Symptoms of cerebellar dysfunction
What are the signs and symptoms of cerebellar dysfunction?
movements that fall short of or go past the intended target. Hypometria = premature arrest; hypermetria = failure to arrest movements. Dysmetria is examined by the finger-to-nose test or great toe-to-examiner’s finger test (using only hip movement).
This is a disturbance in rapid alternating movements, tested by rapid supination/pronation of the forearm on a tabletop or the lap to evaluate the rate, range, force, and accuracy of voluntary movements. This should not be confused with bradykinesia.
ataxic speech has an irregular pattern, caused by interference from articulation, respiration, and phonation.
Also: adiodochokinesis (slow and deliberate speech), explosive-hesitant speech (syllables can be explosive and produced at incorrect points of emphasis), or scanning speech (stretching of the syllables, which also sharply cut off).
decreased resistance to passive limb manipulation. There may be a greater than normal range of motion in the first 7 to 10 days after cerebellar injury.
nystagmus (gaze-evoked, rebound, downbeat, or positional), skew deviation, saccadic dysmetria, impaired smooth pursuit, and impaired optokinetic nystagmus.
wide-based and staggering steps, possibly stiff-legged due to disturbed postural reflexes.
Impaired tandem gait and truncal swaying may be present. Patients generally fall to the side of the lesion.
Ataxia does not significantly worsen when visual input is removed (e.g., Romberg test is negative) whereas in sensory ataxia, a patient may compensate for proprioceptive defects by visual guidance (positive Romberg).
This worsens as the target is approached (“intention tremor”) during finger-to-nose testing.
A “static tremor,” manifested as titubation of the head or trunk, can be observed while holding the arms or legs parallel to the floor and observing rhythmic movements at the shoulder or hip.
A Holmes or rubral tremor is a combination of rest, postural, and action tremors of 3 to 4 Hz, often due to midbrain lesions in the vicinity of the red nucleus.
Large amplitude proximal tremors (tested in the wing-beating position) are characteristic, enhanced with posture and aggravated with movement.