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1/58. The coincidence of schizophrenia and Parkinsonism: some neurochemical implications.

    The hypothesis has recently been advanced that increased activity of central dopaminergic mechanisms underlies the symptomatology of the schizophrenias. The evidence that dopaminergic transmission in the corpus striatum is impaired in Parkinson's disease suggests that observations on the relationship between Parkinson's disease and schizophrenia may illuminate the patholophysiology of the latter disease. Four cases are reported in which an illness with schizophrenic features developed in the setting of longstanding Parkinson's disease; attention is drawn to earlier reports of schizophrenic illnesses occurring as postencephalitic sequelae in the presence of a parkinsonian syndrome. These observations appear to conflict with the view that increased dopamine release in the striatum is necessary for the expression of schizophrenic psychopathology, but do not exclude the possibility that increased transmission may occur at other dopaminergic sites in the brain, for example the nucleus accumbens, tuberculum olfactorium or cerebral cortex. Similarly the dopamine receptor blockade hypothesis of the therapeutic effects of neuroleptic drugs cannot be maintained with respect to an action in the striatum in view of the differences between the actions of thioridazine and chlorpromazine in this structure, but may be tenable for actions at extra-straital sites.
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2/58. Diffuse lewy body disease presenting as multiple system atrophy.

    OBJECTIVES: The majority of patients with diffuse lewy body disease have cognitive or psychiatric manifestations as part of their initial presentation. A sizable minority present with parkinsonian features alone. Autonomic features may also occur, typically after the development of cognitive changes. We aim to demonstrate that diffuse lewy body disease may rarely also present with parkinsonism accompanied by marked autonomic dysfunction in the absence of significant cognitive or psychiatric abnormalities. methods: Case report based on a retrospective chart review and neuropathological examination. RESULTS: We report on a patient in whom a clinical diagnosis of multiple system atrophy was made based on a presentation of parkinsonism with prominent and early autonomic involvement. The former included postural tremor, rigidity and bradykinesia, while the latter consisted of repeated falls due to orthostasis and the subsequent development of urinary incontinence midway through the course of her illness. She was poorly tolerant of dopaminergic therapy due to accentuated orthostasis. Benefit from levodopa was limited and only evident when attempted withdrawal resulted in increased rigidity. There was no history of spontaneous or drug-induced hallucinations, delusions or fluctuating cognition, and in contrast to the prominence and progression of her parkinsonian and autonomic features over the first several years, cognitive impairment did not occur until the final stages of her illness, seven years after the onset of initial symptoms. Neuropathological examination revealed numerous lewy bodies in both neocortical as well as subcortical structures consistent with a diagnosis of diffuse lewy body disease. There was marked neuronal loss in the substantia nigra as well as the autonomic nuclei of the brainstem and spinal cord. CONCLUSIONS: In addition to cognitive, psychiatric, and parkinsonian presentations, diffuse lewy body disease may present with parkinsonism and prominent autonomic dysfunction, fulfilling proposed criteria for the striatonigral form of MSA.
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ranking = 1665.1826684264
keywords = tremor
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3/58. Chronic subdural haematomas and Parkinsonian syndromes.

    We describe three men with parkinsonian syndromes caused or aggravated by chronic subdural haematomas. A 63-year-old man developed tremor at rest, rigidity and bradykinesia one week after he fell and hit his head. A 70-year-old patient suffering from tardive dyskinesia and drug-induced parkinsonism experienced deterioration of his bradykinetic symptoms over two weeks. There was no history of trauma. The third patient, a 82-year-old man with idiopathic Parkinson's disease had a marked increase of his left-sided parkinsonian symptoms. Again, there was no history of trauma. In all three patients chronic subdural haematomas were demonstrated by computed tomography. Evacuation of the chronic subdural haematoma resulted in disappearance respectively improvement of the movement disorder. Diagnostic evaluations appear to be delayed and initial misinterpretations are frequent. The findings of our report and review of the literature point out that a favourable outcome after appropriate surgical treatment is achieved in most instances.
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keywords = tremor
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4/58. chloroquine induced parkinsonism.

    A case of parkinsonism is reported in a 5-years-old male child following prolonged use of chloroquine. The patient presented with reduced spontaneous movements and speech with an expressionless face and a parkinsonian gait but no tremors. His investigations including CT scan brain, CSF study and serum ceruloplasmin were normal. chloroquine was discontinued and the patient was started on oral trihexyphenidyl. The patient showed gradual recovery and the drug was successfully withdrawn. The toxic manifestations were only transient and reversible.
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keywords = tremor
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5/58. Parkinsonism as an initial manifestation of brain tumor.

    Parkinsonism secondary to neoplasm is uncommon. We report two patients with bilaterally symmetric parkinsonism as the initial presentation of their brain tumors. The first patient was a 71-year-old woman who presented with a gradual onset of bilateral resting tremor, bradykinesia and rigidity. Computerized tomography (CT) of the brain revealed a large parasagittal tumor in the left frontal lobe. The patient completely recovered from the parkinsonian symptoms after removal of the brain tumor. The second patient, a 74-year-old man with a history of renal cell carcinoma of the right kidney suffered from an insidious onset of bilateral bradykinesia, rigidity and gait difficulty. Cerebral metastasis was noted on the brain CT scan. Early recognition of intracranial tumor as the cause of parkinsonism is important for the management of this type of movement disorder. Moreover, brain CT scanning plays an important role in the differential diagnosis of patients with parkinsonian symptoms.
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ranking = 22528.32296719
keywords = resting tremor, tremor
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6/58. 5: movement disorders I: parkinsonism and the akinetic-rigid syndromes.

    The major features of akinetic-rigid syndromes are bradykinesia (small, slow movements), rigidity and tremor, often summarised as "parkinsonism". Approximately 80% of akinetic-rigid syndromes are due to Parkinson's disease. Treatment of Parkinson's disease should be determined by level of disability and handicap. The combination of levodopa and peripheral dopadecarboxylase inhibitor is the most efficacious symptomatic treatment for Parkinson's disease. Motor fluctuations appear after 2-3 years of levodopa treatment, and affect at least 50% of patients after five years. Surgery can relieve refractory tremor and dyskinesias, but does not alter disease progression or need for drug therapy.
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ranking = 3330.3653368528
keywords = tremor
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7/58. Vascular Parkinsonism: a case report and review of the literature.

    Vascular Parkinsonism (VP) is characterised by sudden onset and rapid progression of clinical symptoms, absent or poor response to dopamine substitution therapy, and postural instability with shuffling gait and absence of tremor, making it a clinically distinct entity from idiopathic Parkinson's disease (IPD). Furthermore, it displays certain typical findings in neurological investigations. We report on a patient presenting features of VP associated with an intracerebral lesion not ascribed to VP to date, namely an isolated ischaemic focal lesion located in the left cerebral peduncle between the substantia nigra and nucleus ruber as evidenced by magnetic resonance imaging (MRI). The pathophysiological organic correlate for contralateral extrapyramidal symptoms in this patient may be an interruption of nigro-thalamic projection, interrupting the final subcortical station in the cortic-striato-pallido-nigro-thalamico-cortical loop central to the pathophysiology of parkinsonian syndromes. Non-response t o levodopa therapy could be a consequence of disruption of the cortico-basal ganglia-cortical loop on account of ischaemic destruction of subcortico-cortical axons, the underlying pathology, therefore, not being the result of a loss of nigral dopaminergic neurons or striatal dopamine deficiency pathogonomonic of IPD. To our knowledge, this is the first case of clinically manifest VP to be described with a single lesion in the contralateral cerebral peduncle between the substantia nigra and nucleus ruber, and suggests alternative intracerebral patterns for the distribution of disease-causing lesions in VP, and possibly new pathophysiological explanations for the nature of this disease.
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keywords = tremor
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8/58. gaucher disease and parkinsonism: a phenotypic and genotypic characterization.

    Among the many phenotypes associated with gaucher disease, the inherited deficiency of glucocerebrosidase, are reports of patients with parkinsonian symptoms. The basis for this association is unknown, but could be due to alterations in the gene or gene region. The human glucocerebrosidase gene, located on chromosome 1q21, has a nearby pseudogene that shares 96% identity. Immediately adjacent to the glucocerebrosidase pseudogene is a convergently transcribed gene, metaxin, which has a pseudogene that is located just downstream to the glucocerebrosidase gene. We describe a patient with mild gaucher disease but impaired horizontal saccadic eye movements who developed a tremor at age 42, followed by rapid deterioration of her gait. A pallidotomy at age 47 was unsuccessful. Her motor and cognitive deterioration progressed despite enzyme replacement therapy. Sequencing of the glucocerebrosidase gene identified mutations L444P and D409H. Southern blot analysis using the enzyme SspI showed that the maternal allele had an additional 17-kb band. PCR amplifications and sequencing of this fragment demonstrated a duplication which included the glucocerebrosidase pseudogene, metaxin gene, and a pseudometaxin/metaxin fusion. Gene alterations associated with this novel rearrangement, resulting from a crossover between the gene for metaxin and its pseudogene, could contribute to the atypical phenotype encountered in this patient.
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ranking = 1665.1826684264
keywords = tremor
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9/58. parkinson disease and its differentials. Diagnoses made easy.

    BACKGROUND: parkinson disease is a common neurological disorder that is both underdiagnosed and inaccurately diagnosed. There is no reliable biological marker or test that can differentiate between causes of parkinsonism. Even for experienced clinicians, the clinical diagnostic accuracy compared to post mortem findings is about 80%. OBJECTIVE: To discuss the clinical features that differentiate parkinson disease from other important causes of parkinsonism. DISCUSSION: Although parkinson disease is a common cause of parkinsonism, other candidates such as drug reactions, benign essential tremor, vascular disease and Lewy body dementia need to be differentiated. Incorrect diagnosis can result in complications related particularly to the use of levodopa and antipsychotic agents. Diagnostic accuracy is important to ensure appropriate management, to avoid complications and to assist patients to have realistic expectations and prognostic information about their condition.
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ranking = 1665.5160017597
keywords = tremor, action
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10/58. Development of parkinsonian symptoms after discontinuation of carbamazepine in patients concurrently treated with risperidone: two case reports.

    SUMMARY: We report here the development of parkinsonian symptoms after carbamazepine discontinuation in two patients concurrently treated with risperidone. They had been receiving combined treatment of carbamazepine and risperidone for the control of aggressive behavior and psychotic symptoms. The parkinsonian symptoms had not occurred before carbamazepine discontinuation, and have achieved complete remission after the dose reduction of risperidone. These findings suggest that the development of parkinsonian symptoms may be associated with pharmacokinetic interaction between carbamazepine and risperidone.
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