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PubMed1983

[Familial paroxysmal ataxia responsive to acetazolamide].

From their early twenties, a 56 year-old french woman and her 33 year-old son suffered from paroxysmal attacks of gait ataxia, incoordination of both hands, dysarthria and nystagmus. These attacks lasted from one to three hours and occurred at the rate of one to seven per week. On examination between attacks, there was only a bilateral horizontal and upward-beating gaze nystagmus. This was documented by E.O.G. Biological investigations were normal with the exception of a mild elevation of glucose blood level. Treatment with acetazolamide 250 mg daily, completely abolished the attacks in both patients. These cases meet the criteria of familial paroxysmal ataxia, a disorder only described in the United States up to the present. Although rare, this disease should be recognized because of its dramatic response to acetazolamide.

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PubMed1981

Effect of acetazolamide in blood acid-base and electrolyte values in dogs.

The effects of acetazolamide administration on arterial blood acid-base equilibrium and electrolyte concentrations were evaluated in 13 clinical patients and in a 4-week experiment in 6 conditioned mixed-breed dogs. Findings included persistent acidemia characterized by hyperchloremic metabolic acidosis, elevated partial pressure of oxygen, and mild depletion of potassium. Changes in the partial pressure of carbon dioxide were variable, and there was no change in plasma sodium concentration or osmolality. Measured disturbances were apparent within 12 hours of the commencement of acetazolamide administration, peaked at between 1.5 and 5.0 days, and thereafter stabilized. Abnormalities were restored to normal within 1.5 days following termination of drug administration.

Acetazolamide↗
PubMed1982

Acetazolamide and CO2 in hyperbaric oxygen toxicity.

The role of CO2 in hyperbaric oxygen toxicity was investigated by administering acetazolamide (Diamox), Tris buffer [tris(hydroxymethyl)aminomethane], and sodium bicarbonate by i.p. injection, and by exposure of other groups of animals to an atmosphere of 5% CO2 and 95% O2. All animals were placed in a pressure chamber and maintained at 50 psig in 100% O2 until death. The Tris buffer and the sodium bicarbonate buffer significantly extended time to onset of convulsions and to time of death. Acetazolamide and also 5% CO2 shortened time to onset of convulsions and significantly shortened survival time. These results suggest that increased tissue levels of CO2 play an important role in hyperbaric oxygen toxicity. The cause of death in our animals exposed to hyperbaric oxygen was pulmonary edema secondary to a systemic hypertension.

Acetazolamide↗
PubMed1982

Central sleep apnea. Improvement with acetazolamide therapy.

Respiratory rhythm during sleep may be dependent on blood pH with apneas being associated with alkalosis. Acidification may therefore have therapeutic value in some forms of sleep apnea. We administered acetazolamide to six patients with symptomatic central sleep apnea, a disorder of respiratory rhythm with little or no upper airway obstruction. Sleep studies were carried out before and after one week of drug therapy, during which time the mean arterial pH decreased from 7.42 to 7.34. All six patients had significant improvement, demonstrating a 69% reduction in total apneas. Five of the six patients reported better-quality sleep and decreased daytime hypersomnolence. Subsequent studies in normal subjects showed that acetazolamide, like other agents known to produce a metabolic acidosis, shifted the hypercapnic ventilatory response to the left 5 +/- 0.54 mm Hg. This may be important in mediating the observed decrease in apneas.

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PubMed1978

Changes in the surface of fine structure of choroid plexus epithelium following chronic acetazolamide treatment.

Surface changes in the epithelium of the choroid plexuses of the lateral and third ventricles of rats induced by chronic administration of acetazolamide have been studied by scanning electron microscopy. After 3 weeks atrophic changes were evident, the microvilli and blebs normally seen on the ventricular surface of the cells appeared attenuated, and in extreme cases they disappeared, leaving the cell surface completely denuded. Localized areas of hypertrophy, indicated by secondary spherical budding, were occasionally observed. The atrophic changes accord with the known inhibitory effects of acetazolamide on CSF formation: perhaps the small number of cells undergoing hypertrophy compensate to some extent for the atrophic ones and maintain some CSF secretion.

Acetazolamide↗
PubMed1981

[Immediate effects of intravenous acetazolamide on intracranial pressure (author's transl)].

Nineteen patients with hydrocephalus or head injury were subjected to a continuous intraventricular pressure monitoring and received acetazolamide. Seven mg per Kg body-weight were infused intravenously in one minute. Three patterns of reactions were recorded: 1. a sharp and large rise in cerebrospinal fluid pressure 2. a moderate rise 3. no significant change in C.S.F. pressure. The mechanisms of these responses are investigated: metabolic CO2, which is normally converted rapidly to HCO3- through mediation of carbonic anhydrase within erythrocytes, builds up to produce an immediate effect of cerebral vasodilatation and increases C.S.F. pressure of patients with disturbed compensatory mechanisms. Intravenous acetazolamide may be used as a functional test in patients with ventricular enlargement and normal intracranial pressure. This technique provides useful data about the remaining compensatory capacity for further increases in intracranial volume.

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PubMed1980

Treatment of refractory congestive heart failure and normokalemic hypochloremic alkalosis with acetazolamide and spironolactone.

Combination therapy with a loop diuretic and an aldosterone antagonist can produce normokalemic hypochloremic alkalosis, a complication not previously documented in the literature. This report describes 74 patients who had severe congestive heart failure treated with a combination of furosemide and spironolactone in whom this complication developed. Acetazolamide corrected the metabolic abnormality. The combination of furosemide and spironolactone with intermittent courses of acetazolamide was very effective in the treatment of severe congestive heart failure complicated by normokalemic hypochloremic alkalosis.

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PubMedDate not supplied

[Acetazolamide treatment of a newborn infant with posthemorrhagic cerebral ventricular dilatation].

We report a case of a male newborn delivered by vacuum at 40 weeks of gestation, who presented perinatal asphyxia, neonatal seizures and ventricular posthemorrhagic dilatation. The newborn was treated with Acetazolamide for 45 days until the reduction of the ventricular dilatation. This case shows the efficacy and the absence of collateral effects of Acetazolamide. This therapy suggests that it may be used as an alternative or an adjunct to lumbar punctures. The pharmacol treatment in the posthemorrhagic ventricular dilatation has not been well studied and there are a few related cases in the literature.

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PubMed1994

Evaluation of cerebral vasoreactivity by SPECT and transcranial Doppler sonography using the acetazolamide test.

rCBF SPECT with 99mTc-HMPAO was performed prospectively in 29 patients (3 controls and 26 stroke patients) as well as TCD studies in 20 patients (3 controls and 17 stroke patients) before and after 1 g i.v. acetazolamide. The sensitivity of rCBF SPECT increased from 62% to 77% after acetazolamide provocation in stroke patients. In patients with a reversible neurological deficit, the sensitivity under resting conditions was 50% which increased to 71%, while in cases with a permanent deficit it increased from 75% to 83%. In the evaluation of the cerebrovascular reserve capacity the results of rCBF SPECT and TCD coincided in 91% of the hemispheres. The correlation was statistically significant.

Acetazolamide↗
PubMedDate not supplied

[Idiopathic cupulolithiasis: vasomotor reactivity evaluation of the vertebro-basilar artery by transcranial doppler ultrasonography and acetazolamide test].

Benign paroxysmal positional vertigo (BPPV) or cupulolithiasis is one of the more common peripheral vestibular disorders. Diagnosis is made on the observation of typical positioning nystagmus brought about by the Hallpike manoeuver. In most cases of BPPV, etiology is unknown. Microcirculatory disorders have often been considered responsible for idiopathic BPPV. Few reports have been published on this specific aspect of the problem. In our study we evaluated vertebro-basilar haemodynamics and vasomotory reactivity after Acetazolamide administration in 12 patients with idiopathic BPPV. The results obtained reveal the absence of macrocirculatory impairment in the vertebro-basilar district in basal conditions, but significative vasoreactivity variation after acetazolamide, both in vertebral and basilar arteries. Poor vasomotor reactivity in one vertebral artery was observed in 5 patients and, in two cases, in the basilar artery. Altered vasoreactivity in the middle cerebral arteries was not observed in any case. In the light of these findings, we suggest that a possible inadequate response if microcirculation in the labyrinth, in some particular haemodynamic situations, might cause otolithic damage.

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PubMed1993

Acetazolamide-responsive hereditary paroxysmal ataxia: report of a new family.

Five family members were examined because of occurrence since childhood of recurrent episodes characterized by vertigo, dysarthria and gait ataxia. Analysis of the pedigree was consistent with an autosomal dominant mode of inheritance. Though asymptomatic between attacks, all the patients presented on examination a gaze-evoked and rebound nystagmus associated with a saccadic pursuit, a deficient optokinetic response and an inability to suppress the horizontal oculo-vestibular reflex by fixation; hypermetric saccades and truncal ataxia were also present in most of them. A sixth family member, aged 6 years, was found to present a gaze-evoked nystagmus but was completely asymptomatic. Response of the attacks to acetazolamide therapy (250 mg twice a day) was assessed in two patients and was either partial or complete. A positron emission tomography (PET) study was realized between ataxic spells in one patient and demonstrated a decrease of glucose metabolism in the whole cerebellum, the inferior part of the temporal lobes and the thalami. These PET data as well as the detailed neuro-ophthalmological findings bring new informations about acetazolamide-responsive hereditary paroxysmal ataxia, a rare but probably often misdiagnosed and treatable disorder.

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PubMed1977

The response of the choroidal and cerebral circulations to changing arterial PCO2 and acetazolamide in the baboon.

Having established control values for choroidal and cerebral blood flow in twelve baboons, the response of both circulations to changing arterial PCO2 and intravenous acetazolamide was studied. The blood flow in both circulations varied directly with the PACO2, the magnitude of the response being very similar. There was a 3.6 percent change in both choroidal and cerebral blood flow per millimeter of mercury change in PACO2. Intravenous acetazolamide (25 mg./kg.) produced an increase in flow lasting approximately 50 minutes in both cerebral and choroidal circulations.

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PubMed1996

Cerebral blood flow effects of piracetam, pentifylline, and nicotinic acid in the baboon model compared with the known effect of acetazolamide.

In normal aging humans there is a progressive decrease of oxygen and glucose consumption with a reduction of cerebral blood flow (CBF), which could be responsible for age-related changes in cognitive functions. A baboon model under anaesthesia using single photon emission computed tomography (SPECT) of the brain and the radiopharmaceutical hexamethylpropylene amine oxime (99mTc-HMPAO) has been developed and found to be sensitive to the effects of drugs that are known to increase CBF. In the present study, the effect of two haemorrheologically active drugs, viz a combination of pentifylline (CAS 1028-33-7) and nicotinic acid (CAS 59-67-6) vs. piracetam (CAS 7491-74-9) were compared with the known effect of acetazolamide (CAS 59-66-5) on CBF in the baboon model using the 99mTc-HMPAO split dose method. Acetazolamide (p < 0.05) and the combination of pentifylline and nicotinic acid (p < 0.01) increased the CBF when compared with the control baseline. The CBF was not significantly increased upon treatment with piracetam, pentifylline alone and nicotinic acid alone, when compared with the control values for total brain ratios (p > 0.05). However, an increased regional effect was observed for piracetam. These results indicate that the above haemorrheologically active drugs exhibit specific but different effects on cerebral blood flow with possible clinical implications.

Acetazolamide↗
PubMed1996

[Cerebrovascular reactivity in insulin dependent diabetes mellitus studied by an acetazolamide test].

The aim of this study was to investigate, whether the cerebrovascular reactivity (CR) was altered in diabetes mellitus and to evaluate the influence of diabetes's duration on cerebrovascular reactivity. Transcranial Doppler-Acetazolamide tests were performed on 20 insulin-dependent diabetics and in 19 controls. Patients were divided into two groups, each group consisted of 10 patients: diabetics with > 10 years disease duration and with < 10 years diseases duration. Middle cerebral artery mean velocities were measured at rest and after i.v. administration of Ig Acetazolamide (AZ). There were no differences in the absolute velocities between controls and diabetics. The percentual increase of the mean velocity after AZ was slower and less intensive in longterm diabetics (means +/- SE: 5 min: 19.4 +/- 2.8%, 10 min: 28 +/- 3.6%, 15 min: 25.7 +/- 3.8%, 20 min: 23.9 +/- 4.3%), than that in controls (5 min: 32.3 +/- 4.3% -p < 0.05-, 10 min: 45.1 +/- 4.9% -p < 0.05-, 15 min: 47.5 +/- 4.3% -p < 0.01-, 20 min: 46.5 +/- 4.7% -p < 0.01) as well as in diabetics with < 10 years disease duration (5 min.: 39.5 +/- 7% -p < 0.05-, 10 min.: 49.2 +/- 6.5% -p < 0.05-, 15 min.: 53.9 +/- 8.6% -p < 0.01-, 20 min: 32.9 +/- 5.9% -n.s.). The cerebrovascular reactivity is impaired in diabetics after long duration of the disease. The altered cerebrovascular reactivity might be caused by angiopathy of the cerebral arterioles.

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PubMed1997

Acute hemorrhagic gastritis associated with acetazolamide intoxication in a patient with chronic renal failure.

Acetazolamide (Diamox) is a carbonic anhydrase inhibitor commonly used in patients with glaucoma in order to reduce intraocular pressure. Acetazolamide (AZ) is mostly excreted in the urine, therefore, the blood levels of AZ often tend to increase in patients with chronic renal failure. We experienced a case of chronic renal failure in a patient suffering from acute hemorrhagic gastritis associated with AZ intoxication. A 66-year-old female with chronic renal failure was referred to our hospital because of drowsiness and an acute deterioration of renal function. She had been treated with AZ, 500 mg per every day for eleven days for the treatment of glaucoma. Laboratory studies showed leukocyturia, thrombocytopenia, severe anemia, and tarry stools. The serum concentration of AZ was elevated to a maximum of 76.5 mg/ml. She was thus diagnosed as having AZ intoxication. On further examination, acute extensive hemorrhagic gastritis was also found by gastroscopy. Despite of the administration of intensive therapies, she died of disseminated intravascular coagulation (DIC) and septic shock due to bone marrow depression 6 days after admission. It is generally known that excessive blood levels of AZ inhibit not only the gastric juices but also prostaglandin levels and HCO3- excretion in the gastric mucosal barrier. We thus concluded that an excessive dose of AZ had probably destroyed the gastric mucosal barrier or thrombocytopenia due to bone marrow disorder and thus eventually led to the development of hemorrhagic gastritis. As far as we know, this is the first case report of acute hemorrhagic gastritis associated with AZ intoxication. Even though AZ tends to strongly bind to plasma protein and its clearance is generally poor by hemodialysis (HD), in our patient, HD was observed to be rather effective since the clearance of AZ was 45.8 ml/min on HD and 66 ml/min on direct hemoperfusion (DHP). DHP often reduces the number of platelets, also DHP needs a lot of heparin, therefore, we should have performed HD alone instead of DHP. In patients with an impaired renal function, AZ should therefore be administered very carefully in order to avoid an accumulation of the drug. In addition, HD alone should be used to remove any excessive amounts of AZ from the blood.

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PubMed1997

Reversible pontine ischemia caused by acetazolamide challenge.

We report the findings in a patient with a midbasilar artery stenosis in whom reversible ischemic neurologic deficits developed during cerebral blood flow imaging with acetazolamide challenge. The potential for ischemic complications from acetazolamide challenge is discussed.

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PubMed1976

A comparison between an acetazolamide test and weight tonography in pathological and apathological circulation of the aqueous humor.

In a total of 92 eyes in 46 individuals the outflow facilities obtained by weight tonography, Cton correlated curvilinearly with those estimated by an acetazolamide test, Cacet. The presumed apathological pairs of eyes were those with Cacet above (or equal to) 0.15 and pressure symmetry (right/left). Twenty-one patients referred for glaucoma suspicion (and three normal test persons) showed these characteristics. The eyes appeared clinically healthy even if the pressure range reached 30 mm. Hg. Here Cacet averaged 0.32 but Cton only 0.16; the discrepancy is possibly caused by the outflow obstruction brought about by the high pressures during weight tonography. The presumed pathological eyes (33 from 20 individuals referred for glaucoma suspicion or manifest glaucoma) were those with Cacet below 0.15. They generally showed pressure asymmetry and in some cases pressure values above 30 mm. Hg, and there were in several cases other glaucomatous signs. In this group Cton and Cacet were similar; both averaged 0.09. The acetazolamide test is considered more informative than weight tonography because the test provides at the same time an estimate of the outflow facilities in the normal- or low-pressure range as well as an accurate comparison between the pressures and outflow facilities of the two eyes. The test is time-consuming, however (1 to 11/2 hours).

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PubMed1998

[Beneficial effects of acetazolamide on paroxysmal attacks of girdle sensation in multiple sclerosis].

A 56-year-old woman with a 40-year history of multiple sclerosis (MS) developed paroxysmal attacks of girdle sensation in the Th5-6 dermatomes. The attacks lasted 20-60 minutes and occured up to three times per week. T2-weighted MR imaging of the spinal cord showed high intensity area from Th5 to Th8. Electrocardiography, echocardiography and laboratory findings did not indicate ischemic heart disease; therefore, the paroxysms were attributed to the spinal cord lesions. Attacks were successfully suppressed by acetazolamide 250 mg/day. Although carbamazepine is frequently used to treat paroxysmal attacks in MS, we would like to suggest that acetazolamide may also be beneficial in some patients with paroxysmal symptoms.

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