![]() The mechanisms underlying these have been discussed thereafter because they are important both clinically and pathophysiologically from a movement disorder perspective. Dystonia and paratonia have altered tone secondary to network disruption in the basal ganglia, the thalamocortical circuits, and their connections. In the motor control system, spasticity and rigidity are predominantly an output system problem, while dystonia is a system level processing problem. ![]() The other two disorders of altered tone, namely dystonia and paratonia, are not exactly related to the physiological dysfunction of the tone pathways. Spasticity and rigidity, the two types of hypertonia, have been elaborated in the context of the dysfunction in the supraspinal pathways and the interaction between spinal cord and muscle spindle. In this review, we have discussed the controversies regarding the definition of muscle tone and its classification, followed by the mechanisms and pathways responsible for maintaining tone. This hierarchy of motor control includes cortex (extensive processing capability with highest degree of freedom), basal ganglia (learning and teaching of context dependent tasks with less degrees of freedom), cerebellum (fine-tuning), brainstem reticular system (common pathway for ascending and descending tracts), spinal cord (the main pathway for ascending and descending tracts), and muscle spindle (final common pathway with least degree of freedom). Tone is basically a construct of motor control, upon which power is intrinsically balanced. It is regulated by its input and output systems and has critical interplay with power and task performance requirements. In the dark or with eyes closed they have problems.Muscle tone is a complex and dynamic state, resulting from hierarchical and reciprocal anatomical connectivity. The patient does not know where their joint is in space and so uses their eyes. It is a sign of a disturbance of proprioception, either from neuropathy or posterior column disease. NOTE: THE ROMBERG TEST IS NOT A SIGN OF CEREBELLAR DISEASE. NOTE: patients with disease of the vermis and flocculonodular lobe will be unable to stand at all as they will have truncal ataxia–they may not be able to sit. ![]() (See "Gaits" section to learn more about acute cerebellar ataxia and other gaits.) Gait (Acute Cerebellar Ataxia)Īcute cerebellar ataxia is a wide based and staggering gait. “Pendular” knee jerk, leg keeps swinging after knee jerk more than 4 times (4 or less is normal). Abnormal exam occurs when they are unable to keep their foot on the shin. Have patient run their heel down the contralateral shin (this is equivalent the finger to nose test). (Be careful that you protect the patient from the unarrested movement causing them to strike themselves.) Heel to shin test However in cerebellar disease this response is completely absent causing to limb to continue moving in the desired direction. A positive sign is seen in a spastic limb where the exaggerated "rebound" occurs with movement in the opposite direction. ![]() Normally the antagonists muscles will contract and stop their arm from moving in the desired direction. Have the patient pull on your hand and when they do, slip your hand out of their grasp. Rapid alternating movementsĪsk patient to place one hand over the next and have them flip one hand back and forth as fast as possible (alternatively you can ask the patient to quickly tap their foot on the floor as fast as possible) if abnormal, this is called dysdiadochokinesia. You increase the difficulty of this test by adding resistance to the patient's movements or move your finger to different locations. Finger to nose & finger to finger testĪsk patient to fully extend arm then touch nose or ask them to touch their nose then fully extend to touch your finger. Causes enunciation of individual syllables: “the British parliament” becomes “the Brit-tish Par-la-ment.” Nystagmusįast phase toward side of cerebellar lesion.
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