Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Medicine III > Overview of Nervous System Pathology > Flashcards

Overview of Nervous System Pathology Flashcards

1
Q

How can the nervous system be damaged

A
  • Disease: pathogenic infections (meningitis), metabolic, or autoimmune (MS), certain type of tissue is affected throughout CNS
  • Trauma: affects tissue in a local area, can have wide ranging effects ( spinal cord injury, TBI)
  • Congenital reasons: pre-, peri-, post-natal complications (cerebral palsy)
  • Genetic mutation: predisposition to developmental malformation (Down syndrome)
  • Aging: decrease in brain size, weight, nerve conduction becomes slow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define necrosis

A
  • severe injury, cellular swelling (osmosis), fragmentation of structure & cell disintegration, inflammatory response leading to cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define apoptosis

A
  • programmed cell death
  • no inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can necrotic and apoptotic mechanisms be triggered by

A
  • excitotoxicity and free radical accumulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define excitotoxicity

A
  • when neurotransmitters rise above normal levels –> opens
    ion channels leads to excessive entry of Ca2+ ions –> triggers all kinds of harmful cellular pathways –> cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define free radicals

A
  • highly reactive molecule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the key aspect of noting signs and symptoms

A
  • pattern recognition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Components of the illness script

A
  • Pathophysiology
  • Epidemiology
  • Time course
  • Symptoms and signs
  • Diagnosis
  • Treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical manifestations of sensory impairments of neurological disorders

A
  • Somatosensory impairments
  • Visual impairments
  • Vestibular impairments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When do sensory impairments occur in neurological disorders

A
  • when the afferent system is affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of somatosensory impairments

A
  • lack of touch
  • proprioception
  • temperature
  • pain
  • paresthesia (numbness, tingling)
  • can lead to posture & balance problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of visual impairments

A
  • blindness
  • visual field cuts (stroke)
  • optic ataxia (dorsal stream disruptions)
  • visual agnosia (ventral stream disruptions)
  • visual hallucinations (disruptions of optic radiations in stroke/MS)
  • can also lead to balance problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Examples of vestibular impairments

A
  • dizziness/ vertigo
  • nystagmus
  • gaze stabilization problems (oscillopsia)
  • can also lead to balance problems)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When is dizziness more likely a vestibular problem versus cardiovascular problem

A
  • Vestibular: room/head/world is spinning
  • Cardiovascular: faint or lightheadedness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What could be one of the first signs of MS and/or ALS

A
  • lack/loss of sense of smell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What side of the body is effected when there is a brain injury for sensation, pain, temperature, proprioception, etc.

A
  • contralateral side because all pathways have crossed over
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Patterns of somatosensory deficits

A
  • Unilateral (hemiplegic) distribution = cerebral or brainstem pathology
  • Para/tetraplegic distribution = all of the lower half of body
  • Non-specific peripheral distribution
  • Stocking & glove distribution = peripheral neuropathies (diabetic neuropathy)
  • Dermatomal distribution = root impingement (nerve root is affected)
  • Sporadic distribution = MS (multiple sclerosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define anesthesia

A
  • loss/absent of all sensory modalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define hypoesthesia and hyperesthesia

A
  • Hypo = partial loss of sensory modalities
  • Hyper = hypersensitive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define paresthesia and allodynia

A
  • Para = unpleasant sensations like burning, tingling, pricking, numbness with/without sensory stimulus
  • Allo = painful sensation to a normal stimulus that should not be painful
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define hyperalgesia

A
  • increased painful sensations to normally painful stimulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Visual field cuts

A
  • Central Scotoma = dot in the middle of visual field, lesion is the eye
  • Monocular vision loss = one eye blindness, lesion right before the eye
  • Bitemporal hemianopia = tunnel vision, lesion in the optic chasm
  • Contralateral homonymous hemianopia = L/R sided blindness, lesion right before optic chasm
  • Contralateral superior quadrantopia = pie in the sky (can’t see part of upper field), lesion in the optic radiations specifically Meyers loop
  • Contralateral inferior quadrantopia = pie on the floor, lesion in the optic radiations specifically the dorsal optic radiation
  • Contralateral homonymous hemianopia with macular sparing = L/R sided blindness with vision of the middle dot, lesion of both upper/lower bank of calcarine with occluded cerebral artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Peripheral vestibular disorders

A
  • Nerve problems: vestibular neuritis, perilymph fistula, Meniere’s disease
  • Canal problems: BPPV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Central vestibular disorders

A
  • stroke in brainstem/cerebellum
  • cerebellar degeneration
  • Arnold-Chiari malformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Characteristics of nystagmus from peripheral lesions

A
  • direction fixed beating
  • follows Alexander’s & Ewald’s laws: beating increases when eye moves toward fast phase & beating occurs in the plane of impaired canals
  • able to fixate with gaze stabilization
  • habituates rapidly with time
  • good outcomes with vestibular rehab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Characteristics of nystagmus from central lesions

A
  • pure vertical/torsional or direction changing beating
  • does not follow Alexander’s law
  • unable to fixate with gaze stabilization
  • takes longer to habituate/compensate
  • worse outcomes than peripheral
27
Q

Tests for determining peripheral versus central nystagmus

A
  • Head impulse test: Positive for peripheral
  • Nystagmus is directional: Peripheral
  • No askew deviation: Peripheral
28
Q

Patterns of motor deficits for upper motor neuron (UMN) disorders

A
  • paresis/paralysis
  • abnormal tone: spasticity
  • abnormal reflexes: hyper
  • loss of fractionated movement/abnormal synergies
  • no atrophy
  • abnormal co-contractions: cerebral palsy (CP)
29
Q

Patterns of motor deficits for lower motor neuron (LMN) disorders

A
  • paresis/ paralysis
  • decrease in muscle tone: flaccidity
  • decrease in reflex activity: hypo
  • neurogenic atrophy: due to lack of trophic support to muscles
30
Q

Where do upper and lower motor neurons run

A
  • UMN: motor cortex and stops short of LMNs in spinal cord
  • LMN- spinal cord to the muscles
31
Q

Patterns of weakness from motor cortex/UMN problems

A
  • reduced descending drive from motor cortex (corticospinal tracts)
  • inability to recruit enough motor units on contralateral side (semi-) or to one (mono-) or both (bi-) extremities
  • for hemiparesis most weakness on the contralateral side but some evidence of weakness on both sides
  • Degree of involvement can be either paresis or plegia
  • distal muscles are more affected than proximal muscles
32
Q

Define tone, hypertonia, and hypotonia

A
  • Tone: resistance to passive stretch
  • Hypertonia: increased toe, can manifest as spasticity, rigidity, dystonia
  • Hypotonia: floppy muscles, lowered resistance to passive movement, manifest as flaccidity
33
Q

What does hypertonia result from

A
  • increased baseline muscle sensitivity to stretch through mechanisms like loss of descending inhibitory control on motor neurons, loss of presynaptic inhibition, denervation hypersensitivity, etc.
34
Q

What does hypotonia result from

A
  • decreased LMN activity on muscles due to damage to peripheral nerve or due to other subcortical lesions in cerebellum or from developmental delays
35
Q

Patterns of tone problems in UMN vs LMN vs extrapyramidal lesions

A
  • Spastic paralysis caused by UMN lesions: velocity dependent hypertonia
  • Flaccid paralysis can be caused by LMN lesions
  • Rigidity caused by extrapyramidal lesions: velocity independent hypertonia
36
Q

Loss of selective muscle activation (fractionation/individuation)

A
  • loss of ability to selectively activate related muscles
  • abnormal synergies: abnormal coupling of related muscles
  • abnormal stereotypical patterns of movements that cannot be adapted: movements inn spastic patterns
  • typical flexion & extension synergies of UE & LE, person perform voluntary movements I these patterns
  • typically associated with stroke
37
Q

Abnormal co-activation of muscles

A
  • simultaneous activation of agonist & antagonists
  • seen in cerebral palsy (CP)
  • could be due to inadequate pruning of connections during development
38
Q

Movements problems associated with cerebellum

A
  • delayed timing
  • errors in force, ROM, direction (dysmetria)
  • incorrect sequence of muscle activation (dyssynergia)
  • difficulty with RAM/rapid alternating movements (dysdiadokokinesia)
  • intention tremors (involuntary rhythmic oscillations)
  • inability to terminate movements (rebound phenomenon)
  • together known to present as ataxia
39
Q

Other movement disorders associated with cerebellum

A
  • Speech problems: dysarthia/scanning speech - words are pronounced slowly separately, broken into syllables
  • Asthenia: generalized hypotonia, weakness
  • Gait problems
40
Q

Movement problems associated with basal ganglia

A
  • known as dyskinesia
  • Hyperkinesias: involuntary exaggerated high-amplitude movements
  • Types of hypokinesias: bradykinesia & akinesia
  • Types of hyperkinesias: chorea (twitching/jerking), athetosis (twisting), ballismus (violent, flinging), resting tremors
41
Q

Which tremors are mostly related to Parkinson’s

A
  • resting tremor: when the body is supported & relaxed
42
Q

What tremors are mostly related with cerebellar tremors

A
  • most tremors other than resting tremor
43
Q

Define ataxic gait

A
  • cerebellar lesions
  • wide based staggering gait
  • excessive trunk movements
  • arms wide out
  • lack of arm swing
  • LOBs (loss of balance) towards ipsilateral side
  • difficulty in maintaining a line
44
Q

Define Parkinsons gait

A
  • short shuffling gait with destinations, freezing, difficulty turning, tremor in arms at times
45
Q

Define scissoring gait

A
  • in spastic cerebral palsy (CP) due to adductor spasticity
  • knees bent with toes turned inward and walks one toes/ball of the feet
46
Q

Define hemiplegic gait

A
  • circumducting or hip hiking due to LE extensor spastic synergies, arm in flexor synergy
47
Q

Define neuropathic gait

A
  • high steppage gait due to DF weakness and diminished sensation from feet
  • example: diabetic neuropathy
48
Q

What is the frontal lobe responsible for

A
  • responsible for the highest levels of cognitive processing, emotional control, behavior, & personality
49
Q

Symptoms of a frontal lobe lesion

A
  • changes in personality
  • lack of judgement
  • irritability
50
Q

Right hemisphere deficits for cognitive function disorders

A
  • Spatial deficits: hemineglect, tactile extinction (more common with right-sided lesions)
  • Non-spatial deficits: reduced levels of arousal, attention, orientation to stimuli, emotional disturbances
51
Q

Left hemisphere deficits for cognitive function disorders

A
  • problems with reading, writing, and understanding of speech
52
Q

Define apraxia and agnosia

A
  • Apraxia: inability to perform skilled movements in spite of intact sensory & motor systems
  • Agnosia: lesions in sensory cortices for seeing/hearing/feeling - could be one modality, can compensate using remaining modalities
53
Q

Describe persistent vegetative state (PVS)

A
  • if the link from cortex to brainstem is destroyed, eyes may open, have sleep-wake cycles & show random movements, but still unconscious & unresponsive to any stimulus
54
Q

Describe locked-in-syndrome

A
  • damage to pons, opposite of PVS (persistent vegetative state), cognitively fully aware w/o any mental deficits, but cannot move any body parts, except eyes & blink
55
Q

Cognitive function disorder with emotional or memory deficits

A
  • Emotional deficits: limbic system, anxiety disorders like PTSD
  • Memory deficits: hippocampus & thalamus, amnesia
56
Q

Process of diagnosing a neurological disorder

A
  • generate hypothesis regarding site & nature of injury to the nervous system
  • take thorough Hx of onset, signs/Sx, physical exam, tests & measures assist in differential diagnosis
  • deficits in function & gait provide clues to location of damage
  • diagnostic tools include imaging, labs, etc. provide additional insight
57
Q

Describe a CT scan

A
  • detects disorders affecting blood flow, MS, neoplasm
  • dense material appear white, less dense appear darker
  • excellent tool for detecting intracranial hemorrhage
  • can differentiate cytotoxic edema (tumor) from vasogenic edema (stroke)
58
Q

Describe an MRI (magnetic resonance imaging)

A
  • tool of choice for all kinds of lesions in brain & spinal cord
  • contraindicated with intraorbital foreign bodies, pacemakers, some kinds of implants, artificial heart valves
  • tissues with lots of water/protons appear lighter/white and areas that lack protons/water appear darker (air or bone)
59
Q

Describe a functional MRI

A
  • provides functional images of brain during activities
  • based on blood oxygen level detection: activity needs oxygenated blood
  • allows clinicians/surgeons to navigate the precise boundaries of a tumor by staying away from other important functional regions
60
Q

Describe prognosis

A
  • links diagnosis to anticipated outcomes
  • helps educate patient & family about potential for recovery
  • helps identify need for effective treatment options
  • identifies if available treatment options are ineffective
  • helps allocate treatment resources, time, & money in cases of neurological disease with extensive disabilities
  • should include a persons personal, social, & environmental status
61
Q

Different types of pharmacological management for neurological conditions

A
  • neuromodulation: modifying the action of neurotransmitters
  • enhancing or inhibiting neurotransmitters: Synthesis (Levodopa), Release (amphetamines), Reuptake (SSRIs/SNRIs), Blocking/degradation (Gabapentin)
    -Stem cell therapy: attempting to regenerate lost neurons
  • Neuroprotective drugs: against oxidative damage
  • Drugs to reduce inflammation & immune response in demyelinating diseases
  • Antiviral drugs for infections
62
Q

Surgical interventions for neurological conditions

A
  • laminectomies
  • surgical repair of nerves
  • tumor excisionn
63
Q

Implications for physical therapy

A
  • use neuroplasticity based intervention strategies to reestablish lost neuromuscular connections for functional recovery (incorporate principles of neuroplasicity in rehab interventions)
  • restoration vs compensation
  • treatment of affected non-neural tissues due to complications
  • modification of environment & assistive devices as needed
64
Q

What are the principles of neuroplasicity

A
  • practice of relevant tasks
  • intense practice
  • high volumes of therapy
  • forced use techniques: CIMT
  • appropriate patterns of practice
  • appropriate feedback patterns

Clinical Medicine III (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions