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Brain and Behavior > Exam 3 Deck 2 > Flashcards

Exam 3 Deck 2 Flashcards

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1
Q

What is dementia?

A

Clinical syndrome marked by progressive cognitive impairment in clear consciousness

Represent a decline from previous level of functioning

Involves multiple cognitive domains

Interferes significantly with social or occupational functioning

Small percentage is reversible

(Common in elderly)

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2
Q

What is Major Neurocognitive Disorder?

A

Dementia

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3
Q

What are the diagnostic criteria for dementia (major neurocognitive disorder)?

A
  • Significant cognitive decline from previous level of performance in one or more cognitive domains
  • Cognitive defects interfere with independence
  • They do not occur exclusively in context of delerium
  • Not explained by something else
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4
Q

What is the course of dementia?

A

Generally insiduous onset with duration of 6 months to 15 years

Progressive cognitive and functional decline that eventually leads to death

Neuropsychiatric symptoms typically worsen with dprogression

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5
Q

What is the prognosis for dementia?

A

Leads to death

Identifying correctable causes can improve symptoms

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6
Q

What is the number 1 risk factor for dementia?

A

AGE

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7
Q

Which gender suffers from dementia more?

A

Females

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8
Q

What are risk factors for dementia?

A

Age

Female

Vascular (HTN, CV disease, obesity, hyperlipidemia, CHF, A.fib. …)

Environmental (alcohol, diet)

Genetics

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9
Q

What are some factors associated with the reversal of dementia or the slowing of its progression?

A

Education

Social networks

Cognitive stimulating activities/leisure activities

Exercise

Being male

Statins, perhaps; broadly, control of vascular risk factors

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10
Q

What non-cognitive symptoms are observed in dementia?

A

Affective and motivational symptoms

Psychotic symptoms

Disturbances of basic drives

Inappropriate/disinhibited behaviors (wandering)

Sleep disturbance

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11
Q

What symptoms of dementia lead to increased caregiver burden/stress, increased institutionalization, increased cost of care, increased bad outcomes for caregivers, increased bad outcomes for elders (abuse, neglect), danger, and worse medical care?

A

Non-cognitive symptoms-

affective & motivational, psychotic symptoms, disturbances of basic drives, socially inappropriate/disinhibited behaviors (aggression, wandering), sleep disturbance and neurological findings.

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12
Q

What are features of cortical dementia?

A

Memory impairment (recall and recognition)

Language defecits

Apraxia

Agnosia

Visuospatial deficits

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13
Q

What are features of subcortical dementia?

A

Greater impairment of recall memory

Decreased verbal fluency without anomia

Bradyphrenia (slowed thinking)

Depressed mood

Affective lability

Apathy

Decreased attention/concentration

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14
Q

What are some features that distinguish cortical from subcortical dementias?

A

Cortical have recall and recognition memory impairments; Subcortical is more recall impairments

Cortical dementias lack prominent motor signs; subcortical typically feature them

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15
Q

What are some etiologies of dementia?

A

Alzheimer’s

Dementia with Lewy bodies

Vascular

Frontotemporal (Pick’s disease)

Mixed

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16
Q

What is the most common cause of dementia?

A

Alzheimer’s

followed by Lewy Body / Vascular

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17
Q

What are core features of lewy body dementia?

A

Fluctuating cognition with pronounced variations in attention and alertness

Visual hallucinations

Spontaneous parkinsonism

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18
Q

What type of dementia presents with recurrent visual hallucinations and spontaneous parkinsonism?

A

Lewy Body Dementia

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19
Q

What is the major constituent of the cause of the dementia that causes visual hallucinations and parkinsonism?

A

α-synuclein - This is Dementia with Lewy Bodies

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20
Q

What causes vascular dementia?

A

Ischemic or hemorrhagic injury to the brain, consequence of cerebrovascular or cardiovascular disease

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21
Q

What are etiologies of vascular dementia?

A

Stroke

Small vessel ischemic disease

Hemorrhage

Chronic hypoperfusion

Genetic

Cerrebral amyloid angiopathy

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22
Q

What are frontotemporal dementias?

A

Group of disorders with shared clinical features - deterioration of language and personality changes

Includes Pick’s Disease

Earlier onset than AD, with insiduous onset, gradual progression

Executive Dysfunction, attentional defecits, loss of insight

3-5 years before death

TAUOPATHY

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23
Q

What do you find on neuropathology of frontotemproal dementials?

A

Atrophy and Pick bodies (tau-containing deposits)

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24
Q

What type of dementia is seen here?

A

Frontotemporal - Atrophy!

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25
Q

What characterizes Creutzfeldt-Jakob Dementia?

A

Prion disease that is invariably fatal

Incidence = 60-64 years

Rapidly progressive

Myoclonus, extrapyramidal signs, cerebellar signs

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26
Q

How do you evaluate a patient with dementia?

A

Physical and mental status/cognitive exams

Lab testing to check for reversible etiologies (thyroid, LFTs, metabolic, CBC, Vit. B12, folate, infectious…)

Maybe CXR, EKG, Brain imaging, EEG…

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27
Q

What are the activities of daily living?

A

Toileting

Bathing

Dressing

Eating

Transferring

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28
Q

What are the independent activities of daily living?

A

Telephone use

Shopping

Laundry

Transportation

Food prep

Managing meds

Finances

Housekeeping

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29
Q

What are non-pharmacological treatments of dementia?

A

Psychotherapy, behavioral management, cognitive skills training, education, legal & financial planning, safety, caregiver support

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30
Q

What are some pharmacological treatments of dementia?

A

Antipsychotics if symptoms exist

Anticonvulsants, SSRIs for behavioral disturbance

SSRIs for depression

Cholinesterase inhibitors (i.e. donepezil)

NMDA Receptor antagonist (Memantine)

Anti-amyloid therapies (experimental)

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31
Q

What is delerium?

A

Disturbance of consciousness with reduced ability to focus, sustain, or shift attention

Change in cognition not better accounted for by dementia

Over short period of time and fluctuates

Epidemic in hospitalized patients

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32
Q

Where do you most commonly see delerium?

A

Hospitalized patients

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33
Q

What is psychology?

A

Study of the mind, occuring partly via the study of behavior

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34
Q

What is psychological testing?

A

Formal assesment of emotionality, intellecutal abilities, personality, and psychopathology

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35
Q

What is neuropsychology?

A

Specialized discipline within psychology that mostly focuses on cognition in relation to the effects of brain damage or organic brain disease

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36
Q

What is neuropsychological testing?

A

Formal assessment of cognitive function, behavior, functional impairment - helps localize lesion

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37
Q

What is an objective psychological test?

A

Responses are analyzed according to universal standard

Minnesota Multiphasic Personality Inventory

Intelligence Tests/WAIS

Achievement (SAT, MCAT, USMLE, etc)

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38
Q

What is a projective psychological test?

A

Personality test designed to let a person in an open ended way respond to ambiguous stimuli, revealing hidden emotion and internal conflicts

Rorschach
Thematic Apperception Test

Sentence Completion Test

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39
Q

What does the Patient-Health Questionaire (PHQ-9 or PHQ-2) screen for?

A

Depression

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40
Q

What are some neuropsychological tests?

A

WAIS-R, Stanford-Binet (IQ tests)

Neurocognitive battery (e.g. Halstead Reitan) that assesses various aspects of cognition

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41
Q

What does IQ measure?

A

Mental Age/Chronological Age x 100

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42
Q

What defines mental retardation on IQ?

A

IQ < 70

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43
Q

What is the borderline intellectual functioning score on IQ?

A

70-79

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44
Q

What is the WAIS-R?

A

Adult intellegence test

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45
Q

What is the Stroop Test?

A

Changing words and colors to measure selective attention, cognitive flexibility, problem solivng, processing speed (executive functioning)

e.g.

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46
Q

What is the Wisconsin Card Sorting Test?

A

Tests set-shifting (executive function)

Sensitive to frontal lobe dysfunction (DLPFC in particular)

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47
Q

What tests are useful in assessing executive function?

A

Stroop Test

Wisconsin Card sorting

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48
Q

What is the California Verbal Learning Test?

A

Tests ability to acquire, store and retrieve verbal information for more than a few minutes

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49
Q

What is the MMSE?

A

Bedside dementia screen - look for changes over time

Does not assess executive function

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50
Q

What is the MoCA?

A

Montreal Cognitive Assessment

Good for testing dementia - includes executive function

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51
Q

What are cognitive changes seen in normal aging?

A

Slowed info processing

Decreased info retreival

Decreased fine motor coordination

Learning, verbal fluency and abstraction are in tact

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52
Q

What are physiologic changes associated with aging?

A

Innate immune function (increased MHC in brain)

Reduced plasticity

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53
Q

What are neuropathologic changes seen in normal aging?

A

Decreased volume and weight - widened sucli and large ventricles

Loss/shrinkage of neurons

Lipofuscin pigment accumulation and maybe neurofibrillary tangles

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54
Q

Are lipofuschin pigments normal to be found in an aging brain?

A

Yes

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55
Q

What is an example of amyloidoses?

A

Alzheimer’s disease

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56
Q

What is an example of a tauopathy?

A

Progressive supranuclear palsy

Pick’s Disease

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57
Q

What is an example of synucleinopathy?

A

Parkinson’s Disease

Dementia with Lewy Bodies

Multiple System Atrophy

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58
Q

What is an example of TDP-43 proteinopathies?

A

Frontotemporal lobar degeneration

Amyotrophic Lateral Sclerosis (ALS)

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59
Q

What is found neuropathologically in AD?

A

Neurofibrillary tangles (tau- intracellular) and neuritic plaques (amyloid core- extracellular)

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60
Q

What is a major distinction between neurofibrillary tangles and neuritic plaques?

A

Neurofibrillary tangles are tau protein aggregates intracellularly

Neuritic plaques are plaques found extracellularly with amyloid core

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61
Q

What finding is essential for a diagnosis of AD?

A

Dementia

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62
Q

What characterizes Pick’s Disease (Fronto-temporal lobar degeneration)?

A

Lobar atrophy, particularly in the frontal, anterior temporal areas

Deposition of Pick bodies - round structures in the neuronal perikaryon

Tau protein aggregates, as well as ubiquitin and tubulin

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63
Q

What are “Balloon” or “Pick” cells?

A

Chromatolytic neurons seen in Pick’s Disease (Frontotemporal lobar degeneration)

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64
Q

What characterizes ALS?

A

UMN and LMN degeneration

Pathology findings include bunina bodies in anterior horn cells (small, eosinophilic)

Contian hyaline inclusions and skeins seen in immunohistochemistry

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65
Q

When do you see skeins?

A

ALS

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66
Q

What characterizes progressive supranuclear palsy?

A

Supranuclear opthalmoplegia, akinesia, rigidita, nuchal dystonia, pseudobulbar palsy and dementia

Neuronal loss and NF tangles in brainstem - CNIII, IV, X and XII and other structures

Different tangles than in AD

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67
Q

How do the neurofibrillary tangles seen in progressive supranuclear palsy differ from those in AD?

A

They are straight filaments rather than paired helical filaments

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68
Q

What is Capgras Syndrome?

A

Patients can recognize faces but are unable place emotional valence to them

Para-amnesia

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69
Q

What are focal pathologies of cerebrovascular disease?

A

Arteriosclrosis

Congophilic angiopathy

Aneurysm

Vasculitis

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70
Q

What are global pathologies of cerebrovascular disease?

A

Hypoperfusion

Hypoxia/anoxia

Hypoglycemia

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71
Q

What is a stroke?

A

Prolonged ischemia to vascular territory resulting in tissue necrosis

Can be caused by thromboembolus (often hemorrhagic) - particularly carotid territory

Can be caused by thrombosis (over local plaque) - particularly in posterior circulation

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72
Q

What is the most common cause of cerebral infarcts?

A

Thromboembolus - originating in the carotids

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73
Q

What is the most common cause of cerebral infarct in the posterior circulation?

A

Thrombosis

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74
Q

Where is the most common location of in situ atherosclerosis in the Circle of Wilis?

A

Posterior circulation

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75
Q

What are causes of cerebral hemorrhage?

A

Trauma

Vascular malformation (berry aneurysm)

HTN

Cereberal amyloid angiopathy

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76
Q

What are highly vulnerable brain regions to global brain hypoxia?

A

Neurons > oligodendrocytes > astrocytes

Hippocampal formation

Cortical layers 3, 5, 6 via damage to pyramidal neurons

Arterial border zone territories

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77
Q

What are characteristics of an acute infarct?

A

Pallor, edema swelling, sometimes hemorrhage

Activation of PMNs

This can lead to herniation if untreated

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78
Q

What are characteristics of a subactue infarct?

A

Macrophage infiltration - lipid laden or filled with hemosiderin

Vascular proliferation (VEGF)

Demarcation, organization, contraction

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79
Q

What can be seen in chronic infarcts?

A

Wallerian degeneration of damaged axons

Cystic cavity

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80
Q

What is different in brain death from vegetative states?

A

Brain death requires respirator

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81
Q

What is a vascular cause of brain death?

A

Diffuse cerebral edema that increases ICP

Arterial inflow ceases, while extracranial structures are still perfused

Patient requires respirator

NO functional recovery

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82
Q

What is the prognosis for a brain dead patient?

A

Poor - no functional recovery

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83
Q

What are modifiable risk factors for stroke?

A

Previous stroke or TIA

HTN

Cardiac disease

Diabetes

Hyperlipidemia

CAD

Smoking

Obesity, inactivity, drugs

Oral contraceptives

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84
Q

What are non-modifiable risk factors for stroke?

A

Age over 55

Hispanicity

Diabetis

African Americanicity

Male

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85
Q

What is the most common cause of ischemic stroke?

A

Thromboembolism

Acute therapy includes thrombolysis

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86
Q

What is the acute therapy for most ischemic strokes?

A

Thrombolysis - because most commonly caused by thromboembolism

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87
Q

What is the ischemic penumbra?

A

The tissue at risk for injury, but still salvagable. The target for acute stroke therapy

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88
Q

What is amaurosis fugax?

A

Painless monocular blindness that can be caused by anterior circulation TIAs or stroke

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89
Q

What is the distribution of deficits seen in anterior circulation strokes/TIAs?

A

Face-hand-arm-leg contralateral hemiparesis and hemisensory loss

Leg more than arm in ACA; arm more than leg in MCA

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90
Q

In which artery, ACA or MCA does a TIA or stroke cause more leg involvement than arm involvement?

A

ACA (think about the homonculus)

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91
Q

What symptoms would a patient with a stroke or TIA to the left cerebral hemisphere present with?

A

Aphasia

Left gaze preference

Right visual field deficit

Right hemiparesis

Right hemisensory loss

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92
Q

Where could a TIA or stroke be localized in a patient presenting with aphasia, left gaze preference, right visual field deficits, right hemiparesis, and right hemisensory loss?

A

Left cerebral hemisphere

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93
Q

What symptoms would a patient with a TIA or stroke to the right cerebral hemisphere present?

A

Neglect (left hemi-inattention)

Right gaze preference

Left visual field deficit

Left hemiparesis

Left hemisensory loss

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94
Q

Where could you localize a TIA or stroke to in a patient with Neglect (left hemi-inattention), right gaze preference, left visual field deficits, left hemisensory loss and left hemiparesis?

A

Right cerebral hemisphere

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95
Q

What is the result of an internal carotid artery occlusion?

A

ACA and MCA syndromes

May be preceded by amaurosis fugax

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96
Q

What are deficits that you see in posterior cerebral artery strokes or TIAs?

A

Contralateral homonymous hemianopsia with macular sparing

If dominant - alexia without agraphia (can’t read, but can write)

If bilatera, can get Anton’s Syndrome

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97
Q

What is Anton’s Syndrome?

A

Bilateral posterior cerebral artery syndrome that causes patients to have blindness without knowing it

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98
Q

What are the characteristic signs you see in brainstem strokes/TIAs?

A

Crossed signs

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99
Q

Where do emboli occur more frequently in the cerebral circulation?

A

Anterior (posterior is less frequent)

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100
Q

What can cause cerebellar infarction?

A

SCA, AICA, or PICA occlusions

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101
Q

What is a life threatening sequellae of cerebellar infarcts?

A

Edema

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102
Q

What are lacunar strokes?

A

Small, sub-cortical strokes

Most common in the basal ganglia, thalamus, internal capsule, corona radiata, pons

Can cause pure motor stroke (thalamus), pure sensory stroke (posterior limb of internal capsule), ataxic hemiparesis, dysarthria

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103
Q

What are TIAs?

A

Transient ischemic attacks

By definition, symptoms last less than 24 hours

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104
Q

What is subarachnoid hemorrhage?

A

Bleeding around the brain

Usually caused by ruptured aneurysm

surgical emergency

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105
Q

What is needed for a definitive diagnosis of subarachnoid hemorrhage?

A

CT or LP

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106
Q

What is a berry aneurysm?

A

Congenital weakness aneurysm often seen in Circle of Willis

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107
Q

What is the most common location for a Berry aneurysm

A

Acomm

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108
Q

What is a mycotic aneurysm?

A

Caused by infection, usually due to bacteremia or septic embolization

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109
Q

What is a Charcot-Bouchard aneurysm?

A

Microaneurysm usually in the lenticulostriates, associated with chronic hypertension

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110
Q

What type of aneurysm are you likely to see in chronic hypertensive patients?

A

Charcot-Bouchard

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111
Q

What type of aneurysm are you likely to see in bacteremic patients?

A

Mycotic

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112
Q

What is the most common cause of intracerebral hemorrhage?

A

Chronic hypertension

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113
Q

Where are hemorrhages caused by hypertension most commonly found?

A

Thalamus

Putamen

Caudate

Pons

Cerebellum

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114
Q

What percentage of strokes are ischemic?

A

85%

Most of these result from clot occluding an artery

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115
Q

What are treatment options for acute stroke?

A

IV tPA (tissue plasminogen activator)

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116
Q

What drug do patients need to take for life afer having a stroke?

A

Aspirin - warfarin not shown to be more effective

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117
Q

Which cortical regions are important in autonomic control?

A

Insular cortex - viscero-motor and sensory cortex

Amygdala- emotional autonomic output

Anterior cingulate - goal-directed behavior autonomics

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118
Q

What are subcortical regions that are important in autonomic control?

A

Hypothalamus and pre-optic area - integrate autonomic + endocrine responses

Lateral and para-ventricular nuclei provide output to brainstem and spinal cord

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119
Q

What brainstem structures are important in the autonomic system?

A

Solitary tract nucleus - relay for visceral afferents and medullary reflexes

Ventrolateral medulla - nucleus ambiguus and dorsal motor vagus nucleus

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120
Q

What are the main parasymapthetic outflows?

A

Cranial = vagus

Sacral = sacral parasympathetic nucleus (distal GI, pelvic organs)

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121
Q

What is the nucleus of origin for the nerves that constrict the pupil?

A

Edinger-Westphal (parasympathetics of CNIII)

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122
Q

What is Horner’s Syndrome??

A

Clinical triad of:

Drooping eyelid (ptosis)

Miosis (small pupil)

Anhidrosis (lack of sweating)

Can be caused by a pancoast tumor (lesion at apex of lung)

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123
Q

What type of tumor can cause a Horner’s Syndrome?

A

Pancoast tumor (at apex of lung)

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124
Q

What is seen in a CN III palsy?

A

Down and out eye

Ptosis

Dilated pupil due to involvement of parasympathetics

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125
Q

What is the afferent limb of autonomic control of blood pressure?

A

Baroreceptors in heart and major vessels sense pressure

Chemoreceptors in carotid body sense O2 and CO2 levels

Convey this information via branches of CN IX and X to the nucleus of the solitary tract

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126
Q

What nucleus is important in receiving autonomic information about blood pressure?

A

Solitary Tract nucleus (gets info from chemoreceptors in carotid body - blood gases - and from baroreceptors)

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127
Q

Lesions to which areas can cause dysfunction of BP control?

A

Both CNS and PNS

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128
Q

What are sequellae of dysfunctional BP control?

A

Orthostatic hypotension and syncope

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129
Q

What brain regions are involved in the regulation of body temperature?

A

Preoptic area

Anterior Hypothalamus

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130
Q

Is sweating under sympathetic or parasympathetic control?

A

Sympathetic

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131
Q

What is hyperhidrosis?

A

Too much sweating

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132
Q

What is hyophidrosis?

A

Too little sweating (anhidrosis if not at all)

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133
Q

What provides the sympathetic innervation of the pelvic structures?

A

Hypogastric nerves from thoracic cord levels

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134
Q

What provides the parasympathetic innervation of the pelvic structures?

A

Sacral plexus nerves

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135
Q

What provides somatic innervation for pelvic structures?

A

Sacral spinal cord - pudendal nerve

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136
Q

What is overflow incontinence?

A

Atonic or “flaccid” bladder

Fails to empty, fills to capacity, then overflows

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137
Q

What is the term for a bladder that fails to empty, fills to capacity, then overflows?

A

Overflow incontinence

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138
Q

What are symptoms of overflow incontinence?

A

Inability to sense bladder fullness

Stress incontinence
Frequency, urgency, nocturia, UTIs, renal impairment

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139
Q

What are neurologic causes of overflow incontinence?

A

Disruption of detrusor reflex leading to de-afferented and/or weak detrusor

From cauda equina/conus medullaris

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140
Q

What nerve is implicated in overflow incontinence and what is its origin?

A

Detrusor - from cauda equina/conus medullaris

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141
Q

What is detrusor hyperreflexia?

A

Automatic or “spastic” bladder

Bladder contracts while patient is attempting to inhibit micturition

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142
Q

What is the term for when a bladder contracts while a patient is attempting to inhibit micturition?

A

Detrusor hyperreflexia (spastic bladder)

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143
Q

What are symptoms of detrusor hyperreflexia?

A

Urgency

Frequency

Nocturia

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144
Q

What are common neurologic causes of syncope?

A

Neurodegeneration (central as in Parkinsons, or peripheral as in Diabetes, amyloid)

Benign or syndromic (vasovagal, vasodepressor, postural orthostatic tachycardia syndrome)

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145
Q

what is orthostatic hypotension?

A

Caused by a ndurodegenerative disorder

Drop in BP on tilt test - may have compensatory tachycardia if early

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146
Q

At what stage of orthostatic hypotension do you see a compensatory tachycardia?

A

Early

Late you do not see it

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147
Q

What is vasovagal syncope?

A

“The common faint”

Sudden increase in vagal tone that causes bradycardia and hypotension

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148
Q

What is postural orthostatic tachycardia syndrome (POTS)?

A

Symptoms of orthostatic intolerance upon standing with increase in HR and no change in BP

Common in young women

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149
Q

What do we see here?

A

POTS

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150
Q

What do we see here?

A

Vasovagal syncope

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151
Q

What do we see here?

A

Orthostatic hypotension

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152
Q

What are chronic autonomic neuropathies commonly associated with?

A

Peripheral neuropathies

E.g. from DM, amyloid, hereditary, Sjogren’s…

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153
Q

What are acute/subacute autonomic neuropathies associated with?

A

Toxicities (chemo)

Guillain-Barre

Immune-mediated/post viral

Paraneoplastic

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154
Q

How do you treat orthostatic intolerance?

A

Reveiw meds

Salt, and water

Compression stockings

Elevate bed

Strengthen legs

Florinef midodrine

Pyridostigmine and β-blockers for POTS

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155
Q

What is the central controller of the ANS in the brain?

A

Hypothalamus - connects to cortex and nuclei in thoracic and lumbar spinal cord; sacral spinal cord; brainstem

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156
Q

What is HRDB?

A

Heart Rate response to Deep Breathing

Test of autonomic function

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157
Q

What is Valsalva maneuver?

A

Forced rapid exhalation that produces hemodynamic chagnes that tests parasympathetic and sympathetic systems

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158
Q

What are Central causes of ANS dysfunction?

A

Parkinson’s disease spectrum (PD, MSA)

Neurodegeneration

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159
Q

What are main peripheral causes of ANS dysfunction?

A

Diabetes

Amyloidosis

Hereditary with sensory loss

Connective tissue (Sjorgen’s, RA, SLE)

Toxic

Guillain-Barre

Immune

Paraneoplastic

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160
Q

What is the limbic system?

A

The vague term used to describe a variable collection of forebrain regions that are important for emotions and memory

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161
Q

What are the regions of the brain that are involved in the limbic system?

A

Hippocampus

Amygdala

Anterior thalamic nuclei

Septum

Limbic cortex and fornix

Prefrontal cortex

Nucleus accumbens

Bed nucleus of stria terminalis

Lateral habenula

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162
Q
A
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163
Q

What is the function of the hippocampus?

A

Important in memory and emotion - especially declarative memory

Necessary for new memory formation - but they are stored elsewhere

Major inhibitory control of HPA axis

Brief bursts of cortisol promote hippocampal function

Sustained bursts damage hippocampus, leading to feedforward pathological loop

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164
Q

What happens to a patient if you remove their hippocampus?

A

They develop profound anterograde amnesia

Procedural or habit memory is normal

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165
Q

What role does the hippocampus play in governing cortisol secretion?

A

Inhibitory ia HPA axis

Short bursts of cortiosl promote hippocampal function to inhibit cortisol production

Long bursts damage the hippocampus and diminish its ability to inhibit - therefore causing feedforward pathological loop

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166
Q

What is the major output nucleus of the hippocampus

A

Subiculum

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167
Q

What carries most of the axons of the output nucleus of the hippocampus?

A

The fornix

(the output nucelus of the hippocampus is the subiculum)

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168
Q

In the hippocampal circuit, which neurotransmitters are used?

A

ALL are glutamatergic, although GABAergic interneurons and cholinergic neurons modulate the circuitry

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169
Q

What is the function of the amygdala?

A

Involved in associative memory and emotion

Important in fear and reward conditioning

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170
Q

Which part of the limbic system plays an important role in associative memory?

A

Amygdala

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171
Q

Which part of the limbic system plays an important role in declarative memory?

A

Hippocampus

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172
Q

What is Kluver-Bucy Syndrome?

A

Bilateral lesions of the amygdala induce placidity, loss of fear, hypersexuality and hyperphagia

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173
Q

What type of lesion can induce placidty, loss of fear, hypersexuality and hyperphagia?

A

Bilateral lesions of the amygdala

Kluver-Bucy Syndrome

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174
Q

What are major foci of epilepsy?

A

Amygdala and Hippocampus

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175
Q

What is the funciton of the prefrontal cortex?

A

Working memory (keeping things “in mind”)

Executive function

Cognition

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176
Q
A
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177
Q

What is the function of the nucleus accumbens?

A

Major reward region of the brain

Pleasure, laughter, addiction, aggression, fear and placebo effect

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178
Q

What is the function of the septal nuclei?

A

Important in reward

Provides strong cholinergic innervations of hippocampus, which is crucial for cognition

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179
Q

What is the function of the bed nucleus of the stria terminalis?

A

Major output of the amygdala and innervates hypothalamus, septal nuclei and thalamus

Implicated in anxiety

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180
Q

What brain structure is implicated in anxiety?

A

Bed nucleus of the stria terminalis

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181
Q

What is the function of the lateral habenula?

A

Forms important interconnections with most limbic structures

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182
Q

What is the molecular basis for long-term memory?

A

Requires gene expression changes

Accompanied by plasticity (LTP & LTD) and changes in spines

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183
Q

What is declarative memory?

A

Explicit

Semantic and episodic

Characterized by exquisite temporal features

Hippocampus + Amygdala

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184
Q

What is procedural memory?

A

implicit memory

Habit or motor memory

Involves Striatum (caudate-putamen)

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185
Q

What type of memory is associated with the hippocampus and amygdala?

A

Declarative

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186
Q

What type of memory is associated with the striatum (caudate putamen)?

A

Procedural

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187
Q

What type of memory is associated with the prefrontal cortex?

A

Working memory

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188
Q

What is emotional memory?

A

Memories with strong emotional meaning that are strong and long lived

Mediated by monoamine systems (DA from VTA; NE from locus ceruleus; 5-HT from dorsal raphe)

Orexin too

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189
Q

What type of memory is mediated by the monoamine systems (DA, NE, 5-HT)?

A

Emotional memory

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190
Q

What part of the limbic system is important for emotions and drives?

A

Amygdala

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191
Q

What part of the limbic system is important for memory?

A

Hippocampus

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192
Q

What part of the limbic system is important for homeostasis?

A

Hypothalamus

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193
Q

What is the dorsolateral PFC involved in?

A

Important in executive function, working memory, decision making….

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194
Q

What is the anterior cingulate cortex involved in?

A

Reward, anticipation, empathy, emotional processing, motivation

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195
Q

What is the orbitofrontal cortex involved in?

A

Corrects and inhibits maladaptive emotional responses, mediates socially appropriate behavior

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196
Q

What part of the prefrontal cortex is important in executive function, working memory, decision making, etc?

A

Dorsolateral PFC

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197
Q

What part of the PFC is important in mediating reward, anticipation, empathy, emotional processing, and motivation?

A

Anterior cingulate cortex

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198
Q

Which part of the PFC is important in correcting and inhibiting maladaptive emotional responses, mediating socially acceptable behavior?

A

Orbitofrontal cortex

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199
Q

Which psychiatric disorders are associated with lymbic dysfunction?

A

Psychosis

Fear/Anxiety

Drives/Reward/Addiction

Sociopathy

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200
Q

What is the believed role of dopamien in schizophrenia?

A

Hyperactivity of dopamine neurons in the mesolimbic pathway may mediate positive symptoms of psychosis

Hypoactivity of dopaminergic neruons in mesocortical pathway may mediate negative acnd cognitive symptoms

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201
Q

What neurons mediate the positive symptoms of psychosis in schizophrenia?

A

Hyperactive dopaminergic neurons of the mesolimbic pathway

202
Q

What neurons mediate the negative and cognitive symptoms of schizophrenia?

A

Hypoactivity of dopaminergic neurons in the mesocortical pathway

203
Q

What is the neurophysiologic basis of cognitive dysfunction and disorganization in schizophrenia?

A

Decreased activity of dorsolateral PFC and dorsal anterior cingulate

Decreased hippocampal activity

204
Q

What is the neurophysiologic basis of emotional dysregulation in schizophrenia?

A

Inability to engage amygdala, anterior cingulate and hippocampus in processing emotional stimuli

Dysfunctional interconnectivity b/w frontal and temporal regions

205
Q

What is learning?

A

The strengthening of existing responses/behaviors or formation of new ones to existing stimuli taht occurs because of practice or repetition

206
Q

What is habituation?

A

Repeated stimulation results in a decreased response (tuning things out)

207
Q

What is sensitization?

A

Repeated stimulation results in increased response

208
Q

What is classical conditioning?

A

The association of a neutral stimulus with an unconditioned stimulus, such that the neutral stimulus comes to bring about a response similar to that originally elicited by the unconditioned stimulus

209
Q

What is the unconditioned stimulus?

A

A stimulus that, without training, automatically produces reflexive, unlearned response

210
Q

What is the unconditioned response?

A

Response that occurs spontaneously to the unconditioned stimulus

211
Q

What is the conditioned stimulus?

A

A neutral stimulus that elicits a conditioned response following learning

212
Q

What is the conditioned response?

A

Behavior that is learned by an association made between conditioned stimulus and unconditioned stimulus. The response elicited by the conditioned stimulus

213
Q

What is acquisition, with respect to classical conditioning?

A

Conditioned response is acquired or learned

214
Q

What is extinction, with respect to classical conditioning?

A

Reduction of frequency of a learned response as a result of the cessation of reinforcement

215
Q

What is spontaneous recovery, with respect to classical conditioning?

A

The increase in strength of an extinguished behavior after the passage of a period of time

216
Q

What is stimulus regeneration, with respect to classical conditioning?

A

Conditioned response as a result of a new stimulus that resembles a conditioned stimulus

217
Q

What is learned helplessnes?

A

Association (by classical conditioning) between aversive stimulus and the inability to escape

leads to hopelessness and apathetic response during subsequent exposures

218
Q

What is imprinting?

A

Learning occuring at a particular age or life stage that is rapid and independent of the consequences of the behavior

219
Q

What is operant conditioning?

A

Trial-and-error learning

Learning occurs because of the consequences to the individual of a previous behavior

Consequence determines whether behavior continues or not.

220
Q

What is positive reinforcement?

A

Introduction of stimulus that results in an increase of the rate of a behavior

221
Q

What is negative reinforcement?

A

Removal of an aversive stimulus that results in an increase in the rate of behavior

222
Q

What are three types of fixed schedules of reinforcement?

A

Continuous - each time

Fixed ratio - reward given after set number of responses

Fixed interval - reward given after fixed amount of time

223
Q

Describe the rate of learning and extinction in fixed schedules of reinforcement?

A

Rapid learning and rapid extinction

224
Q

Describe the rate of learning and of extinction when you use variable schedules of reinforcement?

A

Slower learning, and more resistant to extinction

225
Q

Which schedule of reinforcement is more resistant to extinction?

A

Variable

226
Q

What are variable schedules of reinforcement?

A

Variable ratio - reward given after random and unpredectable number of responses

Variable interval - reward given at random and unpredictable amount of time

227
Q

What neurons are activated after conditioned stimulus or primary reward is introduced? What neurotransmitter is used?

A

Nucleus basalis

ACh

228
Q

What neurotransmitter plays a role in both positive reinforcement learning and aversive learning?

A

Dopamine

229
Q

What brain regions do all drugs of abuse activate that triggers the reward pathways?

A

Mesolimbic dopamien system

Also increase dopamine levels in nucleus accumbens and elsewhere

230
Q

What is Urbach-Wiethe disease?

A

Rare autosomal recessive disease

Bilateral calcification of anterior medial temporal lobes, especially amygdala

Cannot properly rate intensity of emotion or recognzie fearful stimuli

231
Q

What is sociopathy/antisocial personality disorder?

A

lack of respect for social norms, obligations, and irresponsibility

Reckless, irritable, impulsive, aggressive behavior

Lack of remorse/guilt, empathy, compassion, fear

Repeated lying/conning

Onset before 15 yo

232
Q

What limbic structures are associated with sociopathy?

A

Hypoactiviyt of the amygdala and orbitofrontal cortex

Ventromedial prefrontal cortex dysfunction

233
Q

What is limbic encephalitis?

A

Autoimmune disorders that affect limbic system

Cardinal sign is subacute onset of short term memory loss

can have behavioral, psychiatric, confusion, seizures, or other neurological symptoms

234
Q

What is subacute onset of short term memory loss a cardinal sign of?

A

Limbic encephalitis

235
Q

What is the etiology of limbic encephalitis?

A

Autoimmune - associated with antibodies against intracellular antigens or neuronal surface antigens

Also may or may not be associated with neoplasms

236
Q

What is the treatment for limbic encephalitis?

A

Immunotherapy, tumor removal and screening

237
Q

What are the three major groups of limbic encephalitis?

A

LE associated with classical intracellular neuronal antigen antibodies - associated with neoplasm

LE associated with antibodies against neuronal surface antigens (+/- neoplasm)

LE associated with no known antibody (many associated with neoplasm)

238
Q

What may you find in the CSF of a patient with limbic encephalitis?

A

Anti-neuronal antibodies, elevated lymphocytes and proteins, oligoclonal bands

Not always though

239
Q

What strain of HSV typically causes Herpes simplex encephalitis?

A

HSV-1

240
Q

how do you treat herpes simplex encephaitis?

A

Acyclovir

241
Q

What are clinical features of medial temporal lobe dysfunction?

A

Impaired memory

Inabilty to judge emotional intensity

Inability to recognize fear

Dysregulation of fear

Altered sexuality

Mood changes

Normal intelligence

242
Q

What is temporal lobe epilepsy?

A

Recurrent epileptic seizures from temporal lobes

Hallucinations, illusions, deja vu, out of body sensations, amnesia, mood chagnes, fear, anger, unusual behaviors

Hyper-religiosity ,circumstantiality, hypermorality, intensified mental life, altered sexuality, hypergraphia

243
Q

What type of brain dysfunction is associated with hyper-religiosity, hyper-morality, intensified mental life, altered sexuality, and hypergraphia?

A

Temporal lobe seizures

244
Q

What defines a seizure?

A

Release of excessive and uncontrolled electrical activity in the brain

245
Q

What defines epilepsy (vs seizure)?

A

Neurological condition that in different times produces brief disturbances of the electrical functions of the brain

Epilepsy is 2 or more unprovoked seizures

246
Q

What age demographics does epilepsy usually present in?

A

Childhood and the elderly

247
Q

What is the major cause of seizures in children?

A

Developmental and infections

248
Q

What is the major cause of seizures in the elderly?

A

Stroke

249
Q

What are the two main categories of epilepsy?

A

Primary (idiopathic) generalized epilepsy - genetic; entire brain at once

Localization-related (Focal/Partial) epilepsy - specific part of brain

250
Q

What type of seizure starts with the whole brain at once?

A

Primary (idiopathic) generalized epilepsy

251
Q

What type of epilepsy starts in a specific part of the brain?

A

Localization-related (Focal/Partial) epilepsy

252
Q

What type of epilepsy is caused by visual cues, mental actions (thinking), stimuli such as reading, writing, etc?

A

Reflex epilepsy

253
Q

What is the main concern of a physician when evaluating an epileptic patient?

A

That it may be symptomatic of a treatable cerebral lesion

254
Q

What is the frequency of delta waves and when are they found?

A

<4Hz - sleep

255
Q

What is the frequency of theta waves?

A

4-8 Hz

256
Q

What is the frequency of alpha waves and when are they found?

A

8-13 Hz; found in an awake, relaxed state

257
Q

What is the frequency of beta waves?

A

>13 Hz

Increased in people on benzos and barbituates B!!!

258
Q

What type of seizures are epilepsy auras indicative of?

A

Focal

Characterized by sudden intense fear, deja vu, olfactory hallucinations, rising abdominal sensation

259
Q

A patient is experiencing intense fear, deja vu, olfactory and gustatory hallucinations, and rising abdominal sensation, what do you think might happen to him/her?

A

Epilepsy

These are classic aura symptoms

260
Q

Do generalized tonic-clonic seizures have auras?

A

No!

261
Q

Is there loss of consciousness in generalized tonic-clonic seizures?

A

Yes

May last 2-3 minutes, characterised by amnesia for the event

262
Q

How long do generalized tonic-clonic seizures last?

A

2-3 minutes, followd by post-ictal period of confusion

263
Q

What is happening here?

A

Generalized tonic-clonic seizure

264
Q

What are some things you see in a seizure that involves the motor cortex?

A

Rhythmic movements of contralateral limb

265
Q

What are some things you see in patients with seizures in their visual cortex?

A

Complex figures or colors in part of the visual field

266
Q

What are absence seizures??

A

Sudden behavioral arrest characterized by staring, unresponsiveness, eye-blinking at 3Hz

Mostly young children

267
Q

A young child is staring off into space and blinking at ~3Hz. What do you think?

A

Absence seizures

268
Q

What are myoclonic seizures?

A

Brief, lightning-like whole body or portion seizures, often without loss of consciousness

269
Q

A patient is jerking with brief, lightning-like motions, without loss of consciousness. What do you think?

A

Myoclonic seizure

270
Q

What is juvenile myoclonic epilepsy?

A

5-10% of all epilepsies

Usually present with family history of epilepsy, with myoclonis early in the day (drops things in the mornings)

Requires anti-epileptic tx for life

271
Q

What is mesial temporal sclerosis?

A

Hippocampal sclerosis causing temporal lobe epilepsy

Important cause of refractory complex partial epilepsy

Neuronal loss in CA1, CA3, CA4

Aura of risign epigastric sensation, intense fear, impaired consciousness and automatisms

272
Q

Patient presents with aura of rising epigastric sensation, intense fear, impaired consciousness, and lip-smacking, chewing, and button picking. What are you thinking?

A

Mesial Temporal Sclerosis

273
Q

Where do most focal seizures begin?

A

Temporal lobe

274
Q

What auras are common in temporal lobe seizures?

A

Epigastric rising feeling, intense fear, deja vu, olfactory hallucinations

275
Q

What are automatisms?

A

Lip-smacking, cheiwng, button picking often seen in patients having seizures

276
Q

What is the second most common focal seizure?

A

Frontal lobe seizures (temporal is first)

277
Q

What seizures can be bilateral without loss of awareness?

A

Frontal lobe seizures (only ones)

278
Q

Which seizures feature a jacksonian march?

A

Frontal lobe seizures (myoclonus begins in one part of the body and migrates along the pattern of the motor homunculus)

279
Q

What is a Jacksonian March?

A

myoclonus begins in one part of the body and migrates along the pattern of the motor homunculus

280
Q

What are features of occipital lobe seizures/

A

Poorly formed colors with lights

May see stereotyped, complex forms

281
Q

A patient has a seizure featuring poorly formed colors with lights, and sees complex, stereotyped forms. What are you thinking?

A

Occipital lobe seizure

282
Q

What is Todd’s Paralysis?

A

Post-ictal condition of focal weakness in one part of the body. Helps discriminate between primary and secondary generalized seizures, because region of weakness will correspond to the epileptic foci

If localized = secondary

If diffuse = primary

283
Q

What are Rolandic seizures?

A

Unilateral parasthesia (tingling) and clonus of the tongue, lip, pharynx

Often see dysarthria, drooling

Commonly undiagnosed and occur shortly after falling asleep

Resolve by adolescence

284
Q

Young patient presents with tingling and drooling of mouth with impaired speech shortly after falling asleep. What are you thinking?

A

Rolandic seizures

285
Q

What are Lennox-Gaustat seizures?

A

Triad of mental retardation, slow spike and wave, and multiple seizures

Generally less than 8 years old

Tonic seizures out of sleep

Tx is difficult

286
Q

What is the difference between tonic vs clonic seizures?

A

Tonic = tighten up and lose consciousness

Clonic = spasmic, no loss of consciousness

287
Q

What are febrile seizures?

A

Benign seizures accompanying fever in children 3 months - 5 years old

288
Q

Where do brain tumors occur that are generally not associated with seizures?

A

Cerebellum and brainstem

289
Q

When should withdrawal of pharmacotherapy be considered in an epileptic patient?

A

When a patient is seizure-free for three years - must weigh benefits with potential for seizures and the impact it could have on employment, etc

290
Q

What is status epilepticus??

A

Seizure lasts more than 30 minutes or multiple seizures lasting 30 minutes without recovery in between

May be life-threatening

291
Q

What do the chemical structures of drugs of abuse all have in common?

A

NOTHING!

292
Q

What defines drug addiction?

A

Loss of control over drug use

Compulsive drug seeking and taking despite horrendous adverse consequences

293
Q

What tolerance, with regards to drug use?

A

Reduced drug effect after repeated use

294
Q

What is sensitization with respet to drug use?

A

Increased drug effect after repeated use (opposite of tolerance)

295
Q

What is dependence, with respect to drug use?

A

Altered physiological state that leads to withdrawal symptoms upon cessation of use

296
Q

How can you know if a patient is dependent on drugs?

A

If they experience withdrawal symptoms upon cessation

297
Q

What causes drug addiction??

A

Drug-induced changes in reward or reinforcement of drug use

Includes tolerance, sensitization, or dependence in reward-reinforcement mechanisms

298
Q

What is reinforcement?

A

A stimulus that causes a response to be maintained and increased

299
Q

What are examples of positive reinforcement?

A

Food, sex, etc

300
Q

What are examples of negative reinforcement?

A

Pain, starvation, etc

301
Q

What neurons in the brain are the “rheostats” of reward?

A

VTA dopaminergic neurons

302
Q

What is the function of the VTA dopaminergic neurons?

A

They are the “rheostats” of reward

Activated by rewards, expectations of rewards

Absence of expected reward inhibit these neurons

Hyperactivated by unexpected rewards

303
Q

What brain region is activated by rewards? What is the effect of an unexpected reward?

A

VTA dopaminergic neurons

Unexpected rewards activate it even more

304
Q

What is the difference between drugs of abuse and natural rewards?

A

Drugs of abuse activate the same regions better (VTA dopaminergic neurons)

305
Q

What is the mesolimbic pathway?

A

VTA to Nucleus Accumbens pathway that is very important in reward

The NAc can influence behavioral by virtue of its connection with the ventral pallidum (basal ganglia).

306
Q

What is the mesocorticolimbic pathway?

A

The meso-corticolimbic pathway enables integration of information about the reward, retrieval of internal motivational states for action planning, learning about the reward, and focusing of attention on the reward and the context in which it is being given

307
Q

What are long-lasting changes in the brain that occur in addiction?

A

Reduced resopnses to natural rewards

Sensitization of responses to drugs of abuse and associated cues

Impaired cortical control over more primitive reward pathways

308
Q

What are cortical changes seen in addiction (e.g. cocaine abusers)

A

Hypofrontality

309
Q

What drugs block the dopamine pump?

A

Cocaine - blocks it

Amphetamine - reverses it

310
Q

What drug reverses the action of the monoamine transporter?

A

Amphetamine

311
Q

Where do opiates act?

A

All are agonists or partial agonists at the μ opioid receptor

312
Q

What is the difference between opiates (e.g. morphine and heroin, or methadone, oxycontin, buprenorphine)?

A

Pharmacokinetics - all have similar activity

313
Q

What does the activity of opiates mimic?

A

Endogenous opioid peptides (enkephalins, endorphins, dynorphins)

314
Q

What are opioid receptor antagonists?

A

naloxone, naltrexone

315
Q

How do you treat opiate overdoses?

A

Naloxone, naltrexone

316
Q

What are the effects of opiates?

A

Analgesia, euphoria, sedation, constipation, respiratory depression

Can cause profound dependence, and tolerance, but are addictive

317
Q

Where do stimulants act?

A

On monoamine systems - their action depends on monoamine transporters (cocaine, amphetamine, …)

318
Q

What is the net effect of stimulant use?

A

Increase monoaminergic transmission (bocking pump, reversing pump, etc)

319
Q

What are the effects of stimulants?

A

Euphoria, increased arousal, suppression of fatigue, increased confidence, appetite suppression

320
Q

What action of stimulants deveops tolerance?

A

Euphoria, tachycardia

321
Q

What action of stimulants experiences sensitization?

A

Activation, paranoia, psychosis, irritability

322
Q

What are the actions of nicotine?

A

Causes increased alertness, muscle relaxation, analgesia, nausea, psychomotor activation

323
Q

What is the action of PCP and ketamine?

A

Non-competitive NMDA glutamate receptor antagonists

324
Q

What addictive drugs are NMDA glutamate receptor antagonists?

A

PCP, ketamine

325
Q

Under what circumstances does alcohol have effects in the brain?

A

At very high concentrations

326
Q

What explains alcohol’s complex and concentration dependent effects? (Anxiolytic<< dissociative, psychotogenic << coma, death)

A

It’s effects on transmembrane proteins (receptors/channels)

GABA-A << NMDA << voltage-gated chanels

327
Q

What is the mechanism of opiate tolerance and dependence?

A

Upregulation of the cAMP-CREB pathway

328
Q

What is the importance of upregulated cAMP-CREB pathway proteins?

A

Common adaptation to drug exposure seen in many brain locations that explains the long-term effects of opiates

329
Q

What are treatment avenues for drug addiction?

A

Replacement therapy (with partial agonists or longer-acting agonists)

Antagonist therapy (e.g. naltrexone/naloxone) - less efficacious

Antidepressants - only in depressed patients

Behavioral therapies

330
Q

What are functions of the hypothalamus?

A

Regulates:

Homeostasis

Body Temp

Hunger, thrist, metabolism

Emotional states

Circadian rhythms

Sleep/wakefulness

Reproductive functions

331
Q

How does the hypothalamus exert its broad regulatory effects?

A

Neuroendocrine control of the pituitary gland

ANS control

Diverse projections to various other brain and spinal cord regions

332
Q
A
333
Q

Identify teh paraventricular nucleus

A
334
Q

Identify the supraoptic nuclei

A
335
Q
A
336
Q
A
337
Q
A
338
Q

What key feature of the CNS is not well developed in the hypothalamus?

A

The Blood-Brain barrier

339
Q

What is the function of the preoptic area and anterior hypothalamus?

A

Thermoregulation - cytokines acting here cause fever by activating prostaglandin synthesis here

Regulation of fluid and electrolyte balance

Regulation of sexual behavior

Ventrolateral preoptic area is crucial for sleep

340
Q

What causes fever?

A

Peripheral cytokines acting on the preoptic area and anterior hypothalamus, activating prostaglandin synthesis

341
Q

What is the ventrolateral preoptic area crucial for?

A

Sleep

342
Q

What is the function of the suprachiasmatic nucleus?

A

Master circadian clock that entrains with environmental light

343
Q

Where is the site of the master circadian clock that entrains with environmental light?

A

Suprachiasmatic nucleus

344
Q

What is the function of the arcuate nucleus (a.k.a. infundibulum)

A

Regulation of feeding and body weight (Neuropeptide Y, agouti-related peptide, and melanocortin)

Neuroendocrine regulation via anterior pituitary (dopaminergic regulation of prolactin, GHRH regulates growth hormone)

345
Q

What is another name for the arcuate nucleus?

A

Infundibulum

346
Q

What is the infundibulum?

A

Arcuate nucleus

347
Q

What is the function of the ventromedial nucleus?

A

Regulates feeding, drinking and body weight (reduces)

Thermoregulation via CNS projections

Sexual behavior

348
Q

What is the function of the dorsomedial nucleus?

A

Regulation of feeding, drinking and body weight (reduces)

349
Q

What is the function of the lateral hypothalamus?

A

Regulation of feeding and body weight (increases)

Regulation fo seep-wakefulness

350
Q

What is the function of of the magnocellular neurons in the paraventricular nucleus?

A

Make oxytocin and vasopressin (ADH)

Project directly to posterior pituitary

351
Q

Which paraventricular nuclei cells make oxytocin and vasopressin, projecting to the posterior pituitary?

A

Magnocellular

352
Q

What is the function of the parvocellular paraventricular nuclei cells?

A

Make “releasing factors” that go directly to the anterior pituitary

CRH - corticotropin

TRH - thyrotropin

GnRH - gonadotropin

353
Q

Which paraventricular nucleus cells make the “releasing factors”

A

Parvocellular

354
Q

What is the difference between the magno and parvo cellular paraventricular nucleus cells?

A

Magno - posterior pituitary - oxytocin/vasopressin

Parvo - anterior pituitary - releasing factor

355
Q

What do magnocellular cells of the hypothalamus make?

A

Vasopressin - project direclty to hte posterior pituitary

(paraventricular nuclei cells aso make oxytocin; supraoptic nucleus cells only make vasopressin)

356
Q

What is the function of the paraventricular nucleus?

A

Magnocellular neurons - oxytocin + vasopressin to posterior pituitary

Parvocellular neurons - releasing factors to anterior pituitary (CRH, TRH, GnRH)

357
Q

What is the function of the supraoptic nucleus?

A

Magnocellular neurons make vasopressin, and project to the posterior pituitary

358
Q

Where do parvocellular cells of the paraventricular nucleus project to?

A

Anterior pituitary

359
Q

Where do magnocellular cells of the paraventricular nucleus project to?

A

Posterior pituitary

360
Q

What is the function of the mammillary nuclei?

A

Important in memory - including olfactory memories

Fornix is the major output of the hippocampus

361
Q

Which brain region is important in memory, particularly olfactory memories?

A

Mammillary nuclei

362
Q

What is the function of the tuberomammillary nucleus?

A

Only source of histamine in the brain

363
Q

What is the only source of histamine in the brain?

A

Tuberomammillary nucleus

364
Q

What are the inputs to the HPA axis?

A

Hippocampus (negative)

Amygdala (positive)

To parvocellular cells of the paraventricular nucleus - release releasing factors

365
Q

How does the hypothalamus control the ANS?

A

Reciprocal connections

Inputs from the nucleus of the solitary tract and the reticular formation

Outputs to medulla (parasympathetic vagal nuclei; preganglionic sympathetics in IML nuclei of spinal cord) from hypothalamus

366
Q

What are the inputs to the hypothalamus important in controlling the ANS?

A

Nucleus of the solitary tract

Reticular formation

367
Q

What are the outputs of the hypothalamus important in controlling ANS?

A

To medulla including parasympathetic vagal nuclei, preganglionic sympathetic neurons in the IML nuclei of the spinal cord

368
Q

What nucleus is critical to entrain circadian rhythms in the body to environmental light?

A

The suprachiasmatic nucleus (SCN)

Innervated by optic nerve directly and indirectly

SCN innervates superior vervical sympathetic ganglia which innervate the pineal gland - releases melatonin

369
Q

Is melatonin released during light or dark?

A

Dark only

370
Q

How is melatonin release achieved?

A

Information about light travels via the optic nerve and then directly and indirectly activates the suprachiasmatic nucleus.

This innervates the superior cervical sympathetic ganglion, which in turn innervates the pineal gland.

Pineal gland releases melatonin when not inhibited (norepinephrine inhibits pineal gland)

Light results in inactivation of pineal gland and no melatonin release

371
Q

What is the molecular clock of the circadian rhythms?

A

Clock/Period/Bmal is the molecular circadian clock found in all cells in the body

Functional endpoint of the suprachiasmatic nucleus cells regulation

This clock will function autonomously even in the absence of SCN entrainment

372
Q

How does hte molecular clock work?

A

Clock/Bmal continuously degrades Period/cry and vice versa

373
Q

How do organs differ with respect to their circadian rhythms?

A

Specific tissues are differentially sensitive to the regulation of the molecular clock by the suprachiasmatic nuclei

374
Q

What is orexin/hypocretin?

A

Expressed solely in lateral hypothalamus

Promotes wakefulness, arousal, and reward; this produces pro-feeding effects

375
Q

What neurotransmitter produces pro-feeding effects and is important in wakefulness, arousal and reward?

A

Orexin

376
Q

What is narcolepsy?

A

Sleep disorder that features abnormal switches between REM and non-REM sleep, featuring intrusive periods of REM sleep during awake periods

Normal amount of sleep per 24 hours

377
Q

What is the role of orexin in narcolepsy?

A

Orexin knockouts are narcolepsy-like

Narcolepsy is associated with a loss of orexin neurons in the hypothalamus

378
Q

How is temperature associated with sleep/wakefulness/REM/NREM sleep?

A

Cool during sleep

Warm during wakefulness

Warming induces NREM sleep

379
Q

How is BMI calculated?

A

weight (kg)/ (height in m)^2

380
Q

What is anorexia nervosa?

A

Syndrome of self-starvation seen much more commonly in females

Body weight 15%+ below normal

Intense fear of being fat

Grossly distorted body image

Often accompanied by amenorrhea

10% mortality

381
Q

Is anorexia nervosa fatal?

A

10% mortality

382
Q

What is bulimia?

A

Syndrome of binge eating and purging, seen much more commonly in females

Requires recurrent episodes of binge eating (loss of control), with regular purging; persistent over-concern with body weight

Body weight can be normal, high or low

Can be fatal (electrolyte abnormalities)

383
Q

What percentage of the risk for obesity can be attributed to genetic factors?

A

70% !!!

384
Q

What parts of the brain are pro-appetite (orexigenic)?

A

Lateral hypothalamus

Lesions cause starvation

385
Q

What parts of the brain are anti-appetite (anorexigenic)?

A

Medial hypothalamus

Lesions cause hyperphagia and obesity

386
Q

What would be the result of a lesion to the lateral hypothalamus?

A

Starvation

387
Q

What would be the result of a lesion to the medial hypothalamus?

A

Hyperphagia and obesity

388
Q

What role does the hypothalamus play in feeding behavior?

A

Physiological need for food (hunger)

389
Q

What role does the mesolimbic dopamine system play in feeding behavior?

A

Desire for food as a rewarding substance

(appetite)

390
Q

What role does the cerebral cortex play in feeding behavior?

A

Control over behavior - integration with psychological and social factors

(top-down control)

391
Q

What is the lipostat model of weight control?

A

Adipocytes produce leptin in response to weight gain (leptin levels are a relative marker of body adiposity)

Leptin then promotes anorexigenic factors and inhibits orexigenic factors in order to reduce food intake, increase energy use, and increase sympathetic tone

This works backwards in response to weight loss

392
Q

What is leptin?

A

Peptide synthesized in adipocytes that is made proportionally to the volume of fat

Acts on hypothalamus to decrease feeding, increase energy utilization, and decrease energy storage

393
Q

What are the targets for leptin?

A

Arcuate nucleus of the hypothalamus

Inhibits orexigenic factors (NPY, agouti-related peptdie)

Stimulates anorexigenic factors (α-MSH, aka melanocortin; CART, a.k.a. cocaine- and amphetamine-regulated transcript)

394
Q

How do we go from leptin to body-wide effects?

A

Leptin acts on the arcuate nucleus of the hypothalamus, causing neuropeptide Y and agouti-related protein (orexigenic) and melanocortin and CART (anorexigenic) to be released

These act in the lateral and medial hypothalamus to regulate further anorexigenic factors (CRH, TRH - medial) and orexigenic (Melanin concentrating hormone - lateral)

395
Q

Are neuropeptide Y and agouti-related protein anorexigenic or orexigenic?

A

Orexigenic

396
Q

What is neuropeptide Y?

A

Most prevalent neuropeptide in the brain

Powerfully orexigenic (most powerful)

Gi linked receptor function

Act on medial hypothalamus (paraventricular nucleus), inhibiting anorexigenic peptides; and on lateral hypothalamus where they stimulate orexigenic peptides

397
Q

What is melanocortin?

A

Derived from POMC

Expressed in pituitary and in arcuate nucleus

Gs linked

398
Q

Are anorexigenic peptides generally Gs or Gi linked?

A

Gs

399
Q

Are orexigenic peptides usually Gs or Gi linked?

A

Gi

400
Q

What is the receptor for melanocortin?

A

MC4 receptor (Gs linked)

Agouti-related peptide is a natural antagonist (orexigenic)

401
Q

What is melanin-concentrating hormone?

A

Expressed in lateral hypothalamus

Major orexigenic peptide (knockouts are lean)

Actions via MCH receptors (Gi linked)

402
Q

Are CRF and TRF orexigenic or anorexigenic?

A

anorexigenic

403
Q

Is CART orexigenic or anorexigenic?

A

Anorexigenic

cocaine- and amphetamien-regulated transcript

404
Q

What other peptides (aside from leptin) regulate feeding and satiety?

A

Insulin, glucose

405
Q

What is ghrelin?

A

Peptide secreated by stomach as a function of fasting (more fasting = more ghrelin)

Strongly orexigenic

406
Q

When is bariatric surgery recommended?

A

Only for extreme cases of obesity

407
Q

Are amphetamines appetite suppressants or appetite enhancers?

A

suppressors

408
Q

What is the function of agents that enhance serotonin (i.e. SSRIs) with respect to eating?

A

Appetite suppressants

409
Q

Are cannabinoids appetite suppressants or enhancers?

A

Enhancers

CB1 receptor activation stimulates appetitie

410
Q

What are medical complications of eating disorders?

A

Gastric reflux, ulcers, dehydration, cardiac arrhtyhmia, constipation, osteoporosis, dental erosion

411
Q

What is the distinguishing feature of anorexia (with purging) vs bulimia?

A

Low weight!

412
Q

What is binge eating disorder?

A

Recurrent binges (eating larger amount of food than others in period of 2 hours; sense of lack of control)

Associated with eating more rapidly; uncomfortably full; eating when not hungry; eating alone; feeling disgusted with self

Not associated with inappropriate compensatory behaviors

413
Q

What objectively defines a binge?

A

Eating an abnormally large amount of food - 3 meals’ worth

414
Q

What behaviors do individuals with eating disorders exhibit?

A

Establishment of rigid rules or exercise rituals

Restricting diet , etc

Breaking rules leads to further restrictions

415
Q

What is the critical period for the development of anorexia nervosa?

A

Adolesence - has gonadal hormones that affect developing brain. Highly sensitive

416
Q

What proportion of individuals recover rom anorexia nervosa?

A

30%

417
Q

Which has a higher incidence in men, anorexia nervosa or bulimia nervosa?

A

Bulimia (only 5:1); Anorexia is 10:1

418
Q

What personality traits do anorexic individuals typically exhibit?

A

Obsessive, preservative and rigid personality styles with difficulty shifting attention

Do well with goal-directed behavior; Do poorly with incorporating feedback and modifying behviors

419
Q

What do neurophysiological models suggest for the basis of anorexia nervosa?

A

Sensitivity of 5-HT system

Neuroendocrine system may fail to adapt back to normal weight during critical window of adaptation (adolescence)

420
Q

What is the role of 5-HT in bulimia?

A

Predisposition of 5HT dysregulation can be implicated

Difficulty regulating the internal drive to eat -> binge

421
Q

What defines sleep?

A

Normal reversible recurring behavioral state of disengagement and unresponsiveness to the environment that is characterized by typical changes in the EEG

422
Q

What is the function of sleep?

A

Ecological/environmental advantage

Physical restoration

Optimization of waking neurocognitive and emotional function

Learning, emotional processing

Health and survival

423
Q

What are the stages of sleep?

A

Waking - alpha waves (8-12 Hz)

Stage 1 - light sleep w/ theta waves (4-7 Hz)

Stage 2 - theta waves w/ sleep spindles and K complexes

Stage 3 & 4 - Deep sleep w/ delta waves (0.5-2 Hz)

424
Q

Which sleep stage do you see sleep spindles and k complexes?

A

Stage 2 of NREM sleep

425
Q

What happens to HR during REM sleep?

A

Increases

426
Q

What is the sleep cycle?

A
427
Q

What is sleep latency?

A

Time from “lights out” to the first NREM stage 1 (usually 10-20 minutes)

428
Q

What is REM latency?

A

Time from sleep onset to ferst REM (usually 90-100 minutes)

Narcolepsy goes right to REM

429
Q

What is sleep efficiency?

A

Amount of sleep/amount of time in bed X 100

430
Q

What is a typical time for sleep latency?

A

10-20 minutes

431
Q

What is a typical amount of time for REM latency?

A

90-100 minutes

432
Q

How do sleep patterns change with age?

A

Infants sleep 2/3 of day; 50% REM

Adults sleep 1/3 of day; less REM

433
Q

What changes do we see in sleep with aging?

A

Increased sleep latency, awakenings, NREM stage 1

Decreased Delta sleep, REM sleep, REM latency, efficiency

434
Q

What are dyssomnias?

A

Too little or too much sleep

435
Q

What are parasomnias?

A

Abnormal behaviors or physiologic events that arise during specific sleep stages or during transitions between wakefulness and sleep

436
Q

What are the primary sleep disorders?

A

Dyssomnias and parasomnias

437
Q

What is sleep apnea?

A

Repetitive episodes of complete or partial cessation of air flow during sleep that often results in oxygen desaturation and terminates with brief arousals

Can be result of reduction of respiratory drive or obstruction

438
Q

What is central sleep apnea?

A

Results from reduction of respiratory drive

439
Q

What is obstructive sleep apnea?

A

Resulting from upper airway obstruction

440
Q

How long must airflow be stopped for it to qualify as apnea?

A

>10 seconds

441
Q

What is hypopnea?

A

Reduction of airflow for > 10 seconds

442
Q

What is a respiratory event-related arousal?

A

Reduction in ariflow for < 10 seconds that results in arousal

443
Q

What is the apnea-hypopnea index (AHI)?

A

Number of apneas and hypopneas per hour

444
Q

What are signs and symptoms of obstructive sleep apnea?

A

Excessive daytime sleepiness unexplained by other factors

Also associated with loud, disruptive snoring; choking/gasping while sleeping; pauses in breathing while sleeping

445
Q

What are the consequences of obstructive sleep apnea?

A

increase in all-cause mortality (3-6x)

CHF (right sided), stroke, HTN

Increased car accidents

Decreased vigilence, executive functioning, coordination

446
Q

Which demographics are more likely to get obstructive sleep apnea?

A

Increasing incidence with age up until 55-65 years old

Males

Obesity is big risk factor

447
Q

What are therapies for obstructive sleep apnea/

A

Weight loss

Positional therapy

Surgery

CPAP masks (positive airway pressure)

Exercises

Avoiding alcohol, sedatives

448
Q

What is different in central sleep apnea from obstructive sleep apnea?

A

There is no respiratory effort during apneic periods

Seen in patients with lower brainstem lesions

449
Q

What is the classic tetrad of narcolepsy?

A

Excessive daytime somnolence, cataplexy, sleep paralysis, and hypnagogic or hypnopompic hallucinatoins

450
Q

What is sleep paralysis?

A

Inability to move when falling asleep or upon awakening

451
Q

What are hypnagogic/hypnopompic hallucinations?

A

Vivid hallucinations during transitoin between wakefulness and sleep

452
Q

What is cataplexy?

A

Sudden intrusions of REM sleep into wakefulness, resulting in emotionally-triggered transient muscle weakness

453
Q

Who gets narcolepsy?

A

Male = Female

Usually in teens, but may occur <10 or >50

454
Q

What is the pathophysiological basis for narcolepsy?

A

Dysfunction of the hypothalamic neuropeptide orexin (hypocretin) - reduced levels

455
Q

What is ondine’s curse?

A

Total loss of automatic breathing, especially during sleep

Apneic periods followed by awakenings

Caused by absent external arcuate nuclei of medulla and depleted neuronal population in medullary respiratiory areas

456
Q

What is shift-work sleep disorder (SWSD)?

A

Excessive sleepiness during work hours that are scheduled during usual sleep period

Insomnia when trying to sleep during usual wake period

Commonly seen in night and early morning shift schedules

Decreased total sleep time, poor sleep quality

457
Q

How do you treat SWSD?

A

(Shift-work sleep disorder)

Maintenence of regular and comperable sleep-wake schedule during work and non-work days

Exclude other causes

Some people can’t handle such schedules

Phototherapy (expose to light to combat somnolence)

Stimulants

458
Q

What demographic gets NREM parasomnias more than REM parasomnias?

A

Children

Older men get REM parasomnias more than NREM parasomnias

459
Q

What sleep stage are NREM parasomnias present in?

A

Delta sleep (NREM 3 or NREM 4)

460
Q

What stage are REM parasomnias present in?

A

REM

461
Q

Are patients with NREM sleep disorders dreaming?

A

NO

462
Q

Are patients with REM parasomnias dreaming?

A

Yes!

463
Q

What are REM parasomnias?

A

Nightmare disorder, REM behavior disorder

464
Q

What are NREM parasomnias?

A

Sleepwalking disorder

Sleep terror disorder

465
Q

Is sleep walking a REM parasomnia?

A

NO! NREM

466
Q

What are LP findings in patients with acute bacterial meningitis?

A

Elevated opening pressure

Low glucose

Elevated protein

Elevated WBC

467
Q

Elevated opening pressure on LP. Low glucose, high protein and high WBC. What are you thinking?

A

Acute bacterial meningitis

468
Q

What are the most common causes of meningitis in adults?

A

S. pneumoniae

N. meningitidis - scariest

H. influenzae

469
Q

What are the most common causes of meningitis in adults 60 yo or older?

A

S. pneumoniae

L. monocytogenes

470
Q

What are the most common causes of meningitis in neonates?

A

Group B Strep

E. coli

Listeria monocytogenes

Other gram-negatives

Not N. meningitidis

471
Q

What is a serious complication of acute bacterial meningitis?

A

Secondary vasculitis

Can cause infarcts

472
Q

What are predisposing factors for meningococcal meningitis?

A

Close contact

Crowding (college dorms, barracks, etc)

473
Q

How do you treat meningococcal meningitis?

A

Rifampin to those exposed

474
Q

What is this petichial purpura rash indicative of?

A

Meningococcal septicemia

475
Q

What is waterhouse-friderichsen Syndrome?

A

Bleeding into adrenal gland due to severe bacterial infection

Usually N. meningitidis

leads to adrenal failure and hypotension

476
Q

How can you prevent bacterial meningitis?

A

Vaccination!

H. flu, N. meningitidis, S. pneumoniae are available

477
Q

How do you treat bacterial meningitis?

A

Antibiotics immediately

3rd or 4th gen cephalosporin + ampicillin; PCN

HIV = add RIPE therapy

Meningococcal = Rifampin

Corticosteroids can help vasculitis

Must cross BBB

478
Q

What signs would you see in a neonate with bacterial meningitis?

A

Signs may be absent

Can see bulging fontanelles due to elevated ICP

Caused by GBS, E. coli

479
Q

In which patients would you expect to not see meningeal signs in bacterial meningitis?

A

Neonates

Alcoholics

Elderly

Immunosuppressed

480
Q

In a patient with a subacute meningitis, what are you thinking?

A

Abscess

Atypical infection (syphilis, lyme, TB)

Fungus

Protozoa

parasite

481
Q

What are the most common causes of viral meningitis?

A

Coxsackie B

Echovirus (enterovirus)

HIV

HSV-2

West Nile Virus (arbovirus)

482
Q

What is seen in the CSF of a patient wtih viral meningitis?

A

Lymphocytes

Glucose and protein are normal / slightly decreased

483
Q

What do abscesses mimic?

A

Brain tumors

focal neurological signs

40% don’t present with fever

Obtundation

Herniation

484
Q

What do you see on LP in tuberculous meningitis?

A

Very high protein

Very low CSF glucose (extremes)

High WBC

485
Q

What are the symptoms of neurosyphilis?

A

Cranial nerve lesions

Peresis with psychological symptoms

486
Q

What do you see in the CSF of a neurosyphilis patient?

A

Positive CSF VDRL

Negative VDRL does not rule out

Negative CSF FTA rules out neurosyphilis

Positive CSF FTA doesn’t make diagnosis

487
Q

What are the primary pathogens that cause fungal infections?

A

Cyrptococcus neoformans

Histoplasma capsulatum

Coccioides immitis

Paracoccidioides barziliensis

Blastomyces dermatitidis

Apsergillus, candida, mucorales (opportunistic)

488
Q

When do you see cryptococcal meningitis?

A

AIDS patients or immunosuppressed

489
Q

What do you see on CSF of cryptococcal meningitis?

A

Elevated OP

elevated WBCs

Low glucose

Elevated protein

Budding yeast

490
Q

What is mucormycosis?

A

Most aggressive fungal infection

Seen in diabetics: ketoacidosis, not hyperglycemia

Spreads via cavernous sinu

491
Q

What type of infection would you suspect in a patient with diabetes in ketoacidosis presenting with cavernous sinus thrombosis?

A

Mucormycosis

492
Q

What would you suspect in a patient presenting with meningitis/neurological symptoms who had been swimming in warm ponds?

A

Naegleria fowleri

“Brain Eating Amoeba”

Directly spread from nasal cavity

493
Q

What infectious agent is associated with transmission from domestic cats and other felines and can present with multiple ring enhancing lesions on CT?

A

Toxoplasmosis

494
Q

What are causes of encephalitis?

A

Virauses

Enterovirus, HSV-1, arbovirus

495
Q

Does HSV-1 or HSV-2 cause encephalitis?

A

HSV-1

496
Q

Does HSV-1 or HSV-2 cause meningitis?

A

HSV-2

497
Q

What are signs of herpes simplex encephalitis? What causes it?

A

Aphasia

Impaired memory

Temporal lobe sharp waves on EEG

Get PCR to confirm

Tx with acyclovir

HSV-1 causes encephalitis

498
Q

What are localizing symptoms of brain tumors?

A

Aphasia

Weakness

Visual field cut

Seizures

Hemi-neglect

Gait disturbances

Incoordination

499
Q

What are non-localizing sympoms of brain tumors?

A

Headache

N/V

Mental status changes

Caused by increased ICP

500
Q

What is the location of most adult brain tumors?

A

Supratentorial

Brain and Behavior (9 decks)

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