Outline

Brain Tumors: General Overview

Discuss:

Lisa C. Smith MSN, FNP, AOCN Cancer Centers of the Carolinas Greenville, SC

– Normal brain anatomy and function – Pathophysiology of malignant brain tumors – Epidemiology of malignant brain tumors – Classification of brain tumors and factors in prognosis – Presenting symptoms often seen with malignant brain tumors

The Brain

Hemispheres of the Brain

A soft, spongy mass of nerve and supportive tissues It is connected to the spinal cord Central nervous system = brain and spinal cord Consists of two cerebral hemispheres – the largest area of the brain

Each hemisphere has four sections: Frontal lobe – voluntary movement, language and writing

Temporal lobe – hearing and vision pathways

Parietal lobe – sensory perceptions

Occipital lobe – vision, recognize and identify From A Primer of Brain Tumors: A Patient’s Reference Manual (7th ed.) (p.26), By G. Segal, 2003, Des Plaines, IL: American Brain Tumor Association. Copyright 2003 by the American Brain Tumor Association. Reprinted with permission.

The Brain – The Cerebellum Cerebellum is second largest area of the brain – Located at the back of the head – Consists of two hemispheres – Connected to the brain stem

Function of Cerebellum – Center for balance – Coordination of movement (gross and fine) – Fine movement control – Ability to correct movement – Coordination of muscle contraction/expansion

The Brain – Brain Stem Brain stem is the bottom portion of the brain – Connects the brain to the spinal cord – Includes the midbrain, pons, medulla oblongata, and reticular formation – Cranial nerves IIIIII-XII originate here

From A Primer of Brain Tumors: A Patient’s Reference Manual (8th ed.) (p, 25), by G. Segal, 2004, Des Plaines, IL: American Brain Tumor Association, Copyright 2004 by the American Brain Tumor Association. Reprinted with permission.

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The Brain - Ventricles

The Brain - Ventricles Choriod plexus

Four ventricles:

produces the CSF Function of ventricles

Two lateral ventricles – One in each hemisphere

– To produce CSF – Transport it throughout CNS

Third ventricle is beneath the corpus callosum, callosum, surrounded by thalamus Fourth ventricle is an expansion of central canal of medulla oblongata

CSF is the clear, watery fluid that bathes and cushions the brain and spinal cord From A Primer of Brain Tumors: A Patient’s Reference Manual (8th ed.) by G. Segal, 2004, Des Plaines, IL: American Brain Tumor Association, Copyright 2004 by the American Brain Tumor Association. Reprinted with permission.

Malignant Brain Tumors Neoplasms that originate in the brain itself

Brain Tumors: Malignant

– Can occur in brain parenchyma, meninges, cranial nerves, other intracranial structures – pituitary and pineal glands

Invade and destroy healthy tissue Lack distinct borders – tend to send “roots” roots” Can metastasize to other parts of brain and spine via the CSF

Incidence

Surveillance, Epidemiology, and End Results (SEER)

Among adults, primary brain tumors rank 6th to 8th in frequency of all neoplasms Epidemiologic studies show that brain tumors are becoming increasingly more prevalent

Traditional source for data = Surveillance, Epidemiology, and End Results (SEER) program by the NCI

– As population ages – Appears to be in excess of the improvement in detection rates

Annual incidence of malignant brain tumors for all races from 19951995-1999 was 7.7 per 100,000 personperson-years

Encompasses only malignant tumors In 2004, estimated 18,400 new primary brain tumor cases in the US

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Central Brain Tumor Registry of the United States Central Brain Tumor Registry of the United States (CBTRUS) includes benign and malignant lesions in its data collection In 2002, CBTRUS estimated 39,550 new cases of malignant and benign brain tumors Malignant gliomas are the most common = about 50% of all primary brain tumors

Incidence Gender

Age

– Slight male predominance – 8.0 vs 5.5 per 100,000 personperson-years 199719972001

– Peak incidence age 50

Temporal trends

Race – – –

– Rising incidence rates in industrialized countries, etiology unclear

Caucasians 8.8 vs 4.9 in men 6.1 vs 3.2 in women Surawicz, TS, McCarthy, BJ, Kupelian,V, et al. Descriptive epidemiology of primary brain and CNS tumors: results from the Central Brain Tumor Registry of the US, 1990-1994. Neuro-oncology 1999; 1:14.

Incidence – Tumor Type Gliomas – most common type – approx. 50% of all brain tumors

Glioblastoma multiforme – most aggressive type – 4040-50% of all gliomas

Astrocytomas (grade III) – second most aggressive – 3030-35% of all gliomas

Meningiomas – – 2525-30% of all primary brain tumors

Pituitary tumors – usually benign – 1010-20% of all primary brain tumors

Mortality and Prognostic Factors Overall survival has not improved significantly over the past 50 years (Michaud et al., 2004) Survival rates vary according to: – – – –

Age Histologic grade Duration of symptoms Neurologic performance at presentation (Karnofsky score) – Tumor site – Completeness of resection

Mortality and Prognostic Factors Brain tumors account for only 2% of all cancers, but result in disproportionate share of cancer morbidity and mortality Annual ageage-adjusted mortality rate in the US (1997(1997-2001) = 4.6 per 100,000 personperson-years Five year survival rate for all ages and races = 33 percent According to Jemal et al., about 12,690 patients will die from malignant brain tumors in 2004

Prognostic Factors Favorable prognostic factors = – Young age – High performance status – Lower pathologic grade

Increasing recognition of the influences of inherited and acquired gene alterations on prognosis – Still require prospective survival studies

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Acquired Gene Alterations

Molecular Classification

The genetic epidemiology of CNS tumors is at an exciting phase

Formation of brain tumors involves an accumulation of lesions in genes that regulate cell proliferation, differentiation, and cell death

– Two mechanisms seemed to be involved: – Loss of tumor suppressor genes (deter cells from duplicating) – Activation of protoproto-oncogenes and growth factors

Oncogenes and tumor suppressor genes play critical roles in the pathogenesis of gliomas Example: Glioblastoma multiforme (GBM) may arise de novo, usually in older patients, or evolve from a low grade glioma (secondary GBM) in younger patients

Amplification of the protoproto-oncogene for EGFR has been reported in 2525-50% of glioblastomas and 9% of astrocytomas

Genetic Changes Associated with Gliomas

Other Genetic Abnormalities

Consistent set of genetic changes has been identified in the progression from lowlow-grade to highhigh-grade gliomas: gliomas: – – – – – – – –

Several cytogenetic studies of CNS tumors have shown abnormalities:

P53 = tumor suppressor, 33% of all grades of astrocytomas MDM2 = tumor suppressor, 10% of GBM p15 & p16 = tumor suppressor, deleted in 67% of glioma CDK4 & CDK6 = promoter of cell proliferation, amplified in 15% of cases without p15 or p16 mutations Retinoblastoma = tumor suppressor, 33% of high grade astrocytoma EGFR = oncogene, 3333-50% of high grade astrocytomas PDGFR = oncogene, expressed in all grades of astrocytoma PDGFR = tumor suppressor, in 80% of all GBM

Rasheed, BK, Wiltshire, RN, Bigner, SH, Bigner, DD. Molecular pathogensis of Malignant gliomas. Curr Opin Oncol 1999; 11:162.

– Loss or translocation of parts of chromosome 22 in familial meningioma and acoustic neuroma – Progression to anaplastic astrocytoma is associated with loss of heterozygosity on chromosome 19q and alterations in the retinoblastoma tumor suppressor gene – Gain of one or more copies of chromosome 7 found in 80% of GBM – p53 mutation occurs 4040-80% with GBM p g i i

Giles, GG, Gonzles, MF (1997). Epidemilogy of brain tumors and factors in Prognosis. In A. Kaye & Laws Jr (Eds.), Brain tumors an encyclopedic approach (pp. 47-67). New York: Churchill Livingstone.

Inherited Gene Alterations

Environmental Risk Factors

Only 5% of primary brain tumors are known to be associated with hereditary factors

Literature contains many instances of associations between environmental agents and increased risk of CNS tumors:

– – – – – –

LiLi-Fraumeni syndrome p53 defects (usually associated with LFS) Tubular sclerosis Neurofibromatosis 1 and 2 von HippelHippel-Lindau syndrome Turcot’ Turcot’s syndrome Familial polyposis

– Ionizing radiation – Occupations in electrical and electronics, oil refining, rubber, airplane manufacturing, machining, farming, and pharmaceutical and chemical industries – Diet, this association remains unproven

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Classification of Brain Tumors Reasons for Tumor Grading: – facilitates communication – helps plan treatment – can predict outcome

Grade indicates the degree of malignancy All grading systems have inherent difficulties: – Criteria used is subject to interpretation by pathologist – Tumors are not uniform, sample examined may not be representative of the entire tumor

Histopathologic Classification Done by light microscopy according to the predominant cell type Histologic attempts at developing a classification system date back to the 1830s – German pathologist, Rudolf Virchow, first introduced the term “glioma” glioma” in 1860 – He was the first to attempt a correlation of microscopic to macroscopic features of CNS tumors – Kernohan & colleagues, in 1949, were first to suggest that different histopathologic appearances do not represent separate tumor types, rather, rather, varying degrees of histologic differentiation

WHO Grading System First commissioned in 1976 First published in 1979 encompassing all central nervous system tumors not just intracranial lesions Revised in 1993 and 1997 Recognizes 10 major categories and 107 subcategories of brain tumors Current system combines a tumor nomenclature with an implied grading system – Actual histologic diagnosis directly correlates with the histologic grade of the tumor

Tumor Grading Grade assigned is based on tumor’ tumor’s microscopic appearance: – Atypia: Atypia: similarity to normal cells – Mitotic index: index: rate of growth – Necrosis: Necrosis: indications of uncontrolled growth – Infiltration: Infiltration: potential for invasion and/or spread based on whether tumor has a definitive margin (diffuse or local) – Vascularity: Vascularity: blood supply

The Evolution of Histopathologic Classification In 1950, the Ringertz system was based on the idea that different brain cells give rise to different histologic types of brain tumors – Proposed that astrocytoma consisted of three grades: astrocytoma (Gr 1), astrocytoma with anaplastic foci (Gr 2), glioblastoma multiforme (Gr 3)

In 1981, the St. AnneAnne-Mayo system was based upon the absence or presence of four criteria: – – – –

Nuclear atypia Mitoses Endothelial cell proliferation necrosis

WHO Grading System Grade 1: – Least malignant, usually assoc. longlong-term survival, slowly growing tumors, surgery alone may be effective treatment, ex. Pilocytic astrocytoma

Grade 2: – Relatively slow growing but slight abnormal appearance microscopically, can invade adjacent normal tissue and recur, sometimes as higher grade

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WHO Grading System Grade 3: – By definition these are malignant, actively reproducing abnormal cells and infiltrate adjacent normal brain tissue, recur usually as higher grade

Grade 4: – Reproduce rapidly, irregular appearance under microscope, infiltrate widely, induce growth of blood vessels, also areas of necrosis, glioblastoma multiforme most common

Examples of WHO system Gliomas = 80% of primary CNS malignancies, refers to tumors derived from “glial cells” cells” (i.e. astrocytes, oligodendrocytes, and ependymal cells) Examples of gliomas: gliomas: – Astrocytic tumors – Oligodendroglial tumors – Mixed gliomas

WHO Glioma Grading Astrocytic Tumors: – Astrocytomas: Astrocytomas: low grade, increased cellularity and atypia, no mitoses, endothelial proliferation, or necrosis (Gr 1 & 2) – Anaplastic Astrocytoma: Astrocytoma: exhibit mitoses, no endothelial proliferation or necrosis (Gr 3) – Glioblastomas: Glioblastomas: high mitotic activity with either endothelial proliferation or necrosis (Gr 4)

Oligodendroglial Tumors: – Appear on light microscopy as round cells with perinuclear halos (a (a “fried egg” egg” appearance) appearance) and acutely branching (chicken (chicken-wire) wire) capillary pattern – Anaplastic oligodendrogliomas (malignant): increased cellularity, high mitotic rate, pleomorphism – Manifest with endothelial proliferation and/or necrosis – Considered glioblastomas

Symptom Presentation with Primary Brain Tumors Symptoms present according to: – Location – Tumor size – Amount of edema or mass effect assoc. with the tumor – Degree of infiltration into brain tissue – Whether tumor is located on right or left side of brain Remer, S., Murphy, ME. (2004). The challenges of long-term treatment outcomes in Adults with malignant gliomas. Clinical Journal of Oncology Nursing, 8, 368-376.

Presenting Signs and Symptoms

Neurologic Symptoms Four mechanisms can cause the neurologic symptoms associated with brain tumors: Focal symptoms 1. Invasion of brain parenchyma 2. Brain compression

Generalized symptoms 1. Cerebrospinal fluid obstruction (hydrocephalus) 2. Herniation

DeAngelis, LM, Gutin, PH, Leibel, SA, Posner, JB. (2002) Chapter 3: Principles of diagnosis In LM. DeAngelis, PH Gutin, SA Leibel, & JB Posner (Eds). Intracranial tumors: Diagnosis and treatment (pp 65-80).

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Neurologic Presentation of Brain Tumors Generalized: Headaches – – – –

Seizures Nausea/Vomiting Plateau Waves Neurocognitive dysfunction

Focal: Seizures – – – –

Weakness Sensory Loss Aphasia Visual Spatial dysfunction

Headaches Common initial symptom An exact relationship has not been established between the location of the headache and the location of the tumor Usually intermittent, not throbbing Can be worse in morning or at night Can wake the patient from sleep Worsen with coughing, exercise, or change in position such as bending or kneeling

Generalized Presenting Signs and Symptoms

Seizures The most common symptoms of gliomas and cerebral metastases Can be focal with clinical presentation depending on tumor location – Frontal lobe tumor may cause focal tonictonic-clonic movements involving one extremity – Occipital lobe tumor may cause visual disturbances – Temporal lobe seizure may cause abrupt personality changes with or without typical preseizure auras

Common feature = repetitive nature Presenting symptom in about 2020-60% of patients with brain tumors

Nausea and Vomiting

Neurocognitive Dysfunction: Plateau Waves

Present in approx. oneone-third of patients at presentation

Plateau waves – normally occurring sustained pressure waves within the brain

Result of increasing the ICP at the area postrema of the medulla (Wong et al. 2003)

With brain tumor the baseline ICP can be raised to a level that reduces brain compliance

Usually associated with other neurologic changes such as headache, may be subtle

– Caused by activities that transiently raise ICP – i.e. Valsalva maneuver

– With any additional increase in intracranial fluid volume, even slight, there can be a dramatic elevation in ICP

A significant rise in ICP can temporarily cut off cerebral perfusion, leading to loss of consciousness

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Neurocognitive Dysfunction: Plateau Waves The syncopal episode may trigger a seizure Plateau wavewave-related episodes of loss of consciousness identify patients who require urgent corticosteriods These patients may require neurosurgical intervention

Neurocognitive Dysfunction Most of these deficits are subtle Can include memory problems, mood and/or personality changes Presenting symptom in 3030-35% of patients with brain metastases Patient complaints include: low energy, fatigue, urge to sleep, and loss of interest in everyday activities – Symptoms can be confused with depression

Focal Symptoms

Focal Presenting Signs and Symptoms

Can help identify the location of the tumor Include:

Symptoms by Tumor Location: Brain Stem

Symptoms by Tumor Location: Cerebellum

Brain Stem Tumor:

– Hearing problems, ringing or buzzing sounds or hearing loss – Decreased muscle control – Lack of coordination, balance problems – Decreased sensation, weakness or paralysis – Difficulty walking or with speech – Double vision

Cerebellum Tumor: – Most common symptoms:

– – – – – – – –

Vomiting (usually just after awakening Clumsy, uncoordinated walk OneOne-sided smile or drooping eyelid Difficulty swallowing Slurred or nasal speech Double vision Headache – worse after awakening Symptoms may develop gradually

Headaches Nausea/Vomiting Swollen optic nerve due to increased intracranial pressure

– – – – –

Clumsy, uncoordinated walk Dizziness, tremors Difficulty with coordination and speech Double vision Nerve irritation can cause pain in back of head or neck

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Symptoms by Tumor Location: Frontal Lobe Frontal Lobe Tumor: – May initially be silent – Can cause oneone-sided paralysis – Seizures – ShortShort-term memory loss – Impaired judgment, personality, or mental changes

Symptoms by Tumor Location: Parietal Lobe Parietal Lobe Tumor: – If tumor is in dominant hemisphere – seizures and language disturbances – Loss of ability to read – Spatial disorders – Difficulty with calculations – Difficulty knowing left from right

Sensory Loss Sensory deficit can vary with location of tumor – Graphesthesia seen in patients whose tumors involve primary sensory cortex

Do not follow a dermatomal or peripheral nerve distribution Can include loss of spatial orientation, tingling, discoordination

Symptoms by Tumor Location: Occipital Lobe and Temporal Lobe Occipital Lobe Tumor: – Blindness in one direction – Other visual disturbances can occur – Seizures

Temporal Lobe Tumor: – Seizures – most common symptom – Ability to recognize sounds – Vision can be affected

Weakness Muscle weakness common complaint in brain tumor patients Upper motor neuron lesions produce weakness more pronounced in the flexors of the lower extremities and in the extensors of the upper extremities This weakness responds to highhigh-dose dexamethasone – Especially with tumors near the motor cortex or its descending fibers

Response to dexamethasone usually indicates that the weakness is due to edema and not direct tumor involvement

Aphasia Disorder of language function, not vocalization A specific sign of a lesion in the dominant hemisphere (usually left frontal or parietal) Lesions in nondominant hemisphere can produce constructional apraxia – An inability to perform purposeful movements

Patients with aphasia may be confused with dementia, psychosis, or depression

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Visual Spatial Dysfunction VisualVisual-spatial disconnection syndromes can occur in patients with tumors located in visual association cortex Optic nerve head is good measure of ICP, papilledema TumorTumor-related compression of optic chiasm = bitemporal hemianopsia – In early stage can be unilateral

Brain Edema With brain tumors there is a “breakdown” breakdown” in the bloodblood-brain barrier, not total loss Brain edema = “an increase in brain volume resulting from an increase in water and sodium content” content” (Thapar et al, 1997) In 1967, Klatzo distinguished two types – vasogenic or cytotoxic Fishman (1975) added a third type – hydrocephalic or interstitial

Vasogenic Edema Due to the rigid cranium, unchecked cerebral edema can lead to fatal herniation The amount of preoperative edema provides some indication of the potential for edemaedema-related complications postoperatively

Brain Edema BloodBlood-brain barrier – Permeability barrier between the blood and brain and the blood and CSF – The brain endothelial cell is the anatomic site of the bloodblood-brain barrier (Reese & Karnovsky 1967) – It is a complex regulatory interface – part structural, part biochemical, part enzymatic, part pharmacologic, part electrical, and part immunologic

Brain Edema Vasogenic edema is the dominant form of tumortumor-associated edema – spreads more rapidly in the white matter extracellular space – Can disrupt synaptic transmission – Contributes to headaches, seizures, and encephalopathy – Readily detectable on CT and MR imaging

Treatment of Brain Edema Most patients with peritumoral edema can be managed with corticosteroids – Reduction in elevated ICP may take several days

Dexamethasone has been standard agent Usual regimen consists of 10 mg loading dose, followed by 4 mg four times per day Biologic halfhalf-life is sufficient for twice daily dosing Most patients symptomatically improve within 2424-72 hours

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Emergency Treatment of Brain Edema Occasionally peritumoral edema gets out of control – This can result in imminent brain herniation

Symptom Management Related to Disease and Treatment

Emergency treatment includes: – Mannitol – Hyperventilation – Tumor resection

Seizures Presenting symptom: an alteration in the normal electrical potential of cells caused by the tumor, which then results in hyperactivity (Remer, S., Murphy, M.E., 2004). Classified as: Generalized or partial Occurs in 2020-60% of adult patients with brain tumors

General Seizure General or Grand Mal Seizure: – May begin as partial seizure but progresses – Produces tonictonic-clonic muscle contractions – Associated with shallow breathing, tongue biting, possible loss of body functions – Onset is sudden – May last several minutes – Followed by limpness, confusion, fatigue This may last several hours to days (postictal)

Lisa C. Smith MSN, FNP, AOCN Cancer Centers of the Carolinas Greenville SC

Partial Seizures Simple Partial – May involve any of the senses – Or movement of a part of the body – No loss of consciousness – Generally lasts a few seconds

Complex Partial: – Involves loss of consciousness – Accompanied by purposeless automatic movements – Followed by confusion – May last few seconds or a full minute

Seizure Management Initial Therapy – Standard first line anticonvulsants: Phenytoin Carbamazepine Valproic acid Treat with lowest effective dose, monitor serum levels, avoid polytherapy

Second Line Therapy – Before adding second drug, dose escalate monotherapy and verify serum concentrations Should titrate the 2nd drug to therapeutic level before tapering original agent

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Effects of Drug Management Incidence of adverse events ranges from 3030-40% Drug rash often associated with phenytoin – Seen more while undergoing radiation – Small % develop StevensStevens-Johnson syndrome

DrugDrug-drug interactions – Several anticonvulsants have clinically significant interactions with agents used in brain tumor treatment BCNU – decreases serum phenytoin

– Stimulation of cytochrome P450 enzyme system accelerates metabolism of several chemotherapeutic agents Nitrosoureas Irinotecan Cyclophosphamide Doses of these agents needs to be higher to be effective

Headache Usually result of increased ICP Can be secondary to XRT Dexamethasone decreases the edema – Usual dose 16 mg/day

Analgesics may be necessary

Prophylactic Anticonvulsants Prospective studies have failed to show the efficacy of prophylactic anticonvulsants for patients with brain tumors who have not had a seizure One instance when they are used – perioperative period – Retrospective studies have shown either no benefit or short term benefit (up to 10 weeks) – Phenytoin and carbamazepine have been the agents of choice

Nausea and Vomiting Associated with headaches as presenting symptom Can be treatment related – Acute toxicity from chemotherapy or radiation Symptom of encephalopathy

Assess volume status – Hydrate as needed

Administer antiemetics – Serotonin antagonist Ondansetron Granisetron Dolasetron

– Phenothiazines – Dexamethasone

Relaxation techniques

Weakness

Steroid Myopathy

Muscle weakness common complaint in brain tumor patients, can be presenting symptom or treatment related This weakness can respond to highhigh-dose dexamethasone (dex) Response to dex usually indicates that the weakness is due to edema and not direct tumor involvement

Steroid myopathy is also common in brain tumor patients, contributes to weakness – Incidence 22-21% – Proximal weakness between 9th and 12th weeks of steroid tx – Ideally d/c steroid, if not feasible, use lowest possible dose – Recovery can be expected 22-3 months after steroid d/c

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Treatment Related Side Effects: Radiation Therapy

Radiation Effects Alopecia

Hair loss Skin irritation Hearing deficits Nausea/Vomiting Appetite Changes

Drowsiness/Fatigue Decreased libido Neurologic Effects – Acute reactions – Early delayed reactions – Late reactions

Endocrine dysfunction

– Usually involves treatment area – Patient education: cut hair short, mild shampoo, avoid harsh products (hair color, curling irons, etc), get wig

Skin Irritation – Treatment area becomes reddened, flaky, pruritic – Patient education: mild shampoo, avoid sun exposure, do not apply any creams/lotions to scalp before checking with radiation oncologist

Radiation Effects: Neurologic

Radiation Effects: Neurologic

Acute Reactions: days to weeks

Late delayed: more than 6 months to many years

– Encephalopathy: usually appears in first 2 weeks of XRT and lasts 66-8 weeks N/V, drowsiness, headache, impaired speech, worsening of preexisting deficits Dexamethasone is used

Early Delayed: 11-6 months after XRT – Result of temporary demyelinating processes and alterations in bloodblood-brain barrier Somnolence syndrome, temporary cognitive impairment, subacute rhombencephalitis, and worsening of preexisiting symptoms Steroids may help, symptoms generally improve over a few weeks to months

Treatment Related Side Effects: Chemotherapy Bone marrow suppression Stomatitis, esophagitis Diarrhea/Constipation Nausea/Vomiting

Skin reactions Hair loss Fatigue

– Radiation necrosis Usually 11-2 years after XRT, difficult to distinguish from recurrent tumor (PET can), Treatment includes surgical debulking, anticoagulation, pentoxifylline (Trental), and Vitamin E

– Cognitive impairment Significant longlong-term risk

Chemotherapy Effects Bone marrow suppression: – Anemia Erythropoietin growth factor If iron deficient, oral iron supplementation Transfuse as needed

– Neutropenia Monitor for infection GMGM-CSF or GG-CSF

– Thrombocytopenia Monitor for bleeding Transfuse as needed

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Chemotherapy Effects: Mucositis Stomatitis/Esophagitis: – Patient education: good oral hygiene, use soft toothbrush, floss regularly, salt water or baking soda mouth rinses, drink plenty of fluids – Assess for oral candidiasis – Treatment options: Lidocaine rinse 55-15 cc Magic mouthwash (benadryl, maalox, viscous xylocaine) 151530 cc Nystatin oral suspension fluconazole

Chemotherapy Effects: Constipation/Diarrhea Constipation: – Stool softners – Diet with highhigh-fiber foods, plenty of fluids – Exercise

Diarrhea: – Recommend Immodium AD or Lomotil – Administer fluids and electrolytes if patient becomes dehydrated – Initiate BRATT diet (bananas, rice, applesauce, white toast, decaffeinated tea) – Low residue diet – Skin care

Establishing Diagnosis

Current Treatments for Primary Malignant Gliomas Kara Penne RN, BSN, OCN The Brain Tumor Center at Duke Durham, NC

“Gold” Gold” Standard of Treatment

MRI of brain Biopsy vs resection PATH! PATH! PATH!

Malignant Glioma: Outcome with Conventional Therapy Newly Diagnosed

Recurrent

Surgery External beam radiotherapy With and without chemotherapychemotherapycontroversial

J Clin Oncol 19:509,2001

J Clin Oncol 17:2572,1999

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Surgical Prognostic FactorsFactorsEvidence

Surgery Stereotactic biopsy: inoperable tumors, confirmation of diagnosis !Needle biopsy via burr hole !Stereotactic frame “halo” halo” placement Craniotomy: !Subtotal resection !Gross total resection !Surgical resection with cortical mapping

Surgical Prognostic FactorsFactorsEvidence Extent of Tumor Resection