Analysis of B-cell clonality in the hepatic tissue of patients with Sjögren's syndrome.

OBJECTIVE: We investigated the incidence of B-cell clonality in the minor salivary gland and liver (extra-glandular lesion) of patients with Sjögren's syndrome (SS). We also compared B-cell clonality in the minor salivary gland and liver in the same individuals, and compared its incidence among patients with various liver diseases, such as primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH). METHODS: A minor salivary gland biopsy was performed on 35 patients with SS (30 patients with primary SS, and five patients with secondary SS). A liver biopsy was performed on nine patients with SS associated with bile duct lesions, two patients with PBC, one patient with AIH, one patient with drug-induced liver dysfunction, and three patients with viral hepatitis. DNA was extracted from each tissue sample and then subjected to Polymerase Chain Reaction (PCR). B-cell clonality was analysed by assessing the rearrangement of the immunoglobulin heavy chain (IgH) gene by PCR. RESULTS: B-cell clonality was confirmed in the minor salivary gland biopsy sample in 23 of the 35 patients (65.7%), and in the liver biopsy sample (non-exocrine organ involvement) in seven of the nine patients (77.8%). The presence or absence of B-cell clonality was investigated in both the minor salivary gland and liver in seven patients, but B-cell clonality was confirmed in both tissues in only one patient, and the pattern of clonality in the minor salivary gland differed from that in the liver. B-cell clonality was detected in the liver of the PBC and AIH patients. CONCLUSION: B-cell clonality is a phenomenon that is observed frequently in SS lesions in the salivary glands and liver. The appearance of B-cell clonality was shown to be attributable to antigen-driven clonal expansion.

Protective effect of benidipine against the abnormal electrical activity in single ventricular myocytes of the guinea pig under simulated ischemic conditions and reperfusion.

Induction of electrical abnormalities (EAs) under simulated ischemic conditions and after reperfusion was measured from single cardiac myocytes isolated from guinea pig ventricle using whole-cell voltage or current clamp with perforated patch variation. Conditions of simulated ischemia were produced by the exchange of medium from the standard one oxygenated with 95% O2-5% CO2 gas (pH 7.4) to the modified one, which contained no glucose, 8 mM K+ and 30 mM sodium-D,L-lactate and was gassed with 90% argon-10% CO2 (pH 6.6). Under the simulated ischemia for 20 min, EAs such as delayed afterdepolarization, early afterdepolarization, automatic activity or transient inward current were observed in about 37% of myocytes driven electrically at 1 Hz. Irreversible hypercontracture occurred in myocytes of 10% or less. Upon reperfusion with the standard solution, EAs and hypercontracture were observed in about 43% and 22% of cells, respectively. Glibenclamide-sensitive current was detected during ischemia, but tended to be enhanced during reperfusion. Amplitude of Ca2+ current and ATP-sensitive K+ current after reperfusion varied widely with time and from cell to cell. When myocytes were pretreated for 10 min with 10 nM benidipine, a 1,4-dihydropyridine derivative Ca2+ blocker, the incidence of EAs and hypercontracture was markedly reduced, suggesting the protective effect of benidipine against cardiac cell injury during ischemia and reperfusion.

[A male case of Sjögren's syndrome presenting with generalized lymphadenopathy and swelling of both lacrimal and salivary glands which responded remarkably well to an administration of corticosteroids].

A 68-year-old man noticed severe oral dryness and a submandibular swelling. Sjögren's syndrome (SS) was diagnosed based on microscopic findings of a labial salivary gland biopsy although both anti-SS-A and anti-SS-B antibodies were negative. In addition, hypergammaglobulinemia (IgG 7940 mg/dl) and hypocomplementemia were pointed out and he was admitted to our department. On admission cervical, mediastinal, and abdominal lymph nodes swelling were detected together with enlargement of lacrimal and salivary glands. Lymphoproliferative disorders associated with SS were highly suspected. Biopsied specimens of his lacrimal gland and cervical lymph node disclosed neither malignant cells nor monoclonal proliferation of lymphocytes. An administration of corticosteroids caused rapid diminution in size of lacrimal glands, salivary glands, and lymph nodes. Both lacrimation and salivation recovered, and hypergammaglobulinemia and hypocomplementemia returned to normal after treatment. The characteristics of this case were an atypical onset in an elderly man, the negativity of anti-SS-A and anti-SS-B antibodies, and reversibility of dryness by corticosteroid treatment. These findings suggest that the pathogenesis of this case may be different from typical SS.

Effects of lactate on intracellular pH and hypercontracture during simulated ischemia and reperfusion in cardiac ventricular myocytes of the guinea pig.

Effects of lactate on changes in intracellular pH (pHi) and contractility during simulated ischemia and reperfusion were examined in single myocytes of the guinea pig cardiac ventricle. The conditions of simulated ischemia were produced by the exchange of perfusion medium from the standard one oxygenated with 95% O2-5% CO2 gas (pH 7.4) to one containing no glucose, 8 mM K+, and 0-30 mM sodium-D,L-lactate and was gassed with 90% argon - 10% CO2 (pH 6.6). The pHi was decreased by the simulated ischemia from approx. 7.3 to approx. 6.9 regardless of lactate concentration, while the rate of pHi decrease was increased by lactate in a concentration-dependent manner. The contraction induced by electrical stimulation disappeared faster in the presence of lactate. The incidence of irreversible hypercontracture of myocytes was significantly reduced by 20-30 mM lactate. The overshoot of pHi to approx. 7.7 and excess contractions were induced by withdrawal of lactate during the reperfusion, but not observed when lactate was continuously present. The recovery of normal contractility during reperfusion was facilitated by lactate. It can be concluded that lactate added to or removed from the perfusion medium increases the rate of pHi change under the simulated ischemia and reperfusion, respectively, and that the continuous presence of lactate reduces cell injury under these conditions.

Effects of K+ channel modulators on the relationship between action potential duration and Ca2+ transients in single ventricular myocytes of the guinea pig.

Effects of K+ channel modulators, cromakalim and E4031 [1-[2-(6-methyl-2-pyridyl)-ethyl]-4-(4-methylsulfonylaminobenzoyl) piperidine], on the relationship between the action potential duration (APD) and Ca2+ transients were examined in single myocytes isolated from guinea pig cardiac left ventricle. Application of cromakalim decreased APD at 90% repolarization (APD90) and Ca2+ transient elicited at 0.5 Hz (IC50s=0.6 and 3 microM, respectively). Application of 0.3 microM E4031 increased these parameters by 110% and 45%, respectively. Under voltage-clamp, the relation between the duration of depolarization to 0 mV and Ca2+ transients could be described by the sum of two exponential components; the time constants were approximately 5 and 280 msec, respectively. The first component was abolished by 10 microM ryanodine, suggesting the involvement of Ca2+-induced Ca2+ release (CICR). Neither cromakalim nor E4031 directly affected Ca2+ current and Ca2+ transients under voltage clamp. When APD was changed by K+ channel modulators, the relation between APD90 and Ca2+-transients was almost similar to that obtained by changing the depolarization duration under voltage-clamp. CICR was changed significantly only when APD90 was markedly shortened by cromakalim. The extensively prolonged AP and Ca2+ transient in the presence of E4031 were reduced by an addition of cromakalim. It is concluded that these two K+ channel modulators can significantly alter the AP-induced Ca2+ transient mainly by changing APD, which regulates both Ca2+ influx and extrusion.

[A case of systemic lupus erythematosus overlapping with progressive systemic sclerosis accompanied by deposition of AA amyloid in the stomach].

A 52-year-old woman was admitted to our department because of fever and dysphasia in November 1994. She had noticed Raynaud's phenomenon, arthralgia, and stiffness in the skin for the past 20 years without receiving specific treatment. A diagnosis of progressive systemic sclerosis (PSS) was made based on the presence of sclerosis of the skin, sclerodactyly, pulmonary fibrosis, and the dilatation of the lower esophagus. It was also confirmed that systemic lupus erythematosus (SLE) overlapped based on the presence of an oral ulcer, polyarthralgia, leukocytopenia, renal dysfunction, positive tests for antinuclear antibodies and anti-DNA antibodies. A gastric biopsy specimen revealed amyloid deposits which showed green birefrigence by Congo red staining under polarized light microscopy. The disappearance of the green birefrigence after potassium permanganate treatment indicated that the deposits consisted of AA amyloid. No amyloid deposits were detected in the rectum or the kidney. The average of the SAA level in active SLE patients is 174 micrograms/ml in our department and the SAA level in the present case was 280 micrograms/ml. Although AA amyloidosis is rarely associated with SLE and PSS, a long-term elevation of SAA level could cause the development of amyloidosis even in the cases of SLE and PSS.

[A case of dermatomyositis associated with asymptomatic pneumomediastinum].

A 20-year-old woman initially presented with edematous erythema in the upper eyelids in December 1995. She was admitted to our department in January 1996 because of fever and multiple arthralgia. She was given a diagnosis of dermatomyositis (DM) on the basis of characteristic eruption, elevated serum level of creatine kinase, and increased inflammatory reaction. Chest computed tomography (CT) revealed faint interstitial changes in the left lower lung. The administration of corticosteroid caused improvement in the patient's condition and the interstitial lesion in the lung. Although she was asymptomatic, chest CT showed pneumomediastinum in the pretracheal space and concomitant pneumothorax around left bronchus. Those changes spontaneously disappeared 4 weeks later without treatment. The occurrence of pneumomediastinum in patients with DM has been well documented as an indicator of poor prognosis in the literature. It seems that a severe pulmonary disorder could secondary cause pneumomediastinum. In our case, however, the pneumomediastinum developed in spite of the low grade severity of the pulmonary lesion. This finding suggested that the pneumomediastinum may be associated with the development of DM itself.

[A case of Sjögren's syndrome associated with inflammatory pseudotumor of the liver].

A 71-year-old man had noticed a dry sensation in the mouth with swelling of bilateral parotid glands in 1988. He was given a diagnosis of Sjögren's syndrome (SS) on the basis of characteristic findings of sialography and a minor salivary gland biopsy. He was admitted to our department in Febuary 1995 because of general fatigue of 2 month's duration. Laboratory data showed both positive anti-SSA and anti-SSB antibodies, liver dysfunction, hypoalbuminemia, and thrombocytopenia. Abdominal CT and MRI demonstrated a 2-cm intrahepatic mass (S 6) with enhanced areas at the periphery. The liver biopsy yielded fragments from the intrahepatic mass and hepatic parenchyma. The former was composed of plasma cells, lymphocytes, and histiocytes, compatible with the diagnosis of inflammatory pseudotumor of the liver. The pathological diagnosis of the latter specimen was primary biliary cirrhosis, although antimitochondrial antibody was negative. The intrahepatic mass gradually decreased in size without treatment. Inflammatory pseudotumor is considered to be a benign inflammatory condition simulating a neoplasma and the possibility of an autoimmune reaction is suggested on the basis of etiology. This is the first report of an inflammatory pseudotumor associated with Sjögren's syndrome developing in the liver. The inflammatory pseudotumor should be considered as a possible diagnosis in cases where the tumor is embedded in the liver.

[Isolated infranuclear oculomotor nerve palsy caused by traumatic midbrain hemorrhage: case report].

Traumatic brain stem hemorrhage is often associated with severe head injury and has a high mortality rate. When these patients survive, the midbrain syndromes are usually complicated. The authors report an unusual case with isolated oculomotor nerve palsy caused by acute traumatic midbrain hemorrhage. A 50-year-old woman was brought to Kobe City General Hospital because she had fallen off a bicycle and hit the face severely on the ground. On admission, she was drowsy. Neurological examination revealed normal muscle tone in all extremities without motor or sensory disturbance. Deep-tendon reflexes were symmetrical and there were no Babinski signs present. The left eye lid dropped and the left pupil was 5.5 mm in diameter without responses to light. The eye ball was slightly deviated to the left side on neutral position. There were no extraocular movements except for abduction to the left side. The right pupil measured 3 mm in diameter and was reactive to light promptly. Plane skull films failed to show fractures. Computed tomography (CT) scan 30 minutes after the accident suggested the existence of a hemorrhage in the anterior tegmentum of the left midbrain. Four hours later, a midbrain hemorrhage was diagnosed by consecutive CT scans. She was alert on the next day, although the third nerve palsy remained. The left blephaloptosis disappeared gradually during the next month. At 6 months after the accident, the left pupil was still dilated and did not react to light, either directly or indirectly. Medial gaze recovered almost fully, while both upward and downward movements were still limited. The mechanism of the isolated oculomotor nerve palsy in this case was discussed with a review of the related literature.

Effects of ONO-1101, a novel beta-antagonist, on action potential and membrane currents in cardiac muscle.

Direct effects of ONO-1101 ¿(-)-[(S)-2,2-dimethyl-1,3-dioxolan-4-yl]methyl-3-[4-[(S) -2-hydroxy-3-(2-morpholino carbonylamino)ethylamino] propoxy]phenylpropionate monohydrochloride), a novel beta-antagonist, on action potential parameters and membrane currents, and its beta adrenoceptor antagonism were examined in cardiac muscle. Action potential-parameters in papillary muscle of reserpinized animals and membrane currents recorded from single myocytes obtained from guinea pig and rabbit hearts were not affected by 1 to 100 microM ONO-1101. On the other hand, ONO-1101 markedly inhibited the potentiation of Ca current by isoproterenol in single cardiac myocytes of the guinea pig. The concentration-response relationship of Ca current for isoproterenol was shifted to the right. This effect resembled that of esmolol, which is also a beta adrenoceptor antagonist. A Schild plot analysis revealed the slope and pA2 value of each antagonist (ONO-1101, 0.94, 8.0; and esmolol, 0.98, 7.3, respectively) and demonstrated that ONO-1101 is about 5 times more potent than esmolol as a beta-antagonist. Two other effects of isoproterenol: 1) potentiation of delayed rectifier K current and 2) activation of chloride current, were also inhibited by ONO-1101. The time required for 50% removal of beta-antagonism of ONO-1101 and esmolol after the washout was estimated as 4 and 6 min, respectively, in depolarized papillary muscle. These results suggest that ONO-1101 is a potent beta-antagonist whose effects were removed quickly by washout. When applied at what is thought to be a clinical dosage, ONO-1101 had no direct effects on action potential-parameters and membrane currents in cardiac muscle. These characteristics of ONO-1101 suggest that this agent may be effective in clinical use.

[Bilateral chronic subdural hematomas presented with subarachnoid hemorrhage: report of two cases].

Computed tomography (CT) findings of chronic subdural hematomas are usually diagnostic, unless hematomas are isodense and bilateral. The authors report two cases of bilateral chronic subdural hematomas, in which CT scans on admission were both misdiagnosed as delayed subarachnoid hemorrhage (SAH). The first case was a 43-year-old woman who suffered from a sudden onset of headache and nausea. She had no past history of head injury. CT scans on admission did not clearly reveal the Sylvian fissures and the mesencephalic cistern, without any mass effects. A lumbar puncture demonstrated xanthochromic cerebrospinal fluid (CSF), which was considered to be responsible for her headache. Cerebral angiography performed on day 4 failed to demonstrate any cerebral vascular disorders. Follow-up CT scans on day 7 demonstrated a high density lesion in the left subdural space. Magnetic resonance images (MRIs) confirmed a diagnosis of bilateral chronic subdural hematomas. Removal of the hematomas cleared all signs and symptoms smoothly. The second case was a 44-year-old man who was referred from another hospital because of xanthochromic CSF found by lumbar puncture. He began to suffer headache and be subject to vomiting 6 weeks earlier and these symptoms were still present on the day of admission. CT scans did not clearly show the cerebral cisterns without mass effects. Because the second lumbar puncture showed xanthochromic CSF again, SAH from aneurysm was suspected. However, emergency cerebral angiography failed to demonstrate cerebral aneurysms. MRI performed two days later demonstrated bilateral chronic subdural hematomas. Following surgery, the patient improved immediately and was discharged from hospital without any complications. In both cases, a retrospective study of the angiograms revealed the evidence of bilateral avascular areas over the convexities in the venous phase. The reason why these subdural hematomas were missed at the time of angiography was due to too much attention being paid to the arterial phase in an effort aimed only at identifying cerebral aneurysms. There are no reports of chronic subdural hematoma which demonstrated sudden onset of headache associated with xanthochromic CSF.

[Benign intracranial hypertension and continuous CSF pressure monitoring: case report].

The authors report a case of benign intracranial hypertension (BIH) treated with a ventriculoperitoneal shunt. A 62-year-old man was referred to the Kobe City General Hospital with several episodes of transient visual obscuration. Neurological examination on admission revealed bilateral papilledema and a right lower quadrantic homonymous hemianopsia. Computed tomography (CT) showed normalized ventricles and a low-density area in the left occipital lobe without mass effects. From the findings of magnetic resonance images (MRIs) the occipital lesion was diagnosed as a chronic intracerebral hematoma. Because the hematoma did not show mass effects. BIH was suspected to be responsible for the papilledema. In spite of intravenous administration of dexamethasone and glycerol for a week, a lumbar puncture showed an opening pressure of 360mm H2O. Several subsequent lumbar punctures failed to improve intracranial hypertension. The mean opening pressure of the last 6 punctures was 392mm H2O. The mean terminal pressure dropped to 32mm H2O after removal of 10m/ of cerebrospinal fluid (CSF). A spinal subarachnoid drainage was inserted at the level of L4-L5 interspace for continuous CSF pressure monitoring. The mean CSF pressure ranged from 20 to 40mmHg. The continuous recording showed typical B waves frequently and plateau waves (A waves) occasionally. Removal of only 8m/ of CSF caused significant pressure reduction immediately. Then, pressure returned to the predrainage level about 35 minutes later. These findings supported the diagnosis of BIH. A ventriculoperitoneal shunt was inserted, which resulted in rapid and complete resolution of the papilledema. Postoperative CSF monitoring returned to normal pressure and waves. This case emphasizes the usefulness of continuous CSF pressure recording for the diagnosis and subsequent therapy of BIH.

Electrophysiological changes in substantia nigra after striatal infarction.

The GABAergic efferent pathway from the striatum exerts inhibitory control on the substantia nigra pars reticulata (SNR) neurones. We studied sequential changes in spontaneous single-unit activities in the ipsilateral SNR 1 h, 1 day, 7 days and 14 days after striatal infarction induced by middle cerebral artery occlusion (MCAO) in rats. Compared with a sham-operated group, there was no change in the firing rate 1 h after MCAO, and one day after MCAO the mean firing rate decreased. The firing rate of SNR neurones at 7 and 14 days after MCAO was significantly reduced compared with the sham-operated group. Only two neurones (sham-operated group and 1 h after MCAO group) fired with high frequency. Histological examination revealed degeneration of the ipsilateral SNR 7 and 14 days after MCAO. Our results indicated that SNR neuronal degeneration accompanied by striatal ischaemia does not simply depend on hyperexcitation due to the activation of a disinhibition mechanism.

[Leiomyosarcoma metastatizing to the sphenoid bone presenting exophthalmos: a case report].

A rare subcutaneous leiomyosarcoma metastatizing to the sphenoid bone and presenting exophthalmos is reported. A 56-year-old female presented with protrusion of the right eye and a slowly growing lump on the right temporal region. Six years previously, she had undergone removal of a subcutaneous mass in the back, which was histologically diagnosed in another hospital as leiomyosarcoma. She had undergone four other operations, including removal of local recurrences and a right renal metastasis. On admission, physical examination showed no neurological deficits. Craniogram revealed an osteolytic lesion without marginal sclerosis in the right sphenoid bone. CT showed an inhomogeneously enhanced mass with irregular expansion of the diploic space, which was partly invading the right orbit. MRI demonstrated an extradural mass in the right sphenoid region, which was slightly low-intense in T1-weighted image, high-intense in T2-weighted image, and inhomogeneously enhanced by Gd-DTPA. Right external carotid angiogram showed a highly vascular stain fed by meningeal arteries. Radionuclide bone scintigram showed multiple high-uptake areas in the left femoral head, the ribs, and the sphenoid bone. Preoperative embolization of the tumor vessels fed by the external carotid artery was performed. Following this procedure, the tumor stain disappeared completely. The tumor was totally excised with minimal bleeding through an orbitozygomatic approach. The tumor was loosely adherent to the dura and periorbit. The bone defect was covered with a methylmethacrylate resin plate. the histological examination demonstrated fascicular arrangement of the spindle shaped cells with mitotic figures. Immunohistochemical studies showed that most tumor cells were positive for actin and myosin, but negative for desmin.(ABSTRACT TRUNCATED AT 250 WORDS)

[Primary oculomotor nerve palsy due to head injury: analysis of 10 cases].

Ten cases of primary oculomotor nerve palsy due to head injury are presented. All ten patients had a dilated, non reactive pupil. Seven had complete oculomotor palsy. Two had partial extraocular palsy or blepharoptosis and one had neither extraocular palsy nor blepharoptosis. The initial ophthalmoplegia was recognized immediately after trauma. Nine patients had severely impaired consciousness on admission, but eight patients recovered fully within two months after the traumatic event, while one patient remained disoriented. Emergency CT scan on admission showed mass lesions in no patients except one who had a hematoma measuring 3 cm in the frontal lobe, but had no herniation sign. Patients with complete oculomotor palsy had a high incidence of traumatic SAH (71%) or skull fracture (57%). Recovery from third nerve palsy was not so good. The follow-up period extended from 3 months to 18 months. Of the 10 patients, none recovered completely from third nerve palsy. The prognoses of blepharoptosis, external ophthalmoplegia and internal ophthalmoplegia were analyzed separately. The recovery rates were 78%, 44% and 20%, respectively, the internal ophthalmoplegia showing poorest recovery. We discuss the mechanism of direct injury to the oculomotor nerve.

[A case of deep sylvian meningioma presenting temporal lobe epilepsy].

A rare case of deep sylvian meningioma is presented. A 62-year-old woman was admitted to our hospital because of one year history of temporal lobe epilepsy. She had no neurological deficit except for EEG abnormality. CT scans showed a small calcified mass in the left temporal lobe adjacent to the sylvian fissure with no enhancement by contrast medium. The mass was low-intense in both T1- and T2-weighted MR images. The T1-weighted image after the infusion of gadolinium revealed enhancement of the middle cerebral artery adjacent to the mass, similar to dural tail sign. Left external carotid angiography did not show any tumor stain nor the dilatation of the middle meningeal artery. Left internal carotid angiography disclosed enlarged middle cerebral artery without tumor stain. A left frontotemporal craniotomy was performed and the mass was totally removed. The tumor was located deep in sylvian fissure without any connection to the dura or ventricular system, which was firmly adherent to the middle cerebral artery. The histological examination of the surgical specimen revealed a psammomatous meningioma. Meningiomas are believed to originate from the arachnoid cap cells and can arise from various intracranial locations where arachnoid cap cells exist. The majority of them are attached to the dura, choroid plexus, or the tela choroidea. Only eleven cases of deep sylvian meningiomas have been presented in the literature. We have reviewed the clinical and radiological findings in such meningiomas. MR findings in deep sylvian meningioma have not been described.(ABSTRACT TRUNCATED AT 250 WORDS)

[Non-traumatic cerebrospinal fluid rhinorrhea associated with hydrocephalus: a case report].

We report an unusual case of non-traumatic cerebrospinal fluid rhinorrhea associated with aqueductal stenosis and hydrocephalus. The patient was a 10-year-old girl who suddenly developed massive CSF rhinorrhea following severe edema of the left side of her face. CT scan showed marked dilatation of the lateral and third ventricles and enlarged sphenoid sinus of water density, extending to the lateral wall of the left orbit and to the left pterygoid fossa. Immediately after the onset of CSF rhinorrhea, ventricular drainage was performed, but the rhinorrhea persisted. Ventriculography revealed predominant flow of the contrast medium into the left temporal horn and abnormal collection in the sphenoid sinus. Coronal CT scan did not show any focal bony defect, but a thin layer was seen in the base of the left middle fossa. Exploration of the skull base in the left middle fossa was performed through a left frontotemporal craniotomy. An irregular bony defect measuring 7 x 12mm was then found in the anterolateral floor of the middle fossa and the dura was also perforated there. Brain tissue including the temporal horn protruded through the bony defect into the sphenoid sinus. After excision of the herniated brain tissue, repair was accomplished by packing muscle into the bony defect and covering the dural defect with fat reinforced by coating with fibrin glue. Postoperatively, the CSF rhinorrhea has stopped and the edema of her face has disappeared. We discuss the etiology of this unusual spontaneous CSF leakage through the middle fossa and the abnormally enlarged sphenoid sinus.

[Traumatic anterior cerebral artery aneurysm difficult to distinguish from congenital cerebral aneurysm: case report].

We report the case of a 29-year-old woman in whom a saccular aneurysm of the distal anterior cerebral artery developed following head trauma due to a car accident. She was semicomatose on admission but had no lateralizing motor signs. Reflexes were symmetrical, with bilateral extensor toe sign. X-ray of the skull showed no fracture but CT scans demonstrated a large frontal hematoma and interhemispheric bleeding. Initial cerebral angiography performed within 12 hours of trauma showed a small protrusion on the pericallosal portion of the left pericallosal artery with no branching point nearby. Angiography was repeated on the 9th day after admission and confirmed the presence of a saccular aneurysm of the pericallosal artery, which had been visible as a small protrusion on the initial angiogram. Traumatic aneurysm was suspected and successful neck clipping of the aneurysm was performed on the 14th day. Preoperative CT and angiographic findings could not rule out a congenital aneurysm but the histological study of the specimen confirmed that it was a traumatic false aneurysm. We discussed the diagnosis and the etiology of posttraumatic aneurysm.

Functional changes in thalamic relay neurons after focal cerebral infarct: a study of unit recordings from VPL neurons after MCA occlusion in rats.

We evaluated neuronal and histological changes of thalamic neurons 1, 4, 7, and 14 days after middle cerebral artery (MCA) occlusion in rats. After the somatosensory evoked potentials (SEPs) were measured from the cerebral cortex, the thalamic relay neuronal activities were recorded with a glass microelectrode following repetitive electrical stimulation of the contralateral forepaw at frequencies ranging from 1 to 50 Hz. In approximately 95% of the occluded rats, the ipsilateral somatosensory cortex and/or the subcortical somatosensory pathway developed infarct, resulting in SEP loss. We evaluated unit data from rats with abolished SEPs. The average firing rate of the nucleus ventralis posterolateralis (VPL) neurons in response to 25 stimulations at 30 Hz was significantly reduced to 0.1 spike/stimulus 1 day after MCA occlusion. In sham-operated rats, the same stimulation produced 0.7 spike/stimulus. The firing rate recovered to 0.4 spike/stimulus at 30-Hz stimulation 4 and 7 days after occlusion. This was followed by resuppression (0.1 spike/stimulus) 14 days after occlusion. Histological study revealed some abnormal neurons in the ipsilateral thalamus 7 days after occlusion. We were unable to find normal-shaped neurons in the VPL 14 days after occlusion. The present study demonstrates that cortical infarct produces functional and morphologic changes that gradually and progressively affect the ipsilateral thalamus, although incomplete transient recovery of somatosensory transmission may occur.