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Pathophysiology > 15. Neuro: Cognitive Systems & Cerebral Hemodynamics > Flashcards

15. Neuro: Cognitive Systems & Cerebral Hemodynamics Flashcards

1
Q

absence of voluntary movement

A

akinesia

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2
Q

damage between fibers of language center – may not be able to control tone and emotions of language

A

transcortical dysphasia

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3
Q

muscle resistance to passive movement of a rigid limb that is uniform in both flexion and extension throughout movement

A

rigidity

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4
Q

ICP may not change in this stage due to compensatory mechanisms

A

Stage 1 IICP

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5
Q

Cause of hydrocephalus

A

interference of CSF flow - decreased reabsorption - increased production - obstruction within ventricular system

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6
Q

AD hereditary degenerative disorder that causes severe degeneration of basal ganglia and frontal cerebral atrophy -> depletion of basal ganglia GABA (inhibitory NT)

A

Huntington disease (HD or Chorea)

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7
Q

inability to remember instructions and information needed to guide behavior

A

working memory deficit

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8
Q

broad-based gait where person walks in small steps and the head and body are flexed -> due to basal ganglion dysfunction and seen in Parkinson disease

A

basal ganglion gait

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9
Q

weakness/paralysis of lower extremities as a result of lower spinal cord injury

A

paraparesis/paraplegia

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10
Q

Broca vs Wernicke

A
  • Broca’s area: helps in producing coherent speech - Wernicke’s area: helps in speech processing and understanding language
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11
Q

Explain the rhythm of Cheyne-Stokes respiration

A
  • increased levels of CO2 -> tachypnea - CO2 levels decrease -> leads to apnea until CO2 accumulates again
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12
Q

agnosia is commonly associated w/ what neurological problem

A

CVA

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13
Q

Clinical manifestations of stage 3 IICP

A
  • decreased levels of arousal - widened pulse pressure (systolic increases) - bradycardia - small, sluggish pupils
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14
Q

4 criteria for brain death

A
  • unresponsive coma (no motor or reflex movements) - no spontaneous respiration (apnea) - no brainstem functions (dilated, fixed pupils; no gag or corneal reflexes) - isoelectric EEG
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15
Q

loss of emotional language (aprosody); inability to understand emotional in speech and facial expression or inability to express emotion

A

hypomimesis

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16
Q

result due to damage of descending motor pathways

A

upper motor neuron syndromes

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17
Q

associated w/ upper motor neuron syndromes; mainly the flexors of the arms and extensors of the legs are affected

A

pyramidal motor syndrome

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18
Q

involves an inability to understand written or spoken language; speech is fluent but words and phrases have no meaning

A

Receptive dysphasia or Wernicke’s/sensory/fluent dysphasia

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19
Q

defect of pattern recognition -> failure to recognize the form and nature of objects (can be tactile, visual, or auditory)

A

Agnosia

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20
Q

more severe form of dysphasia and an inability to communicate using language; usually associated w/ CVA involving the middle cerebral A.

A

aphasia

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21
Q

Indicates the presence and level of brainstem dysfunction

A

pupillary changes

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22
Q

causes of increased intracranial pressure (IICP)

A

increased intracranial content - tumor growth - edema - excessive CSF - hemorrhage

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23
Q

excessive, purposeless movement (broad category of abnormal movements)

A

hyperkinesia

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24
Q

neurodegenerative disorder that diffusely affects upper and lower motor neurons of the cerebral cortex, brain stem, and spinal cord (corticospinal tracts and anterior roots)

A

amyotrophic lateral sclerosis (ALS or Lou Gehrig disease)

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25
Q

acquired mental disorder characterized by deficits in attention and coherence of thought and action; secondary to intoxication, metabolic disorders, or nervous system disorders

A

acute confusional states (ACS); may also be called delirium

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26
Q

complete unawareness of the self or surrounding environment and complete loss of cognitive function; can be seen in survivors of cerebral death

A

persistent vegetative state (VS)

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27
Q

complete paralysis of voluntary muscles except for eye movements; person cannot communicate through speech or body movement but is fully conscious w/ intact cognitive function

A

locked-in syndrome

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28
Q

isolated contraction of a single muscle fiber because of metabolic changes I denervated muscle -> not clinically visible

A

fibrillation

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29
Q

individuals may follow simple commands, manipulate objects, gesture or give yes/no responses, have intelligible speech, and have movements such as blinking/smiling

A

minimally conscious state (MCS)

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30
Q

loss of motor function so that a muscle group is unable to overcome gravity

A

paralysis

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31
Q

muscle rippling or quivering under the skin

A

fasciculations

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32
Q

sustained involuntary muscle contraction that causes twisting movement

A

dystonia

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33
Q

Clinical manifestation of ALS

A

progressive muscle weakness leading to respiratory failure and death; pt has normal intellectual and sensory function until death

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34
Q

resistance to passive movement which varies in direct proportion to force applied

A

paratonia

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35
Q

Classic manifestations of PD

A
  • resting tremor - rigidity - bradykinesia/akinesia - postural disturbance (stooped) - short shuffling steps - cognitive-affective symptoms
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36
Q

occurs when the brain is damaged so much that it can never recover (irreversible) and cannot maintain internal homeostasis

A

Brain death

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37
Q

large motor neurons in ventral horn of spinal cord -> bring nerve impulses from upper motor neurons to the skeletal muscle through anterior spinal roots and cranial nerves

A

lower motor neurons

38
Q

NT necessary to make muscle tone smooth

A

dopamine

39
Q

normal ICP

A

5-15 mmHg

40
Q

posture/response caused by severe injury to the brain/brainstem

A

decerebrate posture/response

41
Q

sleep-wake cycle are present, eyes open spontaneously, and BP and breathing are maintained without support; brainstem reflexes intact but cerebral function lost

A

persistent vegetative state (VS)

42
Q

stage of IICP where brain tissue herniates from compartment of greater pressure to compartment w/ less pressure -> blood supply compromised -> further hypoxia in herniated tissues

A

Stage 4 IICP

43
Q

paralysis of corresponding parts of both sides of the body as a result of cerebral hemisphere injuries

A

diplegia

44
Q

cerebral edema caused by increased permeability of capillary endothelium of brain after injury to vascular structure (BBB is disrupted)

A

vasogenic edema

45
Q

paresis/paralysis of the upper and lower extremities on one side

A

hemiparesis/hemiplegia

46
Q

inability to form new personal or factual memories but memories of distant past are retained

A

anterograde amnesia

47
Q

executive attention deficits are associated w/ alternations to which area of the brain?

A

frontal and prefrontal cortex

48
Q

death of the cerebral hemispheres exclusive of the brain stem and cerebellum (no behavior or environmental responses but brain can maintain homeostasis)

A

Cerebral death (irreversible coma)

49
Q

excess fluid within the cranial vault, subarachnoid space, or both -> causes dilation of ventricles and IICP -> severe headache

A

hydrocephalus

50
Q

posture/response characterized by increased tone in extensor muscles and trunk muscles w/ active tonic neck reflexes (head is neutral and all 4 extremities are rigidly extended)

A

decerebrate posture/response

51
Q

inability to set goals and recognize when an object meets a goal

A

sustained attention deficit

52
Q

progressive deterioration of cerebral functions due to neurofibrillary tangles and plaques -> lead to neuronal death and brain atrophy

A

Alzheimer’s disease (AD)

53
Q

decreased amplitude of movement

A

hypokinesia

54
Q

stage with continued expansion of intracranial contents and pressure may compromise neuronal oxygenation and systemic arterial vasoconstriction may occur to overcome IICP

A

Stage 2 IICP

55
Q

At what stage of IICP is surgical or medical intervention the best?

A

Stage 2 IICP

56
Q

loss of ability to perform activities that a person is physically able and willing to do -> brain is unable to make and deliver correct movement instructions to the body

A

dyspraxia/apraxia

57
Q

follows an epileptic seizure and can last hours or 1-2 days; includes headache, confusion, dysphasia, memory loss, and fatigue/deep sleep

A

postictal state

58
Q

state of continuous seizures lasting more than 5 minutes or rapidly recurring seizure before the person has regained consciousness

A

status epilepticus

59
Q

Diagnostic hallmark of PD? What does it lead to later in disease?

A
  • Lewy body formation in neurons (protein misfolding and accumulation of alpha-synuclein) - Lewy body dementia later in disease
60
Q

gait associated w/ bilateral upper motor neuron injury and spasticity -> when walking, legs swing around the body and then cross in front of each other

A

scissors gait

61
Q

posture/response that occurs when the brainstem is not inhibited by the cerebral cortex motor area

A

decorticate posture/response

62
Q

Clinical manifestations of stage 4 IICP

A
  • progression to deep coma - ipsilateral dilation and fixation of pupils -> bilateral dilation and fixation of pupils - abnormal breathing (Cheyne-stokes, ataxic, or central neurogenic hyperventilation) - pulse pressure begins to decrease (as brain herniates and ICP decreases) - pulse slightly irregular
63
Q

Motor signs that indicate loss of cortical inhibition

A

primitive reflexes and rigidity (paratonia)

64
Q

5 patterns of neurologic function that are critical to evaluate

A
  • level of consciousness - pattern of breathing - pupillary reaction - oculomotor responses - motor responses
65
Q

exaggerated emotional response; excessive crying (left hemisphere) or laughing (right hemisphere); may not be appropriate to environment

A

hypermimesis

66
Q

2 symptoms of the preictal phase of a generalized tonic-clonic seizure

A
  • prodroma: hours to days before (anxiety/depression, inability to think clearly) - partial seizure: immediately precedes generalized seizure
67
Q

difficulty retrieving past personal history memories or past factual memories

A

retrograde amnesia

68
Q

gradual increase in tone causing increased resistance until tone suddenly diminishes

A

spasticity

69
Q

severe degeneration of basal ganglia involving dopaminergic nigrostriatal pathway -> dopamine deficiency (inhibitory NT) and unopposed cholinergic activity (promotes muscle tone)

A

Parkinson disease (PD)

70
Q

posture/response characterized by upper extremities flexed (held close to body) and lower extremities that are externally rotated and extended

A

decorticate posture/response

71
Q

stage where ICP begins to reach arterial pressure and brain tissues experience hypoxia and hypercapnia -> rapid deterioration

A

Stage 3 IICP

72
Q

increased fluid (intracellular or extracellular) within the brain

A

cerebral edema

73
Q

decreased speed of movement

A

bradykinesia

74
Q

abnormal, involuntary movements that occur in spasms

A

paroxysmal dyskenisias

75
Q

Clinical manifestations of stage 2 IICP

A

subtle and transient - confusion - restlessness - drowsiness - slight pupillary and breathing changes

76
Q

involves loss of ability to produce spoken or written language w/ slow or difficult speech

A

Expressive dysphasia or Broca’s/motor/nonfluent dysphasia

77
Q

wide-based gait w/ increased body sway and falls, loss of truncation motion, and shuffling

A

frontal lobe ataxic gait

78
Q

passive movement of a muscle mass w/ little to no resistance

A

hypotonia

79
Q

temporary loss of all spinal cord functions below the lesion

A

spinal shock

80
Q

gait associated w/ unilateral upper motor neuron injury -> manifests by a shuffling gait w/ leg extended and held stiff (scrapes floor surface)

A

spastic gait

81
Q

impairment of comprehension or production of language w/ impaired communication

A

dysphasia

82
Q

Clinical manifestations of lower motor neuron syndromes

A
  • flaccid paralysis (both involuntary and voluntary movements affected) - hyporeflexia or areflexia (loss of tendon reflexes) - fibrillation
83
Q

partial paralysis w/ incomplete loss of muscle power

A

paresis

84
Q

clinical manifestations of AD

A
  • forgetfulness - emotional upset - confusion - lack of concentration - decline in abstraction, problem solving, and judgement
85
Q

explain the phases of a tonic-clonic seizure

A
  • neurons are hypersensitive (fire more frequently and w/ greater amplitude - when intensity reaches a threshold point -> cortical excitation spreads - tonic phase (muscle contraction w/ increased muscle tone) - clonic phase (alternating contraction and relaxation of muscles) -> begins when inhibitory neurons in cortex react to excitation
86
Q

gait that is wide-based w/ feet apart and often turned inward for greater stability (person staggers) -> due to cerebellar dysfunction

A

cerebellar (ataxic) gait

87
Q

inability to maintain sustained attention and a working memory deficit

A

executive attention deficits

88
Q

involuntary movement of the face, lips, tongue, trunk, and extremities

A

tardive dyskinesias

89
Q

increased muscle resistance to passive movement

A

hypertonia

90
Q

paresis/paralysis of all 4 extremities as a result of upper spinal cord injury

A

quadriparesis/quadriplegia

Pathophysiology (20 decks)

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