Brain biopsy to aid diagnosis of neuro-Behçet's disease: Case report and literature review.

Central nervous system involvement in Behçet's disease (Neuro-Behçet's disease: NBD) has been reported to present diverse clinical and pathological manifestations. A few cases presenting with neurological symptoms preceding other systemic features are difficult to be diagnosed. Here we suggest the clinical benefit of brain biopsy with a case of NBD initially presenting neurological symptoms.

[Slowly progressive expanding hematoma in the Basal Ganglia: a report of 3 cases and a literature review].

We demonstrate and discuss slowly progressive expanding hematoma (SPEH) in the basal ganglia, which expands over 2 weeks. To our knowledge, there have been only 5 cases of sudden-onset SPEH of the basal ganglia. To this, we add 3 cases admitted our hospitals because of putaminal hemorrhage within 1.5 hours of onset. All hematomas exhibited "2 components of hematoma sign" on initial CT scans, which we termed the "TCH sign" characterized as an anterolateral fluid portion and a posteromedial solid portion. Follow-up CT scans revealed gradual expansion of the fluid component of the hematoma without rebleeding for the subacute phase. Two cases were treated surgically. The first case, a 47-year-old man, underwent ultrasonically guided hematoma aspiration on day 17 and the second case, a 37-year-old man, underwent hematoma removal by craniotomy on day 23 after onset. Their postoperative courses were uneventful. The third case, a 57-year-old man, improved without surgical treatment and the hematoma dissolved completely within 2 months. To an extent, the TCH sign on a CT scan can be related to SPEH. We reviewed previous reports, including those an chronic expanding intracerebral hematomas and chronic encapsulated intracerebral hematomas, and concluded that it requires approximately 1 month for encapsulation of the hematoma to emerge. We suggest a possible progressive mechanism of SPEH. At first, the hematoma is divided into a fluid and a solid portion. Local generation of osmotically active molecules by clot degradation may allow intravascular fluid to escape into the fluid portion of the hematoma. Edema fluid with leakage via the disrupted blood-brain barrier may also aggravate the fluid portion of the hematoma. The continuing inflammatory response leads to the emergence of a hematoma capsule similar to the membrane observed in cases of chronic subdural hematoma, followed by the secondary causes of hematoma expansion. We discuss feasible timing and surgical treatment methods.

Efficacy of the American Heart Association/American Stroke Association guidelines for ultra-early, intentional antihypertensive therapy in intracerebral hemorrhage.

Whether the intentional antihypertensive therapy recommended by the American Heart Association/American Stroke Association (AHA/ASA) guidelines has clinical benefit for patients who have acute spontaneous intracerebral hemorrhage (ICH) has yet to be proven. We retrospectively reviewed the clinical charts of 175 patients with putaminal or thalamic ICH with acute hypertension to examine the correlation between the efficacy of antihypertensive therapy within 3 hours of onset, hematoma expansion (HE) after hospitalization and clinical outcome. The aim of the antihypertensive therapy was to achieve and maintain a systolic blood pressure of 120 mm Hg to 160 mm Hg until the second CT scan. The mean arterial pressure (MAP) after admission was the average MAP values measured every hour for the first 3 hours of hospitalization or until the second CT scan, if this was performed within the same timeframe. Thirty-two (18.3%) patients were found to have HE. Prior to the second CT scan, antihypertensive medications were administered to all patients without any major complications. A multiple logistic regression analysis revealed that a MAP of >110 mm Hg after admission was the only variable independently associated with HE (odds ratio [OR] = 3.455; 95% confidence interval [CI] = 1.510-8.412; p = 0.004). Modified Rankin Scale scores of < or = 3 on day 30 were significantly more common in those patients without HE (p = 0.002). Our findings suggest that there are clinical benefits, by the prevention of subsequent HE, in maintaining a MAP level lower than that recommended by the AHA/ASA (110 mm Hg) after hospitalization for patients who have ICH.

[Dysfunction of multiple cranial nerves in cephalic tetanus--case report].

A 77-year-old man non-immunized to tetanus suffered head trauma on the right side when he tumbled from a height of approximately 2m. Five days later, he experienced difficulty in opening his mouth and developed right ptosis. He was referred to our hospital 2 days post-ictus. The patient suffered trismus, and developed right Horner's syndrome with in a week. Symptoms due to multiple cranial nerve palsies were observed: right inferior oblique muscle weakness, reduced right corneal reflex, right facial palsy, dysphagia, and abnormal tongue movements. Neuroimages (computed tomography, magnetic resonance imaging, and angiography) of the basal skull and internal carotid arteries revealed no abnormalities. From the symptoms associated with his infected head wound and clinical follow-up, we suggested that he had cephalic tetanus. We subsequently conducted the following treatments: debridement of the wound, intravenous infusion of antitetanus human immunoglobulin (AHI), intrathecal AHI infusion, and systemic administration of benzylpenicillin. His condition improved with these treatments, and without any complications such as autonomic nervous system dysfunction or classical tetanic spasms. This case suggests that we should consider the possibility of cephalic tetanus when we observe a patient with cranial nerve palsy associated with injury.

Brain uptake, pharmacokinetics, and tissue distribution in the rat of neurotoxic N-butylbenzenesulfonamide.

The pharmacokinetics, cerebrovascular permeability, and tissue distribution of the neurotoxic plasticizer N-butylbenzenesulfonamide (NBBS) were determined in rats. A stable isotope-labeled form ([(13)C(6)]NBBS) was used to circumvent ubiquitous contamination that was evident whenever the native form was measured. Plasticizer decline in plasma, following an iv dose of 1 mg/kg, was described by a triexponential decay function. NBBS was cleared from plasma at a rate of 25 ml/min/kg, and 24 h after administration, plasma concentrations represented 0.04% of the administered dose. These data suggest rapid elimination and uptake into tissue; however, NBBS was not accumulated by any of the tissues studied (i.e., liver, kidney, muscle, adipose tissue, and brain). Given the critical interest in NBBS neurotoxicity, the brain uptake of [(13)C(6)]NBBS was further explored in experiments using the in situ brain perfusion technique. During perfusion with protein-free saline for 15-30 s, the single-pass brain extraction for free [(13)C(6)]NBBS was very high (73-100%) with a unidirectional blood-brain barrier transfer constant (K(in)) of > 0.08 ml/s/g. No significant differences were found in [(13)C(6)]NBBS content among the measured brain regions. Plasma protein binding (70%) only slightly lowered the single-pass brain extraction to 48%. In summary, the results demonstrate that NBBS distributes rapidly to tissues, including brain. Though highly lipophilic with a Log octanol/water partition coefficient of 2.17 +/- 0.09, brain:blood ratios (2:1) for NBBS were consistent throughout the experimental duration, with little indication of accumulation.