Features of UMN lesion Positive features Hyperreflexia Due to: Formation of new synaptic connection from axonal sprouting

Pre & post synapses (increase or abnormal sensitivity) Inactive synapse becomes active

Exaggerated Cutaneous reflexes Positive babinski Extensor / Flexor spasms Flexor withdrawal reflex Exaggerated Proprioceptive (stretch) reflexes deep tendons Clasp knife phenomenon Increased deep tendon reflexes (DTR) Ankle & patella Clonus series of involuntary muscular contractions & relaxations

Hypertonicity/ spasticity Hypertonicity increase resistance to passive movement Non velocity dependent change in muscle tone Spasticity Increase resistance to passive movement (ie stretch) velocity dependent change in muscle tone

Spasticity refers to a velocity-dependent increase in excitability of phasic and tonic muscle stretch reflexes that is present in most patients with UMNS. Clinically, the defining characteristic is excessive resistance of muscle to passive stretch. In spasticity, normally latent stretch reflexes become obvioustendon reflexes have a lowered threshold to tap, the response

of tapped muscle is increased, and muscles besides the tapped one usually respond; tonic stretch reflexes are affected in the same way. In addition to the tonic stretch reflex, hyperactivity of phasic stretch reflexes (exaggerated tendon jerks and clonus) is also considered a spastic phenomenon. Clonus is an exaggerated phasic stretch reflex characterized by repetitive, rhythmic contractions observed in 1 or more muscles of a single limb segment or multiple limb segments. Spasticity depends on muscle stretch, and its onset occurs after movement has begun when some stretch-related displacement has already taken place. Other phenomena associated with UMNS include co-contraction, characterized by simultaneous activation of agonist and antagonist muscles during voluntary movement; associated reaction, which refers to involuntary activity in one limb that is associated with a voluntary movement effort made by other limbs; flexor and extensor spasms, which represent disinhibited reflexes; spastic dystonia, which is characterized by tonic muscle contraction at rest in the absence of passive stretch or voluntary effort.3,4,8 Increased rheologic (resistive) properties of soft tissues also create or contribute to joint or limb deformity in the UMNS.2-4

Negative features Loss of coordination & dexterity Effect: Inability to coordinate to perform motor task Effect: Inability to use individual muscles groups to move independently (loss of fractionation of movement) Slowness of movement Eg standing up, push off at stance phase Effects: Muscle forces needed cannot rise to peak force fast enough to generate power needed to move effectively

Weakness and paralysis (decrease max voluntary output) Usually distal muscles more affected Because of decreased MU recruitment Effect : unable to activate & sustain muscles needed to generate movement Because of decreased MU firing rates

Effect: unable to regulate muscle force production with speed and skill Adaptive features Increase weakness Increase stiffness Decrease length Refers to Altered mechanical and functional properties of muscle Partly caused by Negative features UMN lesion Because negative features may cause further decrease muscle activity / inactivity leading to increase weakness and disuse. Partly caused by positive features of UMN lesions (eg spasticity & hypertonicity) Because positive features may cause further physical and morphological changes (e.g. shortening and contracture) that further increases stiffness and decrease length Rehabilitation To concentrate on rehabbing the negative features Improve muscle strength Prevent muscle disuse Improve coordination Regain motor control