Cases reported "Parkinson Disease"

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1/28. Parkinson's syndrome after closed head injury: a single case report.

    A 36 year old man, who sustained a skull fracture in 1984, was unconscious for 24 hours, and developed signs of Parkinson's syndrome 6 weeks after the injury. When assessed in 1995, neuroimaging disclosed a cerebral infarction due to trauma involving the left caudate and lenticular nucleus. Parkinson's syndrome was predominantly right sided, slowly progressive, and unresponsive to levodopa therapy. reaction time tests showed slowness of movement initiation and execution with both hands, particularly the right. Recording of movement related cortical potentials suggested bilateral deficits in movement preparation. Neuropsychological assessment disclosed no evidence of major deficits on tests assessing executive function or working memory, with the exception of selective impairments on the Stroop and on a test of self ordered random number sequences. There was evidence of abulia. The results are discussed in relation to previous literature on basal ganglia lesions and the effects of damage to different points of the frontostriatal circuits.
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2/28. intracranial hypotension with parkinsonism, ataxia, and bulbar weakness.

    OBJECTIVE: To describe a case of spontaneous intracranial hypotension with a previously unreported constellation of presenting features. DESIGN: Case report. SETTING: Tertiary care center. MAIN OUTCOME AND RESULTS: We describe a patient with intracranial hypotension who presented with a parkinsonian syndrome and later development of ataxia and prominent bulbar symptomatology. headache was not a feature of her initial presentation and was only reported after repeated questioning during later evaluations. magnetic resonance imaging of the patient's head revealed findings characteristic of intracranial hypotension. An [18F]fluoro-m-tyrosine positron emission tomographic scan showed normal striatal activity, suggesting intact presynaptic nigrostriatal function. Opening pressure on lumbar puncture was reduced at 40 mm H2O. A source of cerebrospinal fluid leakage was not identified on nuclear cisternography and the patient underwent lumbar epidural blood patching, which resulted in complete resolution of her signs and symptoms as well as in a marked improvement in her imaging findings. CONCLUSIONS: The clinical spectrum of intracranial hypotension can be broadened to include parkinsonism, cerebellar ataxia, and prominent bulbar dysfunction. As with more common manifestations of the disorder, these features may resolve after appropriate treatment.
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3/28. Mutations producing premature termination of translation and an amino acid substitution in the sterol 27-hydroxylase gene cause cerebrotendinous xanthomatosis associated with parkinsonism.

    OBJECTIVES: Mutational analysis of the sterol 27-hydroxylase (CYP27) gene was performed on three patients from two Japanese families who had cerebrotendinous xanthomatosis (CTX) associated with parkinsonism. methods: Clinical evaluations, brain MRI studies, and laboratory analyses were completed on the three patients. The CYP27 gene was analysed for mutations by PCR amplification of gene segments followed by direct sequencing. RESULTS: Two different, homozygous mutations were identified in these families. One is a novel transition, substituting T for G at Glu162 (GAG) resulting in a stop codon (TAG). The other is also a transition, substituting T for C at Arg441 (CGG) resulting in Trp (TGG). The second is located in two amino acids ahead of the heme ligand binding site (Cys443) of the protein likely rendering it non-functional. It is the most common CTX mutation in Japanese patients. CONCLUSIONS: CTX with parkinsonism is caused by mutations with a severe impact on enzyme function. The two mutations described here are likely to cause loss of function because they are chain terminating or affect an essential site in the protein.
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4/28. 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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5/28. The dropped head sign in parkinsonism.

    We describe seven patients who exhibited the dropped head sign in parkinsonism. These included six females and one male between the ages of 53 and 74. Three patients were clinically diagnosed as probable Parkinson's disease and four were diagnosed with probable multiple system atrophy. None had weakness in the posterior neck muscles or spasms in the anterior neck muscles. When the patients attempted to extend the head voluntarily or passively muscle contraction that was not seen in the dropped-head condition appeared. Surface electromyography of the neck indicated that the anterior neck muscles had rigidity. A gamma-block of the SCM muscles reduced the muscle activity when the head was elevated and improved the dropped-head condition slightly. These findings seem to indicate that the dropped head sign in parkinsonism could be associated with anterior neck muscle rigidity. Although the severity of the dropped head condition was affected by medication or by the clinical course in three patients, there was no clear relationship between the severity of the dropped head condition and the parkinsonism. We suspected that unbalanced muscle rigidity between the anterior and the posterior neck muscles could cause the dropped head sign.
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6/28. Focal myopathy as a cause of anterocollis in Parkinsonism.

    We present a patient with levodopa-responsive Parkinsonism who developed disproportionate anterocollis over a period of 4 to 5 weeks. A neurological evaluation, including EMG and muscle biopsy, demonstrated the presence of a focal myopathy typical of the so-called "dropped head syndrome" or "isolated neck extensor myopathy." Parkinsonian patients presenting with disproportionate anterocollis should be evaluated for focal myopathy, as this may represent one possible cause.
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7/28. Postural asymmetries following unilateral subthalomotomy for advanced Parkinson's disease.

    Two cases of postural asymmetries following unilateral stereotaxic subthalamotomy were observed with head and body tilting to the side contralateral to the STN lesion, which corrected itself completely or partially with levodopa treatment. After subsequent contralateral STN surgery, the postural asymmetry disappeared in both patients. Possible mechanism is discussed.
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8/28. Myopathic camptocormia in a patient with levodopa unresponsive parkinsonism.

    Camptocormia may be seen in Parkinson's disease. As no changes in paraspinal musculature are found, it is attributed to dystonia or extreme rigidity. However, several cases of parkinsonism and dropped head due to neck extensor myopathy have been reported. We report the first patient with levodopa unresponsive parkinsonism and camptocormia of muscular origin.
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9/28. Co-occurrence of essential tremor and Parkinson's disease: clinical study of a large kindred with autopsy findings.

    A multigenerational family complex with an admixture of essential tremor (ET) and PD is presented. Medical information obtained either by historic documentation and/or examination was available for five generations and included 36 members. Of these, 11 family members had tremor of the limbs and/or head. In all these instances ET made its first appearance at an early age, usually prior to the second decade of life. In one case focal dystonia of the hand, a possible prelude to PD occurred, while in three brothers of the third generation, two of them identical twins, classical Parkinson's disease (PD) developed. They had ET develop at an early age, which persisted and in their 50s began showing evidence of PD. Two decades later the twin brothers succumbed to cancer of the colon and at autopsy typical findings of PD with cell loss in the substantia nigra and Lewy-body formation positive for alpha-synuclein by immunohistochemistry was found. Additionally, more than the usual number of senile plaques and neurofibrillatory tangles were present without clinical evidence of dementia or significant decline in cognitive function. This unusual set of clinical and pathological circumstances can hardly be attributed to chance occurrence and raise the question of a specific genetic mutation and/or clustering, which may link ET with PD.
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10/28. Clinical effects of elastic bandage on neurogenic orthostatic hypotension.

    Neurogenic orthostatic hypotension (OH) often causes troublesome symptoms such as dizziness, syncope and falling, interfering active daily life or various therapies in rehabilitation. Nonpharmacologic measures for treating patients with OH include wearing elastic leotard, head-up tilting at night, etc. Elastic garment or antigravity suits is certainly effective, but it may be uncomfortable and not practical. Although elastic bandage (EB) bound on the lower limbs has been thought to be useful, there is few clinical report about its beneficial evidence. We investigated short-term clinical effects of commercially available EB on OH, and estimated the mechanism of its effectiveness by measuring some blood pressure-related humoral variables in neurodegenerative patients with OH.
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