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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histochemical demonstration of iron and the iron content was examined in the brain of a case of the special type of hepatocerebral encephalopathy (HCE). The patient had suffered from a liver disease since 36 years old. At 44 years old, she experienced the first attack of twilight state with flapping tremor. She had predilection for eating beans. Her personality gradually became euphoric with the recurrent episodes of unconsciousness. At 54 years old, she died of the complication of melena, renal insufficiency and pneumonia. The liver showed cirrhotic changes and iron content of liver was 0 or 1 after MacDonald's criterion scale. The histopathological findings of the brain showed the characteristic changes of HCE, which were incomplete softening and spongy state pseudolaminarilly extending in the deep layer of the cerebral cortex, the proliferation of the severely changed Alzheimer 2 type glia with or without intranuclear carmine positive substance. The deparaffinized sections, 20 mu in thickness, which were not fastened on slides were used for the histochemical study of iron, because iron deposits displaced inside of the brain tissues when the paraffin sections were fastened on slide glasses in the constant-temperature bath. The iron deposition was found in the central gyrus, superior temporal gyrus, medial and lateral occipito-temporal gyrus and middle temporal gyrus of occipital lobe. The iron accumulated in the ground substance, glia cell bodies, glia nuclei and unknown bodies in the 3-6 layers of cerebral cortex of these gyri. The iron accumulation demonstrated histochemically in other parts of the brain were group 1, 2 by Spatz, mammillary body, glia cell bodies in cerebellar white matter and pons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Iron deposition in the brain of a case of the special type of hepatocerebral encephalopathy]. 280 22

1. The effect of tetrahydroaminoacridine (THA) on cholinergically mediated behaviour in the rat and mouse has been investigated. In addition the actions of this compound on cholinesterase activity and on muscarinic and nicotinic receptors has also been examined. 2. Administration of THA (5-20 mg kg-1, i.p.) produced a dose-dependent increase in tremor, hypothermia and salivation in both rats and mice. A similar profile of activity was seen following physostigmine (0.1-0.6 mg kg-1) administration. 3. THA was approximately fifty fold less potent than physostigmine in inducing behavioural change but its effects persisted for over twice as long as those of physostigmine. For example THA-induced hypothermia was still present at 4 h in the mouse and 8 h in the rat. 4. In vitro THA was a potent non-competitive inhibitor of rat brain cholinesterase (IC50: 57 +/- 6 nM) and bovine erythrocyte acetylcholinesterase (IC50: 50 +/- 10 nM) but was a more potent inhibitor of horse serum butyrylcholinesterase (IC50: 7.2 +/- 1.4 nM). 5. Radioligand binding studies indicated that THA binds non-selectively but with moderate potency to both M1 (Ki: 600 nM) and M2 (Ki: 880 nM) muscarinic receptors. THA also interacted with the allosteric site present on cardiac M2 receptors. 6. It is concluded that THA is a reversible non-competitive inhibitor of cholinesterase with a long half life (compared with physostigmine). It also may antagonize muscarinic receptors at high doses. The long half life may account for its reported efficacy in the treatment of Alzheimer's disease.
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PMID:The cholinergic pharmacology of tetrahydroaminoacridine in vivo and in vitro. 280 55

While dementia in Parkinson's disease (PD) is well described, PD features in Alzheimer's disease (AD) are being increasingly recognized. In 20 neuropathologically confirmed AD brains, 11 cases (55%) showed PD changes (Lewy body formation, neuronal loss, and gliosis of pigmented nuclei), with no significant difference in age or symptom duration between those cases with and without PD pathology. A history of rigidity in the absence of neuroleptic medication was noted in 80% of those with PD pathology but only 14% of those without PD pathology. Tremor was not observed in either group. This suggests that extrapyramidal signs, especially rigidity, noted in many AD patients are related to coexistent PD pathology.
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PMID:Neuropathologic and clinical features of Parkinson's disease in Alzheimer's disease patients. 303 44

A 66 year-old woman presented with severe memory disorders followed several months later with tremor of Parkinsonian type of the right upper limb totally relieved by treatment with levodopa-benserazide. Four years later she was admitted with memory disturbances, temporospatial disorientation, constructional and ideatory apraxia, dressing apraxia and language difficulties. Eight years later she had become bed-ridden, with deviation of head and eyes towards the left, hypertonus tremor and stereotyped movements. Neuropathologic examination showed neuronal loss in substantia nigra and left locus ceruleus, dorsal nucleus of the pneumogastric nerve and Meynert's basal nuclei on both sides. Neurofibrillary tangles affected the peri-aqueductal grey matter and Lewy's bodies were observed in the substantia nigra. Neurofibrillary tangles and granulovacuolar degeneration together with senile plaques were numerous in the hippocampus, but senile plaques and neurofibrillary tangles were rare in the remainder of the cortex. Combined Alzheimer's disease and Parkinson's disease could be due to simple coincidence, one of the diseases possibly predisposing to the appearance of the other.
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PMID:[Alzheimer's disease with early association of a hemi-parkinsonian syndrome]. 318 6

To explore the nature of the olfactory dysfunction associated with Parkinson's disease (PD), 81 PD patients who scored well on a cognitive screening test were administered the 40-odorant University of Pennsylvania Smell Identification Test; 38 were additionally given a forced-choice phenylethyl alcohol odor detection threshold test. Clinical ratings of 11 neurologic symptoms (three bilateral) were obtained at the time of testing, and odor identification was retested in 24 patients at intervals ranging from 5 to 39 months. Relative to matched controls, the PD patients exhibited consistent and marked decrements on both types of olfactory tests (ps less than 0.0001). The odor identification deficit was not restricted to any subset of odorants and did not evidence longitudinal change. A factor analysis of the intercorrelations among the variables yielded six easily interpretable factors: general motor, oral motor, olfactory function, cognitive function, tremor, and gender. Olfactory test scores were independent of all other measures, including disease stage and duration. Seventy-two percent of the PD patients were unaware of a smell disorder before testing; those who were aware had significantly lower test scores. A statistical comparison of PD patients' olfactory test scores to those obtained from Alzheimer's disease patients found the olfactory disorders of these diseases to be indistinguishable. The data support the hypothesis that the olfactory deficit of PD is a general and stable one which likely occurs early in the disease process.
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PMID:Olfactory dysfunction in parkinsonism: a general deficit unrelated to neurologic signs, disease stage, or disease duration. 339 75

The human neurological disorders--amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD)--share certain features: they occur in later stages of adult life; are slowly progressive; and involve specific groups of nerve cells. Different clinical syndromes result from dysfunction and death of these specific groups of neurons. In ALS, patients are weak due to disease of motor neurons in the spinal cord. The clinical features of PD, e.g. slow movements, tremor and rigidity, are attributed, in part, to degeneration of dopaminergic neurons of the substantia nigra. Impairments of cognition and memory in AD result from disease of neurons in a number of regions, including brainstem, basal forebrain, amygdala, hippocampus, and neocortex. In each of these diseases, affected neurons exhibit abnormalities of the neuronal cytoskeleton: in ALS, neurofilaments accumulate and distend proximal motor axons; in PD, nigral perikarya show Lewy bodies-intracytoplasmic inclusions containing neurofilament antigens; in AD, neurons develop neurofibrillary tangles, Hirano bodies, granulovacuolar degeneration and filament-filled neurites in plaques. Certain features of ALS, PD and AD are recapitulated in animal models, three of which are described in this review. Hereditary canine spinal muscular atrophy (HCSMA), a dominantly inherited motor neuron disease, shows many clinical and pathological features in common with ALS, including weakness, muscle atrophy, neurofilamentous swellings of proximal axons, impaired transport of neurofilament proteins, and degeneration of motor neurons. In primates, intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a parkinsonian syndrome due to injury of nigral dopaminergic neurons and associated denervation of the striatum. Finally, aged macaques exhibit memory deficits, and their cerebral cortices show senile plaques and filament-filled neurites derived from a variety of transmitter-specific populations of nerve cells. In human diseases, the causes and mechanisms leading to dysfunction and death of nerve cells are unknown. Investigators have begun using a variety of techniques derived from neurobiology to study animal models in an effort to clarify the mechanisms, evolutions, and consequences of structural-chemical abnormalities occurring in different neuronal systems implicated in human disease. Understanding such processes in these models should provide important new insights into the pathogeneses of similar processes occurring in ALS, PD and AD.
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PMID:Dysfunction and death of neurons in human degenerative neurological diseases and in animal models. 355 88

Amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD) are human neurological disorders which occur in middle and late life. These three diseases share certain features: they are slowly progressive; transmitter-specific groups of neurons are selectively affected by disease processes; and affected nerve cells exhibit cytoskeletal pathology. The causes and mechanisms of cell injury are unknown, and there are no treatments which directly affect the disease process. Dysfunction and death of these specific cell groups account for different clinical syndromes. In ALS, patients become paralyzed, at-risk cholinergic motor neurons in the spinal cord develop neurofilamentous swellings of proximal axons, and distal axons atrophy. In PD, affected individuals show slowed movements, tremor, and rigidity. These clinical findings are attributed to regeneration of dopaminergic neurons of the substantia nigra, a cell group showing abnormal accumulations of neurofilament antigens in the form of Lewy bodies. In AD, patients develop dementia (a syndrome of cognitive and memory impairment), and cholinergic neurons of the basal forebrain and certain other populations of nerve cells develop abnormalities of the cytoskeleton. These include perikaryal neurofibrillary tangles and enlarged distal axons which appear as neurites in senile plaques. Certain features of ALS, PD, and AD are recapitulated in three animal models described in this review. Hereditary Canine Spinal Muscular Atrophy (HCSMA), a dominantly inherited motor neuron disease, shows many clinical and pathological features in common with ALS. Affected dogs are clinically weak, have denervation atrophy of muscles, and develop neurofilamentous swellings of proximal axons, atrophy of distal axons, and degeneration of motor neurons. These abnormalities of axonal caliber are associated with impaired transport of the neurofilament triplet proteins and a maldistribution of phosphorylated neurofilaments. Intoxication of macaques with 1-methyl-4-]henyl-1,2,3,6,tetrahydropyridine (MPTP) produces a Parkinsonian syndrome due to selective injury of dopaminergic neurons in the substantia nigra and associated denervation of the striatum. Finally, aged rhesus monkeys (older than 23 years of age) show cognitive and memory deficits and exhibit senile plaques whose neurites are derived from cholinergic and other transmitter systems. Although these macaques do not have AD, they do provide a model for examining the relationships between age-associated cognitive deficits and pathological changes occurring in certain transmitter systems of primates.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Animal models of degenerative neurological disease. 360 87

Abnormal findings on a standardized neurologic examination were compared between patients with a clinical diagnosis of probable Alzheimer's disease (AD) and healthy control subjects. Aside from mental status findings, the most useful examination findings for differentiating AD from control subjects were the presence of release signs, olfactory deficit, impaired stereognosis or graphesthesia, gait disorder, tremor, and abnormalities on cerebellar testing. These abnormalities probably reflect the different areas of the central nervous system that are affected pathologically in AD. In the clinical diagnosis of AD, particular attention should be given to these aspects of the neurologic examination.
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PMID:The neurologic examination in patients with probable Alzheimer's disease. 361 12

Because patients with Alzheimer's disease often develop clinical manifestations of Parkinson's disease, we examined the substantia nigra in 40 cases of pathologically confirmed Alzheimer's disease for the changes of Parkinson's disease (neuronal loss, Lewy bodies, or neurofibrillary tangles). Eighteen patients had one or more of these changes in the substantia nigra. Subsequently, we reviewed their clinical records and found that rigidity, with or without tremor, had been noted in 13 patients, and nine patients had a second diagnosis of possible or definite Parkinson's disease. Eleven (85%) of these patients had the pathologic changes of Parkinson's disease. These findings suggest that the majority of patients with Alzheimer's disease with extrapyramidal signs have the pathologic changes of Parkinson's disease in the substantia nigra.
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PMID:Parkinson's disease in patients with Alzheimer's disease. 372 42

The effects of the compound RS 86 (2-ethyl-8-methyl-2,8-diazaspiro-[4,5]-decan-1,3-dion hydrobromide) in a number of in vitro and in vivo test systems for muscarinic cholinergic activity were analyzed and compared to those of classical muscarinic receptor agonists. In radioligand binding assays RS 86 presented high nanomolar apparent affinity only for sites labeled by 3H-muscarinic receptor agonists while its apparent affinity for sites labeled by 3H-muscarinic receptor antagonists including [3H]QNB, [3H]NMS and [3H]pirenzepine was in the micromolar range. RS 86 had no or only low affinity (IC50 greater than 10 microM) for other neurotransmitter or drug receptor sites. The compound induced scopolamine-sensitive contractions of the isolated guinea-pig ileum showing a pD2 of 6 in this model. In the isolated rat superior cervical ganglion RS 86 was also an agonist with a pD2 of 6.7. When given to mice or rats by different routes RS 86 induced central and peripheral effects typical of a muscarinic receptor agonist, such as hypothermia, tremor, mydriasis, salivation, lacrimation, diarrhoea and modification of behavior as observed in an open field. In several of these tests RS 86 was about 10 times less potent than oxotremorine but more potent than arecoline, pilocarpine, aceclidine or the compound (cis) AF-30. The ED50 values for some central effects, including the induction of hypothermia and alert non-mobile behavior were lower than those for tremor and peripheral effects. Some of the effects lasted for up to 6 h, depending on the dose. Finally, RS 86 administration resulted in modifications of brain acetylcholine turnover and high affinity choline uptake typical of a central muscarinic receptor agonist. Taken together these results demonstrate clearly that RS 86 is a potent, centrally acting, selective muscarinic receptor agonist. RS 86 appears to be an adequate tool for the clinical examination of the cholinergic hypothesis of Alzheimer's disease.
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PMID:The pharmacological assessment of RS 86 (2-ethyl-8-methyl-2,8-diazaspiro-[4,5]-decan-1,3-dion hydrobromide). A potent, specific muscarinic acetylcholine receptor agonist. 373 91


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