CCR5 deficiency in aged mice causes a decrease in bone mass

The CC chemokine receptor 5 (CCR5) is a G protein-coupled receptor that regulates chemotaxis and effector functions of immune cells. It also serves as the major co-receptor for the entry of human immunodeficiency virus (HIV). Recently, CCR5 inhibitors have been developed and used for the treatment or prevention of HIV infections. Additionally, it has been identified that CCR5 controls bone homeostasis by regulating osteoclastogenesis and the communication between osteoblasts and osteoclasts. However, the effects of CCR5 inhibition on bone tissue in elderly patients are unknown. This study aimed to examine the bone phenotype of aged CCR5 knockout (KO) mice. Femoral and tibial bones were isolated from 12-month and 18-month old wild-type (WT) and CCR5 KO mice, and microcomputed tomography and histology analyses were performed. Twelve-month-old CCR5 KO mice exhibited a decreased trabecular bone mass and cortical bone thickness in both femoral and tibial bones compared with age-matched WT mice. Eighteen-month-old mice also showed a decreased trabecular bone mass in femurs compared with control WT mice, but not in tibial bones. Unlike in 12-month-old mice, the cortical margin of femurs and tibias in 18-month-old mice were rough, likely because they were aggravated by the deficiency of CCR5. Overall, our data suggest that the deficiency of CCR5 with aging can cause severe bone loss. When CCR5 inhibitors or CCR5 inactivating technologies are used in elderly patients, a preventive strategy for bone loss should be considered.

A Case of Seizure Induced by Levothyroxine Intoxication in Euthyroidism

No abstract available.

The central conduction time in posterior tibial and pudendal nerve somatosensory evoked potentials

The somatosensory evoked potentials (SEPs), following stimulation of both the posterior tibial nerve (PTSEP) and pudendal nerve (PNSEP), comprise of the lumbar negative, subcortical and cortical potential. These can be used to assess the long somatosensory pathway, including peripheral, intraspinal and intracranial conduction along the entire length. This study aimed to compare the central conduction time between the PTSEP and the PNSEP, and to investigate the relationship between the intraspinal and intracranial conduction time in the SEP pathway. The SEPs following stimulation of the posterior tibial nerve at the ankle and the pudendal nerve at the shaft of the penis were analyzed in 20 normal male subjects. The central conduction of the PNSEP was found to be slower than that of the PTSEP (p <0.05). This difference is due to a delay in conduction rather than that of intracranial conduction.

Paraplegia in Leptospirosis

Leptospirosis is an acute generalized infectious disease caused by spirochetes of the genus Leptospira. The clinical forms of leptospirosis in Korea include asymptomatic form, influenza like form, pulmonary form, hepatic form, renal failure form, Weil's disease, and rash form. However, neurological involvement in leptospirosis is rare. We have recently experienced an interesting case of leptospirosis with flaccid paraplegia. A 73 year-old man presented with walking difficulty, voiding difficulty, fever, and myalgia for 10 days. A positive serologic test for leptospirosis was demonstrated by a passive haemagglutination test. An electrophysiological study showed evidence of denervation with minimal motor nerve conduction slowings, indicating an axonal degeneration. The weakness improved gradually after conservative treatment.

Temporal Bone Magnetic Resonance Imaging Study in Hemifacial Spasm

BACKGROUND: Hemifacial spasm (HS) has been attributed frequently to vascular compression of facial nerve root exit zone from brainstem. A recent brain CT scan study showed that patients with HS had narrower posterior fossa than normal controls. However, cause relationship between narrowed posterior fossa and vascular tortuosity is unknown. METHODS: In 25 patients with HS and 29 controls, using temporal bone MRI, we measured petrous angle (PA) and pons diameter index (PDI) to define correlation between severity of posterior fossa narrowing and compression to brainstem. We compared severity of narrowing of posterior fossa between patients with and without tortuous arteries in posterior fossa. We also compared degree of narrowing of posterior fossa and clinical severity of HS. RESULTS: The mean (+/-standard deviation) of PA of 24 patients with HS (115.5 +/-6.0 degree) was significantly smaller than that of controls ( 118.6 +/- 4.8 degree). The mean (+/-standard deviation) of PDI of patients with HS (82.5 +/-4.7%) was significantly greater than that of controls (77.3 +/-3.7%). However, there was no correlation between PA and PDI in patients with HS. There was no correlation between degree of narrowing of posterior fossa and clinical severity of HS. CONCLUSIONS: Patients with HS have narrower posterior fossa as compared with controls. However, narrow posterior fossa does not seem to be a single important factor causing deformity of brainstem or tortuous arteries in posterior fossa.

Single oral levodopa challenge test in de novo patients with idiopathic Parkinson's disease and multiple system atrophy

BACKGROUND: In the previous literature, single oral levodopa challenge test has been reported as one of the methods differentiating multiple system atrophy (MSA) from idiopathic Parkinson's disease (IPD). However many of the patients included in these studies had been on levodopa treatment for a variable period when they were examined. We performed this study to determine the value of single oral levodopa challenge test in differential diagnosis between IPD and MSA. METHODS: After a single oral dose of SinemetR(25/250), we assessed the improvement of motor function in 54 de novo patients with parkinsonian symptoms (33 with IPD and 21 with probable MSA). We measured the time taken to finish 20 taps with unilateral hand on two marks separated 20 cm apart and to walk 10 meter from a sitting position and return. Such performances were assessed 5 times before the medication, every 15 min for first 2 hrs after the medication, and then every 30 min for the next 4 hrs. RESULTS: The mean of the age, mean of the duration of disease and mean of the Hoehn and Yahr scale score were not significantly different between the patients with IPD and those with MSA. The mean of the unified Parkinson's disease rating scale score between the patients with IPD and MSA was not significantly different. Baseline scores of the hand and the walking performance were not significantly different. The median of the time interval between the levodopa intake and maximum beneficial effects, mean of the objective improvement at the peak, and mean of the amount of maximum subjective improvement comparing to the baseline was not significantly different between the patients with IPD and MSA. Also there were no significant differences in all measurements between the patients with striatonigral and olivopontocerebellar type of MSA. CONCLUSIONS: These findings suggest that single oral levodopa challenge test is not so helpful for the differential diagnosis between de novo patients with IPD and MSA.