Pathophysiology of spasticity

The term "spasticity" describes the velocity-dependent increase in tonic stretch reflexes. The symptom is commonly seen in patients with injury to the central nervous system. It is rarely isolated but, instead, part of a set of symptoms that is sometimes confusing. However, the pathophysiology of the symptom has evolved over the past three decades, and it is now considered part of a global process that includes not only spinal reflex loop modifications, but also changes in the biomechanical properties of muscle fibers. Finally, recent studies of changes in the membrane properties of motor neurons and the occurrence of plateau potential have opened new perspectives. This review aims to describe these new pathophysiological models.     

Outcome measures of spasticity

Spasticity is characterized by a velocity-dependent increase in muscle resistance, in response to a passive stretch. Whilst clinical scales probably represent the most common approach to its measurement, these are limited by poor reliability and difficulties with some definitions. However, recently, a simple system has been used to provide the clinician with a measure of the force applied during the Ashworth Test. The Wartenberg Pendulum Test has been devised for measuring spasticity at the knee, but has been shown to be unsuitable for measuring more severe spasticity. Powered systems have been used in research studies, but are rarely considered suitable for routine clinical use. However, one method of interest, using a low inertia torque motor to measuring stiffness at the wrist, has been shown to provide rapid measurements which correspond to the degree of spasticity defined by other scales. Clinical gait analysis may have an important role to play in assessing spasticity – since there are clear associations between lower limb spasticity and gait problems – but it does not provide a true measure of the condition. In summary, while scales remain the most common method of measuring spasticity, there is considerable potential in instrumented techniques that can provide greater reliability and precision of measurement.     

Electromyographic assessment of spasticity

We define the concept of muscle tone and describe the signs and symptoms of its alteration in spasticity. In assessing muscle tone it is important to consider all the inputs and outputs affecting it, using biomechanical-EMG techniques for measuring active tone. We list the various features of the myotatic and defence reflexes that are altered in spastics and analyze the altered parameters in relation to the tonic reflexes. The degree of displacement, the position from which it is initiated and the velocity of displacement constitute a specific, sensitive and reliable criterion. We report the results of a personal study of these reflexes and of the shortening reflexes.

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Sommario Dopo aver definito, anche in senso semeiologico, il concetto di tono muscolare, gli AA sottolineano l'importanza di una valutazione che tenga calcolo al momento stesso dell'esame di tutti gli apporti afferenti e discendenti che influiscono su di esso. Ciò può essere fatto adottando le tecniche biomeccaniche-emg di misura del tono attivo. Dopo aver elencato i vari aspetti dei riflessi miotatici e di difesa che vengono modificati nella spasticità gli AA analizzano i parametri alterati in rapporto ai riflessi tonici. Di valore specifico, sensibile e attendibile appare il grado di spostamento, la posizione iniziale dal quale viene effettuato nonché la velocità di spostamento. Vengono poi illustrati i risultati ottenuti a carico di tali riflessi e di quelli di accorciamento sulla base di ricerche personali.

     

Physical management of spasticity

Physical management of people with spasticity is a complex task requiring the collaborative work of a multidisciplinary team. This article reviews some of the most commonly used treatment techniques and theories that lay the framework for the physical management of spasticity. Most crucial to the management of the person with spasticity is the skillful application of the techniques and theories discussed. Given the complexity in the standardized evaluation of children with spasticity, it is recommended that existing outcome measures or standardized scales be applied wherever possible as an adjunct tool to the clinician's assessment and interventions. One must recognize the benefits of such scales and their limitations. Therefore, it is recommended that further development of standardized assessments be supported by funding agencies to develop both quantitative and qualitative measurement tools that will address the particular needs of the person with spasticity. Review of the literature supports the many interventions that are listed; however, further research is recommended by the consensus group.     

The pathophysiology of spasticity

Spasticity is only one of several components of the upper motor neurone (UMN) syndrome, known collectively as the `positive' phenomena, that are characterized by muscle overactivity. Other components include tendon hyper-reflexia, clonus, the clasp-knife phenomenon, flexor and extensor spasms, a Babinski sign, and spastic dystonia. Spasticity is a form of hypertonia due to hyperexcitable tonic stretch reflexes. It is distinguished from rigidity by its dependence upon the speed of the muscle stretch and by the presence of other positive UMN signs. Hyperactive spinal reflexes mediate most of these positive phenomena, while others are due to disordered control of voluntary movement or abnormal efferent drive. An UMN lesion disturbs the balance of supraspinal inhibitory and excitatory inputs, producing a state of net disinhibition of the spinal reflexes. These include proprioceptive (stretch) and nociceptive (flexor withdrawal and extensor) reflexes. The clinical syndrome resulting from an UMN lesion depends more upon its location and extent, and the time since it occurred, than on the pathology of the lesion. However, the change in spinal reflex excitability cannot simply be due to an imbalance in supraspinal control. The delayed onset after the lesion and the frequent reduction in reflex excitability over time, suggests plasticity in the central nervous system. Knowledge of the electrophysiology and neurochemistry of spinal reflexes, together with the action of antispasticity drugs, helps us to understand the pathophysiology of spasticity.     

Energy requirements of spasticity

Direct measurement of energy expended by spasticity in children with severe spastic quadriparesis is difficult. Insertion of an intrathecal baclofen pump in a 13-year-old boy with severe spasticity and profound mental retardation resulted in an estimated 30 to 40% decrease in his spasticity. As he had been on a carefully calculated ketogenic diet and fed by gastrostomy, his precise caloric intake was known. Decrease in spasticity, on the same caloric intake, led to marked weight gain. Reduction of 100 calories intake resulted in new weight stability. It was possible therefore, to estimate indirectly energy used by his spasticity. This 100 calories, representing 34% of calories above his resting energy requirement, corresponded to an independently estimated 30 to 40% of caloric expenditure of his spasticity. It was concluded that when calculation of calories is critical, energy utilization by spasticity must be taken into consideration.     

Pathophysiology of dystonia

Understanding of the pathophysiology of dystonia derives primarily from studies of focal dystonias. Physiological investigations have revealed a number of abnormalities that may reflect the genetic substrate that predisposes certain individuals to develop dystonia. There is a loss of inhibition in the central nervous system, and a loss of surround inhibition specifically. Plasticity is increased, and there are sensory abnormalities. Which of these disorders is primary is uncertain.     

Pathophysiology of syncope

Clinical Autonomic Research - Syncope or near-syncope is a not uncommon effect of gravitational or other stresses and it occurs when cerebral blood flow falls to below about half the normal value....     

Pathophysiology of migraine

Neurological Sciences - The exact pathogenesis of migraine remains to be determined. In particular there is increasing evidence for the neural basis of migraine. We now have a body of data...     

Pathophysiology of dystonia

Dystonia is a diverse movement disorder characterized by involuntary muscle co-contraction of the agonist and antagonist, which may cause twisting and repetitive movements or abnormal posture. Dystonia is the least understood movement disorder associated with the basal ganglia dysfunction. While dysfunction of cortico-striatal-thalamo-cortical motor circuits is likely to play a fundamental role in the pathophysiology of dystonia, the disorder does not easily fit into the hypokinetic or the hyperkinetic category of basal ganglion diseases. There was evidence of widespread impairment of the inhibition involving multiple levels of the nervous system. There was also significant data to support the notion that the sensory function and sensorymotor integration were debit in patients with dystonia. The reciprocal inhibition curves between the forearm muscles were abnormal at the spinal cord level, as well as the blink reflex recovery curves at the brain stem level. The motor cortex excitability was enhanced while the transcranial magnetic stimulation. The dystonia showed decreased inhibition of the intracortical inhibition and facilitation and short cortical silent period. The pre-movement gating of the somatosensory evoked potentials and the somatosensory homunculus were abnormal in dystonia. This review provides an overview of the recent studies of the pathophysiology of dystonia, with an emphasis on the cortical plasticity. The possible beneficial effects of the transcranial magnetic stimulation (TMS) and repetitive transcranial magnetic stimulation (rTMS) with new paradigm are also discussed.     

Pathophysiology of epilepsy

This work reviews the current knowledge on epileptogenesis and pathophysiology of epilepsy. Recently, gene defects underlying four monogenic epilepsies (generalized epilepsy with febrile seizures, autosomal dominant nocturnal frontal lobe epilepsy, benign familial neonatal convulsions and episodic ataxia type 1 with partial seizures) have been identified, shedding new light on the pathophysiology of epilepsy as these diseases are caused by ion channel mutations. Although epileptic syndromes differ pathophysiologically, common ictogenesis-related characteristics as increased neuronal excitability and synchronicity are shared as well as mechanisms involved in interictal-ictal transition. Emerging insights point to alterations of synaptic functions and intrinsic properties of neurons as common mechanisms underlying hyperexcitability. This work also reviews the neurochemical mechanisms of epilepsy. An imbalance between glutamate and gamma-aminobutyric acid neurotransmitter systems can lead to hyperexcitability but catecholaminergic neurotransmitter systems and opioid peptides were shown to play a role in epileptogenesis as well. An overview of currently available anti-epileptic drugs and their presumed mechanisms of action is given as an illustration of the neurochemistry of epileptogenesis. Most anti-epileptic drugs exert their anti-epileptic properties through only a few neurochemical mechanisms that are meanwhile basic pathophysiological mechanisms thought to cause seizures.