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FISHER RS 717 MANUAL DEXTERITY







FISHER RS 717 MANUAL DEXTERITY

 
10/14/2017adminComents are closed

Prognosis for patients with brain metastasis remains poor. Whole brain radiation
therapy is the conventional treatment option; it can improve neurological
symptoms, prevent and improve tumor associated neurocognitive decline, and
prevents death from neurologic causes. In addition to whole brain radiation
therapy, stereotactic radiosurgery, neurosurgery and chemotherapy also are used
in the management of brain metastases. Radiosensitizers are now currently being
investigated as potential treatment options. All of these treatment modalities
carry a risk of central nervous system (CNS) toxicity that can lead to
neurocognitive impairment in long term survivors. Neuropsychological testing and
biomarkers are potential ways of measuring and better understanding CNS
toxicity. These tools may help optimize current therapies and develop new
treatments for these patients.

This product is for an ORIGINAL 31 page 1993 service manual for the FISHER
RS-717 MODEL AM/FM STEREO RECEIVER. This service manual. This product is for an
ORIGINAL 31 page 1993 service manual for the FISHER RS-717 MODEL AM/FM. Fisher
Service Manuals User Manuals Printed Reproductions.

This article will review the current management of brain metastases, summarize
the data on the CNS effects associated with brain metastases and whole brain
radiation therapy in these patients, discuss the use of neuropsychological tests
as outcome measures in clinical trials evaluating treatments for brain
metastases, and give an overview of the potential of biomarker development in
brain metastases research. Brain metastases, the most common intracranial tumor
occurring in approximately 10–30% of adult cancer patients and 6–10% of children
with cancer, are a major cause of morbidity and mortality [ ]. The majority of
these tumors metastasize from lung carcinoma, breast carcinoma and melanoma.
Patients often present with headaches, nausea and/or vomiting and seizures. Many
patients also suffer from some form of neurological and/or neurocognitive
impairment which can cause emotional difficulties and affect quality of life.
The prognosis for these patients is poor and without therapeutic intervention
the natural course is one of progressive neurological deterioration with a
median survival time of one month [ ]. Patients treated with whole brain
radiation therapy (WBRT) have a median survival of 3–6 months [ – ].

The addition of WBRT can relieve neurologic symptoms and prevent death from
neurological causes [ ]. Abbreviations: KPS = Karnofsky Performance Status; CNS
= central nervous system.

Methods to increase the efficacy of treatment but limit CNS toxicity are
currently being investigated. To measure the effectiveness of these emerging
treatment modalities various tools will need to be incorporated into clinical
trials. Neuropsychological testing and biomarkers are two such useful tools that
will assist in optimizing radiation delivery methods and in evaluating agents
that modify the effects of radiation. Biomarkers and neuropsychological testing
also may aid in making earlier diagnoses, monitoring disease progression, and
determining prognosis. This review will briefly summarize the current treatment
options available for brain metastases and will review the literature on
neuropsychological outcome measures and biomarkers in this patient population.
Treatment options. WBRT is considered the standard treatment option for patients
who present with multiple brain metastases.

It results in a median survival of 3–6 months [ – ], reduces the recurrence rate
of metastases, and prevents death from neurological causes [ ]. By controlling
and improving neurological symptoms, it improves quality of life in 75 to 85% of
patients [ ].

In addition, WBRT is used in patients with metastases that impinge on important
brain structures or are too numerous for either surgery or SRS to be effective.
WBRT is used in conjunction with surgery and SRS and its combination has been
shown to improve local control [ ]. WBRT is effective and, unlike surgery and
SRS, it treats both gross and microscopic disease. Fahn Tolosa Marin Tremor
Rating Scale Pdf To Autocad.

Table lists the randomized trials that have been performed to determine doses
and fractionation schedules of radiation for patients with brain metastases [, –
]. The results from these studies showed that the differences in dose, timing,
and fractionation do not have a statistically significant difference in median
survival. Currently the most common radiation dose in the United States for
brain metastases is 30 Gy in ten 3 Gy fractions over two weeks.

Surgical resection is used as a treatment option for patients with a favorable
prognosis, surgically assessable metastases and who have minimal extracranial
disease [ ]. In patients with tumor(s) elsewhere in the body under control, the
resection of one or more closely situated metastases can increase survival
significantly. Four randomized trials that have been completed to address the
role of surgical resection of brain metastases are summarized in Table. Three of
the trials demonstrated that combining surgery and WBRT for patients with a
single metastasis significantly extends survival and improves quality of life
when compared to WBRT alone [ – ]. One of the randomized trials failed to show
an increase in survival or a benefit in quality of life [ ]. However, in this
study the patients had lower KPS and a higher incidence of extracranial disease
which may have affected the outcome. Overall these results support the position
that surgical treatment should be utilized in patients with limited extracranial
disease and in those patients with good performance status.

Abbreviatio n: S = Surgery Stereotactic radiosurgery SRS is an alternative to
neurosurgery, in which multiple convergent beams of high energy x-rays, gamma
rays, or protons are delivered to a discrete radiographically defined treatment
volume. SRS can be used to treat single lesions or multiple lesions (usually up
to 3) and can be used to treat deep-seated surgically inaccessible lesions. It
has been shown in several large retrospective analyses to be equivalent to
surgery [, ]. Results from one randomized trial and several retrospective
studies have shown that when SRS is used after WBRT there is a survival benefit
as well as stabilization or improvement in KPS [, ]. There is no clear consensus
on the survival advantage of using SRS followed by adjunct WBRT. A randomized
trial by Aoyama et al [ ], comparing SRS alone to WBRT plus SRS, did not
demonstrate a survival difference in patients with 1 to 4 brain metastases. In
this study intracranial relapse occurred more frequently in those who did not
receive WBRT [ ].

In a phase II trial looking at patients treated with SRS for renal cell
carcinoma, melanoma, or sarcoma found that there was a high degree of failures
within the brain (approximately 50% of patients by 6 months) with the omission
of WBRT [ ]. The role of WBRT after SRS remains unclear. Some investigators
advocate the omission of WBRT after SRS because SRS has excellent local tumor
control for single metastasis and withholding WBRT will spare the patient from
the neurocognitive deficits associated with WBRT.

Others argue that many patients initially treated with SRS either have
micrometastases or will develop recurrent brain metastasis and thus should
receive WBRT for local and distant tumor control. Radiosensitizers and WBRT.
Radiosensitizers are chemicals or biological agents that increase the lethal
effects of radiation on the tumor without causing additional damage to normal
tissue. Efaproxiral (RSR13) is one example of a radiosensitizer that has shown
some promise [ ]. It is an allosteric modifier of hemoglobin that works by
decreasing the binding affinity of hemoglobin to oxygen thus permitting greater
oxygenation of hypoxic tumor cells and enhancing the effect of radiation. In
addition to this example, other agents have been investigated in clinical trials
(Table ) [ – ]. Overall these studies have produced mixed results, some have
shown a slight survival benefit, while the majority of studies have not shown a
difference in survival.

These results have not been strong enough to bring any of these agents into
routine clinical care. At this time there are several clinical trials underway
involving other potential radiosensitizers. Study (ref) Year n Radioenhancer
(Gy)/number of fractions Median Survival (months) WBRT + RS vs WBRT Eyre et al.

[ ] 1984 111 metronidazole 30/10 3.0 vs 3.5 DeAngelis et al. [ ] 1989 58
lonidamine 30/10 3.9 vs 5.4 Komarnicky et al.

[ ] 1991 779 misonidazole 30/6-10 3.9 Phillips et al. [ ] 1995 72 BUdR 37.5/15
4.3 vs 6.1 Mehta et al. [ ] 2003 401 motexafin gadolinium 30/20 5.2 vs 4.9 Shaw
et al. [ ] 2003 57 efaproxiral 30/10 7.3 vs 3.4 Suh et al. [ ] 2006 515
efaproxiral 30/10 5.4 vs 4.4 Knisely et al.

[ ] 2008 183 thalidomide 37.5/15 3.9 vs 3.9. Abbreviations: RS = Radiation
Sensitizer, BUdR = bromodeoxyuridine Chemotherapy for brain metastases The role
of conventional chemotherapy has traditionally been limited by the presence of
the blood brain barrier and by the potential resistance to chemotherapeutic
agents. Conventional chemotherapeutic agents include topotecan, cisplatin,
paclitaxel and temozolomide. Temozolomide, a second-generation alkylating agent,
has 100% bioavailability and readily crosses the blood-brain barrier.

Phase II results show that temozolomide is well tolerated and gives an
improvement in response rate [ ]. Preclinical data has also shown that
temozolomide could be combined with radiation to enhance its effect [ ]. Agents
that are being currently investigated include gefitinib, lapatinib, valproic
acid and thalidomide. Future success of chemotherapy will hinge on the
development of new agents that have improved penetration into CNS. CNS effects
of radiation therapy for brain metastases. WBRT, the standard of care for brain
metastases, decreases the tumor burden, which delays neurocognitive decline and
maintains quality of life.

However, WBRT also can cause brain injury and neurologic complications. There is
risk of dementia in long term survivors of brain metastases treated with WBRT [,
], which is thought to be dependent on the total dose of radiation, the size of
the irradiated field, and the fraction size. Understanding and measuring the
neurotoxicity associated with WBRT as well as SRS is important for evaluating
different treatment regimens beyond the effects on survival and time to disease
progression. Pathophysiology of radiation induced CNS toxicity Radiation
predominantly causes vascular endothelial damage and demyelination of white
matter leading to white matter necrosis [ ]. Clinically, radiation injury of the
brain can be divided into three categories: acute, subacute and late. Acute
effects occur within the first few weeks of radiation treatment and are likely
caused by cerebral edema and disruption of the blood brain barrier. Symptoms
include drowsiness, headache, nausea and vomiting.

Subacute encephalopathy occurs at one to six months after the completion of
radiation and its mechanism of damage is believed to be due to diffuse
demyelination. Symptoms, which resolve in several months, include headache,
somnolence, fatigability, and a transient impairment in cognitive functioning.

Late effects are seen six months after radiation and are usually due to damage
of the white matter tracts caused by injury to vascular endothelial cells,
axonal demyelination, and coagulation necrosis. These late effects usually cause
permanent and progressive memory loss and can lead to severe dementia [ ]. The
incidence of radiation induced dementia is not well studied. The most commonly
cited study is from a retrospective review of 47 patients who survived more than
one year treated with WBRT [ ]. Five (11%) of those patients were reported to
develop severe radiation-induced dementia at one year.

However, four of these five patients were treated with high radiation fractions
(5 or 6 Gy) that are not routinely used. Another study by the same authors
reports an incidences of 1.9 to 5.1%, but once again this retrospective review
included patients treated with unconventional fractions (4 – 5 Gy) [ ]. Rengou
Vs Zaft 2 Plus Isometric Exercises. Contrast enhancing CT findings in these
patients reveal cortical atrophy and hypodense white matter. Autopsies on
patients with severe radiation induced dementia reveal diffuse chronic edema of
hemispheric white matter in the absence of tumor recurrence [ ].

The pathophysiology of late radiation injury is a complex process involving
damage to oligodendrocytes, endothelial cells, neurons, microglia and astrocytes
and the depletion of stem and progenitor cells. It also is a dynamic process
that involves recovery/repair responses with release of various cytokines and
the involvement of secondary reactive processes that result in persistent
oxidative stress [ ]. Vascular damage leading to ischemia and consequently white
matter necrosis is thought to be a major mechanism for late delayed
neurocognitive impairment caused by WBRT. This mechanism is supported by animal
experiments designed specifically to study the long-term cognitive effects of
rats treated with whole brain radiation.

Using this model, investigators found that loss of vessel density appeared
before cognitive impairment with no other gross brain pathology being present,
suggesting cognitive impairment arose after brain capillary loss [ ]. Damage to
the subgranular zone of the hippocampal dentate gyrus also has been suggested as
a mechanism of long term radiation induced cognitive impairment. Recent animal
experiments have shown that this area is extremely sensitive to whole brain
radiation [ ]. Dosimetric planning for WBRT to spare the hippocampal region is
already underway [ ]. Neuropsychological functioning of patients treated with
radiation for brain metastases For many patients with brain metastases,
controlling neurological symptoms, preventing cognitive dysfunction, and
maintaining functional independence are just as important as prolonging
survival. Multiple factors, however, may negatively impact the neurocognitive
functioning of these patients including the presence of the tumor, WBRT, SRS,
neurosurgical procedures, chemotherapy, and other drugs that have neurotoxic
effects such as steroids and anticonvulsants [, ]. Research investigating the
effects of treatment, including WBRT, on the neurocognitive functioning of
patients with brain metastases is limited.

While many studies have evaluated the neurocognitive outcome of patients treated
with radiation, particularly children [, ] and long term survivors of gliomas [,
], the data from these populations are not directly comparable to patients
undergoing WBRT and/or SRS for brain metastases. To examine the neurocognitive
functioning of patients with brain metastases treated with radiation, some
studies used the Folstein Mini-Mental State Examination (MMSE) [ ] while more
recent trials administered a battery of neuropsychological tests. Neurocognitive
impairments prior to radiation Neurocognitive impairment in patients with brain
metastases is common prior to receiving radiation treatment. In studies using
the MMSE to assess neurocognitive status, 8 to 16% of patients were classified
as having dementia [ – ] prior to receiving radiotherapy. Lower MMSE scores at
baseline were associated with greater tumor volume [, ] and death [ ].
Neuropsychological testing was used in a phase III randomized trial to evaluate
whether motexafin gadolinium administered with WBRT could improve neurologic and
neurocognitive outcome and survival in patients with brain metastases [, ].

This trial administered a brief battery of standardized neurocognitive tests as.




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