“Things are not right since he/she left hospital”

The National Parkinson Foundation (parkinson.org) has a good online forum where you can ask MDs questions. Most of the questions are about PD. Occasionally people ask questions about PSP or CBD.

Recently, someone on the NPF Forum asked about the use of general anesthesia during spinal surgery. Dr. Michael Okun (from the University of Florida) indicates that anesthesia in PD is being studied now, and there is concern that symptoms worsen by surgery. The rest of the MD’s answer is an excerpt from a document on hospitalization and PD. I copied the parts of the excerpt that deal with people having worsened motor symptoms or worsened confusion after being in the hospital. There’s also a small paragraph on anesthesia.

http://forum.parkinson.org/forum/viewtopic.php?t=6996

Anonymous
Posted: Mon Mar 09, 2009 5:06 am
Post subject: General Anesthesia

I have spinal stenosis… My orthopedic surgeon wants to do a laminectomy… My neurologist tells me that “the Parkinson brain does not do well under general anesthesia. It can cause cognitive impairment.” … What have you heard and what is your opinion regarding general anesthesia and the Parkinson Brain?…

Dr. Okun
Posted: Fri Mar 13, 2009 7:07 am

Thanks for the nice message. Cate Price at University of Florida has a NPF funded research project in this area. Indeed we are worried about worsening with any type of surgery with PD and we need a better understanding of how to do surgery and anaesthesia for patient safety, because people need these operations!

Here is some information we have written over the years on PD and surgery that may be helpful. …

Be aware that for unclear reasons some symptoms worsen following general or local anesthesia, and some patients have even reported feeling as if they never return to their baseline. In general, local anesthesia is thought to be safer than general anesthesia, and if you have problems with thinking and memory, they should be evaluated prior to surgery as they may also worsen (Chou 2007).

My mother has Parkinson disease and was recently hospitalized. However, she seems to be moving much worse in the hospital than at home. Why is that?

Several explanations are possible. When patients with Parkinson’s disease have an infection of some kind, whether it is the common cold, pneumonia, or a urinary tract infection, they often feel like their symptoms worsen. Increased tremor or more difficulty walking may be noted. When the infection is treated and resolves, the symptoms generally return to baseline. Another symptom that may worsen when patients with Parkinson’s disease have an infection is swallowing. When swallowing is impaired and patients are weak, the food may go down into the lungs, causing an “aspiration pneumonia”, which in turn, may further impair swallowing ability. In these situations, a speech pathology consultation can be useful to formally assess swallowing and make dietary recommendations. In addition, a respiratory therapist consultation for “chest PT” may be helpful. Chest PT consists of several minutes of chest clapping to help mobilize the sputum and make it easier to cough.

Another possibility is – new medication. Common offenders include antipsychotic drugs or anti-nausea drugs. Haloperidol (Haldol) is a common antipsychotic drug that is used in hospital settings. This drug blocks dopamine receptors and worsens Parkinson’s disease. Other commonly used antipsychotics include risperidone (Risperdal), olanzapine (Zyprexa), and aripiprazole (Abilify). The only antipsychotics that can be used safely in PD patients are clozapine (Clozaril) and quetiapine (Seroquel). Common anti-nausea medications that can worsen symptoms of Parkinson disease include prochlorperazine (Compazine), promethazine (Phenergan), and metoclopramide (Reglan). These medications have similar structures to the antipsychotics and should not be used. Trimethobenzamide (Tigan) and ondansetron (Zofran) are suitable alternatives that can be used without fear of worsening symptoms.

Regardless of the cause, all patients with Parkinson disease should be as active as possible while in the hospital. Moving around not only tones muscle, it allows faster recovery and prevents decomposition of the skin, which can happen when staying in one position for too long. Depending upon your condition, however, you may not have a choice and your doctor may order you to bed rest. In that case, physical therapy should be ordered as soon as possible. Some patients may also need rehabilitation at a rehabilitation hospital or a nursing facility before being discharged to home.

There are multiple explanations for worsening of Parkinson disease while in the hospital. Infections should be sought and treated. Drugs that block dopamine, like haloperidol and certain anti-nausea drugs, should be avoided. Chest PT, speech pathology, and physical therapy may all be useful in the recovery process (Chou 2007).

My husband has Parkinson’s disease and became confused in the hospital last time he was there. How can I prevent this?

Many things happen in the hospital that can contribute to confusion. Any infection in a patient with Parkinson’s disease can be enough to tip a patient “over the edge” mentally. Similarly, infections can adversely affect motor function as we discussed above. The introduction of new medications frequently results in disorientation and memory problems, especially pain medications. Lack of sleep while in the hospital can also contribute to a confusional state. Continuous alarms from IV machines and hallway lights can all result in frequent awakening. Nurses also may regularly enter the room overnight to take vital signs, give medications, or to check on a patient. In some patients, especially in the elderly with intermittent confusion at home, just the fact that they are placed in a different and unfamiliar environment may tip them into a delirious state. Finally, confusion is commonly seen following a surgical procedure. The combined effects of anesthesia and medications to treat surgical incision pain are contributing factors in this situation.

Confusion will often disappear once the underlying cause is treated, whether it is addressing the infection or withdrawing the offending medications. Diagnostic testing is rarely necessary. Frequent reassurance, support and comfort may be all that is needed to assist the patient through this period. However, sometimes confusion can lead to behavioral problems, such as aggression, refusal to take pills, and even hallucinations or delusions. In these cases, physical restraints are sometimes necessary to prevent self-injury. Some hospitals have bed or wheelchair alarms to alert nurses when patients attempt to wander, while other hospitals may use a sitter to promote safety. If there are psychotic symptoms, such as visual hallucinations, antipsychotics may be used. Remember in nearly all cases, clozapine (Clozaril) and quetiapine (Seroquel) are the only antipsychotics that should be used in patients with Parkinson disease. Occasionally, lorazepam (Ativan) or diazepam (Valium) can be helpful. These drugs, by themselves, may worsen confusion, but they also can calm the patient. These medications are only temporary and may be discontinued when the confusion resolves.

In very severe cases of confusion with hallucinations and behavioral changes, it may be necessary to temporarily discontinue dopamine agonists, MAO inhibitors, amantadine, benzodiazepines, and pain medications if possible. Treatment with carbidopa/levodopa and either clozapine or quetiapine will usually result in improvement. Later, once patients are stable, they may be slowly titrated back onto previous doses if tolerated (Chou 2007).

Infection and medications are common causes of confusion in the hospital, and when the underlying cause is addressed it usually improves dramatically. …

Michael S. Okun, M.D.

“A Life Worth Living” – Radio Interview and Book

Sadly, the loved ones of five local support group members died in March; one support group member (caregiver) died too. At least one group member was involved in end-of-life treatment decisions, and relied on her husband’s written wishes when he was no longer able to communicate.

Along these lines, I heard a book author interviewed today (Thursday 4/2/09) on NPR’s “Fresh Air” program, and wanted to pass the info along to all of you. The book is “A Life Worth Living,” and the author is Robert Martensen, MD. Dr. Martensen was an ER and ICU MD for many years; he’s also a bioethicist.

In his book he talks about his father’s hospital death, and “argues that safeguarding the quality of a patient’s life sometimes trumps the urge to sustain life at all cost.” He also addresses his father’s death in the “Fresh Air” interview as well as his mother’s impending death. His mother lives in Santa Cruz. In the story about his mother, he describes one of his mother’s first MDs in these final weeks who wanted to place a pacemaker. Dr. Martensen worries that it’s only because he is an MD that he was able to know the right questions to ask the treating physician. Ultimately, he’s very fortunate that both of his parents had given such clear advance directives about what sort of treatment they wanted, given certain circumstances. He contrasts his mother with another elderly woman also suffering from dementia.

I would recommend listening to the 40-minute “Fresh Air” interview. You can find it online here:

The interview is titled “The Ethical Way To Heal American Health Care,” which doesn’t really capture the interview.

“Treating an Illness Is One Thing. What About a Patient With Many?”

This is a good article in a recent New York Times (nytimes.com) about patients with many illnesses, not just one.  A key problem is that these patients end up on many medications.  Here’s an excerpt:

“Doctors know that it’s not right for someone to be on 15, 18, 20 medications,” said Dr. Tinetti, the Yale geriatrician. “But they’re being told that that’s what’s necessary in order to treat each of the diseases that the patients in front of them have.”

Here’s a link to the full article:

http://www.nytimes.com/2009/03/31/health/31sick.html

Treating an Illness Is One Thing. What About a Patient With Many?
Brendan Smialowski
The New York Times
March 30, 2009

Thanks to online friend Joe Blanc for making me aware of this article.

Robin

 

 

Progression of dysarthria + dysphagia in PSP, CBD, etc

I’ve posted some of the info in this article previously and the PubMed ID# but have never posted these excerpts.

This 2001 study is of dysarthria and dysphagia in autopsy-confirmed cases of DLB, CBD, MSA, PSP, and PD. According to the article, all atypical parkinsonism patients develop either dysarthria or dysphagia within one year of disease onset. (I thought dysarthria meant slurred speech. But, according to this article, it can also mean hypophonic speech or monotonic speech.)

Here’s the citation and abstract:

Archives of Neurology. 2001 Feb;58(2):259-64.

Progression of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders.

Muller J, Wenning GK, Verny M, McKee A, Chaudhuri KR, Jellinger K, Poewe W, Litvan I.
Cognitive Neuropharmacology Unit, Bethesda, MD

BACKGROUND: Dysarthria and dysphagia are known to occur in parkinsonian syndromes such as Parkinson disease (PD), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Differences in the evolution of these symptoms have not been studied systematically in postmortem-confirmed cases.

OBJECTIVE: To study differences in the evolution of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders.

PATIENTS AND METHODS: Eighty-three pathologically confirmed cases (PD, n = 17; MSA, n = 15; DLB, n = 14; PSP, n = 24; and CBD, n = 13) formed the basis for a multicenter clinicopathological study organized by the National Institute of Neurological Disorders and Stroke, Bethesda, Md. Cases with enough clinicopathological documentation for the purpose of the study were selected from research and neuropathological files of 7 medical centers in 4 countries (Austria, France, England, and the United States).

RESULTS: Median dysarthria latencies were short in PSP and MSA (24 months each), intermediate in CBD and DLB (40 and 42 months), and long in PD (84 months). Median dysphagia latencies were intermediate in PSP (42 months), DLB (43 months), CBD (64 months), and MSA (67 months), and long in PD (130 months). Dysarthria or dysphagia within 1 year of disease onset was a distinguishing feature for atypical parkinsonian disorders (APDs) (specificity, 100%) but failed to further distinguish among the APDs. Survival time after onset of a complaint of dysphagia was similar in PD, MSA, and PSP (15 to 24 months, P =.7) and latency to a complaint of dysphagia was highly correlated with total survival time (rho = 0.88; P<.001) in all disorders.

CONCLUSIONS: Latency to onset of dysarthria and dysphagia clearly differentiated PD from the APDs, but did not help distinguish different APDs. Survival after onset of dysphagia was similarly poor among all parkinsonian disorders. Evaluation and adequate treatment of patients with PD who complain of dysphagia might prevent or delay complications such as aspiration pneumonia, which in turn may improve quality of life and increase survival time.

PubMed ID#: 11176964

These results were the most interesting (and depressing):

“Dysarthria or dysphagia within 1 year of disease onset was a distinguishing feature for atypical parkinsonian disorders (APDs).”

“Median dysarthria latencies were short in PSP and MSA (24 months each), intermediate in CBD and DLB (40 and 42 months), and long in PD (84 months).”

“Median dysphagia latencies were intermediate in PSP (42 months), DLB (43 months), CBD (64 months), and MSA (67 months), and long in PD (130 months).”

“Survival time after onset of a complaint of dysphagia was similar in PD, MSA, and PSP (15 to 24 months).”

On this last point, here are the CBD and PSP data from the article:

Survival Time After Onset of Dysphagia, months
CBD 49 (25-89…..including a single patient with dysphagia but without dysarthria)
PSP 18 (6-96)

Here are some excerpts from the article’s Comment section:

“(Early) dysarthria and perceived swallowing dysfunction are not features of PD.”

“Dysarthria) as a presenting symptom has been described in clinical series of CBD, MSA, and PSP. In PD and DLB, hypphonic/monotonous speech represented the most frequent type of dysarthria, whereas imprecise or slurred articulation predominated in CBD, MSA, and PSP.”

“In a clinical study of CBD, Rinne et al described dysarthria as one of the initial symptoms in 11% of the patients, which is close to our findings. At follow-up, on average 5.2 years, dysarthria was diagnosed in 70% of the patients… According to our findings, dysarthria occurred in almost every patient with CBD.”

“In both PSP and MSA, progressive dysarthria is believed to represent a manifestation of brainstem and cerebellar involvement. In fact, PET studies revealed marked hypometabolism in the cerebellum and brainstem of patients with MSA, which correlated with dysarthria.”

“In our study, dysphagia was associated with concomitant dysarthria in all parkinsonian patients except one. This sequence of dysphagia following dysarthria has also been reported in clinical studies of PD, MSA, and PSP.”

“…Golbe et al reported dysphagia after a median of 1 year after the onset of dysarthria in PSP.”

In all these disorders, “bronchopneumonia has been reported as a leading cause of death, which may be subsequent to silent aspiration resulting from dysphagia.”

“Most of our patients with MSA and PSP complained of a swallowing dysfunction, in contrast to patients with PD, CBD, and DLB… Impaired lingual proprioception is hypothesized to contribute to the unawareness of swallowing difficulties in PD and might in part explain significantly longer latencies to dysphagia in our PD cases. In contrast, patients with PSP were reported to be keenly aware of swallowing problems, including those with cognitive impairment.”

“(The) similarly short remaining survival time in PD and PSP after the onset of perceived dysphagia suggests that this symptom represents a reliable marker for the onset of functionally relevant swallowing abnormalities in both disorders.”

Robin