[Diagnosis of acute cerebral infarction using diffusion-weighted imaging by low field (0.2 T) magnetic resonance image].

The purpose of this study is to confirm the diagnosis of acute cerebral infarction on diffusion-weighted imaging using low field (0.2 T) magnetic resonance image(MRI). Acute cerebral infarctions in 51 patients were examined on diffusion-weighted imaging using low field MRI within 48 hours after clinical symptoms. Diffusion-weighted imaging was examined using line scan method. Twenty-four cases were cortical infarction, and twenty-two cases were perforating infarction. In five cases out of 51 cases, ischemic regions were not detected as abnormal high signal intensity area on diffusion-weighted imaging. Four cases of no abnormal detection were transient ischemic attack, and the other one was a perforating infarction. The earliest detection time in cortical infarction cases was 1 hour and 20 minutes. On the other hand, the earliest detection time in perforating infarction cases was 3 hours. Detective ability for acute cerebral infarction on diffusion-weighted imaging by low field MRI was depending on both size and lesion of infarction. That is to say, either small size or brain stem infarction was hard to detect. Thin slice and vertical slice examination for the infarction may improve to diagnose in low field MRI. Our conclusion is acute cerebral infarction was able to be diagnosed on diffusion-weighted imaging by low field as well as high field MRI.

[Serial changes of SPECT and MRI findings in a patient with herpes simplex encephalitis].

We report a case of herpes simplex encephalitis in which the patient was repeatedly examined by magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT). The patient was a 36 year-old woman who had been transferred to our institution 6 days after the onset of symptoms with mild consciousness disturbance, nuchal rigidity, and high fever. Cerebrospinal fluid examination revealed an elevated mononuclear cell count with normal sugar concentration. Intravenous aciclovir was started 7 days after the onset of symptoms. The initial plain computed tomography (CT) scans did not reveal any abnormal findings, but contrast enhanced CT the next day showed a slight enhancement effect around the affected middle cerebral artery. Serial MRI showed the initial high intensity lesion starting on the medial cortex of the temporal lobe, then spreading to throughout the entire temporal lobe. During this period SPECT showed a marked, broad hot spot in the temporal lobe. The medial temporal lobe was high density on the CT 15 days after the onset. As the encephalitic lesion spread more laterally, the hot spot on SPECT moved laterally and then decreased in activity. Eleven weeks after the onset, the MRI showed intracerebral vacuolization of the lesion and it appeared as a wide cold spot on SPECT. The cause of the hot spot seen in the acute period was thought to be vasoparalysis of the affected area rather than breakdown of the blood-brain barrier, or impaired washout of the isotope, because the SPECT images after acetazolamide administration showed the cold spot even in the subacute phase.

[Therapeutic effect of a mineralocorticoid in patients with hyponatremia of central origin].

Patients with hyponatremia of central origin were treated with a mineralocorticoid, and the therapeutic effect assessed. The subjects of this study were 14 patients (5 with subarachnoid hemorrhage, 2 with hypertensive intracerebral hemorrhage and 7 with head injury) who developed hyponatremia as a complication during their hospital stay for treatment of their intracranial lesions between March 1993 and April 1994. Hyponatremia of central origin was defined as serum Na+ levels below 135 mEq/l for at least two consecutive days with no other discernible etiology. The mineralocorticoid used was fludrocortisone acetate, and as a rule administration was started the day after the onset of hyponatremia. The mean interval until the onset of hyponatremia was 7.5 days, and the mean minimum serum sodium level was 125.7 mEq/l. The dose of fludrocortisone was 0.3 congruent to 0.6 mg/day, the mean period of administration 5.8 days, and route was via a stomach tube in 3 cases and by mouth in 11 cases. The therapeutic effect was good (improvement within 5 days) in 11 cases and fair (improvement in 5 to 8 days) in 3 cases. None of the patients manifested side effects. All of the patients had lower urinary sodium excretion than before administration, with the mean rate of decrease of 66.9%. Mineralocorticoids, which suppress natriuresis, are safe and effective in the treatment of hyponatremia of central origin. It appears that mineralocorticoid therapy may be aggressively tried in severe cases in which NaCl loading is ineffective.

[Subacute subdural hematoma: findings in CT, MRI and operations and review of onset mechanism].

Subacute subdural hematoma was investigated in terms of findings in CT, MRI and operations and of onset mechanism. The subjects were 7 cases of subacute subdural hematoma in which CT and MRI were performed during the past 5 year period. Subacute subdural hematoma here was defined as a nonoperated case with acute subdural hematoma, accompanied by subacute exacerbation 1-3 weeks after head trauma. The time from the injury to the onset averaged 13.7 days. CT revealed mixed density in 4 cases, low density in 3 cases and cerebral atrophy in all cases, with increasing mass sign due to the enlarged low density area. MRI revealed mixed intensity in 5 cases and high intensity in 2 cases, with increasing mass sign due to the enlarged high intensity area. Operation disclosed the outer membrane of the hematoma only in 1 case, but the inner membrane could not be identified in any case. Analysis of the hematoma contents showed a low hemoglobin concentrations and a high level of methemoglobin. Lack of outer membrane in cases with subacute subdural hematoma suggests that this is a different disease entity from chronic subdural hematoma. It is surmised that subacute subdural hematoma is the result of subdural effusion in the subacute stage, because, judging from the findings of CT and MRI each performed over time, cerebrospinal fluid is considered accountable for the increase in the mass sign.

[Therapeutic effect of mineralocorticoid in patients with hyponatremia of central origin].

Patients with hyponatremia of central origin were treated with a mineralocorticoid, and the pathogenetic mechanism of the hyponatremia was assessed based on the therapeutic effect obtained. The subjects were 14 patients (6 with subarachnoid hemorrhage, 3 with hypertensive intracerebral hemorrhage, 2 with cerebral infarct and 3 with head injury) who developed hyponatremia, as a complication during their hospital stay for their intracranial lesions from April to December 1992. Patients with serum Na levels below 135 mEq/l for more than 2 days with no other discernible etiology were defined as having hyponatremia of central origin. The mineralocorticoid used was fludrocortisone acetate, and as a rule administration was started the day after the onset of hyponatremia. When improvements occurred within 3 days, in 3 to 7 days, or 8 days or more efficacy was rated "excellent", "good" or "poor", respectively. The mean interval until the onset of hyponatremia was 10.4 days, its mean duration was 5.7 days, and the mean minimum serum sodium level was 129.5 mEq/l. The dose of fludrocortisone administration was 0.1 mg/day except for one patient who was treated with 0.3 mg/day. The mean period of administration was 3.7 days (range: 3 to 6 days), and the route was via a stomach tube in 5 cases and oral in 9 cases. The therapeutic effect was excellent in 9 cases, good in 3 cases and poor in 2 cases, the efficacy rate being 86%. None of the patients manifested side effects. Plasma atrial natriuretic peptide levels were above 100 pg/ml in 2 patients and 50-100 pg/ml in 8 patients and neither of the former 2 patients exhibited "excellent" efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

[Subacute subdural hematoma--reexamination of mechanism by CT and MRI findings].

We have already reported about the importance of establishing the concept of subacute subdural hematoma. But the mechanism by which this disease develops has not as yet been elucidated fully. In one case of subacute subdural hematoma, we were able to perform CT and MRI over time and obtained findings which were of use in studying the mechanism of development. The case was a 56-year-old male. He developed with seizure. CT on admission revealed acute subdural hematoma and subarachnoid hemorrhage. But neurological deficits were absent. So he was treated conservatively. On the 16th hospital day there appeared seizure, anisocoria and an increase in the mass sign due to subdural hematoma was noted on CT, so a diagnosis of subacute subdural hematoma was made. Cerebrospinal fluid was considered accountable for the increase in the mass sign judging from the findings of CT and MRI each performed over time. It was surmised that subdural effusion developed concurrently in the subacute stage. Three conditions, namely, presence of (1) arachnoid tear, (2) clots, (3) no intracranial hypertension are considered important as the mechanism by which subacute subdural hematoma develops.

[A study of plasma atrial natriuretic peptide, antidiuretic hormone and cerebral vasospasms in patients with aneurysmal subarachnoid hemorrhage].

The relationship between plasma atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) both of which show high values after subarachnoid hemorrhage and cerebral vasospasm was studied. The subjects were 23 patients who were admitted because of aneurysmal subarachnoid hemorrhage during three years from March, 1989 to March, 1992 and in whom plasma ANP and ADH levels could be determined over time. Cerebral vasospasm was evaluated by the finding of cerebral angiography, clinical symptoms, and presence or not of low density areas on CT. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less for two days or more. Angiographical vasospasm was found in 17 patients (85%), symptomatic vasospasm in 15 patients (65.2%), low density areas on CT in 9 patients (40.9%) and hyponatremia in 8 patients (34.8%). Symptomatic vasospasm was noted in 7 of the 8 patients (87.5%) with hyponatremia, low density areas on CT in 4 patients (50%), the detection rate being high. The plasma ANP and ADH levels were 76.7 +/- 32.1 pg/ml and 2.2 +/- 0.7 pg/ml respectively in the patients with symptomatic vasospasm against 38.3 +/- 21.3 pg/ml and 2.4 +/- 0.6 pg/ml respectively without symptomatic vasospasm, the plasma ANP level being significantly high in the patients with symptomatic vasospasm (p < 0.01). The plasma ANP and ADH were 71.2 +/- 33.8 pg/ml and 2.0 +/- 1.1 pg/ml respectively in the patients with low density areas on CT against 51.2 +/- 31.3 pg/ml and 1.8 +/- 0.5 pg/ml respectively without low density areas on CT.(ABSTRACT TRUNCATED AT 250 WORDS)

[Hyponatremia and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage].

We studied retrospectively the relationship between hyponatremia and cerebral vasospasm in 121 consecutive patients with aneurysmal subarachnoid hemorrhage. In 19 patients sodium levels fell below 130 mEq/l on at least two consecutive days. Hyponatremia developed at average 8.9 hospital day and lasted for 4.4 days. It was mild (126 to 130 mEq/l) in 15 patients, moderate (121 to 125 mEq/l) in 3 patients, and severe (116 to 120 mEq/l) in 1 patient. Cerebral vasospasm was evaluated by angiography, symptoms and CT finding. Angiographical vasospasm was found in 57 patients, symptomatic vasospasm in 38 patients and low density area on CT in 20 patients. Angiographical vasospasm developed in 15 of the 19 patients (78.9%) with hyponatremia, symptomatic vasospasm in 16 patients (84.2%), low density area on CT in 8 patients (42.1%), the difference being significantly high. (respectively, p < 0.01, p < 0.001 and p < 0.01 by chi-square test) Polyuria of 2500 ml or more immediately before the onset of hyponatremia developed in 14 patients (87.5%). When symptomatic vasospasm and hyponatremia coincided, there were only 4 patients in which symptomatic vasospasm was preceded by hyponatremia. So, it is difficult to predict the development of vasospasm from that of hyponatremia. This study found incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage to be significantly higher in patients who developed hyponatremia, which raised suspicion about the presence of dehydration. Hyponatremia with central origin generally remains asymptomatic, but it is important to treat positively when the pathology of cerebral vasospasm is taken into consideration.

[A study of plasma atrial natriuretic peptide, antidiuretic hormone and aldosterone levels in a series of patients with intracranial disease and hyponatremia].

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.

Subtemporal transpetrosal approach to ruptured midbasilar trunk aneurysm.

Aneurysms arising from the midbasilar trunk are not common, and surgical management of these aneurysms remains a difficult challenge to neurosurgeons because of its anatomic characteristics. The authors report on a patient with a ruptured aneurysm arising from the basilar artery at the origin of the anterior inferior cerebellar artery and projecting to the right and upward. The aneurysm was successfully treated by a subtemporal transpetrosal approach in an acute stage.

[CT and 123I-IMP SPECT findings of head injuries with hyponatremia].

CT and SPECT findings were examined and the relationship between development of hyponatremia and lesions was studied in cases who developed hyponatremia following head injury. Six cases of hyponatremia after head injury in the last two years were used as the subjects. SPECT was performed by the 123I-IMP intravenous injection method using Tomomatic 64. Slice 2 of 4 to 6 cm on the OM line in the early image was used as the subject site. The data of development of hyponatremia was 5.8 patients days, duration 9.2 days, minimum serum Na level 117.2 mEq/l and minimum plasma osmotic pressure 247.6 mOsm/lH2O. CT findings in the hyponatremic stage showed frontal subdural effusion in all the cases. SPECT findings revealed a decrease of CBF in the frontal region on both sides and in the central region. CBF in the central region also tended to improve at a time when hyponatremia improved. In hyponatremia after head injury, lesions are often found in the frontal region on CT, and CBF in the central region is also decreased bilaterally on SPECT, which is presumed to be concerned with the development of hyponatremia.

[Internal carotid artery stenosis and external carotid artery occlusion with unusual extracranial collateral pathway: case report].

A patient with stenosis of the internal carotid artery and occlusion of the external carotid artery associated with an unusual extracranial collateral pathway is presented. A 63-year-old man was hospitalized for sudden onset of black-out after urination. He was alert, and no neurological deficit was found. MRI showed multiple lacunae in the bilateral putamens. Cerebral angiogram demonstrated severe stenosis of the left internal carotid artery at its cervical segment and complete occlusion of the left external carotid artery at its origin. The ascending pharyngeal artery originated from the left internal carotid artery above its stenotic lesion and the superior thyroid artery originated from the left common carotid artery. The sternocleidomastoid branch from the left superior thyroid artery and the muscular branch from the left vertebral artery anastomosed with the muscular branch of the ascending pharyngeal artery. The ascending pharyngeal artery maintained patency of the internal carotid artery. It is important to perform vertebral angiography when there is proximal occlusion and severe stenosis of the internal carotid artery, and when the ascending pharyngeal artery has not been clearly identified as a branch from the ipsilateral external carotid artery on the common carotid angiogram.

[Serum ANP and ADH after subarachnoid hemorrhage and hyponatremia].

We determined serum atrial natriuretic peptide (ANP) and anti-diuretic hormone (ADH) on a time course basis in cases of subarachnoid hemorrhage and studied their influence on the development of hyponatremia. Twenty six cases of subarachnoid hemorrhage were admitted to our hospital in the past 1 year, and by the site of ruptured aneurysms, there were Acom 6 cases, ICA 6 cases, MCA 5 cases and VA BA 4 cases. Serum ANP and ADH levels were determined in the acute phase on Day 1-4, in the hyponatremia phase on Day 5-14 and in the chronic phase on Day 15 downward. Levels of not more than 130 mEq/l were regarded as hyponatremia. Cases showing other evident causes such as heart failure and renal insufficiency were excluded. In the normal control group (n = 20) which was admitted to this hospital for a close check-up, serum ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of more than 50 pg/ml were regarded as being abnormally high. 1) Hyponatremia was observed in 7 cases (26-9%); the day of onset was 11.9 hospital day. The duration was 5.0 days and the minimum serum Na level was 126.4 mEq/l. 2) The serum ADH level was high regardless of whether or not there was the development of hyponatremia in the acute phase but tended to decrease gradually and became normal in the hyponatremia phase. 3) The serum ANP level in the cases of hyponatremia was 40.7 +/- 9.1 pg/ml in the acute phase, 69.0 +/- 25.7 pg/ml in the hyponatremia phase and 40.2 +/- 21.5 pg/ml in the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

[An interesting case of pituitary apoplexy showing abnormality in water-electrolyte before and after surgery].

Cases which present abnormality in water-electrolyte before and after operation of pituitary adenoma are occasionally reported. The authors have encountered a case in which neurological symptoms became aggravated abruptly with pituitary apoplexy after admission, hyponatremia was noted before operation and polyuria, not hypotonic urine was observed after operation. As a result of an endocrinological examination which may have an influence on water-electrolyte (ADH, aldosterone, ANP, etc.) the ADH level in hyponatremia before operation was high at 6.8 pg/ml; so, it was taken as SIADH. According to a study at the time of polyuria after operation, the ADH level was normal at 2.4 pg/ml, the ANP level was abnormally high at 140 pg/ml and the specific gravity of the urine was kept at 1.010 or more. So, polyuria was considered due to abnormally increased content of serum ANP. In polyuria due to abnormally increased content of serum ANP, the osmotic pressure of the urine is maintained relatively well, which is a clinical feature evidently different from diabetes insipidus. After operation for pituitary adenoma, water-electrolyte should be controlled with polyuria due to abnormally increased content of serum ANP in addition to diabetes insipidus taken into consideration.

[Infarction in the territory of the anterior choroidal artery due to embolic occlusion of the internal carotid artery--report of two cases].

A case with infarction in the territory of the anterior choroidal artery (AChA) due to embolic occlusion of the internal carotid artery (ICA) is rare. We described two cases and investigated the mechanism of the territory of the AChA. Case 1 was a 69-year-old man. Case 2 was a 71-year-old woman. The neurological examination in both cases showed left homonymous hemianopsia, left facial palsy, left hemiparesis and left hemisensory disturbance. CT scan in these cases showed infarctions of the right uncus, amygdaloid nucleus, genu and posterior limb of the internal capsule, globus pallidus, lateral geniculate body and tail of the caudate nucleus. The right common carotid angiogram showed a complete occlusion of the ICA at its cervical segment in case 1 and at its carotid siphon in case 2. In both cases, the left carotid injection visualized the right anterior cerebral artery and right middle cerebral artery via the anterior communicating artery well, but the right AChA was not visualized. In case 1, the collateral pathways from the right external carotid artery (ECA) and the right posterior communicating artery (PCoA) to the right ICA were not supplied and the precommunicating segment of the right posterior cerebral artery was hypoplastic. In case 2, the collateral pathway from the right ECA to the right ICA was not supplied.(ABSTRACT TRUNCATED AT 250 WORDS)

[Campylobacter pylori in patients with gastroduodenal disease].

Recent advances of Campylobacter pylori (C. pylori) in human gastric disease and peptic ulcer were reviewed. C. pylori is a microaerophilic, motile, gram negative spiral rod bacterium. And all strains of C. pylori has a strong urease activity. In our experience. 91% of duodenal ulcer, 88% of gastric ulcer and 43% of control have C. pylori associated gastric mucosa. Patients of peptic ulcer with C. pylori infection were high relapse than patients of peptic ulcer without C. pylori, C. pylori is now known to be the most common and important case of pathologic gastritis, and C. pylori infection have been associated with gastric ulcer, duodenal ulcer, and non-ulcer dyspepsia. Although it has been only possible to culture C. pylori for about 6 yr in Japan, there are already sufficient data available to allow us to develop the basic framework that relates C. pylori gastritis to the causation of peptic ulcer disease.

[Subacute subdural hematoma--report of 4 cases and a review of the literature].

Subdural hematoma is divided roughly into two types acute and chronic. The two show an entirely different mode of illness. The authors have encountered 4 cases of subacute subdural hematoma in which characteristics of both types coexisted. These cases are characterized by the following. 1) The disease develops in the elderly persons with a history of trauma unknown or after minor head injury. 2) There is a relatively long period of clear consciousness and they visit a hospital when they are in the subacute stage, 3) They have a history of drinking alcohol heavily as a habit and there is a high risk of hypertension and diabetes. 4) Brain CT findings sometimes reveals mixed density hematoma. 5) Hemorrhage from the cortical artery is occasionally noted as the operative findings. Hematoma membrane is absent. 6) The outcome is generally poor because of systemic complications. As described above subacute subdural hematoma was similar to chronic subdural hematoma in the clinical course and CT findings. But operative findings of this disease indicated acute subdural hematoma. Repeated minor hemorrhage, related to coagulation disorder and brain atrophy would be important as the mechanism of subacute subdural hematoma. The effectiveness of perforation craniotomy as radical operation was low and removal of hematoma by major craniotomy was needed. The concept of subacute subdural hematoma is considered important in deciding on a therapeutic policy.

[Evaluation of CT-guided stereotaxic aspiration for thalamic hemorrhage by single photon emission CT].

Sixteen patients with thalamic hemorrhage (hematoma volume greater than or equal to 10 ml and CT classification greater than or equal to IIa) were included in this study. In sixteen patients, ten were treated conservatively (conservative group) and six were subjected to CT-guided stereotaxic aspiration (aspiration group). Stereotaxic aspiration was performed at the acute stage within five days after the onset. We measured cerebral blood flow (CBF) using Single Photon Emission CT (Tomomatic 64) and 133-Xe inhalation method. In both groups, CBF was measured at the onset (day 1-5), acute stage (day 7-13), subacute stage (1 month from the onset) and chronic stage (2-4 months from the onset). In this study, mean hemispheric cerebral blood flow (mCBF) was calculated from the middle slice 2, positioned 5cm above the orbitomeatal line. Regional devision of slice 2 in the hematoma side was made as follows. rCBF-A: regional cerebral blood flow in the anterior area of the hematoma. rCBF-L: regional cerebral blood flow in the lateral area of the hematoma. rCBF-P: regional cerebral blood flow in the posterior area of the hematoma. In both groups, age, neurological grading, CT classification and hematoma volume had no significance. In the conservative group, mCBF of the hematoma side in the subacute stage was 68 +/- 7%, and in the aspiration group it was 85 +/- 17%. This difference was statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)