注射后臀肌挛缩症的分型及手术治疗

目的 探讨注射后臀肌挛缩症的分型、分型与病变的关系和手术范围。方法 根据臀肌挛缩症特有的临床表现.分为轻型、中型、重型：根据分型术中分别显露髂胫束、臀大肌、臀中肌、臀小肌至髋关节囊后方。结果 153例均手术治疗，随访141例、随访时间1～10年，平均6．8年，优良率96．5％。结论 将臀肌挛缩症进行分型？更有利于准确的区别病情轻重程度，选择相应的手术范围和评估预后。     

Improvements in healthcare and cost benefits associated with botulinum toxin treatment of spasticity and muscle overactivity

Spasticity is a widespread, disabling form of muscle overactivity affecting patients with central nervous system damage resulting in upper motor neurone syndrome. There is a range of effective therapies for the treatment of spasticity (e.g. physical, anaesthetic, chemodenervation and neurolytic injections, systemic medication and surgery), but all therapies must be based on an individualized, multidisciplinary programme targeted to achieve patient goals. Appropriate therapy should be based on the extent and severity of spasticity, but spasticity and its consequences, regardless of presentation or cause, are commonly treated with systemic agents. This may be ill-advised as systemic treatment is associated with many undesirable effects. In particular, elderly patients with post-stroke spasticity are at risk from the central adverse effects of systemic medication (e.g. sedation and gait disturbance), which make them more susceptible to falling, with an associated increased risk of fracture. The rising costs of fracture care and its sequelae are fast becoming an international problem contributing to high healthcare expenditure. Botulinum toxin type-A (BoNT-A) treatment is highly effective for some of the more common forms of spasticity and muscle overactivity, and has a favourable profile when compared with systemic agents and other focal treatments. Therefore, the clinical benefits of BoNT-A treatment outweigh the apparent high costs of this intervention, showing it to be a cost-effective treatment.     

Treatment of muscle spasticity in patients with cerebral palsy using BTX-A: a pilot study

This study was designed to verify the safety and efficacy of botulinum toxin type A (BTX-A) used as a neuromuscular block on spastic masticatory musculature of children with cerebral palsy. Six patients who had spastic-tetraplegic cerebral-palsy, aged 5 to 20 years were selected. All patients had spasticity of the jaw muscles, bruxism, lower lip trauma, limited mouth opening, and difficulties in cleaning the oral cavity. The patients were sedated under general anesthesia, while the dentist injected the masseter and temporalis muscles bilaterally with 150 and 75 units of BTX-A each. Clinical examinations were conducted at 7, 14, 30, and 90 days after the initial appointment. We found statistically significant decreases in muscle spasticity and bruxism ( p = 0.002), improved inter-incisal opening ( p = 0.002), improved oral hygiene ( p = 0.031), and less lower lip trauma ( p = 0.060) after the neuromuscular blocking.     

Mechanisms of tizanidine action on spasticity

This investigation estimated the mechanisms of tizanidine action on spasticity using a battery of neurophysiological methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with tizanidine-mean daily dose 15.8 ± 5.6 mg for a mean of 23.3 ± 4.8 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of neurophysiological methods was used to analyze different mechanisms of spasticity: for alpha motoneuron excitability – the F wave parameters; for presynaptic inhibition – the ratio of H reflex amplitudes before and after vibration of the achilles tendon (Hvibr/Hmax); for common interneuron activity – the flexor reflex parameters. Our results revealed that tizanidine reduces spastically increased muscle tone, but has no influence on muscle force, tendon reflexes, Babinski sign and ankle clonus. Tizanidine is supposed to act by increasing the presynaptic inhibition and decreasing of alpha motoneuron excitability. When spasticity has decreased presynaptic inhibition and increased motoneuron excitability, it is better to treat with tizanidine.     

Botulinum toxin injection in patients with hereditary spastic paraparesis

In an open label study, we analyzed the efficacy of botulinum toxin injection at the lower limbs of patients with hereditary spastic paraparesis (HSP). Fifteen patients who showed disabling spasticity with no or poor effect of oral treatment were recruited consecutively. Botulinum toxin was injected (400 U; Botox^®) into the spastic muscles identified by clinical examination (equinus, varus, and pathological hip adduction). Patients were regularly assessed from the first day to the fifth month: spasticity (Ashworth), motor strength, range of movements, Functional Ambulation Categories (FAC), gait parameter, Rivermead Motor Assessment, self-analysis of benefit and satisfaction. We observed a moderate and significant ( P  < 0.05) reduction of ankle plantar flexor and hip adductor spasticity, with a partial increase in the range of the active and passive motion at the ankle and in gait velocity. At an individual level, six of 15 patients showed an increase in gait velocity. The FAC and RMA did not change. Patients often reported partial improvement in foot position and lower limb propulsion, and fair satisfaction. In conclusion, botulinum toxin injection can be effective in HSP patients with relatively ancient spasticity. This technique can be introduced into the therapeutic panel, which also includes physiotherapy, oral treatment and baclofen pump.     

围套式显微血管减压术治疗面肌痉挛

使用围套式显微血管减压术治疗面肌痉挛５０例。采用耳后斜行小切口，分离压迫血管后，用涤沦片包绕面神经根起始部并用银夹固定，术后４９例痉挛停止。本法并发症少，无死亡。术后随访３个月至１０年均无复发。根据术中发现将“责任血管”分为４型：接触型、压迫型、粘连包绕型和贯穿型。讨论了手术适应证、要求及并发症的预防等。     

New type of spinocerebellar degeneration syndrome in a northern Swedish population

A follow-up investigation of 24 patients with hereditary spasticity in a geographically isolated northern Swedish population, first examined by Böök (1953), was performed. Fifteen of them were dead. During the period from 1950–1972 five new cases of spastic syndromes were diagnosed in this population. The patterns of clinical symptoms and the genetic associations between the new and 24 previously reported patients with spastic syndromes were analyzed. Three of the five new cases had a specific syndrome. This starts in the first years of life with ataxia, which is followed by dysarthria, spasticity and jerky intention tremor. Initially the patients are mentally normal, but there seems to be slight mental deterioration through the years. The disorder is a progressive spinocerebellar degeneration with autosomal recessive inheritance.