Npte Study Flashcards
Cerebrum is derived from what?
Prosencephlon or forebrain
What does grey matter do?
Cortex responsible got process and cognition
What does frontal lobe do?
Higher intellect, personality, mood, social conduct,and language
Parietal lobe
Language, calculation and visuals Spatial 2 pt discrimination p
Temporal lobe
Memory and language and primary auditory
This disease affected the descending motor tracts within the cerebral motor cortex,. Symptoms include: hypertonicity, hyperreflexia, and abnormal reflexes. Damaged tracts are in the lateral white column.
Upper motor neuron
Examples of UMN
CP, ALS, CVA, birth injuries, hydropchephalus, Huntington’s, MS, TBI, brain tumors, pseudobulbar palsy
These diseases occur when the nerves or axons below the level of the brain stem are affected. The ventral gray column of SC may also be affected. Flaccidity, or weakness, decreased tone, fasiculations, muscle atrophy or absent reflexes.
LMN
Examples of LMN
ALS, GB, tumors of SC, trauma, poliomyelitis, infection, Bell’s, progressive muscle atrophy, carpal tunnel, MD, spinal muscular atrophy
Damage to Anterior horn cell causes what? What diseases?
Sensory intact, motor weakness and atrophy, fasiculations, decreased reflexes
ALS, poliomyelitis (LMN)
Muscle impacted with UMN vs LMN
Sensory intact, motor weakness, no fasiculations, normal or decreased DTR
MD (LMN)
NMJ affects in LMN vs UMN
Sensory intact, motor fatigue, normal DTR
MG LMN
Affects of peripheral nerve or mononeuropathy LMN vs UMN
Sensory loss along nerve root, motor weakness and atrophy may have fasiculations
Trauma (LMN)
Peripheral polyneuropathy LMN vs UMN
Sensory impairments stocking glove, motor weakness and atrophy, dista to proximal, decreased DTR
Diabetic peripheral neuropathy
Spinal roots and nerve LMN vs UMN
Sensory will have corresponding dermatomal pattern, motor weakness via innervation, decreased DTR
Herniated disc
Athetosis
Slow, twisting writhin movements large amplitude
Seen in face tongue and trunk and extremities
Typically associated with spasticity (CP and BG pathology)
Chorea
Hyperkinesia, brief irregular contractions, rapid
Damage to caudate nucleus, fidgeting,
Ballism(form) large amp jerks-damage to subthalamic nucleus
Huntington’s
Dystonia
Sustained muscle contractions, twisting and abnormal postures, or repetitive movements
All muscles can be affected during volitional movement
Genetic, acquired, SE meds,
Present sustained of agonist/antagonist,
Parkinsons CP and encephalitis
Tics
Sudden brief repetitive coordinated movements at irregular intervals
Vocal, jerks or repetitive sounds
Tourette’s
Tremors
Involuntary rhythmic oscillatory movement 3 groups
Resting: pill rolling Parkinson’s
Postural: rapid tremor in hyperthyroidism, fatigue or anxiety and benign tumor
Intention: increase as target approaches, cerebellum efferent pathway MS
Inability to initiate a movement
Akinesia
General weakness cerebellum pathology
Asthenia
Clasp-knife
Resistance during range of motion of hypertonic joint, greatest resistance at initiation or range lessens with movement through range
Rigidity where resistant to movement is physical quality
Cogwheel
Inability to perform rapid alternating movements
Dysdiadochokinesia
Inability to control ROM and force of muscular activity
Dysmetria
Closely related to athetosis, larger axial movement than appendicular muscles
Dystonia
Rigidity where there is uniform constant resistance often associated with lesions of BG
Lead pipe rigidity
Inability to interpret information
Agnosia
Inability to recognize symbols letters or numbers traced on skina
Agraphesthesia
Inability to write (typically found with aphasia)
Agraphia
Inability to read, within dominant lobe
Alexia
Denial or unawareness of illness (unilateral neglect)
Anosognosia
Inability to communicate or comprehend
Aphasia
Inability to perform purposeful learned movements no sensory or motor impairment
Apraxia
Inability to recognize objects by sense or touch
Astereognosis
Inability to reproduce geometric figures, inability to visually analyze how to perform task
Constructional apraxia
Characteristic or corticospinal lesion at level or brain stem extension of trunk and all extremities
Decerbrate rigidity
Corticospinal lesion at diencephalon where trunk and LE position in extension and UE in flexion
Decorticating rigidity
Slurred speech motor deficit of tongue
Dysarthria
Impairment or Rhythm and inflection of speech
Dysprosody
Right hemisphere infarct where there is inability to control emotions and outbursts of laughing or crying
Emotional lability
Characteristic of receptive aphasia where speech produces functional output with articulation but lacks content
Fluent aphasia
Inability to formulate initial motor plan and sequence of tasks where proprioceptive input necessary for movement is impaired
Ideational apraxia
Condition where person plans a movement or task but cannot volitionally perform, cannot impose additional movements on command
Ideomotor apraxia
Substitution within a word that is so severe that is makes the word unrecognizable
Neologism
Characteristic of expressive aphasia speech is non-functional, effortful and contains paraphasia
Non-fluent aphasia
Cauda equina injury
Below L1 (LMN)
A surgical procedure that severs certain tracts within SC to decrease spasticity and improve function
Myelotomy
A surgical removal of a segment of nerve in order to decrease spasticity and improve function
Neurectomy
Bladder is flaccid as result of cauda equina or conus medullaris lesion. Sacral reflex arc is damaged
Neurogenic nonreflexive bladder
Lowest segment of spinal cord with intact strength and sensation. Grade of fair.
Neurological level
A form of abnormal breathing that is common in tetraplegia where the abdomen rises and the chest is pulled inward during inspiration, then opposite
Paradoxical breathing
An incomplete lesion where son of teh innermost tracts remain Innervates, Saddle area, toe flexors, rectal sphincter
Sacral sparing
Poor or trace motor or sensory function for up to 3 levels below the neurological level of injur
Zone of preservation
Pusher’s syndrome
Can occur due to posterolateral thalami stroke, deficits with perception of orientation
Correction for Pusher’s syndrome
Allow patient to utilize cane and lower height, will encourage WB through uninvolved side, visual cueing for upright
DO NOT allow patients sound extremities to drift into abduction and or extension and push
ALLOW patient to problem solve
