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85 Cards in this Set
- Front
- Back
foramen magnum
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largest foramen in the skull located at base where SC meets medulla called the cervicomedullary junction
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anterior fossa
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anterior compartment in cranial cavity that contains FLs
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middle fossa
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contains TL, edges marked by lesser wing of sphenoid bone anteriorly and petrous ridge of temporal bone posteriorly
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posterior fossa
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posterior compartment of cranial cavity that contains cerebellum and brainstem
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dura
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outermost layer of meninges, has 2 layers: periosteal layer adheres to skull and is fused with inner meingeal layer. inner meningeal layer forms falx and tentorium
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falx cerebri
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flat sheet of dura suspended from roof of cranium and runs interhemispherically separating L/R hemis.
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tentorium cerebelli
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tentlike sheet of dura that covers upper surface of cerebellum and together with petrous portion of temporal bone, divides the posterior fossa from rest of cranial vault. OL and part of TL rest on upper surface.
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tentorial notch (aka tentorial incisura)
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narrow opening in the tentorium cerebelli where the midbrain passes thru
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arachnoid membrane
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middle meningeal layer, csf percolates over brain surface in this layer.
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pia
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innermost meningeal layer, adheres to brain surface and surrounds the initial portion of each blood vessel as it enters brain, forming a perivascular space (Virchow-Robin space) and the fuses with vessel wall.
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epidural space
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b/w dura and skull which contain middle meningeal artery, which is a branch of the external carotid that supplies the dura
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subdural space
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a potential space b/w dura and arachnoid which contains bridging veins (drain hemispheres and pass thru space to several dural venous sinuses)
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subarachnoid space
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b/w arachnoid and pia. csf and major arteries travel thru
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path of csf
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produced by ependymal cells in lat ventricles, pass thru foramen of munro in each hemis to 3rd ventricle (in diencephalon), tthru sylvian aqueduct into 4th ventricle (surrounded by pons, medulla and cerebellum), out thru foramen of Luschka and Magendie, into subarachnoid space, up to arachnoid granulations to be reabsorbed by bloodstream
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foramen of Munro
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where lateral ventricles communicate with 3rd
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cerebral aqueduct (aka aqueduct of Sylvius)
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where 3rd ventricle communicates w/ 4th, travels thru midbrain
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4th ventricle
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roof is formed by cerebellum and floor is formed by pons and medulla
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foramina of Lushka
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one of several foramina where csf leaves ventricular system thru 4th ventricle (lateral foramina)
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foramn of Magendie
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midline forman where csf leaves 4th ventricle - csf percolates around brain and SC in SA space and is reabsorbed by arachnoid granulations
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total volume of csf in adult
amount produced per hour amount produced per day |
150 cc
20 cc/hr 500 cc/day |
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csf cisterns
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where SA space widens to form csf collections: e.g., ambient cisterns (lateral to midbrain), quadrigeminal cistern (posterior to midbrain)cistern magna (beneath cerebellum near foramen magnum), lumbar cistern ( in lumbar portion of SC where LP are done)
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circumventricular organs
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specialized brain regions in BBB where there are interruptions that allow the brain to respond to changes in chemical milieu of remainder of body and secrete neuropeptides in response (e.g., meidan eminence and area postrema)
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area postrema
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paired circumventricular organ in BBB located in caudal wall of 4th ventricle in medulla. a chemotactic trigger zone, it is involved in detecting circulating toxins that cause vomiting
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vasogenic edema
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excessive extracellular fluid resulting from BT, infections, trauma, etc. extravasation of fluid into interstital space
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cytotoxic edema
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excessive intracellular fluid accumulation in brain cells caused by cellualr damage (e.g., infarct).
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headache
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no pain receptors in brain, pain caused by mechanical traction, inflammaiton, irritation of other structures in head that are innervated, including blood vessels, meninges, scalp, and skull. supratentorial dura innervated by trigeminal nerve, posterior fossa dura innervated by CN X and IX and first 3 cervical nerves
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vascular headache
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includes migraines, thought to involve inflammatory, autonomic, serotinergic, neuroendocrine and other influences on blood vessel caliber in the head.
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complicated migraine
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transient focal neurological deficits (sensory, motor defs, visual loss, brainstem findings in basilar migraines and impaired eye movement in opthalmoplegic migraines)
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cluster h/a
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1/10 as common as migraine, 5x more common in men. one to several h/a per day over a period of weeks and then vanishes for several months. severe, behind one eye, unilateral autonomic sxs (tearing, redness, Horner's syndrome (ptosis and miosis), flushing, nasal congestion).
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tension h/a
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described as band-like sensation, steady, dull ache, possibly related to excessive contraction of neck and scalp muscles. can occur continuously for years, and can occur as posttraumatic h/a
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idiopathic intracranial HTN aka pseudotumor cerebri
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condition of unknown cause charac by h/a and elevated ICP w/ no mass lesion.
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temproal arteritis aka giant cell arteritis
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more common in elderly, vasculitis affects temproal arteries, including those supplying eye
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intracranial mass lesion
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anything occupying volume in cranial vault (tumor, hemorrhage, abscess, edema, hydrocephalus, etc)
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mass lesion complications
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compression.destruction of adjacent brain regions,raise ICP, displacement of brain structures and herniation. can compress blood vessels leading to h/a or infarct/hemorrage, disruption of BBB, causing extravasation of fluid and vasogenic edema, hydroceph, szs, midline shift, dsisplacement of RAS causes coma
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effacement
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mild flattening of brain sulci, produces no sxs.
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cerebral perfusion pressure
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mean arterial pressure - intracranial pressure (CPP = MAP-ICP). as ICP increases, cerebral perfusion decreases. Increased ICP can lead to ischemia, herniation, irreversible brain damage and death.
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sxs of ICP
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h/a worse in morning, altered MS esp irritability and depressed alertness/attn, nausea, vomiting, and projectile vomiting (i.e., w/o nausea). papilledema (engorgement and elevation of optic disc), increased blind spot, concentric visual field defict, diplopia, cushings triad (HTN, bradycardia, irreg respirations).
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normal ICP
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less than 20 cm H2O in adults, or less than 15mm Hg
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transtentorial herniation (aka tentorial)
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herniation of MTL, esp uncus inferiorally thru tentorial notch. clinical triad of blown pupil, hemiplegia, and coma. dialted pupil is ipsilateral 85% of cases due to compressed CN III, progresses to impaired eye mvmt. comp of cerebral peduncles = hemiplegia (contra or ipsi)
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central herniation
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downward displacement of brainstem caused by ICP (e.g., hydroceph or edema). lateral rectus palsy (uni or bilat), can also lead to uncal herniation, or can progress downward to foramen magnum- called tonsillar herniation (of cerebellar tonsils).
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tonsillar herniation
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herniation of cerebellar tonsils thru foramen magnum. leads to compression of medulla, respiratory arrest, BP instability and death. may only be a postmortem phenomenon?
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subfalcine herniation
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herniation of cingulate gyrus and other structures under falx cerebri. ACA can be occluded under falx leading to infarct
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concussion
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reversible impairment of neurological fx for a period of minutes to hrs after head trauma. PCS can last several months w/ lethargy, dullness, h/a, etc.can cause carotid or vertrebral dissection
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DAI
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widespread or patchy damage to WM and CN, petechial hemorrhages, larger hemorrhages, cerebral contusion.
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epidural hematoma (EDH)
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in tight potential space b/w dura and skull. usually rupture of middle meningeal artery due to fx of temporal bone.rapidly expanding arterial bleed peels dura away, forms lens-shaped biconvex hematoma. pt may have no sxs initially but may lead to herniation and death w/o tx.
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subdural hematoma (SDH)
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b/w dura and subarachnoid layer, usu rupture of bridgin veins vulnerable to shear injury as they cross from arachnoid to dura, makes a crescent-shaped hematoma. acute or chronic
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chronic SDH
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usu in elderly, usu shearing injury. may not be assoc w/ trauma. venous blood collects from weeks to months, vague sxs- h/a, cog imp, unsteady gait, focal defs, and mb szs.
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acute SDH
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for sig bleed to occur, usu assoc w/ high impact velocity trauma, usu assoc w/ other injury such as SAH and contusion. prognosis is often worse as a result than chronic SDH or EDH.
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acute blood on CT scan vs. older bleed (1-2 weeks, 3-4 weeks)
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hyperdense- i.e. bright spot on CT when new. 1-2 weeks it is isodense due to clotting, 3-4 weeks hypodense. will be of mixed density if new/old blood mixture and may produce hemocrit effect
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SAH
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in CSF-filled space b/w arachnoid and pia which contain major blood vessels of brain. can be nontraumatic (spontaneous) or traumatic
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spontaneous SAH
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"worst h/a of my life" sudden, catastrophic; in 75-80% of cases it is a ruptured arterial aneurysm, 4-5% of time it is a ruptured AVM. risk factors atherosclerosis, congenital abnormalities, PKD, connective tissue d/o
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saccular (berry) aneurysms
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usu near circle of willis, 85% in anterior circulation (carotid) such as AComm, PComm, MCA
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scan for SAH
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CT w/o contrast as contrast and SAH look white on CT. CT initially better than MRI for detecting SAH, although it may disappear after a few days. angiogram needed to find aneurysm
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cerebral contusions
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occur in regions where cortical gyri abut the ridges of bony skull, usu at F and T poles. usu occur in coup/contrecoup fashion
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hypertensive hemorrhage
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usu small penetrating vessels in BG (usu putamen), thalamus, cerebellum, and pons.
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lobar hemorrhage
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bleeding in cortical lobes, usu caused by amyloid angiopathy- deposits of smyloid in vessel walls of older pts cause vascular fragility. also caused by HTN
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types of vascular malf
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AVM (abnormal direct connections of arteries/veins that tangle and present as flow voids on MRI), cavernoma, capillary telangiectasias (angiomas), developmental venous abnormalities
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cavernoma
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abnormally dialted vascular cavities lined by only 1 layer of vascular epithelium. oft present w/ szs and risk of hemorrhage increase .1-2.7% per year per lesion
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hydrocephalus causes
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excessive csf prod (rare), obstruction of csf, decrease in reabsorbtion in arachnoid granulations
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communicating hydroceph vs noncommunicating
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communicating caused by impaired absorption , obstruction of flow in subarachnoid space or rarely by excessive csf prod. noncommunicating is obstruction
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sxs hydrocephalus
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h/a nausea, vomiting, cog imp, decreased consciousness, papilledema, decreased vision, ventricular dilation , unsteady magnetic gait (feet don;t leave floor), incontinence, 6th nerve palsies, limited vertical gaze w/ downward and inward deviation of eyes.
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normal pressure hydrocephalus
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chronicaly dilated ventricles, gait difficulties, urinary incontinence, mental decline. usu in elderly. measurement of csf pressure is not elevated, altho pressure elevations may be intermittent. may be reabsorption prob. pts do better after large volume LP or shunting
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primary vs met CA
relative incidence |
primary originates in CNS; mets arise from neoplasms somewhere else in the body.
mets 5-10x more common than all primary types combined |
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benign vs malignant tumors
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benign if they do not infiltrate or disseminate widely thru CNS, malignant if they can spread. malignant BT rarely spread outside of CNS.
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gliomas
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types- GBM, atrocytoma oligodendroglioma, ependymoma, others). grade of GBM refers to lvl or malignancy w/ 4 being most malignant
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meningiomas
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arise from arachnoid villus cells, occur over lateral convexities, in falx, and in basal regions of cranium. grow slowly, appear as homogenous enhancing areas arising frm meningeal layers.
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pituitary adenomas
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cause endocrine disturbance, compress optic chiasm, can result inbitemporal visual defect
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lymphoma
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arises from B lymphocytes, commonly involves regions adjacent to ventricles, dxd by CSF cytology, median survival rate of 4 yrs
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pineal region tumors
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<1% of CNS tumors; pinealomas, germinoma, teratoma or glioma
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brain mets
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most commonly from lung, breast carcinoma or melanoma
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ped brain CA
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most often infratentorial (70%), cerebellar astrocytoma (better prognosis, b/w 2-20 yrs old), medulloblastoma (worse prog, usu before age 10) ependymoma (also bad prognosis)
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paraneoplastic syndrome
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rare neurologic disorder caused by remote effects of CA in body, leading to abnormal autoimmune response. e.g., limbic or brainstem encephalitis, cerebellar Purkinje cell loss, SC anterior horn cell loss, neuropathy, impaired neuromusc transmission, opsoclonus myoclonus (irreg jerky movement of eyes and limbs). us caused by smal cell lung carcinoma, breast CA, ovarian CA.
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infectious meningitis
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infect of csf in subarachnoid space. cd be bacteria, virus, fungi or parasites.usu heralded by sxs of meingeal irritation (meningimus) such as h/a, lethargy, sesnitivity to light and sound, fevel and nuchal rigidity (neck muscles involunarily contracted and resistant to flexion). onset is hrs to weeks to months. LP necessary for dx.
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bacterial meningitis
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csf has high WBC, high protein and low glucose. needs immediate tx; complications include szs, cranial neuropathies, edema, hydroceph, herniation, infarcts, death
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brain abscess
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bacterial infection of CNS. presents like a tumor but very rapidly progresses, small ones can be txd w/ antibiotics. larger ones need needle aspirationb or surgical removal
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epidural abscess
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can occur esp in spinal canal. sxs of backache, fever, high WBC, h/a and signs of nerve root or SC compression. txd w/ drainage, antib
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subdural empyema
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collection of pus in SD space, resulting from direct extension of nasal sinus infection or inner ear. txd by urgent surgical drainage and antib.
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tuberculous meningitis
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h/a, lethargy, meningeal signs, inflammatory response in basal cisterns which can affect circle of willis and cause infarcts. IVDA, HIV, and regions of tuberculosis common. results from reactivation of tuberculosis infect.
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neurosyphilis
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spirochetal infection transmitted sexually occurs following primary infection, resurgence w/ HIV
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viral meningitis
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less fulminant than bacterial, recovery in 1-2 weeks spontaneously. h/a fever lethargy, nuchal rigidity. when brain parenchyma involved, its called viral encephalitis, usu caused by HSV type 1, preference for limbic cortex, w/ bizarre psychotic behav, confusion, lethargy, h/a, memory loss, aphasia, szs, hemiparesis. can cause necrosis of TL and FL structures
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HIV-related encephalitis
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herpes, varicella-zoster, cytomegalovirus, PML (progressive multifocal leukoencephalopathy) leads to gradual demyelinaiton of brain and death in 3-6 months, HAART improves.
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toxoplasmosis
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parasitic infection oft in HIV, exposure in cat feces, undercooked meat, MRI shows ring-enhancing lesions and edema
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creutzfelt-jakob disease
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prion disease causes rapidly progressing dementia, exaggerated startle response, myoclonus, visual distortions or hallucinations and ataxia. mri-increased signal in BG, progressive neurologic deterioration and death in 6-12 months. can have incubation period of 2-15 years. not synonymous with BVE, but that is what cows have to cause CJD in person.
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impairment in consciousness 2 causes
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lesions directly affecting brainstem-diencephalic reticualr activating system (either directly, thru compression and distortion of nearby lesions) or by lesions affecting cerebral hemispheres bilaterally. impaired consciousness with a dilated, unreactive pupil is characteristic of uncal transtentorial herniation causing midbrain compression.PCA infarct can occur w/ uncal herniation as it passes thru tentorial notch
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acute stroke on CT
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can take 6-24 hrs to be visible on CT
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