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
2
Q
Define necrosis
A
- severe injury, cellular swelling (osmosis), fragmentation of structure & cell disintegration, inflammatory response leading to cell death
3
Q
Define apoptosis
A
- programmed cell death
- no inflammatory response
4
Q
What can necrotic and apoptotic mechanisms be triggered by
A
- excitotoxicity and free radical accumulation
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
6
Q
Define free radicals
A
- highly reactive molecule
7
Q
What is the key aspect of noting signs and symptoms
A
- pattern recognition
8
Q
Components of the illness script
A
- Pathophysiology
- Epidemiology
- Time course
- Symptoms and signs
- Diagnosis
- Treatment
9
Q
Clinical manifestations of sensory impairments of neurological disorders
A
- Somatosensory impairments
- Visual impairments
- Vestibular impairments
10
Q
When do sensory impairments occur in neurological disorders
A
- when the afferent system is affected
11
Q
Examples of somatosensory impairments
A
- lack of touch
- proprioception
- temperature
- pain
- paresthesia (numbness, tingling)
- can lead to posture & balance problems
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
13
Q
Examples of vestibular impairments
A
- dizziness/ vertigo
- nystagmus
- gaze stabilization problems (oscillopsia)
- can also lead to balance problems)
14
Q
When is dizziness more likely a vestibular problem versus cardiovascular problem
A
- Vestibular: room/head/world is spinning
- Cardiovascular: faint or lightheadedness
15
Q
What could be one of the first signs of MS and/or ALS
A
- lack/loss of sense of smell
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
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)
18
Q
Define anesthesia
A
- loss/absent of all sensory modalities
19
Q
Define hypoesthesia and hyperesthesia
A
- Hypo = partial loss of sensory modalities
- Hyper = hypersensitive
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
21
Q
Define hyperalgesia
A
- increased painful sensations to normally painful stimulus
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
23
Q
Peripheral vestibular disorders
A
- Nerve problems: vestibular neuritis, perilymph fistula, Meniere’s disease
- Canal problems: BPPV
24
Q
Central vestibular disorders
A
- stroke in brainstem/cerebellum
- cerebellar degeneration
- Arnold-Chiari malformation
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
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
