The process of recovery after hemiplegia.
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Two groups of rats were used to evaluate the results of nerve repair using fibrin tissue adhesive. In one group of 10 rats, a simple neurotomy of the sciatic nerve was performed. In the second group of 10 rats, a 1-cm segment of sciatic nerve was excised bilaterally and used as an autogenous nerve graft. The neurotomy and the nerve graft were repaired on one side by microsurgical suture technique using 10-0 nylon suture. The opposite side was repaired using fibrin adhesive. The results of the repair were assessed at 12 weeks. Functional assessment of nerve regeneration was performed in those rats with intact repair sites. Nerve-muscle twitch strengths were not significantly different (p greater than 0.05) between nerves repaired using suture and fibrin adhesive; however, compound active potential parameters were significantly better in nerve grafts repaired using suture technique (p less than 0.05).
The authors present a case of methaemoglobinaemia of acute onset, with an unusually protracted course. The long persistence of this disorder led to a search for the cause which was eventually traced to medication with dapsone. The latter was found to be inappropriately being taken by the patient instead of an antispasmodic that had been prescribed for a spinal condition; this was because the tablets had been incorrectly labelled and dispensed in a pharmacy. The patient took increasing doses of the presumed 'antispasmodic' tablets as they seemed to lack clinical effect, thus further exacerbating the toxic consequences. Moreover, the patient brought his wrongly labelled tablets into hospital and was allowed to use them there, contrary to normal hospital policy. As treatment for the methaemoglobinaemia both bolus and continuous infusions of methylene blue were used, which probably contributed to the severe haemolysis which followed. Furthermore, the development of a rare side effect of dapsone toxicity, namely that of a sensorimotor neuropathy, is reported.
BACKGROUND: Cannabis, in herbal form, is widely used as self-medication by patients with diseases such as HIV/AIDS and multiple sclerosis suffering from symptoms including pain, muscle spasticity, stress and insomnia. Valid clinical studies of herbal cannabis require a product which is acceptable to patients in order to maximize adherence to study protocols. METHODS: We conducted a randomized controlled crossover trial of 4 different herbal cannabis preparations among 8 experienced and authorized cannabis users with chronic pain. Preparations were varied with respect to grind size, THC content and humidity. Subjects received each preparation on a separate day and prepared the drug in their usual way in a dedicated and licensed clinical facility. They were asked to evaluate the products based on appearance (smell, colour, humidity, grind size, ease of preparation and overall appearance) and smoking characteristics (burn rate, hotness, harshness and taste). Five-point Likert scores were assigned to each characteristic. Scores were compared between preparations using ANOVA. RESULTS: Seven subjects completed the study, and the product with highest THC content (12%), highest humidity (14%) and largest grind size (10 mm) was rated highest overall. Significant differences were noted between preparations on overall appearance and colour (p = 0.003). DISCUSSION: While the small size of the study precludes broad conclusions, the study shows that medical cannabis users can appreciate differences in herbal product. A more acceptable cannabis product may increase recruitment and retention in clinical studies of medical cannabis.
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The authors report a Chinese boy with a DYT1 gene mutation having muscle stiffness, severe painful muscle spasm, myoclonus, and dystonia compatible with stiff child syndrome. Autoantibodies to glutamic acid decarboxylase (anti-GAD) were absent. His asymptomatic mother had a DYT1 mutation. His asymptomatic sister has diabetes mellitus and antibodies to glutamic acid decarboxylase but no DYT1 mutation.
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In an attempt to clarify the neurophysiologic changes that may follow a cerebral lesion in man, we have studied patients with recent and with long-standing hemiplegia from cerebral infarction. In patients with recent cerebral lesions, inhibition of the monosynaptic reflex by vibration is enhanced. In patients with long-standing cerebral lesions, this inhibitory mechanism is less effective and a comparison of the electrically and mechanically induced monosynaptic reflexes suggests that fusimotor drive may be increased. Related clinical findings are reduced muscle "tone" immediately after the lesion and increased muscle "tone" and exaggerated tendon jerks in patients with long-standing hemiplegia.
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We report a woman with Guillain-Barré syndrome who developed a flexion posture of the right arm and hand resembling upper motor neuron dysfunction. EMG demonstrated that involuntary peripherally generated continuous motor unit discharges caused the posture.
Spontaneous activity on the EMG examination is traditionally ascribed to disease of the lower motor neuron when present in muscles well below the level of para- or quadriplegia despite the absence of any detectable peripheral nerve injury. It is uncertain whether it reflects transient paralysis of transmission (related to clinical spinal shock) or irreversible postsynaptic damage. We performed serial EMG studies of lower extremities and paraspinal muscles on eight young, previously healthy adults, commencing 2 to 9 weeks after acute cervical cord injury. All had stimulated single-fiber EMG (SFEMG) studies at 6-month intervals to determine whether irreversible postsynaptic damage of the anterior horn cell had occurred. MRI and nerve conduction excluded patients with evidence of distal cord injury or peripheral neuropathy. All patients had spontaneous activity in all muscles tested, persisting after spinal shock had resolved. Jitter was present on SFEMG in three of eight patients 6 months after injury. Four of five patients retested 12 months after injury had abnormal jitter, including three who initially had normal SFEMG studies. We conclude that there is electrophysiologic evidence of trans-synaptic distal cord dysfunction following acute spinal cord injury. SFEMG studies suggest that anterior horn cell dropout occurs during the 1st year after injury.
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The author presents a discussion of research on cerebral arterial spasm. Arterial smooth muscle contraction, receptor and relaxation mechanisms are presented in the context of what is known about cerebral arterial spasm and the biochemistry of vascular smooth muscle. Several new experimental approaches are suggested and a theoretical biochemical basis for the idea that damage to the artery alone could cause cerebral arterial spasm is postulated. Methods of determining cerebral arterial spasm and the need for a quantitative, in vivo method are discussed and the question of an irreversible stage of cerebral arterial spasm is considered. Finally, the problems associated with the delivery of a potentially successful treatment to the cerebral arterial smooth muscle cells are examined.
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Muscular fatigue mechanisms were partially analyzed in patients with pyramidal lesions by using a computer device on line with a conventional electromyograph. Both the normal and the affected side were compared with control groups. The recordings were done throughout a ten minutes period and the maximal M wave was also measured at the starting and at the end of the procedure. The findings suggested that central events play a major role in the development of muscular fatigue in spastic muscles due to pyramidal damage.
Using reaction time paradigm, the effect of repetitive passive motion (RPM) on the initiation of fast knee extension was analyzed in seven normal subjects and 10 patients with paraparesis. Before and after 5 min RPM of the responding lower extremity, i.e., alternate flexion and extension of the knee and the hip with frequency of 0.5 Hz, the following five variables were examined: premotor time (PMT), latency from sound stimulus to initiation of EMG activities of the rectus femoris; tension lag time (TLT), period between onset of EMG activities and rise of tension; contraction time (FTmax); maximum tension (Tmax); and rate of tension development (RTD, Fmax/FTmax). In the normal group, PMT decreased significantly after RPM, whereas the other four variables did not show any change due to RPM. In the patient group, shortening of both PMT and FTmax after RPM was significant and Fmax tended to be small. These results suggested that RPM of an extremity induces behavioral alertness when the afferent pathway from moving parts to the higher center is not interrupted and also that RPM modulates abnormal pattern of motor neuron activities at the spinal level.
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