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In an animal where the cortical areas or the midbrain have been "cut off" from the neural axis, this reflex is hyperactive and the animal will maximally extend all four limbs. This phenomenon is known as decerebrate rigidity. In humans, true decerebrate rigidity is rare since the damage to the brain centers it might be caused by usually are lethal.
Decerebrate posturing is commonly seen in pontine strokes. A patient with decorticate posturing may begin to show decerebrate posturing, or may go from one form of posturing to the other. [1] Progression from decorticate posturing to decerebrate posturing is often indicative of uncal (transtentorial) or tonsilar brain herniation.
The MLR was first described by Shik and colleagues in 1966 when they observed that electrical stimulation of a region of the midbrain in decerebrate cats produced walking and running behavior on a treadmill. [3] Twenty-eight years later, Masdeu and colleagues described the presence of a MLR in humans. [4]
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Decorticate posturing, with elbows, wrists and fingers flexed, and legs extended and rotated inward. Brain herniation frequently presents with abnormal posturing, [2] a characteristic positioning of the limbs indicative of severe brain damage.
Opisthotonus is also described as a potential CNS symptom of heat stroke along with bizarre behavior, hallucinations, decerebrate rigidity, oculogyric crisis, and cerebellar dysfunction. [citation needed] Opisthotonus is a symptom of "lavender foal syndrome", a lethal genetic disorder in horses. [4]
Decerebrate cats were made to walk on a level surface with their heads level, tilted up or tilted down. Comparing the decerebrate cats to normal cats showed similar EMG patterns during level walking and EMG patterns that reflected downhill walking with the head titled up and uphill walking with the head tilted down.
A change of gait also results from a change in the signal of CPGs. However, there is an asymmetry in the control of cycle periods in the spinal rhythm generator. The cycle period of fictive locomotion in decerebrate cats is predominantly altered by modifying the extension phase, rather than the flexion phase. [14]