Midbrain Hemorrhage Research Articles

Variations of Tentorial Notch Anatomy in Autopsy and NCCT of Head Injury Patients to Correlate Its Impact over Brainstem—An Observational Study

Abstract Background Tentorium cerebelli divide cranial cavity into supratentorial and infratentorial compartment. Tentorial notch is a gap in tentorium cerebelli located centrally and anteriorly, related to upper brainstem, first six cranial nerves, cerebrum, and cerebellum. The aim of this study was to analyze morphometric variation in tentorial notch anatomy in autopsy and computed tomography (CT) of head injury patients and to find out correlation between tentorial notch anatomy and uncal herniation and changes over brainstem surface in case of uncal herniation. Materials and Methods Autopsy examination of head injury patients was done between July 1, 2021, and Jan 31, 2023. Skull was opened in a standard manner and midbrain sectioned at the level of tentorial edge. Tentorial notch parameters (anterior notch width, maximum notch width, notch length, posterior tentorial length, apicotectal distance, interpedunculoclival distance) were measured using geometry compass and vernier caliper. These parameters were also measured on noncontrast computed tomography (NCCT) head of same patients. Evidence of uncal herniation was sought for in both NCCT head and autopsy examination. Impact of uncal herniation over brainstem in form of indentation over lateral surface of midbrain and macroscopic brainstem hemorrhage was noted. Results In 65 autopsy cases, there were 56 male and 9 female specimens; their mean age was 40.63 ± 16.78 years (range: 7–86 years). The most frequent type of tentorial notch observed in our study was typical type (32.30%). Relative frequency of uncal herniation was present predominantly (75%) in large type of tentorial notch and least (20%) in small type of tentorial notch. A significant correlation (p-value < 0.01) was found between uncal herniation and indentation over lateral surface of midbrain, while no significant correlation (p-value > 0.05) was found between uncal herniation and macroscopic brainstem hemorrhage in autopsy specimens. Conclusion The results of our study provide a baseline data about tentorial notch anatomy and it may facilitate neurosurgical decision making as well as help in deciding the best trajectory for lesions approaching in the vicinity of the tentorial notch

Ruptured brainstem arteriovenous malformation associated with a thalamoperforating artery aneurysm arising from the P1 segment of the right posterior cerebral artery: illustrative case.

Cerebral aneurysms of perforating arteries are rare and can be difficult to detect on computed tomography angiography (CTA) and digital subtraction angiography. Treatment is challenging and associated with a significant risk of morbidity. Endovascular treatment of a thalamoperforating artery (TPA) aneurysm within the midbrain has not previously been reported. A 13-year-old girl with no previous medical history presented with unconsciousness and anisocoria. Head computed tomography showed a right midbrain hemorrhage. CTA showed a midbrain arteriovenous malformation fed by a TPA aneurysm arising from the P1 segment of the right posterior cerebral artery. The feeder had a small distal aneurysm, which increased in size over time. Endovascular embolization was then performed. Cerebral aneurysms of perforating arteries are rare and can be difficult to treat. This is the first report of the endovascular treatment of a TPA aneurysm within the midbrain. Understanding the individual patient's brainstem perforator anatomy and the associated blood flow is essential before occluding a TPA aneurysm to avoid causing ischemia or infarction. Arteriovenous malformation embolization within the brainstem should be avoided because of interperforator anastomoses.

Flow diversion jet: A dangerous mechanism in the flow diversion treatment of giant intracranial aneurysms.

Cerebral hyperperfusion syndrome (CHS) occurs after the restoration of blood flow to a previously low-flow, low-pressure region of the cerebral vasculature, which subsequently responds with chronic compensatory vasodilation, leading to a dysregulated state. Sudden restoration of normal blood flow can overwhelm the vasculature leading to intracranial hemorrhage (ICH). Separately, the Windkessel phenomenon describes the capacity for elastic vessels to expand with systolic pressure and decompress with diastole, thereby suppressing distal pulse pressure. We encountered a case involving giant basilar aneurysms in which we believe the Windkessel phenomenon precipitated a catastrophic manifestation of CHS at treatment. We present a 60-year-old female found to have marked dolichoectasia of the right cervical internal carotid, vertebral, and basilar arteries concurrent with two large vertebrobasilar dissecting-type fusiform aneurysms. Managed conservatively for ten years before developing gait ataxia, new imaging revealed dramatic interval growth of the larger aneurysm. Flow diversion with partial coiling of the aneurysms was pursued. The patient suffered intra-procedural catastrophic thalamic and midbrain hemorrhage with intraventricular extension. A meticulous review of the case data was undertaken. Our findings suggest that giant aneurysms can act as a Windkessel reservoir, depressing the distal pulse pressure. Flow diversion bypasses the reservoir, increasing the distal pulse pressure beyond the autoregulatory capacity, resulting in ICH analogous to CHS. CHS and Windkessel phenomenon can contribute to catastrophic sequelae in the treatment of giant intracranial aneurysms with flow diversion. Awareness of this mechanism can protect future patients from harm.

Abstract Number ‐ 121: Flow Diversion Jet: A Dangerous Mechanism in the Flow Diversion Treatment of Giant Intracranial Aneurysms

Introduction We present a patient with a giant vertebrobasilar system aneurysm. This case provides an in‐depth analysis of the pathologic mechanism resulting in catastrophic distal hemorrhage following stent deployment due to the shared effects of normal perfusion pressure breakthrough (NPPB) and the Windkessel phenomenon. The Windkessel phenomenon and NPPB occur before and after treatment of various vascular malformations, respectively. These phenomena are hypothesized to contribute to the loss of cerebrovascular autoregulation. High flow lesions and giant aneurysms reduce blood flow in downstream vessels, causing chronic distal vasodilation to protect against ischemia. Sudden restoration of normal pulsatile flow, following treatment, compromises the integrity of distal vessels leading to potential catastrophic intracerebral hemorrhage. Methods A retrospective review of the patient’s medical record was performed. Results A 60‐year‐old female initially presenting with pulsatile neck mass was found to have dolichoectasia of the right cervical internal carotid artery and two large, irregular, vertebrobasilar aneurysms. Managed conservatively for 10 years before developing gait ataxia, new imaging revealed growth of the now giant, more distal aneurysm. Flow diversion with partial coiling of the aneurysms was pursued. Following deployment, DynaCT demonstrated catastrophic thalamic and midbrain hemorrhage with intraventricular extension. A review of intra‐aneurysmal pressure measurements, angiography, MRI, and neuromonitoring data strongly suggests rupture of multiple deep perforators following the conversion to laminar flow when the flow diverting chain was finalized. This suggests giant aneurysms chronically depress the distal pulse pressure by acting as a Windkessel reservoir. Flow diversion bypasses the reservoir increasing pulse pressure distal to the aneurysm, exceeding autoregulatory capacity, leading to hemorrhage. Conclusions This is the first case in the literature to describe NPPB and the Windkessel phenomenon in the attempt to treat giant aneurysms with flow diversion. Flow diversion bypasses the reservoir, suddenly changing turbulent flow to laminar flow. The resultant dramatic rise in pulse pressure distal to the aneurysm can exceed the autoregulatory mechanisms of small distal vessels such as perforating branches. While demonstrating a poor outcome, awareness of these mechanisms and meticulous intra‐operative blood pressure management may reduce or prevent complications. Further modeling of flow dynamics both before and following treatment of these aneurysms may lead to altered guidelines in the temporality of treatment due to potential catastrophic sequelae.

Split-Tendon Medial Transposition of Lateral Rectus for Pediatric Complete Oculomotor Palsy.

Split-tendon medial transposition of lateral rectus (STMTLR) for complete oculomotor palsy can correct large angles of exotropia in adults, but outcomes are variable, and complications are frequent. Only a few pediatric cases have been reported, and further insight is needed to assess the child's alignment outcomes and ability for postsurgical gain of function. The aim of our study is to report the outcomes of this surgical procedure in pediatric cases of complete oculomotor palsy. A retrospective review of outcomes was conducted on 5 consecutive patients with complete oculomotor palsy treated with STMTLR by a single surgeon (V.S.S.) between 2015 and 2021 at tertiary referral centers. Primary outcome was postoperative horizontal alignment, and secondary outcome was demonstration of gain-of-function activity in the field of action of the paretic medial rectus muscle. Five cases of pediatric complete oculomotor palsy underwent surgical treatment with STMTLR. Subjects averaged 5.3 years old (range 10 months-16 years). Two were female. Etiologies were heterogeneous, and all presented with unilateral (n = 2) or bilateral complete oculomotor palsy with exodeviations ranging from 45 to >120 prism diopters. Two subjects had bilateral disease secondary to military tuberculosis with CNS involvement. A third subject presented iatrogenically with complete bilateral third nerve palsies secondary to removal of a nongerminomatous germ cell tumor (NGGCT) of the pineal gland. The 2 remaining subjects had monocular involvement in their right eye, 1 from compressive neuropathy after a cavernoma midbrain hemorrhage, and 1 from a congenital right oculomotor palsy. All patients were observed to have stable ocular alignment for a period of at least 6 months before surgery. Unilateral STMTLR was performed in all cases except the subject with NGGCT, in which bilateral STMTLR was performed. Measurement of alignment permanence out to 1-3 years postop resulted in an average correction of 40.83 prism diopters (range 37.5-45 prism diopters) per operated eye. Four of 5 subjects regained limited but active adduction eye movements, and the 2 unilateral cases demonstrated improved convergence. None of the subjects experienced significant complications. STMTLR was a safe and effective approach for the surgical correction of complete pediatric oculomotor palsy in our case series. In addition, pediatric patients may benefit from STMTLR with immediate gain-of-function activity in the transposed lateral rectus muscle, which supports the hypothesis that children have a dynamic and adaptive neuroplasticity of visual target selection that predominates established agonist/antagonist neural signaling.

A rare long-term undetected pheochromocytoma leading to Takotsubo syndrome in an older male patient: a case report

BackgroundTakotsubo syndrome is an uncommon, acute, and reversible cardiomyopathy that occurs primarily in postmenopausal females. The clinical presentation of the syndrome resembles acute coronary syndrome, but coronary angiography reveals no obstructive coronary artery disease. Rarely, a catecholamine surge due to pheochromocytoma may induce Takotsubo syndrome. The clinical features of pheochromocytoma include paroxysmal hypertension, headache, palpitations, and profuse sweating. However, owing to the episodic, rather than continued, symptoms and signs of pheochromocytoma, its timely diagnosis poses a challenge for clinicians. Here, we report a rare case of long-term undetected pheochromocytoma leading to Takotsubo syndrome in an older male patient.Case presentationA 70-year-old man presented with paroxysmal chest distress and chest pain. Examinations revealed acute coronary syndrome with normal coronary arteries, heart failure, reversible left ventricular regional wall motion abnormalities, labile blood pressure, a giant left adrenal mass, and extremely high levels of metanephrine and normetanephrine. Clinical manifestations, laboratory reports, and imaging findings suggested a diagnosis of Takotsubo syndrome caused by pheochromocytoma. Supportive therapy, administration of alpha- adrenergic receptor blockers, and left adrenal mass resection resolved the patient’s symptoms. A histological examination confirmed the presence of pheochromocytoma. We reviewed his history of midbrain hemorrhage 6 years prior and found a mass in the left adrenal region by reviewing the computed tomography images of the lung that were also taken 6 years prior, on which the pheochromocytoma was evident.ConclusionsOur case illustrates the importance of understanding the link between pheochromocytoma and Takotsubo syndrome. A diagnosis of pheochromocytoma-induced Takotsubo syndrome should be considered during the differential diagnosis of acute coronary syndrome, especially in patients with labile blood pressure and normal coronary angiography findings; meanwhile, assessments of catecholamines and its metabolites and abdominal computed tomography scan should be performed at the right time. Clinicians should also be alert to potential pheochromocytoma in patients with unexplained cerebral hemorrhage, even in the absence of symptoms of catecholamine excess.

Brainstem hemorrhage is uncommon and is associated with high morbidity, mortality, and prolonged hospitalization.

Objectives:To determine the frequency, risk factors, and outcomes of patients with brainstem hemorrhage in stroke center at King Abdulaziz Medical City, Riyadh.Methods:A retrospective, observational cohort study including all patients with brainstem hemorrhage from January 2014 to December 2017. The clinical presentation, location of hemorrhage, complications and clinical outcomes were analyzed.Results:Of 1921 stroke patients, 219 had hemorrhagic stroke (11.4%), of whom only 10 (4.6%) had brainstem hemorrhage, comprising 0.5% of all stroke patients. All patients were men; mean age was 58.5 years. Most frequent presenting symptoms were headache (70%), unilateral weakness (60%), and loss of consciousness (50%). All patients had hemorrhage in pons, 5 had concomitant cerebellar hemorrhage (50%), one had medullary hemorrhage, and one midbrain hemorrhage (10% each). Mean ICU stay was 17 days; mean hospital stay was 58 days. At the time of discharge, three (30%) had mRS of 0-2, 5 (50%) had mRS of 3-5, whereas 2 (20%) had died. Glasgow coma scale (GCS) of >8 at presentation was associated with a good outcome at three months (p=0.03). Presentation within six hours of symptom onset (p=0.233), hypertension on presentation (p=0.233), and age less than 60 years (p=0.065) did not affect discharge outcomes.Conclusion:Brainstem hemorrhage occurred in 0.5% of all stroke patients. It was associated with high morbidity and mortality. Low Glasgow Coma Scale at presentation was associated with poor outcomes.

Surgical Treatment for Primary Brainstem Hemorrhage to Improve Postoperative Functional Outcomes

It remains controversial whether primary brainstem hemorrhage (PBH) should be managed conservatively or treated promptly by surgical evacuation of the hematoma. In the present study, we discuss 5 cases of PBH that were treated surgically and the ability of surgical management to improve postoperative functional outcomes. The 4 patients with pontine and medullary hemorrhage underwent surgery via the lateral or midline suboccipital and trans-rhomboid fossa approach in the half-sitting position. The patient with a midbrain hemorrhage underwent surgery via the subtemporal approach in the supine lateral position. We analyzed the postoperative functional outcomes 1 week after surgery and the modified Rankin scale scores 6 months after discharge. Three patients with disturbance of consciousness experienced improvement in their level of consciousness. Four patients with hemiparesis improved in motor function. Oculomotor nerve function improved in 2 of 3 cases. Facial nerve function improved in 2 of 2 cases. Spontaneous respiration improved in 1 patient. The postoperative modified Rankin scale scores improved in all 5 cases. Because of the good results with these 5 patients with PBH, this surgical strategy could be encouraged with exclusion criteria for early initiation of rehabilitation strategies. We hope to increase our number of patients to accumulate further evidence.

Large Basilar Apex Aneurysms Treated with Flow-Diverter Stents.

The treatment of wide-neck, large basilar apex aneurysms is challenging with either an endovascular or a surgical approach. The aim of the present study was to report our experience treating basilar apex aneurysms with flow-diverter stents and to evaluate their efficacy and safety profile in this specific anatomic condition. We retrospectively analyzed data from all consecutive patients treated with flow-diverter stents at our institution between January 2011 and January 2015. Patients with large basilar apex aneurysms treated with a flow-diverter stent were included in the study. Clinical presentations, technical details, intra- and perioperative complications, and clinical and angiographic outcomes were recorded, with a midterm follow-up. Of the 175 aneurysms treated with flow-diverter stents at our institution, 5 patients (2 women and 3 men; age range, 44-58 years) received flow-diverter stent for basilar apex aneurysms. The mean follow-up after stent deployment was 21 months (range, 15-24 months). One patient died on day 31 from an early postprocedural midbrain hemorrhage. One patient had a right cerebellar hemispheric ischemic lesion with a transient cerebellar syndrome resolved within 24 hours without neurologic sequelae at the latest follow-up. The mRS was 0 in 4 patients and 6 in 1 patient at last follow-up. Flow diversion is a feasible technique with an efficacy demonstrated at a midterm follow-up, especially in the case of basilar apex aneurysm recurrences after previous endovascular treatments. Concern about its safety profile still exists.

Brainstem Hemorrhage after Evacuation of Chronic Subdural Hematoma: A Case Report and Review of Literature

Brainstem hemorrhage following evacuation of chronic subdural hematoma is extremely rare and its pathogenesis is unclear. In our case report, we present a rare case of brainstem hemorrhage following evacuation chronic subdural hematoma. Our patient was a 50-year-old man, with no comorbidities, presented with dorsal midbrain hemorrhage with ventricular extension and symptomatic progression of contralateral small chronic subdural hematoma following evacuation of chronic subdural hematoma. Contralateral subdural hematoma was evacuated and midbrain hemorrhage was managed conservatively. He was discharged with minimal neurologic deficit. Review of literature and pathogenesis of remote hemorrhage after evacuation of chronic subdural hematoma were discussed.

Isolated unilateral oculomotor paresis in pure midbrain stroke

Background and purposePure midbrain stroke can cause isolated unilateral oculomotor paresis. We attempted to determine whether there is a difference in the oculomotor paresis pattern between pure midbrain infarction and midbrain hemorrhage. MethodsPure midbrain stroke patients who presented with isolated unilateral oculomotor paresis were identified from a group of 2447 consecutive patients hospitalized for acute cerebral infarction or hemorrhage during the period May 2008 through April 2014. Detailed oculomotor findings were evaluated in the identified patients per the cause of the stroke. ResultsFive patients with infarct and 1 with hemorrhage became our study subjects. Lesions were located in the paramedian area of the midbrain involving the oculomotor fascicles. The pupillary sphincter and inferior rectus muscles were selectively spared in the infarct patients, whereas these muscles were selectively affected in the hemorrhage patient. ConclusionFibers in the oculomotor fascicle that innervate the levator palpebrae, superior rectus, and inferior oblique muscles appear to be more susceptible to ischemic damage than those that innervate the pupillary sphincter and inferior rectus muscles. Isolated impairment of the pupillary sphincter and inferior rectus muscles may be suggestive of a non-ischemic process.

Motor Recovery Via Transcallosal and Transpontine Fibers in a Patient with Intracerebral Hemorrhage

Little is known about the motor recovery mechanisms via transcallosal or tranpontine fibers in stroke patients. In the current study, an attempt was made to demonstrate motor recovery via transcallosal and transpontine fibers in a patient with intracerebral hemorrhage using diffusion tensor tractography and transcranial magnetic stimulation. A 39-yr-old male patient presented with complete weakness of the right extremities at the onset of a left midbrain hemorrhage. His motor weakness had shown slow recovery for 4 mos to the point that he was able to grasp and release using the right hand. Diffusion tensor tractography and transcranial magnetic stimulation were performed at 2 wks and 4 mos after onset. Discontinuation of the left corticospinal tract below the left midbrain was observed on the 2-wk diffusion tensor tractography and no motor evoked potential was elicited in the right hand on the 2-wk transcranial magnetic stimulation study. Four-month diffusion tensor tractography showed that the discontinuation of the left corticospinal tract had not been restored; however, a new neural pathway was observed, which originated from the left primary motor cortex and descended to the left corticospinal tract at the pons through the transcallosal and transpontine fibers. In the 4-mo transcranial magnetic stimulation study, the latency of motor evoked potential obtained at the right hand by stimulation of the left motor cortex was delayed by 9 msecs, compared with the opposite motor evoked potential, which seems to be compatible with transcallosal and transpontine conduction time. The results suggest that the motor function of the affected extremities in this patient was recovered through the transcallosal and transpontine fibers from the left motor cortex.

Hemiparkinsonism after unilateral traumatic midbrain hemorrhage in a young woman.

The relationship between head trauma and parkinsonism has been debated since James Parkinson's first description of the shaking palsy in the late 19th century. We observed in our outpatient clinic a young woman in whom hemiparkinsonism developed within 3 weeks of sustaining closed head trauma with loss of consciousness. The patient had a discrete unilateral midbrain hemorrhage on head MRI which involved the contralateral substantia nigra. The condition responded well to carbidopa/levodopa. This patient is a convincing example of posttraumatic midbrain hemorrhage causing parkinsonism.

Aggressive course of multiple de novo cavernous malformations

The risk of hemorrhage from an intracerebral cavernous malformation has been estimated at 2%-4% per year. In patients with multiple cavernous malformations, typically there are 1 or 2 dominant lesions that result in symptoms. This report highlights an unusual case of recurrent hemorrhage from de novo cavernous malformations. This 35-year-old man had a generalized seizure in 2007. Magnetic resonance imaging performed at the time showed multiple hemorrhagic lesions suggestive of cavernous malformations. Two years later, the patient had clinical symptoms referable to a midbrain hemorrhage. This lesion was not present on 2007 standard and gradient echo images. One year later, the patient had another clinical hemorrhage at the cervical medullary junction. This lesion was also not present on earlier imaging. Genetic testing was negative for the known familial types of cavernous malformation. A lesion was biopsied to ensure correct diagnosis, and the results were pathologically consistent with a cavernous malformation. The patient had a fourth clinical hemorrhage in 2011 from a separate lesion. All hemorrhage symptoms were mild, and he returned to normal functioning and work after each hemorrhage. This case highlights several unusual features of the known natural history of intracerebral cavernous malformations. In this case, resection of the hemorrhagic lesion would not have altered future hemorrhage risk since each new hemorrhage was from a de novo lesion.

Dramatic response to zonisamide of post-subarachnoid hemorrhage Holmes’ tremor

Holmes’ tremor is an unusual combination of 2–5 Hz resting, postural, and kinetic tremors affecting the unilateral upper extremity, which is usually caused by stroke, trauma, vascular malformations, or tumors involving the midbrain [1]. Abnormal involuntary movements such as tremor affect the quality of life by interfering with simple motor tasks and daily activities. Pharmacotherapy for Holmes’ tremor does not usually achieve satisfactory results and some patients require thalamic surgery to control this tremor [2]. Zonisamide (ZNS), 3-sulfamoylmethyl1,2-benzisoxazole, was originally developed as a broadspectrum antiepileptic drug. Recent clinical studies have suggested several new indications for ZNS, including Parkinson’s disease, essential tremor, and psychiatric diseases [3]. Here we report a patient in whom delayed Holmes’ tremor after subarachnoid hemorrhage responded dramatically to ZNS. A 68-year-old, right-handed woman with a history of hypertension developed headache and drowsiness. Neurological examination revealed dysarthria, right oculomotor nerve paralysis, and left hemiparesis [2/5 by manual muscle testing (MMT)]. On admission, brain computed tomography and magnetic resonance imaging (MRI) showed subarachnoid hemorrhage together with right midbrain hemorrhage (Fig. 1a–c). An aneurysm of the basilar artery/right superior cerebellar artery was detected by MRI and digital subtraction angiography (Fig. 1d, e), and was treated by coil embolization (Fig. 1f, i, j). During follow-up for 15 months, her right oculomotor nerve palsy improved slightly and her left hemiparesis improved to 4/5 on MMT. She was able to look after herself without assistance. However, a slow, strong, and large-amplitude tremor affected her left upper limb. The tremor was worsened by emotional stress and disappeared during sleep. It was exhausting and rendered her left arm useless. T2-weighted and fluid attenuated inversion recovery MRI of the brain showed a low intensity to hyperintense area in the right midbrain, corresponding to the site of hemorrhage, without any evidence of additional vascular pathology in the basal ganglia (Fig. 1g, h). A diagnosis of Holmes’ tremor was made. Her tremor was assessed by employing item 20 (tremor at rest) and item 21 (action or postural tremor) of the Unified Parkinson’s Disease Rating Scale (UPDRS). Initial treatment with levodopa (150 mg/day) and a dopamine agonist (pramipexole at 1.5 mg/day) improved the subscore from 3 to 1 for the resting component of her tremor, but the postural and kinetic components were unchanged (subscore of 4). She refused to take dopaminergic agents because of nausea. Therefore, ZNS was started at a dose of 100 mg twice daily. After a few days, her resting and postural/kinetic tremors were markedly improved from 3 to 1 and from 4 to 1, respectively, and she was able to perform most daily activities by herself, such as cooking, eating meals, changing clothes, and cleaning. ZNS therapy has been well tolerated, and improvement of her tremor persists after 8 months of follow-up. S. Suda (&) M. Yamazaki K. Katsura T. Fukuchi M. Ueda H. Nagayama Y. Katayama Divisions of Neurology, Nephrology, and Rheumatology, Department of Internal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan e-mail: suda-sa@nms.ac.jp

Intracranial Hemorrhage Revealing Pseudohypoparathyroidism as a Cause of Fahr Syndrome

Pseudohypoparathyroidism is an infrequently encountered disease. It is one of the causes of Fahr syndrome which also is a rare clinical entity caused by multiple diseases. A 4-year-old man hospitalized for sudden onset left hemiparesis and hypertension was diagnosed to have right thalamic and midbrain hemorrhage on plain CT scan of the head which also revealed co-existent extensive intracranial calcifications involving the basal ganglia and cerebellum bilaterally. General physical examination revealed features of Albright hereditary osteodystrophy, goitre, hypertension, left hemiparesis, and signs of cerebellar dysfunction. Laboratory findings suggested hypocalcemia, hyperphosphatemia along with high TSH, low FT4, low FT3, and high anti-TPO antibody. Though bilateral intracranial calcifications are usually encountered as an incidental radiological finding in the CT scan of brain, in this case, the patient admitted for thalamic and midbrain hemorrhage was on investigation for associated intracranial calcification, and goitre was also found to have coexisting pseudohypoparathyroidism and autoimmune hypothyroidism.

A Prospective, Randomized Clinical Trial to Compare the Effect of Hyperbaric to Normobaric Hyperoxia on Cerebral Metabolism, Intracranial Pressure, and Oxygen Toxicity in Severe Traumatic Brain Injury

This study from Hennepin County Medical Center examined 74 patients with severe traumatic brain injury (TBI). They were the subjects in a prospective, randomized clinical trial to look at the effect of hyperoxia on cerebral metabolism and intracranial pressure (ICP). All patients in the study had sustained severe TBI (Glasgow Coma Scale score<8), and were included in the study within 24 h of injury. Five of the initial 74 patients were excluded when they met the exclusion criteria: brain death, midbrain hemorrhage with fixed midpoint pupils, narcotic overdose with anoxic injury or an inability to follow commands.

Midbrain hemorrhage mimicking pituitary apoplexy in patient using anticoagulation therapy

Pituitary apoplexy represents a hemorrhage or infarction of the pituitary gland and has its occurrence often related in the context of a pituitary adenoma1. In classical pituitary apoplexy, headache, usually of sudden and severe onset, is the most common presenting symptom and hypertension and anticoagulation have been described as relevant predisposing factors1,2. The risk of cranial nerve palsies leading to double vision and/or vision loss and the risk of acute panhypopituitarysm leading to death in the event of apoplexy have [...]

CT Demonstration of Dorsal Midbrain Hemorrhage in Traumatic Fourth Cranial Nerve Palsy

A 21-year-old man who suffered a traumatic brain injury from a motor vehicle accident recovered brain function except for an isolated left fourth cranial nerve palsy. Brain CT showed a focal hemorrhage in the right dorsal midbrain, directly in the brainstem path of what would become the left fourth cranial nerve. Although there has been previous imaging documentation of midbrain and cisternal hemorrhage in patients with isolated post-traumatic fourth cranial nerve palsy, this is the first report to show a large midbrain hemorrhage on CT. The mechanism is likely to be concussive impact of the dorsal midbrain on the tentorium cerebelli.

Periprocedural Bleeding Complications of Brain AVM Embolization with Onyx

The advent of Onyx has provided a new method for neurointerventional therapists to treat brain AVMs. Although some retrospective studies have reported complications for AVM embolization with Onyx, periprocedural bleeding complications with Onyx embolization have not yet been described in detail. The aim of this retrospective study was to analyze the factors of Onyx-related bleeding complications and to find a way to avoid and manage these complications.From January 2003, patients with AVMs recruited in our institution started to be treated by Onyx embolization. From January 2007 to July 2009, 143 consecutive interventions were performed in 126 patients using flow-independent microcatheters and Onyx as embolic agents. Seven patients encountered bleeding complications (5.4% per patients and 4.7% per procedures) during or after the endovascular procedures. Among them, five bleeding episodes occurred during procedures, the other two after procedures. Details of the seven patients' clinical presentations, imaging presentations, speculative reasons and management of these complications were recorded. Follow-up data, including postoperative course, clinical symptoms and duration of follow-up were documented. The five active bleedings discovered in procedures were managed in time, and the patients recovered without any new neurological symptoms compared with preoperation. However, of the two bleeding episodes that occurred after interventional procedures, one was detected half an hour later: the patient was remained comatose two months later after resection of right occipital hematoma; the other who encountered intraventricular and midbrain hemorrhage was treated conservatively and suffered Parinaud syndrome and hemianesthesia. Periprocedural bleeding of AVMs embolization is considered a severe and devastating complication. The clinical course and prognosis of bleeding mostly depends on prompt detection and management. Interventional embolization is an effective method to manage bleeding during procedures, and the detection of risk factors and imaging signs of bleeding is extremely important.