Confronting Boundaries in the Treatment of Movement Disorders

Movement disorders is a term that is broadly applied to the group of diseases and syndromes affecting a person’s ability to produce and control movement; however, the clinical presentations of these disorders can be highly heterogeneous and complex in older patients. Symptoms vary depending on the underlying etiology of the condition, and effective treatment becomes paramount when these symptoms significantly affect patients’ quality of life and impede their ability to perform activities of daily living to the point of requiring placement in a long-term care (LTC) facility.

Medication is typically at the crux of care, but many of the existing therapies for movement disorders are limited when applied to elderly persons residing in LTC settings. Annals of Long-Term Care^® (ALTC) had the opportunity to discuss the challenges of treating movement disorders in older adults with Vanessa Hinson, MD, PhD, associate professor of neurology and director of movement disorders, Medical University of South Carolina, Charleston, SC. Hinson is also the chief of neurology at the Ralph H. Johnson VA Medical Center, Charleston, SC. ALTC asked Hinson for her clinical opinions on the findings of several recent studies that have evaluated alternative, nonpharmacological approaches to care, such as psychotherapy, deep brain stimulation, and nutrition. 

ALTC: In a report that you recently coauthored in Parkinsonism and Related Disorders, you note that no uniformly successful treatment strategies for psychogenic movement disorders have been identified. What are the limitations of existing therapies for movement disorders in older adults?

Hinson: There are two big limitations towards effective therapy for psychogenic movement disorders (PMDs): proper recognition and patient acceptance of the diagnosis. As movement disorders specialists, we are often the third or fourth physician seeing these patients. Because symptoms typically do not fit into the well-known patterns of organic illness, patients often remain undiagnosed. It is an important job for specialists to educate general neurologists and geriatricians about the diagnostic criteria for PMDs. According to the Fahn and Williams criteria for PMDs, a diagnosis is considered clinically established, when the patient displays abnormal movements that are either inconsistent or incongruent with an organic movement disorder, and suffers from other psychogenic symptoms or somatizations, or has a documented coexisting psychiatric disorder. Clinical “red flags” for the presence of PMDs are abrupt onset outside of a vascular cause, episodic or fluctuating symptoms, symptoms affecting multiple body parts, and distractibility on examination.

Sensible delivery of the diagnosis is a major key for successful treatment. I have found it useful to first validate the movement disorders phenomenology (ie, “You suffer from tremor”), and then go over the differential diagnosis (ie, “There are different causes for people to have tremor”), including an explanation of why I am convinced that the basis of the patient’s movement disorder is psychogenic. The patient needs to understand that similar to depression, there is a biological basis for the body’s reaction towards past or current stressors, and that a treatment plan is in place with both psychiatry and neurology on board. The biggest hurdle towards effective psychotherapy is if the patient is feeling dismissed and abandoned by the neurologist.

It seems that in light of these limitations, the importance of an interdisciplinary care team and nonpharmacologic approaches to care are coming to the forefront. One of these approaches is psychotherapy. Can you briefly discuss the benefits of psychotherapy in improving the symptoms of PMDs in your experience?

My colleagues and I conducted a 6-month randomized cross-over design study in which we assessed the impact of immediate versus delayed (after 3 months) weekly psychodynamic psychotherapy in 15 patients with PMDs. The psychiatric treatment arm in this study involved a so-called “short-term” (1 hour per week for 12 weeks) psychodynamic psychotherapy. This treatment focuses on historical and early life experiences, links between those and current stressors, and examines problematic emotions and behaviors. The goal is to help the patients recognize unconscious conflicts and help them work through them. This intervention is not manualized or standardized, and therefore will have to be individualized for each patient.

What we found in this study is that the patient’s movement disorder, as well as coexisting anxiety and depression, improved with both the immediate and delayed psychiatric intervention. But improvement was also seen in the control group, who were being maintained in the medical system with as-needed access to the neurologist. The take-home message is that psychotherapy has an important role in treating PMDs, but that there is also a role for the neurologist to follow the patient along and be available for patient questions and concerns. The benefit of this team approach between neurology and psychiatry is that the neurologist can continue to monitor symptom severity and evaluate potential newly emerging symptoms, whereas the psychiatrist will deliver the actual psychiatric care.

Could a similar psychotherapeutic intervention be tried in the elderly LTC population?

Short-term psychodynamic psychotherapy is certainly appropriate for the LTC population, and is probably underutilized at this point in time. One reason for this might be the misconception that PMDs and other forms of conversion and somatization disorder are disorders of younger people and do not occur in the elderly population. However, in a tertiary care university-based movement disorders center, and at the VA Medical Center where I also practice, we see PMDs very commonly in the older population. Especially in the VA system, there is a strong association with a psychiatric history of posttraumatic stress disorder and later development of PMDs. If cognitive impairment precludes an elderly patient from psychodynamic psychotherapy, then cognitive behavioral therapy would be a good alternative treatment approach, with evidence of efficacy in the treatment of conversion disorders in general.

There has been some discussion in the literature recently that environmental factors, such as nutrition, may play a role in the progression of Parkinson’s disease. Do you recommend any nutritional strategies to older patients for either reducing the risk of Parkinson’s or for delaying its progression? 

Our current understanding of the etiology of Parkinson’s disease is a combination of a predisposing genetic risk and exposure to certain environmental factors. Some of these environmental factors have been well defined, such as exposure to the common pesticides dipyridylium and rotenone. The role of nutrition in Parkinson’s disease is still poorly understood, and the literature is largely based on epidemiological observations without proof of causation. In addition, all studies on disease modification with vitamins and other nutritional supplements, (most recently, vitamin E, coenzyme Q10, and creatine), have been negative. While we generally recommend a healthy diet high in fruits, vegetables, and lean protein, there is not a “Parkinson’s diet” per se, with data for disease prevention or modification.

There have been a number of recent studies evaluating the use of deep brain stimulation (DBS) to treat the symptoms of movement disorders. For example, Pellaprat and colleagues found that DBS of the subthalamic nucleus improves pain in patients with Parkinson’s disease. For whom is the DBS procedure recommended, and what are the risks?

DBS of the subthalamic nucleus, globus pallidus, or ventralis intermedius nucleus of the thalamus is a highly effective surgical procedure for the treatment of Parkinson’s disease, essential tremor, and dystonia. The primary determinant of its success rate is patient selection. In Parkinson’s disease, DBS is appropriate for patients with motor fluctuations (eg, changes in their functional state between akinetic off-time and hyperkinetic on-time), or treatment-refractory tremor. It is important to exclude patients with atypical parkinsonism (eg, dementia with Lewy bodies, progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration), and those with more than minimal cognitive impairment secondary to Parkinson’s disease. DBS can also improve the symptoms of essential tremor. Surgery is offered to those who fail or are intolerant of standard pharmacological approaches to essential tremor (eg, primidone, propranolol, topiramate) and have significant functional impairment. DBS is also used to treat generalized dystonia, or severe forms of torticollis. While age alone is not a contraindication for DBS, an appropriate medical and neuropsychological clearance has to take place before elderly LTC residents can be considered for DBS.

In a recent review, Martino and colleagues spoke to the growing number of progressive heredodegenerative conditions that mimic the presentation of Huntington’s disease (HD) but test negative for the pathological genetic marker. The authors assert that there is much overlap in the clinical phenotype of HD and HD-like syndromes, but the differential diagnosis is complex and may lead to costly and unnecessary investigations. In patients with suspected HD, do you think it is important to differentiate the etiology? How would treatment be different in patients with HD or with an HD-like syndrome?

In my opinion, a precise diagnosis of chorea or a suspected HD-like condition is very important. First of all, some HD-like conditions might be treatable, and need to urgently be identified so appropriate treatment can be initiated. One example for this would be Wilson disease, which is identified by a typical clinical constellation of abnormal movements, psychiatric disturbance, and liver failure, as well an abnormal 24-hour urine copper test. Chelation therapy and mettalothionein inducer drugs approved for treating Wilson disease include penicillamine, trientine, and zinc acetate; these agents should be considered as soon as the diagnosis is made.

Second, the rate of progression and symptom constellation varies considerably between the HD-like conditions, and necessary patient counseling cannot be done without a precise diagnosis. Finally, genetic counseling is an important element of caring for patients and families with these disorders and also relies on diagnostic accuracy. The recent review by Martino and colleagues highlights the complexity of the work-up of HD-like conditions and gives the clinician useful practical tips to narrow down the differential diagnosis before costly genetic tests are considered.