index cards neuro 2 part 1

8/3/2019 Index Cards Neuro 2 Part 1

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The Human Hypothalamus – Torres

Hypothalamus functions: feeding, fighting, F’ing. Water and

electrolyte balance, food intake, blood pressure, circadian rhythms,

sexual drive. 3rd ventricle encapsulates hypothalamus.

– Anatomic location – middle of brain and encapsulates ventralportion of 3rd ventricle.

– Regulation of Autonomic responses

– Baroreceptor reflex – regulates BP from aortic arch and

carotid sinus

Hypothal. Neurons(*paraventricular nucleus) next to the

3rd ventricle and projects to the dorsal vagal nucleus of

medulla(area resp. for auton. Resp.)

– Temperature regulation reflex:

. heat dissipation(dilation) – rostral hypothalamus

Hypthalamic Functions Continued..

– Anterior Hypothalamus: (pre-optic region) – impt. Inregulating INTERNAL body temperature Lesion =

Hyperthermia – EXAM!!

– Posterior Hypothalmus: resp. for generating and conserving

heat. Responsible for keeping you warm. Lesion: patient

cannot thermoregulate.

– Retinal Hypothalamic Tract: Direct pathway btw.

Hypothalamus and hypophysis this connection is resp. for

circ. Rhythms. As photons from the outside impinge upon

retina, direct connection btw. Eyes and hypothalamus

– Water Balance reflex: osmolarity monitored by osm.sensitive

neurons in ant. Hypothalamus(near POA – pre-optic area andPVN)

– Arginine/Vasopressin - produced in 2 areas both also

roduce ox tocinCortisol release feedback onto PVN to stop making CRF.

Clinical depression – high levels of cortisol

Dexamethasone suppression test – normally suppresses but

with clinical depression no suppression

Pancreas – can secrete ectopic ACTH

FSH ovarian follicles estrogens

LH corpus luteum progesterone

Hypothalamic hormones: arginine/vasopressin, oxytocin, orexin

cells(hypcretin cells – def. in narcolepsy), CRF, GnRH(mutation in

Kallman’s cells fail to migrate to arcuate nucleus in hypothal.)

Obesity – twins concordance 70-90% in monozygotic/35-45%



Arcuate nucleus – impt. In terms of hormone secretion and

obesity

Adipose tissue makes: TNF-alpha, IL-6, Leptin

Fat cells come in two types: size of adipocytes increases as you

gain weight

– Brown – non shivering thermogenesis

– White – responsible for lipid storage

EXAM KNOW THESE TWO AREAS:

– Lateral Hypothalamus: (hunger center) – lesions here

weight loss

– Ventromedial hypothalamus(satiety) – lesion obesity

– OB gene = Leptin – its a type 1 cytokine receptor/ Ob gene

crosses the BBB, goes to the hypothalamus and tells you to

stop eating

– Db = Leptin RECEPTOR

– Leptin – appetite suppressing hormone that crosses the BBB

and can be used in Hypothalamic Amenorrhea injected.

Leptin is synthesized in brown adipose tissue.

Ob/Ob Mice vs. Db/Db Mice(Diabetes gene, Leptin Receptor)

– Parabiosis experiment: If you take an Ob mouse and you

Melanocortin Receptors and food intake:

– Neurons in the arcuate nucleus of hypothalamus with high

levels of peptides derived from pro-opiomelanocortin(POMC)

– POMC - Specifically synth. In hypophysis with no biological

activity but it is a precursor to ACTH, alpha, beta, and gamma

MSH(mel.stim.horm.) these are all essential for food intake

but also skin pigmentation

– Melanocortin Receptors:5 g-protein receptors mediating

melanocortin

. MC3R and MC4R – found in brain – most impt. For food

intake specific. 4

. MC1R – found in melanocytes

. MC2R – responds to ACTH in adrenal cortex

Interstitial nucleus of

anterior hypothalamus

is dimorphic. INAH-3,4

show sexual diff. btw. Male



MC4R deficient humans: humans and mice null of this are obese

and hyperphagic

Agouti normally expressed in skin, hair follicles and brain

Ghrelin – displays GH releasing activity

– Stomach and proximal small intestine

– Appetite stimulating hormone

– Everytime you are about to eat, ghrelin goes up

– Associated with gastric bypass surgery

PYY – is in small intestine and decreases feeding

CART(cocaine and amphetamine regulated – suppress feeding

Neurochemistry and Neuropharmacology – Torres

Most diseases are loss of function. Some are gain of function such

as Huntingtons.

Catecholamines: Dopamine, NE(locus ceruleus), Epi(found in

medulla). Serotonin NOT catech.

– Dopamine – synth. In substania nigra, midbrain, VTA, retina,

hypothalamus, tubuloinfundibular system

– D2 receptor – found exclusively pre-synaptically(autoreceptor)

as opposed to post synaptic receptor.

– Diseases ass. With Dopamine:

. Bipolar

. Schizophrenia – too much dopamine, as you treat this you see

Serotonin: synth. In raphe nuclei in back of brain, pons, brainstem

and has pre. And post synaptic receptors. Only good animal model

we have for this is drug addiction.

– Also found outside CNS in: platelets, placenta, when produced

here it is unable to cross BBB.

– It has at least 15 receptors

Too much serotonin:

– Cardiac problems, GI problems, Insomnia, anxiety, sexual

dysfunction

Not enough serotonin:

– Bulemia, Panic attacks, OCD, depression

– Females are most susceptible to depression and schizophrenia



NO: founds in CNS, GI, testes, ovaries

Endocannabinoids: synth. By brain. Marijuana has Delta-9-

THC.CNS makes this as well(endocannabinoids)

– Anandamide– similar to and mimicks THC has two receptors:

. CB1 – in the CNS, immune cells, spinal cord, testes, ovaries

. CB2 – outside the CNS, everywhere else

– Dronabinol – synth. THC used to eat more with AIDS, cancer,

nausea, chemo, prevents emetic reflex

Ketamine – works on Glutamate system and targets and is very

effective at treatment of depression. It targets NMDA glutamate

receptor. In pediatric patients it is a dissociative anesthetic

Epilepsy criteria – two or more seizures and EEG and brain scans

are MC Dx. Test.

Temporal lobe epilepsy: hippocampus(dentate gyrus) plays a key

role in initiating seizures

Voxel based morphometry – lateral hypothalamus is vulnerable to

epileptic attacks, also rostral area, it shows hippocampal atrophy in

pts. With epileptic seiures originating in left or right temporal lobe.

Epileptogenesis – excessive excitation due to lower threshold. 2

ways to induce attack: excessive excitation(depolarization) or

hyperpolarization can be inhibited.

– GABA – valproate and tiagabine(enhance GABA)

. found in interneurons **remember in early fetal development

GABA is both inhibitory and excitatory, when brain rechesmaturity only inhibitory

– Glutamate – felbamate, topiramate, lamotrogine: inhibits

NMDA rece tor(N-meth l-D-as artateSchizophrenia – hallucinations are positive symptoms, most

treatments don’t treat negative symptoms OR COGNITIVE

impairment

– It is a subtle disorder of plasticity

– Risk genes: dysbindin, neuroregulin 1, DISC 1, COMT. DISC 1

EXAM for psychosis! CN V copy # variations

– Peds kids(may not be on exam) – loss of gray matter in frontal

cortex early on.

– They will have Enlarged Lateral Ventricles

– Drugs diminishing + effects:

. 1st gen. – haloperidol, perphenazine – inhibit D2,D3 patients

get parkinsons like symptoms: rigidity, dystonia, dyskinesia

. 2nd gen. – clozapine, olanzapine – no motor side effects,

causes OBESITY particularly olanzapine, compliance a problem.

. target: histamine, NE, dopamine, serotonin receptors – non



ADHD: brain abn. In frontal, and temporal lobes as well as basal

ganglia

– Hypoactive frontal-striatal regions due to deficient

dopamine

– Methylphenidate to treat which prevents reuptake of dopamine

– Patients have low levels of dopamine– Temporal and frontal lobes affected

Depression etiology:

– Stress(HPA axis), and sytokines(IL-1, IL-6, TNF-alpha)

– Signaling pathways that regulate neuro-plasticity

– Olfactory bulb and hippocampus – only areas of brain

undergoing mitosis all the time, hypothesis is tht these people

are unable to synth. New cells

– Treatment:

Duloxetine – inhibits NE reuptake

Symbrax – combo. Of SSRi and antipsychotic also works on

dopamine and Ach.

Lithium – can cause depletion by inositol monophosphatase

Anti-seizure drugs like valproate, lamotrigine, carbamazepine can be

used for depression

Fluoxetine – SA is impotence

OCD – autoimmune following childhood infection or roguegenes(EXAM)

Know the following for the exam!!!

Gilles de la Tourette syndrome – more common in males and part

of PANDA syndrome, one of most impt. Causes of childhood tics.

. etiology is strep.(PANDA)

. simple – motor and vocal tics

. full blown has coprolalia, copropraxia, echolalia, echopraxia

GTS “plus” ADHD,OCD,depression

– Treatment sulpride, clozapine, clonidine, SSRI, ceftriaxone

Gain of function diseases:

– Huntingtons(CAG repeats) coding glutamine

– Spinal and bulbar muscular atrophies(Kennedys disease

– 7 forms of spino-cerebellar ataxia



Blood Supply of the CNS – Leheste

Stroke – 3rd MCCOD in industrial nations

Intra-axial hemorrhage – within the brain

Extraaxial – within the meninges

Berry aneurysm is within circle of willis while Charcot Bouchard

aneurysm is deep within brain tissue ass. With untreated HTN

AV malformation – happens embryologically and is malf. Of

capillary beds where arterioles and venules meet

Ruptured berry aneurysm location – btw. Arachnoid and pia mater

and most common artery is anterior communicating artery

lumbar puncture shows blood in CSF with stiff neck, neurosurgical

emer encHow many anterior spinal arteries are there? 1 2/3rds blood

supply while posterior spinal artery is only 1/3rd blood supply

Anterior spinal artery and posterior spinal artery merge at each level

of each spinal nerve with posterior radicular artery

Venous drainage: We only have 1 anterior and 1 posterior vein and

they run into a venous plexus.

Anterior external venous plexus(outside spinal column) and

anterior interior venous plexus(inside spinal column) merge

on the inside of the venous plexus into the Intervertebral vein

this is what takes the blood away from the spinal cord

2 vertebral arteries near the site where they merge form an anterior

spinal artery and 2 posterior spinal arteries. Then they merge and

become the basilar which runs in the basilar groove on the ventral

PICA – supplies more interior structures while AICA which supplies

more area supplies more on the cortical surface of the cerebellum,

along with upper medulla and lower pons. There is physical overlap

btw. The 2.

Labrynthine artery(internal acoustic artery) – goes to inner ear

supplies internal acoustic meatus which is a space that allows

blood vessels to goto the inner eat and also the vestibule then it

supplies sense of balance, proprioception and hearing

Basilar artery pontine artery classified as:

– Paramedian(short) supplies medial basilar

pons(corticospinal tract), pontine nuclei, pontocerebellar

fibers(stability, ipsilateral)

– Circumferential(long) supplies lateral pons, middle

cerebellar peduncle, lateral pontine tegmentum



PCA supplies: occipital lobe and splenium(post. 1/5th of corpus

collosum)***EXAM!!!, supplies all the primary and some of the

association cortex for vision in combination with motor.

Locked in syndrome: infarction of ventral pons. Patient is

conscious but cannot move or speak due to complete paralysis of all

voluntary muscles except eyes. MLF spared along with reticularpathway.(MLF: oculomotor sends info through MLF) corticospinal

fibers are affected on Right and left side.

Medial medullary syndrome: occluded vessels:

Anterior spinal artery, medullary branch of vertebral

artery

– These structures supply pyramids of CST, DCML, CN-12

– Pts. Get contralateral spastic hemiparesis, contralateral loss of

proprioception, vibratory sense and tactile discrimination fromLateral medullary syndrome(Wallenburg) – medullary branch

of PICA

– Nystagmus away from side of lesion, vertigo, nausea, vomiting

– Ipsilateral cerebellar signs

– Ipsilateral loss of pain and temp. to face

– Contralateral loss of pain and temp. to body

– Horners syndrome

Medial pontine syndrome: occluded vessel: paramedian

branches of basilar artery

Deficits: ipsilateral medial strabismus, contralateral body spastic

paresis(UMN), contralateral body loss of position and vibration

Lateral pontine syndrome: occluded vessel – AICA(caudal pons),

SCA(rostral ons)PCA – main supply is occipital lobe – PCA syndrome will present

with visual field defect, and ***Alexia without agraphia(pt. can

still write)**. Patient can see the letters but cannot interpret them.

They also get:

– Disconnect syndrome – left visual cortex is unable to receive

info the right eye is trying to convey. This happens because

PCA supplies caudal 1/5th of corpus collosum.

Raymonds syndrome(occluded pontine branch of basilar

artery): medial strabismus of ipsilateral eye, loss of visual tracking,

object fixation, contralateral hemiparesis. Similar to medial pontine

syndrome.

Millard Gueblers Syndrome: occluded pontine branch of

basilar artery with more dorso-lateral extension of lesion. Patients

will get contralateral hemiparesis and paralysis of ipsilateral facial



Some questions

– 25 year old medical student had an excruciating headache and

looked in the mirror and noticed eyes were drooping, diplopia

and eyeball was looking down and out. What artery?Posterior communicating artery

– Wallenburgs is ass. With nystagmus, vertigo, ataxia,

ipsilateral laryngeal paralysis, loss of gag reflex, horners

syndrome. Which artery is to blame? PICA supplying the

cerebellum

– 56 year old man presents with dropping of corner of mouth on

right side and weakness of muscles on that side of face.

Patient has full blown left pupil, cant adduct the eye during

gaze or convergence. Drooping of left upper eyelid and both

Part II Vascular Supply of Diencephelon and Cerebrum

Internal carotid artery: merges blood supply that comes from

vertebral arteries. Merges at the Circle of Willis.

-4 sections: cervical, petrous(goes right through foramen lacerum),

cavernous, cerebral

- Internal carotid artery gives rise to MCA and ACA

Ant. Communicating artery – connects both ACA’s, most common

site of berry aneurysm***

MCA – emerges from brainstem and then carries blood into the

sylvian fissure and then supplies most of lateral aspects of brain

supplies lateral cortical areas

ACA – branches are medial striate arter and ant. CommunicatinMiddle cerebral artery – dips into lateral fissure to supply internal

structures and comes out of sylvian fissure. Meanders around 3

lobes(frontal,parietal,temporal)

– Primary motor and premotor cortex and primary

somatosensory area and frontal eye field, cortical areas of

language, post. 4/5th of internal capsule, most of basal ganglia

through striate arteries



From picture we can see that ACA supplies most of interior cortical

areas in primary motor cortex lower limbs, stretches into central

fissure

MCA occlusion facial deficits, lingual defects because wernickes

and brocas messed up

PCA occipital lobe, primary and associated visual cortex,

splenium(post. 1/5th of corpus collosum disconnect syndrome

Posterior communicating artery problems visual field defects

Lesions of ACA unilateral contralateral motor and sensory in

lower limb with transcortical apraxia of left limbs if corpus

collosum involved

Bilaterally b/l like above but impaired memory(because fimbria

Lenticulostriate artery problems: will lead to basal ganglia

defects – motor movements, eye movements, emotions

Venous drainage of brain:

– Cerebrum: external venous system drains hemispheres while

internal drains core of cerebrum

(If have time, look over veins from notes)

Some questions:

50 year old HTN woman complains of numbness and weakness in leftleg and foot, occlusion of what artery? Right ACA

63 year old man comes in and says dad can no longer read or write.

He can speak normally and execute simple motor commands but

when examining him he cant subtract or add. What is the syndrome?

What artery compromised? What anatomical site? Gertsmann

syndrome/Left ACA/Angular Gyrus

Berry aneurysm puts pressure on optic chiasm in anterior/posteriorplane resulting in bitemporal hemianopia. Where is aneurysm found?

Anterior communicating.

60 year old man is suddenly unable to swallow or speak and is

tetraplegic. He can only move eyes vertically and blinks bilaterally.

Able to read and understand whats being said to him. He responds



50 year old woman with dizziness and hearing loss in left ear with left

ear hearing loss, loss of pain and temp on right side of body but left

side of face, palate drooping, diff. swallowing, dryness of left side of

face and left pupil constriction. What affected structure is most likely

responsible?/hearing loss and nystagmus indicate lesion of what

structure? What blood vessel is occluded? Nucleus

ambiguous/vestibular and cochlear nuclei/occlusion of PICA

Wallenburg syndrome

index cards neuro 2 part 1

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