A case of meningococcal meningitis that was difficult to treat owing to concurrent ventriculitis.

A 64-year-old male came to our hospital emergency department with fever and consciousness disturbance. Culture tests of blood and spinal fluid samples revealed meningococci (Neisseria meningitidis), and we made a diagnosis of meningococcal meningitis. Brain magnetic resonance imaging (MRI) findings revealed ventriculitis. Ceftriaxone was administered for 17 days, however, relapse was noted after that was discontinued, with neutropenia and renal impairment thought to be adverse reactions to the beta-lactam antibiotic. Hence, treatment was switched to oral administration of moxifloxacin for a total of 12 weeks, including in an outpatient setting. After moxifloxacin was discontinued, no side effects or relapse were seen, and treatment was ended. Although antibacterial agents generally show favorable effects for meningococcal meningitis, we consider that sufficient antimicrobial therapy is difficult in cases complicated with ventriculitis.

[A case of alien hand syndrome after right posterior cerebral artery territory infarction].

We report a 63-year-old right-handed man who presented an alien hand syndrome (AHS). He complained of clumsiness of his left hand and admitted to our hospital. On the first examination, he presented left homonymous hemianopia, left spatial neglect and left limb ataxia, but neither paralysis nor sensory impairment. A few days after, he complained that his left hand was controlled by someone else, and we considered this phenomenon as AHS. At that time, he lost sensation of almost all modalities including deep sensation on his left upper and lower limb. Magnetic resonance image examination was performed, and it showed acute cerebral infarction at right posterior cerebral artery territory including right thalamus (ventral posterior lateral nucleus). Generally, AHS is caused by left mediofrontal and callosal lesion (frontal type AHS), or by callosal with bilateral frontal or without frontal lesion (callosal type AHS). However, some cases were reported that they presented AHS after damage of the basal ganglia, right thalamus, right occipital or inferior parietal lobe. Some authors described this phenomenon as "sensory" or "posterior" type AHS. In such cases, included our case, we speculate that sensory impairment causes AHS. Especially in our case, AHS might be caused by not only the sensory impairment but also by left homonymous hemianopia and left spatial neglect. So, because of these symptoms, our patient could not recognize the motion of the left hand, and presented AHS. We think that this "sensory" or "posterior" type AHS should be distinguished from frontal and callosal type AHS.

[A case of relapsing myelitis associated with hypocomplementemia, presenting with Lhermitte sign enhanced by truncal flexion].

A 36-year-old woman suffered from steroid-responsive relapsing myelitis associated with hypocomplementemia, thrombocytopenia, and anti-cardiolipin antibody. At the second attack of paraplegia, neck flexion in a supine position induced uncomfortable dysesthesia radiating into the ulnar side of the bilateral forearms. Both truncal and neck flexion resulted in painful dysesthesia down into both lower limbs also. Cervical MRI showed 2 gadolinium-enhanced dorsal-dominant lesions in the spinal cord at C 5/6 and C 6/7 disc levels. Enhancement of Lhermitte sign by truncal flexion might be useful to detect multiple lesions in the dorsal column.