Neuro unit 3

what part of the nervous system conserved energy

Parasyspathetic

• anabolic and rest and relax

location of rewards and punishment center

limbic system

what part of the autonmoic nerverous system does catabolic function

Sympathetic nervous system

catabolic= break wodn mean expends energy

PNS cranial nerve system

•CN 3—pupillary constriction/accommodation

•CN 7—lacrimation and salivation (submandibular gland)

•CN 9—salivation(parotid gland)

•CN 10—thoracic and abdominal viscera

PNS fibers arise from

sacral nerves and brainstem

saracal nerves innervate colon, rectum, bladder, uterus

parasympathetic nervous system releases what NT

Ach

sacral nerve S2-S4

PNS innervation of the colon, rectum, bladder, uterus

what dilates the iris

sns

what parts of the brain of the limbic system

•Portions of the thalamus*

•Relays sensory and motor functions

•Consciousness and alertness

•Hippocampus

•Encodes memory—who, what, where, and when

•Spatial navigation

•Amygdala

•Fear and anxiety

•Emotional memory

•Moral learning

•Hypothalamus

•Thirst  and hunger

•Involuntary changes in HR, RR, Bp, diversion of  blood to skeletal muscle

•

•

•Portions of

•Frontal Lobe

•Helps to refine and adapt primitive reaction to stimuli

•Prefrontal cortex is the primary area involved

•Executive functions—memories, flexible thinking, self-control

•Medial temporal lobe

•Cerebral cortex

•Basal ganglia*

•Motor learning

•Emotions

•Rewards

role and location of the limbic system

The limbic system is a network of structures deep inside the brain that regulates emotions, behavior, motivation, and memory. Located on both sides of the thalamus beneath the cerebral cortex and above the brainstem

self stimulation causes a release of

norepinephrine

doapmine

examples are yoga, reading, mindful breathing

wenickes syndrome seen in

alcoholics and malnutrition

wenickes syndrome is causes by

B1 def aka thiamine

what does lack of B1 impair

CHO metabolism

alcholo effects of thiamine

absorption, transport, and utlization of thiamine

Sx of wernike syndrome (triad)

1. nystagmus

2. ataxic gait

3. altered conssciousness

what type of nystagumus is seen in wernike syndrome

hortizontal are most common and resolve after treatment

up beat is more common

when is downbeat nystagmus seen in wernikes syndrome

later in disease

what does conjugate gaze palsies reflect

lesion in occular motor, abducens, and vestibular nuceli (a neurological condition where a person cannot move both eyes together in a single horizontal or vertical direction

CT/MRI findings of wernikes syndrome

hemmorhages in the maillary bodes, periaqueductal grey matter, and hypothalamus

hemorrhages in wernikes are caused by

caused by leaky capillaries and breakdown of blood brain barrier (lactic acidosis, oxidative stress, excitotoxicity, and loss of astrocyte)

Amygdala

fear and anxiety

emotional memory

moral learning

hippocampus does

encodes memory like who, what, where, when

spatail neavigation

hypothalamus

thirst and hungar

involentary changes in HR, RR, BP diversion of blood into skeletal muscle

what does the thalamus do

relays sensory and motor function

Korsakoff syndrome sx

• retrogrades anemia

• antergrade amnesia

• confabulations

others: tremors, vision problems, coma

tx of korsokoff

thiamine 500mg IV 2 days and 250 for three days

proper nutrtion

hydration

cessation of alc

Kluver Bucy syndrome

behavioral imapirment causing hyperorality

affects temporal lobes b/l primaily the hippocampus and amygdala

what is hyperolity

kulver bucy syndrome

what types of the brain does the kluver bucy syndrome

b/t temporal lobes primarily and the hippocampus alnd amygdala

what are the sx of kluver bucy

• docile behavior as they loss loss of fear and anger response

• hypersexual

• hyperoality

• complusive attentiveness

• visual agonisa

what is visual agonisa

unable to idenitfiy object by sign

MRI findings of kluver bucy

lesions of the amygdala and hippocampus

causes of KBS

• TBI

• herpes simplex

• alzheimers dx

• CVA affecting b/l temporal lobes

• brain tumor affecting b/l temporal

what are the tx of KBS syndrome

• mood stabilizers aka carbazepine

• SSRI

• antipsychotics: haldol, carbamazepine (works best TBI), and leuprlide

haldol

treats the behavioral abnormailites

carbamazepine

reduces sexual behavior abnormalites

leuprolide

reduces sexual bahvior abnormailites

is BSV with an infection

treat the infectionn

where is the pituitary gland

pea shaped gland attached to hypothalamus

lives in the sella turcica

anterior pituitary hormones

• GH

• Prolcatin

• ACTCH

• TSH

• FSH

• LH

pituitary tumors

•Prolactinoma

•Somatotroph Adenoma

•Corticotroph Adenoma

•Thyrotroph Adenoma

•Gonadotroph Adenoma

•Nonfunctioning Adenoma

sx for

slide 27 ?>

what do nnon functiong adenomas cause

VA changes

HA

decreased release in hormones due to compression: hypopituitarism

posterior pituitary releases

vasopression

ocytocin

what does vasopression do

• osmotic control

• BP reg

• sodium control

• kidney function

where is vasopression synthesized

hypoathalmus

what can go wrong with vasopression

• SIADH

• Centrral DM insipiduis;

• nephrogenic DM

what is the difference between central DM insipidiu and nephrogenic DM insipidius

• central= decrease ADH secretion

• nephrogenic DM= normal ADH but kidney unresponsive

what are the autonomic sx disease

•Diabetes Insipidus

•Precocious Puberty

•Horner’s Syndrome

•Pituitary Tumors

•Hirschsprung’s Megacolon

•Shy-Drager Syndrome

pt who pees up 20 quartes a day with constant thirst polydipsia

diabetes insipidus is a disorder of increased urine output

what is gestational DM insipidis

increased placental production of enzyme that breals down ADH

what are the primary causes of DM insipidious both central and nephrogenic

hereditary

what are the secondary causes of central DM insipidisis

• pituitary/hypothalamic surgery

• head trauma

• tumors

• idopathic

nephrogenic DM incipidious secondary causes

• Med

• electrolyte disorders

• obstructive uropathy

• amylydosis, sjogrens, myeloma

what is the MCC med to cause nephropgenic DM insipidis

lithium causes secondary

what electrolyte abnormaility can cause secondary nephrgenic DM I

hypercalcemia and hypokalemia

what are sx of DM I

• thirst

• poilyuria

• dry mnouth

• fatigue

• nausea

• syncope

• intense thirst

• Dizzy

what is the work up for DM I

• 24 urine

• BMP

• copeptin bases testing or water deprevation test

• vasopression stimulation test

• MRI

what can help determine between DM I nephrogenic and central

vasopression stimulation test

what would you see in vasopressin stimulation test in DM I central v neph

in central dx there will be more concentrated urine

in nephro there will be no change to urine cause kidneys do not respond

copeptin

is released with ADH

copeptine in neph

will be normal level cause ADH is still being made

copeptin in centrral

willl be decrease cause no ADH is being produced

water deprivation test

no water for 8 hours if you have DM insipidis then you will not see a change in urine

what are the complications to DM I

•Dehydration

•Tachycardia

•Hypothermia

•Hypotension

•Weight loss

•Fatigue

•HA

•Nephropathy

•Brain damage

what is the tx of DM I central

DDAVP

what is the tx of DM I nephro

• low Na diet

• thaizide diuretics

• NSAID

• stop taking lithium

Low sodium diets helps to reduce urine out, thiazide diuretics help increase sodium and water resorp in proximal tubule (paradoxical effect), NSAIDs limits prostaglandin synthesis which helps sensitize kidneys to vasopressin, lithium damage kidney’s response to vasopressin

what to do when patient had DM I nephro caused by lithium but still needs to take the meds

add amilloride

what is precocious puberty

early onset of secondary sexual characteristics

what is consider precocious puberty

females at 8 and males 9

what is the mc of precocious puberty male f female

idopathic in females and males pathologic

wwhat are cental causes of precocious

•CNS tumors

•Hypothalamic hamartoma most common

•CNS injury

• Trauma

• Radiation

• Cerebral Palsy

• Infections

•Neurofibromatosis Type I

•Genetic inheritance

what is hamartoma

Abnormal growth of tissue from where it develops from

hypothalamic hamartoma

abnormal growth of hypothalamic cells

cafe au lait spots

think neurogibromatosis type 1 which is dominant benign tumor growth on nerves

peripheral cause of precocious puberty

•Due to production of sex hormones from endo/exogenous sources

•Less frequent than central

I think the following:

•Congenital adrenal hyperplasia

•McCune-Albright Syndrome

•Genetic d/o

•Gonadal tumors

•Exogenous exposure to sex steroids

review slide 48

what labs for precocious w/u

•LH/FSH

•Testosterone

•DHEA-S  (dehydroepiandrosterone)

•17-OH progesterone levels

•Thyroid function

what is the intial test for precocious

x- rays

what is gold standard for prococious

GnRH

what imaging for peripheral cause of precocious

• US of the ovary tumors and cyst in females

• U/S for leydig cell tumors in males

central imaging for percocioous puberty

MRI to r/o hypothalamic lesion

tx

slide 52

what is horner syndrome

disruption of sympathetic nerve supply results in partial ptosis, misosis, facial anhidrosis

facial anhidrosis

lack of sweating on one ot both part of the face

miosis

constricted pupil

sx of horner syndrome what side of injury

ipsilateral

where can PNS fibers that cause horners syndrome be affected

• hypothalamus

• C8-T2

• cervical sympathetic chain to superior cervical ganglion

• along course of cartoif artery

where is first order neuron located horner syndrome

hypothalamus to brain stem (midbrain, pons, and medulla down cervical spin cord C8

2nd neuron order for horner syndrome

C8-t2 to paravertebral sympathetic chain close to lung apex

3rd order neuron for horner syndrome

superiod cervical gnaglion to the internal artery, cavernous sinus to orbital fissure

causes 1st order neuron

• CVA

• MS

• arnold-chiari malformation

• mengitis/ encephalitis

causes 2nd order neuron

•Pancoast tumors (apex of the lungs)

•Subclavian artery aneurysm

•Dental abscess

3rd order neuron

•Carotid cavernous fistula

•ICA dissection/aneurysm

•Cluster HA/Migraines

•Herpes Zoster infection

•Temporal arteritis

skiped to slide 70

hirschsprung megacolon

congenital absence of parasympathetic ganglions in wall of colon means it has poor motility and dilated colon

sx at birth of hirchsprung megacolon

• faluire to have leconium in firsdt 48 hrs

• abdominal distention

• fever

• n/f

• obstipation

children hirsprung mega colon sx

• preogessivley gets worse

• loss of apppetite

• delayed growth

• small watery stools

• abdominal distention

sx of hirsprung megacolon depends to

amount of colon that is not innervated

rectal biopdy for H megacolon

shows absence ganglion cells and hypertrophic nerve trunks