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Iloprost, a stable prostacyclin analog, was evaluated clinically for its ability to ameliorate the symptoms of peripheral neuropathy associated with diabetes. In an open, nonrandomized trial, 13 diabetic patients with neuropathy but without proliferative retinopathy received an intravenous infusion of Iloprost at a dose of 10 micrograms, at a rate of 0.1 micrograms/kg/h, twice daily for two weeks. The administration of Iloprost relieved the majority of such subjective symptoms as pain, numbness or sensation of cold and to a lesser extent, such autonomic symptoms as dizziness. In contrast, there was little evidence of objective improvement, e.g., in motor nerve conduction velocity. Iloprost treatment significantly inhibited the platelet aggregation rate stimulated by collagen in vitro. In the one patient tested, thermography revealed an increase in skin temperature by more than 2 degrees C. Side effects associated with Iloprost included headache (3 patients) or aggravation of pain in the extremities (2 patients) and could be ameliorated by slowing the infusion rate or by discontinuing the drug (one patient). Iloprost appears to be safe and effective for relieving the symptoms of diabetic neuropathy. Our results provide the rationale for a double-blind, clinical trial in larger populations of diabetics with peripheral neuropathy.
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PMID:Clinical efficacy of a stable prostacyclin analog, iloprost, in diabetic neuropathy. 170 9

A study of neurological disorders and services is presented. The ten most common neurological diagnoses were headache, back disorders, neuropathy, cerebrovascular disease, dizziness/insomnia, myopathies, soft tissue disorder, intracranial injury, neurological symptoms (numbness, etc.), and Parkinson's disease. The pattern of diseases is similar to that reflected in the prevalence of those in the US. The annual beneficiary rate was 1.6% of the population, the median age was 45 years, and the majority (52%) served were females. There were 1.8 annual services per beneficiary and the median hospital stay was 9 days. Ambulatory care accounted for the majority (62%) of services and 64% of the inpatient services were delivered by neurosurgeons. The majority of the admissions (61%) and of the ambulatory services (55%) were provided in Regina.
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PMID:Neurological disorders and services in Saskatchewan--a report based on provincial health care records. 326 99

Seven cases of subacute central and peripheral neurologic dysfunction developed in 18 workers employed in the manufacture of reinforced plastic bathtubs. Cases were characterized by weight loss, dizziness, paresthesias, muscle weakness, incontinence, memory loss, and loss of peripheral, color, and night vision. Neuropathies began distally, involved both sensory and motor function, and were associated with prolonged sensory latency, muscle fibrillation, and reduced numbers of functioning motor units. One patient developed posterior lenticular cataracts. Slow improvement occurred on removal from exposure, but residual neuropathies persisted for as long as two years. Epidemiologic investigation disclosed that the first case developed approximately two weeks after introduction of a new plastic foaming agent, 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH). All cases occurred in workers exposed directly to BHMH. No new cases developed after use of BHMH was discontinued. A survey of the firm which produced BHMH and of 68 user firms found two additional clusters of mild neuropathy which may have been caused by BHMH. BHMH was withdrawn from distribution following discovery of these cases. Subsequently, BHMH has been shown in rats to be a potent neurotoxin. Adequate premarket testing could have averted this outbreak.
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PMID:Neurologic dysfunction from exposure to 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH): a new occupational neuropathy. 398 40

We defined sudden vertigo as a sudden, unilateral peripheral vestibular dysfunction. The criterion for its diagnosis is a single episode of vertigo without cochlear and central symptoms. Among 20 patients with sudden vertigo there was no difference in clinical aspects between those with CP (canal paresis) (CP% > or = 25%) and those without CP (CP% < 25%). This suggests that sudden vertigo with CP is due to sudden vestibular dysfunction with predominant involvement of the lateral semicircular canal. Basically, vestibular neuronitis is considered to be due to acute unilateral neuropathy of the vestibular nerve. However, since we have no routine examination for evaluating vestibular nerve function, sudden vertigo with CP should be diagnosed as vestibular neuronitis. We then assessed the prognosis of sudden vertigo with CP (vestibular neuronitis). About two years after the onset of CP 4 of 10 patients had recovered. However, patients with persistent CP had a handicap in their everyday life because of the dizziness induced by head movements. The possibility of recovery of vestibular function in response to steroid therapy may improve the prognosis in vestibular neuronitis.
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PMID:[Diagnostic and therapeutic problems in vestibular neuronitis: clinical implications for sudden vertigo]. 762 48

Twenty five diabetics (all insulin dependent) and 20 age and sex matched controls were studied to assess peripheral nerve functions and autonomic (cardiovascular and urinary bladder) nerve functions. Impotence was the commonest symptom followed by postural dizziness, atonic bladder, shooting pains in the limbs and gustatory sweating. Cardiac autonomic neuropathy was found in 60% of the diabetics while 68% of them had diabetic cystopathy. Peripheral nerve dysfunction was present in 80% of the patients. Forty percent of the diabetics had all the three forms of neuropathies (cardiac, urinary bladder and peripheral), while another 40% of the patients had at least two forms of neuropathy.
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PMID:Autonomic and peripheral neuropathy in insulin dependent diabetics. 830 10

Epalrestat is a carboxylic acid derivative which inhibits aldose reductase, an enzyme of the sorbitol (polyol) pathway. Under hyperglycaemic conditions epalrestat reduces intracellular sorbitol accumulation, which has been implicated in the pathogenesis of late-onset complications of diabetes mellitus. Epalrestat 150 mg/day for 12 weeks improved motor and sensory nerve conduction velocity, and vibration threshold compared with baseline and placebo in patients with diabetic neuropathy. Subjective symptoms including pain, numbness, hyperaesthesia, coldness in the extremities, muscular weakness, dizziness, and orthostatic fainting were also improved. Similar benefits were seen in a comparison with historical controls. Epalrestat 300 mg/day for 1 or 3 years was also significantly superior to placebo or no treatment in improving electroretinogram parameters and photo stress recovery time in patients with diabetic retinopathy. Improvements were also documented by funduscopy and fluorescein angiography. Epalrestat appeared most effective in patients with less severe diabetes mellitus and more recent development of late-onset complications. Epalrestat is apparently well tolerated with predominantly minor adverse events reported in clinical trials. Liver enzyme elevations were most commonly reported but generally resolved spontaneously on dose reduction or discontinuation. The effects of age and renal impairment on the efficacy and tolerability of epalrestat require clarification, and data on its use in other late-onset complications of diabetes such as nephropathy are also lacking. Comparisons with other aldose reductase inhibitors are also required to fully determine the role of epalrestat. The suggested ability of epalrestat to prevent the onset of diabetic complications should also be investigated. Thus, available data suggest epalrestat produces some improvement in the late-onset neuropathy and retinopathy associated with diabetes mellitus, although additional trials are required to determine whether ongoing therapy is necessary to maintain the improvements achieved and to confirm tolerability in the long term. Nevertheless, preliminary results suggest that epalrestat may be a useful drug in an area where there is a need for effective therapy.
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PMID:Epalrestat. A review of its pharmacology, and therapeutic potential in late-onset complications of diabetes mellitus. 831 78

Diseases that cause malfunction of the sympathetic nervous system provide insight into how the sympathetic nerves normally modulate responses to stress. This paper discusses insight from a number of such diseases. Transection of the cervical spinal cord leads to autonomic dysreflexia. This syndrome causes episodic hypertension in quadriplegic patients from excess sympathetic activity reflexly activated by bowel or bladder distention. These patients lack cerebral control of spinal sympathetic reflexes. Radiotherapy to the neck can destroy the arterial baroreceptors that monitor blood pressure fluctuations. Patients who lack baroreceptors have exaggerated blood pressure responses to stress. They have episodes of hypertension and hypotension that cause headaches and dizziness. Diabetics and uremics often develop a peripheral sympathetic neuropathy. They have postural hypotension and diminished blood pressure responses to stress. They are often unable to tolerate heat, exercise, or fluid deprivation. Patients with heart failure deplete sympathetic neuronal norepinephrine stores. The continual stress of heart failure diminishes their ability to respond to further stresses such as standing upright or exercising. Patients with diseases of the sympathetic nervous system illustrate that everyday occurrences such as a change in posture or ambient temperature are stresses requiring a marked change in sympathetic nervous activity. Both physical and psychological stresses elicit large initial sympathetic neuronal responses that are subsequently damped by feedback inhibition from structures such as the baroreceptors. Damage to part of these feedback loops leads to exaggerated pressor responses to stress.
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PMID:Abnormal stress responses in patients with diseases affecting the sympathetic nervous system. 841 84

A cross-sectional study was designed to identify a relationship between the presence of symptoms usually related to nervous system involvement as well as other chronic complications of diabetes with three objectively defined degrees of autonomic neuropathy (AN). Symptoms usually related to peripheral sensitive neuropathy and AN were assessed using a questionnaire applied to 132 diabetics (38 IDDM and 94 NIDDM), 65 without and 67 with AN. AN was classified as follows according to 5 cardiovascular autonomic tests described by Ewing: 1) early involvement-1 abnormal test (N = 27); 2) definite involvement-2 or 3 abnormal tests (N = 26); 3) severe involvement-4 or 5 abnormal tests (N = 14). A statistically significant association was observed between degree of autonomic involvement and the presence of the following symptoms: dizziness on standing, dysphagia, vomiting, diarrhea, fecal incontinence, gustatory sweating, urinary retention, numbness and hyperesthesia of the feet or legs. Constipation and cystitis were not significantly related to cardiovascular AN. Only 3% of the patients without neuropathy and with early involvement had four or more than four of the symptoms. The prevalence of proliferative retinopathy and nephropathy was increased among patients with more severe degrees of AN. For IDDM patients there was a positive correlation between the degree of cardiovascular AN and the duration of diabetes. We conclude that: 1) severe cardiovascular AN is usually related to 4 or more of the evaluated symptoms and those patients usually have the other complications of diabetes; 2) severe AN could be a risk factor or an indicator of the same underlying process that determines the beginning of proliferative retinopathy and/or nephropathy.
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PMID:Relationship between the degree of cardiovascular autonomic dysfunction and symptoms of neuropathy and other complications of diabetes mellitus. 858 Aug 65

We evaluated the question of whether the chemosensitizers verapamil and quinine given orally to breast cancer patients failing combination chemotherapy alone would result in additional clinical responses. In vitro studies reported here showed verapamil sensitization of Adriamycin resistance in 18.8% of fresh human breast cancer specimens tested. Patients (27) were first treated with cyclophosphamide, vincristine, Adriamycin and dexamethasone (CVAD) alone. Verapamil and quinine were added in patients with tumors failing to respond or progressing on CVAD alone. Following treatment with CVAD alone there were no complete remissions and 3 patients (11%) developed partial remissions lasting 5.5, 8, 10.5 months. With the addition of verapamil and quinine to the CVAD regimen, one patient (4%) developed a complete remission of 11.8 months duration and 4 additional patients (15%) developed partial remissions lasting 2.8, 17.3, 19 and > 40 months. Thus, the overall rate of CVAD sensitization by verapamil and quinine was 19%. Treatment with CVAD plus verapamil and quinine was generally well tolerated with observed toxicities including: myelosuppression, neuropathy, Cushingoid symptoms and tinnitus and/or dizziness due to quinine. We conclude that addition of the non-cytotoxic chemosensitizers verapamil and quinine to CVAD in patients failing CVAD alone results in additional clinical responses in a small percentage of patients, some with long term durations. The results of this study lend credence to the notion that non-cytotoxic chemosensitizers can enhance the clinical activity of combination chemotherapy and the search for more effective and less toxic chemosensitizers continues.
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PMID:Combination chemotherapy with cyclophosphamide, vincristine, adriamycin, and dexamethasone (CVAD) plus oral quinine and verapamil in patients with advanced breast cancer. 911 20

Patients with acoustic neuromas have several treatment options. The appropriate individual treatment decision and expected control rates and risks for the individual techniques have been outlined in several texts [1-4, 6-8]. This article describes radiosurgery toxicity in those patients with acoustic neuromas who have intracanalicular disease. 52 patients with 54 acoustic neuromas were treated between September 1993 and April 1997. 14 tumors were intracanalicular lesions, with a mean diameter <1 cm and volume <1 cm3. Dose to the periphery of the intracanalicular lesion extension ranged from 12-18 Gy (mean 16 Gy). The margin isodose was 40-60% (mean 47%). 32 isocenters were used to treat the 14 intracanalicular tumors (mean 2.3 isocenters per patient). At a mean follow-up of 18 months (range 1-39 months), 12/12 or 100% of the intracanalicular lesions demonstrated regression or no change in size on subsequent imaging. The following acute side effects were observed posttreatment in intracanalicular tumors: diminished hearing 14%, facial neuropathy 43%, trigeminal neuropathy 21%, balance disorder 14%, dizziness 7%, and headache 7%. Facial and trigeminal neuropathy, balance disorder, dizziness, vertigo and headaches were more common in patients with intracanalicular tumors than those with an extracanalicular extension. Although it has been suggested that small acoustic neuromas (i.e. <1 cm3) tolerate doses of 18 Gy with acceptable toxicity, when the lesion is located in the auditory canal a lesser dose may be warranted to minimize potential side effects. For now, our center has established a protocol that limits radiosurgical stereotactic intracanalicular peripheral doses to 12 Gy until further toxicity studies have been collected and reviewed.
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PMID:Stereotactic radiosurgery toxicity in the treatment of intracanalicular acoustic neuromas: the Seattle Northwest gamma knife experience. 978 39


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