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.     

Two classes of spontaneous GABA-mediated miniature synaptic currents in cultured rat hippocampal neurons.

Amplitude and time course of spontaneous gamma-aminobutyric acid (GABA)-mediated miniature postsynaptic currents (MPSCs), recorded in cultured embryonic hippocampal neurons in presence of either tetrodotoxin (TTX) or increased external [Mg2+/Ca2+] ratio, revealed that they form two classes. The distribution of the most commonly recorded MPSCs was skewed both in terms of peak amplitude and rise-time (skew-MPSCs, mode: 70-120 pS). Another, less frequent class (mode: 1-3 nS) formed bell-shaped (bell-MPSCs) amplitude and rise-time distributions. MPSC initial slope did not correlate with rise time, indicating that smaller MPSCs were not electrotonically attenuated. Bell-MPSCs did not result from the integration of skew-MPSCs and both classes appeared to be composed of subunits.     

Cortical Reorganization Allows for Motor Recovery after Crossed Cerebrocerebellar Atrophy

The authors report the case of a 33-year-old woman who exhibited, at the age of 17, a left-sided hemiplegia, which was followed by good motor recovery, though with a permanent deficit in fine finger movements. She had a widespread loss of neural tissue in the right hemisphere (crossed cerebrocerebellar atrophy), including (1) marked atrophy and thinning of the precentral and postcentral gyri; (2) widespread deep white matter destruction, including the corticospinal tract; and (3) crossed cerebellar atrophy. Except over the supplementary motor area (SMA), transcranial magnetic stimulation did not elicit motor evoked potentials in the affected hand. Nevertheless, during opening and closing of the affected hand, functional magnetic resonance imaging showed an activation of the lesioned primary sensorimotor cortex (SMC), as well as of the intact SMA and the parietal areas, but not of the ipsilateral motor areas. The authors speculate that recovery was achieved by a motor command generated in the SMC and the parietal cortex, passing through corticospinal axons originating in the SMA.