Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasmodic torticollis, once thought to be psychogenic, is now recognized as an extrapyramidal movement disorder. A patient with onset of classical torticollis after closed head injury and intracranial hypertension is described. The patient had no clinical or radiologic evidence of brain stem dysfunction, but brain stem auditory evoked potentials suggested pontomesencephalic conduction disturbance ipsilateral to head and neck movements. This finding accords with some previous clinical and experimental evidence that pontomesencephalic structures ipsilateral to the movements may be involved in torticollis. The observation suggests that spasmodic torticollis may develop as a sequel to trauma in head-injured patients and should be differentiated from posttraumatic seizures.
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PMID:Spasmodic torticollis after closed head injury. 358 52

We studied the relative etiologic importance upon the development of Parkinson's disease (PD) of occupational exposure to herbicides and other compounds, ionizing radiation exposure, family history of PD and essential tremor, smoking, and history of various viral and other medical conditions. We identified patients (n = 130) with neurologist-confirmed idiopathic PD through contacts with Calgary general hospitals, long-term care facilities, neurologists, the Movement Disorder Clinic, and the Parkinson's Society of Southern Alberta, and selected two matched (by sex and age +/- 2.5 years) community controls for each case by random digit dialing. We obtained lifetime work, chemical, radiation, medical, and smoking exposure histories and family histories of PD and essential tremor by personal interviews, and analyzed the data using conditional logistic regression for matched sets. After controlling for potential confounding and interaction between the exposure variables, using multivariate statistical methods, having a family history of PD was the strongest predictor of PD risk, followed by head trauma and then occupational herbicide use. Cases and controls did not differ in their previous exposures to smoking or ionizing radiation; family history of essential tremor; work-related contact with aluminum, carbon monoxide, cyanide, manganese, mercury, or mineral oils; or history of arteriosclerosis, chicken pox, encephalitis, hypertension, hypotension, measles, mumps, rubella, or Spanish flu. These results support the hypothesis of a multifactorial etiology for PD, probably involving genetic, environmental, trauma, and possibly other factors.
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PMID:Parkinson's disease: a test of the multifactorial etiologic hypothesis. 817 May 64

We report a patient who developed an acute, reversible, generalized choreiform disorder from lithium (Li) intoxication. This medication was prescribed for manic-depressive disorder, and serum levels became elevated after the addition of a diuretic for the treatment of hypertension. There were no other apparent causes for the movement disorder, and it was associated with other known features of Li intoxication, including ataxia and encephalopathy. There was a delay between the initial symptoms of Li intoxication and the onset of chorea. The chorea improved as serum Li levels diminished, with some lag time. This represents the eleventh case report of Li-induced chorea, but only the sixth in a patient without concomitant neuroleptic therapy, and the first presented with videotape confirmation. A review of these other cases is included, and possible mechanisms are discussed.
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PMID:Chorea caused by lithium intoxication: a case report and literature review. 891 4

Movement disorders following midbrain haemorrhage are infrequently encountered in rehabilitation, and are uncommonly corrected by pharmacologic means. This report describes a 20 year-old male with a prior history of cocaine abuse who presented with a 4 day history of dysarthria and blurred vision following methamphetamine abuse. Physical examination demonstrated hypertension, left facial hemispasm, bilateral upward gaze paresis and ataxic gait. Magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) showed multifocal parenchymal haematomas in the mesencephalic tegmentum, subcortical left front region and right anterior thalamus consistent with cavernous angiomas. The patient was transferred to rehabilitation on hospital day 5. The following day, he developed choreoathetoid movements, dystonia, and aphasia, secondary to an extension of the midbrain haemorrhage. Cogentin was initiated with slight improvement in choreoathetoid movements. The patient began intensive multidisciplinary rehabilitation therapy but after 18 days of therapy, the patient remained totally dependent in activities of daily living (ADLs), transfers, mobility and was unable to communicate in any manner. A trial of Sinemet was initiated, with resultant steady improvement in functional ability over the next month. By discharge, the patient was independent in ADLs and ambulation. By 9 months post discharge follow-up, the patient was fully independent with normal cognition, and had self tapered all medications without ill effect. Dopamine agonist trials of appropriate duration appear indicated in cases of movement disorder (paucity or excess) following midbrain lesions.
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PMID:Pharmacologic management of movement disorder after midbrain haemorrhage. 965 26

We studied the neurological comorbidity of parkinsonism in 368 consecutive patients from the Lausanne Movement Disorders Registry. Only 6 patients had no neurological comorbidity. We found that 23p.100 of our patients had ischemic strokes, especially large vessel strokes, i.e three times more than in an age-matched control study performed in a recent survey in our country, which is a new finding in contradiction with previous reports mentioning that Parkinson's disease may be a protective factor against stroke. This finding opens new directions for further studies concerning some shared mechanisms in both diseases associated with age. Predominantly tremulous parkinsonism (46p.100) and progressive supranuclear palsy patients (PSP) (40p.100) had the highest prevalence of cerebrovascular disease of all subgroups of parkinsonism, especially lacunar infarcts, which is in accord with a higher frequency of hypertension in these subgroups according to a recent study of ours. Transient ischemic attacks or hemorrhages were not more frequent than in the general population. We did not find a higher frequency of head trauma except for Parkinson's disease, but a trend for a higher frequency of headache and migraine. Brain tumors were more frequent in Parkinson's disease and hydrocephalus and radiculopathies in parkinsonism in general when compared to age-matched populations from the literature. Polyneuropathies were more frequently observed in familial parkinsonism only, but myopathies and cranial neuropathies were not more frequent in our patients. Epilepsy was significantly less frequent in parkinsonism, especially in Parkinson's disease, infectious diseases of the nervous system were rarely encountered, and restless legs syndrome was surprisingly not more frequent than in a normal population. Dementia was associated in 20p.100, but multiple sclerosis is noticeably absent.
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PMID:[Neurological comorbidity in parkinsonism]. 1124 May 47

Vascular parkinsonism (VP) is characterized by predominantly lower body involvement with gait impairment and postural instability, often without tremor, and by relative levodopa unresponsiveness. Neuroimaging studies demonstrate multiple infarcts or ischemic changes in periventricular white matter. Anticardiolipin antibodies (ACLA) are associated with hypercoagulable states and increased stroke risk. Review of our Movement Disorders Clinic records identified 44 individuals with a diagnosis of VP. ACLA have been obtained in 22 of these patients (mean age, 78.3 years; mean Mini-Mental Status Exam score, 25.8). Gait disturbance was the initial clinical feature in 82% of the patients, and levodopa responsiveness was present in 18% of those treated. In 9 of the 22 (40.9%), ACLA immunoglobulin G was positive. No significant differences in clinical features or risk factors (hypertension, diabetes, coronary artery disease, and clinical stroke) were evident between ACLA+ and ACLA- groups. Since the presence of ACLA in individuals with stroke is usually treated by full-scale anticoagulation with warfarin, our findings raise the question whether such treatment should also be used in persons with VP who are ACLA positive.
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PMID:Anticardiolipin antibody in vascular parkinsonism. 1236 May 48

Symptoms or signs of abnormal autonomic nervous system function occur commonly in several neurological disorders. Clinical evaluations have depended on physiological, pharmacological, and neurochemical approaches. Recently, imaging of sympathetic noradrenergic innervation has been introduced and applied especially in the heart. Most studies have used the radiolabeled sympathomimetic amine, (123)I-metaiodobenzylguanidine. Decreased uptake or increased "washout" of (123)I-metaiodobenzylguanidine-derived radioactivity is associated with worse prognosis or more severe disease in hypertension, congestive heart failure, arrhythmias, and diabetes mellitus. This pattern may reflect a high rate of postganglionic sympathetic nerve traffic to the heart. Many recent studies have agreed on the remarkable finding that all patients with Parkinson's disease and orthostatic hypotension have a loss of cardiac sympathetic innervation, whereas all patients with multiple system atrophy, often difficult to distinguish clinically from Parkinson's disease, have intact cardiac sympathetic innervation. Because Parkinson's disease entails a postganglionic sympathetic noradrenergic lesion, the disease appears to be not only a movement disorder, with dopamine loss in the nigrostriatal system of the brain, but also a dysautonomia, with noradrenaline loss in the sympathetic nervous system of the heart. As new ligands are developed, one may predict further discoveries of involvement of components of the autonomic nervous system in neurological diseases.
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PMID:Imaging of the autonomic nervous system: focus on cardiac sympathetic innervation. 1508 63

Neuroleptic malignant syndrome (NMS) is an uncommon potentially fatal side effect of neuroleptic drugs, characterized by movement disorder, altered mental status and autonomic instability. A single dose of clotiapine was administered to an 11-year old male with acute psychosis. The previously healthy child had signs consistent with NMS including hyperthermia, hypertension, motor and mental changes. Repeat examination performed two weeks later, demonstrated that while his hyperthermia subsided, his mental status deteriorated. Olanzapine was administered, after which the child had hyperthermia, dystonia and more pronounced restlessness, once again consistent with NMS. He developed respiratory failure and was intubated and mechanically ventilated. Lorazepam, dantrolene and bromocriptine were administered as treatment of possible NMS. His mental condition, movement disorder and autonomic dysfunction improved significantly. Two weeks later, the patient was discharged in good general condition without the need for any ongoing medical treatment. There are only few case reports of NMS in children treated with olanzapine, an atypical antipsychotic. In children, caution must be exercised when prescribing antipsychotics, particularly atypical antipsychotics as these drugs may cause NMS. Because of the low incidence of NMS, a high index of suspicion is needed to identify cases so prompt treatment can be undertaken.
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PMID:Neuroleptic malignant syndrome in a child treated with an atypical antipsychotic. 1553 33

We discuss 2 cases presenting clinically with disabling orthostatic hypotension and severe supine hypertension. This is a common presentation of autonomic failure, and one that challenges conventional treatment. Clinical findings of isolated autonomic failure were the most prominent manifestation in case 1, whereas a movement disorder was the key finding in case 2. The differential diagnosis and treatment of orthostatic hypotension is discussed from a pathophysiological approach. Understanding of the underlying mechanisms of disorders of the autonomic nervous system is fundamental for an effective management of these patients and provides insight into more common disorders such as essential hypertension.
Hypertension 2005 Apr
PMID:Management of hypertension in the setting of autonomic failure: a pathophysiological approach. 1586 34

An 88-year-old female with atrial fibrillation and hypertension, was admitted to our hospital with sudden onset diplopia and somnolence. She had right hemiparesis with bilateral positive Babinski's sign. Additionally, there was bilateral blepharoptosis with right esotropia. With regard to extraocular movement, the patient demonstrated conjugate upgaze palsy and left monocular down gaze palsy (vertical one-and-a-half syndrome: VOHS). Horizontal gaze in the left eye was completely impaired and there was limited abduction of the right eye. Magnetic resonance imaging of the brain showed left thalamo-mesencephalic infarction. On day 4, the vertical eye movement developed into conjugate upgaze and down- gaze palsies. Magnetic resonance imaging of the brain indicated high signal lesion extending into the dorsal portion of the midbrain. It was suggested that the pathway to contralateral downgaze neurons could have been damaged due to the unilateral (left) dosal midbrain lesion before its decussation with the unilateral interstitial nucleus of Cajal, the oculomotor nucleus and the rostral interstitial nucleus of the medial longitudinal fasciculus. This case is considered to be important because there has been no previous report of bilateral vertical gaze palsy due to VOHS in the same patient. Since there are various patterns of ocular movement disorder in the thalamo-mesencephalic portion, careful observations are required to localize the lesions.
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PMID:[Case of unilateral thalamo-mesencephalic infarction with enlargement to bilateral vertical gaze palsy due to vertical one-and-a-half syndrome]. 1823 38


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