[Campylobacter jejuni meningitis in an immunocompetent adult male].

A 51-year-old man with no underlying disease was referred to our hospital, complaining of mild headache. In May 2004 he developed headache of sudden onset in the occipital region and neck pain. He visited our hospital the following morning. At the first visit, there was no fever and only an analgesic was prescribed. The headache alleviated, with only occasional mild episodes thereafter. However, 2 days later, the headache aggravated again, associated this time with elevated body temperature (38 degrees C). The patient visited our hospital and a lumbar puncture was performed; examination of the cerebrospinal fluid revealed marked elevation of the cell count (mononuclear cell-dominant). The patient was admitted to the hospital and started on treatment with cefotaxime and acyclovir. However, the symptoms persisted and 10 days later, the cerebrospinal fluid culture yielded a growth of Campylobacter jejuni (C. jejuni). The antibiotic was therefore changed to panipenem, which resulted in prompt resolution of the symptoms. To the best of our knowledge, meningitis caused by C. jejuni in an immunocompetent adult is extremely rare. This case highlights the importance of bearing in mind the possibility of C. jejuni meningitis in a patient of meningitis associated with mononuclear cell-dominant pleocytosis of the cerebrospinal fluid.

[A case of herpes simplex virus encephalitis recurring after a seven-year interval].

In January 2008, a 59-year-old man with a history of diabetes mellitus was admitted to our hospital with herpes simplex virus (HSV) encephalitis of his right temporal lobe, which was diagnosed by PCR testing of his cerebrospinal fluid (CSF). He was treated with intravenous acyclovir for three weeks and made a full recovery. On discharge, his CSF was negative for HSV on PCR testing. Seven years later, in March 2015, the man was readmitted to our hospital with fever, disorientation, and nominal dysphasia. Diffusion-weighted MRI of his head revealed a high-intensity area in his left temporal lobe. Testing of his CSF revealed a moderately increased monocyte count and HSV on PCR testing, so he was diagnosed with recurrent HSV encephalitis. He was treated with intravenous acyclovir for three weeks. On discharge, his CSF was negative for HSV on PCR testing, but he had mild residual amnesia. There have been few reports of HSV encephalitis with viral reactivation recurring after a long remission period in adults. This case illustrates the need for prolonged follow up of individuals with HSV encephalitis in order to detect recurrences.

Diabetic neuropathy and nerve regeneration.

Diabetic neuropathy is the most common peripheral neuropathy in western countries. Although every effort has been made to clarify the pathogenic mechanism of diabetic neuropathy, thereby devising its ideal therapeutic drugs, neither convinced hypotheses nor unequivocally effective drugs have been established. In view of the pathologic basis for the treatment of diabetic neuropathy, it is important to enhance nerve regeneration as well as prevent nerve degeneration. Nerve regeneration or sprouting in diabetes may occur not only in the nerve trunk but also in the dermis and around dorsal root ganglion neurons, thereby being implicated in the generation of pain sensation. Thus, inadequate nerve regeneration unequivocally contributes to the pathophysiologic mechanism of diabetic neuropathy. In this context, the research on nerve regeneration in diabetes should be more accelerated. Indeed, nerve regenerative capacity has been shown to be decreased in diabetic patients as well as in diabetic animals. Disturbed nerve regeneration in diabetes has been ascribed at least in part to all or some of decreased levels of neurotrophic factors, decreased expression of their receptors, altered cellular signal pathways and/or abnormal expression of cell adhesion molecules, although the mechanisms of their changes remain almost unclear. In addition to their steady-state changes in diabetes, nerve injury induces injury-specific changes in individual neurotrophic factors, their receptors and their intracellular signal pathways, which are closely linked with altered neuronal function, varying from neuronal survival and neurite extension/nerve regeneration to apoptosis. Although it is essential to clarify those changes for understanding the mechanism of disturbed nerve regeneration in diabetes, very few data are now available. Rationally accepted replacement therapy with neurotrophic factors has not provided any success in treating diabetic neuropathy. Aside from adverse effects of those factors, more rigorous consideration for their delivery system may be needed for any possible success. Although conventional therapeutic drugs like aldose reductase (AR) inhibitors and vasodilators have been shown to enhance nerve regeneration, their efficacy should be strictly evaluated with respect to nerve regenerative capacity. For this purpose, especially clinically, skin biopsy, by which cutaneous nerve pathology including nerve regeneration can be morphometrically evaluated, might be a safe and useful examination.

[A case of pure-sensory-type Guillain-Barré syndrome with galactocerebroside antibody].

A 67-year-old man noticed paresthesia in both legs in July 2011. Three days later, he was found on a street where he was unable to stand up. On admission, the deep sensation in both legs was severely disturbed, but their muscle strength remained normal. Cranial nerves and autonomic functions were normal. The deep tendon reflexes were diminished in both legs. Magnetic resonance imaging of the spine was normal. Motor nerve conduction studies revealed normal conduction velocity, amplitude, and F-wave latency. However, sensory nerve conduction studies revealed severe reduction of amplitude in the upper and lower extremities. Cerebrospinal fluid analysis showed normal cell counts but elevated protein levels. Screening for glycolipid antibodies showed a selective increase of galactocerebroside (Gal-C) IgG antibody. We diagnosed him with pure-sensory-type Guillain-Barré syndrome (GBS). We administered intravenous immunoglobulin (IVIG) for 5 days. After IVIG therapy, his gait disturbance improved slightly but the disturbance of deep sensation remained severe and he was transferred to a rehabilitation ward 53 days after admission. To the best of our knowledge, this is the first report of a case of pure-sensory-type GBS with Gal-C antibody alone. This case suggests a close relationship between Gal-C antibody and sensory nerve disturbance.

[Bilateral ageusia caused by right thalamic infarction].

A 58-year-old man noticed left hemiparesis at 01:00 pm on a particular day in March 2006. Because his symptoms developed gradually, he was referred to the emergency room of our hospital at 05:00 pm and was admitted with the diagnosis of cerebral infarction. While he presented slight left hemiparesis involving the face, impairment of sensation was not apparent. Diffusion-weighted magnetic resonance imaging of the head showed a high-intensity area in the ventromedial area in the right thalamus. The patient was treated with anticoagulant and edaravone, and his symptoms resolved on hospital day 3. When he began eating, he noticed that he was unable to distinguish tastes. On day 5, we performed taste examination using a commercial kit. The taste sensation on both sides of his tongue was severely affected, while the touch sensations in the mouth and olfaction were preserved. His symptoms improved spontaneously and resolved on hospital day 15. This is the second case report of bilateral ageusia caused by right thalamic infarction. Our study indicates the importance of the right thalamus in taste sensation involving both sides of the tongue.