account as possible of symptoms including timeline –

  • what came first?
  • how long and far between onset of other symptoms?
  • are symptoms rapidly progressing?
  • are they progressing in a step like manner – meaning worsening then plateauing then declining again?

Third, equally important, especially when symptoms are very early and unclear, is to have continuity of care by same doctor for several months until picture is cleared- sometimes unfortunately we become impatient and want to know what is wrong with us so desperately that we jump from doctor to doctor giving them only a glimpse into the real pathology. Thus, each doctor only sees just one moment in time instead of the whole picture making diagnosis more difficult for any one person until it becomes so obvious. However, by the time it is easy to diagnose even by none experts frequently so much time has been lost that treatments may be ineffective due to advancing disease ultimately robbing us of not only our peace of mind but also diminishing our quality of life.

Characteristics of common dementias with/without Parkinson’s:

Alzheimer’s disease is loss  of speech& language, along with memory loss. Immediate or recent memory is impaired while remote memory is preserved. Patient’s usually  get lost in familiar places, do not recognize familiar faces, experience loss of previously acquired skills- complex motor skills. Initial presentation includes loss of smell, irritability, depression, personality changes, and apathy. Withdrawal is a common presenting characteristics along with fender benders  – these patients ARE NOT hallucinating when they first present. If diagnosed earl, they respond well to acetylcholinesterase inhibitor (e.g. Aricept, Razadyne, Exelon) and Namenda (Memantine) which can not only improve quality of life but delay hospitalization into a facility. It is a chronic progressive disease which occurs over 20-30 years. The incidence increases with age- although not typically hereditary there are two Alzheimer’s genes which are familial Presenilin 1 & 2. Risks of developing ALZHEIMER’S are illiteracy, low education, low socioeconomics, and lack of exercise, high blood pressure and diabetes.




Lewy body dementia – main characteristic is hallucinations (e.g. auditory, olfactory, visual, tactile, and gustatory) at the onset of disease, along with vivid dreaming, severe REM behavior, and early visuospatial impairment in absence of memory loss along with stiffness, slowness, marked bowel, & bladder problems. The key is that introduction to dopamine agonists and dopamine exacerbates or brings to the forefront the hallucinations. Also Namenda usually given for dementia /Alzheimer’s will worsen symptoms of hallucination, becoming psychotic delusional and extremely agitated.  However, other memory medicines can improve quality of life. Incidence of LBD is. 21/100,000.  This type of illness is a rapidly progressive disease 5-8 years. More common in men 4 to 1 usually in their 70’s.


Fronto-Temporal dementia a.k.a. Pick’s disease– they have significant behavioral and personality changes, interpersonal relationships, including language disturbances and alterations in muscle/motor function. They are caused by disorders involving the protein called TDP43  or the tau protein– why the lobe frontal lobe no one really knows. They usually occur in the 50’s and 60’s however some people may develop as early as their 20’s or as late as their 80’s.  there is a behavior variant  and a language variant. both the behavioral variant and the language variant are much less common than Alzheimer’s disease in those over 65 years of age. However, in the 45-65 year range both of these are as common as young onset Alzheimer’s.  Currently it is estimated that around 60,000 people have FTD the majority of whom are in the young age group. the thing that will distinguish Alzheimer’s and FTD is progression and genetic abnormalities. However,what is interesting is the fact that within the realm of  FTD’s we have PSP (Progressive Supranuclear Palsy) and CBGD.

  •  CBGD (corticobasal ganglionic degeneration) presentation includes more personality and behavior changes at the beginning of disease like FTD’s, even in absence of memory loss. Patients have trouble producing and comprehending language. Both of these have a quick rapid progression. FTD is closer to Alzheimer’s so no PD symptoms unlike CBGD which commonly is unilateral (even when it becomes bilateral there is an obvious dominance); has alien hand. Typical duration of CBGD is 6 years. Patients with CBGD usually are between 50- 70 years of age and it comprises about 1% of population. Tremors, rigidity, muscle spasm, involuntary eyelid spasm, sensory loss, significant swallowing difficulty are also part of the presentation and clinical picture. There is no good treatment  for these patients; they poor response to both Alzheimer’s drugs and to PD meds because they have both cortical and subcortical dementia. The best treatment especially early on is speech  and physical therapy ; when started early in disease process it can significantly improve quality of life particularly since dysphasia and dysarthria (slurred speech) are early signs leading to frequent aspiration and aspiration pneumonias.  These patients also have significant apraxia – this is the inability to perform purposeful movements especially when asked such as making an “okay” sign with your hands.


  • PSP-a.k.a.- Steele-Richardson-Olswenski syndrome- progressive supranuclear palsy-initial symptom in 2/3 of cases is loss of balance , difficulty walking-fast walking bumping into objects or people, and changes in posture- lunging forward when mobilizing. the other common early signs include general slowing of movement, change in personality and visual symptoms due to restricted eye movements especially in the vertical plane-because they can look down very well people fall frequently because cant see especially when stepping off a curb or are increasingly messy when eating because can’t see the food. Later dementia develops affecting loss of inhibition  and difficulty organizing information. They also have  muscle stiffness, swallowing difficulty (usually cause of demise), slurring of speech. Men and women affected equally, about 6/100,000. A poor response to dopamine along with symmetrical onset is the big CLUE along with abnormal eye function which includes eyelid apraxia.

Parkinson’s dementia -early presentation is classic Parkinson’s symptoms which include tremors, slowness, stiffness, and gait impairment; only after 10 plus years do patients get dementia of PD which occurs in up to 50% of individuals. – These patients respond well to PD meds and to acetylcholinesterase inhibitors as well as to Namenda. Exelon works great as do combination of Aricept and Namenda extended release or short acting (now in single formulary called Namzaric). Treatment at early signs is key preceded by adjustment of dopamine levels because the brain is also a muscle and just like the muscles get stiff and slow due to lack of dopamine so does the brain resulting in slow retrieval and weak connections- sometimes all it needs is an extra kick dose of dopamine. Presentation is usually depression, apathy and forgetfulness which is remedied by giving cues. Hallucinations do not occur until late stage and typically are visual. Most visual hallucinations in advance stages are usually benign. A common theme is that of children which typically do not require medication.

Recommended treatment for PD dementia with antipsychotics like Seroquel or Clozaril only if hallucinations are frightening or interfering with care or activities of daily living but first recommend adjusting PD doses then adding acetyl cholinesterase inhibitor if not better then antipsychotic as last result. I recommend that if there is question of memory problems talk to your doctor ASAP and obtain a neuropsych evaluation if necessary which will point to type of dementia cortical/subcortical or both? If have any memory problems or problems with speech, language, gait, coordination, tremors, stiffness or slowness seek first attention of a neurologist who can assess whether a movement disorder specialist is needed.

In summary, knowing the facts will aid in early detection and treatment. In order to achieve this we must be proactive and practice self advocacy because after -all no one knows your capabilities better than you or your spouse/partner so don’t delay seeking medical attention from a NEUROLOGIST if you or loved one have any of these symptoms or have family history of cognitive problems. Plus, do not forget to exercise at least 15 minute walk 3x a day  because can significantly decrease risk of Alzheimer’s dementia especially in women. It may also possibly improve or decrease risk of those with subcortical dementia’s like PD involving basal ganglia by increasing blood and oxygen perfusion to this area.  Also because the brain is a muscle we must remember that if we don’t use it atrophies. Therefore, the more you stimulate it and challenge it the more connections it will develop and the lower the risk for getting dementias of any type.

     So as we approach anew year make a resolution to Go ahead learn a new language, travel more, take up a new hobby, play with your grandkids, and socialize with your friends outside of social media. These things will not cure our illnesses or prevent us from getting them in the first place but can greatly shift the balance to our favor by decreasing risk of becoming severely cognitively impaired.

alzheimers, dementia, dopamine and parkinsons, parkinson's disease, Parkinson's Health, parkinsons treatments, parkinsons y tratamientos

Tips to dealing with Apathy : by Dr. De Leon

Scientists announced today that they have discovered a cure for apathy. However, they claim that no one has shown the slightest interest in it.” ~ George Carlin

I hear the word apathy tossed around all over the place from different places and people who use this term loosely to imply “lack of interest,” or ‘deep depression.’

However, as a neurologist the word apathy has not only a very special meaning but it also carries with it a specific diagnosis.

So, what does apathy really mean. Apathy as described by the Webster dictionary as  “a state of perfunctoriness.” I love that word.  It is a state of complete and total indifference in all realms of our being, emotional, spiritual, and social. People who suffer from apathy are completely and utterly devoid of concern, emotions, and feelings. Not because they don’t want to but because they are incapable of caring due to disconnect of fronto-cortical pathways.

Therefore, the term “apathy”  in neurology is always a harbinger of  brain illness particularly organic etiologies such as head injury, strokes, tumors, schizophrenia (although the latter usually considered a mental illness -I maintain it is an organic neurological disease because of involvement of dopamine- in this case too much) and of course the number one cause and almost synonymous with term of apathy is dementia – (e.g. Alzheimer’s, Parkinson’s, vascular, Lewy body, fronto temporal, etc.)

Therefore, giving someone a diagnosis of apathy in of itself is a poor prognosis which implies typically a rapid cognitive decline.

Having said this, one must always identify the cause and try to treat it as best as possible and prevent further cognitive decline.

Medications employed in the treatment of apathy:

1) [of course are] medications used to treat dementia – i.e the acetylcholinesterase inhibitors like Exelon (Rivastigmine), Aricept (Donezepil), Razadyne (Galantimine), and Namenda (Memantine) an NMDA inhibitor. Several of these compounds have extended release doses and come either in patch or liquid as well or both.

Other medications include:

2) Dopamine replacement– no better feel good drug than dopamine especially if deficiency is what is causing the apathy but it is not always as easy as that in dementia patients particularly those who have dementia of Parkinson’s disease or other dementias associated with parkinsonism because the addition of dopamine will increase visual hallucinations and other hallucinations and worsen confusion. therefore, this has to be measured in scale of risk and benefits but usually in the majority of cases in PD associated apathy combined with other medications like antichlolinerasterase and antipsychotics.

3) Stimulants like Provigil (Modafinil)/ Nuvigil – used in the treatment of Narcolepsy but also for hypersomnolance or increased sleepiness.  I prefer  this class as first line of treatment over amphetamines after dopamine replacement.  In my practice, I  had a moderate  to great success with them.  Other stimulants include amphetamine derivatives such as those employed in the treatment of attention deficit disorder (Methylphenidate-e.g. Concerta, Ritalin; Aderall; Straterra).

4) Antipsychotics are also a good source to combat apathy but best if use atypical drugs like Clozaril or Seroquel because of decrease potential for extrapyramidal side effects like tardive (late onset) dyskinesias and parkinsonism. This is especially crucial if already dealing with apathy related to Parkinson’s or Parkinson’s plus syndrome. We don’t want to make motor symptoms worse resulting in freezing and falls or increase dyskenesias.

5) Anti -depressantsSsri’s/SNri’s -E.g. Zoloft, Lexapro, Effexor, Cymbalta, etc.

6) ECT– electro convulsive therapy when all else fails -it works tremendously well despite all of the bad the media has given it based on past history and  portrayal of patient abuse in movies like One Flew Over the Cuckoo’s Nest. Currently, there are several state of the art centers in the country which provide these much needed services which can help patients  have a higher quality of life than the would otherwise -one may be near you. The alternative is earlier institutionalization.

As always early recognition of apathy is Key to improved quality of life by securing proper diagnosis followed by prolonged watchful supervision and treatment by a team of experts which include Neurologist, Neuropsychologist, counselors, social workers, therapist and loved ones to help with financial issues of caring for a chronically ill patient as well as help prolong nursing home admittance for as long as possible.

dementia, memory loss, parkinson's awareness month, parkinson's disease, parkinsons dementia, parkinsons health and beauty tips, parkinsons y tratamientos, sleep disorders in parkinson's

The Conundrum of PD: Are Memory Problems due to Disease, Medications or Both?: By Dr. De Leon

The Conundrum of PD: Are Memory Problems due to Disease, Medications or Both?: By Dr. De Leon.

chronic illness, dementia, parkinson's disease, parkinsons dementia, parkinsons health and beauty tips

Visual Hallucinations in PD: What do they look like? by Dr. De Leon

Someone asked not long ago if Parkinson’s hallucinations had a particular pattern or flavoring to them? The truth is that there are common trends seen in PD patients who experience hallucinations. First, a hallucination is a strong perception of something that is not real or does not exist. Any and all of the senses can be involved in a hallucination meaning that one can feel, taste, touch, see or hear something that is not real. Hallucinations are purely imaginary as opposed to illusions which are distortions of real things/ objects/ people/ and sounds. The second most common hallucination in my experience is olfactory (smell) hallucinations …I frequently think something is burning. other people have told me same thing. this may be related to olfactory neurons dying out.

It is estimated that at some point up to 75% of PD individuals will experience this phenomena of hallucinations particularly-visual.

It is also important to note that the timing of such events can be a huge diagnostic clue. In typical PD, these symptoms do not occur until more than 10 years into diagnosis and can be exacerbated by medications but are a part of the disease itself. So, if symptoms present at onset or within a few years of Parkinson’s symptoms then we are most likely NOT dealing with regular garden variety PD but rather a disease in the spectrum of Parkinson family like Lewy body dementia or CBGD ( corticobasalganglia degeneration) to name a few.

The most common type of hallucination in PD individuals is a visual one, as I stated earlier.  These can be either black and white or in full color and typically involve children or animals. The perceptions can last a brief period of time or hours. however, important to note that usually the images do not speak or make sounds and thus are not ordinarily distressing to the individual who for the most part remain aware that this is a hallucination (not real). In fact, a lot of my patients, as do many other PD individuals, rather enjoy seeing the children and find comfort in these images. However, although it is usually not the norm some patients can find the hallucinations distressing, anxiety provoking, and even frightening at times, these typically occur with more violent or frightening images- typically of demons and such.  When a person cannot distinguish reality from make- belief or if the images are too frightening or causing distress, this is the time for intervention.

What can you do to help?

1)  Make note as to when hallucinations are more likely to occur to try to prevent. Confusion, hallucinations and a full moon usually go hand in hand! So, keep those neuroleptic drugs handy just in case you may need during a full moon or lunar eclipse. In my experience, more patients were brought to ER because of psychosis during these days.  Typically, I would recommend pre-medicating a patient during those days if I knew they were prone to hallucinate and get distressed over the event.

2)  People that sleep a lot during the day seem to be more prone to visual hallucinations. Try to maintain normal sleep wake cycle as much as possible and prevent excess daytime sleep. On the other hand, sleep deprivation can also trigger these episodes. Therefore it is important  to discuss with your physician any sleep problems.

3)  Also be aware that certain medications like anti- cholinergics (e.g.amantadine), anti- histamines (Benadryl), anti- anxyolitics (e.g. klonopin)  even dopamine medications, more the agonists than levodopa, can induce hallucinations.

4) Other triggers for hallucinations are acute infections. In the elderly population urinary infection is the number one culprit. So maintain your loved ones well hydrated.

Even though, PD individuals may experience auditory hallucinations this is not the norm and if this is highly prevalent, one must consider other causes triggering these events, such as brain tumors, strokes, medications, etc.

Often, my grandmother who had Parkinson’s in her final stages would hallucinate. She frequently saw children playing and thought of them as the children she had lost when they were infants or toddlers. Seeing them made her happy. In this scenario I did not need to give her any type of medication for psychosis or hallucinations for its not always necessary to medicate a loved one just on the basis that they are having hallucinations. However,  there were times when she thought the house was being flooded and caused a great deal of distress thinking that she and we were going to drown especially my daughter who was only a toddler then.  At those times, I would have to give medication to decrease her anxiety.

How to handle patient when hallucinating?

1) You never want to be confrontational or argumentative or even try to change their belief about their hallucination; it would only escalate to violence.

2)  Also do not try to give medication when they are agitated or again will only cause you the caregiver increased heartache.

3) Best to walk away if they are not in imminent danger let them settle down then bring a medication best if it’s something quick acting like an orally disintegrating compound. Another good technique that works unless extremely agitated is distraction with books, pictures, coloring, games, etc.

Fortunately, we now have a new medication on the market just for PD psychosis from Acadia called Nuplazid (Pimavanserin). Medications which I frequently employed for this problem were atypical antipsychotics( neuroleptics) such as Seroquel and Clozaril since they would not interfere with motor symptoms of PD, there are other medications which can be given in smaller quantities but used because they are IV or orally disintegrating.

Finally, since rarely do hallucinations in PD occur in absence of dementia this needs to be treated.  Look for other underlying causes such as strokes, or vitamin B12 deficiency. Adjust dopamine levels and best to remove Amantadine and dopamine agonists which can exacerbate problem and start treatment with an anticholinesterase inhibitor, like Aricept. In my experience combination treatment with Namenda and Exelon or another one of its class went along way to curbing dementia and hence hallucinations.

Make sure you consult your physician regarding any changes in mental status including hallucinations.





Dr. M. De Leon is a movement disorder specialist on sabbatical, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at you can also learn more about Parkinson’s disease at or at;, All materials here forth are property of Defeatparkinsons. without express written consent, these materials only may be used for viewers personal & non-commercial uses which do not harm the reputation of Defeatparkinsons organization or Dr. M. De Leon provided you do not remove any copyrights. To request permission to reproduce release of any part or whole of content, please contact me at contributor Contributor

alzheimers, dementia, parkinson's disease, parkinsons health and beauty tips

Health & Beauty tip # 23 :Things to know when doing a sleep study By Dr. De Leon

Health & Beauty tip #    :Things to know when doing a sleep study By Dr. De Leon

To Sleep perchance to dream“- William Shakespeare, Hamlet

Equipment not working…..wondering from room to room ..finally getting started at close to 2 a.m.
Have to repeat!!!what?!
Fortunately, second time around a whole lot better…but not happy had to redo….

Sleep study! Wow what an ordeal?

I have ordered over a hundred sleep studies in my career as a professional and I had an EEG done as resident as part of my training ( so I KNOW how messy and sticky your hair can get especially if you have as much hair as I do!).
But, I never had to undergo a sleep study myself… of course I was aware of what it entailed….
One thing is to have KNOWLEDGE of something another is to EXPERIENCE it yourself….it was not until the time I volunteered for a research study in Parkinson’s whose primary objective is understanding sleep disorders in said disease- Parkinson’s.
but I was ready so, I thought…

As I was preparing, I remembered that you must avoid all sleeping aids including antiaxiolytic medications known as benzodiazepines which include meds like Klonopin ( clonazepam), Valium ( diazepam ), Xanax ( alprazolam ) etc. for at least 3 days prior to study better if its a week. Because the effect of these meds can change the findings of the brain recording (EEG). Also, avoid caffeinated drinks and alcohol for at least 24 hours prior to study. These too can alter the brain waves…

The doctors and techs will usually give you a very comprehensive list of DO’s & Don’ts!
Take it seriously to obtain best results!

If you can, avoid taking a nap the day of the sleep test so you can sleep …because remember you will have wires everywhere on your face, head, arms, legs, breathing monitor, oxygen tube, heart monitor and these compounded with fact you are in strange place being recorded can be very anxious provoking! Just simply go about your night time routine! Bring a book to read or watch T.V. until they tell you is time to turn off lights -usually around 9 p.m.

Make sure you bring your favorite comfortable sleep ware and pillow if you like and a loved for moral support if you must!. He or she can accompany you and sleep in next room over.
If you are one that has to frequent the bathroom during night time avoid any beverages after 5 p.m. and also ask for a room with own private bathroom so if you DO have to Go it will be less disruptive to you and others..since each time you have to go you MUSt be disconnected and recording stopped!

This, unfortunately, is what happened to me the first go around….
After spending an hour getting hooked up…finally allowed to return to room but since I had been at doctor all day with study I had been off meds most of the day so by time I took before bed I had severe nausea and could not lay down without feeling like I was about to throw up – I had forgotten my nausea pill! ( Make sure YOU BRING ALL your meds with you even if you don’t usually take in the evening just in case!
Finally, stomach settling already past my bed time per their protocol. I went to bathroom before bed got set up which took at least 30 minutes. Then, lo and behold not even a couple of hours later, I had to go again…I held as long as I could because I knew I would have to be unplugged…but difficult to sleep when you have an urge…so, I gave in…well, little did I know that this action set a whole wreck ball in motion!

Once, I returned to my bed the switching back on was no longer a simple matter….the sleep techs began the process of connecting me but there seem to be a malfunction in the equipment! Oh, NO!

They stripped me of all belts etc. and put NEW oNEs in the dark with a small flash light trying to not arouse me! But connections were determined to cause problems- no input…of course with each attempt I kept getting more and more awake …initially they tried to do in the dark as to not wake or rid of my sleepiness but that only caused more fumbling and frustration on the part of techs. With each failed attempt, I could only chuckle inside knowing full well this was the Karma of being a neurologist! But secretly prayed they could make things work for the sake of their own jobs! Knowing their frustration was mounting, I gave permission for them to turn lights on to try to expedite process and lessen irritation hoping to sleep soon and NOT HAVE TO RETURN – alas it was not to be…they then switched EEG board still no input!
Next, I was moved to another suite with different bed…still interference!
2 a.m. nearly on to third room ( felt something like ‘ Goldie Locks) finally Eureka things were working …I dared not move a muscle to avoid irritating the forces that be and Prayed earnestly that I would NOT HAVE To POTTY AGAIN!

I was up by 5am when recording is scheduled to stop but obviously I spent more than half the night playing musical beds…so I would have inconclusive data and therefore had to repeat the blessed ordeal!….

Thus, You can imagine my great trepidation of having to repeat the whole ordeal.
I was very reluctant to repeat because what if they actually found something…I MIGHT have to COME BACK a THIRD time!

But, then I laughed and thought about Karma, AGAIN!.. They say that doctors make the worst patients and have the most complications …well this seemed to be holding true to dogma. Could not argue with it!

But, before you get all panicked by my story and refuse to ever have one done…REMEMBER, I am a rare case..
and I am used to having things happen …as I said Doctor’s Karma so I am used to it…
this rarely occurs but you should nevertheless be prepared for possible delays and mild inconveniences as to avoid increase of blood pressure, anxiety or getting overly upset! take deep breaths and laugh it off if similar things should ever happen to you….

The second (sleep study) go around…
guess the techs knew I might be ‘ difficult’ so I was given a suite with my own bathroom and this time the EEG leads ( head wires) were mounted on track that could be easily disconnected as a whole and carry with me without having to manually switch each individual lead to another track.
I was pleased to see that they had learned from situation.
Life was so much sweeter! Thank goodness because try as I might to not have to go to bathroom in middle of night, I still had to be unplugged at least once…..

My advice:
Take your other medications as you would normally ..
Maintain a sleep diary before you come to study and fill out questionnaire of activities, sleepiness, medications, medical issues and night time problems like cramps in legs, frequent urination, trouble staying awake or asleep…etc.
Do Not schedule other activities or doctors appointments same day…may get you off your game being overly tired or stressed!
Also bring warm clothes or blanket if you are cold natured because they don’t want leads falling so they keep rooms very cold or fans blowing!
Tell them if you need assistance with dressing, bathing, going to restroom, or difficulty turning in bed or have increase risk for falling…to avoid any mishaps especially since you will be covered in wires…

Also if you are allergic to adhesive let them know…although I believe most centers use baby adhesive so not to cause irritation.
Also, most centers will give you baby shampoo to wash your hair off from all the goo placed for brain wave recording…but just incase bring some BABY Shampoo ( it is the best thing to get that jell out of your hair even when you have bunches of hair like me!)
If someone does not go with you, consider having someone drop you off and pick you up next morning in case you do not sleep well and are sleep deprived …would not want you getting into an accident!

I, also, highly recommend that every Parkinson’s patients talks to their doctor about getting a sleep study because so many of us suffer from sleep disorders caused by Parkinson’s disease. This can be an intrinsic part just like tremors or stiffness but is a non-motor abnormality. Treating sleep disorders is vital because they can lead to increase memory loss, fatigue, pain, increase dizziness, headaches, high blood pressure and falls if not diagnosed properly or in a timely matter. Hence, need for sleep monitoring!

After all sleep disorders is one of the most common non motor symptoms in Parkinson which can cause severe disruptions in a persons life but fortunately can also be treated with good success most of the time if problem is adequately and promptly diagnosed.

Sleep is even more crucial than we thought since according to a recent new study published in Science …it appears that sleeps helps the brain eliminate waste which is a critical function in maintaining metabolic homeostasis ( equilibrium by getting rid of trash like beta amyloid proteins that accumulate during wakeful hours and are believed to be the cause for many NEURODEGANERATIVE diseases like Parkinson’s and Alzheimer’s ).

Good luck and happy dreams!


To learn more about the function of sleep in eliminating waste from brain go to-
Xie L, et al. ” Sleep drives metabolite clearance from the adult brain.” Science 2013; 342:373-377.

Dr. M. De Leon is a retired movement disorder specialist, PPAC member and research advocate for PDF (Parkinson’s Disease Foundation); Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at you can also learn more about Parkinson’s disease at or at;,
may also contact me at

alzheimers, dementia, parkinson's disease, parkinsons dementia

Health & Beauty tip # 18: 10 Common Drugs to Worsen Memory! By Dr. De Leon

Health & Beauty tip #  10 Common Drugs to Worsen Memory! By Dr. De Leon

Since September is known as Alzheimer’s month and the East Texas Chapter of Alzheimer’s along with the participation of the Nacogdoches Pilot Club will be kicking off another walk-a-thon to END Alzheimer’s in just a few weeks…. I thought it might be good idea to discuss some of the commonly prescribed medications that can lead to or possibly worsen memory loss mimicking Alzheimer’s:

After all memory loss could be caused by none other than the medications in your drug cabinet rather than your AGE!
Since according to one publication over 90% of people over the age of 65 take at least ONE medication more than any other age group and usually several medications which are likely to interact with one another increasing the risk of memory loss due to drug reactions.

New studies have revealed a direct correlation between commonly prescribed and over the counter medications used to treat anxiety, insomnia, itching or allergies or colds and loss of concentration and poor memory particularly in the elderly population. More important is the fact that the effect of these medications maybe overlooked in an otherwise healthy individual!
Here is a list of commonly used drugs which could mimic Alzheimer’s …… common factor is that MOST block the activity of the chemical CHOLINE –crucial chemical in making memories and learning!

Therefore, if any one is taking drugs in any of these categories and are experiencing PROBLEMS with Memory make sure to consult a physician ASAP……

1) Statin (cholesterol) medications- These are drugs used to lower cholesterol like Lipitor….The brain contains a quarter of the body’s cholesterol, and lipids (fats) are crucial to the connection between nerve cells. According to study published in a journal of pharmacotherapy in 2009 3/4 people using these drugs experience some type of cognitive decline. 90% of patients who stopped therapy reported improved cognition within days!

2) Anti-anxiety medications – in the class of benzodiazepines…medications like Valium, Xanax, Klonopin….all of these drugs are metabolized (broken down in the liver) but, as we age our metabolism takes longer and it is slower therefore the effects of the medications linger on for a longer period of time and varies from person to person. The elderly take longer to metabolize which can lead to more interactions if taking other medications as well…dulling the senses.

3) Anti-seizure medications- all drugs that depress signal of central nervous system can potentially cause memory loss! (e.g. Topamax, Tegretol..)

4) Antihistamine (allergy) medications- this class includes medicines like Benadryl. They are also used to relieve nausea, dizziness, motion sickness as well as colds and allergies. These medications block cholinergic activity which is crucial for memory and learning!

5) Antidepressant medications- especially the older antidepressants in the class of tri-cyclic example of this is elavil (amitryptiline)-these cause memory loss by blocking action of a chemical called serotonin ( important in mood and sleep) and norepinephrine.

6) Parkinson’s medications- the dopamine system which is what a lot of these drugs target is involved in motivation, pleasure- seeking behavior, fine motor control, cognition and memory , & learning. Therefore any disruption to this system can alter our perception of the world impacting learning which is then directly encoded into our permanent memory banks. Other Parkinson drugs work on the cholinergic and glutamate system same systems that are believed to be disrupted in Alzheimer’s therefore causing great memory disturbances. (especially medications like ARTANE, AMANTADINE & COGENTIN)

7) Pain pills-class of opioids/ narcotics – these hamper the signal to flow of pain and blunt emotional reaction to pain…both of these reactions are mediated by chemical messengers that are involved in various aspects of cognition so they can with interfere with both long and short -term memory.

8) Sleeping aids- these also work on chemical messengers like pain pills therefore interfering with memory processing and have similar problems with withdrawal and addiction.

9) Incontinence (bladder) medications- In the brain these medications block cholinergic activity which is crucial for memory and learning!

10) Hypertension medications (blood pressure)-interfere with both norepinephrine and epinephrine key chemicals in the brain.

Always Important to KNOW WHAT YOU ARE TAKING!


Dr. M. De Leon is a retired movement disorder specialist, PPAC member and research advocate for PDF; Texas State Assistant Director for PAN (Parkinson’s Action Network). You can learn more about her work at you can also learn more about Parkinson’s disease at or at;,,
may also contact me at

This information is provided for general educational purposes only and is not intended to constitute i) medical advice or counseling, ii) the practice of medicine or the provision of health care treatment or diagnosis, iii) or the creation of a physician-patient relationship. If you have or suspect a medical problem, contact your physician promptly!