Brain Exam 2 Flashcards
1
Q
Thalamus: origin and location
A
- develops from diencephalon
- located on either side of 3rd ventricle
- supplied by proximal branches of PCA
2
Q
Thalamus: function
A
- relays info to cortex: receives input from subcortical structures
- important for sensory motor integration
- important for alert and conscious state
- allows for modulation of signals before they enter cortex = selective attention
3
Q
Internal medullary lamina
A
- streaks of white matter that run through thalamus that form Y shape & divide thalamus
4
Q
Medial geniculate body (MGB)
A
- input: inferior colliculus
- cortex: auditory cortex (Heschl’s gyrus)
5
Q
Lateral geniculate body (LGB)
A
- input: optic tract
- cortex: visual cortex
6
Q
Ventral posterior lateral nucleus (VPL)
A
- input: dorsal column and spinothalamic tracts (body)
- cortex: somatosensory
7
Q
Ventral posterior medial nucleus (VPM)
A
- input: trigeminal (face)
- cortex: somatosensory
8
Q
Ventral lateral geniculate body (VL)
A
- input: cerebellum
- cortex: motor, premotor, supplementary motor
9
Q
Ventral anterior geniculate body (VA)
A
- input: basal ganglia
- cortex: motor, premotor, supplementary motor
9
Q
Anterior nucleus
A
- input: mammillary body, hippocampus
- cortex: cingulate gyrus
10
Q
Dorsomedial nucleus (DM)
A
- input: amygdala
- cortex: prefrontal cortex
11
Q
Pulvinar nucleus
A
- associated
- input: parietal, temporal, occipital corticies
- cortex: parietal, temporal, occipital corticies
12
Q
Intralaminar nuclei
A
- input: diverse sources including brain stem, reticular formation
- cortex: diffuse (reticular activating system)
13
Q
Pure sensory stroke
A
- thalamic syndrome
- lacunar infarct in VPL/VPM
- often accompanied by small vessel disease assoc. w/ HTN and DM
- typified by microatheroma and lipohyalinosis
- loss of all sensation from body and face
14
Q
Thalamic hemorrhage
A
- spontaneous and usually assoc. w/ HTN
- involvement of adjacent internal capsule dominates clinical picture
- numbness and sensory deficits on contralateral side sometimes developing into thalamic pain
- hemiparesis
15
Q
Thalamic coma
A
- infarcts in both reticular activating systems
- top of basilar artery occlusion
16
Q
Hypothalamus: function
A
- whole body homeostasis via regulation of ANS, endocrine system, and somatic motor activity (behavioral drives)
- ensures survival of the individual and survival of the species
- effects behaviors required to meet basic needs including feeding, drinking, reproduction
17
Q
Circumventricular organs
A
- select regions where BBB is interrupted allowing chemical communication between brain and systemic circulation
- 3 in hypothalamus
18
Q
Hypothalamic disturbances may result from
A
- inflammation
- tumors (intrinsic or extrinsic)
- vascular disorders
- hydrocephalus
19
Q
Clinical disorders associated with hypothalamic lesions
A
- hypothermia and hyperthermia
- obesity and wasting
- Diabetes Insipidus
- disturbances of sleep
- emotional disorders
- hypogonadism and early puberty
- altered growth patterns
20
Q
The hypothalamus regulates the ANS through descending connections with the ____ and ____. Sites associated with ____ function tend to be located in anterior and ____ function in posterior.
A
- brainstem
- spinal cord
- parasympathetic
- sympathetic
21
Q
Magnocellular system
A
- neural; posterior lobe of hypothalamus
- made of paraventricular (PVN) and supraoptic (SON) nuclei
- synthesizes oxytocin [milk letdown] and vasopressin [water resorption] and transports to posterior pituitary for release
- large diameter neurons
22
Q
Parvicellular system
A
- humoral; anterior lobe of hypothalamus
- secretes releasing and inhibiting factors that regulate secretion from anterior pituitary via hypophyseal portal vessels
- small diameter neurons
23
Q
Major hypothalamic substances that stimulate or inhibit release of anterior pituitary hormones
A
- GnRH -> FSH and LH
- GHRH -> growth hormone
- SS -| growth hormone
- TRH -> TSH
- DA -| prolactin
- CRH -> ACTH
24
Q
Hypothalamus: food intake and metabolism nuclei
A
- ventromedial hypothalamus (VMH) [satiety center]
- lateral hypothalamus (LH) [feeding center]
- arcuate nucleus (ARC)
- paraventricular nucleus (PVN)
- dorsomedial nucleus (DMH)
25
Q
Hypothalamus: day-night rhythms nuclei
A
- suprachiasmatic nucleus (SCN)
26
Q
Hypothalamus: temperature regulation nucleus
A
- anterior hypothalamus (AH)
- preoptic area (POA) [heat dissipation]
- posterior hypothalamus (PH) [heat conservation]
27
Q
The input to the hypothalamus to control the physiological manifestation of emotion comes from ____.
A
- limbic structures
28
Q
Limbic lobe
A
- forms rim of cortex at junction between diencephalon and cerebral cortex
- includes Papez circuit (hippocampus, fornix, mammillary bodies, anterior nucleus of thalamus, and cingulate gyrus)
- and orbital and medial prefrontal cortex, amygdala, septal nuclei, dorsomedial nucleus of the thalamus, ventral striatum, hypothalamus
29
Q
Hippocampus subsystem
A
- has primarily an indirect role in emotion
- essential for factual or declarative memory
- specifically involved in consolidation process that requires sleep
- bilateral damage results in profound anterograde amnesia
- 3 layer cortex: dentate gyrus, hippocampus proper, subiculum
- one way info flow: though dentate gyrus, CA3, CA2, CA1, to entorhinal cortex
- CA1 sensitive to anoxia
- impacted by chronic stress (a little stress enhances)
30
Q
Amygdala
A
- central to emotion and participates in acquisition, consolidation, and recall of emotional memory, aggression
- important for determining affective perception of sensory stimuli: good or bad
- plays central role in fear and fear conditioning
- attaches emotional significance to various stimuli perceived by assoc cortex
- 3 subnuclei: medial, basolateral, and central
- 2 pathways: through sensory cortex or skip
31
Q
Habituation
A
- decreasing response to a sensory stimulus
- molecular basis: repeated stimulation causes depletion of glutamate vesicles at atonal terminal = less depolarization
32
Q
Sensitization
A
- increasing response to a sensory stimulus
- molecular basis: interneuron releases serotonin, activating sensory neuron receptors. cAMP activates PKA -> more Ca influx = increased glutamate release
- short term and long term
- long term requires protein phosphorylation and protein synthesis
33
Q
Associative conditioning
A
- associating 2 sensory stimuli
- aka Pavlovian conditioning
- leads to formation of an associative memory
34
Q
Early LTP molecular mech
A
- increase in Ca
- activation of protein kinases
- phosphorylation of receptors
35
Q
Late LTP molecular mech
A
- increase in Ca
- activation or protein kinases
- phosphorylation of CREB
- increased gene expression and protein synthesis
36
Q
Learning and memory requires changes in ____.
A
- synaptic strength
37
Q
Short-term memory depends on ____ but not ____. ____ depends on both.
A
- protein phosphorylation
- protein synthesis
- long-term memory
38
Q
____ are essential for associative conditioning.
A
- NMDA receptors
39
Q
Frontal lobe functions
A
- cognition, executive function, motor strip, execution of movement, frontal eyefields, Broca’s (dominant hemisphere) essential for spoken word, working memory
- lesions: nonfluent aphasia
40
Q
Parietal lobe functions
A
- integrate sensory info, contains primary sensory strip, reading and math functions
- lesions: contralateral neglect; Gerstman’s syndrome
41
Q
Temporal lobe functions
A
- auditory perceptions, primary auditory cortex, Wernicke’s essential for understanding speech, hippocampus and amygdala
- lesion: fluent aphasia-dominant hemisphere
42
Q
Cortex cellular organization
A
- 6 layers
I molecular layer: relatively free of cells; mostly axons
II external granule layer: small cell bodies (sensory)
III external pyramidal layer: big cell bodies (motor)
IV internal granule layer
V internal pyramidal layer
VI polymorphic layer: mix of things - not uniform throughout cortex
43
Q
Occipital lobe functions
A
- processing and integrating visual information, primary & association visual cortex
44
Q
Cortical connectivity: input to cortex
A
- thalamic sensory and relay nuclei: layer IV
- intrathalamic nuclei: layer VI
- intracortical input (corpus callosum): layers II and III
45
Q
Cortical connectivity: output from cortex
A
- layer III: other cortical areas
- layer V: striatum, brainstem, spinal cord
- layer VI: thalamus
46
Q
Association fibers vs. commissural fibers
A
- association: stay w/in same hemisphere (superior longitudinal fasciculus, arcuate fasciculus, cinculum)
- commissural: project from one hemisphere to the other (corpus callosum)
47
Q
blood supply: MCA
A
- primary motor
- primary sensory
- frontal eye fields
- association sensory
- Broca’s and Wernicke’s
- supramarginal and angular
48
Q
Blood supply: ACA
A
- paracentral lobule
- cingulate gyrus
49
Q
Blood supply: PCA
A
- visual cortex
- visual association cortex
50
Q
Retina cell layers
A
- ganglion cells
- bipolar cells
- photoreceptors cells: stacks of discs of membranes that generate electrical signals from light absorption
51
Q
Rods vs. cones
A
- black and white vs. color
- blunt tip vs. tapered tip
- more vs. less
- none in fovea (concentrated around) vs. throughout retina and concentrated in fovea
- dimly-lit vs. well-lit
- many receptors vs. few receptors
- poor acuity vs. excellent acuity
- excellent sensitivity vs. poor acuity
52
Q
Visual cortex organization
A
- forward and medial regions: motion and spatial relations (where)
- lateral regions: form and color (what)
- cuneus (upper) processes lower visual field
- lingula (lower) processes upper visual field
53
Q
Fovea vs. peripheral retina
A
- high vs. low threshold
- cones only vs. rods and cones
- limited or no convergence vs. extensive convergence
- photopic vs. scotopic illumination
- central, color, detail vision vs. peripheral, achromatic, poor detail vision
54
Q
Age Related Macular Degeneration
A
- early stage: no symptoms
- middle stage: blurred central vision, straight lines appear distorted and wavy, blurred or dark spot in center of vision gradually gets larger
- later stages: patient might not recognize faces
- does not typically affect peripheral vision or cause complete blindness
- dry stages: drusen deposits and retinal pigment epithelium cells and neighboring photoreceptors degenerate
- wet stages: new vessels invade subretinal space and they leak blood and plasma causing more degeneration
55
Q
Retinitis Pigmentosa
A
- usually in younger people (genetic disease)
- symptoms: decreased vision in low light, loss of peripheral vision causing tunnel vision, loss of central vision in advanced cases
- slow progression; complete blindness uncommon
56
Q
Diabetic Retinopathy
A
- symptoms: blurred vision, gradual vision loss, floaters, shadows or missing areas of vision, difficulty seeing at nighttime, cotton wool spots
- usually none until damage is severe
- nonproliferative stage: microaneurysms and retinal hemorrhages cause fluid leakage
- proliferating stage: new fragile blood vessels form and hemorrhage; small scars develop; vision loss
57
Q
Glaucoma
A
- leading cause of blindness worldwide
- caused by buildup of pressure leading to damage of optic nerve head
- open angle (majority), closed angle (emergency), and congenital (children)
- open angle symptoms: none until damage severe; slow loss of peripheral vision that can lead to blindness
- closed angle symptoms: sudden/severe pain in one eye, decreased or cloudy vision, nausea and vomiting, rainbow halos around lights, red eye
58
Q
If neither pupil constricts, suspect ____. If only one pupil constricts, suspect ____. If discrete area missing in one eye with no affront pupillary defect, suspect ____.
A
- optic nerve involvement
- oculomotor involvement
- lesion on retina
59
Q
Motor neuron lesion locations
A
- CNS (cerebral cortex, subcortex, brainstem, spinal cord)
- anterior horn cell
- peripheral nerve
- neuromuscular junction
- muscle
60
Q
UMN weakness
A
- increased tone (spasticity)
- increased deep tendon reflex; clonus
- upper extremities tend to be flexed; lower extremities tend to be extended
- Babinski sign present
- less atrophy
61
Q
LMN weakness
A
- decreased tone (flaccidity)
- decreased deep tendon reflexes
- fasciculations
- Babinski sign absent
- more atrophy
62
Q
Sensory lesion locations
A
- CNS (cerebral cortex, subcortex, brainstem, spinal cord)
- peripheral nerve
63
Q
Peripheral sensory etiologies
A
- symmetric “stocking glove” distribution (neuropathy) or
- fits individual nerve or root pattern
64
Q
Central sensory etiologies
A
- spinal sensory level?
- loss of touch/vibration on one side and pain/temp on other side?
- hemisensory loss with face, arm, and leg?
65
Q
Altered mental status/cognition lesion location
A
- CNS (cerebral cortex, subcortex, brainstem)
66
Q
Prosopagnosia
A
- inability to identify faces
- bottom of temporal and occipital lobes on both sides of cortex
67
Q
Frontal lobe syndrome
A
- behavioral changes: lack of responsibility/insight, indifference; abulia (slowed response to environment); hyper sexuality, incontinence, emotional lability
- frontal release signs: suck, snout, palmomental, grasp reflexes; Gegenhalten (variable resistance to passive limb movement)
68
Q
Parietal lobe syndromes
A
- visuospatial deficits
- sensory integration: agraphesthesia, astereognosis, neglect
- visual field deficit: pie in the floor
69
Q
Gerstmann syndrome
A
- dominant parietal lobe syndrome
- finger agnosia
- acalculia
- left-right confusion
- agraphia
70
Q
Non-dominant parietal lobe syndrome
A
- denial of deficit (anosognosia)
- spatial difficulty (drawing, assembling blocks; hemineglect [almost always left side])
- extinction on double-simultaneous stimuli
71
Q
Occipital lobe syndromes
A
- contralateral homonymous hemianopia
- cortical blindness: Anton’s syndrome (denial of blindness) and Balint’s syndrome (bilateral occipitoparietal; simultagnosia, optic ataxia, oculomotor apraxia)
72
Q
Temporal lobe symptoms
A
- auditory integration
- memory disturbance (bilateral hippocampus)
- visual field deficit (Meyer’s loop - pie in the sky)
- Wernicke’s aphasia
73
Q
ICA
A
- internal carotid artery; large vessel
- contralateral weakness
- ipsilateral monocular vision loss (amaurosis fugax)
74
Q
ACA
A
- anterior cerebral artery; large vessel
- leg more than arms weakness/sensory deficit
- language spared
75
Q
MCA
A
- middle cerebral artery; large vessel
- arm more than leg weakness; sensory deficit
- aphasia on left, dysprosody on right
- contralateral homonymous hemianopia/quadrantanopia
- gaze deviation towards side of lesion
76
Q
PCA
A
- posterior cerebral artery
- contralateral homonymous hemianopia
- alexia without agraphia (left PCA involving splenium)
77
Q
Pure motor hemiplegia
A
- lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis
- internal capsule or ventral pons
78
Q
Pure hemisensory loss
A
- lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis
- thalamus
79
Q
Sensorimotor loss
A
- lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis
- thalamocapsular
80
Q
Clumsy hand dysarthria
A
- lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis
- internal capsule, ventral pons, or corona radiata
81
Q
Ataxia hemiparesis
A
- lacunar syndrome; assoc. w/ chronic HTN/lipohyalinosis
- ventral pons or internal capsule
82
Q
Watershed strokes
A
- Acute hypoperfusion (i.e. cardiac arrest, vascular stenosis)
- ischemia in distal areas of vascular supply: ACA-MCA -> proximal > distal weakness in arm and leg; MCA-PCA -> visuospatial deficits (Balint’s)
83
Q
Acute management of stroke
A
- head CT
- MRI brain with MRA head and neck
- cardiac evaluation
- check for diabetes, cholesterol
- tPA if within 4.5 hours, thrombectomy
84
Q
Long term stroke management
A
- antiplatelet agent
- anticoagulation if indicated
- statin
- risk factor modification
85
Q
Intracerebral hemorrhage
A
- causes: HTN**, AVM, tumor, amyloid angiopathy, hemorrhagic conversion of ischemic stroke
- location: basal ganglia > pons > thalamus > cerebellum
- may have sudden onset w/ smooth progression of deficit
86
Q
Aneurysms
A
- outpouching due to weakness of vessel wall
- occur at bifurcation
- rupture leads to subarachnoid hemorrhage
87
Q
Subarachnoid hemorrhage
A
- sudden onset terrible headache, stiff neck, photophobia, nausea/vomiting, transient LOC
- spectrum of classification (1 to 5)
88
Q
Epilepsy
A
- at least 2 unprovoked seizures; tendency to recurrent, unprovoked seizures
89
Q
Focal seizure
A
- aka partial
- simple: focal seizure w/ no impaired consciousness
- complex: dyscognitive; impairment of consciousness
- more likely to have a focal lesion
90
Q
Generalized seizure
A
- refers to onset
- spasm affects both sides of body almost contemporaneously
- absence (petit mal): staring and lack of awareness; generalized spike and wave EEG
- myoclonic
- generalized clonic, tonic, tonic-clonic (grand mal): body stiffening and rhythmic activity
- causes: genetic; metabolic derangement
91
Q
Brain tumor classification
A
- intra-axial: in brain substance
- gliomas: astrocytoma/glioblastoma multiforme, epemdymoma, oligodendroglioma
- neuronal tumors: DNET;favors temporal lobe; seizures
- metastasis
- extra-axial: from outside brain
- meningioma
- schwannoma (acoustic neuroma)
- neurofibroma
- sella masses (pituitary adenoma, craniopharygioma)
- metastasis
92
Q
Gliomas
A
- astrocytoma: pilocytic (pediatric, benign, usually cerebellar); diffuse [low grade] (malignant but good prognosis, no enhancement); anaplastic (malignant, poor prognosis); glioblastoma multiforme (worst prognosis, most common glioma, likes to cross corpus callosum, pseudopallisading necrosis)
- ependymoma: originates in ventricles, hydrocephalus common, low grade and slow growing
- oligodendroglioma: slow-growing, good prognosis, “fried egg” histology, seizures common
93
Q
Meningiomas
A
- extra-axial
- signs due to compression
- can be removed
- slow-growing
- good prognosis
94
Q
Stellar masses
A
- extra-axial
- headaches, bitemporal hemianopia
- pituitary adenoma (hormonal symptoms)
- craniopharyngioma (cystic)
95
Q
The ectoderm becomes the ____ (induction), which becomes the ____ (neurulation), which forms the ____.
A
- neural plate
- neural tube
- CNS
96
Q
Failure of cranial neuropore closure results in ____. Failure of caudal neuropore closure results in ____. What else are neural defects associated with?
A
- anencephaly
- spina bifida
- folate deficiency
97
Q
The neural crest forms ____.
A
- PNS, ANS, & many more tissues
- in conjunction w/ mesoderm, it contributes to calvarium and meninges of brain
98
Q
Vesicles formation
A
- prosencephalon -> telencephalon (cerebral hemispheres) and diencephalon (thalamus, hypothalamus, optic nerves)
- mesencephalon -> midbrain
- rhombencephalon -> metencephalon (pons, cerebellum) and myelencephalon (medulla)
99
Q
Malformations of cortical development
- neuronal and glial proliferation -> ____.
- neuronal cortical organization -> ____.
- neuronal migration -> ____.
A
- lissencephaly: abnormal decrease in cell proliferation; less gyri
- polymicrogyria: cortex too thick; increased gyri
- heterotopias: gray matter did not migrate out properly
100
Q
MS classification
A
- relapsing-remitting: reverts back to baseline between attacks; inflammation
- relapsing-progressive: reverts not quite back to baseline between attacks; inflammation; neurodegenerative
- secondary progressive: coverts to a progressive course; neurodegenerative
- primary progressive: progressive course from onset; neurodegenerative
101
Q
MS evaluation
A
- demonstrate lesions in space and time: brain and spine MRI; clinical symptoms
- evoked potentials (electrical testing)
- lumbar puncture: >2 oligoclonal bands, increased IgG synthesis/IgG index, WBCs < 50
102
Q
Types of dementia
A
- Alzheimer’s: loss of memory, executive function, visuospatial impairment, language, behavior
- Lewy body: hallucinations, psychosis
- vascular: stepwise progression of cognitive decline
- frontotemporal: social disinhibition, abulia
103
Q
Alzheimer’s pathology
A
- senile plaques: beta-amyloid
- neurofibrillary tangles: Tau protein
104
Q
Alzheimer’s disease types
A
- unknown: ApoeE-4, age, female, head trauma
- down’s syndrome
- familial: early onset; autosomal dominant (APP, presenillin 1)
105
Q
Concussion
A
- altered awareness/consciousness without gross injury
- acute symptoms are transient (< 6 hrs)
- post-concussion syndrome: residual symptoms lasting weeks to months or longer; headache, dizziness, fatigue, mild cognitive symptoms, mood changes
106
Q
Hematoma: epidural
A
- middle meninges artery rupture
- between dura and skull
- skull fracture
- lucid interval
- biconvex
107
Q
Hematoma: subdural
A
- rupture of bridging veins
- between dura and brain
- can be both acute and chronic
- involved trauma can be mild (especially in elderly)
- lens shape
108
Q
Coup injury
A
- site of impact is directly over contusion
109
Q
Countrecoup injury
A
- site of impact is on opposite side of head
110
Q
Classification of consciousness
A
- alert
- somnolence: state of drowsiness or near sleep
- obtundation: mild to moderate reduction in alertness; accompanied by a lesser interest in environment
- stupor: condition of deep sleep or similar behavioral unresponsiveness from which the subject can be aroused only with vigorous and continuous stimuli; responds to voice/pain
- coma: both arousal and awareness are severely depressed (> 1 hr); cortical and subcortical (no eye movement)
- encephalopathy: syndrome of global brain dysfunction
111
Q
Coma causes
A
- compressive: cerebral (bilateral subdural hematoma); diencephalon (thalamus hemorrhage, hypothalamus tumor); brainstem (uncial herniation, cerebellum)
- destructive: cerebral hemisphere (cortex [acute anoxia], subcortical [delayed anoxia], diencephalon [bilateral thalamic injury/stroke], brainstem [midbrain, pons stroke])
112
Q
Persistent vegetative state
A
- patient may open eyes, but no interaction with environment
- brainstem is working, but cortex is not
- diagnosis after 1 month; 1 year in trauma cases
113
Q
Minimally conscious state
A
- between PVS and normal
- can follow simple commands
- may gesture or verbalize yes/no responses
- may have intelligible verbalization
- demonstrates purposeful behavior rather than reflexive
114
Q
Locked-in syndrome
A
- patient is awake but incapable of movement and speech
- eye movements possible
- ventral pontine lesion
- respiration can be normal due to sparing of chemoreceptors in ventral medulla
115
Q
Glasgow coma scale
A
- eye opening (1-4): 1 = no response, 2 = noxious stimulus, 3 = voice, 4 = normal
- verbal response (1-5): 1 = no response, 2 = incomprehensible; 3 = inappropriate words, 4 = confused, 5 = normal
- motor response (1-6): 1 = no response, 2 = extensor, 3 = flexor, 4 = withdraws to noxious stimulus, 5 = localized to pain only, 6 = normal
- 8 or less is serious head injury
117
Q
Management of ICP
A
- elevate head
- hyperventilation
- osmotic diuretics
- barbiturate coma
- CSF drainage (ventriculostomy)
- hemicraniectomy
118
Q
cortical lesion
A
- behavioral/personality changes
- language disorder
- visual field deficit
- higher cortical sensory deficit
- apraxia
- neglect
- hemiparesis (part of side)
- hemiesthesia (part of side)
- seizure
119
Q
subcortical lesion
A
- pure motor deficits (may be whole side)
- pure sensory deficits (may be whole side)
- movement disorders
- absence of cortical deficits
120
Q
brainstem lesion
A
- crossed signs
- CN deficit
- vestibular, visual field deficits
- cerebellar signs
- could be bilateral signs
121
Q
spinal cord lesion
A
- usually bilateral motor/sensory
- no involvement above neck
- UMN/LMN combo
- bowel/bladder dysfunction
- autonomic dysfunction
