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142 Cards in this Set
- Front
- Back
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Describe anatomical location of thalamus
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Medial border: 3rd ventricle
Later border: posterior limb of internal capsule Superior: lateral ventricle Ventral: midbrain, subthalamic nuclei, hypothalamus |
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Thalamus: optic tract
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optic tract -> lateral geniculate body -> calcarine gyri via optic radiations
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Thalamus: auditory
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inferior colliculus -> medial geniculate body -> Heschl's gyri (primary auditory cortex in temporal lobe deep in Sylvian fissure)
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Thalamus: somatosensory body
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Ventro-posterior lateral (VPL)
From spintothalamic and posterior column tracts To post-central gyrus |
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Thalamus: somatosensory face
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trigeminal system -> ventro-posterior medial nucleus -> inferior part of sensory strip
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Thalamus: motor
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Basal ganglia: globus pallidus -> ventral anterior -> motor cortex
Cerebellum: deep nuclei -> ventrolateral -> motor association |
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Thalamus: limbic
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Mamillary body -> anterior nucleus -> cingulate gyrus
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Thalamus: association nuclei (2)
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Dorsomedial: frontal cortex -> DM -> frontal
Pulvinar: parieto-temporal-occipital -> pulvinar -> p/t/o |
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Pure hemisensory stroke
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Lacune in VPL (body) or VPM (face)
No associated brainstem or cortical signs |
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Bilateral thalamic infarcts (commonly occur where?)
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Infarcts of both reticular activating systems
Occurs at top of basilar artery |
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Anatomical location of hypothalamus
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Below thalamus
Surrounds lower part of 3rd ventricle |
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Main functions of hypothalamus (6)
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Autonomic regulation
Endocrine regulation Somatic motor regulation Detects body temp Circadian rhythms Feeding/satiety |
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Hypothalamus: autonomic functions
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Through descending connections w/ brainstem and spinal cord
Output to parasympathetic ganglia (from ant hypothal) and intermediolateral cell column (from post hypothal) |
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Hypothalamic control of cardiac function
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Preoptic area and anterior hypothal - decrease heart rate/bp
Lateral and posterior hypothal - increase heart rate/bp |
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Magnocellular neurosecretory cells (from which nuclei in hypothalamus?)
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Magnocellular - posterior lobe, paraventricular and supraoptic nuclei, synth hormones (vasopressin + oxytocin) transported to post pituitary (neurohypophysis)
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Parvicellular neurosecretory cells
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Release inhibiting and releasing factors for anterior pituitary via portal system
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Hypothalamus: medial preoptic area
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temperature regulation
male sex behavior |
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Hypothalamus: suprachiasmatic nucleus
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Circadian rhythms (b/c input is from retina hence suprachiasmatic)
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Hypothalamic feeding center
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Lateral hypothalamic nuclei
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Hypothalamic satiety center
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Ventromedial hypothalamic nuclei
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Response to elevated leptin (3)
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Stimulation of anorexic peptides
Inhibition of feeding behavior Increase in metabolism |
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Korsakoff's syndrome (3)
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Associated w/ destruction of mamillary bodies
Results in confabulatory amnesia Associated w/ poor diet and alcoholism |
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Limbic structures (7)
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Cingulate and parahippocampal gyri
Hippocampal formation Amygdala Septal area Hypothalamus Midbrain reticular formation |
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Kluver-Bucy syndrome (4 signs)
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Behavioral syndrome from removal of temporal lobe ->
Fearless and placid Hypersexuality Excessive sniffing Examine objects incessantly Can also occur due to removal of amygdala alone |
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Major roles of hippocampus (2)
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Emotion (via limbic system)
Essential for factual and declarative memory |
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Stria terminalis
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Output of amygdala to thalamus
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Hippocampal formation
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Input -> subiculum -> dentate gyrus -> CA3-2-1 -> fornix
(CA1 is most prone to hypoxia) |
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Papez circuit
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Proposed anatomical substrate of emotional experience
-> hippocampus -> via fornix -> mamillary bodies -> via mammillothalamic tract -> anterior nucleus of thalamus -> cingulate and parahippocampal gyri ------> |
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Roles of amygdala
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EMOTIONAL EXPERIENCE
Fear conditioning |
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Components of basal ganglia (4)
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Striatum (caudate and putamen)
Globus pallidus (internal and external) Subthalamic nuclei Substantia nigra |
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How does dopamine regulate basal ganglia function?
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Activates direct pathway (D1R)
Inhibits indirect pathway (D2R) Ultimately promotes movement |
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Direct motor pathway (basal ganglia)
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Striatum --| GPi --| thalamus -> cortex -> Movement
Activating striatum inhibits GPi which releases the inhibition on the thalamus to the cortex Dopamine from substantia nigra activates D1 receptors in striatum |
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Indirect motor pathway (basal ganglia)
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Striatum --| GPe --| STN --> GPi --| thalamus --> cortex
Activating striatum releases the GPe inhibition of the STN which is encouraging overall inhibition by activating the GPi |
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Parkinson's (age of onset, etiology, treatment)
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55-60
Loss of dopamine producing cells in SN -> less DA to activate direct pathway -> decreased activation of cortex -> HYPOKINESIA Treatment - give more DA |
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Main clinical features of Parkinson's (5, symmetrical or not?)
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Bradykinesia
Resting tremor Rigidity Postural instability Asymmetry of symptoms |
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Huntington's (age of onset, pathology, treatment)
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Middle-aged
Neuronal and glial loss in striatum -> Activation of direct pathway Also neuronal loss in cortex Treatment - supportive, DA blockers for chorea, benzos, psych support |
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Huntington's clinical features (4)
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Movement disorder
Chorea Dementia Depression/psychosis |
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Orientation of motor and sensory strips
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Face is on inferior part of gyrus
Body/hand on superior part Lower extremity on interior/medial surface |
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What sensations are intact in someone w/ a sensory cortex lesion? What are lost?
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Pin, temperature, vibration
Deficits in: two point discrimination, direction of passive movement, agraphesthesia, point localization, astereognosis |
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Gerstmann syndrome (4)
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Agraphia
Acalculia Finger agnosia Right-left confusion Dominant (usually left) parietal lobe lesion |
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Non-dominant parietal lobe lesion (4)
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Denial of deficits (anosagnosia)
Visual, tactile, auditory extinction Spatial disorganiztion Neglect of left space |
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Wenicke's aphasia (location, 3 features)
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Temporal lobe: posterior region of superior temporal gyrus
Comprehension deficits No awareness of deficit Comprehension of non verbal commands is intact |
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Broca's aphasia (location, 3 features)
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Frontal lobe - inferior frontal gyrus
Intact comprehension Telegraphic speech Awareness of deficit |
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Conduction aphasia
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Lesion in arcuate fasciculus connecting Wernicke's to Broca's
Fluent speech, intact comprehension Unable to repeat phrases w/ grammatical connectives |
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Global aphasia (location and why, 3 features)
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Most common b/c all language areas are perisylvian and in distribution of MCA
Non-fluent aphasia w/ no comprehension and no repitition |
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Tile syndrome (cause?)
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Alexia w/o agraphia
PCA infarction All visual info goes only to right occipital Written words cannot be transferred from occipital lobe to Wernicke's (alexia) Left homonymous hemianopia |
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3 Main mechanisms for Parkinson's drugs
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Replace dopamine
Slow dopamine conversion to other substances Stimulate dopamine receptors |
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Main side effects of Parkinson's drugs (5)
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Central: agitation, confusion, hallucination
Peripheral: nausea and orthostasis |
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Levodopa/Carbidopa (mechanisms and main warning)
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Levodopa is converted to DA
Carbidopa inhibits peripheral dopa decarboxylase and doesn't cross BBB If given w/ MAOi -> too much E and NE -> HTN crisis (Also note tolerance and toxicity) |
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COMT Inhibitors (2 drug names, MOA, side effects)
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Entacapone, tolcapone
Use w/ levodopa/carbidopa Reduce levodopa -> methyldopa in periphery Minimize peripheral side effects SE: diarrhea, LFT up, nausea, dyskinesia |
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Dopamine agonists (use, 2 examples of non-ergots, unique SE (4))
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Milder SE but take longer to work
Pramipexole + Ropinirole Unique SE: pulmonary fibrosis, skin rxns, heart valve damage, compulsive behaviors |
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Apomorphine
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Dopamine agonist for hypomobility
Typical SE of dopamine: nausea/vomiting, orthostasis, cardiovascular, priapism |
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Anticholinergics for Parkinson's (2 examples, MOA, special SE)
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To correct imbalance b/w DA and Ach
Trihexyphenidyl, Benztropine Typical cholinergic SE: heart rate up, constipation, dry mouth, blurred vision Particular glaucoma risk due to increased pressure |
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Amantadine (use, SE)
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Unknown mechanisms of action
Treats rigidity, tremor, akinesia SE: mostly CNS, some GI |
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Selegiline, Rasagiline (MOA)
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MAO type B inhibitors -> Results in accumulation of DA
Parkinson's drugs |
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Distribution of ACA
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Medial surface of brain
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Distribution of MCA (3)
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Lateral surface of brain
Basal ganglia Internal capsule |
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Distribution of PCA (3)
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Medial surface of occipital lobe
Primary visual cortex and visual association cortex Thalamus |
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Blood supply to sensory and motor strip
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ACA supplies leg area medially
MCA supplies arm and face laterally |
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Lenticulostriate arteries (in basal ganglia?)
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Branches of MCA that supply internal capsule
Prone to lacunar infarcts from arteriovascular disease Lacune in basal ganglia -> corticospinal tract deficit w/ no sensory loss, pure motor hemiplegia |
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Vascular syndromes that can cause hemiplegia (3)
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MCA - more arm than leg, language difficulty on left, dysprosody on right
ACA - more leg than arm Lenticulostriate - arm = leg, language spared |
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MCA infarcts (2 main types)
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Superior division supplies motor/sensory strip and Broca's -> contralateral hemiparesis worse in arm/face, Broca's aphasia if on left, contralateral hemisensory loss
Inferior division supplies Wernicke's -> no weakness, Wernicke's aphasia, pie-in-the-sky due to interruption of Meyer's loop (homonymous superior hemianopia) |
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ACA infarcts (2)
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Contralateral weakness and sensory loss worse in legs than arms
Frontal lobe syndrome possible |
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PCA infarcts (4)
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Hemianopia contralateral to lesion
Alexia w/o agraphia Anton's syndrome: cortical blindness w/ denial of deficit Thalamic infarcts |
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Watershed infarcts (3)
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Occur at areas of overlap b/w arterial territories
Classically at junction of ACA and MCA where sensorimotor strip of prox arm and leg is Man in the barrel syndrome Often bilateral |
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Cerebral hemorrhage (main causes (3) and locations)
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Causes: HTN, small vessel disease, arteriolar necrosis
Locations: basal ganglia >> thalamus/pons/cerebelum/lobar |
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Difference between cerebral and systemic aneurysms?
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Cerebral - Saccular (Berry) b/c intracranial arteries lack external elastic lamina
Systemic - fusiform, due to atherosclerosis in large arteries |
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Cerebral aneurysms: Location, Diagnosis, Treatment
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Usually at bifurcation at anterior or posterior communicatings
Exert pressure and are usually asymptomatic until they rupture into sub-a space Hemorrhage symptoms: sudden headache Treatment: prevent further hemorrhage by clipping artery |
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Arteriovenous malformation
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Direct connection between arterial and venous circulation w/o intervening capillary bed puts veins at arterial pressure -> hemorrhage
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Stroke modifiable risk factors (4)
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HTN
Smoking Diabetes Mellitus Cholesterol |
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Stroke symptoms (5)
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SUDDEN:
blurred/decreased vision numbness/weakness difficulty speaking dizziness headache |
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Stroke definition
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Sudden onset neurological deficit in a vascular territory
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Common mechanisms of cerebral ischemia (3)
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Small vessel disease
Embolism Decreased perfusion through fixed stenosis |
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Acute stroke treatment (2, time course)
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Revascularization via intravenous tPA (MUST BE < 180 min AFTER SYMPTOM ONSET)
Prevent damage from ischemic cascade |
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Default state for direct and indirect pathways
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Direct: net activation of cortex
Indirect: decreased activation of cortex Dopamine activates direct (steps on gas) and inhibits indirect (releases brake) leading to net activation of cortex via both pathways |
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Layers of retina (7)
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Pigment epithelium
Rods + Cones Outer limiting membrane Horizontal cells + bipolar cells Amacrine cells Ganglion cells Nerve fiber layer |
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Relation of fovea and optic nerve
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Fovea is lateral to optic nerve
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Photopic vs scotopic vision
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Photopic - in high light levels -> colors via cones
Scotopic- low light levels -> black and white via rods |
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Convergence in the retina
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Convergence in fovea is 1:1 photoreceptors : ganglion cells
Convergence in periphery is very high (100:1) for high sensitivity to light |
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Age related macular degeneration (age of onset, symptom, stages)
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age of onset > 65
Blurred central vision that grows Dry (early): retinal pigment epithelium generates Wet (late): new blood vessels in choroid invade subretinal space |
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Retinitis pigmentosa
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Symptoms: decreased vision in low light, tunnel vision
Genetic disease |
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Course of optic radiation
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From LGN -> pass near cerebral peduncles -> fibers from inferior retina (superior visual field) loop down into temporal lobe (Meyer's loop). Superior fibers (from inferior visual field ) pass up into parietal lobe.
Lesion in radiation -> incongruous defect |
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Congruous vs Incongruous visual field defects
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Congruous - lesion from calcarine cortex where info is retinotopic
Incongruous - lesion from optic radiation where info from adjacent parts of visual field are not adjacent |
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Homonymous hemianopia
Bitemporal hemianopia Identical defects in both eyes |
Homonymous hemianopia - optica tract
Bitemporal hemianopia - optic chiasm Identical defects in both eyes - calcarine cortex |
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Define Epilepsy + Seizure
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Two or more spontaneous/unprovoked seizures
Seizure: interruptions in neurologic function accompanied by abnormal hypersynchronous discharge |
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Partial (simple vs complex) vs Generalized seizure
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Refers to onset:
partial - starts at a specific focal point partial simple vs complex - in simple able to respond |
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Clonic seizure vs Tonic seizure
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Clonic - repetitive, synchronous, rhythmical whole body jerks
Tonic - whole body stiffening Tonic-Clonic seizure: tonic stiffening followed by whole body jerking |
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Temporal lobe epilepsy
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Hallmark seizure: complex partial
75% w/ auras 50% w/ uni or bilateral tonic clonic |
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Main mechanism of AEDs
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Modulate gating of Na+ channels
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Drugs by seizure type (generalized, focal, don't know)
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Generalized - valproate
Focal - carbamaazepine Don't know - valproate |
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Treatment for status epilepticus
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Lorazepam
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Status epilepticus definition (mechanistic and operational)
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Failure of normal factors that serve to terminate a typical GTC seizure
5 minutes of continuous seizures or 2+ discrete seizures b/w which there is incomplete recovery of consciousnes |
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Carbamazepine (which seizures? 2 SE)
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Most common drug for epilepsy
Good for focal but not absence or generalized SE: benign leukopenia/mild hyponatremia |
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Valproate (which seizures?, SE)
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1st choice for generalized seizures
SE - hepatic failure, increased appetite |
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Oxcarbazepine (which seizures? SE)
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Partial seizures
SE - hyponatremia |
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Lamotrigine (which seizures? SE)
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Partial or generalized
SE: severe rash Highest QOL |
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Levetiracetam (which seizures? SE)
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Partial > generalized
SE: irritability |
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Phenytoin(which seizures? SE, key fact)
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2nd choice
Zero order kinetics Lots of SE: coursened facial features |
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AEDs: name a drug for partial and generalized
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Partial - carbamazepine
General - valproate |
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Meningioma (age, prognosis)
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Adults
Good prognosis |
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Diffuse astrocytoma (age, features, localization, prognosis)
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Wide age range
Any site but most supratentorial Diffuse and extensive, poorly circumscribed Tendency to progress: mostly grad II |
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Glioblastoma (age, symptoms, localization, prognosis, imaging finding)
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Usually > age 50
Usually supratentorial Poor prognosis (18 mo survival) Seizures, > IP, focal deficits Rim enhancement |
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Pilocytic astrocytoma (age, symptoms, imaging, localization, prognosis)
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Most frequent glial tumor in children
Cerebellum, thalamus, hypothal, optic nerve Well circumscribed/cystic > IP, headaches, cerebellar signs Good prognosis |
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Medulloblastoma (age, features, localization, prognosis)
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Most common CNS tumor in children
Posterior fossa, 75% in vermis Ataxia and > IP Histology: rosettes |
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2 examples of interventricular tumors
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Central neurocytoma - good prognosis
Ependymoma - children and young adults, well circumscribed, 60% live 5 yr |
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Anatomical basis of conscioussness
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Arousal - ascending reticular activating system (pons and midbrain)
Awareness - cerebral and subcortical substructure |
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Coma (time course?)
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Failure to be aroused upon stimuli
> 1 hr |
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Stupor
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Arousable upon repeated stimuli
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Encephalopathy and delirium
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Encephalopathy - acute confusional state interchangeable w/ delirium
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Persistent vegetative state (better prognosis?)
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State of complete unawareness in which patient may open eyes spontaneously or to verbal stimuli but w/ no recognition
Can't make diagnosis too soon after TBI Poor prognosis (50% recover w/in 6 mo), better recovery if PVS due to TBI |
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Locked-in syndrome (location of infarct?)
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Pontine infarct
Consciousness and respiration preserved but de efferetation of all extremities and cranial nerves |
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Prerequisites for brain death (4)
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Cause is known and irreversible
No severe overlying med condition No drug intox or poisoning Core temp > 32 C |
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Cardinal features of brain death (3)
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Unresponsive/comatose
No brainstem reflexes (pupillary, corneal, oculovestibular, gag/couch) Apnea test |
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Acute disseminated encephalomyelitis (ADEM) (time course, lesion, mechanism
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Pediatric, starts w/ varicella
Lesion: Perivascular demyelination Ag from virus stimulates T-cells that cross BBB and attack myelin |
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Leukodystrophy (pathogenesis and histo)
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Metabolic errors involving myelin
Histo: diffuse continuous demyelination w/ preserved u fibers |
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Progressive multifocal encephalopathy
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In immunosuppresed patients
Papova viruses Histo: oligodendroglial cells at end edges of demyelinated zones w/ intranuclear inclusions filled w/ viral particles |
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MS etiology (3) and lesions (2)
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Patchy Plaques w/ sharp demarcation
Reactive astrocytes and lymphocytes Etiology: genetic or geographic or immunologic |
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MS symptoms, course, age
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Symptoms: weakness, sensory abnormality, visual blurring
Course: many brief events that get worse over time (relapse-remitting) Age: usually 20-50 (f > m) |
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Key feature of demyelinating disease
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Axons intact
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MS diagnosis (2) and treatment (3)
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Dx: imaging (periventricular lesions), abnormal CSF (high IgG, protein, myelin basic protein)
Treatment: corticosteroids, ACTH, B-interferon to intervene w/ T cells Anti lymphocyte drugs |
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Causes of secondary dementia
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Infections (meningitis)
Vitamin deficiency (B12) Hypothyroidism Subdural hematomas Poisoning Brain tumors Anoxia |
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Types of primary dementia (3)
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Multi-infarct dementia - small strokes, progressive
Lewy Bodies - alpha synuclein buildup neuron nuclei -> visual hallucinations and Parkinsonism Frontotemporal - atrophy of frontal lobes -> behavioral changes |
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Alzheimer's: pathology
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Starts in hippocampus then spreads to cortex and basal forebrain
Cholinergic neurons affected first then all NTs |
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Alzheimer's: genetics (late vs early)
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Late onset is associated w/ APO-E4 but low penetrance
Early onset associated w/ APP and PSEN w/ high penetrance (these mutations increase AB42 to AB40) |
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Alzheimer's: treatment
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Currently only treat symptoms:
Cholinesterases inhibitors NMDA receptor agonists to prevent excitotoxicty For pathogenesis: drug development against beta and gamma secretases to reduce AB Vaccines to AB to improve clearance |
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Mechanism of LTP (short term memory?)
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Induced by brief burst of high frequency activity to presynaptic afferents
Causes cell depolarization which pushes Mg++ out of NMDA channel Phosphorylation dependent for single trial short term memory |
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Four properties of LTP
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Rapid onset - 2-3 seconds
Long-lasting - 8 hours Synapse specificity - Associativity - pairing weak and strong synapse w/ LTP strengthens both |
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Alar vs basal plate
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Alar -> sensory + dorsal
Basal -> motor + ventral |
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Several endpoints for neural crest cells (3)
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Inner layers of meninges
Dorsal root ganglia Sensory and autonomic ganglia of cranial nerves |
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Improper closing of neural tube (4)
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Posterior defects:
Spina bifida -> incomplete closure of neural tube -> bladder/leg dysfunction Meningocele/myelomeningocele - meninges or spinal cord plus meninges extrude Anterior - anencephaly -> no brain, encephalocele -> meninges and brain herniate through midline scalp defect |
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Histogenesis (2 phases)
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Cellular differentiation -> neuroblasts (neurons) + glioblasts (macroglia)
Cellular maturation in concentric zones |
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Concussion
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Immediate and transient impairment of neural function occurring after head trauma
Post concussive syndrome can last for weeks (headache, dizziness, nausea, memory . . ) |
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Contracoup contusions and common sites
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180 degrees from site of impact
Frequently frontal lesions after people hit their occiput |
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3 categories for Glasgow Coma Score ( < 8 means?)
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Eye opening, verbal response, motor response
< 8 = seriously injured patient -> ER and IP monitoring |
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Herniation syndromes
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Expanding mass lesion causes headache fatigue
If herniation is over tentorial edge -> Ipislateral CN III compression (blown/dilated pupil) and contralateral hemiparesis |
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Kernohan's notch
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Opposite cerebral peduncle is compressed against free tentorial edge -> ipislateral motor deficit and ipsilateral blown pupil
ALWAYS USE PUPILLARY FINDING TO LATERALIZE LESION |
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Raccoon's eye and Battle's sign indicate . . .
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Basilar fracture
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How is glutamate involved in cell death?
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In hypoxia or ischemia lots of glutamate is released -> lots of Ca++ enters neuron -> cell death
B/c of ionotropic not metabotropic receptors |
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What ligand is required for NMDA channel opening
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Glycine
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Cortex layers for sensory and motor
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Motor: II + IV - granular
Sensory: III + V - agranular |
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Stimulation vs lesion of frontal eye fields
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In posterior middle frontal gyrus
Stim - eyes deviate to opposite side Lesion - eyes deviate to side of lesion |
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Primary visual area vs visual association cortex lesion
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primary -> homonymous hemianopia w/ macular sparing
association cortex -> vision intact but w/ oddities like prosopagnosia or color loss |
