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104 Cards in this Set

  • Front
  • Back
when a neuron is at rest, only ______________ are open
leaky K+ channels
voltage-gated Na+ channels are quick to open, slow to close; as they start to close, ____________________ open
delayed K+ channels open

falling phase ~~ max amount of delayed K+ open
"nuclei" =
neuronal bodies = GRAY matter
diencephalon, on top of midbrain, =

(3)
thalamus + hypothalamus

(+ pineal gland, in b/w superior colliculi)
cortex: inner portions =
white matter

(AXONS + oligodendrocytes)
BG = nuclei =

(3)
caudate + putamen + gp
striatum =
caudate + putamen
lenticulate nucleus =
putamen + gp
limbic system =

(4)
hippo + fornix + mamillary bodies + amygdala
2 features of the Corticospinal tract:
1. motor (~~precentral gyrus)

2. *decussates in caudal medulla*
Medial side of CS tract is supplied by:

Lateral side, by:
ACA;

MCA
5 symptoms of UMN lesion:
1. weakness

2. spasticity

3. hypertonia

4. hyperreflexia

5. + Babinski
paresis =
partial weakness;

plegia = complete
5 symptoms of LMN lesion:
1. weakness

2. flaccid paralysis

3. fasciculations (twitching)

4. HYPOreflexia

5. atrophy
CN's 2 and 8 have NO:
motor component
3 features of the ST tract:
1. conveys PTLT

2. *decussates in the SC*

3. thalamus => PLIC => postcentral gyrus
3 features of the DC/ML:
1. FT/pos/vib

2. *decussates in the caudal medulla*

3. thalamus => PLIC => postcentral gyrus
2 components of the DC/ML:
fasciculus gracilis + cuneatus
fasciculus gracilis:

(2)
1. ~ LE's

2. Medial
fasciculus cuneatus:

(2)
1. UE's

2. Lateral
pyramidal neurons =
cortical/cerebral neurons = UMN's
**CN nuclei and spinal MN's = **
LMN's
what kind of injury pattern does a SC injury show?
MIXED pattern of injury;

UMN fibers below lesion, LMN's AT lesion don't work
deep tendon reflex
stretch reflex
"primitive" reflexes ~~

(2)
1. infants

2. secondary to UMN injury/abnl development
(called "pathological reflex" in this case)
primitive reflexes are also subcortical, and some don't go away;
e.g. knee-jerk = "lifespan" reflex
encephalopathy =
cerebral dz
myelopathy =
SC dz
radiculopathy =
nerve root dz
vertigo MAY be a problem in:
BS

(apart from inner ear, 8th nerve, or cerebellum)
***if deficits occur in a DIFFERENT half of the head than in the body, the lesion is most likely in the:***
BS
***if deficits are bilateral and affect the entire body below a specific horizontal line, lesion is most likely in the:***
SC
if a deficit manifests in a strip or blob, lesion is likely in:

(3)
1. nerve root

2. CN

3. peripheral nerve
left side of brain ~~ ________________. right side ~~ __________________
language;

visual-spatial (==> hemineglect)
lesion in Broca's:

(4)
1. frontal lobe

2. ~~ MOTOR aphasia

3. nl comprehension

4. abnl naming/rep, fluency
lesion in Wernicke's:

(4)
1. temporal lobe

2. ~~ SENSORY aphasia

3. comprehension, naming/rep abnl

4. fluency nl but nonsensical
- paraphrasic errors (similar word subbed)
- neologisms
Broca's and Wernicke's are connected by:
the arcuate fasciculus
lesion of arcuate fasciculus =>
CONDUCTION aphasia
features of conduction aphasia:

(2)
1. comprehension, fluency nl

2. naming/rep abnl
motor cortex => CS tract, Corticobulbar tract;

CB pathway =
fibers to LMN's of CN's
sensory cortex receives:

(3)
1. ST tract

2. DC/ML

3. trigeminal tract
**the ACA supplies motor and sensory cortices of:**
the **LE's**
lesion in ACA =>
contra weakness/sensory deficits of LE's
distal/cortical branches of the MCA supply:
UE/face sections of motor and sensory cortices
lesion of distal/cortical branches of MCA =>

(3)
1. contra weakness, sensory deficits of UE's and face

2. aphasia/apraxia is left side

3. hemineglect if right
apraxia =
inability to perform purposeful action
lesion in proximal/deep branches of the MCA =>

(2)
1. weakness/sensory deficits in UE's, LE's, and face

(via lenticulostriate branches to PLIC)

2. visual field deficits

(via branches to optic radiations)
CN 3 innervates:

(5)
superior, medial, and inferior rectus;

inferior oblique;

levator palpabrae superioris
lesion in CN3 =>

(3)
1. eye down and out

2. ipsilateral ptosis

3. ipsi dilated pupil
CN 4 innervates:

lesion =>
superior oblique (intorsion, depression)

- controls CONTRA eye

lesion => up and out
CN 6 innervates:
lateral rectus
CN locations:

(3)
3-4 in midbrain

5-8 in pons

9-12 in medulla
cerebral peduncles are comprised of:
descending motor pathways

=> CS, CB tracts
2 parts of the midbrain (mesencephalon):
1. substantia nigra

2. red nuclei
***trigeminal pathway provides:***
P/T/LT *AND* FT/pos/vib from CONTRA face (wrt cerebral cortex that gets those sensory signals)

(= DC/ML and ST tract for the face)
**crossed syndrome** =
ipsi CN deficit + contra extremity deficit (motor OR sensory)
only CN 4 decussates; it exits:
posteriorly, at the inferior colliculi
CS and DC/ML =
Medial tracts

- ST and descending, sympathetic fibers = Lateral tracts
meningomyelocele =
sac of meninges AND neural tissue (SC or nerve root)
***Horner's syndrome***

(3)
loss of sympathetic innervation:

1. ptosis
(loss of Muller's muscle)

2. miosis
(pupil constricted from loss of pup. dilator musc)

3. anhydrosis
(dec. sweating in ipsi face and neck)
Arnold-Chiari =
herniation of cerebellar tonsils through foramen magnum

~~ meningomyeloceles
spina bifida can be prevented by taking folic acid;
= neural tube defect/ vertebral arches fail to fuse
**lesion in optic nerve shuts down:**
visual field of the eye on the SAME SIDE
the right visual field is processed by the LEFT side of each eyeball;
right visual field = left temporal nerves + right nasal nerves

(check)
nucleus ambiguous innervates:
pharynx and larynx
nystagmus =
rapid involuntary movement of the eyes
Lesions in the optic nerve lead to:
total blindness in the same eye.
Lesions of the optic tract lead to:
contralateral hemianopsia
Lesions in the parietal portion of optic radiation lead to:
lower quadrantic hemianopsia
lesions in the visual cortex lead to:
contralateral hemianopsia with visual sparing
the PREmotor area coordinates:
movement of the hands
Immediately superior to Broca's area are regions for:
personality and memory storage
exiting fibers of the occulomotor nerve pass through the _____________ on their way to the cavernous sinuses
cerebral peduncles
spinocerebellar tracts ~~
unconscious proprioception
diplopia =
double vision
MLF carries information about:
which direction the eyes should move
when the eyeball faces the nose, only the _________________________ can depress it
superior oblique
when the eyeball faces out, only the ____________________________ can depress it
inferior rectus
levator palpabrae ~~
eyelid
palatal rise is caused by ____________________ MUCH more than ____________________
CN 10 much more than to CN 9
taste in anterior 2/3 of tongue innervated by:
facial nerve
functions of CN 9:

(7)
1. posterior 1/3 taste

2. sensation over the palate,

3. tonsils

4. pharynx

5. the middle ear;

6. receptors in the carotid body.

7. Parasympathetic component ~~ salivary secretion from the parotid gland
astrocytes =
fibroblasts of the CNS, which react to anything pathological insult by _____________ check
microglia =
macrophages of the CNS
olidodendroglia = oligodendrocytes =
myelinating cells of the CNS

(Schwann ~~ PNS)
ependyma =
simple epithelium that separates brain matter from CSF
Wallerian degeneration =
deg. of an axon DISTAL to site of injury
cytotoxic edema =
water crossing an *intact* BBB due to osmotic forces
m.c.c. of noncommunicating hydrocephalus =
complete obstruction of cerebral aqueduct
non-communicating hydropcephalus ==> ____________________ subarachnoid space
DECREASED subarachnoid space

(opposite in communicating hydrocephalus)
communicating hydrocephalus is caused by:
failure to reabsorb CSF
in communicating hydrocephalus, _______ _____ __________________ dilate
ALL the ventricles dilate

- can be inc. P or nl. Pressure
Nl pressure (communicating) hydrocephalus =
*gradual* enlargement of ventricles, leading to dementia, incontinence, and gait impairment in the ELDERLY
hydrocephalus ex vacou =
enlargement of ventricles due to loss of brain parenchyma
syringomyelia =
deg. of the SC that manifests in a fluid-filled cyst
holoprosencephaly =
forebrain does not divide

= one mass instead of two hemispheres
lissencephaly =
a type of congenital microcephaly that results in a smooth brain surface due to no gyri
periventricular leukomalacia
damage to deep periventricular white matter due to pre/neonatal hypoxia
choroid plexus: found within:
ventricles

- produces CSF
arachnoid villi function:
reabsorb CSF

==> dural venous sinuses
what is measured in the amniotic fluid and maternal blood to detect neural tube defects?
aFP

(abnl amounts)
prosencephalon ==> forebrain =>
cerebral cortex
The prosencephalon subdivides early, shortly after the neural tube closes. Problems with this subdivision can cause a spectrum of abnormalities called:
holoprosencephaly (indicating that they affect the entire cerebrum)

=> absent corpus callosum and a single ventricle that spans the midline

Effects on the skull and face are almost the opposite of those seen in anencephaly: dorsal and posterior parts of the skull are present but baby has marked facial abnormalities (e.g. cyclops)
any lesion before the optic chiasm will only show up in:
ONE eye