Parkinson Disease: Gilman S

Vilensky JA, Mukhamedzyanov RZ, Gilman S. · Department of Anatomy and Cell Biology, Indiana University School of Medicine, Fort Wayne, IN 46805, USA. · Eur Neurol. · Pubmed #18628628 No free full text.

Abstract: Although encephalitis lethargica (EL) appeared in epidemic form in the Soviet Union during the 1920s as it did in most of the world, the Western literature, particularly English, contains little information about the manifestations of the disease there. Here we summarize articles by prominent Russian neurologists who wrote about the disease as they viewed it during the epidemic period. As in the West, Russian clinicians found EL to be remarkably polymorphic, although some signs and symptoms, especially those pertaining to the psychological aspects of the disease, seemed to be more prevalent or were described better and perhaps more frequently by these clinicians. Some Russian clinicians emphasized an increased prevalence of EL among Jews and a relationship with illness and trauma, whereas others found strong evidence for contagion, especially in rural areas.

McCall S, Vilensky JA, Gilman S, Taubenberger JK. · Department of Clinical Pathology, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA. · J Neurovirol. · Pubmed #18569452 No free full text.

Abstract: Since encephalitis lethargica's (EL) prevalence in the 1920s, epidemiologic and clinical debate has persisted over whether EL was caused by, potentiated by, or merely coincident with the Spanish influenza pandemic. Epidemiologic analyses generally suggest that the disorders were coincidental. Beginning in the 1970s, modern experiments on archival brain samples mainly failed to confirm a direct relationship between influenza and EL. These experimental studies have technical limitations, e.g., the appropriateness of antibodies, polymerase chain reaction (PCR) primers and controls, and the extreme paucity and age of available material. These factors render the case against influenza less decisive than currently perceived. Nevertheless, there is little direct evidence supporting influenza in the etiology of EL. Almost 100 years after the EL epidemic, its etiology remains enigmatic, raising the possibility of a recurrence of EL in a future influenza pandemic.

Gilman S. · Department of Neurology, University of Michigan, Ann Arbor, MI 48109-0489, USA. · J Neural Transm. · Pubmed #16082507 No free full text.

Abstract: Although the current guidelines for the clinical diagnosis of multiple system atrophy (MSA) do not require structural or functional brain imaging, investigations utilizing positron emission tomography (PET) have been helpful diagnostically in differentiating between MSA and primary autonomic failure; idiopathic Parkinson's disease; and sporadic olivopontocerebellar atrophy. These investigations have demonstrated different patterns of cerebral glucose utilization and of nigrostriatal projection abnormalities among these disorders and between the cerebellar and parkinsonian forms of MSA. Most of the studies have focused upon patients with well-established disease and none have examined the utility of PET imaging in early stage patients with follow-up of clinical course and autopsy verification to ensure accuracy of diagnosis and to determine the sensitivity and specificity of PET techniques for diagnosis. Recent PET studies have revealed denervation of myocardial post-ganglionic sympathetic neurons in some MSA patients, indicating that this disorder can affect the peripheral autonomic as well as the central nervous system. Investigations utilizing ligands to quantify central nervous system dopaminergic and cholinergic terminals have begun to provide insight into the neurochemical disorders that may underlie two of the sleep disturbances common in MSA, rapid eye movement sleep behavior disorder and obstructive sleep apnea.

Gilman S, Low PA, Quinn N, Albanese A, Ben-Shlomo Y, Fowler CJ, Kaufmann H, Klockgether T, Lang AE, Lantos PL, Litvan I, Mathias CJ, Oliver E, Robertson D, Schatz I, Wenning GK. · Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316, USA. · J Neurol Sci. · Pubmed #10223419 No free full text.

Abstract: We report the results of a consensus conference on the diagnosis of multiple system atrophy (MSA). We describe the clinical features of the disease, which include four domains: autonomic failure/urinary dysfunction, parkinsonism and cerebellar ataxia, and corticospinal dysfunction. We set criteria to define the relative importance of these features. The diagnosis of possible MSA requires one criterion plus two features from separate other domains. The diagnosis of probable MSA requires the criterion for autonomic failure/urinary dysfunction plus poorly levodopa responsive parkinsonism or cerebellar ataxia. The diagnosis of definite MSA requires pathological confirmation.

Gelb DJ, Oliver E, Gilman S. · Department of Neurology, University of Michigan, Ann Arbor, USA. · Arch Neurol. · Pubmed #9923759 links to  free full text

Abstract: The clinical diagnosis of Parkinson disease (PD) is based on the identification of some combination of the cardinal motor signs of bradykinesia, rigidity, tremor, and postural instability, but few attempts have been made to develop explicit diagnostic criteria. We propose a clinical diagnostic classification based on a comprehensive review of the literature regarding the sensitivity and specificity of the characteristic clinical features of PD. Three levels of diagnostic confidence are differentiated: Definite, Probable, and Possible. The diagnoses of Possible and Probable PD are based on clinical criteria alone. Neuropathologic confirmation is required for the diagnosis of Definite PD in patients with the clinical diagnosis of Possible or Probable PD. Criteria for histopathologic confirmation of PD are also presented.

Lipp A, Sandroni P, Ahlskog JE, Fealey RD, Kimpinski K, Iodice V, Gehrking TL, Weigand SD, Sletten DM, Gehrking JA, Nickander KK, Singer W, Maraganore DM, Gilman S, Wenning GK, Shults CW, Low PA. · Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. · Arch Neurol. · Pubmed #19506134 No free full text.

Abstract: OBJECTIVE: To report preliminary results of a prospective ongoing study of multiple system atrophy (MSA) and Parkinson disease (PD), with a large subset of patients with PD with autonomic failure (25%), to evaluate autonomic indices that distinguish MSA from PD. METHODS: We used consensus criteria, detailed autonomic studies (Composite Autonomic Symptom Scale, Composite Autonomic Scoring Scale, thermoregulatory sweat test, and plasma catecholamines), and functional scales (Unified MSA Rating Scale [UMSARS] I-IV and Hoehn-Yahr grading) on a prospective, repeated, and ongoing basis. RESULTS: We report the results of a study on 52 patients with MSA (mean [SD], age, 61.1 [7.8] years; body mass index (calculated as weight in kilograms divided by height in meters squared), 27.2 [4.6]; Hoehn-Yahr grade, 3.2 [0.9]; UMSARS I score, 21.5 [7.4]; and UMSARS II score, 22.7 [9.0]) and 29 patients with PD, including PD with autonomic failure (mean [SD], age, 66.0 [8.1] years; body mass index, 26.6 [5.5]; Hoehn-Yahr grade, 2.2 [0.8]; UMSARS I score, 10.4 [6.1]; and UMSARS II score, 13.0 [5.9]). Autonomic indices were highly significantly more abnormal in MSA than PD (P < .001) for the Composite Autonomic Scoring Scale (5.9 [1.9] vs 3.3 [2.3], respectively), Composite Autonomic Symptom Scale (54.4 [21.8] vs 24.7 [20.5], respectively), and thermoregulatory sweat test (percentage anhidrosis, 57.4% [35.2%] vs 9.9% [17.7%], respectively). These differences were sustained and greater at 1-year follow-up, indicating a greater rate of progression of dysautonomia in MSA than PD. CONCLUSIONS: The severity, distribution, and pattern of autonomic deficits at study entry will distinguish MSA from PD, and MSA from PD with autonomic failure. These differences continue and are increased at follow-up. Our ongoing conclusion is that autonomic function tests can separate MSA from PD. Autonomic indices support the notion that the primary lesion in PD is ganglionic and postganglionic, while MSA is preganglionic.

Koeppe RA, Gilman S, Junck L, Wernette K, Frey KA. · Division of Nuclear Medicine, Department of Radiology, The University of Michigan, Ann Arbor, MI, USA. · Alzheimers Dement. · Pubmed #18632004 No free full text.

Abstract: BACKGROUND: Several progressive neurologic disorders begin with cognitive decline or parkinsonism, notably Alzheimer's disease (AD), Parkinson's disease (PD), and dementia with Lewy bodies (DLB). We used positron emission tomography (PET) in attempts to differentiate these disorders. METHODS: We performed PET with (+)-[11C]dihydrotetrabenazine ([11C]DTBZ) to examine blood-to-brain ligand transport (K(1)) and striatal monoaminergic presynaptic binding (distribution volume [DV]) in 25 DLB, 30 PD, and 25 AD patients and 57 elderly controls (NC). RESULTS: [11C]DTBZ DV was decreased significantly in caudate nucleus, anterior putamen, and posterior putamen in DLB and PD compared with AD and NC. DLB and PD groups showed an anterior-to-posterior gradient of binding loss relative to NC, least in caudate nucleus and largest in posterior putamen. The gradient was significantly steeper in PD than DLB. Both PD and DLB showed significantly greater interhemispheric striatal binding asymmetry than NC, and PD had greater asymmetry than DLB. Cerebral cortical [11C]DTBZ K(1) was decreased diffusely by 4% to 8% in PD. Larger K(1) deficits occurred in AD and DLB temporoparietal and prefrontal association cortices and posterior cingulate cortex. Greater reduction of K(1) occurred in occipital cortex in DLB than AD. Receiver operating characteristic curve analyses distinguished DLB from AD more effectively on the basis of striatal DV than occipital K(1) and distinguished DLB from PD more effectively on the basis of cerebral cortical K(1) than striatal DV patterns. Overall, 90% of cases were properly classified by combining these measures. CONCLUSIONS: PET with [11C]DTBZ can differentiate DLB from both PD and AD in a single neuroimaging study.

Vilensky JA, Foley P, Gilman S. · Department of Anatomy and Cell Biology, Indiana University School of Medicine, Fort Wayne, Indiana 46805, USA. · Pediatr Neurol. · Pubmed #17675021 No free full text.

Abstract: Between 1917 and the late 1920s, encephalitis lethargica was an epidemic and often lethal neurologic disease. In adults, it typically elicited severe somatic effects, and in particular, various forms of cranial nerve and motor dysfunction. In children, the psychiatric effects were often as severe as the physical consequences. Approximately one third of affected children underwent a rapid transformation from normal behavior to delinquency, often leading to institutionalization. Many neurologic and psychological theories were advanced to explain these severe behavioral changes, and the therapeutic approaches employed ranged from training in dedicated schools to frontal leucotomy. Whereas epidemiologic associations provide both positive and negative support for an etiologic relationship between encephalitis lethargica and the approximately contemporaneous "Spanish" influenza epidemic, previously unutilized data from children provide some of the strongest links between influenza and encephalitis lethargica. Encephalitis lethargica triggered behavioral changes in children that are not duplicated by any other neurologic condition, with the possible exception of traumatic brain injury. These unique behavioral abnormalities may provide the earliest clear indication of new encephalitis lethargica cases, whether alone or in concert with an influenza epidemic.

Vilensky JA, Goetz CG, Gilman S. · Department of Anatomy and Cell Biology, Indiana University School of Medicine, Fort Wayne, Indiana 46805, USA. · Mov Disord. · Pubmed #16200538 No free full text.

Abstract: Encephalitis lethargica (EL; epidemic encephalitis; von Economo's disease) often presented with a movement disorder, and the motor consequences of postencephalitic parkinsonism (PEP) were characteristic of the chronic sequelae of this condition. PEP was similar to Parkinson's disease but was more variable and had some distinct features such as oculogyric crises. Although two previous publications have included video images of the movement disorders associated with EL and PEP, the sequences presented were typically short, showed only a few patients, and did not include the work of several neurologists who had the foresight to preserve filmed images of their patients. We describe the most complete record of EL and PEP moving images that have been preserved and make them available in edited form.

Mintzer S, Hickenbottom S, Gilman S. · No affiliation provided · N Engl J Med. · Pubmed #10328712 No free full text.

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