TY - JOUR
T1 - The cognitive side of essential tremor
T2 - What are the therapeutic implications?
AU - Janicki, Sarah C.
AU - Cosentino, Stephanie
AU - Louis, Elan D.
N1 - Funding Information:
Future studies are needed to better characterize the cardinal neuropsychological features of ET to aid in accurate clinical diagnoses and appropriately categorize patients for inclusion in clinical treatment trials. Additional case-control and longitudinal studies are needed to examine the potential relationships between ET and the mechanisms contributing to cognitive, personality and psychological change. Autopsy studies and genetic susceptibility studies are also critical for exploration of potential common biologic and genetic pathways between ET and neurodegenerative diseases associated with cognitive impairment such as AD, PD, DLB and PSP. Neuroimaging studies present another modality for examining these potential relationships. Finally, once these patterns and relationships are better characterized, clinical trials could examine the potential utility of cholinesterase inhibitors and memantine for treatment of cognitive impairment in ET. Funding S.J. is funded by the Louis V. Gerstner Jr. Scholars Foundation and NIH-NIA (grant number 5P50AG008702). S.C. is funded by a Paul B. Beeson Career Development Award in Aging (grant number NIH K23 AG032899). E.D.L. is supported by the National Institutes of Health (grant numbers NIH R01 NS039422 and NS042859). Declaration of Conflicting Interests The authors declare no conflicts of interest and no competing financial interests in preparing this article.
PY - 2013/11
Y1 - 2013/11
N2 - While essential tremor (ET) has traditionally been categorized as a pure motor disease, cross-sectional and longitudinal studies of cognition in ET have demonstrated that these patients may have cognitive dysfunction. Recent epidemiological studies demonstrate an association between ET (particularly with onset after age 65) and increased risk for cognitive impairment and dementia. Although existing studies have generally conceptualized cognitive changes in ET as consistent with a ‘frontosubcortical' or ‘corticocerebellar' profile, results from these same studies suggest that cognitive impairment in ET may in fact be heterogeneous. Furthermore, the underlying mechanisms remain uncertain. Cognitive changes could be a byproduct of the cerebellar dysfunction of ET itself; alternately, they may be a feature of concomitant neurodegenerative diseases that have been associated in several studies with ET, including Alzheimer's disease, Parkinson's disease or progressive supranuclear palsy. While the study of cognitive dysfunction in ET has received research attention in recent years, the results of these studies have not been translated into the clinical domain and clinical practice. This review first summarizes the current literature on the potential relationships between ET and cognitive change. We then suggest areas of further clinical evaluation and treatment; these suggestions are directed at physicians caring for ET patients who may demonstrate or complain of cognitive impairment. As we discuss, clinicians should ideally screen ET patients for possible signs or symptoms of cognitive impairment in addition to assessing for psychiatric comorbidity and quality of life. These recommendations are in contrast to most current clinical practice, which does not routinely include such assessment among ET patients. To our knowledge, there have been no pharmacotherapeutic trials to date of any agent for cognitive change associated with ET. We believe that studies for this indication are now called for. Future efforts in this direction will also need to take into account the pathobiology of cognitive changes in ET, which itself is an area that is ripe for future investigations.
AB - While essential tremor (ET) has traditionally been categorized as a pure motor disease, cross-sectional and longitudinal studies of cognition in ET have demonstrated that these patients may have cognitive dysfunction. Recent epidemiological studies demonstrate an association between ET (particularly with onset after age 65) and increased risk for cognitive impairment and dementia. Although existing studies have generally conceptualized cognitive changes in ET as consistent with a ‘frontosubcortical' or ‘corticocerebellar' profile, results from these same studies suggest that cognitive impairment in ET may in fact be heterogeneous. Furthermore, the underlying mechanisms remain uncertain. Cognitive changes could be a byproduct of the cerebellar dysfunction of ET itself; alternately, they may be a feature of concomitant neurodegenerative diseases that have been associated in several studies with ET, including Alzheimer's disease, Parkinson's disease or progressive supranuclear palsy. While the study of cognitive dysfunction in ET has received research attention in recent years, the results of these studies have not been translated into the clinical domain and clinical practice. This review first summarizes the current literature on the potential relationships between ET and cognitive change. We then suggest areas of further clinical evaluation and treatment; these suggestions are directed at physicians caring for ET patients who may demonstrate or complain of cognitive impairment. As we discuss, clinicians should ideally screen ET patients for possible signs or symptoms of cognitive impairment in addition to assessing for psychiatric comorbidity and quality of life. These recommendations are in contrast to most current clinical practice, which does not routinely include such assessment among ET patients. To our knowledge, there have been no pharmacotherapeutic trials to date of any agent for cognitive change associated with ET. We believe that studies for this indication are now called for. Future efforts in this direction will also need to take into account the pathobiology of cognitive changes in ET, which itself is an area that is ripe for future investigations.
KW - clinical
KW - cognition
KW - essential tremor
UR - http://www.scopus.com/inward/record.url?scp=84887832669&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84887832669&partnerID=8YFLogxK
U2 - 10.1177/1756285613489591
DO - 10.1177/1756285613489591
M3 - Article
C2 - 24228071
AN - SCOPUS:84887832669
SN - 1756-2856
VL - 6
SP - 353
EP - 368
JO - Therapeutic Advances in Neurological Disorders
JF - Therapeutic Advances in Neurological Disorders
IS - 6
ER -