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PubMed2002

Stiff man syndrome and related conditions.

The stiff man syndrome (SMS) and its variants, focal SMS, stiff limb (or leg) syndrome (SLS), jerking SMS, and progressive encephalomyelitis with rigidity and myoclonus (PERM), appear to occur more frequently than hitherto thought. A characteristic ensemble of symptoms and signs allows a tentative clinical diagnosis. Supportive ancillary findings include (1) the demonstration of continuous muscle activity in trunk and proximal limb muscles despite attempted relaxation, (2) enhanced exteroceptive reflexes, and (3) antibodies to glutamic acid decarboxylase (GAD) in both serum and spinal fluid. Antibodies to GAD are not diagnostic or specific for SMS and the role of these autoantibodies in the pathogenesis of SMS/SLS/PERM is the subject of debate and difficult to reconcile on the basis of our present knowledge. Nevertheless, evidence is emerging to suggest that SMS/SLS/PERM are manifestations of an immune-mediated chronic encephalomyelitis and immunomodulation is an effective therapeutic approach.

Adult↗
PubMed1990

Blockade of excitatory neurotransmission in the globus pallidus induces rigidity and akinesia in the rat: implications for excitatory neurotransmission in pathogenesis of Parkinson's diseases.

Bilateral microinjections of the selective N-methyl-D-aspartate (NMDA) antagonist, (-)-2-amino-7-phosphonoheptanoate (AP7), 0.02-0.5 nmol, into the globus pallidus and ventral-posterior portions of the caudate-putamen result in an increase in the muscle tone (rigidity) and catalepsy (akinesia) in rats. NMDA blocked the actions of AP7 on motility in sensitive regions of the globus pallidus and caudate-putamen. Topographical differences in the action of AP7 in the striatum were detected in the dorsal-ventral and rostral-caudal direction. Microinjections of AP7 into the nucleus accumbens induced neither an increase in the muscle tone nor catalepsy in rats, while ventral regions of the caudate-putamen were sensitive to both actions of AP7. Microinjections of AP7 into the dorsal caudate-putamen resulted in a moderate or no increase in the muscle tone. AP7 failed to induce catalepsy from dorsal regions of the caudate-putamen. These data identify the globus pallidus and a defined subregion of the caudate-putamen as crucial sites where excitatory neurotransmission acts to regulate the final set-point of the respective output neurons providing modulation of the passage of motor information through the basal ganglia.

2-Amino-5-phosphonovalerate↗
PubMed1975

Motor responses to sudden limb displacements in primates with specific CNS lesions and in human patients with motor system disorders.

Central feedback pathways for motor control were studied by recording EMG responses to sudden upper limb displacements in humans and monkeys using a precision torque motor to generate step load changes. Normal human subjects showed three short-latency EMG responses (M1, M2 and M3) which appear to correspond to those recorded from trained monkeys. The M2 and M3 components, thought to represent feedback in supraspinal pathways, were significantly increased when the subjects were instructed to actively compensate for the load changes. Parkinsonian patients with rigidity showed evidence of markedly increased feedback over the interval for the M2 and M3 responses and appeared to have lost the ability to modulate feedback according to the motor task being performed. The results are discussed with reference to recent research on motor control mechanisms in primates and a tentative model for the basis of Parkinsonian rigidity is proposed.

Animals↗
PubMed1981

Baclofen in the treatment of stiff-man syndrome.

Baclofen, 90 mg daily, was given to a patient with stiff-man syndrome diagnosed by electromyography and clinical criteria. The patient, bedridden for three years, experienced a decrease in rigidity, cramping, stiffness, and spasm and was able to walk on the thirtieth day of treatment.

Aged↗
PubMed1997

Spinal rigidity following acute myelitis.

A patient with a 2(1/2)-year history of painful spasms and rigidity of both lower limbs is described. Symptoms began after an episode of acute myelitis. The spasms--which were spontaneous and stimulus sensitive and occurred on voluntary action--involved the repetitive grouped discharge of motor units. Continuous motor unit activity was present at rest in the muscles of both legs, and cutaneomuscular reflexes were abnormal. This patient is similar to those recently reported as having stiffness and spasms of the legs due to a possible chronic spinal interneuronitis and provides further evidence that this kind of movement disorder may be caused by spinal cord pathology.

Acute Disease↗
PubMed1994

Portable device for quantifying parkinsonian wrist rigidity.

The need for objectivity in the assessment of parkinsonism prompted the development of a portable transducer capable of quantifying muscular rigidity. This paper describes the development and use of a device for measuring wrist rigidity and reports the preliminary findings from 25 normal healthy controls and 29 patients, many of whom were undergoing antiparkinsonian treatment to alleviate rigidity or antipsychotic treatment, which produced parkinsonian rigidity. An objective rigidity score, representing the degree to which motor activity increases muscular stiffness in the wrist, correlates highly with clinical ratings of parkinsonian rigidity and demonstrates 89% specificity and 82% sensitivity. Unlike previous techniques for quantifying rigidity, this transducer offers greater portability and apparent face validity.

Adult↗
PubMed1997

Reciprocal inhibition in Parkinson's disease.

We studied the inhibition of median H-reflex by conditioning stimuli on the radial nerve in 14 normal controls, 6 patients with unilateral and 1 patient with predominantly left-sided Parkinson's disease. In normal controls, the electrophysiological studies were performed on their right hands, yet both hands were examined in patient group. In the controls, we identified three inhibitory phases, with maximal inhibition at conditioning-test intervals of 0 ms (41.66 +/- 4.73%), 20 ms (45.19 +/- 4.33%), and 100 ms (44.55 +/- 6.84%), respectively. In the less- or a- symptomatic side of the patient group, the inhibitory patterns are similar to those of the controls. However, in the symptomatic arms, loss of inhibition, or even mild potentiation, was observed in the third inhibitory phase. When the symptomatic and asymptomatic sides of patients were compared, in contrast to the striking phenomenon found between symptomatic side and the controls, no difference was observed in the third phase. The current results imply that, although no obvious rigidity can be detected on the asymptomatic sides, subtle functional corruption may have occurred within the contralateral basal ganglia in patients with unilateral Parkinson's disease. The remarkable change of the third phase on the symptomatic sides of patients suggests the perturbation of the polysynaptic long latency reflex pathway may somehow play a role in the rigidity pathogenesis.

Adolescent↗
PubMed1983

Physiological mechanisms of rigidity in Parkinson's disease.

Electromyographic responses of triceps surae and tibialis anterior produced by dorsiflexion stretch were studied in 17 patients with Parkinson's disease. Most patients showed increased muscular activity when attempting to relax. A few patients showed an increase of short-latency reflexes when relaxed and when exerting a voluntary plantarflexion prior to the stretch. Many patients showed long-latency reflexes when relaxed and all but one showed long-latency reflexes with voluntary contraction; and these reflexes were often larger in magnitude and longer in duration than those seen in normal subjects. Unlike the short-latency reflex, the long-latency reflex did not disappear with vibration applied to the Achilles tendon. The long-latency reflexes and continuous responses to slow ramp stretches were diminished at a latency similar to the beginning of long-latency reflexes when the stretching was quickly reversed. Dorsiflexion stretch also frequently produced a shortening reaction in tibialis anterior. Of all the abnormal behavior exhibited by the Parkinsonian patients only the long-latency reflex magnitude and duration correlated with the clinical impression of increased tone. The mechanism of the long-latency reflex to stretch which is responsible for rigidity is not certain, but the present results are consistent with a group II mediated tonic response.

Adult↗
PubMed1976

Tonic inhibition of dorsal pontine neurons during the postural atonia produced by an anticholinesterase in the decerebrate cat.

1. Experiments performed in precollicular decerebrate cats indicate that neurons located in the caudal part of the locus coeruleus and locus subcoeruleus as well as in the surrounding reticular formation were greatly depressed during the cataplectic episodes induced by i.v. injection of 0.1 mg/kg of eserine sulphate. 2. These units actually showed a slow regular firing rate when the rigidity was present. Moreover their firing rate greatly decreased during the episodes of postural atonia produced by the anticholinesterase. In some instances a complete abolition of firing occurred during these episodes. The depression of unit discharge anticipated the onset of postural atonia and lasted throughout the episodes. 3. Some of the neurons described above responded with steady changes in their discharge rate to natural stimulation of macular labyrinthine receptors during postural rigidity. However, the response of these neurons to lateral tilts was suppressed during the episodes of postural atonia induced by the anticholinesterase, This and other arguments suggested that these units were tonically inhibited during the induced cataplectic episodes. 4. The time course of the rate deceleration shown by these neurons during transition from postural rigidity to muscular atonia represents a mirror image of the rate acceleration which affects most of the pontine reticular neurons located in the gigantocellular tegmental field (FTG) during the induced cataplectic episodes. These reciprocal rate relations suggest that a functional interaction exists between the two cell groups. In particular it is postulated that the pontine FTG neurons are self-excitatory and excitatory to the locus coeruleus neurons, while the last neurons may be self-inhibitory and inhibitory to FTG neurons. These findings can be related to previous observations showing that neurons located in the region of locus coeruleus undergo a rate deceleration during desynchronized sleep which mimics the time course of firing to the pontine reticular neurons. 5. In conclusion it appears that the decerebrate rigidity is present in so far as the cholinergic reticular neurons, which trigger the bulbospinal inhibitory system, are tonically inhibited by neurons located in the monoaminergic structures of the dorsolateral pontine tegmentum. On the other hand the suppression of the decerebrate rigidity ,which occurs during the cholinergically induced cataplectic episodes results from activation of the cholinergic reticular neurons, which escape tonic inhibition from monoaminergic structures.

Animals↗