Effects of a dual L/N-type calcium channel blocker cilnidipine on blood pressure, pulse rate, and autonomic functions in patients with mild to moderate hypertension.

The current study was conducted to examine the effects of cilnidipine, a dual L/N-type calcium channel blocker, on blood pressure, pulse rate, and autonomic functions in patients with mild-to-moderate hypertension. Sixteen patients with mild-to-moderate hypertension (8 males and 8 females; 44-72 years of age) were treated with cilnidipine (10 mg/day) for 3 months. Before and after the treatment, the following measurements were conducted; beat-to-beat blood pressure during late phase II and overshoot phase of the Valsalva maneuver, the Valsalva ratio, heart rate response to deep breathing, systolic and diastolic blood pressure, and pulse rate. The head-up tilt test was also performed before and after the treatment. Cilnidipine significantly decreased either the systolic or diastolic blood pressure from 151 +/- 15 mmHg to 129 +/- 14 mmHg or 84 +/- 11 mmHg to 71 +/- 9 mmHg, respectively. For pulse rate, there were no significant changes during therapy. Beat-to-beat blood pressure during late phase II and overshoot phase of the Valsalva maneuver indicated significant improvements in both figures. The heart rate response to deep breathing and the Valsalva ratio indicated no significant differences during therapy. Before and after the treatment, no orthostatic hypotension was observed during the head-up tilt test. The current study revealed that cilnidipine significantly decreases blood pressure with improving autonomic functions while having no adverse effects on heart rate response and pulse rate.

[Acute meningoencephalitis caused by Streptococcus pneumoniae, mimicking acute disseminated encephalomyelitis].

A 57-year old woman had a five-day history of cough and high fever followed by abnormal behavior and headache with signs of meningeal irritation. A cerebrospinal fluid (CSF) exam revealed polymorphonuclear pleocytosis. Streptococcus pneumoniae was cultured from the patient's CSF and serum. Clinical features and laboratory investigations supported a diagnosis of pneumococcal meningoencephalitis. After treatment with intravenous meropenem (MEPM), the patient's laboratory data improved and her neck stiffness disappeared, but a brain MRI showed white matter lesions in the bilateral frontal and temporal lobes. The patient responded to pulse therapy with intravenous methylprednisolone (1 g/day), carried out over three days: she recovered neurological function and her MRI lesions resolved. We report a case of acute meningoencephalitis caused by Streptococcus pneumoniae, mimicking acute disseminated encephalomyelitis (ADEM). We suggest that pneumococcal infection is one of the pathogenetic factors in ADEM.

[Vasospastic cerebral infarction induced by smoking: a case report].

A 31-year-old man was admitted to our hospital because of frequent transient ischemic attacks (TIAs). The first episode involved right amaurosis fugax and left hemiparesis at the age of 26. Treatment with aspirin did not reduce frequency of TIA. Cerebral angiography at the age of 29 showed a significant stenosis in the right internal carotid artery with a string-of-beads-like appearance. This pattern suggested fibromuscular dysplasia. TIAs persisted despite of prophylactic medication with ticlopidine. When cerebral angiography was repeated at age of 28, stenosis in the right internal carotid artery had almost disappeared. At the present admission, MR angiography showed stenoses of bilateral internal carotid arteries and middle cerebral arteries, which had disappeared when the study was repeated after 5 days. Vasospasm was suspected based on reversibility of changes in both conventional and MR angiographies. The patient was treated with a calcium antagonist to prevent vasospasm as well as cessations of smoking. The patient had a history of 20 cigarettes a day for 12 years and neurologic deficits often occurred after smoking. Therefore, smoking is considered to be a main trigger for TIAs in this patient.

[Internal ophthalmoplegia in acute oropharyngeal palsy with anti-GQ1b and anti-GT1a IgG antibodies].

A patient with acute oropharyngeal palsy associated with internal ophthalmoplegia was reported. A 13-year-old boy had fever and diarrhea for two days. Ten days after resolution of these symptoms, he noticed difficulty in speaking (day 1). Neurological findings on day 4 included bilateral mydriasis, right abducens nerve palsy, nasal voice with absent pharyngeal reflex. Although superficial sensation was preserved, vibratory sensation was reduced in distal limbs. Tendon reflexes were generally absent. Neither ataxia nor dysautonomia was seen. Serum anti-glycolipid antibody assay on day 4 disclosed elevated IgG antibodies to GQ1b and GT1a. His cerebrospinal fluid on day 21 contained 6 mononuclear cells/microl with 137 mg/dl of total protein. Nerve conduction study on day 5 showed minimal sensory nerve involvement. Quantitative sudomotor axon reflex test was normal in the lower extremities. Low dose pilocarpine eyedrops dilated his pupils. Although mild cerebellar-like ataxia appeared on day 5, intravenous immunoglobulin (0.4 g/kg/day for four days) rapidly improved his neurological abnormalities. IgG anti-GQ1b antibody might contribute not only oropharyngeal weakness but also internal ophthalmoplegia in this patient.

Intravenous immunoglobulin preparation attenuates neurological signs in rat experimental autoimmune neuritis with the suppression of macrophage inflammatory protein -1α expression.

To clarify the mechanism of action of an intravenous immunoglobulin (IVIG) preparation in chronic inflammatory demyelinating polyneuropathy, the effects of IVIG were investigated using an experimental autoimmune neuropathy model in the rat. IVIG significantly suppressed the progression of neurologic signs and sciatic nerve conduction velocity with the inhibition of inflammatory cell infiltration, mainly of macrophages, to the peripheral nerves. A significant suppressive effect on the expression of macrophage inflammatory protein 1-α (MIP-1α) was simultaneously observed in the nerves. These results suggest that IVIG is effective for inflammatory demyelinating polyneuropathy by inhibiting the chemotactic factor of macrophages.