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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Here, we report a rare case of an anaplastic astrocytoma masquerading as a hypertensive basal ganglia hemorrhage. A 69-year-old woman who had been under medical management for hypertension during the past 3 years suddenly developed right hemiparesis with dysarthria. Brain computed tomography (CT) scans with contrast and CT angiograms revealed an intracerebral hemorrhage (ICH) in the left basal ganglia, without an underlying lesion. She was treated conservatively, but underwent a ventriculoperitoneal shunt operation 3 months after the initial attack due to deteriorated mental status and chronic hydrocephalus. Three months later, her mental status deteriorated further. Magnetic resonance imaging (MRI) with gadolinium demonstrated an irregular enhanced mass in which the previous hemorrhage occurred. The final histological diagnosis which made by stereotactic biopsy was an anaplastic astrocytoma. In the present case, the diagnosis of a high grade glioma was delayed due to tumor bleeding mimicking hypertensive ICH. Thus, a careful review of neuroradiological images including MRI with a suspicion of tumor bleeding is needed even in the patients with past medical history of hypertension.
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PMID:Glioma mimicking a hypertensive intracerebral hemorrhage. 2417 27

The authors report a very rare presentation of traumatic carotid-cavernous fistula (CCF) with extensive edema of the basal ganglia and brainstem because of an anatomical variation of the basal vein of Rosenthal (BVR). A 45-year-old woman was admitted to the authors' institution for left hemiparesis, dysarthria, and a comatose state caused by right orbital trauma from a thin metal rod. Brain MRI showed a right CCF and vasogenic edema of the right side of the brainstem, right temporal lobe, and basal ganglia. Digital subtraction angiography confirmed a high-flow direct CCF and revealed a hypoplastic second segment of the BVR responsible for the hypertension in inferior striate veins and venous congestion. Endovascular treatment was performed on an emergency basis. One month after treatment, the patient's symptoms and MRI signal abnormalities almost totally disappeared. Basal ganglia and brainstem venous congestion may occur in traumatic CCF in cases of a hypoplastic or agenetic second segment of the BVR and may provoke emergency treatment.
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PMID:Extensive basal ganglia edema caused by a traumatic carotid-cavernous fistula: a rare presentation related to a basal vein of Rosenthal anatomical variation. 2452 15

A 59-year-old woman who had been diagnosed with systemic lupus erythematosus (SLE) was admitted to our hospital due to paralysis in all of her limbs. The patient presented with dysarthria, cerebellar ataxia and hypoxia. Magnetic resonance imaging (MRI) revealed vasogenic edema in the brain stem and the cerebellum. She was diagnosed with neuropsychiatric lupus syndrome (NPSLE) and pulmonary arterial hypertension (PAH), and was successfully treated using immunosuppressive therapy. To our knowledge, this is the first reported case of simultaneously developing NPSLE and PAH.
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PMID:Successful use of intensive immunosuppressive therapy for treating simultaneously occurring cerebral lesions and pulmonary arterial hypertension in a patient with systemic lupus erythematosus. 2463 36

A 59-year-old man with end-stage renal disease was brought to our emergency department with complaints of headache, nausea, dysarthria, tic, and weakness involving the bilateral arms and legs. He had the similar episode 4 month before, when he was treated elsewhere. The patient had received hemodialysis three times per week. His medications included for hypertension. On examination at his arrival, he was alert with reduced concentration and incoherent thoughts. The blood pressure was 181/87 mmHg and other vital signs were normal. Neurological findings showed slight dysarthria and slow movements but no other abnormalities. Laboratory data showed increased serum creatinine and potassium presumably for a session of periodical hemodialysis but normal sodium concentration. His cerebrospinal fluid examination was normal. We treated him by hemodialysis. Diagnosis of PRES was most likely because of the clinical features and the MRI findings. His symptoms had disappeared immediately and completely after we controlled high blood pressure. MRI on 13 days after admission showed the improvement of the abnormal findings. Although the pathophysiology of PRES is incompletely understood, renal failure was known as one of the risk factors. A relative lack of sympathetic innervation of posterior circulation could not protect the area when severe hypertension makes auto-regulatory control collapsed. However, PRES of the brainstem is uncommon although the posterior circulation involves it. Because control of his hypertension was not appropriate in the outpatient settings before this event, it could have contributed to the recurrence in this patient.
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PMID:Recurrent posterior reversible encephalopathy syndrome of the brainstem in a hypertensive patient with end-stage renal disease. 2511 39

A 76-year-old woman presented with difficulty in speech and weakness on right arm and leg. Her medical history was remarkable only for uncontrolled hypertension for a long period. Dysarthria, right central facial paralysis, right hemiparesis and hypoactive deep tendon reflexes were noticed on neurological examination. Moderate degree aortic insufficiency with aortic diastolic reverse flow was detected on transthoracic echocardiography. Thrombosed aortic aneurysm on descending thoracic aorta, and an acute hemorrhagic infarction in the distribution of the left middle cerebral artery were depicted on thorax, and brain computed tomography scans, respectively. Cerebrovascular event was medically managed and whereas conservative management was offered for thrombosed descending thoracic aorta aneurysm.
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PMID:A morbid coexistence: thrombosed descending thoracic aorta aneurysm and aortic insufficiency with aortic diastolic reverse flow. 2539 31

A 22-year-old male student with no past medical illness, presented with acute onset dysarthria, binocular diplopia, and dysphagia over 10 hours. On examination, he had tachycardia, hypertension, generalized hyper-reflexia, and bilateral pupil sparing oculomotor, troclear, abducens, trigeminal, facial, glossopharyngeal, and vagus nerve palsy. Rest examination was unremarkable. Facial nerve conduction study (NCS) showed decreased amplitude bilaterally and neurogenic pattern on electromyography. Limb NCS, repetitive nerve stimulation, neostigmine test, brain magnetic resonance imaging, cerebrospinal fluid, and biochemical tests were normal. Only positive tests were low thyroid-stimulating hormone (TSH) (<0.01), high free T3 (19.2 pmol/L), and high free T4 (39.2 pmol/L). Thyroid ultrasonography, anti-thyroid peroxidase, and anti-thyroglobulin antibody were normal. Patient was treated with anti-thyroid drugs, with which he completely recovered in 2 months. Though many cases with thyrotoxic myopathy have been reported, only few mention neuropathic cause of dysphagia or polyneuritis cranialis. Getting done thyroid function tests may be helpful in patients with polyneuritis cranialis of uncertain etiology.
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PMID:Polyneuritis cranialis with generalized hyperreflexia as a presenting manifestation of thyrotoxicosis. 2601 29

Non-syndromic, multi-organ mitochondrial disorders (MIDs) are frequently missed if treating physicians are not aware of them. We report a 85 years old Caucasian male, referred for tonic-clonic seizures, presenting with a plethora of abnormalities, including neurodermitis, atopic dermatitis, diabetes, hypertension, renal insufficiency, non-specific colitis, urine bladder lithiasis, bilateral cataracts, atrial fibrillation, diverticulosis, polyneuropathy, vitamin-D-deficiency, renal cysts, left anterior hemi-block, right bundle branch block, pulmonary artery hypertension, and heart failure. Neurological investigations revealed ptosis, quadriparesis, fasciculations, dysarthria, dysdiadochokinesia, tremor, hyperkinesia, ataxia, leukoencephalopathy, and basal ganglia calcification. Based upon this combination of abnormalities a non-syndromic mitochondrial multi-organ disorder syndrome (MIMODS, encephalo-myo-cardiomyopathy) was diagnosed.
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PMID:Multiorgan disorder syndrome (MODS) in an octagenarian suggests mitochondrial disorder. 2653 Feb 6

A 78-year-old Caucasian man was admitted in the Department of Neurology for visual disturbances, started two days before. The next day the patient experienced headache, fever and gait disturbances. He had hypertension, diabetes mellitus, an ischemic stroke 13 years ago, longstanding seronegative rheumatoid arthritis (17 years), polynodular goiter, right ischio-pubian fracture and right femoral vein thrombosis a year ago due to a car accident, since he is treated with oral anticoagulants associated to antiaggregant, hypotensors, statin and oral antidiabetics. The neurologic examination had evidenced nuchal rigidity, left homonymous hemianopsia, left central facial palsy, ataxia of the inferior limbs with wide-based gait, achilean reflexes abolished bilaterally, bilaterally abolished plantar reflexes, ideomotor apraxia, dysarthria, hypoprosexia, and preserved consciousness patient. A non-contrast cerebral CT scan had shown right temporal and parieto-occipital intraparenchymatous hemorrhages, a right frontal sequelar lesion, multiple old lacunar infarets, cortical atrophy. Laboratory findings included an inflammatory syndrome, absence of rheumatoid arthritis positive serology, normal coagulogram, an elevated proteinuria. The cerebral IRM performed on the seventh day of hospitalisation was suggestive for subacute right parietal hemorrhage, old cerebral infarction in the right anterior cerebral artery area, old lacunar infarcts and cerebral atrophy. The anticoagulant and antiaggregant treatment was stopped after a generalized tonic-clonic seizure occurred. Antiedematous, hypotensor, anticonvulsivant, beta-blocker, and symptomatic treatment was started, while the antidiabetic treatment was continued. All symptoms remitted. Arguments for amyloid angiopathy in our patient are previous non-cardioembolic ischemic stroke and a chronic inflammatory disease- rheumatoid arthritis in his personal medical history.
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PMID:Multiple Intracerebral Hemorrhages in an Old Patient with Rheumatoid Arthritis. 2693 15

Neuroleptic malignant syndrome (NMS) is associated with the administration of antipsychotic agents and other drugs such as l-dopa, antidepressants, and antihistaminic agents. Unexpected changes in mental status, new-onset catatonia, episodic tachycardia, tachypnea, hypertension, dysarthria, dysphagia, diaphoresis, sialorrhea, incontinence, low-grade temperature elevations, and rigidity should arouse suspicion. Several lines of evidence provide support for the involvement of dopamine. Most of the drugs implicated in NMS are D2 dopamine receptor antagonists. Central noradrenergic activity is also possibly related to the disorder, as sympathetic hyperactivity is associated with the active phase of NMS. Currently, the definitive role of GABA deficiency in NMS is yet to be established. Differential diagnosis should include malignant hyperthermia, lethal catatonia, lithium toxicity, serotonin syndrome, and heat stroke. A high degree of suspicion and the discontinuation of antipsychotic agents even if the diagnosis is not established are essential for the safety of the patient. Treatment of NMS should be individualized and be based empirically on the character, duration, and severity of the clinical signs and symptoms noted. The initial step in the treatment of NMS is the removal of the offending agent. Full-blown NMS is a serious condition and requires immediate supportive, nutritive, and electrolyte therapies. The administration of drugs that can improve NMS, such as IV dantrolene and/or oral bromocriptine, may also be taken into consideration, based on the severity and nature of the NMS.
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PMID:Neuroleptic malignant syndrome: risk factors, pathophysiology, and treatment. 2698 10

An 85-year-old woman with hypertension was admitted with a sudden onset of gait disturbance and dysarthria. On admission, the patient showed severe bilateral cerebellar ataxia with moderate right medial longitudinal fasciculus (MLF) syndrome. Magnetic resonance (MR) imaging showed an acute infarction in the lower and medial part of midbrain. Diffusion tensor imaging (DTI) started from both cerebellar peduncles revealed that the lesion of the acute infarction matched the decussation of superior cerebellar peduncle where crossing of tract was seen and a part of its tract was interrupted at the site. Interruption of the cerebellum red nuclear path at the medial part of midbrain was considered to be the reason for bilateral cerebellar ataxia and visualization of cerebellum red nuclear path by DTI can give better understanding of the neurological symptom.
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PMID:A case of midbrain infarction with acute bilateral cerebellar ataxia visualized by diffusion tensor imaging. 2747 72


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