Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To establish the difference of mechanism between irritative and paralytic nystagmus, alterations of Na-K-ATPase and succinic dehydrogenase activity in the vestibular sensorineural elements were investigated for 20 guinea pigs, and glucose uptake of the vestibular nuclei for 13 guinea pigs were measured by the [14C]-2-deoxy-D-glucose method. Irritative and paralytic nystagmus were experimentally provoked by introducing K+ into the perilymphatic space. From the results it was concluded that irritative nystagmus is provoked by increased excitability of vestibular sensory cells, while paralytic nystagmus is provoked by decreased excitability. However, the direction of nystagmus was eventually decided by the tonus imbalance between the bilateral vestibular nuclei. The ipsilateral vestibular nucleus was predominant during irritative nystagmus, while the contralateral vestibular nucleus was predominant during paralytic nystagmus.
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PMID:The mechanism of irritative nystagmus and paralytic nystagmus. A histochemical study of the guinea pig's vestibular organ and an autoradiographic study of the vestibular nuclei. 192 91

A study of the brainstem of the rat during horizontal nystagmus using the quantitative 2-deoxy-D-glucose technique reflected changes in the functional activity of cell groups based on their glucose utilization rates. Horizontal nystagmus was induced by unilateral crista ampullectomy of the horizontal canal. Comparisons of glucose utilization rates were made between experimental and control groups as well as from side to side within each group. There was a decrease of the ipsilateral medial and superior vestibular nuclei with a concomitant increase in the contralateral medial vestibular nucleus when compared to control. The medial rectus motor division of the ipsilateral oculomotor nucleus showed an increase whereas the ipsilateral abducens and the ipsilateral nucleus prepositus hypoglossi exhibited a decline in their utilization rates. The extra ocular motor nuclei responsible for the excitatory fast phase of nystagmus utilizes more substrate than those involved in the slow phase. An increase was also measured in the ipsilateral lobule of the cerebellar nodulus. The lateral reticular nucleus showed a bilateral decrease in its glucose utilization rate when compared to control.
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PMID:A quantitative [14C]-2-deoxy-D-glucose study of brain stem nuclei during horizontal nystagmus induced by lesioning the lateral crista ampullaris of the rat. 405 67

Intrathecal ketamine, which has not previously been described in man, has been administered to 16 patients with war injuries of the lower limbs. The first five received varying doses from 5 to 50 mg in a volume of 3 ml of 5% dextrose, to determine a dose-response curve (Group 1). The optimal dose was then administered to a further 11 patients who received ketamine 50 mg in a volume of 3 ml in 5% dextrose with the addition of adrenaline 0.1 mg (Group 2). A distinct sensory level was obtained in all patients. In Group 2, nine of the eleven patients obtained satisfactory surgical analgesia and two required supplementation with local anaesthetic. Central effects (drowsiness, dizziness, and nystagmus) also occurred in nine patients, but they remained conscious throughout; one patient experienced no central effects, and one patient developed dissociative anaesthesia. Central effects were more intense the higher level of block. There were no significant changes in mean systolic arterial blood pressure, pulse, or respiratory rates. Surgical analgesia for the blocked dermatomes lasted for a mean of 58 minutes (range 45-90), and recovery was complete and uncomplicated; mild generalised analgesia persisted for a further one to three hours following return of sensation. Ketamine alone did not produce motor block, but addition of adrenaline resulted in complete motor block, and may have intensified sensory blockade. Motor loss persisted for the same duration as surgical analgesia. Adrenaline neither delayed the onset of central effects, nor reduced their intensity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intrathecal ketamine for war surgery. A preliminary study under field conditions. 649 99

Monocular optokinetic stimulation ( OKS ) in Long-Evans rats enhances the uptake of [14C]2-deoxy-D-glucose (2-DG) in the pretectal nucleus of the optic tract (NOT) and superior colliculus (SC) contralaterally to the open eye regardless of the movement direction. Metabolic increases in NOT and SC are therefore found to be unrelated to the ocular nystagmus that in monocularly viewing rats follows only to OKS nasalward for the seeing eye. Since the oculomotor asymmetry has been attributed to the directional selective properties of NOT neurons responding to nasalward movement in the contralateral visual field but being inhibited by opposite ( temporalward ) movement, the enhanced 2-DG uptakes observed in the present experiments seem to represent the NOT excitatory metabolic work in the case of nasalward movement and the NOT inhibitory metabolic expenditure in the case of temporalward movement.
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PMID:[14C]deoxyglucose uptake of the rat visual centres under monocular optokinetic stimulation. 672 19

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

We report a 65-year-old woman with paraneoplastic cerebellar degeneration (PCD) who showed reduced cerebellar metabolism with preserved blood flow. She was admitted to Gunma University Hospital because of progressive gait and speech disturbances. Neurologic examination revealed nystagmus, dysphagia, explosive speech, reduced muscle tone in limbs, and marked truncal and limb ataxia, and mild hypesthesia in hands and feet. Cranial MRI demonstrated slight cerebellar atrophy. Laboratory findings disclosed high levels of serum CA19-9 and other tumor markers, and positive anti-Yo antibody, indicating that she had PCD. A specimen obtained from an axillary lymph node revealed metastasis of poorly differentiated adenocarcinoma, although systemic and vigorous checkup failed to find its origin. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured using positron emission tomography (PET) 15 months after the onset. CMRO2 was clearly decreased in the cerebellum, while CBF was almost normal. Moreover, PET with 2 18F-fluoro-2-deoxy-D-glucose (FDG) revealed that glucose metabolism was also reduced in the cerebellum. Single photon emission tomography using 99mTc-ethyl cysteinate dimer (ECD) showed a normal blood flow pattern in the whole brain. These results indicated that uncoupling of circulation and metabolism in the cerebellum of this patient. There are several reports showing uncoupling of cerebral perfusion and metabolism in ischemic disorders, encephalitis, mitochondrial diseases, brain tumors, epilepsy and Gaucher disease, although its pathophysiology is not elucidated. Because anti-Yo antibody evidently gives a suppressive influence on the cerebellar neurons, understanding the way the autoantibody acts may give a clue to the mechanism of reduced cerebellar metabolism with preserved perfusion in PCD.
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PMID:[Uncoupling of cerebellar blood flow and metabolism in paraneoplastic cerebellar degeneration: report of a case]. 936 81

We report the case of a patient who experienced a postoperative Wernicke encephalopathy 8 days after a left hepatectomy performed for metastasis related to a rectal cancer. During the six months before surgery the patient lost 10 kg of weight (15%). Moreover, in the postoperative period the patient received exclusively 5% dextrose solution intravenously. On the 8th postoperative day, an alteration of consciousness, a vertical nystagmus and an ataxia led to consider the diagnosis of thiamine deficiency that was then established by the decrease in the transcetolase activity of the red blood cells. Vitamin B1 supply improved the clinical status rapidly and completely. This observation allows to review aetiologies and clinical forms of thiamine shortage. In addition, it stresses the detection of exposed patients and the prevention methods.
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PMID:[Postoperative encephalopathies: thiamine deficiency, an unrecognized etiology]. 1123 77

Alpha-mannosidosis is a disease caused by the deficient activity of alpha-mannosidase, a lysosomal hydrolase involved in the degradation of glycoproteins. The disease is characterized by the accumulation of mannose-rich oligosaccharides within lysosomes. The purpose of this study was to characterize the peripheral nervous system (PNS) and central nervous system (CNS) myelin abnormalities in cats from a breeding colony with a uniform mutation in the gene encoding alpha-mannosidase. Three affected cats and 3 normal cats from 2 litters were examined weekly from 4 to 18 wk of age. Progressively worsening neurological signs developed in affected cats that included tremors, loss of balance, and nystagmus. In the PNS, affected cats showed slow motor nerve conduction velocity and increased F-wave latency. Single nerve fiber teasing revealed significant demyelination/remyelination in affected cats. Mean G-ratios of nerves showed a significant increase in affected cats compared to normal cats. Magnetic resonance imaging of the CNS revealed diffuse white matter signal abnormalities throughout the brain of affected cats. Quantitative magnetization transfer imaging showed a 8%-16% decrease in the magnetization transfer ratio in brain white matter of affected cats compared to normal cats, consistent with myelin abnormalities. Histology confirmed myelin loss throughout the cerebrum and cerebellum. Thus, histology, electrodiagnostic testing, and magnetic resonance imaging identified significant myelination abnormalities in both the PNS and CNS that have not been described previously in alpha-mannosidosis.
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PMID:Histopathology, electrodiagnostic testing, and magnetic resonance imaging show significant peripheral and central nervous system myelin abnormalities in the cat model of alpha-mannosidosis. 1148 56

We present a case of a 25-year-old woman with drowsiness, nystagmus, severe ataxia and areflexia, which developed six weeks after admission to an obstetric clinic for hyperemesis gravidarum. She had been treated with intravenous dextrose and electrolyte solutions and antiemetics. Magnetic resonance imaging (MRI) performed on the fifth day of her neurologic symptoms showed increased intensity in both thalami, periaqueductal grey matter, the floor of the fourth ventricle and superior cerebellar vermis in T2 weighted and FLAIR images. Clinical signs and MRI findings were consistent with the diagnosis of Wernicke's encephalopathy. On the third day of thiamine replacement, neurologic signs improved dramatically In addition to our case, we review 29 previously reported cases of Wernicke's encephalopathy associated with hyperemesis gravidarum, and emphasize the importance of thiamine supplementation to women with prolonged vomiting in pregnancy especially if they are given intravenous or parenteral nutrition.
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PMID:Wernicke's encephalopathy due to hyperemesis gravidarum: an under-recognised condition. 1178 26

Thiamin is a water-soluble vitamin also known as vitamin B1. Its biologically active form, thiamin pyrophosphate (TPP), is a cofactor in macronutrient metabolism. In addition to its coenzyme roles, TPP plays a role in nerve structure and function as well as brain metabolism. Signs and symptoms of thiamin deficiency (TD) include lactic acidosis, peripheral neuropathy, ataxia, and ocular changes (eg, nystagmus). More advanced symptoms include confabulation and memory loss and/or psychosis, resulting in Wernicke's encephalopathy and/or Wernicke's Korsakoff syndrome, respectively. The nutrition support clinician should be aware of patients who may be at risk for TD. Risk factors include those patients with malnutrition due to 1 or more nutrition-related etiologies: decreased nutrient intake, increased nutrient losses, or impaired nutrient absorption. Clinical scenarios such as unexplained heart failure or lactic acidosis, renal failure with dialysis, alcoholism, starvation, hyperemesis gravidarum, or bariatric surgery may increase the risk for TD. Patients who are critically ill and require nutrition support may also be at risk for TD, especially those who are given intravenous dextrose void of thiamin repletion. Furthermore, understanding thiamin's role as a potential therapeutic agent for diabetes, some inborn errors of metabolism, and neurodegenerative diseases warrants further research. This tutorial describes the absorption, digestion, and metabolism of thiamin. Issues pertaining to thiamin in clinical practice will be described, and evidence-based practice suggestions for the prevention and treatment of TD will be discussed.
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PMID:Thiamin in Clinical Practice. 2556 26


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