Pituitary apoplexy is a syndrome characterized by the sudden onset of headache accompanied by ocular motility disturbances and a variable degree of pituitary insufficiency. The cause is usually a rapidly growing pituitary mass secondary to a vascular event (infarction or hemorrhage). General symptoms may range from vomiting or nausea to meningeal irritation. Compression on the chiasm and optic nerve can cause various campimetric deficits (usually greater bitemporal hemianopsia in the superior quadrants) and decreased visual acuity, even blindness. If the mass grows lateral to the sella turcica it can compress the oculomotor nerves, with the common motor ocular nerve being the most frequently affected, because of its more medial course in the cavernous sinus. The test of choice for the diagnosis of pituitary apoplexy is MRI, as CT may not distinguish the region clearly enough to distinguish degenerative or cystic changes from previous bleedings. The finding of erosion of the anterior clinoid processes in the skull CT may support a chronic lesion, which as a result of an acute vascular phenomenon has caused the symptoms. The management of these patients involves strict control of water and electrolyte disturbances and correction of hormonal deficits. In unstable situations as in the case described, with significant visual disturbances, surgical intervention is usually of choice, with transsphenoidal decompression.

A 51-year-old woman comes to the emergency department with a sudden decrease in visual acuity, severe headache, nausea and vomiting. Hypotensive and afebrile. She presented right ophthalmoparesis due to involvement of the third cranial nerve. A cranial CT scan shows a mass in the hyperdense selar region with erosion of the anterior clinoid processes. What is the best approach to follow?

Suspect chemical meningitis derived from a ruptured epidermoid tumor and start immediate treatment with corticosteroids.

It would indicate the performance of a cerebral angiography to rule out an aneurysm, since it is most likely that we are facing a case of subarachnoid hemorrhage and the mass that is evident in the CT is a thrombosed parasellar aneurysm.

Admission to ICU and treatment of the shock suffered by the patient and once stabilized perform brain MRI for scheduled surgery.

Urgent biochemistry and hemogram, initiation of high-dose corticosteroid therapy and urgent transsphenoidal surgery.

Lumbar puncture to rule out bacterial meningitis after starting empirical antibiotherapy. Once the patient was stabilized, study of the selar mass.

Pituitary apoplexy can mimic acute meningoencephalitis or subarachnoid haemorrhage.

Pituitary apoplexy is an uncommon but life-threatening condition that is often overlooked and underdiagnosed. We report a 45-year-old man who presented to our emergency department with a sudden onset headache, acute confusion, signs of meningeal irritation and ophthalmoplegia. An initial diagnosis of acute meningoencephalitis was made, which was amended to pituitary apoplexy following thorough investigation within the emergency department.A 45-year-old man was brought to our emergency department by ambulance with a history of sudden onset of frontal headache and acute confusion. His wife provided the history. There was no significant past medical history of diabetes, hypertension, recent travel abroad, exposure to sick contacts, involvement in outdoor pursuits such as hiking/cave diving, or trauma. He worked in a bank and had been well until 24 h prior to the onset of sudden headache, which was gradually worsening in nature and associated with increasing confusion. The patient's wife reported that he had neither experienced any fevers, night sweats, or coryzal symptoms nor received any recent vaccinations. He was not on any regular medications. He was a non-smoker and occasionally consumed alcohol. There was no significant family history. On examination in the ED, his temperature was 37.6°C, his pulse was 110/min, and he was normotensive and normoglycaemic. A macular blanching rash was noted over the patient's trunk. The patient was disoriented to time and place. Neurological examination revealed reduced GCS (11/15-E3, M6, V2), marked neck stiffness, a positive Kernig's sign and a right sixth nerve palsy.A provisional diagnosis of acute meningoencephalitis was made and the patient was started on a course of intravenous antibiotics with benzyl penicillin 1.2 g, cefotaxime 2 g and acyclovir 750 mg. Baseline blood investigations revealed hyponatraemia (122 mmol/l), a white-cell count of 11 × 109/l and a C-reactive protein > 250. Due to the sudden onset of the symptoms and lack of prodrome, an urgent CT head scan was performed to rule out a cerebrovascular event. The scan demonstrated an enlarged pituitary gland (3 cm in diameter) with impingement of the optic chiasm. The centre of the enlarged pituitary gland was noted to be hypodense in comparison to its periphery, which was consistent with a diagnosis of pituitary apoplexy. A subsequent MRI confirmed the diagnosis (Figure 1) of an enlarged sella containing abnormal soft tissue with increased signal intensity suggestive of haemorrhage (Figure 1A).Post-MRI a lumbar puncture was performed revealing glucose 3.4 mmol/l, protein 1.0 g/l, red cells of 53/mm3 and white cells of 174/mm3 with predominant neutrophilia. No organisms were seen, and CSF cultures and HSV DNA tests were found to be negative. Endocrinological investigations demonstrated low concentrations of thyroid hormones [TSH: 0.14 mIu/l (0.35-5.5 mlU/l), FT3: 1.1 nmol/l (1.2-3.0 nmol/l), FT4: 9.6 pmol/l (8-22 pmol/l)], gonadal hormones (LH: < 1 u/l) and prolactin: 16 u/l (<450 u/l). Serum FSH was 2.9 u/l (0.8-11.5 u/L) and cortisol 575 nmol/l (450-700 nmol/l). The patient was treated for hypopituitarism based on clinical and radiological findings with intravenous fluids, hydrocortisone (100 mg) and thyroxine (50 μg) as loading doses in the ED.Within 24 h of commencement of therapy the patient's GCS rose to 15, and within 48 h there was marked improvement in the right sixth cranial nerve palsy. Formal visual field assessment demonstrated temporal visual field loss in the left eye. The patient was discharged to his usual residence a week later and follow-up was organised with both the endocrinologists and ophthalmologists. Follow-up MRI demonstrated that there was no significant change in either size or signal characteristics of the pituitary fossa mass (Figure 1B).

InternalMed_Harrison

When bacterial meningitis is suspected, blood cultures should be immediately obtained and empirical antimicrobial and adjunctive dexamethasone therapy initiated without delay (Table 164-1). The diagnosis of bacterial meningitis is made by examination of the CSF (Table 164-2). The need to obtain neuroimaging studies (CT or MRI) prior to LP requires clinical judgment. In an immunocompetent patient with no known history of recent head trauma, a normal level of consciousness, and no evidence of papilledema or focal neurologic deficits, it is considered safe to perform LP without prior neuroimaging studies. If LP is delayed in order to obtain neuroimaging studies, empirical antibiotic therapy should be initiated after blood cultures are obtained. Antibiotic therapy initiated a few hours prior to LP will not significantly alter the CSF WBC count or glucose concentration, nor is it likely to prevent visualization of organisms by Gram’s stain or detection of bacterial nucleic acid by

Subarachnoid hemorrhage

Angiography After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below). In emergency department patients complaining of acute-onset headache without significant risk factors for SAH, evidence suggests that CT scanning of the head followed by CT angiography can reliably exclude SAH without the need for a lumbar puncture. The risk of missing an aneurysmal bleed as the cause of SAH with this approach is less than 1%. Lumbar puncture

Pituitary abscess presenting with cranial nerve paresis. Case report and review of literature.

Non-adenomatosus lesions of the pituitary represent a small part of the intrasellar processes and they have heterogeneous presentation. Making a precise diagnosis is of great importance, as it may lead to more efficient management. A 65-year-old man was admitted to the hospital because of headache and right cranial nerve III palsy. Basic laboratory work-up was normal whereas endocrinological assessment revealed hypopituitarism without diabetes insipidus. Plain radiography showed an enlarged sella and frontal and paranasal sinusitis. Computed tomography (CT) and magnetic resonance imaging (MRI) of the sella revealed an intrasellar lesion with extension to the sphenoid and cavernous sinuses as well as the suprasellar region, exerting pressure on the optic chiasm. On T1-weighted images the mass had a low-intensity signal with a smooth enhancing rim with bright signal. Given the presence of multiple sinusitis and imaging characteristics a pre-operative diagnosis of pituitary abscess was made. The patient was operated via transphenoidal route and purulent material was drained out. Cultures of the material were positive for Staphylococcus aureus. Antibiotics as well as cortisol replacement therapy were given. Three months later hypopituitarism persisted but there was significant improvement in the neurological findings. We report a case of an unusual presentation of a pituitary abscess. High index of suspicion, the presence of associated conditions such as pituitary tumors, meningitis or sinusitis, as well as diabetes insipidus and specific imaging features are the main diagnostic clues. Pre-operative diagnosis, which will lead to prompt antibiotic therapy and transphenoidal drainage, can decrease high mortality and morbidity associated with this disease.

[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.

[Cerebral abscess. Clinical review of 26 cases].

The introduction of new diagnostic and therapeutic techniques has changed the clinical attitude and consequences of brain abscesses (BA). To analyse clinical-radiological features, therapy, prognostic factors and evolution of BA in our institution. Retrospective study of all clinical records of patients diagnosed with BA from 1982 to 1992. Twenty-six patients with a mean age of 46.2 years were selected. The incidence was 2.6 patients/10,000 admission/year. Among 17 patients (65%) some extraprenchymatous infectious focus was found, which was located at the otorhynolaryngeal area in twelve patients. Mean duration of symptoms was 12.9 days, headache being the most common of them (69%). With CT 18 patients had a single mass, eight patients multiple masses, and 21 patients a ring enhancement when the contrast material was introduced. The causative organism was recovered from 15 patients. The organism recovered more frequently were Streptococcus spp, Enterobacteriaceae and Staphylococcus aureus. Twenty patients (77%) underwent surgical therapy, which consisted in ablation (12) or drainage (8). All patients received antibiotics for a mean of 37 days: the most frequent antibiotic combination used was penicillin+chloramphenicol. Six patients died (23%) and 7 remained with sequelae. Although statistically non-significant, the acute presentation was associated with a higher mortality rate, and the use of dexamethasone was associated with a lower mortality rate (p = 0.053 and 0.062, respectively). BA is associated with a high mortality rate and a high sequelae rate despite appropriate diagnostic and therapeutic measures. ORL infection is the most frequent predisposing factor. The use of dexamethasone is not associated with a higher mortality rate.

Headache

One recommended diagnostic approach is as follows. If any urgent red flags are present such as visual loss, new seizures, new weakness, new confusion, further workup with imaging and possibly a lumbar puncture should be done (see red flags section for more details). If the headache is sudden onset (thunderclap headache), a computed tomography test to look for a brain bleed (subarachnoid hemorrhage) should be done. If the CT scan does not show a bleed, a lumbar puncture should be done to look for blood in the CSF, as the CT scan can be falsely negative and subarachnoid hemorrhages can be fatal. If there are signs of infection such as fever, rash, or stiff neck, a lumbar puncture to look for meningitis should be considered. If there is jaw claudication and scalp tenderness in an older person, a temporal artery biopsy to look for temporal arteritis should be performed and immediate treatment should be started. Neuroimaging

[Operative treatment of anterior cranial base meningiomas].

The aim of the study is to assess outcome of surgical treatment of anterior cranial base meningiomas with special emphasis on the evaluation of visual skills after surgery. A series of 52 consecutive patients operated on for anterior cranial base meningioma in the last ten years is reported. 18 patients had decreased visual acuity on admission, 6 experienced blindness in one eye, and 4 were totally blind; defects of visual fields were found in 17 patients. Primary optic atrophy and secondary optic atrophy were noted in fundcoscopy in 20 and 2 patients, respectively. Papilloedema was found in 3 patients. Meningiomas were resected radically (Simpson I surgery) in 13 patients and in 34 patients Simpson II surgery with coagulation of the dural attachment was made; meningiomas were partially removed in 5 patients (Simpson IV surgery). In one patient dense hemiparesis occurred after the surgery, and 3 others presented adynamic syndrome, one of whom made a good recovery in follow-up examination. Two patients died: the first one due to a large brain oedema and the second one due to myocardial infarction after uncomplicated postoperative course. The postoperative course in the other 46 patients was uneventful with good outcome. Visual acuity improved in 15 cases and did not change in 10 patients; visual acuity further decreased in 3 patients. Visual recovery is significantly related to preoperative visual acuity values of no less than 0.3 D and to the presence of normal optic discs on fundoscopic examination additionally tumour size less than 3.5 cm favourably affects visual prognosis in meningiomas of tuberculum sellae.

Sudden headache, third nerve palsy and visual deficit: thinking outside the subarachnoid haemorrhage box.

A 75-year-old lady presented with sudden severe headache and vomiting. Examination was normal, and CT and lumbar puncture not convincing for subarachnoid haemorrhage. Shortly thereafter, she developed painless diplopia. Examination confirmed right third cranial nerve palsy plus homonymous left inferior quadrantanopia. Urgent cerebral MRI with angiography was requested to assess for a possible posterior communicating artery aneurysm, but revealed an unsuspected pituitary mass. Pituitary adenoma with pituitary apoplexy was diagnosed. Pituitary apopolexy is a syndrome comprising sudden headache, meningism, visual and/or oculomotor deficits, with an intrasellar mass. It is commonly due to haemorrhage or infarction within a pituitary adenoma. Treatment includes prompt steroid administration, and potentially surgical decompression. While subarachnoid haemorrhage is an important, well-recognised cause of sudden severe headache, other aetiologies, including pituitary apoplexy, should be considered and sought.

Painful ophthalmoplegia: the role of imaging and steroid response in the acute and subacute setting.

Although reports of single cases of painful ophthalmoplegia (PO) are common, studies considering larger case series are lacking. Here, we aimed to determine the relative frequencies of ocular neuropathies, the causes, the usefulness of diagnostic procedures and the role of steroid treatment in PO. Between January 2006 and September 2012, 149 patients' charts who presented with diplopia in our emergency department were studied retrospectively. 34 of them met the inclusion criteria that included recent (≤3 days) symptom onset and a minimum of diagnostic work. 32% of single or combined ocular motor nerve palsies were of diabetic microvascular etiology and most of them were IIIrd or VIth nerve neuropathies. The most useful, in terms of sensitivity and specificity of diagnostic test in the acute setting was ESR, whereas MR-angiography and focused cavernous sinus imaging led to diagnosis in the post-acute phase. Pain response to steroids was non-specific, in contrast to palsy improvement after steroid administration which was indicative of Tolosa-Hunt syndrome or temporal arteritis. Although acute and subacute PO might be intuitively associated with Tolosa-Hunt syndrome or sinister pathology such as aneurysmal hemorrhage, our data show that these causes are far less common than diabetic microvascular palsies. Brain CT, MR-imaging of brainstem, cerebellum or hemispheres, CSF analysis and pain response to steroids are nonspecific and hence less helpful in order to arrive at a diagnosis. Instead, improved ocular motility after steroid treatment, as well as MR-angiography and cavernous sinus imaging appear more useful for this purpose.

Mollaret's meningitis

Investigations include blood tests (electrolytes, liver and kidney function, inflammatory markers and a complete blood count) and usually X-ray examination of the chest. The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid (fluid that envelops the brain and the spinal cord) through lumbar puncture (LP). However, if the patient is at risk for a cerebral mass lesion or elevated intracranial pressure (recent head injury, a known immune system problem, localizing neurological signs, or evidence on examination of a raised ICP), a lumbar puncture may be contraindicated because of the possibility of fatal brain herniation. In such cases, a CT or MRI scan is generally performed prior to the lumbar puncture to exclude this possibility. Otherwise, the CT or MRI should be performed after the LP, with MRI preferred over CT due to its superiority in demonstrating areas of cerebral edema, ischemia, and meningeal inflammation.

Review of 1,000 consecutive cases of severe head injury treated before the advent of CT scanning.

This is a review of 1,000 consecutive cases of severe head injury admitted to our Neurosurgical Department between January 1973 and August 1976, before the advent of CT scanning. All patients were comatose following head injury (GCS less than or equal to 8) and were treated homogeneously by the same neurosurgical team by a protocol that included immediate resuscitation on arrival, diagnosis of intracranial lesions by angiography, early surgery when needed, mechanical ventilation, steroids, and mannitol. Extracranial lesions, even if preponderant, were treated by various specialists in the Neurosurgical Department, which for all practical purposes operated as an Emergency Department. Admission criteria were very broad with no preadmission selection. The overall mortality for this series was 45%. A little less than half the patients made good recoveries or remained moderately disabled (47%); 6% were severely disabled, and 2% survived in a persistent vegetative state. More than two-thirds of the patients were brought to our Neurosurgical Department after a short stay at a general hospital; 72% were admitted within 6 hours of injury; 71% were traffic accident victims; and 34% had significant associated extracranial injuries. Carotid angiography was performed in 78% of the patients and indicated the presence of an intracranial haematoma requiring surgery in 36% of the whole series. Mortality was significantly higher in operated than in unoperated patients (56% versus 39%); those treated surgically, however, were older, in worse clinical condition, and showed a higher incidence of acute subdural haematomas associated with brain contusion. Carotid angiography proved very effective in revealing the presence of an expansive lesion but failed to reflect the severity of brain damage, since the group with "negative" angiograms showed a high mortality (52%). Patients with a lucid interval had a higher percentage of surgical lesions than those with immediate coma (58% versus 26%); but fully 42% of them did not require surgery, and 25% had negative angiograms. From the prognostic point of view the clinical data elicited after initial resuscitation were highly predictive of the outcome: some individual neurological signs, such as mydriasis, posturing and eye movements, were not inferior to the GCS score in that respect. Age also proved a strong predictor, since elderly patients are more likely to have severe subdural and parenchymal lesions and their clinical severity is accordingly greater.(ABSTRACT TRUNCATED AT 400 WORDS)

Intracranial aneurysm

Subarachnoid bleed If an aneurysm ruptures, blood leaks into the space around the brain. This is called a subarachnoid hemorrhage. Onset is usually sudden without prodrome, classically presenting as a "thunderclap headache" worse than previous headaches. Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm. Symptoms of a ruptured aneurysm can include: a sudden severe headache that can last from several hours to days nausea and vomiting drowsiness, confusion and/or loss of consciousness visual abnormalities meningism dizziness Almost all aneurysms rupture at their apex. This leads to hemorrhage in the subarachnoid space and sometimes in brain parenchyma. Minor leakage from aneurysm may precede rupture, causing warning headaches. About 60% of patients die immediately after rupture. Larger aneurysms have a greater tendency to rupture, though most ruptured aneurysms are less than 10 mm in diameter.

[Indication of neuro-imaging for the initial management and the follow-up of acute community-acquired bacterial meningitis].

Lumbar puncture is the best way to prove bacterial meningitis. It should be performed without any delay if the diagnosis is suspected. Herniation is a rare complication of LP. CT is normal in most cases of purulent meningitis, including those complicated by a subsequent herniation; normal CT results does not mean that performing a LP is safe. Three main clinical features can help determine which patient is at risk of herniation and should have a CT before LP. This risk has to be determined rapidly in the emergency ward while assessing anamnestic data, localization signs or symptoms, and level of consciousness. Cranial imaging (mainly MRI) is useful in the course of bacterial meningitis. Patients who do not respond well to treatment or with atypical presentation, persistence of fever, or new neurological signs should undergo brain imaging; MRI and CT may identify subdural effusions, brain abscesses, empyemas, hydrocephaly, or brain parenchymal changes (cerebritis, infarction, hemorrhage). CT and MRI are useful to screen for an ENT cause of bacterial meningitis, and mandatory in case of pneumococcal meningitis. Numerous MRI sequences are useful to identify bacterial meningitis complications: SE T1 without and with gadolinium injection, SE T2, FLAIR, gradient-echo T2, diffusion weighted imaging, MR angiography.

Aneurysm

Diagnosis Diagnosis of a ruptured cerebral aneurysm is commonly made by finding signs of subarachnoid hemorrhage on a computed tomography (CT) scan. If the CT scan is negative but a ruptured aneurysm is still suspected based on clinical findings, a lumbar puncture can be performed to detect blood in the cerebrospinal fluid. Computed tomography angiography (CTA) is an alternative to traditional angiography and can be performed without the need for arterial catheterization. This test combines a regular CT scan with a contrast dye injected into a vein. Once the dye is injected into a vein, it travels to the cerebral arteries, and images are created using a CT scan. These images show exactly how blood flows into the brain arteries.

A point-of-care evaluation after visual loss following paraclinoid aneurysm repair: the role of sonographic and pupillometer assessment.

Visual complications represent common deficits following surgical or endovascular repair of paraclinoid aneurysms. Different etiologies should be investigated to prevent devastating consequences. Herein we present a point-of-care evaluation to investigate sudden visual loss after coiling of paraclinoid aneurysms. A 20-year-old male was admitted for a sudden headache. Head computed tomography showed a subarachnoid hemorrhage and subsequent angiography revealed a 9-mm left supraclinoid aneurysm of the internal carotid artery treated with endovascular coil embolization. Thirty minutes after intensive care unit admission, the patient reported a left amaurosis. To exclude secondary etiologies, an immediate evaluation with point-of-care devices (color-doppler and B-mode ultrasound and automated pupillometry) was performed. Sonographic evaluations were negative for ischemic/thrombotic events and neurologic pupil index within physiological ranges provide evidence of third cranial nerve responsiveness. The symptomatology resolved progressively over 120 minutes with low-dose steroid therapy, 30° head-of-bed elevation, and blood pressure management. Visual deficits can occur after endovascular procedure and should be investigated. Suspected visual loss is a neurological emergency that deserves a prompt evaluation. Ultrasound and automated pupillometry have proved to be an effective, rapid, reliable, and non-invasive combination for a clinical decision-making strategy in the management of post-procedural acute visual deficits.

[Two cases of cerebral aneurysms combined with polycystic kidneys].

Two cases of cerebral aneurysm combined with polycystic kidneys (PCKs) were presented. Case 1, a 24-year-old hypertensive male, was referred to our clinic owing to sudden onset of severe headache at August 20, 1982. Neurological findings on admission were stuporous, right vitreous hemorrhage (so-called Terson's syndrome), and hypertension. CT scans showed subarachnoid hemorrhage, and right MCA bifurcation aneurysm with marked vasospasms by cerebral angiography was revealed. Intentional delayed operation with V-P shunt was performed. He discharged with mild left upper limb paresis, and visual impairment on the right. Bilateral PCKs were confirmed by postoperative DIP and CT scan. Case 2, a 51-year-old female, who suddenly complained of severe headache, was referred to our department 3 days after subarachnoid hemorrhage. One year previously, she had been pointed out PCKs. Neurological findings on admission at February 29, 1980, were drowsy, left third cranial nerve palsy, and hypertension. Cerebral angiography showed multiple aneurysms (bilateral IC-PC & A-com). Neck clipping (1-IC-PC & A-com) and coating (r-IC-PC) were performed at the next day of admission, and V-P shunt operation was followed about 8 weeks after first operation. About 2 weeks after discharge, she suddenly became loss of consciousness and expired. Autopsy revealed intracerebral hemorrhage in left basal ganglia and thalamus. Both kidneys were PCKs of Potter type 3 and cysts of the liver were also noted. In young hypertensive patients with cerebral aneurysms, it should be in mind whether PCKs may be combined or not, and cerebral angiography in PCKs were reasonable to find out harbored cerebral aneurysm.(ABSTRACT TRUNCATED AT 250 WORDS)

[Pituitary abscess, treated by medication].

Pituitary abscesses are rare. The case reported here concerns a 28-year old African. Gradual development of diplopia over 6 months was the first clinical manifestation. Three months later this development had reached a more severe and infectious context, with complete right ophthalmoplegia, meningitis and coma (GCS = 9). CT scan showed an image in favour of a pituitary abscess with suprasellar extension, associated with thrombophlebitis of the cavernous sinus. An antibiotic therapy consisting of cefotaxime and metronidazole administered for 1 month, and netilmicin for 15 days succeeded in controlling the infectious syndrome. This resulted in cure of visual disorders, reduction in size of the CT scan image and reconstruction of the pituitary sella which had been destroyed. The diagnosis of pituitary abscess should be made when confronted with an infectious syndrome (unexplained fever, repeated meningitis). CT does not recognize the nature of the hypophyseal mass it shows: necrosis of a pituitary adenoma, giant aneurysm or craniopharyngioma may mimic local infection. Surgery confirms the diagnosis and is regarded as the best treatment. The patient's life is threatened when meningitis is present, and the functional prognosis is poor when recovery from visual disorders is compromised due to late diagnosis. In this paper a comparative analysis of the clinical course of the disease and therapeutic data in our patient is presented and compared with other reported cases.

[Acute spontaneous subdural hematoma associated with multiple aneurysms--a case report].

A case of acute spontaneous subdural hematoma associated with three aneurysms is reported. On March 12, 1984, a 47-year-old woman experienced the sudden onset of severe headache over the bilateral frontal region and vomiting. Three hours later, she was transferred to our hospital by ambulance car because of continuous headache and vomiting. She had no history of head trauma. She had been medicated hypertension for five years. On admission she suffered from headache and nausea. But there was no clinical sign in physical and neurological examinations. The meningeal irritation was not present, but lumbar puncture showed slightly pinky CSF with normal pressure. A plain computed tomographic scan showed a thin high density mass in the left temporal extra-axial region and the slight deviation of the midline structures to the right. Left carotid arteriogram showed an avascular region over the left cerebral convexity, an aneurysm of the left A2-A3 junction and a questionable aneurysm of the bifurcation of left middle cerebral artery. Right carotid arteriogram showed an aneurysm of the bifurcation of right middle cerebral artery. We diagnosed this case as an acute subdural hematoma by CT scan and arteriogram. We were perplexed preoperatively whether this bleeding was spontaneous or secondary to the rupture of aneurysm, and we could not deny the possibility of a ruptured aneurysm. On March 15, 1984, three days after onset, operation was performed. At operation, a small subdural hematoma was removed, and the underlying cortex was normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Isolated Posterior Spinal Artery Aneurysm Presenting with Spontaneous Thrombosis After Subarachnoid Hemorrhage.

The cause of subarachnoid hemorrhage is more likely to be intracranial than spinal. Bleeding, although common with spinal arteriovenous malformations and spinal cord tumors, rarely occurs with ruptured isolated spinal artery aneurysms. Here, we report a case of isolated thoracic posterior spinal artery aneurysm presenting with thrombosis after subarachnoid hemorrhage. A 67-year-old woman presented with sudden-onset nausea and low back and right thigh pain that worsened with movement. Computed tomography (CT) and magnetic resonance imaging (MRI) scans of the head suggested a small subarachnoid hemorrhage in the high-convexity sulcus, and lumbar puncture showed bloody cerebrospinal fluid. There was no apparent intracranial aneurysm on CT angiography; however, spinal MRI showed a lesion on the right side of the spinal cord at Th10. Contrast-enhanced CT showed an enhancing lesion at this site on day 7 that was not present on day 15. Selective right Th10 intercostal artery angiography on day 22 showed no evidence of aneurysm. The lesion was suspected to be a thrombotic spinal artery aneurysm. Given the unclear natural history of this entity, surgery was performed on day 36. After right Th10 hemilaminectomy and opening the dura, the arachnoid and adhesions were found to be thickened. A fusiform-shaped thrombosed aneurysm continuous with the radiculopial artery was removed. The patient was discharged without neurologic deterioration. Isolated spinal artery aneurysm is a rare cause of subarachnoid hemorrhage. It is expected that additional cases will clarify the natural history and indications for treatment.

[Brain abscess. Clinicomicrobiologic study and prognostic analysis of 59 cases].

Clinical, microbiological, therapeutic and prognostic characteristics of brain abscesses were analyzed as well as the influence of CT in their evolution. Retrospective study of 59 patients with the diagnosis of brain abscess of bacterial source before (group A) and after (group B) the introduction of CT (25 and 34 patients, respectively). The most common symptom was headache (76.3%) and the most common abnormality in physical examination was a decrease in the level of consciousness (61%) and this abnormality was associated with a higher mortality rate (13% versus 41.6%; p < 0.05) and also a higher proportion of neurologic sequelae (50% versus 85.7%; p < 0.05). The diagnosis was obtained earlier in group B. The hematogenous source predominated (32.2%); an adjacent source was identified in 28.8% and an apparent source was not recognized in 27.2% (40% in group A versus 17.6% in group B). Anaerobic and microaerophilic streptococci were the bacteria recovered most frequently. Gram-negative aerobic bacteria were the most common in otogenic abscesses. The use of corticosteroids had no influence upon mortality, but it was associated with a lower percentage of neurological sequelae (40% versus 14%; p < 0.05). The introduction of CT decreased mortality (40% in group A versus 23.5% in group B, although this difference was not significant) and also sequelae (86.6% in group A versus 57.6% in group B; p < 0.05). Leaving apart cases of bacterial endocarditis, in which death was due to the underlying heart disease and a systemic sepsis picture, mortality attributed to brain abscess was 20.3%. The introduction of CT has meant a significant breakthrough for the diagnosis, treatment and follow-up of these patients and has contributed to improvement in survival. In our series, the diagnosis of brain abscess was obtained earlier and the number of brain abscesses with no apparent source has decreased since the introduction of CT. Moreover, CT sensitivity is really good for locating multiple abscesses. Overall, the prognosis of these patients has improved since the introduction of this technique. Nevertheless, brain abscess is still associated with a relevant morbi-mortality rate.

[Rupture of intracranial aneurysm due to cerebral angiography (author's transl)].

The authors report a case of rupture of intracranial aneurysm by angiography which was done four hours after the subarachnoid hemorrhage. Case; A thirty-one year old male patient was brought to our outpatient's clinic by ambulance because of conscious loss and convulsive seizure on Feb. 5th, 1974. Lumbar puncture showed grossly hemorrhage in the CSF. Immediately he was hospitalized and administered anticonvulsants, hypotensive drugs, antibrinolytic agents and corticosteroid. His signs and symptoms on admission were mild headache, nausea, nuchal rigidity, anisocoria (right greater than left) and left hyper reflexia. This attach was his second. (He first noted the bleeding attack on January 30, 1974). Four hours after this attack cerebral angiography was done under local anesthesia with heavy premedication. Puncture of common carotid arteries were uneventful. Three injections of 60% Conray, at the dose of 8 ml each, were performed and three films were taken. Few minutes after injections, he suddenly became unconscious and ceased respiration for a few seconds. Blood pressure was 210 mmHg at systolic, although 120 mmHg two minutes before. Immediately resuscitation started. His respiration reappeared within 0.5 minute and his vital signs gradually improved. We stopped examination. When returned to his bed, right pupil dilated and optic fundi showed bleeding bilaterally. Arteriography showed a large dumbbell shaped aneurysm at the trification of the right middle cerebral artery but no finding of hematoma (Fig. 1). We decided emergency operation at once. When started the operation his both sides pupil dilated, B.P. was very low. OPERATION: Right side large frontolateral craniectomy was done. Large subdural hematoma (Fig. 2), severe diffuse subarachnoid hemorrhage (Fig. 3) and intracerebral hematoma were found. Aneurysmal neck clipping was successfully done. His level of consciousness was semicomatous. But gradually his state deteriorated and died one week after the operation. There was severe edema in both sides cerebrum. The brain stem, especially interbrain, and pons, had fallen into softening, so called respirator brain. This complication of angiography is very rare. This case is the 24th reported case of the ruptured aneurysm by angiography.

Neurology_Adams

The initial elevation of intracranial pressure and threatening temporal lobe or cerebellar herniation can be managed by the use of intravenous mannitol (or hypertonic saline) and dexamethasone, 6 to 12 mg q6h. If improvement does not begin promptly, it becomes necessary to aspirate the abscess stereotactically or remove it by an open procedure that also allows precise etiologic diagnosis by Gram stain and culture. The decision regarding aspiration or open removal of the abscess is governed by its location and the course of clinical signs and by the degree of mass effect and surrounding edema as visualized by repeated scans.

[A 64-year-old woman with severe headache and progressive disturbance of consciousness].

We report a 64-year-old woman who developed nausea, headache, and consciousness disturbance. She was well until four years before the onset of her neurologic illness when (April of 1990 at her 59 years of the age) she was found to have an early cancer in her anterior wall of the lower stomach. Subtotal gastrectomy was performed and the operative result was reported as curative. Four years after the surgery (December of 1994 at her 64 years of the age), she noted suboccipital headache and nausea which had become progressively worse and she was admitted to our service on May 24, 1995. On admission, she appeared chronically ill but general physical examination was unremarkable with normal vital signs. Neurologically she was alert and not demented, and the higher cerebral functions were intact. Cranial nerves were also unremarkable. She was able to walk in tandem and on heels. No motor weakness or ataxia was noted. Deep tendon reflexes were moderately increased, however, no Babinski sign was noted. Although she had headache, no meningeal signs were seen. Slight superficial and vibratory sensory loss was noted in both feet. Routine blood work was again unremarkable except for slight increase in CEA to 8.3 ng/dl (N < 5 ng/dl). The opening pressure of lumbar CSF was 180 mm H2O and the CSF contained 39 cells/microliter, 79 mg of protein, and 10 mg/dl of glucose. Approximately half of the cells were atypical malignant cells. Plain CT was unremarkable, however, tentorial border showed enhancement after contrast infusion. FGS showed no malignant tumors in the stomach. She was treated with intravenous glycerol and whole brain radiation, however, she continued to complain of severe headache, and her sensorium started to be disturbed one month after the admission. Follow-up cranial CT scan revealed enlargement of the lateral and the third ventricles. Her consciousness progressively deteriorated and she became comatose three months after the admission. Repeated cranial CT scan showed enlargement of the ventricles, but no mass lesions were seen within the brain. She developed respiratory arrest on September 25 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had a gastric cancer with meningeal seeding developing meningeal carcinomatosis. The cause of deep coma was ascribed to damage of cerebral cortical areas secondary to metastatic carcinoma cells and fibrinous materials in the surface of the brain. Postmortem examination revealed thickening and clouding of leptomeninges of the cerebral convexity. On histologic observation, patchy areas of fibrous thickening were seen in the cerebral leptomeninges; in such areas, adenocarcinomatous cells were seen scattered. The basal meninges were free of carcinoma cells, however, leptomeninges of the cerebellum and brain stem tegmentum contained scattered carcinoma cells. The lateral and the third ventricles were enlarged, however, insides of the brain were free of pathologies; the ependymal layer were intact. In the stomach no carcinoma cells were remaining. Pneumonic changes were seen in the right upper and the left lower lobes which appeared to be the direct cause of her death. No evidence of tentorial herniation was noted. The cause of her deep coma was not clearly determined, however, combination of hydrocephalus and cortical malfunction due to leptomeningeal carcinoma cell infiltration and fibrinous material accumulation appeared to have played a role.

[A case of favorable outcome of conservative treatment of acute otogenic cerebellar abscess].

The authors report a case of conservatively cured abscess in the left cerebellar hemisphere demonstrated by CT. The patient was admitted in serious condition to a neurotraumatology centre. After pharmacological treatment a quick improvement of patient's health was achieved and control CT examination during his stay in hospital and after discharge from hospital confirmed the relation between clinical improvement and regression of changes in CT. The presented case points to the possibility of conservative treatment of brain abscesses if the patient meets certain clinical criteria, and CT provides the possibility of repeated checking of the dynamics of intracranial lesion.

Recurrent Chemical Meningitis Due to Parasellar Epidermoid Cyst.

Intracranial epidermoid cysts are exceedingly rare lesions that result from a disorder of gastrulation. They are seen only in the pediatric patient population. We describe a 44-year-old Hispanic woman who presented with acute confusion. The family reported two months of progressive headaches and two weeks of fever, blurred central vision, and restricted visual fields. On examination, the patient appeared ill, with a low-grade fever and stiff neck. Neurological testing was limited but grossly non-focal. Computerized tomography (CT) of the head and magnetic resonance imaging (MRI) of the brain showed a large cystic mass arising in the sella, where it displaced the normal pituitary gland. Cerebrospinal fluid (CSF) showed mildly elevated opening pressure with high protein, low glucose, and neutrophilic pleocytosis. Extensive serum and CSF evaluation were negative for infectious agents. The patient was initially started on empiric treatment for presumed infectious meningoencephalitis. As tests for bacterial and viral pathogens were normal, she was switched to fluconazole. The mental status returned to normal and she was discharged home with close follow up. She returned one month later with a recurrent headache, nausea, and stiff neck. The examination showed meningismus but was otherwise non-focal. MRI of the brain showed no change in the parasellar mass. Repeat CSF showed an even higher white blood cell (WBC) count and protein with continued hypo-glycorrhachia. She underwent trans-nasal trans-sphenoidal hypophysectomy and pathology revealed a squamous epithelium-lined keratin-filled cyst suggestive of an epidermoid cyst. The patient responded well to surgery and was discharged on pituitary hormone supplements alone. To our knowledge, this is a first adult case of recurrent chemical meningitis secondary to a ruptured epidermoid cyst in the sella.

Subtentorial subdural empyema: report of two cases and review of the literatures.

Subtentorial subdural empyema is a rare form of intracranial suppuration. We     present two cases treated at our department within the last 11 years. The common     source was an ear infection. Both patients presented with headache, fever,     vomiting and stiff neck. Only one patient had disturbed consciousness. Both     patients received aggressive antibiotic therapy. The first patient was treated     with suboccipital craniectomy and evacuation of pus collection, while the second     patient was treated conservatively with antibiotics and ventriculoperitoneal     shunt for his associated supratentorial hydrocephalus. Both blood cultures and     empyema collection were sterile. Neuroimaging with computed tomography and     magnetic resonance imaging permitted accurate diagnosis and localization of the     purulent collections. At follow up of 11 years for the first case and 10 months     for the second, both patients had complete neurological recovery except for     right mild sixth nerve palsy in the patient with conservative treatment.

Rupture of Thrombosed Cerebral Aneurysm During Antithrombotic Therapy for Ischemic Stroke: Case Report and Literature Review.

Thrombosed cerebral aneurysm (TCA) can cause cerebral infarction. However, treatment of cerebral infarction due to embolism from TCA is controversial because of the risk of rupture, and no consensus has been established for the treatment of patients with this condition. A 75-year-old woman suffered left hemiparesis. Computed tomography (CT) showed a high-density round mass in the right sylvian fissure, which was suspected to be a nonruptured TCA. Magnetic resonance (MR) angiography and CT angiography demonstrated an aneurysm in the distal part of the right middle cerebral artery with poor opacification of most of the aneurysm, suggesting partial thrombosis. Diffusion-weighted MR imaging revealed high intensity in the right frontal lobe, in a distribution distal to the aneurysm. The diagnosis was cerebral infarction due to embolism from a partially thrombosed aneurysm. She was treated with antithrombotic therapy. On day 4, she suddenly became comatose. CT and CT angiography revealed subarachnoid hemorrhage (SAH) and enlarged opacification in the aneurysm, respectively. She underwent neck clipping of the aneurysm, but her neurologic improvement was poor. TCA causing ischemic stroke followed by SAH is extremely rare, with only 4 previous reported cases. All patients had received antithrombotic therapies, and most aneurysms had ruptured within a few days after starting antithrombotic therapy. The outcomes were extremely poor. We suggest that antithrombotic therapy might be avoided for these patients. Early surgical treatment without antithrombotic therapy is recommended to prevent aneurysm rupture and recurrent distal embolism from the TCA.

[Clinical onset of meningitis in chromophobe adenoma of the pituitary: 2 cases].

Two cases of purulent meningitis in subjects with misinterpreted chromophobe adenoma of the hypophysis are presented. Radiography in the acute stage revealed typical enlargement of the sella turcica and thus established the diagnosis, which was eventually confirmed histologically during surgery. The frequency with which this complication has occurred in a personal series is contrasted with its rarity in the literature, particularly neurosurgical works. It is felt, therefore, that the association of adenoma and meningitis is more common than is generally supposed. Routine cranial radiography is recommended in all cases of purulent meningitis, especially in young subjects and adults, from the outset. This will reveal hypophyseal involvement and enable replacement hormonal therapy with cortisone to be added to symptomatic and antibiotic management in cases of concomitant hypophyseal and adrenal insufficiency.

[A case of delayed subrachnoid hemorrhage from vertebrobasilar artery dissecting aneurysm].

We report a case of delayed subarachnoid hemorrhage (SAH) from a vertebrobasilar artery dissecting aneurysm (VBA-DA). The patient was a healthy 32-year-old woman with a sudden onset of severe occipitalgia. Next day, her headache improved gradually, and she consulted with our department. Although we initially suspected that she was suffering from SAH, neurological findings, CT, and cerebrospinal fluid examination did not reveal any abnormal conditions, including SAH. Therefore, she was treated conservatively with analgesics. Twelve days after the initial onset of the headache, she was admitted because of severe re-attack of headache, rt. hemiparesis with rt. oculomotor nerve palsy and loss of consciousness. CT revealed moderate SAH and cerebral angiograms showed VBA-DA. After the cerebral angiography, bleeding reoccurred two times and she lost her life. We present the case, review the literature and discuss the relationship between presenting symptom of headache and non-hemorrhagic VBA-DA. A few cases of non-hemorrhagic VBA-DA have been reported in the literature in which the only presenting symptom was headache, followed by delayed SAH from non-hemorrhagic dissecting aneurysm. Consequently, we concluded that her initial symptom of headache was due to dissection of vertebrobasilar artery, and that SAH was due to delayed hemorrhage of non-hemorrhagic VBA-DA. Even when neurological findings, CT and cerebrospinal fluid examination reveal no abnormalities in the early stage after the sudden onset of headache, especially in the occiptal or nuchal regions, non-hemorrhagic VBA-DA, which has a risk of fatal hemorrhage, cannot be ruled out with certainty. Therefore, MRI, MRA, three-dimensional CT, or cerebral angiography should be performed in such cases.

[A case of multiple septic intracranial aneurysms--successful treatment with surgical and conservative therapy in the same case].

Here reported is a case of multiple septic intracranial aneurysms which were successfully treated with surgical and conservative therapy. A 44-year-old man was admitted to our hospital because of headache, vomiting and visual disturbance. He had had a fever and had been under treatment for a respiratory tract infection during the preceding 3 months. Physical examination on admission revealed pansystolic heart murmur over the cardiac apex. Neurological examination revealed neck stiffness, papilledema and right homonymous hemianopsia. Laboratory data showed the presence of inflammatory process. A CT scan showed a high density area in the left occipital region, and vertebral angiography showed a saccular aneurysm on a distal branch of the left occipitotemporal artery. Fourteen days after admission, the operation of clipping the neck of the aneurysmal artery was performed and the hematoma evacuated to lower the increased intracranial pressure. He had been well after the operation until 3 weeks later when a follow-up angiography showed a new unruptured aneurysm on a distal branch of the right middle cerebral artery with a relapse of the infection. Then, he was treated with appropriate antibiotics and antifibrinolytic agents. A repeated angiography 1 month later showed resolution of the aneurysm. The mechanism of resolution of septic aneurysm and its treatment are discussed.

Recurrent painful ophthalmoplegic neuropathy

Magnetic resonance angiography (MRA) or CT angiography (CTA) can be used to examine cerebral blood vessels and to rule out vascular abnormalities, such as an aneurysm. In cases where intracranial vascular lesions, for example, subarachnoid hemorrhage cannot be completely ruled out after performing MRA or CTA, physicians may consider using traditional digital subtraction angiography (DSA) for more detailed investigation. Laboratory tests Lumbar punctures and blood tests might be performed on those with RPON to identify other possible causes of cranial neuropathy, including diabetes, inflammatory diseases, infections, tumors, and other systemic diseases that involve either the central nervous system or the peripheral nervous system. The detection of abnormalities in these tests suggests that RPON is highly unlikely to be the culprit in cranial neuropathy, and more diagnostic tests should be done to find out the underlying condition.