nervous

Question 1

Define consciousness

Answer 1

The state of awareness of self and the environment, and of being able to orient to new stimuli

Question 2

Consciousness is divided into what two components?

Answer 2

Arousal (wakefulness) & awareness (content of consciousness)

Question 3

3. What parts of the brain are required for a normal state of arousal (wakefulness)? What must be damaged in order for loss of arousal to occur?

Answer 3

Reticular activating system = diffuse network involving brainstem, medulla & thalamus, and functioning cerebral cortex

Direct injury to the RAS or to both cerebral hemispheres

Question 4

4. What is included in “awareness”?

Answer 4

All cognitive functions (awareness of self and environment, moods, reasoning, judgement)

Question 5

5. List and know general meaning of levels of consciousness

Answer 5

Coma = completely not arousable

Stupor = arousable only to pain

Obtundation = lower level of arousal, sleepy

Delirium = restlessness, hallucinations, delusions

Confusion = disorientation, fuzzy thinking, poor response to current stimuli

Question 6

6. Name and describe the scale used to commonly assess level of consciousness. (You don’t have to memorize meaning of numbers, just identify each category, the response at the top and bottom end of each scale, the fact that it is a total score, and whether a high score is a good or a bad result.)

Answer 6

Glasgow coma scale (15 is normal, 13-14 is associated with mild head injury, 8 – 12 is associated with moderate head injury, < 8 is associated with severe head injury)

Eye opening: 1 = no response, 2 = to pain, 3 = to command, 4 = spontaneously

Best verbal response: 1 = no response, 2 = incomprehensible sounds, 3 = inappropriate words, 4 = confused, 5 = oriented appropriate words, phrases

Best motor response: 1 = no response, 2 = extension (decerebrate), 3 = abnormal flexion (decorticate), 4 = withdraws from pain flexion, 5 = localizes pain, 6 = obeys commands

Question 7

7. Define brain death, and be familiar with how it is determined.

Answer 7

Irreversible loss of brain function; brain cannot maintain internal homeostasis; no recovery possible

Well established underlying pathology, deep unresponsive coma & absence of motor reflexes, absent brainstem reflexes, requires mechanical ventilation “apnea test”, lack of other causes e.g. drugs, shock

Question 8

8. Define: persistent vegetative state, minimally conscious state, locked-in syndrome.

Answer 8

Complete unawareness of self or surrounding environment. Sleep-wake cycles are present, brain stem reflexes are intact, but there is bowel and bladder incontinence

Individuals may follow simple commands, manipulate objects, gesture, have intelligible speech, but are consistent with these actions

Complete paralysis of voluntary muscles with the exception of eye movement. Individual is fully conscious with intact cognitive function, but cannot communicate through speech or body movements

Question 9

9. Describe Cheyne-Stokes breathing and neurogenic hyperventilation, including the possible location of brain damage that would cause these two patterns of breathing.

Answer 9

Higher brain injury can result in Cheyne-stokes breathing: alternating periods of apnea and tachypnea, due to response to levels of carbon dioxide in blood (loss of smoothing out of breathing pattern usually performed by higher brain centres)

Injury to midbrain: > 40 breaths per minute when inspiratory/expiratory centres are continuously stimulated

Question 10

10. What alterations can occur with pupillary response, and what information can this yield?

Answer 10

Upon being exposed to light, pupil response can range from combinations of fixed, dilated, pinpoint, and unequal (pupils responses differ). Can help determine location/extent of brain damage

Question 11

11. What is the normal oculomotor “doll’s eye” response in a comatose patient? What are two abnormal oculomotor responses?

Answer 11

Normal response is movement opposite from head movement. Abnormal is following head movement, or independent movement (assessable only in comatose patients)

Question 12

12. What general types of motor responses may occur with neurological damage? Be familiar with examples.

Answer 12

May be purposeful, absen4t or inappropriate (e.g. associated with decreased consciousness are several reflexes: grasping, sucking, palmomental, snout

Abnormal responses in the upper and lower extremities: decorticate / decerebrate postures

Question 13

13. Describe decorticate and decerebrate postures and location of brain damage they indicate.

Answer 13

Upper extremities are flexed at the elbows and held close to the body and lower extremities that are externally rotated and extended. May occur with severe cerebral hemisphere damage

Increased tone in extensor muscles and trunk muscles, with clenched jaw and extended neck = head in neutral position, all for limbs rigidly extended. Occurs with brain stem lesions

Question 14

14. Define seizure. Be familiar with causes.

Answer 14

A sudden, explosive, disorderly discharge of cerebral neurons, that produces a temporary change in brain function, usually involving motor, sensory, autonomic or psychic clinical manifestations and a temporary altered level of arousal

Cerebral lesions, biochemical disorders, cerebral trauma or epilepsy (these factors can result from many causes, including fever, brain tumors, infections, genetic predispositions)

Question 15

15. Differentiate between a seizure and a convulsion.

Answer 15

Convulsions is jerky, muscle contraction – relaxation cycles whereas seizures are sudden, explosive, disorderly discharge of neurons

Question 16

16. Define agnosia, hemineglect, dysphasia, aphasia (Wernike’s and Broca’s).

Answer 16

Failure to recognize the form/nature of objects; usually only affects one sense. Caused by any damage to a specific part of the brain

Inability to attend to and react to stimuli coming from the contralateral (to site of damage) side of space. Won’t visually track, orient or reach to the neglected side. May not use those limbs, or take care of them

Understanding (receptive) and use (expressive) of symbols (written or verbal) is disturbed or lost. Caused by dysfunction in left cerebral hemisphere (stroke, cancer)

Inability to communicate

(receptive) aphasia: result of damage to the centre of the brain responsible for the comprehension of language. Individual speaks in a “word salad” - uses nonsense words in long, meandering sentences

(Expressive) aphasia: result of damage to the centre of the brain responsible for the production of language. Individual has difficulties “findings” the correct word

Question 17

17. Name 3 general alterations that can occur if the neuromotor function of the nervous system is affected.

Answer 17

Alterations in muscle tone, alterations in movement, alterations in complex motor performance

Question 18

18. What is muscle tone and what does it do? How is it controlled?

Answer 18

Muscle tone is the normal state of muscle tension which allows for controlled movement and maintenance of posture. It is controlled by the stretch reflex (which can be inhibited by the CNS – otherwise any stretch of an antagonist muscle (which allows the agonist muscle to act) would be inhibited and we wouldn’t be able to perform large movements that require a full range of movement).

Alterations in muscle tone can be caused by injury to any section of motor pathway: peripheral nerve, NMJ, spinal cord, brain

Question 19

19. What changes in muscle tone are brought about by injuries to the upper motor neurons vs the lower motor neurons?

Answer 19

An injury in the upper motor neurons generally produces increased tone as the inhibitory effect of the brain on the spinal cord reflexes is removed (rigidity = hypertonia)

An injury in the lower motor neurons produces decreased tone (flaccidity = hypotonia)

Question 20

20. Define hypotonia and hypertonia.

Answer 20

Hypotonia = decreased muscle tone

Hypertonia = too much muscle tone so that arms or legs are stiff and difficult to move

Question 21

21. Define paresis, paralysis and hyperkinesia.

Answer 21

Weakness of muscle due to alteration in how the motor units are activated (muscle strength depends upon order and number of motor units recruited)

Loss of motor neuron function so that a muscle group is unable to overcome gravity (total loss of movement)

Excessive movements (tremors)

Question 22

22. Is the influence of the location of the lesion (whether upper or lower motor neuron) the same for the flaccidity/spastic nature of paresis/paralysis as it is for muscle tone?

Answer 22

Upper motor neuron lesion: produces spastic (stiff/rigid) paresis/paralysis: spinal reflexes remain intact but there is loss of cortical (brain) inhibition. (although the muscle will eventually atrophy due to loss of use, since the muscle reflexes are still intact, the atrophy takes longer)

Lower motor neuron lesion: produces flaccid (limp) paresis/paralysis since muscle excitation is lost (muscle atrophy occurs faster, since spinal reflexes are lost)

Question 23

23. Define the terms hemi-, para- and quadri-, as applied to paresis and paralysis.

Answer 23

Weakness or inability to move on one side of the body, making it hard to perform everyday activities

When you’re partially unable to move your legs (paraparesis) & complete inability to move legs (para-paralysis)

Condition in which you have muscle weakness in all 4 of your limbs

Question 24

24. What is the cause of contralateral hemiparesis/hemiparalysis?

Answer 24

80% of upper motor neurons cross over to the opposite side of the body (decussation) giving rise in many cases to contralateral hemiparesis which occurs on the side of the body opposite to the side of the brain in which the causal lesion occurs

Question 25

25. Describe 3 groups of disorders that are included under the category of alterations in complex motor performance.

Answer 25

Disorders of posture: an inequality of tone in muscle groups, because of a loss of normal postural reflexes. Decorticate and decerebrate postures & basal ganglion posture (stooped, hyperflexed)

Disorders of gait: spastic gait - (unilateral UMN injury) a shuffling gait with leg extended and held stiff; basal ganglion gait – small steps with decreased arm swing

Disorders of expression: hypermimesis, dyspraxia/apraxia

Question 26

27. Define hypermimesis, dyspraxia/apraxia, dysarthria and agraphia.

Answer 26

inappropriate laughter or crying

Inability to perform tasks that require learned motor skills (problem is with use of muscles, not with comprehension)

Speaking

Writing

Question 27

28. Describe open and closed brain trauma, and what type of action would cause each.

Answer 27

Open = there is a break in the dura, resulting in exposure of the cranial contents to the environment (penetrating trauma)

Closed = dura remains intact. May result in both focal brain injuries (affecting one area), or diffuse axonal injuries (involving more than one area) (blunt trauma)

Question 28

29. Describe what is meant by primary and secondary stages of brain trauma.

Answer 28

Primary = the damage is caused by impact

Secondary = the damage is caused by subsequent swelling, infection or hypoxia

Question 29

30. Define focal brain injury.

Answer 29

Specific, grossly observable brain lesions that occur in a precise location

Question 30

31. Define contusion, and differentiate between coup and contrecoup injury.

Answer 30

Bruises in brain tissue (blood leaking from injured blood vessels

Coup: impact against the object, causing direct trauma to brain at point of impact

Contrecoup: from rebound of brain against opposite inside area of skull, causing impact injury at area opposite to object, and shearing forces through the brain

Question 31

32. Describe the possible sequence of events involved in the occurrence of a contusion.

Answer 31

Immediate loss of consciousness (no longer than 5 mins), loss of reflexes (individual falls to ground), brief period of no respiration, bradycardia, decrease in BP. Vital signs may stabilize in a few seconds, reflexes and consciousness return. Residual effects may persist

Question 32

33. Describe a hematoma and differentiate between the 3 types of hematomas as to location, cause and timing.

Answer 32

Extradural (epidural) hematoma: injury causes bleeding between the dura mater & skull, predominantly due to arterial bleeding. There may be a delay before symptoms are evident: lucid period of 2 – 3 hours between the trauma and clinical signs, then a rapid deterioration as intracranial pressure rises, hence the importance of maintaining head-injury observations

Subdural hematoma: typically venous, low pressure, slow bleeding. If acute and post-traumatic, can still develop within hours (clinically resembles epidural). If chronic and related to other conditions – cerebral atrophy from alcoholism, develops over weeks or months

Intracerebral hematoma: bleeding within the brain. Penetrating injury or shearing forces traumatize small blood vessels. May be delayed, appearing 3 – 10 days after injury. Signs and symptoms depend upon location in the brain

Question 33

34. Define a diffuse brain injury, its causes and effect.

Answer 33

Diffuse and widespread damage to neural axons in the brain

Result of shaking, rotational and twisting movements (e.g. car accidents, shaken baby syndrome)

Reduces the speed of informational processing

Question 34

35. Differentiate between mild concussion and classic cerebral concussion.

Answer 34

Mild: no loss of consciousness, but CSF pressure increases, confusion lasts for several minutes, retrograde amnesia

Classic: loss of consciousness for up to 6 hours, confused state lasts for several hours, headache, nausea, retrograde amnesia

Question 35

36. What determines the category (i.e., mild to severe) of a DAI?

Answer 35

Mild: 6-24 hour coma – may display decerebrate or decorticate posturing with extended periods of stupor/restlessness

Moderate: > 24 hour coma – may display above posturing with unconsciousness lasting days or weeks. On awakening, often permanent deficit in memory, reasoning, language

Severe: usually emerge from coma in the first 3 months after injury, initial injury eventually results in compromised coordinated movements, verbal and written communication skills, inability to learn and reason

Question 36

37. Describe what is meant by a secondary brain trauma.

Answer 36

Brain damage occurs hours to days after primary trauma

Mechanisms include: release of excitatory neurotransmitters that interfere with normal neuronal metabolism, cerebral edema, hydrocephalus, IICP

Question 37

38. What does IICP stand for, and what does it mean?

Answer 37

Increased intracranial pressure

An increase in the pressure inside the skull that can result from and cause further injury

Question 38

39. What can cause IICP?

Answer 38

May result from anything that takes up volume in the brain (e.g. tumour, edema)

Question 39

40. What 3 things can be adjusted in order to compensate for changes in ICP? In what order are these adjusted, if needed?

Answer 39

To adjust for increased pressure, there must be a reduction in some other cranial content. This can include blood volume, CSF volume, tissue volume

The brain adjusts initially through loss of CSF, as it is most easily decreased in response to increased intracranial pressure

If this does not remedy pressure, cerebral blood volume and flow are altered

Question 40

41. Describe the 4 stages of IICP (know the significant changes in the brain within each stage (the compensations, what is happening to the ICP and perfusion of the brain, and the accompanying presentation of the patient).

Answer 40

stage 1: the brain attempts to further compensate for IICP with vasoconstriction. This mechanism may be effective and often patients are asymptomatic during this stage.

Stage 2: continues to be an increase in the amount of contents inside the intracranial vault. By this stage the increased pressure has surpassed the ability of the brain to compensate. Cellular hypoxia worsens and the body responds by causing a systemic arterial vasoconstriction. This is the body’s attempt to increase the cerebral perfusion pressure and overcome the increased ICP. During the second stage the person begins to show signs of increased ICP. These clinical manifestations include confusion, restlessness, lethargy, pupil and breathing changes. A decreased level of consciousness is the first sign of an increased intracranial pressure

Stage 3: the intracranial pressure approaches arterial pressure. Cellular hypoxia and hypercapnia become worse. The person decompensates very quickly. Clinical manifestations include: a decreased LOC, widening pulse pressure, bradycardia, pupils small and sluggish

Stage 4: characterized by the occurrence of a herniation and the equalization of arterial pressure and ICP. The equalization of these 2 pressures prevents cerebral perfusion, worsens cellular hypoxia, causes cell death and increases ICP. A herniation is present when the brain tissue moves from an area of high pressure to an area of low pressure.

Question 41

42. Describe cerebral edema (definition, be familiar with causes and effects)

Answer 41

An increase in the fluid content, causing increase in brain tissue volume

Occurs after trauma, infection, hemorrhage, tumour, ischemia, infarct or hypoxia

Distorts blood vessels, displaces brain tissues, causes herniation

Question 42

43. Name and describe the mechanism of the two types of cerebral edema.

Answer 42

Vasogenic edema: increased permeability of BBB (plasma proteins leak out of capillaries, drawing water to them = increased water content of tissue. Occurs mainly in the white mater – easily separated fibres)

Cytotoxic edema: toxins, hypoxia, etc cause failure of transport mechanism of cells = more sodium inside cell = more water inside cell. Occurs mainly in the gray matter

Question 43

44. What is hydrocephalus, and what is its cause?

Answer 43

Excess fluid in ventricles, subarachnoid space, or both

Caused by too high production, or too low reabsorption, of CSF

Question 44

45. Name and describe the two types of hydrocephalus and give an example of each.

Answer 44

Noncommunicating (obstructive): obstruction (tumour, inflammation, hemorrhage) prevents CSF from reaching arachnoid villi and being reabsorbed

Communicating: failure of reabsorption due to too few, or scarring (due to meningitis) of arachnoid villi. Adenomas of choroid plexus can also cause overproduction of CSF (much less common)

Question 45

46. Define cerebrovascular disease and be familiar with examples of causes.

Answer 45

Any abnormality of the brain caused by a pathologic process in the blood vessels (vessel wall lesions, occlusion of the vessel lumen by thrombus or embolus, rupture of the vessel)

Question 46

47. What are the two possible results of cerebrovascular disease?

Answer 46

Result can be either ischemia (causing the development of a penumbra (an ischemic area of cells that could survive if blood flow is re-established) with possible infarction of cells, usually in the centre of the penumbra), or hemorrhage

Question 47

48. What does CVA stand for?

Answer 47

Cerebrovascular accident

Question 48

49. Define CVA/stroke.

Answer 48

An acute focal neurological deficit from a vascular disorder, that injures brain tissue

Question 49

50. Be familiar with the risk factors for a CVA, and related long-term deficits.

Answer 49

Risk factors: age, sex (higher risk in men when younger, in women when older), race, family history, hypertension, smoking, diabetes mellitus, hyperlipidemia, atrial fibrillation

Long term deficits: motor deficits, dysarthria and aphasia, cognitive and other deficits

Question 50

51. Differentiate between thrombotic and lacunar strokes as to cause, part of vascular system affected, area of brain affected and usual effect(s).

Answer 50

Occlusions formed by thrombi developing in arteries within the brain (thrombi develop often as a result of atherosclerosis, after plaque ruptures and a clot is formed). Piece of thrombus may detach and lodge in vessel upstream. Either way, thrombus causes acute ischemia. Usually, a single cerebral artery is affected, often affecting the cortex (symptoms: aphasia, neglect, visual field defects) & usually seen in older persons with atherosclerosis causing CAD or PAD

Very small infarctions deep in the brain that leave behind small cavities (“lakes”), can be due to emboli, small hemorrhages, vasospasm. Because of location (internal capsule, basal ganglia, brain stem), effects are different than large vessel strokes (which tend to affect cortex), sensory or motor hemiplegia, dysarthria (more sensory/motor based effects)

Question 51

52. What does TIA stand for? Describe a TIA, its likely cause and what it will likely lead to, with no treatment. Be familiar with manifestations.

Answer 51

Transient ischemic attack

A brief episode of neurologic dysfunction caused by a focal disturbance of brain with symptoms lasting less than 1 hr, with no evidence of infarction and complete clinical recovery

Likely a result of platelet clumps or vessel narrowing with spasm, causing an intermittent blockage of circulation (“brain angina”)

Manifestations: numbness in face, arm or leg, trouble speaking or understanding, poor vision in one or both eyes, confusions, FAST

With no treatment, high risk for repeat occurrence and eventual stroke

Question 52

53. Differentiate between a thrombotic and an embolic stroke as to nature of blockage and timing.

Answer 52

Occlusions formed by thrombi developing in arteries within the brain, piece of thrombus may detach and lodge in vessel upstream causing acute ischemia. Not associated with activity (may occur with rest)

Involves fragments that break from a thrombus formed outside the brain (thrombus usually within the left heart, but could be within carotid artery). Sudden onset with immediate maximum deficit

Question 53

54. Know the most frequent site for embolic stroke, and be familiar with conditions that can lead to formation of embolus.

Answer 53

Middle cerebral artery (terminus of carotid artery)

Rheumatic heart disease, atrial fibrillation, recent heart attack

Question 54

55. Describe a hemorrhagic stroke as to cause, timing, nature, manifestations, and why it is the most frequently fatal type of stroke.

Answer 54

Usually occurs suddenly, with activity

Involves rupture of a blood vessel (usually an aneurysm), bleeding into tissue (intracerebral) or into CSF (subarachnoid), forming a growing mass of blood (hematoma)

Causes include hypertension, ruptured aneurysms, trauma

Focal manifestations of intracerebral hemorrhage depend upon area of brain affected. Usually, hemorrhage is onto basal ganglia, which produces contralateral hemiplegia

Greater danger is increased intracranial pressure, which could lead to coma and death

Question 55

56. What is the most common manifestation of a stroke? Be familiar with other manifestations.

Answer 55

Contralateral weakness of arm and face, sometimes leg

Usually sudden and one sided

Initial flaccidity replaced by spasticity after 6-8 weeks

May also include loss of vision in one eye (monocular blindness), hemianopia, aphasia, dysarthria, ataxia

Motor defects are most common, followed by deficits of language, sensation and cognition

Sensory deficits affect the body contralateral to the lesion and can include: paresthesias, neuropathic pain, numbness

Question 56

57. Define hemianopia and ataxia.

Answer 56

Hemianopia: when you lose sight in half of your visual field

Ataxia: presence of abnormal, uncoordinated movements

Question 57

58. Describe the pathophysiology of Parkinson’s disease, its 3 cardinal symptoms and the basis for using levodopa for treatment.

Answer 57

Loss of dopamine producing cells in substantia nigra that communicate with cells of the basal ganglia (group of nuclei that surround the thalamus and provide control of initiating muscle movement). End result is inability to easily begin desired movements, and inability to reduce undesired movements

Resting tremor, bradykinesia, muscle rigidity

Treatment includes levodopa, which metabolizes to dopamine in the brain. Reduces symptoms but produces other motor side effects

Question 58

59. Describe the mechanism behind neuron death in Alzheimer Disease, progression of disease symptoms and treatment.

Answer 58

Protein containing structures called plaques form between neurons, and protein containing tangles form inside neurons, damaging and killing neurons, disrupting nerve impulse transmission

Initial clinical manifestations often attributed to forgetfulness, emotional upset or illness. Memory loss increases over time; confusion increases; problem solving, language and math skills decrease. Behavioural changes occur (irritability, depression, mood swings)

No cure – treatment is using devices to compensate for impaired cognitive function, improving general state of nutrition and health (drugs that boost neurotransmitter function may help temporarily)