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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subarachnoid hemorrhage can increase intracranial pressure, causing significant morbidity. Acute gastric dilation and delayed gastric emptying are commonly seen in patients with intracranial hypertension, and correction of these gastric abnormalities can facilitate the recovery of patients with brain injuries. We conducted a literature review of both national and international health sciences medical journals and electronic libraries spanning the last twenty-eight years and focused on the brain, gut motility and gastric emptying functional axis either in experimental animal models of brain injury or patients with acute cerebral injuries. Decreased parasympathetic tonus is a potential cause of intracranial hypertension-related food intolerance. Changes in gastrointestinal transit after a brain injury follow a biphasic pattern: an initial phase of accelerated gastric emptying and a late stage of intestinal lethargy. Changes in the physiology underlying gut motility may be essential for homeostatic stabilization in hemodynamically unstable patients. Research studies are necessary to understand the difficult management of intensive care patients with intracranial hypertension secondary to subarachnoid hemorrhages resulting from traumatic brain injuries or rupture of a cerebral aneurysm. Increased intracranial pressure induces massive increases in sympathetic activity, which is responsible for many of the peripheral systemic and gastrointestinal symptoms. Brain injuries leading to significant increases in intracranial pressure result in delayed gastrointestinal emptying due to autonomic nervous system changes.
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PMID:Influence of acute brain injuries on gut motility. 2529 60

Rupture of spontaneous dissecting aneurysms of the middle cerebral artery (MCA) is rare and its etiology remains obscure, although the risk of rebleeding is greater than with saccular aneurysms. Most reports concerning the treatment of a ruptured dissecting aneurysm of the anterior circulation involve surgical trapping or wrapping. Here, we report on a case of an MCA dissecting rupture treated with endovascular procedures. A 22-year-old female presented with sudden stuporous mental change following severe headache and left side hemiparesis. A computed tomography scan showed a diffuse subarachnoid hemorrhage and diffusion MR showed diffusion restriction at the right putamen and internal capsule. A 3-hour follow-up digital subtraction angiography (DSA) showed a dissecting aneurysm, which was not seen on an initial DSA. A stent assisted coil embolization was performed and double stents were applied to achieve flow diversion effects. A small remnant area of the dissecting aneurysm had disappeared at 60-day and was not observed on 12-month follow-up DSA.
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PMID:Endovascular Treatment in Ruptured Middle Cerebral Artery Dissection Preservation of Arterial Continuity. 2615 90

This report details a case of unexpected, severe post-operative cerebral edema following cranioplasty. We discuss the possible pathological mechanisms of this complication. A 50-year-old female was admitted to our department with sudden onset of stuporous consciousness. A brain computed tomography (CT) revealed a subarachnoid hemorrhage with intracranial hemorrhage and subdural hematoma. Emergency decompressive craniectomy and aneurysmal neck clipping were performed. Following recovery, the decision was made to proceed with an autologous cranioplasty. The cranioplasty procedure was free of complications. An epidural drain was placed and connected to a suction system during skin closure to avoid epidural blood accumulation. However, following the procedure, the patient had a seizure in the recovery room. An emergency brain CT scan revealed widespread cerebral edema, and the catheter drain was clamped. The increased intracranial pressure and cerebral edema were controlled with osmotic diuretics, corticosteroids, and antiepileptic drugs. The edema slowly subsided, but new low-density areas were noted in the brain on follow-up CT 1 week later. We speculated that placing the epidural drain on active suction may have caused an acute decrease in intracranial pressure and subsequent rapid expansion of the brain, which impaired autoregulation and led to reperfusion injury.
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PMID:Unexpected Severe Cerebral Edema after Cranioplasty : Case Report and Literature Review. 2627 18

To investigate the nature of the headache accompanying aneurysmal subarachnoid hemorrhage, a retrospective study was conducted. Fifty-four patients and 54 controls completed questionnaires regarding headache, medical history, and family history, in an attempt to derive further information regarding symptoms and factors that might be predictive of aneurysmal subarachnoid hemorrhage. Factors that appear to be of importance in evaluating headache caused by subarachnoid hemorrhage include ominously severe headache, a history of vigorous physical activity precipitating headache, syncope or transient lethargy accompanying headache, previous medical attention for headache, a family history of aneurysmal subarachnoid hemorrhage, or catastrophic central nervous system event at an early age. An algorithm for the management of serious headache is suggested.
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PMID:Headache characteristics in aneurysmal subarachnoid hemorrhage. 2648 56

We report a case of multiple symptomatic cerebral infarctions from a traumatic vertebral artery dissection (VAD) after cervical fractures. A 73-year-old man was admitted with stuporous mentality and left hemiparesis after a motor-vehicle accident. A brain computed tomography (CT) scan at admission showed a traumatic subarachnoid hemorrhage on the left parietal lobe. A cervical CT scan showed left lateral mass fractures on C2, C5, and C6, involving the transverse foramen. Cervical spine magnetic resonance imaging (MRI) revealed loss of signal void on the left vertebral artery. Neck CT angiography showed left VAD starting at the C5 level. Brain MRI revealed acute, multiple cerebral infarctions involving the pons, midbrain, thalamus, corpus callosum, and parietal and frontal lobes on diffusion weighted images. The patient was treated conservatively at the intensive care unit in the acute stage to prevent extent of stroke. Aspirin was started for antiplatelet therapy in the chronic stage. The possibility of symptomatic cerebral infarctions due to traumatic VAD following cervical fracture should be considered.
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PMID:Multiple Cerebral Infarctions due to Unilateral Traumatic Vertebral Artery Dissection after Cervical Fractures. 2718

In the last years, a shift from the microsurgical treatment to an endovascular therapy in patients with basilar apex aneurysm has been settled, part of this phenomenon is related to the significant tendency of vital perforators to be involved in the aneurysm dissection and clipping, which can implicate unfavorable outcomes. Nevertheless, microsurgical treatment remains the treatment that can provide the superior rates of stable and durable aneurysm occlusion, which is most important to young patients.In this video, we present the case of a 45-yr-old female patient who complained of a sudden and severe headache and presented with progressive lethargy during the following 3 d.At admission, computed tomography did not show abnormal findings. However, cerebrospinal fluid analysis showed erythrocytes and corroborated the clinical suspicion of spontaneous subarachnoid hemorrhage. The patient signed the Institutional Consent Form, which allows the use of his/her images and videos for any type of medical publications in conferences and/or scientific articles.Angiography and magnetic resonance imaging revealed a saccular basilar apex aneurysm. It showed a wide neck as well as a lobulated dome with upward and slightly left projection. The aneurysm did not involve angiographically visible thalamoperforator arteries, which allowed the microsurgical treatment by the fronto-orbitozygomatic approach. However, during the interpeduncular cistern dissection, an intraoperative rupture of the aneurysm occurred. This video exemplifies the steps required to manage an intraoperative rupture of a basilar apex aneurysm.
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PMID:Microsurgery for Upper Basilar Tip Aneurysm With Intraoperative Rupture: 3-Dimensional Operative Video. 3006 Feb 22

A 50-year-old woman reported to the emergency department with thunderclap headache and vomiting. Non-enhanced brain computed tomography (CT) showed a subarachnoid hemorrhage of Hunt-Hess Grade II and Fisher Grade III. Brain angiography CT and transfemoral cerebral angiography (TFCA) revealed an aneurysm of the anterior communicating artery. A direct neck clipping was performed using the pterional approach. The post-operation CT was uneventful. Six days postoperatively, the patient became lethargic. The mean velocity (cm/s) of the middle cerebral artery peaked at 173 cm/s on the right side and 167 cm/s on the left. A TFCA revealed decreased perfusion in both recurrent arteries of Heubner (RAH), but no occlusion in either. Intra-arterial nimodipine injection was administered. On the 7th postoperative day, CT demonstrated a newly developed low-density lesion in the RAH territory bilaterally. The cause of the infarction was attributed to decreased perfusion caused by cerebral vasospasm. The patient was discharged with no definite neurologic deficit except for mild cognitive disorder.
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PMID:Bilateral Infarction of the Recurrent Arteries of Heubner Following Clipping of an Anterior Communicating Artery Aneurysm. 3037 Feb 37

Reversible cerebral vasoconstriction syndrome (RCVS) is a disorder of dysregulation of cerebrovascular tone resulting in transient segmental vasoconstriction which resolves in 1-3 months. Cerebral edema is an underrecognized complication in RCVS. It is likely multifactorial. This edema can lead to intracranial hypertension that can be refractory to medical management. Limited evidence exists regarding surgical management of intracranial hypertension in RCVS. We present a 29-year-old Caucasian right-handed female patient with a medical history of migraine, polysubstance abuse presented to the emergency department (ED) daily for 3 days with the chief complaint of recurrent thunderclap headache. She declined neuroimaging and lumbar puncture. She was treated for migraine with abortive medications with no improvement. During the third ED visit, she became lethargic with right-sided homonymous hemianopia. Computerized tomography of the brain showed left parietal intracerebral hemorrhage with intraventricular extension, cortical subarachnoid hemorrhage, and diffuse cerebral edema. Digital subtraction angiography showed multifocal moderate-to-severe segmental vasoconstriction suggestive of vasculopathy. Oral verapamil was initiated. Continuous intracranial pressure monitoring showed uncontrolled intracranial hypertension, despite maximal medical management with hyperosmolar therapy, induced coma, and hypothermia. Decompressive hemicraniectomy with duraplasty was performed for refractory intracranial hypertension. We provisionally diagnosed her with RCVS. She was discharged to inpatient rehabilitation with residual right homonymous hemianopia. Transcranial Doppler study during follow-up showed improved mean flow velocities. She continued to have residual cognitive deficits with complete resolution of headache.
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PMID:Decompression Hemicraniectomy for Refractory Intracranial Hypertension in Reversible Cerebral Vasoconstriction Syndrome. 3100 Oct 36

A 17-year-old female in a lethargic state with mild dysarthria was transferred to our hospital after experiencing a generalized tonic seizure immediately after giving birth. Head CT showed a cortical subarachnoid hemorrhage(cSAH)in the left frontoparietal convexity. Three-dimensional rotational angiography(3D-RA)revealed multifocal narrowing of the cortical branches of the left middle cerebral artery(MCA)and severe stenosis of the left M1 segment with plexiform collateral networks, suggesting the presence of reversible vasoconstriction syndrome(RCVS)and aplastic or twig-like MCA(Ap/T-MCA). When 3D-RA was repeated on day 17, the narrowing of the cortical artery had resolved, and a new constriction of more proximal blood vessels was observed. The arterial spasm disappeared within 3 months, confirming the diagnosis of RCVS and Ap/T-MCA. Although non-aneurysmal SAH due to Ap/T-MCA is extremely rare, RCVS often complicates cSAH in the frontal/parietal region. It is suggested that RCVS triggers cSAH in the presence of incidental Ap/T-MCA. Ap/T-MCA is thought to be caused by developmental abnormalities during the embryonic period, but only 11 cases in children or adolescents have been reported. This suggests that there are a considerable number of asymptomatic young patients whose condition has not been detected. The majority of patients with Ap/T-MCA are from East Asia, suggesting that racial and genetic background differences are a factor. As this anomaly is more likely to present as a stroke in adulthood, long-term follow-up is recommended if it is found at a young age. There is no evidence that revascularization is effective in preventing stroke. Further studies are needed on how to manage this condition appropriately.
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PMID:[Aplastic or Twig-like Middle Cerebral Artery with Cortical Subarachnoid Hemorrhage and Reversible Cerebral Vasoconstriction Syndrome during the Postpartum Period in a Juvenile Female:A Case Report]. 3243 55

Traumatic subarachnoid hemorrhage (SAH), a common finding following head trauma, is usually a benign condition with a favorable outcome, seldom requiring surgical intervention. Unlike nontraumatic aneurysmal SAH, most cases of traumatic SAH occur in the sulci of the cerebral convexities, and only rarely arise at the base of the brain. Basal traumatic SAH can be life-threatening and is primarily associated with rupture of vertebrobasilar arteries. We herein present a rare case of basal traumatic SAH resulting from rupture of the posterior communicating artery (PCoA). A 77-year-old male was taken to the emergency department in a semicomatose state. Upon arrival at emergency room, the patient had a Glasgow coma scale (GCS) score of 6 (E1M3V2), and the neurologic examination demonstrated no focal neurologic deficit. Although the trauma history was evident from abrasions and bruising on the face and chest, brain computed tomography (CT) demonstrated basal SAH, which is typical for nontraumatic aneurysmal SAH. Subsequent digital subtraction angiography (DSA) disclosed a traumatic rupture at the mid-portion of right PCoA and ongoing extravasation of contrast media. Despite emergent trapping of the right PCoA by endovascular surgery, the patient's clinical condition only minimally improved. The patient remained bed-ridden with stuporous mentality and persistent hydrocephalus. To the best of our knowledge, this is the first reported case of basal traumatic SAH originating from rupture of the PCoA. This case demonstrates that a meticulous vascular workup is mandatory for every patient with basal SAH, even though a trauma history is clear.
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PMID:Traumatic Subarachnoid Hemorrhage Resulting from Posterior Communicating Artery Rupture. 3261 22


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