5. PATH Cerebrovascular Disease and Infections

Question 1

What artery when blocked causes deficits in upper motor neuron type weakness, cortical type sensory loss and contralateral hemiplegia intially, contralateral leg more than arm or face, and causes alien hand syndrome- movements of the contralateral arm not under voluntary control?

Answer 1

Anterior Cerebral Arteries ACA

Question 2

Posterior cerebral A blockage causes contralateral homonymous hemianopia. What artery is the MC artery for infarcts and ischemia, causing aphasia*, hemineglect, hemianopia, face-arm sensorimotor loss, *GAZE TOWARDS side of lesion, and lacunes which are small deep infarcts involving pentrating branchs and other vessels?

Answer 2

Middle Cererbral A. - MC

Question 3

Cerebrovascular dz is the 3rd leading cause of death and has 3 major categories; thrombosis, embolism, and hemorrhage, stroke designtation applies to all these conditions especially acute symptomology, what is the resultant lesions of the brain parenchyma?

Answer 3

Infarction

Question 4

The MC Cerebrovascular disorders include global ischemia (whole brain), embolism, ruptured aneurysm and MC- hypertensive intraparenchymal hemorrhage, when blood flow is reduced, survival depends on collateral circulation, duration of ischemia and magnitude?

Answer 4

and rapidity of flow reduction

Question 5

There are two types of reduction in blood flow 1) global ischemia-generalized reduction of perfusion such as carddiac arrest, shock and severe HTN, and 2) focal ischemia-localized area, usually due to embolic or thrombotical arterial occlusion, but MC due to?

Answer 5

Athersclerosis in hypertesion

Question 6

What infarcts occur in most distal regions of the brain or SC of the arterial blood supply to two adjacent cerebral arteries, causing the region between the 2 vessels to become very susceptible to ischemia and infarction- causing a sickle shaped band of necrosis over the cerebral convexit a few centimeters lateral to the interhemispheric fissure?

Answer 6

Watershed (border zone) infarcts

Question 7

Occlusion of internal carotid artery or hypotension in a patient with carotid stenosis causes ACA-MCA susceptibility to infarct causing proximal arm and leg weakness and transcortical aphasia - language issues, what watershed area if damaged would cause higher order visual processing issues- less common?

Answer 7

PCA MCA overlap area

Question 8

Watershed areas are at the border zone between major cerebral arteries and are due to hypoperfusion, cortical border zone infarcts are due to ACA-MCA-PCA issues and what border zone infarcts are of deep white matter of centrum semiovale and corona radiata at the border zone between lenticulostriate and deep penetrating cortical branches of MCA?

Answer 8

Internal border zone infarcts

Question 9

The most sensitive areas of the brain to ischemia will be the ‘watershed’ areas between anterior and middle cerebral arterial circulations. The neurons, and the large pyramidal neurons in particular, are the most sensitive to what kinda of stress?

Answer 9

hypoxic/hypoglycemic

Question 10

• There is little demarcation between the grey and white matter cut surface
• there is ongoing liquefactive necrosis
• Early changes (12-24 hours after):
• Red neurons: microvacuolization, eosinophilia of the neuronal cytoplasm, and later nuclear pyknosis and karyorrhexis
• Similar changes will occur later in astrocytes and oligodendroglia – reactive gliosis?
• After the acute injury the reaction to damage begins with infiltration of neutrophils
• Subacute changes (24 hours to 2 weeks):
• Tissue necrosis, influx of macrophages, vascular proliferation, and reactive gliosis
• Repair (mainly after 2 weeks):
• macrophages can persist for months
• Removal of necrotic tissue, loss of normal CNS architecture, and gliosis
• The pattern of neuronal loss and gliosis are uneven in the neocortex, with preservation of some layers and destruction of others that is called pseudolaminar necrosis
• fibroblastic proliferation with collagen deposition is uncommon in the CNS, except around organizing abscesses

Answer 10

MEOW

Question 11

Atherosclerosis commonly leads to stenosis of the internal carotid artery just beyong the carotid bifurcation, a carotid bruit continues into diastole- thrombi formed here can embolize distally esp in MCA,ACA and opthalmic A, a angioplasty and stenting or endarterectomy are needed to fix, symptoms associated with a lesion here include contralateral face arm weakness, contralat sensory changes and visual defects and ?

Answer 11

Aphasia/ Neglect

***Most likely at MCA

Question 12

Thrombotic occlusions are mostly due to atherosclerosis sites of primary thrombosis include carotid bifurcation, origin of MCA and either end of the basilar artery, rupture ulcertion or erosion of plaque exposes blood to thrombogenic substance causing thrombosis/clot… what is an intimal lesion that has a lipid core covered by a fibrous cap?

Answer 12

Atheroma

Major causes of stroke = thrombus or embolus

Question 13

Sources of emboli include cardioembolic infarcts such as AFib: left atrial appendage, Myocardial infarction: hypokinetic or akinetic areas, valvular disease: thrombi formed on prosthetic valves, artery to artery emboli: emboli from stenosed interna l carotidA or vertebral stenosis, what structure can causes a thromboembolus formed in the venous system bypassing lungs via it and goes straight to the brain aka PARADOXICAL EMBOLUS?

Answer 13

Patent Foramen Ovale

Question 14

Other sources of emboli include air emboli due to deep sea divers or iatrogenically, septic emboli due to bacterial endocarditis, fat/cholesterol emboli d/t long bong trauma and what emboli which is proteinaceous emboli ffrom marantic (non-bacterial thombotic) endocarditis (NBTE) due to hypercoagulable states like amniotic fluid emboli during child birth?

Answer 14

Marantic Emboli

Question 15

What causes shower embolization, which affected individuals manifest generalized cerebral dysfunction with disturbances of higher cortical function and consciousness, you see widespread white matter hemorrhages which is characteristic after trauma?

Answer 15

Bone marrow/fat embolization

Question 16

Hypercoagulability also causes emboli including heritable conditions such as protein S/C deficiency and antithrombin II def, dehydration, adenocarcinoma/malignancies, surgery, trauma, childbirth, DIC, hematologic dz such as sickle cell, leukemia, and vasculitis such as temproal arteritis, SLE, infections and neoplasms which are inflam processes which lead to?

Answer 16

BV vasculitis and luminal narrowing

Question 17

What has symptoms either positive or negative, motor, somatosensory, visual, auditory, olfactory, kinesthetic, emotional or cognitive and commonly caused by migraines, seizures and non-neuro conditions like cardiac arrhythmia or hypoglycemia in elderly, described as neurological deficit of less than 24 hours caused by temporary brain ischemia**?

Answer 17

Transient Ischemic Attacks TIA

Question 18

Transient Ischemic Attacks TIA >1hr are usually small infarcts but complete functional recovery can occur in 1 day, they are WARNING SIGNS for larger ischemic injury to the brain (stroke) and is a neuro emergency**, 15% of TIA pts have a stroke causing persistent deficits in 3 months, half of those in first 48 hours*, main mech for TIA is emoblus temporarily occludes and then disolves, an in situ thrombus formation and or?

Answer 18

Vasospasm

Question 19

Stoke is a major cause of death in US- and major cause of permanent disability, there are two types, 1) hemorrhagic (RED) are more likely to occur when emboli partially occlude vessel/undergo dissolution- red d/t reperfusion of damaged vessels 2) is what? which is pale/bland/anemia-bloodless and is thrombus (over athero-plaque) associated?

Answer 19

Ischemic Infarction

tPA is contraindicated in hemorrhagic infarcts

Question 20

Ischemic stroke is d/t inadequate blood supply causing infarciton/death of brain tissue– with many mechanisms including embolic: material from one location travels to another, thrombotic- locally formed clot, large vessel: MCA, small vessel: deep structures-BG/thalamus, and what which are small vessel infarcts resemblind small lakes?

Answer 20

Lacunar Infarcts- most commonly occur in lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nuc and pons

usually due to hypertension

Question 21

Ischemic infarcts are due to thrombus or emboli, or hypoxia, and hemorrhagic are due to rupture aneurysm or hypertension in which there is a SAH or intracerebral hemorrhage respectively, note with reperfusion after ischemia there is injury which can be seen as ?

Answer 21

Punctate Hemorrhages

Question 22

What infarcts are from deep penetrating arteries and arterioles developing arteriolar sclerosis in lenticulostriate arteries, see lake like single or multiple small cavitary infarcts, localized infarcts causing pure motor hemiparesis - posterior limb internal capsule**, thalamic lacune causing contra somatosensory deficits and BG lacune causing hemiballismus?

Answer 22

Lacunar Infarcts

Question 23

What hemorrhages happens during HTN that causes small caliber penetrating vessels and the development of small hemorrhage- which is reabsorbed and leave small slit like cavities that are surrounded by brownish discoloration, w focal tissue destruction, pigment laden mø and gliosis?

Answer 23

Slit Hemorrhages

Question 24

What type of encephalopathy is a clinicopathologic syndrome of malginant HTN manifested by eye and kidney pathology, HTN risk factor assoc with deep brain parenchymal hemorrhages, comes with HA, confusoin, vomiting convulsions and coma, brain is edmatous and can lead to herniation of tonsil, petichiae and fibrinoid necrosis of arterioles in grey/white matter seen?

Answer 24

Hypertensive Encephalopathy

Question 25

What dementia is a stepwis decline in cognitive function, affects patients w bilarteral grey and white matter infarcts over the years, presents as dementia, gail abnls, pseudobulbar signs and other neuro deficits, caused by cerebral athersclerosis, vessel thrombosis/embolus and cerebral arteriorlar sclerosis from chronic HTN?

Answer 25

Vascular Multi-Infarct Dementia

Question 26

Binswanger dz is a vascular dementia assoc with large area of subcortical white matter with myelin and axon loss. What microaneurysms are associated with chronic hypertension and can cause minute aneurysms in the basal ganglia?

Answer 26

Charcot-Bouchard Microaneurysms

NOTE: saccular berry aneurysms occur in large intracranial vessels in subarachnoid space

Question 27

Intraparenchymal hemorrhage is rupture of a small vessel in the brain associated with sudden onset of neuro symptoms (stroke), can see ganglionic and lobar hemorrhage caused by HTN and cerebral amyloid respectively, what is the risk factor MC associated with deep brain parenchymal hemorrhages?

Answer 27

HYPERTENSION

Question 28

What angiopathy is MC assoc with lobar hemorrhage due to the same AB amyloid depositied in the walls of vessels as in AD, producing microbleeds, pts that have E2/4 allele will increase risk for repeat bleeding (E4 high risk in AD), typically related to ONLY the leptomeningeal and cerebral cortical arterioles and capillaries?

Answer 28

Cerebral Amyloid Angiopathy CAA

Question 29

What AD ateriopathy is associated with NOTCH3 mutation leading to misfolding and collection of the receptor protein which is expressed in vascular smooth muscle, it is characterized by recurrent strokes usually infarcts and dementia, white matter changes at 35, stroke at 45, see thickening of media/ adventitia, loss of SM cells and basophilic PAS+ deposits?

Answer 29

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy CADASIL

Question 30

Stroke risk factors include HTN/DM, hypercholesterol, cigarette smoking, +family hx, cardiac dz- valvular/Afib/PFO, prior hx, and hypercoagulability… Stroke in young patient: think arterial dissection, PFO or hypercoagulability; also?

Answer 30

Sickle Cell!

Question 31

An aneurysm is a localized abnormal dilation of a blood vessel or the heart, the MCC of clinically significant subarachnoid hemorrhage is rupture of what aneurysm in the cerebral artery (ACA= MC)- usually in circle of willis so begins as basilar SAH (base of brain)?

Answer 31

Rupture of Saccular (Berry) Aneurysm

absence of SM or intimal elastic lamina at birth

Question 32

Anerysms can also come from extension of hematoma, as well as trauma, mycotic, saccular and dissection which are all most often in anterior circulation, atherosclerotic fusiform (not saccular) is mc in basilar A., most are not present at birth but develop overtime due to underlying defect in the medial of the vessel, as seen in ADPKD, ehlers danlos type IV, NF1, and MC?

Answer 32

MARFANS

RISK: smoking/HTN (DUH)

Question 33

Mycotic aneursym is caused by an infected artery wall and is fairly rare, caused by bacteria/fungus in the blood- such as mucor, aspergillus and?

Answer 33

Candida

Question 34

2% of population has saccular aneurysms, 90% saccular found near major branch points of anterior circulation, rupture usually occurs in 5th decade slightly more frequent in females, 1/3 of ruptures are assoc with acute increases in ICP such as straining stool or sexual orgasm, aneurysms larger than what in diameter have a 50% risk of bleeding per year?

Answer 34

> 10mm

Question 35

With saccular or berry aneurysms, blood rushes into subarachnoid space* and causes a thunderclap headache or the WORST HEADACHE IVE EVER HAD**, 20-50% die w rupture, repeat bleeding is common in survivors, in the first few days after SAH- there is an inc. risk of additional ischemic injury from what?

Answer 35

Vasospasm affecting vessels bathed in extravasated blood

Tx with clipping or coiling

Question 36

There are four main groups of vascular malformations including cavernous, capillary telangiectasias, venous angiomas and what, which most often occur in cerebral hemispheres of young adult, can involve both vessels of subarachnoid space and may extend into brain parenchyma?

Answer 36

Ateriorvenous malformations AVM

Question 37

Ateriorvenous malformations AVM (*MC) are tangeled vessels that show prominent pulsatile ateriovenous shunting with high blood flow- bypass a capillary bed (arteries to veins), they can often be complete resected without complication, 2x mc in men, present as seizure disorder in 10-30s, intracerebral hemorrhage orSAH, with the most common vessel affected being?

Answer 37

Middle Cerebral Artery - esp posterior branches

(AVM/cavernous malf asso w hem)

(nonfunctional cortex under AVM, tx w embolization prior to surgery or radiation tx to reduce size and bleeding)

Question 38

There are 4 routes of infection 1) direct implantation via trauma or congenital malformations such as myelomenigocele 2) local extension via sinuses/teeth, cranial or spinal osteomyelitis, 3) peripheral NS- viruses (rabies/herpes zoster) and 4) the MC ?

Answer 38

Hematogenous spread of infection- MC is arterial primarily but retrograde venous spread via anastomosis with facial veins is possible

Question 39

Infections can organize with scarring of foramina to produce a noncommunicating hydrocephalus or it could scar the vertex and impair reabsorption of CSF at the arachnoid granulations which would produce?

Answer 39

Communicating HydroCephalus

Question 40

The meninges include dura mater, arachnoid and pia, 15% diffusion across the meninges, CSF-85% produced by choroid plexus of lateral third and fourth ventricles, complete exchange of CSF every 3-4hours, what is inflam process of the leptomeninges (inner two meniges, arachnoid and pia mater) and CSF within the subarachnoid space caused by microbes?

Answer 40

Meningitis

acute pyogenic= bacteria
aseptic= acute or subacte viral
chronic= Tb/spirochetal/cryptococcal

Question 41

Acute pyogenic meningitis: neonates: ecoli and Group B strep, Adolescents: N. meningitidis, elderly: strep pneumo** (MC overall) and listeria, immune supressed = klebsiella/anaerobic, H. Influenza - vax so no longer a common cause in 3m-2yo, clinical presentation of meningitis is HA, photophboia, irritable, cloudy consciousness and neck stiffness, LP shows cloudy/purulent CSF under pressure and it has what protein/glucose?

Answer 41

HIGH protein, LOW glucose

Question 42

What type of meningitis develps by seeding of the CSF from subepidural or submeningeal granulomas,- CSF has no lymphatics, however lymphatics are in the epidural space- infections of the retropharyngeal, posterior mediastinal or retroperitoneal spaces may produce spinal epidural abcesses?

Answer 42

Tuberculus Mengingtis

Question 43

Rabies (rhabdovirsu) binds at acetylcholine receptors at the NMJ and ASCENDS to CNS viA MOTOR NERVES, what virus produce latent infection of sensory ganglia, replicate in schwann cells, and ASCEND to the CNS in sensory* nerves,?

Answer 43

Herpes Simpelx and Zoster

Question 44

Capillaries do NOT have fenestrations or intracellular clefts in the CNS/brain, they are surrounded by foot processes of adjacent astrocytes, molecules move across mainly by active transport and lipid solubility, there is relative IMPERMEABILITY to immunoglobulins, complement and antibiotics*** which is an important factor in pathogenesis of CNS infections and in the selection of abx tx… why?

Answer 44

The chosen ABx MUST be able to cross the BBB

Question 45

Widespread infection, involving all tissue elements, characteristic of bacterial meningitis and many viral encephalitides, functional specialization of different cell populations and of specific neuro-anatomical regions determines the characteristic neurological sxs when specific cell types or anatomic areas are involved by the?

Answer 45

Infectious agent

Question 46

Meningoencephalitis is inflam of the meninges AND brain parenchyma, chemical meningitis is NONBACTERIAL irritant in subarachnoid space (chemo), pyogenic is bacterial, aseptic is viral, an chronic meningitis is MC due to Tb, spirochetes such as neurosyphilis/neuroborreliosis or?

Answer 46

Cryptococcus

tb/neurpsyphilis has predilection for base of brain

Question 47

Cerebral edema is assoc w infection- and inflammation cause loss of capillary integrity and loss of BBB** with transudation of intravascular fluid into brain or spinal cord, development of edem is accelerated by products released by both living bacteria and antibiotic lysed bacteria, and it is slowed and reversed by what only?

Answer 47

CORTICOSTEROIDS

Question 48

Symptoms of acute meningitis (suppurative) include HA, meningeal irritation signs such as kernig (extend leg keeping hip flexed) and brudzinski (flex neck= flexed hip/kness if+), high fever* confusion and coma, full syndrome develops in several days however it may develop over a few hours with fulminant course, what should NOT be done?

Answer 48

DONT send pt home!

Question 49

Acute meningitis locations: pneumococcal meningitis often denset over convexities near sagittal sinus, H. influenza usually basal location, what material can be seen obscuring vessels in the sulci?

Answer 49

Purulent/Cloudy material grossly

Question 50

Acute meningitis suppurative is associated with what type of immune cell which fills the subarachnoid space, and follow leptomeningeal vasculature which when fulminant- inflam may extend to ventricles producing ventriculitis, phlebitis may lead to venous thrombosis and hemorrhagic infarction of brain, and focal cerebritis is inflam cells infiltrating walls of the veins and extend into brain substance?

Answer 50

BACTERIAL = Polymorphonuclear cells = NEUTROPHILS

Question 51

What syndrome may occur and is associated wtih meningitis associated with septicemia with hemorrhagic infarction of the adrenal glands and cutaneous petechiae- occurs MC with meningococcal and pneumococcal meningitis?

Answer 51

Waterhouse-Friderichsen Syndrome

Question 52

Leptomeningeal fibrosis can happen after pyogenic meningitis and lead to hydrocephalus– the capsular polysaccharide of the microbe (in pneumococcal meningitis for example) can make a gelatinous exudate that promotes arachnoid fibrosis forming what is known as chronic?

Answer 52

Adhesive arachnoiditis

Question 53

Complications of bacterial pyogenic meningitis include seizures, encephalitis, hearing loss, blindness, paralysis, fulminant especially with meningococcemia**- rash and adrenal hemorrhage leading to death which is?

Answer 53

Waterhouse-Friderichsen Syndrome

Question 54

Lumbar Puncture (between 3rd/4th lumbar vertebrae) is done to check for meningitis and to get a gram stain of CSF, culutre CSF/blood, antigen detection in CSF/ urine, and PCR is done with the CSF. Match the following gram stain with bacteria....
Gram neg diplococci
Gram pos diplococci
Gram neg pleomorphic
Gram pos cocci
Gram Neg bacilli

H. Influenza
S. Pneumoniae
N. Meningitidis
S. Aureus/S Epi/ Streptococci
E. Coli

Answer 54

Gram neg diplococci = N. Meningitidis
Gram pos diplococci = S. Pneumoniae
Gram neg pleomorphic =H. Influenza
Gram pos cocci = S. Aureus/S Epi/ Streptococci
Gram Neg bacilli = E. Coli

Question 55

Glucose is typically decreased and protein is increased with bacterial infection, and neutrophils are assoc with bacteria, gross appearance is cloudy/turbid(chunky) with HIGH pressure. For virus, gross appearance is clear, normal pressure on puncture, NO neutrophils, instead you see lymphs (lymphocytic pleocytosis), and what with protein and glucose?

Answer 55

Protein is moderately inc

Glucose is normal

Question 56

There is an increased risk of meningitis in people aged <5 or >60, in diabetes, HIV, contiguous infection (sinusitis), IV drug abuse, bacterial endocarditis and ?

Answer 56

Sickle Cell Anemia

Question 57

Acute focal suppurative infections- brain abscess has same route as meningitis- acute bacterial endocarditis predisposes to multiple abscesses, congenital heart disease = r to l shunt removes pulmonary filtration of organisms, chronic pulmonary sepsis, systemic dz w immunosuppression, non immunosupressed MC is due to? 2

Answer 57

Strep and Staph

Question 58

Acute focal suppurative infections causes abscesses- patients present with progressive focal neuro deficits and signs/sxs of increased intracranial pressure, CSF has high WBC (neutrophils), High protein and NORMAL glucose (acute), complications include abscess rupture with ventriculitis or meningitis and venous sinus thrombosis.. tx with surgical drainages and?

Answer 58

antibiotics

Question 59

ON MRI/CAT scan with Acute focal suppurative infections you can see brain abscesses with central liquifactive necrosis and edema/fibrosis surrounding, outer margin has exuberant granulation tissue with neovascularization which leads to vasogenic edema- ringed by fibroblasts depositing collagen, and will show as?

Answer 59

ring enhancement on CT d/t increase vascularity from capillary proliferation and disrupted BBB

Question 60

What is caused when bacterial or fungal infections of the skull bones (mastoiditis) or sinuses spread to subdural space to produce this, the arachnoid and subarachnoid spaces are usually unaffected, large ones can produce mass effect or thrombophlebitis of bridging veins that can cross subdural space and result in venous occlusion and **infarction of the brain?

Answer 60

Subdural Empyema

Question 61

Subdural Empyema as signs and sx of where the infection is, fever, HA, stiff neck, CSF is similar to brain abscesses (NL glucose, high WBC, High protein) if left untreated causes focal neuro signs and sx, lethargy and coma, tx involves surgery, and after tx, residuum is usually only residual evidence wwhich is also called?

Answer 61

Thickened Dura

Question 62

What abscess is MC associated with **osteomyelitis- and comes from another source of infection from surgery or sinusitis, the absecess of the spine may cause cord compression and constitute a neurosurg emergency?

Answer 62

Extradural Abscess (like in epidural space)

Question 63

What bacterial colonized the oropharynx and rhinpharynx of asymptomatic carriers, spread by direct contract via resp droplets, more common in crowded populations like dorms/ barracks, Gram NEG diplococci assoc w rapid septicemia, fever, hypotension, DIC and petechial/purpuric lesions, hemorrhage infarction of adrenals and purpura fulminans which is hem skin lesions which progress to gangrene?

Answer 63

Neisseria Meningitidis

*Chocolate Agar (same w H influenza)

Question 64

Chronic meningitis has sx of fever headache, lethargy, confusion, N/V and stiff neck, CSF shows elevated protein, low glucose, and lymphocytic pleocytosis (sometimes w neutrophils), diagnosis made if sx and csf abnormalities persist or progress for more thatn 4WEEKS, mc due to Tb, neuroborreliosis (lyme) and?

Answer 64

Neurosyphilis

Question 65

M. Tuberculosis is located in base of the brain (arachnoiditis) obliterates cisterns and encases cranial nerves, subarachnoid space contains gelatinous or fibrinous exudate causing arachnoid fibrosis leading to hydrocephalus (and CN symptoms), also associated with what which is inflam of vessel walls, causing intimal thickening, arterial occlusion and infarction of underlying brain?

Answer 65

Obliterative Endartitis

May see tuberculomas= well circumscribed intraparenchymal mass w central caseous necrosis – may cause calcification if inactive

** GET CULTURE IN ADDITION TO SMEAR OF CSF

Question 66

M. Tuberculosis causes diffuse meningoencephalitis- see white areas on leptomeninges, remember to look for acid fast staining with Tb- turns pink, and once can see on histo- reactive astrocytes and lymphocytic infiltrate, the swollen reactive astrocytes are known as?

Answer 66

Gemistocytes

Question 67

What bug causes chronic meningitis with neuro sxs that follow a characteristic rash about 4 weeks later, see cranial nerve palsies (bells) and peripheral neuropathy, CSF WITH antibodies*, via PCR see that antibodies cross react with infectious mono, rheumatoid arthritis, SLE and syphilis, caused by ixodes tick?

Answer 67

Lyme dz or Borrelia Burgdorferi or Neuroborreliosis

Question 68

Neurosyphilis is the tiertary stage of treponema pallidum, only seen in 10% pts, presents with meningovascular neurosyphilis , paretic neurosyphilis and or tabes dorsalis, most will have a mixture of the three but most often a combination of paretic neurosyphilis and?

Answer 68

Tabes Dorsalis

Syphilis much higher due to AIDs

Question 69

Which T. Pallidum neurosyphilis is assoc with chronic meningitis involving the base of the brain and sometimes cerebral convexities and spinal leptomeninges (pia/arachnoid mater), , causes communicating hydrocephalus, obliterative endarteritis aka Heubner arteritis assoc w perivascular inflam rich in plasma and lymphs, cerebral gummas (plasma cell rich mass lesions) may occyr in meninges and extend to parenchyma?

Answer 69

Meningovascular Neurosyphilis

Question 70

Which T. Pallidum neurosyphilis is insidious but progressive mental deficits that results in mood disturbances (delusions of grandeur**) that terminate in severe dementia (general paresis of the insane), assoc w perivascular iron deposits, also granular ependymitis = proliferationof subependymal glia under damaged endymal lining (hydrocephalus)?

Answer 70

Paretic neurosyphilis (invasion of brain by spirochete)

Question 71

Which T. Pallidum group of sx is damage to sensory nerves (loss of myelin/axons) in the dorsal roots, impaired joint position sense and resultant ataxia (locomotor ataxia= widened gait), loss of pain sensation, joint damage=charcot joints, lightening pains and absence of deep tendon reflexes**?

Answer 71

Tabes Dorsalis

causes pallor and atrophy in the dorsal columns of the spinal cord (cuneate fasiculus, gracile fasciculus)

Question 72

What type of meningitis is assoc with absence of recognizable organism in patient with meningeal irritation, fever, and alterations of consciousness, 80% causes by enteroviruses, clinical course less fulminant than pyogenic, CSF shows *Lymph pleocytosis (inc cell count), moderate inc in protein and glucose near normal, usually self limiting and tx symptomatically?

Answer 72

Aseptic Viral Meningitis

(note: An aseptic meningitis-like picture may develop subsequent to rupture of epidermoid cyst into the subarachnoid space or the introduction of a chemical irritant (chemical meningitis). In these cases, CSF is sterile with pleocytosis of neutrophils & ↑ protein concentration with normal glucose.)

Question 73

Viral Meningitis is a CNS infection that may occur following hematogenous dissemination of viruses, they may reach the CNS through nerves* (olfactory/trigeminal sensory or motor nerves), brain mounts inflam response w population of lymphocytes, what is an important facet for several viruses including herpes, progressive multifocal leukoencephalopathy, etc?

Answer 73

LATENCY

Question 74

Characteristic findings of viral encephalitis are perivascular cuffs of lymphocytes and microglial nodules, NOT neutrophils. What causes epidemic encephalitis via misquito vectors such as west nile - involves SC producing polio like syndrome w paralysis, CSF is colorless, inc pressure/protein, NL glucose, intially CNS is neutrophils and then converts to lymphocytes- multiple foci of necrosis in white /gray matter?

Answer 74

Arthropod Borne viral Encephalitis

Question 75

Arthropod Borne viral Encephalitis such as west nile presents with seizures, confusion delirium, ocular palsies, reflex asymmetry and stupor/coma, can see microglial cells forming small aggregates around the foci of necrosis called microglial nodules, and what - which are particularly single cell neuronal necrosis with phagocytosis of the debris?

Answer 75

Neuronophagia (FYI)

Question 76

What viral encephalopathy is MC in children and young adults, presents as mood, memory and behavior disturbances, some progress with weakness, lethargy, ataxia and seizures that take 4-6 weeks to resolve, associated with defect in TLR3 signaling pathway, is NECROTIZING AND HEMORRHAGIC?

Answer 76

Herpes Simplex-HSV-1

Question 77

Herpes Simplex-HSV-1 has a tropism for inferior and medial temporal lobes, orbital gyri of frontal lobes as well, hemorrhagic lesions of the temporal lobes are characteristic of herpes simplex virus encephalitis, there is perivascular inflam with viral inclusion bodies in neurons and glial cells known as?

Answer 77

Cowdry Type A intranuclear inclusion bodies

HSV-2= 50% neonates born by vag delivery to women w active primary HSV = severe encephalitis

Question 78

Herpes Simplex-HSV-1 encephalitis of the temporal lobe* – can also see cingulate gyrus destruction, massive temporal lobe destruction, hemorrhagic necrotizing loss is characteristic, can also see intranuclear inclusions with migration of chromatin, ground glass nuclei which are multinucleated and what type of nodules?

Answer 78

Microglial nodules

Question 79

What virus is the chickenpox cutaneous infection, latent phase is in sensory neurons of dorsal root or trigeminal ganglia, reactivation occurs and is shingles- painful vesicular skin eruption limited to a single or limited dermatome, also assoc w persistent postherpetic neuralgia syndrome where there is persistent pain as well as painful sensation following nonpainful stimuli (brushing clothes)?

Answer 79

Herpes Zoster (varicella-zoster)

Question 80

What virus occurs in fetuses (TORCHES) and immunocompromised patients, in utero causes periventricular necrosis/leukomalacia is characteristic, leading to severe brain dysfunction causing microcephaly and periventricular calcification, in IC - see subacute encephalitis, tends to localize in paraventricular subependymal regions causing severe hemorrhagic necrotizing ventriculoencephalitis and chroid plexitis?

Answer 80

Cytomegalovirus CMV

Question 81

Cytomegalovirus CMV can cause radiculoneuritis in the lower spinal cord and roots, and is assoc with prominent enlarged cells with intranuclear and intracytoplasmic inclusions*** both- CMV infection is confirmed via?

Answer 81

immunohistochemistry

Question 82

What acutely has mononuclear cell perivascular cuffs and neuronophagia of the anterior horn motor neurons causing flaccid paralysis, and may extend to post horns and produce cavitations, and has a post syndrome which develops 25-35 years later assoc with progressive weakness with decreased muscle mass and pain?

Answer 82

Poliomyelitis

enterovirus transmitted fecal oral

Question 83

What virus is lyssavirus genus of the rhabdoviridae family has an incubation period of 1-3 months and causes degen and inflam of the brainstem, infections ascend* along peripheral nerves from the wound site, and symptoms include malaise, fever, HA with local Paresthesias around the wound (needles and pins) which is diagnostic?

Answer 83

Rabies distinct bullet shape virus

Question 84

Rabies causes extraordinary CNS excitability leading to violent motor responses progressing to convulsions, there is flaccid paralysis and resp center failure, see foaming of the mouth due to contracture of pharyngel muscles that produce aversion to swallowing, what is a PATHOGNOMONIC finding of round to oval eosinophilic cytoplasmic inclusions that are found in the pyramidal neurons of the hippocampus and purkinje cells of cerebellum***?

Answer 84

Negri Bodies

Question 85

What is an aseptic meningitis occuring within 1-2 weeks of seroconversion acute phases include mild lymphocytic meningitis, perivascular inflammation and some myelin loss, chronic shows *microglial nodules with multinucleated giant cells, vessels have abnormal prominent endothelial cells and perivascular fomay or pigment laden mø and the white matter shows diffuse areas of myelin palor axonal swelling and gliosis?

Answer 85

HIV Aseptic Meningitis

Question 86

HIV Aseptic Meningitis associated w dementia via inflam activation of microglial cells- no specific pathologic lesion or its correlate, what syndrome is characterized by paradoxical deterioration after starting therapy from the exuberant reconsitituted immune system/ inflammatory response?

Answer 86

Immune Reconstruction Inflammatory Syndrome IRIS

Question 87

HIV is also associated with an increase incidence of WHAT CANCER**?

Answer 87

Primary CNS Lymphoma

Question 88

What leukoencephalitis is caused by JC polyomavirus and has tropism for oligodendrocytes and there fore demyelination is its principle pathologic effect, primary infxn is a-sx but reactivation during immunosuppresion** exclusively occurs in IC patients (such as HIV+), causing irregular ill defined destruction of white matter- subcortical area of demyelination with lipid laden mø in center w dec # of axons?

Answer 88

Progressive Multifocal Leukoencephalopathy PML

Question 89

Progressive Multifocal Leukoencephalopathy PML on histo stained for myelin shows *irregular, poorly defined areas of demylination which may become confluent in places, with enlarged oligo nuclei (represents effect of viral infection), white matter demyelination leading to loss of coordination and weakness, see reactive astrocytes and oligo nucleus filled with?

Answer 89

Glassy amphophilic Viral inclusions

Question 90

Subacute sclerosing panencephalitis SSPE is a rare progressive clinical syndrome that occurs in NON-immunized kids or young adults months or years after initial infection by measles virus (rubeola), see cognitive decline, spasticity of limbs and seizures, what virus?

Answer 90

Paramyxovirus

spread via resp droplets

Question 91

Subacute sclerosing panencephalitis SSPE due to paramyxovirus/rubeola/measles shows widespread gliosis and myelin degeneration ** viral includsion of oligos and neurons, variable inflammation of white and gray matter, and what which is also see in alz?

Answer 91

neurofibrillary Tangles

Question 92

FYI: Three to five days after symptoms begin, a rash breaks out. It usually begins as flat red spots that appear on the face at the hairline and spread downward to the neck, trunk, arms, legs, and feet. Small raised bumps may also appear on top of the flat red spots. The spots may become joined together as they spread from the head to the rest of the body. When the rash appears, a person’s fever may spike to more than 104° Fahrenheit.
After a few days, the fever subsides and the rash fades.
Measles vaccine is usually combined with mumps and rubella (MMR), or combined with mumps, rubella and varicella

Answer 92

MEOW

Question 93

Fungal meningoencephalitis is only seen in immunocompromised pts, via hematogenous dissemination, MC- candid, mucor, aspergillus and crypto, Diabetes = MUCORMYCOSIS, vasculitis = Mucor/aspergillosis, thrombosis causes hemorrhagic infarction that may become septic, endemic pathogens after pulmonary/cutaneous infxn affect CNS and include histo/coccidiodes and?

Answer 93

Blastomyces

Question 94

Brain parenchymal infection causing granulomas is MC due to candida and cryptococcus, crytpo meningitis is MC in AIDS patients and may be fulminant and fatal in 2 weeks or may take years, on histo of the brain there are numerous areas of tissue destruction seen as what, associated with spread of organims in perivascular space?

Answer 94

Soap Bubbles * - high mag see cryptococci

Question 95

crytpo meningitis may obstruct outflow of CSF via foramina of luschka and magendie leading to hydrocephalus, cellular immune dysfunction predisposes to it, (chronic), CSF stained via INDIA INK PREP, also do culture of CSF, urine, sputum blood and stools- What antigen is crypto CSF assoc with?

Answer 95

Cryptococcal Polysaccharide Antigen via india ink

Question 96

What opporutnistic infection is MC in HIV or IC pts ( early in pregnancy, spreads to fetus resulting in severe brain damage (multifocal necrotizing brain lesions that may calcify).* ), is it as protozoa, causes brain abscess located near grey-white junction of cerebral cortex and deep grey nuclei, histo show central foci of necrosis, petechial hemorrhages surround by acute/chronic inflam, mø infiltration and vascular proliferation?

Answer 96

Toxoplasmosis Gondii

Question 97

Toxoplasmosis Gondii is assoc with free tachyzoites and encysted (pseudocyst with) bradyzoites at the periphery of necrotic zones- may be ring enhancing lesions, again shows ring enhancement on imaging with central necrosis- seen on H/E and giemsa but most commonly?

Answer 97

Immunohistochemical

Question 98

What protozoal dz is caused by naegleria (quick death necrotizing encephalo) or acanthamoeba (chornic granulomatous meningoencephalitis), naegleria fowleri- brain eating ameba, infects people when contaminated water enters brain through nose- via warm freshwater such as lakes, rivers hot springs and soil?

Answer 98

Cerebral Amebiasis

best seen PAS or methenamine silver

Question 99

What protozoal dz is caused by plasmodium falciparum- resulting in long term cognitive defects in survivors/ see reduced cerebral blood flow, ataxia, seizures and coma in acute phase?

Answer 99

Cerebral Malaria

Question 100

What is the MC prion disease (which is abnormal forms of cellular protein that cause rapidly progressive neurocognitive DOs that may be sporadic/familial or transmitted- all dz are assoc w PrP prion protein and PRNP gene, heterozygosity at codon 129 protects against disease, see spongiform change- intracellular vacuoles in neurons and glia?

Answer 100

Creutz-Jakob Disease CJD (mad cow- rapidly progressive dementia) along w many others

Question 101

Creutz-Jakob Disease CJD is he MC prion disease and 90% of cases in appear in 70s, caused via iatrogenic transmission via corneal transplant, brain implantation of electrodes and contam human growth hormone, presents with subtle changes in memory/behavior followed by RAPID dementia and startle?

Answer 101

**Myoclonus - involuntary jerking muscle contractions (die in 7 months) - 100% fatal

Question 102

What kind of CJD comes from exposure to bovine spongiform encephalopathy from contaminated food or blood transfusion, in young adults, see behavioral changes early, and assoc w kuru plaque which are extracellular deposits of aggregated abnl protein which is CONGO RED AND PAS+?

Answer 102

Variant CJD 1995 - UK young adults

Question 103

What fatal prion disease is associated with sleep disturbances initially, less than 3 year survival- caused by aspartate substitution at codon 129, presents with ataxia, autonomic disturbances, stupor and then coma and deatH?

Answer 103

FFI - Fatal Familial Insomnia

Question 104

CJD and prion disease are assoc with spongiform change in cerebral cortex with neurons with vacuoles, cerebellar cortex shows kuru plaques via PAS stain, which represents aggregated PrPSC prions and cortical plaques surrounded by spongiform change seen in vCJD, in advanced cases there is severe neuronal loss, reactive gliosis and sometimes status* spongiosus = cyst like spaces with NO WHAT?

Answer 104

NO INFLAMMATION