Christopher G. Goetz

Bio: Christopher G. Goetz is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: Parkinson's disease & Rating scale. The author has an hindex of 116, co-authored 651 publications receiving 59510 citations. Previous affiliations of Christopher G. Goetz include Brigham and Women's Hospital & University of Louisville.

Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS): scale presentation and clinimetric testing results.

Abstract: We present a clinimetric assessment of the Movement Disorder Society (MDS)-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS). The MDS-UDPRS Task Force revised and expanded the UPDRS using recommendations from a published critique. The MDS-UPDRS has four parts, namely, I: Non-motor Experiences of Daily Living; II: Motor Experiences of Daily Living; III: Motor Examination; IV: Motor Complications. Twenty questions are completed by the patient/caregiver. Item-specific instructions and an appendix of complementary additional scales are provided. Movement disorder specialists and study coordinators administered the UPDRS (55 items) and MDS-UPDRS (65 items) to 877 English speaking (78% non-Latino Caucasian) patients with Parkinson's disease from 39 sites. We compared the two scales using correlative techniques and factor analysis. The MDS-UPDRS showed high internal consistency (Cronbach's alpha = 0.79-0.93 across parts) and correlated with the original UPDRS (rho = 0.96). MDS-UPDRS across-part correlations ranged from 0.22 to 0.66. Reliable factor structures for each part were obtained (comparative fit index > 0.90 for each part), which support the use of sum scores for each part in preference to a total score of all parts. The combined clinimetric results of this study support the validity of the MDS-UPDRS for rating PD.

Diagnosis and management of dementia with Lewy bodies: Third report of the DLB Consortium

Abstract: The dementia with Lewy bodies (DLB) Consortium has revised criteria for the clinical and pathologic diagnosis of DLB incorporating new information about the core clinical features and suggesting improved methods to assess them. REM sleep behavior disorder, severe neuroleptic sensitivity, and reduced striatal dopamine transporter activity on functional neuroimaging are given greater diagnostic weighting as features suggestive of a DLB diagnosis. The 1-year rule distinguishing between DLB and Parkinson disease with dementia may be difficult to apply in clinical settings and in such cases the term most appropriate to each individual patient should be used. Generic terms such as Lewy body (LB) disease are often helpful. The authors propose a new scheme for the pathologic assessment of LBs and Lewy neurites (LN) using alpha-synuclein immunohistochemistry and semiquantitative grading of lesion density, with the pattern of regional involvement being more important than total LB count. The new criteria take into account both Lewy-related and Alzheimer disease (AD)-type pathology to allocate a probability that these are associated with the clinical DLB syndrome. Finally, the authors suggest patient management guidelines including the need for accurate diagnosis, a target symptom approach, and use of appropriate outcome measures. There is limited evidence about specific interventions but available data suggest only a partial response of motor symptoms to levodopa: severe sensitivity to typical and atypical antipsychotics in ∼50%, and improvements in attention, visual hallucinations, and sleep disorders with cholinesterase inhibitors.

MDS clinical diagnostic criteria for Parkinson's disease

Abstract: This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD). The Movement Disorder Society PD Criteria are intended for use in clinical research but also may be used to guide clinical diagnosis. The benchmark for these criteria is expert clinical diagnosis; the criteria aim to systematize the diagnostic process, to make it reproducible across centers and applicable by clinicians with less expertise in PD diagnosis. Although motor abnormalities remain central, increasing recognition has been given to nonmotor manifestations; these are incorporated into both the current criteria and particularly into separate criteria for prodromal PD. Similar to previous criteria, the Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity. Explicit instructions for defining these cardinal features are included. After documentation of parkinsonism, determination of PD as the cause of parkinsonism relies on three categories of diagnostic features: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow diagnosis of PD), and supportive criteria (positive features that increase confidence of the PD diagnosis). Two levels of certainty are delineated: clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity). The Movement Disorder Society criteria retain elements proven valuable in previous criteria and omit aspects that are no longer justified, thereby encapsulating diagnosis according to current knowledge. As understanding of PD expands, the Movement Disorder Society criteria will need continuous revision to accommodate these advances.

Clinical diagnostic criteria for dementia associated with Parkinson's disease.

Abstract: Dementia has been increasingly more recognized to be a common feature in patients with Parkinson's disease (PD), especially in old age. Specific criteria for the clinical diagnosis of dementia associated with PD (PD-D), however, have been lacking. A Task Force, organized by the Movement Disorder Study, was charged with the development of clinical diagnostic criteria for PD-D. The Task Force members were assigned to sub-committees and performed a systematic review of the literature, based on pre-defined selection criteria, in order to identify the epidemiological, clinical, auxillary, and pathological features of PD-D. Clinical diagnostic criteria were then developed based on these findings and group consensus. The incidence of dementia in PD is increased up to six times, point-prevelance is close to 30%, older age and akinetic-rigid form are associated with higher risk. PD-D is characterized by impairment in attention, memory, executive and visuo-spatial functions, behavioral symptoms such as affective changes, hallucinations, and apathy are frequent. There are no specific ancillary investigations for the diagnosis; the main pathological correlate is Lewy body-type degeneration in cerebral cortex and limbic structures. Based on the characteristic features associated with this condition, clinical diagnostic criteria for probable and possible PD-D are proposed.

Clinical research criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) Report of the NINDS-SPSP International Workshop*

Abstract: To improve the specificity and sensitivity of the clinical diagnosis of progressive supranuclear palsy (PSP, Steele-Richardson-Olszewski syndrome), the National Institute of Neurological Disorders and Stroke (NINDS) and the Society for PSP, Inc. (SPSP) sponsored an international workshop to develop an accurate and universally accepted set of criteria for this disorder. The NINDS-SPSP criteria, which were formulated from an extensive review of the literature, comparison with other previously published sets of criteria, and the consensus of experts, were validated on a clinical data set from autopsy-confirmed cases of PSP. The criteria specify three degrees of diagnostic certainty: possible PSP, probable PSP, and definite PSP. Possible PSP requires the presence of a gradually progressive disorder with onset at age 40 or later, either vertical supranuclear gaze palsy or both slowing of vertical saccades and prominent postural instability with falls in the first year of onset, as well as no evidence of other diseases that could explain these features. Probable PSP requires vertical supranuclear gaze palsy, prominent postural instability, and falls in the first year of onset, as well as the other features of possible PSP. Definite PSP requires a history of probable or possible PSP and histopathologic evidence of typical PSP. Criteria that support the diagnosis of PSP, and that exclude diseases often confused with PSP, are presented. The criteria for probable PSP are highly specific, making them suitable for therapeutic, analytic epidemiologic, and biologic studies, but not very sensitive. The criteria for possible PSP are substantially sensitive, making them suitable for descriptive epidemiologic studies, but less specific. An appendix provides guidelines for diagnosing and monitoring clinical disability in PSP.

Diagnostic and Statistical Manual of Mental Disorders

Abstract: Given the recent attention to movement abnormalities in psychosis spectrum disorders (e.g., prodromal/high-risk syndromes, schizophrenia) (Mittal et al., 2008; Pappa and Dazzan, 2009), and an ongoing discussion pertaining to revisions of the Diagnostic and Statistical Manuel of Mental Disorders (DSM) for the upcoming 5th edition, we would like to take this opportunity to highlight an issue concerning the criteria for tic disorders, and how this might affect classification of dyskinesias in psychotic spectrum disorders. Rapid, non-rhythmic, abnormal movements can appear in psychosis spectrum disorders, as well as in a host of commonly co-occurring conditions, including Tourette’s Syndrome and Transient Tic Disorder (Kerbeshian et al., 2009). Confusion can arise when it becomes necessary to determine whether an observed movement (e.g., a sudden head jerk) represents a spontaneous dyskinesia (i.e., spontaneous transient chorea, athetosis, dystonia, ballismus involving muscle groups of the arms, legs, trunk, face, and/or neck) or a tic (i.e., stereotypic or patterned movements defined by the relationship to voluntary movement, acute and chronic time course, and sensory urges). Indeed, dyskinetic movements such as dystonia (i.e., sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions) closely resemble tics in a patterned appearance, and may only be visually discernable by attending to timing differences (Gilbert, 2006). When turning to the current DSM-IV TR for clarification, the description reads: “Tic Disorders must be distinguished from other types of abnormal movements that may accompany general medical conditions (e.g., Huntington’s disease, stroke, Lesch-Nyhan syndrome, Wilson’s disease, Sydenham’s chorea, multiple sclerosis, postviral encephalitis, head injury) and from abnormal movements that are due to the direct effects of a substance (e.g., a neuroleptic medication)”. However, as it is written, it is unclear if psychosis falls under one such exclusionary medical disorder. The “direct effects of a substance” criteria, referencing neuroleptic medications, further contributes to the uncertainty around this issue. As a result, ruling-out or differentiating tics in psychosis spectrum disorders is at best, a murky endeavor. Historically, the advent of antipsychotic medication in the 1950s has contributed to the confusion about movement signs in psychiatric populations. Because neuroleptic medications produce characteristic movement disorder in some patients (i.e. extrapyramidal side effects), drug-induced movement disturbances have been the focus of research attention in psychotic disorders. However, accumulating data have documented that spontaneous dyskinesias, including choreoathetodic movements, can occur in medication naive adults with schizophrenia spectrum disorders (Pappa and Dazzan, 2009), as well as healthy first-degree relatives of chronically ill schizophrenia patients (McCreadie et al., 2003). Taken together, this suggests that movement abnormalities may reflect pathogenic processes underlying some psychotic disorders (Mittal et al., 2008; Pappa and Dazzan, 2009). More specifically, because spontaneous hyperkinetic movements are believed to reflect abnormal striatal dopamine activity (DeLong and Wichmann, 2007), and dysfunction in this same circuit is also proposed to contribute to psychosis, it is possible that spontaneous dyskinesias serve as an outward manifestation of circuit dysfunction underlying some schizophrenia-spectrum symptoms (Walker, 1994). Further, because these movements precede the clinical onset of psychotic symptoms, sometimes occurring in early childhood (Walker, 1994), and may steadily increase during adolescence among populations at high-risk for schizophrenia (Mittal et al., 2008), observable dyskinesias could reflect a susceptibility that later interacts with environmental and neurodevelopmental factors, in the genesis of psychosis. In adolescents who meet criteria for a prodromal syndrome (i.e., the period preceding formal onset of psychotic disorders characterized by subtle attenuated positive symptoms coupled with a decline in functioning), there is sometimes a history of childhood conditions which are also characterized by suppressible tics or tic like movements (Niendam et al., 2009). On the other hand, differentiating between tics and dyskinesias has also complicated research on childhood disorders such as Tourette syndrome (Kompoliti and Goetz, 1998; Gilbert, 2006). We propose consideration of more explicit and operationalized criteria for differentiating tics and dyskinesias, based on empirically derived understanding of neural mechanisms. Further, revisions of the DSM should allow for the possibility that movement abnormalities might reflect neuropathologic processes underlying the etiology of psychosis for a subgroup of patients. Psychotic disorders might also be included among the medical disorders that are considered a rule-out for tics. Related to this, the reliability of movement assessment needs to be improved, and this may require more training for mental health professionals in movement symptoms. Although standardized assessment of movement and neurological abnormalities is common in research settings, it has been proposed that an examination of neuromotor signs should figure in the assessment of any patient, and be as much a part of the patient assessment as the mental state examination (Picchioni and Dazzan, 2009). To this end it is important for researchers and clinicians to be aware of differentiating characteristics for these two classes of abnormal movement. For example, tics tend to be more complex than myoclonic twitches, and less flowing than choreoathetodic movements (Kompoliti and Goetz, 1998). Patients with tics often describe a sensory premonition or urge to perform a tic, and the ability to postpone tics at the cost of rising inner tension (Gilbert, 2006). For example, one study showed that patients with tic disorders could accurately distinguish tics from other movement abnormalities based on the subjective experience of some voluntary control of tics (Lang, 1991). Another differentiating factor derives from the relationship of the movement in question to other voluntary movements. Tics in one body area rarely occur during purposeful and voluntary movements in that same body area whereas dyskinesia are often exacerbated by voluntary movement (Gilbert, 2006). Finally, it is noteworthy that tics wax and wane in frequency and intensity and migrate in location over time, often becoming more complex and peaking between the ages of 9 and 14 years (Gilbert, 2006). In the case of dyskinesias among youth at-risk for psychosis, there is evidence that the movements tend to increase in severity and frequency as the individual approaches the mean age of conversion to schizophrenia spectrum disorders (Mittal et al., 2008). As revisions to the DSM are currently underway in preparation for the new edition (DSM V), we encourage greater attention to the important, though often subtle, distinctions among subtypes of movement abnormalities and their association with psychiatric syndromes.

The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease

Abstract: The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia.