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405 Cards in this Set
- Front
- Back
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CT - what color is bone/fluid/brain
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Bone = white / blood = white
Fluid = black / CSF = black Brain = Gray |
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MRI T1 Sequence - what color is bone/fluid/brain
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Used for high anatomical resolution
CSF = black Brain gray matter = gray Brain white matter = white Bone = complicated |
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MRI T2 Sequence - what color is bone/fluid/brain
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Used to identify pathology
CSF = white / edema, fluid from inflammation = white Brain gray matter = Gray Brain white matter = black Bone = complicated |
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MRI - Diffusion weighted T2
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Used to identify ischemia earlier and more clearly
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Epidural Hematoma
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Blood b/w dura and skull
Usually arterial due to impact - acutely life threatening |
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Subdural Hematoma
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Blood b/w arachnoid and dura
Usually venous, associated w/ elderly and head shaking |
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Lissencephaly
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Smooth brain, no gyri or sulci - mutations in genes involved w/ tubulin dynamics
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Pachygyria
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Large (elephant) gyri + 2 abnormal large clefts, do not extend all the way to ventricle
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Polymicrogyria
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Too many small gyri + mixed patches of pachygyria
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Double Cortex
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Second rim of cortical cells in periventricular area - migration failure
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Schizencephaly
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Large gyral cleft, lined w/ gray matter, extends to connect w/ ventricle
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Beningn Familial Neonatal Convulsion
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Mutation in KCNQ2 or KCNQ3 gene
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Meroanencephaly
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Neural tube closure defect - partial absence of brain
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Anencephaly
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Neural tube closure defect - complete absence of brain
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Exencephaly
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Neural tube closure defect - exposure and possible extrusion of brain
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Otx2 -/- mice
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Anencephaly - defect of anterior nervous tissue differentiation
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Wnt1 -/- mice
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Deletions of specific midbrain and hindbrain regions - expressed at boundary
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Holoprosencephaly
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Defect in forebrain bifurcation - caused by defects in Shh signaling
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ROBO3 human mutation
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Horizontal gaze palsy: unable to look move eyes to either side
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Frog Eye Patterning
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Nasal retina = Low EphA --> Posterior Tectum = High Ephrin A (repulsive)
Temporal retina = High EphA --> Anterior Tectum = Low Eph A (repulsive) |
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Familial advanced sleep-phase syndrome
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PER2 mutation, PER2 protein builds up quicker, earlier feedback, wake up too early
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Delayed sleep-phase syndrome
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Delayed cycle (4am-noon), may involve PER3
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Ventral Horn Rexed Laminae
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VIII and IX
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Dorsal Horn Rexed Laminae
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I-VI
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I/A-α sensory nerves
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Ia - muscle spindle / Ib - GTO : large, fast, sensitive to anoxia, resistant to anesthesia
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II/A-β sensory nerves
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Innervate cutaneous mechanoreceptors and muscle spindles
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III/A-δ sensory nerves
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Free nerve endings, respond to sharp pain and cold
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IV/C fiber sensory nerves
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Free nerve endings, respond to dull pain and warmth
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Sensory Nerve medial division
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Ia, Ib, IIA. Touch, vibration, pressure, proprioception
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Sensory nerve lateral division
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IIIA, C. Pain and temperature
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Corticospinal Tract
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Cell bodies in frontal lobe - Primary motor cortex, precentral gyrus, pre-motor area
Cell bodies in parietal lobe - primary and secondary somatosensory cortex Descend in internal capsul through midbrain, pons and medulla 90% cross at pyramidal decussation in Medulla--> Lateral Corticospinal Tract in Lateral Funiculus 10% stay ipsilateral --> Anterior Corticospinal Tract |
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Rubrospinal Tract
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Cell bodies in Red Nucleus - magnocellular division
Decussate in Ventral Tegmental Area - Midbrain Terminate in Cervical Cord - contralateral Anterior Horn Lower Motor Neurons Control movement of contralateral limbs |
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Medial / Pontine Reticulospinal Tract (MRST)
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Cell bodies in pontine reticular formation
Descends ipsilaterally in antero-lateral spinal cord Terminates in all cord levels in Laminae VII and VIII - anterior horn LMN Anti-gravity muscles |
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Lateral / Medullary Reticulospinal Tract (LRST)
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Cell bodies in medullary reticlar formation
Descends bilaterally in antero-lateral spinal cord Terminates in all cord levels on anterior horn LMN Extensor muscles for postural support |
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Medial Vestibulospinal Tract
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Cell Bodies in Medial Vestibular Nucleus
Descend bilaterally in Medial Longtiudinal Fasciculus Terminate in Cervical cord and Upper Thoracic Cord Inntervate α-LMN Control neck and upper limb muscles in response to vestibular stimuli |
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Lateral Vestibulospinal Tract
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Cell Bodies in Lateral Vestibular Nucleus
Receive input from labyrinth, cerebellum, and neck proprioceptors Descend ipsilaterally in anterior quadrant of spinal cord Terminatres in all levels of spinal cord Innervates α-LMN in Anterior Horn Facilitate anti-gravity reflexes, controls balance |
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Tectospinal Tract
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Cell bodies in Superior Colliculus
Decussates in Dorsal Tegmental Area - Midbrain Terminates in Cervical Cord Coordinate visual input to visual musculature orientation |
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LMN Lesions - Flaccid Paralysis
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Paralysis and suppressed reflexes, fasiculations, atrophy. Ipsilateral and at level of lesion
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UMN Lesion
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Paresis (weakness) and hyperactive refelxes
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Dorsal Column Medial Lemniscus Pathway
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Proprioception and discriminative touch modalities
1st order cell body in DRG Axons enter in medial division, ascend ipsilaterally in posterior funiculus 2nd order cell body in Medulla - nucleus gracilis / cuneatus Axon crosses midline in medial lemnisucs, ascends contralaterally to thalamus 3rd order cell body in Ventral posterolateral (VPL) nucleus of thalamus Axon ascends to Primary somatosensory cortex |
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Fasciculus Gracilis
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Medial, lower body - GRacilis / Ground
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Fasciculus Cuneatus
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Lateral, upper body
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Romberg Test
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Patient sways w/ eyes open = cerebellar vermis lesion - motor ataxia
Patient sways w/ eyes closed = DCML lesion - sensory ataxia |
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Anterolateral Spinothalamic Pathway
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Pain and temperature
1st order cell body in DRG Enter spinal cord in medial pathway Ascend/descend 2 segments in Lissauer's tract 2nd order cell body in Dorsal horn - Laminae I and V Axons cross ventral to central canal at same level Axons ascend contralaterally in Ventral part of lateral funiculus 3rd order cell bodies in Ventral posterolateral nucleus of thalamus Axons terminate in primary somatosensory cortex |
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Dorsal Spinocerebellar Tract
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Unconscious proprioception - lower limb
1st order cell body in DRG, Ia and Ib axons enter spinal cord 2nd order cell body in Clark's nucleus - Lamina VII Axons ascend ipsilaterally to cerebellum T1-L2 |
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Cuneocerebellar Tract
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Unconscious proprioception - upper limb
1st order cell body in DRG, Ia and Ib axons enter spinal cord 2nd order cell body in Cuneate Nucleus Axons ascend ipsilaterally to cerebellum |
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Horner's Syndrome
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Compression / Lesion of superior cervical ganglion
Ipsilateral facial symptoms Miosis - pupillary constriction Ptosis - drooping eyelid Anhidrosis - lack of sweating Orthostatic hypotension - drop in systemic blood pressure upon standing |
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Supraspinal Bladder Disorder - Cortical Lesion
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Infantile bladder
Fills normally, empties suddenly and completely Loss of sympathetic inhibition of detrusor contraction |
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Supraspinal Bladder Disorder - Spinal Cord Lesion above Sacral cord
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Spastic bladder
Detrusor contracts in response to mimumum amount of stretch Loss of inhibition on parasympathetic innervations of detrusor |
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Supraspinal Bladder Disorder - Spinal Cord Lesion at Sacral Cord or Cauda Equina
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Atonic Bladder
Fills to capacity, dribbles out continously Loss of parasympathetic innervation to detrusor, fails to contract in response to filling |
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Spinal Muscular Atrophy
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Progressive loss of motor neurons - others not affected
Loss of SMN gene - SMN1 gene copy mutated or replaced by SMN2 gene copy SMN2 copy has defective splicing <10% of transcript is translated |
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Most common level for Radiculopathy
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C5,C6,C7,C8,L4,L5,S1
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PMP22
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2 copies = normal
1 copy = Hereditary neuropathy w/ liability to pressure palises (HNPP) 3 copies = CMT1A, inherited demyelinating neuropathy |
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Glutamate Synthesis
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Glutamine --> Glutamate via Glutaminase
Glutamate --> Glutamine via Glutatmine Synthetase (in Glial cells) |
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ACh synthesis
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Glucose --> pyruvate --> Acetyl CoA
Acetyl CoA + Choline --> ACh via Choline Acetyl-transferase ACh --> Acetate and Choline via ACh Esterase |
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4 classical congential myopathies
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Nemaline myopathy, Centronuclear/myotubular myopathy, Central core disease, Multi/minicore myopathy
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Nemaline Myopathy
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Nemaline rods seen on biopsy, red staining inclusions, derived from Z disk components
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Muscular dystrophy histology
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Degeneration, regeneration, and connective and fatty tissue infiltration
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Gowers' Maneuver
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Indicates proximal muscle weakness
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Trendelenberg sign
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Excessive hip swiging due to proximal muscle weakness
Brought out when climbing stairs Compensates for weak hip abductors and knee extensors |
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Dystrophin Gene
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Out of frame mutations --> truncated protein --> Duchenne Muscular Dystrophy
In frame mutation --> internally deleted protein --> Becker Muscular Dystrophy Therapeutic exon skipping to convert DMB --> BMD Inject oligonucleotides, mask splicing site, skip out of fram exons, restore reading frame |
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Limb-Girdle Muscular Dystrophy
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Reduced Sarcoglycan complex - normal dystrophin
Autosomal recessive --> affects both sexes equally Proximal muslce progressive weakness Presents early in childhood |
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FSHD clinical presentation
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Asymmetric weakness in face, scapula, biceps, and distal leg (foot drop)
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FSHD genetics
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Deletion of DUX4 repeats from long end of chromosome 4 - only A version
Larger deletion / fewer remaining repeats --> more severe disesae Total deletion / no remaining repeats --> no disease Deletions alter chromatin structure, open polyA sequence Remaining DUX4 genes are transcribed and polyadenylated --> stable protein DUX4 protein probably is toxic to muscle cells |
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Acetylcholine synthesis rate limiting step
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Choline uptake
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Nicotinic ACh-R localization
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Post-synaptic in autonomic ganglia and skeletal muscle
Pre-synaptic in CNS --> promote vesicle release |
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AChE inhibitors - Alzheimers
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Reversible competitive inhibitor - tertiary amine, hydrophobic, crosses BBB
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Pyridostigmine
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Carbamylates active site serine on AChE
Inhibits for 30 min - ACh normally acetylates active site serine for 10s Used to treat myasthenia gravis |
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Nerve Gas
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Permanently phosphorylates AChE active site
Treat w/ pyridostigmine to temporarily block active site from irreversible inhibition Treat w/ 2PAM to displace organophosphate before phosphate ester is hydrolyzed |
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ACh - Nicotonic receptor interaction
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π/cation interactions
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ACh - ACh-E interaction
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π/cation interactions
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ACh - Muscarinic Receptor interaction
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Negative charge aspartate binds positive charge quarternary amine
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mAChR downstream effectors
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m2, m4 – inhibit adenylate cyclase, reduce cAMP - αi competes w/ αs
m1,3,5 - activate PL-C - IP3 and DAG second messengers - αq/11 and βγ mediate activation m2,4 - activate inward rectifying K+ channels (GIRKs) - βγ mediate activation |
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Prolonged ACh exposure - nACh-R
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Desensitization - conformation change to high affinity but closed channel
Increased receptor expression on membrane |
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Prolonged ACh exposure - mACh-R
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Desensitization - internalization of receptors
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nACh-R primordial type
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(α7)5
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nACh-R Fetal Muscle Type
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(α1γ)(α1δ)β1
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nACh-R Adult Muscle type
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(α1ε)(α1δ)β1
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nACh-R Major Brain subtype - high affinity for nicotine
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(α4β2)2β2
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nACh-R Major Autonomic Ganglia Subtype
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(α3β4)2β4
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Lambert-Eaton Myasthenic Syndrome
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Autoantibodies against v-gated Ca2+ channels - disrupt release of ACh
Paraneoplastic immune response to small cell lung carcinoma |
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nACh-R subtype important in tobacco addiction
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(α4β2)(α6β2)β3
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What level is LP performed at
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L4/L5
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Upper Motor Neuron Lesions - Signs and Symptoms
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Slowness, stiffness
Spasticity (increased muscle tone), hyperactive reflex, pathological reflexes Babinski sign - extensor plantar response |
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Lower Motor Neuron Lesions - Signs and Symptoms
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Weakness, cramps
Muscle atrophy, fasciculations, hyoactive reflexex, decreased muscle tone |
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Spinal Cord Arterial Blood Supply
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Anterior Spinal Artery --> Ant 2/3 = Corticospinal and ALST
Posterior Spinal Arteries --> Post 1/3 = DCML |
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Complete Cord Transection - Deficits
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Motor - loss of all motor function below lesion
Sensory - loss of all modalities below lesion Autonomic - bowel and bladder dysfunction Acute spinal shock - flaccid weakness, numbness, urinary retention, constipation Chronic spastic weakness, spastic bladder and rectal sphincter |
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Complete Cord Transection - levels and ablities
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C1-C3: require ventilatory support
C4 and below: may have partial ventilatory independence Spare C7: retain ability to independently transfer body |
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Hemisection of Cord / Brown - Sequard Syndrome deficits
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Motor - lpsilateral spastic weakness below lesion (CST)
Sensory - Ipsilateral loss of touch and proprioception below lesion (DCML) Sensory - Contralateral loss of pain and temp 1-2 levels below lesion (ALST) Segmental ipsilateral LMN and sensory signs (anterior horn damage) Autonomic - bladder and bowel function spared, under bilateral control Acute spinal shock - flaccid weakness Chronic spastic weakness below lesion (UMN) / flaccid segmental weakness (LMN) |
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Central Cord Lesions
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Motor - Segmental bilateral LMN findings (anterior horn damage)
Sensory - Bilateral thermoanesthesia (crossing ALST fibers) Damage starts centrally, spreads centrifugally |
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Classic Cervical Syrinx
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Cape-like bilateral thermoanesthesia
Weakness and atrophy of arm and hand muscles |
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Syringomyelia / Hematomyelia
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Cavity filled w/ CSF or blood
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Tabes Dorsalis / Posterior Column Syndrome
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Bilateral Destruction of Posterior Columns from untreated Syphillis
Bilateral impaired vibration and proprioception Sensory ataxia - positive Romberg's sign Lancinating pain in legs, absent reflexes in legs Argyll Robertson pupils - small, miotic, unreactive to light, normal accomodation reflex |
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Posterolateral Column Syndrome / Subacute Combined Degeneration
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B12 deficiency results in myelin degeneration w/o inflammation
Affects posterolateral and corticospinal pathways Loss of proprioception and vibration in legs - Sensory ataxia, positive Romberg's sign Spasticity and hyperreactive reflexes - positive Babinski's sign |
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Anterior Horn Cell Disease
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Segmental LMN findings - flaccid paralysis
Caused by spinal muscular atrophy disorders Caused by poliomyelitis, West nile, enterovirus, echovirus, coxsackie virus |
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ALS
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Combined Anterior Horn Cell - Pyramidal Tract Syndrome
Combined UMN and LMN findings in same segment Flaccid and Spastic Paralysis |
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Anterior Spinal Artery Occulsion
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Acute flaccid weakness - Chronic spastic paraparesis below lesion (UMN)
Bilateral LMN findings at level of lesion (LMN) Bilateral loss of pain and temperature below lesion Impaired bowel and bladder control |
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Intramedullary Lesion
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Lesion inside spinal cord - parenchyma involvement
Redicular sensory and motor findings Causes: Ependymoma, Astrocytoma, Glioblastoma, Myelitis, Abscess |
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Intradural Extramedullary Lesion
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Lesion inside dura / outside spinal cord - extraparenchyma involvement
Redicular LMN findings reflect root compression Myopathy develops w/ increasing lesion size Causes: Schwannoma, Meningioma |
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Extradural lesion
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Lesion outside dura - extraparenchyma involvement
Redicular LMN findings reflect root compression Myopathy develops w/ increasing lesion size Causes: Disc disease, Epidural metastasis, Primary Bone Tumor, Lymphoma, Epidural Abscess |
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Lumbar Disk Herniation
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LMN lesion of compressed root - flaccid paralysis
Dermatomal sensory loss Depressed segmental reflexes Radicular pain No bowel / bladder involvement |
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Cauda Equina Syndrome
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Sudden onset - severe pain
Lesion of multiple roots at L4 and below Severe radicular pain Flaccid weakness in legs, loss of reflexes Global sensory disturbance including saddle region (S3-S5) Bowel / Bladder dysunction and impotence |
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Proximal weakness seen commonly in…
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Muscle disorders
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Distal weakness / length dependent weakness seen commonly in…
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Peripheral nerve disorders
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Tensilon Test
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Diagnostic test for myasthenia gravis
Inhibits ACh-E Causes brief increase in strength in patients w/ NMJ disorders |
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CK test
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Creatine Phosphokinase
Catalyzes ADP + Pi --> ATP + Creatine Elevation in blood indicates damage to muscle membrane Trauma, inflammation, disorder |
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CK extremely high in….
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Disorders of skeletal muslce - damage
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CK mildly elevated (<1000) in …
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Muscle damage secondary to peripheral nerve or anterior horn cell denervation
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Fibrillation potentials
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Nonspecific abnormality in both nerve and muscle disease
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EMG - Decreased amplitude and duration of Motor Unit Action Potential
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Myopathic - muscle fibers drop out - size of motor unit is reduced
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EMG - Increased amplitude and duration of Motor Unit Action Potentials
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Neuropathic - muscle denervation and compensatory sprouting
Motor units are larger and more clustered |
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EMG - Early full recruitment
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Myopathic - smaller motor units
Muscle fires all available units to generate adequate force Loss of orderly progression |
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Dermatomyositis
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Immune-mediated inflammatory disorder of muscle
Skin rash present Cellular infiltration, perifascicular atrophy Abs directed against endothelial cells --> capillary necrosis Associated w/ cancer in 30% of patients - paraneoplastic syndrome |
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Nerve conduction studies - prolonged distal motor and F wave latencies
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Demyelinating polyneropathy - slows conduction velocity
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Albumino-cytologic dissociation
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Elevated CSF protein w/o cellular reaction
Typical but not diagnostic of Guillian-Barre Syndrome |
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Upper Motor Neuron Syndrome
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Weakness, Spasticity, Hyperreflexive, Babinski's sign, loss of fine voluntary movement
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Lower Motor Neuron Syndrome
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Weakness, Flaccid paralysis, hyporeflexive,
decreased tone, fasciculations and fibrillations, atrophy |
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Fasciculation
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Involuntary but synchronized contraction of all fibers in a motor unit
Indicates denervation and resprouting |
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Fibrillations
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Spontaneous contraction of single muscle fiber
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Paresis
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Weakness
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Plegia
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Paralysis
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Golgi Stain
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Random selectin of entire cells
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Nissl Stain
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Cell bodies
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Weigert Stain
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Myelinated axons
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BA 4
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Primary Motor Cortex
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BA 6
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Premotor Cortex
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BA 8
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Supplementary Motor Cortex
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Premotor Cortex
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Projections to primary motor cortex and spinal cord
Involved in selecting, planning, and prepareing movements Mental rehersal invokes activity Activity decreases w/ practice as movements become more automatic |
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Traditional view of motor cortex function
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Individual neurons encode activation of specific muscles
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Population code view of motor cortex function
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Individual neurons encode a particular direction of movement of specific muscle
Vector average of directions determines muscle movement |
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Prolonged stimulation of motor cortex
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Results in goal-oriented movement
Move monkey's hand away from mouth but to any other spot Prolonged stimulation induces monkey to bring hand to mouth |
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Cerebellar Lesions - Clinical Syndromes
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Hypotonia - diminished resistance to passive limb movement
Ataxia - lack of coordinated / ordered movement Intention tremor |
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Dysmetria
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Errors in range of movement - touching finger to nose, overshoot / undershoot
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Dysdiadochokinesia
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Inability to sustain regular rhythm or amount of force
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Ataxia - components
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Lack of coordination of eye movements during walking
Delay to initiate movements Dysmetria Dysdiadochokinesia Decomposition of movement |
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Cerebrocerebellum
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Lateral zone / hemispheres
Involved in motor preparation and planning Mossy Fiber Input from Cortex --> Pons --> Mid Cerebellar Peduncle Purkinje Cell output --> Dentate nucleus --> Sup Cerebellar Peduncle --> VL Thalamus Decussates to contralateral Cortex --> regulates ipsilateral muscles |
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Spinocerebellum
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Intermediate zone and medial zone / paravermis and vermis
Regulates posture and limb movement / medial muscles (vermis) and limbs (paravermis) Mossy Fiber Input from Spinal Cord Clark's Nucleus --> Inf Cerebellar Peduncle Output from vermis --> Fastigial nucleus --> Vestibular nuc and pontine reticular formation Output from Paravermis --> Interposed nucleus --> Red Nucleus No decussation --> ipsilateral muscles |
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Vestibulocerebellum
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Flocculus and Nodulus
Regulates balance and coordination of head and eyes Input from Vestibular (Scarpa's) ganglion and superior colliculus Purkinje Cell output --> Vestibular Nuclei iin brainstem |
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Deep Cerebellar Nuclei
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Cerebrocerrebellum --> Dentate Nucleus
Vermis --> Fastigial Nucleus Paravermis --> Interposed Nuclei Vestibulocerebellum --> project directly to vestibular nuclei in brainstem |
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Cerebellar Cortical Layers - Superficial to Deep
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Molecular - most superficial
Purkinje - middle Granular - deepest |
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Granular Layer cell types
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Granule Cells - excitatory glutamate
Golgi cells - inhibitory GABA |
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Purkinje Layer cell types
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Purkinje cells - Inhibitory GABA
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Molecular Layer cell types
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Basket cells - Inhibitory GABA
Stellate cells - Inhibitory GABA |
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Cerebellar Circuitry - Mossy Fibers
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Inputs from Cerebral Cortex (pontine nuclei), spinal cord, and vestibular system
Excitatory input to deep cerebellar nuclei and granule cells |
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Cerebellar Circuitry - Granule Cells
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Excitatory input from mossy fibers
Axons ascend into molecular layer, branch to form T-junction, extend as parallel fibers Axons are parrallel to cortical surface, perpendicular to Purkinje cell dendrites Excitatory glutamate input to Purkinje cells - simple spikes High degree of convergence and divergence Weak individual input - many inputs per cell |
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Cerebellar Circuitry - Climbing Fibers
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Axons from Inferior Olive - enter through contralateral inferior cerebellar peduncle
Excitatory input to single or few Purkinje Cells Strong input - high safety factor - high probablity of eliciting AP (complex spike) in purkinje cell |
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Cerebellar Circuitry - Golgi Cells
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Inhbit Granule Cells
Negative feedback fo mossy fiber input pathway |
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Cerebellar Circuitry - Basket and Stellate Cells
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Local inhibitory interneurons
Fine tune Purkinje Cell response to mossy fiber input |
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Cerebellar Circuitry - Purkinje Cells
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Weak excitatory input from Granule Cells - Simple spikes
Strong excitatory input from climbing fibers - Complex spikes Inhibitory output to deep cerrebellar nuclei (or vestibular nuclei in brainstem) Strong activation of Purkinje cell results in decreased activation of deep cerebellar nuclei |
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Purkinje Cell Simple Spikes
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Na+ mediated action potentials
Stimulated by excitatory input from parallel fibers Frequency of 50-60 Hz Related to external environmental stimulus |
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Purkinje Cell Complex Spikes
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Ca2+ mediated action potentials - several consecutive, longer lasting spikes
Stimulated by excitatory input from single climbing fiber Frequency of 1 Hz Not related to external environmental stimulus Regular intervals, may be timing signal to motor coordination |
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Effects of inactivating (cooling) deep cerebellar nuceli
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Delayed, oscillatory movements
Overshoot target, take abnormally long to stop Unable to anticipate and compensate for changes in force |
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Neural Computation functions of Cerebellum
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Anticipate and compensate for force
Cognitively evaluate sensory input - discrimination of sensory features Classical conditioning - plasticity to couple US w/ CS Motor Learning - Vestibulo Occular Reflex Addiction - Drugs induce hyperresponsiveness in cerebellum --> reduce prefrontal activity |
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Cerebellum Cognitive Functions
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Increased activity when subject is mentally active - sensory discrimination
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Posture
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Muscle tone sufficient to maintain desired body position against pull of gravity
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Balance
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Maintenance of center of body mass above base of support
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Anticipatory Postural Control - Feedforward
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Motor cortex elicits coordinated limb movement - Lateral Corticospinal Tract
Anticipatory Postural Adjustments controlled by Anterior (uncrossed) Corticospinal Tract, Reticulo Spinal Tract and Vestibulo Spinal Tract from Brainstem Predicts disturbances and produces pre-programmed responses - fastest response Modifiable with experience |
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Compensatory Postural Control - Feedback
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Stimulated by Proprioceptors - Muscle Spindles and Golgi Tendon Organs
Feeback directly influences spinal motor circuits Feedback projects to cerebellum and brain stem to alter subsequent feedforward movements Adjustments evoked by loss of posture and/or balance during movement - slower response Modifialbe with experience |
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Lateral Motor System
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Spinal motor neurons located dorso-laterally in ventral gray of spinal cord
Propriospinal and local interneuorns located in lateral intermediate spinal gray zone Propriosonal interneurons extend only a few segments, independent control of muscles Descending axons of Lateral Corticospinal Tract and Rubrospinal Tract Controls muscles of distal limbs |
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Medial Motor System
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Spinal motor neurons located in antero-medial spinal gray matter
Propriospinal and local interneurons located in medial intermediate spinal gray zone Propriospinal interneurons extend many segments, link functional agonists Descending axons of Reticulospinal, Vestibulospinal, and Anterior Corticospinal tracts Control postural / axial muscles |
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Step Cycle - Muscle contraction patterns
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Extensors contract during stance phase
Flexors contract during swing phase Same type muscles contract in temporally overlapping sequential pattern - not simultaneously Extension/stance = constant length Flexion / swing = variable length |
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Central Pattern Generator - Locomotion
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Generates rhythmic repeating motor pattern in response to non-rhythmic input
Located in Spinal Cord segments that control relevant muscles Regulated by descending Reticulospinal projections Regulated by sensory feedback from limbs, joints, and skin |
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Descending Control of Spinal Locomoter Central Pattern Generator
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Initiated in motor / premotor cortex --> Mesencephalic Locomotor Region (MLR)
MLR --> Medullar Reticular Formation (MRF) MRF axons descend in Reticulospinal Tract --> Spinal Locomoter CPG CPG --> motor neurons innervating limb muscles |
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Feedback from Spinal Central Pattern Generator
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CPG --> Brainstem
Modulates activity of Reticulospinal Tract Converts RST tonic activity to rhythmic |
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Spinal Central Pattern Generator - circuitry
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Reciprocally inhibitory populations of functionally antagonistic interneurons
Interneurons stimulate flexor and extensor motor neurons Interneurons inhibit eachother - rhythmic alternation |
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Strength of Descending Activity - CPG
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Increasing strength of tonic stimulation of MLR increases speed of locomotion
Slow walk --> Fast walk --> trotting --> galloping Change in L/R coordination - not simply same pattern but faster Increased stimulation --> gait pattern change |
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Locomotor Central Pattern Generator Location
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Bilaterally symmetric network in Medial aspect of intermediate gray zone
Candidate CPG members must demonstrate rhythmicity related to locomotor rhythm Cadidate CPG members must demonstrate altered rhythm in their absence HB9 interneurons - fire burst of AP in rhythm w/ extensor motor neurons |
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Nerve Conduction Velocity
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Stimulate neuron distally, record latency to muscle response
Stimulate neuron proximally, record latency to muscle response (Proximal - Distal) / (Proximal Latency - Distal Latency) = Time / Distance = Velocity |
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Nerve Conduction Study - Normal Velocity, Decreased CMAP
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Axonal Neuropathy
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Nerve Conduction Study - Conduction block
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Focal demyelinating neuropathy
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Nerve Conduction Study - Decreased Velocity, Normal Amplitude
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Uniform Demyelinating neuropathy
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Genetic Peripheral Demyelinating Disorders - mutant genes
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Peripheral myelin protein 22
Myelin P Zero Connexin 32 Combined account for 95% of disorders |
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Repetitive Nerve Stimulation Studies
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Electrically stimulate nerve 6-10 times at 2/3 Hz
Record Compound Muscle Action Potential over muscle Normal muscle - No change in CMAP after repetitive stimulation Endplate potential will decrease, but stay above muscle AP threshold |
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Repetitive Nerve Stimulation - Decremental Response
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Neuromuscular transmission disorders
Seen in Myasthenia Gravis Reduced initial end plate potential - further reduction falls below muscle AP threshold |
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Neonatal Hypotonia - Localization: Central v Peripheral Lesion
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Other brain abnormality: C +++ P+/-
Organ Malformation: C+ P+/- Tendon Reflexes: C - brisk/normal P - depressed/absent Postural Reflexes: C - preserved P - Depressed/absent Fisting of hands: C + P - Facial Weakness: C - P +/- Limb Weakness: C +/- P +++ Fasciculation: C - P +/- |
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Neonatal Hypotonia - Anterior Horn Cell Lesion - Pattern of Weakness
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Face +/-
Arms and Legs ++++ Proximal > Distal DTR absent |
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Neonatal Hypotonia - Muscle Lesion - Pattern of Weakness
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Face variable
Arms and Legs +++ Proximal > Distal DTR normal/decreased/absent |
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Neonatal Hypotonia - NMJ Lesion - Pattern of Weakness
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Face +++
Arms and Legs +++ Proximal >/= Distal DTR normal/decreased/absent |
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Neonatal Hypotonia - Peripheral Nerve Lesion - Pattern of Weakness
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Face -
Arms and Legs +++ Proximal < Distal DTR decreased/absent |
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Neonatal Hypotonia - Nerve Conduction Study and EMG results - site of involvement
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Central: NCS - normal EMG - normal
Anterior Horn: NCS - normal EMG - Fasciculation/fibrilation Peripheral Nerve: NCS - abnormal EMG - fibrilation NMJ: NCS - normal/decremental/incremental EMG - Normal / Short duration small amplitude Muscle: NCS - normal EMG - short duration small amplitude |
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EMG - Neurogenic Lesion - LMN
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Insertional activity - increased
Spontaneous activity - Fibrilation / Positive waves Motor Unit Potential - Large amplitude / duration, limited recruitment Interference Pattern - Reduced / fast firing rate |
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EMG - Neurogenic Lesion - UMN
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Insertional activity - normal
Spontaneous activity - None Motor Unit Potential - Normal Interference Pattern - Reduced / slow firing rate |
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EMG - Myogenic Lesion - Myopathy
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Insertional activity - normal
Spontaneous activity - none Motor Unit Potential - small amplidue / duration, early recruitment Interference Pattern - Full / Low amplitude |
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EMG - Polymyositis
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Insertional activity - increased
Spontaneous activity - Fibrilation / Positive waves Motor Unit Potential - Small amplitude / duration, early recruitment Interference Pattern - Full / Low amplitude |
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Myotubular Myopathy
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MTM1 gene mutation
X-linked Severe phenotype - truncating and splicing mutations Mild phenotype - missense mutations and 3' mutations |
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Midline Cerebellar Lesion
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Truncal and Proximal limb dysfunction
Titubation - Truncal tremor Ataxic gait - wide based, lurching, short unequal steps, asynchronous arm swing Symptoms more prominent w/ sudden change of direction Patient unable to perform tandem gait (heel to toe) |
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Hemispheric Cerebellar Lesion
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Limb Ataxia: Arms > Legs
Complex and fast movements worse Decomposition of movement, delayed initiation Dysmetria, Dysdiadochokinesis Oscillatory intention tremor |
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Rebound - Cerebellar Dysfunction
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Inability to stop an ongoing movement
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Nystagmus
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Abnormal jerking eye movements
Fast phase and slow correcting phase |
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Ocular Dysmetria
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Inacurate occular fixation on target, overshoot and oscillate
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Ataxic Dysarthria
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Disruption of metrical structure of speech
Phenomes and intervals too long/shor Incorrect emphasis on syllables Harsh and monotonous speech Scanning speech - slow and deliberate production of syllables |
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Signs of Cerebellar Dysfunction
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Gait ataxia, titubation, tremor, dysmetria, dysdiadochokinesis, rebound, nystagmus
Ocular dysmetria, scanning speech, cognitive dysfunction |
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Acute v Chronic Cerebellar Damage - muscle tone
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Acute hypotonia
Chronic normal tone |
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Sensory v Cerebellar Ataxia
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Sensory Ataxia - loss of input to cerebellum
Appendicular ataxia and wide based gait Position and vibration impaired --> dependent on visual feedback Positive Romberg sign Cerebellar Ataxia - may be restricted to gait or limbs Gait more lurching, staggering Titubation Position and Vibration sense are spared Dysarthria |
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Vestibular dysfunction v Cerebellar damage
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Vestibular dysfunction - Vertigo
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Corticospinal Tract Disease v Cerebellar damage
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CST disease - UMN signs present
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Proximal limb weakness v Cerebellar damage
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Proximal Limb Weakness - Weakness, rhythmycity preserved
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Superior Cerebellar Artery
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Branches off Basilar Artery -
Supplies superior surface of cerebellum Fastigial, interposed, and dentate nuclei Sup Cerebellar Peduncle and Mid Cerebellar Peduncle |
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Anterior Inferior Cerebellar Artery
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Branches off Basilar Artery
Supplies lateral regions of infereior surface of cerebellum Flocculus Part of Mid Cerebellar Peduncle Caudoventral Dentate nuclei Labyrinth of ear (branches) |
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Posterior Inferior Cerebeller Artery
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Branches off each vertebral artery
Supplies medial regions of infereior surface of cerebellum Nodulus Dorsolateral medulla |
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Superior Cerebellar Artery Syndrome
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Ipsilateral Cerebellar Ataxia
Nausea, vomiting, dysarthria Loss of pain and temperature sensation contralateral Partial deafness, arm tremor +/- ipsilateral Horner's Syndrome |
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Anterior Inferior Cerebellar Artery Syndrome
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Vertigo
Ipsilateral Deafness Ipsilateral facial weakness Ataxia |
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Posterior Inferior Cerebellar Artery Syndrome
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Wallenburg Syndrome
Sensory and sympathetic disturbances Cerebellar and pyramidal tract signs Dysfunction of CN V, IX, X, and XI |
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Cerebellar Vascular Disease - Causes
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Ischemic Stroke
Aneurysms - occur at sites of structural weakness, vascular junctions Ateriovenous malformations - no capillary bed --> high blood pressure in venous system Global hypoxemia |
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Cerebellar Mutism
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Commonly seen after surgery in posterior cranial fossa
Decreased / absent speech, irritability, hypotonia, ataxia Severe incoordination of volitional motor aspects of speech May be immediate or delayed |
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Most common location for brain tumor in children
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Posterior Cranial Fossa
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Cerebellar Malformations - Chiari I
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Static herniation of medulla and cerebellar tonsils through foramen magnum
4th ventricle in normal position |
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Cerebellar Malformations - Chiari II
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Neural tube closure defect --> inadequate 4th ventricl formation / small posterior fossa
Herniation of medulla, cerebellar tonsils, and vermis through foramen magnum Towering cerebellum, tectal beaking, myelomeningoecele, aqueductal stenosis |
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Cerebellar Malformations - Chiari III
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Herniation of medulla, cerebellar tonsils and vermis, and 4th ventricle through foramen magnum
Associated w/ encephalocele or myelomeningocele |
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Dandy Walker Malformation
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Cerebellar malformation - neonatal presentation
Cystlike dilation of 4th ventricle Cerebellar vermis absent Enlarged posterior fossa |
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Joubert Syndrome
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Cerebellar malformation - neonatal presentation
Hypoplasia of cerebellar vermis Midbrain appears like "molar tooth" on imaging Breathing abnormalities, hypotonia, eye movement abnormalities Ataxia, mental retardation |
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Medulloblastoma
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Midline Cerebellar tumor
Causes truncal instability and gait ataxia |
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Dysarthria - clumsy hand syndrome
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Due to infarction in superior cerebellar artery
Ipsilateral dysmetria and intention tremor Slurred speech - slow and deliberate |
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Post-infectious cerebellitis
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Acute cerebellar ataxia - explosive onset of gait ataxia and nystagmus
Antecedant viral infection - commonly varicella Typically seen in children < 5 years Full recovery after weeks / months |
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Multiple Sclerosis
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Chronic inflammatory disease of CNS
Inflammation, demyelination, glial scarring Cerebellum involvement common |
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Paraneoplastic cerebellar degeneration
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Tumor associated degeneration - associated w/ specific anti-neuronal antibodies
anti-Hu - small cell lung carcinoma anti-Yo - ovarian or breast cancer anti-Ri - breast and lung cancer Opsoclonus-myoclonus syndrome - associated w/ neuroblastoma |
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Toxic Cerebellar Disease
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Acute or chronic
Alcohol Anti-epileptic drugs - carbamazepine, phenytoin |
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Spinocerebellar Ataxia
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Group of autosomal dominant disorders
Slowly progressive gait and limb ataxia Akinesia, rigidity, tremor, hyporeflexia Many associated w/ triplet repeat expansions |
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Basal Ganglia - Input nuclei
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Striatum - Caudate and Putamen
Caudate receives input from cortical association areas - premotor cortex and supplementary motor areas Putamen receives input from motor cortex Seperated by white matter of internal capsule |
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Basal Ganglia - Output nuclei
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Substantia nigra Pars Reticularis and Globus Pallidus Interna
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Basal Ganglia - Intrinsic nuceli
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Globus Pallidus Externa, Substantia Nigra Pars Compacta, and Subthalamic Nuclei
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Lenticular Nucleus
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Putamen and Globus Pallidus
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Substantia Nigra
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Dopmaine oxidizes to form quinones --> polymetize into neuromelanin (black)
Pars compacta - dopaminergic neurons --> striatum Pars reticularis - receives input from striatum and STN --> projects to thalamus |
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Basal Ganglia - Direct Pathway
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Initiation of movement - learning positive outcomes associated w/ behaviors
Excitatory signal from cortex (ACh) --> striatum Excitatory signal from SNc (DA) --> striatum (D1 receptors) Striatum activation increases inhibitory output (GABA) to GPi / SNr Gpi/SNr inhibition decreases inhibitory output (GABA) to thalamus Disinhibition of thalamus results in excitatory signal to motor cortex |
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Basal Ganglia - Indirect Pathway
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Termination of movement - learning negative outcomes associated w/ behaviors
Excitatory signal from cortex (ACh) --> striatum Inhibitory input from SNC (DA) --> striatum (D2 receptors) Striatum activation decreases inhibitory output (GABA) to GPe GPe inhibition decreases inhibitory output (GABA) to STN Disinhibition of STN results in excitatory signal (Glu) to GPi/SNr GPi/SNr activation increases inhibitory output (GABA) to thalamus Inhibition of thalamus reduces excitatory signal to motor cortex |
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Parkinson's Disease - Histology
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Aggregation of α-synuclein into cytoplasmic Lewy Bodies
Loss of neurons in Substantia Nigra Glial proliferation, microglial inflammation |
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Parkinson's Disease - Signs and Symptoms
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Bradykinesia - slow initiation of voluntary movement / lack of spontaneous movement
Rigidity - increased muscle tone, ratchet resistance to movement Resting tremor Stooped and unstable posture Depression, constipation, urinary symptons, sleep disorders, hyposmia |
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Parkinson's Disease - Pathology
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Loss of dopamine input to striatum
Reduced activity through direct pathway --> less thalamic disinhibition Increased activity through indirect pathway --> more thalamic inhibition Deep brain stimulation of STN or GPI can improve symptoms |
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Huntington's Disease - Signs and Symptoms
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Chorea - brief, jerk-like movements
Athetosis - slow, writhing movements Mental decline - executive dysfunction, slowness, memory decline Personality changes - irritable, anxious, depressed |
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Huntington's Disease - Genetics
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Triplet repeat expansion - CAG
Autosomal dominant - anticipation Protein product functions in axonal transport, vesicle exocytosis and endocytosis |
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Huntington's Disease - Pathology
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Selective loss of medium spiny GABAergic neurons in striatum
Reduced activity through indirect pathway --> disinhibition of thalamus Increased thalamic stimulation of cortex |
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Motor defects - Cerebellar / Pyramidal / Basal Ganglia
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Brainstem / Cerebellar injury --> Ataxia
Pyramidal system injury --> weakness, spasticity, hyperreflexia Basal ganglia injury --> Bradykinesia, Rigidity, postural instability, hyperkinesis, no weakness |
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Striatum Interneurons
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95% medium spiny - GABA - Inhibitory
5% large spiny - ACh - inhibits direct pathway (M4-R) / stimulates indirect pathway (M1-R) ACh inhibits activity of thalamus |
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Dopamine Biosynthesis
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Tyrosine --> L-DOPA --> Dopamine
Rate limiting step: Tyrosine --> L-DOPA via tyrosine hydroxylase |
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Parkinson's Pharmacology - Levodopa
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Levodopa replacement of dopamine - crosses BBB
Converted to Dopamine by Dopa Decarboxylase (DDC) - present in brain and peripherally Co-administer w/ carbidopa and benserazide - peripheral inhibitors of DDC, do not cross BBB Side effects due to peripheral conversion to DA - nausea, orthostatic hypotension Peak-dose chorea / End of dose dystonia |
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Parkinson's Pharmacology - DA receptor agonists
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Longer lasting effects than L-DOPA, more selective receptor stimulation
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Parkinson's Pharmacology - inhibit DA breakdown
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Inhibitors of monoamine oxidase (MAO-B) and catechol-O-methyltransferase (COMT)
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Parkinson's Pharmacology - ACh muscarinic antagonists
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Block ACh-M receptor activity in striatal interneurons - relieve inhibition on thalamus
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Parkinson's Therapy - Deep brain stimulation
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Inactivate GPi or STN
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Huntington's Disease Pharmacology
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Nothing available to halt disease progression
Dopamine inhibition for symptomatic treatment Antidepressants / antipsychotics for personality and mood changes |
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Tremor
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Rhythmical and sinusoidal movement
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Parkinson's Disease v Essential Tremor
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PD: Asymmetrical, Rest > postural/action
Bradykinesia, cogwheel rigidity, shuffling gait Micrographia - small handwriting ET: Symmetrical, Postural/action > rest No bradykinesia, no rigidity, normal gait Shaky graphia - large, jagged, messy handwriting |
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Chin Tremor and Facial Masking
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Parkinson's Disease
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Head tremor
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Essential Tremor
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Chorea
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Irregular, random, abrupt, flowing movement
Hereditary - Huntington's, Spinocerebellar ataxia, neuroacanthocytosis Secondary - Hyperthyroid, stroke, SLE, acute renal failure, drugs |
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Athetosis
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Low amplitude chorea - affects distal muscles
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Ballismus
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High amplitude chorea - affects proxmial muscles
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Hemiballismus
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Unilateral High amplitude chorea - affects proximal muscles
Usually due to structural lesions - STN |
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Myoclonus
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Irregular shock-like movements
Fast and slow phase Hereditary - Essential Tremor, epileptic, degenerative Secondary - Metabolic, drugs, lesions, degenerative Toxic Metabolic Myoclonus - worsens w/ attempted action |
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Tic
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Abrupt, brief, stereotyped movement
Partial voluntary control - can be temporarily suppressed Motor and vocal |
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Dystonia
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Sustained muscle contractions w/ twisitng posutres
Repetitive movements w/ fixed posture |
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Writer's Dystonia
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Task-specific
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Parkinsonism
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Core common features - Rigidity, Akinesia / Bradykinesia, Basal Ganglia Pathology
Seen in Parkinson's, Mutiple systems atrophy, Progressive supranuclear palsy |
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Multiple Systems Atrophy
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Parkinsonism + Autonomic Failure
More symmetric, less prominent tremor |
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Progressive Supranuclear Palsy
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Parkinsonism + opthalmoparesis (weakness in eye movement muscles)
"surprised" facial expression |
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Corticobasal Degeneration
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Parkinsonism + Apraxia and Dystonia
Very Asymmetric, myoclonus features, not tremor |
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Wilson's Disease
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Parkinsonism + Dystonia (young onset)
Facial and voice dystonia Disorder of Copper Metabolism |
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Diencephalon subdivisions
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Dorsal Thalamus - Thalamus
Epithalamus - includes pineal gland Subthalamus - includes subthalamic nuclei Hypothalamus |
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Thalamus boundaries
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Anteriorly - interventricular foramen
Superiorly - transverse cerebral fissure and floor of lateral ventricles Inferiorly - hypothalamic sulcus (seperates thalamus from hypothalamus) Posteriorly - overlaps w/ midbrain Laterally - internal capsule Medially - 3rd ventricle |
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Thalamus anatomy - myelinated fibers
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Internal Medullar Lamina
Divides thalamus into medial and lateral division Splits to surround anterior division |
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Thalamus anatomy - Lateral Division - nuclei / function
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Dorsal Tier:
Lateral Dorsal - Limbic Pulvinar / Lateral Posterior - Association Ventral Tier: Ventral Anterior (VA) / Ventral Lateral (VL) - motor relay Ventral Posterolateral - body sensory relay Ventral Posteromedial - head sensory relay Medial Geniculate - auditory relay Lateral Geniculate - visual relay |
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Thalamic relay nuclei
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VPL/VPM - sensory relay for body / head
LGN - visual MGN - auditory VA/VL - motor Anterior Nucleus - Limbic system - input from mammilary bodis output to cingulate gyrus |
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Thalamic association nuclei
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Dorsomedial Nucleus:
Input from prefrontal cortex, limbic system, and amygdala Functions in affect and foresight Pulvinar / Lateral posterior Nucleus Inpyt from parietal-occipital-temporal association cortex Functions in visual perception |
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Thalamic neurons - types
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Thalamocortical - glutaminergic excitatroy projection neurons
Local interneurons - GABA inhibitory local collaterals Nucleus Reticularis Neurons - GABA inhibitory local neurons - rim around dorsal/lateral aspect |
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Thalamo-cortico-thalamic circuit
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Thalamocortical (TC) projection neurons (Glu) to cortex - no TC-TC connections
Reciprocal excitatory projections (Glu) from cortex to TC neurons TC and CT neurons send collaterals to Reticular Nucleus Reticular Nucleus sends inhibitory (GABA) projections to multiple TC cell bodies TC neurons communicate w/ eachother via Reticular Nucleus Inhibitory interneurons (GABA) synapse on TC cell bodies |
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Thalamocortical neuron electrophysiology
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Tonic: Vm = -55mv --> depolarization causes sustained discharge
NA+ mediated AP frequency proportional to inuput Silent: Vm = -60mv --> depolarization insufficient to reach firing threshold Bursting: Vm = -70mV --> T-Type Ca2+ channels no longer inactivated Depolarization causes Ca2+ influx --> burst of 2-5 Na+ spikes |
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Thalamocortical Tonic-Burst Transition
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Tonic firing = relay mode --> faithfully relays prethalamic input to cortex
Burst mode = interuption of sensory info flow --> burst not related to pre-thalamic input Brainstem / basal forebrain produce ACh and NEPI --> neuromodulatory effects on brain Awake - high ACh/NEPI levels - close K+ leack channels - TC Vm near -55 mV --> Tonic Sleep - low ACh/NEPI levels - TC Vm near -70 mV --> Bursting threshold |
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CNS Acetylcholine source
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Nucleus Basalis of Meynert, brainstem reticular formation
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CNS Noradrenaline source
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Locos coeruleus
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CNS serotonin source
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Periacqueductal Gray, Dorsal Raphe Nucleus
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CNS dopamine source
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Substantia Nigra Pars Compacta
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Human Paleocortex
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Base of telencephalon - involved w/ olfaction
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Human Archicortex
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Hippocampus
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Agranular Cortex
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Apparent lack of stellate (granule) cells
Areas that give rise to many projection axons - Many large pyramidal cells Motor cortex |
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Granular Cortex
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Many small cells (pyramidal and non-pyramidal)
Areas that receive lots of input - do not give rise to projection axons Primary Sensory Cortices |
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Homotypical / Heterotypical Cortex
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Homotypical - 6 distinct neocortical layers
Heterotypical - Granular and Agranular cortex |
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Cortical Columnar Orientation
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Cells arranged in column perpendicular to cortical surface
Respond to same type of stimulus |
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Cortical Pyramidal Cells
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Excitatory, glutaminergic projection neurons
Axon collaterals to adjacent pyramidal and local interneurons Apical dendrite ascends through layers - basal dendrites w/in same layer High and varying density of spines on dendrites - sites of excitatory input Layers 2-6 |
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Cortical Spiny Stellate (granule) cells
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Excitatory, glutaminergic interneurons
Layer 4 - target of thalamic input Multipolar dendritic tree Ascending axon bundles into layers 2 and 3 |
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Cortical Basket Cells
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Inhibitory GABAergic interneurons
Smooth non-spiny cells Axons stay in local network |
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Regular Spiking (RS) Cortical Cells
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Generate sustained firing proportional to depolarizing input
Most excitatory cells - pyramidal and spiny stellate |
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Fast Spiking (FS) Cortical Cells
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Thin action potentials, brief spike afterhyperpolarizaton (HAP)
Output frequency proportional to depolarizing input Higher firing frequency compared to RS in response to same input Most inhibitory cells - Baskey/non-spiny |
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Bursting Cells
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All-or-none bursr of high frequency spikes
Subpopulation of pyramidal cells |
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Properties of local cortical circuits
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Recurrent excitatory input b/w neighboring excitatory cells - synapse on spines
Excitatory input drive feedforward and feedback inhibiotry input - don't synapse on spines |
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Route of information flow through cortex
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Thalamus --> L4 --> L2/3 <--> L5 --> L6 --> Thalamus
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Somatosensory nerve endings
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Generate graded potentials - behave like dendrites
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Somatosensory free nerve endings
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Tuned for pain, temperature, and crude touch
All other somatosensory receptors are mechanoreceptors |
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Slow adapting somatosensory receptors
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Signal sustained presence of stimulus
Free nerve endings, Merkel's disks, Ruffini's corpuscles, Muscle Spindles, Golgi Tendon Organs |
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Fast adapting somatosensory receptors
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Signal onset and offset of stimulus
Meissner's corpuscles, Pacinian corpuscles, Muscle Spindles |
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Lateral / Surround Inhibition
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Stimulation of receptor excites cell - axon collateral to recurrent inhibitory interneurons
Inhibit adjacent receptor cells Enhance contrast b/w signal and noise Occurs at every level where synapse has occurred |
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Cortical Representation - Receptive Fields
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Increased cortical representation --> increased receptor density, 2 point discrimintation
Decreased receptive field size |
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Primary SS cortex - body representation - stimulus type
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3a - muscle afferents
3b - cutaneous receptors 2 - deep pressure receptors 1 - rapidy adapting cutaneous receptors |
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Cranial Nerves Exiting at Ponto-Medullary Junction
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VI, VII, and VIII
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Laterally exiting cranial nerves
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V, VII, IX, and X - all mixed sensory / motor
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Medially exiting cranial nerves
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III, IV, VI, and XII - all motor
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Medial Lemniscus Position in Brainstem
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Moves from medial to lateral position while ascending
"Stands on Pyramids" in Medulla - midline, D/V axis Ventral end rotates laterally in Pons - drift away from midline Elongated medial-lateral orientation in Midbrain - far from midline |
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Anterolateral System Position in Brainstem
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Courses in lateral aspect - does not change location
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Descending Hypothalamic Fiber Position in Brainstem
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Courses in lateral aspect w/ ALST - does not change position
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Brainstem Anatomy - 4th ventricle in…
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Pons and Rostral Medulla
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Brainstem Anatomy - Cerebral aqueduct in…
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Midbrain
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Brainstem Anatomy - Central canal in…
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Caudal Medulla
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Brainstem Anatomy - Cerebellar Peduncles in…
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Medulla - ICP
Pons - ICP / MCP / SCP Midbrain - SCP |
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Brainstem Anatomy - Olives in…
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Rostal Medulla
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Brainstem Anatomy - Pyramidal Decussation in…
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Caudal Medulla - Medullary-cervical junction
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Brainstem Anatomy - Caudal Medulla Structures
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Pyramidal Decussation
Central Canal Nucleus Gracilis / Fasciculus Gracilis Nucleus Cuneatus / Fasciculus Cuneatus Beginings of Medial Lemniscus Dorsal to Pyramids |
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Brainstem Anatomy - Rostral Medulla Structures
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Inferior Olivary Nuclei - Dentate Cerebellar Nuclei looks similar but on dorsal aspect
4th Ventricle Medial Lemniscus Dorsal to Pyramids Vestibular Nuceli - CN VIII Inferior Cerebellar Peduncle Hypoglossal Nuclei / Nerve - CN XII |
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Brainstem Anatomy - Caudal Pons Structures
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Transverse Pontine Fibers - Pontocerebellear fibers
4th ventricle Cranial Nerves VI, VII, and VIII Sup / Mid / Inf Cerebellar Peduncle Medial Lemniscus is diagonal and lateral from midline |
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Brainstem Anatomy - Rostral Pons Structures
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4th Ventricle
Cranial Nerve V Transverse Pontine Fibers - Pontocerebellar fibers Superior Cerebellar Peduncle Dorsal Longitudinal Fasciculus Medial Lemniscus elongated and lateral to midline |
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Brainstem Anatomy - Caudal Midbrain Structures
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Inferior Colliculi
Cerebral Aqueduct - Periaqueductal Gray Decussation of Superior Cerebellar Peduncles Cerebral Peduncles Medial Lemniscus elongated - dorsal to cerebral peduncle Lateral Lemniscus surrounding Inferior Colliculi |
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Brainstem Anatomy - Rostral Midbrain Structures
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Superior Colliculi
Cerebral Aqueduct - Periaqueductal Gray Red Nucleus and Substantia Nigra Cerebral Peduncles Cranial Nerve III exiting in interpeduncular fossa Ventral Tegmental Area |
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Brainstem Anatomy - Arrangement of CN VI and CN VII
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CN VI nuclei located dorso-medial to CN VII nuclei
CN VII axons project medially and loop around CN VI nuclei before projecting laterally and exiting |
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Facial Weakness - UMN v LMN
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Most cranial nerve LMN receive bilateral UMN input - except some LMN in facial nerve (VII)
Facial LMN in Pons --> ipsilateral facial muscles Bilaterally innervated LMN --> ipsilateral upper face / shut eyes and wrinkle forehead Uni/Contralateral Innervated of LMN --> ipsilateral lower face / nose, mouth, and chin UMN Lesion - usually unilateral --> contralateral weakness of lower face LMN lesion --> ipsilateral total facial weakness (Bell's Palsy) |
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Brainstem Nerve Fiber Classification
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G / S: General - whole body / Special - Head or Neck only
V / S: Visceral - smooth muscle, glands, heart / Somatic - skeletal muscle or skin A / E: Afferent - sensory / Efferent - Motor |
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Neural Tube - Brainstem Patterning
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Neural Tube - Dorsal = Sensory / Ventral = Motor
D/V seperated by Sulcus Limitans Brainstem - Neural tube split at roof, rotates Medial = Motor (Neural Tube Ventral) / Lateral = Sensory (Neural Tube Dorsal) |
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Brainstem Cranial Nerve Nuclei Organization
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Discontinous columns of functionally similar motor nuclei
Midline -GSE - GVE - SVE - Sulcus Limitans Continuous columns of sensory nuclei Sulcus Limitans - SVA - GVA - SSA - GSA - Lateral |
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Brainstem Cranial Nerve Nuclei - GSE
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Column 1 next to midline - Innervated Skeletal Muscle
Occulomotor Nuc - CN III - Midbrain - Adduct eye and raise eyelid (Ips except contra sup rect) Trochlear Nuc - CN IV - Midbrain - Depress eye (Contralateral) Abducens Nuc - CN VI - Pons - Abduct eye (Ipsilateral) Hypoglossal Nuc - CN XII - Medulla - Moves tongue (Ipsilateral) |
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Brainstem Cranial Nerve Nuclei - GVE
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2nd column from midline - Pre-ganglionic Parasympathetics
Edinger-Westphal Nuc - CN III - Midbrain - Pupil constriction and near response (ipsilateral) Sup Salvatory Nuc - CN VII - Pons - Lacrimal gland (ipsilateral) Inf Salivatory Nuc - CN IX - Medulla - Parotid gland (ipsilateral) Dorsal Motor Nuc of Vagus - CN X - Medulla - gut viscera |
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Brainstem Cranial Nerve Nuclei - SVE
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3rd column from midline - Pharyngeal arch derived muscles
Motor Trigeminal Nuc - CN V - Pons - Muscles of mastication (ipsilateral) Motor Facial Nuc - CN VII - Pons - Muscles of facial expression (ipsilateral) Nucleus Ambiguus - CN IX,X - Medulla - Palate, pharynx, larynx muscles (ipsilateral) |
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Brainstem Cranial Nerve Nuclei - SVA / GVA
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1st column from Sulcus Limitans - visceral sensory
Solitary Nuc and Tract - Medulla - Gustatory and Cardiorespiratory Nuc Gustatory Nuc - CN VII, IX, X - Rostral Medulla - Taste (SVA) Cardiorespiratory Nuc - CN IX, X - Caudal Medulla - Carotid sinus / body - CV regulation (GVA) |
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Brainstem Cranial Nerve Nuclei - SSA
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2nd column from Sulcus Limitans - Vestibulocochlear sensory
Vestibuluar Nuclei - Sup and Lat in Caudal Pons - Med and Spinal in Medulla Cochlear Nuclei - Rostral medulla - Pontomedullay junction - info from cochlea Cochlear Nuclei displaced laterally from vestibular nuclei |
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Brainstem Cranial Nerve Nuclei - GSA
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3rd column from Sulcus Limitans - Continuous column of Trigeminal Nuclei (V)
Mesencephalic Nuc and Tract of V - Midbrain - Proprioceptions, jaw muscles Principle Sensory Nuc of V - Pons - touch Spinal Trigemincal Nuc - Caudal Pons through Medulla - Pain and temperature |
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Trigeminal Nerve - Sensory - Touch
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Large diameter afferents - cell bodies in Trigeminal Ganglion or Mesencephalic Nucleus
Afferents terminate in Principle Sensory Trigeminal Nucleus Axons decussate - ascend in Medial Lemniscus to VPM thalamus Some axons project to Trigeminal Motor nucleus - masseter stretch reflex |
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Trigeminal Nerve - Sensory - Pain and Temp
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Small diameter afferents - cell bodies in trigeminal ganglion
Afferents descend to terminate in spinal trigeminal nucleus Nucleus Oralis - Facial Touch Nucleus Interpolaris - Tooth Pulp Pain Nucleus - Caudalis - Face Pain and Temperature Axons decussate at level of cell bodies - ascend in Antero Lateral System to VPM thalamus |
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Nucleus Caudalis - Topography
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Spinal Trigeminal Nucleus - Facial Pain and Temperature - Onion Skin Pattern
Most Caudal cell bodies - neck and head behind V3 territory Most Rostral cell bodies - mouth and nose Intermediate cell bodies - intermediate layers of facial territory |
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Babinski Sign
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Stroke planta surface of foot
Flexor Plantat Response - absent sign - normal in adults Extensor Plantar Response - Present sign - normal in neonates, abnormal in adults (UMN Lesion) |
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Unilateral Babinksi Sign
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Lesion of contralateral corticospinal tract
Lesion usually in cerebral hemispheres - distance b/w both CST |
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Bilateral Babinksi Sign
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Lesion of both corticospinal tracts
Lesion usually in spinal cord or brainstem - close proximity |
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Spasticity
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Increased tone
Resistance to external movement increases w/ increasing speed of stretch Resistance rises before giving way to lower level of tone - clasp knife phenomenom Typically occurs in Lesion of CST |
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Rigidity
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Increased tone
Resistance to external movement does not vary w/ speed of imposed movement Typically seen in lesions of extrapyramidal descending tracts (non-CST) |
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EMG - Spontaneous Activity
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Normal Muscle - Silent
Recently denervated - fibrillations (spontaneous action potentials) |
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Primary Olfactory Sensory Neurons
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Located in nasal neuroepithelium
Axons travel in olfactory nerve bundles Pass through cribiform plate Project to ipsilateral olfactory bulb in brain |
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Olfactory Bulb projections
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Lateral Olfactory Tract - Ipsilateral Targets
Pyriform Cortex - Olfactory perception Amygdala - odor associated emotions Anterior Olfactory Nucleus - send axons to contralateral olfactory bulb Olfactory Tubercle Entorhinal Area |
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Olfactory Neuroepithelium Cells
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Olfactory Sensory Neurons - ciliated bipolar receptor cells
Supporting Cells - Glial-like Basal Cells - stem cell, generate new receptors and supporting cells |
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Olfactory Signal Transduction
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Odorant binding to GPCR in cilia of sensory neuron
Golfα activates adenyly cyclase --> cAMP --> opens cAMP gated channel --> Na and Ca influx Ca influx activates Ca-gated Cl channel --> Cl efflux Depolarization --> action potential |
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Sensory Neuron Receptor Expression
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Single nuerons expresses single receptor type
Single receptor can bind multiple odorants - different affinity Single odorant can bind multiple receptors |
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Odor quality and intensity coding
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Combinatorial coding from multuple receptors
Detect different parts of odorant molecule |
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Olfactory Coding in Bulb
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Axons of sensory neurons expressing same receptor converge onto same glomerulus
Mitral/tufted cell send primary dendrite into single glomerulus (receive OSN input) Each glomerulus contains primary dendrite from 25-30 MT cells Single odorant activates mutliple glomeruli / multiple odorants activate single glomeruli Odor stimulus represented by spatial coding and/or temporal coding of multiple glomeruli |
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Olfactory Bulb - Cell types
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Mitral/Tufted cells - excitatory glutaminergic projection neuron - excitatory input from OSN
Periglomerular cells - inhibitory GABAergic local interneuron - modulate OSN Granule cells - inhibitory GABAergic local interneuron - lateral inhibition |
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Olfactory Bulb Lateral Inhibition
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M/T cell firing - secondary dendrites release glutamate --> excited granule cells
Grannule cells release GABA to inhibit original and nearby M/T cells Excitation of M/T cell results in greater inhibiton of neighbor M/T cell - enhances contrast Lateral Inhibition changes response elicitted by repertoire of odorants |
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Cortical Olfactory Coding
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M/T cells project to olfactory cortex - Piriform (Paleocortex - 3 layers)
Divergent and Convergent input to cortical cells Odorant activates unique but disperesed group of cortical neurons No spatial organization - neighboring cortical cells have discontinuous receptive fields |
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Anosmia
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Absence of smell sensation - general or specific
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Hyposmia / Hyperosmia
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Decreased smell sensation / abnormally acute smell sensation
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Dysosmia
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Distortion of smell sensation
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Phantosmia
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Olfactory hallucination - dysosmia in absence of stimulus
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Olfactory agnosia
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Inability to recognize odor sensation - common in stroke patients
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Odorant Qualities
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Volatile organic molecules
Non-inoni Hydrophobic |
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Taste Bud Location
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Clustered in circumvallate, foliate, and fungiform papillae on tongue
Filiform papillae are mechanically gated - non gustatory |
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Taste Bud Innervation
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Anterior 2/3 of tongue - Facial Nerve VII - Chorda Tempani - Geniculate Ganglion
Posterior 1/3 of tongue - Glossopharyngeal Nerve IX - Lingual Branch - Petrosal ganglion |
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Taste Information to Cortex
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Sensory fibers in Geniculate and Petrosal Ganglion
Fibers enter solitary tract in medulla Synapse on neurons in rostral and lateral part of solitary nucleus Axons project to VPM thalamus Relay to ipsilateral primary gustatory cortex (anterior insular and frontal operculum) |
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Primary Gustatory Cortex
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Anterior Insular Cortex and Frontal Operculum
Input from VPM thalamus (ipsilateral) |
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Gustatory Transduction - Salt
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Na+ stimulus
Opens "Amiloride-sensitive" Na+ channel Na+ influx depolarizes cell |
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Gustatory Transduction - Sour
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H+ stimulus
H+ sensitive cation channels H+ influx depolarizes cell TRP - Transient Receptor Potential proteins can serve as acid channels |
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Gustatory Transduction - Sweet, Umami, Bitter
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GPCR
Gustducin - Taste cell specific G-protein Activates Phospholipase C Opening of TRPm5 channel Cation influx depolarizes cell |
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Taste Cells - Receptors and Released products
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Each cell has single type of receptor (Salt, Sour, Sweet, Bitter, Umami)
Depolarization of cell causes release of ATP-containing vesicles at synaptic terminals ATP excites downstream cell - generates action potential |
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Gustatory Receptors - Sweet, Umamia, Bitter
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Sweet = T1R2 + T1R3
Umami = T1R1 + T1R3 Bitter = T2Rs All are GPCR --> Gustducin --> TRPm5 channel --> Cation influx |
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Ageusia
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Absence of taste sensation
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Hypoguesia
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Decreased sensation to tastants
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Dysgeusia
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Distortion of taste sensation
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Gustatory agnosia
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Inability to recognize taste sensation
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Chemosensation Overview
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Integration of Olfactory, Gustatory, and Somatosensory input
Olfactory - CN I - volatile molecules Gustatory - CN VII, IX, X - Salty, sour, sweet, bitter, umami Somatosensory - CN V - texture, spice, mint, temperature |
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Umami
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MSG - monosodium glutamate
Amino acids Meaty - signals protein enriched food |
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Sweet
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Sucrose, Lactose, Fructose
Signals carbohydrate enriched food |
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Medulla Cranial Nerves
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IX, X, XI, XII
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Pons Cranial Nerves
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V, VI, VII, VIII
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Midbrain Cranial Nerves
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III, IV
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Characteristic Finidng of Brain Stem Disorder
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Crossed hemiparesis
Neurologic Deficit on opposite side of a cranial palsy Cranial palsy ipsilateral to lesion Neurologic Deficit contralateral to lesion |
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Medially Located Brainstem Cranial Nerves and Tracts
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CN III, IV, VI, XII
Corticospinal Tract DCML (pons and medulla) |
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Laterally Located Brainstem Cranial Nerves and Tracts
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V, VII, VIII, and X
ALST DCML (Midbrain) |
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Crossed Hemiparesis - Lesion of CN…
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III, VI, VII, XII
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Involvement of multiple cranial nerves on same side of body
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Suggests lesion outside brainstem - extraaxial
All CN must pass through subarachnoid space surrounded by CSF |
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Pupillary Light Reflex
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Tests integrity of Midbrain
Light stimulus to one eye --> contraction of both pupils Optic Tract --> Ipsilateral Pretectal Nucleus --> Bilateral Edinger-Westphal Nucleus --> Ciliary Ganglion --> Iris Constrictor Muscles EW nucleus projects pre-ganglionic parasympathetic fibers - course on periphery of CN III |
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Corneal Reflex / Blink Reflex
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Tests integrity of Pons
Touch cornea w/ cotton ball --> eyelid blinking Afferent - V1 - nasociliary branch of opthalmic branch of trigeminal nerve Efferent - VII |
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Vestibulo-Occular Reflex
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Tests integrity of brainstem from medulla to midbrain
Patient fixates eyes in center - turn head --> eyes rotate in opposite direction to compensate Vestibular Nerve (VIII) --> ipsilateral Vestibular nuclei --> contralateral Abducens Nuclei (VI) --> Ipsilateral Lat Rectus and Contralateral Occulomotor Nerve --> Ipsilateral Medial Rectus VI --> III courses in MLF Coordinated movements of both eyes |
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Internuclear Ophthalmoplegia
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Disorder of Conjugate Lateral Gaze
Indicates Damage to MLF Unilateral in older patients - commonly vascular accident Bilateral in younger patients - commonly multiple sclerosis |
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Brainstem Vasculature
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Midline vessels branch of Basilar or Vertebral Arteries
Vertebral Paramedian Arteries only supply one side --> unilateral defects |
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Isolated CN III palsy
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Dilated pupil - Down and Out
Aneurysm until proven otherwise Commonly at branch point of Posterior Communicating Artery |
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CN III palsy + Head Trauma
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Temporal Lober herniation into midbrain
Compresses CN III Pupil findings earliest sign of herniation |
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Wernickes - Korsakoff's Disease
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Triad of Double Vision, Confusion, and Ataxia
Deficiency of Thiamine (vitamine B1) Chronic deficiency results in midbrain hemorrhage Presents as CN VI palsy Patients commonly alcoholic or malnourished |
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CN V palsy
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Jaw deviates TOWARDS weak side
Wasting of ipsilateral Temporalis Muscle Impaired Corneal Reflex (V-->VII) Localizes lesion in Pons |
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Wallenberg Syndrome
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Lesion to Dorsal-Lateral Medulla
Caused by occlusion of PICA or Vertebral Artery Lateral Branches Ipsilateral Facial Numbness - CN V Contralateral Body Numbness - ALST Ipsilateral Horner's Syndrome Ipsilateral laryngeal, pharyngeal, and palatal hemiparalysis - CN IX, X, XII |
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CN IX or X palsy
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Palate hemiparalysis
Palate deviates AWAY from weak side |
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CN XII palsy
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Ipsilateral tongue atrophy
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Brain major vascular supply
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Receives 20% of cardiac output
80% from Internal Carotid Arteries --> anterior circulation 20% from Vertebral Arteries --> posterior circulation |
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Brain Vascular Anatomy - Internal Carotid Artery
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Enter skull through Foramen Lacerum
1st major branch - Ophthalamic Artery to eye 2nd major branch - Anterior Choroidal Artery 3rd major branch - Post Communicating Artery - connects to post cerebral artery - joins Ant-Post circulation Terminates into Anterior Cerebral and Middle Cerebral Artery |
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Brain Vascular Anatomy - Vertebral Artery
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Enter skull through Foramen Magnum
Ant and Post Spinal Artery branches - supply spinal cord Post Inf Cerebellar Artery branch - caudal cerebellum and lateral medulla Both vertebral arteries join to form Basilar Artery |
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Brain Vascular Anatomy - Circle of Willis
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Posterior - Vertebral Arteries join to form Basilar Artery
Basilar Artery branches: AICA, SCA Basilar A divides into two Posterior Cerebral Arteries Post Communicating Artery branches off PCA --> connects w/ Internal Carotid Artery ICA divides into Middle and Anterior Cerebral Arteries ACAs connected by Anterior Communicating Arteries |
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Brain Vascular Anatomy - Middle Cerebral Artery territory
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Lateral Frontal Lobe, Parietal Lobe, Temproal Lobe, Insular Cortex, Putamen, and Internal Capsule
Spares midline territory, occipital lobe, and most ventral aspects of frontal lobe |
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Middle Cerebral Artery occlusion
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Contralateral hemiparesis - face and arms affected more than legs (central in homonculous)
Aphasia - if in dominant hemisphere Neglect - if in non dominant hemisphere Contralateral visual hemifield / quadrand defect - optic radiations Deviation of gaze - frontal eye fields Cortical sensory deficits |
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Ophthalamic artery occlusion
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Ipsilateral monocular blindness
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Brain Vascular Anatomy - Anterior Cerebral Artery territory
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Medial Frontal Lobe, Cingulate, Corpus Callosum, Caudate
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Anterior Cerebral Artery occlusion
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Contralateral lower extremity weakness - medial homonculous
Behavioral changes - frontal lobe involvement (alien limb syndrome) |
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Brain Vascular Anatomy - Posterior Cerebral Artery territory
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Medial Temporal lobe, Occipital Lobe, Anteromedial Thalamus
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Posterior Cerebral Artery occlusion
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Contralateral visual field loss (hemianopsia) - occipital
Contralateral hemiparesis - thalamus and capsular involvement Behavioral changes - thalamus and capsular involvement |
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Weber / Medial Midbrain Syndrome
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Ipsilateral CN III palsy w/ contralateral hemiparesis
Occlusion of Basilar Artery - infarct in midbrain or pons Commonly involves proximal PCA and short circumfrential basial branches Damage to CN III nerves and CST in peduncles |
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Locked In / Pontine Syndrome
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Occlusion of proximal or midbasilar artery - infarct in pons - Bilateral damage
Damage to ventral pons - descending motor pathways --> paralysis Sparing of dorsal pons - reticular activating system --> consciousness Mild - CN VI palsy w/ contralateral hemiparesis Severe injury - coma or death |
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Wallenberg / Lateral Medullary Syndrome
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Occlusion of PICA
Contralateral loss of pain and temperature in body - ALST Ipsilateral loss of pain and temperature in face - spinal trigeminal nucleus and tract Ataxia, nausea, vomiting, vertigo - damage to vestibular nuclei and/or ICP Ipsilateral Horner's Syndrome - descending sympathetic hypothalamospinal tract |
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Signs common to Cerebellar Infarction
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Sudden onset ataxia, vertigo, nausea and vomiting
Hiccups and/or restelessness may be first signs of IV ventricle compression --> hydrocephalus |
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Major Clinical Finidings - Lacunar (small vessel) occlusion
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Contralateral motor OR sensory deficit
No cortical signs |
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Penumbra
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Viable brain tissue
Target of acute stroke therapy - save penumbra |
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Brain Vascular Anatomy - Venous Drainage
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Sup and Inf Sagital Sinus in midline
Sup sagittal, straight, and transverse sinuses meet at torcular herophili (confluence of sinuses) Drain throuhg sigmoid sinuses into jugular veins |
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Brain Vascular Anatomy - Cavernous Sinus
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Located on each side of sella turcica
CN III, IV, V1 and V2 course in lateral wall CN VI and carotid artery run in center Drain blood from orbits and anterior base of brain |
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Venous Sinus Thrombosis
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Swelling --> hemorrhage
Swelling --> increased intracranial pressure --> reduced arterial perfusion --> infarction Present w/ Headache, papilledema, seizures, sudden focal deficits, encephalopathy |
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Inferior Cerebellar Peduncle
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Connects Medulla to Cerebellum - Afferent
Dorsal Spinocerebellar tract - from ipsilateral Clark's nucleus Cuneocerebellar Tract - from ipsilateral lateral Cuneate nucleus Olivocerebellar Tract - from contralateral inferior olive Vestibulocerebellar Tract - from ipsilateral vestibular ganglion and nucleus Reticulocerebellar Tract - |
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Middle Cerebellar Peduncle
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Connects Cortex to Cerebellum (via Pons) - Afferent
Pontocerebellar Tract - from contralateral basis pontis --> mossy fibers |
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Superior Cerebellar Peduncle
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Connects Cerebellum to Red Nucleus and VA/VL thalamus - Efferent
Project to contralateral targets Fibers decussate at level of infereior colliculus |
