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Patho 2 > Neuro > Flashcards

Neuro Flashcards

1
Q

Cranial Nerve I

A

Olfactory

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2
Q

Cranial Nerve II

A

Optic nerve

Sensory nerve: Visual information

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3
Q

Cranial Nerve III

A

Oculomotor

Motor: movement of pupil, lens, eyelid, visual tracking and gaze fixation

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4
Q

Cranial Nerve IV

A

Trochlear

Motor: movement of eye’s superior oblique muscles to move eye downward and inward

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5
Q

Cranial Nerve V

A

Trigeminal Nerve

Sensory and motor: chewing, clench teeth, give sensation to muscles in tympanic membrane of ear.
Sensation to eyes, nose, eyelid, forehead, teeth, tongue

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6
Q

Cranial Nerve VI

A

Abducens nerve

Motor: lateral rectus muscle - moves gaze outward

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7
Q

Cranial Nerve VII (7)

A

Facial nerve

Motor and sensory: facial expressions, sensation of external ear, taste

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8
Q

Cranial Nerve VIII (8)

A

Vestibulocochlear nerve

Sensory: Hearing and balance

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9
Q

Cranial Nerve IX (9)

A

Glossopharyngeal nerve

Motor and sensory: throat, tonsils, middle ear, taste on posterior 1/3 of tongue. Swallowing, gag reflex

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10
Q

Cranial Nerve X

A

Vagus nerve

Motor and sensory: taste, throat, heart, abdominal organs. Motor to throat and soft palate. Regulates heart rhythm and smooth muscle of airway, lungs, GI tract

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11
Q

Cranial Nerve XI

A

Accessory Nerve

Motor: sternocleidomastoid and tapezius muscles for flexing neck and shoulders

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12
Q

Cranial Nerve XII

A

Hypoglossal Nerve

Motor: tongue muscles (speaking, swallowing)

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13
Q

Neural Tube Defects

A

Caused by an arrest in normal development in the brain and spinal column during first month of pregnancy

Most common is spina bifida, a posterior defect.

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14
Q

Spina Bifida

A

Neural tube defect — posterior

Failure if vertebrae to close.

Spina Bifida occulta: No protrusion, just abnormal opening in bone

Meningocele: Cyst of meninges filled with spinal fluid - minor form - does not involve spinal column. May not have neuro symptoms. Occurs equally in cervical, thoracic, and lumbar regions

Myelomeningocele: Hernial protrusion of saclike cyst - contains meninges, spinal fluid, and a portion of spinal cord. 80% lumbar/sacral

85% have hydrocephalus

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15
Q

Seizures

A

75% of seizures have unknown origin

Causes: trauma, lesions, infectious diseases of brain, generic (low threshold for stimuli), epilepsy (abnormal neurons), Metabolic disorders (withdrawal), degenerative diseases (dementia)

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16
Q

Tonic phase

A

Muscle contraction with increased tone

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17
Q

Clonic phase

A

Alternating contraction and relaxation of muscles

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18
Q

Simple Partial seizure

A

No aura
Sudden onset
Unusual taste in mouth, vomiting, sweating, facial twitching

Focal seizure: only affects one area of brain

Will not lose consciousness. 1-2 mins in length. Localized area. Feeling that something is not right

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19
Q

Absence - Petit Mal

A

Generalized. Common in children. Sudden onset. Impaired responsiveness.
<30 sec.

Blank out for a few seconds <15 secs

Can be set off by hyperventilating

Brief abnormal electrical activity. Both sides of brain.

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20
Q

Tonic Clonic - Grand Mal

A

•Generalized
•Loss of consciousness
•Increased muscle tone
•Muscle jerking
•Usually starts on both sides of brain
•1-3 min long
•Can start as partial seizure or aura

4 phases:
Prodromal: Feeling or sensation. Can be hours or days before (20% will have a prodromal feeling)

Early Ictal: Aura (65% have an aura)

Ictal: Actual seizure. Muscle movements

Post Ictal: Recovery phase. Some immediately, some take minutes, hours, or days. Weak, sore, tired

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21
Q

Myoclonic

A

•Generalized
•Sudden muscle contractions
•Often occurs in limbs or face
•Brief shock-like jerks of a muscle or group of muscles. Lasts a few seconds
•Sensation of electrical shock, clumsy, jerking movements
•Person is awake and can think clearly
•Both side of brain affected

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22
Q

Epilepsy

A

•A chronic seizure disorder with recurrent unprovoked seizures

•Oxygen consumed 60% greater than normal during a seizure. O2 and glucose rapidly depleted, lactate accumulates in brain tissue

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23
Q

Status Epilepticus

A

Seizure activity lasting longer than 30 min - or rapidly recurring seizures before the person regains consciousness.

Medical emergency that can cause brain death

Release of epinephrine and norepinephrine cause physiological changes

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24
Q

Febrile Seizure

A

Benign seizures with high body temp

Loss of consciousness, twitching/jerking of arms/legs, breathing difficulties, foaming at mouth, cyanosis, eye rolling, 10-15 min to wake properly, outgrow by age 5

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25
Q

Forebrain

A

Includes diencephalon (sleep/wake cycle, endocrine system, relaying sensory/motor info to cerebral cortex)

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26
Q

Midbrain

A

Connects the pons to diencephalon

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27
Q

Hindbrain

A

Cerebellum, pons, medulla

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28
Q

Upper Motor Neurons

A

Completely contained within CNS - control fine motor movement influences spinal reflex arcs

29
Q

Lower motor neurons

A

Project into periphery- directly influences muscles - cell body is in the grey matter of spinal column & brainstem, but they extend into peripheral nervous system

30
Q

Damage to upper vs lower motor neurons

A

Damage to upper neurons = initial paralysis followed by partial recovery

Damage to lower neurons = paralysis unless peripheral nerve damage is followed by nerve regeneration

31
Q

Meninges layers from inside (brain) to outside (skull)

A

(brain), pia, arachnoid, dura, (then skull)

32
Q

Subarachnoid space

A

space between arachnoid and pia. Contains cerebralspinal fluid

33
Q

Cerebrospinal fluid amount

A

125-150ml circulates through subarachnoid space and ventricles

600ml produced daily

produced in ventricles and reabsorbed through arachnoid villi

34
Q

CSF pressure (intracranial pressure)

A

5-14 mmHg laying down
doubles when standing up

35
Q

Vertebral column

A

8 cervical
12 thoracic
5 lumbar
5 sacral
1 coccygeal

36
Q

Blood supply (brain)

A

20% of cardiac output
800-1000 ml/min

Carbon dioxide = vasodilator. ensures adequate blood supply

Blood supply from corotid arteries and vertebral arteries

Circle of willis provides alternative route for collateral blood flow if one of the contributing arteries is occluded (safety valve for brain)

37
Q

Do cranial nerves cross over?

A

No

damage to right = effects on right

38
Q

Alterations in arousal/consciousness

A

Structural: vascular alterations, neoplasms, tbi, degenerative, polygenic traits

Metabolic: Infection, inflammation, hypoxia, electrolytes disturbance, hypoglycaemia, renal or liver disorders

Psychogenic: psychiatric disorders

39
Q

Glasgow Coma Scale

A

Eyes:
Spontaneous
To sound
To Pressure
Nome

Verbal:
Orientated
Confused
Words
Sounds
None

Motor:
Obeys commands
Localize to pain
Normal flexion (to pain)
Abnormal flexion (decorticate)
Extension (decerebrate)
None

40
Q

Terms describing altered loc
(confusion, disorientation, lethargy, obtubdation, stupor, coma)

A

Confusion
Beginning of not knowing what’s going on. Not quite disoriented

Disorientated
Progressive confusion, comes with anxiety, restlessness, losing time, place, person

Lethargy
Alert and oriented but sluggish. Sleep frequently hut wakens to voice/shaking

Obtundation
Extreme drowsiness, minimally responsive, barely follows commands (but able to), requires vigorous stimulation, stays awake only minutes

Stupor
Minimal movement, responds in moans, cannot follow commands or open eyes (passed out drunk)

Coma
No response at all
GCS 3

41
Q

Pupillary changes

A

Indicate level of brainstem dysfunction. Brainstem control of arousal is adjacent to areas that control pupils - some meds also affect pupils

Metabolic: Equal pupil changes
Trauma: Unequal pupils on side of injury

42
Q

Oculomotor responses

A

Resting spontaneous, and reflexive eye movements change with LOC. Meds should not change reflexes but destructive or compression injuries to brainstem cause specific abnormalities.

Eyes should move together. Dysconjugate movement - or no eye movement - is a sign of brain injury

43
Q

Selective attention

A

Ability to focus. We can choose what we are going to pay attention to.

Selective attention deficit can be caused by seizures, contusions, subdural, hematomas, stroke, neoplasms, and Alzheimer’s disease.

Temporary, permanent, or progressive

44
Q

Memory: Amnesia, retrograde amnesia, anterograde amnesia

A

Amnesia: mild or severe loss of memory

Retrograde amnesia: difficulty remembering past memory

Anterograde amnesia: inability to form new memories

Can be temporary or permanent

45
Q

Data processing deficits (Agnosia, Dysphasia)

A

Agnosia:
failure to recognize form and nature of objects. can be tactile, visual or auditory. Usually only one sense is affected. Associated with damage from cerebral accidents.

Dysphasia
impaired comprehension or production of language.

Aphasia = more severe form of dysphasia. inability to communicate using language.

Dysphasia is associated with cerebral vascular accident involving specific areas of the brain:

Broca’s area: can’t create speech

Werbicke’s area: can’t understand/comprehend speech

46
Q

Broca’s area

A

Can’t create speech

47
Q

Wernicke’s area

A

Can’t comprehend/understand speech

48
Q

Primary vs secondary injury (hemodynamics)

A

Primary: initial trauma

Secondary: consequence of the alterations in cerebral blood flow, intracranial, pressure and oxygen delivery. Occurs in seconds or days.

49
Q

Cerebral Perfusion Pressure

A

MAP - ICP = CPP

50
Q

Cushing’s Triad

A

occurs in late stages of a cute head injury (increased ICP) indicates brainstem herniation is imminent.

Patient with with 2 of the 3 signs have 2X higher mortality rate.

  1. Increased systolic BP with decreased diastolic BP or widening pulse pressure
  2. Decreased heart rate (HR)
  3. Decreased respirations (RR)
51
Q

Intracranial Pressure

A

increased ICP causes: tumours edema, excess CSF or hemorrhage, causing intracranial hypertension.

First stages - body trying to compensate:

Stage 1: vasoconstriction, and external compression. Attempting to decrease ICP.

Stage 2: continued expansion of intracranial content = increase in ICP. Begins to compromise neuronal oxygenation. Systemic vasoconstriction, episodes of headache, confusion, restlessness, lethargy.

Second stages - body now decompensating:
Stage 3: ICP approaches arterial pressure, brain tissue starting to become hypoxic and hypercapnic. Condition deteriorates rapidly. Inability to stay awake, pupils, small, but still reactive, RR slowing, pulse pressure expanding, pulse rate decreasing. Intervention required STAT.

Stage 4: brain tissue herniates to areas of lesser pressure. Herniated brain, tissue compromises blood supply. Further hypoxia and ischemia = further herniation. Peoples no longer reactive to light and may have “ blown pupil” eventually both peoples for dilate. Intervention is futile

52
Q

Cerebral Edema

A

Causes: distortion of blood vessels, displacement of brain tissues, increase in ICP.

Cytotoxic/metabolic:
•Early stages - blood brain barrier stays intact
• Failure of the active transport systems. Cell lose potassium and gain sodium (water follows sodium) so cells swell

Interstitial Edema
Caused by blockage of CSF pathways

Vasogenic edema
•Late stages - caused by increased permeability of the capillary endothelium of the brain, caused by injury of the vascular structures.
•Plasma proteins leak into extracellular spaces, drawing water to them.
•Starts in area of injury and spreads to white matter of the same side
•Edema promotes more edema due to ichemia

Signs and symptoms (for all)
• headache, stiffness, nausea, vomiting, dizziness, vision loss, memory loss, loss of muscle coordination

53
Q

Hypotonia

A

Decreased muscle tone - passive movement of a muscle has little resistance. Caused by:
•Cerebral damage (causing ataxia snd tremor)
•Spinal cord injury or cerebrovascular accident, where the nerve impulses are lost.

Signs and symptoms:
Weak and tires easily, difficulty rising from sitting, walking upstairs, joints become hyper flexible, loss of muscle mass. Look flabby and flat.

54
Q

Hypertonia

A

increased muscle tone. Passes muscle movement with resistance to stretch.

Caused by:
•Upper neuron damage
•Spasticity, paratonia (inability to relax muscle during assessment), dystonia (contract uncontrollably) or rigidity

Signs and symptoms
•Tire easily, weakness, passive and active affected equally, can see either atrophy, or hypertrophy dependent on decrease in muscle use or overstimulation of muscle fibres.

55
Q

Hyperkinesia

A
56
Q

Dyskinesia

A
57
Q

Hypokinesia

A
58
Q

Spinal shock

A

Temporary loss of all spinal cord function beneath area of lesion.

Initially: complete paralysis, absence of reflexes, motor, sensory, including disturbances in bowel and bladder function. Can last hours to weeks. Caused by sudden destruction of efferent pathways.

Overtime spinal shock will resolve - damage to spinal cord remains - so initially they may have lost of all function.

As reflex return, we get a clearer picture of what damage has been done.

Return of spinal reflex is marked the end of spinal shock, deficits that remain are what has been caused by the original injury.

59
Q

Paresis

A

Muscle weakness caused by nerve damage or disease.

Partial paralysis: confined to one area

60
Q

Paralysis

A

Loss of muscle function in part of the body

61
Q

Hemiperesis/Hemiplagia

A

Upper and lower on one side. Usually from stroke

62
Q

Diplegia

A

Paralysis of corresponding parts on both sides of the body. Cerebral hemisphere injuries of specific parts of the brain (both arms paralyzed but both legs still work)

63
Q

Brain death

A

Damaged beyond recovery
Cannot maintain body. Brainstem functions stopped.

No motor response, no spontaneous respirations, no brain functions, tests performed to confirm brain death: Dolls eyes, corneal reflex, ice in ears,

64
Q

Cerebral death or irreversible coma

A

Death of hemispheres, not of the brain stem and cerebellum. Damage permanent. Brain stem maintains homeostasis. Person cannot speak, open eyes, or make purposeful movements. They will not recover, and they are not candidates for organ donation.

65
Q

Vegetative state

A

unawareness of self or surrounding environment. Does not speak or understand speech, cannot follow commands, sleep-wake cycle’s present, spontaneous, eye-opening. Vegetative states that last longer than 12 months are considered permanent.

66
Q

Astrocytoma

A

•Most common brain tumour across lifespan
•35-50% of all brain tumours
•Most grade 1-3 astrocytomas are in younger people
•Grade 4 = glioblastoma - most common and most lethal type. Most common in older adults, and more in men.
•Glioblastomas are highly vascular so surgery is difficult

67
Q

Extracerebral Neoplasms (Meningiomas)

A

•Growth in meninges
•34% of intracranial tumours are meningiomas
•Usually originate from meningeal cells in dura mater
•Adapts to shape it occupies
•Slow growing
•>50% survival rate

68
Q

Nerve Sheath Tumours

A

Autosomal dominant disorder - neurofibromas - can occur peripherally (type 1) or centrally (type 2)

Slow growing - S&S depend on location

69
Q

Metastatic brain cancer

A

Secondary tumour that metastasized to the brain

10X more common than primary tumours. 20-40%. Primary sites include lung, breast, kidney, colon, skin.

Higher incidence than any primary brain cancer.

Poor prognosis since there is cancer somewhere else in the body that has already progressed to stage 5. Average survival 6 months.

Patho 2 (6 decks)

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