Step 1 - Neuro 1

denniskwinn's version from 2015-04-25 16:11


Question Answer
Sleep stage 1Light sleep - 5%
Sleep stage 2Deeper sleep - bruxism - 45%
Sleep stage 3-4Deepest non-REM - sleepwalkings; night terrors; bedwetting (slow-wave sleep)
REM sleep25% - Dreaming, loss of motor tone, possibly a memory processing function, erections, ↑ brain O2 use
Key to initiating sleepserotonergic predominance of raphe nucleus
NE and REM sleep reduces REM sleep
Extraocular movements during REM are due toActivity of PPRF (paramedian pontine reticular formation/conjugate gaze center)
Paradoxical sleep (desynchronized sleep)REM sleep having same EEG pattern as while awake and alert
Benzodiazepines and sleepshorten stage 4 sleep = useful for night terrors and sleepwalking
Imipramine and sleeptreats enuresis because it ↓ stage 4 sleep
REM sleep characteristics (61. ↑ and variable pulse 2. REM 3. ↑ and variable BP, 4. Occurs every 90 minutes. 5. Ach principal neurotransmitter involved 6. ↓ with age.
Narcolepsy (6)1. Disordered regulation of sleep-wake cycles. 2. May include hypnagogic or hypnopompic hallucinations 3. Sleep episodes start with REM sleep 4. Cataplexy (loss of all muscle tone) in some patients 5. Strong genetic component 6. Treat with stimulants
Circadian rhythm (3)1. Driven by suprachiasmatic nucleus (SCN) of hypothalamus which is regulated by light 2. Controls ACTH, prolactin, melatonin, nocturnal NE release. 3. SCN→Ne release→pineal gland→melatonin
Neuroectoderm products ( 3)1. CNS neurons 2. Ependymal cells (inner lining of ventricles, make CSF) 3. oligodendroglia, astrocytes
Neural crest products (2)Schwann cells, PNS neurons
Mesoderm productsMicroglia
Nissl substanceRER in cell body and dendrites, not in axon
Astrocytes (1. Physical support, repair 2. K+ metabolism 3. Removal of excess neurotransmitter 4. Maintenance of BBB 5. Reactive gliosis in response to injury. 6. marker = GFAP
Microglia (5)1. CNS phagocytes - mesodermal origin 2. Not discernible in Nissl stains 3. Small irregular nuclei and relatively little cytoplasm 4. HIV-infected microglia fuse to form multinucleated giant cells in the CNS 5. Turn into large ameboid phagocytic cells when there is tissue damage
Oligodendroglia (5)1. Myelinates multiple CNS axons 2. In Nissl stain they appear as small nuclei w/dark chromatin and little cytoplasm 3. Predominant glial cell in white matter. 4. Destroyed in MS 5. Look like fried eggs on H&E stain
Schwann cell (1. Myelinates only 1 PNS axon 2. Promote axonal regeneration 3. Derived from neural crest 4. Destroyed in Guillain-Barre syndrome
Acoustic neuromaschwannoma - typically located in internal acoustic meatus CNVIII)
Free nerve endings (4)1. C=slow 2. Aδ=fast, myelinated 3. All skin, epidermis, some viscera 4. Sense pain and temperature
Meissner’s corpuscles (3)1. Large, myelinated fibers 2. Located in hairless (glabrous) skin 3. Sense position, dynamic fine touch, adapt quickly
Pacinian corpuscles (3)1. Large myelinated fibers 2. Deep skin layers, ligaments and joints 3. Sense vibration and pressure
Merkel’s disks (1. Large myelinated fibers 2. Found in hair follicles 3. Sense position, static touch (shapes, edges, textures), 4. adapt slowly
Endoneuriuminvests single nerve fiber - (inflammaton- infiltrate in Guillain-Barre)
Perineurium (Permeabilily barrier) —surrounds a fascicle of nerve fibers. Must be rejoined in microsurgery for limb reattachment.
Epineuriumdense connective tissue that surrounds entire nerve (fascicles and blood vessels).
NE synthLocus ceruleus
NE in disease↑ in anxiety, ↓ in depression
Dopamine synthVentral tegmentum and SNc
Dopamine in disease↑ in schizophrenia, ↓ in parkinsons and depression
5-HT synthRaphe nucleus
5-HT in disease↓ in anxiety and depression
Ach synthbasal nucleus of meynert
Ach in disease↓ in Alz, Huntington’s, REM sleep
GABA synthNucleus accumbens
GABA in disease↓ in anxiety, huntington’s
Locus ceruleusassoc with stress and panic
Nucleus accumbens and septal nucleusreward center, pleasure, addiction, fear
BBB (4)1. 3 structures: tight junctions b/w endo, Basement membrane, astrocyte processes 2. Glucose and aa cross slowly by carrier mediated transport 3. Nonpolar cross rapidly 4. A few specialized regions have fenestrated cappilaries
TAN HATShypothalamus - Thirst and water balance, Adenohypophysis control, Neurohypophysis, Hunger, Autonomic regulation, Temperature regulation, Sexual urges
Inputs to the hypothalamus sense change in osmolarity, area postrema (responds to emetics)
organum vasculosum of the lamina terminalis (OVLT) =supraoptic nucleus - makes ADH
Paraventricular nucleus makesoxytocin
Lateral hypothalamus1. Hunger center 2 .Inhibited by leptin 3. Destruction leads to anorexia, failure to thrive in kids
Ventromedial hypothalamus1. Satiety center 2. Destruction leads to hyperphagia 3. Stimulated by leptin
Anterior hypothalamusCooling - parasympathetic
Posterior hypothalamusHeating - sympathetic
Septal nucleussexual urges
Suprachiasmatic nucleuscircadian rhythm
Posterior pituitary (reveives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (Oxytocin) nuclei
Thalamusmajor relay for ascending sensory information that ultimately reaches cortex
Thalamus Lateral geniculate nucleus (LGN)Visual - projects via optic radiations to occipital cortex
Thalamus Medial geniculate nucleus (MGN)auditory
Thalamus Ventral posterior nucleus lateral (VPL)body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract)
Thalamus ventral posterior nucleus medial (VPM)facial sensation (via CN V) -
Thalamus ventral anterior/lateral (VA/VL) nucleimotor
Thalamus blood supplyPCOM, Posterior cerebral, ICA (anterior choroidal arteries)
Limbic systems 1. Includes cingulate gyrus, hippocampus, fornix and mammillary bodies 2. Responsible for (5 Fs) Feeding, fleeing, fighting, feeling and sex
Cerebellum (4)1. Receives contralateral cortical input via middle cerebellar peduncle 2. ipsilateral proprioceptive information via inferior cerebellar peduncle. 3. Input nerves = climbing and mossy fibers 4. Provides stimulatory feedback to contralateral cortex to modulate movement.
Cerebellum input nervesclimbing and mossy fibers
Cerebellum output fibersPurkinje fibers output to deep nuclei of cerebellum which then output to cortex via superior cerebellar peduncle
Deep nuclei of cerebellum (starting laterally)(4) Dentate, Emboliform, Globose, Fastigial (Don’t eat greasy foods)
Lateral cerebellumvoluntary movement of extremities
Medial cerebellumbalance, truncal coordination, ataxia, propensity to fall toward injured side
Basal ganglia (2)1. Important in voluntary movements and making postural adjustments 2. Receives cortical input, provides negative feedback to cortex to modulate movement.
Basal ganglia Excitatory pathwaySNc's dopamine binds to DI receptors in the excitatory pathway, stimulating the pathway (↑ motion). Therefore, loss of dopamine in Parkinson's inhibits the excitatory pathway (↓ motion).
Inhibitory pathwaySNc's dopamine binds to D2 receptors in the inhibitory pathway, inhibiting the inhibitor)' pathway (↑ motion). Therefore, loss of dopamine in Parkinson's excites (i.e., disinhibits) die inhibitory pathway (↓motion).
SncSubstantia nigra pars compacta
Snr Substantia nigra pars reticulata
Gpe Globus pallidus externus
GpiGlobus pallidus internus
STNSubthalamic nucleus
DI Dopamine DI receptor (excitatory)
D2Dopamine D2 receptor (inhibitory)
Parkinsons1. Degeneration of CNS 2. Lewy bodies (composed of alpha synuclein-intracellular inclusion) and depigmentation of substantia nigra pars compacta) 3. Loss of dopaminergic neurons.
Parkinson’s sxTremor (at rest) Rigidity, Akinesia, Postural Instability
Hemiballismus (2)1. Sudden, wild flailing of 1 arm +/- leg. 2. Characteristic of contralateral subthalamic nucleus lesion - loss of inhibition of thalamus through globus pallidus
Huntington’s disease (5)1. Autosomal dominant trinucleotide repeat disorders 2. Chromosome 4 3. Neuronal death via NDMA-R binding and glutamate toxicity 4. Chorea, depression, progressive dementia. 5. Expansion of CAG repeats - caudate loses ACH and GABA
Chorea1. Sudden jerky purposeless movements 2. Basal ganglia lesion s.a. Huntingtons
Athetosis1. Slow, writhing movemets, especially of fingers. 2. Characteristic of basal ganglia lesion (Huntingtons)
Myoclonussudden, brief muscle contraction - jerks, hiccups
Dystoniasustained involuntary muscle contraction
Essential tremor/postural tremor (4)1. happens with action or when holding position. 2. Autosomal dominant 3. patients self medicate with alcohol which ↓ tremor 4. Treat with beta blockers
Resting tremormost noticable distally. Seen in parkinsons
Intention tremorslow zigzag motion when pointing toward a target, associated with cerebellar dysfunction
Frontal lobe functionsExecutive functions: planning, inhibition, concentration, orientation, language, abstraction, judgement, motor regulation, mood. Lack of social judgement is most notable in frontal lobe lesion
Homunculustopographical representation of sensory and motor areas in the cerebral cortex. Used to localize lesions - leading to specific defects.
Amygdala (bilateral) lesionKluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior)
Frontal lobe lesionDisinhibition and deficits in concentration, orientation and judgement; may have reemergence of primitive reflexes
R parietal lobe lesionspatial neglect syndrome (agnosia of the contralateral side of the world)
Reticular activating system (midbrain) lesionreduced levels of arousal and wakefulness (e.g. Coma)
Mamillary body lesionWernicke-Korsakoff syndrome (Wernicke = confusion, ophthalmoplegia, ataxia. Korsakoff = memory loss, confabulation, personality changes)
Ophthalmoplegiaparalysis of one or more extraocular muscles
Confabulationspontaneous narrative report of events that never happened. It consists of the creation of false memories, perceptions, or beliefs about the self or the environmentspontaneous narrative report of events that never happened. It consists of the creation of false memories, perceptions, or beliefs about the self or the environment
Basal ganglia lesiontremor at rest, chorea or athetosis
Cerebellar hemisphere lesionintention tremor, limb ataxia, damage to the cerebellum results in ipsilateral deficits; fall toward side of lesion (cerebellum→SCP→contralateral cortex→corticospinal decussation = ipsilateral)
Cerebellar vermis lesiontruncal ataxia, dysarthria
Subthalamic nucleus lesioncontralateral hemiballismus
Hippocampus lesionanterograde amnesia - inability to make new memories
Paramedian pontine reticular formation (PPRF) lesionEyes look away from side of lesion
Frontal eye fields lesioneyes look toward lesion
Central pontine myelinolysis (6)1. Acute paralysis 2. dysarthria 3. dysphagia 4.diplopia 5.loss of consciousness 6.Commonly caused by very rapid correction of hyponatremia
Recurrent laryngeal nerve injuryloss of all laryngeal muscles except cricothyroid - hoarsness
Aphasiahigher order inability to speak
Dysarthriamotor inability to speak
Broca’s aphasianonfluent aphasia w/intact comprehension, Broca’s area = inferior frontal gyrus
Wernickes aphasiaFluent aphasia w/ impaired comprhension - Wernicke’s area = superior temporal gyrus
Global aphasianonfluent aphasia w/ impaired comprehensions - both broca’s and wernickes
Conduction aphasia (3)1 .Poor repetition but fluent speech 2. intact comprehension. 3. arcuate fasiculus - connects broca’s, wernickes