Nervous System Flashcards

1
Q

List 3 factors that, when altered, may change arousal. Give one example of how each could be altered.

A

Structure: through infections, neoplasms, trauma, etc.
Metabolism: through hypoxia, drugs, electrolyte disturbances
Psychogenic: uncommon, through psychiatric disorders

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2
Q

What is the Glasgow coma scale used for, and what 3 responses does it measure?

A

Widely accepted “Glasgow coma scale” – a method for assessing level of consciousness in a person with brain injury: numbered scores are given to responses of eye opening, verbal utterances and motor responses.

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3
Q
  1. What does the pattern of breathing depend upon when consciousness decreases and what information can this yield?
A

When consciousness decreases, lower brain stem centers respond only to levels of PCO2 . The pattern of breathing can yield information as to the location of brain damage.

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4
Q
  1. What is the normal oculomotor response in a comatose patient? What are two abnormal oculomotor responses?
A

may be purposeful, absent or inappropriate (e.g., associated with decreased consciousness are several reflexes: grasping, sucking.)

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5
Q
  1. Describe the 5 outcomes of alterations in arousal.
A

Brain death – no recovery possible and brain cannot maintain internal homeostasis
Cerebral death – irreversible coma. Brain stem may continue to maintain homeostasis, but the individual will never be able to respond in any significant way to the environment.
Persistent vegetative state – complete unawareness of self or surrounding environment. Sleep-wake cycles are present, brain stem reflexes are intact, but there is bowel and bladder incontinence.
Minimally conscious state – individuals may follow simple commands, manipulate objects, gesture, have intelligible speech.
Locked-in syndrome – 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

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6
Q
  1. What are 3 properties involved in awareness?
A

Selective attention – ability to select specific information to be processed (youtube video)
Memory – the ability to store and retrieve info
Executive attention deficits – ability to maintain sustained attention and remember instructions

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7
Q
  1. Define awareness in the context of neurological function.
A

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

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8
Q
  1. Differentiate between a seizure and a convulsion.
A

Sudden temporary change in motor, sensory, autonomic or psychic clinical manifestations and a temporary altered level of arousal.
Convulsion – jerky, contract/relax movement associated with some seizures
Results from a sudden, explosive, disorderly discharge of cerebral neurons
Generally caused by cerebral lesions, biochemical disorder, cerebral trauma and epilepsy (which can result from many causes, including fever, brain tumors, genetic predispositions, etc.)

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9
Q
  1. Define agnosia, dysphasia, aphasia, acute confusional state, and dementia.
A

Agnosia – failure to recognize the form/nature of objects; usually only affects one sense (e.g., can recognize a safety pin by touching it, but not when looking at it). Caused by any damage to a specific part of the brain.
Dysphasia – understanding (receptive) and use (expressive) of symbols (written or verbal) is disturbed or lost (e.g., cannot find words, or uses words, but meaningless). Caused by dysfunction in left cerebral hemisphere (stroke, cancer, trauma, etc.)
(Aphasia = more severe form of dysphasia = inability to communicate (often used interchangeably with dysphasia))
Acute confusional states – highly distractible, unable to concentrate on incoming sensory information (e.g., delirium, hallucinations, seizures). Secondary to drug intoxication, nervous system disease, trauma, surgery, withdrawal from drug, etc.
Dementia - progressive failure of many cerebral functions, including orienting, memory, language, judgment and decision making. Because of declining intellectual ability, is accompanied by behavioural alterations. Caused by neuron degeneration, atherosclerosis, trauma, infection, etc.

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10
Q
  1. What is cerebral hemodynamics, and what determines its rate?
A

Cerebral blood flow is normally maintained at a rate that matches local metabolic needs of the brain.
Alterations in cerebral blood flow may be related to 3 injury states:
Inadequate cerebral perfusion
Normal cerebral perfusion with an elevated intracranial pressure
Excessive cerebral blood volume

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11
Q
  1. What does IICP stand for?
  2. What can cause IICP?
  3. What 3 things can be adjusted in order to compensate for changes in ICP? In what order are these adjusted, if needed?
A

Increased Intercranial Pressure
May result from anything that takes up volume in the brain, e.g., a tumour, edema, excess CSF or hemorrhage.
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.

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12
Q
  1. Describe the 4 stages of intracranial hypertension.
A

Stage 1: Vasoconstriction and external compression of the venous system occur in order to decrease the ICP (may be asymptomatic).
Stage 2: When continuing swelling exceeds this compensatory mechanism, oxygenation is compromised (confusion, restlessness, drowsiness), and systemic vasoconstriction occurs to increase systemic blood pressure in order to overcome decreased flow in the brain.
Stage 3: With continued swelling, when ICP begins to equal arterial pressure, cerebral perfusion pressure falls, and hypoxia and hypercapnia of brain tissue occur (rapid deterioration: decreased level of arousal, small, sluggish pupils). At this point, all compensatory mechanisms have been used, so there can now be a dramatic rise in ICP over a very short period of time.
Stage 4: Brain tissue shifts (herniates) from the compartment of greater pressure to a compartment of lesser pressure. This increases pressure in the lower pressure compartment, as well, impairing its blood supply. This increases ICP markedly to where it equals systolic arterial pressure, at which point cerebral blood flow ceases

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13
Q
  1. Describe cerebral edema (definition, causes, effects)
A

An increase in the fluid content of brain tissue.
Occurs after trauma, infection, hemorrhage, tumour, ischemia, infarct or hypoxia.
Distorts blood vessels, displaces brain tissues, causes herniation.

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14
Q

What three events can lead to cerebral edema?

A

increased permeability of BBB (plasma proteins leak out of capillaries, drawing water to them = increased water content of tissue. Occurs mainly in the white matter – easily separated fibers)
Toxins cause failure of transport mechanism of cells = more sodium inside cell = more water inside cell. Occurs mainly in the gray matter.
Obstruction of circulation of CSF in ventricles = fluid leaks into surrounding brain tissue (usually seen in children)

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15
Q
  1. What is hydrocephalus and what two events can cause this? Give an example of each event.
A

Excess fluid in ventricles, subarachnoid space, or both
Caused by too high production of CSF (e.g., tumour in choroid plexus), obstructed flow through ventricles (e.g., aqueduct stenosis - more in children), too low reabsorption of CSF (interference with arachnoid villi - more in adults)
Usually develops slowly over time, but can occur rapidly as a result of brain injury (presents with signs of rapidly developing IICP)

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16
Q
  1. Define hypotonia, hypertonia and dystonia, and what alteration in neuromotor function can result in these.
A

Alterations in muscle tone (364)
Normal muscle tone produces slight resistance to movement, which results in controlled movements.
Depending upon where damage in the brain has occurred, an alteration in this resistance can result in a spectrum from flaccidity (hypotonia) to rigidity (hypertonia).

17
Q
  1. Define paresis, paralysis and hyperkinesia, and what alteration in neuromotor function can result in these.
A

Paresis/paralysis (365)
Paresis: Partial paralysis = weakness
Paralysis: Loss of motor neuron function so that a muscle group is unable to overcome gravity
Can occur in both upper (brain and spinal cord) and lower (cranial/spinal nerves) motor neurons
For upper motor neuron (brain and spinal cord) – The condition can be classified as: hemiparesis/hemiplagia, paraparesis/paraplagia, quadriparesis/quadriplegia.
Hyperkinesia (369)
Excessive movements (e.g., tremors, tics)
Due to physical or chemical (e.g., insufficient dopamine) causes

18
Q
  1. Define the terms hemi-, para- and quadri-, as applied to paresis and paralysis.
A

Paresis/paralysis (365)
Paresis: Partial paralysis = weakness
Paralysis: Loss of motor neuron function so that a muscle group is unable to overcome gravity
Can occur in both upper (brain and spinal cord) and lower (cranial/spinal nerves) motor neurons
For upper motor neuron (brain and spinal cord) – The condition can be classified as: hemiparesis/hemiplagia, paraparesis/paraplagia, quadriparesis/quadriplegia.

19
Q
  1. Name and describe 2 disorders of posture, and the type of brain damage that can cause each posture.
A

Decorticate posture - upper extremities 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.
Decerebrate posture – increased tone in extensor muscles and trunk muscles, with clenched jaw and extended neck = head in neutral position, all four limbs rigidly extended. Occurs with brain stem lesions.

20
Q
  1. Define hypermimesis, dyspraxia/apraxia, dysarthria and agraphia.
A

Hypermimesis – inappropriate laughter or crying
Dyspraxia/apraxia – inability performing tasks that require learned motor skills (speaking (dysarthria), writing (agraphia), using tools, following instructions). Problem is with use of muscles, not with comprehension

21
Q
  1. Describe open and closed brain trauma.
A

Closed – dura remains intact. May result in both focal brain injuries (affecting one area), or diffuse axonal injuries (involving more than one area)
Open – there is a break in the dura, resulting in exposure of the cranial contents to the environment.

22
Q
  1. Define focal brain injury.
A

Focal brain injury – specific, grossly observable brain lesions that occur in a precise location

23
Q
  1. Define contusion, and differentiate between coup and contrecoup injury.
A

Contusions (bruises in brain tissue)
blood leaking from injured blood vessels
Coup injury: impact against the object, causing direct trauma to brain at point of impact
Contrecoup injury: (from head bouncing off object of initial impact) impact within skull, causing impact injury at area opposite to object, and shearing forces through the brain.
Both type of injuries occur in one continuous motion

24
Q
  1. Describe the sequence of events involved in the occurrence of a contusion.
A

Sequence of events: immediate loss of consciousness (no longer than 5 min), loss of reflexes (individual falls to the ground), brief period of no respiration, brachycardia, decrease in BP. Vital signs may stabilize in a few seconds, reflexes and consciousness return. Residual effects may persist.

25
Q
  1. Describe 3 types of hematomas and their causes.
A

Extradural (epidural) hematomas (379)
Injury causes bleeding between the dura mater and the skull, predominantly due to arterial bleeding
Subdural hematomas (380)
Bleeding between the dura mater and the brain
Acute caused by traumatic injury develop rapidly, commonly within hours, chronic (due to accompanying condition, e.g., alcoholism) develop over weeks to months.
Intracerebral hematomas
Bleeding within the brain
Penetrating injury or shearing forces traumatize small blood vessels.
May be delayed, appearing 3-10 days after injury

26
Q
  1. Define a penetrating brain trauma.
A

Projectiles and debris from scalp and skull injury/fracture penetrate dura mater

27
Q
  1. Define a diffuse brain injury, its causes and effect.
A

“concussion”
Result of shaking, rotational and twisting movements
Involves widespread area of the brain, with damage to axonal fibers. Can be observed only with microscope.
Reduces the speed of informational processing

28
Q
  1. Name and differentiate between the 5 types of diffuse brain injury.
A

Mild concussion – no loss of consciousness, but CSF pressure increases, confusion lasts for several minutes, retrograde amnesia
Classic cerebral concussion – loss of consciousness for up to 6 hr. Confused state lasts for several hrs, headache, nausea, retrograde amnesia.
Mild DAI – (6-24hr coma) may display decerebrate or decorticate posturing with extended periods of stupor/restlessness
Moderate DAI – (> 24hr coma) may display above posturing with unconsciousness lasting days or weeks. On awakening, often permanent deficit in memory, reasoning, language, etc.
Severe DAI – (usually emerge from coma in the first 3 months after injury), however, initial injury eventually results in compromised coordinated movements, verbal and written communication skills, inability to learn and reason.

29
Q
  1. Name 3 mechanisms of secondary brain trauma.
A

Indirect result of primary trauma
Mechanisms include cerebral edema, IICP, decreased cerebral perfusion pressure, ischemia and brain herniation.
Brain damage occurs hours to days after primary trauma

30
Q

Define cerebrovascular disease and name 2 examples.

  1. What are the two possible results of cerebrovascular disease?
  2. What does CVA stand for?
  3. What are 3 risk factors for a CVA?
A

Any abnormality of the brain caused by a pathologic process in the blood vessels is referred to as a cerebrovascular disease (vessel wall lesions, occlusion of the vessel lumen by thrombus or embolus, rupture of the vessel, alteration in blood quality such as increased blood viscosity)
Result of cerebrovascular disease can be either ischemia with or without infarction, or hemorrhage.
These lead to a cerebrovascular accident (CVA) otherwise known as “stroke”
Risk factors include: arterial hypertension, smoking, diabetes, insulin resistance, polycythemia.

31
Q
  1. Name and describe 3 types of stroke.

1. What does TIA stand for? Describe a TIA, its likely cause and what it will likely lead to.

A

Thrombotic stroke – occlusions formed by thrombi developing in arteries supplying the brain. (Thrombi develop often as a result of atherosclerosis, after plaque ruptures and a clot is formed). Piece of thrombus detaches and lodges in vessel upstream, causing acute ischemia.
TIA – “transient ischemic attack” is a brief episode of neurologic dysfunction caused by a focal disturbance of brain with symptoms lasting less than 1 hr, 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. With no treatment, high risk of repeat occurrence and eventual stroke.
Embolic stroke – involves fragments that break from a thrombus formed outside the brain. Embolus may plug lumen of small vessel entirely, or may shatter. A second stroke usually follows because the source of emboli continues to exist.

Hemorrhagic stroke (intracerebral hemorrhage, a type of intracranial hemorrhage) – associated with significantly increased systolic and diastolic pressures over several years. A mass of blood (from the size of a pinhead to several cm in diameter) forms and grows to displace adjacent brain tissue. Causes include hypertension, ruptured aneurysms, trauma.

32
Q
  1. Describe the events involved in an intracranial aneurysm and associated signs/symptoms.
A

Often the first indication is an acute subarachnoid hemorrhage and/or intracerebral hemorrhage.
Rupture through thin areas, causing hemorrhage, producing local changes in cerebral cortex. Bleeding ceases when platelet plug forms. Blood undergoes reabsorption within 3 weeks.
Produces excruciating headache or unconsciousness, or both (depending upon location/size of bleed). If achieve a deep unresponsive state, poor prognosis. If survive, recovery of function often is possible.

33
Q
  1. Describe multiple sclerosis: its physiological cause, most common initial symptoms, and usual progression.
A

Acquired autoimmune inflammatory disorder
Involves destruction of axonal myelin in the CNS
Onset usually between 20-40 yrs / more common in women
Interaction between genes and environment
A viral infection is followed by inflammation, resulting in injury to oligodendrocytes and demyelination. Axons degenerate and scars (sclerosis) are formed.
Most common initial symptoms are paresthesias of the face, trunk or limbs, weakness, visual disturbances or urinary incontinence.
Early cognitive changes are common and may include poor judgement, apathy, depression.
Physical and emotional stress can trigger attacks (paresthesias (“pins and needles”, dysarthria and ataxia (lack of coordination) that may persist for weeks, followed by progressive symptoms of MS (spastic paralysis, incontinence, etc.)

34
Q
  1. Describe Alzheimer’s disease: the mechanism behind neuron death, progression of disease symptoms and treatment.
A

One of the most common causes of severe cognitive dysfunction in older persons and the leading cause of dementia. Most common type is late-onset AD.
Exact cause unknown (some connections to genetic makeup have been discovered.)
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.