Fig. 7.1
Motor pathways, upper motor neuron pathway (the brain and spinal cord), and lower motor neuron pathway in nerve root and peripheral nerve (Source: Henry Gray (1918) Anatomy of the Human Body, a public domain image – http://en.wikipedia.org/wiki/Upper_motor_neuron#/media/File:Gray764.png)
Fig. 7.2
The spinal reflex arc, tendon stretch, is transmitted via a sensory neuron into the spinal cord, where it activates the motor fibers to quadriceps and at the same time inhibits the motor fibers to hamstrings, in order to extend the knee (knee jerk). This reflex can be facilitated or inhibited by descending central influences
Lower Versus Upper Motor Neuron Injury
Injuries to peripheral nerves and spinal segments result in partial or complete weakness of innervated muscle and interruption of associated spinal reflex arcs. Such lower motor neuron lesions are easy to recognize and localize based on the pattern of weakness and interruption of the appropriate local reflex arc. For example, both radial nerve and C7 nerve root lesions will cause weakness of wrist and elbow extension and an absent triceps reflex, but the C7 nerve root lesion will also cause wrist flexion weakness through its contribution to the median nerve.
Upper motor neuron lesions are more complicated. First, many such lesions selectively affect the pyramidal pathway with loss of fine motor skills in the affected limb in the absence of complete paralysis. Affected patients will subconsciously keep the upper limb flexed and lower limb extended based on unopposed activity via the unaffected descending extrapyramidal pathways (Fig. 7.3). Second, in addition to loss of motor function, upper motor neuron lesions will also lead to loss of modulation (inhibition) of the local spinal reflexes. Uninhibited, these myotactic reflexes become overactive leading to exaggerated resistance to passive stretching (spasticity) and loss of reciprocal inhibition. In other words, muscle weakness from an upper motor lesion can stem from both loss of volitional activation and also failed relaxation or resistance to passive stretching of the antagonistic muscles, somewhat akin to driving with the hand brake on. Multichannel dynamic EMG recordings can be helpful in sorting this out (Fig. 7.4). Treating the spasticity – or releasing the hand brake – can be enough to improve function in some patients. Other patients require more complicated procedures to improve function. In extreme cases, this can involve lesioning and neurotization. In other words, this converts an upper motor neuron lesion into a simpler lower motor neuron lesion and then fixes the lower motor neuron lesion.
Fig. 7.3
“Pyramidal” distribution weakness. This stroke patient has a spastic right hemiparesis from selective involvement of the pyramidal tract. Unopposed descending input from the extrapyramidal pathways results in disproportionate flexion in the upper extremity and extension in the lower extremity
Fig. 7.4
Spasticity with loss of central inhibition. This patient has a spastic arm with weakness of extension and flexion at the wrist and elbow. Multichannel EMG recording shows that biceps is activated during attempted elbow extension; the “weakness” is from persistent activity in the flexor muscles (i.e., a failure to relax antagonistic groups)
Spasticity
Clinical Features
Spasticity is an involuntary increase in muscle tone that can cause pain and deformity in addition to exacerbating upper motor neuron pattern weakness. This increased tone results from interruption of descending inhibition of myotactic stretch reflexes. Spasticity is velocity-dependent: the resistance will build up as the muscle is stretched faster until it suddenly gives away, known as the “clasp knife phenomenon.” This velocity-dependent change in tone is what distinguishes spasticity from other positive motor phenomena like the rigidity seen in Parkinson’s disease, the sustained dystonic movement seen in Wilson’s disease, or the neuropsychiatric phenomenon of catatonia. Spasticity can also cause reflexive painful grouped muscle spasms in response to a somatic or visceral trigger or change in posture. The increased tone from spasticity can be so severe as to appear as a fixed contracture. This distinction is important, since the latter will not respond to medical therapy. An examination under anesthesia may be necessary to differentiate the two.
Treatment
Treating spasticity not only improves motor function but also can relieve pain, improve posture and positioning (and hence prevent pressure sores), and facilitate hygiene. Treatment modalities can include physical therapy, splinting, and medical and surgical interventions, depending on the extent and severity of the symptoms (Fig. 7.5). This necessitates a multidisciplinary approach to spasticity management, beginning with the identification of reasonable outcome goals.
Fig. 7.5
Algorithm for treating spasticity based on extent and severity of symptoms
Physical Therapy
Spastic limbs can be passively stretched using bands, splints, or pressure garments (dynamic fabricated orthoses) to reduce tone and prevent fixed contracture [2]. Fixed contractures can be slowly stretched out using progressive splinting (Fig. 7.6). Standing frames allow paraplegic patients to remain upright for prolonged periods, using gravity to reduce spasticity and prevent contractures. Strengthening exercise regimens for weak muscles can make it easier to overcome spasticity and improve function; in particular, forced use of a hemiparetic limb by constraining the unaffected side in stroke patients can reduce spasticity [3].
Fig. 7.6
An adjustable wrist splint can be adjusted to provide gradual correction of spastic tone and soft tissue contracture from progressive splinting
Oral Medications
Oral drugs used to treat spasticity work by increasing GABA-mediated inhibition of spinal reflexes (baclofen and benzodiazepines), suppressing the release of the excitatory neurotransmitter glutamate (tizanidine via activation of alpha-2 adrenergic receptors) or blocking calcium release in muscle cells to reduce contractility (dantrolene) (Table 7.1). Drug regimens can be very helpful in specific situations. For example, a dose of clonazepam at bedtime can reduce nocturnal spasms and improve sleep. However, although widely prescribed to spastic patients, for the most part, these drugs have limited efficacy and cause such significant side effects including drowsiness and worsening weakness that most patients are noncompliant with prescribed doses [4–6].
Table 7.1
Oral drugs commonly prescribed for spasticity
Drug | Mechanism of action | Dose | Side effects |
|---|---|---|---|
Baclofen | GABA agonist | 5 mg three times daily, increased by 5–10 mg weekly up to a max dose of 90–120 mg in 3 divided doses
Related posts: Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
Get Clinical Tree app for offline access
|
