Bilateral Putaminal Hemorrhages Research Articles

Intracerebral hemorrhage in methanol toxicity patients during COVID-19 pandemic: case report and review of literature.

The aim of this study is to examine the clinical and imaging manifestations of methanol toxicity during the COVID-19 pandemic, as well as to review existing studies on this topic.The most common cause of methanol intoxication is methanol-adulterated liquor. The primary metabolite of methanol, formic acid, is responsible for pathological changes. Symptoms typically present within 6-24h of consumption and can include visual disturbances, acute neurological symptoms, and gastrointestinal issues. During the initial year of the COVID-19 pandemic, methanol poisoning cases increased significantly. In this study, We present six different patients with methanol intoxication and their clinical and imaging features. In the literature review, the most common clinical presentation was loss of consciousness and obtundation and the other was vision loss. CT scan findings showed bilateral putaminal necrosis and hemorrhage in 55% of methanol toxicity patients. Methanol intoxication, causing bilateral putaminal involvement and a 50% mortality rate in intracerebral hemorrhage patients, warrants urgent toxicological analysis due to potential putaminal hemorrhage.

Abstract Number ‐ 222: Spontaneous Simultaneous Bilateral Putaminal Hemorrhages in a Young Woman

Introduction Spontaneous simultaneous bilateral basalganglia hemorrhage is an exceedingly rare condition with significant morbidity and mortality. Hypertension is the most common underlying etiology followed by intoxication and metabolic causes1. Methods Here we describe a 39‐year‐old woman with a spontaneous simultaneous bilateral putaminal hemorrhages believed to be secondary to amphetamine (Adderall) use and undiagnosed hypertension. Results A 39‐year‐old right‐handed woman with history of attention‐deficit/hyperactivity disorder (ADHD) on dextroamphetamine‐amphetamine (Adderall), white coat hypertension and prior gestational hypertension was brought to the emergency department due to sudden‐onset left hemiparesis, left foot numbness, gait instability, and an abnormal sensation in her right ear. On arrival, blood pressure was 239/139 mmHg. Patient was noted to be somewhat drowsybut was consistently regarding,able to respond, and had anosognosia, hypophonia, a right gaze preference, mild dysarthria, left arm and leg hypotonia, left hemiparesis and hypoesthesia involving face, arm and leg and brisk reflexes on the left side.Head CT revelated bilateral putaminal hemorrhages measuring 10mL on the right and 3mL on the left,with no intraventricular hemorrhage and minimal right‐to‐left midline shift.Patient was admitted to the neuro ICU and treated with a nicardipine infusion. CTA/MRI/MRV/MRA and catheter angiography revealed no underlying structural pathology. Furthermore, patient had a normal platelet count and coagulation profile. Urine drug screen was positive for amphetamines, and serum metanephrines (0.59 nmol/L) and normetanephrines (1.2nmol/L) were elevated in the setting ofAdderall use. Nicardipine infusion was discontinued on day one and she was started on carvedilol 12 mg bid and amlodipine 5mg daily. Adderall was discontinued and patient was counseled on avoiding stimulant medications use. At time of discharge her dysarthria had resolved but her left hemiplegia remained unchanged. She was discharged on day 5 of hospital stay to an inpatient rehabilitation facility. She was started on fluoxetine 20 mg daily for motor recovery at the rehabilitation facility. At her two months follow‐up visit, she was noted to have significant improvement in her left‐sided strength, hypoesthesia and left facial droop but had developed left arm and leg spasticity. She was started on a trial of dry needling with physical therapy prior to consideration of anti‐spasmodic medications or Botox injections. At her office visit, her blood pressure had been well controlled on lisinopril 10 mg and amlodipine 10 mg daily. Conclusions Overall, this case report highlights that amphetamine (Adderall) use is a potential cause of spontaneoussimultaneousbilateralbasalgangliahemorrhage.

A Case Report of Putaminal Hemorrhage Due to Methanol Toxicity; is Hemodialysis the Offender?

Introduction: Methanol toxicity is a life-threatening condition which is rare in developed countries but common in developing countries. Bilateral putaminal necrosis and hemorrhage are potentially two lethal consequences of methanol toxicity which may be due to direct neurotoxicity of methanol metabolites, especially formic acid, or the consequences of acidosis and hypoxemia in the course of poisoning. Hemodialysis is an important part of the treatment of methanol toxicity and some researchers believe that heparin which is administrated during the hemodialysis may be the cause of putaminal hemorrhage Case report: We report a-32-year old man who presented with acute symptoms of methanol toxicity. A day after hemodialysis he suffered from seizure and Parkinsonism, and the neuroimaging revealed bilateral putaminal hemorrhage. Treatment with Levodopa-carbidopa was introduced for the management of Parkinsonism and finally the patient was discharged with marked improvement of symptoms and relative independency in daily activities Discussion and Conclusion: Our patient suffered from a late manifestation of methanol intoxication, bilateral putaminal hemorrhage, and necrosis. This appearance along with subcortical white matter involvement are the most common abnormalities of methanol toxicity in the brain imaging which can be associated with peripheral enhancement. Based on the reported case and review of present evidences, it is suggested that putaminal hemorrhage in methanol toxicity can be due to anticoagulant agents used in hemodialysis

Cortical Deafness and Tinnitus Following Sequential Bilateral Putaminal Hemorrhage.

Cortical Deafness and Tinnitus Following Sequential Bilateral Putaminal Hemorrhage.

Owl Eye Appearance: Simultaneous Bilateral Hypertensive Putaminal Hematoma

Basal ganglia hemorrhage, one of the most devastating forms of cerebrovascular disease, is often as a result of poorly controlled long standing hypertension. Hypertension often leads to development of solitary intracerebral hematoma. The occurrence of multiple simultaneous intracerebral hemorrhages due to hypertension in same or different vascular territories is rare. We report the occurrence of simultaneous bilateral hypertensive putaminal hemorrhage appearing as mirror image (Owl eye appearance) in a 60 years old gentleman and discuss the probable pathophysiological mechanisms

Bilateral putaminal hemorrhages: Serious complication of methanol intoxication

Context:Methanol intoxication is a life-threatening condition. Hallmark of clinical presentations include severe wide anion gap metabolic acidosis with very high serum osmolar gap and visual complication.Case Report:We report a case of severe methanol intoxication with bilateral putaminal hemorrhage, an uncommon serious complication. A 56-year-old man presented with altered mental status. Fundus examination showed optic disc edema. Arterial Blood Gas (ABG) revealed severe anion gap metabolic acidosis with osmolal gap. Head computed tomography (CT) showed hypodense lesions in basal ganglia bilaterally. Hemodialysis and intravenous fomepizole were initiated. Serum methanol level was significantly elevated. Unfortunately, patient was lethargic 2 weeks after discharge. Repeated CT of head demonstrated new putaminal hemorrhages.Conclusion:Bilateral putaminal hemorrhage is an uncommon but serious complication in methanol intoxication. Clinicians should have high index of suspicion for putaminal hemorrhage when patients with recent methanol intoxication present with altered mental status.

両側被殻出血を発症した結節性多発動脈炎の1例

両側被殻出血を発症した結節性多発動脈炎の1例

A Case of Simultaneous Bilateral Putaminal Hemorrhage

Simultaneous occurrence of multiple intracerebral hemorrhages is a rare condition. Here we report a case of simultaneous bilateral putaminal hemorrhage. A 74–year–old woman suddenly collapsed on the street. She had been medicated for hypertension for thirty years. She was receiving an angiotensin receptor blocker, a long–acting calcium antagonist and aspirin. On admission, she was comatose (Glasgow Coma Scale E1V1M2). The size of her right pupil was 4.0 mm, the left pupil was 5.0 mm. Computed tomography of her brain identfied hematomas in bilateral putamen. The right putaminal hemorrhage was 7×4×7cm, and the left hemorrhage was 5×2×4cm. As the hematomas were large and her neurological condition was severe, no surgical intervention was attempted. She died on the sixth day after admission. An autopsy of her brain was performed with the permission of her family. However, her brain was severely autolytic; therefore, pathological findings were difficult to detect.We identified 27 cases of simultaneous bilateral putaminal hemorrhage in the literature. We summarized these cases and ours. The mean age was 56.75 years old. Nineteen cases had a history of hypertension. Twenty–five cases were comatose or semi–comatose at onset. Fifteen cases (55.6%) died. Many of surviving cases were severely disability. Multiple intracerebral hemorrhages occur in patients with hypertension, coagulation defects, neoplasm, multiple small aneurysms, or angiopathies. However, the underlying mechanism for simultaneous bilateral putaminal hemorrhages is not clear.

Bilateral Putaminal Hemorrhage in a Young Female: A casereport

Bilateral Putaminal Hemorrhage in a Young Female: A casereport

Simultaneous bilateral hypertensive putaminal hemorrhages

The simultaneous occurrence of bilateral putaminal hemorrhages is a rare clinical event. We report a case of spontaneous bilateral putaminal hemorrhages in a patient with chronic hypertension and review the clinical presentation and outcome of other reported cases of this type of hypertensive cerebral hemorrhage. All patients have presented with an alteration in level of consciousness, and clinical outcome has been uniformly poor. Simultaneous bilateral putaminal hemorrhages are associated with a poor prognosis. Copyright © 2003 by National Stroke Association

Auditory agnosia restricted to environmental sounds following cortical deafness and generalized auditory agnosia

We encountered a case of auditory agnosia restricted to environmental sounds, which was associated with the development of bilateral subcortical lesions after suffering a bilateral putaminal hemorrhage. The patient had a history of a putaminal hemorrhage on her left side without any major disability. Three years later, she suffered a putaminal hemorrhage on the other side. The clinical picture started with cortical deafness, then changed to generalized auditory agnosia for verbal and environmental sounds, and finally developed into auditory agnosia confined to the perception of environmental sounds. Her errors in a test of sound recognition were discriminative rather than associative in nature. Neuro-radiological examinations revealed bilateral subcortical lesions involving the fibers from the medial geniculate body to the temporal lobes after bilateral putaminal hemorrhage. This case suggested that the subcortical lesion involving bilateral acoustic radiation could cause either cortical deafness, auditory agnosia of all sounds, or auditory agnosia restricted to environmental sounds.

Putaminal hemorrhage: Clinical-computed tomographic correlations

Ninety-two percent of 100 patients with putaminal hemorrhage were hypertensive. Of the eight normotensive patients, seven were substance abusers or had bilateral putaminal hemorrhages. The one other normotensive patient was less than 40 years old. The 100 hemorrhages had the following locations: 1. medial putaminal (17 cases; six were normotensive and less than 40 years old and five were substance abusers); 2. lateral putaminal extending through the external capsule (eleven cases); 3. putaminal-capsular and subcortical white matter (32 cases); 4. putaminal cerebral hemispheric (19 cases); 5. putaminal-thalamic (19 cases); 6. bilateral (two cases). A disproportionate number of black patients suffered hematoma extension to the cerebral hemispheres or thalamus (46%) compared to Caucasians (23%). Overall mortality was 20% (17 blacks and three Caucasians) and occurred in patients with hematoma extension to the thalamus or cerebral hemispheres. Contrast-enhanced CT was performed in all 100 patients and provided no additional diagnostic yield. This indicates limited use for enhanced CT in hypertensive patients with putaminal hemorrhage who have a characteristic appearance of the acute hemorrhage on the nonenhanced CT.

Spontaneous Bilateral Intracerebral Hemorrhage Occurring Simultaneously

A 45-year-old male suffered from bilateral putaminal hemorrhages that occurred simultaneously, followed by pseudo-bulbar palsy. Administration of anticoagulants appeared to have caused the bleeding. Cerebral blood flow was markedly decreased in both hemispheres disproportionally to the small size of the hemorrhages, probably due to a bilateral “diaschisis phenomenon, ” and the patient experienced severe neurological sequelae.