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Thalamic nuclei:
VPL, VPM
LGN, MGN
VL

VPL - STT (pain & temp) & dorsal column/medial lemniscus (touch, etc)
VPM - Facial sensation & taste (trigeminal, gustatory tracts)

LGN = "Light"/vision; MGN = "Music"/hearing
VL = motor (from basal ganglia to motor cortex)

1

Hypothalamic nuclei
- Lateral vs. Ventral
- Anterior vs. Posterior
- SCN

Lateral (hunger) vs. Ventral (satiety)

Anterior (cooling "A/C" - parasymp) vs Posterior (heating- sympathetic)
SCN = circadian rhythm

2

Limbic systems structures

= hippocampus, amygdala, fornix, mammillary bodies, cingulate gyrus

for the "5 Fs" (Feeding, Fleeing, Fighting, Feeling, & Fornication/Sex)

3

Direct pathway in basal ganglia

disinhibits thalamus => STIMULATES mvmt
striatum (D1 from SNc) --l Globus Pallidus interna
=> thalamus free to transmit signal

4

INdirect pathway in basal ganglia

INhibits motion by inhibiting thalamus, using GABA.
striatum (D2 from SN) --l GPe => STN not inhibited -> GPi --l thalamus

5

Function of therapeutic hypOventilation

decrease ICP (brain pressure/edema) by decreasing cerebral perfusion
*bc blood flow = controlled by PCO2 level
(ie: in case of stroke or trauma)
*Hypoxemia only influences cerebral perfusion when PO2 > 50 mmHg!

6

Brown-Sequard Syndrome

= hemisection of spinal cord, so mixed sensory, motor & pain Sxs
- IPsilateral: AT level of lesion - LMN & all sensation lost; below - UMN & touch/vibration/proprioception lost
- Contralateral: below lesion - pain & temp sensation lost
AND Horner's S. if lesion above T1!

7

Horner's syndrome
(Sxs, scenario)

Sxs: Ptosis, Miosis, Anhydrosis (all controlled by descending sympathetics from superior cervical ganglion, via IML in spinal cord)
When: lesion to spinal cord above T1

8

CNs that innervate the eye muscles

CN III (occulomotor) = SR, IR, MR, IO --> "down & out" if damaged
CN IV (trochlear) = SO
CN VI (abducens) = LR

9

Uvula, tongue & jaw deviations w/ CN damage...

1. Uvula deviates AWAY from lesion (CN X)
2. Tongue deviates TOWARD lesion (CN XII)
3. Jaw deviates TOWARD lesion (CN V)

10

muscles that move the jaw

Open: Lateral Pterygoid (only, "Lateral Lowers")
Close: Medial pterygoid, Masseter, teMporalis

11

Glaucoma:
Acute angle closure vs. chronic/open

= optic neuropathy w/ increased IOP
Acute angle closure: painful! sudden vision loss, HARD eyeball, headache *do NOT give epinephrine!!*

Chronic/open: gradual, not painful

12

Case:
Infant born w/ port wine stains in V1 distribution, hemiparesis, and mental retardation...
What other risks should be checked for?

= Sturge Weber syndrome (sporadic)
Risks: ipsilateral leptomeningeal angiomas, pheochromocytomas, Glaucoma, and seizures.

13

Case:
Child with mental retardation, ash leaf spots, and cutaneous angiofibromas ("adenoma sebaceum").
What other risks should be expected?

= Tuberous Sclerosis (AD)
Other risks:
- Hamartomas in CNS & skin, seizures
- mitral regurgitation & cardiac rhabdomyoma
- renal angiomyolipomas.

14

Case:
Infant born with cafe-au-lait spots. Look for what other problems?

= NF1, NeuroFibromatosis/"vonRecklinghausen's disease" (AD)
Mut: NF1 gene on chrom. 17
Other risks: Lisch nodules (iris hamartomas), neurofibromas in skin (from neural crest tissue), optic gliomas, pheochromocytomas

15

Case:
Infant born w/ cavernous hemagiomas on skin. Has family Hx of neuro disorder(s).

= von Hippel-Lindau disease (AD), VHL mut on chrom. 3
Other problems:
- hemangioblastomas in retina, brainstem, or cerebellum
- pheochromocytomas
- bilat. renal cell carcinoma

16

Case:
Young boy can't keep up with classmates when playing. To stand up from the ground he "climbs" himself up with his arms. Muscle hypertrophy apparent in both legs.

Duchenne Muscular Dystrophy, X-linked recessive
= deleted dystrophin gene (muscle structural protein)
=> proximal muscle weakness ("Gower's sign" to stand)
Histo: necrotic muscle tissue

17

Case:
Young child with kyphoscoliosis, dysarthria, and ataxia.
What neural pathways are affected? What other risks?

= Freidrich's ataxia (AR) trinucl. repeat in Frataxin gene
(mitochondrial impairment --> excess free radicals)
=> degeneration of spinocerebral tract, dorsal column & DRG.
Risks: hypertrophic cardiomyopathy, DM, foot deformities.

18

Neural crest derivatives

1. PNS
2. Ganglion cells (of ANS & CNs)
3. Pia mater & arachnoid ("leptomeninges")
4. Melanocytes
5. Chromaffin cells (adrenal medulla)
6. Parafollicular cells (make calcitonin)
7. Bone & CT of pharyngeal arches

19

Alar plate vs. basal plate

(Embryological components of spinal cord)
Alar => sensory neurons
Basal => motor neurons

20

Spinal cord level for ankle jerk reflex

S1 (gastrocnemius m.)

21

Spinal cord level for knee jerk reflex

L2 - L4 (quadriceps m.)

22

Spinal cord level for biceps jerk reflex AND forearm jerk reflex

C5, C6

23

Spinal cord level for triceps jerk reflex

C7, C8

24

Cranial nerves with Parasympathetic fibers (4)

III - ciliary ganglion of occult motor n.
VII - pterygopalatine & submandibular ganglia of facial n.
IX - otic ganglion of glossopharyngeal n.
X - terminal/intramural ganglion of vagus n.

25

Spinal cord levels w/ sympathetic ganglia

T1 - L3,
Superior cervical ganglion for head-C8

26

Succinylcholine:
- pattern of f(x)
- SEs/Complications

= ACh R antagonist => muscle relaxant (ie: for intubation)
2 parts to f(x):
1. phase I = prolonged depolarization, No antidote. *constant train of 4
2. phase II = desensitized ACh Rs, CAN reverse w/ neostigmine
*fading train of 4
SEs: hyperK+, hyperCa2+, malignant hyperthermia

27

Antidote to organophosphate poisoning

Atropine AND pralidoxime (regenerates active AChE)
Sxs of organophosphate poisoning:
DUMBELSS (or SLUD) bc organophosphates irreversibly --l AChE!

28

General function of each of the 3 types of Parasympathetic Rs
(muscarinic - M1, M2, M3)

M1: gastric & CNS
M2: heart
M3: smooth muscle (peristalsis, bronchoconstriction, vascular endothelial release of NO)