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2013-10-06 18:51:42

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  1. What are extraneural factors affecting the blood supply to the brain?
    • low or high blood pressure (variable)
    • Cerebrovascular resistance
    • Atherosclerosis
  2. What is a thrombis and when may it take place?
    • a blood clot (narrowing of artery)
    • in a few minutes or take hours or even days to fully evolve.
  3. what is an embolus?
    a traveling blood clot
  4. A _____ may break off from ____ and be carried to other places in the bloodstream. When the embolus reaches an artery too narrow to pass through and becomes _____ blood flow distal to the fragment ___ and the result is ____
    • small clot
    • a larger thrombus
    • lodged
    • ceases
    • infarction of distal brain tissue due to lack of nutrients and oxygen.
  5. What does a lack of glucose and oxygen cause?
    depletion of the celluar engery stores required to maintain electrical potentials and ion gradients.
  6. What is a penumbra
    • Tissue around the infarctio that is alive but the function is questionable.
    • Dark area surrounding dead tissue
  7. In Ischemic (____) brain tisuuse, what happens?
    • injured
    • the membrane that surrounds each affected neuron becomes "leaky" and the cell loses potassium and atp the tissues medium for energy exchange.
  8. when a membrane is leaky, what happens?
    sends warning to glial cells to clean up biproduct or eat bad cells so they eat up cells and death is the result.
  9. The lower the blockage....
    The greater the problem
  10. The blood brain barrier does what?
    • Protects teh brain from "foreign substances" in the blood that may injure the brain
    • Protects the brain from hormones and neurotransmitters in the rest of the body
    • Maintains constant pure environment for the brain.
  11. What is the blood brain barrier?
    army of enothielial cells that form wall that only certain things can pass.
  12. What is the arachnoid barrier layer?
    the arachnoid barrier later is a part of the arachnoid meningeal layer, it is formed by tight junctions between the endothelial cells of cerebral capillaries in the arachnoid mater.
  13. what did we used to think about the BBB and what do we know now?
    • We used to think that the only way that a chmical could leave the blood and enter the brain was by being small enough to sneak through the tight junctions,
    • but now e know that there are myriad molecular passageways embedded in the membrain of the endothelial cells that block some chemicals and actively push others through
  14. Microglia do what?
    patrol the brain and spinal cord for invaders that are trying to get in, or thet have alrady succeeded in getting inside. they also look for damaged or cancerous cells and remove them.
  15. What are nerves.
    Bundle of peripheral axons that are found in PNS.
  16. Axons that travel together are
  17. What are cranial nerves vs spinal nerves
    • Cranial nerves are nerves that emerge directly from the brain stem
    • Spinal nerves emerge from segments of the spinal cord. 2221
  18. How many nerves are involved in speech and swallowing?
  19. There are ___ pairs of cranial nerves
  20. all cranial nerves exit from front of brainstem except
    for the IV it exits from the back.
  21. What are UMN
    • Upper motor neurons originate in the cortex (precentral gyrus)
    • Axons synapse on cell bodies of lower motor neurons in brainstem and spinal cord. 
    • Cell bodies and axons totally contained within CNS
  22. What are LMN
    • Originate in the brainstem and spinal cord
    • Receive information from upper motor neurons 
    • axons synapes on muscle fivers
    • cell bodies contained with CNS and axons leave CNS
    • Form a final common pathway for information descending from cerebrum to periphery.
  23. What is the corticobulbar tract, Explain.
    • A bundle of fibers that go from the cortex to another area of the brain in the spinal nerves
    • UMN from cortex terminate on LMN nuclei in the brainstem that give rise to CN V, VII, IX, X, XI, and XII
    • Corticobulbar fibers from each hemisphere project bilaterally to brain stem nuclei (except for parts of CN VII:Facial Nerve)
  24. The corticobulbar tract is ..... (unilateral or bilateral)
  25. UMN travel together in...
    LMN travel together as...
    • corticobulbar tract
    • cranial nerve.
  26. What nerves are involved in smell and vision
    I, II, II, IV, VI
  27. Describe the Olfactory Nerve
    • Purely sensory
    • Receptors located in mucous membrane of nose
    • Together, receptors and their unmyelinated axons comprise CN I
    • Pass through several holes in cribriform plate of themoid bone
    • Terminate in olfactory bulbe
    • information about olfaction processed in temporal lobe
    • Olfaction is only sense not mediated by thalamus.
  28. The olfactory nerve is not...
    mediated by the thalamus like all other sensations.
  29. What is the difference between sensation and perception
    Sensation is the physical stimuli and perception is your interpretation of the sensation.
  30. Describe the Optic Nerve
    • II
    • Purely sensory
    • Visual information from retina is carried back to superior colliculus of midbrain on optic tract
    • From superior colliculus information passed on to lateral geniculate body of thalamus and then to cortex of occipital lobe
  31. Where do the visual fields merge?
    • Optic chiasm
    • Goes to the thalamus and ends up in the cortex of occipital lobe.
  32. Optic nerve exits..
    back of eye in orbit and enters cranium via the optic canal (foramen)
  33. Describe the Oculomotor nerve
    • A motor nerve
    • nucleus located in midbrain
    • mediates eyeball movements, pupil constriction, and eyelid elevataion
  34. What are the two components of the oculomotor nerve and their functiosn
    • somatic motor: controls muscles responsible for precise movement of eyes for visual tracking or fixation
    • Visceral motor: mediates pupillary light and accomodation reflexes.
  35. the oculomotor nerve exits...
    back of eye in orbit and enters cranium via superior orbital fissure.
  36. Describe the troclear nerve
    • A motor nerve
    • Nucleus located in the midbrain
    • Nerve mediates eye movements (damage will cause diplopia or double vision
    • supplies one extraocular muscle: contralateral superior oblique (moves eye down from medial position)
    • Only a cranial nerve that exits brain dorsally.
  37. trochlear nerve exits..
    back of eye in orbit and enters cranium via superior orbital fissure
  38. Describe the Abducens nerve.
    • VI
    • A motor nerve
    • nucleus located in pons
    • mediates eye movement 
    • opposit the trochlear nerve
    • innervates ipsilateral lateral recuts muscle (move eyes out laterally)
  39. Abducens nerve exits..
    back of the eye in orbit and enters the cranium via superior orbital fissure.
  40. What cranial nerves are involved in speech, hearing and swallowing
  41. Describe the Trigeminal nerve
    • V
    • A mixed nerve
    • Nucleus located in the pons
    • A large sensory component:
    • -Sensation from face and scalp; mucous membranes of mouth, tongue, nose, paranasal sinuses, and gums, teeth most of dura (pain, touch, temperature)
    • A smaller motor component
    • -innervates masseter and temporalis muscles (mastication), tensor veli palatini muscle(Eustachian tubes), and tensor tympani muscle of middle ear (dampens sound through middle ear).
  42. How many branches does the trigeminal nerve have and what are they?
    • 3
    • Ophthalmic (sensory)
    • Maxillary (sensory)
    • Mandibular (sensory and motor)
  43. the branches of the V nerve enter where?
    • Opthalmic branch enters via superior orbital fissure.
    • Maxillary branch enters via foramen rotundum
    • Mandibular branch enters and exits cranium via foramen ovale
  44. When damage occures to the sensory aspect of the CN V...
    • Numbness or loss of senstion of areas intervated 
    • Absent corneal reflex when affected eye is stimulated (sensory component mediated by opthalmic branc of the ipsilateral trigeminal nerve, Motor component mediated by bilateral facial nerve)
    • Trigem
  45. Describe trigeminal neuralgia (V2 and V3)
    • Mild touch (usually to areas innervated by V2 or V3  produce severe electrical pain
    • Pain believed to be caused by ephatic transmission (cross talking happening between nerves-result of demyelination)
  46. Damage to CN V motor parts results....
    • in atrophy of muscles supplied by CN V 3
    • Masseter and temporalis musch = difficulty with mastication and speech
    • Tensor veli palatini = impaired opening of eustachian tube
    • Tensor tympani = heightened sensitivity to sound
    • Absent jaw jerk reflex = sensory (proprioceptive) and motor (innervation to masseter and temporalis muscles) components mediated by CNV
  47. Describe the facial nerve
    • often classified as motor nerve but has sensory components also. 
    • nucleus located in pons
    • Sensory = mediates taste from anterior two-thirds of tongue.
    • Motor: Innervates all muscles of facial expression including those in forehead, cheeks and lips.
    • upper part of face: bilateral innervation from UMN
    • Lower part of face: only ipsilateral (unilateral) innervation from LMN
    • Supplies stapedius muscle of inner ear
    • Sends motor impulses to rest of ear (wiggling ears)
    • There are also parasympathetic fivers fro lacrimation and salivation ( fivers travel to perifpheral ganglion, Postganglionic fibers innervate lacrimal glands and sumbandibular sublingual salivary glands.
  48. The upper part of VII is ____ the lower is ____
    • bilateral
    • Ipsilateral and unilateral
  49. The facial nerve enters and exits cranium via..
    internal acoustic meatus
  50. What happens when there is damage to CN VII
    • Sensory: Diminished taste on anterior two thirds of tongue
    • Motor: Lacrimal and salivary glands have inability to control lacrimation and salivation
    • and the stapedius musle has heightened sensitivity to sound. 
    • Facial paralysis depending on where lession is.
  51. A lession on the umn of CN VII causes
    weak or paralyzed lower face with a spared forehead.
  52. A lesion of the lmn of CN VII causes
    weakness or paralysis of all ipsilateral facial muscles.
  53. Damage to the neuronal cell bodies in the corticobulbar tract of CN VII
    means loss of voluntary control over lower muscls of facial expression on the contralateral side.
  54. Describe Bell's Palsy LMN
    • Acute unilateral facial nerve paralysis
    • Mononeuropathy
    • Thought to be caused by inflammation of CN VII
    • Treated with anti-inflammatory or antiviral drugs.
  55. Damage to a LMN of CN VII means
    there is paralisis on whole side of face.
  56. CN VIII
    • Vestibulocochlear Nerve
    • A sensory nerve with the nucleus located in the medulla
    • Has two branches: cochlear branch (hearing), and vestibular branch (balance)
  57. The vestibulochochelar nerve enters the cranium via...
    the internal acoustic meatus.
  58. What happens when there is damage to the CN VIII
    • Cochlear branch: unilateral or bilateral hearing loss that depends on locatio nof lesion (along peripheral or central auditory pathway) Possible tinnitus
    • Some causes: acoustic neuromas, ototoxic drugs
    • Vestibular branch: impaired balance, meniere's disease
  59. Describe the Glossopharyngeal nerve
    • IX
    • Mixed
    • Nucleus located in the medulla
  60. Describe the motor component of IX
    • innervates stylopharyngeus muscle that elevates pharynx during a swallow. 
    • Parasympathetic fibers for salivation, fivers travel to a peripheral ganglion, postganglionic fivers innervate parotid salivary gland
  61. Describe the sensory component of IX
    • Supplies pain, temerpature and tactile information from posterior one-third of tongue, mucosa of upper pharynxx including velum and tonsils, eustachian tube and middle ear.
    • Supplies carotid sinus baroreceptors and carotid body chemoreceptors which monitor blood pressure and blood oxygen concentration.
    • Posterior 1/3 of tongue
  62. The carotid sinus receptors help ...
    mediate bp by receiving sensory information and sending that information to the brain.
  63. The glossopharyngeal nerve enters and exits..
    via jugular foramen.
  64. That happens when there is damage to CN IX
    • Motor: difficulty swallowing and controlling salivation
    • Sensory: loss of senstation to areas, loss of taste on posterior one third of tongue (hard to test clinically)
    • Absent gag reflex,
    • Normally tocuing either side of the posterior pharynx leads to bilateral contration of muscles and bilateral elevation of the soft palate. Sensory component mediated by ipsilateral glossopharyngeal nerve, motor component mediated by bilateral vagus nerves.
  65. Describe glossopharyngeal neuralgia
    • Like trigeminal neuralgia
    • sudden paroxysms of severe electric pain in back and side of throat
    • pain can spread down from side of neck to front of ear to back of mandible
  66. Describe CN X
    • Vagus nerve
    • A mixed nerve
    • Nucleus located in medulla
  67. What is the motor component of the vagus nerve
    • innervates soft palate, pharynx, larynx and esophagus
    • There are also parasympathetic fibers projecting to thracic and abdominal viscera
    • three branches: Palatal (glossopalatine and levator veli palatine)
    • Superior laryngeal (cricothyroid)
    • Recurrent laryngeal (all intrinsic laryngeal muscles except cricothyroid.
  68. What is the sensory component of the vagus nerve?
    • Sensory fivers arise from baroreceptors and chemoreceptors in aortic arch and aortic bodies and from thoracic and abdominal viscera
    • Taste
    • Somatosenstion from lower pharynx, larynx, esophagus and ear (including external auditory canal and tympanic membrane)
  69. The vagus nerve enters and exits via
    the jugular foramen
  70. Damage to CN X means that
    Sensory: Loss of taste and loss of somatosensation from intervated areas (risk of aspiration)

    Motor: Visceral motor areas affected. 3 branches, palatal, superior laryngeal, recurrent laryngeal.
  71. Damage to the Palatal branch
    • unilateral weakness of soft palate (no elevation of soft palate on affected side when saying ah)
    • Impaired gage reflex (soft palate will not elevate on affected side)
    • Dysphagia (difficulty swallowing)- decreased palatal elevation and closure of nasopharynx, decreased pharynx constriction 
    • Hypernasal speech
  72. Damage to superior laryngeal brang
    inability to raise pitch because you can't contract the cricothyroid to lengthen vocal folds. Your ability to lower pitch preserved
  73. Damage to recurrent laryngeal branch
    • rough vocal quality (if damage is unilateral, one vocal fold may flap around and create noise)
    • Breathy speech
    • Difficulty phonating (shorter duration of phonation because air is escaping)
  74. Spinal Accessory Nerve
    • XI
    • A motor nerve
    • 2 branches 
    • 1. central branch (nucleus in medulla)- assists cn x supplies motor innervation to larynx, pharynx and soft palate
    • 2. Spinal accessory branch (cell bodies arise from ventral horn of first 5-6 cervical segments of spinal cord)
    • Innervates trapezius and sternocleidomastoid muscles of the neck and back
  75. Spinal accessory nerve exits cranium via.
    Jugular forament
  76. Damage to CN XI is
    • weakness of sternocleidomastoid muscle (difficulty turning head, direction of weak head turn indicates contralateral muscle weakness and contralateral CN XI injury
    • Weakness and atrophy of trapezius muscle causes droopy shoulder on ipsilateral side and difficulty shrugging shoulders
  77. What is jugular foramen syndrome>
    • CN IX X an XI leave together at base of skull with jugular veinn
    • Lesion at skull base can lead to....ipsilateral weakness of pharynx and larynx (X) decreased sensation of ipsilateral pharynx (IX) Weakness of ipsilateral trapezius and sternocleidomastoid muscles.
  78. XII
    • Hpyoglossal nerve 
    • Motor nerve
    • Nucleus located in medulla
    • Controles tongue movement
    • Innervates all intrinsic and extrinsic tongue muscles except one extrinsic tongue muscles.
  79. the hypoglossal nerve exits cranium via
    hypoglossal canal in occipital bone
  80. Damge to CN XII equals
    Decreased tongue movement
  81. A LMN lesion on CN XII
    muscular atrophy and ipsilateral weakness of tongue, fasiculations (twitches), tongue deciates to weak side when protruded, tongue pushes into cheek on weak side with normal strength
  82. An UMN lesion on CN XII
    • mild tongue weakess without atrophy
    • difficulty with fast, alternating tongue movements
    • tongue deviates to weak side.
  83. if you have an umn lesion on left the tongue ...
    deviates to the right.
  84. Is the whole brain used to pump the heart?
  85. what are ways to divide the brain
    • landmarks
    • structrue-function
    • cellular makeup of the 6 layers of the cortex
  86. There are 4 lobes of the brain plus the 5th
    • frontal
    • parietal
    • temporal 
    • occipital
    • limbic love
  87. The limbic lobe is
    white matter
  88. What are the 6 inner structures of the brain
    • basal ganglia
    • thalamus
    • hypothalamus
    • midbrain
    • pons
    • medulla oblongata
  89. The thalamus is the relay station for what?
    all sensory info except smell
  90. What are the three structural divisions of the brain and the parts under them
    • the forebrain: telencephalon and diencephalon
    • midbrain: mesencephalon
    • hindbrain: metencephalon and myelencephalon
  91. Damage to the mesencephalon means
    you will be unconscious.
  92. what does the mesencephalon do?
    processing of visual and auditory data, generation of reflexive somatic motor responses and maintenace of consciousness.
  93. Pons
    relatys sensory information to cerebellum and thalamus, subconscious somatic and visceral motor centers
  94. Medulla oblongata.
    • relays sensory information to thalamus and to other portions of the brain stem 
    • autonomic centers for regulation of visceral function
  95. Describe cytoarchitechtonics
    korbinian broadmann segmented the cerebral cortex into 52 distinct regions based on histological characteristics (cell patterning)
  96. What is diaschisis
    a sudden loss of function in a portion of the brain connected to but at a distance from a damaged area.
  97. What is a functional region and perfusion mapping
    mapping how blood flows through brain and the area is structurally intact but function is not optimal
  98. area 44 on right side of brain is
    not broca's area but a homologue of working memory.
  99. what are the sensory areas?
    • primary sensory area
    • secondary sensory area
  100. what are the motor areas?
    • primary motor area
    • secondary motor area
    • supplementary motor area
  101. What are the association areas and why do we have them
    • parietal, occipital and temporal cortex (conceptual elaboration of sensory data)
    • Prefrontal (frontal) cortex (judegment, foresight)
    • Allow you to interpret sensory information and make response to it.
  102. The primary somatosensory cortex is
    • BA 1,2,3 
    • postcentral gyrus of parietal lobe (allows conscious awarenss of sensation and the ability to localize it :where the sensation is from)
  103. The somatosensory area is
    • behind it (BA 5 & 7)
    • the meaning of what is being felt
  104. BA 34
    • Smell (olfactory sense)
    • Deep in temporal love along medial surface
  105. BA 4
    • Primary motor areas (precentral gyrus of frontal lobe)
    • Precise, conscious or voluntary movement of skeletal muscles
    • Their axons: from massive pyramidal or corticospinal tracts descend through brain stem and spinal cord 
    • cross to contralateral (the other side) in brainstem.
  106. BA 44 and 45
    • Broca's area
    • specialized motor speech area at base of pre central gyrus just above lateral sulcus in only one hemishere usually the left
    •  word articultion and the movements necessary for speech
  107. Damage to brocas area means...
    expressive language deficits (could be receptive too) or if can still speak words are right but difficult to understand.
  108. Area 6
    • Premotor cortex 
    • Complex movements associated with highly processed sensory info; also planning of movements
  109. Inferior 8
    • voluntary movements of eyes.
    • frontal eye fields
  110. Area 17
    • The primary visual cortex area handles info from contralateral retina (right visual field-->left side)
    • Receives input from the optic tract via the thalamus (LGN)
  111. If the primary visual cortex is damaged
    functinally blind because no conscious awareness of sight
  112. Area 18&19
    • Visual association area
    • Rreceives projections from area 17, process stimulus features including form, color, and motion.
  113. What are the two visual systems in the occipital cortex?
    • "where" pathway (dorsal)
    • -occipital-parietal
    • -spatial location
    • "what Pathway"
    • -Occipital to temporal
    • -Object recognition (object naming)
  114. Area 41
    Area 22
    • Primary Auditory Cortex
    • Auditory association area: interpretation of auditory input.Has shown to be modality independent language deficit.
  115. Damage to 41/22
    has shown to cause comprehension deficits for deaf individuals b/c auditory processing has been linked to comprehension.
  116. Association Areas do what?
    • Control our ability to understand sensory information and coordinate a response. 
    • somatic sensory association area
    • visual association area
    • somatic motor association area
    • Interpretation will be individualized even when the stimulus is the same.
  117. Prefrontal cortex:
    • Cognition
    • This area is remodeled during adolescence until the age of 25; it coordinates the brain/body and inter-personal world as a whole
    • Executive funcitoning (working memory)
  118. 5,7,39,40 are found in the parietal lobes, what do they do?
    • 5,7,39,40
    • In addition to processing sensory information (123) the parietal lobe is responsible for spatial cognition as well as some aspects of reading and writing.
  119. What happens when damage occures on right superior parietal?
    • Damage here causes neglect (hemi-inattention) 
    • Lesion to the parietal love (usually RH) individuals do not respond to meaningful information presented to the side opposite of the brain lesion. They do not process the left field.
  120. 40 & 39 are found in the parietal lobes, what do they do?
    Alexia with agraphia
    Alexia without agraphia
    • Supramarginal (40)
    • Angular (39)
    • Reading and writing.
    • Acquired disorder of reading due to brain damage
    • Acquired disorder of writing due to the brain damage
    • .
    • Cannot read, but can write and understand words spelled alloud.
  121. Visual stimuli goes from 17-__- to ___ to ___ to 4 for verbal output.
  122. What are the areas involved in processing auditory information and semantics (the what)
  123. What is Heschel's gyrus?
    • 41 aka primary auditory cortex
    • processing auditory stimuli
    • projects to BA 42 for more detailed analysis of auditory information.
  124. What is agnosia.
    visual agnosia
    • Bilateral lesion to occipital temporal cortex- inability to recognize objects
    • Cannot recognize object presented in visual modality, but can recognize objects when presented in auditory/tactile modality
    • Bilateral/unilateral lesion to occipital-temporal cortex (FFA) -inability to recognize familiar faces.
  125. Damage to posterior area in temporal lobe means
    they don't have multiple representations of the same item.
  126. Area 22
    • Wernike's area
    • Involved in semantics/word meaning
    • comprehension of auditory/visual languag
  127. What is aphasia?
    acquired disorder of language due to brain damage.
  128. Brodmann areas 6,8,9,10,11,44,45
    • In addition to outputting motor information (4) the frontal lobe is involved in higher cognitive functions (executive function, planning, reason) as well as the coordination of motor movements for the production of speech sounds and syntax.
    • Programming motor sequences (6)
    • Frontal eye fields (8) involved in planning eye movements.
  129. 9,10,11
    • prefrontal cortex 
    • involved in executive functioning, reasoning and judging
  130. What is frontal lobe dysfunction
    apathetic/indifferent, difficulty changing strategies, social disinhibition, perseveration or repetition of an old behavior despite a demand for a new behavior.
  131. 44,45
    • Broca's area
    • involved in language output.
  132. lesion in 44 or 45
    results in slow effortful speech with prominent articulatory errors.
  133. What are the subcortical structures>
    • Thalamus
    • Hypothalamus
    • Limbic system
    • Basal ganglia
  134. The thalamus AKA does what
    • inner chamber
    • process and relay sensory information
    • the relay station of the brian
    • processes all sensory information (except smell)
    • Projects motor information to cortex
    • Plays a role in memory.
  135. What is the input and output for thalamus
    • input: sensory tracts (except olfactory)
    • output: projects to the cortex and other subcortical regions
    • Integration of motor information from cerebellum and basal ganglia
    • Crude sensations
  136. There are how many thalamic nuclei?
  137. What do lesions to the ventral posteriomedial nucleus and ventral posterolateral nucleus cause
    loss of all forms of sensation, including light touch, tactile localization and discrimination and muscle joint sense from the opposite side of the body.
  138. What is Korsakoff's syndrom
    • Damage dorsomedial nucleus of the thalamus and the mammillary bodes 
    • Amnesia
    • confabulation
    • Apathy
    • meager content in conversation
    • *from alcoholism*
  139. what are two groups of structures that form a cohesive functional unit
    • Basal ganglia 
    • limibic system
  140. what is the limbic system
    • is a complex set of brain structures in the telencephalon and diencephalon that lies on both sides of the thalamus, right under the cerebrum
    • It directly connects the lower and hight brain functions
    • It influences emotions, the visceral responses to those emotions, motivations, mood and sensations of pain and pressure.
    • Your ability to have and interpret behaviors
  141. What structures are in the limbic system?
    • Hippocampus
    • Amygdala
    • Fornix
    • Mammillary bodies
    • hypothalamus
    • cingulate gyrus
  142. Describe the hippocamus...
    what results from damage here?
    • involved with converting recent memory to long term memory.
    • Anterograde amnesia
    • injury to both amygdala nucleus and the hippocampus produces a greater memory loss than injury to either one alone.
  143. Describe the function and what happens with lessions for the Amygdala.
    • Processing emotion and memory
    • Learned emotional responses (mainly fear)
    • Lessions
    • -tameness-reduced emotional excitability
    • -normalization of behavior in patients with severe urbach-wiethe disease.
  144. What is a fornix?
    fiber bundle that carries part of the outflow of the hippocampus to the mammillary bodies.
  145. Describe the function of the hypothalamus
    • A collection of nuclei with a variety of functions 
    • controles the release of 8 major hormones by the pituitary gland (just inferior to the hypothalamus
    • Temperature regulation
    • control of food and water intake
    • sexual behavior and reproduction
    • circadian rhythm and daily cycles of physiological state and behavior
    • mediation of emotional responses.
  146. Describe the role between the hypothalamus and temperature regulation
    • When body temperature is elevated, neurons in the anterior part of the hypothalamus turn on mechanisms for heat dissipation 
    •      With a lesion = hyperthermia
    • When body temperature is depressed, neurons in the posterior part of the hypothalamus are responsible for heat production
    •      With a lesion= hypothermia
  147. Describe the cingulate gyrus
    • Recieves input from the thalamus and neocortex
    • highly influential in linking behavioral outcomes to motivation
    • This role makes the cingulate cortex highly important in disorders such as depression and schizophrenia
    • It plays a role in executive function
  148. For schizophrenia, the tx is...
    blocking limbic receptors to dopamine acceptors
  149. Alzheimer's disease is an abnormality in the
  150. Rabies virus attacks
    The hippocamus and infected patients show changes in emotional state.
  151. Describe the basal ganglia
    • Functional network of structures connecting the cerbreal cortex and thalamus
    • the basal ganglia are associated with a variety of functions including, voluntary motor control, procedural learning relating to routine behaviors or habits
  152. The basal gangia is made of the
    • Striatum (caudate nucleus and putamen)
    • Globus Pallidus
  153. Where is the basal ganglia?
    Found on both sides of the thalamus, outside and above the limbic system but below the cingulate gyrus and within the temporal lobe.
  154. Describe the Caudate nucleus
    • C shaped gray matter lateral to the thalamus:
    • 1: head: continouus with the putamen or lentiform nucleus
    • body: forms the floor of the body of the lateral ventricle.
    • tail: terminates in the amygdaloid nucleus.
  155. Describe the Putamen
    • The shell
    • the putamen lies just under and behind the front of the caudate
    • It appears to be involved in coordinating automatic behaviors such as riding a bike, driving a car, or working on an assembly line. 
    • Problems with the putamen may account for the syndrome of Tourette's
  156. Describe the Globus Pallidus
    • Located just inside the putamen with an outer part and an inner part
    • It receives inputs from the caudate and putamen and provides outputs to the substantia nigra (function is to control eye movements)
  157. Describe the motor pathway
    • Thalamus--resting state, inhibits movement (neurotransmitters called GABA tell neurons to fire) Released from inhibition-->cortical activation-->movement
    • Inhibitied-->cortex not activation ---> no movement.
  158. What are the 2 pathways that control movement through the BG... Describe both.
    • Direct pahtway (excitatory to movement)
    • -disinhibit thalamus--->activates cortex ---->movement (if you damage this your overly disinhibit the thalamus)(end state is hyperkinetic)

    • Indirect Pathway
    • 0Inhibitory to movement
    • -Inhibits thalamus --->inactiveated cortex -->No movement (end state is hypo kinetic)
    • *These two systems have competing effects of movement- so there is a balance between the two systems.
  159. Describe cause of parkinsons disease and symptoms
    steady loss of the dopaminergic function of the substantia nigra pars compacta

    bradykinesia, akinesia, rigidity, tremors, cognitive deficits, shuffling gait
  160. Describe the cause of Huntington's disease and symptoms
    • hyperkinesia, dyskinesia, uncontrollable/jerky movements, dementia, impaired cognitive abilities, personality disorders
    • Degeneration of the caudate nucleus of putamen
  161. Hemiballisums
    • Symptoms: flailing movements of one arm and leg
    • Cause: damage to the subthalamic nucleus
  162. ADHD is associated with...
    reduced globus pallidus size
  163. What does FAST stand for
    • Face
    • Arms
    • Speech
    • Time
  164. How many people have a strok and how any have a second?
    • 795000
    • 185000
  165. Stroke is the _____ cause of serious long term disability in the US and the _____ cause of death
    • leading
    • third
  166. Define Stroke
    Define TIA
    Acute disruption of blood flow to the brain leading to focal neurologic deficits (not a build up over time but an immediate change

    Transient Ischemic Attach= acute disruption of blood flow to the brian leading to focal neurologic deficits lasting less than 24 hours (usually 10-30 minutes)
  167. What is a hemmorage?
    A small break in the artery that causes a small bleed
  168. Although the term TIA implies transient ischemia...
    it is not infrequent that the pahtology of a TIA is an infarction or a small bleed with rapid recovery.
  169. For TIA, it is extremely important to be aware that
    • Clinically it is hard to distinguish between bleeds and infarctions
    • it is hard to distinguish between embolus and thrombosis
    • It is often difficult to distinguish between lesions of the anterior circulation and of the posterior circulation
    • It is often difficult to determine if a TIA is merely reversible ischemia or a completed stroke with rapid recovery.
  170. What conditions can mimic a stroke?
    • Unrecognized siezures, systematic infections, brain tumor.
    • In addition, there are two relatively common syndromes especially in elderly patients that mimic TIAs and ahve both positive and negative phenomena
    • 1. late-life migrain accompaniments
    • 2. transient focal symptoms associated with cerebral amyloid angiopathy.
  171. What are the 4 steps for a migrane? can it be connected to a stroke later?
    • Prodrome: before pain, light and sound sensitivity, depression, irritability, lack of appetite.
    • Aura: changes in visual perception, flashing lights and geometric patterns that obscure vision.
    • Headache: Pain, nausea, vomiting, speech problems
    • Postdrome: Migraine hangover. mood changes, sensitive scalp.

    Can lead to stroke later. 

    Inflammation is reason of pain.
  172. What is cerebral amyloid angiopathy
    is a disease of the elderly and usually presents as a spontaneous intracerebral  hemorrhage rather than as a transient focal neurological syndrome
  173. What are risk factors of a stroke?
    • Hypertension
    • Cigarette smoking
    • Alcohol use
    • Physical activity
    • diet
    • High cholesterol (hyperlipidemia)
    • Atrial fibrillation
    • Transient ischemic attacks.
  174. What is the effect of hypertension on large vessels?
    • predisposes to accelerated formation of plaque 
    • more common to formation of plaque (atheroma) in large arteries
  175. What is the effect on small vessels?
    deep areas of brain recieve their blood supply from end arteries, hypertension results in damage to small vessel wall and eventually occlusion resulting in infarction of a small area which at post mortem is visible to the naked eye as a small hole. May reuslt in aneurysms in basal ganglia and when they burst massive bleeding is the result.
  176. what are the three major pathological processes stroke is caused by?
    • Thrombosis: a blood clt forms within a blood vessel in the brain 
    • Embolus: a blood clot forms within the heart or a major blood vessel of the brain (outside brain or major artery)
    • Bleed: hemorage, weakness of artery and blood leaks out.
  177. Often, only two groups are considered.
    • 1. thrombo-embolus- infarctions
    • 2. bleeds
  178. What is a lacunar?
    A very small blood vessel of the brain progressively narrows until completely occluded.
  179. For the purposes of stroke, the brain is divided into what two areas?
    • Anterior circulation: the part of the brain which recieves blood supply from the carotid circulation which therefore includes the territory of the middle cerebral artery and the anterior cerebral artery.
    • Posterior circulation: the region of the brain which receives its blood supply from the vertebral, basilar and posterior cerebral arteries.
  180. MCA infarction involves...
    cortical branches and deep perforating leticulo-striate arteries.
  181. Embolism
    • Emboli(objects) derive from the following sources. 
    • heart: left atrium and ventricle (fif patient foramen ovale, then right sided circultion also
    • Aorta: Atheroma of the aorta may five raise to emboli
    • Carotid: This gives rise to platelet-fibrin emboli or cholesterol emboli and is probably the commonest cause of embolisation to the brain.
  182. Describe the subarachnoid hemorrahage
    Rupture of a cogenital malformation the berry aneurysm. These are most commonly found in the region of the circle of willis and its neighboring vessels, one important syndrome is that of a posterior communicating artery aneurysm which gives rise to complete third nerve palsy with pupil dilation
  183. Describe a hypertensive bleeds
    these typically occur in the basal ganglia and give raise to a massive hemorrhage causing coma and contra-lateral hemiplegia. The may also occur more superficially.
  184. Amyloid angiopathy
    this disorder of elderly people giving raise to hemorrhage hemorrhage particularly in the posterior regions of the brain.
  185. What is an arteriovenous Malformations
    are defects of the circulatory system that are generally believed to arise during embryonic or fetal develompent or soon after birth (can be anywhere in spinal cord or brain.)
  186. A middle cerebral artery infarct
    • results in contralateral hemiparesis
    • contralateral upper motor neuron facial weakness
    • contralateral sensory loss 
    • higher function cortical impairment - will be aphasia if left MCA infarction and possibly a neglect syndrome if right MCA infarftion.
    • loss of visual field in on the same side as weakness.  (homonymous hemianopia: blind spot in right visual field of both eyes)
  187. Anterior cerebral artery Infarction
    • Classically this causes weakness of the leg
    • damage to medial frontal lobe and cingulate gyrus you get akinetic mutism: patient who is extremely apathetic and often will not move unless forced to do so.
    • Weakness of right lower limb (right side of face spared and right upper limb less affect
    • Speech disturbance (dysphasia)
    • Apraxia of left side of body (inability to properly execute movements despite normal strength)
    • Disturbance of bladder control
    • Confusion initially, later personality change may occur
    • depends on where the blockage or hemorage is as to the size of the watershed area.
  188. PCA infarct
    • Deep or proximal strokes cause ischemia in the thalamus and or midbrain as well as in the cortex
    • involve only cortical structures
    • if on the left, a patient with acute vision loss in the right half of the visual field.
  189. Describe the Infarct of the basilar artery
    Obstruction usually causes death quickly-
  190. Posterior cerebral artery
    • loss of half of the field of vision on the side opposite to the stroke
    • Ischemic injury to the thalamus may result in unpleseant burning pain over opposite side of body (thalamic syndrome)
  191. Vertebral artery
    • vertigo at onset
    • cerebellar incoordintion of arm and leg on the same side.
    • Loss of pain and temperature sense of the half of the face that is on the same side as the stroke, and of the trunk and limbs on the side opposite to the stroke 
    • difficulty in swallowing and speaking.
  192. Describe horner's syndrome
    small pupil, mild drooping of eyelid and lack of sweating of face on same side as stroke)
  193. Lacunar Stroke
    • Caused by occlusion of a single deep penetrating artery arising directly from the circle of willis. 
    • looks like swiss cheese in brain.
  194. What are the 5 syndromes of lucunar strokes
    • Pure motor stroke: face arm or leg
    • Ataxic heiparesis: hours or day honest- legs mostly
    • Dysarthria/clumsy hand: hand weakness
    • Pure sensory stroke: numbness or unpleasant sensation
    • Mixed sensorimotor stroke: ipsilateral sensory impairment with weakness or paralysis.
  195. Which is most common
    Pure motor stroke/hemiparesis
  196. What are 5 stroke scales used
    • Glascow coma scale: 1= dead to 5=good recovery
    • Barthel index 0-100 100 being good
    • Modified Rankin Scale 0=no symptoms 6- death
    • Hunt Hess Scale I= good V= Coma or death
    • NIH stroke scale - very very in-depth.
  197. What is tratment of acute stroke patients?
    • urgent general supportive care
    • Management of serum glucose
    • Management of hypertension
    • seizure management
    • Magagement of brain edema

    • Medications
    • -intravenous t-PA
    • -Intra-arterial t-PA
    • Anticoagulation
  198. The aim of treatment of the acute stroke is to
    limit the extent of ischemia or to reverse the process completely.
  199. What is recombinant tissue plasminogen activator?
  200. tPA is a thrombolytic or a “Clot Buster” drug. This clot buster is used to break-up the
    • clot (by breaking down proteins used to form the clot) that is causing a blockage or
    • disruption in the flow of blood to the brain and helps restore the blood flow to the
    • area of the brain. It has a high risk of associated bleeding. TPA may only be given
    • within 3 hours of the onset of the stroke and if a CT Scan has excluded a bleed or a
    • large stroke. Large infarcts are excluded, because they have a high risk of becoming
    • hemorrhagic
  201. Prevention of emboli
    Heart: anti-coagulation is given routinely for atrial fibrillation, particularly if associated with mitral valve lesions, or if clot is seen in the left atrium or ventricle on echocardiograph
  202. What is the treatment for bleeds?
    • Hypertensive basal ganglia bleeds are generally untreatable
    • AVMs and Berry Aneurysms are treated surgically before rupture.