• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/127

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

127 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
4 divisions of the diencephalon
- Hypothalamus
- Subthalamus
- Epithalamus
- Dorsal Thalamus THALAMUS
Anterior Nucleus
PAPEZ CIRCUIT:
Mammillary bodies to Anterior Nucleus to Cingulate Gyrus to Hypocampus to Fornix to Mammillary Bodies

{Learning/Memory: Anterior cingulated gyrus}
Dorsomedial nucleii
Connected to Frontal Lobe

{Connects Limbic areas: Prefrontal cortex}
Ventral Anterior nucleii
{Premotor}
Ventral Lateral
{M1. Primary motor cortex}
Ventral Posterior Nucleii
1) VPL: from trunk/limbs via Spinothalmic and Medial Lemniscus
2)VPM: from Trigeminal

{Somatosensory input}
Medial Geniculate
{Auditory input: A1}
Lateral Geniculate
{Vision: V1}
Motor Nucleii
Somatosensory
PTO Cortex
Motor Nucleii : VA, VL
Somatosensory: VPL, VPM
PTO Cortex: Pulvinar
Subcortical nucleii
Have NO CORTICAL PROJECTIONS (project back to other thalmic nucleii)
Thalamus irrigated by
1) Thalamoperforating a.
2) Thalamogeniculate a.
3) Posterior choroidal aa.

{HTN>Contralateral hemiplegia}
Internal capsule irrigated by
1) Lenticulostriate a. {HTN>Contralateral hemiplegia}

2) Medial striate a. (from ACA)

3) Anterior choroidal (from MCA)
VPL/VPM Lesion
Contralateral Somatosensory disturbance
LGN lesion
Contralateral Visual field defects
VA/VL lesion
Disturbances in motor control
Pulvinar lesion
Visual-spatial, perceptual, language disturbances
Anterior nuc. lesion
Memory loss
DM nuc. lesion
Executive or frontal lobe deficits
Intralaminar nuc. lesion
Attention/arousal deficits
Multiple nucleii lesion
Neglect
Ventral posterior nuc. lesion
Dejerine-Roussy Syndrome

Sx: Feeling lingering pain after $ removed. Minor $ can cause stron and persistent pain
Function of THALAMUS
Funnels through all sensory input (except olfactory sense)

SELECTIVE ATTENTION, thalamus prioritizes what is important
Four subtypes of cortical architecture
"CAMI"

1) Corticoid
2) Allocortex
3) Mesocortex
4) ISOCORTEX
Isocortex
- 6-layered neocortex
- 2 subtypes
+ Idiotypic/Heterotypic: Layers diff to differentiate
> Granular (sensory cortex)
> Agranular (Motor cortex-pyramids)
+ Homotypic: Easier to differentiate
> Posterior
* Unimodal 2*
* Heteromodal 3*
> Frontal
6 Layers of Isocortex
1) Molecular: acellular
2) External granular:
3) External pyramidal
4) Internal granular: TERMINATION OF PRIMARY THALAMIC INPUTS
5) Internal pyramidal
6) Multiform (polymorphic)
Brodmann's Areas
S1 - 3, 1, 2
S2 - 5, 7

M1 - 4
M2 - 6

A1 - 41, 42
A2 - 22

V1 - 17
V2 - 18, 19
3 types of cortical pathways
"ACP"
1) Association
2) Commissural
3) Projection
Association pathways
>Within same hemisphere
>(1) Arcuate fasciculus: frontal cortex to superior temporal cortex {ant & post speech}
>(2) Cingulum: septal frontal lobe to cingulated/parahippocampal gyrus {limbic}
Commissural pathway
>Left hemisphere to right
> {Spatial info}
> Ex: Corpus collosum
Projection pathways
>Up and down cortex to non-cortex
>(1) Internal capsule: Corticobulbar/spinal/pontine
>(2) Optic radiations: Geniculocortical fibers
Watershed/Border zone
Anastomosis between ACA and MCA in medial frontal and parietal lobes

LESION: Nebulous cortical probs like diff calculating and reading (no motor deficits)
ACA irrigates
Medial frontal and parietal lobes
MCA irrigates
Runs in lateral sulcus; supplies lateral frontal, parietal, and temporal lobes
PCA irrigates
Occipital lobe, part of inferior temporal lobe
Triune Brain
1) Posterior cortex: Info gathering, processing, integration

2) Frontal lobe: Executive, decision making

3) Hypothalamus/limbic: Emotion/motivation
Lesion to primary posterior cortex
No sensory deficits
Cannot recognize objects.

Can open door when given key but doesn't know what it is
Lesion to secondary posterior cortex
Apperceptive agnosia
Lost ability to associate things with multiple concepts.

Knowing what a hat looks AND feels like.
Lesion to tertiary posterior cortex
Associate agnosia
Left frontal cortex
Speech, motor skills
Right frontal cortex
Emotion, expression, perception, social skills
Inability to recognize own fingers
Lesion of left angular gyrus
Gerstmann's Syndrome
Pt. unaware of own disease/deficit
Ansognosia
Pt. cannot name colors, cannot read, can see in ipsilateral visual field and can write
Lesion to left or right PCA>damaging ipsilateral occipital lobe and ipsilateral corpus callosum
Alexia (without agraphia)
Inability to carry our a discrete previously learned movement

"How do you use a hammer?"
Lesion to supramarginal gyrus, arcuate fasciculus, left premotor area > bilateral deficit

Also from injury to corpus collosum or right premotor area > left side deficit only
Ideomotor apraxia
Pt can speak but cannot repeat things. Difficulty naming objects, reading aloud, writing, and occasionally will substitute sounds for words
Disconnection between Broca's (speaking) & Wernicke's areas (comprehension)
Conduction aphasia
MRI of swiss cheese brain
Arteriovenous malformation, no Sx. other than headaches and seizures
MRI with giant fucking cyst
Subarachnoid cyst
Three types of headaches
1) Tension
2) Cluster
3) Migraine
>With/Without Aura
Tension Headaches
> Most common
> Head in vise
> 30 min to 7 days
> Chronic if >15days over one month
Tx: Stress relief

Chronic
>NSAIDS,
>ASA-Caffeine-Bulbital (barbituate!)
>Phenacetin

also
>Anti-depressants
>Muscle relaxant
Cluster Headaches
>Severe unilateral pain in and around orbit
>Icepick into face
>15 min to 2 hours
Tx:
>Pure oxygen
>5-HT agonists (serotonin agonists)
>Intranasal lidocaine

also
>Ca++ channel blockers
>Bellergal
>Lithium
>Steroids
>Antihistamines


Migraine Headaches
>Unilateral
>Pulsation rather than icepick stab
>Females experience more
>Peak between 30s and 50s
>Can present with anorezia, nausea, vomiting (and photo- and phono-phobia)
Tx
ACUTE
>Analgesic, triptans (serotonin agonists)

PROPHYLACTIC
>Antiepileptics
>Beta-blocker
>Antidepressant

BEHAVIORAL
>Limiting caffeine/stress
>Inc exercise
>Sleep
Migraine stages
Prodrome
Aura
Headache
Postdrome
Three theories of migraine causes
1) Spreading wave: Brainstem to cortex like epileptic seizure

2) Trigeminal: Efferent vasospasms (why serotonin agonists work)

3) Allodynia theory: Hypersensitivity
Memorize syndrome chart:
BROCA
WERNICKE
CONDUCTION
ANOMIA
GLOBAL
TRANSCORTICAL (Motor&Sensory)
Irrigation to language part of brain
MCA
Left M1 loss yields...
Loss of entire left side of brain
>Contralateral hemiplegia and sensory loss
> Homonymous hemianopia
>Eye deviation toward affected side
>Global aphasia (if left)
>
>Neglect and Anosognosia (if right)
M2 loss yields...
>Eye deviation
>Contalateral motor loss
>Broca's aphasia
ACA problems
Echolalia: Pt repeats back what you said to them
Parts of Frontal lobe
1) Superolateral cortex
2) Orbitofrontal area
Superolateral cortex
>Executive center
>Working memory/Scratchpad
>Processes things
>Only area to produce actions without external $

-X- Pathological inertia
>Can't move from one task to another without a $
>Easily distracted
Orbitofrontal cortex
>Prone to injury from falls
>Center of social self
>Inhibits impulses that are socially unacceptable

"Oh Fuck" - OF
Types of Memory
1) Immediate
2) Short term
3) Recent
4) Remote
Memory pathway
>Sensory memory
+Attn or +Forget
>Working memory
+Encode or +Forget
>Longterm memory
+Declarative (facts_
*Semantic (knowledge,meaning)
*Episodic (events,times,places)
+Procedural (skills)
Constructional ability
Ability to reproduce drawings (right brain)
Abstract reasoning
Math, proverbs, similarities/differences
Apraxia
Manifestation of dysfxn in multiple areas. Inability to do somethin on command
Neglect
Usually right brain problem (and neglect left side)
Types of neglect
>Hemibody
>Motor
>Sensory
>Visual
>Auditory
Lesion to dominant angular gyrus
>Gerstmann's Syndrome
>MCA dz.
Acalculia
Can't calculate
Agraphia
Can't write sentence
Finger agnosia
Don't know which finger is ring finger
R/L Confusion
Can't determine which is R or L
R frontal eye field drives eye to _____
Left

Eye looks to side of destruction
PCA dz.
Can write but not read
Three things to look for in a neurological exam
1) Localize the lesion
2) Determine the tempo (onset/duration)
3) Get demographics (exposure, hazards to help Dx)
Two pathological processes that can impair consciousness
1) Bilateral cerebral hemisphere dysfxn

2) Rostral brainstem-thalmic dysfxn in
>Diencephalon
>Midbrain
>Rostral pons
>Disruption os ARAS (ascending reticular activating system)

{Consciousness, sleep/wake cycles}
Delirium
>Acute onset, fluctuating course
>Impaired attn and arousal
>Agitated/altered sleep cycle

Dementia is more global
Delirium risk factors
SHE DIES
I WATCH DEATH

[Seizure, hemodynamic, endocrine, drugs, infection, electrolytes, stroke]

[Infections, Withdrawal, acid/base disturbance, trauma, CNS pathology, hypoxia, deficiency in vitamins, endocrinopathies, acute vascular, toxins/drug, heavy metals]
Pupillary response in CN exam (Symp vs Parasymp)
Pupillodilator - Symp damage causes constricted pupil and ptosis (like horner)

Pupilloconstrictor PS damage causes unreactive dilated pupil
>Uncal herniation
Sluggish light reactivity retained until all other brain stem reflexes lost
Diffuse cellular cerebral dysfxn (toxic-metabolic encephalopathy)
Unilateral papillary dilation, pupil unreactive to light
3rd CN compression (like transtentorial herniation) usually due to ipsilateral lesion
Pupils fixed in midposition
Midbrain dysfxn due to structural damage (infarction, hemorrhage)
Central herniation
Prolonged metabolic depression by drugs or toxins
Pupils tiny (1mm wide)
Massive pontine hemorrhage
Toxicity due to opoids or certain insecticides (organophosphates, carbamates)
General CN by test
Ocular mvmt
Facial grimacing
Corneal reflex
Gag reflex
General CN by test
Ocular mvmt [3, 4, 6] LR6SO4R3
Facial grimacing [5, 7]
Corneal reflex [5, 7]
Gag reflex [9, 10]
Doll's eyes
Oculocephalic reflex

If absent eyes stay static
Calorics
Oculovestibular reflex

Cold water turns eyes away
Warm water attracts
Arms flexed and legs extended
Decorticate rigidity, problem above midbrain
Arms and legs extended
DEcErEbratE rigidity, prob at or below midbrain

E - all limbs ExtEntEd
Compartments of cranial vault, must be balanced to maintain intercranial pressure
Monroe-Kellie Doctrine

1) Parenchyma (80%)
2) CSF (10%)
3) Blood (10%)
**Cerebral perfusion pressure eqn (CPP)
CPP = Mean art press - Intercranial press

CPP = MAP - ICP
**Uncal herniation
From high to low pressure

Uncus and/or hippocampus shifts from Middle cranial fossa to posterior fossa.
Compression of ipsilateral CN3, contra CN2, and mesencephalon
Uncal herniation stages
1)Early: drowsy/sluggish
2)Herniation of midbrain/poins: coma, babinski
3)Later herniation of medulla (IRREVERSIBLE)
Persistent vegetative state
No awareness, communication, response to $, voluntary mvmt, control
Locked in syndrome
Due to basilar artery thrombosis

Awake and alert but tetraplegic, can only blink

RAS and oculomotor nerve fine but other motor (cortico____ not)
Mental status chart:
COMA
PVS
MinCS
LIS
Brain death
Loss of fxn of entire cerebrum and brain stem, resulting in coma, no spontaneous respiration, loss of ALL BRAINSTEM REFLEXES (some spinal reflexes such as deep tendon, plantar flexion, and withdrawal remain)

No recovery.

Core temp will be more than 32C
How to confirm brain death
Must confirm absence of brain stem reflexes

>Pupils don't respond to brigh light
>No oculocephalic reflex
>No oculovestibular reflex
>No corneal reflex
>No grimacing due to pain
> No jaw jerk
>No cough response to bronchial suctioning
Only fibers from the _____ project directly into the thalamus
Spinothalmic (duh, look at the name)
What are the three somatosensory systems
1) DCMLS (M>L as ^) foot is medial {VPL}
2) Trigeminal
3) ALS (L>M as ^) foot is lateral {VPL}
Loss of discrimination in

>3B
>1
>2
>3B: severe deficit in texture and shape discrimination

>1: Deficit in texture disc

>2: Deficit in Finger coordination, shape, and size discrimination
Receptive field and what determines amount of discrimination
A single neuron area

Size and density as well as contrast (affected by lateral inhibition)
The fastest most dense sensory pathway to the cortex is _______
ML
The four fundamental properties for a $
"MIDL"

1)Modality: Class of $ (Touch,temp,pain)
2)Intensity
3)Duration
4)Location

All affect RECRUITMENT
Modalities and type of receptor

MR. PM
Modalities and Receptor types
MR.PM
Dynamic/fast adapting receptors
Pacinian corpuscles and Meissner

LOW freq, discontinuous APs
Slowly adapting receptors
Merkel cells and Ruffini ends

HIGH freq, continuous APs
Thermoreceptors
"Combo"

Adapt quickly then fire steady state APs for entire duration of temperature stimulus
Nociceptors

>Types of fibers
A-delta: myelinated, fast pain, localized, sharp {mechanosensitive, mechanothermal}

C fibers: nonmyelin, slowpain, diffusem aggravating
Encapuslation effects
WITH: receptor potention only when skin undergoes change (rapidly adapting)

WITHOUT: slowly adapting receptor
Basal Ganglia functions
1) Preparation
2) Smooth transitioning
3) Inhibiting
4) Monitoring
5) Initial learning
6) Adapting
Basal ganglia derived from ______
Telencephalon
Basal ganglia comprised of
Caudate
Globus pallidus
Putamen
(all together considered Corpus striatum)

Last two are lentiform/lenticular nucleus
Excitatory NT
Inhibitatory NT
+Glutamate
-GABA
Receiving Nucleii
Caudate and putamen
Processing nucleii
GPe and subthalmic nucleus
Output nucleii
GPi and SNr

(SNc - mixed fxn nucleus)
MOTOR LOOP
LIMBIC LOOP
COGNITIVE LOOP
OCULOMOTOR LOOP
Blood supply to basal ganglia
>Lenticulostriate (from M2 of MCA)
>Medial striate aa.
>Ant. choroidal aa.
Motor basal ganglia disorders
Hypokinetic: Parkinsons, prob direct system


Hyperkinetic: Huntington's prob of indirect inhib system
Parkinson's disease
> degen of SNc
> less dopamine (which inhib inhib paths, if less would inhib)
Huntington's disease
>Striatum diminished cap to inhib GPe, less inhibition of thalamus, increasing unwated cortical activatio
Hemiballism
Lesion of subthalamus (stim inhib GPi in thalamus)

Yields excessive cortical activation