NBEO: Boards: Neuroscience Flashcards
NTs
- Which NT is the most widely distributed INHIBITORY transmitter?
- Which NT is found in the brainstem, spinal cord, and RETINA and is INHIBITORY?
- Which is found in Skeletal muscle and blocked by CURARE?
- Which is found in Sm. Muscle?
- Which are found in the SNS?
- What Receptors are TARGETED by a-Bunagarotoxin (snake Venom)?
- GABA
- Glycine
- Cholinergic: Nicotinic
- Cholinergic: Muscarinic
- Adrenergic NTs
- Nicotinic Ach Receptors (NMJ and PSNS)
Define the Following: PNS
- Ganglia
- Nerves
- Sensory Division
- Somatic Motor Division
- Autonomic Motor Division
- collection of nerve cell bodies
- bundles of axons
- Ganglia that lie near the spinal cord or brainstem
- neurons that innervate skeletal muscle
- Neurons that innervate cardiac and SM and glands. SNS and PSNS
CNS: Define
- Nuclei
- Cortex
- Frontal Lobe
- Parietal Lobe
- Occipital Lobe
- Temporal Lobe
- Collection of neurons (like ganglia)
- layers of cells
- Premotor cortex (Planning and execution of motor tasks). Personality (reasoning, planning). Broca’s AREA (speech conduction)
- Sensory and Recognition
- Vision
- Perception and Sensory Recognition (auditory, speech) and Memory. *Hippocampus; Wernicke’s Area (speech recognition)
Spinal Nerves
- Cervical
a. 1-4?
b. 5-8? - Thoracic
a. 1-12? - Lumbar
a. 1-4?
b. 4-5? - Sacral
a. 1-3?
b. 2-4? - Coccygeal?
- a. Neck
b. Upper Extremities - a. Upper extremities
- a. Thigh
b. Thigh,leg,foot - a. thigh, leg, foot.
b. pelvis - Coccygeal nerve
Brainstem
- Medulla: purpose?
- Pons?
- Midbrain?
- Autnomonic stuff (hear rate, digestion, breathing)
- coordinates movement info b/w cerebral hemispheres and cerebellum
- sensory and motor functions: COORDINATION of EYE MOVEMENT and VISUAL REFLEXES!
Medulla
- Upper medulla: 2 main structures it contains and what tracts do they have?
- The latter part has what tracts and what info do they carry?
- What does the MLF relay?
- Lower/Middle Medulla: Location of what Nuclei?
- Pyramids (Ventral and Descending) and Medial Lemniscus (Ascending Dorsal Tracts)
- Gracilus (lower body info) and Cuneate Fasciculi (Trunk info) (tracts) **Start to see 4th Ventricle
- Vestibular info to EXTERIOR EYE MUSCLES; Coordinates the VOR
- Vestibular Nuclei and Olivary Nuclei (Learning and memory)
Pons
- Purpose?
- What nuclei are found here?
- What else is the pons involved in?
- CNs found here?
- Relay info b/w midbrain and Medulla
- Pontine Nuclei (relay stations for motion-related info that goes b/w the cortex and cerebellum)
- Controls respiration and sleep
- Nuclei for CNs 5-8
Midbrain
- Upper Midbrain: Location of what?
- Lower Midbrain: Contains what?
- a. Superior Colliculus (has motor neurons that control orientation of the HEAD/EYES)
b. Red Nucleus (Controls arm movement and Oculomotor nuclei)
c. EW-Nucleis (CN 3): PSNS innervation to the IRIS! - a. Inferior Colliculus (reflex response of head/neck to auditory stimuli)
b. CN 4 nucleus (C/L SO)
c. Start to see Cerebellar peduncles (Tracts going to Cerebellum)
Neural Tube
- 3 General Areas?
- Which differentiates into the TELENCEPHALON and DIENCEPHALON?
- What gives rise to the Cerebral Hemispheres?
- Forebrain, Midbrain, Hindbrain
- Forebrain
- Telencephalon
* So, forebrain gives rise to the diencephalon and cerebral hemispheres.
Midbrain
- Diencephalon
- Epithalamus
- Thalamus
- Subthalamus
- Hypothalamus
- Epithalamus, Thalamus, Subthalamus, and Hypothalamus
- Pineal Gland (melatonin)
- Relays sensory info to Cortex; also has Nuclei for voluntary motor movements
- communicates w/basal ganglia: helps control muscle movement
- regulates body temperature, eating, and sleep behavior.
Cerebral Hemispheres
- Dominant Hemisphere
- Non-Dominant Hemisphere
- More control over understanding, processing language, intermediate and long-term memory, word retrieval, and emotional stability
- Facial expression recognition, Vocal intonation, music, visual learning
Cerebellum
- Purpose
- fine motor movements, posture, balance
Blood Supply
- Main Blood supple by what 4 arteries?
- Vertebrals
a. Originate from what Arteries?
b. Rt and Lt join to form what ARTERY? Supplies what?
c. This artery then joins the Carotids at what? - Internal Carotids
a. Arise from what arteries in the neck?
b. These branch into what and supply what area of the brain? - Circle of Willis
a. Joins what arteries?
- Internal Carotids and Vertebral Arteries…all meet by the Pituitary gland
- a. Subclavian arteries (blood to spinal cord)
b. BASILAR ARTERY (blood to pons)
c. Circle of Willis - a. Common carotid arteries in the neck; Lt common comes off the AORTIC ARCH; the Rt Common comes off the Braciocephalic Trunk
b. ICAs branch into ANTERIOR and MIDDLE CEREBRAL ARTERIES: supply blood to FOREBRAIN - a. ICAs, Basilar, and Anterior and Posterior Communicating Arteries
- What tests help us determine if ON damage is present (2)?
2. What test is used to evaluate for Macular Damage?
- Brightness comparison and Red-Cap Desaturation
2. Photostress Test
Name 3 ways an ON that’s unhealthy can present itself
- Atrophic (Excavated or Pallid (Primary = not previously edematous))
- Edematous
- Normal (Retrobulbar Optic neuritis, PION)
Disc Edema
- Posible Signs (6)
- Pathogenesis: Cause?
- What are the most common causes (7)
- APD, VF defect, decreased acuity, blurred disc margin, nerve fiber elevation, hemes.
- PRE-CHIASMAL DISRUPTION of Axoplasmic Flow
- a. AION (AAION and NAION)
b. CRVO
c. Compressive Lesion (Meningioma, TED, Lymphoma, Hemangioma)
d. Diabetic Papillopathy
e. Hypotony
f. Optic Neuritis (Papillitis (Anterior) and Retrobulbar (Post. 2/3 of nerve): Causes: MS, Viral, Toxoplasmosis, Sarcoid, Syphilis, Tb, Non-infectious uveitis, Idiopathic
g. Papillophlebitis
PAPILLEDEMA
- Signs: Blurred disc margins, elevated/opaque NFL, No Spontaneous Venous Pulsation, and What else?
a. How is VA in the early stages? - Pathogenesis: ?
- Most Common Causes (5)
- Splinter hemes, Paton’s Folds (circumferential retinal folds), exudates, CWS, Venous distention, and hyperemia of the disc.
a. Normal - Increased Cerebrospinal fluid pressure in Subarachnoid space of the intraorbital part of the ON. This causes AXOPLASMIC Stasis
- a. Malignant HTN
b. Post-Chiasmal Tumor
c. Inflammatory (Infectious (Meningitis) and Non-Infectious (Sarcoidosis)
d. Pseudotumor Cerebri
e. Compromised or Obstructed Venous Outflow
Atrophic Optic Nerve (U/L or B/L)
- Pathogenesis
- Types of ON Atrophy (2)?
- Causes of Pallor of the Rim: Primary Optic Atrophy (5)
- 2ndary Optic Atrophy Causes?
- Destruction or degeneration of the optic nerve axons
- Excavated (Glaucoma) and Pallid (Flat/whitish in color)
- a. Hereditary (Leber’s, Dominant Optic Atrophy)
b. Orthograde Degeneration (Eye to Brain)
c. Retrograde Degeneration (brain to eye)
d. Toxic/Nutritional
e. Trauma - Previously Edematous
What is a way you can tell if the Pt has Papilledema vs. B/L Disc Edema?
- In Disc Edema, ACUITY will be DECREASED!
AAION
- Cause of AAION?
- Major Symptoms?
- Test for Dx?
- **Elevated ESR for Men
- Elevated ESR for Women
- Occlusion of SHORT POSTERIOR CILIARY ARTERIES
- SUDDEN vision loss in ONE EYE w/other symptoms (HA, Malaise, Jaw claudication, etc…)
- Increased ESR and CRP, also increased Platelets; TABs.
- Age/2
- (age +10)/2
NAION
- What is it?
- Usually seen in whom?
- Risk Factors?
- Symptoms?
- VF Loss.
- Tests (Sedimentation rate, CRP, Platelet count)
- Ischemia to Anterior part of Optic Disc.
- > 50 y/o; M=F
- HTN, DM, Hypercholesterolemia, Disc at risk (Small disc…not cause, but is a RISK)
- sudden, painless, irreversible, non-progressive vision loss in 1 eye, usually noticed after waking up.
- Varies, but MOST COMMON: Inferior Altitudinal Defect
- All NORMAL, and no systemic symptoms.
- Define DIABETIC PAPILLOPATHY
- Type of NAION WITHOUT VISION LOSS in a Pt w/Diabetes.
OPTIC NEURITIS
- What is it?
- Usually seen in whom?
- Symptoms?
- Signs?
- After ACUTE EPISODE: What tends to happen?
- Associated w/what Dz?
- Primary inflammation of the ON
- Age: 20-45; Females > Males
- U/L sudden vision loss (VA: 20/20 to NLP), PAIN ON EYE MOVEMENT is seen in 90%
- 2/3: Retrobulbar Optic Neuritis w/NORMAL APPEARING ON. 1/3: Papillitis w/Disc Edema. BOTH HAVE APD!
- Vision usually Returns to NORMAL w/DECREASED CONTRAST SENSITIVITY and OPTIC NERVE PALLOR
- MS! (56% of cases) *MS can also have an INO (MLF lesion)
Neuroretinitis
- What kind of Optic Neuritis is it?
a. What is SEEN with it on the RETINA?
b. Type of Dz: Infectious or Non-infectious; Immune or non Immune-mediated?
c. Causes (3)
- Anterior
a. STELLATE MACULAR STAR (cause: Optic Disc Vasculopathy and leakage into the Macula)
b. Infectious and Immune-Mediated
c. Cat Scratch Dz, Histoplasmosis and Toxoplasmosis
Papillophlebitis
- Who is it seen in?
- Vision?
- Systemic Dzs associated?
- What does it look like?
- Young, healthy peeps
- Good
- None
- Looks like a CRVO in a young, healthy person.
Thyroid-Related Ophthalmology (Graves’ Ophthalmology)
- Type of Dz?
- Characterized by what 3 things?
- Signs: Multiple…list some.
- Which RECTI are usually affected FIRST?
- AI
- Edema of the EOMs, Orbital Adipose tissue prolapse, and ON Compression.
- UPPER EYELID RETRACTION, EXOPHTHALMOS, Disc Edema, APD, Decreased acuity and color vision, VF Defects
- INFERIOR and MEDIAL RECTI.
(I think it goes: I, M, S, L)….LOOK THIS UP!
Malignant (SEVERE) Hypertension
- What is it?
- Papilledema due to HBP: >220/>120. ER.
Foster Kennedy Syndrome
- Rare condition due to what?
- Causes what to occur?
- FRONTAL LOBE TUMOR
- Disc Edema in one eye; Disc Pallor w/Decreased Vision in the OTHER EYE.
* May also have POOR SACCADIC FUNCTION towards the Swollen Nerve Side
Pseudotumor Cerebri
- Who?
- Signs/Symptoms?
- Diagnosis of Exclusion: What do we test to see if this is the case?
- Some things that could cause it (CANT)
- Fat Fertile Myrtle
- Papilledema, ENLARGED BLIND SPOT ON VFs. CN 6 Palsy, HAs.
- Normal MRI, Normal CSF content, BUT, HIGH OPENING PRESSURE on LP (>200 mm water)
- Contraceptives, Vitamin A, Naladixic Acid, Tetracyclines
Toxic/Nutritional Optic Neuropathy
- What is the CLASSIC Sign seen?
- Symptoms?
- CAUSES?
- TEMPORAL PALLOR of the Optic Nerves
- B/L, Painless, Progressive Vision Loss and CENTRAL or CENTROCECAL VF LOSS
- Alcoholism, Malnutrition, Tobacco Abuse, Toxicity from MEDS!
Papilledema: Tests
- HTN:
- Tumor
- Brains/Veins
- What else?
- BP
- MRI
- MRV
- LP
Leber’s Hereditary Optic Neuropathy
- Cause?
- Get this from whom?
- Affects mostly whom?
- Onset?
- MAIN CHARACTERIZED SYMPTOM?
- Early Signs?
- Late Signs?
- Mitochondrial DNA Mutations
- MOTHER
- Mostly MALES (85%)
- Late Teens/Early 20s
- Sudden DECREASED CENTRAL VISION (20/200 to CF)
- Disc Hyperemia
- Optic Disc Atrophy
Dominant Optic Atrophy
- Most common type of what?
- When does it develop?
- CHARACTERIZED BY WHAT SYMPTOM?; What Signs?
- Hereditary Optic Atrophy
- YOUNG (childhood)
- Insidious Onset of Mild to Moderate Visual Loss (20/30-20/70);
* Temporal PALLOR and EXCAVATION (Optic Nerves)
Congenital Anomalies: Optic Nerve Pit
- What is it?
- Main Location?
- Pt is at RISK for what?
- Symptoms?
- U/L Depression of Optic Disc
- Inferior/Temporal
- SEROUS RD
- Asymptomatic, unless Macula is involved
Congenital Anomalies: Morning Glory Syndrome
- Uni/Bi?
- Characterized by what 3 things?
- What symptom is seen?
- U/L
- Enlarged, Funnel-Shaped, Excavated ON
- Poor VAs
Congenital Anomalies: Optic Nerve Hypoplasia
- Uni/Bi
- What is it?
- Major SIGN?
- Symptoms?
- Associated with what 2 maternal issues?
- Either
- Optic Nerve doesn’t completely form
- DOUBLE RING SIGN (Disc is Hypoplastic w/a Ring of Sclera and a Ring of Hyperpigmentation)
- Mild to Severe Vision Loss
- FAS and Maternal Drug Use
Congenital Anomalies: Optic Nerve Coloboma
- What is it?
- Cause?
- Usual Location
- What other defects do Pts have?
- a Large, abnormal shaped Disc
- Incomplete closure of the Embryonic Fissure
- INFERIOR/NASAL
- Systemic Defects
Congenital Anomalies: Optic Nerve Head Drusen
- What is it?
- They Appear HYPER-REFLECTIVE on what test?
- HYALINE BODIES in Optic Disc. We start seeing them more as we AGE. Can cause VF Defects
- on B-SCAN
Optic Nerve Tumors
- Melanocytoma
a. What is it? (Benign/Malignant; Pigmented/Non-pigmented)
b. More common in whom? - Optic Nerve Sheath Meningioma
a. Benign/Malignant?
b. Uni/Bi?
c. Seen more in whom?
d. What happens to the ON? - Optic Nerve Glioma
a. Benign/Malignant?
b. Can be associated with what Dz?
- a. Benign, Darkly Pigmented tumor. Adjacent to or on TOP of the Optic Nerve.
b. AAs
* DOES NOT AFFECT VISION - a. Benign mostly
b. U/L
c. Young-Middle Aged women
d. Starts Edematous, then leads to SECONDARY OPTIC ATROPHY and Progressive Vision Loss - a. Benign if starts in CHILDHOOD; MALIGNANT if starts in ADULTHOOD.
b. Neurofibromatosis
- Explain REVERSE APD
- Good Eye: Pupil will CONSTRICT on APD testing. Good to know when Bad Eye has a Corneal Opacity, traumatic pupil, etc…
- Anisocoria: % that is physiological?
- 20%
Aniso: Pupil Size
- 3 Dzs where the ABNORMAL Pupil will be SMALLER in the DARK? (Miotic pupil: larger difference b/w the 2 eyes in the dark)
- 4 Times when the ABNORMAL Pupil will be LARGER in the LIGHT (Abnormal Pupil is Miotic: Larger difference b/w the pupil size in the light)
- Horners, Itis, AR
2. 80s (0.125% pilo), CN3 (1% pilo), Trauma, Pharmacological
Aniso: Adie’s Tonic Pupil
- What is it?
- What causes it?
- Seen mostly in whom?
- U/L or B/L?
- The iris has what kind of MOVEMENT?
- Will pupil constrict to light?
- Will pupil constrict to near object?
- What % of Pilocarpine will cause a Pupil constriction due to HYPERSENSITIVITY of the Cholinergic Receptors on the Iris Sphincter Muscle?
- ADie’s Pupil = ?
- Acute Dilated pupil.
- Lesion in the CILIARY GANGLION or Ciliary nerves
- Young (20-40) FEMALES (30-70%)
- U/L…then becomes B/L at a rate of 4%/yr.
- VERMIFORM MOVEMENT (seen in SLE)
- Slow and minimal to no constriction in response to light
- Slow Constriction to a near object.
- 0.125%
- Acute Dilated pupil due to a CG lesion.
Aniso: Argyll Robertson Pupil
- MIOTIC Pupil associated with what 3 dzs?
- Due to a LESION in what?
- U/L or B/L?
- Characterized by what?
- How does it respond to light?
- How does the pupil respond to near objects?
a. Why is this? - Argyll Robertson Pupil…=?
- NEUROSYPHILIS, Diabetes, Alcoholism
- in the TECTOTEGMENTAL TRACT (Pretectal Nuclei to I/L and C/L EW Nuclei)
- U/L…then becomes B/L w/time
- LIGHT-NEAR DISSOCIATION
- little to no constriction to light.
- Constricts Normally to convergence/accommodation
a. this is mediated by FRONTAL EYE FIELDS that send input to EW nuclei. - Accommodative Response Present
Aniso: Horner’s Syndrome
- Miotic Pupil most notable in dim illumination due to a LESION where?
- What TRIAD do patient’s present with?
- Cocaine Test: Horners: Dilates or not?
a. What does this tell us? - Hydroxyamphetamine: 1%: normally dilates normal EYES. What kind of lesion do we think of when it does not dilate Horner’s pupil?
- 1% APRACLONIDINE: What will it do in Horner’s?
- Sympathetic pathway… (Pancoast Tumor at apex of lung)
- Miosis, Anhydrosis (no sweating), and Ptosis on the affected side.
- NO DILATION (normal eyes: dilates eyes by blocking re-uptake of norepi)
a. Helps us decide if it’s pre or postganglionic lesion - POSTGANGLIONIC LESION suspected
- PUPIL DILATION (Adrenergic Receptors on Iris Dilator muscle are HYPERSENSITIVE)
Coma Pupils: Hutchinson’s Pupil
- What is it?
- Due to what?
- U/L Dilated pupil in a comatose Pt
2. Ipsilateral Tumor or Subdural Hematoma compressing on Pupillary Fibers on surface of CN 3!
Coma Pupils: Miosis
- Why does early stages of coma induce Miosis?
- Inhibitory Cortical Input to the EW nucleus is ABSENT. Put they still respond to LIGHT!
CN 3:
- Superior Division innervates what?
- Inferior Division innervates what?
- What will a Complete CN 3 Palsy look like?
- Symptoms
- Etiology
- Pupil Involvement in what kind of lesion?
a. No pupil involvement in what kind of lesion? - If the pupil is involved or the Pt has an INCOMPLETE CN 3 Palsy, what test should be done!?
- Levator and SR
- IR, MR, IO; Parasympathetic Fibers travel with it to Ciliary Muscle and Iris Sphincter Muscle
- Down and Out and Ipsilateral Ptosis (is that right???)
- could have diplopia
- Microvascular Infarct, Trauma and Aneurysm (LOOK THIS INFO UP!)
- Compressive (tumor/Aneurysm): FIXED and DILATED
a. Ischemic Palsy - MRI/CT and MRA to r/o Aneurysm (most commonly at the POSTERIOR COMMUNICATING ARTERY!)
CN 4: Trochlear
- CN4 Palsy presents w/what type of Deviation?
- Symptoms
- Etiology
- Congenital will have what? (vs. Acquired)
- Dx?
- HYPERDEVIATION w/a Torsional Component.
- VERTICAL DIPLOPIA; maybe torsional Diplopia; HEAD TILT AWAY from SIDE of LESION to MINIMIZE diplopia
- Trauma/Congenital. *Most susceptible to Trauma due to longest course in the body of all the CNs.
- Congenital: LARGE VERTICAL VERGENCE RANGES
- Park’s 3 Step; Double Maddox rod for Torsional
CN 6: Abducens Nerve
- *Most common of the 3 CN Palsies affecting EOMs. Symptom?
- Etiology?
- Differential Dx?
- Horizontal Diplopia
- Microvascular Infarction; Pseudotumor cerebri, Trauma, Tumor, Horner’s Syndrome
- Duane’s Syndrome and Infantile or Accommodative Esotropia
EOM Palsy: Most common causes
- CN3
- CN4
- CN6
- What kind of cause will usually resolve w/in 3 Months?
- Aneurysm
- Trauma, Congenital
- Increased ICP
- Microvascular
What 2 DZs should ALWAYS be considered for ALL ocular motor palsies?
- MG and TED
Ocular Myasthenia
- What is this?
a. 90% of Pts w/Systemic MG will have what? - What is going on here?
- Symptoms?
- Dx?
- MG in the eye. Involves the muscles of the eye.
a. ocular signs at some point; 70% of cases will have ocular signs as the initial sign of MG. - Ach receptors are blocked or altered at the NMJ, causing weakness of skeletal muscles
- Levator and EOMs are susceptible to a deficiency in innervation causing Ptosis and Diplopia. Signs vary and are worse at the end of the day or when the patient is tired.
- Tensilon test or high serum levels of Ach Receptor Antibodies. *Injected IV. Inhibits breakdown of Ach in Synaptic cleft, prolonging its duration of action. (tensilon uses Edrophonium)