SleepScout’s role in Dental Sleep Medicine

February 5th, 2010 by Jerusha Michael

CleveMed’s SleepScout is a compact, portable sleep monitor used to aid in assessment of sleep disordered breathing outside the traditional sleep lab: in a hospital setting (with iPSG™), or typically perfect for self-administered home sleep testing (even remotely attended with DreamPort™) right in the patient’s home. But here is another way to use the SleepScout: Dentists with an interest in sleep, snoring (sleep disordered breathing), and remedies for snoring through oral appliances and surgeries can use SleepScout to perform take-home sleep tests for their patients.

    Here’s why the SleepScout is a great option when considering a sleep recorder for the dental office:

  • SleepScout uses AASM recommended Type 3 channel set
  • SleepScout’s accessories are very cost-effective
  • SleepScout can monitor effectiveness of treatment with CPAP and oral appliances
  • SleepScout gives an easy-to-read report with auto-scoring of respiratory events
  • SleepScout records EMG to monitor Bruxism
  • With SleepScout you have next day results

These are just a few reasons to consider the SleepScout, and you can read more details here. Also, see a sample report from the SleepScout portable sleep monitor at www.CleveMed.com/DentalSleep. And if you haven’t seen the SleepScout overview video, check it out!

Smallest, lightest home sleep monitor: SleepView

January 25th, 2010 by Jerusha Michael

The SleepView™ is the smallest, lightest home sleep monitor following AASM guidelines for portable monitoring. The SleepView is ergonomically designed for patients to perform a self test at home. SleepView works hand in hand with the e-Crystal PSG Web Portal, where sleep studies are uploaded for review and scoring by sleep technologists and interpreted by a board certified sleep physician. This practical and efficient patient monitoring system, allows physicians to provide a continuum of care. (For more information on the SleepView call 216-791-6720)

Optimizing Drug-Induced Side Effects in Parkinson’s Disease

January 15th, 2010 by Thomas Mera

Significant strides have been made in the management of Parkinson’s disease (PD) motor symptoms such as tremor, slowness of movement, and rigidity; however, treatment side effects pose a key therapeutic challenge. Upon initial onset of the disease, patients are typically prescribed levodopa, a drug taken orally several times a day to increase dopamine levels in the brain to alleviate motor symptoms.

As the disease progresses, changes in the body’s response to levodopa give rise to therapy complications such as delayed onset and decreased duration of motor symptom relief per dose. Chronic treatment can also lead to side effects such as dyskinesias, which can take on various debilitating forms: irregular brief rapid movements (chorea) during the “On” state at peak dose and sustained twisting movements (dystonia) during the “Off” state when the medication has worn off. Approximately 30% of patients diagnosed with PD exhibit levodopa-induced dyskinesia within 5 years of treatment[1] and 59-100% by 10 years[1-3]. Quality of life has been shown to be negatively impacted by dyskinesias[4], specifically mobility[5], activities of daily living[5, 6], communication[5, 6], and bodily discomfort[6].

Figure 1: Blood Levodopa Concentration

Figure 1: Blood Levodopa Concentration

Adjustments in medication to reduce drug side effects often sacrifice control of motor symptoms, and balancing this tradeoff poses a significant challenge for management of advanced PD. Alternate strategies to better control motor fluctuations have aimed efforts at developing drug administration methods to minimize swings in blood levodopa concentration. Figure 1 highlights the typical drug cycles that patients may experience throughout the day when taking levodopa in discrete intervals[7]. Over time this approach shrinks the size of the “On” state window requiring higher doses to achieve the same effect and increasing the frequency and severity of dyskinesia. The ideal scenario would be to maintain levodopa concentration in the “On” state where levodopa is effective at alleviating motor symptoms without inducing dyskinesia. Studies have suggested that continuous drug administration may better mimic the normal physiological release of dopamine in the brain in order to attain more stable therapy benefits[8, 9].

1. Van Gerpen, J.A., et al., Levodopa-associated dyskinesia risk among Parkinson disease patients in Olmsted County, Minnesota, 1976-1990. Arch Neurol, 2006. 63(2): p. 205-9.
2. Colosimo, C., et al., Motor fluctuations in Parkinson’s disease: pathophysiology and treatment. Eur J Neurol, 1999. 6(1): p. 1-21.
3. Grandas, F., et al., Risk factors for levodopa-induced dyskinesias in Parkinson’s disease. J Neurol, 1999. 246(12): p. 1127-33.
4. Pechevis, M., et al., Effects of dyskinesias in Parkinson’s disease on quality of life and health-related costs: a prospective European study. Eur J Neurol, 2005. 12(12): p. 956-63.
5. Chapuis, S., et al., Impact of the motor complications of Parkinson’s disease on the quality of life. Mov Disord, 2005. 20(2): p. 224-30.
6. Damiano, A.M., et al., Evaluation of a measurement strategy for Parkinson’s disease: assessing patient health-related quality of life. Qual Life Res, 2000. 9(1): p. 87-100.
7. Keijsers, N.L., et al., Online monitoring of dyskinesia in patients with Parkinson’s disease. IEEE Eng Med Biol Mag, 2003. 22(3): p. 96-103.
8. Olanow, C.W., et al., Continuous dopamine-receptor treatment of Parkinson’s disease: scientific rationale and clinical implications. Lancet Neurol, 2006. 5(8): p. 677-87.
9. Olanow, C.W., Levodopa/dopamine replacement strategies in Parkinson’s disease–future directions. Mov Disord, 2008. 23 Suppl 3: p. S613-22.

Benefits of Exercise for Parkinson’s Disease

January 7th, 2010 by Thomas Mera

Parkinson’s disease (PD) is characterized by cardinal motor symptoms of tremor, slowness of movement, and rigidity [1]. Symptoms directly affect quality of life and activities of daily living by impeding coordination of multiple limbs and fine dexterity. This can be extremely debilitating, leading to decreased mobility and independence with increased risk for falling.

Current clinical PD therapies are designed to address disease motor symptoms; however, there are limitations associated with these approaches. Drug therapy (e.g., levadopa) effectiveness may decrease over time and lead to side effects such as dyskinesias (involuntary irregular movements) [2]. Patients may eventually consider surgical procedures such as deep brain stimulation when increased drug dose side effects outweigh the benefits. This procedure, however, has limitations and risks, such as improper lead placement, decreased effectiveness over time, and not being appropriate for all patients [3].

While treatments such as drug therapy and surgical procedures are clinical standards, new research suggests exercise as a potentially less invasive alternative/adjunct treatment. It has been well established that exercise reduces risks of developing chronic diseases such as cancer, obesity, and heart disease [4-6]. Such benefits of exercise can also be translated to motor improvement in PD [7, 8]. The general concept behind the benefit of exercise in PD suggests that physical exercise may stimulate specific biochemical changes to induce production of dopamine, a neurotransmitter involved in allowing the body to perform smooth controlled movements [9]. The sedentary lifestyle associated with PD promotes further motor symptom impairment through muscle weakness, postural imbalance, and increased risk of falling [10]. Thus, there exists an urgency to develop PD-specific exercise regimens early in disease progression in an attempt to break or delay this debilitating cycle.

1. Pflanzer, R.G., et al., Human Physiology. 1996, Saunders College: Forth Worth.
2. Encarnacion, E.V., et al., Levodopa-induced dyskinesias in Parkinson’s disease: etiology, impact on quality of life, and treatments. Eur Neurol, 2008. 60(2): p. 57-66.
3. Beric, A., et al., Complications of deep brain stimulation surgery. Stereotact Funct Neurosurg, 2001. 77(1-4): p. 73-8.
4. Dugan, S.A., Exercise for preventing childhood obesity. Phys Med Rehabil Clin N Am, 2008. 19(2): p. 205-16, vii.
5. Kelley, G.A., et al., Efficacy of aerobic exercise on coronary heart disease risk factors. Prev Cardiol, 2008. 11(2): p. 71-5.
6. Knobf, M.T., et al., Exercise and quality of life outcomes in patients with cancer. Semin Oncol Nurs, 2007. 23(4): p. 285-96.
7. Ridgel, A.L., et al., Forced, not voluntary, exercise improves motor function in Parkinson’s disease patients. Neurorehabil Neural Repair, 2009. 23(6): p. 600-8.
8. Crizzle, A.M., et al., Is physical exercise beneficial for persons with Parkinson’s disease? Clin J Sport Med, 2006. 16(5): p. 422-5.
9. Tillerson, J.L., et al., Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson’s disease. Neuroscience, 2003. 119(3): p. 899-911.
10. Ashburn, A., et al., A randomised controlled trial of a home based exercise programme to reduce the risk of falling among people with Parkinson’s disease. J Neurol Neurosurg Psychiatry, 2007. 78(7): p. 678-84.