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PubMed1980

Stiff-man syndrome with abnormalities in CSF and computerized tomography findings. Report of a case.

We report a case of stiff-man syndrome with abnormal spinal fluid. Serum protein values were normal, but the spinal fluid levels of immunogammaglobulin G and acute-phase proteins were elevated. We discuss the possibility of an inflammatory process of the nervous system as a cause for these findings. Another interesting observation in our patient was that of local atrophies seen on computerized tomography, indicating hemispheral and especially brainstem lesions. Furthermore, as a new therapeutic possibility, we demonstrated the improvement of spasms and rigidity under the influence of heat.

Atrophy↗
PubMed1996

Prepharyngeal dysphagia in Parkinson's disease.

Dysphagia in patients with Parkinson's disease (PD) is most often attributed to pharyngeoesophageal motor abnormalities. In our study of patients with idiopathic PD, attention was focused on prepharyngeal symptoms and motor functions. Using the Hoehn and Yahr disease severity scale, patients were grouped into those with mild/moderate disease [subgroup I (n = 38)] and those with advanced disease [subgroup II (n = 34)]. Dysphagia symptoms were present in 82% of all patients, but subgroup I patients voiced significantly more complaints. Conversely, many prepharyngeal abnormalities of ingestion, including jaw rigidity, impaired head and neck posture during meals, upper extremity dysmotility, impulsive feeding behavior, impaired amount regulation, and lingual transfer movements were statistically more frequent in subgroup II patients. Impaired mastication and oral preparatory lingual movements were the most common aberrations observed during dynamic videofluoroscopy (48/71), with most patients being concordant for both. The motor disturbances of ingestion reported herein reflect the disintegration of volitional and automatic movements caused by PD-related akinesia, bradykinesia, and rigidity.

Aged↗
PubMed2001

Lesions as therapy: rigidity and Parkinson's disease.

Since James Parkinson (1817) first characterized the shaking palsy as a unique condition, significant confusion has remained concerning the causes and treatments of Parkinson's disease (PD). Through the 19th century, a wide variety of approaches were attempted in an effort to reduce its cardinal signs--rigidity, tremor, and bradykinesia--but to little effect. Today, approaching 200 years after Parkinson's seminal work, this disorder is commonly treated by surgical means, inducing a lesion in one specific portion of a small nucleus in the central nervous system (Desaloms et al., 1998, Lang et al., 1999). The notion of providing a lesion to the nervous system as a therapy for PD, however, began in earnest at the beginning of the 20th century. The first attempt to alleviate the symptoms of PD through surgical means involved a section of the dorsal roots of the spinal cord supplying the affected limb (also known as dorsal rhizotomy). Although ultimately resulting in disastrous effects, these early surgical attempts proceeded from a firm body of clinical and experimental research on both the central and peripheral nervous systems. After briefly reviewing the use and failure of dorsal rhizotomy as a treatment for parkinsonian rigidity, this paper will examine the manner in which clinicians and scientists justified the procedure.

Decerebrate State↗
PubMed1988

Delayed respiratory depression following fentanyl anesthesia for cardiac surgery.

High-dose fentanyl anesthesia is widely used in cardiac surgery. Its immediate side-effects are well known. However, its late adverse effect manifested by extreme truncal rigidity, decreased chest wall compliance, hypoventilation, respiratory acidosis and hemodynamic instability is not sufficiently appreciated. Of 380 patients who underwent aortocoronary artery bypass under high-dose (100 micrograms/kg) fentanyl anesthesia, 29 (7.6%) developed the sudden onset of extreme thoracic and abdominal rigidity, leading to respiratory depression 2 to 6 h postoperative, after an apparently normal recovery from the anesthesia. In 15 patients, a high plasma level of fentanyl (5.2 to 7.8 ng/ml) correlated with the clinical events. Administration of naloxone or a muscle relaxant rapidly reversed this late complication of fentanyl, thought to be due to re-entry of fentanyl into plasma from deposits in adipose tissue, muscle and the GI tract, leading to a secondary peak in plasma fentanyl. It is more likely to be encountered when hypothermia, rewarming, and acidosis occur in the postoperative period. Awareness of this life-threatening complication is critical in patients undergoing surgery with fentanyl anesthesia.

Aged↗
PubMed2002

[Quantitative assessment of Parkinsonian rigidity by vessel Doppler ultrasonography].

OBJECTIVE: To investigate the value of quantitative assessment of parkinsonian rigidity by vessel Doppler ultrasonography. METHODS: The diameter of the rigid limbs, including radial artery and vein, ulnar artery and vein, brachial veins, popliteal vein, anterior tibial vein, and posterior tibial vein in twelve individuals with PD and twelve age matched controls were measured by ultrasonography in both "on" and "off" states. Meanwhile the UPDRS unified Parkinson's disease rating scale for rigidity were also recorded both in "on" and "off " states by experienced neurologists. RESULTS: The mean diameter of radial vein, ulnar vein, brachial vein, popliteal vein, anterior tibial vein and posterior tibial vein, were 1.14, 1.13, 2.47, 3.85, 1.89, and 1.33 mm respectively in "off " state (group "A"), and were 1.58, 1.54, 2.88, 4.65, 2.27, and 1.69 mm respectively in "on" states (group "B") among the PD patients. The diameters of corresponding vessels in the controls (group "C") were 2.07, 1.69, 4.15, 5.07, 2.63, and 1.99 mm respectively. The data increased from group "A" to "C" gradually. Paired samples t tested showed a significant difference between the data of group A and group B (P = 0.00 approximately 0.03) and between group A and group C (P = 0.00 approximately 0.02) and no significant difference between group B and group C (P > 0.05, except for brachial vein with P = 0.02). The data of vein diameters in rigid limbs were correspondent to the UPDRS scores for rigidity with the correlation coefficient of 0.71, 0.82, 0.91, 0.73 (all P < 0.01), 0.60 P < 0.05 , and 0.77 P < 0.01) for the above mentioned vessels respectively. CONCLUSION: The diameter of distant veins in limbs can be adopted as objective and quantitative indicators for parkinsonian rigidity and contribute to the evaluation of therapeutical effects.

Aged↗
PubMed1989

Rigid spine syndrome. Report of 4 cases.

Four cases of rigid spine syndrome are reported for the first time in China. They are 2 males and 2 females. One girl has a positive family history. Limitation of flexion of the cervical and dorsolumbar spine, contractures of joints, especially the elbow joints, extreme flattening of the chest and scoliosis are the prominent symptoms of this syndrome. The clinical criteria for this rigid spine syndrome tally with those described by Dubowitz (1965). Symptomatology, diagnosis, differential diagnosis and genetics are discussed. However, the question whether rigid spine syndrome is a single, well defined disease entity remains to be explored.

Adolescent↗
PubMed1986

Some pathophysiological aspects of the parkinsonian rigidity.

The neurophysiological mechanisms explaining parkinsonian rigidity are still poorly understood. Its reflex nature is well established but the peripheral afferents causing it are likely multiple and not restricted to IA afferents. Few modifications appear in spinal cord reflex mechanisms and are limited to some interneurones (reciprocal inhibition and flexor reflex). At present, the most plausible explanation of rigidity relies on hyperactivity in long loop reflex pathways relaying in the brain.

Electromyography↗
PubMed1997

Measurement of rigidity in Parkinson's disease.

Clinical assessment of rigidity in parkinsonian patients is largely qualitative. The reliability and validity of the assessments are sometimes in doubt. Several "engineering" methods of quantifying rigidity have been described, but none has been adopted into general clinical practice. A possible reason is that these methods differ in crucial aspects from the clinical exam. We therefore tackled the problem by monitoring the clinical exam itself, using small sensors to measure the forces and displacements applied. Limb impedance (Z) was computed using parameter identification methods and compared to raters' verbalized ratings of rigidity based on a 5-point scale: the Unified Parkinson's Disease Rating System. The qualitative and quantitative estimates of impedance covaried over a fourfold range, depending on the forces imposed and the subject's motor set. Raters differed by up to 1 full point in their mean qualitative ratings and sometimes disagreed on whether levodopa reduced rigidity. This was not due to any significant differences in the overall range of rigidity they evoked, but rather to the way they scored this range [the ratio of mean rating to mean impedance (R/Z) varied between raters and subjects]. On the other hand, the R/Z ratio was reproducible over separate sets of ratings and may therefore serve to convert measured impedance into a standardized rating. Our results indicate that the current clinical exam may be too abbreviated to detect the sometimes quite small reductions in rigidity after levodopa. We conclude that a device that conveniently quantifies the clinical assessment of rigidity is now available and will lead to more standardized protocols for rating rigidity in the near future.

Antiparkinson Agents↗