neurologic disorders
Weakness
Pathophysiology of Weakness
Voluntary movement is initiated in the cerebral motor cortex, at the posterior aspect of the frontal lobe. The neurons involved (upper motor or corticospinal tract neurons) synapse with neurons in the spinal cord (lower motor neurons). Lower motor neurons transmit impulses to the neuromuscular junction to initiate muscle contraction. Common mechanisms of weakness thus include dysfunction of Upper motor neurons (corticospinal and corticobulbar tract lesions) Lower motor neurons (eg, due to peripheral polyneuropathies or anterior horn cell lesions) Neuromuscular junction Muscle (eg, due to myopathies) The location of certain lesions correlates with physical findings: Upper motor neuron dysfunctiondisinhibits lower motor neurons, resulting in increased muscle tone (spasticity) and increased muscle stretch reflexes (hyperreflexia). An extensor plantar (Babinski) reflex is specific for corticospinal tract dysfunction. However, upper motor neuron dysfunction can decrease tone and reflexes if motor paralysis is sudden and severe (eg, in spinal cord transection, in which tone first decreases, then increases gradually over days to weeks) or if the lesion damages the motor cortex of the precentral gyrus and not nearby motor association areas. Lower motor neuron dysfunctiondisrupts reflex arcs, causing hyporeflexia and decreased muscle tone (flaccidity), and may cause fasciculations; with time, muscles atrophy. Peripheral polyneuropathiestend to be most noticeable in the longest nerves (ie, weakness is more prominent in the distal limb than the proximal and in legs more than arms) and produce signs of lower motor neuron dysfunction (eg, decreased reflexes and muscle tone). — Myasthenia Gravis —typically causes fluctuating weakness that worsens with activity and lessens with rest. Diffuse muscle dysfunction(eg, in myopathies) tends to be most noticeable in the largest muscle groups (proximal muscles). 