Neuro Flashcards

Question

Forebrain

Answer 1

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

Answer 2

Connects the pons to diencephalon

Answer 3

Cerebellum, pons, medulla

Answer 4

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

Answer 5

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

Answer 6

Damage to upper neurons = initial paralysis followed by partial recovery Damage to lower neurons = paralysis unless peripheral nerve damage is followed by nerve regeneration

Answer 7

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

Answer 8

space between arachnoid and pia. Contains cerebralspinal fluid

Answer 9

**125-150ml** circulates through subarachnoid space and ventricles 600ml produced daily produced in ventricles and reabsorbed through arachnoid villi

Answer 10

**5-14 mmHg** laying down doubles when standing up

Answer 11

8 cervical 12 thoracic 5 lumbar 5 sacral 1 coccygeal

Answer 12

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)

Answer 13

No damage to right = effects on right

Answer 14

Structural: vascular alterations, neoplasms, tbi, degenerative, polygenic traits Metabolic: Infection, inflammation, hypoxia, electrolytes disturbance, hypoglycaemia, renal or liver disorders Psychogenic: psychiatric disorders

Answer 15

**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

Answer 16

**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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

**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

Answer 21

**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

Answer 22

Can’t **create** speech

Answer 23

Can’t **comprehend/understand** speech

Answer 24

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

Answer 25

MAP - ICP = CPP

Answer 26

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)

Answer 27

**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

Answer 28

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

Answer 29

**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.

Answer 30

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.

Answer 31

**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.

Answer 32

Muscle **weakness** caused by nerve damage or disease. Partial paralysis: confined to one area

Answer 33

Loss of muscle **function** in part of the body

Answer 34

Upper and lower on one side. Usually from stroke

Answer 35

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)

Answer 36

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,

Answer 37

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.

Answer 38

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.

Answer 39

•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

Answer 40

•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

Answer 41

Autosomal dominant disorder - **neurofibromas** - can occur peripherally (type 1) or centrally (type 2) Slow growing - S&S depend on location

Answer 42

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.

Neuro Flashcards

(69 cards)