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Brain and Behavior Part 2 > Week 1 Lectures > Flashcards

Week 1 Lectures Flashcards

1
Q

It is composed of two layers of dense collagenous connective tissue with large venous sinuses formed where the various leaves of the mater come together

A

Dura

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2
Q

A thin membrane containing a mixture of fibroblasts and arachnoidal cells, also known as meningothelial cells, and forms a continuous sheet subjacent to the dura and, in most places, joined to it to form one physically continuous tissue.

A

Arachnoid

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3
Q

It anchors delicate strands of the arachnoid trabeculae, which connect the arachnoid to it.

A

Pia

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4
Q

Subdural space

A

Normally the arachnoid matter is adherent to the dura. However, unlike the tight adherence between the inner table of the skull and the dura (only disrupted by high pressure such as arterial flow from a traumatized middle meningeal artery), this interface is more readily disrupted by minor injuries. Typically trauma results in tearing of the bridging veins that traverse this space as they pass between the cortical surface and the overlying dura resulting in the accumulation of blood in the subdural space (subdural hematoma).

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5
Q

Subarachnoid space

A

an actual (not potential) cavity between the arachnoid mater and the pia mater, which contains vascular structures and CSF.

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6
Q

Virchow Robin space

A

Since the pia mater is tightly attached to the brain and follows the vessels into the brain parenchyma, so does the subarachnoid space, creating the Virchow Robin spaces that surround vessels within the brain.

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7
Q

Dural sinuses

A

In specific locations, the dural leaflets form the draining structures named dural sinuses.

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8
Q

Dural sinuses are penetrated by ________ whose function is:

A

arachnoid villi (or arachnoid granulations); structures that conduct CSF back into the circulation

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9
Q

T/F Arachnoidal cells are found distributed throughout the arachnoid membrane, but are most concentrated over the arachnoid villi.

A

T

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10
Q

____________ have a distinctive histologic appearance, forming small multicellular clusters with prominent whorls and occasional ________ bodies

A

arachnoidal cells and psammoma bodies –> oval nuclei with fine, even dispersed chromatin and occasional pseudo-inclusions

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11
Q

Arachnoidal cells are thought to be the basis for a slow growing tumor seen in older adults called _______.

A

meningioma

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12
Q

T/F Normally clear, the arachnoid may become opacified with age due to thickening from the deposition of collagen in the subarachnoid space.

A

T –> opacification of the leptomeninges

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13
Q

3 components of a neuron

A
  1. dendrites – multiple elongated processes specialized in receiving stimuli
  2. perikaryon (soma or cell body) – trophic center, i.e. center of nutrition, support and supply, also receptive to stimuli
  3. axon – single process specialized in generating or conducting nerve impulses. Axons end in specialized terminal arborizations, each branch of which terminates on the next cells in dilatations called boutons, which form part of the synapse.
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14
Q

T/F most neurons have a prominent nucleolus.

A

T –> finely dispersed chromatin in nucleus too

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15
Q

T/F Axons have nissl and dendrites don’t.

A

F –> axons don’t have nissl, dendrites do.

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16
Q

T/F RER projects into axons.

A

F

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17
Q

Astrocytes (A) and oligodendrocytes (O) are commonly referred to as _______ cells.

A

glial –> common precursors but different functions in CNS

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18
Q

_______ are located in both gray and white matter and have long processes that are rarely visible as they merge into a feltwork of axons and dendrites called _______.

A

astrocytes and neuropil

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19
Q

Bare nuclei appearance

A

astrocytes

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20
Q

White matter vs. Gray matter astrocytes

A

In the gray matter astrocytes have numerous short highly branched processes (protoplasmic astrocytes). In the white matter astrocytes tend to have fewer and relatively straighter processes (fibrous astrocytes)

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21
Q

Protoplasmic astrocytes

A

Gray matter

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22
Q

Fibrous astrocytes

A

White matter

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23
Q

Astrocyte function

A

extend numerous fine foot processes towards both the pial surface, around the basement membrane of blood vessels, and the non-synaptic regions of neurons. Astrocytes thus have an important structural role, as well as functional significance as mediators of metabolic exchange between neurons and blood

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24
Q

Astrocytes contain an abundant amount of an intermediate filament known as __________ which can be used to highlight the presence of these fine processes, as well as to confirm the astrocytic nature of particular glial cells.

A

GFAP: glial fibrillary acidic protein

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25
Q

, these cells can only be identified histologically by their dense darkly stained nuclei and lack of conspicuous cytoplasm.

A

oligodendrocytes

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26
Q

___ are the predominant type of glial cell in the white matter

A

oligodendrocytes

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27
Q

T/F Likeastrocytes, there is no immunohistochemical stain (like GFAP) that can be used in tissue sections for ready identification of these cells.

A

F

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28
Q

In the gray matter oligodendroglial cells are often found in small groups of 2-3 cells in close proximity to neurons in a process called ______.

A

satellitosis

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29
Q

T/F A single oligodendrocyte can contribute to the myelination of up to 50 axons that may belong to the same or different fiber tracts.

A

T

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30
Q

The cytoplasm of the oligodendroglial cell is packed with _____, which makes sense for a cell type that makes lots of glycolipid membrane material

A

Golgi

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31
Q

The ______ lines the ventricles of the brain and the central canal of the spinal cord.

A

ependyma

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32
Q

Ependymal cell appearance

A

cuboidal with elongated nuclei, microvilli (thought to be involved in absorptive and secretory activity) and cilia (may be involved in propulsion of CSF through the ventricular system). Like other epithelial cells in the body, they are bound together by junctional complexes at their luminal surfaces. However, they do not rest upon a basement membrane. Instead, the base of ependymal cells breaks up into fine branches that interdigitate with an underlying layer of astrocytic processes. Specialized ependymal cells have elongated processes that extend to the subependymal vasculature, thus linking the ventricular, vascular and intraparenchymal compartments of the CSF. A similar pattern may be observed in tumors derived from ependyma (ependymoma) that often have prominent perivascular processes.

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33
Q

T/F Ependyma has no basement membrane.

A

T

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34
Q

Projections of vascular stroma derived from the meninges are covered with a low cuboidal epithelium that secretes _____.

A

CSF

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35
Q

_______ cells have numerous long microvilli with only a few cilia. They also have many mitochondria, large Golgi complexes and basal nuclei, which is consistent with their secretory activity.

A

Choroid plexus –>lateral ventricles and fourth ventricle

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36
Q

Cells found in layers of neocortex

A
  1. a relatively acellular outer molecular layer,
  2. external granular layer comprised of small round darkly staining neurons
  3. external pyramidal layer comprised of larger triangular shaped neurons
  4. internal granular layer
  5. internal pyramidal layer
  6. a polymorphous or multiform layer with a mixed populations of neurons, including large pyramidal type cells.
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37
Q

pyramidal cells give rise to ________ that point upwards towards the pial surface, and axons that are the efferent output of the neocortex which project downwards towards the ____________.

A

apical dendrites and subcortical white matter

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38
Q

large pyramidal cells are the efferent output of the neocortex and are located primarily in layers ______

A

3 and 5 –> external and internal pyramidal

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39
Q

. For example, the pyramidal cells of layers 3 and 5 are very large (Betz cells) in the primary __________cortex.

A

motor (precentral)

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40
Q

_______ cortex has small pyramidal cell layers but markedly expanded granular cell layers.

A

the primary sensory (postcentral)

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41
Q

Ammon’s horn

A

hippocampus proper

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42
Q

three-layered cortex that connects the hippocampus to the parahippocampal gyrus

A

subiculum

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43
Q

Sommer Sector

A

CA1 –> most sensitive to various insults including ischemia, seizures, and degenerative changes from Alzheimer’s

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44
Q

Each cerebellar _____ is comprised of a relatively hypocellular molecular layer (ML) that contains the complex dendritic processes of ______ cells

A

folia and purkinje

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45
Q

the greatest number of cerebellar neurons are actually contained in the densely packed _______.

A

granular layer (GL)

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46
Q

What cells are associated with: acute ischemic injury, chronic cell loss, and inclusions

A

neurons

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47
Q

What cells are associated with: reactive gliosis

A

glial cells

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48
Q

What cells are associated with: microglia and inflammatory infiltrates

A

inflammatory cells

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49
Q

“Red” neuron

A

cells that have experience irreversible ischemic injury. They are characterized by a shrunken cell body, intense cytoplasmic eosinophilia with complete loss of Nissl basophilia. They can be seen about 12-24 hours after the ischemic insult. The nucleus is frequently darkly stained without an evident nucleolus.

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50
Q

Red neurons can be seen about _____ hours after ischemic injury.

A

12-24 hours

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51
Q

Which regions of the brain are more vulnerable to ischemic injury?

A

the pyramidal neurons of the CA1 region in Ammon’s horn (hippocampus) and the Purkinje cells of the cerebellum

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52
Q

One of the most common subcellular alterations in neurons is the accumulation of _______, especially in large/small motorneurons of the spinal cord/brainstem/cortex.

A

lipofuscin in large motorneurons of the spinal cord

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53
Q

lipofuscin

A

This is a normal age-related process. Oxidized fatty acids from cell membrane breakdown accumulate as a fine light brownish retractile material, typically located along the perikaryal edge.

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54
Q

neuromelanin

A

by-product of neurotransmitter synthesis in these catecholaminergic neurons.

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55
Q

3 catecholaminergic areas of neurons that produce neuromelanin

A

These include the substantia nigra of the midbrain, locus ceruleus of the rostral pons and the dorsal motor nucleus of the vagus.

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56
Q

T/F Viral infections can lead to abnormal inclusions

A

T –> CMV (nuclear, cytoplasmic), herpes (nuclear), rabies (cytoplasmic)

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57
Q

T/F Many neurodegenerative disorders are associated with neuronal inclusions

A

T –> neurofibrillary tangles in AD, Lewy bodies in Parkinson’s

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58
Q

______ are the main effector of reaction to injury in the CNS: through both hypertrophy and hyperplasia they cause ______, a common denominator for diverse causes of injury.

A

astrocytes cause gliosis

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59
Q

_______ react to injury by hyperplasia and by developing elongated nuclei and increased elongated cytoplasmic processes

A

microglia

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60
Q

Microglial nodules are aggregates of microglial cells that are often seen in some inflammatory conditions including _______.

A

viral encephalitis

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61
Q

5 most common routes of access to the CNS (by infections)

A

hematogenous spread, local extension (paranasal sinuses, middle ear), retrograde PNS transport, direct implantation (trauma, surgery)

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62
Q

T/F Virulence and tropism of certain organisms for neural and glial elements determines “homing” to the nervous system.

A

T

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63
Q

Spread of infection into layers of the dura mater

A

Pachymeningitis

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64
Q

Inflammation of the pia and arachnoid

A

Meningitis/Leptomeningitis

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65
Q

Inflammation (usually viral) of the brain parenchyma

with mononuclear cells

A

Encephalitis

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66
Q

Inflammation (usually bacterial) of the brain parenchyma

with neutrophils

A

Cerebritis

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67
Q

Inflammation of the spinal cord

A

Myelitis

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68
Q

Inflammation of spinal gray matter

A

Poliomyelitis

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69
Q

Inflammation of the dorsal root ganglia

A

Ganglionitis

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70
Q

Inflammation of the intradural spinal nerve roots

A

Radiculitis

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71
Q

Immune response associated with: Acute (bacterial) meningitis, cerebritis, abscess

A

Neutrophils (acute inflammation)

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72
Q

Immune response associated with: Chronic (“aseptic” viral) meningitis, encephalitis

A

Mononuclear cells (lymphocytes and plasma cells, chronic inflammation)

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73
Q

Immune response associated with: Micobacteria, spirochetes, fungi, parasites

A

Granulomatous inflammation

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74
Q

Immune response associated with: Viral encephalitis

A

Microglial nodules

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75
Q

T/F Bone, dura mater, arachnoid and pia mater delineate four compartments that tend to inhibit the spread of infection from one compartment to another

A

T

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76
Q

Most common area of bacterial CNS infection

A

Subarachnoid space –> meningitis/leptomeningitis

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77
Q

Epidemics of bacterial meningitis are common/rare and almost always associated with ______.

A

rare and Neisseria meningitidis.

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78
Q

Long term complications of bacterial meningitis

A

hydrocephalus due to leptomeningeal scarring blocking basal cisterns and arachnoid granulations and hearing loss

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79
Q

3 bacteria that cause the majority of bacterial meningitis.

A

S. pneumoniae, N. meningiditis and H. influenzae

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80
Q

Which age of patients are affected by: Group B Streptococcus, Escherichia coli, Listeria monocytogenes

A

neonates

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81
Q

Which age of patients are affected by: Streptococcus pneumoniae, Listeria monocytogenes

A

Adults >60 years and immunosuppressed

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82
Q

Which age of patients are affected by: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae

A

Children and Adults (6 mos to 60 years)

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83
Q

Macroscopic findings of bacterial meningitis

A

purulent exudate, opacification of leptomeninges

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84
Q

bacteria causing basal exudate in bacterial meningitis

A

H. Influenza

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85
Q

bacteria causing convexity exudate in bacterial meningitis

A

S. Pneumoniae

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86
Q

Microscopic findings of bacterial meningitis

A

neutrophils in leptomeningeal space, pia effective barrier to parenchymal spread, occasional cerebritis when infection crosses parenchyma

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87
Q

____are focal, destructive lesions (occasionally multifocal) of the brain parenchyma due to necrosis mediated by acute inflammation in response to bacterial infection.

A

Abscesses

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88
Q

2 sources of abscess forming CNS infections

A

Local (sinusitis otitis, mastoiditis) or hematogenous (septic emboli or cyanotic congenital cardiac disease-PFO)

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89
Q

Most common bacteria in abscess formation

A

S. aureus, Streptococci, often polymicrobial

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90
Q

T/F Bacterial endocarditis can cause
infectious emboli to travel to the brain
and cause abscesses

A

T

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91
Q

T/F Mass effect from a CNS abscess can cause herniation.

A

T

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92
Q

T/F abscesses in the CNS have surrounding fibrotic capsules.

A

T

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93
Q

4 features of early abscess formation

A

vascular congestion, early necrosis, edema and initiation of inflammation –> neutrophils

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94
Q

After approximately ______, neovascularization and collagen fibers start to create the abscess capsule that will eventually isolate the area of necrosis (eventually a cystic cavity) from the surrounding preserved parenchyma.

A

10 days

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95
Q

Features of late abscess formation

A

neutrophil debris and fibroblastic collagenous capsule

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96
Q

Typically, tuberculous meningitis involves the ____ aspect of the brain and presents with cranial nerve involvement

A

basal

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97
Q

CSF findings of TB meningitis

A

lymphocytosis, hypoglycemia, increase in protein

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98
Q

Acid fast stain

A

identify filamentous mycobacteria like TB

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99
Q

Which condition? chronic basal meningitis with associated obliterative endarteritis. Perivascular inflammatory infiltrate, rich in plasma cells and lymphocytes. Cerebral gummas (mass lesions) may also occur.

A

Meningovascular neurosyphilis

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100
Q

Which condition?invasion of the brain byTreponema pallidum.Inflammatory lesions associated with parenchymal damage in the cerebral cortex with loss of neurons, proliferations of microglia (rod cells), gliosis, and iron deposits. The spirochetes can, at times, be demonstrated in tissue sections.

A

Paretic neurosyphilis

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101
Q

Which condition? damage by the spirochetes to the sensory nerves in the dorsal roots and posterior columns. Organisms are not demonstrable in the cord lesions.

A

Tabes dorsalis

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102
Q

T/F In neurosyphilis, CNS is affected in the primary stage

A

F –> tertiary stage

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103
Q

Stage at which chancres form

A

primary syphilis

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104
Q

Stage of neurosyphilis with hematogenous spread, generalized lymphadenopathy, maculopapular rash, condyloma lata, mucous patches

A

secondary syphilis

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105
Q

Which organism causes lymphocytic meningitis, cranial nerve palsies, and polyradiculitis, and occurs several months after a skin rash known as erythema chronicum migrans?

A

Borrellia burgdorferi –> Lyme

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106
Q

Viral Inflammation restricted to the meninges

A

aseptic meningitis

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107
Q

Viral disease restricted to the grey matter

A

polioencephalitis, poliomyelitis

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108
Q

Viral disease of both grey and white matter

A

panencephalitis, panmyelitis

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109
Q

Viral disease of white matter

A

leukoencephalitis

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110
Q

What kind of viral meningitis? enterovirus

A

aseptic meningitis

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111
Q

What kind of viral meningitis? poliovirus, coxsackie, arbovirus, echovirus, tick-borne, rabies

A

polioenceph/myelitis

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112
Q

What kind of viral meningitis? HSV, HIV

A

panenceph/myelitis

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113
Q

What kind of viral meningitis? JC, PML, HIV

A

leukoencephalitis

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114
Q

T/F Viral meningitis is generally less severe than bacterial meningitis.

A

T

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115
Q

One form of recurrent aseptic meningitis ______ that was previously regarded as non-infective has been linked to infection with herpes simplex virus (HSV), especially HSV-2.

A

Mollaret’s

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116
Q

What kind of viral meningitis? acute infection of meninges + lymphocytes in CSF,

A

aseptic meningitis

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117
Q

T/F Survivors of viral CNS infections involving the parenchyma can subsequently develop permanent neurological disease.

A

T

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118
Q

Which of the following are seasonal in nature? Arbovirus, HSV

A

Arbovirus Acute Viral Encephalitis

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119
Q

Most common cause of epidemic encephalitis.

A

Arbovirus (arthropod borne) –> birds, horses, small mammals, arthropods –> incidental/terminal hosts in humans

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120
Q

T/F The majority of human arbovirus infections are asymptomatic or may result in a nonspecific flu-like syndrome.

A

T

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121
Q

Site of arbovirus replication in humans

A

The virus replicates at the site of host inoculation and then spreads to regional lymph nodes and other lymphoreticular tissues (primary viremia) where it proliferates before disseminating hematogenously (secondary viremia) to systemic tissues, including, in some cases, the CNS.

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122
Q

General pathologic features of acute viral encephalitis

A

perivascular lymphocytic infiltrate, microglial nodules (gray or white matter + rod cells, macrophages, lymphocytes), neuronophagia, intranuclear cytoplasmic inclusions, gliosis

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123
Q

Bilateral, asymmetrical, hemorrhagic necrosis of temporal lobes is classical in _____ encephalitis.

A

HSV (but diff dx includes infarction and contusion) –> temporal involvement = seizure

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124
Q

_____ is the most common cause of acute necrotizing encephalitis in immunocompetent individuals.

A

HSV1 (sometimes CMV or VZV)

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125
Q

The initial HSV1 infection involves the _____

A

oropharyngeal mucosa

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126
Q

The putative routes of HSV1 CNS infection are

A

Centripetal spread of virus along olfactory nerve fibers and tracts, and reactivation of latent virus in the trigeminal ganglia

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127
Q

_____ virus replicates within skeletal muscle at the site of inoculation before being taken up by axons and transported centripetally to the CNS.

A

Rabies

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128
Q

Negri bodies are the hallmark of _____

A

rabies —>sharply delineated round to oval eosinophilic inclusions in neuronal cytoplasm

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129
Q

3 sites for negri bodies

A

Purkinje cells, hyppocampal pyramidal neurons, cortical neurons and brain stem nuclei

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130
Q

Which polio vaccine can revert to wildtype through back mutation?

A

live attenuated oral vaccine can revert and cause paralytic disease

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131
Q

Features of acute poliomyelitis

A

intense chronic perivascular inflammation of parenchyma and meninges, microglial nodules and neuronophagia, blood vessel congestion and possible hemorrhage

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132
Q

Diffuse encephalitis with space occupying lesions, septic infarcts, leptomeningitis, and hemorrhage are associated with _____

A

fungal infection

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133
Q

____ fungus often affects ACA, MCA territories causing early hemorrhagic infarcts and late abscesses

A

aspergillosis –> feature of chronic infection (from direct spread vs. hematogenous)

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134
Q

Grocott silver stain demonstrates thin filamentous fungal forms with branching in _____

A

aspergillosis

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135
Q

_____ usually starts with nasal or unilateral facial swelling and hyperemia.

A

Rhinocerebral mucormycosis with focal ulceration and necrosis of skin/mucosa –> The infection extends rapidly into the orbit, producing unilateral ophthalmoplegia, proptosis, edema of the lids, corneal edema, and blindness in some cases

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136
Q

2 classical presentations of mucormycosis

A

diabetic ketoacidosis, rhinocerebral disease

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137
Q

Hyphae are nonseptate in _____

A

mucor

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138
Q

Hyphae are wider in aspergillus/mucor

A

mucor

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139
Q

_____, has been isolated from fresh water, soil, sewage, heating, ventilation and air conditioning units, dental units, gastrointestinal washings, and dust and is a cause of meningoencephalitis.

A

Naegleria fowleri –> infection from swimming in fresh water at high temperature –> nasal cavity–> CNS

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140
Q

Which organism causes Fulminant, acute meningoencephalitis with cerebral swelling and hemorrhagic necrosis frontal lobes and olfactory bulbs ?

A

Naegleria fowleri

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141
Q

Most common helminthic CNS disease

A

cysticercosis

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142
Q

Cysticercosis is caused by _______

A

Taenia solium

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143
Q

______ cause of CNS infection is associated with epilepsy.

A

cysticercosis

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144
Q

Clinical features of cysticercosis

A

Manifestations can include focal and generalized seizures, papilledema, headache, vomiting and ataxia (which may be intermittent), vertigo produced by abrupt movements of the head, focal motor and sensory deficits, dementia, acute hydrocephalus due to obstruction of the ventricular system, and occasionally, sudden death.

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145
Q

T/F cysts formed in cysticercosis result in robust inflammatory responses.

A

F –> almost non response –> Shortly after the cysticerci die, the cysts are surrounded by neutrophils, lymphocytes, macrophages, foreign body giant cells, and eosinophils and then enclosed by a zone of granulation tissue, which eventually produces a dense collagenous capsule and eventually some of the cysts become calcified.

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146
Q

Most common cause of fungal meningitis

A

Cryptococcus neoformans

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147
Q

T/F Cryptococcomas (Cryptococcal abscesses) are much less common than cryptococcal meningitis and usually occur in patients who are not immunocompromised.

A

T

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148
Q

T/F in cryptococcus is usually pulmonary with subsequent hematogenous spread to the CNS.

A

T –> The pulmonary lesions have often resolved before the neurologic disease manifests.

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149
Q

Which organism is visible in India Ink?

A

Cryptococcus

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150
Q

Collections of _______ produce gelatinous pseudocystic dilations of Virchow – Robin spaces (“bubbles”) with little surrounding inflammation or gliosis

A

Cryptococcus

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151
Q

_______ is an opportunistic infection common in the setting of HIV caused by the protozoan, an obligate intracellular parasite with a propensity to infect the nervous system. The definitive hosts for this parasite are domestic cats and other feline species.

A

Toxoplasmosis

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152
Q

T/F In toxoplasmosis, symptomatic neurologic disease is unless associated with depression of cell-mediated immunity, particularly in AIDS, and is probably due to reactivation of dormant infection.

A

T

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153
Q

Which organism? Most common pattern is brain abscesses, presenting as multiple ring-enhancing lesions

A

Toxoplasma gondii

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154
Q

Which organism? Free tachyzoites and encysted bradyzoites may be found at the periphery of centrally necrotic lesions.

A

Toxoplasma gondii

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155
Q

3 areas affected by HIV encephalitis

A

Involves subcortical white matter, basal ganglia and brainstem

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156
Q

Which condition? Widespread low-grade inflammation with perivascular and parenchymal lymphocytes and microglial nodules, multinucleated giant cells, and leukoencephalopathy

A

HIV encephalitis

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157
Q

T/F In the CNS, HIV infects mainly microglial cells or macrophages.

A

T

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158
Q

Which organism has a tropism for oligodendroglia?

A

JC virus/polyoma

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159
Q

Which organism? Ill-defined demyelinating lesions, lipid-laden macrophages, intranuclear viral inclusions, bizarre atypic astrocytes.

A

JC virus/polyoma

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160
Q

glass nuclei are associated with _____

A

JC virus/polyoma

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161
Q

T/F concussion is equivalent to mild TBI

A

T

162
Q

mTBI are due to ______

A

mild axonal injury

163
Q

T/F Genetic risk factors for concussion are the strongest factor

A

T

164
Q

Inertial loading is due to hit/rotation of the head due to _____ of axons called _____

A

rotation and tensile elongation of axons called viscoelasticity

165
Q

Neuropathology of inertial loading

A

diffuse axonal injury and swelling of white matter, disconnection, variscose-like veins: 1. bulb evolution, 2. axonal swelling evolution

166
Q

A spirochete like axons suggest _____ damage

A

initial mechanical damage

167
Q

Microtubule catastrophe

A

during trauma, secondary chemical damage results in destruction of microtubueles

168
Q

Axonal varicosities are due to damage of microtubules at single/multiple sites

A

multiple

169
Q

The gold standard for diagnosing tbi is _____

A

amyloid protein

170
Q

____ inhibits relaxation of undulations along axons post-injury by stabilizing microtubules.

A

Taxol –>stabilize microtubules by reducing relaxation and degeneration of microtubules in axons

171
Q

Calcium influx due to increasing axonal strain is a result of _____ channels

A

Sodium–> inactivation gate –>unremitting entry of sodium into cell –> reversal of sodium/calcium exchanger = massive calcium influx

172
Q

Can block calcium influx with TTX or ______ inhibitors.

A

protease inhibition of calpain (which proteolyzes the inactivation gate

173
Q

Period of vulnerability

A

another mild injury is thought to trigger a greatly exaggerated response –
> repetitive mTBI

174
Q

Repetitive mTBI results in exaggerated responses due to ______ sodium channels

A

hyperexpressed –> restoring axonal function may involve increasing # of channels –> NaChO

175
Q

Immediate loss of consciousness and coma following brain trauma is due to ______.

A

DAI

176
Q

______ is the current standard for non-invasively evaluating DAI

A

diffusion tensor imaging

177
Q

T/F TBI is the highest epigenetic risk factor for developing AD-like dementia

A

T

178
Q

The hallmark pathologies of AD, _____ are also found in CTE

A

amyloid plaques and neurofibrillary tangles

179
Q

T/F mTBI can result in CTE

A

F –> moderate to severe or repetitive TBI

180
Q

T/F In AD, amyloid is secreted intracellularly.

A

F –> extracellularly resulting in neuritic or diffuse plaques extracellularly

181
Q

Abnormal hyperphosphorylated intra-neuronal accumulation of tau is called _____

A

neurofibrillary tangles

182
Q

T/F axonal disconnection is permanent

A

T

183
Q

T/F CNS tumors are classically classified by morphologic appearance including constituent cell type and tissue pattern

A

T

184
Q

7 major histopathological categories of CNS tumors

A

neuroepithelial, cranial and spinal, meninges, lymphomas and hematopoietic neoplasms, germ cell, sellar, metastatic

185
Q

Tumors of neuroepithelial tissue

A

astrocytomas, oligodendromas, ependyomas, embryonal tumors, neurocytomas (neurons), mixed neuronal-glial tumors

186
Q

Most frequent primary CNS tumors are ____

A

neurepithelial origin

187
Q

Astrocytoma categories

A

diffuse, infiltrating and relatively circumscribed

188
Q

Diffuse, infiltrating astrocytoma

A

diffuse astrocytoma (II), anaplastic astrocytoma (III), glioblastoma (IV)

189
Q

Relatively circumscribed astrocytomas are grade _____

A

I or II –> pilocytic, pleomorphic, subendymal giant cell

190
Q

Grade II astrocytomas are diffuse/circumscribed and are characterized by _____

A

diffuse –> atypia no mitoses

191
Q

Grade III Anaplastic astrocytomas are characterized by _______

A

atypia with mitoses

192
Q

Grade IV glioblastomas are characterized by _____

A

atypia, mitoses, and vascular proliferation/necrosis

193
Q

Glioblastomas are more common in old/young people

A

older –> higher grades are more common in older people

194
Q

T/F diffuse astrocytomas are encapsulated.

A

F –> poorly defined

195
Q

Which tumor? Elongated, irregular, angulated, hypochromatic nuclei in a meshwork of fibrilllary processes and no mitoses.

A

diffuse fibrillary astrocytoma –> grade II

196
Q

Which tumor? Plump cells with glassy pink cytoplasm.

A

Diffuse astrocytoma, gemistocytic variant –> Grade II

197
Q

Which tumor? Foci of increased cell density, hyperchromatism, and pleomorphism with mitotic figures.

A

Anaplastic astrocytoma –> Grade III

198
Q

Which tumor? Necrosis, high cellularity, mitoses, and variable vascular supply with both glomeruloid tufts (neovascularization) and vessel death.

A

Glioblastoma –> Grade IV

199
Q

Two types of GBM

A

primary –> EGFR and secondary –> IDH1/IDH2 and P53

200
Q

Astrocytomas have a propensity for anaplastic transformation of diffuse Grade II to ____ or _____.

A

grade III anaplastic or grade IV GBM

201
Q

T/F Neoplastic progression is associated with sequential acquisition of multiple genetic abnormalities.

A

T

202
Q

BRAF/KIAA tandem duplications are associated with _____

A

pilocytic astrocytoma –> children and young adults

203
Q

Which tumor? Well demarcated, solid, cystic lesion with rosenthal fibers, biphasic architecture with compact and spongy patterns and eosinophilic granular bodies//no mitoses or necrosis.

A

pilocytic astrocytoma

204
Q

T/F In oligodendrogliomas, the neoplastic cells maintain certain features of normal oligodendroglial cells which form and support the myelin sheath in the CNS.

A

T

205
Q

Which tumor? Well differentiated, infiltrating tumor, expanding gyri and deep white matter, fried egg appearance, chicken wire capillaries.

A

Oligodendroglioma

206
Q

Most common genetic alteration in oligodendroglioma.

A

1p/19q –> genetically favorable for chemo/radiotherapy (grade II or III but no IV)

207
Q

T/F rosettes and canals are found in the majority of ependyomas.

A

F

208
Q

Which tumor? neoplastic cells clustered around blood vessels producing pseudorosettes due to perivascular arrangement of elongated cytoplasmic processes of neoplastic cells

A

Ependymoma

209
Q

Which grade IV tumors are predominant in children?

A

Embryonal tumors like medulloblastoma, supratentorial PNET, AT/RT, and medulloepithelioma

210
Q

Which tumor? high-grade cerebellar vermal tumor with extension to the 4th ventricle and opacification of the SA (sugar icing) with CSF dissemination//well circumscribed, gray/pink, gelatinous, limited necrosis//ovoid nuclei, highly packed cells with frequent mitoses

A

medulloblastoma

211
Q

Some medulloblastomas are considered to originate from ____ neurons that produce the external granule layer.

A

Granule neurons

212
Q

T/F homor wright rosettes are present in 40% of medulloblastomas and are regarded as signs of neuronal differentiation.

A

T

213
Q

3 groups of cranial and paraspinal nerves?

A

schwannomas (neurilemmomas), neurofibromas, malignant peripheral nerve sheath tumors

214
Q

Which tumor? slowly growing neoplasms of schwanna cells with effects on CNS, especially CN 8

A

Schwannoma –> cerebellar pontine angle

215
Q

Patients with NF2 may have _____ acoustic/vestibular schwannoma

A

bilateral –> neurofibromatosis type 2

216
Q

Which tumor? dermal nodular lesion of skin or intraneural, solitary, or plexiform neoplasm.

A

Neurofibroma

217
Q

The presence of multiple neurofibromas is usually seen with _____

A

neurofibromatosis type 1

218
Q

Which tumor? arise from meningothelial cells of leptomeninges with increased inceidence with age and associated with females//composed of whorls and cords of neoplastic cells and identified by EMA.

A

Meningiomas (ofen with NF2)

219
Q

Which tumor? numerous compact whorls with psammoma bodies.

A

Psammomatous meningioma

220
Q

The most common primary sites for metastic CNS tumors are ____

A

lung, breast, skin, kidney, colon

221
Q

T/F Metastatic tumors are 50% likely to be solitary.

A

T

222
Q

T/F Gliomas and embryonal tumors occur more frequently in males

A

T

223
Q

T/F Meningiomas preferentially affect females

A

T

224
Q

T/F Most primary brain tumors are sporadic and of unknown origin

A

T

225
Q

T/F More than 5% of brain tumors are associated with heriditary syndromes that predispose to neoplasia.

A

F <5%

226
Q

Neurofibromatosis Type 1 is associated with 4 tumors:

A

neurofibroma, malignant nerve sheath tumor, optic nerve astrocytoma, meningioma

227
Q

Neurofibromatosis type 2 is associated with 3 tumors:

A

schwannoma, meningioma, ependymoma

228
Q

Tuberous sclerosis is associated with 1 tumor

A

subependymal giant cell astrocytoma

229
Q

T/F X-irradiation increases risk of brain tumors

A

T –> meningiomas and astrocytomas or other tumors of neurepithelial origin in children treated b/c of ALL

230
Q

Headache (postural, nocturnal, early morning), vomiting, papilledema, and clouding of consciousness/coma are signs of _____

A

increased intracranial pressure

231
Q

Which kind of herniation? cingulate below falx cerebri

A

subfalcine

232
Q

Which kind of herniation? parahippocampal gyrus of medial temporal lobe across tentorium cerebelli

A

transtentorial

233
Q

Which kind of herniation? anteromedial part of temporal lobe

A

uncal

234
Q

Which kind of herniation? diencephalon through tentorium cerebelli

A

bilateral/central/diencephalic

235
Q

Which kind of herniation? tonsils

A

tonsillar

236
Q

Which kind of herniation? cerebellum through tentorium

A

superior cerebellar

237
Q

secondary hemorrhages due to transtentorial herniation is called ____

A

duret hemorrhage

238
Q

Which nerve is compressed against petrous ligament?

A

abducent

239
Q

Which nerve is implicated in uncal herniation?

A

Oculomotor

240
Q

What structure is compressed against the tentorium with ipsilateral hemiparesis?

A

cerebral peduncle

241
Q

Which familial syndrome is related to CN 8?

A

NF2

242
Q

Complete turnover of CSF occurs every _____ hours

A

5-7

243
Q

Adults produce ____ ml/day CSF

A

500

244
Q

Approximate CSF volume in ventricles is ____ and in SA space is ____

A

30 and 120 ml

245
Q

Choroid plexus

A

located in ventricles, specialized ependymal cells (cuboidal glial cells)

246
Q

Blood to the choroid plexus is provided by _____ arteries

A

anterior/posterior choroidal arteries

247
Q

Stages of CSF production

A
  1. ultrafiltration of plasma across fenestrated capillaries, 2. secretion/transport of components into ventricle from choroid epithelia (isoosmotic)
248
Q

T/F Capillary ultrafiltrate is outside the blood-brain barrier

A

T –> choroid plexus epithelia employ tight junctions to create a barrier against free diffusion

249
Q

CSF has high/low protein

A

low

250
Q

CSF has high/low amino acids vs. plasma

A

low

251
Q

CSF has high/low K+ vs. plasma

A

low

252
Q

CSF is absorbed into the venous blood supply of the_______

A

superior sagittal sinus and spinal veins

253
Q

Small arachnoid evaginations are called

A

villi

254
Q

Large arachnoid evaginations are called

A

granulations

255
Q

T/F CSF can enter venous blood but venous blood can’t enter CSF

A

T –> one way valve

256
Q

What mechanism is likely to be implicated in absorption of CSF?

A

transcytosis via large fluid containing vacuoles

257
Q

T/F Since there is no lymphatic system in the brain, CSF serves an excretory waste function.

A

T

258
Q

2 routes into CNS and function

A

blood brain barrier, regulated at capillaries –> O2, CO2, glucose; blood-CSF barrier, regulated at choroid plexus –> Ca2+ influx

259
Q

3 reasons for integrity of BBB

A
  1. tight junctions between non-fenestrated capillaries, 2. thick basement membrane, 3. astrocyte endfoot “insulation”
260
Q

Which molecules are excluded from the BBB?

A

large, charged molecules

261
Q

Which molecules cross the BBB more readily?

A

uncharged and lipid soluble molecules

262
Q

T/F BBB is permeable to water

A

T

263
Q

Circumventricular organs

A

areas around ventricles that lack definitive BBB b/c have leaky capillaries –> part of neuroendocrine control system for monitoring temp/plasma concentration and for hormone release

264
Q

Collect the CSF specimen from the patient in the __________ position

A

lateral recumbent –> CSF pressure changes with posture

265
Q

In LP, needle insertion occurs at what level?

A

L3-L5

266
Q

Normal adult opening pressure

A

90-200 mm water

267
Q

Normal pediatric opening pressure

A

10-100 mm water

268
Q

contraindication to LP

A

raised intracranial pressure could lead to cerebral herniation

269
Q

Most common complication of LP

A

headache

270
Q

What’s in the CSF? Cloudy

A

elevated WBC

271
Q

What’s in the CSF? Bloody

A

RBC due to SAH

272
Q

What’s in the CSF? Yellow/Xanthochromic

A

orange from carotene ingestion, brown due to metastatic melanoma

273
Q

What’s in the CSF? Viscous

A

metastatic mucinous adenocarcinoma

274
Q

Normal CSF glucose

A

60 mg/dL

275
Q

What’s in the CSF? Low glucose

A

neutrophils reliant on anaerobic glycolysis –> low glucose due to infection

276
Q

Normal CSF protein

A

30 mg/DL

277
Q

T/F for detecting Cryptococcus, India ink has a lower sensitivity than latex agglutination antigen assay

A

T

278
Q

5 classical symptoms of meningitis

A

fever, headache, AMS, stiff neck, photophobia

279
Q

What kind of meningitis? elevated opening pressure, elevated WBC, most neutrophils, high protein

A

bacterial

280
Q

What kind of meningitis? normal opening pressure, mainly lymphocytes, normal glucose and protein

A

viral

281
Q

What kind of meningitis? variable opening pressure, mostly lymphocytes, elevated protein

A

fungal

282
Q

Liptotechoic acid

A

S. pneumoniae –> cell wall protein that links to PAF to enter CNS

283
Q

Layers of head

A

scalp, periosteum/outer and inner table of skull, potential epidural space, dura, potential subdural space, arachnoid, subarachnoid, pia mater, brain

284
Q

T/F Extent of external lesion is not reliable indicator of deeper lesions.

A

T

285
Q

T/F Lethal lesion(s) of skull/brain may be small or absent.

A

T

286
Q

What fracture? Secondary to contact with large flat object. Fracture begins along inner table.

A

Linear

287
Q

What fracture? Fx associated with scalp laceration.

A

Compound

288
Q

What fracture? Fx involving multiple bones

A

Complex

289
Q

What fracture? Secondary to contact with small objects. (e.g. bullet, hammer)

A

Depressed

290
Q

What fracture? Located distant from point of injury.

A

Contrecoup

291
Q

What kind of hemorrhage? Between skull and dura, arterial bleeding

A

Epidural

292
Q

What kind of hemorrhage? below dura with venous bleeding

A

Subdural

293
Q

T/F SDH is more common in people with brain atrophy

A

T

294
Q

Fracture contusion/laceration

A

at site of fracture and tend to be severe

295
Q

Coup contusion

A

caused by bending/rebound of skull at site of injury

296
Q

Contrecoup contusion

A

located distant, usually opposite from point of impact –> impact vs. impulsive loading

297
Q

_____ contusions are most common on orbito-frontal surfaces and temporal poles.

A

Contrecoup

298
Q

Elevated glutamate, activation of ATP Na/K pump, elevated intracellular Ca, and elevated lactic acid are signs of ____

A

severe concussion

299
Q

Black Brain

A

Classical “Black Brain” of abused infant representing total brain necrosis secondary to shock a/o severe concussion.

300
Q

GCS <= 8 is severe/moderate/minor

A

severe

301
Q

Seizure

A

transient dysfunction of all/part of brain due to excessive discharge of a group of neurons causing sudden and transient symptoms of a motor, sensory, autonomic, or psychic nature

302
Q

A seizure with an immediate precipitant such as fever, acute head trauma or CNS infection.

A

provoked seizure

303
Q

A seizure without an immediate precipitant.

A

Unprovoked seizure

304
Q

Recurrent unprovoked seizures.

A

Epilepsy

305
Q

Motor seizure propagating along primary motor cortex

A

Jacksonian march

306
Q

Drug for epilepsy that inhibits neurotransmission via GABA-A receptors.

A

Phenobarbitol

307
Q

Which seizure? subtle, staring spells, no shaking/falling, no strange vocalizations

A

absence general

308
Q

Which seizure? quick jerks, symmetrical, short

A

myoclonic general

309
Q

Which seizure? grand mal

A

tonic-clonic general

310
Q

Which seizure? quick body stiffening, fall

A

tonic general

311
Q

Which seizure? bilateral rhythmic jerking

A

clonic general

312
Q

Which seizure? loss of tone, slumping

A

atonic general

313
Q

Seizures that “Start deep down in the center of the brain and spread quickly to both sides” are ___ seizures

A

generalized

314
Q

T/F Focal seizures can occure with or without impairment of awareness

A

T

315
Q

Seizures that start in a spot of the brain and may or may not spread are ____ seizures

A

focal

316
Q

Which seizure? clonic shaking of contralateral limbs

A

motor strip focal

317
Q

Which seizure? complex, bilateral hypermotor activity

A

anterior to motor strip near midline focal

318
Q

Which seizure? arrest of activity, hypomotor

A

fronto-polar focal

319
Q

Which seizure? aura, arrest of activity, unresponsiveness, motor automatisms

A

temporal lobe focal

320
Q

Which seizure? sensory signs based on propagation to other lobes

A

parietal focal

321
Q

Which seizure? visual signs

A

occipital lobe focal

322
Q

3 mechanisms of reduced inhibition in epileptic brain

A
  1. gaba receptor change, 2. loss of interneurons, 3. change of interneuron activity
323
Q

3 mechanisms of excitation in epileptic brain

A
  1. mossy fiber sprouting, 2. changes in EAA receptors, 3. presynaptic changes
324
Q

general processes occurring in the brain before a patient develops spontaneous seizures after an insult is called ______

A

epileptogenesis

325
Q

Paroxysmal depolarization shift

A

cellular correlate of focal interictal epileptiform spike/sharp wave –> prolonged Ca depolarization leading to sodium-mediated action potentials –> prominent after hyperpolarization due to opening of ca dependent k channels

326
Q

T/F seizures involve loss of inhibitory control and runaway excitation (e.g. paired pulxse facilitation)

A

T

327
Q

Sustained repetitive firing

A

mechanism of seizure generation similar to spikes in PDS but without Ca inward current–> voltage gated Na channels maintain threshold for spike generation

328
Q

Mutations of what system might lead to absence epilepsy/generalized epilepsy

A

t-type calcium channel –> alterations in oscilllatory circuitry including changes in interaction between GABAb receptors, calcium channels, k channles in thalamus –> abnormal thalamocortical volleys between cortical layer 5 neurons and intralaminar nucleus of thalamus

329
Q

Burst firing

A

hyperpolarization –> activation of TCa channel –> voltage dependent Na channel activation –> burst firing

330
Q

GABA is excitatory/inhibitory during development

A

excitatory –> NKCC1 maintains high Cl in cell –> GABA activation leads to flow of Cl out of cell and depolarization

331
Q

NMDA receptor in development

A

more readily expressed than AMPA –> GABA excitation more readily removes Mg block in NMDA receptors –> hyperexcitable state

332
Q

Are GABA agnonists like benzodiazepines less useful during development?

A

No –> already in state of transition from excitatory GABA to inhibitory GABA so there is some benefit

333
Q

_____ synchronized synaptic development across brain regions

A

giant depolarizing potentials

334
Q

MOA: Na channel blockers

A

block voltage dependent Na channels @ high firing frequency –> inhibit sustained repetitive firing, indicated in focal epilepsy, oxcarbazepine, lamotrigine, phenytoin,

335
Q

MOA: GABA agonists

A

increase inhibitory transmission –> prolong GABA mediated Cl channel opening (barbituates), increase frequency of GABA mediated Cl channel opening (benzodiazepines)

336
Q

MOA: Ca channel blockers

A

blocks or modulates t-type calcium channels –> main effect on thalamic neurons –> prevents abnormal thalmo-cortical interaction –> absence seizures (valproic acid and ethosuximide)

337
Q

MOA: EAA transmitter antagonists

A

multiple mechanisms to restore excitation/inhibition balance by reducing excitation –> 1. antagonize glutamate at AMPA/kainaite receptors (topiramate), 2. block voltage dependent t channels and Na (zonisamide), modulate NMDA receptor via strychnine-insensitive glycine receptor (felbamate)

338
Q

MOA: Synaptic mechanisms

A

GABA reuptake inhibitors (vigabatrine, tiagabine), increase GABA (pregabalin), vesicle binding (Levetiracetam)

339
Q

Ketogenic diet

A

high fat/low carb/low protein diet –> increase GABA production, ketones directly anti-epileptic

340
Q

T/F B6 is a cofactor for gABA production and may support seizure therapy

A

T

341
Q

Infections that trigger MS

A

EBV, HHV6, chlamydia, mycoplasma

342
Q

T/F MS most often affects women

A

T

343
Q

Which gene has the strongest association with MS?

A

HLA DRB1501 (MHC II)

344
Q

Risk for MS among identical twins

A

30%

345
Q

Risk for MS in fraternal twins

A

4%

346
Q

Risk for MS among first degree relatives

A

4%

347
Q

What symptom? painful inflammation of optic nerve

A

optic neuritis

348
Q

What symptom? flexion of neck causing parasthesia

A

Lhermitte’s

349
Q

What symptom? symptoms exacerbated by overheating

A

uhthoff’s

350
Q

4 clinical patterns of MS

A

relapsing-remitting, secondary progressive, primary progressive, progressive relapsing

351
Q

T/F MS respects vascular territories

A

F

352
Q

Gadoliniumenhancing lesions suggest:

A

acute inflammation in MS

353
Q

white matter lesions in MS suggest:

A

demyelination

354
Q

black holes in MS suggest:

A

axonal loss, gliosis

355
Q

Dawson’s fingers

A

characteristic periventricular ovoid FLAIR hyperintense MSlesions

356
Q

oligoclonal bands

A

if not present in serum, indicative of igg production in cns

357
Q

Acute treatment of MS

A

corticosteroids, treat underlying infection

358
Q

Disease modifying treatment of MS

A

inteferon 1a/b, natalizumab, etc.

359
Q

The ____ is the master biological clock.

A

suprachiasmatic nucleus

360
Q

Circadian clocks are based on _____ feedback loops

A

negative

361
Q

Which two systems coordinate sleep temporally?

A

circadian system and homeostatic need for sleep

362
Q

The circadian rhythm drives wakefulness/sleep

A

wakefulness

363
Q

T/F Sleep drive is an oscillator.

A

F –>Sleep drive is a homeostatic system—not an oscillator—and as such it builds up and dissipates relative to the quantity and quality of sleep we obtain. It therefore promotes sleep to varying degrees. If sleep is not adequately satisfied physiologically, the homeostatic drive for sleep can build to a point at which the circadian system cannot maintain wakefulness. At this point, microsleeps and sleep attacks can occur when what people are trying to stay awake and engage in motivated behavior.

364
Q

melanopsin cells—in our retinal ganglion cell layers transmit information about the environmental timing of Earth’s light via the _____ tract to the hypothalamic suprachiasmatic nucleus (SCN).

A

retinohypothalamic

365
Q

T/F Night shift work is better than longer shifts.

A

F –> night shifts not only build up sleep pressure but also force you to sleep in the wrong cycle which leaves you more exhausted because you can’t sleep as fully.

366
Q

Stages of sleep

A

waking –> sleepy, alpha activity –> stage 1 non-REM, theta –> stage 2, non-REM, sleep signals, delta wave –> stage 3/4 SWS, delta waves –> REM

367
Q

During what stage of sleep do we give up thermoregulation?

A

REM

368
Q

Declarative memory consolidation requires what kind of sleep?

A

non-REM

369
Q

Emotional and procedural memory consolidation requires what kind of sleep?

A

REM

370
Q

Cholinergic input from the ______ and the _____ nuclei project through the thalamus and facilitate thalamocortical transmission of arousal signals.

A

laterordorsal tegmental and pedunculopontine nuclei

371
Q

Sleep switch

A

This internal biological clock originates in the suprachiasmatic nucleus (SCN), projects through the dorsomedial hypothalamus (DMH) sending inhibitory signals to the GABA(γ-aminobutyric acid)ergic (grey) ventrolateral preoptic nucleus of the hypothalamus (VLPO)

372
Q

During the early hours of dark periods the pineal gland (Pin) releases melatonin (red), which has______ effects on the SCN and DMH of the melatonergic system.

A

inhibitory

373
Q

With age we have more/less SWS

A

less

374
Q

wake state instability

A

Once the homeostatic drive for sleep is elevated beyond levels typical of a normal waking day (16-18 hours) in a healthy adult, wakefulness can become unstable, as the sleep system turns on in the presence of waking drive, resulting in “lapses,” which refer to sudden unexpected delays in the brain’s responses.

375
Q

The sleep drive accumulator is thought to be in the ____

A

basal forebrain

376
Q

Narcolepsy tetrad

A

hypersomnolence, cataplexy, hypnogogic/hypnopompic hallucinations, sleep paralysis (and impaired sleep quality)

377
Q

Cataplexy

A

sudden loss of muscle tone/partial loss common –> seconds to minutes, spared consciousness, triggered by emotion

378
Q

Neurons secreting ______, produced in the ______, project widely to areas of brain involved in sleep-awake control; this substance is diminished or absent in narcolepsy with cataplexy.

A

hypocretin/orexin in the posterolateral hypothalamus

379
Q

Flipflop switch model

A

awake/sleep is a balance between LC/TMN/Raphe nuclei/VLPO/eVLPO –> orexin supports wakefulness and is inhibited by VLPO

380
Q

Treatment for hypersomnolence

A

stimulants, modafinil, armodafinil, naps

381
Q

Treatment for cataplexy

A

tricyclic antidepressants, SSRI, gamma hydroxybutyrate (Xyrem)

382
Q

An undesirable behavioral,motor, or sensory phenomenon which occurs intermittently during sleep.

A

parasomnia

383
Q

T/F Parasomnias can emerge from rem/non-rem sleep.

A

T

384
Q

Disorders of arousal begin in non-REM/REM sleep.

A

non-REM

385
Q

T/F arousal disorders tend to have positive family history.

A

T

386
Q

Tx for arousal disorders

A

reassurance, secure environment, warning devices, benzodiazepines, avoiding stressors

387
Q

T/F sleepwalking is less likely when sleep deprived.

A

T

388
Q

Dissociated state characterized by violent dream-enacting behavior, increased tonic/phasic EMG in REM, absence of epileptiform activity is ______

A

REM sleep behavior disorder

389
Q

Normally, REM sleep-generating neurons in the _____ actively inhibit spinal interneurons in descending tracts.

A

pons

390
Q

T/F RBD is a neurodegenerative condition

A

T

391
Q

T/F RBD is most common in older men.

A

T

392
Q

T/F RBD is not associated with PD, Lewy Body, or multi-system atrophy.

A

F

393
Q

Tx of RBD

A

clonazepam, melatonin, secure environment

394
Q

REM sleep behavior disorder typically presents in patients 10-20 years after diagnosis of ____

A

PD

395
Q

_____: an awake sensory phenomenon with a volitional motor response.

A

Restless legs

396
Q

____: an involuntary sleep-related motor phenomenon.

A

Periodic leg movements

397
Q

RLS URGE criteria

A

urge to move legs with dyesthesias, onset with rest or inactivity, partial or total relief with movement (Getting up), symptoms worse in evening or night

398
Q

Secondary RLS may be related to 3 conditions

A

iron deficiency anemia, pregnancy, chronic renal failure

399
Q

Link between iron and RLS

A

low iron –> impaired central dopaminergic supra-spinal inhibition

400
Q

RLS/PLM affects sensory afferents.

A

RLS

401
Q

RLS/PLM affects motor efferents

A

PLM

402
Q

Tx of RLS

A

dopamine agonists, opiates, gabapentin, iron, benzodiazepines

Brain and Behavior Part 2 (6 decks)

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