Neuro Exam 3

Front 1

What is the hallmark of HIV encephalitis on MRI?

Back 1

1. symmetrical white matter involvement
2. generalized atrophy of brain, esp cortex
- as result see widened sulci, and increased CSF space

Front 2

What is the primary infection of the brain w/ HIV caused by?

Back 2

lymphocytes brought in by opportunistic infections (such as toxoplasmosis)

Front 3

At what point during the HIV illness does primary infection of the brain occur?

Back 3

during the long, asymptomatic phase of HIV infection

Front 4

What types of cells in the brain are primarily affected by HIV?

Back 4

microglia and macrophages

Front 5

What is the common endpoint of all the ways HIV affects the brain?

Back 5

excitation of neuronal NMDA --> influx of calcium into cell --> death

Front 6

What are the 3 main ways HIV affects the brain?

Back 6

1. gp120 glycoproteins on protein coat shed by virus --> activate uninfected macrophages and cause them to produce various neurotoxins --> affects neurons
2. virus infects macrophages directly
- macrophages can produce neurotoxins and cytokines --> can affect astrocytes adjacent to neurons
3. Shed gp120 can affect astrocytes directly
- affected astrocytes produce NO
- affected neurons --> produce Glu (neurotoxic)

Front 7

What types of neurotoxins are produced by HIV or gp120-infected macrophages? How do they affect astrocytes?

Back 7

NO, arachidonic acid, oxygen free radicals
- normally, astrocytes scavenge excess glutamate; but arachidonic acid inhibits Glu re-uptake

Front 8

What are primary spinal cord diseases caused by HIV?

Back 8

1. vacuolar myelopathy
- small holes in SC due to drop-out of neurons
2. necrotizing vasculitis (inflammatory destruction of bv's) --> can cause SC necrosis

Front 9

Painful sensory neuropathy (in context of HIV)

Back 9

- one of most common symptoms in long-term AIDS patients
- late-phase disease manifestation involving peripheral nervous system
- loss of sensation in hands, arms and feet --> if brush skin there, feel painful sensation
- common among patients w/ severe immunodeficiency
- side effect of retroviral cocktails

Front 10

What are the 3 most common focal or mass lesions in the brain as result of HIV infection?

Back 10

1. toxoplasmosis
2. primary CNS lymphoma
3. progressive multifocal leukoencephalopathy

Front 11

what are the most common pairs of multiple concurrent pathologies in HIV patients?

Back 11

1. PML w/ toxoplasmosis
2. CMV w/ lymphoma
- cytomegalovirus encephalitis

Front 12

archicortex

Back 12

3 layers
made up of hippocampus and dentate gyrus

Front 13

paleocortex

Back 13

3-5 layers
Uncus + subiculum (transitional cortex)

Front 14

isthmus (in context of limbic system)

Back 14

connects the cingulate gyrus w/ the parahippocampal gyrus

Front 15

what structures make up the hippocampal formation?

Back 15

1. hippocampus
2. dentate gyrus
3. subiculum

Front 16

stria terminalis

Back 16

tract connecting the amygdala to other parts of limbic system (major output tract of amygdala)
- follows similar projectory to fornix, exept comes out of amygdala
- Carries reciprocal connections
Has pre and post commisural parts
a. post-comm --> projects down to hypothalamus
b. pre-comm --> swings ant to AWC, and ends in septal region

Front 17

what is the septal region comprised of?

Back 17

1. septal area (aka subcallosal gyrus or septal cortex)
2. septal nuclei
3. septum pellucidum

Front 18

Where do the different fibers of the fornix go to?

Back 18

1. pre-commisural (anterior to anterior comm) --> septal region
2. post-comm --> swing down posterior to ant comm and end in mammillary bodies

Front 19

What are the functions of the septal area?

Back 19

Animals:
- pleasure center (connected to n accumbens by medial forebrain bundle)
- if lesioned --> sham rage (get hostile towards anything in env)

Humans
- brightening of attitude
- feel good sensation

Front 20

Stria medullaris thalamus

Back 20

connects septal region to habenular nucleus
- integrates somatic (habenular), visceral, and emotional info (both in septal region)

Front 21

alveus of hippocampus

Back 21

surface facing the lateral ventricle

Front 22

What structure can cause damage to the uncus?

Back 22

tentorium (runs right under uncus)
- therefore can damage uncus if brain drops a bit due to increased intracranial P

Front 23

Uncal herniation

Back 23

produce "uncinate fits" or "olfactory hallucinations" when uncus is damaged by edge of tentorium

Front 24

What is another name for the hippocampus proper? What are the different areas?

Back 24

aka Ammon's Horn or Cornu Ammonis
1. CA1 (closest to subiculum)
2. CA2
3. CA3
4. CA4 (closest to dentate gyrus)

Front 25

hippocampal sulcus

Back 25

vestigial structure
- separates CA1, CA2, CA3 from dentate gyrus

Front 26

How many layers and lamina make up the hippocampus proper?

Back 26

3 cell layers and 6 lamina
1. Alveus (white matter, vent surf)
2. stratum Oriens (1)
3. " pyramidale (2) --> contains hippocampal pyramidal cells
4.
5.
6. " Moleculare (layer 3)

Front 27

How many layers of dentate gyrus?

Back 27

3 cell layers
1. Stratum Moleculare
2. Stratum Granulosum (granule cell)
3. Polymorphic layer

Front 28

What hippocampal cell area is most sensitive to hypoxia?

Back 28

CA1 aka Somer's sector
- CA1 cells can die in epileptics and are very vulnerable in Alzheimers
- amnesia is common phenomenon after cardiopulm arrest or bypass surgery

Front 29

What hippocampal cell area is resistant to hypoxia

Back 29

CA3 (Spielmyer sector)

Front 30

What hippocampal cell area would be damaged in epileptics or Alzheimer's patients?

Back 30

CA1

Front 31

Schaeffer collaterals in hippocampal lamina

Back 31

interconnect CA3 with CA1

Front 32

What fibers make up the fornix?

Back 32

mostly subicular fibers and some CA3 fibers (via alveus)

Front 33

what are the 2 functions of the hippocampus?

Back 33

1. conversion of short-term --> long-term memory
2. Daily cell addition to dentate gyrus (fn or significance unknown)

Front 34

What are the 2 parts of the amygdala and their general functions?

Back 34

1. basolateral --> conscious processes
- relates to connectivity w/ frontal and temporal lobes
2. corticomedial --> more autonomic fn

Front 35

What are the results of stimulation of the corticomedial amygdala?

Back 35

salivation, licking, chewing, defecation, urination

Front 36

what is the result of stimulation of the basolateral amygdala?

Back 36

arousal, increased attention, fear/rage, pupil dilattion, EEG activation, hallucinations (think more active processes)

Front 37

What is the result of lesions to the basolateral amygdala?

Back 37

tameness, decreased emotionality, decreased aggression, decreased hyperactivity

Front 38

Kluver-Bucy Syndrome

Back 38

due knocking out amygdala via bilateral damage to parahippocampal gyrus or anterior lobe ablation
- agnosia
- hyperorality
- lack of emotion
- hyperphagia (overeating)
- hypersexual
- hyperexploratory

Front 39

what is the only myelinated tract in the hypothalamus?

Back 39

mammillothalamic tract

Front 40

What does the transverse fissure mark (diencephalon)?

Back 40

the space between the pia overlying the diencephalon and the pia underlying the telencephalon

Front 41

periventricular hypothalamus

Back 41

neurons that have relationship w/ anterior pituitary
- axons DO NOT project there

Front 42

medial hypothalamus

Back 42

neurons that have relationship to posterior pituitary
- it's axons do project to pituitary
- also has autonomic role

Front 43

What are the hypothalamic nuclei that deal w/ the anterior pituitary?

Back 43

1. preoptic region (reg male and female sex hormones, and heat dissipation)
2. arcuate nucleus (eating pathway)

Front 44

what would a lesion in the pre-optic nucleus produce?

Back 44

hyperthermia

Front 45

How does the hypothalamus secrete releasing factors to anterior and posterior pituitary?

Back 45

1. anterior via Hypothalamo-Pituitary portal system
- axons from preoptic and arcuate nuclei travel down median eminence and release products into portal system --> drift into antererior pit gland

2. Posterior pituitary
- axons from paraventricular and supra-optic nuclei goe all way from hypothalamus to post pituitary and synapse there

Front 46

suprachiasmatic nucleus
What is its input and output?

Back 46

hypothalamic nucleus
- regulates circadian rhythms
INPUT: from retinal ganglion cells
OUTPUT: 1. to pineal gland (affects rhythm via melatonin release)
2. to other hypothalamic nuclei (influence drinking, eating, temperature control)

Front 47

Which hypothalamic nuclei respond to heat?

Back 47

1. pre-optic nuclei
2. anterior nucleus (parasymp control)

Front 48

What hypothalamic nucleus responds to cold?

Back 48

Posterior nucleus

Front 49

What are the 3 Forces that Create an Infarct?

Back 49

1. hypoxia (global oxygen dep)
2. hypoglycemia
3. ischemia (focal blood deprivation, hence o2 dep)

Front 50

What is the blood flow in a normal brain?

Back 50

50ml/100gm/min

Front 51

At what blood flow points do you start seeing brain damage and cellualr death?

Back 51

1. 18-23ml/100gm/min --> proper neural function (synaptic activity) stops working --> clinical manifestations appear

2. <10ml/100mg/min --> cellular death occurs; at that level is ATPase dependent pump failure and neurons die

Front 52

ischemic penumbra

Back 52

neurons in the 10-18ml/100mg/min blood flow range, usually found around the dead neurons
- are injured/not working, but are not dead

Front 53

TIA (transient ischemic attack)

Back 53

transient ischemic attack
- a transient event that does not cause an infarct (aka no demonstrable lesion on imaging studies)
- aka "ministroke" by lay public

Front 54

what are the 3 ways to cause focal deprecation (ie ischemia)?

Back 54

1. thrombus
2. embolus
3. hemodynamic low-flow mechanism

Front 55

thrombus

Back 55

a clot formed in a diseased blood vessel
- does not go away
- is not found in healthy bl vessels

Front 56

embolus

Back 56

clot that has detached and travels to another site to lodge
- DOES NOT stay forever
- often damages brain tissue and then dissolves

Front 57

what is the most common cause of a subarachnoid hemorrhage?

Back 57

trauma

Front 58

what is the most common cause of an atraumatic subarachnoid hemorrhage?

Back 58

aneurysm burst

Front 59

what part of artery is weak in an aneurysm?

Back 59

tunica media

Front 60

What is the greatest killer of human beings (other than malaria and mosquito)?
what are different types?

Back 60

Arteriosclerosis
1. Artherosclerosis - affects lg arteries, see artheromas (plaques of the neo-intima)

2. Arteriolosclerosis - affects arterioles (0.1-0.4mm)

Front 61

what vessel can be dissected from chiropractors or snapping your own neck? What type of stroke does that result in?

Back 61

vertebral --> results in posterior fossa stroke

Front 62

what are small vessel strokes usually due to?

Back 62

arteriolosclerosis, thrombus in a small vessel

Front 63

What does small vessel thrombosis usually cause?

Back 63

lacunar infarct or lacunar stroke

Front 64

What part of the brain do lacunar strokes typically occur in?
What's the typical presentation?

Back 64

thalamus
- pure weakness or pure numbness on 1 side

Front 65

What is the number 1 cause of cardiac stroke?

Back 65

atrial fibrillation

Front 66

What are 2 possible fates of an arteriolosclerotic lesion?

Back 66

1. if thrombose --> lacunar infarct (if lucky)
2. if rupture --> intracerebral hemorrhage

Front 67

what is the best imaging technique for acute stroke?

Back 67

CAT scan, without contrast

Front 68

Paradoxic emboli

Back 68

clots in veins that can bypass the lungs if there's a hole in the heart (patent foramen ovale) --> are a cause of cardiogenic stroke

Front 69

Myxomas

Back 69

degenerative lesions in heart
- if appear in L atrium --> stroke

Front 70

What are the 2 worst vascular malformations that can result in subarachnoid or ICH and therfore stroke?

Back 70

1. AVM
2. cavernous hemangioma

Front 71

hemorrhagic infarct

Back 71

a cause of bloody stroke
- blocked blood vessel damages downstream blood vessels and clot damages brain
- when clot dissovles --> reperfusion of damaged brain (BBB also damaged) --> diapedesis of RBCs into brain tissue --> infarct w/ hemorrhagic quality

Front 72

what is the best imaging technique for acute stroke?

Back 72

CAT scan, without contrast

Front 73

Paradoxic emboli

Back 73

clots in veins that can bypass the lungs if there's a hole in the heart (patent foramen ovale) --> are a cause of cardiogenic stroke

Front 74

Myxomas

Back 74

degenerative lesions in heart
- if appear in L atrium --> stroke

Front 75

What are the 2 worst vascular malformations that can result in subarachnoid or ICH and therfore stroke?

Back 75

1. AVM
2. cavernous hemangioma

Front 76

hemorrhagic infarct

Back 76

a cause of bloody stroke
- blocked blood vessel damages downstream blood vessels and clot damages brain
- when clot dissovles --> reperfusion of damaged brain (BBB also damaged) --> diapedesis of RBCs into brain tissue --> infarct w/ hemorrhagic quality

Front 77

difference between associative and non-associative learning

Back 77

associative --> organism exposed to > 1 stimulus and its behavior altered on the basis of relation bet stimuli

non-assoc --> org exposed to a stimulus 1 or more times, alters its behavior based on that stimulus and elicits a reflex

Front 78

Habituation vs. sensitization

Back 78

both are nonassoc learning
1. habituation = reflex dimishes w/ successive activation of stimulus (simplest type)
2. sensitization = globally arousing stimulus that increases strength of reflexes and can overcome habituation on relatively short terms

Front 79

What types of memories do we have conscious access to?

Back 79

declarative

Front 80

which memories would be affected by bilateral lesion of hippocampus?

Back 80

declarative memories impaired but procedural memories kept intact

Front 81

Different stages of memory

Back 81

1. sensory memory (high capacity, brief persistence)
2. short term memory (lower capacity, slightly longer persistence)
3. long-term memory (high capacity and long persistence)

Front 82

sensory memory composed of:

Back 82

1. partial-report approach (for short period of time, have access to everything presented to you as the stimulus)
2. destructive read out (once you start reporting info, lose it)

Front 83

what type of memory is resistant to focal damage of the CNS? What kind of damage would be required to lose this type of memory?

Back 83

Long term memory --> need widespread cortical dysfunction

Front 84

imagination inflation/guided imagination

Back 84

asked to imagine false events and think about the context in which they might have happened, in subsequent interviews are more likely to recall that those events actually happened

Front 85

reconsolidation

Back 85

idea that events surrounding the recall of an event can influence subsequent memories of the original event

Front 86

what brain structure is resp for integrating a conditioned stimulus w/ unconditioned stim

Back 86

amygdala

Front 87

what structure recognizes emotional content of facial expression? What happens with a more fearful face?

Back 87

amygdala; the more fearful the face, the more cerebral regional blood flow to the RIGHT amygdala

Front 88

place fields

Back 88

are a property of hippocampal neurons for mapping the world
- neurons become activated in particular regions of space, regions in which cells fire at increased rate (place field)
- an absolute sort of mapping --> new place fields in new environments

Front 89

what are the computational properties of the LTP, making it important for storage of info?

Back 89

1. specificity -> only synapses that were activated during tetanus show potentiation after the fact
2. cooperativity - need a sufficient number of presynaptic cells activated in order to provide enough depolarization for postsyn cell for potentiaion (aka a weak input, only 1 cell, will not show potentiation after tetanus but a strong input will)

3. associativity - tetanizing both pathways simultaneously produces potentiation in both pathways

Front 90

Why do both the weak input and strong input show potentiation after the fact if both are stimulated?

Back 90

in strong pathway, post synaptic cell sufficiently depolarizes
in weak pathway, glutatmate released
(2 criteria met for NMDA activation)

Front 91

what are the 2 major cascades set up by NMDA activation which contribute to maintaining LTP

Back 91

1. insertion of new AMPA receptors into post-syn site --> increases glutatmate sensitivity of postsyn membrane and get a larger post synaptic current

2. synthesis of retrograde messenger (NO or arachidonic acid) that diffuse back to presyn term and increase the amt of transmitter released for a given AP

Front 92

what's the difference between partial and generalized seizures?

Back 92

1. partial - DO have a clear point of origin, and electrical activity reflects its restricted scope
- either preserved (simple) or impaired consciousness (complex), but not total loss

2. generalized - DO NOT have localized onset
- similar activity may be recorded on either side of brain; spread all over
- all involve a loss of consciousness

Front 93

what's the difference between partial complex and partial simple seizures?

Back 93

1. partial complex
- impairs consciousness
2. partial simple
- preserved consciousness

Front 94

status epilepticus

Back 94

defined as > 30min of continuous seizure activity, or 2 or more sequential seizures spanning that period w/o full recovery between seizures
- medical emergency

Front 95

what are the sequence of events in a seizure?

Back 95

1. micro-anatomical and/or electrophysiological abnormality
2. changes in excitation/inhibition ratio
3. critical mass fires spontaneously
4. neighboring cells triggered
- shared refractory period
5. wave spreads via hemichannels

Front 96

what are the 2 types of inhibitory synapse receptors and the difference between them?

Back 96

1. GABA-A - post-synaptic
- specific recognition sites
2. GABA-B pre and post synaptic
- requires cAMP (metabotropic)

Front 97

paroxysmal depolarizing shift

Back 97

depolarization of cortical neurons after post-ictal depression and before the silent period begins preceding an ictal seizure
- characterized by interictal spike if fired in synchronous manner by multiple neurons
- prolonged calcium-dep depolarization --> results in multiple sodium mediated AP's during depol phase
- followed by prominent hyperpolarization (beyond baseline resting pot)

Front 98

what are the mechanisms of anti-convulsants?

Back 98

1. enhanced sodium channel inactivation (CBZ, phenytoin, valproate)
2. enhanced GABA activity (benzos, or barbituates)
- works well for 80-85% of patients

Front 99

are epileptic drugs safe for a pregant woman?

Back 99

NO- are teratogenic

Front 100

What are the cellular mechanisms (ionic and NT) of seizure?

Back 100

1. too much excitation - inward NA and CA currents, and Glutatmate/Asp

2. too little inhibition - inward Cl, outward K currents, GABA

Front 101

what part of the hippocampus does status epilepticus damage?

Back 101

CA3

Front 102

Saltatory conduction

Back 102

phenomenon where nerve impulse jumps from node to node (of ranvier)
- very necessary for motor activity --> increases the speed at which an impulse can go down a nerve (fast propagation)
- due to myelination (insulates the nerve)

Front 103

If one of the nodes of ranvier were denuded, what would happen?

Back 103

conduction block

Front 104

What are the 3 stages/classificaitons of nerve injury?

Back 104

1. neuropraxia (minimal)
- just the myelin is disrupted, body remyelinates region quickly and numbness disappears

2. axonotmesis - myelin disrupted plus crush/cut to axon itself (outer epineurium remains intact)

3. neurotmesis (most severe)
- total dehiscence of the nerve and epineurium
- if nerve not brought back together w/in 24 hrs --> denervation

Front 105

denervation

Back 105

where nerve is totally dehisced, and will retract, therefore lose muscle

Front 106

When does one perform an EMG?

Back 106

to distinguish between denervation (neurotmesis) or myelin/axon injury (axonotmesis)

- must wait 2 weeks to do, because takes about 2 weeks for denervation to show up

Front 107

What are the 3 types of axoplasmic transport?

Back 107

1. fast - deals w/ membrane assoc proteins and lipids
2. slow - resp for transporting cytoskeletal proteins and axoplasmic matrix
3. retrograde - involved w/ uptake by axon terminals
- endocytose trophic factors released by post-syn cell and transport them back to soma

Front 108

Wallerian degeneration

Back 108

aka secondary or anterograde degeneration
- distal part of cut axon whithers and is phagocytized (different mech's in PNS and CNA)
- part connected to soma maintains itself --> swells slightly --> slight degeneration w/in soma itself
- soma will heal and get bulb --> grows back down (anterograde regeneration)

Front 109

abberent reinnervation

Back 109

fibers of nerves innervating multiple muscles get confused and cross
- occurs in bell's palsy --> innervates eyelid and corner of mouth --> blink and smile at same time

Front 110

is there any regeneration of either axons or cell bodies in the CNS?

Back 110

no

Front 111

is there regeneration of either axons or cell bodies in PNS?

Back 111

If cut DRG cell --> no regeneration
If cut peripheral part of DRG (axon) --> usually is regeneration
LMN damage in PNS --> ability to regenerate

Front 112

What are factors dictating the prognosis of a nerve injury?

Back 112

1. the smaller a neuron is, the less likely that it will survive
2. the closer the injury is to the cell body, the worse the outcome is
- metabolically toxic substances into axoplasm are at increased dose to cell body if injury is closer

Front 113

what are the 2 different causes of axon damage?

Back 113

1. mechanical injury (very common)
2. demyelinating diseases (such as MS)

Front 114

What is the worst kind of mechanical nerve injury? The best (prognosis)?

Back 114

worst = evulsion (yanking on nerves)
best = slashing (cut)

Front 115

What is the primary reaction to damage (aka axon reaction)?

Back 115

1. axoplasmic material leaks out
2. cut axon retracts and swells
3. some toxic substances may leak into the axoplasm (calcium, free O2 radicals) --> may be transported retrograde to cell body and kill it

Front 116

What is the initial response of the cell body to damage?

Back 116

1. Disintegration of Nissl substance (chromatolysis)
2. cell swelling
3. nucleus translocates to periphery
- Cell will either lyse or is destined to survive

Front 117

What happens to a cell body after damage if it is destined to survive?

Back 117

1. Reappearance of Nissl material (cell appears hyperchromatic)
2. increase in protein synthesis in attempt to reconstitute axon

Front 118

what is the signal for chromatolysis?

Back 118

elimination of retrogradely transported trophic factors

Front 119

what determines the time it takes for a cell body to respond to injury in retrograde degeneration?

Back 119

rate of retrograde axoplasmic transport

Front 120

Wallerian degeneration in PNS vs. CNS

Back 120

- distal end of axon doesn't survive and is phagocytized by:
1. PNS - macrophages release IL-1--> stimulates Schawann cells --> release NGF and create substrate over which new axons grow
2. CNS - astrocytes and microglia clean up (prospects of regeneration low)

Front 121

which part of a nerve needs to be sutured together if you want to surgically repair it?

Back 121

epineurium

Front 122

what is a peripheral nerve's response to axonal degeneration?

Back 122

schwann cells proliferate w/in endoneurium sheath to create proteins and other things axons prefer to grow on
- these hollow sheath's = Bands of Bungner/fiber bands
- represent a lane going back to the target for the axon to grow back into --> if grow back into tube, then end up at correct target

Front 123

what is the CNS response to axon degeneration?

Back 123

microglia (usually dormant) activated and invade injured region and phagocytize debris and take into vascular system and ventricles
- astrocytes seal off necrotic tissue from healthy tissue --> form astrocytic scars (form barriers for growing axons, impediment to regeneration)

Front 124

Why is there generally failure of axons to regenerate in CNS

Back 124

axons have ability to grow, but growth is aborted due to the presence of astrocytic scars formed by astrocytes trying to seal off necrotic tissue from healthy

Front 125

Anterograde-Retrograde Transneural Degeneration

Back 125

When both the presynaptic and post-synaptic neuron atrophy and disappear due to damage of neuron in between (eliminates neurotrophic factors that support pre and postsyn cells)
- occurs in pathways that have specific non-expansive projections, such as the optic system (if LGN damaged, lose retinal ganglion cells and cortical cells in area 17)

Front 126

What are factors that affect the rate of nerve regeneration?

Back 126

1. temperature - rate of regen in upper forearm is faster than lower forearm, which is faster than hand

Front 127

what are the steps of axonal regeneration (PNS)?

Back 127

1. Damage to axon
2. Schwann cells proliferate w/in endoneurial sheath
3. distal part of axon phagocytized
4. proximal end of axon starts sprouting out new axons/collaterals (Collateral sprouting---many collaterals)
5. axons not making synapses withdraw/retract
6. axons that make synapses are regenerated
7. remyelination

Front 128

Neuroma

Back 128

tangled bulb of axon terminals due to failure of axons to regenerate (usually due to obstruction), occurs in PNS
- reflects aborted/non-functional axonal regeneration and can generate spontaneous pain

Front 129

collateral sprouting

Back 129

occurs in PNS nerve regeneration
- occurs between 2 neurons
ex if presynaptic cell is damaged, then another nearby cell can generate collateral sprout and synapse on the postsyn denervated cell to prevent it from dying (provide trophic factors)

Front 130

What happens to the conduction velocity after regeneration? Why?

Back 130

Conduction velocity is slower than before the damage
1. regenerated axons are 20% thinner
2. Less control of the number of schwann cells that remyelinate axons --> more schwann cells means more internodes which decreases conduction velocity

Front 131

Monocular diplopia

Back 131

- double vision but only in 1 eye
- almost never has neurological cause
- usually due to something in the eye --> refractive error or something in the outer media

Front 132

What is considered the "great mimicker" of ocular cranial nerve palsies? When should it especially be consiered?

Back 132

ocular myasthenia gravis
- autoimmune disease causing weakness of eye muscles and misalignment
- should be considered in the absence of any pain

Front 133

Hering's Law

Back 133

states that in diplopia, images will be furthest apart in the field of action of the weak or paretic muscle

Front 134

Difference between phoria and tropia

Back 134

phoria = the natural misalignment of the eyes, which is held in place by the brain's fusion mechanism (normal)

tropia = manifestation of a misalignment of the eyes, resulting in double vision unless born w/ ocular misalignment

Front 135

Why do children w/ congenital misalignment not have double vision?

Back 135

occurs w/in critical period of plasticity, so brain learns to suppress the 2nd image

Front 136

commitant vs. incommitant strabismus

Back 136

1. misalignment is the same in different positions of gaze
2. degree of misalignment is different in different areas of gaze

Front 137

Paralytic strabismus

Back 137

a type of incommitant strabismus resulting from palsies of either 3, 4, or 6,
- is also seen in Duane's syndrome and ocular myasthenia gravis

Front 138

What is the most common cause of 3rd and 6th nerve palsies?

Back 138

ischemia due to diabetes/hypertension/or both
- gets better on its own and goes away

Front 139

What is the cause of 3rd nerve palsy that's most concerning to physicians?

Back 139

Compression of 3rd nerve by aneurysm
- can be at either junction of Post comm a and ICA, or basilar tip
- pupil is dilated in 90% of cases

Front 140

what is the most common site for abberant regeneration of the 3rd nerve?

Back 140

lid moving upward on downward gaze
- both levator palpebrae and inferior rectus are innervated by same fiberrs

Front 141

What are the most common etiologies of aberrant regeneration of 3rd nerve?
What condition do you need to assume if patient never had 3rd nerve palsy diagnosed?

Back 141

1. only w/ compressive (aneurysmal) or traumatic causes of palsy
2. If never had 3rd nerve palsy diagnosed, assume intercavernous sinus aneurysm or meningioma until proven otherwise

Front 142

Mobius syndrome

Back 142

congenital, a common cause of 6th nerve palsy
- 6th, 7, 12 palsy
- whole face sagging downward, very expressionless

Front 143

What are the 2 mimicker's of 6th nerve palsy?

Back 143

1. duane's syndrome
2. convergence spasm

Front 144

What are the types of duane's syndrome and what distinguishes it from 6th nerve palsy?

Back 144

1. type I - restriction of abduction
2. type II - restriction of adduction
3. type III - restriction of both adduction and abduction

- all will be accompanied by narrowing of interpalpebral fissure when trying to perform the restricted movement

Front 145

convergence spasm

Back 145

mimicker of 6th nerve palsy
- when eyes converge (both looking inward) --> become stuck and cannot abduct
- when cover one eye --> can fully abduct
- key distinguishing factor from 6th nerve palsy = seeing pupils constrict

Front 146

Most common cause of 4th nerve palsy

Back 146

trauma

Front 147

What are the clinical signs of 4th nerve palsy (diagnostic indicators)?

Back 147

1. positive bielchowsky --> if tilt head ipsilateral to lesion, will complain of worsening diplopia
2. excyclotorsion
- whole eye is extorted
- when tilt head opposite lesion, affected eye will intort --> restores normal vision

Front 148

what is the best way to isolate the superior oblique muscle?

Back 148

adduct eye --> only the superior oblique depresses the eye now

Front 149

which oculomotor nucleus gives rise to levator palpebrae superioris

Back 149

central caudal subdivision

Front 150

Weber's syndrome

Back 150

due to lesion of midbrain
- ispi oculomotor palsy (ptosis, mydriasis [pupil dilation], relevant oculomotor muscle atrophy)
- contralateral hemiparesis of limbs, and paralysis of lower face and tongue

Front 151

What are the stabilizing horizontal eye movement reflexes?

Back 151

1. vestibulo-ocular - uses vestibular input to hold images stable on retina during brief or rapid head rotation (insensitive to slow movements)

2. optokinetic - uses visual input to hold images stable on retina during sustained or slow head rotation

Front 152

Vestibulo-ocular reflex

Back 152

eyes rotate in opposite direction of head movement
- during short, unsustained head movement, eyes kept in place by neural integrator
- during long, sustained head movements, vestibular nystagmus (eyes snap back to fwd gaze and position continually reset)

- head turns to left --> left scarpa's ganglion increases firing --> left vestibular nucleus --> right (contra) abducens nucleus
- have contraction of right lateral rectus
- V1 nuc also sends fiber across MLF to left oculomotor to contract left medial rectus, so that the eyes move to the right

- scarpa's ganglion on other side of head decreases firing to depress the antagonizing muscles

Front 153

Optokinetic reflex

Back 153

Scenery moves to right --> head moves to left --> eyes follow scenery (right)
- the vesticular nuclei must be tricked by vestibular cerebellum into thinking there's SC canal movement

- visual input --> retina --> nucleus of the optic tract (before LGN) --> inferior olive --> vestibular cerebellum --> vestib nuclei --> drive the III and VI nuclei again

Front 154

where is the vertical gaze center located?

Back 154

midbrain reticular formation
- includes interstitial nucleus of Cajal

Front 155

what is the frontal eye field's role in saccadic movements

Back 155

it initiates them; appraises the location of targets via input from visual association cortex and thalamic relays
- stimulation of frontal eye field on 1 side causes deviation of the eyes to opposite direction

Front 156

what is the horizontal gaze center in the brain?

Back 156

paramedian pontine reticular formation
- contains an omnipause region responsible for holding things still, then when want to shift gaze, must stop and burst cells increase their activity

Front 157

what would be the result of a stroke defect in the frontal eye field?

Back 157

difficulty moving eyes in opp direction

Front 158

Name the 3 voluntary eye movements for keeping visual target on the fovea w/o moving head

Back 158

1. saccade - simultaneous, quick movements of both eyes in same direction; for looking at unmoving objects
2. smooth pursuit - smoothly tracking an object moving in space w/o head movement
3. vergence - adjusting eyes for different viewing distances in depth

Front 159

what sources does the PPRF get input from for generating saccades?

Back 159

frontal eye field (premotor cortex) and superior colliculus

Front 160

projections of the horizontal saccadic pathway

Back 160

ex. moving eyes to left
R frontal eye field --> L PPRF --> L VI --> lateral rectus and R III --> R medial rectus

Front 161

What happens in lesion of MLF? How do you distinguish from medial rectus paralysis?

Back 161

1. weakness of adduction on attempts of horizontal gaze
2. but no weakness of adduction w/ convergence
ex.) R MLF lesion --> weakness of adduction of R eye on attempted leftward gaze

Front 162

what is the smooth pursuit pathway

Back 162

visual input --> R parieto-occipital junction (assoc cortex) --> R pontine nuclei --> L vestibulocerebellum --> L vestibular nuclei (tricked) --> rest is same as optokinetic

Front 163

What is the center for micturition located and what is its functions?

Back 163

pontine micturition center (2 paired nuclei)
- 1 controls detrusor contraction (contracts during voiding)
- 1 controls contraction/relaxation of striated sphincter (relaxes during voiding)

Front 164

How does damage to pudendal nerve occur and what's the result

Back 164

1. anything damaging to lower sacral cord or pelvic floor (pelvic fracture, difficult childbirth)
2. incontinence

Front 165

What nerves control the different muscles in the bladder and what NT's do they use?

Back 165

1. Pelvic nerves (Parasymp, Ach) --> detrusor
2. Hypogastric nerves (Symp, NE) --> sm. muscle sphincter/trigone of bladder
3. Pudendal nerve (Ach, somatic) --> external/striated urinary sphincter

Front 166

What is treatment for interstitial cystitis and the rationale for it?

Back 166

I.C = contant irritation of bladder
Tx = inserting capaiscin in bladder --> blocks neurokinin receptors --> decreases pain and sensitivity

Front 167

overflow vs. urge incontinence

Back 167

overflow = hi volume in bladder, but some abnormality of sensation so can't feel the fullness; bladder pressure exceeds urethral pressure and urine leaks out

urge = high frequency, low volume
due to some sort of irritation; often exhibit nocturia

Front 168

functional incontinence

Back 168

abnormality of body, not bladder. can't physically move well enough to get yourself to bathroom on time

Front 169

iatrogenic incontinence

Back 169

due to medications
- produce a relative amt of retention in the bladder

Front 170

Hinman bladder (non-neurogenic neurogenic bladder)

Back 170

type of acquired incontinence
"aka schoolteachers' or bus driver's bladder"
- is a result holding back urine when bladder is full --> increase in bladder pressure damages detrusor muscle
- if not functioning, can't contract to expel urine when sphincter is relaxed
- when full and want to empty fast, valsava to push down --> center in sacral SC causes sphincter to tighten when you bear down --> increases resistance you're emptying bladder at

- as result, is an increase in urine going along past of least resistance --> backflow into ureters

Front 171

stress urinary incontinence

Back 171

most common kind of incontinence
- involuntary leakage synchronous w/ exertion, sneezing, laughing, etc

Front 172

dyssynergic voiding, and it's cause

Back 172

as bladder detrusor trying to contract, sphincter is contracting
- due to lesion of spinal cord above Onuf's nucleus (for pudendal --> sphincter), and below pontine micturition center

Front 173

dysreflexia

Back 173

massive sympathetic discharge that can occur w/ lesions at thoracolumbar junction - get really full bladder cause of contraction of symp nerves contracting sm muscle sphincter
- hypertension, increased bp, increased sweating

Front 174

detrusor areflexia

Back 174

due to either sacral SC injury or cauda equina --> patient into spinal shock --> deep tendon reflexes absent (flaccid)
**Sphincter is 1 muscle resistant to shock, therefore will result in huge bladder w/o sensation because detrusor won't work, but sphincter can

Front 175

hoffman reflex

Back 175

if 1st reflex normal and 2nd is delayed --> something wrong w/ conus medullaris (usually demyelination as result of MS)

Front 176

Low volume uninhibited bladder often is due to

Back 176

loss of frontal lobe control over voiding timing (frequent voiding; all other mechanisms are normal)

Front 177

what are the different disconnection syndromes?

Back 177

1. alexia w/o agraphia
2. limb kinetic apraxia
3. callostomy for epilepsy
4. conduction/transcortical aphasias

Front 178

Limb kinetic apraxia

Back 178

due to lesion of anterior corpus callosum (supplied by ACA)
- sends info from dominant hemisphere motor assoc cortex (Left) to right brain to activate left arm
- inability to perform skilled movements w/ left hand on command, but can imitate or use actual objects w/ left hand, no weakness

Front 179

Alexia w/o agraphia

Back 179

- lesion of splenium of corpus callosum supplied by PCA, and left occipital lobe damage
- CC sends visual info from right hemisphere to left hemispheric word-recognition center (angular gyrus)
- inabilty to read (can't recognize words), but can write
- right visual hemianoptic field effect

Front 180

what distinguishes transcortical aphasias from the others?

Back 180

good repetition in transcortical

Front 181

ideomotor vs ideational apraxia

Back 181

ideomotor = inability to perform in response to verbal stimulus
- can imitate
- does improve if given object to perform the action w/ (ex. toothbrush)
- due to dominant parietal lobe lesion

2. ideational = does not improve if given object and can't imitate
- due to diffuse cerebral disease

Front 182

prohormone convertases

Back 182

cleave at PAIRS of basic residues (Arg or Lys)
- post-translational processing of NP precursors

Front 183

carboxypeptidase E

Back 183

removes C-term arg and lys residues

Front 184

Peptidylglycine alpha-amidating monooxygenase (PAM)

Back 184

amidates peptides w/ C-term Gly residues
- req oxygen and ascorbate

Front 185

What is the significance of C-terminal amides in NP's?

Back 185

helps for their biological actiivty, receptor interactions, and in providing resistance to carboxypeptidases

Front 186

Why do NP's have slower transmission than NT's? Why do NP's have slower release following AP?

Back 186

1. Only G-protein coupled receptors are involved in NP signalling

2. law of mass action; mass of NP's much > than NT's

Front 187

List the different melanocortin receptors and their location of selective expression

Back 187

MC1-R = receptor for alpha-MSH (selectively expressed in skin)
MC2-R = receptor for ACTH
(selectively expressed in adrenal cortex and liver)
MC3-R = equal affinity for ACTH, alpha-MSH, gamma-MSH (CNS expression)
MC4-R = equal afinity for alpha and gamma MSH (CNS)
- critically linked to regulation of food intake and energy balance
MC5-R - peripheral tissues and CNS

Front 188

What are leptin's effects on the NP's associated w/ food intake and energy balance

Back 188

1. stimulates beta-endorphin and alpha MSH release in hypothalamus and CNS --> contribute to leptin's effects to decrease food intake and body weight

2. inhibits agouti-related protein's release (normally ARP would inhibit MC4-R)

Front 189

What are the hypothalamic nuclei that deal w/ the posterior pituitary?

Back 189

1. paraventricular nucleus
a. mostly oxytocin, a little vasopressin to posterior pituitary
b. autonomic role - projects to brainstem (pons and medulla) and affects autonomic fn, also projects to SC (preganglionic nymp neurons) --> vasoconstriction

2. supra-optic nucleus
a. mostly vasopressin, a little oxytoc to post pituitary
b. autonomic - regulates BP, osmoreceptors in nuc --> can influence blood volume

Front 190

what hypothalamic nucleus deals w/ emotions?

Back 190

dorsomedial

Front 191

what hypothalamic nucleus has a satiety center for eating and drinking

Back 191

ventromedial nucleus

Front 192

what are the lateral nuclei in the hypothalamus responsible for and what are they connected to?

Back 192

hunger center, thirst center, sympathetic control

Front 193

in what region is the nucleus basilis of Meynert located?

Back 193

septal region

Front 194

What are the symptoms/clinical presentation of Wernicke's?

Back 194

Memory
Opthalmolegia
Nystagmus
Ataxia
Thermal disturbances (rarest) --> if have hemorrhages in hypothalamus and mamillary bodies

Front 195

Involuntary Emotional Expression Disorder

Back 195

- often seen in ppl w/ frontal lobe damage (prevents hyperemotionality)
- pathological laughing or cying

Front 196

Laughing Seizures

Back 196

Seen often in ppl w/ hypothalamic hamartomas (inappropriate growth of brain tissue, not a tumor)

Front 197

Kleine-Levin syndrome

Back 197

possibly psychiatric
periodic somnolence and hyperphagia

Front 198

Prader-Willi syndrome

Back 198

hypothalamic syndrome
- hypomentia, hypogonadism, hypotonicity, and obesity

Front 199

mesiotemporal sclerosis

Back 199

loss of neurons and scarring of the temporal lobe
- ppl who get febrile seizures when they're young may damage temporal lobes, develop epilepsy later on and scarring of temporal lobes
- also could be from bilateral posterior cerebral artery infarcts

Front 200

what happens to the pituitary gland during pregnancy? what is a potential complication?

Back 200

undergoes significant physiological hypertrophy (3-4X normal size)
potential comp = sheehan's syndrome
- pituitary can hemorrhage
- present w/ severe headache and sudden blindness and can die from hemorrhage

Front 201

What did the anterior and posterior pituitary develop from?

Back 201

1. anterior from Rathke's pouch
- pouch of ectoderm in stomodeum (dev mouth) acending towards diencephalon
- ascends through sphenoid bone and meets w/ diverticulum coming from hypothalamus

2. posterior pit from hypothal (hence neurohypophysis)

Front 202

what is loss of vision in lateral half of left and right visual fields a symptom of?

Back 202

pituitary macroadenoma
- bitemporal hemianopsia
(homonymous hemianopsia would be result of occipital lobe pathology)

Front 203

pituitary apoplexy

Back 203

sudden hemorrhage of a pituitary tumor, regression happens very quickly
- often present w/ sudden onset severe headache (much like subarachnoid) and acute loss of vision
- potential structures affected = V1 and V2, 3, 4, 6
- blindness, diplopia, ptosis, sudden pituitary failure, sudden hypopituitarism

Front 204

what is the most common type of functional pituitary tumor, and what are its symptoms?

Back 204

prolactin secreting tumor
1. galactorrhea (spontaneous milk production from breasts, bilateral)
2. amenorrhea - lack of menstrual cycle

Front 205

an ACTH secreting pituitary tumor will result in what?

Back 205

Cushing's syndrome (hypercortisolism)
- weight gain
- purple striae on abdomen due to subQ collagen tissue weakness
- hypertension, hyperglycemia, osteoporosis

Front 206

what is the result of a GH-secreting pituitary tumor?

Back 206

Acromegaly
- lg hands and feet, hypertrophy of resp mucosa
- may present w/ sleep apnea
- in child --> gigantism
- diabetogenic (may even have cardiomyopathy)

Front 207

What are some conditions that can present similarly to pituitary adenoma?

Back 207

1. Rathke cleft cysts (from nest cells)
2. craniopharyngioma (tumor from nest cells)
3. meningioma (of diaphragma sella)
4. carotid artery aneurysm (present's w/ 3rd nerve palsy just like PA)
5. neurofibromatosis (tumor in optic nerve and chiasm)

Front 208

Snowman tumor

Back 208

a type of macroadenoma that is extended in all 3 directions (below, above, and on side of sella) --> sellar, parasellar, and suprasellar extension

- protrudes into cavernous sinus, hypothalamus, and 3rd ventricle

Front 209

pan-hypopituitarism

Back 209

due to macroadenoma --> involvenment of ALL pituitary hormones
- present w/ myxedema (sign of total thyroid failure)

Front 210

What are the different categories of the Glasgow Coma Scale?
What are the ranges for injury severity?

Back 210

1. motor (6 pts)
2. verbal (5 pts)
3. eye opening score (4 points)
- get 1 point automatically for each
a. Mild = 13-15
b. Moderate = 9-12
c. Severe < 9

Front 211

a lucid interval in the case of head trauma is a hallmark symptom of what?

Back 211

epidural hematoma

Front 212

what blood vessel does epidural hematoma typically involve?

Back 212

middle meningeal

Front 213

subdural hematoma

Back 213

more crescent shaped lesion on MRI
spreads along suture lines
often see a midline shift in MRI --> ventricles shifted over
- usually occurs from tentorial tears in bridging veins (in older ppl usually)

Front 214

What are the different types of skull fractures, from least to most severe?

Back 214

1. Linear (2/3 of all skull fractures)
- mostly parietal bone
2. Depressed
- often due to focal impact
- dural lacerations (CSF pooling), ping pong fractures in neonates
3. Complex (most severe)
- usually result of severe injury mech (MVA, high fall)
a. Basilar - battle's signs (behind ear bruising), and racoon eyes
b. Frontal sinus (sinuses exposed to brain - need repair)

Front 215

What is the rule regarding intracranial pressure?

Back 215

sum of intracranial volumes of blood, brain, and CSF is constant
- an increase in any one must be offset by an equal decrease in another, otherwise ICP will increase

Front 216

what are different methods to reduce intracranial pressure?

Back 216

1. EVD (external ventricular drain)
2. Hyperventilation (last-resort, short-term)
- hypocapnia --> vasoconstriction --> decreased cerebral blood flow --> decreased ICP
3. Osmotic agents (mannitol, and hypertonic saline)
4. Seizure prophylaxis
5. craniectomy
6. brain tissue oxygen monitoring

Front 217

What is the negative side effect of mannitol?

Back 217

hypovolemic

Front 218

Signs and symptoms of headache of spontaneous SAH

Back 218

- CAT scan
- meningmus --> meninges irritated by blood
- nuchal rigidity
- uniformly blood stained CSF w/ supernatant xanthochromia
- sudden onset severe headache (worst headache of life)

Front 219

Symptoms of headaches of increased ICP

Back 219

1. headache worst 1st thing in morning
2. projectile vomiting due to activation of medulla vomiting center
3. papilledema - edema of optic nerve head, visible w/ opthalmascope
4. mass lesion on imaging

Front 220

Classic migraine vs. common migraine

Back 220

1. classic - family history, warning sign or aura beforehand, hemicranial headache (most manifestations unilateral), possibly severe vomiting

2. common - many features of classic except NO family history
- usually no visual aura, usually occurs later in life

Front 221

what type of headaches is a migraine?

Back 221

vascular (BV's of brain and scalp)

Front 222

What disturbances in blood vessel homeostasis occur during a classic migraine?

Back 222

- period of vasoconstriction occuring during the aura
- period of vasodilation follows --> headache due to this

- both mech's mediated by number of chemicals (5ht and prostaglandins imp)

Front 223

What are the chronological clinical phases of a migraine

Back 223

1. Prodrome - drowsy or excited, food cravings, yawning, abdominal sensations
2. Aura - visual symptoms, pins and needles (80% don't have aura)
3. Headache - severe, pulsatile, vomiting, photo and phono phobia, 2-72hrs
4. Post-drome - strange sense of well-being when headache lifts, euphoria, then eventually tired (electrolyte imbalance from vomiting, muscle aches from hemorrhage of abdominal wall muscles)

Front 224

most common kind of headache?

Back 224

tension headache
- muscles in occipital and upper cervical region contract and go into spasm, irritating greater occipital nerve and some branches of trigeminal

Front 225

Benign intracranial hypertension

Back 225

severe headache often occurring in young adults w/ obesity
- papilledema, severe headache, amenhorrhea if girl

Front 226

temporal arteritis

Back 226

complaint of severe temporal pain, result of superficial temporal artery, occurs in elderly
- don't want to miss because can affect central artery of retina --> blindness

Front 227

What is the mechanism of pain of trigeminal neuralgia

Back 227

artery is pulsating against the root entry zone of the trigeminal --> myelin can wear off easily because in 1st cm of entry zone is produced by oligodendrocytes (not as strong as schwann myelin) --> short circuiting between axons

- electrical shooting type of pain

Front 228

what are potential roadblocks for assessing cognitive level

Back 228

1. alteration of consciousness
2. aphasia
3. hearing level
4. language spoken

Front 229

difference between stupor and delirium

Back 229

1. stupor - generally lethargic and sleepy; arousable either by verbal or noxious stimuli
2. delirium - not lethargic; cannot attend to stimuli and be focused, extremely attracted to all stimuli

Front 230

coma vs. vegetative state

Back 230

1. coma - closed eyes, severe encephalopathy states, never stay in coma for more than few months, eventually open their eyes (after too much time would enter vegetative state)

2. Vegetative state - OPEN eyes (apparent wakefulness), develop sleep wake cycle, absolutely no awareness of self or environment

Front 231

akinetic mutism/minimally responsive state

Back 231

alteration of consciousness
- higher state of fn beyond vegetative
- DO have awareness --> can look at you and track
- purposeful movements
- dont talk or move too much

Front 232

what is the key difference between dementia and MR?

Back 232

HISTORY
- person w/ dementia must have been normal once and then lost it
- person w/ MR never acheived normalcy

Front 233

Neurologist criteria for dementia

Back 233

- cognitive deficit must be in > 1 domain (judgment, behavior, memory, language)
- can have normal memory and still be cognitively impaired
- diff from psychiatrist criteria --> memory always involved in dementia

Front 234

Locked-In State

Back 234

Lesion in caudal pons --> de-efferentation
- enough RAS to keep brain awake
- can't do anything but move eyes VERTICALLY

Front 235

Findings in a "non-focal" brain lesion exam

Back 235

- must have symmetric qualities to impairments
- Brainstem reflexes intact (no evidence of brainstem dysfunction) --> pupils relax, blink reflex intact, eyes move w/ head movement, gag reflex

Front 236

What is the common symptom presentation of normal pressure hydrocephalus?

Back 236

triad of dementia, incontinence, and gait disturbance (magnetic gait)

Front 237

Fronto-temporal dementia

Back 237

- prob w/ frontal lobe
- tremendousl probs controlling limbic system (infantile activity)
- CHARACTERISTIC SYMPTOM = APATHY

Front 238

Lewy bodies

Back 238

pathological finding in substantia nigra of someone w/ parkinson's disease

Front 239

cortico-basal degeneration

Back 239

asymmetric disease where 1 limb is apraxic; can be an underlying etiology of dementia later on

Front 240

Vascular dementia

Back 240

usually result of multiple cortical or multiple lacunar strokes
- common to have focal neurological lesions, vascular disease risk factors

Front 241

What are the major pharmacological treatment for Alzheimer's?

Back 241

1. cholinesterase inhibitors
2. NMDA receptor antagonist --> first non-cholinesterase to be approved

Front 242

What virus is primary cns lymphoma associated with?

Back 242

epstein barr

Front 243

what is toxoplasmosis and pml caused by?

Back 243

1. intracellular parasite
2. infection of oligodendrocytes by JC papovirus

Front 244

prosopagnosia

Back 244

type of visual agnosia
inability to recognize familiar faces
usually gets better over time
- due to focal lesion involving non-dominant hemisphere PCA or bilateral/diffuse brain disease

Front 245

anosognosia

Back 245

unawareness of own hemiplegia