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Brain and Behavior > Exam 3 Deck 1 > Flashcards

Exam 3 Deck 1 Flashcards

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1
Q

What is the function of the cerebellum?

A

Key structure for motor learning and coordination

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2
Q

What is the main symptom of cerebellar damage?

A

Ataxia - issues synthesizing smooth, well-timed and proportional movements

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3
Q

What are the cerebellar lobes?

A

Anterior, posterior, flocculonodular

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4
Q

What are the Identify the anterior lobe of the cerebellum.

A
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5
Q

Identify the posterior lobe of the cerebellum

A
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6
Q

Identify the flocculonodular lobe of the cerebellum

A
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7
Q

What is a folium?

A

Equivalent to a gyrus in the cerebellum

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8
Q

What is a cerebellar lobule?

A

A combination of multiple folia in the cerebellum

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9
Q

Identify the primary fissure of the cerebellum

A
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10
Q

Identify the postero-lateral fissure of the cerebellum.

A
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11
Q

Idnetify the horizontal fissure of the cerebellum

A
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12
Q

What connections pass through the inferior cerebellar peduncle?

A

Connections fromthe medulla and spinal cord to the cerebellum

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13
Q

What information passes through the middle cerebellar peduncle?

A

Connections from the pontine nuclei to the cerebellum

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14
Q

What information passes through the superior cerebellar peduncle?

A

Exiting efferents from the cerebellum (except vestibular), and afferent ventral spinocerebellar tract axons

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15
Q

Where is the fastigial nucleus found?

A

In the vermis

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16
Q

Where is the interposed nucleus found?

A

Between fastigial and dentate nucleus

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17
Q

Where is the dentate nucleus found?

A

Lateral cerebellum

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18
Q

Identify the fastigial nucleus

A
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19
Q

Identify the interposed nucleus

A
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20
Q

Identify the dentate nucleus

A
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21
Q

What is the spinocerebellum?

A

Vermis and intermediate hemisphere

Contains somatotopic representations of the head nad body and sends efferents to spinal motor nuclear tracts

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22
Q

Which part of the spinocerebellum receives axial body input and projects through medial descending motor systems?

A

Vermis

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23
Q

Which part of the spinocerebellum receives distal body inputs and projects through lateral descending systems?

A

Paravermis (intermediate hemisphere sections)

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24
Q

What are the lateral hemispheres of the cerebellum responsible for?

A

Cerebrocerebellum - receive input from cerebral cortex via the pontine nuclei and do not receive direct somatosensory input

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25
Q

What is the flocculonodular lobe of the cerebellum responsible for?

A

The vestibular cerebellum.

Connectivity breaks all the rules of the other cerebellar structures

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26
Q

What is the part of the cerebellum responsible for vestibular functions?

A

flocculonodular lobe

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27
Q

What are the four spinocerebellar tracts?

A

Dorsal spinocerebellar tract - lower boddy proprioception

Ventral spinocerebellar tract - lower boddy error signal

Cuneocerebellar tract - upper body proprioception

Rostra spinocerebellar tract - upper body error signal

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28
Q

Which spinocerebellar tracts are involved with proprioception?

A

Cuneocerebellar tract (upper body)

Dorsal spinocerebellar tract (lower body)

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29
Q

Which spinocerebellar tracts are involved with transmitting error signals?

A

Rostral spinocerebellar tract (upper body)

Ventral spinocerebellar tract (lower body)

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30
Q

Which spinocerebellar tracts go to the lower body?

A

Dorsal and ventral spinocerebellar tracts

dorsal = proprioception; ventral = error signal

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31
Q

Which spinocerebellar tracts go to the upper body?

A

Cuneocerebellar tract = proprioception

Rostral spinocerebellar tract = error signal

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32
Q

What is the dorsal spinocerebellar tract?

A

Ipsilateral lower body proprioceptive tract

Muscle spindle afferents carry proprioception from lower body climb up the fasciculus gracilus and terminate in Clarke’s nucleus. Project through ipsilateral dorsolateral funiculus and inferior cerebellar peduncle to the intermediate zone of cerebellum

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33
Q

What is the cuneocerebellar tracts?

A

Proprioceptive upper body spinocerebellar tract

Ipsilateral

Muscle spindle afferents carry proprioceptive info to external cuneate nucleus. These axons travel up with teh dorsal spinocerebellar tract and end in intermediate zone of cerebellar cortex

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34
Q

What is the ventral spinocerebellar tract?

A

Lower body error signal spinocerebellar tract

Contralateral ascent, re-cross in cerebellum

GTO afferents project to spinal interneurons. Cross in spinal cord and ascend in the ventrolateral funiculus

Travel through superior cerebellar peduncle and recross midline

Cerebellar projection is ipsilateral

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35
Q

What is the rostral spinocerebellar tract?

A

Upper body error signal tract

GTO to interneurons through inferior cerebellar peduncle to cerebellum

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36
Q

Which spinocerebellar tracts course through the inferior cerebellar peduncle?

A

Cuneocerebellar, dorsal spinocerebellar, rostral spinocerebellar

Ventral spinocerebellar courses through the superior cerebellar peduncle

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37
Q

Which spinocerebellar tract courses through the superior cerebellar peduncle?

A

Ventral spinocerebellar tract

Dorsal, cuneocerebellar, and rostral course through inferior peduncle

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38
Q

What are the inputs to the cerebellum?

A

Spinocerebellar tracts (4 of them)

Reticular formation

Vestibular nerve, nuclei

Pontine nuclei

Inferior olivary complex

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39
Q

What are the layers of the cerebellar cortex?

A

Molecular = closest to pia

Purkinje = middle

Granular = deepest

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40
Q

Which cells are the key to the cerebellar cortex?

A

Purkinje cells

Reside in the purkinje layer

GABAergic, inhibitory neurons

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41
Q

What cells reside in the molecular layer?

A

Purkinje cell apical dendritic trees (perpendicular to long axis)

Climing fiber axon terminals - which provide direct, convergent input to purkinje cells

Stellate cells = inhibitory interneurons to Purkinje dendrites

Basket cells = inhibitory interneurons to Purkinje cell bodies

Excitatory parallel fibers (course parallel to long axis)

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42
Q

What are the climbing fibers?

A

Synapse directly to Purkinje cells and arise from the Inferior Olivary Complex

Provide convergent excitation (one purkinje cell receives input from one climbing fiber; but each climbing fiber innervates only a few Purkinje cells; however, the climbing fibers make thousands of synapses on each Purkinje)

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43
Q

What are mossy fibers?

A

Provide input from all sources except inferior olivary complex

Provide indirect input to purkinje cells. Relayed via parallel fibers of granule cells located in glomeruli

These convey excitatory information to large number of Purkinje cells

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44
Q

What is a cerebellar glomerulus?

A

Located in granular layer

Comprised of mossy fiber axon terminal (excitatory; Golgi cell axon terminal (inhibitory) and several post-synaptic granule cell dendrites

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45
Q

Describe the inputs of cerebellar cortex

A
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46
Q

What are the outputs of the cerebellar cortex?

A

Purkinje cell is the only output

Project to cerebellar nuclei or to the vestibular cerebellum

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47
Q

How doe the cerebellum control pusture?

A

Flocculonodular lobe and vermis project to the vestibular nuclei of the brainstem (bilaterally) with no cerebellar relay. From here goes to reticulospinal and vestibulospinal tracts to the axial, neck muscles

Some vermis projections to the vestibular nuclei relay through the fastigial nucleus

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48
Q

How does the cerebellum control motor control?

A

Paravermis nuclei (interposed nuclei = globulose and emboliform nuclei) project through the superior cerebellar peduncle to the contralateral red nucleus (decussates)

Activate rubro-olivary tract (red nucleus to inf. olivary complex, to cerebellar peduncle and climbing fibers)

Activate rubrospinal tract (red nucleus to midbrain decussation to distal misculature)

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49
Q

How does the cerebellum control motor planning?

A

Lateral hemispheres of the cerebellum project to the dentate nuclei which send axons through superior cerebellar peduncle to the VLp in the thalamus (contralateral). These go to the cerebral cortex which send projections to the distal musculature through corticospinal tract

Dentate nuclei also project to red nucleus , which lets the red nucleus integrate info from paravermal intermediate zone and lateral hemispheres

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50
Q

Why are cerebellar deficits always ipsilateral to the lesion?

A

All outpus (except vestibular) course through the superior cerebellar peduncle. This decussates as it ascends and targets the red nucleus and cerebellar cortex through the thalamus. The resulting descending tracts also cross (back) to the muscles of the ipsilateral side of the lesion

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51
Q

What are cardinal features of cerebellar dysfunction?

A

Ataxia

Decomposition of movement

Dysarthria

Dysdiadochokinesea

Dysmetria

Hypotonia
Nystagmus

Scanning Speech

Tremor

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52
Q

What is ataxia?

A

Reeling, or wide-based gait

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53
Q

What is decomposition of movement?

A

Inability to correctly sequence fine coordinated acts

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54
Q

What is dysarthria?

A

Inability to articulate words correctly with slurring and inappropriate phrasing

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55
Q

What is dysdiadochokinesia?

A

Inability to perform rapid altering movements

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56
Q

What is dysmetria?

A

Inability to control range of movement (abnormal trajectories through space)

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57
Q

What is hypotonia?

A

Decreased muscle tone

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58
Q

What is scanning speech??

A

Slow enunciation with a tendency to hesitate at the beginning of a word or syllable

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59
Q

What is tremor?

A

Rhythmic, alternating, oscillatory movement of a limb as it approaches a target (intention tremor)

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60
Q

What are features of Vermis Syndromes?

A

Symptoms that affect the trunk

Wide-based gait and stance

Truncal titubations (staggering)

Arm and leg coordination are spared

Gait abnromalities not improved by visual orientation (indiscriminate falling)

Eye movement disturbances

Rotated postures of head

Test by tandem toe-heel walking; walking backwards; hop on each foot; romberg

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61
Q

What is the most common cause of midline (vermis) cerebellar syndromes?

A

Chronic alcohol use

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62
Q

What are symptoms of hemispheric cerebellar syndromes?

A

Appendicular ataxia - loss of coordination of limbs ipsilateral to lesion

Impaired rapid alternating movements

Gait abnormalities not improved by visual orientation - fall toward lesion

Dysdiadochokinesia, Dysarthria, Dysmetria

Tremors

Hypotonia

Test with rapidly alternating movements (finger to nose, heel-knee-shin), check and rebound, past pointing

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63
Q

What are common causes of cerebellar hemisphereic syndromes?

A

Metastasis, infarcts, abcesses

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64
Q

What are pancerebellar syndromes?

A

Combination of vermis and hemispheric syndromes

Can be caused by infectious processes, hypoglycemia, paraneoplastic disorders, drunkenness

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65
Q

What oculomotor dysfunctions are commonly seen in cerebellar disorders?

A

Nystagmus (gaze evoked, upbeat, rebound)

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66
Q

What is the Romberg Sign?

A

Close eyes and stand still

Patients will fall with both cerebellar and posterior column disease

With eyes open, patients with cerebellar disease will fall.

Posterior column defecits will present with eyes closed (falling out of shower)

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67
Q

What do cerebellar tremors present as?

A

Intention tremors

Occur during purposeful/directed movement (especially near end)

Usually slow frequency, coarse, and broad

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68
Q

What do non-cerebellar tremors present as?

A

Resting tremors, usually

Occur maximally at rest and decrease with activity

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69
Q

What structures are likely affected in a patient with a resting tremor that improves with motion?

A

Not cerebellum!

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70
Q

What structure is likely affected in a patient with a tremor that worsens with movement and is worse at the end of a movement towards an object?

A

Cerebellum!

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71
Q

What is a resting tremor?

A

Maximal at rest

Decreases with activity

Usually symptom of Parkinson’s

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72
Q

What is a postural tremor?

A

Maximal with limb in a fixed position against gravity

Gradual onset suggests physioloic or essential tremmor

Acute onset suggests toxic/metabolic disorder

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73
Q

What is an intention tremor?

A

Maximal during movement toward a target (finger to nose)

Suggests cerebellar disorder but may be due to somethign else (MS, Wilson’s)

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74
Q

What is asterixis?

A

Flapping “tremor” in wrist due to liver failure (think metabolic)

Caused by interruptions of contraction in wrist extensors

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75
Q

What is a pill-rolling tremor indicative of?

A

Parkinsons!

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76
Q

What do dysfunctions of the basal ganglia present as?

A

Motor behavior and reward seeking deficits

Tremor, rigidity, dyskinesias, loss of postural reflexes, chorea, ballismus, dystonia, addiction

Parkinson’s, Huntingtons, Tourette’s, hemibalismus are diseases

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77
Q

What are the components of the basal ganglia system?

A

Striatum (dorsal = caudate nucleus + putamen; ventral = nucleus accumbens septi)

Pallidum (external, internal, ventral)

Substantia nigra (compacta, reticulata)

Ventral tegmental area

Subthalamic nucleus

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78
Q

What are the major inputs to the basal ganglia system?

A

Cerebral cortex (huge) - glutamatergic

Thalamus - glutamatergic

Midbrain - dopaminergic

Raphe nuclei - serotinergic

Locus ceruleus - noerepinephrine

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79
Q

How is cerebral cortical input to the basal ganglia organized?

A

Topographically

from all areas, but especially the frontal lobe

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80
Q

Where does thalamic input to the basal ganglia originate from?

A

Ventral group (VA/VM; VLa)

Inrtralaminar nuclei (CM)

Medial Dorsal Nucleus (MD)

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81
Q

What are the main efferent cells of the striatum?

A

Medium Spiny Neurons (GABA-ergic)

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82
Q

What are the two subtypes of the medium spiny neurons of the striatum?

A

Substance-P colocalizing neurons with D1 receptors (excitatory)

Enkephalin colocalizing neurons with D2 receptors (inhibitory)

Project to Globus Pallidus and Substantia Nigra

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83
Q

What are the components of the striatum?

A

Dorsal = caudate and putamen

Ventral = nucleus accumbens septi, olfactory tubercule

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84
Q

What is the dorsal striatum?

A

Putamen and caudate nucleus

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85
Q

What is the ventral striatum?

A

Nucleus accumbens and olfactory tubercule

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86
Q

What is the subthalamic nucleus?

A

STN - pod-shaped, located rostral and lateral to substantia nigra

Output is excitatory (Glutamatergic)

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87
Q

What is the globus pallidus?

A

Located lateral to the interanl capsule and medial to the putamen

3 parts: External, internal, ventral

External (GPe) and inner (GPi) are dorsal pallidum; ventral pallidum (VP) is ventral to anterior commissure

All are GABAergic

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88
Q

What is the substantia nigra?

A

Two parts (pars reticulata (SNpr), and pars compacta (SNpc))

SNpr is caudomedial extension of GPi = both are GABAergic

SNpc is midbrain dopaminergic cell group that provides input to striatal MSN

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89
Q

Which are the major output centers of the basal ganglia?

A

GPi, SNpr and VP

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90
Q

Which basal ganglia output center contorls head and neck motor control?

A

SNpr

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91
Q

Which basal ganglia output center controls motor body function?

A

GPi

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92
Q

How does output to the pyramidal system occur from the basal ganglia?

A

GPi/SNpr axons travel to thalamus via ansa lenticularis and lenticular fasciculus

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93
Q

What are the important functions of the ansa lenticularis and lenticular fasciculus?

A

Tracts of output from the GPi/SNpr axons to the thalamus

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94
Q

What are the pathologic hallmark of parkinson’s disease?

A

Lewy bodies

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95
Q

What is a lewy body?

A

Pathologic hallmark for Parkinson’s Disease

Eosinophilic inclusion in neuron made of alpha synuclein and ubiquitin

Classically in Substantia Nigra, but also found elsewhere

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96
Q

How is Parkinson’s diagnosed?

A

Clinically

Cardinal signs:

Bradykinesia, rigidity, tremor, postural instability

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97
Q

What is the characteristic parkinson’s tremor?

A

3Hz, 3-5Hz, pill rolling

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98
Q

How is Parkinson’s treated?

A

Symptomatically - no cure

Levodopa (precursor to dopamine that crosses BBB)

MAOI -B inhibitors - increases dopamine levels

COMT inhibitors - keep plasma levodopa levels high

Amantadine - antiviral agent that keeps endogenous dopamine levels high

Anticholinergics

Deep brain Stimulation

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99
Q

What is Lewy Body Dementia?

A

Parkinsonism, dementia, fluctuations in arousal and attention, myoclonus, visual hallucinations

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100
Q

What is progressive supranuclear palsy (PSP)?

A

Symmetric Parkinsonism

Early postural instability with falls

Typically onset after 70 years old, and no response to levodopa

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101
Q

What is Cortical basal ganglionic degeneration?

A

Rare condition with onset in 60s or 70s with rapid course

Asymmetric, atremulous parkinsonism

Cortical involvement with issues writing, aphasia

no response to levodopa

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102
Q

What is multiple system atrophy?

A

Onset in 40s-60s and can mimic Parkinson’s

parkinsonian, cerebellar, or autonomic

early autonomic dysfunction (orthostatic, incontinence)

symmetrical parkinsonism, with rapid progression

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103
Q

What is Wilson’s Disease?

A

Movement disorders that present at 10-25 years old with liver disease

(liver + neuro/psych = wilsons)

Can lead to renal failure, retardation

Dysarthria, dystonia, tremor, parkinsonism, Kaiser Fleischer rings (copper in cornea),

Autosomal recessive caused by mutations in copper transporter ATPase. Causes copper accumulation

If under 50 with parkinsonism = test for Wilsons!

Treat with chelators!!!!

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104
Q

What is Huntington’s Disease?

A

Chorea - starts as clumsiness/fidgetiness progresses to full chorea

Dysarthria, dysphagia, motor impersistence

Parkinsonism

Depression, psychosis, dementia

Slowed saccades

Atrophy of the striatum - particularly caudate

Initially degenerates indirect pathway, eventually both

Treat with Dopa antagonists and Dopa depleting agents

Autosomal dominant - CAG repeats in huntingtin gene (Chr 4 >38 repeats

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105
Q

What is chorea?

A

Involuntary continual irregualr and unsustained movements

Not predicatable or suppresable

Motor impersistence, mild hypotonia

In Huntingtons, side effect of L-Dopa, antipsychotics

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106
Q

What are tics?

A

Unvoluntary production of movements, sounds

Premonition sensation, suppressible, suggestible, stereotyped

Childhood onset, co-occurs with OCD, ADHD (Tourette’s)

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107
Q

What are tremors?

A

Involuntary rhythmic oscillations, usually 3-12 Hz

Essentail tremor = head, hands voice (6Hz)

Cerebellar dysfunction = 3 Hz

Parkinsonism = 3Hz

Alcohol improves essential tremor

Treat with DBS, botulinum, anticonvulsants

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108
Q

What is dystonia?

A

Slow, twisting, repetitive movements that produce abnormal postures

Task specific, persist over time, spread

Sensory tricks can aleviate

Dopamine, ACh dysfunction in basal ganglia

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109
Q

What happens in hypokinesis?

A

Indirect pathway dominates over direct pathway - net inhibition of thalamus - decreased cortical output - decreased quality of movement

Parkinsons = loss of Dopaminergic SNpc neurons

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110
Q

What happens in hyperkinesis?

A

Direct pathwya predominates over indirect pathway with net disinhibition of the thalamus - increased cortical signals - increased movement

Huntingtons - death of neurons that initiate indirect pathway; D1 Substance P MSNs are spared, but lost over time

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111
Q

What two main category of symptoms is OCD characterized by?

A

Obsessions and compulsions

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112
Q

What are obsessions?

A

Recurrent, persistent thoughts, urges, or images experienced as intrusive and unwanted, usually causing marked distress

Affective individuals attempt to ignore, suppress or neutralize such obsessions with another thought or action

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113
Q

What are compulsions?

A

Repetitive behaviors or mental acts that a person feels driven to perform in response toa n obsession or according to rules that must be rigidly applied

Aimed at preventing or reducing distress or preventing some dreaded event or situation

Usually unrealistic, excessive and may reduce anxiety, but are not pleasurable.

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114
Q

What are the features of obssessions and compulsions that meet the diagnostic critera for OCD?

A

Time consuming, lasting more than one hour per day

Associated with significant distress or impairment

Insight can vary, and OCD patients usually recognize/acknowledge at some point that their obsessions/compulsions are unrealistic or excessive

Some have lifetime history of chronic tic disorder

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115
Q

What is the lifetime prevalence of OCD?

A

2-3%

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116
Q

When is onset of OCD most common?

A

Childhood (over 50% of new cases in children)

Course is typically chronic and sometimes disabling

Men and women are affected equally

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117
Q

What is the gender distribution of OCD?

A

Equal

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118
Q

What are some typical obsessions in OCD patients?

A

Contamination

Aggression

Safety/harm

Sex

Religion (scrupulosity)

Somatic Fears

Need for symmetry or exactness

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119
Q

What are typical compulsions in OCD?

A

Cleaning/Washing

Checking

Ordering/Arranging

Counting

Repeating

Hoarding/Collecting

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120
Q

What is Tourette’s Syndrome?

A

Disorder in which affected individuals have motor and vocal tics that occur many times a day nearly every day for at least one year

Onset is usually before 18 years old

Significant comorbidity with OCD, likely due to the role of basal ganglia and genetic factors that overlap in the two disorders

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121
Q

What are primary headache syndromes?

A

Physiological disruption

Migraine
Tension type

Cluster

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122
Q

What are secondary headache syndromes?

A

Pathology + physiology

Neoplasm

Infection

Aneurysm

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123
Q

What is the most common type of headache?

A

Tension headache

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124
Q

What is the most common type of headache that physicians see?

A

Migraines

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125
Q

What defines a migraine without aura?

A

At least 5 attacks

Headache lasts 4-72 hours

Two of: unilateral, pulsatile, moderate/severe pain, aggravation or avoidance of physical activity

One of: N/V, photophobia and phonophobia

Not attributable to somethign else

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126
Q

What defines a migraine with aura?

A

At least two of:

Aura with fully reversible visual, sensory, or dysphasic speech symptoms

Homonymous visual or unilateral sensory symptoms; 1 aura symptom developing over 5 minutes, or different symptoms in succession over 5 minutes

Headaches fulfill criterea for migraine without aura

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127
Q

How does cerebral blood flow correlate with headache?

A

Prodrome - nothing

Aura - nothing

Headaceh - increased flow

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128
Q

How do you determine whether the origin of a headache is opthalmic?

A

All ocular causes of headache are associated with changes in the external apperance of the eye

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129
Q

How do the timing and topography of cerebral blood flow, aura, and headache relate to each other during migraine attacks?

A

Pain begins during hypoperfusion phase

Hyperperfusion may outlast pain

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130
Q

What is cortical spreading depression?

A

Devleopment of waveform in brain that causes period of activation followed by refractory period of depression

Crawls at 3mm/minute from brainstem, up to occiput, and then forward through brain

I.e. activation = aura; depression = blindness

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131
Q

Describe threshold of transcranial magnetic stimulation of a patient with migraines compared to normal.

A

Migraines - lower thereshold (brain is ‘excitable’)

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132
Q

What brain structures get activated at the onset of migraines?

A

Brainstem centers - periaqueductal grey turns on during migraine attack

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133
Q

What structures is primarily involved in migraines that can explain symptoms?

A

Meninges!

Cortical spreading depression causes release of vasodilatory mediators in the brain that cause meninges to expand/be inflamed

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134
Q

What is the cheiro oral phenomenon?

A

Numbing/tingling of cheek and hand (which then spreads)

Almost pathognomonic for migraines

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135
Q

If a patient walks in with headache symptoms and a tingling/numbing of the mouth and a hand, that progressively spreads up arm, what are you thinking?

A

Migraine

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136
Q

What is the funciton of glial cells, and what about their normal physiology is important to migraines?

A

They redistribute K, Mg, and excitatory amino acids

Lowest numbers in primary occipital cortex (i.e. if glia aren’t working well, the occipital lobe will take a hit)

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137
Q

What is the role of astrocytes in migraines?

A

Astrocyte calcium waves could mediate propagated cortical phenomena of migraine via release of neuroactive and vasoactive messengers

Astrocyte waves can explain cortical activity changes in the absence of cortical spreading depression

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138
Q

What is a tension-type headache?

A

Bilateral, band-like pressing headache

Not aggravated by activity

Little or no nausea, photophobia, or phonophobia

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139
Q

What are the diagnostic criteria for tension-type headache?

A

Essentially: not a migraine

Bilateral, steady non-pulsatile pain, not affected by movement,

Not associated with N/V, nor photophobia nor phonophobia

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140
Q

Can migraines present with neck pain?

A

yes

Migraines are often misdiagnosed because of neck pain leading to the diagnosis of tension headache

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141
Q

What is the physiology of neck pain that can be seen in migraines?

A

It is a referred pain phenomenon

Trigeminal nucleus caudalis extends to dorsal horn C2, C3, C4 => causes neck pain and posterior head pain.

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142
Q

What is the trigeminal autonomic reflex?

A

Irritation of trigeminal nerve causes activaiton of parasympathetic nucleus which causes lacrimation, rhinorrhea, nasal congestion

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143
Q

What is the tearing/sniffling/congestion reaction to cold/spicy/etc called?

A

Trigeminal autonomic reflex

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144
Q

What are some symptoms of children with migraines?

A

Benign paroxysmal vertigo of childhood

Alternating hemiplegia

Cyclic vomiting

Recurring abdominal pain

Benign torticollis

Acute confusional migraine

Car sickness

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145
Q

What is sinus headache?

A

NOT actually a thing.

Commonly diagnosed as headache secondary to sinusitis in the US - leads to overprescription of antibiotics

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146
Q

What are more serious complications of migraines?

A

Progression in severity

Migrainous stroke

Persistent aura without infarction

Epilepsy

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147
Q

What neurological issues does migraine put you at an elevated risk for?

A

Stroke

Epilepsy

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148
Q

What are you likely to see if you order an MRI for a migraine patient?

A

White matter changes that may be misdiagnosed as MS plaques, vasculitis, etc.

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149
Q

Generally speaking, what is the timeframe of primary headache syndromes?

A

Months to years

Shorter is likely to be a secondary headache

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150
Q

Which structures in the head are pain sensitive?

A

Meninges

Neural Structures (Trigeminal, Glossopharyngeal, Vagus CNs)

Scalp + Superficial structures

Vasculature

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151
Q

What are red flags that a headache is not a primary headache syndrome?

A

• A new or different headache

– ≤5 years old

– ≥50 years old

  • Abrupt onset
  • Cancer, HIV, pregnancy
  • Abnormal physical exam
  • Neuro symptoms ≥ one hour
  • Headache onset

– With seizure or syncope – With exertion, sex, or

Valsalva

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152
Q

How do headaches due to brain tumors present?

A

Similar to tension headaches in most patients

Can be migraine like

“Classical” brain tumor headache is only 8%

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153
Q

What type of headache do patients with brain abscesses get?

A

Same as brain tumor

Fever in 1/2 of cases

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154
Q

Patient with frontal headache which increase with straining and are awekening out of sleep. Also papiledema, and dysmenorrhea. What type of headache?

A

Idiopathic intracranial hypertension

Pseudotumor cerebri

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155
Q

What are characteristics of headaches of idiopathic intracranial hypertension?

A

brain tumor headache

Visual complaints (diploplia, TVOs, photopsias)

Cranial bruits, noises in head, pulsatile tinnitus

N/V

radiculopathies

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156
Q

What do you treat idiopathic intracranial hypertension with?

A

Try to correct predisposing factors (weight loss, diuresis, shunting)

Try to preserve vision - optic nerve sheath fenestration

Symptoms

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157
Q

What is a hypnic headache syndrome?

A

Rare disorder in older people (40-84 y/o)

Bilateral throbbing headache

Recurring 1-3 times nightly with no other associated symptoms

Treat with lithium, caffeine, flunarizine

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158
Q

What types of headaches are seen with patients who had strokes?

A

Abrupt or gradual

Severity not associated with size of infarct

Headache can be multifocal or migratory - pain can move down arms, etc)

Not migraine in older patients (would have had a history)

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159
Q

What must you consider in a patient with “complicated” migraine presentation who is older?

A

Not only migraine (but may be less likely due to age)

Consider tumors, strokes, sensory seizures, etc.

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160
Q

How do sub-arachnoid hemmorage present as?

A

Abrupt onset of severe headache (reaches full intensity instantly - or close)

(Aneurysm burst)

Seizures and diploplia can be seen

Perform non-contrast CT, LP

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161
Q

What is thunderclap headache?

A

Headache seen in survivors of Berry aneurysm

Can be caused by aneurysmal or nonaneurysmal subarachnoid hemmorrage

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162
Q

What distinguishes a thunderclap headache from a subarachnoid hemmorrhage?

A

Seizures adn diploplia seen in SAH

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163
Q

What is a cluster headache?

A

Intense, boring (knife-like pain, very severe), unilateral pain

Quicker onset (over span of minutes)

Eyes tear and nose runs - autonomic involvement

Horner’s Syndrome (ptosis and miosis)

Episodic - bouts of headache that last 1-4 months. Follow circadian pattern within and between cycles

Chronic - may evolve from episodic form or be chronic from onset. Absence of circadian patterns

Headaches with manic symptoms - almost opposite of migraine

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164
Q

What is temporomandibular dysfunction?

A

Pain that can be around the ear while chewing

Can go away quickly, but can persist too

Click may be heard over ear while jaw opening.

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165
Q

What type of headache can present with giant cell arteritis (temporal arteritis)?

A

Generalized, throbbing, temporal pain

Claudication - worsens with exertion

Polymyalgia rheumatica in 50% (aches and pains, maybe fever)

Visual scintillations

CRP or ESR abnormalities indicate biopsy

TREAT WITH CORTICOSTEROIDS

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166
Q

What type of headaches can be seen with angina?

A

Jaw, tip of nose, brow, bregma, occiput, palate, …. (anywhere really)

Extremities, shoulder pain

Rarely below umbilicus

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167
Q

What type of headache do you see with sexual activity?

A

Explosive, throbbing, occipital or frontal

Lasts for hours

Confusional state or symptoms of ischemia

(occur with valsalva too)

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168
Q

What symptoms can you see withs pontaneous carotid artery dissection?

A

Seen in young and middle age

Risk factors include trauma, arteriopathies, family history, respiratory infection

Headaches, neck pain, horner’s syndrome

Cerebral ischemia

Tx: anticoagulation

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169
Q

If a patient presents with unilateral throbbing headache with pain of the face, neck, worse with movement, Horner’s Syndrome, and a recent URI; what do you suspect?

A

Spontaneous carotid artery dissection

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170
Q

What can cause low-pressure headache?

A

Meningeal diverticula

Dural root sleeve tears

Excessive coughs

Erosion of dura from adjacent lesions

Head trauma

overshunting/carbonic anhydrase inhibitors

Lumbar puncture (esp. in thin females)

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171
Q

What is a common issue that can develop in thin female patients who have lumbar punctures?

A

Low-pressure headacehs

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172
Q

How do you treat low-pressure headaches?

A

IV Na caffeine benzoate

Epidural blood patch (if post-LP)

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173
Q

What is beta-2-transferrin?

A

Indicator of CSF

If seen in rhinorrhea, indicative of CSF leak

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174
Q

What do you suspect if you identify beta-2-transferrin in rhinorrhea?

A

CSF leak

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175
Q

What is POTS?

A

Postural orthostatic tachychardia syndrome

Seen in young post pubertal females

See orthostatic and non-orthostatic headache

Fatigue, decreased concentration, exercise intolerance, syncope

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176
Q

How do you treat POTS?

A

Hydration and salts

Elastic stockings

Beta blockers, fludrocortisone, minodrine, indomethacin

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177
Q

72 year old male, developed sharp pains in his right cheek and lip. These increased with light touch and he was nearly unable to shave or eat. His neurological examination was entirely normal. What do you suspect?

A

Trigeminal Neuralgia

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178
Q

What is trigeminal neuralgia??

A

Brief paroxysms of electric-like, lancinating pains (stabbing)

Usually affects V2 and V3

Stimulation of trigger points induces attacks

Suggest structural disease - demyelinated nerve-root area

Seen more in older patients. In younger patients think neurodegenerative disease

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179
Q

How does trigeminal neuralgia occur in older patients?

A

Superior Cerebellar Artery rubs against trigeminal nerve root and causes demyelination - origin of pain

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180
Q

How does trigeminal neuralgia occurs in younger patients?

A

Demyelinating process of trigeminal nerve

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181
Q

What is primary stabbing headache?

A

New onset, sharp, shooting pain in temple and behind eye

Not triggered by cutaneous stimuli

Preceded by days of euphoria

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182
Q

What sequence of events occurs during excitotoxicity?

A

Injury (ischemia, trauma, etc) leads to a decreased ATP state in the neuron.

This causes increased Na and Ca levels, depolarizing membrane potential.

Glutamate is increased extracellularly, exciting neighboring neurons.

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183
Q

What is chromatolysis?

A

Apoptosis of neurons

Shown here surrounded by healthy neurons with intact Nissl bodies

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184
Q

What is neurapraxia?

A

Focal demyelination of a neuron

Leads to a loss in conduction velocity of the axon - neuron stays in tact

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185
Q

What is axonotmesis?

A

Axon is cut and the distal part is lost via Wallerian degeneration

Nerve can regrow back to original target (takes months)

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186
Q

What is neurotmesis?

A

Loss of axon and surrounding wrappings (endoneurium, perineurium, epineurium)

Poor prognosis, surgery may help

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187
Q

What is disrupted in neurotmesis?

A

Wrappings of the nerve beyond the myelin (endoneurium, perineurium, and/or epineurium)

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188
Q

What can you see in nerve conduction studies/electromyography in demyelination?

A

Decreased conduction velocity

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189
Q

What do you see in nerve conduction studies/electromyography in axonal loss?

A

decreased action potential amplitude

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190
Q

What occurs during wallerian degeneration?

A

Intra-axonal organelle and microtubule breakdown (mins-hours)

Schwann cells begin breakdown of axons and recruit macrophages

Macrophages do their thing

Then the path is cleared for axons to regrow from proximal to distal

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191
Q

Which is more conducive to nerve regeneration, CNS/PNS?

A

PNS

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192
Q

Does Wallerian degeneration occur in the PNS? CNS?

A

PNS only!

Oligodendrocytes not as good at initiating degradation as Schwann cells

CNS - astrocytes and microglia not as helpful as macrophages

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193
Q

Which cells (PNS/CNS) have greater intrinsic growth potential and why?

A

PNS cells - have greater expression of regeneration-associated genes (RAGs)

PNS neurons possess receptors and signal transduction machinery allowing them to grow in response to neurotrophins - retrograde injury signals

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194
Q

What are neurotrophins?

A

Retrograde injury signals - promote growth towards higher concnetration

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195
Q

What is a growth cone?

A

Very tip of a regenerating axon - sense the milieu and decide to grow or not (sense neurotrophins, for instance) and direct growth of axon

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196
Q

What is the molecular basis of a growth cone?

A

Cytoskeletal rearrangement - actin bundles and microtubules

Attachment of cytoskeleton to the signal transduction machinery is key

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197
Q

What are retraction bulbs (of Cajal)?

A

Failed regeneration growth cones of the CNS

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198
Q

What types of changes are seen in CNS plasticity?

A

Molecular and structural changes

Molecular include synapse, receptor, transmitter regulation

Help adapt instead of regrowing in CNS

199
Q

What opportunities arise from the complexity of neuronal connetions in the brain?

A

Complexity allows for recovery in the case of injury - you can reroute or use other mechanisms - don’t have to fix the original pathway

200
Q

How does activity help lead to neuronal plasticity?

A

Leads to increases in grwoth factors, especially BDNF (important in exercise)

Leading to increased neurogenesis, glial cell support.

Also, angiogenesis, synaptogenesis

201
Q

What parallels are there between normal brain developmenta nd recovery from injury?

A

Birth->child age -> maturity

Injury->regrowth->consolidation

You need to prune the neuronal connections

202
Q

What types of activities are best for helping regrow/recover from neuronal injuries?

A

A variety of skilled, task-specific, repetitive tasks - these are better than general exercise alone

e.g. real life skills (reaching into cupboard)

203
Q

What are natural sources for stem cells?

A

Embryonic - inner cell mass from 4-5d blastocyst - usually from excess IVF cells - plurpotent

Fetal - from extra-fetal or fetal tissue (amniotic, cord blood, placental tissue) - multipotent

Adult - from BM, skin, GI, fat, heart, brain, dental pulp - multipotent or oligopotent - huge advantage is they are autologous

204
Q

What is a difference between adult, fetal and embryonic stem cells?

A

adult - oligo or multipotent - autologous

fetal - multipotent

embryonic - pluripotent

205
Q

What is somatic cell nuclear transfer?

A

Take nucleus from adult somatic cell and insert it into enucleated egg cell - get early embryo

Not 100% autologous - mitochondrial genome is still present

206
Q

What are induced pluripotent stem cells (iPS) and their advantages?

A

Turn on four genes - myc, sox, oct, nanog - in a somatic cell and you get a stem cell

Pluripotent

100% autologous

207
Q

What are the best targets for stem cel therapies?

A

Neurodegenerative diseases - Huntington’s (one type of neuron, isolated), ALS, Parkinson’s, Alzheimers (but it is very diffuse)

Stroke

Traumatic Brain Injury, Spinal Cord Injury

208
Q

How many approved indications are there for pluripotent stem cells?

A

ZERO

Hematopoeitic stemm cells are used in bone marrow transplants

209
Q

What are dysmyelinating diseases?

A

Disease where myelin sheath is abnormally formed (mostly related to inherited metabolic disorders)

210
Q

What are demyelinating diseases?

A

Disease wher ethe myelin sheath is normally formed but is the target of destruction (e.g. MS)

211
Q

What cells comprise the gray matter?

A

Neuron cell bodies

Dendrites

Synapses

Axons

212
Q

What comprises the white matter?

A

Myelinated axons

213
Q

What makes up the myelin of the CNS?

A

Oligodendroglial cells wrapped around the axon

214
Q

Where in the brain are grey and white matter generally located?

A

Cortex - grey matter

Tracts underneath - white matter (including corpus callosum)

215
Q

What are examples of dysmyelinating diseases?

A

Adrenoleukodystrophy - primarily affects white matter

Tay Sachs disease - primarily involves ccumulation of myelin byproducts in neurons

216
Q

What is the general course of MS?

A

Initially begins with relapse/recover periods (something like IBD)

Then morphs into a progressive disease (something like Alzheimers)

217
Q

What is multiple sclerosis?

A

Inflammatory, autoimmune disease of CNS

Characterized by relapsing neurologic symptoms, and progressive impairement of function

Variable symptoms and signs - monocular vision loss, brainstem, motor/sensory impairments, imbalance

218
Q

What are common early features of MS?

A

Motor weakness, parasthesias, impaired vision, double vision, intention tremor, ataxia

These are symptoms common of other diseases, so you must work it up or look back at it later

219
Q

What is Charcot’s triad?

A

Intention tremmor, nystagmus, scanning speech

Points to white matter pathways to and from cerebellum (vulnerable to demyelination)

Common presentation of MS

220
Q

What is the most common form of involvement of the visual pathway of MS?

A

optic neuritis

Inflammation of optic nerve - painful

221
Q

What is a very common first presenting feature of MS?

A

Optic neuritis - inflammation of optic nerve - presents with pain

222
Q

What type of eye involvement is common in MS?

A

Optic neuritis - painful upon movement

Common to have a scotoma - isolated area of visual field with absent vision

223
Q

What is the prognosis of optic neuritis that is seen early in MS?

A

1/3 will recover completely, the rest will improve substantially

Half of patients who present with optic neuritis alone will develop other signs of MS

224
Q

What is RR-MS?

A

Relapsing-remitting MS

Relapses, recovery, and stability between

225
Q

What are the different clinical patterns of MS?

A

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

226
Q

What is secondary progressive MS?

A

Relapse with recovery, then gradual worsening of symptoms over time

227
Q

What is primary progressive MS?

A

gradual worsening of symptoms - no cardinal features of relapses

228
Q

What is the relationship between brain lesions and disability in MS?

A

We can see lesions more readily than attacks, and are indicators of progression of MS

Looking below the surface of symptoms reveals worsening picture of lesions in the brain

229
Q

What is clinically isolated syndrome?

A

First presentation of what is liekly to become MS - (singular sclerosis)

Within 10 years, 50% wil develop secondary-progressive MS

230
Q

Who gets MS?

A

young people: 20-40 (big spread)

Particularly women (3:1)

231
Q

What is the most common cause of medical disability in young adults?

A

MS

232
Q

In what ethnicity is MS more common?

A

North European descent

Seen more common in latitudes further from equator too

233
Q

What are the genetic fators of MS?

A

Complex - but twins at 30% chance of getting MS, siblings 2-5%

Both more common than general population

234
Q

What helps you make the diagnosis for MS?

A

Dissemination in space and time of disease activity

Based on history and neurological exam

No single diagnostic test

MRI can help

235
Q

What is the significance of contrast-enhanced lesions in the brain on MRI?

A

Indicate active inflammation. Lesion associated with MS

In non-contrast MRI - indicate history of MS lesions

236
Q

In non-contrast-enhacned MRI, what is the significant of lesions in white matter tracts?

A

Old MS plaques. Active inflammation can be seen by contrast enhancement

237
Q

What is this MRI indicative of?

A

Multiple Sclerosis

Periventricular lesions - radiating upward and outward from ventricles + white matter tracts

Radiating upwards from corpus callosum

Brainstem, cerebellum lesions

238
Q

How do MRI lesions predict development of MS after presentation with optic neuritis (or other first attack)?

A

Increased likelihood

239
Q

What must you be sure of before diagnosing MS?

A

That there is no better explanation, e.g.:

 Infectious: Lyme, Syphilis, HIV, HTLV-1, PML

 Inflammatory: SLE, Sjogren’s syndrome, vasculitis,

sarcoidosis, Bechet’s syndrome, APLS

 Metabolic: Vitamin B12 deficiency, dysmyelinating

diseases (lysosomal/leukodystrophies), toxins, CPM,

mitochrondrial disorders, Copper deficiency,

 Vascular: CADASIL, susac’s syndrome

 Neoplastic: CNS lymphoma, metastatic disease

 Structural Spine disease: AVMs, degenerative disc

disease, syrinx, arnold-chiari

 Genetic- hereditary spastic paraparesis

Psychogenic-Depression, anxiety, conversion

240
Q

What occurs from an immunological perspective in Multiple Sclerosis?

A

Th1 cells become activated and self-reactive T cells enter brain and mistake myelin for antigens

Without regulatory cells, they are reactivated and release proinflammatory cytokines that increase inflammation, cause edema, and damage myelin and nerves

241
Q

What type of disregulation is thought to occur in MS with respect to Th cells?

A

Th1 more than Th2 (inflammatory more than anti-inflammatory)

242
Q

What do you see in the CSF of MS patients?

A

Oligoclonal bands - identified by electrophoresis of CSF

Two or more bands needed to be seen for it to be useful

IgG bands

243
Q

What are oligoclonal bands?

A

When you electrophorese CSF in MS patients, you will see excess of bands instead of smear, of IgG

244
Q

What is seen in histological sections of MS lesions?

A

Peri-venular inflammatory infiltrates

245
Q

What are the goals of treating MS?

A

Treat relapses and exacerbation

Prevent relapses

Reduce devleopment of disability

Treat symptoms

246
Q

What can be used to directly treat MS relapses/exacerbations?

A

High dose IV steroids - remember, this is an inflammatory event.

247
Q

What are some limitations of treating MS?

A

Disease modifying agents are only partially effective

All injectible (IV)

Side effects of interferons (flu-like, headche, fever)

Risk/Benefit

248
Q

How can you identify an acute exacerbation of MS that you should treat?

A

Must distinguish from Uhthoff’s phenomenon (which is sudden onset of neurological dysfunction as a result of elevated body temperature)

Episode of neurological dysfunction lasting more than 24 hours in the absence of fever or infection

249
Q

What is Uhthoff’s phenomenon?

A

A sudden onset of neurological dysfunction as a result of elevated body temperature

250
Q

What drug do you use to treat acute exacerbations of MS?

A

IV methylprednisone - high dose

251
Q

When is the onset of Tourette’s Syndrome?

A

Before 18 years old

252
Q

What is a common comorbidity seen with Tourette’s Syndrome?

A

OCD

253
Q

What is an effective psychological treatment for COD?

A

Cognitive Behavioral Therapy (CBT)

254
Q

What is the learning theory explanation of OCD?

A

Symptoms are a result of a person developing learned negative thoughts and behavior patterns towards previously neutral situations

255
Q

What is the neurotransmitter based model for the etiology of OCD?

A

Based on the findings clinically that selective serotonin reuptake inhibitors (SSRIs) and glutamate receptor blockers are efficacious

Also that glutamate is found in elevated levels in some brain areas

Not fully well understood

256
Q

What is the circuit-based hypothesis for the etiology of OCD?

A

It is hypothesized that OCD involves an imbalance between the direct and indirect pathways of the basal ganglia, leading to relatively greater excitation of the circuit, and resultant stereotyped behavior

257
Q

What is the infection-triggered hypothesis for the etiology of OCD?

A

It is has been observed that there is a subset of children with rapid onset of OCD symptoms and/or tic disorders and it is hypothesized that these symptoms are caused by group A beta-hemolytic streptococcal infections- an initial autoimmune reaction to the strep infection produces antibodies that interfere with basal ganglia function.

258
Q

What organism has been implicated in the development of some cases of OCD in children?

A

group A beta-hemolytic streptococcus

259
Q

What evidence suggests the role of genetics in the etiology of OCD?

A

Family aggregation studies show it is familial - especially early-onset and tic-related forms

Twin studies

One glutamate transporter gene (SLC1A1) has been associated and replicated

Little from GWAS

260
Q

What are the two well established mainstays of OCD treatment?

A

Serotonin reuptake inhibitors (SRIs) - either clomipramine or fluvoxamine (SSRI)

Cognitive Behavioral Therapy - exposure and response prevention therapies -> shown to have a higher rate of resopnse

261
Q

What proportion of patients respond to OCD treatment (either pharmacologic of CBT)?

A

50% and full remission is uncommon

262
Q

What are some options for OCD patients for whom traditional serotonin therapies or CBT is not working?

A

Changing SSRI

Adding antipsychotic drugs

If all other treatments are not working, deep brain stimulation and in some cases neurosurgery could be attempted - but must get full consent from patient

263
Q

When can DBS be used for the treatment of OCD patients?

A

Failed CBT

Failed multiple medication treatments including SSRIs, clomipramine, and SSRI + antipsychotic

Must get full consent (and often IRB approval, etc) - still experimental/not proven efficacious

264
Q

What are the two major divisions of the cerebral cortex?

A

Allocortex - including the archicortex (e.g. hippocampus) and paleocortex (parahippocampal cortex)

Isocortex - referred to as neocortex nowadays

265
Q

What are the components of the allocortex?

A

Archicortex (hippocampus) and paleocortex (parahippocampal cortex)

266
Q

What is the isocortex?

A

Neocortex

267
Q

Which brain region is primarily responsible for conscious thought?

A

Cerebral cortex

complex sensory processing, motor control, decision making, introspection

268
Q

Which brain region is responsible for complex sensory processing, motor control, decision making, introspection?

A

Cerebral cortex

269
Q

What accounts for over 90% of the cerebral cortex in humans?

A

The neocortex

270
Q

What is the basic unit of information processing in the neocortex?

A

Cortical column - includes all essential cellular and synaptic elements of intrinsic cortical circuitry

271
Q

What is a cortical column?

A

The basic unit of information processing in the neocortex

Includes the essential cellular and synaptic elements of intrinsic cortical circuitry

272
Q

What are the two most important types of projections to a given cortical area?

A

Thalamocortical inputs - provide primary sensory input to the neocortex

Corticocortical input that interconnect functionally linked cortical areas

273
Q

What inputs do thalamocortical connections provide to the neocortex?

A

Primary sensory input

274
Q

What do corticocortical inputs provide to the neocortex?

A

Interconnect functionally linked cortical areas

Establish broad distributed systems that are well suited for complex information processing

275
Q

What are the inputs that the neocortex receives?

A
  • *Thalamus - sensory**
  • *Other neocortical areas - linked functional systems**

Extrathalamic subcortical afferents - regulation of mood and attention

Amygdala - emotional tone to neocortical functions

Parahippocampus - primary association cortex - role in memory

276
Q

Where do cholinergic projections to the neocortex originate?

A

Nucleus basalis

277
Q

Where does the dopaminergic projections to the neocortex originate from?

A

Substantia Nigra/Ventral Tegmental Area

278
Q

Where do the serotinergic projections to the neocortex originate from?

A

Dorsal Raphe nucleus

279
Q

Where do the noradrenergic projections to the neocortex originate from?

A

Locus Ceruleus

280
Q

What is a difference between the organization of thalamic cortical inputs and extrathalamic cortical inputs?

A

Thalamic cortical inputs are highly topographic with a narrow field of termination

Extrathalamic inputs are highly divergent, innervating huge areas of the neocortex and regulating functions such as mood, sleep, wakefulness, attention, alertness, etc.

281
Q

Which inputs to the neocortex are highly topographic and well-organized?

A

Thalamic inputs

282
Q

What are the major efferents of the neocortex?

A

Mostly reciprocal projectiosn of the major afferents:

Extrathalamic afferents are not reciprocal, largely

Major non-reciprocal cortical efferent system from motor and frontal association areas to the caudate.

Also non-reciprocal projections to brainstem nuclei and spinal cord that are important for motor control

283
Q

What are the non-reciprocal efferent tracts from the cortex?

A

Basal ganglia - from the motor and prefrontal cortices

To brainstem and ‘downstream’ motor areas - Pons, brainstem motor nuclei, tectum, spinal cord

284
Q

What are the six layers of the neocortex?

A

I - Molecular (plexiform)

II - External granule layer

III - External pyramidal layer

IV - internal granule layer

V - Ganglionic layer (internal pyramidal)

VI - multiform layer (polymorphic)

285
Q

What is layer IV of the neocortex associated with?

A

Sensory information (inputs)

286
Q

What is layer V of the neocortex associated with?

A

Motor outputs

287
Q

How are cortical layers different in different brain areas?

A

For instance- primary motor and frontal premotor have larger layer V (motor)

Sensory areas (occipital, for example) have larger layer IV (sensory)

288
Q

What is significant about the neocortex in the primary visual cortex?

A

It is highly specialized to receive initial sensory input from teh thalamus

Large layer IV of the neocortex

289
Q

What is significant about the neocortex in the primary motor cortex?

A

Directly drives motor centers of the brain stem and spinal cord - large layer V

290
Q

What are pyramidal neurons?

A

Principal output neurons

The main axon leaves the cortex and they are generally excitatory (signal with glutamate)

Spiny - have great capacity for integration of information form multiple sources

291
Q

What is significant about the spines on pyramidal neurons?

A

They each receive excitatory signals (glutamatergic)

These are modified in the context of learning and memory and are implicated in plasticity and their loss is associated with aging

292
Q

What are non-pyramidal neurons?

A

Interneurons that have fairly local projections

Mostly inhibitory (signal via GABA) - some are excitatory spiny-stellate (in layer IV of visual and somatosensory cortices)

Three types: Chandelier, Basket, and Double Boquet

They modulate excitability throughout the entire receptive surface of pyramidal neurons

293
Q

What are chandelier cells?

A

Inhibitory interneurons (non-pyramidal) that synapse on the axon initial segment and inhibit the action potential

294
Q

What are basket cells?

A

Inhibitory interneurons (GABAergic, non-pyramidal) that synapse on the cell bodies of pyramidal cells

295
Q

What are double bouquet cells?

A

Inhibitory interneurons (GABAergic, non-pyramidal) that synapse on the dendritic shafts and spines

296
Q

What is the basic scheme of columnar organization of the neocortex?

A

Activation of the pyramidal cell via incoming excitatory afferent, which is modulated by the GABAergic interneurons’ inhibitory signals.

Thought to arrange in radial columns of interconnected neurons that form integratory circuit that processes bits of information

297
Q

How do the types of circuits of the brain reflect the neurotransmitters through which they signal (GABA, Glutamate, 5-HT, NE, DA)?

A

Local interneurons control pyramidal cell output via inhibitory GABAergic synapses

Thalamocortical and corticocortical circuits are heirarchical excitatory circuits via glutamatergic synapses

Brainstem projections to the cortex are broadly modulatory via monoamines (5HT, NE, DA)

298
Q

What types of functions do GABAergic neurons play?

A

Locally inhibitory interneurons that modulate pyramidal cell signaling

299
Q

What types of functions do glutamatergic neurons play?

A

Excitatory links of thalamocortical and corticocortical pathways. Heirarchical

300
Q

What types of functions do monoamine (5HT, DA, NE) neurons play?

A

Broadly modulatory from the brainstem to cortical areas.

301
Q

What are association cortices?

A

can be linked to a particular sensory modality (unimodal) or can be a center for convergence of multiple modalities (polymodal)

Required for interpretation and elaboration of sensory information

Prime example is visual cortex

302
Q

What are the two major streams of visual processing?

A

Occipito-parietal stream - processes visuospatial information and motion detection

Occipito-temporal stream - processes form and color

303
Q

What information does the occipito-parietal stream process?

A

visuospatial information and motion detection

304
Q

Which visual processing stream processes visuospatial information and motion detection?

A

Occipitoparietal stream

305
Q

What information does the occipito-temporal stream process?

A

Form and color information for the visual system

306
Q

Which visual processing stream processes form and color information?

A

Occipito-temporal stream

307
Q

What is the “where” visual processing system?

A

Occipito-parietal stream

308
Q

What is the “what” visual processing system?

A

Occipito-temporal stream

309
Q

[…] cells are involved in the processing of “where” visual informaiton (motion, spatial relations)

A

Magnocellular cells are involved in the processing of “where” visual informaiton (motion, spatial relations)

Occipito-parietal stream

310
Q

[…] cells are involved in the processing of “what” visual information (form, color)

A

Parvocellular cells are involved in the processing of “what” visual information (form, color)

Occipito-temorpal stream

311
Q

Which visual processing stream is involved in the recognition of faces?

A

occipito-temporal stream

312
Q

What is visual agnosia?

A

Incapability of recognizing visual stimuli

May be able to recognize objects presented to other sensory modalities

313
Q

What is prosopagnosia?

A

Inability to recognize previously known human faces or to learn new ones

Can perform complex perceptual tasks and do not have visual spatial disturbances

Correlated withd amage to the occipito-temporal region

314
Q

What lesions can cause prosopagnosia?

A

Damage to the occipito-temporal region

315
Q

What is the term for the inability to recognize previously known human faces or to learn new ones?

A

Prosopagnosia

316
Q

What is the term for the inability to recognize objects visually?

A

Visual agnosia

317
Q

What is visual object agnosia?

A

In addition to prosopagnosia, patients have inability to identify or recognize the generic class to which an object belongs

Also correlated with damage to the ventral and medial parts of the occipito-temporal visual areas

318
Q

What is Balint’s syndrome?

A

Three components:

Optic ataxia (impairment of target pointing under visual guidance)

Ocular ataxia (inability to shift gaze at will toward new visual stimuli)

Simultanagnosia (perception and recognition of only parts of the visual field)

– Strongly correlated to bilateral damage of the occipito-parietal region

319
Q

What is optic ataxia?

A

impairment of target pointing under visual guidance

320
Q

What is the term for impairment of target pointing under visual guidance

A

optic ataxia

321
Q

What is the term for the inability to shift gaze at will toward new visual stimuli?

A

Ocular ataxia

322
Q

What is ocular ataxia?

A

The inability to shift gaze at will toward new visual stimuli

323
Q

What is simultanagnosia?

A

Perception and recognition of only parts of the visual field

324
Q

What is the term for perception and recognition of only parts of the visual field?

A

Simultanagnosia

325
Q

What syndrome is related to bilateral damage of the occipito-parietal region?

A

Balint’s Syndrome

326
Q

What types of lesions is Balint’s Syndrome related to?

A

Bilateral occipito-parietal region damage

327
Q

What functions does the prefrontal cortex serve?

A

Working memory

Planning

Executive function

Top-down cognitive control (forming rules)

Modifying these rules

Response inhibition

328
Q

Which area of the brain is more developed in humans than in other species?

A

Prefrontal cortex

329
Q

What modalities send signals to the prefrontal cortex?

A

All higher level association areas project to the prefrontal cortex

Auditory, somatosensory, motor, visual, affective (amygdala)

330
Q

What information about the prefrontal cortex can be elucidated from delayed response task studies in monkeys? (The task consists of a visual cue, then obligated to delay their response but remember the cue’s location and then generate an appropriate response for a reward)

A

Different neurons fire during different parts of this task

The prefrontal cortex neurons are active during the delay phase! (D below)

331
Q

What are key characteristics of prefrontal cortex neurons in delayed-response task studies?

A

They are active duriing the delay

They are spatially selective (others are object selective)

They are resistant to distraction

332
Q

What neurons are important for tasks such as adjusting to cars traveling on the left side of the road when in England (i.e. changing the rules)

A

Prefrontal cortex

333
Q

What cognitive impairments are associated with prefrontal cortex damage?

A

Problem solving deficits

Impaired temporal order judgements

Difficulty in attending to a task

Enhanced sensitivity to distraction

Perservation

Impulsive behavior

Poor planning

Impaired decision making

Working memory defecits

Impaired executive functioning

  • Heavily compromised in disorders such as Alzheimers
334
Q

What brain region is likely damaged in patients presenting with problem solving deficits, impaired temporal order judgments, difficulty in attending to a task, enhanced sensitivity to distraction, perservation, impulsive behavior, poor planning, impaired decision making, working memory deficits and impaired executive functioning?

A

Prefrontal Cortex

As in Alzheimer’s Disease

335
Q

What brain regions is Alzheimer’s Disease associated with?

A

Compromised prefrontal cortex

336
Q

What are the two core clinical components of consciousness?

A

Arousal - level of consciousness - are the lights on?

Awareness - content of consciousness - is anyone home?

337
Q

Which brain structures are important in mediating arousal?

A

Ascending reticular activating system (ARAS) - in brainstem

Thalamus

Thalamocortical Relays

338
Q

What is ARAS?

A

Ascending reticular activating system

Origininates in nuclei in the ponto-mesencephalic junction

Transmits via Acetylcholine

339
Q

What neurotransmitter is used by ARAS?

A

Acetylcholine (ACh)

340
Q

Where are the source nuclei of the ARAS located?

A

Ponto-mesencephalic junction

341
Q

Which brain structure important in mediating arousal has its source nuclei located in the ponto-mesencephalic junction?

A

Ascending reticular activating system (ARAS)

342
Q

Which brain structures are important in mediating awareness?

A

The cerebral cortex

343
Q

How can lesions to the cortex impair consciousness?

A

Large, bilateral lesions

344
Q

What areas, if disrupted, can cause an impairment of consciousness?

A

ARAS

Thalamic relays

Cortex (bilaterally)

345
Q

What are possible etiologoies of consciousness impairment?

A

Structural - trauma, mass lesions (neoplasm, hematoma, abscess)

Functional - ischemia, seizure, metabolic, endocrine, inflammatory, infectious, iatrogenic, toxic

346
Q

What are the six levels of arousal?

A

Awake

Drowsy/somnolent

Lethargic

Obtunded

Stupor

Coma

347
Q

What does it mean to be awake?

A

Full wakefulness

348
Q

What does it mean to be drowsy/somnolent?

A

Able to be stimulated to full arousal by non-noxious stimuli

349
Q

What does it mean to be lethargic?

A

Resonsds to non-noxious stimuli but unable to be brought to full arousal

350
Q

What does it mean to be obtunded?

A

Responds to non-noxious stimuli but more depressed level of consciousness

351
Q

What does it mean to be stuporous?

A

Requires noxious stimuli to raise level of arousal

352
Q

What does it mean to be comatose?

A

Unresponsive, reflexive response to all stimuli

353
Q

What is the Glascow Coma Scale (GCS)?

A

Quantitative scale to asses level of arousal on verbal responsivity, eye opening, motor responsivity

Scores range from 3-15. 3 is deep coma, 15 is fully awake

354
Q

What is a quantitative descriptor of arousal?

A

Glascow Coma Scale

355
Q

What are the components of consciousness?

A

Arousal

Awareness

356
Q

How is awareness described?

A

From alert/attentive to inattentive (distractible or dissociated) to vegetative

357
Q

What are the three principal features used to localize the source of an arousal dysfunction?

A

Respiratory pattern

Eye function

Motor responsivity

358
Q

What is Cheyne-Stokes respiration? What is it indicative of?

A

Crescendo-decrescendo respiratory pattern with apnic period

Indicative of diffuse forebrain dysfunction

359
Q

What type of brain lesion is hyperventilaiton indicative of?

A

Midbrain injury

360
Q

What type of breathing pattern will you see in a diffuse forebrain dysfunction?

A

Cheyne-Stokes

361
Q

What type of breathing pattern will you see in a midbrain injury?

A

Hyperventilation

362
Q

What type of breathing pattern will you see in a rostral pons injury?

A

Apneusis

363
Q

What region of the CNS do you suspect a lesion if a patient’s respiratory pattern is apneusis?

A

Rostral pons

364
Q

What is apneusis? What type of CNS injury is it indicative of?

A

Large breaks of apnea. Rostral pons injury

365
Q

What type of breathing pattern do you expect to see in a caudal pons injury?

A

Ataxia - dyscoordinated, irregular respiratory pattern

366
Q

What type of CNS lesion do you suspect if a patient has an ataxic respiratory pattern?

A

Caudal pons

367
Q

What is the difference in the respiratory pattern of a patient with an injury to the rostral vs caudal pons?

A

Rostral = apneusis - large periods of apnea

Caudal = ataxia - disorganized, irregular

368
Q

What type of respiratory pattern do you expect to see in a patient with a medullary injury?

A

Respiratory arrest

369
Q

Where in the CNS do you expect to find a lesion for a patient in respiratory arrest?

A

Medulla

370
Q

What eye functions are important in helping identify arousal dysfunction?

A

Corneal reflex

Pupil size/reactivity
Extra-ocular movements

371
Q

What is a thalamic pupil?

A

Small, reactive, symmetric

372
Q

What types of pupils are small, reactive, and symmetric?

A

Thalamic

373
Q

What types of pupils are fixed and dilated?

A

Pretectal pupils

(Edinger-Westphal damage)

374
Q

What are pretectal pupils?

A

fixed, dilated

(damage to Edinger-Westphal)

375
Q

What are pontine pupils?

A

Pinpoint

376
Q

What types of pupils are pinpoint?

A

Pontine pupils

377
Q

What types of pupils are fixed at mid-size?

A

Midbrain pupils

378
Q

What is a midbrain pupil?

A

Fixed, mid-size

379
Q

What is a herniation pupil?

A

1 fixed, dilated pupil

This suggests a mass effect and is an emergency

380
Q

What does one fixed, dilated pupil indicate?

A

Herniation pupil - indicates mass effect - emergency

381
Q

What is responsible for the afferent limb of the corneal reflex?

A

CN V1 - localizes to the pons

382
Q

What is responsible for the efferent limb of the corneal reflex?

A

CN VII - localizes to the CNVII nucleus in the pons

383
Q

Which brain structure is important for the corneal reflex?

A

PONS

Afferent - CN V1

Efferent - CN VII

384
Q

What can the vestibulo-ocular reflex tell you about a person’s lesion in arousal dysfunction?

A

VOR requires in tact brainstem

Lateral pontine lesion - PPRF on side of lesion is dysfunctional and the eyes do not move horizontally when the head is turned in the direction that is contralateral to the lesioned PPRF (cold water in ipsilateral ear makes no eye movement)

385
Q

What changes in the VOR would you expect with a lateral pontine lesion?

A

PPRF of lesion side is not functinoal - eyes do not move horizontally when head is turned in contralateral direction

Colt water in ipsilateral ear = no movement; contralateral ear = movement

386
Q

What do you suspect when cold water into the right ear produces no horizontal eye movements?

A

Right lateral pontine lesion - lesion of PPRF on right side

387
Q

Identify the lesion:

A

Right lateral pontine lesion

388
Q

Identify the lesion:

A

Bilateral midbrain lesion

389
Q

Identify the lesion:

A

Brainstem is intact!

390
Q

What occurs in a bilateral midbrain lesion?

A

Bilateral CNIII nuclei are not able to function properly so they are unable ot activate the medial rectus as to adduct the appropriate eye during head turns/calorics

391
Q

What innervates the meninges?

A

Trigeminal nerve

392
Q

What are components of cognition?

A

Attention
Language

Memory
Perceptual processing

Praxis - process of learning

Thought content

Executive function

393
Q

What is akinetic mutism?

A

Medial frontal lobe dysfunction

Loss of initiative/agency/motivation

Anterior cingulate

Can be caused by stroke, medial frontal mass lesion, trauma, degeneration

394
Q

What determines hemispheric dominance?

A

Language lateralization - handedness is an indicator

R-handed = 98% L-hemisphere language dominance

L-handed = 60% L hemisphere language dominance (more likely to have bilateral

395
Q

What cerebral hemisphere is more likely to be dominant for language in all patients?

A

Left

98% in right handers

~60% in left handers

396
Q

Patients with […] handedness are more likely to have bilateral language representation in their hemispheres

A

Patients with left handedness are more likely to have bilateral language representation in their hemispheres

397
Q

What are the three parameters used to evaluate language dysfunction?

A

Fluency (grammar, syntax)

Repetition

Comprehension

398
Q
A
399
Q
A
400
Q
A
401
Q
A
402
Q
A
403
Q
A
404
Q
A
405
Q
A
406
Q
A
407
Q

What is Broca’s Area involved in?

A

Expression of language

408
Q

What is Wernicke’s Area involved in?

A

Understanding spoken language

409
Q

What is the function of Wernicke’s Area?

A

Detects auditory stimuli and identifies them as having linguistic value

410
Q

What is the function of the transcortical sensory areas?

A

They determine what information identified by Wernicke’s area as having linguistic value actually mean

411
Q

What areas of the brain are important in comprehension of language?

A

Wernicke’s Area - identifies auditory stimuli as having linguistic value

Transcortical Sensory Area - determines what this information means

412
Q

What areas of the brain are important for expression of language?

A

Broca’s area - mediates final output for language

Transcortical motor area - assembly of language (syntax, etc)

413
Q

What areas of the brain are important for language repetition?

A

Arcuate fasciculus - connects Broca’s and Wernicke’s area

(it is possible to repeat something without understanding its meaning)

414
Q

Which area of the brain is important for the final output for language?

A

Broca’s Area

415
Q

Which area of the brain is important for assembling language for output?

A

Transcortical motor area

416
Q

What is the function of the transcortical motor area?

A

Assembly of language for production (sends to Broca’s area)

417
Q

What is Broca’s Aphasia?

A

Non-fluent speech

Effortful/frustrated

Missing relational words (articles, conjunctions)

(may indicate emergence of non-dominant hemisphere expressive laguage)

418
Q

What would a lesion like this produce?

A

Broca’s Aphasia

Effortful/frustrated non-fluent speech that misses relational words

419
Q

What is a transcortical motor aphasia?

A

Expressive dysphasia

Impaired fluency

Preserved comprehensoin and repetition

420
Q

What would a lesion like this produce?

A

Transcortical motor aphasia

Impaired fluency (preserved comprehension and repetition)

421
Q

What is Wernicke’s aphasia?

A

Receptive dysphasia (impaired comprehension)

Expressive features are syntactically correct but semantically/lexically empty

Patients circomlocute (talk around words)

Paraphasic errors (semantic, phonemic)

Neologisms

Dictionary/lexicon is embedded in and around Wernicke’s area

422
Q

What would a lesion like this produce?

A

Wernicke’s aphasia

Impaired comprehension and repetition

Expressive features are syntactialy correct but may be circomlocutions (talking around objects) since Wernicke’s area has the dictionary/lexicon in and around it

423
Q

What is Transcortical Sensory Aphasia?

A

Receptive dysphasia with impaired comprehension, but preserved fluency and repetition

424
Q

What would a lesion like this produce?

A

Transcortical Sensory Aphasia

Receptive dysphasia with impaired comprehension, but preserved fluency and repetition

425
Q

What is a conduction aphasia?

A

Impaired repetition but preserved fluency and comprehension

426
Q

What would a lesion like this produce?

A

Conduction aphasia

Impaired repetition but preserved fluency and preserved comprehension

427
Q

What are the steps that go into producing a memory?

A

Attention

Registration

Working memory

Evaluation for reference

Encoding

Storage/consolidation

Retreival of memories

428
Q

What are the different types of memory?

A

Echoic - <5 seconds

Short term - seconds-minutes

Working memory - seconds-minutes

Long term minutes (explicit or implicit) - minutes-years

429
Q

What is echoic memory?

A

Lasts for 5 seconds or less, and is basically a perceptual echo - may facilitate registration

430
Q

What is short term memory?

A

Passively on-line maintenence of information over a period of seconds to minues

431
Q

What is working memory?

A

Complex concept that involves attentional circuits, task control and short term memory systems

Active on-line maintenence over a period of seconds to minutes

432
Q

What is long-term memory?

A

Covers a period of time from minutes to years

2 types:

Explicit/declarative - conscious or preconscious and can be semantic (factual) or episodic (from events)

implicit - non-conscious and includes procedural memory (skilled motor tasks), classical conditional, and emotional

433
Q

What is anterograde amnesia?

A

Impaired ability to form new memories

434
Q

What is retrograde amnesia?

A

loss of old memories (with or without temporal gradient)

435
Q

What is complete unilateral apperception?

A

Perceptual deficit that produces a visual field cut

436
Q

What is attentional asymmetry?

A

Perceptual deficit that produces neglect of one side - have in tact acuity, but need very effortful preservation of lesser preserved side to see what is happening there

437
Q

What is a sensory field cut?

A

Complete unilateral apperception (perceptual deficit)

438
Q

What is neglect?

A

Attentional asymmetry (perceptual deficit)

439
Q

What is extinction?

A

Asymmetry of perception of simultaneously presented stimuli (perceptual deficit)

440
Q

Which parietal lobe mediates attention only to the contralateral hemispace?

A

The dominant one (usually left)

441
Q

What parietal lobe usually mediates attention to bilateral hemispace?

A

The non-dominant one (usually right)

442
Q

To what does your dominant parietal lobe mediate attention?

A

The contralateral hemispace

(usually left parietal lobe)

443
Q

To what does your non-dominant parietal lobe mediate attention to?

A

Bilateral hemispace

(usually your right parietal lobe)

444
Q

What is the neuroanatomical basis for neglect?

A

Lesions to the non-dominant parietal lobe, since it is in charge of bilateral hemispace attentional capacity

Dominant parietal lobe only mediates attention to contralateral hemispace

445
Q

Lesions to which parietal lobe will produce neglect?

A

Non-dominant - it mediates attention to bilateral hemispace

Dominant lobe only mediates attention to contralateral hemispace

446
Q

How do you clinically assess neglect?

A

Line bisection task

Clock-drawing task

Writing

447
Q

What is agnosia?

A

Intact peceptual production but dysfunction of associational sensory processing which leads to impaired recognition

I.e. visual agnosia where there is an inability to visually recognize an object (can sometimes recognize object presented in other sensory modalities)

448
Q

What is anosagnosia?

A

The inability to recognzie one’s own deficit, especially neurological ones

E.g. hemi-body neglect (will only dress half of yourself, etc)

449
Q

What is Anton’s syndrome?

A

Cortical blindness + unaware of deficit due to occipital + parietal association area dysfunction

450
Q

What is dyspraxia?

A

The inability to perform a previously learned motor task

451
Q

What is the praxicon?

A

The store of motor programs (analogue of lexicon, but for actions)

Mostly found in the dominant side in the temporal-parietal regions

452
Q

Where is the praxicon typically located?

A

Dominant parietal lobe

453
Q

What is the neuranatomical basis of praxis?

A

Praxicon (dominant side) sends projections to SMA and other premotor areas

This will then send projections to the motor strips (bilaterally via corpus callosum), which then send projections down corticospinal system and to body

454
Q

What is constructional apraxia?

A

Inability to properly form objects

(i.e. inability to draw intersecting pentagons)

455
Q

How do you asses construction apraxia?

A

Ask patient to draw intersecting pentagons/cubes

456
Q

What are the three subdivisions of the prefrontal cortex?

A

Medial prefrontal cortex/Anterior cingulate - provides go/motivation/initiative/agency (dysfunction can cause aboulia - lack of desire/motivation)

Orbitofrontal cortex - provides brake/no-go (dysfunction = disinhibition syndrome)

Ventrolateral and dorsolateral prefrontal cortex - direct the ‘how to go’ - executive function (dysfunction = dysexecutive syndrome)

457
Q

Which subdivision of the prefrontal cortex is involved with directing motivation, initiative/ “go”?

A

Medial prefrontal cortex (anterior cingulate)

458
Q

Which prefrontal cortex subdivision is responsible for applying the brakes/”no-go”/inhibitoin?

A

Orbito-frontal cortex

459
Q

Which prefrontal cortex subdivision is responsible for providing executive function/”how to go”?

A

Ventrolateral /dorsolateral prefrontal cortex

460
Q

What is abulic-akinetic syndrome?

A

Dysfunction of medial prefrontal cortex/anterior cingulate

Loss of “go”/initiative/motivation center

461
Q

What is disinhibition syndrome?

A

Dysfunciton of the orbitofrontal cortex

Loss of inhibitory/’no-go’ / brakes functionality

462
Q

What is dysexecutive syndrome?

A

Dysfunciton of the dorsolateral prefrontal cortex/ventrolateral prefrontal cortex

Loss of executive function/ “how to go”

463
Q

What is a great test for executive dysfunction?

A

Ask a patient to draw “ten after eleven” on a clock:

464
Q

What is a difference between Alzheimer’s disease memory impairment and age-related memory impairment?

A

Alzheimer’s has significant selective neuron death

Age-associated memory impairment has no significant neuron loss, but the synapse may be the site of the changes leading to functional decline

465
Q

What proteins are in neurofibrillary tangles of AD?

A

Tau

466
Q

What proteins are in the plaques seen in AD?

A

Beta amyloid protein

467
Q

What is thought to disrupt cortical-cortical circuits in AD?

A

Both tangles and plaques

468
Q

Where do tangles appear early in AD?

A

entorhinal cortex and CA1 - then become abundant in association cortex

469
Q

What is the function of the entorhinal cortex?

A

Gets input from the association areas and then informaiton flows through the hippocampus where new memories are laid down

470
Q

Where does neuron death start in AD?

A

Entorhinal cortex

When the circuit dies, access to neocortical information for new memories is compromised

The circuit also suffers in normal aging

Disruption of neocortical circuits is required for the dementia of AD

471
Q

What is required for the development of the dementia of AD?

A

Disruption of neocortical circuits

472
Q

Is it abnormal to find neurofibrilary pathology in the entorhinal cortex in patients over 55 years old?

A

Yes

473
Q

Which circuits are most vulnerable in AD?

A

Cortico-cortical circuits that mediate cognition (especially those in the temproal-prefrontal areas) are most vulnerable

474
Q

What happens to neurons that have tangles form in them?

A

They die

475
Q

What is the basis for the dementia of Alzheimer’s Disease?

A

The inability of cortical regions to funciton together as a cohesive system

Complex thought requires complex circuitry and once the cortical connections deteriorate, it is not possible

(Tau bundles, Beta amyloid plaques)

476
Q

What cognitive functions are more sensitive to decline with age?

A

Prefrontal functions

Memory as mediated by the hippocampus and other medial temporal lobe areas also decline (but not as sensitive)

477
Q

What are prefrontal functions that decline with age?

A

Working memory

Attending to significant events

Reasoning ability

Planning

Guiding goal-directed behavior

Executive function

478
Q

What are some things that individuals with diminished prefrontal functions (due to aging/AD) have difficulty with?

A

Altering daily routine

Learning new strategies

Managing medications

Keeping track of finances and paying bills

Scheduling/keeping appointments

Being efficient at home activities like cooking, cleaning

Interacting socially

Working with their immediate environment

479
Q

What are some tests of medial temporal lobe (MTL) function?

A

Mostly recall tests - word recall after dealy/picture recognition after delay

fMRI with specific tasks - showing decreased activity in hippocampus

480
Q

When do we see deficits in top-down suppression of irrelevant information?

A

In normal aging

Associated with working memory impairment

481
Q

What are large mushroom spines?

A

Spines that have strong AMPAR-mediated currents that contribute to strong, stable synaptic circuits

482
Q

What are thin spines?

A

NMDAR-dominated, highly plastic can expand and stabilize or retract

483
Q

What are the memory spines?

A

Large mushroom spines

484
Q

What are the learning spines?

A

Small thin spines

485
Q

What types of spines and connections are AMPAR-mediated currents associated with/

A

Mushroom - strong, stable circuits

486
Q

What types of spines and connections are NMDAR-dominated currents associated with?

A

Long thin spines - plastic learning spines

487
Q

What occurs on a cellular/molecular level in age-related cognitive decline?

A

Loss of thin spines - age-related loss of structural plasticity

488
Q

What types of spines are lost in age-related cognitive decline?

A

Long thin spines that are associated with learning

489
Q

What is a potential therapeutic target for the preservation of thin spines?

A

Estrogen receptors are present - estrogen may be protective

490
Q

What changes are seen in the hippocampus with aging?

A

No synapse loss or shift in size of total axospinous synapses

Changes in numbers of perforated synapses and multi-synaptic boutons - degree correlated with cognitive decline

491
Q

What are some identifiable pathological changes seen in most elderly individuals?

A

Cortical atrophy

Enlarged ventricles and cerebral cortical sulci

Cell loss

Amyloid plaques

Neurofibrillary tangles

Lewy bodies, etc

492
Q

Does the level of neurological decline correlate with brain pathology?

A

Not necessarily

493
Q

What defines Mild Cognitive Impairment/Mild Neurocognitive Disorder?

A

Impaired cognition in one or more domains and to a lesser degree than in dementia

Do not interfere with capacity for independence in everyday activities

(may be prodromal state of dementia) - most develop

1/3 improve

Brain and Behavior (9 decks)

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