Chronic Brain Disorders Flashcards

1
Q

Transient neurologic event of paroxysmal abnormal or excessive cortical electrical discharges
-Manifested by disturbances of skeletal motor function, sensation, autonomic visceral function, behavior, or consciousness

A

Seizure

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2
Q

Causes: cerebral injury, lesions, metabolic/nutritional disorders, idiopathic (no known cause)

A

Seizure

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3
Q

Recurrent seizures

A

epilepsy

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4
Q

May be triggered by specific stimuli such as flashing lights, fever, loud noises

A

Seizure

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5
Q

Due to an alteration in membrane potential that makes certain neurons abnormally hyperactive and hypersensitive to changes in their environment (epileptogenic focus)

A

Seizure

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6
Q

What’s the prodrome of a seizure?

A

subjective sense of impending seizure

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7
Q

whole brain surface is affected during ______seizure

A

Involvement of thalamus and RAS system results in loss of consciousness

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8
Q

Involvement of thalamus and RAS system results in loss of consciousness

A

Involvement of thalamus and RAS system results in loss of consciousness

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9
Q

Absence (petite mal): occurs in children, staring spells that last only seconds
•Atypical absence: myoclonic jerks, automatisms with the staring spell

A

Generalized seizure

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10
Q

Myoclonic: single/several jerks
•Atonic (drop attack): fall down
•Tonic-clonic (grand mal): jerking of many muscles

A

Generalized seizure

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11
Q

continuing series of seizures without a period of recovery between episodes; can be life-threatening

A

Status epilepticus

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12
Q

abnormal electrical activity restricted to one brain hemisphere

A

Partial seizures

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13
Q

No change in level of consciousness; motor, sensory, and/or autonomic symptoms common in ________ seizures

A

Simple/Partial Seizure

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14
Q

change in consciousness happens in ______ seizures

A

complex/partial

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15
Q

Starts as simple but advances to generalized in _____ seizures

A

Partial with secondary generalization

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16
Q

Electroencephalograms: assess electrical patterns of brain regions
Laboratory studies: identify metabolic/nutritional deficits, infections, and exposure to toxins
diagnose _______

A

Seizure

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17
Q

Lumbar puncture: for CNS infections
CT, MRI: for structural causes
diagnose

A

Seizure

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18
Q

Maintain airway•Protect from injury•Document course

to treat ____

A

Seizure

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19
Q

Continued until no seizures for at least 2 years and then gradually withdrawn•Not a cure

A

Anticonvulsant medications

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20
Q

Avoid triggers

Surgery: removal of foci or neurostimulation to treat ______

A

seizure

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21
Q
Question 1
A patient has a tonic-clonic seizure. What type of seizure did the patient experience?
 A. Petite mal
B. Grand mal 
C. Myoclonic
D. Drop attack
A

B. Grand Mal

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22
Q

Syndrome associated with many pathologies; characterized by progressive deterioration and continuing decline of memory and other cognitive changes

A

dementia

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23
Q

Abrupt onset, may fluctuate often, becoming worse at night; disturbed consciousness, decreased awareness of the environment, incoherence, and hallucinations

A

delirium

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24
Q

Characterized by degeneration of neurons in temporoparietal and frontal lobes, brain atrophy, amyloid plaques, and neurofibrillary tangles

A

Alzheimer disease

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25
Q

Deficient synthesis of brain acetylcholine

A

Alzheimer disease

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26
Q

Cause remains unknown, although genetic factors (family history increases 4x) and environmental triggers suspected
Aging increases risk
Behavioral problems progress from forgetfulness to total inability for self-care
Depression and psychosis may be significant

A

Alzheimer disease

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27
Q

Results from single cerebrovascular insults

Risk factors: stroke, hypertension, and diabetes

A

Vascular dementia

28
Q

Early: memory loss, especially short-term memory, long-term memory may be preserved; thinking ability declines, decreasing ability to function at work and in social settings; anxiety, agitation

A

dementia

29
Q

As the disease progresses, increasing difficulty with judgment, abstract thinking, problem solving, and communication; assistance for completing activities of daily living (ADLs); difficulty with eating and swallowing, weight loss; loss of bladder and bowel control and eventual complete loss of the ability to ambulate; personality and behavior changes

A

dementia

30
Q

Complete blood cell count, chemistry panel, thyroid function, vitamin B12 levels, and syphilis serology
diagnose

A

dementia

31
Q

Chest x-ray, CT, MRILumbar punctureMental status examinations, clock drawing test, and tests of functional status
diagnose

A

dementia

32
Q

Early diagnosis and intervention is key in the management of dementia
Early stages may be able to stay at home; later stages may need nursing home or assisted living

A

dementia

33
Q

tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) are _______ inhibitors. They are indicated for _______. NOT A CURE

A

Acetylcholinesterase; mild to moderate Alzheimer disease and vascular dementia

34
Q

Indicated for the treatment of moderate to severe Alzheimer-type dementia
•Blocks stimulation by the neuroexcitatory transmitterglutamate
•Not a cure, but slows progression of the disease

A

N-methyl-D-aspartate (NMDA) receptor antagonists: memantine (Namenda)

35
Q

May be idiopathic, acquired or drugs

Dopamine deficiency in the basal ganglia (substantia nigra) associated with motor impairment; Lewy bodies

A

Parkinson Disease

36
Q

Difficulty initiating and controlling movements results in akinesia, tremor, and rigidity
Tremor occurs at rest and hand tremors exhibit pill-rolling movements
Attempts to passively move the extremities are met with cogwheel rigidity

A

Parkinson Disease

37
Q

General lack of movement, loss of facial expression, drooling, propulsive (shuffling) gait, and absent arm swing

A

Parkinson Disease

38
Q

Treatment: no cure; restoring brain dopamine levels or activity by administration of dopamine precursors, dopamine agonists, monoamine oxidase inhibitors, and anticholinergics; antidepressant therapy may be NEEDED
*Ablative surgical procedures may be helpful for motor symptoms

A

Parkinson Disease

39
Q

________responsible for smooth, coordinated control of muscle action, excitation and inhibition of postural reflexes, and maintenance of balance

A

Cerebellum

40
Q

Causes: abscess, hemorrhage, tumors, trauma, viral infection, chronic alcoholism
Clinical manifestations: ataxia, hypotonia, intention tremors, disturbances in gait and balance
Treatment: identify and eradicate cause

A

Cerebellum disorders

41
Q

Chronic demyelinating disease of the CNS that primarily affects young adults
Autoimmune disorder that results in inflammation and scarring (sclerosis) of myelin sheaths covering nerves; slowly progressive

A

Multiple Sclerosis

42
Q

Cause unknown, but immunologic abnormalities, genetics, and environmental factors suspected
Demyelination can occur throughout the CNS but often affects the optic and oculomotor nerves and spinal nerve tracts

A

Multiple Sclerosis

43
Q

Marked by exacerbations and remissions; exacerbated by heat, infection, trauma, stress

Manifestations: double/blurred vision, weakness, poor coordination, and sensory deficits; bowel and bladder control may be lost; memory impairment common

A

Multiple Sclerosis

44
Q

Diagnosis: MRI

Treatment: no cure; short-term steroid therapy may be helpful during acute exacerbations and immune-modifying drugs may slow progression of symptoms

A

Multiple Sclerosis

45
Q

Problem of the young
Males 3 to 4x more likely
Usually traumatic, a result of motor vehicle accidents, falls, penetrating wounds (usually gunshot), or sports injuries

A

Spinal cord injury

46
Q

Cord may be compressed, transected, or contused
Mechanisms of injury
Hyperflexion, hyperextension, compression

A

Spinal cord injury

47
Q

_______injury may result from hemorrhage, swelling, ischemia, inflammation

A

Secondary spinal cord

48
Q

________occurs immediately and is characterized by temporary loss of reflexes below the level of injuryMuscles flaccid; skeletal/autonomic reflexes lost

A

Spinal shock

49
Q

End of ______: reflexes return and flaccidity replaced by spasticity

A

spinal shock

50
Q

______shock may occur after SCI due to peripheral vasodilation

A

Neurogenic

51
Q

Hypotension, bradycardia, and circulatory collapse can occur (life-threatening); high spinal cord injuries can affect respiratory muscles, leading to ventilatory failure
results from ________

A

neurogenic shock

52
Q

________is an acute reflexive response to sympathetic activation below the level of injury

A

Autonomic dysreflexia

53
Q

Visceral stimulation (full bladder or bowel) and activation of pain receptors below the injury are common stimuli
Manifestations: hypertension, headache, bradycardia, flushing above the level of injury, and clammy skin below the level of injury
occur in_______

A

Autonomic dysreflexia

54
Q

Prompt removal of the offending stimulus; aggressive blood pressure management may be needed (adrenergic receptor–blocking drug) to amend ____

A

Autonomic dysreflexia

55
Q

Appropriate stabilization of spinal vertebrae•May be accomplished surgically with internal fixation or with external fixation and bracing to treat _____

A

spinal cord injury

56
Q

intensive care to maintain oxygenation and blood pressure to treat ________ shock

A

neurogenic

57
Q

High-dose methylprednisolone may be used to decrease secondary injury
Intensive rehabilitation required to maximize function

A

spinal cord injury

58
Q

Inflammatory demyelinating disease of the peripheral nervous system or a lower motor neuron disorder
Segmental demyelination that is T-cell and B-cell mediated

A

Guillain-Barré Syndrome

59
Q

Also known as acute idiopathic polyneuropathy or polyradiculoneuropathy

A

Guillain-Barré Syndrome

60
Q

Cause unknown; postinfectious immunologic mechanism suspectedSpontaneous recovery usually occurs

A

Guillain-Barré Syndrome

61
Q

Muscle weakness that begins in the lower extremities and spreads to the proximal spinal neurons

Progressive ascending weakness or paralysis, may affect respiratory muscles

Diagnosis: patient history, physical examination, and nerve conduction studies, lumbar puncture

A

Guillain-Barré Syndrome

62
Q

Treatment: supportive; plasmapheresis; immunoglobulin

A

Guillain-Barré Syndrome

63
Q

Idiopathic neuropathy of the facial nerve; paralysis of the muscles on one side of the face
Etiology: virus

A

Bell Palsy

64
Q

Clinical manifestations: develop rapidly over 24 to 48 hrs; unilateral facial weakness, facial droop and diminished eye blink, hyperacusis, and decreased lacrimation
Diagnosis: physical findings, MRI, CT, EMG

A

Bell Palsy

65
Q

Often self-limiting condition within 3 wks
Lubricating drops, ointments, and nighttime eye patching may be necessary
to treat

A

Bell Palsy

66
Q

Corticosteroids improve the likelihood of complete recovery
Antiviral medications: acyclovir or valacyclovir recommended
to treat

A

Bell Palsy