cheese + onion Flashcards
damage where leads to an UMN lesion?
anywhere from motor nerve cells in the precentral gyrus of the frontal cortex, through the internal capsule, brainstem and cord to the anterior horn cells in the cord
what is the typical distribution of an UMN lesion?
pyramidal ie weakness involving physiological extensors of the arm (shoulder abduction, elbow, wrist, and finger extension and the small muscles of the hand) and flexors of the lower limb (hip flexion, knee flexion, and ankle dorsiflexion and everters
how is increased tone in UMN lesions manifested?
clasp knife phenomenon - resistence to a passive movement that can suddenly be overcome
how is hyperreflexia seen in UMN lesions?
brisk reflexes
- plantars are upgoing (+ve babinski sign) +- clonus (elicited by rapidly dorsiflexing the foot <3 rhythmic, downward beats of the foot are normal, more suggest an UMN lesion)
+- positive hoffmans reflex (brisk flexion of thumb and index finger in a pincer movement following a flick ot the pump of the middle finger
damage where leads to the LMN lesion?
from anterior horn cells int he cord, nerve roots, plexia or peripheral nerves
the distrubtion coordinates to the muscles supplied by the cord segment
what are LMN signs?
muscle wasting +- fasciculation
feels soft and floppy, providing little resistance (hypotonia)
reflexes are reduces apart from the plantar flexors remain
what does ACA supply
frontal and medial cerebrum
what does ACA lesions show
weak, contraltaeral numb leg
what does the MCA supply
lateral + external cerebrum
what does MCA lesion show
hemisensory loss of face and arm
contralateral hemiplegia
contralateral homonymous hemianopia
what does PCA supply
occipital lobe
what does PCA lesion show
contralateral homonymous hemianopia (with macular sparing)
