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276 Cards in this Set
- Front
- Back
What arteries supply the anterior and posterior circulation?
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Internal carotid arteries
Vertebral and basilar arteries |
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What is caused by an ACA, MCA, and PCA lesion?
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ACA Lesion – CL leg and foot
MCA Lesion – CL, hand, arm, and face - Language maybe , Vision maybe (ML) PCA Lesion – CL visual disturbance |
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Lesion of what artery causes locked in syndrome?
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basilar artery
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Lesion of what artery causes lateral medullary syndrome?
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Lateral medullary syndrome
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Lesion of what artery causes damage to both the corticospinal and DCML?
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ASA (think medulla)
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What sends blood to internal capsule?
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MCA
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What can result in ambulatory spastic hemiparesis with hemihypoesthesia ?
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Capsular or Lacunar Infarct
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What disease causes Thalamus & BG lit up on MRI?
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CJD
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What disease is associated with enlarged ventricles?
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Huntington's
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From superior medial to inferior lateral, what is the body parts affected?
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HAL
Head Arm Legs |
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What are the 3 dural septa?
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Falx cerebri- fold that lines the longitudinal fissure
Falx cerebelli- runs along the vermis of the cerebellum Tentorium cerebelli- horizontal dural fold extends into the transverse fissure |
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VPL damage results in what type of deficits?
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loss of CL sensation
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What fibers go through the internal capsule, cerebral peduncles, and pontine base?
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CST
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What are the 2 types and 4 subtypes of stroke? What are the majority?
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Main type: Ischemic (80%)
Subtypes: Thrombotic (53%) and Embolic (31%) Main Type: Primary Hemorrhagic (20% of Strokes) Subtypes: Intracerebral Hemorrhage 10%, Subarachnoid Hemorrhage 6% |
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ACA Damage and Clinical Symptoms?
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Paralysis and sensory impairment of contralateral leg and foot
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Focal Ischemia- Left Side (Dominant) MCA?
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Right face, hand and arm weakness, somatosensory deficits and language problems
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Focal Ischemia- Left Side (Dominant) MCA
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Right face, hand and arm weakness, somatosensory deficits and language problems
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What are Broca's and Wernicke's lesions? What lesions will cause Broca's and Wenicke's aphasia?
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Broca’s (expressive aphasia-related to speech production)
Wernicke’s aphasia (receptive aphasia-related to interpretation of speech) left MCA, superior left MCA, inferior |
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A lesion in which region would cause the following symptoms?
Difficulty speaking Slow, labored speech No Prepositions and conjunctions Dysarthria Good comprehension Aware of problem agraphia: |
Broca's area
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A lesion in what area will cause the following symptoms?
deficit of auditory comprehension Cannot monitor conversation Unaware of making mistakes Verbal paraphrasia Phonemic paraphrasia jargon aphasia |
Wernicke's
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Posterior Association Area (parietal portion):lesion to dominant (usually LEFT) hemisphere
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"Gerstmann's syndrome,"
finger agnosia (inability to recognize different fingers) agraphia (inability to write) alexia (inability to read) agnosia (inability to synthesize, correlate or recognize multisensory perceptions) dyscalculia (decreased ability to calculate or use numbers) left-right confusion |
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Posterior Association Area (parietal portion):lesion to nondominant (Usually Right) hemisphere
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hemineglect, contralateral neglect, extinction
constructional apraxia (disturbances in drawing) disturbances in the awareness of the body image anosognosia: denial (ie lack of awareness) that there is anything wrong |
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What is unique about a parietal lobe lesion?
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The brain can recover (see painting)
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What's the disease associated with hemineglect?
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Focal Ischemia- Right Side (non-dominant) MCA
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Posterior Association Area (parietal portion):lesion to nondominant (Usually Right) hemisphere
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hemineglect, contralateral neglect, extinction
constructional apraxia (disturbances in drawing) disturbances in the awareness of the body image anosognosia: denial (ie lack of awareness) that there is anything wrong |
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MCA Damage and Potential Visual System Problems, match lesion to symptoms:
1. frontal lobes 2. radiation in temporal (Meyer's loop) 3. optic radiation in parietal and temporal lobes 4. upper portion of internal capsule and corona radiata |
1. damage to conjugate eye movement to contralateral eye
2. quadrantanopia 3. hemianopia 4. capsular (motor) hemiplegia |
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What infarcts cause Contralateral homonymous hemianopia?
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Focal Ischemia PCA Territory
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What supplies STT in medulla?
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PICA and vertebrals
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What supplies DCML and CST in medulla?
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ASA
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What supplies pons?
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basilar/ SCA
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Damage in the medulla causes contralateral or ipsilateral in the tracts?
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contralateral to all
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What controls this:
Controls ipsilateral tongue (CN XII) Speech and swallowing (CN IX, X nucleus ambiguus) (test with gag reflex) Salivation (CN IX inferior salivatory nucleus) Pain, temp crude touch from ipsilateral face and dura (CN V, VII, IX,X) Vestibular and auditory inputs (CN VIII) Taste (nucleus of solitary tract CN VII, IX, X) Visceral sensory input (blood O2, MAP, CN X) Sympathetics descend from hypothalamus toward preganglionic cell bodies ipsilateral spinal cord |
medulla
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Medial Medullary Syndrome
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DCML and CST contralateral, ipsilateral XII tongue. Deviates toward weak side.
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Hypoglossal lesion
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tongue tilts to affected side
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Lateral Medullary Syndrome- Wallenburg syndrome
What causes it? Symptoms? |
Occlusion of branches of the PICA or Vertebral
STT contralateral ipsilateral lack of eye sympathetics (Horner's Syndrome) ipsilateral loss of facial STT Nucleus Ambiguus (IX and X) dysphagia Vestibular loss- vertigo, nystagmus cerebellum- limb ataxia trigeminal damage (ipsilateral) nucleus ambiguus (IX and X motor nucleus) |
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What does an AICA hit affect? Where?
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rostral medulla
hearing |
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PICA or Vertebral HIT
can affect ________, but not ______. |
balance
hearing |
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Hits in the Pons will be contralateral or ipsilateral to the tracts?
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CL to all tracts
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What CN are in pons?
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Eye Abduction (CN VI)
Mastication (CNV) Facial Expression and eye blink (CN VII facial motor nucleus), Tearing and salivation (CN VII superior salivatory nucleus) Fine touch, vibration, proprioception from face (and dura) CN V trigeminal nucleus Vestibular input (CN VIII) |
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What is caused by basilar artery occlusion (pons)?
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facial- paralyzed ipsilateral face
abducens- lack of lateral gaze in ipsilateral eye and ipsilateral conjugate gaze Main trigeminal nucleus, if lesion extends rostrally- fine touch and sensation ipsilateral Medial lemniscus, if lesion extends anteriorly- Loss fine touch, vibration, and proprioception from CL body Spinothalamic tract, if lesion extends anteriorly &laterally- Loss pain and temp from CL face & body Descending spinal trigeminal tract, if lesion extends sufficiently laterally- Loss pain temp from ipsilateral face |
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Acoustic Neuroma ( vestibular Schwannoma)
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Vestibulocochlear nerve
Vestibular division- vertigo Cochlear division- hearing Facial nerve- face weakness and taste |
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Where are the tracts in the midbrain? Damage would be CL or IL?
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DCML- fine touch, proprioception, and vibration from contralateral body
STT –pain and temperature from contralateral body (contiguous with the ML) CST –descending contralateral motor control in crus cerebri/peduncles |
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What important structures are in the midbrain?
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Periaqueductal gray – component of the intrinsic analgesia system
Substantia nigra (source of dopamine) Red nucleus (rubrospinal tract) Tectum (colliculi contribute to saccadic eye movements, pupillary light reflex, and reflexive orientation to auditory stimuli) |
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What causes locked-in syndrome? Where is the hit? What is spared?
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bilateral ventral pontine infarcts, hemorrhage, tumor, encephalitis, MS, central pontine myelinolysis
hit: Corticospinal Lower corticobulbar Abducens spared: Medial lemniscus Spinothalamic Spinal trigeminal Facial motor |
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What is Central Pontine Myelinolysis?
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Noninflammatory, demyelinating condition associated with rapid correction of hyponatremia (rapid fluctuations in electrolyte status). Originally described in alcoholics and malnourished persons, and now associated with transplant patients
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What would CN damage in the midbrain cause?
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Eye movement control (CN III and IV)
Eye lid retraction (CNIII) Pupil constriction and lens thickening (Edinger-Westphal & PSIII) |
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What's involved in Weber's syndrome?
Artery? Lesion site? Symptoms? |
PCA branches
Site: Cerebral peduncles Corticospinal tracts and descending cortical control of brainstem UMN Symptoms: Hemiparaesis, spastic hemiparalysis, babinski, Loss superficial reflexes in contralateral body Hemiparasis, or hemiparalysis in contralateral lower face, tongue weakness without atrophy deviation away from lesion Site: Oculomotor nerve Symptoms: Paralysis of ipsilateral eye with ptosis, mydriasis (pupil dilation), lateral strabismus –eye rolls down and out |
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Where are the possible lesion sites with a pineal tumor? What are the corresponding signs and symptoms? What is the syndrome?
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Site: Vertical gaze center
Lesion: Loss vertical gaze, eyes deviate downward Site: Vergence center Lesion: Nystagmous on eye convergence Site: Posterior commissure and tectum Lesion: Loss pupillary light response, possibly with accomidation intact Parinaud Syndrome |
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What is Nystagmous on eye convergence and what causes it?
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involuntary movement on eye convergence
midbrain-Pineal tumor, tectal infarct |
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Epidural hematoma?
Blood source: Shape: |
Blood source: Middle Meningeal Artery
Shape: Lens shaped |
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Subdural hematoma?
Blood source: Shape: |
Blood source: bridging veins
Shape: Crescent-Shaped |
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Subarachanoid hematoma?
Blood source: Shape: Where does blood travel? What phrase do they say? |
Blood source: from arteries within pial membrane
Shape: texaco star CSF "worst headache of my life” |
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Who has increased risk of tear to the bridging veins?
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Alcoholics & elderly
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What is the Monro-Kellie Doctrine?
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As the volume of one component increases the volumes of the others compensate to maintain ICP (0-15 mm Hg) and to prevent neurological changes
As an intracranial mass increases in size CSF is displaced into the spinal canal Blood volume is reduced in the brain Displacement of brain tissue = herniation |
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how does cranial perfusion pressure, mean arterial pressure, and intercranial pressure relate to one another? What are normal values?
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CPP = MAP -ICP
CPP Cerebral Perfusion Pressure = 80-100 mm Hg MAP (mean arterial Pressure) = 50 – 150 mm Hg MAP = systolic + (2x Diastolic)/ 3 ICP (intracranial Pressure) = 0-15 mm Hg |
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When a fundoscope indicates high pressure, what do you not do? What do you do?
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do not lumbar puncture (brain will herniate)
monitor ICP and relieve pressure (burr hole) |
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What is the optic disk?
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blind spot where arteries and veins emerge
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What does papilledema look like?
What is it caused by? |
Blurred disc margins
Capillary & venous dilations Striated optic nerve fibers Retinal hemorrhages high ICP |
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What are are two major classes of herniation?
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The supratentorial (occurs above the tentorial notch) Uncal, transtentorial (central), cingulate, and Transcalvarial
The infratentorial (occurs below the tentorial notch) upward transtentorial and tonsillar. |
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Where does CSF travel (production to finish)?
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choroid plexus (red capillary tufts in pictures) --> the ventricles --> the lateral (foramina of Luschka) and median (foramina of megendie) apertures in the walls of the 4th ventricle --> subarachnoid space --> arachnoid granulations --> dural sinus (venous circulation)
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How can you tell the difference between SAH and traumatic tap?
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The presence of erythrocytes can indicate
subarachnoid bleeding (if RBC + then spin serial vials of CSF, if clear = traumatic spinal tap, if xanthrochromatic = SAH ) |
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What distinguishes bacterial meningitis CSF?
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purulent CSF and elevated protein levels
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Where do you put the needle for lumbar puncture?
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between L3 and L4
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What causes higher opening pressure?
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all types of meningitis and SAH (from the bleeding)
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What causes higher PMNs and what causes higher leukocytes in CSF?
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PMNs- bacterial
leukocytes- TB and viral meningitis |
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What causes normal to higher protein levels?
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viral meningitis
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What 2 things cause lower glucose in CSF?
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bacterial and tuberculous meningitits
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What are the generalized symptoms of meningitis?
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Fever, headache, stiff neck & or change in mental status
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What are the cell types of the CNS?
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oligodendrocytes- make myelin
astrocytes: Form support for CNS (lactate) help form Blood Brain Barrier Secrete neurotrophic factors take up K+, neurotransmitters Remove EAATs (excitatory amino acinds-GLUT microglia- scavengers (macrophages) ependymal cells- Form barriers between compartments |
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What are the cell types of the PNS?
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schwann cells- make myelin and secrete neurotrophic factors
satellite cells- support cell bodies |
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In the CST, what layer does neuron 1 start in? Where does LMN (neuron 2) start? Where is crossover?
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Neuron 1 pyramidal cell cell body in layer V of the cortex
Neuron 2 cell body in anterior horn spinal cord = LMN (innervates muscle caudal medulla |
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In the midbrain, pons and medulla, where is motor and where is sensory?
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All motor is anterior
& sensory is posterior |
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How does the CST cross in the caudal medulla?
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Across and up the pyramidal decussation
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What are the medullary pyramids?
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The medullary pyramids are two parallel ridges that run the length of the anterior medulla they have CST axons within
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What is in the precentral gyrus?
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primary motor cortex
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In the cortex, what are the major input and output layers?
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IV = major input layer; V = major output layer
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What cranial nerve is carried in the colliculi?
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CN IV
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What does a PCA hit cause?
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Contralateral paralysis, contralateral tongue hit and visual problems
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What causes the normally uncommon CN XII lesion? What are the 2 types and what symptoms do each cause
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congenital abnormalities
(foramen magnum) UMNL (upper motor neuron lesion) Supranuclear (eg cortex) Contralateral atrophy and deviation LMNL (Lower motor neuron lesion) Peripheral to brain stem Ipsilateral atrophy and deviation |
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What is normally seen in a LMN CN XII lesion?
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LMNL (Lower motor neuron lesion) Peripheral to brain stem Ipsilateral atrophy and deviation
The atrophy seen on the left side of this individual’s tongue would be due to damage to the left hypoglossal nerve |
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What kind of neurons do LMNs use? What is their other name?
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Use large, fast, myelinated axons
ie type A, subtype alpha motor neurons |
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Where are LMN cell bodies located? How do LMN axons leave CNS?
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brainstem (cranial nerve nuclei)
anterior horn of spinal cord Axons leave CNS in cranial and spinal nerves |
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How many LMNs per muscle and vice versa?
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Each LMN innervates several individual muscle fibers within a muscle.
Each individual muscle fiber is innervated by only ONE LMN (During development, LMNs compete for muscle fibers, with only one winner per fiber) |
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What is a motor unit?
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One LMN cell body in the CNS
It’s axon, branches, terminal regions all of the muscle fibers it innervates |
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What type of damage is associated with fasiculations?
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LMN
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Why do fasiculations occur?
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as the LMN cell body dies, it may fire spontaneously
(disorders of spinal roots may also do this) causes its whole motor unit to twitch visible to the naked eye |
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What are Deep Tendon Reflexes? What is the effect of LMN/UMN lesions? What is an inverse myotatic reflex?
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Myotatic (muscle stretch) reflex = DTR
monosynaptic, detects muscle stretch (change in muscle length) through spindle and counters with muscle contraction (homonymous muscle) DTRs lost with lesions of LMN (hyporeflexia or areflexia because reflex circuit broken) DTRs increased with UMN lesions (hypereflexia- because UMN dampen DTRs usually) Inverse myotatic- multisynaptic, detects muscle contraction through golgi tendon organ and counters with muscle relaxation- GTO detects tension |
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What is the other name for Monosynaptic Reflex (DTR)? What are the steps?
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alpha-gamma coactivation
1.Muscle stretch activates Ia/II afferents. 2. Ia/II fibers activate LMN and muscle contracts. Also activate gMN which contract spindle fiber |
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When the muscle is stretched, what increases?
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AP
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What happens to AP during a - g Neuron coactivation?
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constant
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What can cause flaccid paralysis?
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Acute UMN lesion occur rapidly
Flaccid paralysis = no muscle tone The flaccid phase may last days to weeks to months… complete loss of muscle tone, absent DTRs, absent plantar response (?) or, with lesser lesion: weakness, hypotonia, hyporeflexia |
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When will a UMN lesion skip the flaccid period?
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If lesion is subacute or chronic, this initial flaccid paralysis may not occur and hyperreflexive responses will prevail
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What are the 4 main things from UMN damage?
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hyperreflexia - due to loss of modulation of deep tendon reflexes.
clonus - rapid alternating contraction/relaxation of a stretched muscle – often more prominent in ankle reflex clasp knife rigidity (“spastic catch”) - describes resistance to passive movement of a joint when spasticity is present. Muscles first resist the movement strongly ( DTR). Then resistance melts away rapidly (GTO-based reflex kicks in) spasticity - excessive muscle tone (hypertonicity), due to hyperactive stretch reflexes. |
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What neurogenic atrophy?
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LMN damage
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Potential Sites of Disruption of Motor Function
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Upper Motor Neuron Cell Bodies
Projections from UMNs to LMNs Lower Motor Neuron Cell Bodies Projections from LMNs to Muscles Presynaptic, ie Release of Transmitter from LMN Terminals Postsynaptic, ie Receipt of Transmitter (ACh) By Muscles Muscles |
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What causes ALS? What are signs and symptoms?
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Amyotrophic lateral sclerosis (ALS)
Progressive degeneration of corticospinal tracts and a-motor neurons, both upper and lower MN disease. Absence of neurologic or organ system involvement and sparing of voluntary eye muscles and urinary sphincters Symmetric gait disturbance, limb weakness, reflexes increased or depressed, dysarthia and dysphagia with respiratory complications |
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What is a neuropathy?
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functional disturbances and/or pathological changes in PNS
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What is Polyradiculoneuropathy?
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affecting nerve roots
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What are the major categories of peripheral neuropathy?
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Major categories –
Inflammatory-AIDP Hereditary-Charcot-Marie-Tooth Disease Acquired metabolic & toxic (industrial or environmental chemicals)-Diabetic Neuropathy (DPN) Traumatic (lacerations, avulsions, compressions (carpal tunnel syndrome and `Saturday night palsy´-ulnar nerve compression)) Infectious (e.g., leprosy, diphtheria, varicellar‑Zoster), Associated with malignancy (invasion or paraneoplastic) |
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What is Acute inflammatory demyelinating polyradiculoneuropathy? What is it's other name? What initially causes it? What kind of damage, UMN or LMN? What are other signs and symptoms?
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AIDP – (Landry-Guillain-Barré Syndrome)
40% “viral prodrome” (days to wks after URI or GI infection); Causes acute paralytic illness Clinical (acute): Symmetrical glove/stocking paresthesia followed by leg weakness (several days)- and spreads up- ascending paralysis, Pain –bilateral sciatica, or aching pain in thigh muscles and back (“Charley horse”) Difficulty walking bilateral foot drop & unsteady waddling, DTRs absent or reduced Severe cases – respiratory distress Eye movements, swallowing, and ANS functions affected |
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What is a Hereditary Motor and Sensory Neuropathies?
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Charcot-Marie-Tooth Disease
Pes cavus-has high plantar arches with hammer toes and atrophy of foot muscles Weakness/wasting in lower leg and foot producing “stork leg” (inverted wine bottle) (foot drop & stepped gait) |
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What Acquired Metabolic Neuropathy do we know? What are signs and symptoms? What part of the nervous system does it attack? What causes it?
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Diabetic Neuropathy (DPN)
Distal sensory or sensorimotor neuropathy symmetric polyneuropathies (pain, paraesthesias & weakness) Autonomic neuropathy Microvascular damage leads to DPN |
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What are 2 Peripheral Nerve Sheath Tumors?
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Schwannomas (Arise from Schwann cells)
Acoustic neuroma = Vestibular Schwannoma - tinnitus and hearing loss large tumors - pressure on V & VII producing palsies, or brainstem compression & hydrocephalus Neurofibromas (Arise from Schwann cells, perineural cells or fibroblasts) Common cutaneous (Café au lait spots ‑ develop in childhood: Lisch nodules ‑ small yellow/brown elevations), and peripheral nerve manifestations |
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What is the difference between pre and post synaptic Disorders of Neuromuscular Junction?
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Presynaptic disorders are:
- frequently the result of a decrease in ability to release neurotransmitter or the an uncontrolled release of neurotransmitter until the terminal is depleted - characterized by larger response with repeated stimulation warm up phenomenon Postsynaptic disorders are: frequently the result of a decrease in availability of Ach receptors on motor endplate. characterized by fatigueability (smaller response with repeated stimulation) |
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What is a presynaptic disorder?
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Lambert-Eaton, blocks Ca+2 entry and ACh release
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What causes Lambert Eaton? what are symptoms and treatment?
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Cause:
Autoimmune disorder associated with non-neural carcinomas Antibodies produced against VCCCs (voltage-dependent Ca++ channels) Symptoms: muscle weakness & fatigue (proximal) improves with exercise, diminished reflexes autonomic dysfunctions: dry mouth, impotence, hypotension Treatment: plasmaphoresis to remove IgGs, suppress immune system Treat tumor Death is more likely to result from associated cancer than from LEMS |
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What is the postsynaptic disease we learned of? Cause? Symptoms? Normal target?
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Myasthenia Gravis muscle weakness occurs because circulating AChR antibodies cause increased degradation of Ach receptors
Few AChR on the muscle and Ach is broken down before it can stimulate the muscle resulting in muscle weakness 2/3 cases associated with thymic hyperplasia and 15-20% with thymomas (rare neoplasm of the thymus -90% benign) ptosis 20 year old females |
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What CNs are in the midbrain?
Pons? Medulla? |
Midbrain: III and IV
Pons: V - VIII Medulla: VIII - X, XII |
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What are the sensory cranial nerves of solitary tract, rostral and caudal?
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rostral- CN VII, IX, and X
caudal- CN IX, X |
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What are the main cranial nerves with parasympathetics?
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Edinger-Westphal- CN III
Abducens- VI Nucleus Ambiguus- IX, X |
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What are the symptoms of CN III compression? What causes it?
What causes CN III ischemia? |
CN III compression: eye down and out, pupil dilated, eyelid droop-
dilated unresponsive pupil early sign of CN III compression from temporal lobe herniation (because parasympathetic fibers are affected first) CN III ischemia (Diabetes M) extraocular muscle palsy with pupil sparing |
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What are the CN of the corneal nerves?
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sensory (CN V) and motor (VII)
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What are the symptoms of a CN IV lesion?
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IV Lesion- difficulty walking down steps, and reading b/c double vision ( posterior emergence) Come in with head tilt
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What can cause CN VI damage? What are the symptoms?
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VI (and III) susceptible to ICP
VI can not ABduct eye |
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What is the purpose of MLF? What can damage it?
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MLF connects III and VI so you can have movement conjugate eye movement synchronized right and left eye movement (INO =damage MLF -think MS)
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What controls the gag reflex?
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Gag reflex= CN IX (sensory) CN X (motor)
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What CN helps you rotate head and shrug shoulder?
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XI
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What is the effect of CN XII lesion? UMN versus LMN?
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XII hypoglossal innervates ipsilateral tongue protrusion- LMN tongue deviates to side of lesion, UMN tongue deviates to opposite side. Each XII nerve directs tongue to opposite side. After damage the tongue deviates to weak side on protrusion that is towards LMN lesion and away from an UMN lesion
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What handles taste sensation from the tongue?
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Taste sensation from posterior 1/3 of tongue (IX)
Taste sensation from anterior 2/3 of tongue taste (VII) |
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What is a consequence of CN III lesion?
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Eye position: down & out (downward & ABducted)
strabismus (eyes not directed towards same object) diplopia (double vision) Ptosis (lid droop) Pupil dilation (mydriasis) and loss of accommodation Accommodation = the process whereby the eye maintains a clear image (focus) of an object as its distance changes |
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A dilated and unresponsive pupil is an early sign of __________ lesion from a _____________?
Vascular lesions to this CN affect eye movement but spare ________. |
CN III
temporal lobe herniation because of parasympathetics goes first pupils |
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Why is CN VI so susceptible to ICP?
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Cranial Nerve VI has a very long run and is not very thick
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How does abducens nucleus damage effect MLF (CL and IL)?
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Damage to one abducens nucleus causes loss of LR ABduction in ipsilateral side and loss of contralateral eye ADduction (CN III MR)
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What does damage to PRPF show (CL or IL)?
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Damage to PPRF causes selective loss of rapid eye movements to ipsilateral side
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What does damage to MLF cause regarding the MR?
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Damage to one MLF causes selective weakness of the ipsilateral MR – can not ADduct during attempted lateral gaze
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InterNuclear Opthalmoplegia (INO)
Where is the lesion? what is the symptom? |
MLF
affects ipsilateral MR, contralateral LR diplopia, affected eye (right) has impaired adduction, nystagmus in CL eye |
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What is nystagmus and what disease is it associated with in the eye contralateral to the injury?
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Nystagmus: smooth pursuit in one direction, saccadic movement in other direction
INO |
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What lesion and muscle goes with the following symptoms?
Weak eye extorts patient cannot look down & in often becomes obvious when patient goes down stairs Likely vertical diplopia tilt head to good side to ‘fix’ diplopia (torticollis = twisted neck) |
Trochlear and CN IV
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What handles the Circuitry for Voluntary Saccades to each side?
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FEF and Superior Colliculus Trigger Saccades to the Contralateral side
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Why are smooth pursuits slower than saccades?
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Tracking smooth pursuit movements (slower than saccades because uses visual feedback)
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What causes Damage to Frontal Eye Field (right FEF)? What function is lost? What is redundancy?
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Acute Stroke loose Right FEF. Possible “right gaze preference" due to unopposed left frontal eye fields activity.
NOTE: Redundancy- Eyes CAN move left as a tracking maneuver via a brainstem reflex |
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What is fixation?
What 2 reflexes are GAZE STABILIZATION? |
Fixation = keeping the fovea pointed at the target of interest
Optokinetic reflexes: keep the fovea on target during slow, sustained movements of head or target use visual feedback Vestibulo-ocular reflexes: keep the fovea on target during rapid & jerky head movements NO time for visual feedback! Use vestibular inputs |
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What is the point of the VOR?
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Vestibular nuclei input
Allows us to generate eye movements equal and opposite to head movements- The VOR Vestibulo-ocular reflex |
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What is connected in Saccadic Rapid eye movements? What is the purpose?
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Fast
Connections between the Frontal Gaze Center to the PPRF To bring new objects onto fovea |
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what is the connection in Smooth Pursuit movements? What is the purpose?
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Slow
Connections from Parietal-Occipital gaze center via cerebellar and vestibular pathways To keep a moving image Centered on the fovea |
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what is the connection in . Vestibulo-ocular movements? What is the purpose?
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Connections from vestibular system to the nuclei for motor movements
Keeps image steady on fovea during head movement |
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what is the connection in Vergence movements? What is the purpose?
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Optic Pathways to the oculomotor nuclei
To keep image in focus when moving near |
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What are the 2 components of the blink reflex?
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Opthalmic division V1 of CN V, is the sensory component of corneal reflex and branch of VII nerve is the motor component
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|
Blink Reflex Circuitry
|
Touching the cornea tests the integrity of CN V1 (nasociliary branch) and CN VII (contracts the orbicularis oculi muscles via the branchial motor division VII)
|
|
V lesion consequences?
|
Parethesia, neuralgia, hypo- or anesthesia one side of the face, disappearance of the corneal reflex, impaired mastication, mouth becomes oval
|
|
What are the symptoms of facial nerve damage (Bell's Palsy)? What can it be caused by?
|
He has lost control of muscles of facial expression:
He cannot wrinkle his forehead (effects both quadrants=LMN) He cannot close his eye He cannot smile symmetrically Caused by herpes simplex I virus-may disappear spontaneously |
|
Facial (CN VII) Lesions and their Consequences, what are the 2 types?
|
UMNL (upper motor neuron lesion) Supranuclear (cortex)
Contrlateral effects on lower quadrant only Upper quadrant receives input from both hemispheres Whereas lower quadrant only contralateral input LMNL (Lower motor neuron lesion) Lesion of facial nucleus or more peripheral Ipsilateral effects on both upper and lower quadrants of the face |
|
How is control of the upper and lower face organized?
|
Upper face is controlled bilaterally from the cortex;
Lower face is controlled only from the contralateral cortex |
|
Why is the Forehead unaffected, in UMN lesion of CN VII?
|
bilateral cortical control
|
|
What functions do IX and X share?
|
control of speech and swallowing
|
|
Where do the branchial motor components of IX and X originate?
|
nucleus ambiguus in the medulla
|
|
When is DCML contralateral and ipsilateral?
|
CL: cortex to rostral medulla
IL: Spinal cord, all |
|
How are the primary, secondary, and tertiary neurons split in the DCML?
|
Primary sensory neurons
Axons ascend in posterior funiculus bundle = posterior columns Fasciculus gracilis (leg) Fasciculus cuneatus (hand) lateral synapse in medulla Second order sensory neurons Cell bodies in Nucleus gracilis Nucleus cuneatus lateral Axons cross midline as internal arcuate Axons ascend to thalamus as medial lemniscus Third order sensory neurons Cell bodies in VPL of thalamus Axons join internal capsule to project to primary (and secondary) somatosensory cortex |
|
What is the purpose of the DCML?
|
proprioception, fine touch, vibration
|
|
How do we test proprioception?
|
Move big toe up and down (hold on sides of toe)
And the Romberg test |
|
What causes a positive Romberg test?
|
Problem with DCML, OR a problem with afferent sensory information
|
|
What is the pathway of the STT/ Anterolateral system?
|
1˚ afferents (ascend or descend for 2-3 segments ) synapse on second order neurons (PTN)
Cross the midline in anterior white commissure of spinal cord PTN axons ascend in the anterior portion of the lateral funiculus as the anterolateral system STT transmits information from the spinal cord to the VPL of the thalamus to Somatosensory cortex |
|
What are 3 diseases/deficiencies that cause DCML damage?
|
MS, Syphilis, and Vit B deficiency
|
|
What is Bilateral INO pathognomonic for?
|
MS
|
|
If a hit to the spinal cord is at the cervical level, what effect will it have on the STT and DCML of the leg?
|
CL STT loss
IL DCML loss |
|
In the spinal cord, is the CST ipsilateral or CL?
|
ipsilateral, crosses at medulla
|
|
Cause:
Ipsilateral spastic paralysis and loss of vibration, fine touch and proprioception And contralateral loss of pain and temperature beginning one or more segments below the level of damage |
Spinal cord damage
|
|
Damage to the cervical spinal cord causes what loss?
|
causes loss of control of ipsilateral sympathetic preganglionics, resulting in a partial Horner syndrome- Miosis and ptosis affecting the contralateral eye
|
|
Where do sympathetics of the eye emerge?
|
fibers emerge at about T1 and ascend in the sympathetic trunk to synapse in the superior cervical ganglion
|
|
What is Horner's syndrome and what can cause it?
|
Ipsilateral to lesion
Loss sweating Pupil constriction and lid droop Damage sympathetic out-flow to face- Hypothalamus Brainstem (Lat Med Syn) Cervical spinal cord- interrupts descending control or affects sympathetic preganglionic cell bodies Ascending Symp. Trunk (apical lung tumor) Postganglionic symp. Fiber damage (Carotid artery aneurysm) |
|
What is Syringomyelia and what does it cause?
|
a central cavity in the spinal cord
SST (anterolateral sytem) Anterior White Commissure Hit Severe burns- Analgesia and thermanesthesia in both hands -segmented and bilateral -sensory motor ok in legs, Proprioception OK, Fasciculations in both arms (LMN) |
|
Typical findings include: a band of bilateral loss of pain and temperature sensation, and can have weakness and atrophy if damage extends to the anterior horns
|
syringomyelia
|
|
SPLIT – Dissociated Senses
Where is lesion? -Loose pain sensation from CL- right foot, without loss of vibratory sense from right foot. Will loose vibratory sense from ipsi -left foot. |
Thoracic level left half of spinal cord
|
|
Where is this lesion:
Lose pain sensation from CL -right foot, & lose vibratory sense from CL-right foot? |
Brainstem damage exclusively on the left side
|
|
What is the role of basal ganglia?
|
Role of Basal Ganglia is to Select and Suppress Movements-
Selection & initiation of willed movements , and suppression of unwanted movements |
|
What are the 2 pathways of the basal ganglia?
|
The Direct Path releases thalamic activity
This results in increased thalamic activity and increased motor output (Because caudate & putamen inhibit SNr/Gpi) The Indirect Path inhibits thalamic activity This results in decreased thalamic activity, and decreased motor output (Because of increased BG output (SNr/GPi) |
|
Parkinson’s involves loss of what pathway and what are the symptoms?
|
Loss of Da Producing Neurons in Substantia Nigra -Striatal Pathway
Tremor (resting) Rigidity Akinesia (hypokinesia, bradykinesia) Posteral instability (flexed posture- Festinating gate) -Dementia Difficulty getting out of a chair, fall backwards, Cogwheel rigidity, Stiff gate stooped posture, no arm swing, short shuffling steps, Festinating Gate = accelerate the further they walk |
|
What diseases look like Parkinson's?
|
Parkinson’s Disease
Diffuse Lewy Body Disease Drug Induced Parkinson’s -MPTP (synthetic heroine contaminant), -Reglan (antinausea medication), -Haldol (antipsychotic medications) Post Traumatic Parkinsonism |
|
What is Huntingtons Disease?
|
inherited disease
CNS progressive dementia involuntary choreic movements degeneration of the caudate and putamen nuclei |
|
What causes dementia and chorea in HD?
|
dementia (characterized by both cognitive and personality changes) in HD is caused primarily by the degeneration of neurons in the cerebral cortex, and the chorea is caused by degeneration in the basal ganglia
|
|
What are the 4 C's of HD?
|
chorea
CAG repeats caudate cortex |
|
Hemiballismus:
What is hit? Symptoms? |
Subthalamic Nucleus Hit
Contralateral unintentional, forceful flinging movements of the right arm and leg (or rotatory in nature) |
|
Dystonia
|
Persistence of a postural abnormality, a sustained posture or position of any part of the body
|
|
Wilson Disease
What is it? What is the hallmark? What is it associated with? What is it caused by? Symptoms? Treatable? |
Disorder of Copper Metabolism Affecting Brain & Liver
Kayser-Fleischer ring (copper-colored ring around cornea) Associated with a decrease in ceruloplasmin concentration (a blue plasma copper transport protein) Genetic (leads to hepatolenticular degeneration) Movement disorders include: dystonia, tremor, chorea, rigidity & other BG-related signs TREATABLE! |
|
What is the function of the cerebellum?
|
Proper execution of planned motor acts
Establishes direction, timing , force of planned motor acts Compares intended movements with ongoing movement Involved in motor learning |
|
What are the cerebellar tests?
|
Finger to nose
Heel-knee-shin test Rapid alternating movement (Dysdiadochokinesia = inability to perform rapid, alternating movements) Gate examination Alternating pronation-supination test |
|
Is cerebellar dysfunction ipsilateral or contralateral?
|
ipsilateral
|
|
What are the symptoms of Cerebellar Dysfunction-IPSILATERAL?
|
Intention Tremor -during planned motor activity
(ie reaching for target) Hypotonia- loss resistance Disequilibrium- loss balance, gate and trunk dystaxia- jerky, irregular, arrhythmic movement s Dyssynergia- loss coordination, dysmetria, nystagmus. Abnormalities in: - rate of movement = initiation & mvt slowed, - direction or range of movement - force of movement (hypotonia) Ataxia- uncoordinated, voluntary movement |
|
Where does “Alcoholic” Cerebellar Degeneration attack? What are the symptoms? What is a probable cause?
|
Superior vermis more affected than hemispheres
Gait ataxia without limb ataxia Probably a problem relating to malnutrition |
|
What are the Monoaminergic pathways?
|
Serotonergic pathways from several raphe nuclei: project widely rostrally and caudally
Norepinephrine pathways from Locus ceruleus and Lateral tegmental area : project widely rostrally and caudally Dopaminergic pathways from the Substantis nigra pars compacta (SNc) and the ventral tegmental area (VTA) : project to striatum |
|
Where does the serotonergic pathways project from and where to?
|
Serotonergic pathways from several raphe nuclei: project widely rostrally and caudally
|
|
Where are norepinephrine pathwaws run and where do they project?
|
Norepinephrine pathways from Locus ceruleus
and Lateral tegmental area : project widely rostrally and caudally |
|
Where does the dopaminergic pathway come from and where do they project?
|
Dopaminergic pathways from the Substantis nigra pars compacta (SNc) and the ventral tegmental area (VTA) : project to striatum
|
|
What NTs affect sleep?
|
Sleep function is altered by
Norepinephrine (arousal) Serotonin (promotes sleep) Dopamine (arousal) Acetylcholine (in cortex – arousal) Histamine (arousal) GABA (promotes sleep) Opioid/opiates (promote sleep) |
|
What does the Electroencephalogram (EEG) measure?
|
EEGs Measures cortical electrical activity, EPSPS and IPSPS summed from cortex
|
|
What are the characteristics of a normal EEG?
|
Alert with eyes open = asynchronous, low voltage, fast activity EEG
|
|
What are the stages of sleep?
|
stage 1: Theta rhythms
stage 2: Sleep spindles stages 3 and 4: Delta rhythms Stage 5: During REM sleep, the EEG displays a beta rhythm, which is characteristic of the waking state |
|
What is the deepest nonREM stage?
|
stage 4
|
|
SWS versus REM?
|
Deep Slow Wave Sleep
Difficulty waking No eye movement Parasympathetic control dominates (slowed HR) Sleep deprivation causes increased stage 4 sleep Stage 4 suppressed by valium Sleep walking (somnambulism) REM Rapid Eye Movement High freq, low voltage similar to awake beta wave Deepest sleep of all Atonia (muscle paralysis) Wake spontaneously Sympathetic activity dom. Vivid dreaming Suppressed by alcohol, barbiturates, TCAs |
|
What is insomnia?
|
Subjective sense of insufficient sleep. Inability to achieve sufficient sleep or difficulty in falling asleep (>30 min). A symptom, not a disorder per se
|
|
What causes insomnia?
|
Anxiety / depression / stress / pain
Side effect of meds / alcohol / poor sleep habits? Disruption of circadian rhythms? Increasing age? |
|
What are the effects of insomnia?
|
Problems with memory & concentration
Potential link with cardiovascular disease 4-fold increase in likelihood of depression Impaired performance (at home, on the job, driving) |
|
What is Obstructive Sleep Apnea?
What is is accompanied by and more common in? What is sleep apnea? |
Obstructive sleep apnea is the major cause of daytime sleepiness up to 500 awakenings per night!
heavy snoring overweight individuals (physical abnormalities of neck, throat). Sleep apnea = brief periods of interrupted breathing during sleep |
|
What is Narcolepsy?
|
Enter REM sleep directly from the waking state
Excessive daytime sleepiness ((EDS) “sleep attacks” = abrupt transition to NREM sleep Cataplexy -sudden loss of muscle tone in awake state Hallucinations while falling or awakening from sleep and suffer from sleep paralysis(awake but can’t move for several minutes) Narcolepsy is associated with a lack of orexin (hypocretin- a hypothalamic protein)- genetic or autoimmune-related neurodegeneration |
|
What is the purpose of Reticular Formation Functions?
|
Activates the cerebral cortex (arousal and wakefulness)
Integrates cranial nerve reflexes Modulates pain – intrinsic analgesic system Influences voluntary movements Regulates autonomic nuclei Integrates respiration and sleep |
|
What does Consciousness involve? Where?
|
1. Alertness
(pontomesencephalic RF, thalamus and cortex) 2. Attention (same circuits as above plus frontoparietal association cortex) 3. Awareness higher-order integration of multiple brain regions |
|
What causes Persistent Vegetative State? What still functions? What is preserved? What about spontaneous eye movements? What is missing?
|
Cause: severe, diffuse cerebral cortical damage with brainstem function intact (“cerebral death”)
Respiratory system, circulatory system functioning Possible preservation of sleep-wake cycle on EEG Spontaneous eye movements but NO evidence of awareness / responsiveness / interaction with environment NO meaningful responses |
|
How is a vegetative state different from coma?
|
After several weeks of being in a coma a patient
may emerge into a state in which they regain sleep-wake cycles and other primitive orienting reflexes mediated by the brainstem and hypothalamus, but remain unconscious |
|
What happens in a coma over six hours in length?
|
diffuse axonal injury
|
|
What is coma not?
|
Not sleep, which is readily reversible
Not fainting/syncope, which is transient Not Inattention/Confusion/Stupor |
|
Where is there decorticate and decerebrate posture? Flaccid paralysis? Death?
|
Above midbrain
Midbrain (red nucleus) Pons Medulla |
|
The UMN Pathways that Originate in the Brainstem
|
Tectospinal- reflex head turning
a Rubrospinal- arm flexor bias arm flexion seen in decorticate rigidity stems from unopposed rubrospinal tract activity. Reticulospinal- feed- forward extensor bias Vestibulospinal- feed-back adjustments arm and leg extension bias due to unopposed vestibulospinal tract activity – seen in decerebrate rigidity |
|
Of the UMN pathways that originate in the brain, which on is seen in decorticate and which is seen in decerebrate?
|
Rubrospinal- arm flexor bias
arm flexion seen in decorticate rigidity stems from unopposed rubrospinal tract activity. Vestibulospinal- feed-back adjustments arm and leg extension bias due to unopposed vestibulospinal tract activity – seen in decerebrate rigidity |
|
What does a score of 0 and 15 mean on the Glasgow scale?
|
0 = death
15 = okay |
|
Respiratory Patterns and Levels of Lesions in Coma
|
1. Deep forebrain—Cheyne-Stokes
2. Midbrain—central neurogenic hyperventilation 3. Rostral pons—apneustic 4. Midpons—cluster breathing 5. Caudal pons or rostral medulla—ataxic breathing 6. Respiratory centers in mid-medulla—respiratory arrest |
|
Clinical Examination to Assess Brain Death
|
step 1, check motor response and check the eyes do not open when a painful stimulus is applied to the supraorbital nerve or nail bed.
step 2, Assess brain-stem reflexes Absence of grimacing or eye opening with deep pressure on both condyles at the level of the temporomandibular joint (afferent nerve V and efferent nerve VII), the absent corneal reflex elicited by touching the edge of the cornea (V and VII), the absent light reflex (II and III), the absent oculovestibular response (VIII and III and VI), and the absent cough reflex elicited through the introduction of a suction catheter deep in the trachea (IX and X). Step 3, apnea test , disconnect the ventilator -observe and monitor the patient for changes in vital functions |
|
What brain stem reflexes do you check for in brain death?
|
grimacing or eye opening –apply deep pressure on the temporomandibular condyles (afferent V & efferent VII)
corneal reflex - touching the edge of the cornea (V and VII) light reflex (II and III) oculovestibular response (VIII and III and VI) gag reflex – push suction catheter deep in the trachea (IX and X) |
|
Match cause of coma to pupils:
toxic or metabolic midbrain lesion or transtentorial herniation pontine lesion opiate overdose, pontine damage |
Toxic or metabolic- normal sized, reactive
Midbrain lesion or Transtentorial herniation-Unilateral or bilateral blown pupil Pontine lesion- Small, responsive to light bilaterally Opiate overdose, Pontine damage- Bilateral Pinpoint pupils |
|
What is the normal VOR? What can explain its absence?
|
The oculocephalic reflex is present if the eyes move in
the opposite direction of the head movements (doll’s eyes) brainstem dysfunction in coma, or barbiturate overdose, but can be normal in awake state (normal eye movements) |
|
Caloric Testing, indicate the lesion:
Cold Water in Ear --> smooth conjugate eye turn to ipsilateral side and stay cold water in ear --> deviation to side cold water with nystagmus in opposite direction cold water --> 1 eye does not adduct on spontaneous eye movements or in response to reflex maneuvers |
intact brainstem, damage to supratentorial cerebrum
normal INO |
|
What are the necessary preconditions for brain death?
|
acute catastrophic brain injury must be present
Rule out all reversible causes: No hypothermia (BT > 90˚ F or 32˚ C), No drug-related cause, No shock |
|
What are the tests for brain death/coma?
|
no response to verbal or visual command
no movement in response to painful stimuli Absent brainstem reflexes-pupils mid-position and nonreactive,absent corneal reflex, absent oculocephalic (“doll’s eye”) reflex, or absent VOR on caloric test), absent gag reflex Apnea: no spontaneous ventilation EEG is done to confirm brain death- it shows “electrocerebral inactivity” (flat pattern, < 2mV in amplitude) |
|
What is the difference between coma and brain death?
|
brainstem reflexes and non-flat EEG (various fixed patterns)
|
|
How is persistent vegetative state different from coma?
|
presence of sleep wake cycles
|
|
What is the different between locked in syndrome and coma?
|
Eye movements and blinking. Locked in is lesion to anterior pons. that spares CN VII. Also, normal EEG.
|
|
What are simple vs complex partial seizures?
|
Simple Partial Seizures- small local but progress to generalized
vague location, Aura-auditory or visual hallucinations, emotional experience, arms, legs or face may twitch. Does not impair consciousness Complex Partial Seizure (psychomotor or temporal lobe) Altered consciousness, Sensory, motor and ANS symptoms, some have aura (unpleasant odor or taste), Start blank stare, post-ictal- somnolence or confusion, with no recollection of seizure |
|
What is a partial seizure?
|
Involves a limited portion of the brain
Starts on one side (foci = start location) |
|
What is a Jacksonian march?
|
progression of seizure location with march of symptoms a -start in feet and legs goes to arms hand and face
|
|
Generalized Seizures
|
Not localized to one area (no aura)
Travel throughout entire brain on both sides Originates bilaterally and symmetrically |
|
Define the following seizures:
absence myoclonic tonic clonic atonic |
Absence (petit mal) Occur in children, last seconds, loss of activity and not responsive
Myoclonic large jerky movements Tonic clonic- LOC-alternating intense contraction and relaxation, hoarse cry out, post ictal may sleep, confused, sore Atonic (drop attacks) |
|
Status Epilepticus:
|
Continuous series of seizures without reawakening
|
|
generalized seizure consisting clinically of a brief staring spell in conjunction with a characteristic burst of spike-wave complexes on the EEG
|
Absence Seizure
|
|
What is a generalized seizure?
|
Both hemispheres hit – NOT local
|
|
What nerves are parasympathetic?
sympathetic? Note: nerves denote PNS, so the question is really asking, where does parasympathetic CNS become PNS. |
CN (III, VII, IX, X) & S2-S4
T1-L2 |
|
Describe the pre and postganglion action and NT of somatic efferent and the autonomic.
|
Somatic efferent cell bodies in the CNS release Ach onto target skeletal muscle expressing nicotinic Ach receptors.
The ANS innervates smooth muscle, gland cells and cardiac muscle. Sympathetic preganglionic fibers with cell bodies in the CNS release ACh onto postganglionic neurons expressing nAChR. Postganglionic axons release NE on target smooth and cardiac muscles expressing a and b-adrenergic receptors. Parasympathetic preganglionic fibers with cell bodies in the CNS release Ach onto target smooth and cardiac muscles expressing mAChRs. |
|
What 2 actions occur when successfully urinating?
|
contract detrusor, relax sphincters
|
|
What control the bladder?
|
Several regions of cerebral cortex (prefrontal) for voluntary override
Pontine micturition center (Barrington’s nucleus) via the reticulospinal tract for general coordination (similar to UMN) Sympathetic (T10-L2) to STOP Innervation of base of bladder (trigone, neck, internal sphincter) through hypogastric nerve Parasympathetics (S2-S4) to PEE Innervates dome of bladder through pelvic nerve Somatic motor (S2-S4) to Stop voluntarily |
|
“Lower motor neuron bladder” indicates a lesion of sacral spinal cord or cauda equina. What are the clinical symptoms?
|
no parasympathetic ability to initiate micturition = no voluntary control of external sphincter
Detrusor flaccid = large bladder, poor emptying Sphincter has decreased tone = overflow incontinence (cannot withstand additional pressure) |
|
Bladder fills to max capacity, then dribbles,
urinary retention overflow incontinence |
“Lower motor neuron bladder”
|
|
“Upper motor neuron bladder”
Where is the lesion? What are the symptoms? |
Following loss of input from pontine micturition center, i.e. anywhere between pons and S2 (start of parasympathetic output to bladder)
Similar to other UMN lesions, associated with hyperactivity: small, spastic, hypertonic bladder that empties reflexively (1-4 hr), but may not FULLY empty increased sphincter tone? Difficulty initiating stream |
|
When do you have to catheterize a patient with nerve damage to bladder?
|
During the period of spinal shock immediately following injury, one sees atonic bladder
|
|
“uninhibited bladder”
|
Loss of cortical input
Leads to urinary incontinence, but no urinary retention problem because detrusor-sphincter loop is still intact |
|
Urination: Micturation reflex
|
Stretch receptors fire
Parasympathetic neurons fire motor neurons stop firing Smooth muscle contracts Internal sphincter passively pulled open. External sphincter relaxes |
|
what 4 functions of homeostasis does the hypothalamus control?
|
Blood pressure
Body temperature Fluid and electrolyte balance, and Body weight |
|
What does the Anterior hypothalamic nuclei control? What does a lesion lead to?
|
heat dissipation center; triggers sweating, cutaneous vasodilation. (think Anterior Center = AC)
Estrogen receptors! Hot flashes?? Lesion leads to hyperthermia - inability to dissipate heat. Potentially fatal! |
|
Posterior hypothalamic nuclei
What is its purpose and what does a lesion lead to? What kind of lesion? |
heat conservation center, triggers cutaneous vasoconstriction and heat production center, triggers shivering
Bilateral lesion inability to raise core temperature (heat production/conservation) may result in complete loss of ability to thermoregulate (poikilothermia) |
|
What are the Anorexic neuropeptides
that act on the hypothalamus? |
Alpha MSH, cocaine and amphetamine related transcript (CART) prooplomelanocortin (POMC)
Orexigenic Neuropeptides Neuropeptide Y, agout-related peptide (AgRP) Orexins (hypocretins) |
|
What are the Signals from the periphery that cause anorexia?
|
Leptin (adipose), Insulin, Ghrelin, glucocorticoids
|
|
Leptin
What does it do? What happens in its absence? Where are receptors? |
Hormone produced in adipose tissue-product of the ob gene
Leptin infusion into 3rd ventricle inhibits food intake and energy expenditure Absence of circulating active leptin results in obesity, diabetes and sterility Abundent leptin receptors in VMN and lateral hypothalamus |
|
What lesion is indicated by loss of a consensual pupillary light reflex?
|
CN III
|
|
What lesion is indicated by loss of a direct pupillary light reflex?
|
CN II
|
|
What lesion is indicated by a complete lack of pupillary light reflex?
|
CN II
|
|
For the cochlear nerve, what will the following result in:
destruction irritative lesions |
deafness
tininess |
|
Acoustic neuroma (schwannomma)
|
schwann cell tumor of the cochlear nerve that causes deafness and…
|
|
What are the full side effects of an acoustic neuroma?
|
Auditory (VIII):
tinnitus, ipsilateral deafness Vestibular (VIII): vertigo/dizziness, nausea, nystagmus Facial (VII): multiple findings ipsilateral facial paresis/paralysis, loss of corneal reflex, loss of taste (front 2/3 of tongue), loss of salivation, tearing hyperacusis? No! overridden by deafness! Cerebellar signs possible |
|
What Regulates compensatory eye movements (to head movements)?
|
vestibulocochlear nerve
|
|
What nerve is associated functionally with the cerebellum (flocculonodular node) and oculomotor nuclei?
|
vestibulocochlear nerve
|
|
First order sensory bipolar cells in the vestibular ganglion (internal auditory meatus) project to the hair cells of the cristae of the semi-circular canals, and to the hair cells of the uticle and saccule
They also project to the vestibulo nuclei of the brain stem and flocculonodular lobe of the cerebellum Which nerve? |
Vestibulocochlear nerve
|
|
What are the utricle and saccule sensitive to?
|
Uticle sensitive to tilts beginning from upright and responds to acceleration in the horizontal plane, the saccule is sensitive to tilts from sideways position and accelerations in the vertical plane
|
|
What does a Vestibulocochlear nerve
lesion cause? |
Disequilibrium,
Vertigo, and Nystagmus (nystagmus can be physiological or pathological) |
|
What are the 2 forms of deafness?
|
- those that impair the ability of airborne vibrations to reach the organ of Corti (Conductive hearing loss- eg from middle ear infection) only affects ability to hear sounds delivered in air (no effect on skull vibrations) so impaired hearing in one ear by air conduction but normal hearing by bone indicates conductive hearing loss
- those that impair the ability of hair cells or the cochlear nerve to respond (sensorineural hearing loss) Damage from noise exposure or VIII tumor result in impaired hearing no matter what route used to deliver vibrations |
|
What are the three kinds of deafness and the causes attributed?
|
Conductive Hearing Loss
External ear obstructions (wax?, peas?) Middle ear obstructions: Otitis Otosclerosis - commonly causes progressive hearing loss Sensorineural Hearing Loss Degeneration of hair cells Presbycusis (high freqs go first: 20,000 down to 8,000 or 4,000 Hz) Lesion of cochlear nerve Central Hearing Loss Lesion of primary auditory cortex (Brodmann's areas 41 and 42) Lesion of Wernicke's area (Brodmann's area 22) Seizure activity in the auditory cortex (e.g. temporal lobe epilepsy) Tinnitus = the paresthesia of the auditory system |
|
How do you diagnose conductive hearing loss with the weber test? Sensineural?
|
Louder in the bad ear (the conduction problem masks the ambient noise of the room)
Louder in good ear (the affected ear is less effective at picking up sound even if it is transmitted directly by conduction into the inner ear) |
|
How do you diagnose conductive hearing loss with the rinne test? Sensineural?
|
In both cases, with the good ear, AC > BC
With conductive BC > AC with the bad ear (bypasses bad conduction) With sensineural AC > BC (bypass doesn't matter) |
|
Meniere's disease (VERY IMPORTANT)
|
hearing loss and vertigo due to alteration in endolymph pressure (increase)
|
|
What is the difference between dementia and delirium? (Hint: What does David Wong love?)
|
attention (demented people can still attend to you)
onset (dementia is slower) |
|
What are the symptoms and treatment of normal pressure hydrocephalus?
|
Confusion, depression, problems with memory, urinary incontinence and ataxia- worse over a period of weeks
- shunt to divert CSF can reverse the dementia |
|
Alzheimer’s Disease (AD)
definitive diagnosis symptoms |
Definitive diagnosis of AD requires postmortem
examination of the brain and sufficient numbers of plaques and tangles to qualify as affected by AD progressive memory impairment - disordered cognitive function - altered behavior, including paranoia and delusions - progressive decline in language function |
|
What are extracellular and intracellular with alzheimer's?
|
extracellular- plaques
intracellular- tangles |
|
What genotype is protective and which is harmful for alzheimers?
|
ApoE2
ApoE4 |
|
What neurochemistry occurs in alzheimers?
|
50-90% decrease in choline acetyltransferase activity in cerebral cortex and hippocampus – selective loss of ACh neurons (from deep nuclei in septum to hippocampus and basal nucleus of Meynert to the cerebral cortex)
Glutamate may be involved in loss of large neurons in both cortex and hippocampus |
|
Severely enlarged ventricles, cortical & hippocampal shrinkage
|
AD
|
|
What are the general functions of the different areas of the brain?
|
Frontal lobe: personality and higher centers for voluntary motor activities (Primary motor cortex- seen in red)
Parietal lobe: peripheral sensations (primary somatosensory cortex- seen in blue) Temporal lobe: sensations of smell, taste (in insula) & hearing Occipital lobe: vision |
|
What are the parts of the Limbic lobe and their function?
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Hippocampus-involved in memory, and damage results in amnesia
Amygdala is involved with fear and anger and the emotional interpretation of events and visual stimuli Anterior cingulate gyrus -pain |
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What is active during emotional interpretation of visual stimuli?
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amygdala
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Hyperalgesia
definition and types? |
Increased response to painful inputs
Primary hyperalgesia: Increased sensitivity to pain with lowered threshold at mechanical and thermal nerve endings Secondary hyperalgesia: Changes within CNS that cause increased response by [1] lowering the threshold or [2] increasing its magnitude of pain evoked by suprathreshold stimuli. |
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Allodynia
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pain resulting from a normally non-nociceptive stimuli
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Pain can be modulated
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at the brainstem and at the spinal cord dorsal horn
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Endogenous Pain Control Mechanisms
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Enkephalinergic interneurons within the dorsal horn can inhibit pain transmission
Noradrenergic projections from pontine centers terminate on neurons and terminals within the dorsal horn and inhibit pain transmisssion Activation of cannabinoid receptors in the spinal cord dorsal horn can limit pain Serotonergic projections from brainstem raphe nuceli can activate local circuits within the dorsal horn of the spinal cord to prevent pain transmission Endogenous opioids |
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Visceral Pain: Summary
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Visceral nociceptors respond to mechanical stretching (distention), ischemia, chemicals released by tissue damage (H+, bradykinin, PGE2, etc)
Visceral pain transmitted to spinal cord primarily bundled in sympathetic afferents (T1-L2) Visceral pain: poorly localized Visceral pain may be referred to associated somatic region |
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Referred Pain
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Pain of visceral or parietal origin may be perceived as somatic pain by the patient.
The somatic region to which the pain is referred is always a dermatome(s) that is (are) innervated by the same dorsal roots that supply the irritated structure. Thus the site of the referred pain can direct the clinician to appropriate underlying visceral sources. |
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Concerning the STT tract in the medulla, is it CL or IL with the pain, temp, and crude touch from the face?
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Ipsilateral
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What infarct causes a hearing loss?
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AICA
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What is Parinaud syndrome?
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compression of posterior midbrain
Vertical gaze center- Loss vertical gaze, eyes deviate downward Vergence center- Nystagmous on eye convergence Posterior commissure and tectum- Loss pupillary light response, possibly with accomidation intact |
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Who is at a higher risk of tearing bridging veins? What type of aneurysm?
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alcoholics and elderly
subdural |
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What is contained within medullary pyramids?
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CST axons
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