4. PATH Intro to Neuropathology

Question 1

Oligodendrocytes are fried egg appearance and are always round, blue/dark, and can be found closest to neurons, neuropil can be found in the background and is mainly pink, what cells is oval*, and stains with glial fibrillary acidic protein GFAP revealing its perinuclear cytoplasm and well developed processes?

Answer 1

Astrocytes

Astrocytes+ Oligodendrocytes = Glia

Question 2

What neuron reaction to injury occurs in 12-24 hours and is the earliest morphologic indicator of acute insult due to hypoxia, hypoglycemia or trauma, and on histo can see shrinkage of cell body, pyknosis, loss of nucleoulus, loss of nissl substance with INTENSE eosinophilia of the cytoplasm?

Answer 2

Red Neurons (acute neuronal injury = 12-24…>24hrs = irreversible)

Note: pyramidal cells are most sensitive to insult

Question 3

What tpye of neuronal injury is the best indicator of neuronal injury showing cell loss due to reactive gliosis (proliferation of astrocytes in response to brain injury) with apoptosis, you see abnormal protein accumulation– seen most commonly in ALS and alzheimers?

Answer 3

Subacute and chornic neuronal death = Degeneration

Question 4

What is enlargement and rounding up of the cell body, peripheral displacement of the nucleus, enlarged nucleus, increased protein synthesis assoc w axonal sprouting, and where the nissl is moved from the center of cell to periphery (=central chromatolysis)?

Answer 4

Axonal Reaction

Question 5

Neuronal inclusions may occur from aging- intracytoplasmic accumulations of lipids, proteins, lipofusion or carbs, other intraCYTOplasmic inclusions include rabies negri bodies, alz neurofib tangles, parkinson lewy bodies and CJD, *intraNUCLEAR inclusions seen with viruses include what other two?

Answer 5

Herpes Cowdry Bodies

CMV- owls eye nuclear inclusion bodies(in both nucleus and cytoplasm)

Question 6

Note: Chromatolysis = swollen cell body, eccentric displacement of nucleus, loss of nissl substance except along the margins of the cell body- if you see these they are evidence of?

Answer 6

Neuronal system damage

Question 7

What, aka astrogliosis, is the MOST IMPORTANT histopath indicator of CNS injury***, characterized by both hypertrophy and hyperplasia of astrocytes, they act as metabolic buffers and detoxifiers in the brain, foot processes contribute to BBB?

Answer 7

Gliosis (reaction of astrocytes to injury)

Question 8

What is the change in astrocytes that include nuclei enlarge, become vesicular and develop prominent nucleoli, cytplasm expands and becomes BRIGHT PINK and dislocates nucleus centrally- forming stout ramifying processes?

Answer 8

Gemistocytic astrocytes or gemistocytes

Question 9

What type of astrocyte is a gray matter cell with large nucleus, pale staining central chromatin, intranuclear glycogen, and prom nuclear membrane and nucleolus, seen in individuals with long standing hyperammonemia due to chronic liver dz, wilson dz, or hereditary urea cycle dz?

Answer 9

Alzheimer Type II Astrocyte (not related to alzheimers dz)

Question 10

Any tumor that spills contents into/adjacent to brain parenchyma would produce a localized jury and cause astrogliosis

Answer 10

MEOW

Question 11

What are chracteristic of pilocytic astrocytoma- thick elongated, brightly eosinophilic, irregular structures that occur within astrocytic processes, found in regions of long standing gliosis (SEEN IN pilocytic astrocytoma), contains 2 heat shock proteins: ab-crystalline and HSP27, along with ubiquitin?

Answer 11

Rosenthal Fibers- thick pink corkscrew sausages

Question 12

What are aka polyglucosan bodies and are more commonly seen, are round, faintly basophilic, PAS+, concentrically laminated structures located adjacent to astrocytic end processes- especially subpial and perivascular zones, may contain glycosaminoglycan (GAG) polymers with some HSPs and ubiquitin, # increase with age and represent degen change?

Answer 12

Corpora Amylacea (represent indigestible remnants of astrocyte metabolism- common seen in aged brains) - onions**

Question 13

Microglia are mesoderm derived phagocytic cells that serve as resident macrophages of the CNS, have same surface markers as peripheral Mø= CR3/CD68, they respond to injury by proliferating, develop elongated nuclei (rod cells- as seen in neurosyphilis), they congregate around cell bodies of dying neurons (=neuronophagia) and they form aggregates around small foci of tissue necrosis= ?

Answer 13

Microglial Nodules

Question 14

Oligodendrocytes reaction to injury is usually a feeature of acquired demyelinating disease and leukodystrophies which may harbor viral inclusions as seen in progressive multifocal leukoencephalopathy PML, or glial cytoplasmic inclusions (mostly asynuclein) in oligodendrocytes as seen in MSA or?

Answer 14

multiple system atrophy

Question 15

Ependymal cells are ciliated columnar epithelial cells lining the ventricles which dont have a specific reaction but disruption of the ependymal lining and proliferation of subependymal astrocytes causes what, which are small irregularities on the ventricular surfaces, as seen/caused by CMV?

Answer 15

Ependymal Granulations

Question 16

Cerebral edema is accum of fluid in brain parenchyma- two main types include vasogenic and cytotoxic edema. What type is from increased ECF due to BBB distruption and increased vascular permeability, assoc with fluid shift from intravascular compartment to intercellular space, lack of lymphatics impairs resorption of excess ECF, localized edema = adjacent to inflam or neoplasm, generalized= often follows ischemic injury?

Answer 16

Vasogenic Edema (d/t BBB disruption, inflam or neoplasm)

Question 17

What cerebral edema is where the BBB is intact but there is an inc intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury often due to generalized hypoxic/ischemic insult or metabolic derangement- Na/K ATPase is compromised leading to retention of Na and H2O = global processes?

Answer 17

Cytotoxic Edema (d/t ischemia)

Question 18

Often both vasogenic and cytotoxic are seen in clinic, which results in flattened gyri, narrowed sulci, compressed ventricles, ultimately leading to?

Answer 18

Herniation*

Question 19

Hydrocephalus is accumulation of CSF within the ventricular system which is usually absorbed via arachnoid granulations… Response to inc CSF includes dilation of front and temporal horns, elevation of corpus callosum, thinning of cerebral mantle, stretching of septum pellucidum, enlargement of third ventricle and most commonly and importantly?

Answer 19

Papilledema (d/t inc intracranial pressure)

(causes include: inc production d/t chroid plexus papilloma, obstruction: intraventricular foramina-tumors/blood clot, congenital stenosis, secondary to tumors/*infections, or dec. absorption or outflow obstruction)

Question 20

Once cause of hydrocephalus would be due to pyogenic meningitis in which there is a thick layer of suppurative exudate covering the brainstem and cerebellum and thickens the leptomeninges causing obstructive hydrocephalus*, MC seen in neurosyphilis or what? (likes the base of the brain)

Answer 20

Tuberculosis TB!

Question 21

Congenital causes of hydrocephalus include intrauterine TORCH infections, agenesis/atresia/stenosis, AV malformation, arnold chiari, dandy walker, and cranial defects. Acquired causes of hydro include infections such as meningitis and cysticercosis, neoplasms, inflam d/t brain abscess, hypervitaminosis A or post hemorrhage such as?

Answer 21

Intraventricular or subarachnoid hemorrhage

Question 22

The MCC of noncommunicating (obstructive) hydrocephalus in the neonate/infant is aqueductal stenosis, in noncommunicating the ventricular system is obstructed and does not communicate with subarachnoid space (ex: dandy walker/aquaductal stenosis). What hydrocephalus is when the ventricular system is in communication with subarachnoid space but the CSF is not absorbed properly at the dural sinus level and the ventricles become SYMMETRICALLY dilated?

Answer 22

Communicating (non-obstructive) ex: neurosyphilis/arachnoid fibrosis= involves leptomenininges NOT a single point/obstruction

Question 23

Cysticercosis is caused by pork tapework taenia solium- causes 50% of acquired epilepsy cases in developing country and is the MC parasitc nervous system disease in the world, on MRI what can be seen in the brain?

Answer 23

Many calcified cysts

Question 24

What type of hydrocephalus refers to compensatory increase in ventricular volume secondary to loss of brain parenchyma (atrophy), type of communicating- see dilation of ventricles and shrinkage of brain substance due to stroke or injury or neurodegenerative DO (huntington/alz), CSF PRESSURE IS NORMAL?

Answer 24

Hydrocephalus Ex-Vacuo

Question 25

What hydrocephalus is common in >60, develops slowly, CSF drainage is blocked gradually, pressure not as elevated as others, causes dementia similar to alzheimer, gait similar to parkinson, easily reversed, 2 types: idiopathic and secondary (d/t SAH, trauma, tumor, infxn, all less common), presents as classic triad of urinary incontinence, gait disturbance and dementia- wet, wacky and wobbly?

Answer 25

Normal Pressure Hydrocephalus

Question 26

Increased intracranial pressure is generally due to generalized brain edema or focal expanding mass lesions such as tumors, abscesses, or hemorrhages. What is caused by increased pressure beyond the compensatory ability of venous system to compress and displacement of CSF leading to tissue pushing past the rigid dural folds (falx/tentorium) or through openings of the school?

Answer 26

herniation - subfalcine, transtentorial, tonsillar

Question 27

What type of herniation is unilateral or asymmetric expansion of the cerebral hemisphere which displaces the cingulate gyrus under the falx, leading to compression of the ACA and its branches- see contralat LE weakness?

Answer 27

Subfalcine (cingulate) herniation

Question 28

What type of herniation is due to mass effect of a medial temporal lobe compressed against the tentorium, compressing oculomotor N (CNIII palsy) causing a down and out eye along with dilated pupil on same side as lesion?

Answer 28

transtentorial Herniation

Question 29

What type of herniation is displacement of the cerebellar tonsils through the foramen magnum, is life threatening because it compresses the brainsstem and the corresponding vital respiratory and cardiac centers of the brain?

Answer 29

Tonsillar Herniation

Question 30

All of the following are signs and symptoms of what?
headache, nausea, vomiting, lethargy, change in pupil reaction, impaired upward gaze, false localizing signs, seizures, decreased coordination, ataxia, papilledema

Answer 30

Increased Intracranial Pressure

Question 31

What notch phenomenon is a result of compression of the cerebellar peduncle against the tentorium cerebelli due to transtentorial herniation, producing ipsi hemiparesis or hemiplegia, causes a visible notch in peduncle, affects CN6***?

Answer 31

Kernohan’s Notch

***right hemisphere herniation causes LEFT peduncle to be notched which causes RIGHT side motor impairment- paradoxical

Question 32

What hemorrhage is secondary hemorrhagic linear or flame shaped lesions in the midbrain and pons* that often accompany transtentorial herniation, occur in the midline/paramedian regions, again it is a midline hemorrhage into the pons (mesencephalon) that accompany transtentorial herniation?

Answer 32

Duret Hemorrhage

Question 33

Hypoxia means a low partial pressure of oxygen, ischemia means impairment of blood’s oxygen carrying capacity or inhibition of venous blood supply, infarct is area of necrosis resulting from sudden insuff or arterial or venous blood supply… Cessation of blood flow may be due to decreased perfusion pressure (hypotension), or?

Answer 33

small or large vessel obstruction or BOTH

Question 34

Hypoxia first affects prukinje cells of the cerebellum and pyramidal cells of sommer’s sector (CA1/2) in the hippocampus (MOST SENSITIVE), in both cases, the cells will die (pseudolaminar necrosis) and become shrunen, pyknotic and eosinophilic along with a decreased?

Answer 34

number of nuerons in the area

Question 35

Necrosis is the denaturation of intracellular proteins and enzymatic digestion of lethally injured cells, enzymes that digest the cells are derived from the lysosomes of the dying cells themselves, what type of necrosis is digestion of tissue into liquid viscous mass with NO architectural remnants- seen only in CNS and bacterial infections (purulent material)?

Answer 35

Liquifactive necrosis-CNS infarcts only

all other organs undergo ischemic coagulative necrosis where architecture remains

Question 36

Infarcted areas at low mag are shown well by myelin stain.. Acute ischemic injury causes diffuse eosinophilia of neurons (dead red neurons 12-24h) which begin to shrink, infiltration of a cerebral infarct by neutrophils begins at the edges of the lesion where vascular supply has remained intact, after 10 days, area of infarction is charcterized by presence of what and surrounding reactive gliosis?

Answer 36

MACROPHAGES = 10DAYS

After damage is cleaned up you see missing neuropil = pale due to dec number of cells

Question 37

What is known as separartion of arachnoid from dura due to contraction of underlying brain parenchyma status post infarct?

Answer 37

Hygroma

old infarcts destroy cortex and leave cavities

Question 38

Malformations and devel DOs path remains unknown but is a mix between genetic and environmental factors, including toxic compounds and infectious agents with teratogenic effects, medications/drugs (RX, OTC illicit and natural), the earlier the malformation occurs the more severe the phenotype, malformations include forebrain anomalies, post fossa anomalies, syringomyelia, hydromyelia and what - which is the MC?

Answer 38

Neural Tube Defects

Question 39

Neural tube defects are due to failure of the neural tube to close or reopening of a region of the tube after closure which may lead to malformations involving some combination of neural tissue, meningies and overlying bone or soft tissue. NTD account for most CNS malformations, the MCC is what which causes issues with neural tube closing by day 28?

Answer 39

Folate Deficiency* = VitB9 (works w Vitb12/C)

Question 40

What is aka spinal dysraphism, which may be asymptomatic bony defect (oculta) or flattened disorganized segment of cord associated with a meningeal pouch?

Answer 40

Spina Bifida Oculta (a-fetoprotein is not elevated)

Question 41

What is the MC type of spina bifida in which there is extension of CNS tissue thorugh a defect in vertebral column- usually lumbosacral, (meningocele only meninges protrude), leads to motor and sensory deficits in LE with accompanying bowel and bladder dysfunction, complicated by superimposing infection that enters open skin?

Answer 41

Myelomeningocele/ Meningomyelocele (both meniges and CNS tissues)

Question 42

What is a diverticulum of malformed brain tissue that extends out of a defect in the cranium, most often occurs in the posterior fossa, but also happens anterior fossa and through the cribriform plate (mislabeled as nasal glioma)?

Answer 42

Encephalocele

Question 43

What is absence of most of the brain and calvarium to form, forebrain development disrupted at 28 days gestational age, only thing that remains is area cerebrovaculosa = flattened remnant of disorganized brain tissue with admixed ependyma, choroid plexus, and meningothelial cells?

Answer 43

Anencephaly - post fossa may be spared

Question 44

Forebrain anomalies are caused by asymmetric migration of neurons while they are proliferating, excess cells leave the proliferating pool too early= overal generation of neurons is reduced. What occurs when the brain is abnl small or large, with small being more common, assoc w small head circumference, linked to chr abnl, fetal alch syndrome and HIV in utero, most like from a REDUCTION in overall # of neurons that reach neocrotex leading to a simplification of gyral folding?

Answer 44

Microcephaly/Megalocephaly

ZIKA VIRUS (arbovirus) is thought to cause microcephaly

Question 45

What forebrain anomaly is malformation characterized by reduction in the number of gyri or NO gyri pattern = agyria = a severe form of this malf, two types 1)smooth surfaced 2) rough or cobblestoned surface?

Answer 45

Lissencephaly

Question 46

What forebrain anomaly is characterized by small unusually numerous irregularly formed cerebral convolution, grey matter is composed of 4 layers or less (normal 6) with entrapment of meningeal tissue, can be induced by local injury toward end of neural migration or genetically (bilat and symetrical) influenced?

Answer 46

Polymicrogyria

Question 47

What forebrain anomaly is a group of migrational disease that are commonly assoc w epilepsy, defined by presence of collections of neurons in inappropriate locations along pathway of migration- commonly along ventricular surface, on X chr- filamin A protein and DCX (double cortin protein) mutations cause lissencepaly in males and subcortical band heterotopias in females?

Answer 47

Neuronal Heterotopias

Question 48

What forebrain anomaly is caused by incomplete separation of the two hemispheres across the midline- severe forms causing midline facial abnls including cyclopia, arrhinenceophaly = absence of olfactory cranial nerves, associated with trisome 13 (patau), due to defects in sonic HH pathway?

Answer 48

Holoprosencephaly

Question 49

What forebrain anomaly is relatively common, has a bat wing deformity (misshapen lateral ventricles) commonly associated with mental retardation but may occur in clinicall normal people?

Answer 49

Agenesis of the corpus collosum

Question 50

What posterior fossa anomaly is assoc with a small posterior fossa, misshappen midline cerebellum with downward displacement of the vermis through the foramen magnum, tenting of tectal plate, leading to hydrocephalus, assoc w lumbar myelomeningocele (TYPE 2), type 1 less severe w low lying cerebellar tonsils extending down into vertebral canal - silent?

Answer 50

Arnold-Chiari Malformation Type II/I

Question 51

What posterior fossa anomaly is characterized by an enlarged posterior cranial fossa with absent or rudimentary cerebellar vermis replaced by a midline cyst lined by ependymal and is contiguous with leptomeninges on its outer surface, enlargement of the fourth ventricle and hydrocephalus + NO VERMIS?

Answer 51

Dandy Walker Malformation

Question 52

What posterior fossa anomaly is hypoplasia of the cerebellar vermis with apparent elongation of the superior cerebellar peduncles and an altered shape of the brainstem- gives rise to molar tooth sign on imaging- caused by mutations that encode primary nonmotile cilia?

Answer 52

Jourbert Syndrome

Question 53

What is the formation of a fluid filled cavity in the inner portion of the cord that can extend into the brainstem, assoc w arnold chiari, presents in 2/3rd decade, assoc with classic sx of syrinx = isolated loss of pain and temp sensation of the upper extremities due to cross anterior spinal commissural fibers AWC?

Answer 53

Syringomyelia - enlargement of central canal of SC- interrupting fibers that cross through white commisure = pain/temp lost bilaterally UE

Anterolateral System/Spinothalamic Tract

Question 54

What is an expansion of the ependymal lined central canal of the cord, onset and destruction same as syringomyelia?

Answer 54

Hydromyelia

Question 55

NOTE: syrinx == tubular defect that extends laterally, disrupting the spinothalamic tracts (pain and temperature) and anterior horns (lower motor neurons)

Answer 55

MEOW

Question 56

What perinatal brain injury is a term for nonprogressive neurologic motor deficits characterized by combinations of spasticity, dystonia, ataxia/athetosis, and paresis attributable to insults that occured in the pre natal and perinatal periods (present from birth)?

Answer 56

Cerebal Palsy **MC

Question 57

What is the MCC of intraventricular hemorrhage in premature infants which is seen in germinal matrix(thick cellular layer immature cells under ependymal lining of ventricles) hemorrhage can extend into the cerebral ventricles (=intraventricular hem) and from there into the subarachnoid space (SAH), premature bbs between 22-30 weeks most likely- germinal matrix is a region of high cellularity and vascularity and vulnerable to insults from even minor changes in cerebral blood flow- near junction between thalamus and caudate nucleus?

Answer 57

Parenchymal Hemorrhage (germinal matrix hemorrhage)

Question 58

What is a type of perinatal infarct caused by hypoxic-ischemic events/infxns, premature bbs higher risk, infarct of supratentorial periventricular white matter- takes form of chalky yellow plaques consisting of discrete regions of necrosis and calcifications?

Answer 58

Periventricular Leukomalacia

Question 59

What is a type of infarct which is more severe than Periventricular Leukomalacia, in which both grey and white matter are damaged from extensive ischemia damage that leads to large destructive cysts throughout the hemispheres, seen as thinned out gliotic gyri = ulegyria?

Answer 59

Multicystic encephalopathy

Question 60

If someone falls awake= occipital skull fracture, someone loses consciousness = frontal fracture/impact, what is a fracture in which bone is displaced into the cranial cavity more than the thickness of the bone itself?

Answer 60

Displaced/Depressed Skull Fracture

Question 61

A basal skull fracture follows impact to the occiput or sides of the head - orbital and or mastoid hematomas can occur can also see CSF discharfe from nose/ears and infection may follow. What is a fracture that cross sutures of the skull usually caused by kinetic energy-multiple points of impact or repeated blows to the head? (new fracture lines DONT extend across old fracture lines)

Answer 61

Diastatic Fractures

Question 62

Signs of head injury include battle’s sign = bluish discoloration in postauricular region= basilar skull fracture, raccoon eyes = periorbital hematomas suggestive of basilar skull nasal or facial bone fracture and CSF otorrhea = leakage from external auditory canal due to?

Answer 62

Basilar Skull Fracture

Question 63

What type of injury is a category which includes: concussion (clinical syndrome)-altered consciousness secondary to head injury typically brought about by change in momentum of the head- assoc w instantaneous onset of tranisent neurological dysfunction, including loss of consciousness, temp resp arrest and loss of reflexes?

Answer 63

Parenchymal Injuries

-no radiologic findings w concussions but may see degree of axonal damage w LOC

Question 64

TBI/CTE is when there is some level of (nondegenerative/noncongenital) damage to the brain resulting from external mechanical force, such as rapid de/acceleration, impact, etc, there is an assoc diminished or altered state of consciousness*, brain function is temp or permanently impaired, head injury and what are not synonymous?

Answer 64

head injury does NOT equal TBI (can be single event)

Question 65

Chronic Traumatic Encephalopathy CTE from repeated* head blows- could be reason for sxs experienced before death including depression, impulsivity and behavior changes- memory loss/dementia, CTE leads to progressive loss of normal brain matter and an abnormal build up of a protein called?

Answer 65

Tau

Question 66

CTE is a taupathy characterized by deposition of hyperphosphrylated tau proteins as neurofibrillary tangles, astrocytic tangles and neurites in striking clusters around small blood vessels of the cortex at sulcul depths, general features of CTE include possivle microhemorrhages/DAD, focal nueronal loss, **NEUROFIBRILLARY TANGLES/amyloid (beta) and tau deposition and depigmentation of?

Answer 66

Substantia Nigra

along w cerebellar tonsillar scarring

Question 67

Direct parenchymal injury are contusions and lacerations caused by transmission of kinetic injury to the brain- crests of gyri are most susceptible. Contusion is a wedge shaped, broad base at point of impact, coup is a contusion at point of impact (d/t contact beetween brain/skull) and what is diametrically opposed to coup (sudden deceleration)?

Answer 67

Countercoup (from brain striking opposite inner surface of skull after sudden deceleration)

Question 68

What is a depressed, retracted, yellowish brown patch involving crests of gyri- old trauma lesions, often due to countercoup = inferior frontal cortex, temporal and occipital lobes?

Answer 68

Plaque Jaune

Question 69

Morphologically- brain contusions are wedge shaped with the broad base lying along the surface at the point of impact.. Early stages: pericapillary edema and hem, Next few hours: extravasation of blood 24 hours: pyknosis of the nucleus, eosinophilia of cytoplasm and disintegration of the cell which is morphological evidence of what?

Answer 69

Neuronal Injury

Question 70

What injury most often affects the surface but deeper subcortical white matter may be injured as well, microscopically there is axonal swelling** +/- hemorrhagic lesions, morph shows widespread asymmetric axonal swelling in hours of the injury- swelling best demonstrated with silver stain or amyloid precursor protein APP* and alpha synuclein?

Answer 70

Diffuse Axonal Injury DAI

Question 71

Diffuse Axonal Injury DAI is due to the direct action of mechanical forces, angular acceleration alone can produce even in the absence of impact, 50% of individuals who develop coma shortly after trauma, even without cerebral contusions, are believed to have DAI, may also see dilated axons which are also called?

Answer 71

Axonal Spheroids

Question 72

Shaking a child violently stops crying through inducing brain damage, 80% bbs dont die, they just develop brain damage, may be like a second concusion syndrome in which they dont die right away, but they die after hours of brain swelling and?

Answer 72

Diffuse Axonal Injury DAI

Question 73

To recognize shaken impact syndrome there are a constellation of injuries including Diffuse Axonal Injury DAI, cerebral edema, subdural hematomas, retinal hemorrhages, subgaleal hemorrhages, microscopic iron (prussian blue stain) and the child will never be?

Answer 73

Normal again

Question 74

An adult with a severe TBI on the date of injury will show a decrase in ventricle size and global edema, if followed up, 2 weeks post TBI, what can be seen?

Answer 74

Increase ventricle size = DEC parenchymal mass :(

Increased VBR= ventricle to brain ratio

Question 75

Epidural vascular injury is usually due to trauma and associated with a skull fracture in adults, rapidly evolving neurologic symptoms requiring intervention (ARTERIAL). What vascular injury is also due to trauma- may be mild, slowly evolving neurological symptoms, often with delay from time of injury (VENOUS)?

Answer 75

Subdural Vascular injury - d/t bleeding from lowpressure veins - risk greater in elderly

Question 76

Subarachnoid trauma is usually assoc with underlying contusions with involvement of crests of gyri, vascular abnormalities such as AV malformation or saccular berry aneurysms often have rapid neurological deterioration, secondary injury may emerge associated with vasospasm and what type of headache?

Answer 76

SUDDEN onset of SEVERE headache- THUNDERCLAP headache

Question 77

What type of hematoma is due to rupture of dural artery (middle menigeal A. MC), due to skull fracture- between dura and skull, extravastion of blood under arterial pressure can cause dura to separate from inner surface of skull, lens-shaped lenticular lesion w/ LUCID INTERVAL= patient is fine for several hours, then declines as BP causes dura to separate and compress brain?

Answer 77

EPIDURAL HEMATOMA

Question 78

What hematoma occurs when the bridging veins rupture, bleeding occurs into the REAL space between dura and arachnoid mater- see cresecent sign- MC in elderly w brain atropy b/c veins are already stretched?

Answer 78

Subdural Hematoma- much thinner on MRI than epidural

acute= lights up, chronic= dark