Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

We report three children with benign paroxysmal torticollis (BPT) and review the literature. BPT represents a self-limited disorder that occurs mainly in infancy and in females. The condition is characterized by recurrent spells of torticollis which may, or may not, be accompanied by other symptoms such as vomiting, pallor, ataxia, irritability and drowsiness. The diagnosis of BPT should be established clinically, although, in some cases, it is necessary to rule out conditions such as posterior fossa tumor, cervical dislocation, ocular palsy, dystonia due to side effects of drugs, or Sandifer's syndrome. The etiology of the syndrome remains unknown and, at present, there is no effective therapy.
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PMID:[Benign infantile paroxysmal torticollis. Apropos of 3 cases]. 305 50

Ten clinically healthy cats were allotted into 2 groups. Group A was given the low (60 ml), and group B was given the high (120 ml) recommended dose of a commercial hypertonic sodium phosphate enema. Enema retention was enforced. All cats developed clinical and/or laboratory abnormalities, with group B cats being more severely affected. Clinical signs that occurred rapidly included depression, ataxia, vomition, bloody diarrhea, mucous membrane pallor, and stupor; tetany was not seen. One cat in group B died. Laboratory abnormalities included hypernatremia, hyperphosphatemia, hypocalcemia, hyperglycemia, calculated hyperosmolality, and metabolic acidosis with high anion gap probably due to hyperlacticacidemia. There were no significant gross or microscopic lesions associated with enema administration. Therefore, the use of hypertonic sodium phosphate enema at recommended doses is potentially dangerous to cats.
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PMID:Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. 401 52

Bilateral ocular metastatic squamous cell carcinoma was diagnosed in a cat. Ophthalmic signs included bilaterally swollen optic discs, choroidal pallor, and retinal vascular engorgement. A retinal detachment was apparent in the left eye and retinal edema and hemorrhage in the right eye. Systemic signs of progressive visual impairment, ataxia, and weakness were noted. The patient's condition continued to deteriorate despite therapy with systemic antibiotics and corticosteroids, and euthanasia was performed. The diagnosis was made upon histologic examination that revealed metastasis of malignant squamous cells to both globes, the brain, and lungs.
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PMID:Metastatic ocular squamous cell carcinoma in a cat. 651 28

Aqueous and organic extractions of ground seeds of Cassia occidentalis were obtained. Chickens were dosed with extracted material to assess the toxicity of the extracts. Organic extracts with methanol, ethanol, chloroform, ethyl acetate, and benzene were ineffective in removing the toxin from the seeds. Aqueous extractions, using 25 mM sodium bicarbonate or 250 mM sodium citrate, removed the toxin from the seeds, but left the toxin bound to particulate matter in the extract. Addition of Triton X-100 to the aqueous buffers effectively solubilized the toxin from the particulate matter. Signs of intoxication in the chickens were loss of weight, weakness, diarrhea, hypothermia, occasionally ataxia, and recumbency; then death. Gross lesions included paleness of skeletal and cardiac muscles and congestion of the liver. Microscopic lesions in muscle tissue were vacuolation, proliferation of sarcolemmal nuclei, and separation of myofibrils. Electron microscopic examination revealed disruption of mitochondrial cristae and swelling and rupture of mitochondria.
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PMID:Preliminary isolation of a myodegenerative toxic principle from Cassia occidentalis. 688 74

Complications from mydriatic and cycloplegic drugs are rare compared with their extensive use. Adverse effects are often related to dosage or other factors. The ocular complications include increased intraocular pressure, pigmentation of the conjunctiva and cornea, pigment in the anterior chamber, lacrimal duct blockage, macular edema, corneal endothelium damage, hyperemia, allergy, discomfort, and blurred vision. The systemic complications are those common to sympathomimetic and parasympatholytic drugs and include tachycardia, hypertension, headache, faintness. pallor, trembling, excessive sweating, palpitations, arrhythmias, confusion, hallucinations, drowsiness, ataxia, flushed skin, high fever, dysarthria, thirst, dry mouth, convulsions, disorientation, nervousness, coma, and death. An understanding of all possible side effects is of paramount importance to those using these drugs in the treatment of anticholinesterase poisoning. This review is intended as a ready reference to the adverse effects of mydriatic and cycloplegic drugs.
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PMID:Mydriatic and cycloplegic drugs: a review of ocular and systemic complications. 703 29

A previously healthy 10-year-old girl suffered sudden, binocular visual deterioration. During the next few years her neurologic and visual condition progressively worsened and she developed hypertension, seizures, ataxia, and lactic acidemia, leading to death at the age of 16 years. Bilateral optic disk pallor was followed by the loss of the foveal reflex and pigmentary maculopathy, manifested as disorganization of the retinal layers, loss of ganglion cells, degeneration of the photoreceptors and nuclei, and irregular infiltration of the retina by pigment epithelial cells. The optic nerves and tracts showed central axonal loss. Bilateral, multifocal symmetric areas of cerebral atrophy and necrosis of the neuropil and neurons in the cerebral cortex, basal ganglia, and thalamus were observed; neurons persisted in the dorsal medulla, despite neuropil degeneration.
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PMID:Pigmentary macular degeneration with multifocal necrotizing encephalopathy. 729 3

Salt toxicosis was confirmed in a flock of 20,000 thirteen-week-old tom turkeys experiencing an increase in mortality. Clinical signs included polydipsia, diarrhea, ataxia, incoordination, tremors that progressed to depression, sternal and lateral recumbency accompanied by torticollis, and death. Mortality over a 5-day period was 6.7%. Necropsy lesions included pallor and dehydration of pectoral muscles, hepatic congestion, and fluid-filled small and large intestines. Microscopic lesions consisted of bilaterally symmetrical areas of necrosis within the cerebral hemispheres accompanied by vascular congestion and edema, as well as hyalinization of the glomerular capillary walls of the kidney and eosinophilic granular casts in the renal tubules. Average salt concentration in the feed from affected houses with 8.04%.
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PMID:Salt toxicosis in commercial turkeys. 779 77

We present two siblings with hereditary cortical cerebellar atrophy (CCA), who showed peculiar clinical features. Their unaffected parents are cousins. The mode of inheritance in this family was autosomal recessive. Both patients developed involuntary movement and ataxia during the fourth decade. The proband (patient 1) was the elder sister. She developed choreoathetoid involuntary movement and cerebellar ataxia at the age of 32. At the age of 39, she showed mental deterioration and marked gait disturbance due to severe ataxia and amyotrophy. At the age of 40, she took medication for hypertension. At the age of 42, she was bedridden and had generalized convulsions and dysautonomia. Involuntary movement continued until her death at age 44. She had amenorrhea since the age of 25 years. Neuropathological findings. The brain weighed 1,010 g. We found marked degeneration in the cerebellar cortex including the molecular, Purkinje cells, and granular cell layers, and in the inferior olivary nuclei. In the basal ganglia, the putamen and caudate nuclei were moderately affected, but the substantia nigra and globus pallidus were spared. The cerebral cortex was spared, but the cerebral white matter showed diffuse myelin pallor without fibrillary gliosis. In the pons, the volume of the tegmentum was moderately decreased, but the base was spared. The spinal cord was normal. The findings of the patient differed from those of the case originally reported by Gordon Holmes in 1907. Holmes autopsied a case showing severe degeneration in both the cerebellar cortex including all three layers and the inferior olivary nucleus as in our patient. However, the striatum of his case spared and the patient did not develop involuntary movement as did other patients. The patients presented here should be distinguished from Holmes' original case clinicopathologically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Autosomal recessive hereditary cortical cerebellar atrophy with striatal degeneration--two siblings showing choreoathetoid movement, ataxia, dementia, and amenorrhea]. 806 39

This report consists of 13 patients who on retrospective analysis had had periodic symptomatology in the first 2 years of life, and who on later evaluation were determined to have juvenile migraine. The commonest early expression consisted of vomiting, accompanied by behavioral change. Seven of 13 showed some indication of headache. Other symptoms such as sleep relief, pallor, and vertigo or ataxia were relatively common. A family history of migraine, primarily maternal, was found in 11 of 12 patients in whom it could be evaluated.
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PMID:Migraine in the infant and toddler. 815 Oct 93


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