Midterm and final Flashcards

0
Q

How did Hippocrates view brain-behavior relationship?

A

The brain controls all senses. Noted that paralysis occurs on opposite side of head injury.

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1
Q

How did Pythagoras view brain-behavior relationship?

A

The brain is the center of human reasoning and plays crucial role in the soul’s life

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2
Q

How did Aristotle view brain-behavior relationship?

A

The heart is the source of all mental processes and locus of human soul.

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3
Q

What are the three parts of the neuron?

A

Dendrite- gather info
Soma/Cell body- core region; integrates info
Axon- carries info to other cells

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4
Q

What are the different types of neurons?

A

Sensory- bring info to CNS
Interneuron/Associate Neurons- associate sensory and motor activity within CNS
Motor- sends signals from brain and spinal cord to muscles

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5
Q

What are the five types of glial cells?

A
Ependymal
Astrocyte
Microglia
Oligodendroglia
Schwann
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6
Q

What is an ependymal cell?

A

Small, oval shaped; secretes CSF

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7
Q

What is an astrocyte?

A

Star-shaped, symmetrical; nutritive and structural support function, scar tissue; transports substances thru blood-brain barrier

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8
Q

What is a microglial cell?

A

Small; defensive function; originates in blood as offshoot of immune system

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9
Q

What is an oligodendroglial cell?

A

Asymmetrical; forms myelin around CNS axons in brain and spinal cord

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10
Q

What is a Schwann cell?

A

Asymmetrical; wraps around peripheral nerves to form myelin

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11
Q

What is the meninges and what is the order?

A

The protective layer of tissue around the brain:
Dura mater- hard mother
Arachnoid layer- spiders web
Pia mater- soft mother, moderately tough

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12
Q

Symptoms of meningitis? Consequences?

A

Headache, neck stiffness, fever, confusion, vomiting, sensitivity of light/noise
Deafness, epilepsy, hydrocephalus, cognitive

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13
Q

Sympathetic v Parasympathetic Nervous System?

A

Sym- fight or flight, reactive

Para- calm down, relax

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14
Q

What is the somatic nervous system?

A

Part of Peripheral Nervous System. Controls skeletal muscles thru cranial and spinal nerves

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15
Q

What is the autonomic nervous system?

A

Part of Peripheral Nervous System. Comprised of Symp and Parasympathetic. Regulates glands, blood vessels, internal organs.

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16
Q

What is the function of the spinal cord?

A

Controls most body movement. Spinal

Reflex.

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17
Q

Difference between afferent and efferent?

A

Afferent- IN. Carries info away from sensory receptors

Efferent- OUT. Carries info from spinal cord to muscles. (Motor pathways)

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18
Q

What are the lobes of the brain?

A

Frontal, parietal, temporal, occipital

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19
Q

What does the frontal lobe do?

A

Executive function; motor function

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20
Q

What does the parietal lobe do?

A

Sensory integration; tactile functions

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21
Q

What does the temporal lobe do?

A

Auditory, taste, smell, memory, some visual

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22
Q

What does the occipital lobe do?

A

Visual

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23
Q

What is the cerebrum?

A

Major structure of the forebrain, consisting of two virtually identical hemispheres

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24
Q

What is the cerebellum?

A

Involved in coordination of motor and maybe other mental processes

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25
Q

What is the gyrus?

A

Small protrusion or bump formed by the folding of the cerebral cortex

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26
Q

What is a sulcus?

A

A groove in brain matter, usually found in the neocortex or cerebellum

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27
Q

What is a fissure?

A

A very deep sulcus

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28
Q

What are ventricles?

A

There are four ventricles- cavities in the brain that contain CSF.

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29
Q

What is CSF?

A

Cerebral spinal fluid. It’s sodium chloride and other salts. In ventricles, around brain and spinal cord in subarachnoid space. Cushions.

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30
Q

What is the brainstem?

A

Pons- bridge, connects cerebellum to rest of brain; important movements
medulla- rostral tip of spinal cord; breathing and heart rate
reticular formation- regulation of sleep-wake behavior and behavioral arousal

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31
Q

Gray matter versus white matter?

A

Gray matter- areas of the nervous system predominately composed of
Cell bodies and blood vessels
White matter- areas of nervous system rich in fat-sheathed neural axons

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32
Q

What is the tectum?

A

Roof of midbrain; sensory processing (visual and auditory); produces orienting movements (turning head to see source of sound)

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33
Q

What is the tegmentum?

A

Floor of midbrain; eye and limb movements; species-specific behaviors; perception of pain

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34
Q

What is the thalamus?

A

Part of diencephalon. Gateway for channeling sensory info to cortex; primary role is sensory processing; motor processing; integrative functions

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35
Q

What is the hypothalamus?

A

Part of diencephalon. Hormone function thru pituitary; feeding; sexual behavior; sleeping; temp; emotional behavior

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36
Q

What is the basal ganglia?

A

Controls voluntary and involuntary movements; involved in procedural learning and habits; eye movement; some emotion

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37
Q

What is the limbic system?

A

Regulates emotion and behavior that create and require memory
Amygdala, hippocampus, and cingulate cortex (aka limbic cortex, 3-4 layers gray matter)

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38
Q

What is the hippocampus?

A

Longterm memory formation; declarative memory

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39
Q

Amygdala?

A

Emotion, especially fear response

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40
Q

What is the neocortex? How many layers?

A

Neocortex has six layers. Creates and responds to perceptual world

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41
Q

Left hemisphere lateralization?

A

Specialized role in language; logic; sensory-motor cortex is larger on left and so better motor/sensory on right side; Broca’s area- neurons on left hemi have larger dendritic fields than right hemi
Process words/language better if in right visual field

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42
Q

Right hemisphere lateralization?

A

Auditory cortex is larger on right than left; process info related to music and emotional regulation; prosody
Remember objects better if in left
Visual field

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43
Q

Examples of damage in left parietal lobe?

A

Aphasia
Apraxia
Anomia

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44
Q

What is aphasia?

A

Disturbance of comprehension and production of language spoken or written

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45
Q

What is Broca’s aphasia?

A

Loss of ability to produce language; understands it; expressive aphasia

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46
Q

What is wernickes aphasia?

A

Fluent but nonsensical speech; cannot understand; receptive aphasia

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47
Q

Conduction aphasia?

A

Associative aphasia; poor speech repetition

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48
Q

Transcortical motor aphasia?

A

Halting and effortful speech; can repeat

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49
Q

Transcortical sensory aphasia?

A

Poor comprehension and naming; fluent and spontaneous; echolalia- compulsive repetition

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50
Q

Anomic aphasia?

A

Difficulty with naming

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51
Q

Global aphasia?

A

Difficult understanding and producing written and spoken language; most severe

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52
Q

Isolation aphasia?

A

Watershed region damaged; language comp and prod severely impaired but can repeat

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53
Q

What is apraxia?

A

Impairment in voluntary movement. Apraxia of speech- can’t make mouth movements effectively

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54
Q

What is anomia?

A

Naming difficulty.

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55
Q

What are right parietal damages?

A

Difficulty with coping drawings, assembling puzzles, and navigating around familiar places

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56
Q

Functional asymmetry in normal functioning?

A

Auditory pathways- verbal v music

Visual pathways- language v non-verbal (RVF v LVF)

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57
Q

What happens in split brain?

A

Language abilities- if object in RVF, can name. If in LVF, cannot name but can make correct nonverbal responses, such as selecting a matching item with left hand but not right hand.
Spatial tasks- left hand better

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58
Q

Why left hemi for language?

A

Control of fine movements in left hemi

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59
Q

Why right hemi for spatial?

A

Right hemi controls actual movements in space and mental imagery of movements

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60
Q

Difference between learning and memory?

A

Learning- change in behavior as result of experience

Memory- ability to recall or recognize previous experience

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61
Q

What is implicit memory?

A

Procedural/non-declarative; tasks; bottom-down- encoded same way perceived; passive role

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62
Q

What is explicit memory?

A

Declarative; conscious; episodic and semantic (personal v general knowledge); top-down- recognize info before encoded (schema match); active

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63
Q

What parts of brain are involved with explicit memory?

A

Medial temporal region: hippocampus (major! Consolidation), amygdala, entorhinal cortex, parahippocampal cortex, perirhinal cortex
Frontal cortex

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64
Q

What are the neural circuits/brain areas involved in implicit memory?

A

Basal ganglia-
Ventral thalamus-
Premotor cortex

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65
Q

What are the circuits/areas involved in emotional memory?

A
Amygdala!
Medial temporal cortex
Brainstem
Hypothalamus
PAG
Basal ganglia
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66
Q

Why are explicit memories conscious?

A

Bc medial temporal lobe projects back to cortex

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67
Q

Where is the auditory cortex?

A

In Herschl’s gyrus:
Broca’s area in front- motor
Wernickes in back- comprehension
the arculate fasciculus connects the two, projects to Broca’s; repetition

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68
Q

What are the basic parts of the eye?

A

Cornea, lens, iris, retina, fovea

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69
Q

What is the cornea?

A

Clear outer covering of eye

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70
Q

What is the iris?

A

Opens and closes to adjust level of light allowed into eye via the pupil

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71
Q

What is the lens?

A

The lens focuses light and bends to accommodate near and far images

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72
Q

What is the retina?

A

Light sensitive surface at back of eye consisting of neurons and photoreceptor cells. Light becomes action potentials. Color registered.

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73
Q

What is the fovea?

A

The receptive field at back of eye that is highly focused

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74
Q

What is the optic chiasm?

A

Junction of optic nerves from each eye. Point of transfer of information, where information from the left visual field goes to the right side of the brain and the information from the right visual field goes to the left side of the brain.

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75
Q

What is the geniculostriate system?

A

This is the primary really center for visual info received on retina. The lateral geniculate nucleus is the first stop in the system after the optic nerve and is located inside the thalamus. It sends information directly to the primary visual cortex.

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76
Q

What is The difference between the primary visual cortex and the secondary visual cortex?

A

The primary visual is the striate cortex- receives input from the lateral geniculate nucleus. Perception of color shape and motion.
The secondary visual cortex is the extrastriate cortex. Refines perception and information into wholes in order to view objects and guide movement

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77
Q

What are the two pathways of the primary visual cortex?

A

Parietal lobe- this is the dorsal stream. Or the where pathway- faster and more important
Temporal lobe- this is the ventral stream. Or the what pathway

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78
Q

What does damage to the ventral stream lead to?

A

Agnosia

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79
Q

What is agnosia?

A

It is an impairment in recognition of visually presented objects

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80
Q

What are the two types of visual agnosia?

A

Apperceptive agnosia and associative agnosia

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81
Q

What is Apperceptive agnosia?

A

Impaired object recognition- cannot form a whole picture out of visual information

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82
Q

What is associative visual agnosia?

A

Impaired object identification- can see whole object but can’t give meaning to it

83
Q

What are the types of attention?

A

Focused or selective attention
Sustained attention or vigilance
Divided attention or multitasking

84
Q

What is ADHD?

A

Attention deficit hyperactivity disorder. Neurodevelopmental disorder marked by significant problems of attention hyperactivity or acting impulsively. Must be observed in 2 settings for six months or more. Males more likely to be diagnosed. Subtypes- inattentive, hyperactive – impulsive, combined

85
Q

What is the issue of heritability and ADHD?

A

Related to two genes involved with the dopaminergic system. Dysfunction in brain reward cascade which directly links abnormal craving behavior with A defect in the DRD2 dopamine receptor gene

86
Q

What is hyperkinetic disorder?

A

An enduring pattern of severe developmentally inappropriate inattention, hyperactivity and impulsivity across different settings. More impulse control difficulties then ADHD. Onset by age 6 not 12. Symptoms must be directly observed rather than reported history. Cannot be comorbid with mania, depressive, or anxiety disorder. Can be comorbid with conduct disorder.

87
Q

Why is language important in cognitive fx?

A

To categorize info, particularly important in multi step process to organize thoughts

88
Q

Damage to what area causes difficulty generating novel solutions to problems?

A

Frontal lobe

89
Q

What’s Hebbian theory?

A

Neurons that fire together, wire together. Describes basic mechanism for synaptic plasticity where presynaptic cell stimulates post synaptic

90
Q

What is the association cortex?

A

Neocortex outside the primary sensory and motor cotices that functions to produce cognition.

91
Q

How is association cortex different from primary?

A

More highly processed, complex

92
Q

What are the fx of the temporal association regions?

A

Visual and auditory cognition

93
Q

What are the fx of the parietal association cortex?

A

Somatosensory and movement control

94
Q

What are the fx of the frontal association cortex?

A

Coordinates info from parietal and temporal association regions with info coming from sub cortical regions

95
Q

What are fx of the prefrontal cortex?

A

Controlling executive fx, planning movement, specifying goals towards which movement should be made, controlling processes by which we select appropriate movements for the time and context

96
Q

What are specific behaviors of the PFC?

A

Inhibition, Shifting, emotional control, initiating, organization, monitoring, decision-making, working memory, planning, logical reasoning

97
Q

What is and how would a person look with dysfunction of inhibition?

A

Inhibition is what prevents behaviors and resists impulses. STROOP test assesses.

Dysfunction: impulsivity, swearing, blurting out things, acting out aggressively or sexually

98
Q

What is and how would a person look with dysfunction of shifting?

A

Shifting is the ability to move from one task to another. Stroop and trails assess.

Dysfunction: perseveration, rigidity, making mistake over and over again

99
Q

What is and how would a person look with dysfunction of emotional control?

A

Emotional control is ability to modulate emotions.

Dysfunction: lability

100
Q

What is and how would a person look with dysfunction of initiating?

A

Initiating is ability to start tasks.

Dysfunction: hard time getting started, coming up with ideas and responses, passive, needs support and prompts

101
Q

What is and how would a person look with dysfunction of organization?

A

Organization is ability to order info.

Dysfunction: disorganized/messy oral and written expression

102
Q

What is and how would a person look with dysfunction of monitoring?

A

Monitoring is self-monitoring, interpersonal awareness, and ability to assess self.

Dysfunction: multiple errors, lack of self-correction

103
Q

What is and how would a person look with dysfunction of decision-making?

A

Making decisions, especially small ones.

Dysfunction: take long time to make simple decisions

104
Q

What is and how would a person look with dysfunction of working memory?

A

Working memory is capacity to hold info in mind to work or solve problems.

Dysfunction: hard to complete multi step instructions

105
Q

What is and how would a person look with dysfunction of planning?

A

Planning is ability to set goals, plan steps, etc.

Dysfunction: underestimate time, resources needed to complete task, no realistic plan

106
Q

What is and how would a person look with dysfunction of logical reasoning?

A

Logical reasoning is ability to problem solve and think logically.

Dysfunction: problem with solving novel issues, etc

107
Q

Where does the dorsolateral region project? What does it influence?

A

Posterior parietal cortex, cingulate cortex, basal ganglia, and Premotor cortex.

Influences movement and memory.

108
Q

What were they attempting to treat with lobotomy?

A

Schizophrenia, bipolar, ADHD, depression

109
Q

What are the three frontal lobe syndromes?

A

Dorsolateral prefrontal syndrome
Orbitofrontal syndrome
Medial frontal syndrome

110
Q

Describe dorsolateral prefrontal syndrome and how it would affect someone.

A

Pseudo depressed syndrome. Psychomotor apathy and slowing, weakness in contralateral upper extremity, poor problem solving, amotivational, poor organization, impaired shifting, perseveration, reduced working memory and retrieval issues, organization of memories

111
Q

Describe orbitofrontal syndrome and how it would affect someone.

A

Disinhibited syndrome.
Hyperactive, intrusive, pressed behavior, poor impulse control, loss of social insight, poor situation awareness, distractibility, emotional lability

112
Q

Describe medial frontal syndrome and how it would affect someone.

A

Akinetic/apathic syndrome.
Akinetic, apathic, lacking insight, little initiation of movement or speech, lack of interest and indifference, amnesia with confabulation, incontinence, weakness of lower extremities

113
Q

What is cardiovascular disease?

A

Class of diseases that involve heart, blood vessels, or both. Cardiac disease, vascular disease of brain and kidneys, peripheral arterial disease.
Leading cause of death, followed by stroke and cancer

114
Q

What does cardiovascular disease often stem from?

A

Atherosclerosis (buildup on blood vessel walls) and hypertension (hbp)

115
Q

Who is most at risk?

A

Males 25% more likely to get, women 60% more likely to die (due to being older), older adults, stroke belt in SE, poor diet, lack of exercise, smoking, substance abuse

116
Q

What is a stroke?

A

An interruption in blood flow in the brain, either due to blockage or bleeding. Aka CVA (cerebrovascular accident), CVI (cerebrovascular insult), or brain attack.
1 in 6 will have stroke. Men more likely, women more likely to die

117
Q

What does stroke lead to?

A

Ischemia, or lack of blood to brain. Result not cause of stroke. This leads to a cascade effect where damage begins at initial site and then surrounding area.

118
Q

What are the risk factors for stroke?

A

95% 45 and older, 60% over 65, stroke in past, old age, HBP, diabetes, high cholesterol, smoking, genetics, live in stroke belt
Women: pregnancy, birth, menopause

119
Q

3 types of stroke?

A

Ischemic, hemorrhagic, and TIA

120
Q

What is an ischemic stroke and what are the risk factors?

A

Blockage of blood to brain. 87% of strokes. Two subtypes: thrombosis and embolism
Thrombosis- blood clot that develops at clogged part
Embolism- clot that travels to tiny veins in brain
Risks- atrial fib, irregular hb, primary atherosclerosis

121
Q

What is a hemorrhagic stroke and what are the risk factors?

A

When weakened blood vessel ruptures. 13% of strokes. 2 types of weakened blood vessels- aneurysm and malformations
Risks is typically uncontrolled HBP

122
Q

What is a TIA and risk factors?

A

Transient ischemic attack- mini stroke caused by temporary clot blockage. Most strokes not preceded by TIA but TIA leads to 30% of strokes

123
Q

What is Silent Cerebral Infarction?

A

Silent stroke. Brain injury likely caused by blood clot. Related to irregular heartbeat and hypertension

124
Q

What are some cognitive outcomes of stroke?

A

Perceptual, aphasia, dementia, memory issues, anosogosia- not aware of disability

125
Q

What are some emotional outcomes of stroke?

A

Anxiety, panic attacks, apathy, flat affect, psychosis, emotional lability

126
Q

What are some physical outcomes of stroke?

A

Muscle weakness, appetite loss, pain, difficulty with ADLs, apraxia- loss of learned movement

127
Q

Treatments for stroke?

A

Thrombolysis in ischemic, rehab, constriction therapy

128
Q

What is outcome in stroke affected by?

A

Age, baseline IQ, psych history, pre existing conditions

129
Q

What are the types of pediatric strokes?

A

Ischemic 45%, hemorrhagic 55%

130
Q

Risk factors for pediatric stroke?

A

TBI, hypoxia, chemo, being male, in first 2 mos of life, heart disease and prematurity for infants

131
Q

Symptoms of pediatric stroke?

A

Seizures and weakness on one side of body

132
Q

Outcomes of pediatric stroke?

A

Cognitive and behavioral issues, visual deficits, epilepsy

More likely to experience anxiety and depression

133
Q

What are signs of a stroke?

A

Muscular: overactive reflexes, paralysis of one side of the body, difficulty walking, stiff muscles, problems with coordination, or paralysis with weak muscles
Visual: sudden visual loss, double vision, temporary loss of vision in one eye, or blurred vision
Sensory: numbness, pins and needles, or reduced sensation of touch
Speech: speech loss, difficulty speaking, or slurred speech
Limbs: weakness or numbness
Facial: muscle weakness or numbness
Whole body: lightheadedness, vertigo, balance disorder, or fatigue
Also common: inability to understand, mental confusion, headache, difficulty swallowing, or rapid involuntary eye movement

134
Q

What is a TBI and prevalence?

A

Traumatic brain injury. 1.4 million treated a year, many more not. Most common in 15-24 yr old males due to risk taking, also kids and elderly due to falls. Head injury most common form of brain damage in ppl younger than 40.

135
Q

What impacts recovery from TBI?

A

Substance abuse, Rx drugs, pre existing psych and med issues, alcohol

136
Q

TBI due to?

A

Blunt force trauma, acceleration/deceleration force, both

137
Q

Types of TBI?

A

Open and closed. Closed more common

138
Q

Explain coup- countercoup

A

Coupe is the damage at site of impact, counter coup is damage on side opposite of initial impact.

139
Q

How do you classify mild, moderate or severe TBI?

A

Glasgow coma scale-measures level of consciousness through verbal response, eye movement response, and motor response
LOC- loss of consciousness in minutes/days
PTA- post traumatic amnesia in days

140
Q

How do you classify moderate TBI?

A

GCS score of 9-12, LOC of 30 min to one day, PTA of 1 to 7 days

Anything with higher GCS and lower LOC and PTA is mild; lower GCS and higher LOC and PTA is severe

141
Q

In moderate to severe TBI what regions most likely affected?

A

Frontal and temporal

142
Q

What are types of TBI damage?

A

Primary if there is axonal injury (damage to corpus collosum or bundle fibers after severe rotation), vascular injury, or hemorrhage
Secondary from cell damage or secondary systemic processes such as hypotension, hypoxia, ischemia, excitotoxicity (damage of cells due to excessive stimulation by NTs), energy failure in brain metabolism, cell death cascades/necrosis, edema, traumatic axonal injury, inflammation

143
Q

Explain edema

A

Swelling of the brain from contusion, or bruise of brain. Major swelling or collection of blood (hematoma) leads to compression, which might cause hernia (more likely with diffuse edema and hemorrhage)

144
Q

Explain traumatic axonal injury

A

DIA or diffuse axonal injury. Typically in upper brainstem and axons between white and gray matter

145
Q

What are treatments for TBI?

A

Decompressive craniotomy

146
Q

Outcome of TBI?

A

Most recovery in 1st year (most cognitive in 6-9 mos) may continue 2-3 yrs. May have issues of substance use, motor impairment, balance issues, dizziness, mood/sleep/personality issues, psychosis, sexual issues, fatigue, headaches, visual impairment, cranial nerve impairments, lack of awareness, work issues, family/social issues

147
Q

What suggests poor prognosis?

A

Personality, pre existing conditions, chronic pain, depression/anxiety, social psych factors, litigation, and post concussive syndrome

148
Q

What is postconcussive syndrome?

A

Symptoms that occur way after should have been resolved. Risk factors include age, expected outcome, pre existing med or psych, gender.
Symptoms include PTSD, depression, anxiety/stress/somatic issues, substance abuse, insomnia, chronic pain or headache, brain injury, vestibular injury

149
Q

What is mTBI?

A

Mild traumatic brain injury or concussion. 80% of all TBI. Very heterogenous. Medically: a traumatically induced physiological disruption of brain fx manifested by LOC, amnesia, altered mental state, focal neuro deficit, but NOT over 30min LOC, 13-15 GCS, or PTA greater than one day

150
Q

Complicated v uncomplicated mTBI

A

Complicated shows on imaging

151
Q

What is the difference between epilepsy and seizures?

A

Seizure is isolated electrical disturbance in brain; epilepsy is neuro disorder marked by seizures (at least two)

152
Q

What are the prevalence rates and causes for epilepsy?

A

More common in young children and older adults, 1 in 26 or 1-3 million

Causes: brain injury, drug overdose or withdrawal (esp. Alcohol), fever

153
Q

How respond to someone having a seizure?

A

Time it, loosen clothing, remove sharp objects, lay person on side, reassure the audience, stay with them, do not hold down or put anything in mouth. If longer than 5 minutes, keep occurring, or loss of consciousness, call 911

154
Q

Two types of seizures?

A

Focal: simple partial, complex partial, and secondarily generalized

Generalized: absence, atonic, tonic, clonic, myoclonic, tonic-clonic

155
Q

What does a simple partial seizure look like?

A

no loss of consciousness
Few seconds
Involve sensory, motor, autonomic or psychic phenom
AURA

156
Q

What does complex partial seizure look like?

A

Few seconds to few minutes
Loss of consciousness
Starts as simple or aura
Impaired responses to environ stimuli

157
Q

What does secondarily generalized seizures look like?

A

Move from simple to complex to generalized, typically tonic-clonic (grand mal)- stiffening and bilateral jerking of extremities
Less than 3 minutes

158
Q

What do absence seizures look like?

A

Brief episodes- 20sec- of impairment of consciousness with no warning
Children can have many many a day
Onset in childhood or adolescence

159
Q

Atonic seizures?

A

Brief loss of muscle tone of postural muscles- drop head or crumple to floor

160
Q

Tonic seizures?0

A

Sudden onset
Bilateral tonic extension or flexion of head, trunk, or extremities
Several seconds
May fall to group

161
Q

Clonic seizures?

A

Brief rhythmic jerking of muscles
Typically lower and upper extremities
Consciousness impaired

162
Q

Myoclonic seizures?

A
Lightening fast jerks of symmetric movement
Head, distal limbs, axial musculature
Cluster over period of several minutes
No loss of awareness
May evolve to tonic-clonic
163
Q

Primary generalized tonic-clonic?

A

Grand mal
Tonic extension of extremities for 20s
Clonic shaking about 45s
Period of confusion after

164
Q

Which seizures feature impairment of consciousness?

A

Complex partial
Absence
Clonic
Tonic-clonic (after)

165
Q

What are febrile seizures?

A
Seizure associated with fever in children
Between 1 month and 5 years old
No hx of seizure prior to fever
2-5%
Typically generalized
166
Q

What are the typical cognitive findings in epilepsy?

A

Decline in verbal memory, attention, and psychomotor speed

167
Q

What are profiles of epilepsy?

A

Generalized syndromes: generalized, frontal lobe impairment in flexibility, working memory and task shifting
Temporal lobe epilepsy: issues with memory, atten/exec fx, language, visuoconstruction, IQ
Frontal lobe epilepsy: fine motor, attn/exec fx, fluency, sometimes memory

168
Q

Why is NP testing important?

A

Predicting outcomes (cognitive and psychological)
Assisting with lateralization or localization of brain dysfunction
Assessing post surgery
Get baseline assessment of cognitive fx

169
Q

Epilepsy multidisciplinary model?

A
Neurologica exam
EEG interictal- between seizures
Ictal video EEG- during seizures
FMRI
Interictal PET
Intracranial monitoring 
Wada's test
Ictal SPECT
170
Q

Common psychiatric disorders in epilepsy?

A
Mood disorder- 20-50%, higher suicide risk
Anxiety disorder- 10-50%, often comorbid
Psychosis
Personality
Substance abuse
171
Q

Treatment for epilepsy?

A

Meds

Surgery (resection)

172
Q

What is difference between normal aging, MCI, dementia, and delirium?

A

Normal aging: slight decrements in processing speed, memory, movement
MCI: isolated impairments, usually memory, bridge to dementia
Dementia: severe impairments in 2 or more cognitive domains and fx decline
Delirium: medical induced

173
Q

Dementia stats?

A

Rare in young, 60 1%, 65+ 5-8%, 74+ 15-20%, 85+ 30-50%.

Below 65, early onset

174
Q

How are dementias classified in DSM 5?

A

Part of neuro cognitive disorders.

Cognitive deficit primary and acquired rather than development

175
Q

Different dementias?

A
Alzheimer's 
Vascular
Lewy body
Parkinson's
Frontotemporal
TBI
HIV
Substance/med induced
Hunting tons
Prion disease
176
Q

What’s unique about dementia?

A

Acquired illness and degenerative

Either primary degenerative or secondary result of illness

177
Q

Alzheimer’s disease prevalence and onset?

A

35% of all dementias and 15% of mixed, so 50%

Earlier than 65 is early onset

178
Q

Risk factors for Alzheimer’s disease

A

Older, female, lower education, family history especially early onset, down syndrome, head injury, psychiatric illness, alcohol abuse

179
Q

Where does atrophy begin in Alzheimer’s? And where does it spread?

A

Atrophy begins in the medial Temporel lobe. It spreads to the parietal and frontal lobe and eventually most of neocortex

180
Q

Most cellular changes in Alzheimer’s disease are in what two lobes?

A

Temporel and parietal

Ventricles are also enlarged

181
Q

Describe the course of Alzheimer’s disease

A

Early – subtle personality changes such as being withdrawn less energy, depression but depending on environment, minimize cognitive issues
Later on – agitation, confusion, wandering, apathy, decreased sleep and appetite, delusions and hallucinations

182
Q

How does Alzheimer’s affect the brain?

A

Through beta-amyloid plaques and neurofibrillary tangles

183
Q

Describe mild Alzheimer’s

A

Mild memory problems for new events and information, increased difficulty thinking of the word you want to use, or names of acquaintances, if other people notice cognitive difficulties, they consider them minor

184
Q

Describe moderate Alzheimer’s disease

A

Pronounced memory problems, anxiety paranoia or depression, confusion about the date or time, disorientation a familiar places, spatial problems, difficulty with math, difficulty planning and organizing, difficulty multitasking, difficulty recalling details of personal history

185
Q

Describe severe Alzheimer’s disease

A

Serious amnestic memory problems, difficulty with most cognitive abilities, personality changes, behavioral problems, wondering and becoming lost, trouble naming or recognizing family and loved ones, problems naming highly familiar items, difficulty caring for self, changes in sleep wake cycle

186
Q

What is the characteristic of vascular dementia?

A

Stepwise progression

187
Q

What is the prevalence and onset of vascular dementia?

A

Onset age 62 to 75
Slow or abrupt
Second most common dementia, 10% vascular, 15% mixed

188
Q

What are the risk factors for vascular dementia?

A

History of stroke, atherosclerosis, high blood pressure, diabetes, high cholesterol, smoking, obesity, male, older

189
Q

What are the behavioral symptoms of vascular dementia?

A

They vary, depression anxiety, apathy, withdrawal, disinhibition

190
Q

What deficits occur in vascular dementia?

A

Early deficits and processing speed, attention and executive function, visual constructional, memory intact early, poor rapid generative verbal fluency, psychomotor deficits

191
Q

What is frontotemporal dementia?

A

Dementia of the frontotemporal areas.
Frontal variant of FTD is marked by personality and behavior changes
Primary progressive aphasia is the second type of FTD

192
Q

What’s behaviors in the behavioral cluster occur with frontotemporal dementia?

A

Loss of personal awareness, disinhibition, mental inflexibility, perseverations, impulsivity

193
Q

What behaviors are associated with the affective cluster of frontotemporal dementia?

A

Indifference, depression, a spontaneity

194
Q

What behaviors are associated with the speech symptoms of frontotemporal dementia?

A

Repetition of phrases, echolalia, mutism

195
Q

What are the risk factors and prevalence of frontotemporal dementia?

A

Prevalence – 5 to 9%, more common under 60

Risk factors – family history, older, abnormal tau protein gene

196
Q

What is unique about HIV-associated dementia?

A

Languages kept longer than the other dementias

197
Q

What is the prevalence of HIV-associated dementia?

A

Six to 66% of HIV patients

Acquired neurocognitive disorder lasting at least one month in at least two areas

198
Q

What is the course of HAD?

A

Slow with one. Of asymptomatic problems followed by physical and neurocognitive morbidity

199
Q

What are the risk factors for HIV-associated dementia?

A

Higher CSF viral load, hepatitis C infection

200
Q

What are the early neuropsychological deficits in HIV-associated dementia?

A

Processing and psychomotor speed, attention and executive functions, verbal fluency, visuospatial skills, mild memory

201
Q

Mild versus major deficits in executive functioning with dementia

A

Mild – increased effort, fatigue

Major – abandons complex projects, one task at a time, needs others to plan

202
Q

Mild versus major deficits in language and memory with dementia

A

Mild – difficulty with recall, needs occasional reminders, might repeat self

Major – repeat self often, can’t keep track

203
Q

Mild versus major deficits and language with dementia

A

Mild – word finding difficulty, Megas general in place of specific, grammar errors

Major – significant difficult with language, no names or specifics, echolalia and automatic speech proceed mutism

204
Q

Mild versus major deficits and perceptual motor skills with dementia

A

Mile – needs maps and directions more, notes, gets turned around

Major – it’s lost, especially at dusk due to light changing perceptions

205
Q

Mild versus major deficits in social cognition with dementia

A

Mild – subtle personality changing

Major – behavior not acceptable, insensitive, disinhibition, little insight