Neuro Exam 8
TB meningitis treatment
- drugs for TB
acute bacterial clinical manifestation
-Fever -Neck stiffness -Altered mental status
Diagnosis of primary brain tumors
1) MRI or CT •MRI most informative: with assist of gadolinium contrast enhancement can detect tumors even mm in size - can distinguish tumor from surrounding anatomic and neurovascular areas 2) following detection with imaging distinguishing intraaxial or extraaxial is important for differential diagnosis •Intraaxial: within brain and expanding (astrocytoma) •Extraaxial: outside brain and compressing (meningioma) 3) history and other tests to rule out whether metastases to the brain (chest x-ray) 4) needle biopsy 5) endocrine studies
primary vs secondary neoplasms
1) primary: originate from the various cells and structures normally found within 2) secondary: also known as metastatic. originate from structures outside the brain
medulloblastoma incidence
•<2% of primary brain tumors, most common malignant primary CNS tumor in children •Very aggressive in younger children •Age of peak incidence is 45-55 yrs in adults
pituitary adenoma overview
•Benign, derived from cells of anterior portion of pituitary gland
brain abscess
•Occur when microorganisms reach the brain and cause a local infection •Uncommon disorder, 2% of intracranial mass lesions •Circumscribed, enlarging and focal infections •Symptoms similar to other space occupying lesions •Often progress rapidly and frequently affect meningeal structures •Can cause increased ICP
medulloblastoma clinical manifestations
•Often develops in cerebellar vermis •Signs of hydrocephalus and ataxia are common •Tends to metastasize through the CSF
risk factors of brain abscess
•Persons with compromised immune system or persons with systemic illness such as HIV
Medical management: Radiation
•Post-surgery radiation -> increases survival •Radiation for unresectable or partial resection •Side-effects - Acute brain swelling -> increased neuro deficits or increased ICP—often prescribed steroids -Postirradiation syndrome 1-3 mos. post - Radiation necrosis - months to years after -> severe and irreversibleà dementia, deterioration, etc - Other long term complications
neurinoma/neuroma clinical manifestation
•Progressive unilateral sensorineural hearing loss; tinnitus, vertigo, unsteadiness, facial numbness, difficulty swallowing, impaired eye movement •Deformity of 4th ventricle may cause hydrocephalus
infectious disorders of the CNS overview
- Infection of the CNS remains rare •A major cause of mortality and morbidity worldwide •Biologic adaptations of infections agents •Altered modes of transmission a. CSF, emboli, brain parenchyma, etc •Drug resistant strains •Increased travel
pathogenesis of meningitis
- Most common bacteria have neurotropic potential allowing them to invade epithelium > multiply in bloodstream > and cross blood-brain barrier into the CSF (S. Pneumoniae, N. Meningitidis, H. Influenza) 1 Adherence and colonization of mucosa 2 Invasion of bloodstream 3 Multiplication in bloodstream 4 Increased permeability of the blood-brain barrier and bacteria cross the blood-brain barrier 5 Infiltration of CSF by white cells 6 Release or proinflammatory cytokines 7 Uncontrolled replication of bacteria in sanctuary site 8 Bacterial products stimulate inflammatory cascade 9 Activated leukocytes lead to production of matrix metalloproteinase (MMP) and oxidants
encephalitis
- acute inflammatory disease of parnchyma (tissue of brain) from direct viral invasion of hypersensitivity initiated by virus a. primarily in grey matter b. can result in neuronal cell death, cerebral edema and damage to vascular system - cause cannot be identified in 2/3 of viral encephalitis - mosquitos or ticks are responsible for most of the worldwide known cases (west nile virus) - west nile has spread in US since 1994 - west nile primarily from avian host and mosquitos
clinical manifestations of primary neoplasms
- depends on compression on infiltration of specific cerebral tissue, related edema and development of ICP - the initial clinical signs of intracranial tumor are related to increase in ICP •Headache- typically retroorbital, worse in the morning and better later in the day. Increases with stooping, straining, coughing or exercises- activities that increase ICP. •6th CN is commonly involved- weakness of Lateral rectus and report of diploplia •Nausea and vomiting
diagnosis of encephalitis
- detection of IgM antibody in serum of CSF - EEG for seizure activity- in temporal lobe in herpes simplex - lumbar puncture- looking for abnormal proteins and glucose levels - MRI-cerebral and vascular damage a. West Nile: lesions in white matter, pons, substantia nigra, and thalamus b. key finding: focal abnormal signal intensity in the anterior horns; abnormal findings correspond to paralysis - blood samples (days 8-20 will have best yield)
diagnosis of meningitis
- difficult to diagnosis on symptoms alone due to time course of presentation - lumbar puncture: only absolute dx a. viral meningitis: many lymphocytes, normal glucose level, mild increase in protein, absence of bacterial organisms b. TB meningitis: predominance of lymphocytes, glucose level decreased, protein increased c. bacterial meningitis: elevated white blood cell count and protein concentration, glucose possible lower, neutrophil or lymphocytes predominance - CT or MR of brain and spine will show brain abscesses or infarction - gram stain examination of CSF recommended to differentiate type - symptoms can develop a. viral: within hours b. fungal or TB: days to weeks c. bacterial: over 4-24 hours
spinal cord neoplasms
- extradural a. metastases - intradural a. extramedullary - meningiomas - schwannomas, neurofibromas a. intramedullary - ependymomas - astrocytomas
bacterial meningitis
- from organisms found in mucosal surfaces in upper respiratory tract - bacteria in birth canal can be transferred during birth - neonate: at risk for group B streptococcus, Escherichia coli, Listeria monocytogenes - 6-12 mo: at risk for Hib, pneumococcus and meningococcus - adult and geriatric: at risk for streptococcus pneumoniae - inflammation confined to subarachnoid space, and then spreads to brain parenchyma - neurologic sequelae often present
signs and symptoms of brain tumors
- headache - visual changes (double vision, blurred vision) - nausea - vomiting - cognitive changes (impairment of memory, judgment, personality) - lethargy - behavioral changes - seizures - syncope - weakness - hemiparesis, hemiplegia - apraxia - cortical sensory deficits (graphesthesia, stereognosis difficulties) - sensory impairments (tingling, spatial orientation changes) - cranial nerve palsies - aphasia - facial numbness - hearing disturbances - anosmia - swallowing difficulties - paralysis of outward gaze (sixth cranial nerve) - papilledema - incoordination - ataxia - in children, diastases of cranial sutures and enlarging head size
clinical manifestations of encephalitis
- headache, nausea, vomiting, altered consciousness, coma, agitation - focal neurologic signs (hemiparesis, aphasia, ataxia, etc.) - stiffness of back and neck - possible seizure, hallucination and disturbance of memory - west nile virus a. symptoms develop in 20-40% of cases b. incubation period of 2-14 days c. flulike symptoms d. fever, headache, malaise, fatigue, vomiting, diarrhea, +Kerning or Brudzinski sign e. Various patterns of extremity weakness
pathogenesis of encephalitis
- inflammatory response and pathologic changes of brain - cell changes and cell death, destruction of plasma membranes, destruction of vessels - west nile virus a. infection spreads to regional lymph nodes and into the bloodstream b. thought that it invades nervous system through retrograde transport along peripheral nerves c. neuronal cell loss thalamus, brainstem and cerebellar Purkinje cells - herpes simples virus a. virus found in neonates likely from maternal genital infection b. 50% who contract virus will develop CNS disease (other skin, eye, mouth disease) - measles, mumps rubella, varicella or other acute systemic infection-encephalomyelitis - epstein-barr virus, Hepatitis A - parasites, bacteria, and toxic drug reactions
bacterial meningitis treatment
- medical emergency, antimicrobial therapy should begin ASAP - anti-seizure meds to inhibit seizures - corticosteroids to reduce inflammation
viral (aseptic) meningitis
- most common cause of CNS inflammation, however less severe than bacterial - acute febrile illness with signs and symptoms of meningeal irritation - most common causes a. enteroviruses (40% of those 30-60 yrs) or sarcoid tumors or cysts, NSAIDS b. herpes simplex virus 2 (20%) - other causes a. epstien barr virus b. systemic lupus erythematosus c. sarcoid tumor or cysts d. NSAIDs e. chemicals related to surgical procedures - occur days/weeks after exposure - majority of people get better on their own
treatment of encephalitis
- no antiviral treatment except for herpes simplex (Acyclovir) - treatment to manage cerebral edema (surgical decompression or administration of mannitol) - supportive care
pathogenesis- inflammatory cascade (meningitis)
- once across BBB there is less immune protection than in rest of body (1/200 amount of antibody as blood; fewer white blood cells; no lymphatic system to fight infection) - leukocytes, cytokines, chemokines, macrophages, microglia respond to bacterial and viral infections - cells recruited to fight the infection release cytotoxic free radicals and excitatory amino acids (glutamate) - neuronal cell death through apoptosis and necrosis - vasculitis can lead to infarction and decreased blood flow - inflammation can block CSF > hydrocephalus, edema, and inc intracranial pressure
secondary (metastatic) neoplasm overview
- originate outside of the brain and spread to CNS from another site - incidence: •150,000 brain metastases and 80,000 spinal cord/year •Most common intracranial tumor in adults •On the rise - pathogenesis: •Most reach brain through arterial blood system •In distribution of middle cerebral artery (MCA), lesions in frontal and parietal lobes •20% to posterior fossa, primarily cerebellum •Brain metastases: a. primarily from lungs, breast, kidney, GI tract, genitourinary tract or melanoma •Spinal cord metastases: - primarily from lung, breast, prostate, kidney, and lymphomas
CNS neoplasms overview
- presence of any CNS tumor is cause for concern due to the vital functions of the brain and spinal cord - brain is susceptible due to damage to structures or space a. results in ICP, focal neurologic signs, compression and destruction of brain tissue - significant cause of morbidity and mortality - approximately 50% have long term prognosis
CNS neoplasm classification
- purpose is to facilitate communication about tumor behavior and treatment - WHO classification system according to histology •Names a tumor by most likely cell of origin and adding qualifying phrases to describe its behavior. •Graded I-IV with IV being the most aggressive tumor - St. Anne-Mayo system •4 tiered- based on presence or absence of 4 major criteria (nuclear atypia, mitoses, endothelial proliferation and necrosis)
tuberculous meningitis
- rare .5-1% - high mortality and disability among survivors - mycrobacterium tuberculosis enters via inhalation - CNS involvement-abscess or spinal cord disease - diagnosis is based on a. clinical picture b. neuroimaging abnormalities c. CSF changes - treatment includes anti-tuberculosis meds 6-12 months
Low-grade Astrocytomas - Grade I-II presentation
- typically in 3rd and 4th decade of life - frontal lobe is common for adults •Initial symptoms: unilateral headache, possible personality disorder with changes in behavior and emotions, seizures or visual changes - cerebellum is most common in children •Symptoms of unilateral cerebellar ataxia, increased intracranial pressure
more advanced disease clinical manifestation
-Apistinotis -Focal neurologic deficit -Seizures -Reduced level of consciousness -Positive kernig sign -Hip flexion and knee extension (pain) -Inflammation progresses, flexion of neck produces flexion of hips and knees (Burdinski's sign) Untreated means it will hit brainstem (seizures, vomiting, coma, papilidima) Focal nerve signs (cranial nerve palsies and deafness as well)
TB meningitis clinical manifestation
-Focal deficits -Elevated intracranial pressure -Headache -Vomiting -Meningeal signs -Vision loss -Cranial nerve palsies
etiology and risk factors of meningitis
1) bacterial - acquired or congenital immunodeficiency's, hemoglobinopathies (i.e., sickle cell disease, HIV0 - functional or anatomic asplenia a. more susceptible to pneumococcal disease - crowded spaces: day care, dorm rooms, some households - CSF leak - otitis, mastoiditis, and sinusitis - common predisposing conditions 2) bacterial - low socioeconomic status - young children - certain geographic areas and seasonal patterns of mosquito - vaccines have decreased incidence
Spinal Metastases- Medical management
1) diagnosis •Examination and plain film x-rays of the spine, bone scans •MRI or CT then performed for more definitive imaging 2) treatment •Radiotherapy •Chemotherapy •Surgery- for those with worsening neurologic deficit or spinal instability causing cord compression or individuals who have already received max radiation 3) prognosis •Based on degree of loss before radiotherapy
primary neoplasms
1) malignant (ie: astrocytomas) •High growth rate, invasive, infiltrative •Angiogenesis 2) benign (ie: meningiomas, neuinomas and hemangioblastomas) •Slow growth rate, noninvasive, high threat of function due to space occupying lesion. Depending on location may be inoperable or inaccessible- continue to grow, ICP increase, neurologic deficits, herniation and death - may develop in brain, SC or surrounding structures - grade 1-4
anatomical sites: most common CNS tumors
1) supratentorial 2) midline 3) infratentorial 4) spinal cord
Etiology of strokes
Atherosclerosis is a major contributory factor in cerebrovascular disease. Plaque formation occurs at certain sites including: bifurcations, constrictions, dilations, or angulations of arteries. The most common lesion sites for lesions are: at the origin of the common carotid artery or at its transition into the middle cerebral artery, at the main bifurcation of the middle cerebral artery, and at the junction of the vertebral arteries with the basilar artery.
Positive Kernig/Brudzinki sign
Kernig sign: pain in posterior thighs and lumbar area or pain with combined hip flexion and knee extension Brudzinski sign: flexion of the neck will produce flexion of the hips and knees (secondary to progression of inflammation)
glioma risk factors
Possibly related to chromosomal abnormalities •None identified with exception of exposure to ionizing radiation •Effects of carcinogenic viruses are unclear •Associations have been made with Epstein-Barr virus and primary CNS lymphoma •Sustained exposure to certain pesticides and other environmental chemicals has been implicated •Infection, trauma and immunosuppression suspected triggers •Exposure to full mouth dental x-rays •Link to maternal diet for children (nitrates from cured meats)
Hemorrhagic strokes
are the result of rupture of a cerebral vessel or trauma and lead to abnormal bleeding into the extravascular areas of the brain. Hemorrhage results in increased intracranial pressures with injury to brain tissues and restriction of distal blood flow. Clinically, a variety of focal deficits are possible, including changes in the level of consciousness and impairments of sensory, motor, cognitive, perceptual, and language functions Hemorrhage is closely linked to chronic hypertension.
Intracerebral hemorrhage (IH)
is caused by rupture of a cerebral vessel with subsequent bleeding into the brain. o Primary cerebral hemorrhage (nontraumatic spontaneous hemorrhage) typically occurs in small blood vessels weakened by atherosclerosis producing an aneurysm.
Ischemic stroke
is the most common type and results from a thrombosis, an embolism, or hypoperfusion. The resulting lack of cerebral blood flow (CBF) deprives the brain of needed oxygen and glucose, disrupts cellular metabolism, and leads to injury and death of tissues. A differentiating feature of stroke resulting from hypoperfusion, as opposed to other ischemic infarcts, are the neurological deficits are global in nature with bilateral neurological deficits.
Subarachnoid hemorrhage (SH)
occurs from bleeding into the subarachnoid space typically from a saccular or berry aneurysm affecting primarily large blood vessels.
glioma
specific primary tumor - tumor of glial cells (astrocytoma, oligodendroglioma, ependymoma, medulloblastoma) - most common primary brain tumor •30-40% •Men > women 3:2 - divided into: 1.Benign - low grade gliomas- e.g., low grade astrocytoma •7-10% of primary brain tumors, most common in children 2.Malignant gliomas- e.g., anaplastic astrocytoma or GBM •More common in adults, 20-30% of brain tumors 3.Other: oligodendroglioma, ependymomas, medulloblastomas
viral meningitis treatment
symptomatic treatment - rest, fluids, headache management - antiviral for herpes - most recover in 1-2 weeks
Stroke (cerebrovascular accident [CVA]; brain attack)
· Sudden loss of neurological function caused by an interruption of blood flow to the brain · Neurological deficits must persist for at least 24 hours
Strokes are classified by:
· etiological categories (thrombosis, embolus, or hemorrhage) · specific vascular territory (anterior cerebral artery, middle cerebral artery, etc.) · management categories (transient ischemic attack, minor stroke, major stroke, deteriorating stroke, young stroke)
ependyoma prognosis
• •80% 5 year survival rate
Low-grade Astrocytomas - Grade I-II
•10-12% of primary brain tumors of adults •Grade I:slow growing, often cystic; cells uniform and resemble nonanaplastic astrocytes (well diferentiated •Grade II:diffuse, infiltrative, and/or fibrillary (neuroglial fibrials), anaplastic features •Cerebral:solid grey mass with indistinct boundaries; frontal lobe most common site in adults •Cerebellar:cystic and well circumscribed; most common site for children
Oligodendroglioma incidence
•2-3% of gliomas •Occur most frequently in young and middle-aged adult; can also be found in children
TB meningitis prognosis
•20-50% mortality rate; survivors left with neurologic sequelae
meningioma incidence
•34% of all intracranial neoplasms •Second most common primary intracranial tumor in adults •Most common benign brain neoplasm •Ages 40-70, 3x greater in females •Increased in neurofibromatosis, postmenopausal hormone replacement therapy and patients with breast cancer
Bacterial meningitis prognosis
•5-25% mortality rate depending on bacteria and health and age of person •At least one neurologic complication in 75% •Systemic complications, cardiorespiratory failure or sepsis occur about 40% •Cranial nerve palsies and hyponatremia 30% •Children can have long-term neurologic consequences such as developmental impairment, hearing loss, blindness, hydrocephalus and hemiparesis
primary neoplasms info/incidence
•69,720 new primary malignant and benign brain tumors in 2013 •Mean age of onset: 53 yrs •5-year survival rate for 2003-2009 is 33.5% •Survivors: 75% benign, 23% malignant •For intracranial diseases, death from brain tumor is second only to stroke •Primary brain tumors are the second most common form of cancer in children and second leading cause of death from cancer in children •Adult tumors are primarily supratentorial •Child tumors are primarily infratentorial
infratentorial neoplasms
•Adults: acoustic schwannomas, metastases, meningiomas, hemangioblastomas) •Children: cerebellar astrocytomas, medulloblastomas, ependyomas, brainstem gliomas
treatment of brain abscess
•Antibiotics •Possible corticosteroids to control edema- short time frame only •Surgical options include aspiration and excision to drain the abscess and reduce mass effect - needs to be surgically accessible and not damage eloquent tissue
spinal metastases
•Back pain is the most common and prominent symptom- 95% of the cases •Hx of known cancer and new onset of back pain should be screened for cancer •Symptoms: dull ache, worse at night in the recumbent position •Progression without tx includes: increased pain, sensory loss, bowel and bladder sphincter disturbance, possible paraplegia •Dx early is important- those tx while still ambulatory are likely to remain so, if progressed to paraplegia likely will not regain function
medical management: other therapies
•Chemotherapy (many side-effects) •Hormonal therapy, e.g., for pituitary tumor •Immunotherapy - donor serum with preformed antibodies; interferons, interleukin -2 •Osmotherapy - use of Mannitol for quick decrease of brain edema to decrease ICP •Anti-inflammatories (corticosteroids e.g., Decadron, prednisone) to reduce peritumor edema •Anti-seizure meds
pituitary adenoma incidence
•Common, accounting for approximately 13% of all intracranial tumors in adults •Women affected > men, specifically during childbearing years
meningioma prognosis
•Complete resection only possible in <50% •Complete resection: 80-90% 10-year survival rate
pathogenesis of primary neoplasm
•Compress brain tissue and structures •Invade or infiltrate cerebral tissue •Sometimes erode bone •Followed by cerebral edema and increased ICP •Cerebral Edema develops in surrounding tissue - impairs cellular activity in white matter > electrochemical instability > seizures - brain can accommodate slow growing tumors, but eventually herniation and ICP
metastatic tumors medical management
•Corticosteroids; surgery; radiation
neurinoma/neuroma prognosis
•Cure is achieved with surgical resection, hearing may be compromised or possible vestibular complex •May have long term balance/vestibular/hearing issues that need addressed
Paraneoplastic syndrome
•Effects on the nervous system that are not directly related to the primary tumor mass or metastasis •Symptoms - Paraneoplastic cerebellar degeneration, brainstem encephalitis, myelitis of the spinal cord, motor neuron disease •Hypothesized to be caused by an immune mechanism - Response of immune system is misguided and causes neurologic dysfunction •Rare, but severe; often leave patient with severe neurologic disability
pituitary adenoma clinical manifestation
•Excess pituitary hormone release or pituitary insufficiency can lead to various syndromes (amenorrhea, gigantism, acromegaly, Cushing's disease or fatigue, weakness, hypogonadism). •Might also present with regression of secondary sexual characteristics or neurologic findings
pathogenesis of brain abscess
•Extracerebral infection •Blood-borne metastases •Infection from lung or heart •Other infections in cranium such as sinusitis and mastoiditis
clinical manifestation of meningitis
•Fever •Headache •Nausea and vomiting •Altered mental status •Increased ICP •Meningeal signs - Nuchal rigidity- Stiff and painful neck, impaired neck flexion - Positive Kernig sign: pain in posterior thigh and lumbar area or pain with combined hip flexion and knee extension •Cranial nerve palsies •Photophobia •Sleepiness or trouble waking from sleep •Lack of appetite •Lethargy •Seizures •LBP •Vision loss •Reduced level of consciousness •Sepsis
Glioblastoma multiforme (GBM
•GBM aggressive, infiltrative, fast growing, tends to invade both hemispheres via corpus callosum - pinkish grey or multicolored, well-demarcated mass with scattered areas of hemorrhage - highly vascular; many cell types and forms, many mitoses •Most frequently in frontal and temporal lobes •Most often in 5th and 6th decade of life •Presentation: unilateral headache, seizure, lethargy, memory loss, motor weakness, and personality change •Prognosis - with optimum excision and radiation: - anaplastic astrocytoma (Grade III): 70% 1-year survival - Glioblastoma multiforme (Grade IV): 50% 1-year survival
High-grade Astrocytomas - Grade III-IV
•High grade malignant-much more common in adults •Grade III: anaplastic astrocytoma •Grade IV: glioblastoma multiforme (GBM) •Make up 20-35% of primary brain tumors •Often in white matter of cerebral hemispheres
diagnosis of brain abscess
•History of infection or immunosuppression suspicion of abscess rather than neoplasm •MRI preferred over CT •CSF, serologic studies and patient history
location of neoplasm/lesion
•Location of lesion in reference to tentorium or cerebral tissue •Assists in predicting probable deficits •Guides specific treatment strategies along with primary or secondary, metastatic, child hood, etc.
ependymoma incidence
•Low incidence, only 2% of gliomas •More prevalent in children vs adults •3rd most common posterior fossa neoplasm in children
metastatic tumors diagnosis
•MRI and other tests to confirm metastases •Hx of cancer elsewhere, a solitary brain lesion is 90% certainty metastatic
Meningitis
•Meninges of the brain and spinal cord become inflamed •Inflammation can involve all three layers of the membranes (pia, arachnoid and dura mater) and extend into first and second layers of cortex and spinal cord •Increased chance of infarction •Scar tissue can result in restricted flow of CSF >hydrocephalus or subarachnoid cyst •Incidence - 2-6/100,000 adults/yr in developed countries; up to 10x higher in less developed countries - highest among young children <1 y.o. - High rates in Native Americans and Australian aboriginals
supratentorial neoplasms
•Metastases •Meningiomas •Gliomas (malignant gliomas: anaplastic astrocytoma, and gliobastoma multiforme (GBM), astrocytoma, oliogodendroglioma) •60% of tumors in adults
ependyoma clinical manifestations
•More common in 4th ventricle and detected due to signs of increased ICP •Usually surgically excised
prognosis of brain abscess
•Mortality rate is lowered from 65% to 30% with antibiotics and surgery •Nearly 50% will have some neurological sequelae
Medical management: Surgery
•Most important form of initial therapy- allows for histological confirmation •Goal is complete resection (higher survival rates), however partial excision is often performed - Relieves ICP pressure and mass effect and tumor load, reducing symptoms and improving neurologic function, while also enhancing effectiveness of adjuvant therapy (radiation) •Procedures - Craniotomy with tumor resection, computer based stereotactic resection without craniotomy for deep mass lesions, endoscopic procedures
ependyoma pathogenesis
•Neoplasm derived from the ependymal cell lining of the ventricular system •Graded I-IV; reddish, lobulated and well-circumscribed (cauliflower in shape)
clinical manifestations of brain abscess
•Normal body temp, neck stiffness is rare •Symptoms resemble those of expanding intracranial mass, slow growing neoplasm or may be rapid and progress to herniation and brainstem compression à death •Headache most common symptom •If process continues, focal symptoms (hemiparesis or aphasia), decreased level of consciousness, coma •Possible seizures •Lethargy and confusion
meningioma pathogenesis
•Originate in arachnoid later or meninges •Most often located between or over cerebral hemispheres, at skull base, or posterior fossa •Typically well-circumscribed globular masses •Generally do not invade underlying brain parenchyma
midline neoplasms
•Pituitary adenomas •Pineal tumors •Craniopharyngiomas
metastatic tumors prognosis
•Poor; metastasis indicates the primary cancer has already escaped control
medulloblastoma pathogenesis
•Rapidly growing, malignant tumor •Possibly from embryonal external granular layer of the cerebellum •Highly vascular •4 classifications: classic, large cell, desmoplastic and nodular
viral meningitis prognosis
•Self-limiting with less degree of neurologic sequelae
meningioma overview
•Slow growing usually benign •Most commonly occur along dural folds and cerebral convexities •3 classifications 1) grade I- benign (90%) 2) grade II- atypical 3) grade III- malignant
neurinoma/neuroma overview and incidence
•Slow growing, benign tumors originating from Schwann cells •Aka acoustic neurinoma/neuroma, schwannoma •3-10% of all brain tumors •4th-6th decade of life, 2:1 women to men •Most commonly develop on the 8th CN; may impact other cranial nerves (5 and 7) or brainstem
Oligodendroglioma pathogenesis
•Slow, growing, calcified tumor arising from myelin-producing cells in the CNS
meningioma clinical manifestations
•Symptoms evolve over years due to slow growing tumor, can become quite large in "silent" brain areas
metastatic tumors clinical manifestations
•Symptoms similar to primary tumors, but may arise quickly from edema •Headache, seizures, elevated ICP, focal weakness, speech difficulty, focal sensory loss, mental status change, papilledema, etc.
Oligodendroglioma clinical manifestations
•Tend to bleed spontaneously and may present with stroke like syndrome •Located predominantly in frontal lobes •Presentation of seizure and headache
neurinoma/neuroma pathogenesis
•Thickly encapsulated, highly vascular
modes of radiation
•Traditional delivery to localized area of brain •Brachytherapy - radium seeds within tumor (for several days) •Stereotactic radiosurgery, e.g., gamma knife radiotherapy- high energy photon beams; halo device (highly focused) •Cyberknife for extracranial lesions (frameless robotic radiosurgical device)
prognosis of encephalitis
•Varies depending on infectious agent •10-50% recovery rate •Severity of illness does not always predict final outcome •Young children will take longer to recover than adults •Neurologic sequelae are common in 50% of persons
Low-grade Astrocytomas - Grade I-II prognosis
•Varies depending on treatment; categorized benign, but astrocytomas always infiltrative and generally progressive •5-10 year survival rate of 100% if completely excised lesion •Untreated 5 yrs survival 32%, 10 year 11%
pituitary adenoma prognosis
•Very treatable, majority having long-term survival or complete cure -surgery and stereotactic radiotherapy
types of meningitis
•Viral (Aseptic) •Tuberculous •Bacterial •Fungal •Parasitic •Amebic •Noninfectious
Oligodendroglioma prognosis
•With optimal tx: 5 year survival rates are 80-100% •Eventually reoccur, often as more aggressive tumor
medulloblastoma prognosis
•age > 2, no metastases, and at least 75% tumor resection means 60-70% 5-year survival; otherwise: 45% 5-year surviva