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)

A 35-year old woman took 1 gram of isocarboxazide (Marplan) with suicidal intent. She was admitted to hospital approximately six hours later with nystagmus, generalized hypertonia and jaw trismus. Four hours after admission, she became comatose with poor ventilation, increasing rigidity of all muscles and temperature rising to 41.1 degrees C. She was intubated and ventilated. Dantrolen was used for muscular relaxation but because of minor unfavourable experience with dantrolen pancuron was employed instead. After this, the temperature fell and the patient became relaxed. After two days, she was extubated and transferred to psychiatric care in a normal physical state. It is concluded that a non-depolarizing neuromuscular blocking drug should be used in patients with hyperpyrexia caused by MAOI overdose, because of the generally more favourable experience with these drugs and because of the potential hepatoxicity of dantrolen.
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PMID:[Hyperpyrexia following poisoning with a monoamine oxidase inhibitor]. 271 90

Inverse ocular bobbing (IOB) is an uncommon abnormal eye movement. Its characteristics are slow downward eye movement with rapid upward return, a nadir at the extreme of downgaze position and horizontal roving eye movement. We present a case of IOB associated with cerebral embolism and diabetes insipidus. A 69 year-old right-handed woman was admitted because of a consciousness disturbance. She had been well until November 10, 1983, when she was found dysarthric and left hemiplegic. On admission, she was stuporous. There were conjugate deviation to the right, central left facial and hypoglossal palsy, left hemiplegia with spasticity, left hyperreflexia with positive pathologic reflex and anosognosia. A CT scan performed on November 11 showed extensive hypodense area in the region supplied by the right middle cerebral artery. A right carotid angiography revealed multiple occlusions in the top of the right internal carotid artery with poor collateral circulation. After admission, the level of consciousness gradually deteriorated and became comatose on November 18, when the following abnormal eye movements were observed. Following spontaneous horizontal roving eye movement, both eyes deviated downward slowly from midposition, taking 1 to 2 seconds to reach the nadir. The eyes then remained in the position for 1 to 15 seconds, followed by a rapid return to the midposition. These abnormal eye movements are compatible with inverse ocular bobbing (IOB) described by Knobler. Electronystagmography detected typical IOB and spontaneous upward nystagmus. There was no evidence of hypoxia when these abnormal eye movements were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inverse ocular bobbing associated with cerebral embolism and diabetes insipidus--a case report]. 274 84

A 69-year-old male, with a history of a previous subdural hematoma, multistroke dementia and ventricular shunting for hydrocephalus, exhibited while comatose isolated periodic alternating rotatory nystagmus with cyclic pupillary changes and periodic alternating gaze. His simultaneous EEG showed PLEDs and subsequently burst-suppression pattern. The latter abnormality was associated, in addition, to transient eyelid opening, synchronized with the EEG bursts. Complex neuro-ophthalmologic clinical signs, sometimes subtle, may be the sole manifestation of EEG periodic complexes that have potential prognostic and therapeutic implications.
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PMID:Periodic complexes and alternating rotatory nystagmus with cyclic pupillary changes. 279 17

Periods of epileptic nystagmus consisting of rightward eye deviation and right-beating nystagmus, alternating with upward eye deviation and upbeating nystagmus, occurred in a comatose patient with a left hemisphere subdural hematoma and seizures. The periods of upbeating nystagmus were associated with symmetric, low-voltage 3 to 4 Hz bifrontal spikes. Rightward eye deviation and right-beating nystagmus occurred with diffuse, predominantly left hemispheric 4 to 6 Hz sharp waves. No eye movements occurred in the absence of spike and wave activity. These correlations agree with current concepts of the cortical control of saccadic eye movements in monkeys studied by electrical stimulation.
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PMID:Vertical and horizontal epileptic gaze deviation and nystagmus. 279 62

A 67-year-old, non-alcoholic Japanese female case with liver cirrhosis, in the course of admission due to ascites and rupture of the rectal varix, was affected by an unusual type of acute progressive encephalopathy, presenting inattentiveness and slurred speech as initial symptoms. Her consciousness was increasingly clouded. Variable symptoms such as saccadic eye movement, nystagmus, weakness, hyperreflexia, dysmetria, adiadochokinesis and painful dysesthesia were also noted. Laboratory examination disclosed abnormal liver functions, hyponatremia, respiratory alkalosis and normal blood ammonia. Cerebrospinal fluid was xanthochromic and contained slightly increased protein. On CT scan, bilateral symmetrical low density areas were demonstrated in the diencephalon, brainstem and cerebellum. A week after the onset, she was comatose with rigidity of the extremities. Hyperbilirubinemia and severe hyponatremia developed. On the second CT, low density areas extended to the cerebral deep white matter. Her respiration became irregular, and she expired 16 days after the onset. Autopsy disclosed edematous lesions with dark brown discoloration in the medial basal ganglia, ventral diencephalon and mesencephalic tegmentum. Less severely affected lesions with pale yellow discoloration extended into the cerebral white matter, pontine and medullar tegmentum and cerebellar dentate nuclei. In the central lesions, diapedesis of erythrocytes and serum-plasma was marked, with necrosis of the neurons. In the peripheral lesions, diapedesis of less proteinaceous fluid was noted, with less severe neuronal damages. Neither capillary prominence nor gliosis was remarkable. The clinical and pathological features of the present case bore some similarity to those of Wernicke's and Leigh's encephalopathies. However, the patient's age, habitus or clinical course was atypical for the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute encephalopathy with symmetrical, widespread, edematous and necrotic lesions--an autopsy case report]. 280 34

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

We are reporting a rare case of clivus chordoma with fatal hemorrhage in the posterior fossa. A 38-year-old woman afflicted with sudden onset of severe headache and vomiting. On neurological examination, she was mildly lethargic. She had slight dysarthria and nystagmus, but no cranial nerve abnormalities. Craniogram revealed erosive changes in the right petrous bone. CT scan showed a massive intracerebellar hemorrhage and isodense mass in the sphenoid sinus, which were not enhanced by contrast medium. She became comatose and died 3 days later. No operation was performed. Autopsy revealed massive hemorrhage in the posterior fossa and yellowish, gelatinous tumor extending from the right clivus to the sphenoid sinus. Histological examination showed a chordoma. This case demonstrates that the hemorrhage associated with brain tumor, especially in posterior fossa, produces a significant sudden elevation of intracranial pressure and leads clinically to a rapid loss of consciousness and death soon after the onset.
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PMID:[A case of clivus chordoma showing hemorrhage in the posterior fossa]. 306 8

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

In 30 comatose head injured patients vestibulo-ocular responses were elicited by caloric stimulation. Inter- and intra-observer agreement of these responses was studied. The responses were shown in the form of a film to ten doctors who classified them into four categories: no reaction, tonic reaction, paradoxical nystagmus and nystagmus. The level of the coefficient Kappa (a chance-corrected measure of interobserver agreement) was 0.50; this is within the range of levels for most components of clinical examination reported in the literature.
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PMID:Interobserver agreement in assessment of vestibulo-ocular responses. 365 9

A case of spongy glio-neuronal dystrophy is reported. The clinical features included mental and motor retardation in early infancy after a normal birth, and from the age of 4 years increasingly severe attacks of multifocal epilepsy, with prolonged postictal coma, myoclonic twitching and nystagmus, and at times hemiplegia for one to two weeks. Acidosis was present during the periods of postictal coma. Jaundice occurred several days before death at the age of 5 years. Neuropathological examination revealed severe spongy degeneration in the thalamus and dentate nucleus, and the cerebral cortex to a lesser degree, with sparing of the white matter. There was partial necrosis of liver cells and in some areas regenerative nodules. Possible aetiological factors linking the cerebral and hepatic pathology are discussed.
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PMID:Spongy glio-neuronal dystrophy: a degenerative disease of the nervous system. 469 90


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