Syndrom der spastischen Parese

Zusammenfassung

Nach einer akuten zentralen Läsion kommt es zuerst zu einer „Schock”-Phase mit schlaffem Muskeltonus, danach entwickelt sich ein spastisches Syndrom. Dieses ist klinisch durch eine Muskeltonuserhöhung und gesteigerte Reflexe sowie eine charakteristische Bewegungsstörung gekennzeichnet. Neuere Untersuchungen zeigen, dass die spastische Bewegungsstörung wesentlich durch sekundäre Veränderungen der Antigravitationsmuskulatur verursacht ist, die eine spezifische Behandlung erfordert. Die gesteigerten Muskeleigenreflexe spielen eine nur untergeordnete Rolle.

Syndrome of Spastic Paresis

An acute central nervous system lesion is followed by a phase of „shock” with flaccid muscle tone. After some weeks the syndrome of spastic paresis develops which is characterized by increased muscle tone and exaggerated tendon tap reflexes. During the last years it could be shown that the characteristic spastic movement disorder is mainly due to secondary changes of muscle properties which require a specific treatment. Exaggerated reflexes do only little contribute to the movement disorder.

Literatur

• 1 Lance J W. Symposium synopsis. In: Feldmann RG, Young RR, Koella WCP (eds) Spasticity: Disordered Motor Control. Chicago; Year Book Medical Publishers 1980: 485-495
• 2 Hiersemenzel L P, Curt A, Dietz V. From spinal shock to spasticity: neuronal adaptation to a spinal cord injury.  Neurology. 2000;  53 1574-1582
• 3 Leis A A, Zhou H H, Mehta M. et al . Behavior of the H-reflex in humans following mechanical perturbation or injury to rostral spinal cord.  Muscle Nerve. 1996;  19 1373-1382
• 4 Weaver R, Landau W, Higgins J. Fusimotor function: Part. 2: Evidence of fusimotor depression in human spinal shock.  Arch Neurol. 1963;  9 127-132
• 5 Ashby P, Verrier M, Lightfoot E. Segmental reflex pathways in spinal shock and spinal spasticity in man.  J Neurol Neurosurg Psychiatry. 1974;  37 1352-1360
• 6 Schadt J C, Barnes D D. Motoneuron membrane changes associated with spinal shock and the Schiff-Sherrington phenomenon.  Brain Res. 1980;  201 373-383
• 7 O'Dwyer N J, Ada L. Reflex hyperexcitability and muscle contracture in relation to spastic hypertonia.  Curr Opin Neurol. 1996;  9 451-455
• 8 Ibrahim I K, Berger W, Trippel M, Dietz V. Stretch-induced electromyographic activity and torque in spastic elbow muscles. Differential modulation of reflex activity in passive and active motor tasks.  Brain. 1993;  116 971-989
• 9 Dietz V, Quintern J, Berger W. Electrophysiological studies of gait in spasticity.  Evidence that altered mechanical proberties of muscle contribute to hypertonia.. Brain. 1981;  104 431-449
• 10 Dietz V. Neurophysiology of gait disorders: present and future applications.  Electroenceph clin Neurophysiol. 1997;  103 333-355
• 11 Nacimiento W, Mautes A, Töpper R. et al . B- 50 (GAP- 42) in the spinal cord caudal to hemisection: Indication for lack of intraspinal sprouting in dorsal root axons.  J Neurosci Res. 1993;  35 603-617
• 12 Ashby P. Discussion I. In: Emre M, Benecke R (eds) Spasticity. The Current Status of Research and Treatment. Carnforth; Parthenon 1989: 68-69
• 13 Burke D, Ashby P. Are spinal „presynaptic” inhibitory mechanisms suppressed in spasticity.  J Neurol Sci. 1972;  15 321-326
• 14 Faist M, Mazevet D, Dietz V, Pierrot-Deseillingy E. A quantitative assessment of presynaptic inhibition of Ia afferents in spastics: differences in hemiplegics and paraplegics.  Brain. 1994;  117 1449-1455
• 15 Thilmann A F, Fellows S J, Garms E. Pathological stretch reflexes on the „good” side of hemiparetic patients.  J Neurol Neurosurg Psychiatry. 1990;  53 208-214
• 16 Thilmann A F, Fellows S J, Garms E. The mechanism of spastic muscle hypertonus: variation in reflex gain over the time course of spasticity.  Brain. 1991;  114 233-244
• 17 Berger W, Quintern J, Dietz V. Tension development and muscle activation in the leg during gait in spastic hemiparesis: the independence of muscle hypertonia and exaggerated stretch reflexes.  J Neurol Neurosurg Psychiatry. 1984;  47 1029-1033
• 18 Dietz V, Trippel M, Berger W. Reflex activity and muscle tone during elbow movements of patients with spastic paresis.  Ann Neurol. 1991;  30 767-784
• 19 Powers R K, Campbell D L, Rymer W Z. Stretch reflex dynamics in spastic elbow flexor muscles.  Ann Neurol. 1989;  25 32-42
• 20 Jones C A, Yang J F. Reflex behavior during walking in incomplete spinal-cord-injured subjects.  Exp Neurol. 1994;  128 239-248
• 21 Dietz V, Berger W. Normal and impaired regulation of muscle stiffness in gait: a new hypothesis about muscle hypertonia.  Exp Neurol. 1983;  79 680-687
• 22 Powers R K, Marder-Meyer J, Rymer W Z. Quantitative relations between hypertonia and stretch reflex threshold in spastic hemiparesis.  Ann Neurol. 1988;  23 115-124
• 23 Lee W A, Boughton A, Rymer W Z. Absence of stretch reflex gain enhancement in voluntarily activated spastic muscle.  Exp Neurol. 1987;  98 317-335
• 24 O'Dwyer N J, Ada L, Neilson P D. Spastic and muscle contracture following stroke.  Brain. 1996;  119 1737-1749
• 25 Dietz V. Human neuronal control of automatic functional movements: interaction between central programs and afferent input.  Physiol Rev. 1992;  72 33-69
• 26 Rosenfalck A, Adreassen S. Impaired regulation of force and firing pattern of single motor units in patients with spasticity.  J Neurol Neurosurg Psychiatry. 1980;  43 907-916
• 27 Brown J K, Rodda J, Walsh E G, Wright G W. Neurophysiology of lower-limb function in hemiplegic children.  Dev Med Child Neurol. 1991;  33 1037-1047
• 28 Hoogstraten M C, van der Ploeg R J, van der Burg W. et al . Tizanidine versus baclofen in the treatment of spasticity in multiple sclerosis patients.  Acta Neurol Scand. 1988;  77 224-230
• 29 Steinbock P, Reiner A M, Beauchamp R. et al . Randomized clinical trial to compare selective posterior rhizotomy plus physiotherapy with physiotherapy alone in children with spastic diplegic cerebral plasy.  Dev Med Child Neurol. 1997;  39 178-184
• 30 Wright F V, Shei E M, Drake J M. et al . Evaluation of selective dorsal rhizotomy for the reduction of spasticity in cerebral palsy: a randomized controlled trial.  Dev Med Child Neurol. 1998;  40 239-247
• 31 Corry I S, Cosgrove A P, Walsh E G. et al . Botulinum toxin A in the hemiplegic upper limb: a double blind trial.  Dev Med Child Neurol. 1997;  39 185-193