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Biomedical subjects

M W Fox

Publications and source records attributed to M W Fox.

At least 37 records · Page 2Linked to original sources
PubMed1993

Neuroprotection by corticotropin releasing factor during hypoxia in rat brain.

BACKGROUND AND PURPOSE: Corticotropin releasing factor is an endogenous neuropeptide released by the hypothalamus that activates the pituitary-adrenocortical system in response to stressful stimuli. It has been demonstrated that corticotropin releasing factor increases the excitability of hippocampal neurons in both in vitro and in vivo studies, which may contribute to neurological injury during hypoxia. The purpose of this study was to determine the effects of corticotropin releasing factor and its synthetic competitive antagonist, alpha-CRF, on neuronal synaptic recovery after a hypoxic insult using the hippocampal slice. METHODS: Wistar rat hippocampal brain slices (n = 120) were treated with various concentrations (10(-6) to 10(-11)) of corticotropin releasing factor or its synthetic antagonist during a 10-minute hypoxic episode. Extracellular recording of population spikes was used during and after the hypoxic insult to assess neuronal recovery. RESULTS: Corticotropin releasing factor provided dose-dependent neuronal protection with maximum recovery (37.95 +/- 8.71%) occurring at 10(-9) concentrations. The competitive antagonist alpha-CRF provided a similar degree of recovery at 10(-6) concentration, whereas 10(-9) molar concentration of competitive antagonist resulted in 16.84 +/- 7.68% recovery. CONCLUSIONS: Corticotropin releasing factor provides moderate protection to hypoxic hippocampal neurons in the brain slice preparation. The mechanism of action is unknown but appears to be a direct neuronal effect. These results support the hypothesis that corticotropin releasing factor may act as an endogenous neuroprotective hormone during hypoxia.

Animals↗
PubMed1993

The natural history and management of symptomatic and asymptomatic vertebral hemangiomas.

Fifty-nine cases of vertebral hemangioma were seen at the Mayo Clinic between 1980 and 1990. Vertebral hemangiomas were discovered incidentally in 35 patients, while pain was the presenting complaint in 13 patients. Five patients presented directly with progressive neurological deficit requiring surgery, and six patients had surgery elsewhere for spinal cord compression and were referred for follow-up evaluation. To better define the natural history of these lesions, a historical review of these patients was conducted; progression of an asymptomatic or painful lesion to neurological symptoms was found in only two cases (mean follow-up period 7.4 years, range 1 to 35 years). New-onset back pain followed by subacute progression (mean time to progression 4.4 months, range 0.25 to 12 months) of a thoracic myelopathy was the most common presentation for patients with neurological deficit. Initially, all 11 patients with spinal cord compression underwent decompressive surgery with full neurological recovery. Recurrent neurological symptoms were observed in three of six patients following subtotal tumor resection and postoperative administration of 1000 cGy or less radiation therapy (mean follow-up period 8.7 years, range 1 to 17 years). No recurrences were noted in four patients who had subtotal excision plus radiotherapy between 2600 and 4500 cGy. One other patient had gross total tumor removal without radiotherapy and has not had a recurrence. Based on these patients and a review of the literature, the authors recommend annual neurological and radiological examinations for patients with hemangiomas associated with pain, especially young females with thoracic lesions in whom spinal cord compression is most likely to develop. Radiation therapy or embolization is an effective therapeutic alternative for patients with severe medically refractory pain. Regular follow-up monitoring for patients with asymptomatic lesions is unnecessary unless pain develops at the appropriate spinal level. It is concluded that management of patients with a progressive neurological deficit should include preoperative angiography and embolization, decompressive surgery with the approach determined by the degree of vertebral involvement and site of spinal cord compression, and postoperative radiation therapy in patients following subtotal tumor removal. Operative management and complications are discussed.

Adolescent↗
PubMed1993

Neurological complications of ankylosing spondylitis.

Thirty-three patients with ankylosing spondylitis with or without spinal neurological symptoms requiring surgical intervention were identified in a retrospective review of all cases of spinal disorders treated at the Mayo Clinic during the period from 1984 to 1989. Spinal fractures (traumatic or pseudoarthroses), progressive spinal deformity, rotary instability secondary to atlanto-occipital or atlantoaxial subluxation, and spinal stenosis with associated neurological deficit, pain, or spinal instability were the most common indications for surgery. Of the 41 operations performed, there were 17 cervical, 14 thoracic, and 10 lumbar procedures. Eight patients had two or more disorders at separate spinal levels that required surgery. Preoperative neurological deficits were recorded in 13 patients; these improved following surgery in nine and stabilized in four. This review emphasizes the fragility of the ankylosed spinal column and its inherent susceptibility to fracture with attendant neurological compromise. It also identifies the variety of spinal disorders observed in these patients and discusses their surgical management. The experience with this series suggests that thorough radiological evaluation, extreme caution with endotracheal intubation and with halo-vest applications, early surgical spinal immobilization, and aggressive postoperative mobilization of patients are necessary for a successful outcome. It is concluded that outcomes in these patients can be favorable when managed appropriately.

Adult↗
PubMed1992

Dangerous dogs.

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Animal Welfare↗
PubMed1991

Stereotactic ventrolateralis thalamotomy for medically refractory tremor in post-levodopa era Parkinson's disease patients.

Thirty-six patients with Parkinson's disease and medically refractory tremor underwent stereotactic ventrolateralis thalamotomy at the Mayo Clinic between 1984 and 1989. All patients had been or were being treated with carbidopa/levodopa but with unsatisfactory tremor control. Modern stereotactic techniques, including microelectrode recording, were used to treat 36 patients, of whom 31 (86%) had complete abolition of tremor and three patients (5%) had significant improvement. Tremor recurred in two patients within 3 months of surgery; however, the remaining patients suffered no recurrence of tremor during follow-up periods ranging from 14 to 68 months (mean 33 months). Persistent complications (arm dyspraxia, dysarthria, dysphasia, or abulia) were noted in five patients but were a source of disability in only two. It is concluded that thalamotomy in carefully selected patients is a beneficial operation for the control of medically refractory parkinsonian resting tremor.

Adult↗
PubMed1990

Selected neurologic complications of pregnancy.

Many neurologic disorders, such as eclampsia, pseudotumor cerebri, stroke, obstetric nerve palsies, subarachnoid hemorrhage, pituitary tumors, and choriocarcinoma, can develop in the pregnant patient. Maternal mortality from eclampsia, which ranges from 0 to 14%, can be due to intracerebral hemorrhage, pulmonary edema, disseminated intravascular coagulation, abruptio placentae, or failure of the liver or kidneys. Associated fetal mortality ranges from 10 to 28% and is directly related to decreased placental perfusion. Pseudotumor cerebri can be associated with serious visual complications; thus, the therapeutic goal is to prevent loss of vision. The risk of stroke in the pregnant patient is 13 times the risk in the nonpregnant patient of the same age. The major causes of stroke in pregnant patients are arterial occlusion and cerebral venous thrombosis. Lumbar disk prolapse is common in pregnant patients, and lumbosacral plexus injuries can occur during labor or delivery. In addition, peripheral nerve compression or entrapment syndromes are thought to be caused by the retention of fluid during pregnancy. The incidence of subarachnoid hemorrhage during pregnancy is 1 in every 10,000 patients, a rate 5 times higher than in nonpregnant women. Because of a proliferation of prolactin-secreting cells, the pituitary gland can enlarge dramatically during pregnancy, a change that can disclose a previously unknown tumor or cause a known pituitary tumor to become symptomatic. The incidence of choriocarcinoma is 1 in 50,000 full-term pregnancies but 1 in 30 molar pregnancies. This malignant tumor has a high rate of cerebral metastatic lesions. In addition to these disorders that develop during pregnancy, the pregnant state can affect numerous preexisting neurologic conditions, including epilepsy, headaches, multiple sclerosis, myasthenia gravis, spinal cord injury, and brain tumors. We discuss advice for patients with such conditions who wish to become pregnant, recommendations for medical and surgical management, and surgical considerations for neurologic complications during pregnancy.

Female↗
PubMed1989

Animal waste.

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Abattoirs↗