Neuropathology 1 Flashcards

(192 cards)

1
Q

1) The Fasciculus Gracilis exist at _______of spinal cord and DOES contain ______ ____ from the ___
vs.
Fasciculus Cuneatus exist in {__-__} = ____ and ______ and contains _____ ____ from the ___

1B) Which Pathway are these Fasciculus columns associated with?

2) What happens to 2nd order neurons of this Pathway?
2B) Where are these 2nd order neurons located?

3) What happens to 3rd Order neurons of this Pathway?
4) How does [Proprioreception/Vibration/2-point discrimination] get to 2nd order neurons? [5]

**Position/Vibration/2-point discrimination travels from periphery in the ______ ______—–> passes ______—>passes ______ ______ Gray mater–>ultimately travels upwards using ______ ______ or ______ ______
—>travel up into [______ MEDULLA] to synapse 1st time in ______ ______ or ______ ______

A

1) The Fasciculus Gracilis exist at ALL LEVELS of spinal cord and DOES contain [ascending sensory fibers] from the LE
vs.
Fasciculus Cuneatus only exist in {C1-T6} = Thoracic segments (T1-T6) and Cervical segments (C1-C8) and contains [ascending sensory fibers] from UE

**DORSAL COLUMN PATHWAY**

2) 2nd order neurons in [nucleus gracilis] AND [nucleus cuneatus] decussate as [internal arcuate fibers] in LOWER MEDULLA—>cross midline to form [Medial Lemniscus]—>this travels to VPL nucleus of thalamus!
3) 3rd order neurons in [VPL nucleus of thalamus] travel in internal capsule and terminate in [Area 312 POSTcentral gyrus]
4) Position/Vibration/2-point discrimination travels from periphery in [Dorsal Root]—> passes DRG—>passes Dorsal Horn Gray mater–>bends in {Fasciculus cuneatus or gracilis}—>travel up into [LOWER MEDULLA] to synapse 1st time in {nucleus cuneatus or gracilis}

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2
Q

A) [Lateral Dorsal Root] Synapses in ____ _____ of ____ Horn and then becomes the _____ ______ . What sensations is this transmitting? [2]

B) SPINOTHALAMIC TRACT DECUSATES in _____ _______ and BEGINS ASCENT in the __________
—->It then travels ultimately travel up to [VPL nucleus of Thalamus] via the _____ _____ of spinal cord

C) Cutting STT in CORD will affect Pain on ____[same/Opposite] side of Body

A

A) [Lateral Dorsal Root] Synapses in Nucleus Proprius of [Gray Dorsal Lateral Horn] to become SPINOTHALAMIC TRACT= USED FOR PAIN and TEMPERATURE OF THE BODY

B) SPINOTHALAMIC TRACT DECUSATES in [ANT Commissure of Spinal Cord] and begins ascent in the [white Anterolateral Fasciculi] —->STT then ultimately travels up to [VPL nucleus of Thalamus] via [LATERAL FUNICULUS] of spinal cord

C) Cutting STT in CORD will affect Pain on OPPOSITE of Body

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3
Q

A: [Dorsal Spinocerebellar tracts] travel in ____ ______ and synapse either on _____(below C8) OR _____(Above C8). This tract is used for ____ ______ ______

B: Muscle Spindles use Sensory Affarent fibers (which bend in the [Fasciculus ______]) and transmit __ ______ ______ to the [____ _____ _____ nucleus] located in ___ ______

C: What is the [cuneocerebellar tract] ?
**A tract that receives ______ info from ______ nucleus & then ______[contralaterally/Ipsilaterally] sends this to the __ ___ ____ which relays info to ______ ______

D: [Dorsal Spinocerebellar tracts] AND [cuneocerebellar tract] use the__ ___ ____ to enter Cerebellum Vermis

A

A: [Dorsal Spinocerebellar tracts] travel in LATERAL FUNICULUS and synapse either on [Dorsalis Nucleus of Clarke] (below C8) OR lateral accessory cuneate nucleus for UNCONSCIOUS IPSILATERAL PROPRIORECEPTION

B: Muscle Spindles use Sensory Affarent fibers to bend in the [Fasciculus CUNEATUS] and transmit UE unconscious positioning to the LACN [lateral accessory cuneate nucleus] located in Lower Medulla.

C: [cuneocerebellar tract] = tract that receives UNCONSCIOUS positioning info from LACN [lateral accessory cuneate nucleus] & then ipsilaterally sends this to the ICP—> Cerebellum VERMIS

D: [Dorsal Spinocerebellar tracts] use the [inferior cerebellar Peduncle] to enter Cerebellum Vermis

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4
Q

A: How are the Bipolar Cells, Internueonrs & Ganglion cell bodies arranged near the Fovea? What about blood vessels?

B: How does Fovea and surrounding Macula receive metabolic supply?

C: Fovea is an _____[vascular/Avascular] retinal area with the ___[least/most] visual acuity. It has a __ ___ ____layer to prevent light barrier and is EXCLUSIVELY _____. There is a 1:1 ratio with [__:___] -which means ___ are more specific

D: Fovea is only __% of Retina and transmits __[least/most] of visual information to ________

A

A: Near Fovea, Bipolar Cells, Interneurons & Ganglion cell bodies are pushed LATERALLY–>makes a clear path for light = High visual acuity.
**Fovea is also Devoid of any blood vessels for same reason

B: Since Fovea is Devoid of any blood vessels, Fovea and surrounding Macula depend on diffusion from underlying choroid vessels for metabolic needs

C: The Fovea is an AVASCULAR retinal area with the MOST visual acuity. It has a laterally flat inner layer to prevent light barriers and is EXCLUSIVELY CONES. There is a 1:1 ratio with
[ganglion cell body: Cone receptor] –>Cones are more specific!

D: Fovea is only 5% of Retina but transmits MOST of visual information to [Lateral geniculate nucleus of thalamus]

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5
Q

A: What are the 7 Steps of Visual Pathway starting with light entering eye?

B: Light Entering Eye:
[TEMPORAL Field axons] pass _____ [crossed/uncrossed]
vs.
[nasal field axons] pass ____ [crossed/uncrossed], which means what for optic chiasm lesions?

A

A: Pathway of Visual Info from Retina [RN CT L DV]
RN (use) CT (to) Learn Direct Vision”
1st: Light enters —> hits Retina
2nd: Travels in Optic N.
3rd: Optic Chiasm [Temporal Field Axons CROSS HERE]
4th: Optic Tract
5th: [Lateral Geniculate Nucleus of Thalamus]
6th: Optic RaDiations [Meyer’s Temporal Loop vs. Parietal direct path]

7th: [Area 17 -Calcarine Primary Visual cortex]

B: Light Entering Eye:
TEMPORAL Retina Fields pass CROSSED = [Temporal fields] decussaTe at Optic Chiasm
vs.
nasal retina fields pass UnCrossed @ Optic Chiasm = NOT AFFECTED BY Central OPTIC CHIASM LESIONS

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6
Q

A: [P-type] ganglion cell bodies are used by _____. [M-type ganglion cell bodies are used by ______.

B: Describe each of these
[2 each]

A

A: There are 2 MAJOR classes of [innermost ganglion cell bodies]
1. P-Type [USED BY CONES] “Pretty Colors”
ºsmall receptive fields –> BEST with [color/fine detail/high acuity]
ºtons of it near Fovea

  1. M-type[used by rods]
    ºLARGE Bodies and many axons share 1 cell body –> LARGE Receptive fields
    ºBEST with [rapidly transient adaptation] &response to mvmnt or large objects
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7
Q

A: Although Visual Perception begins in ______, collateral visual info enters ____ via Pretectal Area= for ___ _____ and _____ _____ for ________

B: Pretectal Area uses ___ nuclei of _____ for ___ _____ and projects both ipsilateral & contralateral via ____ _____

A

A: Although Perception of vision begins in [Area 17 CPVC-Calcarine Primary Visual Cortex] collateral visual info enters

  • Brainstem via Pretectal Area=FOR PUPILLARY REFLEX and
  • [SUP Colliculus]=For [head&eye movement]

B: Pretectal Area uses [Edinger-Westphal nuclei] of midbrain for PUPILLARY REFLEX and projects both ipsilateral & contralateral via POSTERIOR commissure

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8
Q

What would occur if there was a Lesion in …
1. R Optic N. —->

  1. *Optic Chiasm —–>
  2. R Optic Tract—>
  3. R [lower radiation meyer’s loop] –>
  4. R [Lateral Geniculate nucleus of thalamus]–>
  5. R [upper radiation fibers]
  6. R [Area 17 CPVC]

B: Which 2 lesions present the same Visual sx?

C: Which Visual Field Decussates at Optic Chiasm?

A

Lesion in … (using R side damage as example)

  1. R Optic N. —-> BLIND RIGHT EYE
    - ——————————————————————————-
  2. *Optic Chiasm —–> [Bitemproal Heteronymous hemianopsia] (both temporal fields knocked out) since Temporal fields decussaTe at Optic Chiasm
    - ——————————————————————————-
  3. R Optic Tract—>[CTL homonymous hemianopsia]
    - ——————————————————————————-
  4. R [lower radiation meyer’s loop] –> “Pie in the Sky Lesion’ = [CTL homonymous upper quadrantanopsia]
    - ——————————————————————————-
  5. R [Lateral Geniculate nucleus of thalamus]–>[CTL homonymous hemianopsia]
    - ——————————————————————————-
  6. R [upper radiation fibers]–>[CTL homonymous LOWER quadrantanopsia]
    - ——————————————————————————-
  7. R [Area 17 CPVC]–> [CTL homonymous hemianopsia with macular/fovea sparing]
    - ——————————————————————————-

**Lesions of Optic Tract {4} and [Lateral Geniculate Nucleus of thalamus] {6} - PRESENT SAME VISUAL SX!

C: [Temporal fields] decussaTe at Optic Chiasm

CTL = Contralateral or (Left side in this case)

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9
Q

A: The Pupillary Light Reflex involves a ___ reflex and ____ reflex. Describe each?

B: After light is shone thru 1 eye, BOTH pupils constrict becuz ___ connections to [_____ nucleus] from ____ fibers traveling thru [___ ____]–> activates [Oculomotor CN3] fibers to synapse in the ___ganglion and constrict ____ _____ m.

C: What part of the brain does this test?

D: [Optic Nerve damage] presents how? Why is this?
vs.
E: [Oculomotor Nerve damage] presents how? Why is this?

A

A: DIRECT reflex = light is shone thru L pupil and the L pupil constricts
CONSENSUAL reflex= light is shone thru L pupil BUT R pupil constricts also

B: both pupils constrict becuz bilateral connections to [Edinger-Westphal nucleus] from optic nerve fibers traveling thru [SUP colliculus] activates [Oculomotor CN3] which travels to Ciliary ganglion ipsilaterally—>constrict [sphincter pupillae m].

C: Rostral Midbrain

D: Optic Nerve Damage—-> EQUAL PUPILS becuz signal is NEVER sent to [Edinger-Westphal nucleus]= NO REFLEX on either side
vs.

E: [Oculomotor CN3] damage—>[constricted pupil on 1 side and Dilated pupil on other]. Signal is sent from Optic N. but only 1 [Oculomotor CN3] is working = 1 sided constriction

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10
Q

A: Explain how the [Pupillary Dark Reflex] is transmitted?

B: Explain what causes Horner’s Syndrome and the 4 manifestations?

A

A: Darkness activates [Optic Tract] which –> terminates at hypOthalamus –> hypOthalamus sends its axons to descend in spinal cord and terminate at the [sympathetic preganglionic neurons of the T1-T3 lateral horn]–>sends its axons to [SUP cervical ganglion]–> Postganglionic axons in the [ciliary n.] –> Activate [iris Dilator pupillae m.]

B: Horner’s Syndrome= Damaged [SUP cervical ganglion]

1) loss of [Face Vasculature] –> flushing
2) loss of [Sweat/Lacrimal glands] –> (anhidrosis)
3) loss of [Eyelid Tarsal Muscles]—> (Ptosis)
4) loss of [iris Dilator pupillae m.] –> (miosis)

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11
Q

In order to change gaze & focus on very close objects you need the ____ REFLEX, which involves what 3 things?

A

In order to change gaze & focus on very close object you need the ACCOMMODATION REFLEX which involves..
1. eye convergence via [medial recti m.]

  1. Ciliary m. constriction —>Lens thicken
  2. Constriction of both pupils–>DEC light entering due to greater reflectance from close object
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12
Q

A: What are the 2 ways to Detect Motion?

B: *Motion Perpendicular to orientation axis can be detected by____ ___ ____ but___ ____is needed for more complex movements **

C: What test is used to test for Color Blindness?

A

2 ways to detect Motion
1. Image moves temporarily across retina while eye remains still = “temporal association”

  1. [Head & Eyes] move to fix the [object image] onto the fovea

B: *Motion Perpendicular to orientation axis can be detected by [Area 17 CPVC] but [V5 Temporal area] is needed for complex movements **

C: Ishihara Test

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13
Q

**DIFFERENCES BETWEEN RODS & CONES **
1. ____ are better for DAY Vision with ___[higher/lower] sensitivity to light. They Saturate only in _____ Light

  1. ____ Capture MORE light and are great for _____ Vision and ______ light. ___ have ___[FAST/slow] response time and long integration.
  2. Cones have Less photopigment AND Less amplification per cell
  3. ___ are AChromatic and ____ are Chromatic ! Explain this
  4. Which photoreceptor CAN’T do Bright Light?
A
  1. CONES are better for DAY Vision with Lower sensitivity to light. They Saturate only in INTENSE Light
  2. RODS Capture MORE light and are great for NIGHT Vision and Scattered light. Rods have slooow response time and long integration.
  3. Cones have Less photopigment AND Less amplification per cell
  4. Rods are AChromatic and Cones are Chromatic!
    **Chromatic Cones = 3 types of photopigment in Cones (each sensitive to diff visible light spectrums –> Red/Blue/Green

**AChromatic Rods= ONLY 1 TYPE of photopigment in Rods

  1. RODS CAN’T DO BRIGHT LIGHT (since they capture more light)
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14
Q

A: In the OUTER ear the ___ & ______ direct sound/vibrations to tympanic membrane

B: Once in The MIDDLE ear _______ conduct sound from the tympanic membrane to the ___ _____

C: What does the EUSTACHIAN Tube do and where is it located?

A

A: In the OUTER ear the Pinna & [EAM Ear Canal] direct sound to the tympanic membrane

B: The MIDDLE ear [MIS ossicle bones]–>{Malleus/Incus/Stapes} conduct sound from tympanic membrane to the [Oval vestibular window]

EAM = External Auditory Meatus

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15
Q

A: [Bony Labyrinth] is the __-SHAPED CAVE of the ____ ear that surrounds a bony core called the _______. It’s housed in the ____ _______ bone and has a [_____ Snail Apex]. The [Bony Labyrinth] is divided into 3 canals.

B: These 3 Canals are separated by the ____ ___ _____ & ____ ___.

C: Describe These 3 Canals

A

A: [Bony Labyrinth] is the SNAIL-SHAPED CAVE of the INNER ear that surrounds a bony core called the [MODIOLUS]. It’s housed in the Petrous temporal bone and has a [Helicotrema Snail Apex]. [Bony Labyrinth] is divided into 3 canals.

B: 3 Canals: [Scala are separated by [Reissner’s Vestibular Membrane] & basilar membrane]
1. Scala Vestibuli (Contains perilymph & is continuous with bony labyrinth of vestibular apparatus)

  1. Membranous Labyrinth (contains _endo_lymph and is inbetween 2 Scala)
  2. Scala Tympani (Contains perilymph and separated from Cochlear Duct by Basilar membrane of the round window)
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16
Q

A: [Membranous Labyrinth] is filled with ______ & forms the ___ ____ (or ___ ____) which contains [________]. This is where __________

B: How far does the Cochlear Duct extend throughout the cochlea in the [Membranous Labyrinth]?

A

A: [Membranous Labyrinth] is filled with ENDOLYMPH & forms the COCHLEAR DUCT (or scala media) which contains [Organ of Corti]. This is where sound wave transduction—>nerve impulses occur.

B: Cochlear Duct extends throughout the cochlea, EXCEPT FOR HELICOTREMA

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17
Q

1) The [Organ of Corti] contains __inner row and __ OUTER rose of hair cells. Describe each of these rows (OUTER vs. inner row)
2) What are Stereocilia
3) Is hearing an Active or passive process?

A

[Organ of Corti] contains 1 inner row and [3 OUTER ROWS] of [hair cell cilia]
*OUTER ROW= contain Stereocilia that insert into tectorial membrane & can receive inhibitory inputs via olivocochlear n. fibers= amplifies/sharpens/suppresses responsiveness of inner row

*inner row= When cochlear fluid displaces Basilar membrane–>displaces Tectorial membrane—-> deflects [Stereocilia of inner row to move in endolymph]–> TRANSDUCTS MOST OF SENSORY AFFERENT VIA CN8

2) Stereocilia= [Tethered Hair cell cilia] arranged in a “V” and when 1 is bent –> causes neighboring Stereocilia to bend

3) Hearing is an ACTIVE PROCESS

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18
Q

•Cochlear nerve fibers enter brainstem at ___ _____ and terminate in ___________

B: Ventral cochlear nucleus is ___[smaller/Larger] and it projects to to the _______ nuclei in the _____. What is the TRAPEZOID BODY?

C: dorsal cochlear nucleus terminates in the ___ and ____ nuclei

D: [inferior Colliculus] relays ____ info (via ____) to_____ nucleus in the Thalamus —->sends ______ projections to _______ where it is interpreted

E: [T or F] Auditory Cortex is sensitive to lesions and can easily —> sound discrimination problems

A

•Cochlear nerve fibers enter brainstem at PONTOMEDULLARY JUNCTION and terminate in [Dorsal/Ventral cochlear nuclei]

B: Ventral cochlear nucleus is LARGER and it projects to ipsilateral & contralateral [SUP olivary nuclei] in Pons. **Midline crossing of the [Ventral cochlear nuclei] axons = TRAPEZOID BODY

C: dorsal cochlear nucleus terminates in the [inferior Colliculus] and [lateral lemniscus nuclei]

D: [inferior Colliculus] relays auditory info (via brachium) to [Medial Geniculate nucleus] in Thalamus —->sends auditory projections to [Area 41 Heschl’s Gyri]

E: FALSE! Auditory Cortex Lesions have to be EXTENSIVE in order to affect sound discrimination

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19
Q

C: Where is the Tensor Tympani m. & what is it innervated by?

D: Where is the Stapedius m. & what is it innervated by?
D2: What is the OVERALL PURPOSE of these 2 Middle ear muscles?

A

C: Tensor Tympani m.= Fast Striated m. (middle ear wall fibers) near eustachian tube that attaches to Malleus
{{Innervated by CN5B3}}

D: Stapedius m.= Fast Striated m. (middle ear wall fibers) tht attaches to [Stapes] near its connection with [Incus]
{{{Innervated by Facial CN7}}}

D2: Purpose of these MIDDLE EAR m. is to DEC amplification of sound oscillation—> protect us from LOUD SOUNDS & adjust loudness of voice b4 we speak[using Facial CN7]

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20
Q

A: Describe the Semicircular Canals

C: Utricle and Saccule are Dilations of the __ ___ that contain _____ which allows them to ______ . Why can they do this? How are they related to the Maculae?

D: What’s the difference between Utricle and Saccule in regards to Planes?

E: ºThe ______ [Utricle/Saccule] connects the [3 semicircular canals]

ºThe ______[Utricle/Saccule] is continuous with Cochlea

ºBOTH Utricle & Saccule have an ______ ______ for [______, ______ & ______ detection]

A

A: 3 interconnected tubes positioned at right angles to one another in 3 planes of space (1 horizontal, 2 perpendicular)

C: Utricle and Saccule are Dilations of the [Membranous Labyrinth] that contain [Ca+carbonate Otolithic granules]—>allows them to respond to gravity/acceleration because it Adds weight. They also EACH have a Maculae which contains the [Vestibular sensory Hair cells]
——————————————————————————
1. Utricle = sensory hair cells oriented in HORIZONTAL plane = sensitive to linear acceleration/deceleration in HORIZONTAL DIRECTION

  1. SACcule =sensory hair cells oriented in vertical plane = sensitive to linear/acceleration/deceleration in VERTICAL DIRECTION. “We SAC those dudes Vertically”
    - ——————————————————————————

E:
ºThe Utricle connects the [3 semicircular canals]

ºThe Saccule is continuous with Cochlea

ºBOTH have an Otolithic Membrane for [Gravity, Acceleration & position detection]

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21
Q

[PPRF] Paramedian pontine reticular formation
1. Where is this located?

  1. What happens when this is stimulated?
  2. Describe its projection
    - ——————————————————————————-
  3. Explain what the [mesencephalic reticular formation] does and is located?
  4. A: Vestibuloocular Reflexes (VORs) reflexly move eyes in Direction ____ of Head mvmnt. It uses ____ to get from ____ and ____ to the ____

B: Absent of (VORs) means there is ___ damage

A

[PPRF] Paramedian pontine reticular formation
1. Near abducens nucleus (so sometimes called parabducens nucleus)

  1. Stimulation = Horizontal Eye movement
  2. Receives multiple afferents and projects to Ocular nuclei 3, 4 and 6 using the [Ascending MLF]
    - ——————————————————————————-
  3. [mesencephalic reticular formation] = includes a [Cajal interstitial nucleus] and controls VERTICAL eye mvmnt . Is located in the ROSTRAL [PPRF]
  4. A: Vestibuloocular Reflexes (VORs) reflexly move eyes in Direction OPPOSITE of Head mvmnt. It uses [Ascending MLF] to get from [medial vestibular nuclei] and [SUP vestibular nuclei] —->PPRF—>[CN nuclei 3, 4 & 6]

B: Absent of (VORs) = brain STEM damage

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22
Q

What are the 3 ways we can get “Dizzy”?

A
  1. Vestibular input without vision (i.e. spinning in a chair with eyes closed–> constant motion that eventually results in cupola membrane returning to its baseline)
  2. [Motion detection from Visual system] but WITHOUT [Vestibular confirmation] (looking out car window when an adjacent car moves away= false sense of motion)
  3. [Motion detection from Vestibular system] but WITHOUT [Visual confirmation] (sitting in cabin of a boat during a storm= MOTION SICKNESS)
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23
Q

Nystagmus are __ ___ ___ that have both _ and __ components (but during test refers to ___ component only) *There are 3 types*

B1. SPONTANEOUS Nystagmus is ____[sometimes/always] pathological and is caused by ___ ____ 2º to ______

B2. What are the 3 sx?

A

Nystagmus are OSCILLATING EYE MOVEMENTS that have both slow and Fast components (but test refers to Fast component only) .

B1. SPONTANEOUS Nystagmus is ALWAYS PATHOLOGICAL and is caused by [Vestibular/ Brainstem/ Cerebellum] imbalance 2º to irritating or destructive lesions.

B2: Sx= [N/V] + [bp DEC] + Tachycardia

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24
Q

A: Tracking/Smooth Pursuit involves _____ using ______. Is Tracking/Smooth Pursuit voluntary and can it be done without Visual Stimuli?

B: What is the [Fixation Reflex]? Give example

C: [Optokinetic Railway Nystagmus]? Give example

A

A: Tracking/Smooth Pursuit involves “Locking” eyes onto perceived moving object using [Occipital Eye Fields]. Although These mvmnts are voluntary, smooth sweep of eyes CAN’T be done in ABSENCE of visual stimuli

B: Fixation Reflex = same as smooth pursuit mvmnt but allows us to fix on an object when BOTH person AND object are moving [Ex: Reading road sign while driving on bumpy road]

C: [Optokinetic Railway Nystagmus] = (to-and-from) oscillating eye mvmnts made when ur fixating on moving objects [Ex: Looking @ telephone pole out window of moving train]

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25
A: Frontal eye fields are located in the __ \_\_ ___ and are considered the \_\_\_\_\_\_\_. Frontal eye fields influence ____ nuclei using ___ and \_\_\_\_ B: Lesioned [Frontal Eye Fields] will lead to what?
A: Frontal eye fields are located in the MIDDLE FRONTAL GYRUS and are considered the [center for Voluntary eye Saccades]. FEF influence Ocular nuclei using [SUP colliculus] and PPRF B: Lesioned FEF ----\>inability to look contralaterally (with reflex eye movements intact)
26
ASCENDING Medial Longitudinal Fasciculus (MLF) 1. Arises from what 2 nuclei? 2. Describe where it projects to? 3. what is its purpose? (2) 4. Explain how CROSSED Ascending MLF Fibers are different than UnCrossed Ascending MLF Fibers?
\*\*[**ASCENDING** Medial Longitudinal Fasciculus] (MLF)\*\* 1. Arises from [medial vestibular nuclei] and [SUP vestibular nuclei] 2. Projects BILATERALLY to CN3, 4 and 6's nucleus! 3. Coordinates - [conjugate Eye mvmnts] (via reticular formation) +/- [Head mvmnt = i.e. vestibuloocular reflex] 4. \*\*\*CROSSED Ascending MLF = EXCITES XtraOcular m. vs. \***UN**Crossed Ascending MLF= **inhibits** xtraocular m.
27
Describe the 3 Vestibulospinal Tracts 1. Lateral vestibulospinal tract Arises from [\_\_\_\_\_ nucleus] & descends ___ to ___ spinal cord levels to activate \_\_\_\_\_ 2. MEDial vestibulospinal tract is the MAJOR component of ___ \_\_ and comes from [\_\_\_\_\_ nucleus] . Projects to ___ spinal cord levels to innervate \_\_\_\_\_\_ 3. Spinovestibular tract
1. Lateral vestibulospinal tract Arises from [lateral vestibular nucleus] & descends ipsilaterally to ALL spinal cord levels to activate EXTENSOR motor neurons 2. MEDial vestibulospinal tract is the MAJOR component of DESCENDING MLF and comes from [medial vestibular nucleus] . Projects to CERVICAL spinal cord levels to innervate neck muscles 3. Spinovestibular tract = collaterals of spinoCEREbellar projections
28
A: _____ hair cells of the [Crista ampullaris] produce a gelatinous [\_\_\_\_\_] to cover and protect them. B: How are the Semicircular Canals paired up?
A: Stereocilia hair cells of the [Crista ampullaris] produce a gelatinous [CUPULA] to cover and protect them. B: ANT canal is parallel to POST canal from other side. Horizontal canals from both sides form functional pair together
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A: Equilibrium is Maintained and Controlled by what 3 sensory inputs? How many is needed to maintain Balance ## Footnote B: What are the Sx (3) of Vertigo? B2: Causes of Vertigo (2)?
A: Equilibrium is Maintained and Controlled by 1. Vestibular apparatus of internal ear 2. Vision 3. Proprioreception [It only requires 2 out of the 3! to maintain Balance] ------------------------------------------------------------------------------ B: **Vertigo** Sx = **DNP** = **D**izziness, **N**V and **P**allor B2: Causes: [Degenerated Ca+ Crystal Otoliths] vs. [Acute Labyrinthitis]
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What are the 6 Sensory Receptors that utilize the [Dorsal **Spinocerebellar** Tract] Pathway for ______ \_\_\_\_\_\_ \_\_\_\_\_\_.
5 Sensory Receptors that utilize the [Dorsal **Spinocerebellar** Tract] Pathway for **UNCONSCIOUS IPSILATERAL PROPRIORECEPTION** MMM JRP 1. **M**eissner's Corpuscle 2. **P**acinian Corpuscle 3. **M**erkels Disk 4. **R**uffini 5. **J**oint Receptors 6. **M**uscle Spindles
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Describe This Receptor: [**Free Nerve Ending**] 1. Is it Encapsulated? 3. Function (2) 4. Distribution (2)
[Free Nerve Ending] Receptor: 1. **NOT** Encapsulated ("*Free Hairy Merkel*") 3. Pain/Temp 4. Deep skin & viscera
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Describe This Receptor: [Merkel's Disk] 1. Is it Encapsulated? 3. Function 4. Distribution [4]
[Merkel's Disk] Receptor: 1. **NOT** Encapsulated (*"Free Hairy Merkel​"*) 3. Touch 4. Feet/hands/genitalia / lips
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Describe This Receptor: [Hair Follicles] 1. Is it Encapsulated? 3. Function 4. Distribution
[Hair Follicles] Receptor: 1. **NOT** Encapsulated ("*Free Hairy Merkel*") 3. Touch 4. Anything with Hair
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Describe This Receptor: [Meissner's Corpuscle] 1. Is it Encapsulated? 3. Function 4. Distribution [4]
[Meissner's Corpuscle] Receptor: 1. Encapsulated !! 3. 2 Point Discrimination 4. [hair*LESS* Skin] / joints / ligaments / fingertips
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Describe This Receptor: [Pacinian Corpuscle] 1. Is it Encapsulated? ] 3. Function 4. Distribution [4]
[Pacinian Corpuscle] Receptor: 1. Encapsulated !! 3. Vibration 4. Fingers & Toes / mesenteries / peritoneum
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Describe This Receptor: [Ruffini Ending] 1. Is it Encapsulated? 3. Function 4. Distribution
[Ruffini Ending] Receptor: 1. Encapsulated !! 3. Stretch / pressure 4. Dermis
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Describe This Receptor: [Joint Receptor] 1. Is it Encapsulated? 3. Function 4. Distribution [2]
[Joint] Receptor: 1. Encapsulated !! 3. Joint Position 4. [Joint Capsules] & Ligaments
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Describe This Receptor: [Neuromuscular Spindle] 1. Is it Encapsulated? 3. Function 4. Distribution
[Neuromuscular Spindle] Receptor: 1. Encapsulated !! 3. Limb muscle Stretch 4. Muscles
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Describe This Receptor: [Golgi Tendon Organs] 1. Is it Encapsulated? 3. Function 4. Distribution
[Golgi Tendon Organs] Receptor: 1. Encapsulated !! 3. MUSCLE Tension 4. Muscle tendon Junctions
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[Dorsal Posterior Horn] contains the [Substantia gelatinosa] and [Nucleus Proprius] Describe the [Substantia gelatinosa] (3)
\*\*[Substantia gelatinosa]\*\* ºIs "Pain Gate keeper" & filters sensory information by synapsing on dendrites in [Nucleus Proprius] ºHomologous to [spinal trigeminal nucleus] ºAxons ascend & descend 1 to 4 segments in [Dorsolateral Fasciculus /Zone of Lissauer]
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1. [Pain, temperature, position sense, vibration from skin/body wall and pressure] come from the ___ component 2. [Motor projections to Viscera, Glands & blood vessels] = ____ component 3. Pain, sensations of FULLNESS/STRETCH come from the ____ component \*Alar Plates derive into the \_\_\_\_/\_\_\_\_ root Basal Plates derive into the \_\_\_/\_\_\_\_\_ root
1. [Pain, temperature, position sense, vibration from skin/body wall and pressure] come from the GSA component 2. [Motor projections to Viscera, Glands & blood vessels] = GVE component 3. Pain, sensations of FULLNESS/STRETCH from viscera come from the GVA component \*Alar Plates Derive into SENSORY/DORSAL ROOT {Afferent and Alar = Sensory} \*Basal Plates derive into MOTOR/VENTRAL Root
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A: What's special about the CLOSED medulla? B: What are the Corpora Quadragemini? How is it related to "SLOW AIM" C: Describe the 3 Cerebellar Peduncles and what their attached to D: Which Cerebellar Peduncle DECUSSATES in the Caudal Midbrain?
A: The CLOSED Medulla is the part of Medulla NOT UNDER 4th Ventricle B: [Corpora Quadragemini] are 4 Colliculi tht sit on DORSUM of Midbrain and is AKA [TECUM OF MIDBRAIN]. \*\*SLOW = SUP colliculi talk with [Lateral geniculate] for Optic "WVision" \*\*AIM = Auditory system uses Inferior Colliculi which talks with [MEDIAL geniculate] -------------------------------------------------------------------------------------- C:3 Cerebellar Peduncles 1- \*\*SUP Cerebellar Peduncle = MOSTLY EFFERENT except [Ventral Spinocerebellar tract] and is in midbrain 2-MIDDLE cerebellar Peduncle= LARGEST, is afferent and attaches to Pons 3- inf cerebellar peduncle= afferent and attached to Medulla -------------------------------------------------------------------------------------- D: \*\*SUP Cerebellar Peduncle DECUSSATES inbetween [substantia nigra] of caudal MIDBRAIN ...on its way to [Red Nucleus of midbrain]
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A: [Crus Cerebri Cerebral Peduncles] are on the \_\_\_\_\_\_[Dorsal/Ventral] Midbrain and responsible ...... B: Where does the Infundibulum Stalk sit in relation to the [Crus Cerebri Cerebral Peduncles]? What does it suspend? C: Cerebellar Peduncles would stain ____ with myelin stain. Why?
A: [Crus Cerebri Cerebral Peduncles] are on the VENTRAL Midbrain and responsible for connecting Cerebrum with brainstem/spinal cord B: Infundibulum Stalk hangs Between [Crus Cerebri Cerebral Peduncles] of midbrain and suspends PITUITARY GLAND ventrally C: Cerebellar Peduncles **would stain BLACK** with myelin stain because they're white fibers lol
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A: "Pontocerebellar mossy fibers" -------------------------------------------------------------------------------------- C: Describe the Pathway of [Spinal CN11] -------------------------------------------------------------------------------------- D: What happens when the _____ \_\_\_\_\_\_ ____ squishes [Oculomotor CN3] and why?
A: "Pontocerebellar mossy fibers" = Cortex fibers that travel to [Pontine Gray Nuclei] ---\>then contralaterally travel to [MIDDLE Cerebellar Peduncle] ------------------------------------------------------------------------------- C: [Spinal CN11] goes up thru Foramen Magnum and then goes back out Cranium [Jugular Foramen] -------------------------------------------------------------------------------------- D: When the Temporal Lobe UNCUS squishes [Oculomotor CN3] ---\> LATERAL GAZE! (because CN6 Abducens just takes over)
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1. Which Artery perfuses the [LATERAL Medulla] and what Parent Artery does it come from? 2. What's the Name of Dz that occurs when this Artery becomes occluded? 3. Name the Sx of this dz and what syndrome is causes? (5)
1. The **PICA** (*Daughter of Vertebral a.*) perfuses Lateral Medulla 2. Can Cause [**Lateral Medullary syndrome of Wallenberg**] 3. causes ischmia and ---\> **L**ucy **H**as **2** **VPN** **L**imb Dysmetria *ipsilateral*- from [inf cereberllar peduncle] **H**orner's Syndrome *ipsilateral*- from [descending sympathetic fibers] **2**TVP loss *Contralaterally*-from [medial lemniscus involvement] [**V**ocal Cord/Palatal Weakness] *ipsilateral*- from [nc. ambiguous] [**P**ain & Temp] impairment *ipsilateral face/Contralateral body (STT)*- from [descending CN5, n & t] & STT **N**ystagmus- from vestibular nc.
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1) Where is the [Nucleus of Solitary Tract] [NST] located? 2) What is it responsible for? (2)
1. [NST] Nucleus of Solitary Tract are in the [Medulla] 2. Taste [upper NST] &; GVA Sensation [Lower NST]
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B: What are these Structures PERFUSED By? 6. Olive (2) 7. Basal Bons 8. [Middle cerebellar peduncle] (2) 9. [Crus Cerebri Cerebral Peduncle] 10. .[inf cerebellar peduncle] AKA ___ \_\_\_\_
PERFUSIONS! 6. Olive perfused by [PICA or actual *Parent* Vertebral a.] 7. Basal Pons perfused by Basilar a. 8. [Middle cerebellar peduncle] perfused by [AICA and Basilar a.] 9. [Crus Cerebri Cerebral Peduncle] perfused by PCA {POST cerebral a.} 10 .[inf cerebellar peduncle] (AKA RESTIFORM BODY) perfused by PICA
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A: [Lower Motor Neurons] are Motor neurons of the ___ & _____ They are arranged into 4 columns and release ____ onto _____ receptors of ____ \_\_\_\_\_ Lower Motor Neurons are recruited based on __ & \_\_\_\_ B: What are the 4 Column Arrangements and which muscles do they innervate?
A: Lower Motor Neurons are Motor neurons of the Brainstem & Spinal Cord. They are arranged into 4 columns and release ACETYLCHOLINE onto nicotinic receptors of target m. Lower Motor Neurons are recruited based on size & Force B: 4 Column Arrangement: 1. medial LMN--\>axial trunk m. 2. Lateral LMN---\>Distal Limb m. (extremities) 3. Dorsal LMN---\>FLEXORS 4. venTral LMN-------\>exTensors
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Describe the Descending pathways for Lower Motor Neurons. These all act as 1 of the ___ \_\_\_\_\_\_ in the Spinal Cord A: Corticospinal tract (lateral) B: Vestibulospinal tract [2] C: Reticulospinal tract [2] D: Tectospinal tract E: Rubrospinal tract
Descending pathways = CONTROL SYSTEM in spinal cord LMNs A: Lateral CST=ALL Excitatory (Glutamate is the transmitter) B: Vestibulospinal= Head mvmnt & postural adjustments C: Reticulospinal= locomotion & postural control D: Tectospinal = reflex of turning head in response to visual/auditory stimuli E: Rubrospinal= no significance in humans
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A: CorticoBULBar tract (AKA ___ tract) is an ____ MOTOR NEURON tht descends ANterior to _____ tract. It usually ends on ____ of the ___ \_\_\_\_\_ but sometimes ends on \_\_\_\_\_inside the \_\_\_\_. B: Name the 3 CN nucleus that do NOT receive DIRECT CorticoBULBar innervation.
A: Cortico**BULBar** tract (AKA Cortico**nuclear** tract) is an UPPER MOTOR NEURON that descends ANterior to Corticospinal tract. It usually ends on interneurons of [Reticular formation] but sometimes ends on [motor neurons of CN] inside the brainstem. B: Oculomotor, Trochlear & Abducens nucleus does NOT receive DIRECT CorticoBULBar innervation.
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Describe The Cortex Origin of **Upper Motor Neuron** for CN nuclei involving: 1. Chewing ex. *Upper Motor Neurons for Chewing (CN\_\_) comes from \_\_\_\_[R vs. BOTH] side(s) of the Cortex before reaching the Nucleus* 2. Facial Droop vs. Bell's Palsy 3. [speaking & swallowing] 4. tongue mvmnt
Cortex Origin of Upper Motor Neuron for CN nuclei involving: 1. Chewing ex. UMN for Chewing (CN5) comes from [**Both** BUT More of 1 side] before reaching Nucleus 2. *Facial Droop vs. Bell's Palsy*: UMN come from **BOTH Cortex** before reaching CN7 Nucleus --\> **ONLY 1 LMN** Innervates **Entire** Face *ipsilaterally* * Facial Droop= Lesion of Facial **UMN*** * Be**LL**s Palsy= **Lesion of Facial LMN = complete face droop*** 3. [speaking & swallowing]: UMN come from BOTH Cortex before reaching CN9 and CN10 Nucleus 4. tongue mvmnt: UMN comes from [Both BUT More of 1 side Cortex] before reaching CN12 Nucleus
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What are **Betz** cells?
Make up 3% of [CST-Corticospinal Tract] and are concentrated there Primary Motor Cortex makes up 50% of CST and the rest comes from [Adjacent Frontal motor and Parietal areas]
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Area 44 = \_\_\_\_\_\_ Area 22 = \_\_\_\_\_\_ Area 41 = \_\_\_\_\_\_ Hearing is \_\_\_\_\_\_[unilateral/Bilateral] above the cochlear nucleus \*\*99% of hearing comes from \_\_\_\_\_\_[Outer/inner] row of hair cells What is the Other row for?
Area 44 = Broca’s Area 22 = Wernicke’s Area 41 = Heschel’s Gyrus / Primary Auditory Cortex Hearing is BILATERAL above the cochlear nucleus = why it’s hard to knock out \*\*99% of hearing comes from inner row Outer row = displacement sensitive so controls tectorial membrane
54
A: The _____ Artery (\_\_\_\_\_ circulation) perfuses MOST of the CEREBRUM. It bifurcates into the ______ and ______ artery B: What are the 3 daughter branches of this Artery?
The **INTERNAL CAROTID Artery** (ANTERIOR circulation) **perfuses MOST of Cerebrum** (70%). (*Vertebral a. perfuse 30%*) It bifurcates into..... [Anterior Cerebral a.]----\>medial cortex and [middle cerebral a.]--\>lateral cortex B: Daughter branches: 1) ophthalmic artery 2) ANT Choroidal a. 3) POST communicating a.
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A: The _____ system (\_\_\_\_\_\_circulation) perfuses Brainstem, Cerebellum & Spinal Cord. It Bifurcates into ____ cerebral arteries. B: Describe this system C: What are the daughter branches for each of these Arteries?
The VERTEBROBASILAR system (POSTERIOR circulation) perfuses Brainstem, Cerebellum & Spinal Cord. B: 2 Vertebral a. Join---\> 1 Basilar ARtery--\>Bifurcates into PCA [POST cerebral a.] C: \*Basilar branches = [(AICA) ANT inf. cerebellar a.] & [(SCA)SUP cerebellar a.] \*\*Vertebral branches = PAP! (, ASA PSA, PICA) -ANT Spinal a. -POST Spinal a. -POST inferior cerebellar a.
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A: 80% of Strokes arise from occlusion in the ____ a. which is a bifurcated branch of the ______ Artery. What part of the brain is perfused by this bifurcated branch? B: What part of the Brain does the [POST cerebral a.] perfuse? [2]
80% of strokes\<-----[**middle cerebral a.**] which is a bifurcated branch of INTERNAL CAROTID ARTERY. [**middle cerebral a**.] perfuses lateral cortex B: [POST cerebral a.] perfuses Occipital lobe & Temporal Lobes (memory lost)
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A: The Circle of Willis Interconnects the ____ and ____ circulations. How does it do this exactly? B: How is it related to perfusion of **deep cerebral structures**? (2) C: What are the Anterior/Posterior Perforated Substance?
{Circle of Willis} Interconnects ANTERIOR and POSTERIOR circulations. It forms 1. [ANT communicating a.] between the two [ANT cerebral a.] and [POST communicating a.] between [Internal carotid] and [POST cerebral a.] B: [Circle of Willis] surrounds brain base it gives rise to small perforating ganglion arteries (*via MCA*) called [**lenticulostriate a.**] --*perfuse*---\> **[deep cerebral structures (*internal capsule/basal ganglia/thalamus*)]** C: entry points of perforating a. on Brain Base
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Blood Brain Barriers are formed by _____ \_\_\_ \_\_\_\_\_which use ___ junctions between ____ cells to filter blood coming from \_\_\_\_\_\_\_. B: What are Pericyte? Where is it located (2)?
Blood Brain Barriers are formed by [ASTROCYTE GLIAL CELLS] which use TIGHT junctions between ENDOTHELIAL cells and [ENDOTHELIAL CELL LAMINA] to "gatekeep" blood coming from from CAPILLARIES(which never make direct contact with brain tissue) B: Pleuripotent cell that gives rise to other blood vessels and regulates endothelial cells. Located [under basal lamina] but [ON TOP OF ENDOTHELIUM]
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The Brain is \_\_\_% of Body weight BUT uses \_\_\_% Oxygen! A: metabolic: INC neuronal activity---\>\_\_\_\_\_\_\_\_ released ---\>[\_\_\_\_\_\_ _______ \_\_\_\_\_\_\_ activation]---\>\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_released at feet ---\> applied to vessels to ________ \_\_\_\_\_\_\_\_ in that area B: How is Control of Blood Flow AUTOregulated? C: How is Control of Blood Flow regulated neuronally? D: What is the normal Flow of Blood and what happens when that number is low? [2]
Brain is 2% Body Weight BUT uses 25% Oxygen! *-Control of Blood Flow:* A: metabolic: INC neuronal activity---\>Glutamate released ---\>[astrocyte feet receptor activation]---\>VasoDIOLATES factors released at feet ---\> applied to vessels to DILATE VESSELS IN THAT AREA B: AUTOREGULATION: Arterial & Smooth muscle cell mediated C: neuronally: autonomic fibers innervate Cerebral vessels D: Normally= [55 ml Blood/100 g in 1 minute] 20 ml = neurons stop electrically firing 10 ml = NECROSIS OF BRAIN!
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Valveless Cerebral Veins ---(drain into)---\>\_\_\_\_\_\_\_\_\_\_\_-----(drain into)-----\> _____ \_\_\_\_\_\_ ______ + [Basilar Venous Plexus] B: The [Basilar Venous Plexus] drains mostly ____ \_\_\_\_\_ and communicates with +\_\_\_\_\_\_\_\_\_\_\_\_\_ C: Where does the [Cerebellum and Brainstem] draiiin their veiiiinnns?
Valveless Cerebral Veins---(drain into)---\>[DURA VENOUS SINUSES]----(drain into)----\> [INTERNAL JUGULAR VEIN] + [Basilar Venous Plexus] B: [Basilar Venous Plexus] mostly drains BASE OF BRAIN and communicates with [SPINAL CORD EPIDURAL VENOUS PLEXUS] C: [Cerebellum and BrainSTEM] drain their veins into the [GREAT VEIN OF GALEN]! (along w/Deep Veins)
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Describe the 2 Major Divisions of Cranial Venous Drainage -Superficial Veins (5) vs. Deep Veins (6)
\*\*\*\*Superficial Veins\*\*\* 1. Superficial group = Dumps INto Superior/inferior Sagittal Sinuses 2. Inferior group= empties with transverse AND cavernous sinus ----\>[SUP/inf sagittal sinus]----\> \*\*[SINUS CONFLUENCE]\*\*----\>Transverse sinuses---\>IJV vs. Deep Veins = empty into [Internal cerebral Veins] ---\>[GREAT VEIN OF GALEN]-----\>Straight Sinus----\>\*\*[SINUS CONFLUENCE]\*\*-----\>Transverse sinuses ------\>IJV
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*What does the CT scan delineate?*
**SubArachnoid Hemorrhage** going into the Cisterns
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A: What type of Nystagmus does *Drugs/Metabolic* produce? B: What type of Nystagmus does ***A**natomical lesions* produce? C: Give an example of **Physiological Nystagmus**
A: **Symmetrical** Nystagmus B: **A**symmetrical nystagmus C: Rotating in a swivel chair and then suddenly stopping
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A: MOD for **Bell's Palsy** B: Clinical Manifestation (3) C: Cause D: Short-term tx
A: Be**LL**s Palsy= _Sudden and Non-traumatic_ Lesion of Facial **L**MN = **complete** face droop + [possible taste loss over *ipsilateral* ANT Tongue (*chorda tympani branch*)] + [possible *ipsilateral* hyperacusis (*stapedius branch*)] C: [Facial CN7 inflammation in petrous bone (*possibly viral*)] D: Steroids
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List Clinical Manifestation for these **Facial CN7 lesions** 1. [Facial CN7 LMN] 2a. [*Petrous Bone:* Chorda tympani fibers] 2B. [*Petrous Bone*: Stapedius fiber] 3. [*CAAN-* *C*erebellopontine *A*ngle *A*coustic *N*euroma] 4. [Pontine Lesion]
**FTSDL** ## Footnote [**F**acial Paralysis *ipsilateral* / **T**aste loss / **S**ound sensitivity INC / **D**eafness&Tinnitus / **L**ateral Gaze impairement] 1. [Facial CN7 LMN] = **F** 2a. [*Petrous Bone:* Chorda tympani fibers] = **FT** 2B. [*Petrous Bone*: Stapedius fiber] = **FTS** 3. [*CAAN-* *C*erebellopontine *A*ngle *A*coustic *N*euroma] = **FTSD** 4. [Pontine Lesion] = **FTSDL**
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**Brain Stem Synromes** *Describe:* A: Brain stem lesions (2) B: [R Pontine Infarct] (2)
A. **Brain stem lesion** --\> - ipsilateral CN deficit - *Contralateral* UMN limb weakness B: **R Pontine Infarct**--\> - [R LMN Facial Weakness from CN7 deficit] - [L Hemiparesis from (Corticospinal Pyramidal tract) deficit]
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**Stroke - Brain Stem Syndromes** *Describe:* [**Medial Midbrain of Weber syndrome**]
A. [**Medial Midbrain of Weber syndrome**] \*\*Occlusion of [POST Cerebral a.] --\> 1. *ipsilateral* CN3 lesion 2. *Contralateral* hemiplegia (*Cerebral Peduncle*)
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A: Explain the \*Rinne Test\* [3] B: What two **Auditory Defects** does it differentiate between?
1st: Place vibrating tuning fork on mastoid process of suspected side. Pt should hear vibrations in that ear = **Bone** conduction route intact 2nd: While tuning fork is still vibrating move prongs of fork to [outside ear pinna]--\> where _***A****ir**conduction**is 100x more sensitive** than bone*_ 3rd: Pt should still hear sound for 15 more seconds. If pt can't hear sound for that long = air conduction deafness on that side B: Differentiates between [**Air** and **SensoriNeural: 2nd step**] defects
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A: Explain \*\*WEBER'S TEST\*\* [4] B: What two **Auditory Defects** does it differentiate between?
A: WEBER'S TEST 1st: Tuning Fork placed on Skull midline 2nd: Normally sound is conducted simultaneously by both [ossicular air] and [bone] routes which are out of phase w/each other (1vibration up and 1vibration dwn) 3rd: Being out of phase---\>Cancel each other out on both sides of head--\>sound perceived as coming from midline 4th: If [ossicular air] route loses conduction, cancellation effect on tested ear is DEC and net vibration will be GREATER on the AFFECTED SIDE * can also be caused by [CTL Ear has SensoriNeural defect]* B: Differentiates between [**Air** and **SensoriNeural** **defect: 1st step**]
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A: Clinical Course of **Carbon Monoxide Poisoning** B: Tx C: Which drugs cause **Drug-related Stroke Syndrome** (4)
1st: HA / vomiting / blurred vision 2nd: Coma / Seizures / Cardiopulm arrest (*Amnesia / Parkinsonism*) B: [Hyperbaric O2 chamber] C: [Cocaine (most common) / Amphetamine / PCP / LSD]--\> *vasoconstriction or abrupt HTN--\>cerebral infarct/hemorrhage*
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A: Describe the 2 stages of **EtOH Withdrawal** B: What factors can be _Fatal_ during **EtOH Withdrawal** (2) C: When is a *Brain Scan* during **EtOH Withdrawal** warranted?
1. [**Early Hypersympathetic Stage**] = tremors + sweaty + tachycardia + [limited convulsive *Tonic--\>Clonic* seizures] tht occur 12 hrs-3 days post drinking] 2. [**Later (*3-4 days post drinking*) Delirium Tremen Stage**] = [Fluctuating motor/autonomic activity] + confusion + hallucinations(visual and auditory) B: Coexisting infectio vs. Trauma C: If pt has [Partial / Focal Seizure] this suggest focal lesion
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**_Chronic_ Alcoholism Syndrome** A: Causes (3) B: What type of Head Trauma can it cause? (2) C: Clinical Manifestations (4)
A: - EtOH itself - Malnutrition from EtOH - Vitamin (*B1*) Deficiencies from EtOh B: [Subdural vs. Cerebral Hemorrhage] C: 1. [Wernicke Encephalopathy] ---\> [Korsakoff Psychosis] 2. [Alcoholic (ANT SUP Cerebellar vermis) Degeneration] 3. Peripheral Neuropathy 4. Dementia
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**_Chronic_ Alcoholism Syndrome** A: [Wernicke Encephalopathy] - Sx (4) - Tx B: [Korsakoff Psychosis] -Sx of [Korsakoff Psychosis]
A: **[Wernicke Encephalopathy]** - [Nystagmus vs. Ophthalmoplegia vs. (Gait ataxia) vs. Confusion] - Tx = *Thiamine* *B1 supplement* B: **[Korsakoff Psychosis] = CHRONIC PHASE!** -Amnesia compensated with Comnfabulation
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A: Brain uses **\_\_\_\_\_** metabolism intaking [\_\_\_% Cardiac Output] and [\_\_\_\_% O2 consumption] B: Describe pathogenic course once **Cerebral ischemia** occurs (2) C: Which *brain cells* are **most** ischemia sensitive? (4) D: Which *brain cells* have variable ischemia sensititvity (3)
A: Brain uses **Aerobic** metabolism intaking [20% Cardiac Output] and [15% O2 consumption]. ## Footnote *Brain has NO O2 reserve = SENSITIVE TO ISCHEMIA* B: Post cerebral ischemia --\> [Normal for 8-10 seconds] --\> [**Irreversible Damage** **AFTER** **6-8 minutes!**] C: Neurons \> Oligodendrocytes \> [Endothelial Cells] \> Astrocytes D: 1. Cerebellar Purkinje 2. [(**SHC-S**ommer's **H**ippocampus **C**A1) Pyramidal neurons (*long term memory*)] 3. [Cortex Watershed Layers 3 & 5] Pyramidal neurons (***--\>Laminar Necrosis if pt survives Global ischemia longer than 3 days***)
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A: What type of pathology makes up the lesser porition of **Stroke** cause? Describe its etiologies (2)
A: **Intracranial Hemorrhage** makes up 15% of causes of Stroke (*Cerebral Ischemia is most common*) - Intraparenchymal Hemorrhage (HTN vs. amyloid) - SubArachnoid Hemorrhage (Saccular Aneurysms vs. AVM)
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A: **Brain** **Histology** post *Global Cerebral Ischemia* (3) B: When do these **Histological** changes occur?
A: - [**Red Dead Neurons**] (*neuronal cytoplasm appears red because necrosis attracts eosinophilia*) - DEC Nissl substance - Dark Pyknotic nuclei B: [6-12 hours post insult]
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What type of **Necrosis** most likely occurs in the *Watershed Areas of the Cortex*? B: Describe these *Watershed Infarcts*
**Laminar Necrosis** of [Cortex Watershed Layers 3 & 5] Pyramidal neurons ----\>Laminar Necrosis if pt survives *Global* ischemia longer than 3 days B: Wedge-shaped areas of hyperemia and softening (*particularly in ACA and MCA Watershed Zones*)
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A: **Ischemic** stroke --\> what kind of neuro deficits? A2: Where do [*In-Situ Thrombotic* strokes] typically occur? B: [_Small Vessel_ SubCortical infarct] occurs from _____ (*embolism or thrombosis*). What's the MOD of **Lacunar Stroke**? C: Describe **Lacunar Syndrome** (2)
A: Ischemic Stroke --\> **Focal** neuro deficits (*In-Situ* *Thrombotic vs. Embolic*) A2: Thrombotic= [Bifurcation of Internal Carotid and MCA] B: [_Small Vessel_ SubCortical infarct] occurs from [***In-Situ Thrombosis***] (Large Vessel Dz can be Thrombosis or embolism): * lenticulostriate vessels perfuse [**B**e **TIPC**]* 1) **Lacunar Stroke**= ischemia of lenticulostriate vessels --\> [cystic infarcts \< 1.5 cm (*mostly seen with* *MRI*)] --\> Lacunar Syndrome (listed below) 1A: [*I*nternal Capsule/*P*ons/*C*orona Radiata] Stroke--\> pure Motor stroke (*ataxia vs. hemiplegia vs. clumsy hand*) 1B: *T*halamu**S** Stroke --\> pure **S**ensory stroke 1C: *B*asal Ganglia - not included in Syndrome *Note: Lacunar lesions may be WITHOUT sx*
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A: Describe the Radiographic finding below B: Clinical Presentation (3)
A: MRI Brain: Ischemic hemispheric infarct of the [MCA territory] --\> Midline shift B: 1) CTL [Hemiparesis / Hemisensory loss/ Visual field deficits] affecting lower face and UE \> leg 2) Hemisphere infarct will be associated with [**CTL** **expressive aphasia]** 3) [Non-involved hemisphere *ipsilateral* **neglect syndrome**]
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A: What 2 factors are the **Gross & Micro findings** post **Ischemic infarction** dependent on? B: Describe the Gross findings of the brain from an **Acute Ischemc Infarct** (3) C: What pathology is shown in the image below? Describe its features (3)
A: [Time after insult (*acute vs. subacute vs. remote*)] and [Embolic(**red**) vs. Thrombotic(**pale**)] B: *Brain* *Image on L* 1) Swelling / softening / pallor of brain parenchyma 2) Indistinct border 3) Blurring of Cortex/DEC **White** matter differentiation C: **SUB**Acute Ischemic Infarct = [More Distinct Borders] + [Tissue Liquification] + [Early PMN & Late macrophages/vascular proliferation]
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What type of **Cerebral Infarct** is depicted in image?
**Remote MCA Infarct** (*will have _cystic spaces_*)
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A: What type of **Cerebral Infarct** is depicted in image? B: Features of this infarct (3) C: Which artery is *most commonly* responsible for this type of infarct? D: MOD
**Embolic Infarct** ## Footnote 1) [Usually smaller & centered at gray-white jxn] 2) Can be single or multiple 3) May involve more than 1 vascular territory C: **MCA** D: Can occlude *Large* Artery at origin OR [occlude *Large* Artery and then **embolize** to [*Distal Large A.*]
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A: What type of **Infarct** is depicted in image? B: typical size of infarct C: Where does this infarct (5) D: Cause (2)
**Lacunar Infarct** ## Footnote B: small (*no more than 1.5 cm*) and cystic C: **B**e **TIPC** [(**B**asal Ganglia) /**T**halamus / **I**nternal Capsule/ **P**ons / **C**orona Radiata which all = SubCortical *White* Matter)] D: 1) HTN (*Arterial Hyalinosis*) 2) [small vessel dz]
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A: **Hemorrhagic** _Infarctions_ are usually ______ in nature ***Intracranial hemorrhage*** B: Name the common cause of [**Above** Arachnoid] ***Intracranial hemorrhage***. List 2 examples. C: List the 2 *Types* of [**BELOW** Arachnoid] ***Intracranial hemorrhage*** and what their caused by
A: **Hemorrhagic** _Infarctions_ are usually *Embolic* in nature ***Intracranial hemorrhage*** B: **Above** Arachnoid: Traumatic causes (*Epidural and SubDural Hematomas*) C: **BELOW** Arachnoid: Cerebrovascular Dz is cause - **S**ub**A**rachnoid **H**emorrhage (*usually from Aneurysms*) - Parenchymal Hemorrhage (*usually from HTN*)
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A: List the *Common Locations* for [**Parenchyma** **HTN Hemorrhages**] (4) B: Which vessels contribute to [**Parenchymal HTN Hemorrhages**] and is associated with [***Pseudoaneurysm Rupture***]? (3) What is the name of this particular phenomena?
A: 1. Putamen 2. Thalamus 3. Pons 3. Cerebellum B: [**Charcot Bouchard**]: 1. Lenticulostriate arteries 2. Paramedial pontine vessels 3. Short circumferential vessels of Cerebellum & white matter * similar distribution as lacunar infarcts. Histo with minimal tissue necrosis but does have cystic spaces containing macrophage-laden hemosiderin*
86
**Cerebral Ischemia** manifestation varies based on *Age Of Infarct*: *Describe...* **ACUTE** A: Time period B: Gross (2) C: Micro (2)
A: 6 - 48 hours B: [pale, soft , swollen] + [**in**distinct border/blurred grey-white junction] C: 1. 6-48 hours= [**Dead Red Neurons**] + Pallor Edema 2. 1-3 Days= Neutrophil infiltration + Necrosis
87
**Cerebral Ischemia** manifestation varies based on *Age Of Infarct*: *Describe...* **SubAcute** A: Time period B: Gross (5) C: Micro (3)
A: [2 days - 3 Weeks] B: Gelatinous / Friable / **Distinct** Border / [Tissue liquefaction] / [Glial Scar ( *\>2 weeks*)] C: [early neutrophils]--\> [macrophages in 3-5 days] ---\> [vascular proliferation & reactive gliosis in 1-2 weeks]
88
**Cerebral Ischemia** manifestation varies based on *Age Of Infarct*: *Describe...* **Chronic** A: Time period B: Gross (3) C: Micro (2)
A: [\> 3 Weeks] B: Cystic / [+/- Hemosiderin staining] / [2° Degeneration] C: - [Astrocytic Gliosis] - [Residual Macrophages]
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A: Causes of [**SAH**- ***S**ub**A**rachnoid **H**emorrhage*] (4) B: Labs C: [**SAH**​- ***S**ub**A**rachnoid **H**emorrhage*] MOD D: [**Berry Saccular Aneurysm**] MOD E: What 3 Dz's are [**Berry Saccular Aneurysm**] associated with?
"[**A**n**_T_**i **AA**] led me straight to the **SAH**" A: - **A**neurysm (*Berry Saccular Aneurysm*) = COMMON *NON-TRAUMATIC* CAUSE - **T**rauma = MOST COMMON ***OVERALL*** CAUSE - **A**VM - **A**nticoagulation B: CSF with xanthochromia (*yellow hue from bilirubin*) C: "Berry-like" thin-walled (*no media*) outpouchings from arterial branch points --\> Rupture at the dome --\> Global Vascular spasm --\> Global cerebral ischemia D: Outpouching of [Circle of Willis: **ANT *Communicating* Artery**] 2º to [Tunica media congenital defect]---\> Rupture at the dome --\> **S**ub**A**rachnoid **H**emorrhage = 50% Fatality within first 24 hours, but **most are asx until rupture** - [Auto Dom Polycystic Kidney Dz] - [Ehlers-Danlos] - Marfans
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**Intraventricular Hemorrhage** A: Demographic B: Where does the **Hemorrhage** occur
A: Premature Infants (*RARE IN ADULTS*) B: **Germinal Matrix** beneath ependyma(*easily ruptures into ventricles*)
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**Duret Hemorrhage** MOD (2)
A: _Herniated [**TUMTL**-*Transtentorial Uncal Medial Temporal lobe*]_ from various mass lesions (*hemorrhage/neoplasm*) --\> 1. **Pons Compression** 2. Perforating Arteriole stretching --\> ischemia
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A: What type of **Cerebral Pathology** is depicted in image? B: MOD C: Prognosis
**Epidural Hematoma** ## Footnote B: [Temporal Bone Fracture] --\> [**Middle Meningeal Artery** rupture]--\> [Football/Lens shaped lesion from blood between dura & skull] C: Pt may be lucid b4 any neuo signs manifest *but* Herniation is lethal complication
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A: What type of **Cerebral Pathology** is depicted in image? B: MOD C: Prognosis D: Demographic *and* Why them?
**Subdural Hematoma** ## Footnote B: [Truama vs. Age] -\> [Tearing of bridge veins between Dura & Arachnoid] --\> [*Crescent* shaped lesion] C: Progressive neuro signs but Herniation is lethal complication D: Elderly (*A**ge-related cerebral atrophy stretches bridging veins*)
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Describe: A: **Tonsillar** Herniation B: **Subfalcine** Herniation
A: [Cerebellar tonsils] --*herniates into*--\> [Foramen magnum]--\> Brainstem compression --\> Cardiopulm arrest! B: [Cingulate Gyrus] --*herniates into*--\> [Falx Cerebri]--\> [**ACA** compression] --\> infarct
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Describe: A: **Uncal** Herniation (*including which _3_ vessels it affects*) B: What are the manifestation of each vessel affected C: Which *Letter* in image below is associated with **Uncal** Herniation
[**TUMTL**-*Transtentorial Uncal Medial Temporal lobe*] --*herniates under*--\> [Tentorium Cerebelli]--\> Compression of [**POP- *P****CA / **O**culomotor CN3 / **P**aramedian Pontine vessels*] --\> 1. [Occipital lobe infarct from **PCA** compression] ( ---\>*CTL homonymous hemianopsia w/Macular/fovea sparing*) 2. ["Down and Out" Eye + Dilated Pupil] 3. **Duret Hemorrhage** (*with Pons compression*) C: **{**letter **C****}**=**Duret Hemorrhage**
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*Identify*
A- [**Middle Cerebral Artery** Infarct] B1 - **Subfalcine** Herniation B2 - [**TUMTL**-*Transtentorial Uncal Medial Temporal Lobe*] Herniation C - **Duret Hemorrhage** (*comes from* **TUMTL** Herniation)
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A: [*Snellen Wall Chart*] is used for **Visual Acuity**. What does *20/100 vision* actually mean for a pt? B: What does a **Negative Pinhole Result** (*pt vision does **not** improve when looking through pinhole*) possibly indicate? C: Is the Optic Nerve *lateral or medial*? Identify the structures in the image
A: [Pt reads at 20 feet] what a [normal person would read at 100 feet] in that eye B: Visual problem may be **neurological** C: Optic Nerve is **Medial**. So [R = [Optic Disc w/ Optic N.]] vs. [L = Macula]
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*Describe:* A: **Physiological** Blindspot A2: What happens to this Blindspot during Papilledema B: **Pathological** Blindspot (AKA ____ ) C: How do you differentiate [Glaucoma/Retinal Degeneration] from [Psychogenic Tunnel Vision] in pts with *Constricted Visual Fields*
A: Normal Blind spot that occurs due to **Optic disc having no rods/cones** (*center of vision*). This ENLARGES with papilledema from INC ICP B: **Pathological** Blindspot (AKA **SCOTOMA**) occurs from [Ocular/Retinal/Optic N.] Disorder. Usually in 1 eye. C: - If Pt Visual Field enlarges once you move target away from them = [Glaucoma/Retinal Degeneration] - If Pt Visual Field _continues_ to be *Constricted* even as you move target away from them = [Psychogenic Tunnel Vision]
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A: What type of **Visual Defect** would result from a *Bilateral Outer Chiasm lesion*? B: What type of **Visual Defect** would result from [***PCA-P**ost **C**erebral **A**rtery*] dz (2) B2: This defect would still have what things intact (2)
A: Heteronymous (*Bilateral*) **Nasal** Hemianopsia ## Footnote B: 1. Cortical Blindness from Bilateral Occipital lobe infarct vs. 2. [CTL homonymous hemianopsia w/Macular/fovea sparing] from Unilateral Occipital lobe infarct B2: Normal [Pupillary light reflex] & [No Optic Atrophy]
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A: Nystagmus are __ \_\_\_ ___ that have both _ and __ components (but during test refers to ___ component only) \*There are 3 types\* B1: Describe the [**IPNB- I**nduced **P**ostrotatory **N**ystagmus of **B**arany] B2: What does this test ultimately indicate
Nystagmus are OSCILLATING EYE MOVEMENTS that have both slow and Fast components (*but test refers to Fast component only)* B1.[**IPNB- I**nduced **P**ostrotatory **N**ystagmus of **B**arany] = Rotation of Head by 45º (*Dix-Hallpike maneuver*) sets endolymph of [**Post semicircular canal**] in motion---\>causes deflection of stereocilia hair cells. B2: If Nystagmus occurs after this = overly sensitive [**Post semicircular canal**] on the side being lowered. = Positional Vertigo
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Nystagmus are __ \_\_\_ ___ that have both _ and __ components (but during test refers to ___ component only) \*There are 3 types\* B1. [**Induced CALORIC Nystagmus**] is when irrigation of the ____ \_\_\_ \_\_\_\_with warm/Cold water creates\_\_\_ _____ in the ____ \_\_\_\_\_. This as a result stimulates ______ by \_\_\_\_\_\_ B2: What does [Cold water vs. Warm water] do during *Nystagmus testing*? What test is used for this? C: What does the [Induced CALORIC Nystagmus] test for? (2)
Nystagmus are OSCILLATING EYE MOVEMENTS that have both slow and Fast components (*but test refers to Fast component only)* . B1. **[Induced CALORIC Nystagmus]** is when irrigation of [External Auditory Canal] with Cold/Warm water creates convection currents in *Vestibular labyrinths*---\>stimulates [crista ampullaris] by deflecting stereocilia B2: **COWS** (*ENG-Electronystagmogram*)= * *C**old Water---\>Eyes move **O**pposite direction of irrigation * *W**arm water --\>eyes move in **S**ame direction of irrigation C: test function of individual semicircular canals (_ESPECIALLY LATERAL CANAL_) & [Brainstem normality]
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A: Why is having a *Complete* **Circle of Willis** so important B: Name 3 important **Circle Of Willis** collaterals
A:[Ischemic infarct] 2º to [Cerebral a. occlusion] can be circumvented if competent [Circle of Willis] collateral circulation detours inadequate blood flow. B: Example: *If Internal Carotid becomes occluded....Collaterals =* 1) **Basilar a.** (*via PCA and PICA*) 2) [**Ipsilateral** **External Carotid a.**] (***retrogradely from ophthalmic a.)*** perfusing [Intracranial Internal Carotid A.] 3) [**CTL** **Internal Carotid a.**] (*via ACA and AICA*)
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A: Define [**TIA**-***T****ransient **I**schemic **A**ttack*] B: What usually causes it? C: [**Carotid-area** **TIA]** manifestation (2) D: [**Vertebrobasilar-area TIA]** manifestation (2)
A: **Reversible** **Stroke with sx** that resolve in a [**_less than_ 24 hour period (usually 10-20 min.)**] = 3rd leading Cause of Death in Developed countries! B: Embolus (*fibrin vs. platelets vs. cholesterol*) C: - [**Amaurosis Fugax monocular blindness**] (*lowered dark shade*) - Hemispheric syndromes (*aphasia & hemiparesis*) D: - [Brainstem vs. Cerebellar] ataxia & diplopia - Homonymous Hemianopsia
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Name the most common **Cardiac sources** of **Emboli** to *Large* Arteries (5)
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A1: *Radiographic* evaluation of any **Cerebral Ischemic Infarct** (2). Why? A2: *Vascular* evaluation of any **Cerebral Ischemic Infarct** (2) A3: *Cardiac* evaluation of any **Cerebral Ischemic Infarct** B: What else should be done to work this up (2) C: List Other DDx with similar presentation (4)
*(TIA vs. [Cortical Large Artery Ischemic Infarction]**)* A1: 1st Choice: [Brain **MRI**] = confirms suspected vascular territory involved if infarct occurred 2nd Choice: CT A2: [Carotid US vs. MR/CT/Catheter Angiogram] A3: Echocardiograph B: Also Determine sources of emboli and other infarct causes C:[Atypical tumor] vs. Hemorrhage vs. Abscess vs. Encephalitis
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A: What pathology is depicted in image? B: MOD C: Describe the associated **syndrome** with this pathology (2)
A: Multiple **Lacunar Infarcts** B: **Lacunar Stroke**= ischemia of lenticulostriate vessels --\> [cystic infarcts \< 1.5 cm (*mostly seen with MRI*)] --\> Lacunar Syndrome C: Lacunar Syndrome: * lenticulostriate vessels perfuse [**B**e **TIPC**]* 1) Lacunar Stroke= ischemia of lenticulostriate vessels --\> [cystic infarcts \< 1.5 cm (mostly seen with MRI)] --\> Lacunar Syndrome (listed below) 1A: [**I**nternal Capsule/**P**ons/**C**orona Radiata] Stroke--\> pure _Motor_ stroke *(ataxia vs. hemiplegia vs. clumsy hand)* 1B: **T**halamuS Stroke --\> pure Sensory stroke 1C: Basal Ganglia - not included in Syndrome *Note: Lacunar lesions may be WITHOUT sx*
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A: [Acute Cerebral Infarction] **1st line tx** (2) B: What tx is used if **1st line tx** is not available? (2) C: What *other* management should be done (3)
A: Thrombolytic Drugs (*tPA*) 1. [IV tPA _within 3 hours of stroke_ onset] 2. [intra**A**rterial tPA] to break up clot in stroke center B: Antiplatelet drugs (*or anticoagulant drugs in RARE situations*) C: - Control BP!! - Control Hyperglycemia - Control other complication (*edema / sepsis*)
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A: Which Rx is given to **prevent** **_C_**ardiac Emboli (*especially from aFib*) (2) B: Rx given to **prevent** [TIA/Small vs. Large cerebral ischemic infarct] (3) C: What are 2 other good **preventative** Rx for Cerebral Ischemia. Which has caveots? Describe the caveot.
A: Heparin vs. Warfarin = **Anti**_C_**oagulants** B: [ASA vs. Clopidogrel vs. Dipyridamole] = **AntiPlatelets** C: - Control Atherosclerosis - Carotid Endarterectomy (*only for **symptomatic**-flow limiting [NON-Cranial Internal Carotid A.] with 70-99% Stenosis*)
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**Cerebral** **_Hemorrhage_** A: List Causes (6) A2: Which is MOST COMMON and where does it affect (2) B: Sx (3). *Which Sx helps to differentiate **Cerebral Hemorrhage from Infarct*** C: Radiographic scan used to diagnose
*High arterial pressure --\>blood rupture into brain* ## Footnote A: "Can't hear yo **C**_H_**ATTA**, if I'm Bleeding in Ma Brain!" 1) [**H**TN-Uncontrolled] = MOST COMMON (*can also be from illicit drugs*). Affects basal ganglia & thalamus most commonly 2) **T**rauma 3) [**C**oagulopathy DEC] (*usually accompanied with systemic bleeding*) 4) [**A**VM rupture]-*Use angiography to visualize* 5) [**T**umor vs. Ischemic Infarct] 6) [**A**myloid Angiopathy in Elderly] B: [_Early_ impairment of consciousness] is **not** usually associated with infarct. + HA + [INC ICP/edema --\> potential local ischemia] C: **CT Scan** (*since it'll show location & severity*)
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A: What Afferents travel TO the Thalamic [Lateral Geniculate] nc. (2) B: Where does the **Efferent** fibers of the Thalamic [Lateral Geniculate] nc. project to? C: What type of Thalamic nucleus is the [Lateral Geniculate]
[Lateral Geniculate nc.] "**L** for **L**ight! " A: Aff= Optic Tract & [SUP colliculus] --\> nc B: Eff= nc---\> [Area 17 CPVC] C: [Specific Relay nuclei]
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A: What Afferents travel TO the Thalamic [medial Geniculate] nc. B: Where does the **Efferent** fibers of the Thalamic [medial Geniculate] nc. project to? C: What type of Thalamic nucleus is the [medial Geniculate]
[medial Geniculate nc.] "**M** for **M**usic" A: Aff= [inf colliculus] --\> nc B: Eff= nc---\> Primary Auditory Cortex C: [Specific Relay nuclei]
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A: [Lower Motor Neurons] are Motor neurons of the ___ & _____ They are arranged into 4 columns and release ____ onto _____ receptors of ____ \_\_\_\_\_ Lower Motor Neurons are recruited based on __ & \_\_\_\_ B: What are the 4 Column Arrangements and which muscles do they innervate?
A: Lower Motor Neurons are Motor neurons of the Brainstem & Spinal Cord. They are arranged into 4 columns and release ACETYLCHOLINE onto nicotinic receptors of target m. Lower Motor Neurons are recruited based on size & Force B: 4 Column Arrangement: 1. medial LMN--\>axial trunk m. 2. Lateral LMN---\>Distal Limb m. (extremities) 3. Dorsal LMN---\>FLEXORS 4. venTral LMN-------\>exTensors
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A: Cells of Origin for [Area 4 precentral gyrus] are called the ____ \_\_\_\_ \_\_\_\_. So...Corticospinal Tract is AKA ____ Tract B: CST starts in \_\_\_\_\_\_\_---\>forms ___ \_\_\_\_---\>which travels in _____ Capsule----\> _________ ---\>\_\_\_\_\_\_\_\_ inside Pons -----\> decusates in ___ \_\_\_\_\_---(travels in) --\>\_\_\_\_ ______ as the \_\_\_\_\_\_\_\_---\> synapse on [ANT horn cells] C1: 10% of CST fibers DON'T CROSS AT [\_\_\_ \_\_\_\_] These are called the \_\_\_\_ C2: These ______ cross over at diff levels of the __ \_\_\_\_\_to still synapse on contralateral [ANT horn cells] like the \_\_\_\_\_\_\_\_\_ D: CST Fibers are \_\_\_\_[Upper/lower] Motor Neurons and is the \_\_\_[smallest/Largest] Descending Tract E: CST is used for what type of movements?
A: Cells of Origin for [Area 4 precentral gyrus] = [**Pyramidal Betz Cells**] *So...Corticospinal Tract is AKA Pyramidal Tract* B: CST starts in [Area 4 precentral gyrus]---\>forms [CORONA RADIATA]---\>travels in [**Posterior limb**: Internal Capsule]----\> [Crus Cerebri Cerebral Peduncle] ---\>[Base of the Pontine Gray] -----\> **decusates in medullary pyramid**---(travels in)--\>[Lateral funiculus] as the [Lateral CST]---\> synapse on [ANT horn cells] C1: 10% of CST fibers DON'T CROSS AT [medullary pyramids= [ANT CST] . C2:[ANT CST] crosses over at diff levels of [Ventral Funiculus] to still synapse on contralateral [ANT horn cells] like the [Lateral CST] D: **CST Fibers are Upper Motor Neurons** and is the LARGEST Descending Tract E: CST is used for [**Fine motor movements**] like piano playing/picking up pennies
114
A: **Corticospinal Tract** originates and terminates from \_\_\_origins and consist of \_\_[#] fibers. 50% of it comes from ______ while other 50% comes from \_\_\_\_\_\_\_ B: CST projects to the __ \_\_\_&; \_\_\_\_\_. Its collaterals (both direct & indirect) travel to\_\_\_\_\_, \_\_\_\_, ______ and \_\_\_\_\_ C: CST Passes through the ____ limb of ____ \_\_\_\_\_
A: Corticospinal Tract has MULTIPLE origins and terminations and consist of ~1 million fibers. 50% of it comes from Primary motor cortex while other 50% comes from areas [Adjacent Frontal motor and Parietal areas] B: The CST projects to [Brainstem & Spinal Cord]. Its collaterals (*both direct & indirect*) travel to basal ganglia, thalamus, [reticular formation of midbrain] and sensory nuclei C: CST Passes through **POSTERIOR limb of Internal Capsule**
115
A: Define **Coma** B: **Coma** prognosis (3) C: [**Irreversible** **Brain Death**] - cause (2) - Dx - caveot
A: Sleep like [un**a**rousable *(not **a**lert/**a**wake even after pain)* vs. unresponsive] state where cortex is not functioning B: 1. **Reversible** (*only if treated in time and after a reversible cause*) 2. **Minimal Return** = [Days-weeks post cerebral anoxia] pt may appear awake + [roving eyes] + [pain response] **but still no real interaction** = *Persistent* *Vegetative State* 3. [**Irreversible Brain Death**]: - *mostly from progressive edema & neuron death and can be declared even with heart beat* * -Dx at least 6 hour observation of no imprvmnt + Absent Cerebral blood flow over 10 min on brain scan*) - (Caveot: Muscle reflexes & Babinski can be present in Coma Dx)
116
A: [Ascending Reticular Activating System] or **ARAS** plays a role in \_\_\_\_\_\_\_, \_\_\_\_\_\_\_& \_\_\_\_\_\_\_. It helps to _______ the Cerebral Cortex. B: Other "candidates" that Activate Cerebral Cortex are the...[3] C: Why does the Cerebral Cortex project TO the [Reticular Formation]?
A: [Ascending Reticular Activating System] or **ARAS** plays a role in level of alertness, [sleep-wake] rhythms & "Startle" rxns. It helps to Activate the Cerebral Cortex. B: Other "candidates" for activating Cerebral Cortex... 1. Basal forebrain---\>[Basal nucleus of Meynert]----\>ACH 2. [Orexin of LAT Hypothalamus]----\>tuberomammillary body and STABILIZES WAKE STATE 3. Cholinergic neurons near [locus ceruleus] C: Motor Cortex, influences alertness and allows focusing of attention
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A: Orexin comes from the [\_\_\_\_\_\_\_ Hypothalamus] and is responsible for \_\_\_\_\_\_\_. It makes sure _______ states are TURNED OFF! B: Narcolepsy occurs when \_\_\_\_\_\_\_ B2: What is Cataplexy? C: What are these caused by? D: The part of the Hypothalamus Orexin is synthesized in was previously considered the \_\_\_\_or ____ center
A: Orexin comes from the [Lateral Hypothalamus] and is responsible for STABILIZING WAKE STATE. It makes sure REM/Non-REM states are TURNED OFF! B: Narcolepsy occurs when pt randomly falls asleep and IMMEDIATELY enters REM Sleep. B2: w/ Cataplexy: sudden episode of REM-like muscle Weakness but during FULL CONSCIOUS AWAKEFULLNESS C: Cataplexy is caused by Autoimmune dz: Body destroying Orexin Neurons D: LATERAL Hypothalamus was previously considered the FEEDING or PLEASURE center
118
Name the *common* causes of **Coma** (2)
1. [Upper Brain Stem lesions that interupt (**ARAS**-***A****scending **R**eticular **A**ctivating **S**ystem*] 2. [Bilateral Extensive Cerebral Cortex Damage] a: Unilateral Cerebral lesion --\> Edema which affects CTL hemisphere vs. herniation compresses **ARAS** b: Toxic changes (*Drugs vs. anoxia*) --\> **DIFFUSE DAMAGE**
119
A: How should you *initially* examine an **Unresponsive pt** (4) B: Describe the **MOTOR** testing (5)
A: Examine [Brain Stem Reflexes] (_**ME** then **PB**_ = ***M**otor vs. **B**reathing vs. **P**upils vs. **E**ye mvmnt*) ***Motor** testing* 1. Withdrawal to pain = some cortical function 2. [**DecorTicate** posturing (*UE Flexion & LE Extension*)] = Cerebral Hemisphere damage 3. [**Decerebrate** posture (*ALL EXTREMITIY EXTENSION*)] = [Midbrain *Red Nucleus* lesion] 4. [Myoclonic jerks & Asterixis] = [Toxic metabolic coma] 5. [Spontaneous Nystagmus & Twitching] = [Coma 2° to *electrical status epilepticus*]
120
A: How should you *initially* examine an **Unresponsive pt** (4) B: Describe the **Eye Movement** testing (2)
A: Examine [Brain Stem Reflexes] (_**ME** then **PB**_ = ***M**otor vs. **B**reathing vs. **P**upils vs. **E**ye mvmnt*) ***Eye Movement** testing = Both Test indicate _Normal_* *Brain Stem* 1. [Oculocephalic Doll's Eyes Reflex] = eyes conjugately move in direction opposite from head rotation (*normal brain stem response*) - **RULE OUT CERVICAL SPINE FRACTURE BEFORE DOING THIS** 2. [**Induced CALORIC Nystagmus**] is when irrigation of [External Auditory Canal] with *Cold/Warm water* creates convection currents in Vestibular labyrinths---\>stimulates [crista ampullaris] by deflecting stereocilia * **COWS** (ENG-Electronystagmogram)= * *C**old Water---\>Eyes move **O**pposite direction of irrigation * *W**arm water --\>eyes move in **S**ame direction of irrigation*
121
A: How should you *initially* examine an **Unresponsive pt** (4) B: Describe the **PUPIL** testing (5)
A: Examine [Brain Stem Reflexes] (_**ME** then **PB**_ = ***M**otor vs. **B**reathing vs. **P**upils vs. **E**ye mvmnt*) ***Pupils** testing* 1. Pupil Dilation (*hypothalamus--\>brain stem--\>spinal cord--\> **sympathetic** ganglia*) 2. Pupil Constriction (*Oculomotor CN3 & Parasympathetics*) 3. Pupillary Light Reflex (**Doesn't rule out Metabolic Coma**) 4. Small Pupils ([*Narcotics/Glaucoma Cholinergic Eyedrops*] vs. [*Normal in Awake Elderly*] 5. [Unilateral Large Pupil] (*possible Oculomotor CN3 compression from uncal herniation*) = **EMERGENCY!!!**
122
A: How should you *initially* examine an **Unresponsive pt** (4) B: Describe the **BREATHING** testing (3)
A: Examine [Brain Stem Reflexes] (_**ME** then **PB**_ = ***M**otor vs. **B**reathing vs. **P**upils vs. **E**ye mvmnt*) ***Breathing** testing* 1. **Cheyne-Stokes** = *alternating* tachypnea & apnea from bilateral cortical lesions vs. HF vs. sleeping elderly 2. **Hyperventilation** = mostly from pulmonary congestion 3. [**Irregular Ataxic**] = Lesion at/near [medullary cardiopulmonary control] --\> impending respiratory failure
123
**Emergent** Evaluation of a **Comatose** pt should include what *4 Steps*
1st: **ABC** = **A**irway / **B**reathing / **C**irculation 2nd: Check Blood-glucose --\> Give [50% IV Dextrose] if necessary 3rd: W/u for Toxi-metabolic coma (*don't forget CO poisoning and hypOthermia*) - Myoclonic Jerks & Asterixis 4th: W/u for **Structural** Coma (*hemorrhage / tumor / infarct*) = hemispheric abnormalities
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A: Describe the **Persistent** **Vegetative State** B: Are *Cranial Nerve Reflexes* still intact? C: In a **Vegetative State**, which neural structures are still _intact?_ (2) D: What does this progress from?
*Pt is Arousable but not really **responsive*** ## Footnote A: [Days-weeks post **Cerebral Cortex** anoxia] pt may appear awake + [roving eyes] + [pain response] **but still no real responsiveness** = *Persistent* *Vegetative State* B: Some CN reflexes may still be intact (*Brainstem & Spinal Cord are still intact*) C: Brainstem & Spinal Cord D: Coma --\> Minimal Return
125
A: Describe the **Demented** pt B: How do you approach *Advanced Directives* for these pts C: What is their *Nutritional Status* (2)
A: Pt who is progressively becoming [unaware of problems] and [unable to understand/communicate], typically associated w/behavioral changes B: Establish Directives early! (*since* *family will eventually assume all decision-making*) C: [Olfactory Dysfunction] --\> No Appetite, but pt will still have "basic need" to hydrate. Tx= [**PEG**-**P**ercutaneous **E**ndoscopic **G**astrostomy] vs. feeding tube
126
A: The SCN [Suprachiasmatic Nucleus] is located Above _____ \_\_\_\_\_\_\_ and is used as our ___ \_\_\_ \_\_\_\_& ___ \_\_\_\_\_. It keeps us on a \_\_\_\_\_\_\_. This is 1 of the nucleus from the \_\_\_\_\_. B: What type of EXTERNAL input does the SCN receive? [3] C: What internal Output does it send out? D: Biologic Rhythms by the SCN are not linked exclusively to the _____ and works together with ___ \_\_\_\_\_. Name the 4 Categories, describe their timing and give example E: When does SCN secrete the MOST hormones?
A: The SCN [Suprachiasmatic Nucleus] is located Above Optic Chiasm and is used as our endogenous "biological clock" & CIRCADIAN Pacemaker. It keeps us on a 24 hour cycle, turning some systems on/off. This is a nucleus of the HYPOTHALAMUS. B: Light (reason its near Optic Chiasm), Food & Temperature C: Sleep-Wake ------------------------------------------------------------------------------ D: Biologic Rhythms by the SCN are not linked exclusively to the HIPPOCAMPUS. It works together with Environmental Cues. These are the 4 Categories: 1. Ultradian = less than 24 hours --\>Resp/HR 2. Circadian = 24 hours ---\>Corticosterone rhythm 3. Infradian = More than 24 but less than 1 year--\>menstrual cycles 4. Circannual= every year---\> Hibernation -------------------------------------------------------------------------------------- E: Highest amount of SCN hormone secretion = When ur Sleep
127
A: Disconnection syndromes usually result from _______ matter damage interfering with ____ \_\_\_ or ___ \_\_\_\_ B1: Define **Alexia** B2: Define **Agraphia** B3: Lesions in [*NON**-Dominant* Hemispheres of cortical language center] --\> \_\_\_\_ C: AWA is usually caused by _______ stroke to _______ Lobe. ___ \_\_\_\_ of this area is affected
A: Disconnection syndromes usually result from WHITE matter damage interfering with Corpus Callosum or ANT commissure. B: 1. Alexia = impaired reading (*visual cortex is disconnected from language center*) 2. Agraphia= impaired writing (*motor cortex for dominant hand is disconnected from language center*) 3: [*NON-Dominant* Hemisphere lesions] in the [mirror image locations of **cortical language center**]--\> **Aprosody** (*inability to interpret the [**TIP**-**T**one/**I**nflection**/P**itch] of language*) C: [Alexia ***without*** Agraphia] is usually caused by PCA stroke to Occipital Lobe. Corpus Callosum of this area is affected---\>Seeing object in L eye CAN'T be interpreted in the R brain like normal.
128
*Describe**:* A: **HemiBallismus** B: **Hunt**_I_**ngtons** C: **Parkinsons**
A: Lesion of [**SubThalamic Nucleus**] --\> less Stimulation of [**Globus Pallidus: *internal*]** --\> **HYPER**Kinesia (*specifically* *VIOLENT limb flinging*) B: Hunt**I**ngton's = [Auto Dominant Degeneration of ((**_I)_ndirect** Striatum) 2° to [Chromo 4 trinucleotide repeats]] "*Hunter was way too excited*" C: Parkinson's = [Degeneration of (**Substantia Nigra:*Compact*)** = Loss of All Dopamine] ***DDEM** = **D**opamine & [**D**irect Path] **E**nable **M**ovement*
129
A: [Chorea and Dystonia] are SE of **Dopamine** _____ [*blockers vs. agonist*] B: Name 4 *Movement Disorders* that are **unrelated to Basal Ganglia** C: Name the 5 components of the **Basal Ganglia**
A: A: [Chorea and Dystonia] are SE of **Dopamine** **AGONIST** B: 1. Essential Tremor 2. [Myoclonus vs. Asterixis (*ToxiM**etabolic etiology*)] 3. Dystonia 4. Tic C: [Caudate / Putamen / [Globus Pallidus] / [Substantia Nigra] / [SubThalamic Nucleus]]
130
A: *Primary* Clinical Signs of **Parkinsonism** (4) B: *Secondary* Clinical Signs of **Parkinsonism** (3)
A: **PARK** & **ham** 1. [**P**ill Rolling Resting Tremor] 2. [**R**igidity Cogwheel] 3. Brady**K**inesia 4. [**A**Reflexia posturally] --\> Fall B: - **h**ypOphonic speech - **A**utonomic Dysfunction (*constipation / bladder problems / orthostatic hypOtension*) - **m**icrographia
131
A: Causes of **Parkinsonism** (4) B: Age of onset C: Dx (2) D: Histology
A: 1) Parkinson's Dz 2) [Rare Degenerative Disorders (*progressive supranuclear palsy vs. multiple system atrophy*)= **NOT responsive to levodopa** 3) [Dopamine Blocker (*Haloperidol*) **SIDE EFFECTS**] 4) [Manganese vs. Carbon Monoxide Poisoning] B: onset between 40-70 y/o C: [2 or more *Primary* Clinical Signs --- typically worst on 1 side and progressive] + [Responds to **Dopaminergic** tx] D: *Lewy Bodies* = [alpha synuclein cytoplasmic accumulations tht are eosinophilic]
132
A: **Parkinson's Dz** Tx (5) B: Describe the 3 *aspects* of ***Surgical tx*** specifically
"Eat a **SALAD** after you Park" 1. [**Levodopa** (*Dopamine Precursor*)] 2. **Amantidine** (*_weakly_* *stimulates Dopamine release*) 3. **Anticholinergics** (WEAK effect) 4. [**Dopamine Agonist** *Post synaptic*] (*Ropinirole vs. Pramipexole*): Also has ability to [DEC Long term Dyskinesia if given as monotherapy] 5. **Surgical tx** - Used in Pts refractory to meds - Pallidotomy: Intential Destructive Lesion of the [**Globus Pallidus:*internal***] - SubThalamic nuc. _inhibition_ with implanted electrode
133
**Levodopa** A: *What* is **Levodopa** co-administered with and *why*? B: Describe *How Long* **Levodopa** has an effect. What can be given to mitigate this? (2) C: Side Effects (4)
**Levodopa** = **Parkinson's Dz** tx ## Footnote A: Administered with **Carbidopa** (*decarboxylase inhibitor*), which prevents peripheral **Levodopa** catabolism before it has chance to enter brain B: DEC over time since there will continue to be dopaminergic neuron death. [MAO-B and COMT-_inhibitors_] sustain effective **Levodopa** levels C: [Hallucinations vs. Psychosis vs. Chorea vs. DysTonia]
134
**Lewy Body Dementia** A: Statistics B: Clinical Course (2) C: Describe the Histology. What parts of the brain is it found in (2)?
**Lewy Body Dementia** is the **SECOND** common type of neurodegenerative dementia B: [Dementia + Visual Hallucinations] --\> [**Parkinsonian** sx] C: [alpha synuclein cytoplasmic accumulations tht are eosinophilic] - found in Cortex & Brainstem
135
**Frontotemporal Degeneration** A: Statistics B: Clinical manifestation C: Genetic Cause D: Dx (3)
A:[**Frontotemporal Degeneration**] is the THIRD common type of neurodegenerative dementia *BUT MAY BE CONCOMITANT WITH ALZHEIMER'S*. Typically worst on Left. B: Change in personal/social conduct, associated with **disinhibition** and **language changes** C: [Chromo 17 **Tau** gene mutation] D: *Immunohistochemistry* against: [Tau vs. Ubiquitin vs. TDP43]
136
A: Categorize **Pick's Dz** B: Clinical Presenation C: Histology D: What 2 neural structures are associated
A: *RARE* *SubType* of [**Frontotemporal Dementia**] B: **Aphasia** (*minimal memory loss but may develop Dementia*) C: **Pick Bodies =** _Globose_ neuronal cytoplasmic inclusions made of **Tau**. D: Hippocamps and Cortex
137
**Huntington's Dz** A: Genetic Cause B: What effect does *Caudate nc.* degeneration have? (2) C: In this Dz, what actually causes *Neuronal Death*?
A: Hunt**I**ngton's = [Auto Dominant Degeneration of ((**I**)ndirect Striatum) 2° to [Chromo 4 trinucleotide repeats]] "*Hunter was way too excited*" B: [Degeneration of Caudate nc.] --\> [DEC GABA and ACh] C: [NMDA-R binding and Glutamate]
138
[**Multiple System Atrophy**] A: onset B: Sx (3) C: Histology
A: 40-60 (*Parkinson's Dz Onset = 40-70*) B: *Atrophy of **COPS*** 1. Parkinsonism -***S**ubstantia nigra atrophy* 2. Cerebellar Ataxia - ***C**erebellar atrophy* 3. Autonomic dysfunction -[***O**livary nc./**P**ons atrophy*] C: [**GLIAL** **alpha synuclein** cytoplasmic accumulations tht's eosinophilic]
139
**Friedreich's Ataxia** A: Statistics B: Genetic Cause C: Clinical Manifestation (3)
[Friedrei**CH'S** Ataxia] ## Footnote A: Most common **Hereditary Ataxia** B: [Auto **r**ecessive *GAA Trinucleotide repeat* in Chromo 9 Frataxin gene] *Frataxin is needed for mitochondrial iron* C: [Friedrei**CH'S** Ataxia] 1. [**C**erebellar Degeneration]--\> Ataxia 2. **H**eart Abnormalities --\> 50% of deaths! 3. [**S**pinal Cord Degeneration] --\> [Loss of **2TVP**] + [Muscle Weakness] + [Loss of Deep Tendon Reflex]
140
A: **Mixed Dementia** mostly consist of _____ & [**Vascular Dementia**] B: What are Risk Factors for **Mixed Dementia** (2) C: What is the *most common form of* [**Vascular Dementia**]
A: **Mixed Dementia** mostly consist of **Alzheimer's** & [**Vascular Dementia**] ## Footnote B: 1) [*ApoE4 genotype*] INC risk of Alzheimer's AND CV Dz 2) *Vascular Amyloidosis* INC risk of hemorrhagic strokes --\> [Vascular Dementia] C: CADASIL = involves small arterioles & capillaries
141
**[*Ethanol Tox*: Wernicke's Syndrome]** A: Clinical *Triad* (3) B: This syndrome is characterized by deficiency of what substance? C: What *supplement* *deficiency* is this syndrome caused by?
**TACO** ## Footnote A: **_T_**hiamine deficiency ---\> 1. **_O_**culomotor abnormalities (*ophthalmoplegia vs. nystagmus*) 2. **_C_**erebellar Dysfunction 3. **_A_**ltered Mental Status B: [+/- Korsakoff Psychosis from **mammillary body hemorrhage & atrophy** (*can't recall recent memory so compensates with confabulation*)] C: ****_T_**hiamine** Deficiency
142
A: Toxicity of *what compound* causes [Cortical Atrophy] and [**Central Pontine Myelinolysis**] B: [Central Pontine Myelinolysis] *Histology* C: What *Electrolyte abnormality* causes [**Central Pontine Myelinolysis**] ?
A: **ETHANOL TOXICITY** ## Footnote B: Triangular lesion with myelin loss of the *Pons* C: [Rapid Correction of Chronic hypOnatremia]
143
**Methanol** Toxicity A: MOD (3) B: Clinical Manifestation (4)
A: Hepatic oxidation of [Methanol --\> (Formaldehyde & Formic Acid)]--\> - global hypoxia - *white matter* necrosis & hemorrhage--\> [Putamen & Claustrum hemorrhagic infarct] B: [Vision loss vs. Delirium/Convulsions vs. Coma vs. Death]
144
*Gross Histology* of **Carbon Monoxide** Toxicity (3)
1. [**Bilateral** **Globus Pallidus** Hemorrhagic Necrosis] 2. [*White* Matter Hemorrhagic Petechiae] 3. Cerebral Edema
145
A: *Identify* and *Describe Histology* of image B: Cause
A: [Alzheimer Type 2 Astrocyte] = [Nuclei are large and appear clear] B: liver Failure--\> Hyperammonemia (*Hepatic Encephalopathy*)
146
A: **Speech** consist of ____ and \_\_\_\_ B: Describe each component of **Speech** C: Define **Aphasia**
A: Speech = **Phonation** and **Articulation** - **Phonation**: *making sounds* with vocal cord mvmnt (*Vagus CN10*) - (*Dysphonia = Hoarse vs. whispery*) - **Articulation**: *articulating sounds* with [lips/tongue/palate/pharynx] (*Dysarthria* = *slurred speech 2º to **Articulation** problems*) B: Disorder of [previously acquired language ability] due to [language center lesion in *dominant* hemisphere] --\> **all-around** **impaired** **communication** (*includes gestures & Braille*)
147
A: Where are the *Cortical Language Centers* B: what *perfuses* this center C: Describe the *Function* of **Wernicke** and **Broca** area D: Lesions around this *Center* leads to what guaranteed defect?
A: [Sylvian Lateral Sulcus] of the dominant *(usually L hemisphere**)* hemisphere B: MCA C: 1) Wernicke's area = language **comprehension** 2) Broca's area = language **execution/expression** D: Imperfect Repetition
148
A: **Paraphasia** definition B: Examples (3)
[Word or Syllable Substitutions] ## Footnote - Phonemic or literal = *Sully* for *Silly* - [Semantic or verbal]= *blue* for *Green* * -*Neologism= nonsense word: *scatifang*
149
**Broca's Aphasia** A: Location of Lesion (2) B: Clinical Manifestation (5)
A: [Area 44 Inferior Frontal Gyrus] + [involvement of adjacent motor cortex] B: - [Poor Repetition/Naming/_Fluency_ ([telegraphic **non**fluency ( *"I.....up.....early"*)]] - R Hemiparesis - Facial Weakness
150
**Wernicke's Aphasia** A: Location of Lesion B: Clinical Manifestation (4) C: What *Dx* is this sometimes confused with?
A: [Temporal Lobe (*posterior vs. superior*)] B: - [Poor Repetition/Naming/_Comprehension_ (*They don't comprehend you and You can't comprehend them*)] - Hemiparesis C: Psychiatric disorders
151
**Conductive Aphasia** A: Location of Lesion B: Clinical Manifestation
A: [Arcuate Fasciculus (*tract between Broca & Wernicke*)] B: [**Intermediate** version of *Wernicke**'s* *Aphasia*]
152
**GLOBAL Aphasia** A: Location of Lesion (3) B: Clinical Manifestation (3)
A: [Broca + Wernicke + Arcuate Fasciculus] = ALL! B: [**SEVERELY NONFLUENT / MUTE / poor comprehension**]
153
A: Define **Prosody** B: Lesions of which area --\> **AProsody** C: Name the *2 Types* of **AP**rosody
A: [Semantic & Emotional meaning] conveyed by the [**TIP**-***T**one/**I**nflection/**P**itch*] of Language B: [**Non**dominant Hemisphere lesions] in the [mirror image locations of cortical language center] C: - [Sensory Receptive Aprosodia] - [***Non****Dominant Wernicke's lesion]* - [Motor Expressive Aprosida] - [***Non****Dominant Broca's lesion]*
154
[**Sensory Receptive Aprosodia**] A: Location of lesion B: Clinical Manifestation (3)
A: [**Non**Dominant **Wernicke's** lesion] B: **Speaks with Prosody** but has [Poor prosodic comprehension when listening] and [unable to repeat prosody in others' speech]
155
[**Motor Expressive Aprosodia**] A: Location of lesion B: Clinical Manifestation (3)
A: [**Non**Dominant **Broca's** lesion] B: **DOES NOT SPEAK with Prosody and** **[unable to repeat prosody in others' speech]** but has [Good prosodic comprehension when listening]
156
A: Describe **Gait *Apraxia*** B: Describe **Constructional** ***Apraxia***. What lesion causes this?
A: Pt are only _unable to walk_ when **commanded to** walk, even though they have all the essentials to walk intact B: PARIETAL LOBE LESION --\> pt _unable to draw_ when **commanded to** draw *Apraxia is not due to sensory/motor/language deficit*
157
A: What***Type*** of Ataxic Gait is in image B: **Location** of Lesion causing this (2)
A: [**Broad**-**based** Ataxic Gait] B: 1. [Dorsal Column and its associations] or 2. [Cerebellum (*Gait is _constantly_ bad regardless of eyes open/close*)]
158
A: What***Type*** of Ataxic Gait is in image B: **Location** of Lesion causing this
A: [**Hemiplegic** Ataxic Gait] B: Stroke *UE: [Upper limb flexed at elbow + DEC armswing] on affected side*
159
A: Describe [**Tabetic** Ataxic Gait] B: Associated **Diseases** (2)
A: [**Stomping foot gait**] where pt forcibly plants feet down on ground to "feel" floor & compesnate for impaired sensation B: 1. [Tabes Dorsalis Neurosyphilis] or 2. [Severe Neuropathy]
160
A: What***Type*** of Ataxic Gait is in image B: Causes (3)
A: [**Steppage** Ataxic Gait] B: 1. [peroneal n. lesion] 2. [L5 root lesion] 3. Peripheral Neuropathy to prevent tripping over the toes, the hip is flexed even higher to elevate the drooping foot, which is lowered to the floor toe first
161
A: Describe [**Waddling** Ataxic Gait] B: Associated **Disease**
A: [Pelvic vs. Hip muscles] can't support body when on 1 leg so swaying/leaning when foot is raised helps = alternatively wadduling like a duck! B: Myopathy
162
A: What***Type*** of Ataxic Gait is in image B: **Location** of Lesion causing this C: Disease Associated (2)
A: [**Scissors** Ataxic Gait] B: 1. CST lesions--\> [spastic paraparesis]--\>tightness in adductor muscles and knees--\>legs cross over each other like **scissor blades** C: - Cerebral Palsy - Multiple Sclerosis
163
A: What***Type*** of Ataxic Gait is in image B: Disease Associated C: Describe this gait
A: [**Parkinsonian** Ataxic Gait] B: Parkinson's C: [Slow shuffling gait] with *Stooped forward* *posture* and **festination** (leaning more & more forward to walk and then runs to catch up with center of gravity). Falls a lot.
164
**Cerebellar Function Test**:*How do you use....* A: Speech B: Eye mvmnts C: Limb (4)
A: Dysarthria = slurred speech 2º​ to **Articulation problems** B: [Nystagmus with erratic, jerky mvmnt] C: 1. Kinetic Tremor (*rhythmic oscillations during limb mvmnt*) 2. Dysmetria (*overshooting/undershooting target*) 3. Mvmnt Decomposition (*jerky and broken down*) 4. [Rebound Check response Deficit] (*sudden release of contracted triceps from loss of check response from antagonist muscle--\>pt hits himself*)
165
A1: Describe **Hemispheral Syndrome** A2: Cause B1: Describe **Vermal Syndrome** B2: Cause (2)
A1: ***Ipsilateral*** Limb [kinetic tremor/dysmetria/rebound check response loss] A2: Any Bilateral lesion in degenerative dz (*MS*) B1: ***TRUNK*** [truncal unsteadiness with standing / walking / gait ataxia] B2: - Alcoholic Cerebellar Degeneration (*ANT SUP vermis atrophy*) - Any Bilateral lesion in degenerative dz
166
**Spinocerebellar Degeneration** A: Most common type B: Pgn
A: [Friedreich's Ataxia] B: No curative tx and Older pts become wheelchair-dependent *[Cerebellar and Spinal Cord Nc. and tract are affected]*
167
A: Describe **Choreoathetosis** (2) B: What areas are affected (3) C: Causes (2)
A: [slow continuing limb movements= **Athetosis**] + [Irregular dancelike movements = **Chorea**] B: Limb, trunk and face C: - [Caudate nc. lesion (*Huntington's Dz*)] - [Dopaminergic medications]
168
A: Describe **Tics** B: What disorder is this associated with?
A: Brief repetitive contractions of muscle groups (*facial twitch vs. eye blink vs. sniffs vs. grunts*) B: Tourette's (*inherited with variable penetrance-mostly boys*)
169
A: Describe **Myoclonus** B: Causes (2)
A: Asynchronous rapid shocklike mvmnts of limbs or body bilaterally B: - Diffuse Encephalopathy (*Creutzfeldt Jakob Dz*) - Medical Dz (*Renal/Hepatic Failure vs. Anoxia*)
170
A: Describe **Asterixis** B: Causes (3)
A: **Flapping Tremor** of hand/foot from [postural tone loss] typically bialterally B: - Diffuse Encephalopathy (*Creutzfeldt Jakob Dz*) - Medical Dz (*Renal/Hepatic Failure vs. Anoxia*) - Structural brain lesions - **will be Unilateral**
171
**Tx** for... A: **Essential Tremor** (2) B: **Dystonia** (3)
A: [Beta blockers vs. Barbiturates] B: [Anticholinergics vs. Benzodiazepines vs. Botox]
172
A: [Thalamic RETICULAR nucleus] projects ONLY to _____ and NOT the \_\_\_\_\_. Neurons of this nuclei are ___ \_\_\_\_\_. B: Thalamic Axons passing thru (incoming & outgoing) give off ____ which travel to [Thalamic RETICULAR nucleus]. C: Main Purpose of [Thalamic RETICULAR nucleus] is to inhibit _____ and therefore Enhances activity of \_\_\_\_\_\_\_
[Thalamic RETICULAR nucleus] projects ONLY to other thalamic nuclei and NOT the Cerebral Cortex. Neurons of this nuclei are [inhibitory GABAergic]. B: Thalamic Axons passing thru (both incoming & outgoing) give off collaterals to [Thalamic RETICULAR nucleus]. C: Main Purpose of [Thalamic RETICULAR nucleus] is to inhibit random background sensory activity ---\> Enhances salient activity of 1 area of thalamic neurons.
173
A: What Thalamic Afferents travel TO the [ANTERIOR nc.]? [2] B: Where does the Efferent fibers of the [ANTERIOR nc.] project to? C: What type of Thalamic nucleus is the [ANTERIOR nc.]
[ANTERIOR nc.] A: Aff= Mammillary body & Hippocampus ---\> nc B: Eff= nc---\> projects to Cingulate Gyrus C: [Specific Relay nuclei]
174
A: What Thalamic Afferents travel TO the VA[VENTRAL Anterior nc.]? B: Where does the Efferent fibers of the [VENTRAL Anterior nc.] project to? C: What type of Thalamic nucleus is the [VENTRAL Anterior nc.]
[VENTRAL Anterior nc.] A: Aff= Basal ganglia ( [substantia nigra] ) ---\> nc B: Eff= nc---\> projects to PreFrontal Cortex C: [Specific Relay nuclei]
175
A: What Afferents travel TO the Thalamic [VL\>ant] nc. B: Where does the Efferent fibers of the Thalamic [VL\>ant] nc. project to? C: What type of Thalamic nucleus is the [VL\>ant]
[VENTRAL Lateral nc.]\>ANT part (**VL\>ant**) A: Aff= Basal ganglia ([Globus Pallidus])---\> nc B: Eff= nc---\> projects to Supplementary motor area C: [Specific Relay nuclei]
176
A: What Afferents travel TO the Thalamic [VL\>**PoST**] nc. B: Where does the Efferent fibers of the Thalamic [VL\>PoST] nc. project to? C: What type of Thalamic nucleus is the [VL\>PoST]
[VENTRAL Lateral nc.]\>**PoST** part A: Aff= Cerebellum---\> nc B: Eff= nc---\> MOTOR CORTEX C: [Specific Relay nuclei]
177
A: What Afferents travel TO the Thalamic [VPM] nc. B: Where does the Efferent fibers of the Thalamic [VPM] nc. project to? C: What type of Thalamic nucleus is the [VPM] D: What type of info specifically is this Thalamic nucleus involved with?
[VENTRAL POSTEROMEDIAL nc.] A: (Somatic) Aff= Head --\> nc B: Eff= nc---\> Somatosensory Cortex C: [Specific Relay nuclei] D: Involved with relaying Vestibular information
178
A: What Afferents travel TO the Thalamic [VPL] nc. (2) B: Where does the Efferent fibers of the Thalamic [VPL] nc. project to? C: What type of Thalamic nucleus is the [VPL] D: What type of info specifically is this Thalamic nucleus involved with?
[VENTRAL POSTEROLateral nc.] A: (Somatic) Aff= [Trunk&Limbs] --\> nc B: Eff= nc---\> Somatosensory Cortex C: [Specific Relay nuclei] D: Involved with relaying Vestibular information
179
A: What Afferents travel TO the Thalamic [Lateral Geniculate] nc. (2) B: Where does the Efferent fibers of the Thalamic [Lateral Geniculate] nc. project to? C: What type of Thalamic nucleus is the [Lateral Geniculate]
[Lateral Geniculate nc.] A: Aff= Optic Tract & [SUP colliculus] --\> nc B: Eff= nc---\> [Area 17 CPVC] C: [Specific Relay nuclei]
180
A: What Afferents travel TO the Thalamic [medial Geniculate] nc. B: Where does the Efferent fibers of the Thalamic [medial Geniculate] nc. project to? C: What type of Thalamic nucleus is the [medial Geniculate]
[medial Geniculate nc.] A: Aff= [inf colliculus] --\> nc B: Eff= nc---\> Primary Auditory Cortex C: [Specific Relay nuclei]
181
A: What Afferents travel TO the Thalamic [Lateral Dorsal] nc. B: Where does the Efferent fibers of the Thalamic [Lateral Dorsal] nc. project to? C: What type of Thalamic nucleus is the [Lateral Dorsal]
[Lateral Dorsal nc.] A: Aff= Hippocampus--\> nc B: Eff= nc---\> Cingulate cortex C: [Specific Relay nuclei]
182
A: What Afferents travel TO the Thalamic [LP & Pulvinar] nc. (4) B: Where does the Efferent fibers of the Thalamic [LP & Pulvinar] nc. project to? C: What type of Thalamic nuclei are the [LP & Pulvinar]
[(Lateral POST) & Pulvinar nc.] A: Aff= [SUP colliculus]/[Area 17 CPVC]/ [Primary auditory cortex]/Somatosensory Cortex -----\> nc B: Eff= nc---\> {PPLTAC} "Posterior Parietal and Lateral Temporal Association Cortex" C: [Association nuclei]
183
A: What Afferents travel TO the Thalamic [Dorsomedial] nc. (3) B: Where does the Efferent fibers of the Thalamic [Dorsomedial] nc. project to? C: What type of Thalamic nucleus is the [Dorsomedial]
[Dorsomedial nc.] A: Aff= [Prefrontal Cortex]/Olfactory/Limbic -----\> nc B: Eff= nc---\> PreFrontal Cortex C: [Association nuclei]
184
A: What Afferents travel TO the Thalamic [Intralaminar] nc. (3) B: Where does the Efferent fibers of the Thalamic [Intralaminar] nc. project to? C: **What type of Thalamic nucleus is the [Intralaminar]**
[Intralaminar nc.] A: Aff= [Reticular Formation]/[BasalGanglia]/limbic -----\> nc B: Eff= nc---\> Cerebral Cortex/[BasalGanglia]/limbic C: [**Non-Specific nuclei**]
185
A: What Afferents travel TO the Thalamic [Thalamic RETICULAR nucleus] (2) B: Where does the Efferent fibers of the Thalamic [Thalamic RETICULAR nucleus] project to? C: What type of Thalamic nucleus is the [Thalamic RETICULAR nucleus] D: What is Different of this Thalamic nucleus from the others?
[Thalamic RETICULAR nucleus] A: Aff= Thalamus & Cortex-----\> nc B: Eff= nc---\> ONLY other Thalamus nuclei C: [Non-Specific nuclei] D: Aside from this [Thalamic RETICULAR nucleus], All OTHER thalamic nuclei "decide" where info should go in Cerebral cortex
186
Intralaminar nc. and [thalamic reticular nuclei] are both types of the _______ functional group
Intralaminar nc. and [thalamic reticular nuclei] are both types of the NON-SPECIFIC functional group
187
Lesions of which structures typically produce **Amnesia** (*Anterograde vs. Retrograde*) (3)
"*Amnesia* comes from **H**aving **M**emory **T**roubles!" **Bilateral** lesions in: - **T**halamus 2. **M**amillary bodies (*Thiamine deficiency-Wernicke Korsakoff*) 3. **H**ippocampus (*Herpes Encephalitis / Anoxia / Alzheimer's*)
188
**Agnosia** A: General definition B: *Visual* Agnosia C: *Tactile* Agnosia
A: Failure to identify Object via 1 sensory modality, but can identify objects via others B: Failure to *visually* recognize a bell but can identify when hearing or touching the bell C: Failure to recognize bell *from touch* but can identify in other ways which also = [Severe Astereognosis]
189
Describe the *Clinical Presentation* of **Frontal Lobe Syndrome** (5)
A: **F**rontal Lobe has **D**&**G** on **D**&**G** 1. [**D**isinhibition / Lack of concern] 2. [**D**istractible motor and mental function (*Poor planning & impaired creatitivity*)] 3. [**F**rontal lobe release signs in *(Normal in infants only*)] 4. [**G**egenhalten Paratonia (*resistance to passive limb mvmnt*)] 5. **G**ait Apraxia
190
**Temporal Lobe Syndromes** A: Name the *Bilateral* lesions (3) B: Name the *Unilateral lesions*
A: Bilateral: 1. Amnesia (hippocampal lesions) 2. [Cortical Deafness from Auditory lesions] 3. [Kluver Bucy Syndrome] B: Dominant Hemisphere lesion: *Wernicke's Aphasia*
191
**Parietal Lobe syndromes** A: *Clinical Manifestation* for **Nondominant Parietal lesions**. List and describe 2 examples. B: List and describe an example of **Dominant Parietal Lesions**. What structures are associated with this (2)?
A: Impairment of spatial relationships between body and its surroundings - Anosognosia: Unawareness of hemiparesis or denial of an entire half of your body = **Hemispatial Neglect** - Constructional Apraxia: Inability to **write** when commanded to B1: "*Gerstmann's* **HAD** a *Syndrome*" Gerstmann's Syndrome ([**H**and disorientation + Finger agnosia] /**A**graphia / **D**yscalculia -[Supramarginal vs. Angular Gyrus]
192
**Occipital Lobe** A: *Bilateral* Lesion examples (3) B: *Unilateral* Lesion examples
A: 1. **Anton's Syndrome**: Denial of Cortical Blindness 2. **Visual Agnosia** 3. **Prosopagnosia**: *Inability to recognize previously known faces* = subtype of Visual Agnosia B: [Dominant TemporOccipital lesion] --\> **Color Anomia** (*inability to name colors*)