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Neuroscience final exam > CUMULATIVE STUFF > Flashcards

CUMULATIVE STUFF Flashcards

1
Q

Brodmann’s areas/functions of the cortex

A

Primary motor area: Brodmann’s #4, execution of skilled movement, follows homunculus (UE = lateral, LE = medial)
s/s contralateral UMN
Supplementary motor cortex: Brodmann’s #6, medial cortex, ACA, internally guided movement (lesions: apraxia or motor planning disorder)
Premotor cortex: Brodmann’s #6, lateral cortex, MCA, externally guided movement (lesions: apraxia or motor planning disorder)
Posterior parietal cortex: Brodmann’s #5,7, MCA primarily and PCA (les: ideomotor apraxia)
Primary sensory area: Brodmann’s #1,2,3, detects sensation from opposite side of body, MCA and ACA (les: contralateral sensory motor ataxia)
Cingulate cortex: movement execution during complex behaviors and emotional control of movement
Frontal eye field: voluntary eye movement, activates eyes to look to contralateral side
Prefrontal area: affective behaviors, judgment, foresight, problem solving, social, motor memory and motor learning

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2
Q

cranial nerves

A

I - Olfactory
II - Optic
III - Oculomotor: constriction of the pupil and focusing on a near object, levator palpebrae superioris (keeps eyes OPEN, ptosis)
IV - Trochlear: superior oblique
V - Trigeminal: innervates dura, ½ face
VI - Abducens: lateral rectus
VII - Facial: causes you to BLINK in response to sound (blink reflex), innervates small piece behind ear, anterior ⅔ tongue (bell’s palsy)
VIII - Vestibulocochlear
IX - Glossopharyngeal: innervates posterior ⅓ tongue, upper pharynx
X - Vagus: innervates lower pharynx, larynx, esophagus, parasympathetic cardiac and visceral functions (heart rate, BP, breathing, etc)
XI - Spinal Accessory
XII - Hypoglossal

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3
Q

lesions in CN motor nuclei

A

ipsilateral LMN s/s

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4
Q

ventral trigeminothalamic tract

A
  • pons
    decreased/impaired pain and temperature sensation throughout ½ of face, behind ear, all oral cavity, pharynx, larynx, esophagus, contralateral deficits (crossing occurs lower down)
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5
Q

DCML

A

Light touch, conscious proprioception, 2 point discrimination
1st: dorsal root ganglia → 2nd: nucleus gracilis and nucleus cuneatus → medial lemniscus → 3rd: ventral posterolateral nucleus → thalamus → somatosensory cortex via internal capsule
Fasciculus gracilis: LE; fasciculus cuneatus: UE (T6 and above)
Cross: closed medulla
Above closed medulla: contralateral (has crossed)
Below closed medulla: ipsilateral (has not crossed)

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6
Q

ALS

A

Pain, temperature, coarse touch, tickle
Spinothalamic tract: lesion will reduce ability to feel severe chronic pain
Spinoreticular tract: lesion impacts pain modulation
Spinomesencephalic tract: endogenous pain control
Cross: immediately in ventral white commissure
Partial loss 2-3 segments above and below, then total loss below that
Dorsal horn: ipsilateral (has not crossed)
Anterolateral quadrant: contralateral (has crossed)

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7
Q

dorsolateral pathways

A

descend unilaterally to distal muscles, fine dexterity and fractionation

Lateral corticospinal: cortex → down midbrain, branch off to red nucleus → cross @ pyramidal decussation of closed medulla → down SC (85% -15 to ventral corticospinal)
Les: R cortex controls L side of body. Before CM: contralateral, After CM: ipsilateral
s/s: weakness in distal limbs, impaired ability to fractionate movement, UMN s/s if pathway is lesioned; LMN s/s at level of lesion
Rubrospinal: red nucleus → cross immediately → descend contralaterally
Same function as above, but no clinically significant deficits

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8
Q

ventromedial pathways

A

descend bilaterally to proximal and axial/trunk muscles, posture, balance, stability

Tectospinal: tectum in midbrain → crosses immediately and descends cervical SC
Coordinates head/neck/eye movement
Pontine reticulospinal: reticular formation → descends bilaterally
Les: decerebrate rigidity - extension in UE and LE
Medullary reticulospinal: reticular formation → descends bilaterally
Les: decorticate rigidity - flexion in UE and extension in LE
Medial vestibulospinal: vestibular nucleus → descends bilaterally to cervical and upper thoracic regions
Coordinates head/neck righting reactions
Lateral vestibulospinal: vestibular nucleus → descends ipsilaterally in all SC regions
Causes tone in extensor muscles
Les: Ipsilateral hypotonia, balance issues, motor ataxia

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9
Q

lateral/medial cortex

A

lateral cortex = UE + face, MCA

medial cortex = LE, ACA

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10
Q

brown sequard lesion

A

Lesion in half of the spinal cord
Ipsilateral LMN symptoms at site of lesion
Ipsilateral UMN symptoms below site of lesion

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11
Q

2 pain modulation mechanisms

A
  1. Gate Theory of Pain Modulation: FAST
    Group I touch fibers will inhibit the input from smaller diameter pain fibers
    Pain fibers come in, go down to NP and excite cells there: send signal via ascending pain pathways
    If at same time there is touch AND proprioceptive information coming it and it goes through SG and then to NP giving it inhibitory signal
    Since touch and proprioceptive input is a stronger signal, it can modulate pain and temperature input
    Rubbing a body segment with firm pressure can help alleviate pain
  2. Endogenous pain control: LONG LASTING
    Spinomesencephalic tells brain that something hurts, on the way down it will help give pain relief at that level of pain
    Opiates: serotonin, norepi
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12
Q

basal ganglia - receptive

A 
nucleus accumbens (L)
caudate nucleus (O, E)
putamen (M)
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13
Q

basal ganglia - projection

A 
ventral pallidum (L)
internal globus pallidus (M,O,E)
substantia nigra reticulata (M,O,E)
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14
Q

basal ganglia - modulators

A 
substantia nigra pars compacta (receptive) - parkinsons
globus pallidus externus (projective) - chorea
subthalamic nuclei (projective) - balissmus
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15
Q

modulation

A

dampens excessive movement

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16
Q

lesion in putamen

A

destroys cells projecting to globus pallidus → chorea (involuntary movements that look like fragments of purposeful movements)

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17
Q

cerebrocerebellum - what, composition, nuclei, lesion

A

precise rapid limb movement, dexterity, movement initiation, motor learning
Comp: lateral cerebellar hemispheres
Nuclei: dentate nucleus
Les: ipsilateral dysdiadochokinesia, difficulty motor learning

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18
Q

spinocerebellum - what, composition, nuclei, lesion

A

fined tuned motor control, compensations for load changes, smooth oscillations, corrected deviation of intended movements, mx tone
Comp: vermis and intermediate cerebellar hemispheres
Nuclei: fastigial/vermis and interposed/intermediate nuclei
Les: ipsilateral hypotonic mx tone, ipsilateral coordination difficulties (ataxia, dysmetria, intention tremors)

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19
Q

vestibulocerebellum - what, composition, nuclei, lesion

A

balance, coordination of eye and head movement in relation to space, control axial muscle posture
Comp: flocculus and nodulus
Nuclei: vestibular nucleus
Les: balance and righting problems

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20
Q

muscle spindle

A

Group Ia (velocity of movement) and II afferents (both = proprioceptive info of length of a mx)

Intrafusal: not responsible for mx contractions, make up mx spindles and convey info about length or stretch and change of mx length, gamma motor neurons (stretch the otherwise saggy fiber and produce action potentials thus they increase muscle spindle sensitivity)
Muscle spindles also provide mechanism for stretch reflex, regulating tone, and coordinating/smoothing mx contractions

Extrafusal: responsible for muscle contraction, alpha motor neurons

21
Q

golgi tendon organ

A

Ib afferents
Receives info about muscle force and changes in tension
Tension feedback system

22
Q

hypotonia

A

Caused by certain upper motor neuron lesions and all lower motor neuron lesions. Presents as decreased muscle tone and difficulty producing and sustaining muscle contractions.

***Increased activation/excitation of alpha motor neurons can inhibit spasticity and excite hypotonic muscles.

23
Q

hydrocephalus

A

communicating (no obstruction to flow within ventricles, after subarachnoid hemorrhage), non communicating (obstruction to flow of CSF within ventricles), normal pressure (elderly)

24
Q

meningioma

A

tumor from arachnoid cells, benign brain tumors, cause damage due to compression

25
Q

syringomyelia

A

causes a lesion around central canal of SC, destroys VWC and alpha/gamma motor neurons

usually cervical spine

causes bilateral deficits in pain and temp sensation a few segments about and below lesion

26
Q

spina bifida

A

congenital malformation of neural tube development, incompletely formed SC (occulta, meningocele, meningomyelocele)

27
Q

conditions related to arteries

A

Internal carotid artery – strokes, transient ischemic attacks
Middle cerebral artery – cerebrovascular accident, stroke, aphasia and apraxia
Wallenberg’s syndrome – PICA
Locked In Syndrome – basilar artery, paralysis in all 4 extremities
Thalamic pain syndrome - posterior cerebral artery

28
Q

myasthenia gravis

A

input component of neural signaling affected - muscle weakness, ptosis and diplopia, nasal speech, dysarthria, dysphagia, dyspnea and weak cough

29
Q

guillain-barre

A

myelin sheaths around peripheral nerves are affected - sensory, motor, and autonomic functions of peripheral nerves affected – no cognitive impairments, tingling/numbness and weakness, progressive muscle weakness that may result in full paralysis, often need ventilation, hyper/hyposensation

30
Q

multiple sclerosis

A

myelin sheaths around axons in CNS are destroyed, may affect all CNS functions, progressive

31
Q

MS vs. GB

A

in both, myelin sheaths are destroyed. MS is CNS and GB is PNS. Cognitive impairments are in MS but NOT in GB

32
Q

shingles (herpes zoster)

A

infection of dorsal root ganglia or cranial nerve ganglia. Some unknown stimulus triggers the virus to become infectious again and the virus irritates and inflames the spinal nerve causing pain. The virus is released into the skin from the nerve endings causing painful red eruptions on the skin. Itching and burning or tingling sensations can precede these skin lesions.

33
Q

nerve lesions

A

Peripheral: Impairment of all sensation in the area of skin supplies by that peripheral nerve
Dorsal root/Spinal nerve: Impairment of all sensation in the dermatome supplied by that nerve

34
Q

polio

A

damages the alpha motor neurons in the ventral horn of the spinal cord and cranial nerve motor nuclei in the brainstem due to a viral infection
LMN disorder
s/s = weakness (paresis), hypotonia, hyporeflexia, muscle atrophy, fasciculations, and fibrillations
the virus is self-limiting and pt’s usually recover to a point and live with residual deficits

35
Q

post polio

A
  • seen in pt’s who have been living with residual deficits for many years - likely caused by a combination of aging and overuse of unaffected muscles
    s/s = new muscle weakness and muscle fatigue
    not life threatening, but requires significant lifestyle changes reduce fatigue and conserve remaining muscle energy
36
Q

ALS (lou gehrigs)

A

destroys the alpha motor neurons in the ventral horn of the spinal cord and cranial nerve motor nuclei in the brainstem
classified as LMN disorder, with possible UMN s/s if lateral columns affected
s/s = sames as polio + spasticity (an UMN s/s) if lateral columns affected
progressive disease, usually fatal within 5 years - often due to respiratory issues

37
Q

subacute combined degeneration

A

damages the dorsal and lateral white matter columns due to a B12 deficiency - commonly seen with alcoholism
s/s = DCML affectation due to damage of dorsal columns + UMN s/s due to damage of lateral columns

38
Q

parkinson’s

A

decreased dopamine means that the motor related cortical regions that facilitate movement are not stimulated as much
decrease in activation of motor-related cortex in basal ganglia
supplementary motor cortex is involved with this circuit, so patients have the most difficulty planning and executing movement to command or that are internally guided
this is why pt’s with Parkinson’s are able to produce better movement when prompted by sensory stimuli
Bradykinesia, akinesia, flat affect, resting tremors, shuffling gait, dysarthria and dysphagia, rigidity, flexed, stooped posture, decreased balance reactions, dementia, depression

39
Q

corticobulbar tracts - face/tongue

A

above pons:

  • upper face: no s/s because bilateral
  • lower face: contralateral UMN s/s
    tongue: contralateral UMN s/s, tongue deviates towards lesion

IN pons:
upper and lower face: ipsilateral LMN s/s
tongue: contralateral UMN s/s

in medulla:

  • face: none
  • tongue: ipsilateral LMN
40
Q

lesion in one optic nerve

lesion in one EW nucleus

A

neither eye can restrict in response to light that shines in that eye

that eye cannot constrict no matter which eye the light is in
the other eye has intact pupillary light reflex to light that shines in either eye

41
Q

frontal eye fields

A
  • right FEF activates eyes to look left and vice versa

- lesion: eyes deviate TOWARD side of lesion

42
Q

pontine paramedian reticular formation (PPRF)

A
  • right PPRF coordinates eyes to look right

- lesion: eyes deviate AWAY from lesion

43
Q

apraxia

A

motor planning disorder
*lesions in cortex
- Ideomotor: Unable to perform task on command even though patient can describe how to perform the task and sometimes perform it automatically
(Lesion to left side of pre-motor and supplementary cortex)
- Ideational: Failure of conceptualization of task, Cannot perform task automatically or on command, Cannot explain how to accomplish a purposeful activity, Often attempts to use objects for the wrong purpose
(Lesion to left side of parietal association cortex)
- Constructional
- Dressing

44
Q

ataxia

A

CLARKES NUCLEUS
Lesions of spinocerebellar tracts
Bilateral decreased coordination, decreased balance, and abnormal gait
Similar to being drunk: such as slurred speech, stumbling, falling, and incoordination. These symptoms are caused by damage to the cerebellum, the part of the brain that is responsible for coordinating movement.

45
Q

LMN s/s

A

alpha motor neurons that directly innervate skeletal muscle (in ventral horn of SC at every segment and motor nuclei for cranial nerves in brainstem)
s/s: weakness, hypotonia, hyporeflexia, muscle atrophy, fasciculations and fibrillations

Les: ipsilateral and segmental

46
Q

UMN s/s

A

s/s: weakness, spasticity, no early atrophy, abnormal and hyper reflexes, dec coordination, loss of fractionation

Les: if in cortex, think of homunculus; if in SC: affects all levels below the lesion

47
Q

value for normal intracranial pressure and s/s

A

5-15 mmHg

  • hydrocephalus and cerebral edema
  • s/s: headache, lethargy, nausa/vomitting, weakness, sig changes in vital signs, motor control problems, inc tone
48
Q

flow of CSF

A
  1. produced in choroid plexus/lateral ventricles
  2. interventricular foramen of monro
  3. third ventricle
  4. cerebral aqueduct
  5. 4th ventricle
  6. median aperature and 2 lateral aperatures
  7. subarachnoid space
  8. superior sagittal sinus

Neuroscience final exam (5 decks)

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