Neuro 4/7 Flashcards
Broca’s aphasia
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Wernicke’s aphasia
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Global aphasia
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Dysarthria
Motor speech disorder
Dysphagia
Difficulty swallowing, prone to chocking, poor nutritional status, Modified barium swallow test can determine areas most dysfunctional in the swallowing mechanism
Contraversive pushing
Patient pushes toward paretic side, Often involves lesion in thalamus and/or right sided cortical lesions causing neglect
Can resolve in 6 months.
Perseveration
Continuous repetition of words, lesion of the premotor and prefrontal cortex
Left CVA Behavioral Differences
Right hemiparesis - Difficulties in communication and processing information in a sequential manner. Cautious, anxious and disorganized. Hesitant to try new tasks. Realistic regarding their dysfunctions
Right CVA Behavioral Differences
Left hemiparesis - Difficulty grasping the whole idea of a task, Quick and impulsive, Overestimate their abilities, Safety of more concern with these patients
Early warning signs of CVA
Sudden N/T in face and/or extremities Sudden confusion and trouble speaking Sudden difficulty seeing out of one eye Sudden dizziness and LOB Sudden severe headache F.A.S.T (face, arm, speech, time)
Ischemic umbra (shadow)
Core area of irreversible neuronal damage
Ischemic penumbra
Peripheral area of “damaged” neurons, neurons are vulnerable for expansion of stroke. First 3-4 hours
Lacunar strokes
Can affect neuronal cell bodies in the cerebrum, can affect the internal capsule (capsular stroke)
CVA pure motor symptoms
posterior limb of internal capsule, basal pons, pyramids
CVA pure sensory symptoms
thalamus, thalamocortical fibers
Stage 1 CVA recovery
Initial flaccidity; no voluntary movement
Stage 2 CVA recovery
Emergence of spasticity, hyperreflexia and synergies
Stage 3 CVA recovery
Strong spasticity; voluntary movement possible, but only in synergistic patterns
Stage 4 CVA recovery
Decline in spasticity and synergies; voluntary control in isolated joint movements emerging
Stage 5 CVA recovery
Increased voluntary control out-of-synergies; coordination deficits present
Stage 6 CVA recovery
Control and coordination near normal
Multiple Sclerosis
- De-myelination of axons in CNS between ages 15-50
- (?) d/t immune reaction triggered by viral infection (possibly a form of Epstein-Barr)
- Vitamin D deficiency could be a factor
- Women 3x more affected
Sensory impairments of MS
parasthesias, decreased position sense, decreased pallesthesia, dysesthesias, allodynia, trigeminal neuralgia, pain, lhermitte’s sign
Visual impairments of MS
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Motor impairments of MS
Fatigue, paresis, ataxia, dysmetria, dysdiadochokinesia, dysphagia, dysarthria, dysphonia, UMN signs (spasticity, hyperreflexia, (+) Babinski)
Cognitive/Behavioral impairments of MS
mild to moderate cognitive deficits, bowel/bladder dysfunction, sexual dysfunction
Relapsing/Remitting MS
85% initially this Dx. Onset of sxs with either full or partial recovery followed by periods of no progression of the disease.
When deficits always resolve between episodes = benign MS
Secondary Progressive MS
initial relapsing/remitting course followed by progressive course
50% will develop this form by 10 years; 90% within 25 years
May include minor remissions
Primary Progressive
Disease progresses consistently from initial onset
May have occasional plateaus & minor improvements
Progressive relapsing
Progressive decline with episodes of increased symptoms
Least common form; occurs in those that are > 40 y/o
Clinically isolated syndrome (CIS)
Person has an attack suggestive of demyelination but does not fulfill the criteria for MS
30%-70% will later develop MS
Should be started on immune-modulating drugs immediately
MS signs/Sx exacerbated by
Heat (Uhthoff’s Phenomenon - itcreased body temperature worsens Sxs), stress, viral or bacterial infections
Diagnosis of MS
- Evidence of plaques in at least 2 distinct areas which occurred at different points in time
Amyotrophic Lateral Scerosis
Muscles w/o innervation, lateral gray horn in spinal cord affected, degenerated neurons become sclerosed.
Degeneration and loss of motor neurons in the spinal cord, brainstem and cortex (results in UMN &LMN signs/sx)
Stages of ALS
I) mild focal asymmetric weakness; hand cramping
II) moderate weakness in groups of muscles
III) severe weakness, but ambulatory
IV) severe weakness; predominately uses
w/c
V) severe weakness with loss of head control; spasticity noted
VI) bedridden with progressive respiratory distress
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