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Query: UMLS:C0233565 (
bradykinesia
)
2,352
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
It has been shown that the autosomal recessive mutation, gray tremor (gt) was associated in the homozygous state (gt/gt) with a rapidly fatal spongiform encephalopathy. Heterozygotes (+/gt) developed mild asymptomatic spongiform brain lesions as did recipient inbred mice inoculated with gt/gt brain homogenates, some of whom also showed behavioral abnormalities [Sidman, R. L., Kinney, H. C. & Sweet, H. O. (1985) Proc. Natl. Acad. Sci. USA 82, 253-257]. In these studies, inbred NFS/N mice inoculated intracerebrally at birth or as adults with gt/gt or first passage gt brain homogenates developed a progressive disease characterized by tremor, ataxia, and spasticity. The symptoms were milder and more slowly progressive than in the gt/gt homozygote, in the paralytic syndrome that followed neonatal inoculation of NFS/N mice with a wild murine leukemia virus (Cas-Br-M MuLV), or in the rapidly progressive ataxia and terminal
bradykinesia
that followed scrapie inoculation of NFS/N mice. The noninflammatory spongiform encephalopathy in affected NFS/N mice resembled that observed in gt/gt homozygotes, +/gt heterozygotes, and asymptomatic recipient inbred mice inoculated with gt/gt brain homogenates. Neither infectious MuLV nor MuLV proteins were detected in gt/gt brain homogenates or in affected recipient mouse brains. Scrapie-associated fibrils, readily identifiable in subcellular fractions of brains from scrapie-inoculated NFS/N mice, were not detected in similar brain fractions from NFS/N mice inoculated with gt brain homogenates. These results confirm and extend the suggestion that gt spongiform encephalopathy has both heritable and transmissible properties. Moreover, the transmissible agent of gt disease differs from both Cas-Br-M MuLV and scrapie in its disease-inducing properties in NFS/N mice. The capacity of NFS/N mice to express transmitted gt
encephalopathy
as clinical disease, to rapidly express Cas-Br-M MuLV spongiform encephalomyelopathy, and to develop mouse-adapted scrapie after a very short incubation time suggest a distinct sensitivity of NFS/N mice to transmissible spongiform encephalopathy.
...
PMID:Transmission in NFS/N mice of the heritable spongiform encephalopathy associated with the gray tremor mutation. 347 86
Among children causing educational difficulties there is, according to the author, a much greater number of encephalopaths with BTEC than it is commonly assumed. Better diagnostic methods help more and more often to diagnose organic changes in the so-called difficult children. The present report gives a clinical picture of
encephalopathy
after BTEC. Studies were made on a group of 500 children who had suffered brain trauma of various kinds during their foetal life or early childhood. Symptoms of the infantile psychoorganic syndrome and character disorders were the most significant features of
encephalopathy
after BTEC. Furthermore, the children presented changes in the EEG and a lowered IQ score (not very markedly, as a rule). Focal neurological changes were rare. Basing on the fact that character disorders are a most typical feature of
encephalopathy
, the author classified encephalopaths as belonging either to the group of
bradykinesia
or that of hyperkinesia. Each of these groups has further been subdivided into those comprising the common, the asocial and the anxious type, according to the encephalopaths' attitude toward their environment.
...
PMID:A study on the late consequences of a brain trauma in early childhood (BTEC). 500 90
We investigated the existence, clinical symptoms, and brain pathology of cerebrovascular parkinsonism. In this study, clinicopathological criteria of cerebrovascular parkinsonism was defined as follows: 1) at least 2 or more symptoms from the following 4 symptoms: tremor, rigidity, akinesia or
bradykinesia
, and short stepped gait or freezing, 2) no depigmentation, no Lewy body at the substantia nigra, no other degenerative disease, and 3) existence of cerebrovascular lesions. Among consecutive 4,000 autopsy series in the elderly, clinicopathologically confirmed cerebrovascular parkinsonism was found in 24 patients with mean age of 80 years. Cerebrovascular parkinsonism was characterized by the short-stepped gait as initial symptoms, absence of the resting tremor, lead-pipe rigidity, the symmetry of findings, and negative response to levodopa. Pseudobulbar palsy was observed in 54%, pyramidal findings in 63% of the cases. Most cases had multiple vascular lesions of the basal ganglia, but the distribution of lesions was not different from that in the cases of progressive subcortical vascular
encephalopathy
of Binswanger type without parkinsonism. Diffuse pallor and the loss of oligodendrocytes in the frontal white matter observed in the cerebrovascular parkinsonism suggested that the symptoms of parkinsonism resulted from the white matter damages in the frontal lobe.
...
PMID:[Cerebrovascular parkinsonism--clinicopathologic study]. 875 29
Cyclosporine has been associated with various neurological side-effects including postural tremor, seizures, headaches,
encephalopathy
, cortical blindness, and visual hallucinations. We describe here two patients who developed parkinsonism, with rest tremor and
bradykinesia
, after receiving cyclosporin A following allogeneic bone marrow transplantation. The patients did not have pre-existing neurological disorders, and had not received significant amounts of dopamine-blocking drugs. One patient improved markedly with Sinemet (carbidopa-levodopa), while the other (who did not tolerate Sinemet) improved with decrease in cyclosporine dosage. The relation of the parkinsonian symptoms to cyclosporine therapy and lack of other evident causes for the symptoms, suggests that parkinsonism may be an occasional consequence of cyclosporine.
...
PMID:Parkinsonism during cyclosporine treatment. 887 34
Carbon disulfide toxicity is well characterized. The principal target organ is the nervous system, although cardiovascular, reproductive, ophthalmologic, and other effects are also recognized. The neurotoxicity manifests in three ways:
encephalopathy
, peripheral and cranial nerve dysfunction, and movement abnormalities. This report describes a case of olivopontocerebellar atrophy, a form of multiple system atrophy, developing in an adult after over 30 years of occupational exposure to carbon disulfide. The patient presented with the insidious onset of balance problems, impotence, and irritability, without tremor, cogwheel rigidity,
bradykinesia
, or changes in facial expression. Over the next few years severe ataxia developed, and the clinical diagnosis was confirmed with computed tomography and magnetic resonance imaging scans. The patient experienced multiple medical complications and died approximately 9 years after diagnosis. This case is consistent with a large body of clinical and experimental literature, much of it 50 years old, showing that carbon disulfide can cause movement disorders. It also serves as a reminder that movement disorders, ranging from parkinsonism to dystonia, are associated with a variety of toxic exposures such as manganese, carbon monoxide, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and medications.
...
PMID:Multiple system atrophy following chronic carbon disulfide exposure. 1070 37
Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis,
bradykinesia
, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy, serum ammonia level normalized and examination showed only minimal parkinsonism after 1 week. An abdominal CT scan identified portal vein thrombosis with porto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of
encephalopathy
.
...
PMID:Reversible parkinsonism and hyperammonemia associated with portal vein thrombosis. 1124 May 69
HIV-related
encephalopathy
is an important problem in vertically infected children with HIV. Infected infants may manifest early, catastrophic
encephalopathy
, with loss of brain growth, motor abnormalities, and cognitive dysfunction. Even without evidence of AIDS, infected infants score lower than serorevertors on developmental measures, particularly language acquisition. Children with perinatal or later transfusion-related infection generally are roughly comparable developmentally to their peers until late in their course. Symptoms similar to adult AIDS dementia complex are occasionally seen in adolescents with advanced AIDS, including dementia,
bradykinesia
, and spasticity. Opportunistic CNS infections such as toxoplasmosis and progressive multifocal leukoencephalopathy are less common in children and adolescents than in adults. Increasing evidence suggests that aggressive antiretroviral treatment may halt or even reverse
encephalopathy
. Neuroimaging changes may precede or follow clinical manifestations, and include early lenticulostriate vessel echogenicity on cranial ultrasound, calcifying microangiopathy on CT scan, and/or white matter lesions and central atrophy on MRI. Differential diagnosis of neurological dysfunction in an HIV-infected infant includes the effects of maternal substance abuse, other CNS congenital infections, and other causes of early static
encephalopathy
. Initial entry of HIV into the nervous system occurs very early in infection. The risk of clinical HIV encephalopathy increases with very early age of infection and with high viral loads. Virus is found in microglia and brain derived macrophages, not neurons. The neuronal effect of HIV is probably indirect, with various cytokines implicated. Apoptosis is the presumed mechanism of damage to neurons by HIV.
...
PMID:Neurological and developmental effects of HIV and AIDS in children and adolescents. 1155 37
Parkinson syndrome occurs in the course of chemical intoxication, especially Mn, CS2, CO. It is rarely caused by chronic mercury intoxication. We present the case of 55 year old man who was exposed to metallic mercury vapor during 33 years of working in the chemical plant at the production of chlorine. On several occassions patient was removed from contact with Hg because of the symptoms of increased Hg absorption. At the age of 52 he developed hand tremor, balance and gait disturbance with
bradykinesia
, paresthesias of the upper extremities, neurobehavioral abnormalities, slight memory loss, and spatial disorientation. Psychoneurological examination revealed dementia, Parkinson's syndrome and ataxia of the lower limbs. Mercury excretion in the urine, which equaled 18.3 mu\g creatinine, confirmed exposure to Hg. MRI of the head revealed cortical and cerebellar atrophy. Electroneurography examination found features of subclinical peripheral sensory axonopathy of the upper limbs. Despite atypical clinical course (parkinsonismus) chronic mercury
encephalopathy
was diagnosed based on documented occupational exposure and diagnostic test results.
...
PMID:[Parkinsonism in chronic occupational metallic mercury intoxication]. 1509 29
Secondary parkinsonism is uncommon in children and exceedingly rare after cranial radiotherapy. This report describes a 14-year-old female who presented with growth retardation as a result of a craniopharyngioma, which was partially resected. A secondary hydrocephalus responded well to shunting. She gradually developed a severe hypokinetic-rigid syndrome 6 months after radiotherapy (54 Gray in 30 daily fractions of 1.8 Gray). In addition, her vigilance decreased. Magnetic resonance imaging revealed increased signal intensity on T2-weighted images in the globus pallidus bilaterally. Nuclear scans indicated only a marginal striatal dopaminergic deficit and revealed decreased metabolism in the thalamus bilaterally. Treatment with dopamine agonists resulted in minor improvement in motor function. Magnetic resonance imaging investigations 3 months later disclosed a decrease of signal intensity changes of the globus pallidus. Gradually,
bradykinesia
diminished slightly and vigilance increased little. In conclusion, secondary and partially reversible parkinsonism can occur in children after radiotherapy. We suggest that focal
encephalopathy
resulting from postradiation edema secondary to microangiopathy led to dysfunction of the globus pallidus and thalamus.
...
PMID:Secondary parkinsonism in childhood: A rare complication after radiotherapy. 1676 32
Many cases of coeliac disease, a gastrointestinal autoimmune disorder caused by sensitivity to gluten, can remain in a subclinical stage or undiagnosed. In a significant proportion of cases (10-15%) gluten intolerance can be associated with central or peripheral nervous system and psychiatric disorders.A 38-year-old man was admitted as to our department an inpatient for worsening anxiety symptoms and behavioural alterations. After the addition of second generation antipsychotic to the therapeutic regimen, the patient presented neuromotor impairment with high fever, sopor, leukocytosis, raised rhabdomyolysis-related indicators. Neuroleptic malignant syndrome was strongly suspected. After worsening of his neuropsychiatric conditions, with the onset of a frontal cognitive deficit,
bradykinesia
and difficulty walking, dysphagia, anorexia and hypoferraemic anaemia, SPET revealed a reduction of cerebral perfusion and ENeG results were compatible with a mainly motor polyneuropathy. Extensive laboratory investigations gave positive results for anti-gliadin antibodies, and an appropriate diet led to a progressive remission of the
encephalopathy
.
...
PMID:Gluten encephalopathy with psychiatric onset: case report. 1955 61
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