Neuropsychiatric Symptoms of Patients With Progressive Supranuclear Palsy and Parkinson s Disease

Size: px
Start display at page:

Download "Neuropsychiatric Symptoms of Patients With Progressive Supranuclear Palsy and Parkinson s Disease"

Transcription

1 Neuropsychiatric Symptoms of Patients With Progressive Supranuclear Palsy and Parkinson s Disease Dag Aarsland, M.D., Ph.D. Irene Litvan, M.D. Jan P. Larsen, M.D., Ph.D. Neuropsychiatric symptoms are common in basal ganglia disorders and may have severe clinical consequences. The authors compared the neuropsychiatric manifestations of patients with Parkinson s disease (PD)and progressive supranuclear palsy (PSP). All 103 PD patients and 27 of the 61 PSP patients were taking dopaminergic agents. PSP patients showed significantly more apathy and disinhibition. Patients with PD had higher frequency of hallucinations, delusions, and depression. These results suggest that PSP patients show symptoms compatible with lesioned orbitofrontal and medial frontal circuits, such as disinhibition and apathy, whereas PD patients show symptoms associated with monoaminergic disturbances, such as psychosis and depression. (The Journal of Neuropsychiatry and Clinical Neurosciences 2001; 13:42 49) T he basal ganglia play an important role in the regulation of emotions, mood, motivation, and cognition, in addition to motor control. Although much has been written about the role of the basal ganglia in motor functions, less is known about their role in neuropsychiatric conditions. Idiopathic Parkinson s disease (PD) and progressive supranuclear palsy (PSP) are the most common hypokinetic basal ganglia disorders. Clinically, PD is characterized by unilateral onset of resting tremor, rigidity, and bradykinesia and later development of postural instability, whereas PSP is characterized by prominent postural instability at symptom onset, followed by development of symmetric bradykinesia and rigidity as well as vertical supranuclear ophthalmoparesis. Five frontal-subcortical circuits unite the basal ganglia with regions of the frontal lobe and thalamus in functional systems that mediate motor, cognitive, and emotional behavior. Thus, it is not surprising that behavioral abnormalities, reflecting interruption of these circuits, are present in basal ganglia disorders such as PSP and PD. In both disorders there is involvement of the substantia nigra neurons and striatal dopaminergic depletion, but there are important neuroanatomic and Received February 17, 2000; revised May 22, 2000; accepted May 31, From the Section of Geriatric Psychiatry, Rogaland Psychiatric Hospital, Norway; Cognitive Neuropharmacology Unit, Defense and Veteran Head Injury Program, Henry M. Jackson Foundation, Bethesda, Maryland; and Department of Neurology, Central Hospital of Rogaland, Stavanger, Norway. Address correspondence to Dr. Aarsland, Section of Geriatric Psychiatry, Rogaland Psychiatric Hospital, PO Box 1163 Hillevåg, N-4004 Stavanger, Norway. aarsland@netpower.no Copyright 2001 American Psychiatric Publishing, Inc. 42 J Neuropsychiatry Clin Neurosci 13:1, Winter 2001

2 AARSLAND et al. neurochemical differences between these disorders. Anatomically, PSP patients have greater involvement of additional basal ganglia nuclei (i.e., putamen, globus pallidus, caudate, and subthalamus) and the orbitofrontal and medial frontal circuits than PD patients. Neurochemically, mesocortical dopaminergic, serotonergic, and noradrenergic nuclei are more severely affected in PD than in PSP. 1 We compared the Neuropsychiatric Inventory (NPI) 2 scores in two clearly defined samples of PSP and PD patients to better understand the neurobiological basis for the psychiatric symptoms observed in these two hypokinetic disorders. After considering the differential neuroanatomical and neurochemical involvement, we hypothesized that PSP patients would manifest symptoms associated with disruption of the orbitofrontal (disinhibition) and medial frontal (apathy) circuits, whereas PD patients would exhibit symptoms related to monoaminergic dysfunction (e.g., depression, hallucinations). Because the psychiatric symptoms in these disorders may be secondary to the disease process, to drugs acting on the brain, or to interaction between the disease process and medications, we were careful to control for patients medication and disease stage, in addition to their demographics. METHODS Subjects The PSP patients were 61 consecutive outpatients presenting to the National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, for evaluation and participation in research studies who fulfilled the research criteria outlined by the NINDS Society for Progressive Supranuclear Palsy, Inc., for the diagnosis of definite (n 5), probable (n 44), or possible (n 12) PSP. 3 Definite PSP required neuropathologic confirmation. Mandatory inclusion criteria for the diagnosis of probable PSP included onset after age 40 of progressive vertical supranuclear gaze palsy and severe postural instability during the first year of symptom onset. Possible PSP required onset after age 40 of either progressive vertical supranuclear gaze palsy or progressive severe postural instability during the first year of symptom onset and slowing of vertical saccades. In addition, patients were required to meet exclusionary criteria to rule out features suggestive of other disorders, such as history of encephalitis, severe dysautonomia, or cerebellar symptoms. Thirty-four of these patients were previously reported. 4 The subjects with PD were selected from an epidemiological study of 238 PD patients in the county of Rogaland, Norway. 5 Four years after the primary evaluation, 144 of the 151 surviving PD patients (95.4%) were examined by a neurologist. They received a diagnosis of clinical definite, probable, or possible PD based on the criteria published by Larsen et al. 6 In order to obtain a homogenous population with a high diagnostic specificity for PD, only subjects with definite PD were included. A diagnosis of definite PD required that a patient have resting tremor and at least two of the following three other cardinal signs: 1) akinesia, 2) rigidity, or 3) postural abnormalities. Unilateral symptom onset as well as good to excellent response to dopaminergic agents were required. Atypical features such as early falls, autonomic failure, or dementia and pyramidal signs, cerebellar findings, or supranuclear gaze findings by clinical examination excluded a diagnosis of clinical definite PD. In order to exclude patients with dementia with Lewy bodies (DLB), 7 patients were not included if they had one of the following three features at the baseline evaluation: 1) cognitive impairment, 2) repeated falls, or 3) hallucinations. The PD patients constituted a subset of PD patients in a previous report. 8 Exclusionary criteria for all subjects included other diseases that could explain the symptoms; radiological structural brain abnormalities including significant cerebrovascular disease; a history of alcohol or substance abuse in the past year; head trauma with loss of consciousness; and psychiatric disorders requiring treatment preceding the onset of current disease (other than depression, which several patients had prior to the diagnosis of PD). All participating subjects gave their informed consent. In all, 103 (94.5%) of the 109 PD patients with clinical definite disease and who fulfilled the inclusion criteria agreed to participate in the study. In the PD group, mean age was 74.4 years (SD 7.7), and 56% were female. In the PSP group, mean age was 67.1 years (SD 6.5), and 38% were female. The age and gender distribution differed significantly between the two groups (Table 1). In addition to the main analysis of differences between the PSP and PD groups, we selected a subgroup of PD patients comparable for age and gender with the PSP patients. In this group, PD patients were selected if they matched a PSP patient for gender and age (i.e., not more than 5 years older than the PSP patient) pairwise. Forty-seven PD patients met these criteria. The PSP patients were compared with the total and the age- and gender-matched PD groups. Procedures Neuropsychiatric symptoms were evaluated by administering the NPI, 2 which consists of a structured interview of a caregiver assessing 10 symptoms commonly J Neuropsychiatry Clin Neurosci 13:1, Winter

3 SYMPTOMS IN PSP AND PD found in patients with brain disorders: delusions, hallucinations, agitation, depression, anxiety, euphoria, apathy, disinhibition, irritability, and aberrant motor behavior. Screening questions for each symptom were posed first, and if a positive response was obtained for any of the 10 symptoms, this aspect was then further explored with scripted questions. The product of the frequency (scored 1 4) and severity (scored 1 3) of the particular symptom constitutes the composite score for each symptom (range of scores for each symptom is 0 12). Cognition was assessed on the same day by administering the Mini-Mental State Examination (MMSE). 9 The degree of motor impairment was assessed with the Hoehn and Yahr scale. 10 Dosages of antiparkinsonian and psychotropic drugs were recorded. For dosages of levodopa and dopaminergic agonists, a transformation to a daily dopaminergic measure was performed. The actual daily dosage was calculated as a percentage of defined daily dosages (DDD) based on the Anatomical Therapeutic Chemical Classification (ATC), accepted by the World Health Organization Drug Utilization Research Group 11 for international studies of drug consumption. One DDD corresponds to 600 mg of levodopa, 40 mg of bromocriptine, 3 mg of pergolide, or 1.8 mg of pramipexole. TABLE 1. Characteristic Demographic and clinical characteristics of the study group PD Total (n 103) PD Matched a (n 47) PSP (n 61) Age, years b Duration, years c % female b Education, years c MMSE score Note: Data are expressed as mean SD or percentages. PD Parkinson s disease; PSP progressive supranuclear palsy; MMSE Mini-Mental State Examination. a A subgroup of PD patients matched for age and gender with the PSP group (see text). b Significantly different from the total PD group (P 0.02). c Significantly different from the total PD and matched PD groups (P 0.001). Statistical Analyses Because scores on the NPI items were not normally distributed, nonparametric analyses were used. Mann- Whitney test was used to test differences in severity of NPI scores between PSP and PD patients. Spearman rank correlations were used to test the association between NPI scores and demographic and clinical variables. Normally distributed data were analyzed by using Student s t-test. Proportions were compared by using the Fisher s exact test or the gamma test for ordered categories. Statistical significance was set at a P 0.05 level. For all analyses, tests were two-tailed. RESULTS The PD full data set group was older, included more women, had a longer disease duration, and had fewer years of education than the PSP group (Table 1). MMSE scores did not differ between groups (Table 1). The PSP patients had more advanced parkinsonism (Table 2). To control for the potential influence of disease severity, medication, and age and gender distribution, we first compared the NPI scores for PSP and PD patients at similar Hoehn and Yahr stages. Subsequently, to control for differences in the use of medication, we compared only patients treated with dopaminergic agents. Finally, we compared the PSP group with a gender- and agematched PD group. Neuropsychiatric Symptoms and Disease Stage Linear regression analyses were performed to examine the relationship between total NPI scores and Hoehn and Yahr stages. A significant relationship was found in PD patients (F 10.2, P 0.002), but not in PSP patients (F 1.0, P 0.31). Only one PSP patient had a Hoehn and Yahr stage less than III. NPI scores in PSP and PD patients with Hoehn and Yahr stage III or later were compared (Table 3). In subjects at stage III, a higher total NPI score was found in PSP than in PD patients (z 2.1, P 0.05). In patients at stage IV, the total NPI score was higher in PD patients than in PSP patients (Table 3), but the difference was nonsignificant (z 0.9, P 0.3). A double dissociation of neuropsychiatric symptoms in PSP and PD patients was found: PSP patients showed higher scores on apathy and disinhibition than PD patients, whereas scores for hallucination, delusion, and stage IV depression were higher in PD patients com- TABLE 2. Distribution of patients at different Hoehn &Yahr stages PSP PD Stage n % n % I II III IV V All Note: Different distribution between PSP and PD: gamma 0.5, P PSP progressive supranuclear palsy; PD Parkinson s disease. 44 J Neuropsychiatry Clin Neurosci 13:1, Winter 2001

4 AARSLAND et al. TABLE 3. NPI scores of PSP and PD patients at different Hoehn &Yahr stages NPI All Patients Stage III Stage IV Stage V Subscale PSP (n 61) PD (n 103) PSP (n 23) PD (n 25) PSP (n 29) PD (n 19) PSP (n 8) PD (n 15) Apathy (84) ** (17) (87) ** (20) (86) ** (32) (75) ** (13) Disinhibition (56) ** (8) (48) ** (8) (76) ** (11) (13) (13) Depression (25) (34) (22) (32) (28) * (58) (25) (33) Hallucination (2) ** (26) * (24) ** (63) (13) (47) Anxiety (18) (16) (17) (28) (14) (32) (38) 0 Irritability (20) * (8) (13) (8) (31) (21) (7) Agitation (21) (12) (30) (8) (17) (26) (21) (12) Aberrant motor (9) (10) (4) (8) (10) (21) (13) (27) Delusion (3) * (17) (4) (8) ** (37) (13) (47) Euphoria (1) (5) 0 0 Total NPI score ** * Note: Data are expressed as mean SD (percentage of patients with nonzero score). NPI Neuropsychiatric Inventory; PSP progressive supranuclear palsy; PD Parkinson s disease. Severity of NPI symptoms, PSP vs. PD, Mann-Whitney test: *P **P pared with PSP patients (Table 3). This pattern of neuropsychiatric symptoms was consistent through the Hoehn and Yahr stages III, IV, and V. However, because of a small sample size, only the difference in apathy score reached statistical significance in patients at stage V. Neuropsychiatric Symptoms and Medications Neuropsychiatric symptoms may occur as a side effect of antiparkinsonian drugs. 12 To investigate if the observed difference in neuropsychiatric symptoms between PSP and PD patients was associated with dopaminergic treatment, the NPI scores in PSP and PD patients who were taking antiparkinsonian agents were compared. The number and dosage of antiparkinsonian and psychotropic medications are shown in Table 4. All PD patients were taking levodopa. The mean dose was 632 mg/day (SD 382), and the mean duration of treatment was 10.1 years (SD 4.8). Fifty-nine patients (57%) took one antiparkinsonian agent, 40 patients (39%) took two, and 4 patients (4%) took three. In the PSP group, 27 patients (44%) were taking antiparkinsonian drugs. Twenty-two subjects (36%) were taking levodopa. The mean dose of the PSP subjects taking levodopa was 593 mg/day (SD 300), not significantly different from that of the PD group (t 0.4, P 0.7). Eighteen PSP patients (29%) were taking one antiparkinsonian drug, and 9 (15%) were taking two. Thus, the proportion of patients taking dopaminergic drugs was higher among PD than among PSP patients (gamma 0.85, P 0.001). There were no differences in the average dosage of dopaminergic agents (measured as percentage of DDD) between the 25 PSP subjects who took levodopa and/or a dopamine agonist (93%, SD 55) and the PD subjects (115%, SD 73; t 1.4, df 126, P 0.17). The NPI scores in PSP and PD subjects with similar TABLE 4. Number (%) of patients taking antiparkinsonian and psychotropic drugs Type of Drug PSP (n 61) PD (n 103) Levodopa 22 (36) 103 (100) Selegiline 6 (10) 26 (25) Dopamine agonist 6 (10) 18 (17) Anticholinergic 0 2 (2) Selective serotonergic agent 11 (18) 17 (17) Tricyclic antidepressant 10 (16) 4 (4) Cholinesterase inhibitor 2 (3) 0 Benzodiazepine/hypnotic 4 (7) 12 (12) Atypical antidepressant (buproprion, trazodone) 4 (7) 2 (2) Antipsychotic 1 (2) 9 (9) Methylphenidate 2 (3) 0 Note: PSP progressive supranuclear palsy; PD Parkinson s disease. J Neuropsychiatry Clin Neurosci 13:1, Winter

5 SYMPTOMS IN PSP AND PD disease severity (i.e., Hoehn and Yahr stage III or later), who took one or two antiparkinsonian drugs were compared. The results were similar to those reported above. PSP patients had higher apathy (P 0.001) and disinhibition (P 0.001) scores as well as total NPI score (P 0.001) than PD patients. Hallucination (P 0.001), delusion, (P 0.05), and depression (P 0.05) scores were higher in patients with PD than in those with PSP. Finally, NPI scores in PSP (n 16) and PD (n 59) subjects receiving levodopa monotherapy were compared. Scores for apathy (z 4.3, P 0.001), disinhibition (z 5.1, P 0.001), irritability (z 2.0, P 0.05), and total NPI (z 2.9, P 0.005) were higher in PSP than PD patients, whereas more severe hallucination scores were found in PD (z 2.0, P 0.05). Hallucination and delusion scores were not associated with the number of dopaminergic agents, the daily levodopa dose, or the percentage of DDD in PSP or PD patients. There was no association between duration of treatment and psychotic symptoms in PD patients. Many subjects were treated with psychotropic drugs (Table 4). Twenty-one PSP patients (34%) and 22 PD patients (21%) were taking one or two antidepressants. There were no between-group differences in dosages of selective serotonin reuptake inhibitors or tricyclic antidepressants. Nine PD patients were taking clozapine (n 7, dose range mg/day) or another antipsychotic agent, compared with one PSP patient who was taking neuroleptics prn (Fisher s exact test, P 0.09). To control for the possible confounding effect of antidepressants, PSP and PD patients who were not taking antidepressants were compared. No differences in anxiety and depression scores between PSP and PD patients were found, and the results on other NPI symptoms were also similar to those obtained when all subjects were included. Neuropsychiatric Symptoms in PSP and PD Patients Matched for Age and Gender Subsequently, we selected PD subjects matched with the PSP group according to gender and age. As seen in Table 1, the age- and gender-matched PD subjects had longer disease duration and fewer years of education than the PSP patients. However, with the exception of a high correlation between the disinhibition score and duration of disease in the PD group, (r 0.33, P 0.01), the NPI scores did not correlate with disease duration or length of education in either group of patients. As shown in Table 5, the PSP patients exhibited more neuropsychiatric symptoms, as measured by the total NPI score, than the age- and gender-matched PD group. The same disease-specific pattern of neuropsychiatric symptoms as found above emerged, with higher apathy and disinhibition scores in PSP patients and higher hallucination and delusion scores in the PD group. Fiftysix (92%) of the PSP patients had a positive score on at least one NPI symptom, compared with 25 (53%) of the PD patients (z 3.6, P 0.001). DISCUSSION The main finding in this study was a differential pattern of neuropsychiatric symptoms in patients with PSP and PD. Apathy and disinhibition were more common and severe in PSP patients, whereas hallucinations and delusions were more frequent in patients with PD. Depression was more severe in patients with PD than in those with PSP in subjects with Hoehn and Yahr stage IV, and in those receiving dopaminergic agents. Thus, the results support the hypotheses that neuropsychiatric symptoms are associated with the involvement of selected frontal-subcortical circuits in PSP, and distinct subcortico-cortical monoaminergic nuclei in PD. Neuropsychiatric symptoms were more common and severe in PSP than in PD, possibly due to the more widespread involvement of the basal ganglia in PSP. 1 This is the first study comparing the neuropsychiatric symptoms of patients with these two hypokinetic movement disorders, although the neuropsychiatric features of PSP 4,13 and PD patients 8 have already been previously reported. The relatively large study sample, the use of a standardized and validated instrument to assess psychiatric symptoms in patients with brain disorders, and the use of specific inclusion and exclusion criteria for the diagnoses of PSP and PD 3,6 are the strengths of this study. Although the diagnostic criteria for PSP used in this study is highly specific and reliable, 14 occasion- TABLE 5. NPI composite scores of age- and gender-matched PSP and PD patients NPI Subscale PSP (n 61) PD (n 47) P a Apathy (84) (19) Disinhibition (56) (4) Depression (25) (36) 0.3 Anxiety (18) (17) 0.9 Irritability (20) (13) 0.39 Aberrant motor (8) (11) 0.6 Hallucinations (2) (19) Delusions (3) (11) Agitation (21) (4) Euphoria (2) 0.3 Total NPI Note: Data are expressed as mean SD (percentage of patients with nonzero score). PSP progressive supranuclear palsy; PD Parkinson s disease. a Severity of NPI symptoms, PSP vs. PD (Mann-Whitney test). 46 J Neuropsychiatry Clin Neurosci 13:1, Winter 2001

6 AARSLAND et al. ally it may be difficult to distinguish PSP from PD during the first 2 years of symptom onset when postural instability or ophthalmoplegia present late in the course of PSP. 15,16 To avoid this, several mutually exclusive criteria were used for the diagnoses of PSP and PD in the current study. Patients with a clinical diagnosis of PD and early hallucinations may in fact suffer from dementia with Lewy bodies. 17 Therefore, patients with features compatible with a diagnosis of probable DLB were not included in the PD group. Asymmetrical parkinsonism early in the disease, resting tremor, and excellent levodopa response, which were required for the diagnosis of definite PD in our study, are highly predictive of PD rather than DLB. 15 Inclusion of PSP or DLB patients in the PD group is therefore unlikely. The differences in demographics and case ascertainment limit the interpretation of this study. The PD patients were drawn from an epidemiological study with high case ascertainment, 5 whereas the PSP patients consisted of patients referred to a tertiary care facility. This group may thus not be representative of the general PSP population, but it is difficult to ascertain enough subjects with PSP from the general population. Because only PD patients with a disease duration of at least 4 years were included, PD patients with a short disease duration and mild severity are underrepresented. This factor also limited our ability to explore if depression is more frequent during the early stages in PD than in PSP. On the other hand, because PSP is a rapidly progressing disease with a survival time of only 5 to 7 years, 18 inclusion of earlier and milder PD patients with shorter disease duration and thus less severe parkinsonism would have increased the difference in motor impairment between the two groups. Given the strong association between disease stage and neuropsychiatric disturbances in PD, this would have further increased a stage-dependent difference in neuropsychiatric morbidity between the two groups. Other potential limitations can be noted. The differences in age, gender distribution, and years of education may have had an impact on the observed differences in neuropsychiatric symptoms; there were a few minor associations between NPI scores and demographic variables. However, after controlling for the differences in gender distribution and disease severity, the principal findings of this study were still evident. The NPI raters were not blind to diagnosis, but they were unaware of the hypotheses of the study at the time of assessment. Lack of interrater reliability assessment limits the strength of the findings, but the NPI has been shown to have acceptable reliability in previous studies. 2 Since it is caregiver rated, it may not be as accurate as symptoms rated by a clinician with input from a patient interview. We used the official Norwegian version of the NPI, which has been retranslated into English and authorized by the constructor of the instrument. Finally, no attempt was made to control for multiple comparisons. Accordingly, some statistically significant differences might have occurred by chance. However, the principal findings were robust and occurred in nearly all of the different comparisons performed. Our findings of more severe apathy and disinhibition in PSP than PD are consistent with previous neuroanatomical and neuroradiological reports of a more marked involvement of the orbitofrontal and medial frontal circuits in PSP than in PD. 1 These conclusions extend previous findings of more severe executive impairment in PSP than in PD patients, 19 suggesting a greater involvement of also the dorsolateral frontal-subcortical circuit in PSP. Hallucinations in PD patients are usually considered to represent a side effect of dopaminergic treatment. 12 However, several recent reports have suggested that other factors may be important. Hallucinations in PD were not associated with the number, dosage, and duration of treatment with dopaminergic agents (consistent with previous studies 20,21 ) and do not relate simply to the high levels or sudden changes in plasma levels of levodopa. 22 Almost half of the PSP patients in our study were taking dopaminergic agents, and surprisingly, the dosages of these agents were similar in PSP and PD patients. Dopaminergic agonists, which induce hallucinations more often than does levodopa, were somewhat more frequently administered in PD than PSP patients. Nevertheless, hallucinations were reported in only 1 of the 27 PSP patients who were treated with dopaminergic agents, compared with 27 of the 103 PD patients. Similar results emerged in the subgroup of patients on levodopa monotherapy. PD patients had longer disease duration and had been treated with dopaminergic agents for a longer time than the PSP patients. Theoretically, long-term dopaminergic treatment might increase the risk for hallucinations, possibly via dopamine receptor hypersensitivity. 23 However, in the present and other studies, 20,24,25 there was no association between the duration of levodopa treatment and risk for hallucinations in PD. Thus, although the study design precludes identifying the effect of dopaminergic medication on neuropsychiatric symptoms in the PD group, the results indicate that other factors contribute to hallucinations and delusions in PD. It has been suggested that cortical cholinergic loss, 26,27 imbalance of serotonergic-dopaminergic neurotransmission, 28 or poor visual discrimination 29 might contribute to hallucinations in PD patients. Cholinergic loss occurs in both PSP and PD patients. Although cho- J Neuropsychiatry Clin Neurosci 13:1, Winter

7 SYMPTOMS IN PSP AND PD linergic loss is more severe in PSP than PD 1, there is some evidence suggesting a greater loss of cholinergic innervation to the cerebral cortex in PD, whereas there is a preferential loss of cholinergic innervation to the thalamus in PSP. 30 Monoaminergic nuclei are more involved in PD than in PSP patients. 1 These neurochemical differences are possible explanations for the finding of more frequent hallucinations in PD than in PSP patients. Psychiatric symptoms in basal ganglia disorders are treatable 31 conditions with significant consequences for the care of patients 32 and the well-being of their caregivers. 33 The evaluation and treatment of neuropsychiatric abnormalities in patients with basal ganglia disorders may improve the quality of life for both patients and their caregivers. Our findings provide insight into the neurobiology of psychiatric symptoms in basal ganglia disorders, but neuroimaging and neuropathologic studies are needed to confirm these relationships. The authors thank Neh Geok Lim, M.D., for her contribution to data collection for the study, and the patients for offering their time for research. References 1. Litvan I: Extrapyramidal disorders and frontal lobe function, in The Human Frontal Lobes: Functions and Disorders, edited by Miller BL, Cummings JL. New York, Guilford, 1999, pp Cummings JL, Mega M, Gray K, et al: The Neuropsychiatric Inventory: comprehensive assessment of psychopathology in dementia. Neurology 1994; 44: Litvan I, Agid Y, Calne D, et al: Clinical research criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson- Olszewski syndrome): report of the NINDS-SPSP International Workshop. Neurology 1996; 47: Litvan I, Paulsen JS, Mega MS, et al: Neuropsychiatric assessment of patients with hyperkinetic and hypokinetic movement disorders. Arch Neurol 1998; 55: Tandberg E, Larsen JP, Nessler EG, et al: The epidemiology of Parkinson s disease in the county of Rogaland, Norway. Mov Disord 1995; 10: Larsen JP, Dupont E, Tandberg E: The clinical diagnosis of Parkinson s disease: proposal of diagnostic subgroups classified at different levels of confidence. Acta Neurol Scand 1994; 84: McKeith IG, Galasko D, Kosaka K, et al: Consensus guidelines for the clinical diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology 1996; 47: Aarsland D, Larsen JP, Lim NG, et al: Range of neuropsychiatric disturbances in patients with Parkinson s disease. J Neurol Neurosurg Psychiatry 1999; 67: Folstein MF, Folstein SE, McHugh PR: Mini-Mental State : a practical method for grading the mental state of patients for the clinician. J Psychiatr Res 1975; 12: Hoehn MH, Yahr MD: Parkinsonism: onset, progression, and mortality. Neurology 1967; 17: World Health Organization: Studies in drug utilization, methods, and applications. Copenhagen, WHO Report Publication, European Series, Cummings JL: Behavioral complications of drug treatment of Parkinson s disease. J Am Geriatr Soc 1991; 33: Litvan I, Mega MS, Cummings JL, et al: Neuropsychiatric aspects of progressive supranuclear palsy. Neurology 1996; 47: Lopez OL, Litvan I, Catt KE, et al: Reliability and validity of four clinical diagnostic criteria for the diagnosis of neurodegenerative dementias. Neurology 1999; 53: Litvan I, MacIntyre A, Goetz CG, et al: Accuracy of the clinical diagnoses of Lewy body disease, Parkinson s disease, and dementia with Lewy bodies. Arch Neurol 1998; 55: Litvan I: Progressive supranuclear palsy revisited. Acta Neurol Scand 1998; 98: Goetz CG, Vogel C, Tanner C, et al: Early dopaminergic druginduced hallucinations in parkinsonian patients. Neurology 1998; 51: Litvan I, Mangone CA, McKee A, et al: Natural history of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) and clinical predictors of survival: a clinicopathological study. J Neurol Neurosurg Psychiatry 1996; 61: Pillon B, Dubois B, Lhermitte F, et al: Heterogeneity of cognitive impairment in progressive supranuclear palsy, Parkinson s disease, and Alzheimer s disease. Neurology 1986; 36: Aarsland D, Larsen JP, Cummings JL: Prevalence and clinical correlates of psychosis in Parkinson s disease. Arch Neurol 1999; 56: Sanchez-Ramos JR, Ortoll R, Paulson GW: Visual hallucinations in Parkinson s disease. Arch Neurol 1996; 53: Goetz CG, Pappert EJ, Blasucci LM, et al: Intravenous levodopa in hallucinating Parkinson s disease patients: high-dose challenge does not precipitate hallucinations. Neurology 1998; 50: Klawans HL, Goetz C, Nausieda PA, et al: Levodopa-induced dopamine receptor hypersensitivity. Trans Am Neurol Assoc 1977; 102: Tanner CM, Goetz CG, Klawans HL: Hallucinations in Parkinson s disease: a population study (abstract). Ann Neurol 1983; 14: Klein C, Kompf D, Pulkowski U et al: A study of hallucinations in patients with Parkinson s disease. J Neurol 1997; 244: Kuhl DE, Minoshima S, Fessler JA, et al: In vivo mapping of cholinergic terminals in normal aging, Alzheimer s disease, and Parkinson s disease. Ann Neurol 1996; 40: Minagar A, Shulman LM, Weiner WJ: Transderm-induced psychosis in Parkinson s disease. Neurology 1999; 53: Mellers JDC, Quinn NP, Ron MA: Psychotic and depressive symptoms in Parkinson s disease: a study of the growth hormone response to apomorphine. Br J Psychiatry 1995; 167: Diederich NJ, Goetz C, Raman R, et al: Poor visual discrimination and visual hallucinations in Parkinson s disease. Clin Neuropharmacol 1998; 21: Shinotoh H, Namba H, Yamaguchi M, et al: Positron emission tomographic measurement of acetylcholinesterase activity re- 48 J Neuropsychiatry Clin Neurosci 13:1, Winter 2001

8 AARSLAND et al. veals differential loss of ascending cholinergic systems in Parkinson s disease and progressive supranuclear palsy. Ann Neurol 1999; 46: The Parkinson Study Group: Low-dose clozapine for the treatment of drug-induced psychosis in Parkinson s disease. N Engl J Med 1999; 340: Aarsland D, Larsen JP, Tandberg E, et al: Predictors of nursing home placement in Parkinson s disease: a population-based, prospective study. J Am Geriatr Soc 2000; 48: Aarsland D, Larsen JP, Karlsen K, et al: Mental symptoms in Parkinson s disease are important contributors to caregiver distress. Int J Geriatr Psychiatry 1999; 14: J Neuropsychiatry Clin Neurosci 13:1, Winter

Range of neuropsychiatric disturbances in patients with Parkinson s disease

Range of neuropsychiatric disturbances in patients with Parkinson s disease 492 Section of Geriatric Psychiatry, Rogaland Psychiatric Hospital D Aarsland N G Lim C Janvin Department of Neurology, Central Hospital of Rogaland, Stavanger, Norway J P Larsen K Karlsen E Tandberg Departments

More information

T he prevalence of Parkinson s disease (PD) is nearly 1% in

T he prevalence of Parkinson s disease (PD) is nearly 1% in 708 PAPER Donepezil for cognitive impairment in Parkinson s disease: a randomised controlled study D Aarsland, K Laake, J P Larsen, C Janvin... See end of article for authors affiliations... Correspondence

More information

Clinical Features and Treatment of Parkinson s Disease

Clinical Features and Treatment of Parkinson s Disease Clinical Features and Treatment of Parkinson s Disease Richard Camicioli, MD, FRCPC Cognitive and Movement Disorders Department of Medicine University of Alberta 1 Objectives To review the diagnosis and

More information

Behavioral and psychological symptoms of dementia characteristic of mild Alzheimer patients

Behavioral and psychological symptoms of dementia characteristic of mild Alzheimer patients Blackwell Science, LtdOxford, UKPCNPsychiatry and Clinical Neurosciences1323-13162005 Blackwell Publishing Pty Ltd593274279Original ArticleDementia and mild AlzheimersJ. Shimabukuro et al. Psychiatry and

More information

A wide range of neuropsychiatric disturbances commonly

A wide range of neuropsychiatric disturbances commonly 36 PAPER Neuropsychiatric symptoms in patients with Parkinson s disease and dementia: frequency, profile and associated care giver stress D Aarsland, K Brønnick, U Ehrt, P P De Deyn, S Tekin, M Emre, J

More information

Update on functional brain imaging in Movement Disorders

Update on functional brain imaging in Movement Disorders Update on functional brain imaging in Movement Disorders Mario Masellis, MSc, MD, FRCPC, PhD Assistant Professor & Clinician-Scientist Sunnybrook Health Sciences Centre University of Toronto 53 rd CNSF

More information

DEMENTIA and BPSD in PARKINSON'S DISEASE. DR. T. JOHNSON. NOVEMBER 2017.

DEMENTIA and BPSD in PARKINSON'S DISEASE. DR. T. JOHNSON. NOVEMBER 2017. DEMENTIA and BPSD in PARKINSON'S DISEASE. DR. T. JOHNSON. NOVEMBER 2017. Introduction. Parkinson's disease (PD) has been considered largely as a motor disorder. It has been increasingly recognized that

More information

Parkinsonian Disorders with Dementia

Parkinsonian Disorders with Dementia Parkinsonian Disorders with Dementia George Tadros Consultant in Old Age Liaison Psychiatry, RAID, Heartlands Hospital Professor of Dementia and Liaison Psychiatry, Aston Medical School Aston University

More information

DIFFERENTIAL DIAGNOSIS SARAH MARRINAN

DIFFERENTIAL DIAGNOSIS SARAH MARRINAN Parkinson s Academy Registrar Masterclass Sheffield DIFFERENTIAL DIAGNOSIS SARAH MARRINAN 17 th September 2014 Objectives Importance of age in diagnosis Diagnostic challenges Brain Bank criteria Differential

More information

Parkinson s Disease. Sirilak yimcharoen

Parkinson s Disease. Sirilak yimcharoen Parkinson s Disease Sirilak yimcharoen EPIDEMIOLOGY ~1% of people over 55 years Age range 35 85 years peak age of onset is in the early 60s ~5% of cases characterized by an earlier age of onset (typically

More information

Lewy body disease (LBD) is the second most common

Lewy body disease (LBD) is the second most common REGULAR ARTICLES Lewy Body Disease: Can We Diagnose It? Michelle Papka, Ph.D. Ana Rubio, M.D., Ph.D. Randolph B. Schiffer, M.D. Christopher Cox, Ph.D. The authors assessed the accuracy of published clinical

More information

Non Alzheimer Dementias

Non Alzheimer Dementias Non Alzheimer Dementias Randolph B Schiffer Department of Neuropsychiatry and Behavioral Science Texas Tech University Health Sciences Center 9/11/2007 Statement of Financial Disclosure Randolph B Schiffer,,

More information

Role of Neuropsychiatric Assessment in Diagnosis and Research

Role of Neuropsychiatric Assessment in Diagnosis and Research Role of Neuropsychiatric Assessment 163 11 Role of Neuropsychiatric Assessment in Diagnosis and Research Dag Aarsland, Uwe Ehrt, and Clive Ballard INTRODUCTION Although the basal ganglia have traditionally

More information

Extrapyramidal Motor System. Basal Ganglia or Striatum. Basal Ganglia or Striatum 3/3/2010

Extrapyramidal Motor System. Basal Ganglia or Striatum. Basal Ganglia or Striatum 3/3/2010 Extrapyramidal Motor System Basal Ganglia or Striatum Descending extrapyramidal paths receive input from other parts of motor system: From the cerebellum From the basal ganglia or corpus striatum Caudate

More information

Neurodegenerative Disease. April 12, Cunningham. Department of Neurosciences

Neurodegenerative Disease. April 12, Cunningham. Department of Neurosciences Neurodegenerative Disease April 12, 2017 Cunningham Department of Neurosciences NEURODEGENERATIVE DISEASE Any of a group of hereditary and sporadic conditions characterized by progressive dysfunction,

More information

Health related quality of life in Parkinson s disease: a prospective longitudinal study

Health related quality of life in Parkinson s disease: a prospective longitudinal study 584 Department of Neurology, Central Hospital of Rogaland, Postbox 8100, N-4003 Stavanger, Norway K H Karlsen E Tandberg J P Larsen Department of Psychiatry D Årsland Correspondence to: Professor Jan P

More information

Basal ganglia motor circuit

Basal ganglia motor circuit Parkinson s Disease Basal ganglia motor circuit 1 Direct pathway (gas pedal) 2 Indirect pathway (brake) To release or augment the tonic inhibition of GPi on thalamus Direct pathway There is a tonic inhibition

More information

Mirtazapine improves visual hallucinations in Parkinson s disease: a case report

Mirtazapine improves visual hallucinations in Parkinson s disease: a case report bs_bs_banner doi:10.1111/j.1479-8301.2012.00432.x PSYCHOGERIATRICS 2013; 13: 103 107 CASE REPORT Mirtazapine improves visual hallucinations in Parkinson s disease: a case report Kenji TAGAI, Tomoyuki NAGATA,

More information

Anosognosia, or loss of insight into one s cognitive

Anosognosia, or loss of insight into one s cognitive REGULAR ARTICLES Anosognosia Is a Significant Predictor of Apathy in Alzheimer s Disease Sergio E. Starkstein, M.D., Ph.D. Simone Brockman, M.A. David Bruce, M.D. Gustavo Petracca, M.D. Anosognosia and

More information

Parts of the motor circuits

Parts of the motor circuits MOVEMENT DISORDERS Parts of the motor circuits cortical centers: there are centers in all the cortical lobes subcortical centers: caudate nucleus putamen pallidum subthalamical nucleus (Luys) nucleus ruber

More information

Neuropsychiatric features of corticobasal degeneration

Neuropsychiatric features of corticobasal degeneration J Neurol Neurosurg Psychiatry 1998;65:717 721 717 Neuropharmacology Unit, Defense and Veteran Head Injury Program, Jackson Foundation and the Medical Neurology Branch I Litvan National Institutes of Neurological

More information

Nature, prevalence and clinical significance. Barcelona, Spain

Nature, prevalence and clinical significance. Barcelona, Spain Nature, prevalence and clinical significance Jaime Kulisevsky Barcelona, Spain 1 Non motor (neuropsychiatric) symptoms are an integral part of Parkinson s s disease (PD) Affective disorders And are associated

More information

A prospective study of dementia with Lewy bodies

A prospective study of dementia with Lewy bodies Age and Ageing 998; 27: 6-66 998, British Geriatrics Society A prospective study of dementia with Lewy bodies CLIVE G. BALLARD, JOHN O'BRIEN, KATH LOWERX GARETH A. AYRE, RICHARD HARRISON, ROBERT PERRY,

More information

Parkinson Disease. Lorraine Kalia, MD, PhD, FRCPC. Presented by: Ontario s Geriatric Steering Committee

Parkinson Disease. Lorraine Kalia, MD, PhD, FRCPC. Presented by: Ontario s Geriatric Steering Committee Parkinson Disease Lorraine Kalia, MD, PhD, FRCPC Key Learnings Parkinson Disease (L. Kalia) Key Learnings Parkinson disease is the most common but not the only cause of parkinsonism Parkinson disease is

More information

The Spectrum of Lewy Body Disease: Dementia with Lewy Bodies and Parkinson's Disease Dementia

The Spectrum of Lewy Body Disease: Dementia with Lewy Bodies and Parkinson's Disease Dementia Disclosures Research support, Parkinson Society Canada, Canadian Institutes of Health Research, Ministry of Economic Development and Innovation, Teva Novartis clinical trial, Principal Investigator CME

More information

Psychosis and Agitation in Dementia

Psychosis and Agitation in Dementia Psychosis and Agitation in Dementia Dilip V. Jeste, MD Estelle & Edgar Levi Chair in Aging, Director, Stein Institute for Research on Aging, Distinguished Professor of Psychiatry & Neurosciences, University

More information

The place for treatments of associated neuropsychiatric and other symptoms

The place for treatments of associated neuropsychiatric and other symptoms The place for treatments of associated neuropsychiatric and other symptoms Luca Pani dg@aifa.gov.it London, 25 th November 2014 Workshop on Alzheimer s Disease European Medicines Agency London, UK Public

More information

Original Articles. Calne, resting tremor. Mortimer, Pirozzolo, Hansch, & Webster, postural disturbance III

Original Articles. Calne, resting tremor. Mortimer, Pirozzolo, Hansch, & Webster, postural disturbance III 2004 97-106 Original Articles 1 2 3 1 1 2 3 47 22 III I II muscular rigidity postural disturbance resting tremor bradykinesia Calne, 2001 Mortimer, Pirozzolo, Hansch, & Webster, 1982 Tel: 02-23627076 E-mail:

More information

III./3.1. Movement disorders with akinetic rigid symptoms

III./3.1. Movement disorders with akinetic rigid symptoms III./3.1. Movement disorders with akinetic rigid symptoms III./3.1.1. Parkinson s disease Parkinson s disease (PD) is the second most common neurodegenerative disorder worldwide after Alzheimer s disease.

More information

Acetylcholinesterase inhibitors: donepezil, rivastigmine, tacrine or galantamine for non-alzheimer s dementia

Acetylcholinesterase inhibitors: donepezil, rivastigmine, tacrine or galantamine for non-alzheimer s dementia STEER 2002; Vol 2: No.2 Acetylcholinesterase inhibitors: donepezil, rivastigmine, tacrine or galantamine for non-alzheimer s dementia Bunmi Fajemisin Evidence search date: November 2001 www.signpoststeer.org

More information

The course of neuropsychiatric symptoms in dementia. Part II: relationships among behavioural sub-syndromes and the influence of clinical variables

The course of neuropsychiatric symptoms in dementia. Part II: relationships among behavioural sub-syndromes and the influence of clinical variables INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY Int J Geriatr Psychiatry 2005; 20: 531 536. Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/gps.1317 The course of neuropsychiatric

More information

Use of the Neuropsychiatric Inventory to Characterize the Course of Neuropsychiatric Symptoms in Progressive Supranuclear Palsy

Use of the Neuropsychiatric Inventory to Characterize the Course of Neuropsychiatric Symptoms in Progressive Supranuclear Palsy ARTICLES Use of the Neuropsychiatric Inventory to Characterize the Course of Neuropsychiatric Symptoms in Progressive Supranuclear Palsy Milica Jecmenica-Lukic, M.D., Tatjana Pekmezovic, M.D., Ph.D., Igor

More information

HDSA Annual Convention June 2013 Behavior Issues: Irritability and Depression Peg Nopoulos, M.D.

HDSA Annual Convention June 2013 Behavior Issues: Irritability and Depression Peg Nopoulos, M.D. HDSA Annual Convention June 2013 Behavior Issues: Irritability and Depression Peg Nopoulos, M.D. Professor of Psychiatry, Neurology, and Pediatrics University of Iowa, Iowa City, Iowa The information provided

More information

Neuropsychiatric disturbances such as delusions,

Neuropsychiatric disturbances such as delusions, Differential Neuropsychiatric Responses to Tacrine in Alzheimer s Disease: Relationship to Dementia Severity Daniel Kaufer, M.D. Jeffrey L. Cummings, M.D. Dianne Christine, R.N. Neuropsychiatric symptom

More information

ORIGINAL CONTRIBUTION. Accuracy of the Clinical Diagnoses of Lewy Body Disease, Parkinson Disease, and Dementia With Lewy Bodies

ORIGINAL CONTRIBUTION. Accuracy of the Clinical Diagnoses of Lewy Body Disease, Parkinson Disease, and Dementia With Lewy Bodies Accuracy of the Clinical Diagnoses of Lewy Body Disease, Parkinson Disease, and Dementia With Lewy Bodies A Clinicopathologic Study ORIGINAL CONTRIBUTION I. Litvan, MD; A. MacIntyre, MHS; C. G. Goetz,

More information

Overview. Overview. Parkinson s disease. Secondary Parkinsonism. Parkinsonism: Motor symptoms associated with impairment in basal ganglia circuits

Overview. Overview. Parkinson s disease. Secondary Parkinsonism. Parkinsonism: Motor symptoms associated with impairment in basal ganglia circuits Overview Overview Parkinsonism: Motor symptoms associated with impairment in basal ganglia circuits The differential diagnosis of Parkinson s disease Primary vs. Secondary Parkinsonism Proteinopathies:

More information

A. General features of the basal ganglia, one of our 3 major motor control centers:

A. General features of the basal ganglia, one of our 3 major motor control centers: Reading: Waxman pp. 141-146 are not very helpful! Computer Resources: HyperBrain, Chapter 12 Dental Neuroanatomy Suzanne S. Stensaas, Ph.D. April 22, 2010 THE BASAL GANGLIA Objectives: 1. What are the

More information

Parkinsonism or Parkinson s Disease I. Symptoms: Main disorder of movement. Named after, an English physician who described the then known, in 1817.

Parkinsonism or Parkinson s Disease I. Symptoms: Main disorder of movement. Named after, an English physician who described the then known, in 1817. Parkinsonism or Parkinson s Disease I. Symptoms: Main disorder of movement. Named after, an English physician who described the then known, in 1817. Four (4) hallmark clinical signs: 1) Tremor: (Note -

More information

Coordinating Care Between Neurology and Psychiatry to Improve the Diagnosis and Treatment of Parkinson s Disease Psychosis

Coordinating Care Between Neurology and Psychiatry to Improve the Diagnosis and Treatment of Parkinson s Disease Psychosis Coordinating Care Between Neurology and Psychiatry to Improve the Diagnosis and Treatment of Parkinson s Disease Psychosis Jeff Gelblum, MD Senior Attending Neurologist Mt. Sinai Medical Center Miami,

More information

Screening and Management of Behavioral and Psychiatric Symptoms Associated with Dementia

Screening and Management of Behavioral and Psychiatric Symptoms Associated with Dementia Screening and Management of Behavioral and Psychiatric Symptoms Associated with Dementia Measure Description Percentage of patients with dementia for whom there was a documented screening* for behavioral

More information

Neuropsychiatric Manifestations in Vascular Cognitive Impairment Patients with and without Dementia

Neuropsychiatric Manifestations in Vascular Cognitive Impairment Patients with and without Dementia 86 Neuropsychiatric Manifestations in Vascular Cognitive Impairment Patients with and without Dementia Pai-Yi Chiu 1,3, Chung-Hsiang Liu 2, and Chon-Haw Tsai 2 Abstract- Background: Neuropsychiatric profile

More information

FDG-PET e parkinsonismi

FDG-PET e parkinsonismi Parkinsonismi FDG-PET e parkinsonismi Valentina Berti Dipartimento di Scienze Biomediche, Sperimentali e Cliniche Sez. Medicina Nucleare Università degli Studi di Firenze History 140 PubMed: FDG AND parkinsonism

More information

Pharmacologic Treatment of Parkinson s Disease. Nicholas J. Silvestri, M.D. Associate Professor of Neurology

Pharmacologic Treatment of Parkinson s Disease. Nicholas J. Silvestri, M.D. Associate Professor of Neurology + Pharmacologic Treatment of Parkinson s Disease Nicholas J. Silvestri, M.D. Associate Professor of Neurology + Disclosures n NO SIGNIFICANT FINANCIAL, GENERAL, OR OBLIGATION INTERESTS TO REPORT + Learning

More information

A. General features of the basal ganglia, one of our 3 major motor control centers:

A. General features of the basal ganglia, one of our 3 major motor control centers: Reading: Waxman pp. 141-146 are not very helpful! Computer Resources: HyperBrain, Chapter 12 Dental Neuroanatomy Suzanne S. Stensaas, Ph.D. March 1, 2012 THE BASAL GANGLIA Objectives: 1. What are the main

More information

COGNITIVE IMPAIRMENT IN PARKINSON S DISEASE

COGNITIVE IMPAIRMENT IN PARKINSON S DISEASE 1 GENERAL INTRODUCTION GENERAL INTRODUCTION PARKINSON S DISEASE Parkinson s disease (PD) is a neurodegenerative movement disorder, named after James Parkinson who described some of its characteristic

More information

Behavioral and Psychologic Symptoms in Different Types of Dementia

Behavioral and Psychologic Symptoms in Different Types of Dementia ORIGINAL ARTICLE Behavioral and Psychologic Symptoms in Different Types of Dementia Ming-Jang Chiu,* Ta-Fu Chen, Ping-Keung Yip, Mau-Sun Hua, 1 Li-Yu Tang 2 Background/Purpose: Behavioral and psychologic

More information

Differential Diagnosis of Hypokinetic Movement Disorders

Differential Diagnosis of Hypokinetic Movement Disorders Differential Diagnosis of Hypokinetic Movement Disorders Dr Donald Grosset Consultant Neurologist - Honorary Professor Institute of Neurological Sciences - Glasgow University Hypokinetic Parkinson's Disease

More information

Objectives. RAIN Difficult Diagnosis 2014: A 75 year old woman with falls. Case History: First visit. Case History: First Visit

Objectives. RAIN Difficult Diagnosis 2014: A 75 year old woman with falls. Case History: First visit. Case History: First Visit Objectives RAIN Difficult Diagnosis 2014: A 75 year old woman with falls Alexandra Nelson MD, PhD UCSF Memory and Aging Center/Gladstone Institute of Neurological Disease Recognize important clinical features

More information

Parkinson s Disease in the Elderly A Physicians perspective. Dr John Coyle

Parkinson s Disease in the Elderly A Physicians perspective. Dr John Coyle Parkinson s Disease in the Elderly A Physicians perspective Dr John Coyle Overview Introduction Epidemiology and aetiology Pathogenesis Diagnosis and clinical features Treatment Psychological issues/ non

More information

Transcranial sonography in movement disorders

Transcranial sonography in movement disorders Transcranial sonography in movement disorders Uwe Walter 1st Residential Training of the European Society of Neurosonology and Cerebral Hemodynamics September 7-12, 2008 Bertinoro, Italy Department of

More information

10th Medicine Review Course st July Prakash Kumar

10th Medicine Review Course st July Prakash Kumar 10th Medicine Review Course 2018 21 st July 2018 Drug Therapy for Parkinson's disease Prakash Kumar National Neuroscience Institute Singapore General Hospital Sengkang General Hospital Singhealth Duke-NUS

More information

Pharmacologic Treatment of Parkinson s Disease. Nicholas J. Silvestri, M.D. Assistant Professor of Neurology

Pharmacologic Treatment of Parkinson s Disease. Nicholas J. Silvestri, M.D. Assistant Professor of Neurology + Pharmacologic Treatment of Parkinson s Disease Nicholas J. Silvestri, M.D. Assistant Professor of Neurology + Overview n Brief review of Parkinson s disease (PD) n Clinical manifestations n Pathophysiology

More information

CHAPTER 5 NEUROPSYCHOLOGICAL PROFILE OF ALZHEIMER S DISEASE

CHAPTER 5 NEUROPSYCHOLOGICAL PROFILE OF ALZHEIMER S DISEASE CHAPTER 5 NEUROPSYCHOLOGICAL PROFILE OF ALZHEIMER S DISEASE 5.1 GENERAL BACKGROUND Neuropsychological assessment plays a crucial role in the assessment of cognitive decline in older age. In India, there

More information

The Effect of Pramipexole on Depressive Symptoms in Parkinson's Disease.

The Effect of Pramipexole on Depressive Symptoms in Parkinson's Disease. Kobe J. Med. Sci., Vol. 56, No. 5, pp. E214-E219, 2010 The Effect of Pramipexole on Depressive Symptoms in Parkinson's Disease. NAOKO YASUI 1, KENJI SEKIGUCHI 1, HIROTOSHI HAMAGUCHI 1, and FUMIO KANDA

More information

Revised criteria for the clinical diagnosis of dementia with Lewy. Dementia with Lewy bodies. (Dementia with Lewy Bodies)

Revised criteria for the clinical diagnosis of dementia with Lewy. Dementia with Lewy bodies. (Dementia with Lewy Bodies) Dementia with Lewy bodies First described: Okazaki H, 1961, Diffuse intracytoplasmic ganglionic inclusions (Lewy type) associated with progressive dementia and quadriparesis in flexion. J Neuropathol Exp

More information

Freezing of gait in patients with advanced Parkinson s disease

Freezing of gait in patients with advanced Parkinson s disease J Neural Transm (2001) 108: 53 61 Freezing of gait in patients with advanced Parkinson s disease N. Giladi, T. A. Treves, E. S. Simon, H. Shabtai, Y. Orlov, B. Kandinov, D. Paleacu, and A. D. Korczyn Movement

More information

Correlation between motor and cognitive functions in the progressive course of Parkinson s disease

Correlation between motor and cognitive functions in the progressive course of Parkinson s disease doi:10.1111/ncn3.53 ORIGINAL ARTICLE Correlation between motor and cognitive functions in the progressive course of Parkinson s disease Hidetomo Murakami,* Yoshiyuki Owan,* Yukiko Mori,* Kazuhisa Fujita,*

More information

Movement Disorders: A Brief Overview

Movement Disorders: A Brief Overview Movement Disorders: A Brief Overview Albert Hung, MD, PhD Massachusetts General Hospital Harvard Medical School August 17, 2006 Cardinal Features of Parkinsonism Tremor Rigidity Bradykinesia Postural imbalance

More information

Psychiatric Morbidity in Dementia Patients in a Neurology-Based Memory Clinic

Psychiatric Morbidity in Dementia Patients in a Neurology-Based Memory Clinic Original Articles 179 Psychiatric Morbidity in Dementia Patients in a Neurology-Based Memory Clinic Ching-Sen Shih 1, Sui-Hing Yan 2, Ying-Hoo Ho 1, Yuh-Te Lin 1, Jie-Yuan Li 1, and Yuk-Keung Lo 1 Abstract-

More information

N europsychiatric symptoms can induce marked disability

N europsychiatric symptoms can induce marked disability PAPER Neuropsychiatric profiles in patients with Alzheimer s disease and vascular dementia J-L Fuh, S-J Wang, J L Cummings... See end of article for authors affiliations... Correspondence to: Dr J-L Fuh,

More information

Basal ganglia Sujata Sofat, class of 2009

Basal ganglia Sujata Sofat, class of 2009 Basal ganglia Sujata Sofat, class of 2009 Basal ganglia Objectives Describe the function of the Basal Ganglia in movement Define the BG components and their locations Describe the motor loop of the BG

More information

Parkinson s Disease Update

Parkinson s Disease Update Parkinson s Disease Update Elise Anderson MD Providence Center for Parkinson s Disease October 26, 2017 11/6/2017 1 Disclosures GE Speaker, DaTSCAN 11/6/2017 2 Outline PD diagnosis Motor and nonmotor symptoms

More information

Visualization and simulated animations of pathology and symptoms of Parkinson s disease

Visualization and simulated animations of pathology and symptoms of Parkinson s disease Visualization and simulated animations of pathology and symptoms of Parkinson s disease Prof. Yifan HAN Email: bctycan@ust.hk 1. Introduction 2. Biochemistry of Parkinson s disease 3. Course Design 4.

More information

HDSA welcomes you to Caregiver s Corner. Funded by an educational grant from

HDSA welcomes you to Caregiver s Corner. Funded by an educational grant from HDSA welcomes you to Caregiver s Corner Funded by an educational grant from Caregiver s Corner Webinar, DATE Managing Psychiatric Symptoms Peg Nopoulos, M.D. Professor of Psychiatry, Neurology, and Pediatrics

More information

NEUROPSYCHOMETRIC TESTS

NEUROPSYCHOMETRIC TESTS NEUROPSYCHOMETRIC TESTS CAMCOG It is the Cognitive section of Cambridge Examination for Mental Disorders of the Elderly (CAMDEX) The measure assesses orientation, language, memory, praxis, attention, abstract

More information

P athological examination of the brains of patients with a

P athological examination of the brains of patients with a PAPER How valid is the clinical diagnosis of Parkinson s in the community? A Schrag, Y Ben-Shlomo, N Quinn... See end of article for authors affiliations... Correspondence to: Professor N P Quinn, Sobell

More information

Huntington s Disease Psychiatry. Christopher A. Ross MD PhD HDSA Convention June 6, Many slides adapted from Adam Rosenblatt, MD

Huntington s Disease Psychiatry. Christopher A. Ross MD PhD HDSA Convention June 6, Many slides adapted from Adam Rosenblatt, MD Huntington s Disease Psychiatry Christopher A. Ross MD PhD HDSA Convention June 6, 2008 --Many slides adapted from Adam Rosenblatt, MD Huntington s Disease Society of America The information provided by

More information

Parkinson s Disease Initial Clinical and Diagnostic Evaluation. J. Timothy Greenamyre, MD, PhD

Parkinson s Disease Initial Clinical and Diagnostic Evaluation. J. Timothy Greenamyre, MD, PhD Parkinson s Disease Initial Clinical and Diagnostic Evaluation J. Timothy Greenamyre, MD, PhD Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported

More information

ORIGINAL CONTRIBUTION. Progression of Dysarthria and Dysphagia in Postmortem-Confirmed Parkinsonian Disorders

ORIGINAL CONTRIBUTION. Progression of Dysarthria and Dysphagia in Postmortem-Confirmed Parkinsonian Disorders ORIGINAL CONTRIBUTION Progression of Dysarthria and Dysphagia in Postmortem-Confirmed Parkinsonian Disorders Jörg Müller, MD; Gregor K. Wenning, MD, PhD; Marc Verny, MD; Ann McKee, MD; K. Ray Chaudhuri,

More information

ORIGINAL CONTRIBUTION. Diagnostic Accuracy of Dementia With Lewy Bodies. to be the second

ORIGINAL CONTRIBUTION. Diagnostic Accuracy of Dementia With Lewy Bodies. to be the second ORIGINAL CONTRIBUTION Diagnostic Accuracy of Dementia With Lewy Bodies Ursula Hohl, MD; Pietro Tiraboschi, MD; Lawrence A. Hansen, MD; Leon J. Thal, MD; Jody Corey-Bloom, MD, PhD Background: Diagnostic

More information

Predicting Lewy Body Pathology in a Community-Based Sample With Clinical Diagnosis of Alzheimer s Disease

Predicting Lewy Body Pathology in a Community-Based Sample With Clinical Diagnosis of Alzheimer s Disease Predicting Lewy Body Pathology in a Community-Based Sample With Clinical Diagnosis of Alzheimer s Disease Debby Tsuang, MD, MSc, Kate Simpson, MPH, Eric B. Larson, MD, MPH, Elaine Peskind, MD, Walter Kukull,

More information

History Parkinson`s disease. Parkinson's disease was first formally described in 1817 by a London physician named James Parkinson

History Parkinson`s disease. Parkinson's disease was first formally described in 1817 by a London physician named James Parkinson Parkinsonismm History Parkinson`s disease Parkinson's disease was first formally described in 1817 by a London physician named James Parkinson Definition : Parkinsonism: Parkinsonism is a progressive neurological

More information

White matter hyperintensities correlate with neuropsychiatric manifestations of Alzheimer s disease and frontotemporal lobar degeneration

White matter hyperintensities correlate with neuropsychiatric manifestations of Alzheimer s disease and frontotemporal lobar degeneration White matter hyperintensities correlate with neuropsychiatric manifestations of Alzheimer s disease and frontotemporal lobar degeneration Annual Scientific Meeting Canadian Geriatric Society Philippe Desmarais,

More information

Parkinson s Disease. Prevalence. Mark S. Baron, M.D. Cardinal Features. Clinical Characteristics. Not Just a Movement Disorder

Parkinson s Disease. Prevalence. Mark S. Baron, M.D. Cardinal Features. Clinical Characteristics. Not Just a Movement Disorder Prevalence Parkinson s Disease Mark S. Baron, M.D. Associate Professor of Neurology Movement Disorders Section VCU School of Medicine Common disorder Approaching 1% by 65 yrs of age, 2% by 80 yrs of age

More information

Drug Therapy of Parkinsonism. Assistant Prof. Dr. Najlaa Saadi PhD Pharmacology Faculty of Pharmacy University of Philadelphia

Drug Therapy of Parkinsonism. Assistant Prof. Dr. Najlaa Saadi PhD Pharmacology Faculty of Pharmacy University of Philadelphia Drug Therapy of Parkinsonism Assistant Prof. Dr. Najlaa Saadi PhD Pharmacology Faculty of Pharmacy University of Philadelphia Parkinsonism is a progressive neurological disorder of muscle movement, usually

More information

MAXIMIZING FUNCTION IN PARKINSON S DISEASE

MAXIMIZING FUNCTION IN PARKINSON S DISEASE 1 MAXIMIZING FUNCTION IN PARKINSON S DISEASE September 13, 2016 End Falls This Falls Conference Jan Goldstein Elman One Step Ahead Mobility Toronto, Ontario Outline An overview of Parkinson s disease (PD):

More information

Dementia Update. October 1, 2013 Dylan Wint, M.D. Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, Nevada

Dementia Update. October 1, 2013 Dylan Wint, M.D. Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, Nevada Dementia Update October 1, 2013 Dylan Wint, M.D. Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, Nevada Outline New concepts in Alzheimer disease Biomarkers and in vivo diagnosis Future trends

More information

Making Things Happen 2: Motor Disorders

Making Things Happen 2: Motor Disorders Making Things Happen 2: Motor Disorders How Your Brain Works Prof. Jan Schnupp wschnupp@cityu.edu.hk HowYourBrainWorks.net On the Menu in This Lecture In the previous lecture we saw how motor cortex and

More information

First described by James Parkinson in his classic 1817 monograph, "An Essay on the Shaking Palsy"

First described by James Parkinson in his classic 1817 monograph, An Essay on the Shaking Palsy Parkinson's Disease First described by James Parkinson in his classic 1817 monograph, "An Essay on the Shaking Palsy" Parkinson s disease (PD) is a neurological disorder characterized by a progressive

More information

NeuroPharmac Journal ISSN: Alzheimer s Disease: Pharmacotherapy of noncognitive symptoms Aslam Pathan; Abdulrahman M.

NeuroPharmac Journal ISSN: Alzheimer s Disease: Pharmacotherapy of noncognitive symptoms Aslam Pathan; Abdulrahman M. ISSNISSN ISSN: 2456-3927 NeuroPharmac Journal Alzheimer s Disease: Pharmacotherapy of noncognitive symptoms Aslam Pathan; Abdulrahman M. Alshahrani www. neuropharmac.com Jan-April 2018, Volume 3, Issue

More information

Kinematic Modeling in Parkinson s Disease

Kinematic Modeling in Parkinson s Disease Kinematic Modeling in Parkinson s Disease Alexander Hui Department of Bioengineering University of California, San Diego La Jolla, CA 92093 alexhui@ucsd.edu Abstract Parkinson s disease is a slowly progressing

More information

Management of the Acutely Agitated Long Term Care Patient

Management of the Acutely Agitated Long Term Care Patient Management of the Acutely Agitated Long Term Care Patient 80 60 Graying of the Population US Population Over Age 65 Millions of Persons 40 20 0 1900 1920 1940 1960 1980 1990 2010 2030 Year Defining Dementia

More information

PARKINSON S PRIMER. Dr. Kathryn Giles MD, MSc, FRCPC Cambridge, Ontario, Canada

PARKINSON S PRIMER. Dr. Kathryn Giles MD, MSc, FRCPC Cambridge, Ontario, Canada PARKINSON S PRIMER Dr. Kathryn Giles MD, MSc, FRCPC Cambridge, Ontario, Canada COPYRIGHT 2017 BY SEA COURSES INC. All rights reserved. No part of this document may be reproduced, copied, stored, or transmitted

More information

Evaluation of Parkinson s Patients and Primary Care Providers

Evaluation of Parkinson s Patients and Primary Care Providers Evaluation of Parkinson s Patients and Primary Care Providers 2018 Movement Disorders Half Day Symposium Elise Anderson MD Medical Co-Director, PBSI Movement Disorders 6/28/2018 1 Disclosures GE Speaker,

More information

ORIGINAL CONTRIBUTION. Transcranial Brain Sonography Findings in Discriminating Between Parkinsonism and Idiopathic Parkinson Disease

ORIGINAL CONTRIBUTION. Transcranial Brain Sonography Findings in Discriminating Between Parkinsonism and Idiopathic Parkinson Disease ORIGINAL CONTRIBUTION Transcranial Brain Sonography Findings in Discriminating Between Parkinsonism and Idiopathic Parkinson Disease Uwe Walter, MD; Dirk Dressler, MD; omas Probst, MD; Alexander Wolters,

More information

The motor regulator. 1) Basal ganglia/nucleus

The motor regulator. 1) Basal ganglia/nucleus The motor regulator 1) Basal ganglia/nucleus Neural structures involved in the control of movement Basal Ganglia - Components of the basal ganglia - Function of the basal ganglia - Connection and circuits

More information

A major aim in the management of advanced Parkinson s

A major aim in the management of advanced Parkinson s 396 PAPER Use and interpretation of on/off diaries in Parkinson s disease J Reimer, M Grabowski, O Lindvall, P Hagell... See end of article for authors affiliations... Correspondence to: Peter Hagell,

More information

Baseline Characteristics of Patients Attending the Memory Clinic Serving the South Shore of Boston

Baseline Characteristics of Patients Attending the   Memory Clinic Serving the South Shore of Boston Article ID: ISSN 2046-1690 Baseline Characteristics of Patients Attending the www.thealzcenter.org Memory Clinic Serving the South Shore of Boston Corresponding Author: Dr. Anil K Nair, Chief of Neurology,

More information

symptoms of Parkinson s disease EXCEPT.

symptoms of Parkinson s disease EXCEPT. M. Angele Theard, M.D Asst. Professor, Washington University, St. Louis, MO Quiz team; Shobana Rajan, M.D; Suneeta Gollapudy, MD; Verghese Cherian, M.D, M. Angele Theard, MD This quiz is being published

More information

Objectives. Objectives continued: 3/24/2012. Copyright Do not distribute or replicate without permission 1

Objectives. Objectives continued: 3/24/2012. Copyright Do not distribute or replicate without permission 1 Frontotemporal Degeneration and Primary Progressive Aphasia Caregiver and Professional Education Conference Diana R. Kerwin, MD Assistant Professor of Medicine-Geriatrics Cognitive Neurology and Alzheimer

More information

Parkinson s Disease: initial diagnosis, initial treatment & non-motor features. J. Timothy Greenamyre, MD, PhD

Parkinson s Disease: initial diagnosis, initial treatment & non-motor features. J. Timothy Greenamyre, MD, PhD Parkinson s Disease: initial diagnosis, initial treatment & non-motor features J. Timothy Greenamyre, MD, PhD Involuntary tremulous motion, with lessened muscular power, in parts not in action and even

More information

Can Tango Help Improve Quality of Life for Patients with Parkinson s Disease?

Can Tango Help Improve Quality of Life for Patients with Parkinson s Disease? Philadelphia College of Osteopathic Medicine DigitalCommons@PCOM PCOM Physician Assistant Studies Student Scholarship Student Dissertations, Theses and Papers 2018 Can Tango Help Improve Quality of Life

More information

NIH Public Access Author Manuscript Mov Disord. Author manuscript; available in PMC 2009 May 18.

NIH Public Access Author Manuscript Mov Disord. Author manuscript; available in PMC 2009 May 18. NIH Public Access Author Manuscript Published in final edited form as: Mov Disord. 2008 August 15; 23(11): 1602 1605. doi:10.1002/mds.22161. Emergence of Parkinsons Disease in Essential Tremor: A Study

More information

Parkinson s Disease Psychosis: Hallucinations Delusions and Paranoia

Parkinson s Disease Psychosis: Hallucinations Delusions and Paranoia Parkinson s Disease Psychosis: Hallucinations Delusions and Paranoia Christopher G. Goetz, MD Professor of Neurological Sciences Professor of Pharmacology Rush University Medical Center Parkinson s Foundation

More information

Weight loss in the early stage of progressive supranuclear palsy

Weight loss in the early stage of progressive supranuclear palsy Received: 28 May 2016 Revised: 31 October 2016 Accepted: 2 November 2016 DOI: 10.1002/brb3.616 ORIGINAL RESEARCH Weight loss in the early stage of progressive supranuclear palsy Ayako Tsuge 1 Satoshi Kaneko

More information

Neuropsychiatric symptoms and associated caregiver stress in geriatric patients with Parkinson s disease

Neuropsychiatric symptoms and associated caregiver stress in geriatric patients with Parkinson s disease imedpub Journals http://journals.imed.pub NEUROLOGY AND NEUROSCIENCE Neuropsychiatric symptoms and associated caregiver stress in geriatric patients with Parkinson s disease Abstract Objectives: In Parkinson

More information

Parkinson s disease Therapeutic strategies. Surat Tanprawate, MD Division of Neurology University of Chiang Mai

Parkinson s disease Therapeutic strategies. Surat Tanprawate, MD Division of Neurology University of Chiang Mai Parkinson s disease Therapeutic strategies Surat Tanprawate, MD Division of Neurology University of Chiang Mai 1 Scope Modality of treatment Pathophysiology of PD and dopamine metabolism Drugs Are there

More information

#CHAIR2016. September 15 17, 2016 The Biltmore Hotel Miami, FL. Sponsored by

#CHAIR2016. September 15 17, 2016 The Biltmore Hotel Miami, FL. Sponsored by #CHAIR2016 September 15 17, 2016 The Biltmore Hotel Miami, FL Sponsored by #CHAIR2016 Parkinson s Disease Psychosis: The Latest Evidence for Screening and Treatment Stuart Isaacson, MD FIU Herbert Wertheim

More information

Quality of Life in Patients with Parkinson s Disease

Quality of Life in Patients with Parkinson s Disease Quality of Life in Patients with Parkinson s Disease Seuk Kyung Hong, M.D., Kyung Won Park, M.D., Jae Kwan Cha, M.D., Sang Ho Kim, M.D., Dong Yeol Chun, M.D.*, Chang Kook Yang, M.D.*, Jae Woo Kim, M.D.

More information