It is a headache in the context of papilledema. In this case the papilledema is due to increased intracranial pressure due to a tumor. The headache due to increased intracranial pressure is of positional type (it increases with Valsalva maneuvers and when bending down), so option 2 is not correct. In addition, it is predominantly morning (option 1 is correct) because in the morning intracranial pressure naturally rises. Migraine-type headaches may be associated with photophobia or sonophobia (answers 3 and 4). But this headache is not a migraine headache.

It is a headache in the context of papilledema. In this case the papilledema is due to increased intracranial pressure due to a tumor. The headache due to increased intracranial pressure is of positional type (it increases with Valsalva maneuvers and when bending down), so option 2 is [HIDDEN]. In addition, it is predominantly morning (option 1 is [HIDDEN]) because in the morning intracranial pressure naturally rises. Migraine-type headaches may be associated with photophobia or sonophobia (answers 3 and 4). But this headache is not a migraine headache.

A 59-year-old woman with recent onset of epileptic seizures comes to the emergency department. On examination she presents left pyramidal signs and papillary edema. A brain MRI shows a right hemispheric mass with edema, midline deviation and signs of tentorial herniation. She reports that for the past week she has been suffering from headache that has been progressing in intensity. Which of the following features associated with headache seems most likely for this patient?

Chronic Headaches After a Concussion in an Obese 16-Year-Old Girl.

Jennifer is a 16-year-old Latina girl who is new to your practice. During her first well visit, she mentions that she has had daily headaches for 2 years. They began after sustaining a concussion in a car accident. Typically, her headaches are bilateral and "squeezing"; they occur in the afternoons and last for a few hours. Her concussion also resulted in depressed mood, which has improved over time.When you ask if her headaches have changed recently, she says that they have been worse for the last few days. The quality and severity are unchanged; however, they now occur first thing in the morning, are worse when supine, and no longer remit. In the last 2 days, she has developed new-onset blurry vision, nausea, dizziness, photophobia, and sonophobia. Although she previously experienced sadness with her concussion, she now feels irritable. She has never used tobacco, alcohol, or drugs, and she takes no medications.On examination, her body mass index is above the 99th percentile. You note mild papilledema bilaterally. She has no focal neurological deficits. The remainder of her examination is normal.You send her to an emergency department. Her head computed tomography is normal. A lumbar puncture demonstrates an opening pressure of 32 cm H2O; she feels relief after the procedure. She is admitted with a diagnosis of benign intracranial hypertension and is started on acetazolamide. What is the differential diagnosis of chronic headaches in an obese adolescent? How should a busy community pediatrician manage Jennifer acutely? What follow-up care should Jennifer receive?

Posterior reversible leukoencephalopathy syndrome presenting with global cerebral edema and herniation.

We report a case of global cerebral edema and herniation due to Posterior Reversible Leukoencephalopathy Syndrome (PRES). Case report. A 37-year-old healthy female developed persistent severe occipital headache, and after 1 month of persistent headache, developed an episode of loss of consciousness. CT brain showed diffuse cerebral edema and effacement of the sulci and basal cisterns. Her initial neurological examination was nonfocal but with severe headache. Overnight, she acutely became unresponsive with fixed dilated pupils, tachycardia, and hypertension. She was intubated and treated with hypertonic saline and mannitol with improvement in her clinical status. Intracranial Pressure (ICP) monitor showed elevated ICPs to 37 mmHg which responded to mannitol. MRI brain showed diffuse vasogenic edema predominantly in the white matter without enhancement. Cerebral angiogram was unremarkable. Cerebrospinal fluid including infectious work-up was negative. With supportive care, her mental status improved. On her 3 month follow-up visit, she was asymptomatic and had returned to work. Repeat MRI brain at 3 months showed persistent white matter changes that subsequently resolved at 9 months. Although PRES is typically considered to have a benign clinical course, clinician should be aware that severe cases can present with global cerebral edema and associated complications including intracranial hypertension and herniation.

Acute Headache -- History and Physical

What is the patient's medical history? Does the patient take new medications, or have they recently changed them? Does the patient take "blood thinners"? Is this the worst headache the patient has ever experienced? Was the pain maximal at the onset? Has the patient had any difficulty moving or speaking normally? Did the patient have nausea or vomiting? Does the patient have a fever? Does the patient have any changes in vision or hearing? Does the patient have eye pain? Does the patient have any neck or facial pain? Did the patient have a seizure? Does the patient have dizziness? Does the patient have any sensitivity to light? Does the patient feel generally weak? Is there a weakness in a specific area of their body? Has the patient traveled recently? Has the patient been around sick contacts? Is the patient less than six weeks postpartum? Does the patient have a history of immunosuppression or take immunosuppressive medication?

[Posterior reversible encephalopathy syndrome in systemic lupus erythematosus: a case report].

This case report concerns a 22-year-old woman who had been diagnosed with systemic lupus erythematosus (SLE). She had intermittent fever, butterfly erythema, photosensitivity, oral ulcers, and multiple arthralgia in the past seven years, but she did not adhere to regular treatments. The edema of the lower extremities and face aggravated in the recent two weeks, so she was admitted to our Department of Rheumatology and Clinical Immunology. Meanwhile, we found she had severe hypertension, the maximal blood pressure was 170/120 mmHg. The patient had high SLE disease activity (the disease activity index score was as high as 23) with blood involvement, acute renal insufficiency, multiple serous effusion and rash. After one week treatments of intravenous methylprednisolone 80 mg daily and other drugs, her conditions made some extent improvement. However, she suffered sudden epileptic attacks. No positive neuropathological signs were found, and the blood pressure was up to 190/130 mmHg before the onset of the seizures. Her cerebrospinal fluid (CSF) pressure was 330 mmH<sub2</subO, the CSF protein level was normal value, and the white blood cell count was 0 cell/mm<sup3</sup, with no signs of infection. Cranial MRI showed vasogenic edema at bilateral parietal, occipito-parietal regions, and centrum ovale. We prescribed drugs of decreasing intracranial pressure, intravenous drugs of decreasing blood pressure and midazolam for sedation, without corticosteroid impulse therapy. She recovered consciousness in the next day, without epilepsy recurrence. We eventually diagnosed it as posterior reversible encephalopathy syndrome (PRES), according to the history, laboratory results, imaging featuresand clinical outcome. PRES is a disorder of reversible subcortical vasogenic brain edema in patients with acute neurological symptoms (eg, seizures, encephalopathy, headache, and visual disturbances). PRES is mainly caused by blood pressure changes or endothelial injury, which lead to breakdown of the blood-brain barrier and subsequent brain edema. Most patients have a favourable prognosis. SLE complicated with PRES is not rare, especially in patients with disease activity, hypertension, lupus nephritis and/or renal insufficiency, and use of cytotoxic drugs, early recognition and appropriate treatment remain important. Brainstem involvement, intracranial hemorrhage, renal insufficiency and high disease activity of lupus are risk factors for poor prognosis.

Emergent headaches during pregnancy: correlation between neurologic examination and neuroimaging.

Emergent evaluation of the pregnant headache patient requires rational selection of acute neuroimaging studies, yet guidelines do not exist. We investigated the demographic and clinical features that are predictive of intracranial pathologic lesions on neuroimaging studies in pregnant women with emergent headaches. We conducted a retrospective review of demographic factors, clinical features, and radiologic findings in a consecutive case series of 63 pregnant women emergently evaluated with a chief complaint of headache, including those with previous headache histories. Clinical data were abstracted from emergency department records, hospital course, and discharge summaries. Multivariate logistic regression analysis examined predictors of intracranial pathologic lesions on emergent neuroimaging studies. Multiparous African American women constituted 63% of the case subjects. Headaches were frequently accompanied by photophobia (59%), nausea (52%), vomiting (37%), and occasionally with fever (11%), meningismus (9%), or seizures (7%). A total of 43% of case subjects had abnormal neurologic examination findings. Emergent neuroimaging, including noncontrast head CT and MR imaging, revealed an underlying headache etiology in 27%, including cerebral venous thrombosis, reversible posterior leukoencephalopathy, pseudotumor, and intracranial hemorrhage. The odds of having intracranial pathologic lesions on neuroimaging were 2.7 times higher in patients with abnormal results on neurologic examination (P=.085). Emergent neuroimaging studies may reveal an underlying headache etiology in 27% of pregnant women. Further research with a larger sample size is needed to determine what clinical factors are predictive of a pathologic condition on neuroimaging studies.

[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 young man presenting with acute encephalopathy, hemiparesis, and headache.

Familial hemiplegic migraine (FHM) is a rare type of migraine. Correct diagnosis is challenging for emergency physicians (EPs) due to its variable clinical picture, as well as its lack of diagnostic biological markers. To raise awareness among EPs regarding FHM's diverse clinical picture, and to highlight FHM's diagnostic criteria to facilitate an accurate and timely diagnosis of FHM in patients presenting to the emergency department (ED) with indicative symptomatology. A 24-year-old male student presented to the ED complaining of dizziness, general weakness, and blurred vision that had developed the previous night. The initial physical examination revealed drowsiness, slow speech production, and slight weakness with paresthesia in all limbs. Detailed communication with the patient's aunt revealed that he had experienced several similar attacks since the age of 12 years, and that there was also an extensive family history of the same symptoms. In addition, 2 h after arrival, the patient experienced severe throbbing headache, vomiting, severe dysphasia, and the weakness shifted to the right side. A computed tomography scan of the brain showed no anomalies. He was admitted with a tentative diagnosis of FHM. A diagnosis of FHM should be considered if the patient's clinical features include headache and weakness, with a family history of similar symptomatology. However, atypical symptoms of FHM may present as recurrent episodes of unexplained encephalopathy. Crucial elements for making an accurate and timely diagnosis of FHM include a detailed knowledge of weakness-related diseases and an ability to consider FHM in the differential diagnosis, as well as obtaining a thorough family history with repeated neurologic assessments.

A Rare Case of Cerebral Amyloidoma Mimicking a Hemorrhagic Malignant Central Nervous System Neoplasm.

Cerebral amyloidoma is a rare form of amyloidosis with a localized tumor like an amyloid deposition in the brain composed of insoluble fibrillary protein with cross beta-sheet conformation. Its usual presentation includes vision loss, seizures, behavioral changes, cognitive decline, and recurrent headaches. It has a benign course with a slow progression, and it is not associated with dissemination. We report a case of a 65-year-old Caucasian woman who presented with symptoms of progressively worsening cognitive dysfunction of six months' duration. From CT of the brain, it was found that she had a right frontal and left parietal hemorrhagic mass with a large amount of vasogenic edema and a midline shift. MRI showed heterogeneously enhancing hemorrhagic mass of 5.2 cm x 2.6 cm x 3.6 cm in size, with a satellite lesion. Initially, this was suspected to be a high-grade glioma vs. metastatic hemorrhagic lesions. She underwent stereotactic biopsy of the mass, and histopathology was consistent with cerebral amyloidoma with marked IgA lambda plasma cell differentiation. She did not have any evidence of systemic amyloidosis, and therefore, she is being clinically observed with a regular follow-up and annual CT surveillance. She has remained stable over the past two years, although she has residual cognitive dysfunction. Cerebral amyloidoma can mimic malignant central nervous system (CNS) neoplasms and should be considered as a differential of any single or multiple mass lesions occurring in the white matter region of the brain with a characteristic appearance of "hyperdense lesions" on CT. It is a benign disease with no metastatic potential that usually resolves entirely after resection.

Warning symptoms of sinister headache.

Headache is a common complaint. In most patients, it is usually a problem of migrainous or tension-type headache. It is crucial that a physician is able to differentiate sinister causes of headache from the more benign ones. Six cases are presented to illustrate the fact that there are clues in the history to suggest a sinister cause of headache even though there are minimal or no neurological deficits on physical examination. At some point of time, these cases were examined by a senior physician but they were diagnosed as migrainous or tension-type headaches. The first case is a 41-year-old labourer with cryptococcal meningitis. He presented with severe headaches at a relatively late age. A 20-year-old female complained of the worst headache she ever had and this was due to a subarachnoid haemorrhage. The third case was a young woman with a large parietal meningioma. Her headaches had recently assumed a different character. The fourth case involved an investment manager who developed headaches with transient diplopia and projectile vomiting and investigations revealed an ependymoma. A shipyard worker complained of a constant headache which disturbed his sleep. Two weeks after medical consultation, the character of his headache changed and he developed diplopia in all directions of gaze. He succumbed to pituitary apoplexy. The final case is a 28-year-old woman who had a complicated migraine. CT scan of the brain showed a large arterio-venous malformation.

[Changes of electroencephalographic findings in a case of migraine with various neurological symptoms].

We report here an 1-year-old boy who was diagnosed as sporadic hemiplegic migraine demonstrated transient changes in electroencephalographic (EEG) background activity accompanied with migraine attacks. The attacks were associated with various neurological complications such as impairment of consciousness and hemiplegia and so on, which coincided with the changes of EEG findings. When his first headache developed with fever and impairment of consciousness, diffuse slow waves (1-2 Hz, 250-300 microV) appeared transiently. The slow wave gradually improved thereafter, and disappeared on the 24th day. On the 25th day, when he had the second attack with left hemiplegia and impairment of consciousness and sensation, slow waves, (2-3 Hz, 250-300 microV) appeared on right side of the brain. Constriction of the right middle cerebral artery was found on MR angiography at that time. The EEG change had improved to normal background activity 3 days after the episode. This unique case demonstrated that transient EEG changes seem to be correlated with the existence of unconsciousness and the laterality of the ischemic insult. We may assume that the changes of electroencephalographic findings may represent the cortical dysfunction caused by vascular constriction.

[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma].

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)

Rare clinical findings in a patient with sporadic hemiplegic migraine: FDG-PET provides diminished brain metabolism at 10-year follow-up.

Sporadic hemiplegic migraine (SHM) is defined as migraine attacks associated with some degree of motor weakness during the aura phase and where no first-degree relative has identical attacks. SHM has a wide inter- and intraindividual clinical spectrum and, in case of prolonged aura symptoms and disturbed consciousness, can mimic several other acute neurological diseases. In 1996, during his wedding night, a 28-year-old man developed left face, arm and leg weakness, nausea and a throbbing headache. Neurological examination on presentation revealed stupor, fever, meningism and left hemiplegia. There were no abnormalities on emergency magnetic resonance. Lumbar puncture showed mild lymphocytic pleocytosis and slightly elevated protein. He received symptomatic treatment. Subsequent genetic analysis revealed the T666M mutation in the CACNA1A gene of chromosome 19. He was diagnosed with SHM. In 2005, at the end of another episode of hemiplegic migraine (HM), he for the first time developed an episode of paranoid psychosis with anxiety and visual hallucinations. The psychiatric symptoms resolved within a week. All perfusion SPECT and transcranial Doppler studies performed in the first days of HM attacks were consistent with hyperemia of the hemisphere contralateral to the neurological signs. FDG-PET/CT in January 2013 revealed a diffusely reduced glucose metabolism of the supratentorial cortex and marked asymmetric hypometabolism of the left cerebellum. The finding of progressive cortical metabolic dysfunction over years appears as a new finding. Glucose hypometabolism may indicate primary neuronal dysfunction as the cause of the prolonged deficits.

Atypical presentation in Rasmussen encephalitis: delayed late-onset periodic epileptic spasms.

A five-and-a-half-year-old girl started experiencing progressive left hemiparesis at age two and a half years. At age five years and four months she started presenting clusters of asymmetric periodic epileptic spasms with no hypsarrhythmia. The ictal EEG showed periodic, constant and stereotyped complexes. Serial brain imaging revealed progressive atrophy of the right hemisphere with increased T2 signal on MRI. She underwent a right hemispherotomy, and histological examination showed signs of inflammation and features of focal cortical dysplasia (FCD). She has been seizure-free for 16 months. This case is unique in the following aspects: the presence of typical Rasmussen encephalitis features of progressive unilateral brain involvement without seizures, a delay of almost three years prior to seizure onset; an atypical seizure type presentation with periodic epileptic spasms and the presence of FCD associated with inflammatory changes. [Published with video sequences].

Clinical predictors of significant intracranial computed tomography scan findings in adults experiencing headache disorder.

Radiological assessments for adult headache disorder show significant intracranial findings in 2.5% to 10% of performed computed tomography scans (CT-scans), leading to an overuse consideration for CT-scan requests by physicians in headache-experiencing patients. Therefore, we undertook this study in order to determine predictors of significant intracranial CT-scan findings in adults experiencing headache disorder; in order to help physicians better select patients who need imaging, which would subsequently decrease the costs of headache disorder management and the useless irradiation rates. We carried out a cross-sectional study in the medical imaging departments of Yaounde Central Hospital and Douala Laquintinie Hospital, which are two teaching hospitals in Cameroon, over a period of five months. We consecutively and non-exhaustively included all consenting patients aged eighteen years and above, referred to the radiology department to perform a head CT-scan as aetiological workup of headache disorder, from either a traumatic or non-traumatic mechanism. Patients having a known brain lesion and those with a Glasgow coma scale less than thirteen were excluded. The clinical history of patients was taken and a complete physical examination was performed. Demographic data, clinical characteristics of the headache, results of neurological and physical examinations were collected and correlated to the results of head CT-scan. We enrolled 169 patients in the study, 56.2% were males, with a sex ratio of 1.3; sudden onset of headache increased by two the risk of discovering significant intracranial pathology (p = 0.032). Occipital and cervical location of headache, headache evolving by crisis, and recurrent paroxysmal headache were rather significantly correlated to no structural brain finding. An abnormal neurological examination with specifically abnormal stretch reflexes, aphasia, loss of consciousness, raised intracranial signs, weakness, and meningeal signs were predictive of structural intracranial pathology. Otorrhagia, epistaxis, and periorbital ecchymosis in addition were predictive in post-traumatic headaches. Abnormal results from neurological examination are the best clinical parameters to predict structural intracranial pathology on CT-scan in adult patients experiencing headache disorder. In case of post-traumatic headaches, in addition, otorrhagia, epistaxis, and periorbital ecchymosis are too highly predictive.

[A case of traumatic subacute subdural hematoma presenting symptoms arising from cerebral hemispheric edema].

Traumatic subacute subdural hematoma is a condition in which the major symptoms affecting prognosis most appear in the subacute stage after head trauma, while traumatic acute subdural hematoma is treated conservatively when the symptoms are mild. The cause of the major symptoms occurring in the subacute stage is mostly expansion of the subdural hematoma volume. The authors report a case of traumatic subacute subdural hematoma in which the cause of the major symptoms was cerebral hemispheric edema instead of expansion of the subdural hematoma volume. To our knowledge, only one similar case to the present case has been previously reported. A 44-year-old female fell from the stairs on July 21, 1995 and was suffering from headache. On July 23, she was admitted to our hospital because of generalized convulsion. On admission, she was drowsy but showed no convulsion. Head CT showed an acute subdural hematoma on the right side with a slight midline shift and no other abnormalities. She was treated conservatively because of the mildness of the symptoms and two days later became alert with no symptoms. Thereafter she only complained of occasional headache which was controlled with medicine. On August 3, she suddenly fell into coma. Head CT showed severe cerebral hemispheric edema on the right side without change of the subdural hematoma size. Emergency cerebral angiography showed no definitive abnormalities such as occlusion of the arteries or of the venous sinuses. Craniotomy associated with external decompression was performed. The hematoma was composed of red-brown jelly accompanied with some liquid component and had a thin black-brown outer membrane. While removing the hematoma, bleeding from a vein on the cerebral surface around the sylvian fissure was observed and this location was suspected to be the sources of the bleeding point. Postoperatively, she received steroid and barbiturate therapy associated with moderate hypothermia under hyperventilation. She tolerated this treatment well and left the hospital, on September 26, 1995 with only diplopia during downward gaze. Although the mechanisms of the cerebral hemispheric edema occurring in the subacute stage was unclear, a failure in the cerebral venous circulation arising from compression to the bridging veins, which may be hypoplastic, by the subdural hematoma was suspected to have been the cause.

A Rare Case of Fatal Hemorrhagic Stroke in a Young Female with Early Mixed Connective Tissue Disease.

Mixed connective tissue disease (MCTD) often presents as a slow progressive illness with low morbidity and mortality. Serious central nervous system disease is uncommon, and fatal outcomes are rarely seen. Here, we report a rare case of fatal hemorrhagic stroke in a 43-year-old female with a rapidly progressive MCTD. She presented to primary care with a history of headaches, visual disturbances, and unprovoked lower extremity swelling and pain. A rheumatological workup showed positive antinuclear (ANA) and ribonucleoprotein (RNP) antibodies. Magnetic resonance imaging (MRI) found a 12 mm hemorrhage along a cortical sulcus of the right frontal lobe, and a follow-up magnetic resonance angiography (MRA) and ophthalmological exam showed no definitive signs of vasculitis. Over the course of her workup, she developed swollen hands, Raynaud's syndrome, myalgias, and synovitis characteristic of evolving MCTD. The patient then began to experience severe headaches over one month. Repeat MRI was ordered, but never completed, and the patient presented to the emergency department (ED) with a severe, right-sided headache, and left-sided visual disturbance. In the ED, she began to display evidence of delirium and seizure activity and became unresponsive. A computerized tomography scan (CT) of the brain showed a right parietal lobe intraparenchymal hemorrhage approximately 5 × 3 × 5 cm in size with secondary mass effect including mid- and hind-brain herniation. Computerized tomography angiography (CTA) of the brain showed signs of large vessel vasculitis. A craniectomy was performed; however, the patient never regained consciousness and died several days later. Vasculitis, while rare in connective tissue diseases, should be aggressively assessed for and managed in patients with any early signs and symptoms of cerebrovascular involvement to prevent fatal outcomes.

Post-epileptic headache and migraine.

One hundred epileptic patients were questioned about their headaches. Post-ictal headaches occurred in 51 of these patients and most commonly lasted 6-72 hours. Major seizures were more often associated with post-epileptic headaches than minor attacks. Nine patients in this series of 100 also had migraine: in eight of these nine a typical, albeit a mild, migraine attack was provoked by fits. The post-ictal headache in the 40 epileptics who did not have migraine was accompanied by vomiting in 11 cases, photophobia in 14 cases and vomiting with photophobia in 4 cases. Furthermore, post-epileptic headache was accentuated by coughing, bending and sudden head movements and relieved by sleep. It is, therefore, clear that seizures provoke a syndrome similar to the headache phase of migraine in 50% of epileptics. It is proposed that post-epileptic headache arises intracranially and is related to the vasodilatation known to follow seizures. The relationship of post-epileptic headache to migraine is discussed in the light of current ideas on migraine pathogenesis, in particular the vasodilation which accompanies Leao's spreading cortical depression.

[Three Japanese cases of hypnic headache].

We described three cases of hypnic headache with successful treatment by lithium carbonate or caffeine. This is the first detail report of Japanese cases. An endocrinological test and rhythm analyses of ambulatory blood pressure (ABP) and heart rate variability in a case suggested possible association between hypnic headache and hypothalamic-pituitary dysfunction. Case 1: A 48-year-old female migraineur complained of new-onset nocturnal headaches. Her headache awakened her from sleep between 1 AM and 2 AM. The headache occurred 3-4 times per week and lasted from 1 hour to 2 hours. The headache were moderate intensity and bilateral dull throbbing pain that located in the forehead to temples. There was no accompanying symptoms such as nausea, phonophobia, photophobia, nor the other autonomic features including conjunctival injection or tearing during the headache attacks. Physical and neurological examinations showed normal results except slight weakness and mild dysesthesia of the left arm due to a vertebral disk herniation at C5/6 level. In the pituitary endocrinological test, the prolactin level remarkably increased in response to the TRH loading. The single cosinor analysis demonstrated significant circadian rhythm of ABP parameters. However, the analysis did not demonstrate any significant circadian rhythm of Holter ECG parameters of time domain analysis and frequency analysis. Receiving 200 mg lithium bicarbonate before sleep, her nocturnal headache completely disappeared. Case 2: A 68-year-old woman had been followed up by her chronic tension-type headache since her forties. At her 66-years, she suffered from a new nocturnal headache. She awoke from sleep by the headache about 3 AM and the headache lasted 30 min. Moderate, dull headache located on her left temple to parietal head, 3-4 times/week. She was able to go back asleep without any medication after spontaneous headache cessation. She first complained the nocturnal headache at the 10 months later of the new headache appearance. She received 200 mg caffeine just before sleep and her headache has been disappeared. Case 3: 70-year-old women had been regularly visited our clinics for her migraine and chronic tension-type headache. She received amitriptyline and her headaches was well controlled. At her 69 years, she complained nocturnal headache. It occured every other day. The headache was moderate pulsative dull pain on the occipital region and lasted 90 minutes without any autonomic symptoms. Headache began between midnight and 1 AM. She told us her new nocturnal headache one year later of the onset. Oral caffeine (200 mg) just before sleep did not improve her headache and caused insomnia. Receiving 100 mg lithium before sleep, her hypnic headache disappeared completely. These three cases are compatible with the diagnostic criteria proposed in ICHD-II. There were some patients with hypnic headache in Japan and neurologists should pay attentions to this form of benign headache, because some beneficial treatments are currently available.

Case 284.

History A 36-year-old left-handed woman with a history of developmental delay and medical refractory seizures since birth most recently presented with continuous simple partial seizures and occasional breakthrough complex partial seizures with postictal migraines. These were described as the patient "becoming pale with sinking to the floor and staring for approximately 1 minute with confusion thereafter." The patient had years of reported seizure freedom until 2010 when she was evaluated for intractable headaches, and electroencephalography revealed her focal subclinical status. At that time, ambulatory electroencephalography findings showed asymmetric left parietal-occipital high-amplitude spike-and-wave discharges in her best awake and alert state. Since that time, the patient developed and continues to have complex partial seizures every 2-3 months that are persistent despite the implementation of several medical regimens. At the time of recent presentation, the patient initially underwent unenhanced head CT in the emergency department followed by unenhanced MRI of the brain due to increased seizure activity at the patient's group home despite continued compliance with her antiepileptic regimen. Contrast material-enhanced imaging was not available at the time of recent presentation, so comparison was made with gadolinium-enhanced brain MRI performed approximately 9 years earlier (Figs 1-5).

Paraneoplastic Encephalopathy in a Patient With Metastatic Lung Cancer: A Case Study.

<bCASE STUDY</b RS, a 36-year-old female, presented to the emergency department (ED) of a large academic medical center upon the advice of her primary care provider because of 3 weeks of progressive mental status changes, weakness, and decreased oral intake. According to her husband, RS was diagnosed with stage IIIA large cell lung cancer 8 months earlier and was treated with concurrent chemotherapy (carboplatin, pemetrexed, and bevacizumab) and radiation therapy that was completed 4 months prior to admission. No other specific information about her treatment or outside health records was available. According to her husband, RS had been in her usual state of health until approximately 3 weeks prior, when she began having significant mental status changes. She first exhibited some difficulty finding words and later was noted to be putting food in a coffee maker. This spontaneously resolved after approximately 1 week; however, she rapidly developed slurred speech and began to make nonsensical statements. These manifestations also slowly improved but were followed by worsening speech deficit, difficulty walking, and impaired balance. During one of these episodes, she had an occurrence of incontinence. Her husband also noted an incident where her "eyes were beating back and forth and the left side of her face was twitching." RS also had periods (according to her husband) where she "did not seem to be interacting with her environment." These progressively worsened during the last week, and she completely stopped walking and talking 2 days prior to coming to the ED. According to her husband, RS had rheumatoid arthritis and no surgical history. Her family history was unknown except that RS's mother had "seizures." RS had reportedly not used tobacco, alcohol, or drugs, and she was sexually active with her husband. Home medications included transdermal fentanyl 12 μg/hr patch changed every 72 hours; oxycodone-acetaminophen tablets 5-325 mg, two every 4 hours as needed for pain; prednisone 10 mg, one tablet daily; and megestrol 40 mg/mL suspension, 20 mL once daily for appetite stimulation. RS was admitted to an inpatient medical oncology service and evaluated by the oncology advanced practitioner (AP) on her second inpatient day. Upon exam, RS was nonverbal except for moaning in response to painful stimuli and to her sister's voice. Her vital signs were normal. She appeared ill but well-nourished, and she was mildly diaphoretic. Neurologic examination revealed that her pupils were slightly sluggish but equal, round, and reactive to light. Extraocular muscle movements were intact, but she did not move her eyes in response to commands. She tracked the AP and family members around the room with her eyes. Cranial nerve examination was intact with the exception of cranial nerves IX, X, and XI, which were difficult to examine given her inability to cooperate and open her mouth. Motor examination revealed increased tone throughout and intermittent, inconsistent resistance to passive movement. She was seen to move all four extremities spontaneously although not in response to commands. Deep tendon reflexes were intact and equal in all extremities. Examination of other body systems was as follows: there was dry, peeling skin on her lips, but her mucous membranes were moist and free of erythema or lesions. Her lungs were clear to auscultation bilaterally. Her heart rate and rhythm were regular, there were no murmurs, rubs, or gallops, and distal pulses were intact. Her abdomen was nondistended with normally active bowel sounds in all four quadrants. Her abdomen was soft, nontender to palpation, and without palpable masses. There was no peripheral discoloration, temperature changes, or edema, and examination of her skin was benign. <bWorkup</b On admission to the emergency department, serum laboratory studies were unrevealing for any potential causes of encephalopathy. Kidney and liver function were normal, making diagnoses of uremic and hepatic encephalopathies less likely. Cultures of the urine and blood were negative. Samples of cerebrospinal fluid (CSF) were obtained via lumbar puncture and were unrevealing for any abnormalities. Computed tomography (CT) of the head without contrast was negative for any acute intracranial process. Ultrasound of the right upper quadrant revealed a single, nonspecific, hypoechoic hepatic lesion. Computed tomography scans of the chest, abdomen, and pelvis demonstrated the primary malignancy in the upper lobe of the left lung, as well as possible metastatic disease within the left lung, right lung, and liver, and widespread osseous metastatic disease. Magnetic resonance imaging (MRI) of the brain performed 1 day after admission demonstrated numerous scattered punctate foci of enhancement throughout the supratentorial and infratentorial brain parenchyma, measuring at most 3 to 4 millimeters in diameter. There was no significant mass effect or midline shift. A paraneoplastic panel was sent to an outside laboratory and returned positive for antivoltage-gated potassium channel (VGKC) autoantibodies. <bDifferential Diagnosis</b Clinically, RS was exhibiting signs of encephalopathy, a broad term that indicates general brain dysfunction, the hallmark of which is altered mental status. Diagnosing encephalopathy is challenging, as many differential diagnoses must be considered. The clinician must consider metabolic derangements, toxic and infectious etiologies, psychiatric disorders, and less commonly, prion disorders and progressive dementia. Cultures of RS's blood and urine as well as other specialized endocrine tests were negative, decreasing the likelihood of a metabolic or infectious cause for her presentation. The abnormalities on her brain MRI were reviewed by a neuro-oncology team, who felt that the faint, nondescript nature of the visualized lesions was not suspicious for metastatic disease. Sequelae of seizures was also considered by neuro-oncology but dismissed given a grossly normal prolonged electroencephalogram. Some encephalopathies are caused by autoimmune or inflammatory mechanisms, which are confirmed by the presence of autoantibody markers and/or clear response to immunomodulatory treatment (Vernino, Geschwind, & Boeve, 2007). These types of encephalopathies have been seen in patients with cancer and have thus been termed paraneoplastic. The presence of anti-VGKC antibodies on RS's paraneoplastic panel directed the inpatient medical oncology team toward a paraneoplastic neurologic disorder (PND) as the most likely diagnosis.

Incidence and pattern of headache in cerebral venous thrombosis.

Cerebral venous thrombosis (CVT) is a challenging condition because of the variability of clinical presentations. CVT can present at all ages, but is seen more in young and middle-aged women. CVT does not necessarily occur only when there is an obvious underlying etiology. In almost 30% of cases, the etiology cannot be established. CVT can present with an acute thunderclap headache, fever, seizures, focal deficits, impaired sensorium, or papilloedema. Headache is known to be the most frequently associated initial complaint, and is present in more than 80% of patients, but it is not always remembered that headache can be the sole presenting complaint of CVT and even when early papilloedema is absent. Headache can occur in isolation in up to 5% of CVT cases. There is no identifiable, uniform, recognizable pattern of headache in CVT, but this article discusses the "Headache Profile" that is seen more commonly in this setting with an illustration of one such case where the innocuous headache turned sinister. Magnetic resonance imaging with venography is the investigation of choice to diagnose CVT; computed tomography alone will miss a significant number of cases. One must keep in mind the possibility of CVT in every patient who presents with new-onset headache of any type, any severity, and in any location, particularly when there is worsening in spite of analgesics. Earlier the diagnosis, earlier the treatment, better is the outcome.

Grade III solitary fibrous tumor/hemangiopericytoma: An enthralling intracranial tumor-A case report and literature review.

Hemangiopericytomas account for less than 1% of all intracranial tumors. In 2016, World Health Organization (WHO) unified the two terms into a single medical condition known as solitary fibrous tumor/hemangiopericytoma (SFT/HPC). Our patient is an 80-year-old woman with a past medical history of sick sinus syndrome status post pacemaker placement. She presented to the emergency department with progressive headaches for one month duration. Her headaches worsened at night, waking her up from sleep. They also increased in intensity by bending forward. Review of systems was significant for bilateral lower extremity weakness accompanied by difficulty walking. The motor exam was remarkable for right upper and right lower extremity 3/5 weakness. The gait was ataxic. A Computed tomography scan of the head without contrast revealed a large dural-based right parietal hyperdense mass with surrounding edema, mass effect, and compression of the right lateral ventricle atrium. A right-to-left midline shift was also noted. Given the fact that our patient had a pacemaker, she was not a candidate for a brain MRI. Neurosurgery successfully resected the mass. Histopathological studies confirmed WHO grade III anaplastic solitary fibrous tumor/hemangiopericytoma. The patient was discharged on adjuvant radiation with imaging surveillance given the grade and the extent of resection. This case highlights a rare type of intracranial mass that resembles meningioma on imaging studies. It also illustrates that solitary fibrous tumor/hemangiopericytoma should be kept as a differential diagnosis for brain masses, given its aggressive nature, and its potential of metastasis and recurrence.

Case of the month: April 1997--a 32 year old man with mental status changes and a severe occipital headache.

A 32 year old man with symptoms of an upper respiratory infection one week prior presented with mental status changes, diffuse hyperreflexia, and bilateral extensor plantar responses. An MRI scan showed multifocal areas of high signal intensity predominantly in the parietal and occipital white matter, unassociated with mass affect. Despite aggressive treatment, the patient's symptoms rapidly progressed and he was declared brain dead. Post-mortem examination revealed acute hemorrhagic leukoencephalopathy. The clinical and pathologic features of this disorder are reviewed.

Reversible cerebral vasoconstriction syndrome

Signs and symptoms The key symptom of RCVS is recurrent thunderclap headaches, which over 95% of patients experience. In two-thirds of cases, it is the only symptom. These headaches are typically bilateral, very severe and peak in intensity within a minute. They may last from minutes to days, and may be accompanied by nausea, photophobia, phonophobia or vomiting. Some patients experience only one headache, but on average there are four attacks over a period of one to four weeks. A milder, residual headache persists between severe attacks for half of patients. 1–17% of patients experience seizures. 8–43% of patients show neurologic problems, especially visual disturbances, but also hemiplegia, ataxia, dysarthria, aphasia, and numbness. These neurologic issues typically disappear within minutes or a few hours; more persistent symptoms may indicate a stroke. Posterior reversible encephalopathy syndrome is present in a small minority of patients.

Postpartum trifecta: simultaneous eclamptic intracerebral hemorrhage, PRES, and herniation due to intracranial hypotension.

In the postpartum patient, sudden depression of consciousness may be caused by a number of etiologies and can result in serious consequences. Rapid, accurate diagnosis allows for specific treatments that optimize outcome, but diagnosis can be challenging in this population. We present a case of postpartum herniation due to intracranial hypotension in a patient with eclampsia, posterior reversible encephalopathy syndrome (PRES), and intracerebral hemorrhage (ICH). Case report. A 26-year-old woman developed headache on postpartum day (PD) 1 after cesarean section with epidural anesthesia. Over the next 3 days, she developed progressively worsening headache and hypertension. On PD 5, she had a generalized seizure, leading to endotracheal intubation, propofol infusion, and transfer to our institution. By PD 6, she opened her eyes to voice, followed commands, moved all extremities, and had briskly reactive 4 mm pupils. MRI showed L parasagittal ICH with minimal mass effect, edema consistent with PRES, and brain descent with obliteration of the basal cisterns and tonsillar herniation. Later on PD 6, after diuresis for pulmonary edema, she became unresponsive with a dilated and nonreactive left pupil. She was laid flat for transport to CT, with improvement in arousal and pupil reactivity within 5 min. Intravascular volume was repleted with normal saline and albumin, and she was placed in the Trendelenburg position. Over the subsequent 8 h, she developed a dilated and nonreactive left pupil whenever her head was raised to horizontal. Her head position was gradually successfully raised over 48 h without need for a lumbar epidural blood patch. She was discharged home on PD 13 with only mild left arm dysmetria. Intracranial hypotension may coexist with other potential causes of cerebral herniation in the postpartum period. Establishing this diagnosis is crucial because its treatment is opposite that of other causes of herniation.

[Headache originating front-orbital area].

Headache originating front-orbital area can be divided to (1) Which has no autonomic symptoms such as lacrimation, rhinorrea, rhinostasis. This include psychogenic headache and epileptic headache. In the case of psychogenic headache, pericranial tenderness is not observed, and headache is medium in intensity. Most often patient complains of a headache originating frontal area. There are more than five various symptoms such as general malaise, numbness, tingling sensation, vertigo, sleeplessness. However, although symptoms are multiple, patients spend a life commonly. In other words, a patient is protected by a headache against his or her stress. No medication is needed in such a case. In epileptic headache, pressing type pain is felt over the forehead for several minutes to a few hours. Tremor or convulsion sometimes follow the headache. EEG shows spike and wave activities. In the case of focal epilepsy, headache occurs contralateral to the focus. Anti-epileptic drugs such as VPA or CBZ is a choice in such case, and headache as well as seizure disappears. (2) Front-orbital headache with autonomic symptoms include various trigeminal autonomic cephalalgias. These include cluster headache, episodic paroxysmal hemicrania, hemicrania continua, among others. Precise history taking is necessary for the treatment, because no drug is 100% effective.

Severe cerebral edema following nivolumab treatment for pediatric glioblastoma: case report.

Nivolumab is an immune checkpoint inhibitor (ICI) currently undergoing Phase III clinical trials for the treatment of glioblastoma. The authors present the case of a 10-year-old girl with glioblastoma treated with nivolumab under compassionate-use guidelines. After the first dose of nivolumab the patient developed hemiparesis, cerebral edema, and significant midline shift due to severe tumor necrosis. She was managed using intravenous dexamethasone and discharged on a dexamethasone taper. The patient's condition rapidly deteriorated after the second dose of nivolumab, demonstrating hemiplegia, seizures, and eventually unresponsiveness with a fixed and dilated left pupil. Computed tomography of her brain revealed malignant cerebral edema requiring emergency decompressive hemicraniectomy. Repeat imaging demonstrated increased size of the lesion, reflecting immune-mediated inflammation and tumor necrosis. The patient remained densely hemiplegic, but became progressively more interactive and was ultimately extubated. She resumed nivolumab several weeks later, but again her condition deteriorated with headache, vomiting, swelling at the craniectomy site, and limited right-sided facial movement following the sixth dose. MRI demonstrated severe midline shift and uncal herniation despite her craniectomy. Her condition gradually declined, and she died several days later under "do not resuscitate/do not intubate" orders. To the authors' knowledge, this represents the first case of malignant cerebral edema requiring operative intervention following nivolumab treatment for glioblastoma in a pediatric patient.

Headache in Cerebral Venous Thrombosis: incidence, pattern and location in 200 consecutive patients.

We analyzed the incidence, pattern and location of headache in consecutive 200 patients with proven diagnosis of CVT to identify an association between localization of headache and site of sinus involvement. Headache was present in 136 (68%) patients. The duration of headache (reported in 128 patients) was reported as acute (1-3 days), 81 patients (60%); sub-acute (4-14 days), 33 patients (24%); and chronic (more than 14 days), 14 patients (10%). The quality of headache (reported in 72 patients) was reported as throbbing 12 (9%), band like 27 (20%), thunderclap 7 (5%), and other (pounding, exploding, stabbing, etc.) 26 (20%). The location of headache (reported in 101 patients) was reported as unilateral (one side of head) 48 (37%), localized (frontal, temporal, occipital, and neck) 25 (19%), and diffuse (whole head) 28 (20%). 43 (32%) patients had normal neurological examination (normal mental status, cranial nerves, motor and sensory examination with down going planters). 93 (68%) patients have abnormal findings on neurological examination including papilledema 29 (15%) patients, altered mental status 38 (19%), and focal neurological deficit 45 (22%) patients. There was no association between headache and presence of hemorrhage on CT and MRI (P = 0.1) or hydrocephalus (P = 0.09). There was no association between localization of headache and site of sinus thrombosis except sigmoid sinus thrombosis, where 17 out of 28 patients with involvement of sigmoid sinus alone or in combination with transverse sinus had pain in the occipital and neck region (P < 0.05). There was no association between lateralization of pain and site of thrombosis (P = 0.66).

Status Epilepticus and Blindness in a Patient with Carfilzomib-Associated Posterior Reversible Encephalopathy Syndrome.

Posterior reversible encephalopathy syndrome (PRES) is a neurological condition characterized by headaches, visual disturbances, and seizures. A magnetic resonance imaging (MRI) scan of an affected brain typically shows symmetrical white matter edema in the posterior cerebral hemispheres. The onset of PRES can constitute a medical emergency, especially when accompanied by status epilepticus. If promptly recognized and treated, the clinical syndrome and associated radiological findings are usually resolved in a matter of weeks or months. Carfilzomib is a proteasome inhibitor that is newly approved for relapsing myeloma in a patient who has received one or more lines of therapy. In this paper, we report on a 52-year-old female on carfilzomib for multiple myeloma who developed PRES following her second dose of treatment. She was admitted for chronic obstructive pulmonary disease (COPD) exacerbation, and while she was in the hospital, she developed a severe headache, blindness, and status epilepticus. A brain MRI showed signs consistent with PRES. After carfilzomib was discontinued, her symptoms resolved within three days. Unfortunately, the patient passed away shortly after being discharged, so there was no opportunity to perform a repeat MRI.

Sudden onset headache: a prospective study of features, incidence and causes.

Sudden onset headache is a common condition that sometimes indicates a life-threatening subarachnoid haemorrhage (SAH) but is mostly harmless. We have performed a prospective study of 137 consecutive patients with this kind of headache (thunderclap headache=TCH). The examination included a CT scan, CSF examination and follow-up of patients with no SAH during the period between 2 days and 12 months after the headache attack. The incidence was 43 per 100 000 inhabitants >18 years of age per year; 11.3% of the patients with TCH had SAH. Findings in other patients indicated cerebral infarction (five), intracerebral haematoma (three), aseptic meningitis (four), cerebral oedema (one) and sinus thrombosis (one). Thus no specific finding indicating the underlying cause of the TCH attack was found in the majority of the patients. A slightly increased prevalence of migraine was found in the non-SAH patients (28%). The attacks occurred in 11 cases (8%) during sexual activity and two of these had an SAH. Nausea, neck stiffness, occipital location and impaired consciousness were significantly more frequent with SAH but did not occur in all cases. Location in the temporal region and pressing headache quality were the only features that were more common in non-SAH patients. Recurrent attacks of TCH occurred in 24% of the non-SAH patients. No SAH occurred later in this group, nor in any of the other patients. It was concluded that attacks caused by a SAH cannot be distinguished from non-SAH attacks on clinical grounds. It is important that patients with their first TCH attack are investigated with CT and CSF examination to exclude SAH, meningitis or cerebral infarction. The results from this and previous studies indicate that it is not necessary to perform angiography in patients with a TCH attack, provided that no symptoms or signs indicate a possible brain lesion and a CT scan and CSF examination have not indicated SAH.

Posterior Reversible Encephalopathy Syndrome Causing Vision Loss After Endoscopic Endonasal Resection of Pituitary Adenoma.

Posterior reversible encephalopathy syndrome (PRES) is characterized by headache, altered mental status, visual changes, and seizure combined with brain imaging consistent with cerebral edema without infarction. To the best of our knowledge, we report the first case of PRES after an endoscopic endonasal resection of a pituitary macroadenoma. A 59-year-old woman was diagnosed with a pituitary macroadenoma, for which she underwent endoscopic endonasal extracapsular resection. After an uneventful initial postoperative recovery, the patient experienced sudden onset of emesis, confusion, vision loss, and severe hypertension. Emergent computed tomography showed normal postoperative changes, with no signs of hematoma or infarction. Magnetic resonance imaging (MRI) showed fluid-attenuated inversion recovery changes in the posterior lobes and thalamus, consistent with PRES. Cerebral angiography showed no vascular abnormalities. Blood pressure control was the primary treatment modality. Within 10 days, the patient was neurologically intact except for right homonymous hemianopsia. Follow-up MRI showed resolution of the PRES with an area of infarction in the left occipital lobe. At 5 years follow-up, the patient reported minimal blurred vision. MRI showed encephalomalacia at the old infarct area, and her visual field testing was unremarkable. Although rare in neurosurgical patients, PRES must be considered in patients who develop acute vision loss and mental status changes associated with hypertension after surgery, including endoscopic endonasal surgery. PRES has the potential for significant neurologic morbidity, if not treated in a timely manner. Early recognition and treatment, with blood pressure control mainly, are therefore mandatory after a surgical complication, such as a postoperative hematoma, has been ruled out.

[An unusual case of status epilepticus of simple partial seizure with an occipital lobe focus].

A 45-year-old man developed generalized convulsion and consciousness disturbance at age 43. An X-ray CT revealed hemorrhagic infarction in the left fronto-parieto-temporal area. A conventional angiography disclosed complete occlusion of the left cortical vein. In the chronic stage of the stroke, he had incomplete right quadrantopsia, a mild right hemiparesis and sensory aphasia. The patient has had partial somatosensory seizures since February 1990. Ictal EEG recordings showed epileptogenic discharges in the left parietal region. The seizures were adequately controlled with clonazepam. Since July 27, 1993, he has become aware of blurred vision in both eyes accompanied with headache and dizziness. On August 6, he was admitted to the hospital with right homonymons hemianopsia, sensory aphsia and tonic seizures in the right hand. Ictal EEG recordings demonstrated theta waves of the left parieto-occipital region and epileptogenic discharges in the left occipital region which consisted of spikes, sharp waves and spike-wave complexes. Single photon emission computed tomography (SEPCT) images obtained during seizures showed considerable hyperperfusion in the left occipital temporal lobes, while there was hypoperfusion in the left temporo-parietal area corresponding to the lesion of the old cerebral infarction. A T2-weighted MRI scan showed an abnormal high-intensity area in the left occipital lobe that suggested brain edema. After the admission, the patient was treated with additional anticonvulsant drugs. The tonic seizures in the right hand disappeared and right homonymous hemianopsia and sensory aphasia showed gradual improvement in the next four weeks.(ABSTRACT TRUNCATED AT 250 WORDS)