Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Fahr's Disease" is characterized by bilateral and symmetrical calcifications of the Globus Pallidus (systematically extending to the Commisura Anterior and the Capsula Interna, and less commonly to the Putamen, the Centrum Semi-Ovale and the Cerebral Cortex), and of the Cerebellar Nucleus Dentalus (with spreading to the White Matter and the Cortical Lamellae). Lesions or absence of Parathyroids are frequently related, with subsequent metabolic disorders of Phosphorus and Calcium, but idiopathic cases without hypoparathyroid disturbances are also found. A Morgagni-Morel Hyperostosis Frontalis Interna is often associated with "Fahr's Disease", and there could be a relationship between these two affections. We found in three cases the association between "Fahr's Disease" and Morel's Nodular Dysgenesis of the Frontal Cortex. Most of the cases are sporadic, but observations with a clear familial incidence are also found. Clinically, various Neurological Disorders (cerebellar, extrapyramidal, pyramidal, dysarthria, epileptic seizures) are often but not always observed; the Psychiatric Disorders found in some cases could be fortuitious associations (psychoses), connected to hypothyroidism (oligophrenia), and in aged patients, to unrelated cerebral vascular or degenerative lesions; very seldom, a dementing state could be connected to the spreading of calcifications to the Cerebral Cortex.
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PMID:[Pallido-dentate calcifications (apropos of 7 anatomo-clinical case reports)]. 69 68

We report a patient with idiopathic hypoparathyroidism associated with unilateral calcification of the basal ganglia and contralateral choreic movements. A 66-year-old woman was admitted to our hospital because of involuntary movements of the left limbs. Two years before the present admission, she had operations for bilateral cataracts. Eight months before admission, she had an onset of severe carpal spasms and pain in both arms and legs. These symptoms improved after one month's rest in a hospital. About a month before admission, she noted progressive difficulty in using her left hand, followed by difficulty in walking due to the abnormal involuntary movement of the left lower limb. Two weeks before admission her carpal spasms appeared again, bilaterally. On admission, she was alert. The general physical examination was normal. Neurological examination revealed choreic movements in the left hand, arm, leg and neck, and grimacing of the left face. She also complained of the spasms and pain in her hands, dysarthria and shortness of the breath. Chvostek and Trousseau signs were positive. Laboratory examination revealed marked decrease in serum calcium level (2.57 mEq/ml) and increase in inorganic phosphorus level (6.40 mEq/ml). Serum level of parathyroid hormone was less than 10 pg/ml. Ellthworth-Howard test was positive, in that the infusion of parathyroid hormone (100 u) elicited a marked increment of the urinary excretions of phosphorus and cAMP. X-ray examination of the spine revealed ossification of the posterior longitudinal ligament in the cervical region. CT-scans of the brain revealed calcification in the region of right globus pallidus and putamen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Unilateral choreic movements in idiopathic hypoparathyroidism]. 152 May 67

We reported two families each propositus of which exhibited extrapyramidal signs and dementia with bilateral basal ganglia calcifications (BGC), while some of the other non-symptomatic family members showed BCG on brain CT by further examinations. Family 1) A 49-year-old woman was normal until her mid 40s when her memory began to fail. At age 40, dementia, finger-tremor and rigidity were observed and with brain CT and Magnetic Resonance Imaging, BCG and dentate calcifications were found. Her two daughters (20 years old and 26 years old) were free of any neuropsychiatric symptoms, but with CT examinations disclosed BCG. Family 2) A 40-year-old man. His symptoms started at 33 years old. He noticed gradually increasing finger-tremor, rigidity and dysarthria. At 40 years he showed mild dementia and BCG on Brain CT. His mother (64 years old) was non-symptomatic but CT showed that she had BCG. In the two families the calcium, phosphorous and parathyroid hormone levels, and Ellsworth-Howard test were normal. Other specific etiology including infections and somatic abnormalities was not discovered. Familial idiopathic basal ganglia calcification was considered to be rare. But the main purpose of this report is to point out that we must pay attention to the possibility of BCG of non-symptomatic family members if one showed dementia and extrapyramidal signs, and BCG on Brain CT in middle age.
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PMID:[Two cases of familial idiopathic basal ganglia calcifications (BCG) with non-symptomatic family members]. 204 99

A very rare case of severe calcification in brain is reported. A 49-year-old man was hit and run by a motorcar in acrossing a road on foot, and he died 1 hour later in an emergency hospital. Medico-legal autopsy was done at 5 hours after his death. The cause of death was cerebral contusion caused by a struck on partieto-occipital region. Unusually severe calcification was observed in the right and left cerebral hemispheres, especially basal ganglia, in the border areas between grey and white matters of frontal, parietal and occipital lobes, as well as in the cerebellar nucleus, cortex and medulla. Histological examination showed severe multiple calcification in the brain tissue. Dispersed deposit of pseudocalcium-Ca and edema were observed around the calcifications. Proliferation of glia cells and decrease of nerve cells were also noted. In his past history, he began to speak distinctly and to stagger since 8 years ago. Three years ago, he collided with guardrail while driving his motorcycle, and he was hospitalized. Calcification in the brain was already revealed in the roentogenographic examination. In the laboratory findings, the data of serum calcium, serum phosphorus and Ellsworth-Haward test were normal. The antibody of toxoplasma, however, showed high level more than X 1,024. After he was discharged, dementia, instability of trunk and dysarthria still continued, and he used to across a crowded road unconcernedly. The cause of the calcification might be suspected to be toxoplasmosis, although neither trophozoites, cysts nor oocysts were found in the brain tissue.
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PMID:[Unusual calcification in brain suspected to be caused by toxoplasmosis: a report of an autopsy case]. 277 37

A patient with renal failure developed hypermagnesaemia, with confusion, drowsiness, and dysarthria. Nevertheless, the dietary magnesium content was low, and investigation showed actual intracellular depletion of magnesium. The cause of this state is not known, though it is presumably connected with a failure to maintain the normal concentration gradient of magnesium across the cell wall. The clinical state and the serum magnesium level returned to normal after treatment with calcium gluconate.
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PMID:Hypermagnesaemia in presence of magnesium depletion in acute-on-chronic renal failure. 576 60

We treated a family with idiopathic calcifications of symmetric areas of the brain, including the basal ganglia, dentate, and cerebral white matter. Dementia, progressive dysarthria, incontinence, propulsive-ataxic gait, fixed facies, and cogwheel rigidity without dysmorphic features develop in affected persons. Calcium, phosphorus, and parathyroid hormone levels were normal in the two siblings tested. The literature is reviewed and five other families with a similar syndrome are identified. These six families seem to be clinically distinct from the larger group of idiopathic cerebral calcifications usually referred to as Fahr's disease.
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PMID:Adult onset idiopathic familial brain calcifications. 650 50

Two patients, one with ataxia, internuclear ophthalmoplegia, muscle weakness, atrophy, fasciculations, and bilateral Babinski's signs, the other with dysarthria, dysphagia, muscle weakness, atrophy, fasciculations, and hyperreflexia, had elevated serum calcium and parathyroid hormone levels, establishing the diagnosis of primary hyperparathyroidism (HPT). Removal of a parathyroid adenoma in one patient and three hyperplastic parathyroid glands in the other resulted in remission of the hyperparathyroidism but left both patients with residual neurological damage. Postmortem examination of the second patient showed typical features of amyotrophic lateral sclerosis. The findings in these patients show that hyperparathyroidism may be associated with signs of severe central nervous system disease and that patients with unexplained neurological signs or symptoms should be checked for hyperparathyroidism.
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PMID:Severe neurological disease associated with hyperparathyroidism. 673 92

The clinical, laboratory and EEG findings of 4 uremic patients on hemodialysis who accidently developed acute hypercalcemia were reviewed. An acute central nervous system syndrome developed, associated with the clinical changes of disorientation, dysarthria, seizures, myoclonic jerks, hallucinations, irritability, confusion, memory and judgment defects plus bizarre behavior. The EEG findings demonstrated diffusely severe slow background activity in all tracings. In addition, the EEG abnormalities as well as the clinical findings disappeared when serum calcium returned to normal. Hypercalcemia, a reversible condition, seems to have been the cause of this clinical syndrome which should be differentiated from dialysis dementia, a condition known to be irreversible and fatal.
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PMID:Acute hypercalcemia in hemodialysis patients: distinction from 'dialysis dementia'. 738 36

This communication concerns a 55 year old woman with a 5 year history of chronic progressive multiple sclerosis (MS) in whom a single external application of extremely low magnetic fields (MF) (7.5 picoTesla; 5 Hz frequency) of 20 minutes duration resulted in a rapid improvement in symptoms including vision, cerebellar symptomatology (ataxia and dysarthria), bladder functions, mood, sleep, cognitive functions and fatigue. Improvement in the patient's symptoms was associated with normalization of the pretreatment abnormal visual evoked potential (VEP) latencies within 24 hours after magnetic treatment. The rapid normalization of the VEP latencies suggests that recovery did not occur as a result of remyelination but probably was related to enhancement of neurotransmitter functions. MF have been shown to alter cellular calcium metabolism which may facilitate axonal conduction in demyelinating plaques. Furthermore, as MF affects the release of the pineal gland's principal hormone, melatonin, which influences the release of monoamines, it is also hypothesized that the effects of picoTesla MF in MS are partly mediated by the pineal gland which has recently been implicated in the pathogenesis of MS (Sandyk, 1992 a).
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PMID:Rapid normalization of visual evoked potentials by picoTesla range magnetic fields in chronic progressive multiple sclerosis. 781 17

It has been reported that 50% or more of patients diagnosed with multiple sclerosis (MS) exhibit speech impairment (dysarthria) which in some cases can be exceedingly disabling. Currently there is no effective medical treatment for the dysarthria of MS which occurs as a result of lesions to the cerebellum and its outflow tracts. It was reported recently that extracranial application of brief AC pulsed electromagnetic fields (EMFs) in the picotesla (pT) range intensity produced in patients with MS sustained improvement in motor functions including cerebellar symptomatology. This communication concerns two MS patients with a chronic progressive course who exhibited severe dysarthria which improved already during the initial treatment with pulsed EMFs and which resolved completely 3-4 weeks later. Since application of EMFs has been shown to alter: (a) the resting membrane potential and synaptic neurotransmitter release through an effect involving changes in transmembrane calcium flux; and (b) the secretion of pineal melatonin which in turn influences the synthesis and release of serotonin (5-HT) and gamma-amino butyric acid (GABA) in the cerebellum, it is suggested that the immediate improvement of the dysarthria occurred as a result of changes in cerebellar neurotransmitter functions particularly 5-HT and GABA rather than from remyelination.
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PMID:Resolution of dysarthria in multiple sclerosis by treatment with weak electromagnetic fields. 874 51


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