A 5-year-old Birman cat presented with paraparesis associated with a fracture of the third thoracic vertebra and was managed conservatively. Voluntary function was regained over the next 6 months, but the cat was referred 4 years after the trauma because of recurrence of hindlimb paresis and ataxia. Magnetic resonance imaging (MRI) showed a spinal arachnoid cyst at the level of the fourth thoracic vertebra, which was treated surgically by dorsal laminectomy and durectomy, and hindlimb function subsequently recovered. The cat re-presented 4 years later for recurrent hindlimb paresis. Myelography and computed tomography-myelography (CT-M) showed dorsolateral pooling of cerebrospinal fluid (CSF) at the previous laminectomy site. The neurological signs after the second surgery improved, but not as much as after the first surgery and the cat remained ataxic with moderate paresis. Seven months later repeat CT-M revealed an atrophic spinal cord, but negligible pooling of CSF at the previous site of the arachnoid cyst. The cat could walk, but was being treated for self-induced trauma of the left hindlimb that was thought to be related to paraesthesia. The neurological signs gradually deteriorated over 3 months and the cat was euthanased.

Inferior alveolar nerve (IAN) injury induces persistent ectopic pain which spreads to a wide area in the orofacial region. Its exact mechanism remains unclear. We investigated the involvement of nitric oxide (NO) in relation to ectopic orofacial pain caused by IAN transection (IANX). We assessed the changes in mechanical sensitivity of the whisker pad skin following IANX, neuronal nitric oxide synthase (nNOS) expression in the trigeminal ganglion (TG), and the functional significance of NO in relation to the mechanical allodynia following intra-TG administration of a chemical precursor to NO and selective nNOS inhibitors. IANX induced mechanical allodynia, which was diminished by intra-TG administration of selective nNOS inhibitors. NO metabolites and nNOS immunoreactive neurons innervating the lower lip were also increased in the TG. Intra-TG administration of nNOS substrate induced the mechanical allodynia. The present findings suggest that NO released from TG neurons regulates the excitability of TG neurons innervating the whisker pad skin, and the enhancement of TG neuronal excitability may underlie ectopic mechanical allodynia.

Gas-phase clustering reactions of halide ions (X- = F-, Cl-, Br-, and I-) with ethylene (C2H4) and propylene (C3H6) were studied with a pulsed electron beam mass spectrometer. Bonding energies of all cluster ions were found to be less than 10 kcal/mol, i.e., no anion-initiated polymerization of C2H4 and C3H6 took place. For the cluster F-(C2H4)n, a small gap in the binding energy is observed between n = 4 and 5 suggesting that the first shell is completed with n = 4. For larger halide ions, the bond energies for the clusters X-(C2H4)n were found to be nearly n independent. For Cl-(C3H6)n a steep decrease in binding energies was observed between n = 2 and 3 and n = 3 and 4. The structure of the cluster ions was investigated by ab initio calculations. X-(C2H4)n complexes were calculated to have hydrogen-bond geometries regardless of the identity of the halide ions, and bidentate (chelate) type geometries of X-(C3H6)1 were found.