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Many reports of diabetic ophthalmoplegia have been published from the clinical points of view. However, there have been only three autopsied cases in which the ocular nerves were investigated histopathologically. A 72-year-old housewife was diagnosed to have glycosuria at the age of 67, but no medical treatment was done. She admitted to the hospital, because of acute onset of right eyelid drooping and diplopia for previous four days. She showed complete eyelid ptosis, moderate dilatation of right pupil, loss of light reaction, and extraocular muscle palsy except abduction on the right. Blood pressure was normal. A glucose tolerance test was diabetic and HbA1c was moderately increased. Her diabetes was fairly well-controlled with a diet therapy and injection of lente insulin. Two and a half months after admission, the course of illness became regressive. Seven months later, external ophthalmoplegia was disappeared and only slight anisocoria was seen. She readmitted to the hospital one year and eleven months later, because of anorexia and emaciation. She died of adenocarcinoma of the stomach without chemotherapy. The duration from onset of ocular symptoms to death was two years and one month. At postmortem examination, stomach cancer infiltrated extensively to the abdominal and pelvic viscera, but no metastasis to the nervous system or intraorbital tissues was found. There were mild to moderate atherosclerotic changes in the small-and middle-sized arteries of the kidneys, pancreas and adrenal glands corresponding to her age. Moderate atherosclerosis was found in all of the major arteries including Willis ring, siphon of the right internal carotid artery and Vertebro-basilar one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic ophthalmoplegia--a clinico-pathological study of the first case in Japan]. 269 31

Dose-dependent changes in behavioural patterns and in local cerebral glucose utilization (LCGU) following subcutaneous application of apomorphine were measured in conscious, unrestrained rats by means of a scoring system and of the autoradiographic [C14]2-deoxyglucose technique, respectively. The behavioural patterns of akinesia, ptosis, yawning and penile erections were scored. Akinesia and ptosis were most prominent after 0.02 and 0.07 mg/kg apomorphine but not after 0.18 mg/kg. Maximal scores for yawning and penile erections were obtained after 0.07 mg/kg. LCGU was not significantly changed after 0.07 mg/kg except for decreases in the cingulate cortex and hypothalamus. Apomorphine 0.5 mg/kg decreased LCGU in the cingulate, parietal and occipital cortex, anteromedial and lateral thalamus and lateral habenula but increased it in laminae IV and VI of the sensorimotor cortex, in the parafascicular nucleus of the thalamus, and in some parts of the basal ganglia and related nuclei. Similar changes in LCGU occurred after 2.0 mg/kg apomorphine, which also increased LCGU in the ventral tegmental area. The lower dose did not produce changes in LCGU opposite to those occurring after larger doses. The data obtained with LCGU do not support the idea that behavioural effects after low doses of apomorphine are elicited by activation of dopamine autoreceptors.
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PMID:Alterations in regional energy metabolism in rat brain produced by small and by large doses of apomorphine: possible relations to autoreceptors. 282 Jul 57

1. S-135, 2-(5-methylthien-3-yl)-2,5-dihydro-3H-pyrazolo[4,3-c]quinoline-3- one, bind binds to benzodiazepine receptors with a high affinity and shows pharmacological actions opposite to those of conventional benzodiazepine drugs. 2. S-135 induced no convulsion in mice by itself, but selectively potentiated the effect of subconvulsive dose of pentylenetetrazole. 3. S-135 potentiated rat crossed extensor reflex and Ro 15-1788 completely antagonized this potentiation. 4. S-135 antagonized pentobarbital-induced anesthesia, tetrabenazine-induced ptosis and reserpine-induced hypoactivity and shortened immobilization time in the despair test in mice, indicating that this compound possesses antidepressive properties. 5. S-135 antagonized amnesia in mice and rats in passive avoidance tasks. 6. Glucose utilization in brain areas relating to memory and arousal functions was enhanced following S-135 treatment. 7. These results indicate that S-135 can be a useful drug for activating depressed brain function.
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PMID:Activation of brain function by S-135, a benzodiazepine receptor inverse agonist. 285 84

Effects of dl-1-(4-amino-3-chloro-5-trifluoromethyl-phenyl)-2-tert.-butylamino-etha nol hydrochloride (mabuterol) on the central nervous system, the striated muscle and the carbohydrate and lipid metabolism were investigated in comparison with those of isoprenaline and salbutamol. Mabuterol caused the following changes in behavior: increased touch response (10 mg/kg p.o.), decreased spontaneous movement and ptosis (30 and 100 mg/kg p.o., resp.), observed for 240-300 min. Mabuterol (5 mg/kg p.o. and 2.5 mg/kg s.c.) prolonged the sleeping time induced by hexobarbital Na, but not dose-dependently. Mabuterol depressed reactive movement at 80 mg/kg p.o. and 40 mg/kg s.c. in the rotarod test, at 160 mg/kg p.o. and 40 mg/kg s.c. in the traction test and at 200 mg/kg p.o. and 160 mg/kg s.c. in the inclined plane test in mice, whereas isoprenaline and salbutamol were almost ineffective. Analgesic activity of mabuterol was found in the acetic acid writhing test but not in the bradykinin-induced nociception test. An anticonvulsive effect was not observed. Mabuterol (10 mg/kg i.v.) produced a change in the spontaneous EEG of one of three rabbits, showing synchronization of cortical activity with sedation. Equipotent dose (i.v.) ratios of mabuterol to isoprenaline were 10.2, 30 and 133 in the depression of incomplete tetanic contraction of cat soleus muscle, hypotensive effect and tachycardia respectively, whereas neither indirect nor direct electrical stimulation induced contraction of diaphragm and gastrocnemius muscle was affected. Equipotent dose (s.c.) ratios of mabuterol to isoprenaline were 2.07, 4.64 and 3.21 in increasing plasma levels of glucose, lactic acid and free fatty acids respectively. Mabuterol caused no remarkable change in myocardial glycogen content.
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PMID:Pharmacological studies of mabuterol, a new selective beta 2-stimulant. III: Effects on the central nervous system, striated muscle and carbohydrate and lipid metabolism. 615 58

Seven cases of chronic progressive external ophthalmoplegia (CPEO) have been studied. They all present palpebral ptosis, slowly progressive ophthalmoparesis without diplopia, descending myopathy and hypoacusia. Additional symptoms were small stature in 5 cases, vestibulo-cerebellar dysfunction in 4 cases, cardiac conductive defects in 6 cases, pigmentary degeneration of the retina in 2 cases, endocrine abnormalities in 2 cases. Muscle biopsy displays in all patients numerous ragged red fibers with typical mitochondrial changes, glycogen accumulation and abnormal amounts of lipid droplets. Metabolic studies reveal in all cases abnormal levels of pyruvic and lactic acid both in basal condition and after an oral glucose load. All the patients have been treated with pyridoxine-alpha-ketoglutarate (PAK). This substance is known to reduce pyruvic and lactic acid concentration in normal subjects after muscular exercise. Two months later a reduction of blood pyruvic and lactic acid both in normal condition and after oral glucose load was observed. The AA. discuss the possible physiological mechanism which can explain their findings.
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PMID:Ophthalmoplegia plus: neuropathological and metabolic studies with a therapeutic trial in seven cases. 693 62

A 48-year-old woman was referred to the First Dept. of Int. Med., Nagasaki Univ. Sch. Med., in August, 1979, with a six-month history of recurrent episodes of right-sided painful ophthalmoplegia and diplopia. An epidode affected the right eye, lasted one to two weeks, and relapsed every month. On examination she had a complete ptosis on the right side and pain on the right eye. All extraocular muscle supplied by the 3rd nerve were paralysed. The pupils were equal in size both sides, reacting to light completely. Visual acuity was normal except myopia. All the other cranial nerves and the remainder of central nervous system was normal. Results of thyroid function tests and of lumbar puncture were normal. The glucose tolerance test showed a mild diabetic pattern. Blood and CSF cultures for bacteria, fungi, and acid-fast bacillus were negative. The skull, brain CT scan, and carotid angiogram were within normal limits. A tentative diagnosis of Tolosa-Hunt syndrome was made after an unproductive search for a cause for this woman's painful ophthalmoplegia and unsuccessful treatment of ophthalmoplegia with antibiotics or diet therapy for mild hyperglycemia. The patient was given prednisolone 30 mg daily orally when she had the 9th attack of painful ophthalmoplegia Pain, ptosis, and diplopia disappeared in 5 days and she did not show any recurrence of symptoms over the next 7 months.
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PMID:[The Tolosa-Hunt syndrome: report of a case with recurrent (9 times) painful ophthalmoplegia (author's transl)]. 732 86

A careful history points the urodynamic examination in the right direction and enables the examiner to ask the correct questions. The individual who does the test is the only reliable interpreter of the results of that study. No urodynamic technique is as sensitive or specific as a blood glucose, or even an electrocardiogram. A history of urgency and urge incontinence suggests uninhibited contractility and is a better index of that condition than a cystometrogram. Leakage occurring shortly after a previous operative procedure for stress incontinence suggests type III stress incontinence. A past history of radiation, prior pelvic surgery, neurologic disease, herniated disc conditions, or prior chemotherapy all require a simple cystometrogram to rule out abnormal bladder compliance. Following a simple history and urodynamic evaluation, a physical examination should be performed, searching for urethra hypermobility and genital prolapse. Abdominal leak-point pressure testing is useful to assign broad categories of incontinence. Relatively high leak-point pressures with hypermobility suggest suspension operations will be effective. Low leak-point pressures with hypermobility often require a sling, and very low leak-point pressures with no hypermobility indicate a suitable candidate for a trial of injection therapy.
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PMID:Urodynamic evaluation of stress incontinence. 764 56

The destruction of N-methyl-D-aspartate (NMDA) receptor-bearing neurons by insulin-induced hypoglycemia has long been known to be due to excessively released aspartate and glutamate. In this study, the effects of NMDA-bearing neuron destruction by insulin-induced hypoglycemia on the development of morphine (M) physical dependence, which was found related to functional states of NMDA receptors, were investigated. NMDA receptor antagonists CGP 39551 and MK-801 were used to see whether they could change intensity of precipitated abstinence syndrome by preventing destruction. Therefore, two groups of fasting rats injected IP with physiological saline, and another two groups given IP 10 mg/kg CGP 39551 and 0.5 mg/kg MK-801 received 15 IU/kg crystalline zinc insulin IP. After 2 h, the rats were orally given 2 x 4 ml of 5% glucose solution. On the third day, two pellets containing 75 mg base M were SC implanted to all rats. On the sixth day, they were IP given 2 mg/kg naloxone (NL). Then jumps, wet-dog shakes, and defecation were counted while diarrhea and ptosis were rated for 15 min. The rats given insulin manifested significantly more intense NL-precipitated abstinence syndrome than controls. The rats administered CGP 39551 showed a less intense physical dependence than those injected with only insulin. But, the intensity was still significantly higher than controls. In the rats that received MK-801, the abstinence syndrome was more or less equal to that in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphine physical dependence intensification by hypoglycemia: NMDA receptor involvement. 793 7

Fourteen patients (10 boys, 4 girls) aged from 4 months to 14 years old were diagnosed with mitochondrial disease based on the clinical manifestations together with abnormal muscle mitochondrial morphologies. Their clinical diagnoses included Leigh syndrome, three; Menkes' syndrome, three; Kearns-Sayre syndrome, two; myoclonic epilepsy with ragged fibres, one; and infant-onset progressive myoclonic epilepsy, one; fatal infantile mitochondrial myopathy, one; fatty acid oxidation defect, two; and myopathy with cardiopathy, one. Organs involved other than muscles included central nervous system, ten; heart, six; eye, two; liver, two; and kidney, two. Clinical manifestations varied to include hypotonia, seizures, myoclonus, mental retardation, nystagmus, ataxia, ptosis, ophthalmoplegia, retinal degeneration, muscle atrophy, spasticity etc. Nine had an abnormal rise in lactate after glucose loading. Ragged-red fibres were found in four patients. Abnormal mitochondrial morphology included abnormal accumulation, abnormal cristae pattern of tubular, concentric, or parallel form, some contained osmiophilic inclusion bodies. One patient of Leigh syndrome had had brain necropsy which showed intramyelin splitting of myelinated axons.
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PMID:Clinical manifestation of mitochondrial diseases in children. 821 54

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48


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