61 Muscle tone – an introduction
Tone is the resistance of a muscle to stretch. It is generated by reflex circuits of muscle spindles and Golgi tendon organs projecting onto motor neurons. The motor neurons in turn receive input from the UMN.
There are conduction delays in the feedback loops regulating muscle length and this gives rise to a small oscillation called physiologic tremor. The tremor worsens with any change to the feedback loop or the UMN influences upon it.
If the motor nerve is damaged, the muscle loses tone and becomes flaccid. If inhibition to the motor neurons is removed, muscle tone increases (hypertonia, spasticity).
There are both inhibitory and facilitatory UMN pathways descending through the brainstem and cord to influence the LMN. Lesions of descending UMN pathways produce the clinical picture of ‘release’, i.e. removal of inhibition to the extensor muscles.
In humans, the loss of descending inhibition from the basal ganglia creates a rigid, unchanging hypertonia, whereas loss of other descending UMN inhibition results in a spastic, varying hypertonia. The terms rigid and spastic do not carry such localizing value in veterinary neurology.
Interneurons within the spinal cord are inhibitory to motor neurons limiting their duration, intensity and distribution of discharge. A sudden severe thoracolumbar spinal cord lesion in the dog can remove this inhibition to the forelimbs, resulting in the Schiff–Sherrington syndrome (Table 61.1).
|Rigid extension: hypertonia||Hypotonia|
|Normal reflexes||Normal reflexes|
|Voluntary movement present: stiff gait||Paraplegia|
|Pain perception present||Pain perception absent|
* Proprioception testing is fruitless in a paralysed animal because the animal is unable to move its limb into the correct position. A spinal cord lesion producing paraplegia will also damage the ascending proprioceptive pathways. Lastly, if pain (sensory) perception is absent, proprioceptive testing will also be absent.
Do not confuse this with a severe C1–C5 spinal cord lesion (Table 61.2).
|Increased spinal reflexes||Increased spinal reflexes|
|Pain perception present||Pain perception present|
Schiff–Sherrington syndrome signifies severe spinal cord dysfunction but does not imply its irreversibility. Prognosis is assessed as in other cases of paralysis.
Schiff–Sherrington syndrome usually disappears 10–14 days after onset to be replaced by the usual signs of T3–L3 paraplegia: normal to increased spinal reflexes and muscle tone.
The release of inhibitory neurotransmitters from spinal cord interneurons is prevented by the tetanus toxin tetanospasmin. Similar clinical signs of tetanic muscle spasm occur in strychnine poisoning which also acts on spinal interneurons.
Acute spinal lesions in vertebrates cause a period of spinal shock in which spinal reflexes caudal to the lesion are profoundly depressed resulting in areflexia and atonia. The duration is proportionate to the degree the gait is controlled by the cerebrum. Spinal shock may be present for 1–2 hours in the dog and cat. If areflexia is found in an acutely paralysed animal recheck reflexes frequently thereafter. Hyperreflexia and hypertonia may develop. Spinal shock is rarely encountered in small animal patients.