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Spasticity in the Podiatric Patient

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Spasticity in the Podiatric Patient CHAPTER II SPASTICITY IN TI{E PODIATRIC PATIENT Lwke D. Cicchinelli, DPM The management of the podiatric patient presenting with diseases at this level such as polio effect the classic lower spasticity can be both vexing and rewarding. Content with a motor neuron syndrome. seemingly good outcome at 1 year postoperarively must be This lower motor neuron condition exhibits in tempered wit-h an appreciation for the potential conse- general that individual muscles may be affected, atrophy quences of a growing limb and the complex interplay is pronounced as the muscles do not receive normal between muscles, tendons and osseous factors. The 10 year innervation, flaccidiry and hypotonia of affected muscles follow up outcome might be very different and the patient with loss of tendon reflexes, plantar or babinski reflex if may have other as yet unrecognized functional aberrations. present is of the normal or flexor type, fasciculations may So how does one treat rhese patients? Many be present representing the sporadic discharge of questions come to mind. Do you transfer a spastic muscle fibers due to diseased and irritable axons and muscle? Is the neuromuscular lesion static or progressive? electromyograms reveal reduced numbers of motor units You are a podiatrist, what about the suprastructural and fibrillations representing isolated activity of individ- deformity such as spastic hip adductors, whar is their affect ual muscle fibers. Sensorium is intact. No clonus is on the lower limb function? Is the foot reducible or rigid? Present. Diseases of lower motor neurons or peripheral \fill a muscle tendon transfer shift the muscle power rhe nerves show distal limb weaknesses such as foot drop or a wrong way causing a resultant different deformiry? Are the steppage gait. extrinsic muscles affecting the foot and ankle under In contrast the upper motor neuron pathway (think voluntary control by the patient? Maybe they could actively BRAIN versus spinal cord, cerebral palsy is a grear control tibialis anterior if it were nor for the spastic example!) consists of central nervous system neurons and gastrocsoleus complex. How does one know? their associated descending pathways through the The author continues ro encounter, mull over and brainstem and spinal cord. There are also several indirect search for the answers ro these questions while treating pathways operating through the basal ganglia and related children and adolescents with congenital or acquired subcortical nuclei that influence motor activity on a spastic conditions, particularly during medical mission central level. These indirect pathways are the extrapyra- surgical trips. This chapter represenrs an effort to midal system., while the corticospinal tract constirutes consolidate some thoughts, observations and information the pyramidal system. gleaned from our surgical forefathers while at the same Pyramidal involvement manifests as muscle groups time establish a personal blueprint for the successful that are affected diffusely, never individual muscles, management of these patients that is modifiable as atrophy is slight but strength is decreased, spasticity wirh clinical and didactic experience grows. hyperactivity of the tendon reflexes, an extensor plantar reflex or Babinksit sign and fascicular twitches are not UNDERSTANDING THE produced. The upper motor neuron syndrome is a motor NEUROMUSCUI-A.R LESION neuron disorder characterized by a velociry dependant increase in tonic stretch reflex, (muscle tone) with jerks Upper motor neuron vefsus lower motor neuron, what does exaggerated tendon resulting from hyperexcitability it mean? Is there pyramidal or corticospinal tract involve- of the released or disinhibited spinal motor neurons. ment or is it extrapyramidal? Is the patient with cerebral Clonus is present. Pyramidal involvement is essentially a palsy spastic, athetotic or both? An organized clinical spastic motor dysfunction approach to these patients requires an intimate appreciation Extrapyramidal involvement is characterized by of normal neuromuscular parhways and structure. increase muscle tone or rigidity (although may be In simplest terms the brain or cortex relays informa- hypotonic in infants) with disorders of movement such as tion to the anterior horn cells which then communicate chorea, athetosis or dystonia. Muscle sffength is normal with the motor unit and muscle itself The anterior horn or mild decrease, tendon reflexes are normal or siighdy cells are the location of the lower motor neurons and increased and Babinski is normal or down going. The 48 CHAPTER 11 involuntary movement disorders of extrapyramidal evaluation for general muscular control assessment and involvement are hallmarks. Dystonia is a fast and slow naturally range of motion exams to passive and muscle rwisting movement of the trunk, head and extremities active testing to include deep tendon and superficial or with very slow relaxation intervals. Athetosis is cutaneous reflexes. Alterations of muscle tone such as differentiated from dystonia by the smoorh flow of hypertonicity, spasticity or rigidity are noted. Inspection posture from one position to anorher without sustained for muscle atrophy and/or strength is performed. posturing of the limb. These movements are accentuated Gait is facilitated in the neuromuscular patient by during purposeful movement and involve a peculiar, an extensor synergy thigh adduction and thigh and knee writhing, irregular movement with increased tone in the extension with plantarflexion of the feet and toes. This is lower extremity. Chorea consists of rapid, involuntary more powerful then flexion synergy and this bias toward and nonrhythmic, generalized jerks of various parts of the extension synergy assists weightbearing and walking. The body. Movements occasionally dance from one joint to limbs are checked for symmetry. another and may involve facial grimacing and The presence of tissue contractures or not is noted flexion-extension movements of the extremities. and attempts are made to determine if certain muscle If sensory changes coexist with a flaccid arreflexic groups are being overpowered by spastic groups. Is an paralysis this indicates anterior and posterior horn cell equinus present as a fixed condition or is it a dynamic involvement or in mixed motor and sensory nerves. If only equinus only noted during ambulation secondary to a motor changes exist then the lesion must be at the level of spastic gastrocsoleus that demonstrates a posterior thrust gray matter of the spinal cord, anterior horn cell level, of the knee. motor branches of peripheral nerves or motor axons aione. It is important to remember that the muscles of the Rigidity must be difTerentiated from spasticity and cerebral palsy patient show contracture and weakness due shows the distinction in qualiry of hypertonicity. In to neurological deficit as well as limited use. The atrophy rigidiry there is a heightened discharge of alpha motor of muscles in a clubfoot patient may be due to disuse and neurons and resistance to passive movement of the limb is should be graded on their expected strength. constant and sometimes described as "lead pipe" or Furthermore, spastic muscles undergoing short stretch "plastic". This is an extrapyramidal exhibition and show augmentation of tone while long stretch inhibits maintenance of a flexed position is common. "Cogwheel" tone due to hypertonicity and resistance to passive move- rigidity is common in Parkinson's disease when ment. Athetotic muscles undergoing short stretch inhibits hypertonic muscles show resistance to passive stretching tone and long stretch augments it. by rhythmic jerky movements as though the resistance of The determination of voluntary or involuntary the limb were controlled by a ratchet. Deep tendon muscie action is critical and muscle belly blockade with reflexes are normal. Consistent with the extrapyramidal 1%o lidocaine may be useful. The element of spasticity can involvement is the disorder of involuntary movement. not be determined under general anesthetic and therefore Spasticity however is corticospinal or pyramidal and must be done preoperatively. It is particularly important a hyperactivity of the stretch reflex (a tap on a tendon, to determine if tibialis anterior is under voluntary or stimulates muscle spindles, activates afferent neurons, involuntary control. If it functions with the "mass or transmits impulses to alpha motor neurons, resulting in confusion' reflex which is performed when the patient brief muscle contraction or tendon reflex) secondary to voluntarily flexes the hip and resistance is placed on the central changes but without increased sensitivity of thigh and the anterior tibial muscle responds then it is muscle spindles. Clinically this is seen as a free interval functioning although under involuntary control. The followed by a "clasp knife" or sustained phenomenon patient utilizes the muscle to help dorsiflex the foot where the muscle doesn't contract until stretched a little during gait and with hip flexion. Dosriflexion of the foot and then during the stretch the augmentation in muscle occurs despite the absence ofvoluntary action. tone quickly subsides. Deep tendon reflexes are increased. This maneuver has been termed synkinesia, "confusion or automatic" reflex or Strumpell test. It is CLINICAL EXAM essential to determine if tibialis anterior is under voluntary control and often this can not be elicited with The clinical exam begins with an appreciation of the the knee extended. Likewise, if under
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