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
Deficient synthesis of brain acetylcholine
Alzheimer disease
26
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
Alzheimer disease
27
Results from single cerebrovascular insults | Risk factors: stroke, hypertension, and diabetes
Vascular dementia
28
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
dementia
29
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
dementia
30
Complete blood cell count, chemistry panel, thyroid function, vitamin B12 levels, and syphilis serology diagnose
dementia
31
Chest x-ray, CT, MRILumbar punctureMental status examinations, clock drawing test, and tests of functional status diagnose
dementia
32
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
dementia
33
tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) are _______ inhibitors. They are indicated for _______. NOT A CURE
Acetylcholinesterase; mild to moderate Alzheimer disease and vascular dementia
34
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
N-methyl-D-aspartate (NMDA) receptor antagonists: memantine (Namenda)
35
May be idiopathic, acquired or drugs | Dopamine deficiency in the basal ganglia (substantia nigra) associated with motor impairment; Lewy bodies
Parkinson Disease
36
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
Parkinson Disease
37
General lack of movement, loss of facial expression, drooling, propulsive (shuffling) gait, and absent arm swing
Parkinson Disease
38
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
Parkinson Disease
39
________responsible for smooth, coordinated control of muscle action, excitation and inhibition of postural reflexes, and maintenance of balance
Cerebellum
40
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
Cerebellum disorders
41
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
Multiple Sclerosis
42
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
Multiple Sclerosis
43
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
Multiple Sclerosis
44
Diagnosis: MRI Treatment: no cure; short-term steroid therapy may be helpful during acute exacerbations and immune-modifying drugs may slow progression of symptoms
Multiple Sclerosis
45
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
Spinal cord injury
46
Cord may be compressed, transected, or contused Mechanisms of injury Hyperflexion, hyperextension, compression
Spinal cord injury
47
_______injury may result from hemorrhage, swelling, ischemia, inflammation
Secondary spinal cord
48
________occurs immediately and is characterized by temporary loss of reflexes below the level of injuryMuscles flaccid; skeletal/autonomic reflexes lost
Spinal shock
49
End of ______: reflexes return and flaccidity replaced by spasticity
spinal shock
50
______shock may occur after SCI due to peripheral vasodilation
Neurogenic
51
Hypotension, bradycardia, and circulatory collapse can occur (life-threatening); high spinal cord injuries can affect respiratory muscles, leading to ventilatory failure results from ________
neurogenic shock
52
________is an acute reflexive response to sympathetic activation below the level of injury
Autonomic dysreflexia
53
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_______
Autonomic dysreflexia
54
Prompt removal of the offending stimulus; aggressive blood pressure management may be needed (adrenergic receptor–blocking drug) to amend ____
Autonomic dysreflexia
55
Appropriate stabilization of spinal vertebrae•May be accomplished surgically with internal fixation or with external fixation and bracing to treat _____
spinal cord injury
56
intensive care to maintain oxygenation and blood pressure to treat ________ shock
neurogenic
57
High-dose methylprednisolone may be used to decrease secondary injury Intensive rehabilitation required to maximize function
spinal cord injury
58
Inflammatory demyelinating disease of the peripheral nervous system or a lower motor neuron disorder Segmental demyelination that is T-cell and B-cell mediated
Guillain-Barré Syndrome
59
Also known as acute idiopathic polyneuropathy or polyradiculoneuropathy
Guillain-Barré Syndrome
60
Cause unknown; postinfectious immunologic mechanism suspectedSpontaneous recovery usually occurs
Guillain-Barré Syndrome
61
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
Guillain-Barré Syndrome
62
Treatment: supportive; plasmapheresis; immunoglobulin
Guillain-Barré Syndrome
63
Idiopathic neuropathy of the facial nerve; paralysis of the muscles on one side of the face Etiology: virus
Bell Palsy
64
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
Bell Palsy
65
Often self-limiting condition within 3 wks Lubricating drops, ointments, and nighttime eye patching may be necessary to treat
Bell Palsy
66
Corticosteroids improve the likelihood of complete recovery Antiviral medications: acyclovir or valacyclovir recommended to treat
Bell Palsy