Br Pathology: Nervous System

Front 1

What is done to a patient with head trauma? What happens to brain blood vessels when the body is acidotic?

Back 1

A patient with head trauma is purposely hyperventilated to produce respiratory alkalosis, which causes cerebral vessel constriction. This decreases the risk of increased vessel permeability and cerebral edema. Respiratory acidosis and hypoxemia cause vasodilation of cerebral vessels, which increases cerebral vessel permeability, resulting in cerebral edema.

Front 2

Acidosis has what effect on blood vessels? What about hypoxemia? What is the MOA? What can this lead to?

Back 2

both increase activity of the K+ channels in smooth muscle cells → produces hyperpolarization → relaxes smooth muscle cells (↓ intracellular calcium) producing vasodilation with increased vessel permeability

edema

Front 3

What are causes of intracellular cerebral edema?

Back 3

↓ serum Na+ (SIADH); dysfunctional Na+/K+-ATPase pump (global hypoxia)

Front 4

What causes extracellular edema?

Back 4

1) Acute inflammation (e.g., meningitis, encephalitis)
2) Metastasis, trauma, lead poisoning

Front 5

What are signs of increased intracranial pressure?

Back 5

1. Papilledema
* Swelling of the optic disk
2. Headache, projectile vomiting without nausea
3. Sinus bradycardia, hypertension
4. Potential for herniation

Front 6

Pseudotumor cerebri is a benign cause of intracranial hypertension. What are the signs?

Back 6

papilledema, bradycardia, projectile vomiting without nausea, hypertension

Front 7

How is psuedotumor cerebri characterized? Who is it most commonly seen in?

Back 7

1) ↑ intracranial pressure without evidence of tumor or obstruction
2) No mental status alterations as one would see with cerebral edema
3) No focal neurologic signs
4) Most commonly seen in obese women of childbearing age

Front 8

What conditions predispose someone to psuedotumor cerebri?

Back 8

1) All-trans-retinoic acid used in treating acute promyelocytic leukemia
2) Hypothyroidism; Cushing disease
3) Isotretinoin in treating acne; tamoxifen
4) obese young women (most common)

Front 9

Pathologically what occurs in psuedotumor cerebri?

Back 9

1. Decreased CSF resorption in arachnoid granulations
2. Eventual equilibration occurs with inflow and outflow.

Front 10

What are clinical findings inpseudotumor cerebri?

Back 10

1. Headache
2. Rhythmic sound heard in one or both ears
3. Diplopia; blurry vision
4. papilledema, bradycardia, projectile vomiting, hypertension

Front 11

How is psuedotumor cerebri diagnosed? Which test has 100% positive predictive value?

Back 11

1. MRI shows flattening of the posterior globe (100% positive predictive value)
2. Increased CSF pressure
* Usually >300 mm H2O (normal, 70-180 mm H2O)
3. Decreased CSF protein

Front 12

How can psuedotumor cerebri be treated?

Back 12

1. Carbonic anhydrase inhibitor (acetazolamide) or systemic corticosteroids if visual disturbances (lowers CSF pressure)
2. a) Lumboperitoneal shunt
b) Optic nerve sheath fenestration (regresses papilledema in the eye)

Front 13

Cerebral herniation is the result of what?

Back 13

complication of intracranial hypertension

Front 14

In a Subfalcine herniation what is displaced and what is compressed?

Back 14

1. Cingulate gyrus herniates under the falx cerebri.
2. Causes compression of the anterior cerebral artery (ACA)

Front 15

In an uncal herniation what is displaced? What are complications in vision? What artery is compressed? What lobe is infarcted?

Back 15

1. Medial portion of temporal lobe herniates through the tentorium cerebelli.
2. Complications
a) Compression of the midbrain
o Produces Duret's hemorrhages
b) Compression of oculomotor nerve
o (a) Eye is deviated down and out.
o (b) Pupil is mydriatic (dilated).
+ Compression of parasympathetic postganglionic fibers
+ also have drooping of lid from levator palpebrae superior palsy
3) Compression of posterior cerebral artery (PCA)
o Causes hemorrhagic infarction of occipital lobe

Front 16

When are duret's hemorrhages observed? What lobe is infarcted and what artery?

Back 16

uncal herniation

PCA is compressed causing occiptal lobe ischemia

Front 17

Where does the hernia occur in a tonsilar herniation? What sign is seen? What system is impaired?

Back 17

1. Cerebellar tonsils herniate into the foramen magnum.
2. Causes "coning" of the cerebellar tonsils
3. Produces cardiorespiratory arrest
Note: nucleus ambiguous is compressed which is parasympathetics to heart, lungs, GI
Note: caudal nucleus solitarus is compressed which is sensory from carotid body and aortic body

Front 18

CSF normally is clear and colorless. What can cause it to be turbid?

Back 18

protein, cells, microbial pathogens, or a combination of all three elements

Front 19

What are causes of bloody CSF?

Back 19

1) spinal taps is most commonly iatrogenic
2) pathologic hemorrhage into the subarachnoid space
a. ruptured berry aneurysm,
b. intracerebral bleed near the surface of the brain or ventricles

Front 20

General John Pershing

Back 20

1916 - when Mexican leader Pancho Villa attacked Columbus, New Mexico, killing Americans, Pershing was directed to follow him into Mexico. Pershing met with little resistance but eventually left without finding Pancho Villa in order to ready the U.S. in its war upcoming against Germany. Pershing commanded the U.S. "Expeditionary Forces" in WWI which turned the tide against Germany.

Front 21

What causes CSF to be pink? When does it first occur? peak and subside?

Back 21

1) due to oxyhemoglobin (oxyHb) from ruptured red blood cells.
2) It first occurs 2-4 hours post-bleed, peaks in 24-36 hours, and subsides in 4-8 days

Front 22

What causes a yellow to orange (xanthochromia) CSF? When does it first appear? When does it peak and subside?

Back 22

1) due to oxyHb breakdown into bilirubin
2) It first appears 12 hours post-bleed, peaks in 2-4 days, and subsides in 2-4 weeks

Front 23

What is the normal CSF protein concentration?

Back 23

15-45 mg/dL

Front 24

IgG is made by plasma cells in CNS. When is it increased?

Back 24

1) MS
2) meningitis

Note on electrophoresis Ig makes up 12% of total CSF protein

Front 25

A CSF IgG index (calculated with a formula) is useful in distinguishing acute inflammation from demyelinating diseases. If it is high what does it mean? Low?

Back 25

1) high = CNS origin of the IgG
2) low = acute inflammation

Front 26

What are causes of demyelinating disorders that would increase the IgG index? Besides the index what other protein can be measured in these disorders?

Back 26

1) multiple sclerosis is the most common
2) neurosyphilis
3) Guillain-Barré syndrome
4) myelin basic protein (MBP)

Note: CSF MBP is decreased when a demyelinating disease is in remission.

Front 27

What is the normal CSF glucose level? How can the CSF glucose be estimated based on plasma glucose?

Back 27

1) 50-75 mg/dL
2) by multiplying blood glucose by .66

Ex: blood glucose 100 x .66 = CSF glucose 66

Front 28

What is low CSF glucose called? At what level is it considered low? What does a low CSF glucose level imply?

Back 28

1) hypoglycorrhachia
2) glucose level < 40 mg/dL
3) It implies that there has been increased uptake of glucose by cellular elements in the CSF (e.g., neutrophils in acute bacterial meningitis, malignant cells) or a defect in the glucose carrier system (frequently occurs in bacterial/fungal meningitis)

Front 29

In what conditions is CSF glucose normal?

Back 29

1) viral meningitis
2) neurosyphilis, lyme disease
3) demyelinating disease
4) cerebral abscess

Front 30

What viruses can produce a low CSF glucose?

Back 30

1) mumps
2) herpes simplex
3) lymphocytic choriomeningitis virus

Front 31

What is the normal CSF WBC count? What WBC is normally never in the CSF?

Back 31

1) normally is 0-5 mononuclear cells/mm3
2) neutrophils

Front 32

What CSF WBC infiltrate is seen in bacterial meningitis? viral? fungal? parasitic?

Back 32

1) Bacterial meningitis has a predominance of neutrophils
2) viral meningitis initially has a neutrophil response in the first 24 hours that changes to a lymphocytic response in 2-3 days. 3) Fungal meningitis is characterized by lymphocytes and monocytes.
4) parasitic meningitis has a mixed inflammatory infiltrate (eosinophils suggest a helminth infection)

Front 33

Staining the CSF with india ink is great for what pathogen?

Back 33

Cryptococcus neoformans

Front 34

What does it mean to have communicating hydrocephalus? What are some causes?

Back 34

1. Open communication between ventricles and subarachnoid space
2. Causes
a) Increased CSF production
o Example-choroid plexus papilloma
b) Obstruction in reabsorption of CSF by arachnoid granulations
o Examples-postmeningitic scarring, tumor

Front 35

What are causes of noncommunicating hydrocephalus? What is the most common cause in newborns and what syndrome results?

Back 35

1) Stricture of the aqueduct of Sylvius (Most common cause in newborns)
a) Paralysis of upward gaze (Parinaud's syndrome)
2) Tumor in the fourth ventricle
o Examples-ependymoma, medulloblastoma
3) Scarring at the base of the brain
o Example-tuberculous meningitis
4) Colloid cyst in the third ventricle
5) Developmental disorders

Front 36

What are clinical findings in adults with normal pressure hydrocephalus?

Back 36

1) no increase in head size but dilation of ventricles
2) dementia
3) gait disturbance (wide-base gait)
4) urinary incontinence

Front 37

If someone has Hydrocephalus ex vacuo what disorder might they have? What is the cause?

Back 37

1. Dilated appearance of the ventricles secondary to brain atrohy (decreased mass)
2. Example-Alzheimer's disease

Front 38

What occurs in normal pressure hydrocephalus? How many cases of dementia does it account for? Is the dementia reversible?

Back 38

1) dilated ventricles + triad-dementia, urinary incontinence, wide-based gait
2) Accounts for 5% of dementia cases
3) Potentially reversible cause of dementia

Front 39

What causes normal pressure hydrocephalus?

Back 39

1) Idiopathic (50%)
2) Secondary causes
a) Prior subarachnoid hemorrhage
b) Prior intracranial surgery
c) Prior trauma

Front 40

What produces the symptoms of normal pressure hydrocephalus?

Back 40

1) Increased subarachnoid space volume
2) Ventricular dilation is out of proportion to sulcal atrophy ("ventriculomegaly")
3) Wide-based gait and urinary incontinence due to stretching of sacral motor fibers near the dilated ventricle
4) Dementia due to stretching of limbic fibers near the dilated ventricle

Front 41

How is normal pressure hydrocephalus diagnosed and treated?

Back 41

Diagnosis
1) MRI documents ventriculomegaly and sulcal atrophy.
2) Large volume of CSF is removed at lumbar puncture.
o Symptoms improve with removal of the fluid.

Treatment
Ventriculoperitoneal or ventriculoatrial shunting

Front 42

What is the pathogenesis of neural tube defects? Which structures can fail to fuse?

Back 42

1. Failure of fusion of the lateral folds of the neural plate
2. Rupture of a previously closed neural tube

Front 43

A mother with ancephalic fetus would have what lab findings?

Back 43

1) polyhydraminos
2) increased AFP

Front 44

Spina biffida occulta results from what? superficially how can it be identified?

Back 44

1. Defect in closure of the posterior vertebral arch
2. Dimple or tuft of hair in the skin overlying L5-S1

Front 45

What is a meningocele? What region of body is it most common in?

Back 45

1. Spina bifida with cystic mass containing meninges
2. Most common in lumbosacral region

Front 46

What is a myelomeningocele? What part of body is it most common?

Back 46

1. Spina bifida with cystic mass containing meninges and spinal cord
2. Most common in lumbosacral region

Front 47

What occurs in Arnold Chiari malformation? What happens to skull? What conditions is it associated with?

Back 47

1. Caudal extension of medulla and cerebellar vermis through foramen magnum
2. Noncommunicating hydrocephalus
3. Platybasia (flattening of base of skull)
4. Associations:
a. Meningomyelocele
b. Syringomyelia
5. Treatment
* Decompression surgery

Front 48

What is absent in Dandy Walker malformation? What type of hydrocephalus is it? What happens in the 4th ventricle? How is it treated?

Back 48

1. Partial or complete absence of the cerebellar vermis
2. Cystic dilation of fourth ventricle
3. Noncommunicating hydrocephalus
4. Treatment
* Shunt to treat hydrocephalus

Front 49

what occurs in Syringomyelia? When do symptoms present? What is seen in the neck region?

Back 49

1) degenerative disease of spinal cord
2. Symptoms appear in the third and fourth decades.
3. Fluid-filled cavity (syrinx) within the cervical spinal cord
4. Produces cervical cord enlargement
5. Cavity expands and causes degeneration of spinal tracts.

Front 50

What is the pathogenesis of syringomyelia? what does it often present with?

Back 50

1) enlargement of spinal canal most common at C8-T1
2) Arnold Chiari type II malformation

Front 51

What portions of the spinal tract are interrupted in syringomylia? What senses are lost or retained? What disorder can syringomylia be confused with? What happens to the joints

Back 51

1. Disruption of the crossed lateral spinothalamic tracts from enlargement of the central spinal canal
a) Loss of pain and temperature sensation in the hands
b)Tactile sense preserved
* Patient can burn hands without being aware of the burn.
2. Destruction of anterior horn cells
a) Atrophy of intrinsic muscles of the hands
b) Often confused with amyotrophic lateral sclerosis (ALS)... No sensory changes in ALS
3. Charcot joint at shoulder, elbow, wrist

Front 52

What does phakomatosis mean? Embryologically what is messed up? What are the conditions that occur? Which occurs most?

Back 52

1) neurocutaneous syndromes
2) Disordered growth of ectodermal tissue
3) Malformations or tumors of the CNS
4) Includes the following in descending order of incidence:
* Neurofibromatosis, tuberous sclerosis, Sturge-Weber syndrome

Front 53

Is NF dominant or recessive? Does it affect men or women more? What types are there and which is most common? Which chromosomes are affected? What is the function of each protein mutated in NF?

Back 53

1) Autosomal dominant (AD) disorder with incomplete penetrance
2) No gender predominance
3) Type 1 (NF1; most common) and type 2 (NF2) variants
a. NF1-mutation on chromosome 17 coding for neurofibromin
b. NF2-mutation on chromosome 22 coding for merlin
4) Both proteins act as tumor suppressors.

Front 54

What skin lesions appear in NF-1? What brain tumors occur? What are Lisch nodules? what is seen in the axillary region and the inguinal region?

Back 54

1) Café au lait coffee-colored macules
a) Occur in 100% of children before 2 years of age
2) Optic gliomas (2-5%); astrocytomas
3) Lisch nodules (>90%)
o Hamartoma of the iris
4) Axillary and inguinal freckling (70%)
5) Mild scoliosis

Front 55

What is found in NF1 but not NF2? What can they progress to?

Back 55

6) Pigmented plexiform neurofibromas (not in NF2)
o May progress into neurofibrosarcoma involving large nerves

Front 56

In addition to cafe-alait spots, axillary and inguinal freckling, what else occurs on skin in someone with NF1? Where on the body are they absent? What age do they appear?

Back 56

7) Pigmented cutaneous/subcutaneous neurofibromas
a) Occur anywhere on the body except palms, soles
b) Appear in late adolescence and increase in size with age
c) Focal or diffuse

Front 57

What tumors and cancer are associated with NF1? What leukemia?

Back 57

8) Tumor associations
a) Pheochromocytoma; Wilms' tumor... Both produce hypertension.
b) Juvenile chronic myelogenous leukemia (CML)

Note: they also have Neurodevelopment problems (30-40%)

Front 58

Is NF1 or 2 known as the peripheral type? Which is central?

Back 58

NF1 = peripheral
NF2 = central

Front 59

What special senses are impaired in NF2, why? What symptoms will they have as a result? What tumors do they develop?

Back 59

1) Bilateral acoustic neuromas (schwannoma; >90%)
a) Cranial nerve (CN) VIII tumor
b) Benign tumor
c) Sensorineural hearing loss; tinnitus
2) Meningiomas
3) Spinal schwannomas
4) Juvenile cataracts (∼80%)

Front 60

What is found in both NF1 and NF2?

Back 60

1) café au lait macules
2) Pigmented cutaneous/subcutaneous neurofibromas
a) Occur anywhere on the body except palms, soles
b) Appear in late adolescence and increase in size with age
c) Focal or diffuse

Front 61

Is tuberous sclerosis a dominant or recessive disorder? How are children characterized that have it?

Back 61

1. AD disorder
phakomatosis after neurofibromatosis
2. mental retardation; hamartomas in brain and kidneys

Front 62

What do children with tuberous sclerosis develop during infancy? What do they develop on face? How are skin lesions identified?

Back 62

1. Mental retardation and seizures (infantile spasms) beginning in infancy
2. Angiofibromas (adenoma sebaceum) on the face
3. Hypopigmented skin lesions ("ash leaf" lesions)
a) Best identified with Wood's lamp

Rhabdomyoma of heart: highly predictive of tuberous sclerosis

Front 63

What are the features of tuberous sclerosis?

Back 63

seizures, mental retardation, angiofibromas, ash leaf lesions, shagreen patches, cardiac rhabdomyoma, renal angiomyolipoma

Front 64

What are the hamartomatous lesions in tuberous sclerosis? What do they look like? Where do they occur? What occurs in the kidneys? In the heart?

Back 64

1) Astrocyte proliferations in subependyma (giant cell proliferations)
o Look like "candlestick drippings" in the ventricles
2) Angiomyolipomas in the kidneys (80%)
3. Rhabdomyoma in the heart (50-60%)
* Almost 100% predictive of tuberous sclerosis
a. also cause mitral regurgitation

Front 65

What type of genetic aberration occurs in Sturge-Weber syndrome? What happens in the face? What nerve is damaged? What occurs in the meninges? what do they have early onset of?

Back 65

1. Somatic mosaicism or sporadic
2. Vascular malformation on the face
* In a trigeminal nerve distribution
* port-wine stain (aka nevus flammus)
3. Some patients have ipsilateral arteriovenous malformation in the meninges.
4. early onset of glaucoma, also have seizures

Front 66

Is a cerbral contusion permanent or reversible? What is the most common cause? What are the two types? What lobes of brain are most affected?

Back 66

1. Permanent damage to small blood vessels and the surface of the brain
2. Most often secondary to an acceleration-deceleration injury
3. Coup injuries occur at the site of impact
4. Contrecoup injuries occur opposite the site of impact.
* Common sites are at the tips of the frontal and temporal lobes.

Front 67

Between what structures in the head do acute epidermal hematomas occur? What vessel and bone are typically affected? can it cross suture lines?

Back 67

1) Arterial bleed creates a blood-filled space between the bone and dura that is a BICONCAVE DISK that can cross suture lines
2) temporoparietal skull fracture, and tear of middle meningeal artery

Front 68

How does someone with a cerebral contusion progress? What eventually can cause death?

Back 68

1 Some patients have lucid interval after trauma followed later by neurologic deterioration.
2 Intracranial pressure increases, leading to herniation and death

Note: Hematoma rarely crosses the suture line due to firm attachment of dura at these sites
Note: there is Permanent damage to small blood vessels and the surface of the brain

Front 69

How is a subdermal hematoma characterized? What is a person at increased risk of?

Back 69

1) Venous bleeding between the dura and arachnoid membranes
2) cerebral atrophy

Front 70

What are causes of a subdural hemaoma?

Back 70

a) trauma
b) Medical anticoagulation
c) Hemophilia
d) Child abuse; shaken baby syndrome
e) Spontaneous

Front 71

what are risk factors for subdural hematoma? What is the pathogenesis?

Back 71

a) Elderly patients and alcoholic with atrophy of brain
b) Loss of brain mass leads to excess traction on the inflexible bridging veins

Pathogenesis
1. Tearing of bridging veins between brain and dural sinuses
2. Slowly enlarging blood clot covers the convexity of the brain.
3. occur between meningeal dura and arachnoid layer
4. Forms a CRESENTERIC SHAPE

Front 72

What are clinical findings in someone with a subdural hematoma? How is it treated?

Back 72

1. Fluctuating levels of consciousness
2. Herniation and death may occur.
3. Chronic subdural hematomas may produce dementia.
4. creating burr holes to relieve pressure
Note: gyri are present and hemorrhage can cross suture lines but not Falx or tentorium... remember that epidural can cross falxi and tentorium

Front 73

What is an Adenoma sebaceum? What is a Shagreen patch?

Back 73

1) angiofibroma
2) white skin (leukoderma) with the typical ash-leaf
3) Both occur in tuberous sclerosis

Front 74

Repeated episodes of hypoglycemia have the same effects on the brain as does what?

Back 74

global hypoxic injury

Front 75

What are the complications of global hypoxia? What cerberal layers are damaged? What type of necrosis occurs? What are red neurons?

Back 75

1. Cerebral atrophy
a) Due to apoptosis of neurons in layers 3, 5, and 6 of the cerebral cortex
b) Produces laminar necrosis
2) Neurons are the most susceptible cell to hypoxic injury.
3) Neurons undergo apoptosis ("red" neurons)
4) Cerebrovascular accident (e.g., stroke)

Front 76

Where do watershed infarcts occur? What is an example of a site where this occurs?

Back 76

1) Occur at the junctions of arterial territories
2) Example-junction between the anterior and middle cerebral arteries
3) Cerebrovascular accident (e.g., stroke)

Front 77

When is the peak incidence of strokes? are they more common in men or women?

Back 77

1) 80 and 84 years of age
2) men

Front 78

What are the types of strokes? Which is most common?

Back 78

1) Ischemic (70-80%)
(a) Atherosclerotic
+ Most common type
(b) Embolic
2) Intracerebral hemorrhage
3) Subarachnoid hemorrhage
4) Lacunar stroke

Front 79

How are the infarcts characterized in an atherosclerotic stroke? What type of necrosis occurs? which arteries are primarily involved? Does repurfusion help?

Back 79

1) Usually pale infarcts (liquefactive necrosis)
a) Platelet thrombus develops over a disrupted plaque.
2) Middle cerebral artery (most common) and Internal carotid artery near the bifurcation
* (2) Reperfusion does not usually occur.
o Hemorrhagic infarction develops if reperfusion occurs.

Front 80

What is seen on both gross and microscopic analysis of an atherosclerotic stroke?

Back 80

1) Wedge-shaped area of pale infarction
o Develops at the periphery of the cerebral cortex
2) Swelling of the brain occurs.
3) Loss of demarcation between gray and white mater
4) Myelin begins to break down.
5) Gliosis is the reaction to injury.
6) Astrocytes proliferate at the margins of the infarct.
7) Microglial cells (macrophages) remove lipid debris.
8) Cystic area develops after 10 days to 3 weeks.
o Example of liquefactive necrosis

Front 81

What are most atherosclerotic strokes preceded by? What is it caused by?

Back 81

a) Transient neurologic deficits last <24 hours
* Visual loss, paresthesias, hemiparesis, loss of speech
b) Usually caused by microembolization of plaque material

Front 82

When can a something be called a stroke?

Back 82

When the transient ischemic symptoms last longer than 24 hours

Front 83

What is Amaurosis fugax?

Back 83

Temporary loss of vision due to embolization of atherosclerotic material to bifurcation of retinal arteries; called Hollenhorst plaque
Note: curtain coming down over eye

Front 84

What is a Hollenhorst plaque? What does it lead to?

Back 84

a cholesterol embolus that is seen in a blood vessel of the retina and causes amaurosis fugax

Front 85

How is a transient ischemic attack treated?

Back 85

Aspirin; clopidogrel; ticlopidine

Front 86

What are symptoms of a stroke involving the MCA?

Back 86

a) Contralateral hemiparesis and sensory loss in the face and upper extremity
b) Expressive aphasia
* If Broca's area is involved in the dominant (left) hemisphere
c) Visual field defects
d) Head and eyes deviate toward the side of the lesion.

Front 87

What are symptoms of Strokes involving anterior cerebral artery?

Back 87

1) Contralateral hemiparesis and sensory loss in the lower extremity
2) ACA stroke: contralateral paresis/sensory loss in lower extremity

Front 88

What are symptoms of strokes involving the vertebrobasilar artery system?

Back 88

a) Vertigo, ataxia
b) Ipsilateral sensory loss in face
c) Contralateral hemiparesis and sensory loss in the trunk and limbs

Front 89

How are atherosclerotic strokes prevented?

Back 89

Aspirin; clopidogrel if allergic to aspirin

Front 90

Embolic strokes are also known as?

Back 90

hemorrhagic strokes

Front 91

What is the pathogenesis of an embolic stroke?

Back 91

1. Ischemic type of stroke due to embolization
2. Source of emboli
* Most often originate from the left side of the heart
3. Produces a hemorrhagic infarction
4) Most occur in the distribution of the MCA
5) Vessel reperfusion after lysis of embolic material produces hemorrhage.

Front 92

What is the pathogenesis of an intracerebral hemorrhage? Where do they mostly occur?

Back 92

1) Most often due to stress imposed on vessels by hypertension
2) Branches of lenticulostriate vessels develop Charcot-Bouchard macroaneurysms.
3) Rupture of aneurysms produces intracerebral hemorrhage (hematoma).
o Intracerebral hematoma pushes the brain parenchyma aside

Front 93

Where are the most common sites for an intracerebral hemorrhage?

Back 93

1) Basal ganglia (35-50% occur in the putamen)
2) Thalamus (10%)
3) Pons and cerebellar hemispheres

Front 94

What are causes of a subarachnoid hemorrhage?

Back 94

1) Majority are secondary to rupture of a congenital berry aneurysm.
2) Bleeding from an arteriovenous malformation is a less common cause

Front 95

How do congenital berry aneurysms develop? Where?

Back 95

1) May develop from normal hemodynamic stress or hypertension
2) Most develop at junctions of communicating branches with main cerebral artery
a) Junction lacks internal elastic lamina and smooth muscle.
b) Most common site for berry aneurysm is junction with ACA

Front 96

Blood covers the brain in a subarachnoid bleed. What color is the CSF and why?

Back 96

1 Blood in the CSF is broken down into bilirubin pigment.
2 Imparts a yellow color to CSF called xanthochromia

Front 97

What are clinical findings of a subarachnoid bleed?

Back 97

1) Sudden onset of severe occipital headache
2) "worst headache ever"
3) Nuchal rigidity is present.
4) About 50% of patients die soon after the hemorrhage.

Front 98

What are complications of a subarachnoid bleed?

Back 98

a) Further hemorrhage
b) Hydrocephalus
+ Blockage of arachnoid granulations; block foramina
c) Permanent neurologic deficits

Front 99

How are lacunar infarcts characterized? What is the cause?

Back 99

1) Cystic areas of microinfarction < 1 cm in diameter
2) Caused by hyaline arteriolosclerosis
* Secondary to either hypertension (most common) or diabetes mellitus

Front 100

What are the symptoms of lacunar infarcts?

Back 100

1) Pure motor strokes with or without dysarthria
* Occur if the posterior limb of the internal capsule is involved
2) Pure sensory strokes
* Occur if the thalamus is involved

Front 101

What is the best overall test to diagnose a stroke? What is the best technique to diagnose infarcts of the posterior fossa?

Back 101

CT without contrast because it distinguishes hemorrhagic from nonhemorrhagic strokes

MRI

Front 102

Acutely what can be given to someone with a stroke? Would this same treatment be given to a hemorrhagic bleed?

Back 102

1) Thrombolytic therapy in thromboembolic strokes if <3 hours
2) Usually not implemented if stroke is hemorrhagic
3) In some cases, intracerebral hemorrhages can be evacuated

Front 103

What is the long term treatment in someone that is prone to strokes?

Back 103

1) Antiplatelet treatment (e.g., aspirin, clopidogrel)
2) Warfarin for embolic types of strokes
3) Treat risk factors for strokes (e.g., hypertension, diabetes)

Front 104

A cholesterol embolis in the retinal arteries is characterized how by the patient?

Back 104

painless loss of vision ("curtain coming down") followed in a variable period of time by restoration of vision ("curtain coming up") as the embolus dislodges. This is called amaurosis fugax

Front 105

What does meningitis mean?

Back 105

inflammation of pia mater

Front 106

Where do the majority of organisms originate in the body that cause meningitis?

Back 106

nasopharynx

Front 107

How is viral meningitis transmitted?

Back 107

1. Most transmitted by fecal-oral route
2. Respiratory route less common

Front 108

What are complications of meningitis?

Back 108

1. Seizures; focal neurologic deficits
2. Cranial nerve palsies
3. Sensorineural hearing loss
4. Communicating and noncommunicating hydrocephalus

Front 109

What are CSF findings in viral meningitis?

Back 109

1. Increased CSF protein
* Due to increased vessel permeability
2. Increased total CSF leukocyte count
* Initially neutrophils but converts to lymphocytes in 24 hours
3. Normal CSF glucose
Note: lymphocytes do NOT have to be elevated... this is called aseptic meningitis

Front 110

What are CSF findings in bacterial meningitis?

Back 110

1. Increased CSF protein
2. Increased total CSF leukocyte count
3. Decreased CSF glucose

Front 111

What cause high protein in the CSF? What about glucose?

Back 111

↑ CSF protein (viral, bacterial, fungal);

↓ CSF glucose (bacterial, fungal)

Front 112

What are clinical findings in encephalitis?

Back 112

1. Fever, headache
2. Impaired mental status, drowsiness, coma

Front 113

What is the CSF WBC count in viral meningitis? Which immune cell predominates? What is the glucose level and which viruses are exceptions? What about protein?

Back 113

1) <1000 cells/mm3
2) First 24-48 hours, neutrophils, then switches to lymphocytes/monocytes after 48 hours
3) Normal: exceptions-mumps, herpes can decrease
4) Increased

Front 114

What is the CSF WBC count in bacterial/fungal meningitis? Which immune cell predominates? What is the glucose level? What about protein?

Back 114

1) 1000-20,000 cells/mm3
2) >90% neutrophils (>80%), may be lymphocyte and monocyte response with fungus
3) Decreased (<40 mg/dL)
4) Increased (>50 mg/dL)

Front 115

What is an example of a disease that causes Destruction of normal myelin? Example of Production of abnormal myelin? Causes Destruction of oligodendrocytes?

Back 115

1. multiple sclerosis
2. leukodystrophy
3. multiple sclerosis, slow virus infections

Front 116

What is the most common debilitating disease amongst young adults? Is it more common in men or women? What age?

Back 116

MS more common in women 20-40

Also the most common demyelinating disease

Front 117

What are genetic and environmental factors linked to MS?

Back 117

1) Genetic factors (e.g., HLA-DR2)
2) Environmental triggers and Microbial pathogens (e.g., Epstein-Barr virus, human herpes virus 6, Chlamydophilia pneumoniae), vitamin D, sun exposure

Front 118

What is the pathogenic process of MS? What type of hypersensitivity is MS?

Back 118

1) Environmental trigger activates helper T cells whose antigen-specific receptors recognize CNS myelin basic protein (other antigens as well) as an antigen.
3) T cells release cytokines that activate macrophages, which also release cytokines (e.g., tumor necrosis factor-α) that destroy the myelin sheath as well as oligodendrocytes that synthesize myelin (type IV hypersensitivity).
4) Antibodies directed against the myelin sheath and oligodendrocytes may also be involved (type II hypersensitivity).

Front 119

What are gross and microscopic findings in MS? What WBCs are predominately seen?

Back 119

1) Demyelinating plaques occur in white mater of brain/spinal cord
o White mater looks like gray mater in areas of demyelination.
2) Inflammatory infiltrate in plaques is composed predominantly of CD4 T cells and microglial cells with phagocytosed lipid.

Front 120

Is MS episodic or continuous?

Back 120

Episodic course punctuated by acute relapses and remissions (80-90%)

Front 121

What are sensory deficits that occur in MS?

Back 121

a) Paresthesias
b) Loss of pain/temperature sensation
c) Loss of vibratory sensation

Front 122

What are upper motor neuron deficits that occur in MS?

Back 122

a) Spasticity
b) Increased deep tendon reflexes (DTRs)
c) Muscle spasms
d) Extensor plantar response (Babinski)
e) Weakness
o Shoulder abduction; finger extension; foot dorsiflexion; hip/knee flexion

Front 123

How is the autonomic nervous system affected by MS?

Back 123

a) Urge incontinence
o Hyperactive detrusor muscle
b) Sexual dysfunction
c) Bowel motility problems

Front 124

What happens to vision in MS?

Back 124

a) Inflammation of the optic nerve
o MS is the most common cause of optic neuritis.
b) Blurry vision or sudden loss of vision

Front 125

What happens to balance in MS? speech? eye movement and muscles? What happens during head flexion?

Back 125

1) Cerebellar ataxia
2) Scanning speech (sound drunk)
3) Intention tremor, nystagmus
4) Bilateral internuclear ophthalmoplegia
* Demyelination of medial longitudinal fasciculus (MLF)
5) Flexion of the neck produces an electrical sensation down the spine.

Front 126

What is Bilateral internuclear ophthalmoplegia pathognomonic for?

Back 126

MS

Front 127

What does the CSF of someone with MS show? When it is electrophoresed what is seen? What does MRI show?

Back 127

1) Increased CSF leukocyte count
* Primarily CD4 T lymphocytes
2) Increased CSF protein
* Primarily an increase in γ-globulins
3) Increased CSF myelin basic protein
* Indicates active disease
4) Normal CSF glucose
5) High-resolution electrophoresis shows oligoclonal bands.
a) Discrete bands of protein in the γ-globulin region
b) Sign of demyelination
6) MRI is extremely sensitive in detecting demyelinating plaques (Dawson's claws coming off of ventricles)

Front 128

What indicates active disease in MS? What is the most sensitive test for MS?

Back 128

1) Increased CSF myelin basic protein
2) MRI with gadolinium

Front 129

How is acute MS treated? How is chronic MS treated? What is the name of the monoclonal antibody used in treatment?

Back 129

1) Acute relapse
o High dose methylprednisolone
2) Chronic
a) Disease modifying drugs-e.g., interferon-beta
b) Monoclonal antibody-natalizumab
c) Cytotoxic-cyclophosphamide; methotrexate; azathioprine

Front 130

What is the prognosis of MS?

Back 130

1) Varies with the type of disease
2) On average, ∼70% of patients with MS are alive 25 years after their diagnosis.

Front 131

What is the cause of Central pontine myelinolysis? Who does it occur in? How is it treated?

Back 131

1. Most often occurs in alcoholics who have hyponatremia
2. Rapid intravenous correction of hyponatremia causes demyelination in the basis pontis.
3. Treatment is supportive.

Front 132

What are Viral infections with direct infection of oligodendrocytes?

Back 132

1) subacute sclerosing panencephalitis
2) progressive multifocal leukoencephalopathy

Front 133

What are Leukodystrophies?

Back 133

inborn errors of metabolism.

Front 134

What type of genetic disorder is Adrenoleukodystrophy? What is deficient? What results?

Back 134

1. X-linked recessive (XR) disorder
2. Enzyme deficiency in β-oxidation of fatty acids (FAs) in peroxisomes
* Results in accumulation of long-chain fatty acids
3. Causes generalized loss of myelin in the brain and adrenal insufficiency

Front 135

What type of genetic disorder is Metachromatic leukodystrophy? What results? What is deficient?

Back 135

1. Autosomal recessive disorder
* Lysosomal storage disease (LSD)
2. Deficiency of arylsulfatase A
* Results in accumulation of sulfatides

Front 136

What type of genetic disorder is Krabbe's disease? What is deficient? What results? What type of cells are seen in the brain?

Back 136

1. Autosomal recessive disorder
* LSD
2. Galactocerebroside β-galactocerebrosidase deficiency
* Leads to accumulation of galactocerebroside
3. Brain shows large, multinucleated, histiocytic cells (globoid cells).

Front 137

What do arboviruses cause? What is the vector for all abroviruses? What is the reservoir? How has west nile spread?

Back 137

1) encephalitis
2) Mosquitoes are the vector
3)Wild birds are the reservoir for the virus
4) West Nile virus: crows and other birds have spread the disease from New York to the West Coast
5) Encephalitis can be fatal
Note: examples include flaviviruses (+ssRNA linear), togaviruses (+ssRNA linear), bunyaviruses (-ssRNA 3 segments)

Front 138

What is cockackie virus the most common viral cause of? What genus is it from? What is are common genomic similarities between it and other viruses in this genus? What months of the year is it active?

Back 138

1) meningitis
2) Enterovirus: most common cause of viral meningitis
3) (+)ssRNA viruses (polio)
4) Viral meningitis peaks in late summer and early autumn

Front 139

CMV is the most common infection in people with what? what is seen on microscopic exam? What does it cause in newborns? How is it treated? What does it cause in the CNS?

Back 139

1) Most common viral CNS infection in AIDS (CD4 <50)
2) Primarily intranuclear basophilic inclusions (owls in lungs)
3) Periventricular calcification in newborns
4) Treatment: ganciclovir + foscarnet; or valganciclovir
5) encephalitis

Front 140

What does HSV1 cause in the CNS? Where in the brain does it attack and what results? How is it treated?

Back 140

1) encephalitis and meningitis
2) Causes hemorrhagic necrosis of temporal lobes especially limbic areas
3) Treatment: IV acyclovir

Front 141

What does HIV cause in the CNS? What is it the most common cause of in AIDS patients? What is seen on microscopic exam?

Back 141

1) encephalitis
2) Most common cause of AIDS dementia
3) Microglial cells fuse to form multinucleated cells

Front 142

Lymphocytic Choriomeningitis Virus is endemic in what species? What are clinical findings? What are lab findings? what are characteristics of virus?

Back 142

1) Endemic in the mouse population
2) Transmission: food or water contaminated with mouse urine/feces
3) Meningoencephalitis: combination of nuchal rigidity and mental status abnormalities (encephalitis)
4) CSF findings: increased protein, lymphocyte infiltrate, normal to DECREASED glucose
Note: -ssDNA circular virus with two segments with helical capsid and envelope

Front 143

What does poliovirus cause in the CNS? What is destroyed during the infection? What is post-polio syndrome?

Back 143

1) Encephalitis and myelitis-spinal cord
2) Destroys upper and lower motor neurons. Causes muscle paralysis
a. have fasiculations and hyporeflexia
3) Post-polio syndrome: occurs in ∼ 50% of people with previous poliomyelitis; usually occurs 15-30 years after original infection; increased muscular weakness/pain in muscle groups already affected; excessive fatigue

Front 144

Rabies virus causes encephalitis. What is the vector? What is the viral receptor? Where does replicate and migrate?

Back 144

1) Most often transmitted by raccoon bite (40% of cases)
Other vectors are dog, skunk, bat, and coyote
2) Viral receptor is acetylcholine receptor
3) Initially replicates at site of the bite; moves by axonal transport to the CNS; after CNS replication, it migrates to the saliva
Note: has bullet shaped capsid

Front 145

What is the incubation period of rabies? What are prodrome symptoms? What is hydrophobia and what follows it? What is seen on microscopic exam? How is it treated?

Back 145

1) Incubation period 10-90 days
2) Prodrome: fever, paresthesias in and around the wound site
3) Hydrophobia: due to spasms of throat muscles when swallowing
4) Followed by flaccid paralysis
5) Encephalitis: death of neurons; eosinophilic intracytoplasmic inclusions called Negri bodies; seizures, coma, death
6) Treatment: wash wound site (quaternary ammonium compound); give passive immunization (immune globulin) mostly into wound site (where virus initially replicates); give active immunization (human diploid vaccine)
7) Universally fatal if not treated

Front 146

What is a negri body seen in? What is it called in this same patient if they have spasms of throat muscle spasms and can't swallow?

Back 146

1) death of neurons; eosinophilic intracytoplasmic inclusions called Negri bodies
2) Hydrophobia
3) RABIES

Front 147

What is the cause of Creutzfeldt-Jakob disease? How is it transmitted? What results? Is it fatal?

Back 147

1) encephalopathy due to prions (abnormal PrP)
2) noninfectious prion protein normally found on surface of neurons (function unknown)
3) Transmitted by corneal transplantation, contact with human brain, use of improperly sterilized cortical electrodes, or ingestion of tissues from cattle with bovine spongiform encephalopathy ("mad cow" disease)
4)Brain has "bubble and holes" spongiform change in cerebral cortex
5)Death usually occurs within 1 year

Front 148

Progressive multifocal leukoencephalopathy is caused by what? what cells are affected and what is seen on histologic exam? When does it occur?

Back 148

1) Conventional slow virus encephalitis due to papovavirus
2) Intranuclear inclusion in oligodendrocytes
3) Occurs in AIDS when CD4 TH count < 50 cells/mm3

Front 149

Subacute sclerosing panencephalitis is associated with what? What is seen on microscopy? Is it fatal?

Back 149

1) Conventional slow virus encephalitis associated with rubeola (measles) virus
2) Intranuclear inclusions in neurons and oligodendrocytes
3) Death usually occurs within 1-2 years

Front 150

What can Streptococcus agalactiae cause? What age group is effected? What group is it in? How does it spread? How is it treated?

Back 150

1) Most common cause of neonatal meningitis (49%)
2) Group B streptococcus (bscitracin resistant and beta hemolytic)
3) Spreads from a focus of infection in maternal vagina
4) Empiric treatment (culture negative): ampicillin + cefotaxime

Front 151

What does E coli cause in neonates? How is it treated if the culture is negative? What is the specific treatment?

Back 151

1) second most common cause of neonatal meningitis (18%)
2) Empiric treatment (culture negative): ampicillin + cefotaxime
3) Specific treatment: ceftazidime + gentamicin

Front 152

Listeria monocytogenes can cause meningitis in the neonate. What type or bacteria is it? Where are the pathogens found in nature? How is it treated empirically? What is the specific treatment?

Back 152

1) Gram-positive rod with tumbling motility; actin rockets help organism to move from cell to cell
2) Pathogen found in soft cheese, hot dogs
3) Empiric treatment (culture negative): ampicillin + cefotaxime
4) Specific treatment: ampicillin ± gentamicin
Note: falcultative intracellular microbe and only gram + with endotoxin

Front 153

What type of bacteria is Neisseria meningitidis? What group is most susceptible? How is it treated? What is used for prophylaxis?

Back 153

1) Gram-negative diplococcus; locates in posterior nasopharynx
2) Most common cause of meningitis in those between 1 month and 18 years of age
3) Treatment: ceftriaxone
4) Prophylaxis for people in close contact: ciprofloxacin or rifampin or ceftriaxone

Front 154

What age group does Streptococcus pneumoniae cause meningitis in? How is it treated?

Back 154

1) Most common cause of meningitis in patients > 18 years of age (some authors say N. meningitidis is the most common and S. pneumoniae the 2nd most common)
2) Treatment: penicillin G or ampicillin

Front 155

Mycobacterium tuberculosis can cause meningitis. What part of brain is involved? What occurs there? How is it treated?

Back 155

1) Involves base of brain
2) Vasculitis (infarction) and scarring (hydrocephalus)
3) Treatment: isoniazid, rifampin, ethambutol, pyrazinamide, dexamethasone (prevent scarring)

Front 156

What does Treponema pallidum cause in the CNS? What type of bacteria is it? What are specific neurologic deficits that result? How is it treated?

Back 156

1) Meningitis, encephalitis, myelitis
2) Spirochete
3) Meningovascular: vasculitis causing strokes
4) General paresis: dementia
5) Tabes dorsalis: involves posterior root ganglia and posterior column; causes ataxia, loss of vibration sensation, absent deep tendon reflexes, Argyll-Robertson pupil (pupils accommodate but do not react)
Treatment: penicillin G (difficult to treat)
Note: aseptic meningitis

Front 157

What does Cryptococcus neoformans cause in the CNS? Who does it most commonly occur in? What stain is used? How is it treated?

Back 157

1) Meningitis and encephalitis
2) Most common fungal CNS infection in AIDS
a. causes "soap bubble" appearance in brain
3) Budding yeasts visible with India ink
4) Treatment: fluconazole non-AIDS, amphotericin + flucytosine
Note: latex agglutination detects polysaccharide capsule

Front 158

Mucor species cause what in the CNS? Who does it occur in? How does it spread? How is it treated?

Back 158

1) Frontal lobe abscess
2) Occurs in diabetic ketoacidosis
3) spreads from frontal sinuses
4) Treatment: amphotericin B

Front 159

Naegleria fowleri causes what in the CNS? What type of organism? What part of brain is involved? How is contracted? How is it treated?

Back 159

1) Meningoencephalitis
2) Protozoa (amoeba)
3) Involves frontal lobes
4) Contracted by swimming in freshwater lakes
5) Treatment: amphotericin B
Note: enter brain via cribiform plate

Front 160

Trypanosoma gambiense/rhodesiense cause encephalitis. What type of organism is it? How is it transmitted? How does it spread in body? What is it called in later stages?

Back 160

1) Protozoa (hemoflagellate)
2) Transmission: bite of an infected tsetse fly (Glossina)
3) Trypanosomes invade the blood and lymphatics early in the disease; initial drainage into the posterior cervical nodes produces lymphadenopathy (Winterbottom's sign); encephalitis occurs in later stages
4) Diffuse encephalitis: somnolence ("sleeping sickness") due to the release of sleep mediators by the organisms

Front 161

Why are Trypanosoma gambiense/rhodesiense difficult to treat? What is the most common cause of death? How is it diagnosed? How is it treated?

Back 161

5) Trypanosomes are capable of antigen variation (cyclical fever spike)
6) Starvation is the most common cause of death
7) Diagnosis: trypanosomes in blood, CSF; serologic tests; characteristic increase in IgM early in the disease
8) Treatment: pentamidine early in the disease; melarsoprol in encephalitis stage

Front 162

Taenia solium causes what? what type of organism is it? How is it transmitted? What is intermediate host? What is the lifecycle? How is it treated?

Back 162

1) Cysticercosis
2) Helminth (tapeworm; cestode)
3) pig transmitted disease
4) Patient (intermediate host) ingests food or water containing eggs; eggs develop into larval forms (cysticerci) that invade brain, producing calcified cysts causing seizures; hydrocephalus
5) Treatment: albendazole + dexamethasone
Note: brain looks like swiss cheese

Front 163

Toxoplasma gondii causes what in CNS? What type of organism? How is it identified in CNS? What congenital transmission do? How is it treated?

Back 163

1) encephalitis
2) Protozoa (sporozoan) spread by cat feces or meat
3) Most common CNS space-occupying lesion in AIDS;
4) ring-enhancing lesions on CT
5) Congenital toxoplasmosis produces basal ganglia calcification
5) Treatment: pyrimethamine + sulfadiazine + folinic acid (leucovorin)
Note: congenital triad of chorioretinitis, hydrocephalus and intracranial calcifications

Front 164

What stain are mucor species identified with? How do the hyphae appear?

Back 164

India ink shows aseptate hyphae that have wide-angled branching

Front 165

What can toxoplasmosis infection be confused with?

Back 165

primary central nervous system lymphoma

Front 166

What is the most common overall cause of dementia?

Back 166

Alzheimer

Front 167

What are the types of Alzheimer's? What are the mutations present?

Back 167

1) Sporadic late onset type of AD (most common)
2) Sporadic early onset type of AD (before age 65)
o Related to apolipoprotein gene E, allele ≥4
3) Familial early onset type of AD (<1% of cases)
a) Mutations of amyloid precursor protein (APP) on chromosome 21
b) Mutations in presenilin 1 on chromosome 14
c) Mutations in presenilin 2 on chromosome 1

Front 168

What ages does Alzheimer's occur? What percentage of people have it?

Back 168

1) It is <1% in the 60- to 64-year-old age group.
2) It is 40% to 50% by the age of 95.

Front 169

What CNS disease is occurs in trisomy 21?

Back 169

1) Trisomy 21 (Down syndrome) has a strong association with AD
* By 40 years of age, most Down syndrome patients have AD.

Front 170

Where does the Aβ protein primarily accumulate in the CNS?

Back 170

Aβ is neurotoxic and damages neurons in the following sites:
(1) Medial temporal lobe structures
(2) Frontal cortex, especially the entorhinal cortex and hippocampus

Front 171

What is the Pivotal role of activated glycogen synthase kinase-3β (GSK) in neurotoxicity of Aβ? What type of feedback is there? Where is GSK initially activated?

Back 171

1) Activation of GSK causes phosphorylation of Aβ, which in turn, produces:
a) Neuronal and synaptic dysfunction
b) Signaling for neuronal apoptosis
2) Phosphorylated Aβ also has a positive feedback on GSK; hence, keeping the cycle of neurotoxicity in motion
3) Initial activation of GSK has been traced to dysfunction within the Wnt (Wingless integration pathway), which is a family of genes normally involved in:
a) Neuronal development during embryogenesis
b) Normal neuronal function
4) Normally, the Wnt signaling pathway inactivates GSK, hence preventing phosphorylation of Aβ and its harmful effect on neurons.
5) However, if the Wnt signaling pathway is dysfunctional, GSK remains activated leading to phosphorylation of Aβ and its neurotoxic effects (e.g., apoptosis of neurons).

Front 172

What stain is used for Aβ and how is it visualized?

Back 172

Aβ stains positive with Congo red and has apple-green birefringence with polarization

Front 173

Aβ is a metabolic product of what? What enzyme is needed to prevent Aβ formation? Which enzymes promote it? What occurs in the sporadic early onset type of Alzheimer's disease?

Back 173

1) APP is normally coded for on chromosome 21.
2) Defects in metabolism of APP by secretases cause an increase in Aβ.
3) α-Secretases cleave APP into fragments that cannot produce Aβ.
4) β-Secretases followed by γ-secretases cleave APP into fragments that are converted to Aβ.
5) In the sporadic early onset type of AD, apolipoprotein gene E, allele e4 codes for a product that cannot eliminate Aβ from the brain leading to early onset of neurotoxicity.

Front 174

Is a type I or II diabetic at increased risk for Alzheimer's? Why?

Back 174

1) Involved in the clearance of Aβ
2) Insulin resistance syndromes (type 2 diabetes; metabolic syndrome) have increased risk for AD, because increased insulin lowers insulin degrading enzyme, which increases Aβ.

Front 175

Sporadic early onset of alzheimers is associated with what gene and which allele?

Back 175

Apo gene E, allele ε4

Front 176

What is the normal function of tau?

Back 176

maintain microtubules in neurons.
* Assembles and supports scaffolding important in neuron structure and function

Front 177

What is activated GSK-3β's effect on tau? What is the enzyme that helps to regulate tau?

Back 177

Activated GSK enhances hyperphosphorylation of tau protein
1) This process causes the protein to change shape and cluster into fibers.
2) Fibers appear as neurofibrillary (NF) tangles (twisted fibers) in the cytoplasm.
a. Best visualized with silver stains
3) NF tangles produce neuronal dysfunction including death of the neuron.
4) Pin 1 enzyme (prolyl isomerase) normally strips excess phosphate molecules from NF, restoring it to its original shape; however, in some cases of AD, this enzyme is absent or dysfunctional.

Front 178

What are gross findings in AD? Which lobe of brain is usually spared?

Back 178

Cerebral atrophy with dilation of ventricles (hydrocephalus ex vacuo)
1) Due to loss of neurons in the temporal, frontal, and parietal lobes
2) Occipital lobe is usually spared.

Front 179

How are neurfibrially tangles stained and what part of cell are they in? What other conditions are they seen in?

Back 179

Presence of NF tangles in the cytoplasm of neurons
1) Best visualized with silver stains
2) Elderly patients without dementia, Huntington's disease, Niemann-Pick disease

Front 180

What are senile plaques composed of? Are they located in Gray or White matter? What stains are used? Is this normally present in elderly people?

Back 180

1) Core of Aβ surrounded by neuronal cell processes containing tau protein, microglial cells, and astrocytes
o Located in the gray mater.
2) Aβ stains with Congo red
3) Best visualized with silver stains
4) Are also normally present in the brains of elderly people

Front 181

What is amyloid angiopathy and what results? Who is at risk?

Back 181

1) Aβ is present in cerebral vessels.
2) Causes weakening of vessels with increased risk for hemorrhage
3) people with AD

Front 182

How is AD confirmed?

Back 182

1) Requires postmortem examination of the brain
2) Must be widespread presence of NF tangles and senile plaques

Front 183

What are early signs of AD? What about in patients with mild to moderate disease? What types of focal deficits are present? What do patients usually die from?

Back 183

1. Prominent early sign is the decline in short-term memory.
2. Another early sign is loss of smell.
* Dysfunction in entorhinal cortex
3. Patients with mild to moderate disease have only cognitive defects.
4. Additional deficits accumulate, including changes in behavior, judgment, language, and abstract thought.
5. Even later in the course, functional deficits manifest in the patient not being able to care for themselves.
6. No focal neurologic deficits are present early in the disease.
7. Patients usually die of an infection.
* Example-intercurrent bronchopneumonia

Front 184

How is AD tentatively diagnosed?

Back 184

1. Orientation
2. Attention
3. Verbal recall
4. Language
5. Visual-spatial skills

Positron emission tomography (PET) is useful the differential diagnosis of dementia.

Front 185

How is AD treated?

Back 185

1. Cholinesterase inhibitors
* Increase synaptic transmission
2. Memantine (blocks glutamate receptors)

Front 186

What is parkinsons disease? What parts of brain are affected? Where is dopamine prominent in brain and parkinsons?

Back 186

Group of disorders that alter dopaminergic pathways involved in voluntary muscle movement
1) Striatal system is involved in voluntary muscle movement.
o Substantia nigra, caudate, putamen, globus pallidus, subthalamus, thalamus
2) Dopamine is the principal neurotransmitter in the nigrostriatal tract.
o Connects the substantia nigra with the caudate and putamen

Front 187

The majority of parkinsons cases are idiopathic. What are the known causes?

Back 187

1) Encephalitis, ischemia
2) Chronic carbon monoxide poisoning
o Causes necrosis of globus pallidus
3) Wilson's disease
4) Addiction to MPTP, a derivative of meperidine
o 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
5) Antipsychotic drugs (e.g., phenothiazines)

Front 188

Does idiopathic parkinsons occur more in men or women? In what age group?

Back 188

1) Occurs between 45 and 65 years of age
2) Distribution is equal in men and women.
3) Most cases are sporadic.

Front 189

What is the pathophysiology of parkinsons disease? What do the neurons contain?

Back 189

1) Degeneration/depigmentation of neurons in substantia nigra
2) Causes deficiency of dopamine
3) Neurons contain intracytoplasmic, eosinophilic bodies called Lewy bodies.

* Ubiquinated damaged neurofilaments

Front 190

What are features of parkinsons that involve the muscles?

Back 190

1) Muscle rigidity
a) Slowness of voluntary muscle movement (bradykinesia)
b) Cogwheel rigidity on physical examination

Front 191

Describe the tremor in parkinsons? Facial expressions? Gait? posture? skin?

Back 191

1) Resting tremor
a) "Pill rolling" between thumb and index fingers
b) Illegible handwriting (micrographia)
2) Expressionless face ("poker face"), stooped posture
3) Difficulty in initiating first step; shuffling gait
4) Blepharospasm (involuntary movement of eye muscles)
5) Commonly have severe seborrheic dermatitis
6) Dementia in some cases
7) postural instability

Front 192

How is parkinsons treated?

Back 192

1. Avoid drugs that worsen parkinsonism-neuroleptics, antiemetics, monoamine oxidase (MAO) inhibitors
2. Levodopa-transformed into dopamine
3. Carbidopa, benserazide-dopa decarboxylase inhibitors
4. Bromocriptine, pergolide-dopamine agonists
5. Selegiline, rasagiline-inhibit monoamine oxidase-B, which inhibits breakdown of dopamine
6. Specialized surgical procedures

Front 193

What type of genetic disorder is Huntingtons? At what age does it occur? Does it occur more in men or women?

Back 193

1. Autosomal dominant disease
2. Trinucleotide repeat disorder (CAG) involving chromosome 4
3. Delayed appearance of symptoms until 30 to 40 years of age
4. No gender dominance

Front 194

What parts of the brain atrophy in huntingtons?

Back 194

striatal neuron atrophy of caudate nucleus, putamen, globus pallidus

Front 195

What are clinical findings in huntingtons?

Back 195

1. Chorea
a) Irregular, rapid, nonstereotyped involuntary movements
b) Called choreoathetosis if it has a writhing quality
2. Oculomotor abnormalities
3. Parkinsonism in later stages
4. Depression

Front 196

How is huntingtons diagnosed and treated?

Back 196

1. Genetic testing is available
2. Imaging studies (CT, MRI)
* Atrophy of caudate and putamen
3. No treatment only supportive

Front 197

What type of genetic disorder is Friedreich's ataxia? What is deficient? this deficiency impairs what and cells are prone to what?

Back 197

Autosomal recessive (AR) disease
1) Trinucleotide repeat disorder (GAA)
2) Frataxin deficiency (protein found in mitochondria that aids in Fe metabolism)
(a) Leads to impaired mitochondrial iron homeostasis
(b) Cells are more prone to apoptosis.

Front 198

What is the most common hereditary ataxia?

Back 198

friedreich's

Front 199

What are the sites of degeneration in Friedreich's ataxia?

Back 199

1) Dorsal root ganglia
2) Posterior columns
3) Spinocerebellar tract
4) Lateral corticospinal tracts
5) Large sensory peripheral neurons

Front 200

What are two conditions associated with Friedreich's ataxia?

Back 200

hypertrophic cardiomyopathy; type 1 diabetes mellitus

Front 201

What are clinical findings in Fridreich's ataxia?

Back 201

1. Progressive gait ataxia
2. Loss of deep tendon reflexes
* Initially at the ankles
3. Loss of vibratory sensation and proprioception
4. Muscle weakness in the legs

Front 202

How is Friedreich's ataxia treated?

Back 202

1. Gene testing is available.
2. Imaging (MRI) shows spinal cord atrophy.
3. Treatment is supportive.

Front 203

Lou Gehrig's disease is also known as?

Back 203

amyotrophic lateral sclerosis [ALS]

Front 204

What degenerates in ALS? When do symptoms appear? Are most cases sporadic or hereditary? Where is the mutation in familial ALS?

Back 204

1) Degenerative disease involving upper and lower motor neurons
2) Symptoms usually appear between 40 and 60 years of age.
3) Most cases are sporadic (90-95%).
4) Familial cases involve mutations on chromosome 21.
a. Defective superoxide dismutase 1
b. Produces superoxide free radical injury of neurons

Front 205

What are clinical findings in ALS? What happens to bowel and bladder function?

Back 205

1. Upper motor neuron (UMN) signs
* Spasticity, Babinski's sign
2. Lower motor neuron (LMN) signs
a) Muscle weakness Begins with atrophy of intrinsic muscles of the hands
b) Eventual paralysis of respiratory muscles
3. No sensory changes
4. Preservation of bowel and bladder function

Front 206

How is ALS diagnosed? treated? mean survival?

Back 206

1 Electromyography and nerve conduction studies
2 Riluzole (glutamate antagonist)
3 Average survival time is 3 to 5 years.

Front 207

Who does Werdnig-Hoffmann disease occur in? What is destroyed?

Back 207

1) children
2) LMN disease
3) linked to survival motor neuron (SMN) gene

Front 208

What type of genetic disorder is Wilsons disease? What is the pathogenesis?

Back 208

Autosomal recessive disease
1. Defect in copper excretion in bile
2. Defect incorporation of copper into ceruloplasmin
3. Leads to liver cirrhosis and excess free copper in blood

Front 209

What are CNS findings in Wilsons disease?

Back 209

1. Atrophy and cavitation of basal ganglia, particularly globus pallidus and putamen
2. Lenticular nucleus-putamen and globus pallidus in the basal ganglia
3. Signs of parkinsonism, chorea, and dementia

Front 210

What is the cause of Acute intermittent porphyria? What is deficient? What accumulates?

Back 210

1. Autosomal dominant disorder
2. Defect in porphyrin metabolism
1) Deficiency of uroporphyrinogen synthase (porphobilinogen deaminase)
2) Proximal increase in porphobilinogen (PBG) and δ-aminolevulinic acid (ALA)

Front 211

How does the urine appear in someone with Acute intermittent porphyria? What happens when the person is exposed to light?

Back 211

1) Urine is colorless when first voided.
2) Exposure to light causes oxidation of PBG to porphobilin producing port-wine color.
a) Classic "window-sill test"
b) urine becomes dark with light exposure

Front 212

In Acute intermittent porphyria what feedback is lost that leads to attacks? What else can precipitate attacks?

Back 212

1) Heme has a negative feedback relationship with ALA synthase.
2) ALA synthase is the rate-limiting enzyme of porphyrin metabolism.
3) Decreasing heme precipitates porphyric attacks by increasing porphyrin synthesis.
o Example-drugs enhancing liver cytochrome P-450 system (e.g., alcohol)

Front 213

What are the clinical findings in someone with Acute intermittent porphyria

Back 213

Neurological:
1) Recurrent bouts of severe abdominal pain simulating acute abdomen
2) Often mistaken for a surgical abdomen
o Patient has "bellyful of scars."
3) Psychosis
4) Peripheral neuropathy
5) Dementia

Front 214

How is Acute intermittent porphyria treated?

Back 214

Diagnosis: Enzyme assay in RBCs

Treatment:
1. Avoid drugs that precipitate attacks
2. Carbohydrate loading with glucose Inhibits ALA synthase

Front 215

What is the pathogenesis of vit B12 deficiency?

Back 215

1. Subacute combined degeneration of the spinal cord
* Posterior column and lateral corticospinal tract demyelination
2. Dementia, peripheral neuropathy

Front 216

What are CNS findings in a chronic alcoholic?

Back 216

1) Cortical and cerebellar atrophy
2) Central pontine myelinolysis
3) Wernicke-Korsakoff syndrome

Front 217

Wernicke-Korsakoff syndrome is due to what? What are gross and microscopic findings?

Back 217

1) Most often due to thiamine deficiency (secondary to alcoholism)
2) Gross and microscopic findings
a) Hemorrhages with hemosiderin deposits
b) Mamillary bodies, wall of the third and fourth ventricles
c) Neuronal loss, gliosis, vessel hemorrhage

Front 218

What is Wernicke's encephalopathy? Is it reversible or irreversible?

Back 218

1) reversible
2) Confusion, ataxia, nystagmus, ophthalmoplegia (eye muscle weakness)

Front 219

Is Korsakoff's psychosis permanent? What kind of neurologic dysfunctions occur?

Back 219

(1) Advanced irreversible stage of Wernicke's encephalopathy
* Targets the limbic system
(2) Anterograde amnesia (inability to form new memories)
(3) Retrograde amnesia (inability to recall old memories)
(4) Confabulation
(5) Hallucinations

Front 220

How is acute Wernicke's encephalopathy prevented in alcoholics?

Back 220

Alcoholics receive IV infusion with glucose and thiamine to prevent acute Wernicke's encephalopathy

Front 221

What type of brain lesion can Wilsons disease cause and where?

Back 221

cavitary necrosis of putamen

Front 222

Where in the brain do adult tumors occur? What are the types of tumors in decreasing order of frequency?

Back 222

1. Approximately 70% occur above the tentorium cerebelli.
2. In order of decreasing frequency: glioblastoma multiforme, meningioma, ependymoma

Front 223

Most common primary CNS tumor in adults?

Back 223

glioblastoma multiforme

Front 224

Are brain tumors the most common cancer in children? Where do the tumors arise in head? What are the tumors in order of decreasing frequency?

Back 224

a.Second most common cancer in children
b.Approximately 70% occur below the tentorium cerebelli.
c.In order of decreasing frequency:
■Cystic cerebellar astrocytoma, medulloblastoma, brainstem glioma

Front 225

What are risk factors for developing a primary CNS tumor?

Back 225

◦Turcot's syndrome, neurofibromatosis, cigarette smoking

Front 226

What are general symptoms of a primary CNS

Back 226

a.Headache (20% initially, 60% later)
b) Tend to be worse during the night; wakes person up
c) Accompanied by nausea and vomiting
d) seizures (>30%)
e) Symptoms/signs of intracranial hypertension

Front 227

Astroycytoma Accounts for about what percent of all neuroglial tumors

Back 227

70%

Front 228

What lobes does an astrocytoma involve in adults and in children?

Back 228

a.Usually involves frontal lobe in adults
b.Usually involves the cerebellum in children

Front 229

How are CNS tumors graded?

Back 229

a.Grades I and II are low-grade cancers.
b.Grades III and IV are high-grade cancers.

Front 230

Glioblastoma multiforme is a high grade what? Where do they arise from?

Back 230

astrocytoma

(1) May arise de novo
(2) May arise from dedifferentiation of a low-grade astrocytoma

Front 231

How would you describe a gliobastoma multiforme tumor?

Back 231

grade IV astrocytoma; often crosses corpus callosum; hemorrhagic/cystic

Front 232

Do glioblastomas metastisize? What is the prognosis?

Back 232

a.May seed the neuraxis via the CSF
■Rarely metastasize outside the CNS
b.Generally poor prognosis

Front 233

The Most common benign brain tumor in adults is what?

Back 233

meningioma

Front 234

Do meningiomas occur more in men or women?

Back 234

◦Female predominance (tumors have estrogen receptors)

Front 235

Where do meningiomas derive from and where are commonly located?

Back 235

1. Derived from arachnoidal cells
2. Locations-parasagittal location, olfactory groove, lesser wing of sphenoid

Front 236

What are meningiomas associated with?

Back 236

neurofibromatosis, history of radiation

Front 237

What are gross and microscopic features of meningiomas? Do they invade? What are they a common cause of?

Back 237

a.Firm tumors
1) May indent (not invade) the surface of brain
2) Often infiltrate overlying bone
3) Causes increased bone density
4) Swirling masses of meningothelial cells encompass psammoma bodies (calcified bodies).
5) Common cause of new-onset focal seizures

Front 238

Are Ependymomas benign or malignant? Where do they arise in adults? children?

Back 238

1. Benign tumor derived from ependymal cells
2. Arises in cauda equina in adults
3. Arises in fourth ventricle in children

Front 239

Are Medulloblastomas benign or malignant? Where do they occur? Who do they occur in? Can they spread?

Back 239

1.Malignant small cell tumor of cerebellum
2. Primarily occurs in children
3. Arises from the external granular cell layer of the cerebellum
4.Often seeds the neuraxis and invades the fourth ventricle

Front 240

Oligodendrogliomas occur in who? Where in the CNS? Are they malignant? What happens to the tumor?

Back 240

1.Benign tumor derived from oligodendrocytes
2. Primarily occurs in adults
3. Frontal lobe tumor that frequently calcifies

Front 241

What causes the majority of CNS lymphomas? What are primary CNS lymphomas associated with?

Back 241

1.Majority are metastatic high-grade B-cell non-Hodgkin's lymphomas.
2.Primary CNS lymphomas
a.Most often associated with AIDS
b.Epstein-Barr virus (EBV)-mediated B-cell lymphomas
c.Rapidly increasing due to the increase in AIDS

Front 242

What is the most common brain malignancy from? Where do metastisis come from?

Back 242

1) metastisis
2) In order of decreasing frequency:
◦Lung, breast, skin (melanoma), kidney, gastrointestinal tract

Front 243

What is a tumor that is parasagittal multilobular and is attached to the overlying dura?

Back 243

Meningioma

Front 244

Microscopically what is seen in a meningioma?

Back 244

swirling meningothelial cells and numerous basophilic staining psammoma bodies

Front 245

Demyelination is often segmental resulting in?

Back 245

A glove and stocking feeling (paresthesias)

Front 246

Axonal degeneration leads to?

Back 246

■Muscle fasciculations leading to muscle atrophy

Front 247

What is the Most common hereditary neuropathy? Is it dominant or recessive?

Back 247

Charcot-Marie-Tooth (CMT) disease

■Autosomal dominant disease

Front 248

What does peroneal nerve neuropathy result in?

Back 248

(1) Causes atrophy of muscles of lower legs
(2) Legs have an "inverted bottle" appearance

Front 249

The most common acute peripheral neuropathy is? What else is it the most common cause of?

Back 249

1) Guillain-Barré syndrome
2) acute flaccid paralysis

Front 250

Is Guillain-Barré syndrome primarily motor or sensory?

Back 250

1) Predominantly motor involvement
2) Variants can be motor and sensory

Front 251

Autoimmunity can lead to Guillain-Barré syndrome. What precipitates it? What part of the nervous system gets attacked?

Back 251

Autoimmune demyelination syndrome
(a) Involves nerve roots and peripheral nerves
(b) Common preceding infections are Mycoplasma pneumoniae pneumonia, Campylobacter jejuni enteritis, viral infection (HIV, EBV, cytomegalovirus, influenza)

Front 252

Is Guillain-Barré syndrome rapid or slowly progressive? Is ascending or descending motor weakness present? Which muscles are initially involved? What is the longterm dander?

Back 252

Rapidly progressive ascending motor weakness
1) Less commonly descending motor weakness
2) Usually starts in proximal muscles and eventually includes distal muscles
3) Danger of respiratory muscle paralysis and death

Front 253

Are DTR's affected in Guillain-Barré syndrome?

Back 253

Yes, they are Depressed or absent deep tendon reflexes in arms and legs

Front 254

What are CSF findings in Guillain-Barré syndrome?

Back 254

1) Increased CSF protein
■Oligoclonal bands present on high-resolution electrophoresis
2) CSF glucose, cell count normal

Front 255

How is Guillain-Barré syndrome diagnosed?

Back 255

1) Spinal tap with increased CSF protein
2) Electromyography and nerve conduction studies

Front 256

Hoiw is Guillain-Barré syndrome treated and what is the prognosis?

Back 256

1) Infusion IV immunoglobulin or plasma exchange
2) Mechanical ventilation if required
Prognosis
1) Mortality 5% to 10%
2) Full motor recovery 60%
3) Residual weakness 15%

Front 257

What is the most common cause of peripheral neuropathy? At the cellular level what is it due to?

Back 257

a.Diabetes Mellitus
b.Due to osmotic damage of Schwann cells

Front 258

What toxins can cause peripheral neuropathies?

Back 258

1) Alcohol, heavy metals, diphtheria

Front 259

Is idiopathic Bells palsy a problem with an UMN or LMN? where is the problem? What can bells be associated with?

Back 259

a.Lower motor neuron palsy
b.Inflammatory reaction of facial nerve (CN VII)
■Near the stylomastoid foramen or in the bony facial canal
c.May be associated with herpes simplex virus (HSV, most common), HIV, sarcoidosis, Lyme disease, pregnancy

Front 260

Is bells that is caused by lyme disease unilateral or bilateral?

Back 260

Often bilateral in Lyme disease

Front 261

Idiopathic Bell's palsy is most commonly associated with what?

Back 261

HSV

Front 262

What are clinical findings in bells caused by LMN dysfunction?

Back 262

1) Ipsilateral upper and lower face involvement
2) Drooping of the corner of the mouth
3) Difficulty speaking
4) Inability to close the eye
5) Hyperacusis in some cases

Front 263

What are clinical findings in bells caused by UMN dysfunction?

Back 263

1) Contralateral lower face involvement
2) Contralateral sparing of the upper face

Front 264

What drugs can cause peripheral neuropathies?

Back 264

vincristine, hydralazine, phenytoin

Front 265

What vitamin deficiencys can cause peripheral neuropathies?

Back 265

deficiency of thiamine, vitamin B12, pyridoxine

Front 266

How can peripheral neuropathies and the pain associated be treated?

Back 266

a.Antiseizure medications-gabapentin, carbamazepine, phenytoin
b.Lidocaine patch
c.Tricyclic antidepressants-amitriptyline, nortriptyline

Front 267

What is another name for Schwannoma? Are they benign or malignant?

Back 267

1) (neurilemoma)
2) benign

Front 268

Schwannomas commonly occur in which nerves?

Back 268

a.CN V (trigeminal) and VIII (acoustic) may be involved.
b.Spinal nerve roots, peripheral nerves may be involved

Front 269

Where do the majority of acoustic neuromas form? What do they look like?

Back 269

Majority are located in the cerebellopontine angle.
1) Encapsulated tumors
2) Usually unilateral
3) Microscopic view shows alternating dark and light areas

Front 270

What is acoustic neuroma sometimes associated with? How is it different from the benign form?

Back 270

Associated with neurofibromatosis (NF2) and is BILATERAL

Front 271

What are clinical findings in acustic neuroma? How is it treated?

Back 271

tinnitus and sensorineural hearing loss

surgery

Front 272

microscopically acustic neuromas look like?

Back 272

spindle-shaped cells with alternating dark and light areas

Front 273

What spinal levels are in the ulner nerve? What is fractured and what results?

Back 273

1) C8-T1
2) Fracture of medial epicondyle of the humerus
Injury produces a "claw hand" (loss of interosseous muscles)

Front 274

The radial nerve encompasses what spinal levels? Where can it be damaged and what results?

Back 274

1) C5-T1
2) Midshaft fractures of humerus
Draping the arm over a park bench (called "Saturday night palsy")
3) Injury produces wrist drop

Front 275

The Axillary nerve encompasses what spinal levels? Where can it be damaged and what results?

Back 275

1) C5-6
2) Fracture of surgical neck of humerus; anterior dislocation of the shoulder joint (may also injure the axillary artery)
3) Cannot abduct the arm to horizontal position or hold the horizontal position when a downward force is applied to the arm (paralysis of deltoid muscle)

Front 276

The median nerve is composed of what spinal levels? What are causes?

Back 276

1) C6-T1
2) Most commonly due to entrapment in the transverse carpal ligament of the wrist or between the bellies of the pronator teres muscle
3) Rheumatoid arthritis and pregnancy two most common causes; also overuse of hands and wrist (e.g., in barbers), amyloidosis, hypothyroidism, supracondylar fracture of humerus

Front 277

Clinical how do people present with median nerve damage? What type of hand do they develop?

Back 277

nocturnal pain; pain, numbness, or paresthesias in the thumb, index finger, third finger, and radial side of fourth finger; thenar atrophy produces an "ape hand" appearance and difficulty in opposing the thumb with the 5th finger

Front 278

Which spinal levels comprise the common peroneal nerve? Dorsiflexion is lost, what muscles are weakened?

Back 278

1) L4-S2
2) peroneus longus and brevis muscles

Front 279

What type of gait does someone have if there is peroneal nerve damage? What muscle is lost?

Back 279

Loss of foot dorsiflexion due to weakening of the tibialis anterior muscle produces "slapping gait" or "high-stepping gait" like a horse

Front 280

Toe extension is lost with peroneal nerve palsy. Which muscles are effected?

Back 280

extensor digitorum longus and hallucis longus muscles

Front 281

When does equinovarus deformity occur? What happens?

Back 281

1) peroneal nerve palsy
2) foot is plantar flexed and inverted

Front 282

Sensation is lost with peroneal nerve where? what reflex is lost?

Back 282

1) Sensory deficits involve the anterolateral aspect of the leg and dorsum of the foot
2) Loss of the ankle jerk reflex

Front 283

What is wrong in Erb-Duchenne palsy?

Back 283

Brachial plexus lesion involving C5 and C6
"Waiter's tip deformity"

Front 284

Fibrillary background, Immunoreactivity for glialfibrillary acidicprotein (GFAP), and Diffuse (ill-demarcated) pattern of growth

Back 284

Astrocytomas

Front 285

spindly neoplastic astrocytes with long bipolar processes; tumors
rich in Rosenthal fibers, thick corkscrew-like eosinophilic structures, which
derive from hypertrophic processes of astrocytes

Back 285

pilocytic astrocytoma

Front 286

Pronounced perinuclear halo: "fried-egg" appearance
Prominent capillary network in a chickenwire pattern

Back 286

oligodendroglioma

Front 287

histologically how are ependymal cells characterized?

Back 287

1. Ependymal rosettes: cells organized around a lumen
2. Perivascular pseudo rosettes: cells arranged around small vessels

Front 288

Spindle-shaped cells with indistinct borders (syncytial) with Cells arranged in whorls or fascicles

Back 288

meningioma

these are Psammoma bodies

Front 289

blue,small, round cell tumors, with pseudorosettes

Back 289

primitive neuroectodermal tumors that occur in children

Front 290

Spindly cells arranged in hypercellular Antoni A areas, alternating with
hypocellular Antoni Bareas and Verocaybodies

Back 290

Schwannoma

Verocaybodies:parallel rows of neoplastic Schwann cells